1
Part 1—Forensic Medicine and Pathology
Introduction and History of Forensic Medicine The origin of medicine is as old as civilization. In the early stages the mankind used spirituality, herbs, God worship and witchcraft etc. for the cure. Then they felt the need of formulating certain rules and regulations for these practices that led to the origin of medical jurisprudence with advancement of civilization various legal systems came into force and the knowledge of medicine became necessary for the purpose of law and justice and the concept of legal medicine or Forensic Medicine originated. The term Forensic Medicine, Legal medicine and Medical Jurisprudence are all used in different meanings. Forensic Medicine is an application of medical knowledge for the purpose of law both civil and criminal for example in cases of vehicular accidents. The Forensic expert is able to opinion whether the said injuries are due to vehicular accident or not, duration of injuries, nature of injuries and the cause of death etc. Likewise in case of sexual offences, he is able to give opinion whether the sexual act has been committed or not, the duration and type of injuries etc. The Forensic expert not only expertises in his own field but uses the knowledge of other branches of medical science to solve the problems related to forensic medicine for example while doing postmortem in cases of accidental deaths, criminal abortion and sudden deaths due to medical and surgical causes. Medical Jurisprudence deals with legal aspects of practice of medicine. The concept of doctor patient relationship, rights and duties of doctors, duties towards the patient and the state in particular the medical negligence etc. are all covered by the term Medical Jurisprudence. Medical ethics deals with the moral principles that guide the members of medical profession when
they deal with each other, their patients as well as with the State. Medical etiquette deals with the conventional laws of courtsey observed between the members of the medical profession. State Medicine is a term, which was suggested by Dr. Stanford Emerson Chaille in the year 1949, but now a days it stands rejected worldwide. In India few States like West Bengal, Manipur and Assam etc. use the word and the subject is known as Forensic and State Medicine. Forensic medicine can be divided into a number of sub branches. Forensic pathology deals with morbid anatomy, pathology of injury and different aspects of death with their medicolegal significance. Forensic psychiatry is a very interesting branch where legal aspects of mental disorders are studied. Forensic odontology where the ability of dentistry is undertaken when the question of identification and interpretation of bite marks arise. A number of factors are found in the teeth that are utilized for identification purposes. Forensic anthropology, studied of bodily shape and skeletal formation in legal sense and also for the identification purposes. The branch of forensic science that is a sister discipline of forensic medicine. Now-a-days this is mainly occupied by the non medical scientists mainly a biologist or chemist who deals with the criminal aspects of crime investigations. There is a strong link between the forensic medical experts and forensic scientists as the former collects the evidences during medicolegal autopsy or while examining living persons and the letter carries out the test and gives the opinion. Therefore both these branches are complementary to each other.
2
Textbook of Forensic Medicine and Toxicology
HISTORY OF FORENSIC MEDICINE IN INDIA AND ABROAD The word forensic medicine came from the Latin word ‘forensis’ meaning marketplace, as during ancient days the justice used to be dispensed from marketplaces or common meeting places. The total period of forensic medicine can be divided into three phases. 1. Ancient Phase The law and medicine problems were found as written records in China, India, Egypt and Babylon etc. dating back to 5000 BC to 3000 BC. The Hammurabi code by King of Babylon is the oldest medicolegal code. Chief justice and Chief physician of the King Zoser of Egypt was the first medicolegal expert. Different techniques were developed for the preservation of the dead bodies (mummification). Indian civilization such as excavation remains of the Indus valley civilisation (3200-2000 BC) gives the evidence of the use of medicines like shilajit and use of weapons made of bronze and copper. Manu (3102 BC) was the first lawgiver in India. His “Manusmriti” gives the knowledge about the laws prevalent at that time. Various types of crimes like sexual offences, seduction and adultery have been mentioned. Those who were having mental illness were not allowed to contract. King’s permission was required to practice medicine. Definite rules were laid down to practice and to learn medicine. It can be presumed that the origin of medical jurisprudence can be dated back to 3000 BC. At the same time a Chinese materia medica gives information about poisons. The Vedas of ancient India were composed between 3000 to 1000 BC. The Rig Veda, the oldest one mentions about kings and their administration. Marriage was prohibited in blood relations. The Atharva Veda mentions cures for wounds, snake bite and poisons etc. in the form of mantras or charms while other Vedas mentions crimes like incest, adultery, abortion and drunkenness etc. along with the punishment for them. During this time dead bodies were dissected that can be compared to anatomical dissection as well as pathological autopsy today. At that time Ayurveda was quite advanced. The first treatise was Agnivesh Charaka samhita
supposed to have been composed during 700 BC. Here we find regarding the rules of studying ayurveda, duties and rights of the students, privileges they can avail that can be considered the origin of medical ethics. In addition, there is a mention of poisons, their symptoms with their treatment. Between third and fourth century BC, the Arthashashtra of Kautilya was written. In this book the penal laws are defined and the rules regarding the application of medical knowledge to legal matters has been mentioned which can be considered as the origin of legal medicine in India. The physicians were allowed to practice only after king’s approval, similar to registration with medical council today. They were liable to be punished if there was any negligence during treatment. The other crimes like sexual offences, violation in marriage laws etc. were also punishable. There were provisions for the examination of dead bodies like post mortem examination of today. The body used to be kept in oil for examination in cases of sudden deaths. If any dead body that was swollen with eyes protruding out, marks on the neck, was taken granted that he has been killed by strangulation. Signs of death due to hanging, strangulation, drowning etc have been mentioned. In cases of poisoning the portions of stomach and heart were put in the fire and the nature of flame and sound were noted to determine the nature of poison. Depending on the seriousness of the crimes different types of punishments like whipping and cutting of body parts were awarded. Hippocrates the father of western medicine (460 BC to 377 BC) was first to write the code of medical ethics. He practiced in the island of Kos in Greece and discussed the lethality of wounds at large. During 44 BC Antistius had conducted the autopsy on the body of Julius Caesar who was assassinated. 2. Medieval Phase Justinian court during the 1st to 5th century AD came into existence after the name of Justinian the Roman Emperor who specified the role of medicolegal experts in dealing with medicolegal problems. During the period of 12th to 15th century AD a Chinese treatise was published named His-HuanLu. The inquest was made obligatory in all types of unnatural deaths. Different types of injuries were defined and the manner of investigations to be done in these cases was also suggested.
Introduction and History of Forensic Medicine During the period of 1000 AD to 1600 AD India was invaded by several foreign powers like Dutch, the French and East India Company so as to plunder its wealth and establish their colonies. Chaos and uncertainty prevailed in all spheres of life including law and order situation. Lastly the East India Company conquered and ruled over India in the middle of 18th century until it handed over power to the British crown in 1857. The first medicolegal autopsy was done by Bartoloneo D E Varignana in Bologna (Italy) in the year 1302 AD. The Constitutio Criminalis Carolina was published in Germany in 1532 AD which wrote about different types of homicides that were not punishable for example if a criminal who is deprived of his judgment power was not responsible for the act like a murder committed by an insane. 3. European Phase (1600-1947 AD) Paulus Zacchias was the principal physician to Pope Innocent X and Alexander VII an expert before the court “rota romana”, the court of appeal. His works “medicolegalis“ were published in seven volumes during 1621 to 1635 AD. This work remained an authority in medicolegal matters until the start of 19th century. He was considered as the father of forensic psychiatry as well as of legal medicine. An Italian physician Fortunate Fedele published the first book in forensic medicine in 1602. In 18th century the post of professorship was created in Germany. Orphila, professor of chemistry and legal medicine at Paris is considered as the father of modern toxicology. The British ruled over India till 1947 and introduced their system in every sphere like culture, education, administration, legal system and crime investigation etc. They introduced the allopathic system of medicine. The present legal system in India is a mixture of the English and Roman system, having been modified to suit the Indian conditions. The first medical school was established in Calcutta in 1822 that was later on converted into a medical college in the year 1835. Next medical school established in Madras in 1835, which was converted into a college in 1850. In Bombay first medical college was established in the year 1950. In 1857 AD, the first separate chair in medical jurisprudence was created in Madras medical college. Governor Lord Harris selected Dr Urguhart,
3
a private practitioner and coroner of Madras as the first professor. Among the earlier professors were Dr Mouat, Dr John Moses of Calcutta medical college, Dr A Porter and Lt. D.G. Roy of Madras medical college and Major Collies Barry of Grant medical college, Bombay. The books that were followed were brought from England. The popular English authors books were Taylor’s principles and practice of medical jurisprudence and Capsers medical jurisprudence. The first book for India was written in 1856 by Dr Norman Chevers the other books written in 1888 by Dr I B Lyon named Medical Jurisprudence for India, outlines of Medical Jurisprudence by Lt. Colonel P. Henir and J D B Gribel in 1889 and Legal Medicine in India and Toxicology by Major Collies Berry in 1902. Dr Jaising P Modi, lecturer at Agra Medical College and then at Lucknow Medical College since 1918 was a leading medicolegal expert. His first book the Text Book Of Medical Jurisprudence And Toxicology was published in 1920. The book became popular not only with medical students but also among the lawyers and judges. The British rulers subsequently codified the criminal law in India in 1833. The present Indian penal code (IPC) came into existence in 1860 and superseded all previous laws. The criminal procedure code (CrPC) came into force from 1861. These laws are being followed till today. The procedure for crime investigation was systematized by the introduction of Indian Police Act of 1861 and the coroner system by the Indian Coroners Act 1871. The coroner system was followed in Calcutta, Bombay and Madras whereas the rest of the country followed the police system. The practice of modern medicine was first regulated by the formation of provincial medical councils in 1912 according to which the medical practitioners were required to register themselves in the respective state medical councils. In 1916 the Indian medical degrees act was passed to recognize the qualifications from recognized institutions and to penalise persons having false certificates to practice medicine. The Indian Medical Council Act was passed in the year 1933 and the Indian Medical Council was established to control the state medical councils and to regulate infirmity in medical education throughout the country. One of the greatest contributions India has made to modern criminology is dactylography or fingerprint
4
Textbook of Forensic Medicine and Toxicology
system for personal identification. Towards the later part of 19th century that is in 1860 AD William Herschel, an Indian civil service officer posted at Nadia district of Bengal first used this method for identifying illiterate people while distributing money. After him Edward Richard Henry in 1891 AD developed the method further and published a book entitled “classification and use of fingerprints”. By his recommendation the government of India also adopted this method of identification and established
a fingerprint bureau in Bengal in 1897 AD. Subsequently this method was introduced in criminal investigation department of Scotland Yard in July 1901 by Henry himself who was posted there as assistant commissioner. Then the medicolegal work was undertaken and postmortem centers were established at different places. During the time of East India company a post mortem was conducted in Madras in August 1693 by Dr Buckley in an alleged case of arsenic poisoning. This was probably the first medicolegal autopsy in modern India.
MULTIPLE CHOICE QUESTIONS
1. The first book in Forensic Medicine was written by a physician of: A. U.S.A. B. U.K. C. Italy D. Denmark 2. The first medicolegal autopsy was conducted in: A. Italy B. Greece C. England D. Portugal 3. Who is known as the father of modern toxicology? A. Paulus Zacchias B. Bartolomeo De Varignana
1 C
2 A
3 C
4 B
5 D
C. Orfila D. Fortune Fedele 4. In India the first book of forensic medicine was written in the year: A. 1850 B. 1856 C. 1860 D. 1875 5. The first separate chair in medical jurisprudence was created at: A. Grants Medical College B. Calcutta Medical College C. K.G. Medical College, Lucknow D. Madras Medical College
Part 1—Forensic Medicine and Pathology
2
Legal Procedures The legal procedures should be followed in the cases where death has resulted from some unnatural cause and under suspicious circ*mstance. The investigating agency should be informed who conducts further investigations. Legal procedures in India are based on the Indian Constitution, Code of Criminal Procedure, Indian Penal Code and the Indian Evidence Act etc. The Criminal Procedure Code, 1973 (CrPC) deals with the procedure of investigation and trial of offences within the limitations of the Union Territories of India except Jammu and Kashmir and some other tribal areas. It provides for different classes of Courts and defines their powers. It also formulates duties of police in arresting offenders, dealing with absconders, in the production of documents and investigating offences. It defines offences into two categories; cognizable and non cognizable. Some cases are triable by both magistrates as well as Courts of Sessions as indicated in Section 2 of CrPC. However, when tried by a magistrate the punishment must be limited to magistrate’s powers. The Code also provides for the period of detention undergone by the accused during investigation, inquiry or trial is to be deducted from the sentenced of imprisonment awarded by the Court and the balance period only is to be undergone. A bar of limitation for taking cognizance ranging from 6 months-3 years has been prescribed in certain cases under Sec.468. The Indian Penal Code, 1860 (I.P.C) describes various offences and with their punishments in the Courts of Law. It defines offences and several categories of the same offence are created such as House Trespass (Section 448-460) and theft
(Section 379-382 and 401). These offences are categorised under the I.P.C. to keep the workload low for higher Courts as well as in expensive thus reducing the number of such Courts. Besides this the I.P.C. also provides a chapter on general exceptions in which the right of self defence of person or property and extending to causing deaths in certain circ*mstances is to be found. The IPC describes various punishments such as (i) Death (20 years in prison) (ii) Imprisonment for life including solitary confinement (iii) Simple imprisonment (iv) Forfeiture of property and fine. The Indian Evidence Act, 1872 (I.E.A.) relates to evidence on which the Courts could come to some conclusion about the facts of the case. Criminal law relates to the offences that are against the interest of the public namely offences against the person, property, safety of the public as well as security of the state. Civil law deals with disputes between two individuals or parties called the plantiff and defendant (accused).
INQUEST An inquest is investigation in to the cause of death in cases of sudden, unnatural & suspicious deaths conducted by the legal authorities such as the Police Officer, Magistrate or the Coroner etc. TYPES OF INQUEST Police Inquest (Sec. 174 Cr.P.C.) Police to Enquire and Report on Suicide etc. An officer-in-charge of the police station in whose jurisdiction the death has occurred conducts the
1. 2. 3. 4.
Police inquest Magistrate’s inqu Coroner’s inques Medical Examine
6 Textbook of Forensic Medicine and Toxicology police inquest. On receipt of information of an unnatural death, the police officer informs the nearest magistrate and thereby proceeds to the place of death. The police officer then conducts an inquest in the presence of two or more respectable inhabitants of the neighbourhood (panchas). After the necessary investigation, a report is drawn up on the apparent cause of death as judged by the state of the body, the injuries present on the body, hearsay evidence and circ*mstantial evidence etc., this document is called panchnama or inquest report. This report is signed by the police officers and the persons present at the inquest. If any foul play or unnatural death is suspected, the police officer forwards the body for postmortem examination to the nearest government hospital along with the written request for conducting the postmortem examination and a copy of punchnama (inquest papers). If the autopsy report confirms that the death is due to an unnatural cause, further inquiry and trial of the case is conduced in the usual manner by the magistrate concerned to whom the entire records of the case are transferred by the police officer. Police Inquest is done in cases where a person (i) has committed suicide (ii) has been killed by another man (iii) killed by animal (iv) killed by machinery (v) killed in an accident (vi) died in suspicious circ*mstances raising reasonable suspicion that some other person has committed an offence. 1. In the above situation when the Police Officer gets information, he will immediately informs the nearest Executive Magistrate empowered to hold inquest and then proceeds to the place where the body of such person is found. He makes investigation in the presence of two or more respectable person of the locality, draws up a report regarding the apparent case of death, describing such wounds, bruises, factures etc. found on the body and stating the manner and type of weapon that has caused such injuries. 2. The report shall be signed by such Police Officer and other persons or by so many of them who agree with the same opinion and shall be forwarded to District Magistrate/SDM. 3. When (i) The case involves suicide by a woman within seven years of marriage, or (ii) The case
relates the death of woman within seven years of her marriage raising a reasonable suspicion that some other person has committed the offence in relation to such woman or (iii) The case relates the death of a woman within seven years of marriage and any relative of the woman has made the request in this behalf or (iv) There is any doubt regarding the cause of death (iv) The police officer for any other reason considers it suitable to do so sends the body to the nearest civil surgeon or Medical Officer for examination. 4. The following Magistrates will be empowered to hold inquests, namely any District Magistrate or Sub Divisional Magistrate, any other Executive Magistrate empowered by State Govt. or the District Magistrate. Magistrates Inquest (S.176 CrPC) Inquiry by Magistrate into Cause of Death 1. The inquest is done by any District Magistrate, sub Divisional magistrate or any other executive Magistrate or any Magistrate empowered by the State Government. Following are the indications of Magistrate’s Inquest: i. Custodial deaths ii. Deaths due to Police firing iii. Death inside prison iv. Dowry deaths v. Clause (i) or (ii) of sub Section (3) of Section 174 CrPC. The case involves suicide by a woman within seven years of marriage or the case relates the death of woman within seven years of her marriage raising a reasonable suspicion that some other person has committed the offence in relation to such woman 2. In addition the Magistrate may hold an inquest in the cases done by Police. The proceedings of the Magistrate are not judicial proceedings, they only try to find out the cause of death. After inquest the body is sent for the postmortem examination. The inquest papers must be handed over to the Autopsy surgeon for information. During the investigation, the Magistrate shall inform the relatives of the deceased and also allow them to stay during investigation.
Irritant Poisons 7 Coroner’s Inquest Coroner’s inquest no longer exist in India. However it used to the followed previously in Bombay. It is interesting that in Caltutta still for conducting the inquest, the dual system exists. The presidency town of Calcutta is under the Coroner’s system whereas in rest of Calcutta it is the police inquest. However, the Coroner system is prevalent in countries like U.K and some states of U.S.A. The Coroner’s Court is a Court of inquiry in which the Coroner conducts the inquest in unnatural, sudden and suspicious deaths. In his Court, the jurors are sworn to give a true verdict according to the evidence. Besides this, the Coroner has some judicial powers also.
2. A Sessions Judge may also pass any sentence authorized by law but any sentence of death passed shall be subject to confirmation by the High Court. 3. An Assistant Sessions Judge may pass any sentence authorized by law except a sentence of death or of imprisonment for life or of imprisonment for a term exceeding ten years. POWERS OF MAGISTRATES (Sec. 29CrPC) The Court of Chief Metropolitan Magistrates shall have the powers of the Court of a Chief Judicial Magistrate and that of a Metropolitan magistrate. The powers of the Court of Magistrate are given in Table 2.1.
Medical Examiner’s System
COGNIZABLE OFFENSE (Sec. 2 CrPC)
The Medical Examiner’s system for conducting inquest exists in most of the states in the Unites States. Medical examiner is a medical man who is appointed to perform the duties of a coroner. The medical examiner neither has judicial functions nor does he have authority ordering arrest of any person. In this system, the medical examiner visits the scene of crime and conducts further inquest. This system is superior to that of police or a coroner.
Cognizable offence means an offence for which, and cognizable case means a case in which, a police officer may in accordance with the First schedule or any other law for the time being in force, arrest without warrant. These offences include rape, dowry deaths, ragging, deaths due to rash or negligent act etc.
CLASSES OF CRIMINAL COURTS (Sec. 6 CrPC) Besides the High Courts and the Courts constituted under any law, there shall be in every state: (i) Courts of Sessions (ii) Judicial Magistrates of the first class and, in any Metropolitan area, Metropolitan magistrate (iii) Judicial Magistrate of second class, and (iv) Executive Magistrate. SENTENCE PASSED BY HIGH COURTS AND SESSIONS JUDGES (Sec. 28 CrPC) 1. A High Court can pass any sentence authorized by law.
JURISDICTION IN CASE OF JUVENILES (Sec. 27 CrPC) Any offence not punishable with death or imprisonment for life, committed by any person who at the date when he appears or is brought before the Court is under the age of eighteen years, may be tried by the Court of Chief judicial Magistrate, or by any Court specially empowered under the Children Act, 1960, or any other law for the time being in force providing for the treatment, training and rehabilitation of youthful offenders. SUMMONS (SUBPOENA) It is a written document compelling the attendance of the witness in the Court, to depose evidence, at a particular time and purpose under penalty.
Table 2.1: Powers of magistrate Magistrates
Imprisonment
Chief judicial magistrate First class judicial magistrate Second class judicial magistrate
Up to 7years Up to 3years Up to 1 year
Solitary confinement Yes Yes yes
Fine (Rs) Unlimited 5,000 1000
8 Textbook of Forensic Medicine and Toxicology This is also called subpoena. Literally sub means under and poena means penalty. The provisions regarding summons are dealt in the Sections 61 to 69 CrPC. The summon is issued in duplicate signed by presiding officer of the Court and bears the seal of the Court (Section 61 CrPC). The summons is delivered through a police officer, an officer from the Court or by any other person. The witness signs the carbon copy and returns it to the Court. According to 66 CrPC, if the witness is a government servant the summons can be sent to the head of the office in duplicate and the head in turn serves it to the concerned person. When summons are issued to produce a document or any other article required for investigation or trial (Section 91 CrPC) the person in possession of the said document or article may send it instead of attending personally. If the witness fails to attend the Court without any valid reason he will be penalized in the form of paying damages in civil cases and Criminal cases notice will be served under Section 350 CrPC. After hearing from the witness if the Court thinks that there was no proper reason for not attending the Court, a bailable/non-bailable warrant may be issued to procure his attendance in the Court (Section 172174 IPC and Section 87 CrPC). If a witness receives two summons on the same date from the same type of Court he will attend the Court from which he received the summon first and will inform the other Court. If he receives two summons, one from Criminal Court and the other from Civil Court, he will attend the criminal Court first with intimation to the Civil Court because Criminal Courts have priority over Civil Courts and also the higher Courts have priority over lower Courts. The witness would not leave the Court without the permission of the presiding officer. In civil cases certain amount of money is paid to the witness towards his expenses for attending the Court, which is called conduct money. This amount is paid to the witness while serving the summons. At times the money is paid in the Court. If the witness thinks that the amount is less according to his status he can pray to the presiding officer in the Court for additional amount. Even he can ignore the summon if no amount is paid.
But in criminal cases no conduct money is paid the witness must attend the Court in the interest of the state or in the interest of justice. The government usually pays TA and DA to attend such Courts. If the witness does not attend the Court he will be charged for contempt of Court. After getting the summons the witness appears before the Court on the specified date and time with the records called for. Before deposing the evidence the witness has to take the oath. OATH The witness stands in the witness box and takes the oath. The main aim is that the witness will tell the truth during the evidence. The provision is incorporated in Section 51 IPC. He takes oath as follows. “I swear in the name of God, that what I shall tell, be the truth, the whole truth, nothing but the truth.” (Vide Indian Oath Act 44 1969 Section 4 and 6). The oath is taken in the case of all Courts other than high Courts and supreme Courts, which is administered by the presiding officer. In cases where the witness appear before a bench of judges / oblique magistrates, one of the judges or the magistrate can administer the oath. (Indian Oath Act 44 of 1969 Section 2). Perjury means willfully giving false evidence under oath or unable to tell what he knows or believes to be the truth (Section 191 IPC and Section 344 CrPC) he is liable to be prosecuted for perjury under Section 193 IPC with imprisonment up to seven years and fine. EXAMINATION IN CHIEF (Sec. 137 IEA) After the oath or affirmation the witness will be examined by the lawyer of the party that has called him it is also known as direct examination. In criminal cases the state becomes a party so the burden of proof is always on the prosecution. It is always presumed that the accused is innocent unless otherwise proved. Before giving the evidence the doctor should always see the previously prepared report. If needed he can meet the public prosecutor and go through the files and other records. The doctor should help the public prosecutor to frame the questions so that proper facts are elicited. The medical witness is usually
Irritant Poisons 9 asked questions as to when he saw the body and started the postmortem examination. The question pertaining to description of the injuries, duration of injuries and possibly about the weapon of offence are also asked during examination in chief. Normally leading questions are not allowed where the Court is satisfied that the witness is a hostile one (Section 142 of the IEA). A leading question is the one, which suggests the answer. (Section 141 IEA) for example “did you carry out the postmortem examination”, “did you find a 5 cm laceration on the forehead”. To an ordinary witness, question such as “did you see the accused inside the restaurant” or “ have you seen him beating A” are asked. In civil cases also the same procedure is followed. CROSS EXAMINATION During the cross examination the lawyer of the opposite party i.e. the lawyer of the accused (defence lawyer) examines the witness. The main objectives are: • To elicit facts favourable to his client. • To find out the weak points in the case. • To verify the accuracy of the facts already told. (Section 146 IEA). The defence lawyer always tries to discredit the witness and tries to prove that the report given is not correct and biased one. It is not necessary that the question should be confined to the facts told in examination in chief. (Section 143 IEA). The defence lawyer may even ask questions pertaining to the qualifications, experience etc., especially in the type of the case in question. During this time the Court observes whether a particular question should be answered or not. The Court has power to disallow a question if it is intended to insult or harass the witness but if it is relevant to the case the Court cannot disallow. The witness has to answer the question that relates to the case even if it is harmful to the witness or it exposes his fault or negligence (Section 146 IEA). If a witness is forced to answer that goes against him he cannot be arrested or prosecuted or cannot be taken as proof against him for any criminal proceedings When a question is not audible, the witness can request to repeat the
same and when the question is not understood properly he can again ask to explain. The witness should be clear, direct and precise in his answer. The doctor is an expert witness to the Court, not to either party even though one party has called him. The Court and the society want him to be impartial and assist the Court to reach a proper conclusion for the sake of justice. This has been well put by the famous French medicolegal authority in 19th century Brovardel. He said, “Where the law has made a physician a witness, he should remain a man of science. He should remember that he has no victim to avenge, no guilty person to convict and no innocent person to save.” When a witness is harassed and humiliated he becomes angry, hostile and tense. His intellectual faculties are blunted so as to loose the power of giving proper evidence. He may ask the Court for some time to be in proper shape for further evidence. He may volunteer certain facts that are relevant to the case even if not asked by the lawyer. Here the leading questions are allowed and there is no time limit for cross-examination. RE-EXAMINATION This is done by the lawyer who has called the witness (Section 137 IEA) the main aim is to clarify the points raised in cross examination and correct the mistakes done. However the lawyer should not bring any new points during the examination that has not been raised in the examination in chief. If any new point arises the witness should be cross-examined. Raising a new point should be done after taking permission from the Court. Questions put by the Court The judge may ask any question to clarify doubts in the evidences. The Court is also empowered to recall and reexamine any witness already examined if it is essential to arrive at a decision (Section 165 IEA and Section 311 CrPC). The deposition is handed over to the witness after reading carefully and thoroughly he signs at the end of each page with date. Any mistakes in the deposition should be brought to the notice of the Court and then he can correct it with his initials. He should not leave the Court without prior per-
10 Textbook of Forensic Medicine and Toxicology mission. The TA and DA are usually paid in the Court. CODE OF CONDUCT OF A DOCTOR INSIDE THE WITNESS BOX The doctor in the witness box should appear as a man of professional competence and integrity. He should be well dressed and look sober, prepare the facts of the case and take all relevant records / articles in his custody to the Court. The doctor should never be nervous inside the Court and speak loudly and clearly so that the presiding officer can record the deposition. It is essential that he should use no medical jargon and if medical terms are to be used a short explanation can be added. An expert may refresh his memory by reference to the professional treatise. The writing that is used to refresh the memory can be cross-examined by the opposite party (161 IEA). The doctor should never be over confident or arrogant. He should always use “Sir” or “Your honour” while addressing the Court. He should never use adjectives or exaggerations like very large bruise severe pain etc. And he should never loose the temper even if provoked by the opposite lawyer. The doctor should not avoid any question. If the answer is not known, always say, “I don’t know”. Nobody expects the doctor to know everything. Do not alter your findings to what is said in the statement. The answers should always be brief and to the point. If the lawyer limits the answer to “yes” or “no” which is not possible at times, the doctor can tell the judge that it requires explanation because you have taken the oath not only to speak truth but the whole truth. Always answer “in my opinion but not as I think or imagine or I am not sure etc”. When the answer demands quantity or number, the doctor should not tell the number unless he knows the exact number or quantity such as in cases of age estimation, the answer should be given within certain limits. The doctor should always answer within his own speciality. He should never comment on the points where he has little or no experience at all.
When the lawyer reads a paragraph from the book and asks to comment the doctor should always be careful. He must read the paragraph carefully even the paras before and after it to come to the conclusion. He must see that the book should be recent edition and the views expressed must be latest. He may or may not agree. It’s not necessary to agree upon everything written in the book. It should be remembered that views expressed in the book by reputed authors are taken as evidence even if the witness doesn’t agree to it. When attempts are made to influence the witness by one party or the other he must report to the senior police officer or to the Court so that the corrupt person can be penalized and at the same time he and his family members are given protection. A medical witness cannot claim professional privilege. He has to answer each and every question asked after obtaining the permission of the Court. A witness whether medical or otherwise is completely immune from actions for defamation (libel or slander) for anything he says in the witness box. This is quite important otherwise the witness will not disclose the actual facts because of fear of legal action later on. Volunteering of statements—At occasions the public prosecutor leaves certain ambiguities in the evidence and the advocates for the defence also put ambiguous questions, as a result the witness gives incomplete answers. The defence lawyer takes the advantage of these during an argument. When certain ambiguity is left or a general statement given by him is not applicable to the facts of the case in hand, the medical witness should come forward and volunteer for a statement making the position clear. When such statements are volunteered the Court writes “as statements volunteered” the statement has the same value as other statements given by the witness in response to questions put to him. The advocates of both the parties have a right to cross-examine such volunteer statements. MEDICAL EVIDENCE Section 3 IEA 1972 defines evidence as: All statements, which the Court permits or requires
Irritant Poisons 11 to be made before it by the witness, in relation to matters of fact under inquiry, are called oral evidence. All documents produced for the inspection of the Court are called documentary evidence. Before accepting the documents the Court must be satisfied regarding the identification and the place of seizure. Ordinarily the value of medical evidence is only corroborative. It proves that the injuries could have been caused in the manner alleged and nothing more. The defence makes use of the medical evidence to prove that the injuries could not possibly have been caused in the manner alleged and thereby discredit the eyewitness. Types Documentary Evidence It includes all documents produced before Court during trial. According to Section 29 IPC the word document means “Any matter expressed or described upon any substance by means of letters, figures, marks or by more than one of these means intended to be used or which may be used as evidence of that matter.” The documentary evidences are embodied in the Sections starting from Section 61 to Section 90 of the IEA. The contents of documents may be proved either by primary or secondary evidences (Section 61 IEA). Primary evidence means the document itself produced for inspection of the Court, (Section 62 IEA). The secondary evidence means and include the certified copies, copies made from the original by mechanical process, copies made from or compared with the original and oral accounts of the contents of a document given by a person who has himself seen it (Section 63 IEA). Taperecorded statements are admissible as evidence (K.S. Mohan vs. Sandhya Mohan AIR 1993 Mad 59). Evidence must confirm to the matters in issue and is admitted on the basis of relevance and admissibility. Oral Evidence Section 59 IEA says that all facts, except the contents of documents or electronic records may be proved by oral evidence.
Direct Evidence The oral evidence must be direct (Section 60 IEA) for example when it refers to a fact that could be seen/heard/perceived, it must be the evidence of that person who saw/heard/ perceived it. It must be direct if it refers to an opinion or to the grounds on which that opinion is held. The evidence must confirm to the matters in issue that is a knife that has caused stab injury, a medical prescription that resulted in the ill effects to the patient. Indirect Evidence (Circ*mstantial) At times the other surrounding facts are taken into consideration that are consistent with the direct evidence for example ‘A’ committed murder of ‘B’ with knife at a particular place, date and time. Here ‘C’ will depose that he saw ‘A’ on that day, date and time with a knife in hand just before the murder. This evidence of ‘C’ has a bearing to the fact. Hearsay Evidence Here the persons other than the witness give the statement. For example during the trial ‘A’ told that ‘B’ had told him that he has seen ‘C’ while committing the crime. Here ‘B’ can give the direct evidence as he has seen ‘C’ committing the crime. Varieties of Documentary Evidence Documentary evidence is of the following: Medical Certificate Medical certificates are regarded as the simple form of documentary evidence. They are issued by a registered medical practitioner in respect of ill health, age and mental condition. The certificates are also issued in cases of death, a vital document, may be needed during cremation, transportation outside state and certain claims. It is accepted in the Court of law as a piece of evidence as to the facts stated in the medical certificate. Even the doctor who has • issued it may be summoned to the Court of law to • testify the contents of the certificate on oath and • if needed cross examination can be done. Thus • the medical practitioner must exercise due care and skill in issuing such certificate. The certificate must state the exact nature of illness and should contain doctor’s opinion in clear language. In case of ill health the doctor should write the exact nature of illness, the duration of illness and probable
Medical certificate Death certificate Medicolegal reports Dying declaration.
12 Textbook of Forensic Medicine and Toxicology period of absence in cases of employed persons. The signature of the patient should be at the bottom with the date indicating that he attended the clinic and the doctor has examined him while issuing the certificate. The signature is to be verified by the doctor. Death Certificate It is essential that identification and cause of death is to be determined for the lawful disposal of the dead body. The registration of Birth and Death Act came into force from 1st April 1970. As per the act all the births and deaths are to be registered throughout India. In case of death certificate the doctor must inspect the body and satisfy that the person is dead. He is legally bound to issue the certificate he has attended the patient during his last illness indicating the cause of death. According to the recommendation of Brodrick committee a doctor should not be allowed to issue a death certificate unless he has attended the deceased at least once during seven days preceding death. He cannot charge any fee for issuing a death certificate. He cannot delay or refuse to issue a certificate. He may subsequently sue the legal heirs for his pending dues. He must refuse to give a certificate on the following grounds. (A) if he is not sure about the cause of death. (B) any suspicion of foul play. (C) death by violent and unnatural cause, drugs, poisoning etc. If he is not sure regarding the cause of death and suspects some foul play he should not issue the certificate, instead he should inform the police. Issuing a false certificate under Section 197 IPC is punishable under Section 193 IPC with imprisonment that may extend to 7 years and also fine. In general in obtaining a certificate the public expectations are great because they think by giving some money anything can be written in a certificate and try to produce false certificates for various purposes. Death certificate is a predicament in any doctor’s practice. The relatives of the deceased my plead, persuade, pressurize, offer a price and at times even threaten the doctor. He may be tempted at times on humanitarian grounds to issue a certificate. The doctor may certify death in doubtful cases but must not give a cause of death and he should inform the police. Failure to do so may result in the doctor being prosecuted under
Section 39 CrPC. Under Section 17 (1)(b) of RBD Act 1969, any person may obtain an extract from the registrar relating to any death after paying the requisite fee, though it will not disclose particulars regarding the cause of death as entered in the register. This confidentiality can be overridden in public interest. International format of death certificate: The death certificate recommended by WHO for international use, is in two parts. Part I: Records (a) immediate cause: the disease or condition directly leading to death and (b) antecedent causes viz, the morbid conditions, if any, giving rise to the cause mentioned in (a). (c) is the contributory cause to (a) and /or (b). Thus (a) must be due to (b) which must be due to (c), etc. When many conditions are involved, write the full sequence-one condition per line, with the most recent condition (immediate cause) at the top and the earliest (the condition that indicated the sequence of events between normal health and death) the last. The basic pathological condition is the one, which is mentioned on the lower most line, and this is the one that is used for statistical and epidemiological purposes. Part II: Records other significant conditions contributing to death, but not related to the disease or condition causing it. International forms are used by various municipal authorities in our country and are available for doctors. Doctors should necessarily use their rubber stamp after affixing signature to death certificate. Medicolegal Report These are the legal documents prepared by the doctor at the request of investigating officers usually in criminal cases like injury cases, sexual offences, murder and poisoning cases. These reports are made in both living and dead cases. The request usually comes from police officer or magistrate. It usually comes in two parts. The first part consists of observations and findings of the cases while the second part consists of the opinion and conclusion. The doctor starting the examination should write in detail the name of the individual, date, time and place of examination. The identification marks should be noted and the consent has to be taken because any examination without consent is
Irritant Poisons 13 regarded an assault in law. The victim should be explained the purpose and outcome of such examination before taking the consent. While examining a female, a lady registered medical practitioner should examine (Section 53(2) CrPC). Where the lady doctor is not available a female attendant should be present at the time of examination whose signature should be taken in the report. The findings are observed in detail and a report is prepared. The opinion or conclusion drawn should not be biased one as it is subjected to cross examination in the Court of law. The opinion must be kept pending till the reports are available in cases where necessary investigations are required. The negative findings are also to be pointed out in the report. These reports are produced in the Court of law. The doctor who has made the report should attend the Court to testify under oath, and then only they are taken as evidence. If the doctor is not available someone else can attend the Court to testify his signature and handwriting before being taken as evidences. Dying Declaration This topic is always mentioned in all the textbooks of forensic medicine though it is relatively an unimportant matter. Its major purpose is to render it admissible. Dying declaration is any evidence from a person who dies before the case is heard. Such a dying declaration must have corroborative evidence to support it before it can be accepted (Section 157 IEA). The dying declaration has been incorporated in Section 32 of IEA that reads as “a statement written or verbal of relevant facts made by a person who is dead or who cannot be found, or who has become incapable of giving evidence or whose attendance cannot be procured, without an amount of delay or expenses which under the circ*mstances of the case appears to the Court unreasonable” are themselves relevant facts in the following: (i) When it relates to the cause of death (ii) When a statement made by a person as to the cause of his death or as to any of the circ*mstances of the transaction which resulted in his death. Such a statement are relevant whether the person who made them was or was not at the time when they were made under expectation of
death and whatever may be the nature of proceeding where his cause of death comes in question. The above provisions were made on mainly two grounds: (i) At times the victim being the only eyewitness to the incident, exclusion of his or her statement will not be justified to meet the justice. (ii) Impending sense of death that is taken as equal to oath and the person is believed to tell the truth at that time. Recording dying declaration: If there is time the magistrate should be called to record the declaration in the absence of magistrate the doctor should record it either at the site of accident or when the patient is being taken to the hospital. The police officer can also record it and even anybody like the panchayat head or the relatives can record the declaration depending upon the situation. However the weightage of dying declaration becomes less and less in the descending order. Procedure: In the hospital admitted cases; the treating physician first tries to stabilize the patient and then informs the police. If the doctor thinks that the patient life is in danger he will arrange for the dying declaration. The police inform the area magistrate for the purpose. The doctor first has to certify that the patient is in perfect mental condition to make a declaration i.e. the patient is in “compos mentis”. If the magistrate is not available or there is much delay of his arrival then the doctor will write the declaration. The police should be discouraged to be near the patient so as to avoid the undue influence. The doctor should be there throughout the declaration to check the mental condition. If during declaration the patient becomes unconscious or unfit for a declaration the recordings will be stopped at that time putting the signature of the person who is recording with date and time. The declaration is recorded again when the doctor declares the patient fit. If the dying person is unable to speak but able to make sign in answer to questions this can be recorded and regarded as verbal statement. It can also be recorded in the form of questions and answers. If at any stage a particular point is not clear he can be asked to make it clear. At the end the declaration is read before the patient who puts his signature or thumb impression. It is also signed
14 Textbook of Forensic Medicine and Toxicology by the recording magistrate, the doctor and the witness mentioning the date and time. The declaration may take in the form of first information report of a statement before the police (Section 162 CrPC) during investigation. There is no prescribed form to record a dying declaration and no rigid rule can be formed. When a deceased person makes more than one dying declaration then they should be taken as one for the purpose of conviction. If the subject matter differs efforts should be made to reconcile. If at all the differences exist about the facts that should be covered by the explanation to the Section 161 CrPC and to be considered as a matter of fact in each case. If the person survives after making a declaration then he is called to the Court and his evidence is taken. Therefore the dying declaration recorded earlier acts as corroborative evidence. Dying Deposition There is no provision of dying deposition in the Indian Evidence Act therefore it is not followed in India. Here the magistrate records the evidence after administering oath. The accused or his lawyer is present and they are allowed to cross-examine the victim. WITNESS Section 118 IEA states about the person who may testify as witness in Courts of Law and reads as “All persons shall be competent to testify unless the Court considers that they are prevented from understanding the questions put to them, or from giving rational answers to those questions as a result of tender age, extreme old age, disease of mind or body or any other cause of the same kind.” Even a mentally ill person, lunatic is not incompetent to testify unless he is prevented by his lunacy from understanding the questions put to him.
actually seen the facts. This principle is known as “first hand knowledge rule”. For e.g. ‘A’ told in the Court that he had seen ‘X’ and ‘Y’ fighting in a garden on a particular date and time. Expert Witness Section 45 IEA deals with opinion of experts. They • Common are not only medical experts, but also experts in • Expert other subjects. It reads as when a Court has to form an opinion upon a point of foreign law or of science or art or identity the handwritings and fingerprints that are relevant facts. Such persons because of their professional training and experience are capable of drawing a conclusion on the facts observed by them or by others and are called experts. They also give expert opinion on hypothetical questions as well as on matters of common knowledge. The answer should be given by an expert witness after understanding the questions clearly and whenever possible in a guarded manner, the examples like the findings are consistent with the alleged history, does not mean that another mechanism cannot produce the same findings. Conclusions must be based on the facts because it is more important than the opinions. Hostile Witness Hostile witness is one who purposefully makes statements contrary to the fact or has some interest or motive for concealing truth. Section 191 IPC states that whoever, being legally bound by an oath or by an express provision of law to state the truth, or being bound by a law to make a declaration upon any subject, makes any statement which is false, and which he either knows or believes to be false or does not belong to be true, is said to give false evidence. The common as well as expert witnesses can be hostile.
Types
Long Questions
Common Witness (Ordinary Witness)
1. What is inquest? Discuss different types of inquest prevalent in India and which is the best. 2. Discuss the various types of documentary evidences in medicolegal practices. 3. Discuss the various types of evidences.
Common witness is a person who has seen/ observed the facts. It has to be proved that he/ she was capable of perceiving the facts or has
Irritant Poisons 15 Short Questions 1. 2. 3. 4.
5. Magistrate’s inquest 6. Subpoena. 7. Difference between police and magistrate inquest 9. Expert witness 10. Hostile witness
Cross Examination Dying declaration Powers of magistrates Types of witness
MULTIPLE CHOICE QUESTIONS 1. Section 174 CrPC deals with: A. Inquest B. Murder C. Exhumation D. Inquiry 2. Leading questions are permitted only in: A. Examination –in-Chief B. Cross Examination C. Re Examination D. Dying declaration 3. A Cognizable offence signifies: A. Arrest without warrant B. Imprisonment up to 1 year C. Imprisonment up to 5 years D. Only fine 4. The present Criminal Procedure Code has been enacted in the year A. 1947 B. 1963 C. 1973 D. 1985 5. Code of Civil Procedure which is being followed now a day was amended in the year: A. 1950 B. 1962 C. 1976 D. 1982 6. A second class Magistrate can pass a sentence up to: A. 1 year B. 2 year C. 3 year D. 4 year 7. Chief Judicial Magistrate can pass a sentence up to: A. 5 years B. 7 years C. 10 years D. Life imprisonment 8. Minimum age to be a witness in the court of law is: A. 7 years B. 12 years C. 16 years D. Any age 9. Dying declaration ideally is to be recorded by: A. Police B. Medical Officer C. Magistrate D. Session’s Judge
1 A 12 D
2 B 13 D
3 A 14 A
4 C 15 B
5 C 16 A
6 A
10. In dying deposition which of the following is fulfilled? A. Statement is to be recorded by Magistrate B. Oath is to be taken by the patient C. Cross examination to be done D. All of the above 11. Which of the following document is accepted in the court of law as evidence without being examined the person who has written it? A. Dying declaration B. Expert opinion expressed in a treatise C. Chemical examiners report D. All of the above 12. Conduct money is paid to witness, if he/she comes from a distance of more than: A. 2 kms B. 3 kms C. 5 kms D. Any distance 13. Dying declaration can be recorded by: A. Magistrate B. Police C. Medical officer D. All of the above 14. Before recording the dying declaration, the attending medical officer has to: A. Certify the mental condition B. Make a medicolegal report C. Treat the patient D. All of the above 15. Leading questions are allowed during Examination-in-chief, if the witness: A. Has no previous criminal record B. A hostile one C. Comes to court for 2nd time D. Has a criminal record 16. Summon is a document of the court: A. Compelling attendance of a witness B. Guarantee money of witness C. Providing legal immunity to witness D. That can be attended at will
7 B
8 D
9 C
10 D
11 D
Part 1—Forensic Medicine and Pathology
3
Laws in Relation to Medical Practice The medical profession is guided by a code of ethics which are formulated by the National Medical Council and State Medical Council alongwith World Medical Association. The ethics are nothing but the moral principles that guide the members of medical profession. The enforcement is done by the Medical Council of India and state medical council. INDIAN MEDICAL DEGREES ACT 1916 The Act was passed to grant the title in respect of the qualification of western medical science. According to the Act, we have right to grant medical degrees, diplomas and certificates to practice the western medical science but false use of a title is punishable under the Act. MEDICAL COUNCIL OF INDIA The Medical Council of India was established by the Indian Medical Council Act of 1956 to maintain a medical register for India and for the matters concerned with it. The act is applicable to the whole of India. Constitution and Composition of the Council The council consists of members as follows: 1. One member from each state other than a union territory, to be nominated by the central government in consultation with the state government concerned. 2. One member from each university, to be elected from its medical faculty, by the university senate or court. 3. One member from each state in which a state medical register is maintained, to be elected
from amongst themselves by all the persons enrolled on such register who possess a qualification included in the 1st, 2nd or part II of the third schedule. 4. Seven members to be elected from amongst themselves by persons enrolled on any state medical register and possess a qualification included in part 1 of the third schedule. 5. Eight members to be nominated by the central government. The president and vice president are elected from amongst the members for a term of 5 years or till their membership expires, This is a provision that they can get re-elected or re-nominated. The council meets at least once in a year and all acts of the council are decided by a majority of the members present and voting. An elected or nominated member is deemed to have vacated his seat if he is absent without excuse, for 3 consecutive ordinary meetings of the council or if he is no longer a member of the medical faculty or he/she ceases to be enrolled in the medical register. The council constitutes from amongst its members an executive committee (of not less than seven members) and any other committeesm required. The president and the vice-president of the council are also the president and the vicepresident of the executive committee respectively. It also appoints a registrar who acts as a secretary and if necessary as a treasurer to look after the day to day business of the council. Functions of The Medical Council of India The main functions of the Medical Council of India are as follows:
18 Textbook of Forensic Medicine and Toxicology 1. Maintenance of a Medical Register: The Council maintains a register for the medical practitioners where the names of all the registered doctors are entered. It also contains the names of the doctors who were registered in the State Medical Council. If due to some reason the name of the doctor is erased from the State Medical Register, it is automatically also erased from the Central medical Register maintained by the Medical Council of India. 2. Medical Education: It maintains the uniform standard throughout the country in respect to Undergraduate and Post Graduate courses. There is a Post Graduate Medical Education Committee consisting of nine members to maintain a uniform standard in respect to Post Graduate Qualification imparted by different Universities. They also advice the Universities and give guidance in this respect. Prior approval of M.C.I. is required for starting a PG course in any discipline. If not followed the M.C.I. has power to derecognised the said qualifications. As regards to Under Graduate Medical Education, the Council prescribes minimum standard. It appoints Medical Inspectors to inspect the various colleges before giving sanction either to start a new college or to renew it. Even to increase the numbers of seats in Medical College requires M.C.I.’s prior permission. The inspectors submit the report to the M.C.I. which is considered by the committee formed. Then the committee recommends to the Government to grant permission or not. In cases when the Council is not satisfied, it recommends the Government to withdraw the recognition. 3. Recognition of foreign medical qualifications to an Indian National with foreign degree which is not included in the part II of the third schedule applied to central government along with the full information in respect of the syllabus and duration of course etc. The Central Government forwards the applications to Indian Medical Council which has authority to enter in negotiations with any of the Medical Council of the Foreign Countries and can recognize such qualifications. Then the Central Government by
official gazette notification may amend the part II and includes such qualifications. 4. Appeal against disciplinary action: When name of any doctor is removed from the state medical register, he may appeal to Central Government after exhaustion of all the official remedies under the state medical council. He should apply within 30 days from the date of decisions alongwith all the relevant documents. The Central Government in consultation with the Medical Council of India will decide which is binding on state medical council. 5. Warning notice: The Medical Council prescribes standard of professional conduct and code of ethics for the doctors. If the medical practitioner fails to abide the code he can be issued warning notices in respect to professional misconduct. CODE OF MEDICAL ETHICS The oldest one is the Hippocratic Oath which is being followed till date. It reads as follows: I swear by Apollo the physician, by Aesculapius, Hygiea and panacea and I take to witness all the Gods, all the Goddesses to keep according to my ability and judgment the following oath: “To consider dear to me as my parents him who taught me this art; to live in common with him and if necessary to share my goods with him; to look upon his children as my own brothers, to teach them this art if they so desire without fee or written promise; to impart to my sons and the sons of the master who taught me and the disciples who have enrolled themselves and have agreed to the rules of the profession, but to these alone, the precepts and the instruction. I will prescribe regimen for the good of my patients according to my ability and my judgment and never do harm to anyone. To please no one will I prescribe a deadly drug, nor give advice which may cause his death. Nor, will I give a woman a pessary to procure abortion. But I will preserve the purity of my life and my art. I will not cut for stone, even for patients in whom the disease is manifested I will leave this operation to be performed by practitioners (specialists in this art). In every house where I come I will enter only for
Irritant Poisons 19 the good of my patients, keeping myself far from all intentional ill-doing and all seduction, and especially from the pleasures of love with women or with men, be they free or slaves. All that may come to my knowledge in the exercise or my profession or outside or any profession or in daily commerce with men, which ought not to be spread abroad. I will keep secret and will never reveal. If I keep this oath faithfully, may I enjoy my life and practice my art, respected by all men and in all times; but if I swerve from it or violate it, may the reverse be my lot.” DECLARATION OF GENEVA 1968 It was amended at Sydney in 1968. At the time of being admitted a member of the medical profession: I will solemnly pledge myself to consecrate my life to the service of humanity; I will give to my teachers the respect and gratitude which is their due; I will practice my profession with conscience and dignity; The health of my patient will be my first consideration; I will respect the secrets which are confided in me, even after the patient has died; I will maintain by all means in my power the honour and the noble traditions of the medical profession; My colleagues will be my brothers; I will not permit considerations of religion, nationality, race, party politics or social standing to intervene between my duty and my patient; I will maintain the utmost respect for human life from the time of conception; even under threat, I will not use my medical knowledge contrary to the laws of humanity. I make these promises solemnly, freely and upon my honour. Professional Misconduct It is also known as infamous conduct or disgraceful act. It is the improper conduct of the doctors in the professional aspect. What really constitutes misconduct is controversial. But the M.C.I. has enlisted the acts or behavior that constitutes the
professional misconduct. If the doctor’s act falls in any of the enlisted acts, he is liable for disciplinary action. The conduct of the doctor is judged by the professional omen of good repute and competence. The M.C.I. is also empowered to take action against an act done by the doctor even if it is not included in the list. The use of Red Cross Emblem by the doctors is prohibited. The Medical as well as paramedical staffs use it, which is wrong. They can be penalized under section 13 of Geneva Convention Act 1960 up to Rs.500/- fine and forfeiture of the property on which it has been used. Section 12 of the above act 1960 prohibits its use and allied emblem without the approval of Central Govt. Warning Notice The Medical Practitioner is required to observe certain rules of conduct contained in the code of Medical Ethics prescribed by the M.C.I. and the State Medical Councils. If the doctor fails to observe these, that will be taken as professional misconduct and action can be taken against the doctor. The list of conduct is not a complete one. The doctor can be penalised for a conduct even if not included in the list depending on its nature. He may be issued warning notice or the name may be erased from the register. the following are the few examples for which action can be taken. 1. Adultery: If a doctor has voluntary sexual intercourse with a married woman other than his spouse. 2. Advertisem*nt. A physician should not exhibit publicly the scale of fees except in the waiting hall of the patients or in his chamber. The doctor can publish in the newspapers or journals regarding his change of address maximum two times. Even he can publish regarding his timings, interruption or restarting of the practice, in the press after a long interval. He can write to the lay press in his name on matters of public interest and even can deliver public lectures or can give talks on the radio. He should not use an unusually large signboard and to write on it anything other than his
20 Textbook of Forensic Medicine and Toxicology name, qualification and the name of his speciality. The same should be contents of his prescription paper, which may in addition contain his address registration number and telephone number. It is unethical to fix a signboard on a chemist shop or in places where he does not reside or work. He should not advertise himself through manufacturing firms directly or indirectly. 3. Association: It is unethical to show improper conduct or association with the patient or his family. He should not associate himself with the manufacturing firms in the form of ownership, should not receive any rebates or commission for prescribing medicines. He should not use abbreviations, which can be read in only one particular pharmacy to dispense medicine. 4. Abortion: He should not perform an abortion that is not under the cover of MTP Act or he will not assist any unqualified person for doing a criminal abortion. 5. Alcohol: He should not practice medicine under the influence of alcohol, which interfere the skilled performances. 6. Addiction: He should not use any drugs of addiction that can hamper the practice. 7. Dichotomy or fee splitting, receiving or giving commission or other benefits to a colleague or drugs manufacturer. 8. Using touts and agents for fetching patients. 9. Not informing about the notifiable diseases to Health Authority. 10. Disclosing the patient’s secrets learnt during examination and treatment without consent. 11. Refusal to treat a patient on religious grounds. 12. To run a chemist shop for the sale of medicine or for dispensing prescriptions of other doctors. 13. Issuing false certificates in connection with sick benefit insurance or passport etc. 14. He should not assist a person who has no qualification to attain or treat a patient. The Medical Council of India brought into force the new ethical regulations in year 2002 called the Indian Medical Council regulations, 2002. They
are binding on all doctors in India. Its salient points are as follows: 1. The doctors are free to choose their patients but should not arbitrarily refuse treatment and must not refuse to help in an emergency. 2. Doctor should not refer their patients for consultation to other doctors or clinical investigations unless absolutely necessary. 3. Once a case is taken, the doctor must not abandon or neglect the patient without proper reason and appropriate notice to the patient and his family. 4. Doctors must display their fees and other charges clearly and should write clear prescriptions for dispensing medications. 5. Doctors must not provide any endorsem*nt for medications and equipment with or without any financial gains. 6. Drugs should be prescribed with their generic name as far as possible. 7. No sex determination tests should be done with the intention to destroy the female fetus if present. 8. The patients must not be subjected for trials except under ICMR guidelines. 9. Doctors should keep records for a minimum period of 3 years for in patients and must produce the documents if asked for within 72 hours. 10. The doctors should undergo 30 hours of CME training in every five years for renewal of registration. CONSENT It is defined as voluntary agreement, compliance, and permission. Section 13 of Indian Contract Act defines that “two or more persons are said to consent when they agree upon the same thing in the same sense.” According to Section 14 of Indian Contract Act, Consent is said to be free, when it is not caused by (i) coercion, as defined in section 15, or (ii) undue influence, as defined in section 16 or (iii) fraud, as defined in section 17, or (iv) misrepresentation, as defined in section 18, (v) mistake subject to the provisions of sections 20, 21, 22.
Irritant Poisons 21 Reasons for Obtaining the Consent To examine, treat or operate upon a patient without consent is regarded as assault in law, even if it does not cause any harm and even if it is beneficial and done in good faith, for which the patient may sue for damages. If the doctor fails to give the requisite information to a patient before asking for his consent for a particular operation / treatment he may be charged for negligence. Types of Consent 1. Implied 2. Express • Oral • Written—informed. Implied Consent This type of consent is specifically stated by the patient and is seen in routine medical practice and is quite adequate. Here consent is implied in the mere fact that patient comes to physician with a problem or when a patient holds out his arm for an injection. If the procedure of diagnosis is simple and straightforward, the risk is negligible and uncommon and the conduct of the patient implies willingness to undergo treatment. In spite of everything, if there is the slightest fear of complication, the doctor should seek express consent. Express Consent May be written or verbal, and should be obtained for any procedure beyond the routine physical examination, like operation, collection of blood, blood transfusion etc. The nature and consequences of the procedure should be explained before getting consent. Oral consent in the presence of a disinterested third party is as good as written one. Doctrine of Informed Consent In informed consent, the patient is informed about his/her condition of the disease, nature of the proposed treatment whether surgical or medicinal methods, any alternative procedure available or not, the possible risks and benefits of the proce-
dure and the percentage of chances of success and failure. The patient should be told in a simple language so that he can understand and give consent in the presence of third party. After that any untoward reaction or harm to the patient cannot lead to charge the doctor for negligence. The exceptions to the informed consent are: 1. Emergency—in an emergency it is assumed that the patient gives consent. So the consent is implied in these cases. 2. Incompetence—the incompetent patients may be treated without permission. In general incompetent patients are unable to make rational decisions. In this category the patients of unconscious, delirious, senile or grossly psychotic in nature are included. When patients are in intensive care unit they are treated without informed consent. So it is best either in an emergency or incompetence situation. 3. Therapeutic privilege—in this category the physician can be excused of taking informed consent when disclosure of information could have a detrimental effect on the patient. 4. Waiver—the last exception allows a patient to waive his right to informed consent. In these cases the patient may delegate the right to the physician or to a third party to make the decision for him. If one of the exceptions to the informed consent applies, the physician should document the exception under these circ*mstances how disclosure and consent should occur but in emergency time may not permit disclosure and consent. If patient is incompetent or therapeutic waiver is used, a surrogate should give informed consent for the patient. Informed refusal:The doctor has a duty to inform the patient that he has a right to refuse the treatment/investigations to be done. If after listening to the doctor, he thinks so, he can refuse to consent. Rules of Consent Consent is necessary in every medical examination. Ordinarily, formal consent to medical
22 Textbook of Forensic Medicine and Toxicology examination is not required because the patient conducts himself/herself in a manner which implies consent. Written consent is not necessary in every case. However it should be taken for proving the same in the court if necessity arises. In medico legal cases written consent is a must. Any procedure beyond routine physical examination such as operation, blood transfusion, collection of blood etc. requires express consent. It must be taken before the act and not at the time of admission in to the hospital. The consent should be free, voluntary, clear, informed, direct and personal. There should be no undue influence, fraud, and misrepresentation of the facts, compulsion and threat of physical injury, death or other consequences. The doctor should inform the patient that he has the right to refuse to submit to the examination and that the results may go against him / her. If he/she refuses it is an absolute bar for examination except under S 53 CrPC. Written consent is taken for a specific procedure. It is not same as blanket permission for general procedure where the surgeon can decide in the operation threater itself regarding the type extent of operation. The doctor should explain the object of the examination to the patient and he should be informed that the findings would be embodied in a medical report. In criminal cases the victim cannot be examined without consent. The court also cannot compel a person to get medically examined against his will. If the person is arrested being charged of some offence and the examination of his body will provide some evidences toward the commission of the crime he can be examined by a registered medical practitioner even without his consent and if necessary by using reasonable force. (Under Section 53(1) CrPC) and section 53 (2) CrPC mentions that in case of a female the examination should be done by a female medical practitioner or under her supervision. Under section 54 CrPC and an arrested person can request to be examined by a doctor to detect
any evidences in his favour. Under section 87 IPC a person above 18 years of age can give consent to suffer any harm if the act is not intended and not known to cause death or grievous hurt. Under section 88 IPC a person can give consent to suffer any harm if the act is not intended and not known to cause death or grievous hurt if the act is done in good faith and for the benefit of the person. Under section 89 IPC for a child under 12 years of age or a person of unsound mind cannot give consent to suffer any harm for an act which may cause grievous hurt or death even in good faith, but the consent has to obtained from the guardian of the child or person. Under section 90 IPC consent given by an insane person or given under fear of injury, death etc. or due to misunderstanding of a fact is invalid. Under section 92 IPC any harm caused to a person in good faith even without the person’s consent is not an offence if the circ*mstances were such that it was impossible to obtain consent of the person or his lawful guardian in time for the thing to be done for the benefit of the person, but the act should not extend to intentional causing hurt other than for preventing death or hurt or curing of grievous disease or infirmity. Professional Secrecy In the Hippocratic Oath there is an affirmation by the doctor that whatever in connection with my professional practice or not in connection with my professional practice or not in connection with what I see or hear in the life of men, which ought not be spoken of abroad, I will not divulge, as reckoning that all such be kept secret’. Even the places where oath is not formally given in qualifying ceremony, there is an implied acceptance of its spirit and intentions as the ideal standard of his professional behaviour. Therefore, both on ethical grounds and also because he may be used in the civil courts for breach of confidence, the doctor should respect this professional secrecy to the utmost of his ability. The following examples may be kept in mind: 1. The doctor should not discuss any point with others except with the consent of the patient.
Irritant Poisons 23 2. If the patient is a major a doctor should not disclose anything about his illness even to his parents without getting the consent. 3. In case of husband and wife the facts relating to the nature of illness of one should not be disclosed to the other without the consent. 4. If the doctor examines a domestic servant at the request of the master who is paying the fees still he should not disclose even to the master without the consent of the servant. 5. Doctors in government service are bound by code of professional secrecy even if they are treating the patients free of cost. 6. The criminals in police custody has right not to allow the treating doctor to disclose about the nature of illness to any person. However once the person is convicted he has lost this right and the doctor can disclose to the proper authorities. 7. While reporting about any case in a medical journal care should be taken not to disclose the identity of the person. 8. When somebody submits for medical examination while taking the life insurance the doctor can disclose the result to the proper authorities because of implied consent. 9. A doctor should not disclose any information about the illness of his patient without consent whenever requested by a statutory body except notifiable diseases. 10. The examination of the dead body at times may reveal certain facts that affect the reputation of the deceased as well as the family members so the doctor should not disclose the fact to others. Exceptions to Professional Secrecy Professional secrecy should be broken in certain situations that are known as privileged communication It is a statement made by the doctor to the concerned authority to protect the interest of the community or state. To be privileged it must be made to the concerned person/authority. If the plea of privilege facts is made to more than one
person, then in these situations, the doctor must tell the patient to give the consent. If he fails, then he will tell proper authority to protect the interest of the community. The following are the examples of privilege communications. Infectious diseases: If anybody having infectious diseases gets an employment, she/he should be persuaded not to undertake the job till he becomes cured. If somebody is found to be suffering from infectious diseases, during his employment, he/she should also be told to go on leave till he/she becomes all right. If they refuse, the doctor can tell the employer about it. Example: A schoolteacher with tuberculosis, Cook of the hostel with typhoid. Notifiable diseases: Medical persons has a statutory duties to notify births, deaths and other diseases to the Public Health Authority. Suspected crimes: The doctor must inform the police (U/s 39 CrPC) Servants and Employees: When an employee is suffering from a serious disease like colour blindness in case of drivers, Epilepsy in case of cooks, they should be persuaded to change their profession, otherwise the employer should be informed about the illness. Sexually transmitted diseases: Person having a sexually transmitted disease intending to join in swimming pool or going for marriage, should be persuaded not to join the swimming pool or go for marriage. If he does not listen, then the doctor should inform to the proper person/ authority. In patient’s interest: If the patient having suicidal tendency, the parents/guardians may be informed about, so that, they can take proper care as well as provide proper treatment. Court of Law: In the court of law the doctor cannot claim the privilege about the illness of his patient. When asked he should appeal to the court that he should submit in writing, so that the public cannot know about the facts. If the court rejects he has to tell before the court. But under section 126 and 129 IEA, a lawyer can claim the privilege in a court of law requesting any communication made to him by his client. Negligent suits: When a patient files any suit of negligence against a doctor and he employ
24 Textbook of Forensic Medicine and Toxicology another doctor to examine the patient, the information thus acquired is not privileged and he can divuldge in the court of law. Self-interest: when a patient files a civil or criminal suit, the doctor can disclose evidence.
•
Rights and Privileges of Registered Medical Practitioner • • • • • • •
Right to practice medicine. Right to choose a patient. Right to issue a certificate. Right to add title to his name. Right to recover his fees. Right of appointment to public hospitals. Right to give expert evidence in the Court of law. • Right to dispense medicine.
•
Duties of a Medical Practitioner The registered Medical Practitioner has multiform duties towards the patient, colleagues and state. Some of them are follows:
•
Towards Patients • Duty to exercise necessary care and skill: In a patient comes to a doctor and doctor has right to refuse but when starts treating the patient the duty towards the patient starts. For hospitals, the duty arises when the patient gets admitted to it but in cases emergency the doctor cannot refuse the patient but after giving the first aid can refer with proper precaution to the nearest hospitals where facilities are available. He could use his care and skill according to his knowledge and qualification in cases of minors, the doctor has the duty to exercise care and skill even if the fee is being paid by the guardian. • To examine the patient properly: It is the duty of the doctor to examine the patient thoroughly and take proper history from him or from the attendent. • To prescribe proper medicines: The doctor should prescribe proper medicines after carefully evaluating the patient. In cases of Government Hospitals, if the medicines are not available there, the doctor should advice the patient to
•
•
•
purchase from the market. In case of wrong prescriptions causing harm to the patient, the doctor will be liable for the damages. Duty to inform the risks: The doctor should inform the patient about the disease and possible risks involved. If the patient is not of sound mind the guardian should be informed. After getting the consent the doctor should get his consent for the management. In cases where the doctor thinks that after telling the risks, there will be great psychological upset, he can withhold some of the risks. Duty to give proper instructions: The doctor should give full instructions to the patient or to the attendents regarding the use and type of diet to be taken. He should also mention the dose and frequency of the medicines to be used. In cases of any untoward reaction the patient should be advised to report immediately. Instructions to those patients who cannot take care of themselves: In cases of mental ill patients or comatose patients, their attendents or guardians to be properly instructed about the use of medicine. Duty in relation to operations: After careful diagnosis when the surgeon thinks to operate the patient, he should explain the nature and extent of operation to the patients, the possible risks involved in these cases and any alternative method available. He must obtain consent before operation. He must not experiment on the patient. He should be sure that no swabs, instruments are left inside the body after operation. He must take post-operative care properly to avoid any complication. Inform third parties: In cases of patient suffering from infectious diseases, the doctor should not only warn the patient but also the third party i.e. relatives, friends and co-workers, so that they can take proper precautions. He also has duty to inform the proper Health Authorities. Poisoning case: When the doctor attend a suspected poisoning case, he has to do the stomach wash with plain water so that the sample can be sent for chemical analysis. He has to preserve vomitus, blood and urine for chemical analysis. After that he should treat
Irritant Poisons 25 with suitable anti-dots and take other steps towards treatment. Toward Colleagues • Never criticize: A medical practitioner should never criticize his colleagues. When a patient comes to him after leaving another doctor, he must not tell to the patient about the ills of that doctor or criticize the medicines prescribed by him earlier in order to gain cheap popularity. • Never take fees: When any specialist examine or treats another doctor, he should not demand any fees from him. It is the professional curtesy he has to extend to his colleagues. • Always help: The doctors should always help his fellow colleagues at the time of need specially any professional matters. • Consultation: It is the duty of a doctor to consult another specialist depending upon the type of disease he is treating. In cases of operation or other emergency situations, he has to take consultation from a specialist in the relevant field. In these situations, the patient must be told that he is being referred to a specialist for consultation. The patient will also be told whether it is only consultation, joint participation or he will be on continuous treatment of the consultant and get proper consent for that. In cases where the patient is completely transferred to another specialist, the liability of the referring doctor ceases and the duty of the consultant starts in relation to the liability towards the patient. Towards State • Notifiable diseases. • Geneva Conventions. Notifiable Diseases A doctor is bound to inform the communicable diseases like cholera, plague etc. to the Health Authorities. He is also bound to inform the birth and death to proper authorities. If a doctor fails to inform, a civil suit can be brought against him, but not a criminal suit.
Geneva Convention, 1949 A Medical Practitioner is bound to treat/provide medical aid in cases of person wounded or sick of the armed forces (I Convention), ship wrecked persons (II Convention); prisoner of war (III convention) and civilians of enemy nationalist (IV Convention). All the above categories of person should be treated without any discrimination based on Race, Religion or Political grounds. MEDICAL NEGLIGENCE (MALPRAXIS) Introduction: The law of negligence is applicable to the conduct of all individuals whether layman or professional. In addition certain ethical standards are applied to the professionals. Whenever a privilege is bestored upon an individual, concomieant duties and obligations attach and the physician is no exception. In present times doctors can not be sure that they will never be threaten with an action for negligence. Even patients are ready to sue who have had excellent treatment with complete cure and without cost. There are three reasons for this: 1. Transfer of Hospitals to the State or Central Government. 2. The cost are met out of National funds 3. There is a provision of free legal aid for the patient. It is difficult to appreciate that severe disability resulting from an accident during the course of treatment is not necessarily negligence but unfortunately patient may allege negligence and seek compensation. In Hatcher Vs. Black & Others (1954) Lord Denning compared negligence with a dagger. The doctors’ professional reputation is as much dear to him as his body, perhaps more
26 Textbook of Forensic Medicine and Toxicology so, and an action for negligence could wound his reputation as severely as a dagger to his body. Professional Negligence is defined as “Want of reasonable care and skill or willful negligence on the part of the medical practitioner while treating a patient resulting in bodily injury, ill health or death.” Negligence was first defined by Justice Baron Alderson in 1856 “The omission to do something which a reasonable man could do or doing something which a prudent and a reasonable man could not do”. It could be defined as a failure to perform the duty to exercise a reasonable degree of skill and care in the treatment of patient. In 1934 Lord Wright defined it as . there must be a duty owed . Breach of that duty either by omission or commission. . Direct causation. . Damage To summarize the doctor owes a duty towards the patient, the doctor was in breach of that duty as a result of which the patient suffered damage. there is a direct relationship between the dereliction of duty and a damage. Medical negligence is no different in law from any other type of negligence. Negligence medical or otherwise is a civil wrong than as a “tort”, rarely the medical negligence may be renewed from a civil action between doctor and patient to the criminal courts, where the state prosecutes the doctor for a severe degree of reckless and dangerous action, amounting to criminal negligence. Duty of the doctor to choose a patient: The doctor has right to refuse any patient. So any patient who comes to a doctor, he can either refuse or accept for the treatment. Once the doctor accepts the patient, his duty towards the patient starts. The doctor can refuse to accept the patient in the following circ*mstances (i) Not belonging
to his/her speciality (ii) Facilities are not available at the place. (iii) The doctor is not well or any member of the family is sick. (iv) Busy in important family functions. Duty of the doctor during an Emergency: During emergency he is morally and ethically bound to provide the best of help he can do to save the life of the patient and see that the patient if not accepted by him, can reach the nearest hospital. Here no patient doctor relationship is established. So if some damage occurs, the patient cannot sue the doctor. Absence of reasonable care and skill: The duty to exercise reasonable care and skill exists when a doctor-patient relationship is established. This may be true even if the patient is unconscious and quite unaware of the doctor’s presence. A doctor who deals with a patient with the intent to act as a healer establishes a doctor-patient relationship immediately and from that moment he has a legal obligation to exercise due care and skill. Any breach of that duty is a ground for the negligent action. When a doctor examines a patient for some other purpose than providing advice and treatment, i.e. he is not present as a healer, no relationship is established and there is no duty of care. When a doctor examines a medico legal case like sexual assault, alcoholics, and insurance etc., he is there not as a healer and thus no relationship exists, but there is a duty not to damage, thus if he breaks the needle while taking blood sample, he is liable to pay damages. On the other hand if he reports the findings to the employer and insurance company, no action for damages arises. Degree of Competence A doctor must possess reasonable degree of proficiency and he must apply it while treating the patient. A highly qualified doctor will be held negligent if he fails to apply his greater knowledge with sufficient degree of care. Conversely an in experienced doctor may be negligent if he attempts to do some procedure, which is beyond his capability except in an emergency. The degree of competence is not a fixed quality but varies
Irritant Poisons 27 according to the status of the doctor. There is a minimum level of competence for all doctors who have qualified in the examinations and registered in the state medical councils or the Indian medical council. This minimum level is set to protect the public from insufficiently qualified doctors. Beyond this minimum point there is a whole spectrum of proficiency from a newly graduated doctor to a senior specialist. No doctor is expected to possess all up-to-date knowledge nor he can apply all known diagnostic and therapeutic techniques however a doctor of a particular status as regards his grading and experience is expected to have a standard of knowledge and capability corresponding to his position in the profession for example a house surgeon is not expected to possess the same skills as that of a consultant surgeon. A house surgeon volunteering to perform a major surgical operation (not an emergency) might be held guilty of negligence if he causes damage to his patient. This applies to all other specialities such as anesthesia, medicine and so on. On the other hand if a junior doctor performs any operation or treats a patient in an emergency or where there is no other medical facility available even if there is damage to the patient he will not be held negligent provided that he has acted in good faith. Breach of Duty of Care It will not be incorrect to say that categories of negligence are never closed which means that it is impossible to draw a complete list of things that can cause negligence in action because of the advancement of medical technology day by day. Anything a doctor does can be a ground for negligence if the patient is not satisfied and damage occurs. A doctor is not liable for errors of judgment either in diagnosis or treatment as long as he applied a reasonable standard of skill. Negligence is not a matter of a doctor making a mistake but of not trying hard enough, lack of care and attention for the consequences. A doctor can misdiagnose and mistreat a patient without being negligent even if another practitioner of greater skill and ability
would have had more success. A doctor is not an insurer of as one famous judge said and he doesn’t guarantee to provide the best possible care but only care which is reasonably adequate and consistent with his professional status. Who Sets the Standard? The court will rely upon the evidence of competent practitioner in the relevant field of medical practice. Approved practice is a criterion for reasonable care. In almost all defence cases it is told that what was done, was done in accordance with general approved practice. Court gives much importance to the expert evidence in the relevant field. A doctor is not negligent if he acts in accordance with general accepted practice. The court pronounces the practice negligent if there are some inherent defects in it. It is not enough to repute negligence by saying that he did it what everybody does. A risky practice may well be held negligent not withstanding that it is widely followed. In almost all defence cases it is told that what was done, was done in accordance with general approved practice. Court gives much importance to the expert evidence in the relevant field. A doctor is not negligent if he acts in accordance with general accepted practice. The court pronounces the practice negligent if there are some inherent defects in it. This is not a usual and normal practice. That the practice was not adopted. The practice adopted is one which no professional man of ordinary skill would adopt. A medical practitioner when deviates from normal practice it must be established that he is free to exercise his judgment, discretion and the new procedure was done with the consent of the patient for his benefit. Anyone who adopts a noble course of treatment or omits to use some form of diagnosis or treatment, which has gained general approval, must be able to justify his actions if something goes wrong. In these cases success is the best justification. Duty to Inform the Risks In a hospital, no matter what care is taken there
28 Textbook of Forensic Medicine and Toxicology is always a risk. Always there is some risk in every operation under general anaesthesia; to what extent the doctor is obliged to inform his patient or relatives about these risks? When there is some non-risk they should be informed before taking the consent. Then there is no room for negligence. For example, in an ECT Therapy the risk of fracture of dorsal vertebrae so the written consent must be taken. The doctor is not expected to inform all possibilities. He is not negligent if he has not informed about remote risks. Retention of Swabs, Packs, Instruments and Drainage Tube Etc. Responsibility of recovery of swabs used in operation theatre lies with the surgeon. As he puts the swabs inside he must take them out. He must use degree of care, which is reasonable in the circ*mstances. That must depends upon the evidences. He cannot say, “I relied upon the nurse”. He must ask the nurse if everything is all right. The circ*mstances in which the nurse’s count will be of immense value is that the emergency was so great, the surgeon could not carry out search without endangering the patient’s life. To avoid negligence, the surgeon must satisfy the following: The counting system is efficient and the person working is familiar with it. The system was followed during the operation and the count showed that the number is all right. He must take all reasonable precaution that swabs used were recovered. He must do a visual and manual search of the field. In these cases the plaintiff has only to
prove that he has suffered damage and the onus is upon the surgeon to prove that he is not negligent (Table). Precautions against Medical Negligence 1. Never guarantee a cure. 2. Obtain informed consent from the patient. 3. The diagnosis to be confirmed by proper investigation depending upon the nature of cases. 4. Reasonable skill and care to be taken 5. Proper, accurate and legible records to be maintained. 6. Immunization to be done specially tetanus in cases of injuries. 7. Sensitivity test to be performed before injecting the drugs known to cause hypersensitivity reactions specially in cases of penicillin, streptomycin and antivenins. 8. The patient or his attendant should be advised that the medicine should be given in the proper dosage and in time and no telephonic consultation should be done. 9. Consultation to be undertaken with appropriate specialist in case of need. 10. Never criticise your colleagues regarding his professional ability. 11. The patients should not be left unattended when she is undergoing labour. 12. In case of absence from practice the patient should be informed or qualified substitute should be arranaged. 13. A written informed consent should be
Table 3.1: Differences between civil and criminal negligence Features
Civil negligence
Criminal negligence
Offence
No specific and clear violation of law Simple absence of care and skill Compared to a generally accepted standard of profesisonal conduct Good defence in court of law cannot recover damages Civil court Strong evidence is sufficient Damages to be paid
There is specific violation of a particular criminal law in question Gross negligence, inattention or lack of competency Not compared to a any single test
Negligence Conduct of physician Consent for act Trial Evidence Punishment
Not a defence; can be prosecuted Criminal court Guilt should be proved beyond reasonable doubt Imprisonment
Irritant Poisons 29 obtained before carrying out surgery and anaesthesia and the detailed surgical procedures and possible risks should be explained to the patient. Anaesthesia should be given by an expert in the field. 14. Before a surgical operation, the surgeon should make sure that all the instrument are in good working condition and proper count of the instruments should be done by the nurse before and after completing the operation. 15. Whenever a death occurs from anaesthesia or during surgical operation the doctor should report to the police. 16. For carrying out any research work on the patient his consent should be taken. 17. No female patient to be examined without the presence of a third person preferably a female or by a female registered medical practitioner. 18. The doctor should be well versed with the advanced medical knowledge in the field. Contributory Negligence Contributory Negligence is the absence of reasonable care on the part of the patient or his attendant that combines with the negligent action of the doctor resulting in the damage completed off directly and without which damage should not have occurred. The examples are: Not to provide proper history to the doctor. Failure to follow the line of treatment. Refusal to take up the suggested advice. Leaving the hospital against the doctor’s advice. Failure to seek further medical treatment if the signs/symptoms persists. If the doctor and the patient are negligent simultaneously, the doctor can take a good defence, otherwise the contributory negligence is a partial defence in civil suit only and has no place in criminal negligence. When the patient consents to take the risk of the injuries effects, then he cannot claim damages. When the doctor is not negligent and it is the patient alone who is negligent, it is called “Negligence of the patient”. Limitations of Contributory Negligence 1. Last clear chance doctrine—In this rule the
person who is negligent may recover the damages if the doctor discovered the injury while there was still time to avoid the injury but he failed to do so. 2. Avoidable consequences rule–In these cases the doctor was found to be negligent and he was sued for the same and after that the negligence of the injured person occurs. In these situations the patient is not guilty of contributory negligence since his actions were not the cause of the injury. Therapeutic Misadventure A misadventure is a accident or unexpected damage to the patient which the doctor is attending during the treatment is called Therapeutic misadventure. It can be during diagnosis or during experiment. Almost every therapeutic drug has side effects. So the doctor has to explain the possible side effects while prescribing the drug. When there are more than one drug and there is a choice of treatment for a particular disease, then the doctor should prescribe the drug having lesser side effects. Hypersensitivity to drugs is very common, so when a doctor prescribes a particular drug, he/ she has to be very particular to ask about the history of hypersensitivity before starting treatment and at the same time to be equipped with life saving measures if required. The doctor is not liable for the damages caused by administration of a drug unless the element of negligence exists. Examples: (i) A hot water bottle or heating pads causing burns. (ii) Foetal and neonatal deaths occurring inside uterus while the mother is given some drugs for treatment during pregnancy. (iii) Hypersensitivity reaction caused by administration of Penicillin/streptomycin, tetracycline etc. (iv) Radiological procedures during diagnostic methods can prove fatal. (v) During Barium enema, rupture of rectum causing peritonitis. Error Of Judgement: It is a well established fact that a doctor is not expected to do a miracle. The courts do not
30 Textbook of Forensic Medicine and Toxicology condemn an honest exercise of judgement even though other doctors may disagree. To cover up an error of judgement is held to be negligent conduct. Respondent Superior (Vicarious Liability) The employer is responsible not only for the wrongful deeds committed by him, but also the wrongful deeds of his employees. The doctor usually employs or supervises other members of staff who may be less qualified persons. He distributes the work and supervises them. If one of the member/s does any negligence, then the principal/doctor is held responsible known as Respondent superior. Doctrine of Res Ipsa Loquitur Usually the professional negligence of a doctor must be proved in the Court of Law by the experts in the field. Here the patient has to prove the negligence of the doctor. But in cases of Res Ipsa Loquitur which means “ the facts speaks for itself” the patient need not prove the negligence. The rule will be applicable if the following conditions are satisfied: 1. That in the absence of negligence the injury would not have occur. 2. The doctor had exclusive control over the injury producing instrument or treatment 3. There is no contributory negligence by the patient. Few are the following examples: 1. Breaking of a needle during injection. 2. Failure to remove swabs from the abdomen during operation . 3. Prescribing overdose of medicine. 4. Burns resulting from application of hot water bottle. 5. Failure to give anti-tetanic serum in cases of injury resulting titanus. This Doctrine is applied to both civil and criminal negligence. It can not be applied against several defendants. Doctrine of Common Knowledge:
This Doctrine is based on the assumption that the issue of negligence in a particular case is not related to the technical matters which are within the knowledge of medical profession. It is one type of Res Ipsa Loquitur where the patient need not produce evidences regarding the standard of care but in Doctrine of Common Knowledge the patient must prove the causative factor but he need not produce the evidences to establish the standard of care. Defenses Available in Cases of Negligence No duty owed to the plaintiff. The duty was discharged according to the prevailing standard. It was a therapeutic misadventure. It was error of judgment. Contributory negligence: It can be taken as defence in cases of civil negligence only. Res judicata: Once the case has been decided it cannot be taken to another court. Only appeal can be made. Limitation: The case should be filed within two years from the date of alleged negligence. If it is alleged that there was a breach of duty to take care under some particular contract between doctor and patient, then the period is three years from the date of breach of contract. The following points are not good defences: There was no contractual relationship between the doctor and the patient. Service was rendered free of charge. The medical man had no bad motive. CONSUMER PROTECTION ACT 1986 The consumer protection act 1986 came into force on 15 April 1987 is a welfare legislation mainly tilting towards the consumer like industrial dispute act that favours the workers. The act envisages a three tier quasi judicial machinery i.e. District Consumer Disputes Redressal Forum at the District level, State Consumer Disputes Redressal Commission of the State level and National Consumer Disputes Redressal Commission at the National level. The District Forum consists of three members presided by a retired or serving district judge. It entertains claims up to rupees twenty lacs. The State
Irritant Poisons 31 Commission consists of three members presided a serving or retired high court judge. It entertains claims between rupees twenty lacs to one crore. And the National Commission consists of five members presided by a retired Supreme Court judge, which entertains claims above rupees one crore.
the national commission and finally to supreme court within thirty days of the date of order.
Procedure
Penalties
The complaint can be lodged at any of the places with or without engaging a lawyer by paying a nominal fee. The complaint may be filed with the district forum by • The consumer to whom the service has been provided or had been agreed to be provided. • Any recognised consumer association • One or more consumers where numerous consumers have the same interest. • State or central government. If the complaint relates to any service the district forum shall refer the copy of the complaint to the opposite party directing him to submit a reply within thirty days. Here it is not necessary for the parties to be represented by the lawyers so the disputes are settled on the basis of evidences put before him. The district forum has the same powers as that of a civil court under the code of civil procedure 1908. Every proceeding before the district forum shall be deemed to be a judicial proceeding within the meaning of section 193 and 228 of the IPC 1860. If the district forum is satisfied that the goods supplied were having some defects specified in the complaints and that any of the allegations contained in the complaint about the services are proved, it will issue an order to the opposite party either to remove the defect, replace the goods or provide adequate compensation. But if the complaint is not proved it will be dismissed and the court directs to pay the costs of the opposite party not exceeding more than rupees ten thousand. But there is a provision that the aggrieved party if not satisfied can appeal in the state commission within thirty days from the date of order. If not satisfied any party can appeal to
For the noncompliance of the order made by district forum, State Commission or National Commission the trader or the person shall be punished with imprisonment ranging from one month to three years and fine from rupees two thousand to ten thousand. Interpretation of the act by the Supreme Court Since the enactment of the act there was a controversy whether the provisions of the act are applicable to the persons who are rendering medical service to the patients. In this regard there was a difference of opinion between the State Commissions, National Commission and various high courts. The said controversy came to an end by the landmark judgment delivered by the Supreme Court in the case of Indian medical association council vs V P Shantha and others. The Apex Court arrived at the following conclusions; Service rendered to patient by medical practitioner except where the doctor renders service free of charge to every patient or under a contract of personal service, by way of consultation diagnosis and treatment both medical and surgical would fall within the ambit of service as defined in section 2(1)(0) of the act. The fact that the medical practitioners belong to the medical profession and subject to the disciplinary actions of Medical Council of India or state Medical Council constituted under the provisions of the Indian Medical Council act would not exclude the services rendered by them from the ambit of the act. A ‘contract of personal service’ has to be distinguished from ‘contract for personal service’. In the absence of relationships of master and
Limitation Period The complaint should be filed in all the above forums within two years from the date on which the cause of action has arisen.
32 Textbook of Forensic Medicine and Toxicology servant between the patient and the medical practitioner the service rendered by a medical practitioner to the patient cannot be regarded as service rendered under ‘contract of personal service’ but such services are regarded as being rendered under a ‘contract for personal service’ and is not covered by exclusionary clause of definition of service contained in section 2(1)(0) of the act. The expression ‘contract of personal service’ in Section 2(1)(0) of the Act cannot be confined to contracts for employment of domestic servants only and the said expression would include the employment of a medical officer for the purpose of rendering medical service to the employer. The service rendered by a medical officer to his employed under contract of employment could be outside the purview of ‘service’ as defined in Section 2(1)(0) of the Act. Service rendered free of charge by a medical practitioner attached to a hospital/nursing home or a medical officer employed in a hospital/nursing home where such services are rendered free of charge to everybody, would not be ‘service’ as defined in Section 2(1)(0) of the Act. The payment of a token amount for registration purpose only at the hospital/nursing home would not alter the position. Service rendered at a non-government hospital/ nursing home where no charge whatsoever is made from any person availing the service and all patients (rich and poor) are given free-service is outside the purview of the expression ‘service’ as defined in Section 2(1)(0) of the Act. The payment of a token amount for registration purpose only at the hospital/nursing home would not alter the position. Service rendered at a non-government hospital/ nursing home where charges are required to be paid by the persons availing such services falls within the purview of the expression ‘service’ as defined in Section 2(1)(0) of the Act. Service rendered at a non-government hospital/ nursing home where charges are required to be paid by persons who are in a position to pay, and persons who cannot afford to pay are rendered
service free of charge, would fall within the ambit of expression ‘service’ as defined in Section 2(1)(0) of the Act irrespective of the fact that the service is rendered free of charge to persons who are not in a position to pay for such services. Free service, would also be ‘service” and the recipient a ‘consumer’ under the Act. Service rendered at a government hospital/ health center/dispensary where no charge whatsoever is made from any person availing the services and all patients (rich and poor) are given free service, is outside the purview of the expression ‘service’ as defined in Section 2(1)(0) of the Act. The payment of a token amount for registration purpose only at the hospital/nursing home would not alter the position. Service rendered at a government hospital/ health center/dispensary where services are rendered on payment of charges and also rendered free of charge to other persons availing such services would fall within the ambit of the expression ‘service’ as defined in Section 2(1)(0) of the Act irrespective of the fact that the service was rendered free of charge to persons who do not pay for such service. Free service would also be ‘service’ and the recipient a ‘consumer’ under the Act. Service rendered by a medical practitioner or hospital/nursing home cannot be regarded as service rendered free of charge, if the persons availing service has taken an insurance policy for medical care where under the charges for consultation, diagnosis and medical treatment are borne by the insurance company and such service would fall within the ambit of ‘service’ as defined in Section 2(1)(0) of the Act. Similarly, where, as a part of the conditions of service, the employer bears the expenses of medical treatment of an employee and his family members dependent on him, the service rendered to such an employee and his family members by a medical practitioner or a hospital/nursing home would not be free of charge and would constitute ‘service’ under the Section 2(1)(0) of the Act. HUMAN EXPERIMENTATION
Irritant Poisons 33 All research involving human subjects should be conducted in accordance with three basic ethical principles, which have equal moral force and guide the conscientious preparation of proposals for scientific studies. These are: • Respect for persons—It incorporates at least two fundamental ethical considerations • Respect for autonomy, which requires that those who are capable of deliberation about their personal choices should be treated with respect for their capacity for self determination • Protection of persons with impaired or diminished autonomy, which requires that those who are dependent or vulnerable be afforded security against harm or abuse. • Beneficence—Refers to ethical obligation to maximize benefit and minimize harms and wrongs. This principle gives rise to norms requiring that the risks of research be reasonable in the light of the expected benefits and that the research design be sound enough to safe guard the welfare of the research project. • Justice—Refers to the ethical obligation to treat each person in accordance with what is morally right and proper to him/her. Human experimentation may be: a. Therapeutic experimentation—Is concerned primarily with improving the condition of a particular patient under treatment b. Research experimentation—Is concerned primarily with using a human subject as a means of expanding scientific knowledge for the benefit of humanity c. Innovative experimentation—Are therapeutic procedures that have not yet earned a place in medical practice The Declaration of Geneva: The Declaration of Geneva of the world Medical Association binds the doctor with the words, “The health of my patient will be my first consideration” International Code of Medical ethics: It declares, “Any act or advice which could weaken physical or mental resistance of a human being may be used only in his interest” The purpose of biomedical research involving human subjects must be to improve the
diagnostic, therapeutic and prophylactic procedures and understanding of the etiology and the pathogenesis of the disease. In current medical practices, most of these procedures involve hazards. Medical progress is based on research that ultimately rests in past on human subjects. Special caution must be exercised in the conduct of research, which may effect the environment, and the welfare of animals used for research must be respected. The results of the laboratory experiments must be applied essentially to human beings to further scientific knowledge and to help the suffering humanity. World Medical association has prepared the following recommendations as a guide to every doctor in biomedical research involving human subjects. It must be stressed that the standards as drafted are only a guide to physicians all over the world. Doctors are not relieved from the civil, criminal and ethical responsibility under the laws of their own countries. The code of ethics known as Declaration of Helsinki was drawn in 1964 and revised in 1975 as follows. Basic Principles Biomedical research involving human subjects must conform to the generally accepted scientific principles and should be based on adequately performed laboratory and animal experimentation. It should be based on a thorough knowledge of scientific literature. The design and the performance of each experimental procedure involving human subjects should be clearly formulated in an experimental protocol which should be transmitted to a specially appointed independent committee for consideration, comment and guidance. Biomedical research involving human subjects should be conducted only by scientifically qualified person and under the supervision of a clinically competent medical person. The responsibility for the human subject must always be with medically qualified person and never rest on the subject of the research, even though the subject has given his/her consent.
34 Textbook of Forensic Medicine and Toxicology Biomedical research involving human subjects cannot legitimately be carried out unless the importance of the objective is in proportion to the inherent risk to the subject. Every biomedical research project involving human subjects should be preceded by careful assessment of predictable risks in comparison with foreseeable benefits to the subject or to the others. Concern for the interest of the subject must always prevail over the interest of science and society. The right of the research subject to safeguard his/her integrity must always be respected. Every precaution should be taken to respect the privacy of the subject, to minimize the impact of the study on the subject’s physical and mental integrity and on the personality of subjects. Doctors should abstain from engaging in research projects involving human subjects unless they are satisfied that the hazards involved are believed to be predictable Doctor should cease any investigation if the hazards outweigh the potential benefits. In publication of results of his/her research, the doctor is obliged to preserve the accuracy of his results. Reports of experimentation that are not in accordance with the principles laid down in this declaration should not be accepted for publication. In any research on human beings, the subject must be adequately informed of the aims, methods, anticipated benefits, potential hazards of the study and discomfort it may entail and that he/she is at liberty to abstain from participation in the study and is also free to withdraw consent to participation at any time. The doctor should then obtain the subject’s freely given informed consent in writing. The doctor should be particularly cautious if the subject is in a dependent relationship to him/her or may consent under duress. In that case, an independent doctor who is not engaged in the investigation and is completely independent of his official relationship should take informed consent. In case of legal incompetence, informed consent should be obtained from a legal guardian in accordance with national legislation. If the
person is physically or mentally incapacitated and cannot give informed consent or when the subject is minor, permission from the responsible relative replaces that of the subject in accordance with national legislation. The research protocol should always contain a statement of ethical considerations involved and should indicate that the principles enunciated in the present Declaration are complied with. Medical research combined with professional care (clinical research) In the treatment of the sick person, the doctor must be free to use a new diagnostic and therapeutic measure, if in his/her judgment it offers hope of saving life, reestablishing health or alleviate suffering The potential benefits, hazards and discomfort of a new method should be weighed against the advantages of the best current diagnostic and therapeutic methods. In any medical study, every patient including those of a control group, if any should be assured of the best-proven diagnostic and therapeutic methods. The refusal of the patient to participate in a study must never interfere with the doctor-patient relationship. If the doctor considers it essential not to obtain informed consent, the specific reasons for this proposal should be stated in the experimental protocol for transmission to the independent committee. The doctor can combine medical research with professional care, the objective being the acquisition of new medical knowledge only to the extent that medical research is justified by its potential diagnostic or therapeutic value for the patient. Non-therapeutic biomedical research involving human subjects (Non-clinical biomedical research) In the purely scientific application of medical research carried out on a human being, it is the duty of the doctor to remain protector of the life and health of that person on whom biomedical research is being carried out. The subjects should be volunteers, either healthy persons or patients for whom the experimental design is not related to the patient’s illness. The investigator and the
Irritant Poisons 35 investigating team should discontinue the research if in his/her or their judgment it may, if continued be harmful to the individual. In research on man, the interest of science and society should never take precedence over consideration related to the well being of the subjects Salient features of Helsinki Declaration Extensive animal research is an absolute prerequisite to the use of an innovative technique in the treatment of human beings. The most difficult innovative cases will be those in which prior animal research is impossible or would be uninformative. The treatment should be given cautiously and its after effects noted and appreciated. Experiment on volunteers can only be justified if they do no significant harm to the subject and the results are likely to be beneficial. It would be unethical to do something merely by way of experimentation that is which is not strictly related to cure patient’s illness. There must also be no great risk in proposed experimentation even if the patient consents to run the great risk. In considering whether a new treatment is as efficacious as an old one, side effects of the two treatments and their costs should be considered. ICMR Guidelines for Human Research 1995 The ICMR has laid down certain ethical guidelines for biomedical research on human subjects. It states that medical and related research using human beings should necessarily ensure that: The purpose of such research is directed towards the increase of knowledge about human conditions in relation to its social and natural environment. The research is conducted under such conditions that the subjects are dealt with in a manner conducive to and consistent with their dignity and well being. The research must be subjected to a regime of evaluation at all stages. General Principles Principle of Essentiality Whereby the research is considered absolutely
essential after a due consideration of all factors and options involved. Principle of Voluntariness, Informed Consent and Community Agreement Whereby, the subjects are fully apprised of the research and the impact and risks on him and others; and he retains the right to abstain from further participation in the research irrespective of any obligation they may have entered, subject to only minimal restitutive obligations of any advance consideration received. Principle of Non Exploitation Whereby as a general rule the research subjects are remunerated for their involvement in the research or experiment. Principle of Privacy and Confidentiality Whereby, the identity and records of the subjects are kept confidential as far as possible. Principle of Precaution and Risk Minimization Whereby, due care and caution is taken at all stages of a research to ensure that the subjects are put to minimum risk and generally benefit from the experiment. Principle of Professional Competence Whereby, the research is conducted at all times by competent and qualified persons who act with total integrity and impartiality and who have been made aware of the ethical considerations. Principle of Accountability and Transparency Whereby, the research experiment will be conducted in a fair, honest, impartial and transparent manner after full disclosure of all aspects of their interest. Principle of Maximization of Public Interest and of Distributive Justice
36 Textbook of Forensic Medicine and Toxicology Whereby, the research or experiment and its subsequent applicative use are conducted and used to benefit all human kind. Principle of Institutional Arrangement Whereby, there shall be a duty on all persons connected with the research to ensure that all the procedures required to be complied with and all institutional arrangements required to be made in respect of the research and its subsequent use or application are duly made in a transparent manner. Principle of Public Domain Whereby, the research is brought into public domain so that its results are generally made known through scientific and other publications. Principle of Totality of Responsibility Whereby, the professional and moral responsibility, for the due observance of all the principles, guidelines and prescriptions rests with all those involved in conducting the experiment. Principle of Compliance Whereby, there is a general and positive duty on all persons, conducting with any research entailing the use of a human subject to ensure that these guidelines are adhered in letter and spirit. Long Question 1. What are the functions Indian Medical Council? 2. What are duties of a Registered Medical Practitioners? 3. What is infamous conduct in professional respect? When is warning notice issued to registered Medical Pratitioner? 4. Define negligence and how will you prove it? 5. Describe the precautions one can take to prevent negligence. 6. What is consent? Described the “Doctrine
of informed consent.” 7. Discussed the salient features of consumer protection Act. 8. Define consent, the various types of consent, laws in relation to consent and the general rules to be followed for taking consent. 9. Discuss the professional and ethical duties and conduct of a medical practitioner. 10. Discuss medical negligence in detail. Enumerate the various types of negligence. Short Questions 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12.
Informed consent. Vicarious liability. Professional secrecy. Privileged communication. Contributory negligence. Human experimentation. Consent. Consumer protection Act. Indian Medical Council Act. State Medical Councils. Functions of Medical Council of India. Differentiate between Civil and Criminal Negligence.
Irritant Poisons 37
38 Textbook of Forensic Medicine and Toxicology MULTIPLE CHOICE QUESTIONS
1. In case of an unconscious patient with head injury requiring emergency surgery with no relative to give consent, the doctor should: A. Not operate at all B. Operate only with consent of police C. Operate only with Medical Superintendent’s consent D. Operate without consent 2. Professional death sentence is given for: A. Murder B. Rape C. Infamous conduct D. bestial*ty 3. The law does not consider the following doctrine in a charge of criminal negligence: A. Vicarious Liability B. Novus-actus interveniens C. Contributory negligence D. Res-ipsa-loquitor 4. Which of the following section of I.P.C. deals with criminal negligence? A. Sec.302 B. Sec.304 C. Sec.304-A D. Sec. 306 5. Paternalism means: A. Abuse of medical knowledge, so as to deprive the patient to make a choice B. Absence of reasonable care and skill C. To obtain informed consent D. To operate without patient’s consent 6. Indian Medical Degrees Act was passed in the year A. 1916 B. 1920 C. 1925 D. 1930 7. The functions of Indian Medical Council is to: A. Maintain a medical register B. Maintain the standard of medical education C. Recognize the foreign medical education D. All of the above 8. Warning notice is issued to a medical officer in cases of: A. Adultery B. Conviction by a Court of law for offences
9.
10.
11.
88.
89.
90.
91.
1 D
2 C
3 C
4 C
5 A
6 A
involving moral turpitude C. Dichotomy D. All of the above The Indian Medical Council Act was passed in the year: A. 1932 B. 1956 C. 1960 D. 1972 Warning notices is issued to a medical practitioner in cases of: A. Association with manufacturing firms B. Addiction C. Doing practice under the influence of alcohol D. All of the above Prescribing an overdose of medicine is an example of: A. Doctrine of Res-ipsa-loquitor B. Doctrine of common knowledge C. Medical maloccurence D. None of the above A patient of head injury has no relatives and requires urgent cranial decompression, doctor should: A. Operate without formal consent B. Take police consent C. Wait for relatives, to take consent D. Take magistrate’s consent A boy attempts suicide. He is brought to a private doctor and he is successfully cured Doctor should: A. Inform police B. Reporting not required C. Report to magistrate D. Refer to a psychiatrist Disciplinary action in professional misconduct of an anesthetist may be taken by: A. Surgeon B. Medical Superintendent C. Judicial Magistrate D. State Medical Council Dying declaration can be recorded by: A. Medical officer
7 D
8 B
9 B
10 D
11 A
Irritant Poisons 39
92.
93.
94.
95.
B. Magistrate C. Police officer D. Any of the above ‘Dying declaration’ is: A. Always made to magistrate B. Cross examination is not permitted C. Has more value D. The person is under oath Privileged communication is given for all of the following except: A. Negligence suite B. Preventing a person suffering STD from taking a job as a car driver C. Benefit of society D. A doctor for saving himself in court of law A doctor repeatedly advertising about his professional expertise in newspaper is doing: A. Dichotomy B. Civil negligence C. Infamous conduct D. Privileged communication All the following can be used as defense in a case of criminal negligence by a doctor except: A. Therapeutic misadventure B. Unforeseeable complication C. Error of judgement D. Contributory negligence
40
4
Textbook of Forensic Medicine and Toxicology
Part 1—Forensic Medicine and Pathology
Moment of Death THANATOLOGY Thanatology is the branch of science that deals with death in all its aspects. Death The definition of death created little or no problem for centuries until 1960 when organ transplantation caused minute scrutiny to be director at the phenomenon of death itself. Section 46 I.P.C. states says that death denotes the death of a human being unless the contrary appears from the context. Section 2(b) of the Registration of Births and Deaths Act defines death as ‘permanent disappearance of all evidence of life at any time after live birth has taken place. Black’s law dictionary (Black 1951) in United States defines death as “The cessation of life, the ceasing to exit”, defined by physicians as total stoppage of circulation and cessation of vital functions, there upon such as respiration and pulsation. Shapiro (1969) defined death as ‘the irreversible loss of the properties of living matter. However, it is difficult to appreciate his claim that this definition satisfies the practical requirements for death certification.
Calne (1970) gave a more practical definition that states ‘when destruction of the brain has been established, the individual has died no matter what the state of the rest of his body, giving four signs for such a diagnosis: 1. Deep, irreversible coma with fixed, dilated pupils and absent cranial nerve reflexes. 2. No spontaneous respiration 3. Absence of electrical brain activity 4. Cessation of circulation through the retina. Rentoul and Smith (1973) defined death as ‘complete and persistent cessation of respiration and circulation’ In a case of Smith v/s smith: In a fatal automobile accident both husband and wife sustained injury. Husband died on the spot and the wife was taken to the hospital where she remained unconscious for 17 days and then died. The petitioner argued that the deaths were simultaneous, since there was no evidence of brain activity after accident and the physicians were unsuccessful to revive her by resuscitation. The inference was that resuscitative efforts were maintaining the body in a state of animation although it could not be shown that life existed. The Court did not accept the contention. They quoted Black’s definition of death and stated that breathing though unconsciousness is not dead.
Moment of Death The living body depends upon on the integrity of three principal interdependent systems circulation, respiration and enervation. Failure of one of them will cause failure of the other two. This leads to the death of the individual. There are two phases of death: 1. Extinction of the personality is immediate sign of vital process—Somatic death. 2. Progressive disintegration of the body tissue—Molecular death or cellular death that occurs sometimes later. Somatic Death This is the form of death referred to in common parlance. The issue of its occurrence might have considerable legal implications, but the decision when death has occurred is always a medical one. Its onset is usually not difficult to detect even by lay people if the dying person is under observation during the last minute of life. It is said to have occurred when a final expiration is followed by continuous immobility of the chest, loss of pulse, alteration of the features. These changes indicate that respiration and circulation have been stopped and the brain will stop functioning if it has not been so. Residual heart movement is not of practical importance as they are insufficient to maintain the circulation. Somatic death can be detected by ECG that will stop within minutes. The recent development in medical techniques has posed a number of problems, where as for so many years it was accepted that death has occurred if respiration and circulation have ceased for more then 10 minutes. Now it is possible for methods of cooling the whole body to 15oC or 59oF or less to stop the heart and respiration for an hour or longer and restart them again at will. During this period, ECG and EEG shows no electrical activity and body looks like a corpse. This leads to the view that it is not the cessation
41
of the respiration or circulation but it is their failure to return that indicates death. Thus we are driven from a positive to negative approach. Therefore, the doctor while taking decision must satisfy himself that not only respiration and circulation has stopped, but their failure has persisted to such a period that under no circ*mstances it is possible for the person to come to life again. Finally death can be defined as “Permanent and irreversible stoppage of tripod of life”. The diagnosis of death by auscultation of the chest can be difficult in cases of excessive fat, emphysema, apex beat below the rib, poorly beating heart and shallow diaphragmatic respiration. All these conditions damps the conduction of heart sound with body wall. Diagnosis of recent death is also very difficult whenever the death of the person has not been observed. Whenever a doctor is called to certify a patient as dead that is brought by ambulance, he must insist that the body must be removed to a well-–lit room where he can carry out his examination. Even though the condition is satisfactory, the error can occur in the examination. The signs of life can be detected by special methods like Oscilloscope, ECG, and EEG etc. It can never be assumed that attempted resuscitation is pointless. On the other hand, resuscitative measures should always be continued for half an hour. In cases of electric shock and drug overdose, treatment should continue until death. In a case of a young women 23 years found lying on a beach at 8:10 AM near Liverpool apparently dead, police was informed. The doctor failed to see any movement for 15 minutes and certified her dead. A pathologist came later examined and agreed with the diagnosis. About two hours later when the postmortem was to start, one of the person noticed flickering of eyelids and formation of tear. She was immediately taken to intensive care unit
42
Textbook of Forensic Medicine and Toxicology
where she was survived. On investigation, it was found to be a case of overdose of barbiturate. This case emphasizes the importance of examination of the body by the doctor before certifying it. If the doctor fails to detect heart sound or respiration after adequate auscultation, he must see rectal temperature. When the rectal temperature is below 75oF (23.9oC) it is to be diagnosed as dead. On Ophthalmoscopic examination, there is segmentation of blood in retinal blood columns. If still there is any doubt, the patient should be taken to intensive care unit for further investigation of heart and brain function. Major N.C. Kapoor reports a case of resuscitation after cessation of vital functions for 15 minutes. A Hindu 80 years old male was brought to medical college, Calcutta at 10 PM on July 13, 1925 suffering from severe dyspnoea resulting from laryngeal obstruction due to malignant growth. Tracheostomy was done immediately when he suddenly stopped breathing. No heart sounds were audible on auscultation, pupils were dilated and eyes were fixed. Artificial respiration was started and tracheostomy was performed when he was apparently dead, the chest was being flickered by wet towel, there was no pulse at the wrist. After 15 minutes when every body had given up the hope, patient’s chest was flicked in a forcible manner and the patient took a shallow breath. The heart sounds were audible and pulse was palpable. Molecular Death The occurrence of clinical death implies the failure of the body as an integrated system. For some time afterwards, life continues in the separate tissues, which constitute the body. These only die after varying periods depending upon the ability of the tissue to function without blood supply. This is called molecular or cellular death.
The nervous tissue dies rapidly and the vital centers die in about 5 minutes. The muscle live longer and they will contract to direct electrical stimuli up to 3 hours. The corneal reflex and papillary reflex disappear at the time of death. The pupil reacts to the drugs like atropine that causes dilatation up to 4 hours and esrine that causes contraction up to 1 hour. The cornea can be removed for transplantation up to 6 hours and blood can be transfused for up to 6 hours of death. Therefore, we die in bits and pieces. The legal definition of death depends upon the diagnosis of somatic death. The distinction between somatic and molecular death becomes important because in order to remove essential tissues and organs for transplantation there is a relatively short time for the biological properties of living matter to persist after somatic death. With somatic death, there is complete generalized anoxia of the tissue and consequently stoppage of metabolic process carried out by the tissue cells. The metabolic process of the ganglionic cells stops in minutes, which are most sensitive where as that of connective tissue stops in hours, which are the least sensitive. Errors in Diagnosis of Death Generally, there is no difficulty in the diagnosis of somatic deaths. However, in some cases the heart sounds and breath sounds diminish greatly. Errors occur if proper clinical examination is not done or hurriedly done in patients with kidney failure and Cheyne-stockes respiration etc. Nevertheless, there are occasions when the distinction between death and suspended animation poses a real difficulty. Suspended Animation This is a death like state in which vital functions of the body are at such a low pitch that they can not be determined by ordinary methods of clinical
Moment of Death examination. Practitioners of yoga can induce this death like state voluntarily. In addition it can be involuntarily due to (i) Severe shock following accident (ii) Electrical shock (iii) Poisoning— barbiturate (iv) Drowning (v) Epilepsy (vi) Sunstroke (vii) Cholera and (viii) Hysteria Suspended animation lasts for seconds to hours and by ordinary clinical methods, distinction is not possible. Importance of Moment of Death 1. The classical concept of so called tripod of life does not hold good now as lungs and heart could be maintained on artificial support system. Any attempt to determine the moment of death in such patients by the help of classical criteria results in a stalemate. Dr Christian Bernard did the first heart transplant on 3rd December, 1967 in Cape town. 2. The second major factor responsible for a fresh appraisal of moment of death is the growing practice of organ transplantation. A beating heart, which is the ideal specimen for transplantation can not be taken out of an individual because of i. If we were to apply to classical criteria, because the heart is beating in the prospective donor, he is obviously not dead, ii. On the contrary, if we wait for his heart to stop to resolve the ethical dilemma, the heart becomes useless for transplantation and chances of such a heart surviving in the recipient are very dim. Therefore, the people of all over the world were trying to fine out the legal definition of death, as most of the countries had no such definition. In 1968 Bruce Tucker, a labourer fell down from a multistory building. His heart was taken out by the transplantation team while it was beating being declared brain dead on the ground of extensive Cranio-cerebral damage. His brother William
43
Tucker appealed in the Court in the State of Virginia, USA. The Court verdict was that doctor had not acted lawfully. The jury has directed by the Court decided on the facts of the case and opined that a person having suffered irreparable brain damage and whose bodily function can not be sustained without continuous artificial assistance is dead. Therefore, the loss of brain function was taken into account for declaring a person dead. Before coming to the modern concept of moment of death, we consider two questions. 1. What is it that is so central to your humanity, that when you loose it you are dead? 2. Whether death is an event or process. If we consider death to be an event then the end point of existence is very clear and sharp. Nevertheless, the 50 trillion cells of the body do not die at a time. Probably they die turn by turn. Therefore, how many cells whether 10%, 20% or 90% will die to declare an individual dead? Is there any point of no return after which no artificial means will be able to revive the person and will be called dead? Let us clarify the fact with an example: What we call a person who has just been decapitated but whose heart is still beating. If we go by the concept of point of no return, we would pronounce him dead but if we go by old method, he is not dead. It is absurd to wait for asystole in a decapitated man who has reached the “point of no return”. Therefore, the modern concept of brain death is now taken into account. Brain Death Philadelphia Protocol (1969) It determined death on the basis of: 1. Lack of responsiveness to internal and external environment 2. Absence of spontaneous breathing movements for 3 minutes, in the absence of
44
Textbook of Forensic Medicine and Toxicology
hypocarbia and while breathing room air. 3. No muscular movements with generalized flaccidity and no evidence of postural activity or shivering. 4. Reflexes and responses: i Pupils fixed, dilated, and nonreactive to strong stimuli ii. Absence of corneal reflexes iii. Supra-orbital or other pressure response absent (both pain response and decerebrate posturing) iv. Absence of snouting and sucking responses v. No reflex response to upper and lower airway stimulation vi. No ocular response to ice water stimulation of inner ear. vii. No superficial and deep tendon reflexes. viii. No planter responses 5. Falling arterial pressure without support by drugs or other means 6. Iso-electric EEG (in the absence of hypothermia, anaesthetic deaths, and drug intoxication) recorded spontaneously and during auditory and tactile stimulation. Further, it was added that these criteria shall have been present for at least 2 hours and two physicians other than the physician of a potential organ recipient should certify that death. As the protocol insists on a two hour delay, this precludes the use of any organs for transplantation. The concept of brain death goes back as far as 1959 when two French physicians Moll-ret and Loudon described a condition “Coma depasse” that is literally a state beyond coma. Again, the adhoc committee of Harvard Medical School revived it. The committee was constituted mainly after Bruce Tucker’s case and incorporates surgeons, anesthetists, forensic expert, legal personnel, philosophers etc. It was declared that it is futile to cling to the older concept, as heart and lungs could be maintained indefinitely. It was declared in fact that the brain
was synonymous with the individual, and the death of the brain should be equated with the death of the individual. Brain was considered superior to heart and lungs because 1. Brain is the seat of consciousness and hence of the individuality of the person. 2. Brain cannot be kept on artificial support, making stoppage of its functioning irreversible. 3. Brain controls, integrates and coordinates the whole body system, making it master of the orchestra, so to say. Then it was necessary to formulate criteria, which would indicate brain death known as Harvard Report (1968). Harvard Criteria 1. Unreceptivity and unresponsivity: Total unawareness to externally applied stimuli and inner need and complete unresponsiveness to even the most intense painful stimuli. 2. No movements: No spontaneous muscular movements in response to stimuli such as pain, touch, sound or light for a period of at least one hour 3. Apnoea: Absence of spontaneous breathing for at least one hour and when patient is on ventilator, the total absence of spontaneous breathing may be established by turning off the respirator for 3 minutes and observing whether there is any effort on the part of the subject to breath spontaneously 4. Absence of elicitable reflexes: Irreversible coma with abolition of central nervous system activity is evidenced in part by the absence of elicitable reflexes. The pupils are fixed and dilated and does not respond to a direct source of bright light. Ocular movement and blinking are absent. There is no evidence of postural activity. Corneal and pharyngeal reflexes are also absent. Stretch tendon reflexes also
Moment of Death cannot be elicited. 5. Isoelectric EEG: Has confirmatory value All these tests should be repeated after 24 hours with no change. Further its is stressed that the patient be declared dead before any effort is made to take him off the ventilator if he is then on a ventilator. This declaration should not be delayed until he has been taken off the respirator and all artificially stimulated signs have ceased. By this time all over the world, it was agreed that brain death was indeed equivalent to individual death. However, they did not agree regarding the criteria fixed by Harvard school. There are three distinct school of diagnosing death: 1. French school that is similar to Harvard 2. English school that is similar to Harvard 3. Austro-German school that includes Harvard criteria and bilateral serial angiography of internal carotid and vertebral artery criteria. A negative angiogram for more than 15 minutes proves death. Critical Issues Involving Brainstem Death Since the brain contains 14 billion neurons, how many neurons should be dead to declare a person dead and should one wait until the last neuron is dead? It was argued that even if one neuron is alive that shows electrical activity you cannot pronounce a person dead. Conversations told that yes, even if one neuron is alive, electrical activity could be recorded and the person should not be declared as dead. However, the argument that remained was that how much human one remains after loosing 90% of the brain’s tissue. In addition, it was argued that since we do not know where the seat of consciousness lies, it is only reasonable to assume that some consciousness does remain even if a single neuron is left.
45
Then a new school emerged known as American school, led by Mohandas and Chou in 1971 that summarized the criteria of brain death at the University of Minnesota Health Services Center. Minnesota Criteria (1971) The criteria for brainstem death was formulated by Mohan Dass and Chou as follows: 1. Known but irreparable intracranial lesion. 2. No spontaneous movement 3. Apnea when tested for a period of 4 minutes at a time 4. Absence of brainstem reflexes: i. Dilated and fixed pupil ii. Absent corneal reflexes iii. Absent Doll’s head phenomenon iv. Absent ciliospinal reflexes v. Absent gag reflex vi. Absent vestibular response to caloric stimulation vii. Absent tonic neck reflex 5. EEG not mandatory 6. Spinal reflex not important 7. All the findings above remain unchanged for at least 12 hours Brain stem death can be pronounced only if the pathological processes responsible for states 1 through 4 above are deemed irreparable with presently available means The basic teaching of the American school was not the brain, but the brain stem death, after which there is the point of no return that should be equated as death. There were several reasons for this equation: 1. Medullary neurons are most resistant to anoxia, if they are dead, then higher centers are also dead. 2. Brain stem is responsible for the vital functions because the respiratory center and circulatory center are present. 3. Brain stem is necessary for proper
46
Textbook of Forensic Medicine and Toxicology
functioning of the cortex as all sensory and motor nerves pass through this gateway. Immediately after an individual is put on respirator and other life support system, a systemic examination is done to exclude the possibility of brain stem death. If Minnesota criteria are fulfilled, life support systems to be withdrawn and the person is to be declared dead. Brain Stem Death and Organ Transplantation For centuries, there has been a dread of being declared dead while still alive. However, it is only since 1959 that there have been conceptual and practical problems with the diagnosis of death following the description of “brain death”. The ability to ventilate brain dead bodies in intensive therapy units preceded the developments of transplant surgery. The concept of brain death is not simply a convenience invented to satisfy the demands of transplant surgeons. The diagnosis of death is traditionally made using the triad of Bichat that states that death is “the failure of the body as an integrated system associated with the irreversible loss of circulation; respiration and enervation”. This is also known as somatic death or clinical death. Death is now accepted as synonymous with brain stem death. The brain stem is a small area of the brain that controls respiration and circulation. If this area is dead, the person will never be able to breathe spontaneously or regain consciousness. Molecular death may be defined as “the death of individual organs and tissues of the body consequent upon the cessation of circulation”. Different tissues die at different rates depending on their oxygen requirement. Thus, within four minutes of the blood supply to the brain ceasing the central nervous system is irreversibly damaged. Some authorities recognize a third concept of
apparent death that is also known as a suspended animation. It may occur under certain specialised conditions for example drowning or hypothermia. Severe brain damage which does not involve the brain stem may result in a persistent vegetative state”. These patients breathe spontaneously, open and close their eyes, swallow and make facial grimaces. However, they show no behavioural evidence of awareness. It is in these cases that the moral dilemma of “allowing some one to die” arises. The above dilemma does not apply to those who are brain stem dead. These patients are dead irrefutably and unequivocally. Switching off a ventilator under these circ*mstances would not kill the patient but would discontinue ventilating a corpse. In 1976 the Conference of the Medical Royal Colleges and Faculties of the United Kingdom issued guide lines on the subject of brain stem death. These guide lines are regularly updated and used by doctors in intensive care units throughout the UK. Diagnosis of Brain Stem Death Exclusions 1. Where the patient may be under the effects of drugs e.g. therapeutic drugs or overdoses 2. Where the core temperature of the body is below 35°C e.g. exposure. 3. Where the patient is suffering from severe metabolic or endocrine disturbances which may lead to severe but reversible coma e.g. diabetes. Preconditions of diagnosis 1. The patient must be deeply comatose. 2. The patient must be maintained on a ventilator. 3. The cause of the coma must be known. Personnel who should perform the
Moment of Death tests
47
1. The brain stem death tests must be performed by two medical practitioners. 2. The doctors involved should be experts in this field. Under no circ*mstances are brain stem death tests performed by transplant surgeons. 3. At least one of the doctors should be of consultant status. Junior doctors are not permitted to perform these tests. 4. Each doctor should perform the tests twice.
stem is incapable of reacting to the presence of the carbon dioxide and is thus dead. Once two doctors have performed these tests twice with negative results, the patient is pronounced dead and a death certificate can be issued. It is at this stage that a decision concerning the use of organs for transplantation purposes may be raised and the decision made as to the whether the corpse should be maintained on the ventilator until the organs may be harvested.
Tests to be Performed
Organ Transplantation
Before the tests are performed the core temperature of the body is taken to ensure that it is above 35°C. The diagnosis of brain stem death is established by testing the function of the cranial nerves which pass through the brain stem. If there is no response to these tests the brain stem is considered to be irreversibly dead. 1. The pupils are fixed in diameter and do not respond to changes in the intensity of light. 2. There is no corneal reflex. 3. The vestibulo-ocular reflexes are absent, i.e. no eye movement occurs after the installation of cold water into the outer ears. 4. No motor responses within the cranial nerve distribution can be elicited by painful-or other sensory stimuli, that is the patient does not grimace in response to a painful stimulus applied to or to the limbs. 5. There is no gag reflex to bronchial stimulation by a suction catheter passed down the trachea. 6. No respiratory movements occur when the patient is disconnected from the ventilator for long enough to ensure that the carbon dioxide concentration in the blood rises above the threshold for stimulating respiration i.e. after giving the patient 100% oxygen for 5 minutes the ventilator is disconnected for up to 10 minutes. If no spontaneous breathing of any sort occurs within that 10 minutes the brain
Advances in medicine have enabled the use of several organs for transplant purposes. It is now possible to harvest from a cadaver the eyes, kidneys, liver, pancreas, small intestine, lungs and heart. From the living donor it is possible to transplant one kidney. The cornea of the eye may still be suitable for transplant up to 24 hours after death, other organs such as the heart, are very sensitive to low oxygen levels and deteriorate very quickly following the cessation of circulation. It is this, which has led to the controversy regarding the ventilation of corpses prior to harvesting of organs. To prevent premature declaration of death by the physician eager to obtain organs for his patients, due precautions have been incorporated in The UK Human Tissue Act 1961 and in India, the Anatomy Act 1984 and The Human Organ Transplantation Act 1994 that covers transplantation of human organs. The UK Human Tissue Act 1961 It states that If a person, either in writing at any time or orally in the presence of two or more witnesses during his lifetime has expressed a request that his body or any specified part of his body might be used after his death for therapeutic
48
Textbook of Forensic Medicine and Toxicology
purposes or for purposes of medical education or research, the person lawfully in possession of his body after his death may unless he has reason to believe that the request was subsequently withdrawn, authorize the removal from the body of any part or, as the case may be, the specified part; for use in accordance with the request. British Department of Health has issued cards for donors to carry, indicating their wish to donate organs, if they died. This Act also provides for obtaining permission for postmortem examination when no medicolegal investigation is being carried out. The person who is legally in charge of the body such as hospital authorities may give permission for autopsy if they are satisfied after reasonable enquiry that there are no surviving close relatives and that the deceased had not objected to such an examination during his lifetime. Memorandum of British transplantation society British transplantation society has issued a memorandum that states that Human Tissues Act should be amended to clarify the legal aspects. The society has proposed ‘Codes of Practice’ for organ transplantation with salient features as: 1. Two doctors who are not members of the transplantation team should do the certification of the death of the donor and of the two one should be qualified for at least five years. 2. As far as decision of switching of the respirator is concerned, it should entirely base on the decision of the treating physicians. This decision should have no connection with the requirements for transplantation. 3. When it is decided to switch off the ventilator, the willingness for organ donation should be discussed with the relatives 4. The surgeon of the transplantation team should ensure that the death has already occurred and the deceased had requested for the
donation during his lifetime and that the relatives now has no objection in removal of the organs for the purpose of transplantation. 5. In situations where relatives object to the decision of the deceased for removal of his organs for transplantation, their decision should be respected. 6. In a medicolegal case, the coroner’s permission should be obtained before removing the organs and the surgeon should report any matter of medicolegal significance to the authorities. The Transplantation of Human Organs Act 1994 This Act came into force on February 4, 1995 and gave a legal recognition to brainstem death. 1. The Act defines brainstem death as a stage at which all the functions of the brainstem have permanently and irreversibly ceased but organ can sustain life on life support systems. The salient features of the Act are 2. Section 3 (6) of the Act provides that the organs from the body of a donor can only be removed after the Board of Doctors certify regarding the brainstem death of the deceased. According to Section 3(6): ‘Where any human organ is to be removed from the body of a person in the event of his brainstem death, no such removal shall be undertaken unless such death is certified, in such form and in such manner and on satisfaction of such conditions and requirements as may be prescribed by the Board of medical experts consisting of the following: i. The registered medical practitioner in charge of the hospital in which brainstem death has occurred ii. An independent registered medical
Moment of Death
3.
4.
5.
6.
7.
8.
practitioner, being a specialist, to be nominated by the registered medical practitioner specified in clause (i), from the panel of names approved by the appropriate authority. iii. A neurologist or a neurosurgeon to be nominated by the registered medical practitioner specified in clause (i), from the panel of names approved by the appropriate authority, and iv. The registered medical practitioner treating the person whose brainstem death has occurred Section 3 (1) of the Act provides that any donor can authorize for the removal of his organs and utilisation only for therauptic purposes. Section 3(2): For donation of organs, the donor at the time of his death should request in writing for removal of organs from his body for transplantation in the presence of two or more witnesses, one of whom should be a near relative Section 3 (5) the human organs is to be removed from the body of the deceased person when the brainstem death has occurred and has been certified under sub Section 3(6) The donor who is at least 18 years of age can authorize such removal and parental consent is must in case of a minor. When any unclaimed or unknown body is lying in the hospital for more than 48 hours, the hospital-in-charge can authorize for such removal. When a postmortem examination is mandatory either for medicolegal or pathological purposes, the doctor conducting such an examination can authorize for the removal of organs after satisfying himself that the organs to be removed are not required for such examination. The
9.
10.
11.
12.
13.
14.
49
authorization for removal of organs is subject to no objection from the deceased before his death. The human organs removed from the body of the donor shall only be used for transplantation into the body of his near relative. For transplantation of organs removed from the body of a donor into the recipient other than the near relative, prior approval of authorization committee should be obtained. Registration is mandatory for the hospitals that are engaged in removal, storage and transplantation of human organs. In case, they violate any of the conditions specified in this Act, their registration is liable to be cancelled after proper inquiry. Any person or hospital who are associated in the removal of any human organ without authority shall be liable to punishment with imprisonment up to five years and also fine up to Rs 10,000/-. If a registered Medical practitioner is convicted for violating the conditions of this Act, his name would be removed from the medical register for a period of two years for first offence and permanently for subsequent offences. The Act also provide punishment for commercial dealing in human organs that is imprisonment for at least two years but may extend to seven years and fine not less than Rs 10,000/- extending to Rs 20,000/-.
MEDICAL CERTIFICATION OF DEATH The Registration of Births and Deaths Act, 1970 makes it obligatory for doctors to issue a death certificate certifying the underlying cause of death to the patient whom they have attended during his final illness after examination of the body. In our country, the form of certificate
50
Textbook of Forensic Medicine and Toxicology
required by statistical authorities for this purpose s based on the nomenclature agreed to by WHO in 1950 that has been in use in U.K. since 1927. According to this medical certification of cause of death is divided into two main parts Part I: Disease or condition directly leading to death Part II: Other significant conditions contributing to the death but not related to the disease or condition causing it. Part 1 is categorized into three subsections (a), (b) and (c) that are interrelated to each other and have a direct chain of causation between each other That (a) must be due to or be a consequence of (b) which is due to or a consequence of (c) Part 2 is any condition that is not related to part 1 but which is a significant factor in causation of death. In this certificate, the doctor should specify in part 1 the underlying pathological condition that led to the death. No clinical manifestations or mode of death should be included in part 1. Part 2 of the form should preferably be left blank unless there is any contributory factor in the death. The terms such as syncope, heart failure or cardiac failure should not be used on part 1 of the certificate. Most commonly, the physicians use the term cardio respiratory arrest that should not be used as everyone dies of stoppage of circulation and respiration. It is important to specify the underlying pathological cause of the cardiac or respiratory arrest. Similarly the term ‘coma’ is quite unacceptable as it a clinical symptom and not underlying pathological entity. Also the term ‘asphyxia’ should be avoided especially when it is not qualified by the underlying cause of death. Some of the older textbooks give account of the various modes of death but these are irrelevant in legal medicine. These are:
Bishop’s Classification of Modes of Death Death occurs due to the stoppage of the functions of any of the three main organs (Bishop’s tripod of life) namely heart, brain and lungs. Depending on the functions of these organs, the mode of death comprises of 1. Syncope: Failure of functions of heart with its circulatory system 2. Asphyxia: It comprises of failure of the respiratory system 3. Coma: Failure of nervous system signifies mode of death as coma Bishop laid emphasis on the mode of death or the three proximate causes of death. This classification is useful to the law enforcing agencies and nonprofessionals for interpretation of medical evidence as to cause of death.
EUTHANASIA The word euthanasia is derived from the Greek word ‘Eu’ meaning good and ‘thanatos’ meaning death. It means ‘good death’ or to ‘die well’, with the basic theme of ‘mercy killing. Euthanasia: is the intentional killing by act or omission of a dependent human being for his or her alleged benefit. (The key word here is “intentional”. If death is not intended, it is not an act of euthanasia It may be defined as the doctrine or theory that in certain circ*mstances when owing to disease, senility or the like, a person’s life has permanently ceased to be either agreeable or useful, the sufferer should be painlessly killed either by himself or by another. In the last decade, the use of advanced directives or living wills has become increasingly common. However, with these also problems can arise. All over the world and especially in North American continent, there is increasing support for euthanasia and its
Moment of Death
51
Voluntary euthanasia
Someone provides an individual with the information, guidance, and means to take his or her own life with the intention that they will be used for this purpose. When it is a doctor, who helps another person to kill himself or herself it is called “physician assisted suicide.” Euthanasia by Action: It is intentionally causing a person’s death by performing an action such as by giving a lethal injection. Euthanasia by Omission: It is intentionally causing death by not providing necessary and ordinary (usual and customary) care or food and water. What is not Euthanasia: There is no euthanasia unless the death is intentionally caused by what was done or not done. Thus, some medical actions that are often labeled “passive euthanasia” are no form of euthanasia, since the intention to take life is lacking. These acts include not commencing treatment that would not provide a benefit to the patient, withdrawing treatment that has been shown to be ineffective, too burdensome or is unwanted, and the giving of high doses of painkillers that may endanger life, when they have been shown to be necessary. All those are part of good medical practice, endorsed by law, when they are properly carried out.
When the person who is killed has requested to be killed with his consent
Views on Euthanasia
consequences. The medical profession finds itself caught in a conflict between the Hippocratic Oath and the question “whose life is it anyway?” Euthanasia evolves the strong feelings in every one including doctors. It can be classified based on the acts of induction as active and passive and based on the will of the patient as voluntary, involuntary and non-voluntary euthanasia Active Euthanasia (positive euthanasia) It is a positive merciful act, to end useless suffering or a meaningless existence. It is an act of commission that is when a doctor takes steps to end patient’s life e.g., giving large doses of drugs to hasten death. Passive Euthanasia (negative euthanasia) It means discontinuing or not using extraordinary life sustaining measures to prolong life. It includes acts of omission such as failure to resuscitate terminally ill or hopelessly incapacitated patient or a severely defective infant. It is not using measures that would probably delay death and permits natural death to occur.
Non-voluntary When the person who is killed made no request to be killed such as in persons incapable of making their wishes like persons in irreversible coma. Involuntary Euthanasia When the person who is killed made an expressed wish to the contrary. Assisted Suicide
There are both protagonist and antagonist views on euthanasia: 1. Protagonist views: It advocated euthanasia on the ground that the patient, if willing should be allowed to die a dignified death instead of prolonging the same through the torture of pain and disease. The protagonist plead that it is a tremendous economic and psychological burden on the patient’s relatives to support an incurable patient and have often expressed death wishes for such a patient. They also
52
Textbook of Forensic Medicine and Toxicology
argue that medical sciences too have its limitations and it cannot cure all the diseases. 2. Antagonists claim that Medical science has made such a rapid progress and its capabilities are so great that the disease, which seems incurable today, will become curable tomorrow. They remind the doctor of the code of medical ethics and Hippocratic Oath by which the doctor swears to preserve the life and prevent further damage. They remind that euthanasia is against religion and that the crimes against society would increase and would amount to legalizing murder and suicide. If legalized euthanasia could be misused by doctors coming with hand in hand with relatives for material gains or otherwise. It may also encourage people to commit suicides.
3.
4.
History of Euthanasia 1. About 400 B.C, The Hippocratic Oath was given as “I will give no deadly medicine to any one if asked, nor suggest any such counsel” 2. Swift, in his early 19th century treatise on the laws of Connecticut, stated, “If one counsels another to commit suicide, and the other by reason of the advice kills himself, the advisor is guilty of murder as principal.” This was the well-established common law view, as was the similar principle that the consent of a homicide victim is wholly immaterial to the guilt of the person who caused his death. The right to life and to personal security is not only sacred in the estimation of the common law, but it is inalienable. Moreover, the prohibitions against assisting suicide never contained exceptions for those who were near death. Rather, the life of those to whom life had become a burden, of those who were hopelessly diseased or fatally wounded and
5.
6. 7.
even the lives of criminals condemned to death, were under the protection of law, equally as the lives of those who were in the full tide of life’s enjoyment, and anxious to continue to live. Even the prisoner who persuaded another to commit suicide could be tried for murder, even though victim was scheduled shortly to be executed. The earliest American statute explicitly to outlaw assisting suicide was enacted in New York in 1828, and many of the new States and Territories followed New York’s example. Between 1857 and 1865, a New York commission led by Dudley Field drafted a criminal code that prohibited aiding a suicide and, specifically, furnishing another person with any deadly weapon or poisonous drug, knowing that such person intends to use such weapon or drug in taking his own life. In 1920, the book “Permitting the Destruction of Life not Worthy of Life” was published. In this book, authors Alfred Hoche, M.D., a professor of psychiatry at the University of Freiburg, and Karl Binding, a professor of law from the University of Leipzig, argued that patients who ask for “death assistance” should, under very carefully controlled conditions, be able to obtain it from a physician. This book helped support involuntary euthanasia by Nazi Germany. In 1935 the Euthanasia Society of England was formed to promote euthanasia. In October of 1939 amid the turmoil of the outbreak of war Hitler ordered widespread “mercy killing” of the sick and disabled. The Code named “Aktion T 4,” was the Nazi euthanasia program to eliminate “life unworthy of life” and it at first focused on newborns and very young children.
Moment of Death
8.
9.
10.
11.
12.
Midwives and doctors were required to register children up to age three who showed symptoms of mental retardation, physical deformity, or other symptoms included on a questionnaire from the Reich Health Ministry.” The Nazi euthanasia program quickly expanded to include older disabled children and adults. Hitler’s decree of October, 1939, typed on his personal stationery and back dated to September 1, enlarged ‘the authority of certain physicians to be designated by name in such manner that persons who, according to human judgment, are incurable can, upon a most careful diagnosis of their condition of sickness, be accorded a mercy death.’” In 1973 in America, the Patient Bill of Rights was created that includes informed consent and the right to refuse treatment. In Netherlands, Dr Gertrida Postma received life sentence for giving her dying mother a lethal injection In 1980, Pope John Paul II issued Declaration in euthanasia opposing mercy killing but permitted the use of painkillers to ease pain and the right to refuse life sustaining means. In California, the Hemlock Society founded by Derek Humphery advocated legal change and also distributed how to die information. Also the campaign for assisted dying was launched in America. Right to die societies was also formed in Germany and Canada. In 1984, the Netherlands Supreme Court approved voluntary euthanasia under certain conditions. In 1990, in America, the Medical Association adopted the position that with informed consent, physician can withhold or withdraw treatment from a patient near death. The Hemlock of Oregon introduced
53
the Death with Dignity Act. 13. In 1995 Australia’s Northern Territory approved a euthanasia bill 14. The euthanasia bill went into effect in 1996 and was overturned by the Australian Parliament in 1997. 15. In 1997, the U. S. Supreme Court ruling in the Washington v. Glucksberg was that “More specifically, for over 700 years, the Anglo American common law tradition has punished or otherwise disapproved of both suicide and assisting suicide.” 16. In 1998 the U.S. State of Oregon legalized assisted suicide. In Switzerland the firm Dignitas was established to offer physician -aided -suicide. 17. In 1999 Dr. Jack Kevorkian sentenced to a 10-25 year prison term for giving a lethal injection to Thomas Youk whose death was shown on the “60 Minutes” television program in America. 18. In the year 2000 the Netherlands legalized euthanasia. 19. In 2002 Belgium legalized euthanasia. Legal Scenario Around the World Laws in Australia World’s first law allowing voluntary euthanasia had come in to effect in Australia on July 1, 1996 under the Northern Territory Rights of the Terminally Ill Act. Northern Territory legislative assembly of Australia passed this Act on the morning of May 24, 1995 by a narrow margin of fifteen votes to ten. The first patient on whom this law was used was former carpenter Bob Dent 66 years old male who was suffering from cancer. In this case, a computer-operated machine was used to administer a lethal dose of drug on September 22, 1996. The bill remained until March 1997 and was overturned by the Australian Parliament. Seven patients have made
54
Textbook of Forensic Medicine and Toxicology
formal use of this bill and four died. All these seven patients had cancer and most were in advanced stages with symptoms of depression. The features of this bill were: 1. The patient should be of sound mind, terminally ill and at least 18 years old. 2. The patient must experience unacceptable pain, suffering or distress. 3. Four doctors must be involved in the patient’s decision to die 4. The attending physician must believe that patient has come to his decision voluntarily and he must inform the patient about his illness, prognosis and treatment available. 5. The second physician must confirm the diagnosis made by the first physician and the presence of psychiatrist is must. 6. There must be a seven-day cooling off period between the doctor signing off the decision for euthanasia and another two days before euthanasia procedure is performed. 7. A computerized system knows as the ‘Deliverance programme’ enables a fatal in injection to be administered by a computer and the doctor stands on one side. Laws and Practices in Netherlands In the Netherlands, the word euthanasia has a more limited meaning; it only refers to the deliberate termination of the life of a person on his request by another person that is active voluntary euthanasia. Due to this Netherlands has attracted so much attention and raised so much controversy. According to Dutch Penal code, euthanasia is a crime, however it is not classified as murder that is euthanasia is practically permissible but not legal. Royal Dutch Medical Association after discussion had made certain guidelines to be followed. These are: 1. The request for euthanasia must come from the patient and be entirely free and voluntary,
well considered and patient. 2. The patient must experience intolerant physical and mental suffering, with no prospect of improvement and with no acceptable solutions to alleviate patient’s situation. 3. A physician must perform euthanasia after consultation with an independent colleague who has experience in this field. 4. In 1990, a new procedure was agreed upon, according to which a physician informs the local medical examiner by mean of an extensive questionnaire, then reports to the district attorney. When he is satisfied that the criteria laid down by the Courts are compiled with, the public prosecutor will issue a certificate of no objection to burial or cremation. In other cases, he may order an investigation and decide to prosecute the case.
The medical care of demented patients in the last phase of life is primarily the duty of the physician. Nevertheless, in the year 2000, Netherlands legalized euthanasia Laws in United Kingdom The criminal law in U.K. regards as a potential offence of homicide any wrongful act which results in the loss of life. When life is taken deliberately, the person is charged with murder. If a doctor responds to a request from a patient to end his life and administers a lethal injection, the doctor will have acted with the necessary mens rea for murder. It makes no difference from the legal point of view that the patient gave his consent to the doctor’s act. Consent is no defence to a charge of murder nor does the doctor’s motive make any difference. The fact that there was a case of mercy killing does not affect the status of the cat as one of murder. The criminal law does not require doctors to persist in the treatment of a patient when no medical purpose is served by such persistence. All that is required
Moment of Death from legal point of view is that the patient be given appropriate medical treatment. Scenario in USA In the year 1994, right to die judgment was given in U.S.A when a New York Court struck down the state law prohibiting doctors for helping dying patients commit suicide. In 1997, the U.S. Supreme Court ruling in the Washington v. Glucksberg, opinion written by Chief Justice Rehnquist was ‘That suicide remained a grievous, though no felonious, wrong is confirmed by the fact that colonial and early state legislatures and courts did not retreat from prohibiting assisting suicide. The United States’ assisted suicide bans have in recent years been reexamined and, generally, reaffirmed. It seems that because of advances in medicine and technology, the Americans today are increasingly likely to die in institutions, from chronic illnesses. Public concern and democratic action are therefore sharply focused on how best to protect dignity and independence at the end of life, with the result that there have been many significant changes in state laws and in the attitudes, these laws reflect. Many States, for example, now permit “living wills,” surrogate health care decision making, and the withdrawal or refusal of life sustaining medical treatment. At the same time, however, voters and legislators continue for the most part to reaffirm their States’ prohibitions on assisting suicide Legal Status in India India has not come up with any legislation on euthanasia. Article 21 of the constitution of India has right to live as a natural right embodied in it. Recent Supreme Court judgment has clarified further on that. It says that article 21 guarantees ‘right to live’ but doesn’t in any way imply ‘right to die’
55
and hence extinction of natural life is illegal. As per this verdict suicide, assisted suicide or euthanasia are not permissible. However, Sec 92 of the Indian Penal Code prevents euthanasia. Sec 92 IPC provides immunity to doctors for any act done in good faith for the benefit of a person without his consent. But under the first and second sub clause of this section, which states that this exception doesn’t extend to the intentional causing of death, or attempting to cause death or for an act which is know to cause death. In effect it prohibits euthanasia. Long Questions 1. Discuss the medicolegal significance of thanatology. 2. Discuss in detail the moment of death with special reference to organ transplantation. 3. Define euthanasia. What are the various types? Discuss the legal status in India. Short Question 1. 2. 3. 4. 5. 6.
Brain death. Brain stem death. Suspended animation. Harvard criteria. The Human Organ Transplants Act 1989. Euthanasia.
56
Textbook of Forensic Medicine and Toxicology MULTIPLE CHOICE QUESTIONS
1. The first medicolegal autopsy was done in: A. Germany B . Italy C. India D. U.K. 2. The minimum amount of air required for fatal systemic air embolism is A. 50 ml B . 100 ml C. 150 ml D. 200 ml 3. Substance commonly used for preservation of viscera for toxicological purpose: A. 10% formalin B . Saturated solution of common salt C. 40% formalin D. Alcohol 4. ‘Triad of Bichat’ does not include: A. Respiration B . Circulation C. Innervation D. Reflexes 5. Harvard criteria doesn’t include: A. Unreceptivity and unresponsivity B . No movement for 3 hours C. Apnoea on 3 minutes off respirator D. Iso electric EEG 6. The Minnesota criteria for brain death were formulated in: A. 1960 B . 1964 C. 1971 D. 1976 7. Not a feature of brain death: A. Complete apnea B . Absent Pupillary reflex C. Absence deep tendon reflex D. Heart rate un-responsive to atropine
1 B
2 B
3 B
4 D
5 B
6 C
8. Suspended animation may be seen with: A. Electrocution B . Strangulation / hanging C. Drowning D. Bum 9. Surest sign of death due to antemortem hanging is: A. Cyanosis of face and lips B . Ligature mark around the neck C. Protruding tongue D. Trickling of saliva, down the angle of the mouth 10. Molecular death is: A. Complete and irreversible cessation of brain, heart and lungs function B . Death of individual tissues and cells after somatic death C. Vitals functions are at such a low pitch that can not be detected by routine clinical examination D. Total loss of EEG activity but heart is functioning 11. All are tests for stoppage of circulation except: A. Magnus test B . Winslow’s test C. Icard’s test D. Diaphanous test 12. Suspended animation: A. Is apparent death from which person can be aroused B . Is true death from which person cannot be aroused C. May last for days or weeks D. Cannot be produced voluntarily 7 8
9 10
11
12
6
Part 1—Forensic Medicine and Pathology
Identification Identification means to determine the individuality of a person. It is done by recognizing the physical characteristics. When the person is known by his name with complete address, it is known as complete identification. But in certain circ*mstances only other details like age, sex etc. can be established known as partial identification. The question of identification in living persons arises in criminal cases like assault, murder, rape etc. and even in new born cases when babies get interchanged. In civil cases like marriage, inheritance, insurance and disputed sex etc. identification plays an important role. In the dead especially unknown medicolegal cases, police plays an important role in the matter of identification. He has to investigate and advertise the details in the news media. He has to photograph and also take the fingerprints. He has to find out the relatives who identify the person before bringing the case to the doctors for medicolegal postmortem. Sometimes, the identification becomes very difficult if the body is destroyed or mutilated in fires, explosions and other mass disasters.
The following points are taken into consideration for the purpose of identification in a dead person: (i) Age (ii) Sex (iii) Religion (iv) Complexion (v) General development including stature (vi) Anthropometric measurements (vii) Fingerprints and footprints (viii) Superimposition (ix) Teeth (x) DNA fingerprinting and (xi) Personal belongings. In cases of living person in addition to the above features the following criteria are taken into consideration: (i) Speech and voice (ii) Handwriting (iii) Gait (iv) Habits (v) Memory and education. While establishing identification, it is advisable to use maximum number of criteria. There are methods available by which to establish positive undeniable identification that are: • Fingerprints, footprints, handprints and lip prints. • Dental patterns. • Frontal sinus pattern. • Skull suture patterns and vascular grooves. • Normal and abnormal bone comparisons. • Other fortuitous comparisons.
CORPUS DELICTI
To establish the identity of an individual, estimation of age is to be done that depends on: a. Physical or morphological features. b. Laboratory tests. c. Dental study. d. Ossification activity and growth of bones.
Corpus delicti refers to the body of the criminal offence, which is an essential part of the crime. It not only includes the body of the victim but also the weapon of offence, clothing, drawings and photographs of the deceased. The main purpose of corupus delicti is to establish the identity of the person. However, the Court has passed death penalty even though the body has not been recovered and identification not being established.
AGE
Physical or Morphological Features Physical feature include height and weight of the person. Starting from the intrauterine life up to
Identification certain periods of extra-uterine life, height and weight of the individual has some relationship with the age. Determination of Intrauterine Age Intrauterine age of the foetus can be calculated using the Hasse’s rule and Morrison’s rule. Rule of Hasse (1895): According to this rule the age of the foetus is calculated by the square root of the crown heel length in centimeters. For example if the crown heel length is 16 cm, the age of the foetus is about 4 weeks intra uterine life. Rule of Morrison (1964): On the other hand the rule of Morrison (1964) says that the crown heel length of the foetus in centimeters, divided by five gives the age in months. For e.g. if the length is 40 cm, the age is 8 months. It is applicable after 5 months. Intrauterine age is that period starting from time of conception up till delivery. The various terms used for the products of conception are: 1. Ovum: From fertilization till second week of gestation. 2. Embryo: From second week of gestation till third month of intrauterine life. 3. Fetus: From third month of gestation till full term. The age of the fetus can be determined by some of the features as given below: 1. End of 1st month (4th week): At the end of first month the length is 1 cm and the body is attached to chorion by a short chord weight is about 5 gms. 2 dark spots indicate the eyes and mouth is seen as a cleft. The beginning of formation of limbs is by four bud like processes. Fetus of this age cannot be detected in aborted material. 2. End of 2nd month (8th week): the length is about 4-5 cm and is of the size of hen’s egg. Weight is about 10 grams. At this age the human appearance can be demarcated from the limbs, mouth and nose. Feet and hands are webbed. Anus appears as a dark spot. Placenta starts forming with a longer
87
umbilical cord. Sex is indistinct. 3. End of 3rd month: the length is about 8 – 10 cm and weight about 30 gms. The head is separated from body by neck formation and there is formation of palate. Placenta is fully developed. Heart is 4 chambered. Alimentary canal is situated in the abdominal cavity. Sex bud appears. Limbs, finger and toes are well developed but nails remain as membranes. The centers of ossification for ischium, 1st, 2nd, 3rd sacral vertebras are present. 4. End of 4th month: length is 15 to 16 cm. weight is 100–120 gms. Sex is distinct skin is covered with fine downy lanugo hair. Ear ossicles are ossified. Centre of ossification for lower segments of sacrum appears. Skull bones are partly ossified. Brain convolutions begin to develop. Gall bladder is formed and meconium is found in duodenum. 5. End of 5th month: length is about 25 cms and weight 450 gms. Light hair appear over the scalp and downy lanugo hair cover whole of the body. The nails are distinct and soft. Skin is covered with vernix caseosa. Meconium is present at the beginning of large intestine. Centre of ossification appears for calcaneum and ischium. The germs of permanent teeth are present in jaw. 6. End of 6th month: length is about 30 cm and weight is 800gms to 1 kg. Skin is red and wrinkled. Eyelids are adherent but eyebrows and eyelashes begin to form. Gall bladder contains bile and meconium is present in upper part of large intestine which starts showing sacculation. testicl*s lie close to kidney. Centre of ossification for lower 4 divisions of sternum are present. Cerebral hemispheres cover the cerebellum. 7. End of seventh month (28th week): Length is about 35 cm and weight is 900-1200 gms. Eyelids are separate and eyelashes can be distinguished. The skin is dusky red in colour covered with vernix caseosa. Nails are distinct but do not reach the finger tips.
88
Textbook of Forensic Medicine and Toxicology
testicl*s descend in internal inguinal ring. Caecum is in right iliac fossa and meconium is in entire large intestine. Centre of ossification for talus is present. Cerebral convolutions are present. 8. End of eighth month (32 weeks): Length is about 40 cm and weight is 1.5-2 kg. Scalp hair is thick and skin is rosy red in colour and covered with soft lanugo hair except for the face. Nails reach tips of fingers, but not tips of toes. testicl*s reach external inguinal rings left testicl* may descend in scrotum. Meconium reaches the rectum. Cerebral convolutions are well developed. Centre of ossification for last sacral vertebra appears. 9. End of ninth month (36 weeks): Length is about 45 cm and weight is about 2.5 kg. The scalp is covered with thick dark hair. Downy hairs disappear on the body except on the shoulders. Vernix caseosa may be found in the joint flexures. Scrotum shows wrinkling and contains both the testicl*s. Meconium is found at the end of rectum. Centre of ossification of lower end of femur appears. Nails grow beyond tips of fingers but only tip of toes.
10. End of tenth month (40th week): Length is about 50-53 cm and crown rump length is 30-33 cms. Weight is about 2.5-4 kgs. Head circumference is 33 cms and scalp is covered with 3.5 cm long hair. Anterior fontanelle is 4 × 2.5 cm wide. Posterior fontanelle gets closed. Face is not wrinkled and lanugo hair is absent except on the shoulders. Cartilages are formed in nose and ear. Umbilicus is situated between pubis and xiphisternum. Scrotum contains testicl*s the vulva is closed and labia majora cover the labia minora and cl*tor*s. Rectum contains dark greenish or black meconium. Centre of ossification is present for upper end of tibia and cuboid (Table 6.1). Determination of Extrauterine Age A full term foetus is 19-20 inches (50cm) in length and 6-7 pounds by weight. At six months of age, it is 24 inches (60cm) and by one year of life it is 27 inches (68cm) in length. At the age of four years, the child becomes 40 inches (100cm) in length. Weight has little relation with the age of the person. The weight of the infant increases one pound every month until five months of age when it doubles and trebles by a year.
Table 6.1: Intrauterine age of fetus Age (Months) Length (cms) Weight 1 2 3 4 5 6 7
1 4 9 16 25 30 35
2.5 gms 10 gms 30 gms 120 gms 400 gms 700 gms 0.9-1.2 kg
8 9
40 45
1.5-2 kg 2.5-3 kg
10
50
2.5-5 kg
Features Eyes— two dark spots Mouth as a cleft Anus seen as dark spots; Placenta forms Pupillary membrane appears; Nails appear Sex can be differentiated; Meconium in duodenum Light hairs appear; Meconium beginning of large intestine. Eyelashes and eyebrows appear; Testes close to kidneys. Nails thick; Pupillary membrane—disappears; Eyelids—open; Meconium—whole of large intestine; Testis at external inguinal ring. Placenta 350-400 gms; Gallbladder—bile; Caecum—Rt iliac fossa Nails—tips of fingers; Left testis—scrotum Posterior fontanelle—closed; Scalp hair—4 cm long; Both testis—scrotum. Scalp hair 3-5 cm long, dark; male 100 gms more than female. Meconium—rectum; Ossification centers—lower end of femur, upper end of tibia, cuboid.
Identification Development of Secondary Sexual Characteristics 1. Growth of hair: The appearance and growth of hair in males and females vary with the attainment of maturity. Appearance/graying of hair
Males
Females
Pubic hair Axillary hair Beard and moustache Other body parts Graying of scalp hair Graying of pubic hair Balding
14-15 years 15-16 years 16-17 years 17-20 years 40 years 55 years 45 years
13-14 years 14-15 years Absent Absent 40 years 55 years Less common
Hair start developing in the following stages in males and females over genitalia (after Tanner) (Table 6.2). 2. Development of breasts in girls: There are different stages of growth of breast by 12 to 20 years depending on the nutrition and sexual practices at an early age. The various stages of development are: • Breast and papillae are elevated as a small mound and there is enlargement of areolar diameter at about 11 to 12 years. • There is more elevation of breast and papillae and enlargement of areolar diameter at about 13 years. • Areola and papillae project over the level of breast at about 14 years. • Only papillae project over the level of breast at about 15 years. • Only papillae projects over the surface and areola merges with the breast at about 15 to 16 years. 3. Hoarseness (deepening) of voice occurs in males by 15-17 years.
89
4. Adam’s apple is more prominent in males by 16-18 years. 5. Stature starts decreasing after 25 years of age at the rate of 1mm per year. 6. The Arcus senilis is the circular opacity at the limbus of cornea develops by 40 years. 7. Females achieve menopause by 40-45 years. 8. The cataract never occurs in the eyes before 55 years except when the precipitating factors cause it early. 9. The creased or wrinkled skin develops after 55 years. 10. Partial deafness could develop after 65 years of age. Laboratory Tests 1. Absence of nucleated RBC in the peripheral blood occurs by 24 hours after birth. 2. Fall of reticulocyte count (2%) in the peripheral blood by 10 days after birth. 3. Replacement of foetal hemoglobin by adult hemoglobin is completed by 6 months to two years of age. Dental Study The approximate age of the individual can be determined from the examination of teeth in both the jaws. After birth and during developing years, the close estimation of age can be determined by the presence of deciduous dentition and its stages of eruption, the period of mixed dentition, stages of eruption of permanent teeth and loss of deciduous teeth. There are twenty temporary teeth and thirty-two permanent teeth in human jaw. The deciduous and permanent teeth erupt earlier in the lower jaw except the lateral incisors that erupt
Table 6.2: Tanner’s stages of growth of pubic hair Stages
Growth of hair
Age
Stage 1 Stage 2
Prepubertal no pubic hair, fine brown vellus hair Sparse not extending on to mons pubis, light pigmented at the base of penis Darker, coarse extending on to mons pubis, pigmented and start curling and spreading Covering most parts but not going up to thighs Dense hair extending to the inner thighs and dark mature pubic hair
Less than 12 years 12-13 years
Stage 3 Stage 4 Stage 5
13-14 years 14-15 years More than 15 years
90
Textbook of Forensic Medicine and Toxicology
earlier in the upper jaw. The teeth erupt about a year earlier in the females. The permanent molar erupts first in the lower and on the left side and then on the right side. The eruption of tooth depends on the hereditary, environmental, nutritional and endocrinal factors. There are 32 permanent teeth comprising of four incisors, two canines, four premolars and six molars in each of the jaw. The temporary teeth are twenty in number comprising of four incisors, two canines, and four molars in each jaw. At 6-7 year of life, first permanent molars erupt behind the second temporary molars. The premolars replace the temporary molars. The amount of wearing in the premolars and molars gives some indication of age after complete dentition. Root formation occur after completion of the crown and as the root becomes longer, the crown erupts through the bone and finally comes out of the jaws. The tooth calcifies from crown to neck to roots. When permanent tooth erupts, the overlying root of its deciduous predecessor undergoes resorption until only the crown remains that falls off. By assessing the stage of eruption of teeth and extent of completion of calcification of root fairly accurate estimate of age of the individual can be made. In old age, either the tooth falls off decayed or the crown is worn away to the sockets. Dental Anatomy (Fig 6.1) The development of tooth begins with the formation of cellular tooth germ within the alveolar bone in the shape of the crown. The tooth has a crown,
Enamel Dentin
Crown
Pulp cavity Neck Root canal
Root
Figure 6.1: Different parts of tooth
neck and root that are embedded in the jaw. There certain differences in the appearance of deciduous and permanent teeth (Table 6.3). Incisors—The incisors have chisel shaped crown that is convex on labial surface and concave on lingual surface, with a constricted neck and has single root. They have chewing surface and cutting edge. Canines—The canines are larger compared to the incisors, the crown is conical shaped that is concave on its labial surface but slightly concave on its lingual surface. The masticatory edges tapers and projects beyond the level of other teeth. It has a single root. They have single cusps. Premolars—The premolars are also known as bicuspids. They are smaller and shorter than the
Table 6.3: Differences between primary and secondary dentition Features
Temporary teeth
Permanent teeth
Size and weight Colour Incisors Neck Presence of ridge Root of molars Replacement by Total number Types
Smaller and lighter China white Vertical More constricted Between neck and body Smaller and more divergent Permanent teeth Twenty No premolars, 8 molars
Larger and heavier Ivory white Projected forwards Less constricted No ridge Longer and less divergent Not replaced Thirty two 8premolars and 12 molars
Identification canines and the crown is circular. The chewing surface is bicuspid with a groove between them. They have a single root but may have double root in some of the races. Molars—The molars are the largest of the entire tooth, the crown is cubical that is convex on its lingual and labial surface. In upper jaw, first molar has stable configuration with 4 cusps, second molar is very different individually with 3 cusps and third molar is less mineralized than others and may have chalky spots. Also, upper molar has three roots. In lower jaw, first molar has got 5 cusps, 3 buccally and 2 lingually whereas second and third molars have 4 cusps each. Determination of age from dentition In Children At birth, the rudiments of all temporary teeth and first permanent molars are there. In children and young persons the chronological calcification and eruption of teeth gives their ages. The age of appearance of the permanent and secondary dentition is as give in the Table 6.4 and Figure 6.2. Wisdom tooth: The third molar is also known as the wisdom tooth. During the age of 14-20 years, the stage of development of third molar is of particular importance to determine the age. The lateral oblique X-ray of maxilla and mandible will show the development of third molar and root
completion of second molar. The body of jaw grows posteriorly and the ramus is elongated after eruption of second molar and a space is created for third molar. Mixed dentition: Mixed dentition is the period when both the temporary and permanent are present in the jaw. It is the period starting from 6th year of life when the first molar erupts and till the canine falls that is upto 11 years. Successional teeth: These are ten in each jaw. The permanent teeth replaces the temporary ones except the permanent premolars that erupt in place of deciduous molars. Superadded teeth: These do not have deciduous predecessors and erupt behind the temporary teeth. All permanent molars are superadded as the first permanent molar erupts while other deciduous teeth are present. There are a particular number of teeth in different ages in children that is: 1. At the age of 5 years—There are 20 teeth, all are temporary 2. At the age of 6 years—There is mixed dentition and the number of teeth is 21-24 due to eruption of first permanent molar. 3. At the age of 7-11 years—There are 24 teeth (mixed dentition) with eruption of other permanent teeth replacing the temporary ones. 4. At the age of 12-14 years—The number of teeth is 24-28 due to eruption of second molar.
Table 6.4: Age of appearance of deciduous and permanent teeth Type of teeth Lower central incisor Upper central incisor Upper lateral incisor Lower lateral incisor Canines First premolar Second premolar First molar Second molar Third molar
91
Age of eruption of temporary teeth
Age of appearance of permanent teeth
5-6 months 6-7 months 7-8 months 8-9 months 1½ years Absent Absent 1year 20-30 months Absent
7-8 year 7-8 year 8-9 year 8-9 year 11-12 year 9-10 year 10-11 year 6-7 year 12-14 year 17-25 year
92
Textbook of Forensic Medicine and Toxicology
Figure 6.2: Age of eruption of permanent teeth
5. At the age of 14-17 years—The number of teeth is 28 as there is no eruption. 6. At the age of 17-25 years—The number of teeth is 32 due to eruption of last permanent molar or wisdom tooth. 7. At the age of 25 years and above—The number of teeth is thirty-two. Spacing of the jaw: When the second molar erupts, the ramus of the mandible grows behind and the body of the jaw also increases in length for the eruption of third molar teeth. The eruption of third molar is quite irregular as it can erupt within 17-25 years. The space for third molar should be examined for its hardness, if present whenever dental examination is being carried out. It is to be noted whether the space is half formed or fully
formed by inserting the finger beyond the second molar. Boyde’s formula: Boyde in 1963 suggested a method for determining the age up to a few months after birth from structural features of the enamel. The so-called cross striations of the enamel prism are thought to be daily increments of growth. The numbers of cross striations formed from birth (when a particularly prominent incremental line, the neonatal line is formed) until death is counted. Determination of Age from Dentition in Adults and Older Age Age changes in mandible: In the mandible the center of ossification of jaw appears at second
Identification
93
Table 6.5: Age changes in mandible Features
Infancy
Adult
Old age
Angle formed by ramus with body Body Ramus Condylar process
Obtuse
Right angle
Obtuse
Shallow and small Short and oblique At lower level than coronoid process Placed near to the lower border of ramus and mandible
Thin and elongated Stunted Above the level of coronoid process Midway between upper and lower border
Shallow and big Long and oblique Neck of Condylar process is bent backwards Near the alveolar margin
Mental foramen
month of intrauterine life and symphysis menti fuses by 18-20 years. The changes in mandible with age are (Table 6.5 and Fig. 6.3): When eruption has ended and the person has achieved adult dentition, it is necessary to apply other methods that occur due to the normal wear and tear and age of the person. Gustafson’s method: This method is used for estimation of age in the adults by studying the progressive changes in an individual tooth. Pathological conditions can alter each of the factors separately (Fig. 6.4). • Attrition: It is wearing and tearing on the opposing mastication surface of the teeth of the upper and lower gums due to continuous friction. The four degrees of attrition are: A0—No attrition A0
Figure 6.3: Adult mandible
A1—Attrition within enamel A2—Attrition within dentine A3—Attrition exposes to soft pulp
A1
A2 S1
S0 P0
A3
S2
S3
P1
P2 P3
T0
C0 R0
C1 T1
R1
C2 T2
C3
T3 R2
Figure 6.4: Gustafson’s method
R3
94
Textbook of Forensic Medicine and Toxicology
• Periodontosis: When the maintenance of teeth and gums is bad, there is regression of gums and periodontal tissue. There is loosening of the teeth, exposure of length of root and deposition of stony hard debris over a long period. According to the length of exposure of root, the periodontosis is of following degrees P0—No Periodontosis or no root exposure P1—Exposure of less than 1/3rd of the part of the root next to crown P2—Exposure of more than 1/3rd of the of the root but less than 2/3rd. P3—Periodontosis beyond 2/3rd of the length of the root near the crown. • Secondary dentine: With advanced age there is deposition of secondary dentine tissue in pulp cavity. The process progress until whole of pulp cavity is replenished and the size of cavity decreases. In mandibular teeth, it starts from above and in maxillary from below. It is due to ageing, pathological conditions, dental caries etc. There are four degrees of secondary dentine formation: S0—No deposition S1—Deposition in the upper part S2—Deposition in the half of the pulp cavity from above S3—Almost whole of the pulp cavity is involved. • Root resorption: It is another decaying change involving both cementum and dentine that shows grooves. First apex is involved then extends upwards. R0—No root resorption. R1—Seen only in some parts. R2—Seen over a large area. R3—Involves both cementum and dentine. • Cementum apposition: Cementum deposition increases due to change in the surface of tooth near the end of roof and forms incremental lines. It occurs on the surface of the root in four degrees: C0—Only normal layer of cementum is noticed.
C1—Slightly greater than normal. C2—Thick layer has occurred. C3—When a heavy layer is present. • Root transparency: It occurs in the root from below upwards in the lower jaw and above downwards in the upper jaw due to rarefaction of dentine tissue: R0—No transparency noticed anywhere R1—Transparency noticeable mostly over apical region R2—Transparency up to 1/3rd from the apical region R3—Transparency noticeable up to 2/3rd of the length of the root from apex. Out of the six criteria, transparency of the root is the most reliable one for age estimation. The anterior are most suitable as they erupt early and the changes are present earlier then others. This method is applicable only in dead bodies. The tooth is first examined by naked eye and then sectioned. Before the teeth is extracted, the degree of periodontosis is noted. The tooth is then ground down on a glass slab to about 1 mm size and transparency is noted. Then it is grounded to 1/4 mm for microscopical examination. The preceding factors are assessed and given a point value according to the degree of departure from the normal. The average is ascertained from an erupted tooth, which has not exhibited any of these factors. When the total points have been allotted for particular teeth, then these values are compared with the points obtained from a series of teeth of accurately known age. This comparison is carried out on a graph by drawing regression lines showing the relation of the point values of teeth of known age. The estimated age is usually found within an error of + 3.5 years. Point formula as given by Gustafson is An+Pn+Rn+Cn+Tn+Sn = Total points indicates the Age in years.
Identification Estimation of age from transparency of root: In 1963, Miles stated that transparency of root is a good marker for age and for this purpose anterior tooth are mostly used. The tooth is grounded up to thickness of 1mm and placed on a dotted paper and outline of tooth is made, then the dots visible through transparent root are counted. All dots lying in the area of tooth are counted and the percentage of the two is used to know the age. Estimation of Age from the Bones Skeletal age can be determined from the ossification of bones that is helpful in the determination of age. The human bones develop from a number of ossification centers. At 11-12th week of intrauterine life there are 806 ossification centers that at birth are reduced to about 450. Adult human is made up of 206 bones. The time of appearance of center of ossification and the process of union of the epiphysis with the diaphysis at the metaphysis have a sequence and time that is utilized towards determination of age (Tables 6.6 and 6.7). Ossification centers are studied up to the age of 20-22 years, thereafter the skull vault sutures, union and activity of sternum; changes in shape of mandible, changes in pubic symphysis are taken in to account. The ossification begins centrally in an epiphysis that spreads peripherally and gradually takes up the osteological details of the bony part, it is going to constitute e.g., upper end of femur, lower end of radius and ulna etc. the union of epiphysis with diaphysis in long bones is interpreted as united, recently united, uniting and non-united, depending on the stage of union. When the epiphyal lines persist, it will be called as recently united. The anatomical evidence of bony union differs from radiological union by about three years and radiographs give an earlier time of union. In the living subjects while determining the age of subjects to help the Courts of law in cases of disputes relating to age, the radiological examination of the bones is to be undertaken (Figs 6.5
95
to 6.13). While determining the age of a subject for medico-legal purposes, the standard value obtained from examination of the number of subjects should be the guiding criteria, as individual variations for bony union tend to occur. The degree of growth and development of bones to some extent is affected by the dietary, environmental, hereditary and endocrinal factors in different individuals belonging to different regions and culture. Ossification occurs earlier in tropical climates compared to temperate zones. In females, epiphyseal union occurs 1-2 years earlier than males. Maturation score for estimation of skeletal age: To minimize the errors of epiphyseal union, Mckern and Stewart in 1957 suggested a scheme of scoring involving seven combinations of various segments. The total score is applied to prediction equation for more accurate age estimation. The scoring is given based on the degree of epiphyseal union that is: Degree of union
Scoring
No union 1/4th union 1/2union 3/4th union Complete union
1 2 3 4 5
Figure 6.5: X-ray of shoulder joint showing non union of head and appearance and union of coracoid process (Age = 14-18 years)
96
Textbook of Forensic Medicine and Toxicology
Figure 6.6: X-ray of elbow joint showing appearance of medial epicondyle, capitulum, trochlea, heads of radius and ulna and non union of medial epicondyle, conjoint epiphysis and non appearance of lateral epicondyle (Age = 9-11 years
Figure 6.8: X-ray of wrist joint showing appearance of carpal bones and unossified head of first metacarpal (Age = 12-17 years)
Figure 6.7: X-ray of elbow joint showing appearance of medial epicondyle, lateral epicondyle that are united and ununited heads of radius and ulna (Age = 11-14 years)
Figure 6.9: X-ray of wrist joint showing appearance of carpal bones except pisiform, unossified head of first metacarpal and lower ends of radius and ulna. (Age = < 12 years)
Identification
97
Figure: 6.10: X-ray of pelvis showing unobliterated triradiate cartilage, non union of head and greater trochanter of femur and non appearance of lesser trochanter (Age = 11-14 years)
Figure 6.12: X-ray of knee joint showing non union of lower end of femur and upper ends of tibia and fibula (Age = < 17 years)
Figure 6.11: X-ray of pelvis showing unobliterated triradiate cartilage and non union of head, greater and lesser trochanter (Age = 14-15 years)
The various segments considered for the purpose of scoring are: i. Humerus—Proximal end and medial epicondyle. ii. Radius—Distal end. iii. Femur—Head and distal end. iv. Iliac crest. v. Sacrum—Lateral portion and 3,4 th segments.
Figure 6.13: X-ray of sternum—lateral view showing non union of I, II and IIIrd parts of sternum (Age = 1520 years)
98
Textbook of Forensic Medicine and Toxicology Table 6.6: The important ossification centers and their fusion
Centers of bones
Appearance
Fusion
Clavicle—medial end Sternum Manubrium Body (Ist segment) IInd segment IIIrd segment IVth segment Xiphoid process
15-19 years 5 month IUL 5 month IUL 7 month IUL 7 month IUL 10 month IUL 3 years
20-22 years 60-70 years 14-25 years from below upwards; 3rd and 4th-15 years 2nd & 3rd-20 years 1st & 2nd-25 years >40 years with the body
Humerus (Upper end) • Head • Greater tubercle • Lesser tubercle
1 years All three unite at 6 years 3 years 5 years
18 years 4-5 years with head 5-7 years with greater tubercle
Humerus (Lower end) • Medial epicondyle • Capitulum • Trochlea • Lateral epicondyle
5-6 years 1 year 9-10 years 10-12 (11) years
Capitulum, trochlea & lateral epicondyle form conjoint tendon at 14 years, unites with shaft at 15 years Med. epicondyle unites at 16 years
Radius • Upper end • Lower end
5-6 years 1-2 years
15-16 years 18-19 years
Ulna • Upper end • Lower end
8-9 years 5-6 years
16-17 years 18-19 years
• Head Ist metacarpal • Head other metacarpals
2 years 1½ to 2½ years
15-17 years 15-19 years
Hip bone • Triradiate cartilage • Iliac crest • Ischial tuberosity • Sarcum
11-13 years 14-15 years 15-16 years 8 months IUL
14-15 years 18-20 years 20-22 years 25 years
Femur (Upper end) • Head • Greater trochanter • Lesser trochanter Femur (Lower end)
1 year 4 years 14 years 9 month IUL
17-18 years 17 years 15-17 years 17-18 years
Tibia • Upper end • Lower end
9 month IUL 1 year
16-17 years 16 years
Scapula • Coracoid base • Acromion process
10-11 year 14-15 year
14-15 years 17-18 years
Identification Table 6.7: Age of ossification of hand and foot bones Type of bone Capitate Hamate Triquetral Lunate Scaphoid Trapezium Traphezoid Pisiform Calceneum Talus Cuboid Lateral cuneiform Medial cuneiform Intermediate cuneiform Navicular
Age of ossification 2 months 3 months 3 months 4 months 4-5 months 4-5 months 4-5 months 9-12 years 5 months 7 months 10 months 1 year 2 years 3 years 3 years
Sutural Closure of Skull Closure of sutures of skull has some bearing with the milestone of life. Absence of any signs of closure of any sutures of the skull, points to the strong possibility of the age having not exceeded thirty years. Evidence of commencing union of the sutures is always noticed first in the endo-
99
cranial surface, then on the endocranial one (Figs 6.14 and 6.15). As a rule, inner surface closes several years before the outer. The sutural closure occurs earlier in males than females. Estimation of age from closure of sutures of skull can be given within the range of 10 years between 30-60 years and even more in higher age groups. The chronological ages for sutural closure are as follows: • Lateral and occipital fontanelle closes at 2 months after birth • Posterior fontanelle closes at 6-8month of birth • Anterior fontanelle closes at 1½-2 years of birth • Metopic suture closes at 2-4 years but may extend upto six years. • Basiocciput and basi-sphenoid fuses at 18-20 years. • Sagittal suture is the first to start closing endocranially at about 25 years at its back portion close to parietal eminence. The fusion is complete both ectocranially and endocranially by 35-40 years. • Coronal suture starts closing endocranially by 25-30 years in its lowest part, close to the junction with the sphenoid. It is completely closedCoronal at 40 years. Suture Anterior Fontanelle
50-60 yrs
20 yrs 30 yrs
40-50 yrs
Sagittal Suture
50-60 yrs
50-60 yrs
Posterior Fontanelle 60-90 yrs
Lambdoid suture
3
40-50 yrs
Figure 6.14: Sutures of skull
Figure 6.15: Ages of sutural closure of skull
100
Textbook of Forensic Medicine and Toxicology
• Lambdoid suture starts closing endocranially at 25-35 years and terminal closure occurs by 45-50 years. • Pterion starts closing at 40 years and completely closes by 65 years. • Mastoido-occipital starts closing at 45 years of age and complete closure occurs by 80 years. Asterion also closes by 80 years and parieto-temporal suture closes by 70 years Age Changes in Bones in Adults and Old age Changes in Scapula Scapula is a delicate bone and is often too damaged to be helpful. It requires experience to interpret and also the changes do not seem to be constant. The changes are not as closely identified with age as desired. The changes in the scapula are divided in to two categories: a. Changes due to ossification after maturity: i. Lipping of glenoid fossa begins at 30-35 years ii. Lipping of clavicular facet begins at 35-40 years. iii. Appearance of ‘plaque; or ‘facet’ on the underside of acromial process thus prolonging the acromial tip from 2-8 mm at 35-40 years. iv. Increasing demarcation of the triangular area at the base of scapular spine begins at 4550 years. v. Appearance of crista scapularis that tend to become more broader at the base and prominent at the apices with advancing age. b. Changes due to atrophic process after maturity: i. Surface vascularity: This is seen as number of fine lines in less than 25 years old. This visibility is slowly diminished and finally disappears with advancing age. ii. Deep vascularity: Deep vascularity is seen as fine lines but only by transillumination by the age of 25-30 years and they tend to diminish with advancing age. iii. Atrophic spots are areas of bone atrophy that starts appearing around 45 years and usually start in infraspinous area.
iv. ‘Buckling’ and ‘pleating’ of infraspinous area is due to irregular atrophy of bone and is the result of diminished vascularity. It begins around the age of 40 years and there is absorption of cancellous tissue. Changes in Pubic Symphyseal Surface Ageing is responsible for the fundamental contribution and provides a better guide than skull sutures for age estimation. Todd’s system states estimation of age from 10 stages of metamorphosis. Mckern and Stewart that is a more reliable method have replaced Todd’s system (Fig. 6.16). In this method symphysis pubis is divided in to three components of which, six stages (0-5) are studies of metamorphic changes. A total score of three components is obtained which in turn is translated in to age provided the individual is male. Various changes in the three components are: I. Component 1(Dorsal half of joint surface) Stage 0—Dorsal margin absent. Stage 1—Slight margin formation starts in middle 3rd. Stage 2—Dorsal margin extends over the entire border. Stage 3—Formation of plateau (filling of grooves and resorption of ridges) begins in middle third of the dorsal surface. Stage 4—Visible billowing still present and plateau extends over most of the dorsal surface. Stage 5—Billowing disappears completely and the surface becomes flat and slightly granular. II. Component 2 (Ventral half of joint surface): Stage 0—Ventral beveling absent. Stage 1—Ventral beveling present at the superior extremity and ventral border. Stage 2—Beveling extending downwards. Stage 3—Bony extension (ventral rampart) begins from either or both extremities. Stage 4—Ventral rampart extends still further but gaps are still visible. Stage 5—Ventral rampart is complete. III. Component 3 (Combination of both-whole surface):
Identification
18-19 yrs
20-21 yrs
22-24 yrs
25-26 yrs
27-30 yrs
30-35 yrs
35-39 yrs
39-44 yrs
45-50 yrs
50 yrs
101
Figure 6.16: Age changes in pubic symphsis (after Todd’s)
Stage 0—Symphyseal rim is absent. Stage 1—Dorsal rim appears at superior end of the dorsal margin, it is smooth and raised above the symphyseal surface. Stage 2—Dorsal rim is complete and ventral rim starts forming. Stage 3—Symphyseal rim is complete and the surface is finely granular. Stage 4—Rim begins to break down, is sharply defined. The surface becomes smooth and flat with no lipping of ventral edge. Stage 5—There is further breakdown of rim and rarefaction of symphyseal surface. Joint lipping begins along the vertebral edge during the last two stage of component 3 at about 35-40 years Rough Estimate of Age from Pubic Symphysis 1. When the symphyseal surface is even, age is < 20 years.
2. When the surface is markedly ridged and irregular called billowing, the ridges running transversely across the articular surface, the age is 20-25 years 3. Billowing gradually disappears and the articular surface becomes granular with sharp anterior and posterior margins by 25-35 years of age 4. Articular surface is smooth and oval by the age of 35-45 years 5. Narrow and beaded rims develop in and around the margins of articular surface and some erosion of the surface starts by 45-50 years 6. There is varying degree of erosion with breaking down of ventral margin by > 50-60 years 7. Surface becomes irregularly eroded after about 60 years of age. Age Changes in the Vertebra 1. By the time the deciduous dentition is completed, the arch unites posteriorly and at the same time the arches and bodies of lowest lumbar vertebra begins to fuse.
102
Textbook of Forensic Medicine and Toxicology
2. The posterior parts begins to fuse by 6 years and at the same time the arches of the first cervical vertebra unite posteriorly. 3. The upper and lower surfaces of immature vertebra shows a series of radial furrows up to 10 years. 4. The furrows gradually fades on the upper and lower surfaces between 21-25 years. 5. Lipping of vertebra is seen usually after 45 years. 6. Osteophytic outgrowth from anterior and lateral margins become visible by 40-45 years. The second cervical vertebra up to the age of about three years consists of three pieces that is two lateral portions that constitute the arch, the body and the dens. Age Changes in Internal Bone Structure Two structural components are studied that is: • Cancellous tissue: For studying this, humerus and femur are mainly considered and out of the two, humerus is used on priority basis. The methods used are radiological examination of bones and longitudinal section of bones in which resorption pattern of cancellous tissue is examined. The proximal end of the medullary cavity of humerus assumes a cone shape, the tip of which gradually reaches the surgical neck of the bone during the period of 40-50 years and further ascends up to epiphyseal line by 60-75 years. • Cortical tissue: The cortical elements osteon, osteon fragments, lamellar bones and non haversian canals are studied microscopically and the age could be ascertained with in the margin of 5 years. By counting the osteons in cross section of bone, the age can be ascertained but it is not an accurate and reliable method. Estimation of Age As A Whole from Birth Onwards To know the age of the person, usually horoscopes, hospital birth certificates, school admission certificates and matriculation certificates are
being used. However, in the Courts horoscopes affidavits about age are not relied upon. In all such cases, the age of the individual is to be determined from those certain parameters are used as a whole. These are 1. First 15 days after birth: The changes that occur in the umbilical cord, umbilical vessels and the skin of the newborn helps in determining his age within first 15 days after birth. 2. First 6 months after birth: In the first 6 months after birth the age of the infant can be estimated from the following parameters: • Posterior fontanelle closes within 6 weeks of birth • Pterion and Asterion closes • The temporary teeth start erupting • Foetal hemoglobin is changed to adult type 3. Between 6months-2 years: The following parameters are used • All temporary teeth erupt. • Ossification centers for heads of humerus, femur, all tarsal and carpal bones appear. • Anterior fontanelle closes at 1½ years. 4. Between 2-6 years: The parameters that are undertaken for this age group are: • The two halves of mandible fuse by second year. • The metopic suture close by 2-4 years. • Greater and lesser tubercles of head of humerus appear at 3 and 5 years respectively. • Condylar part of occipital bone fuse with the squamous part and basi-occiput. • Medial epicondyle and upper end of radius appear by 5-6 years. • Head of first metacarpal appear. • Greater trochanter of femur appear at 4 years. • Center for xiphisternum appears at 3 years. 5. Between 6-12 years: The various findings are: • Ischio-pubic ramus fuses by 6-7 years. • Pisiform bone appear between 9-12 years.
Identification • Coracoid process of scapula appear at 10-11 years. • Upper end of ulna appear by 8-9 years. • Trochlea appear at 9-10 years. • Lateral epicondyle appear between 1012 years. • All temporary teeth are shed and permanent teeth erupt except third molars. • The secondary sexual characters appear on the body. 6. Between 12-18 years: The secondary sexual characters are well developed at this age. The bones around elbow joint, shoulder joint, hip joint, ankle and knee joint ossify during this period of life. The various changes are: • Upper end of radius fuses with the shaft. • Olecranon fuses with the shaft. • Third molar teeth erupts between 17-25 years and roots of other erupted teeth calcify. • The head, greater and lesser trochanter of femur fuse with the shaft and lower end of femur, upper and lower end of tibia and fibula unite with their respective shafts. • Coracoid process fuses with scapular body at 16 years and acromion unites by 18 years. • The bony replacement of the cartilage between basi-occiput and basi-sphenoid commences at about 17 years. • The third and fourth part of sternum fuses by 15 years. 7. Between 18-25 years: By this age long bones epiphysis unites with their shaft • Lower end of radius and ulna unite with their respective shafts at 18-19 years. • Iliac crest unites with the ilium and ischial tuberosity unites with the ischium of hip bone by 20 years • The sternal end of clavicle unites with the sternum by 21 years. • Secondary centers in articular facet of the rib is complete by 20-25 years. • The bony replacement of cartilage between basi-occiput and basi-sphenoid is complete by 20-25 years.
103
• Second and third part of sternum fuses by 20 years and first and second part unite by 25 years. • All parts of sacral vertebra unite with each other. 8. Between 25-35 years: • The coronal, sagittal and lambdoid sutures of the skull start closing endocranially by 25-35 years and sagittal sutures closes usually by 30-35 years. • The age changes on symphysis pubis are characteristic after 25 years. 9. Between 35-50 years: The following changes are seen: • The coronal and sagittal suture closes by 35-40 years. • Lambdoid suture closes by 50 years. • The xyphoid process unites with the body at about 40 years. • The age changes in symphysial surface of pubis are seen in this age group. • The articular surfaces of some bones may show changes such as lipping and loss of joint space. The glenoid cavity of scapula first shows such changes whereas bodies of lumbar vertebra and inner border of ischial tuberosities usually show lipping by 40 years and other joints of the body shows lipping 45-50 years. • The hyoid and thyroid cartilages ossify. 10. Above 50 years: • Mastoid, occipital, squamous and parietomastoid sutures close in very old age. Parietal suture may not close throughout the life. • Manubrio-sternal joint fuse by 60 years • Laryngeal and costal cartilages calcify • The long bones become lighter and brittle whereas skull bones become thinner and lighter as the diploe is absorbed. The fractures are common in old age owing to these changes. • Degenerative changes like formation of arcus senilis in the eyes, wrinkling of the skin, silvery white hair deposition of atheromatous plaque in the arteries is
104
Textbook of Forensic Medicine and Toxicology common in old age. The chances of development of osteoporosis in the bone are more with advanced years of life.
Various Ages of Medico-legal Importance 1. Criminal responsibility • Under S. 82 I.P.C., the child of less than 7 years is not held responsible for the crime. • Under section 168 of the Indian Railways Act 1989, If the person under 12 years is guilty of offence under (i) S. 150 (maliciosly wrecking or attempting to wreck a train—punished with death/ imprisonment for life/10 years) (ii) S. 151 (damage to or destruction of certain railway property—punishment with imprisonment for 5 years or fine or both), (iii) S. 152 (maliciosly hurting or attempting to hurt persons travelling by railway—punishment with imprisonment for life/10 years) (iv) S. 153 (endangering safety of persons travelling by railway by willful act or omission—punished with imprisonment for 5 years) and (v) S. 154 (endangering safety of persons travelling by railway by rash or negligent act or omission—punished with imprisonment for one year or with fine or both), the court may require father/guardian of such person to execute a bond for such amount and for such period for good conduct of the aforesaid person. • S. 83 I.P.C.—The child of 7-12 years is presumed to be capable of committing an offence if he has attained sufficient maturity of understanding the nature and consequences of his conduct • S. 89 I.P.C.—The child of less than 12 years cannot give valid consent to suffer any harm what may occur for an act done in good faith for its benefit • S. 87 I.P.C.—The adult of more than 18 years can give valid consent to suffer any harm that may result from an act not intended and not known to cause death
2. Judicial punishment—According to the “Juvenile” Justice Act 2000, juvenile means a boy or a girl who is less than 18 years of age. Delinquent juvenile when commits an offence, no death sentence and no imprisonment is awarded. The juveniles are send to juvenile homes by the Court when they commit an offence. 3. Infanticide—If the baby is of less than 6months of intrauterine life, the charge of infanticide cannot be supported. 4. Criminal abortion—A woman who has passed the childbearing age cannot be charged of procuring criminal abortion. 5. Identification—To identify a person, the age is important. 6. Impotence and sterility—Women is sterile after menopause and the boy is sterile before puberty though not impotent. In India there is no legal limit on age of persons who can be declared impotent. There have even been allegations of rape against people more than 80 year old. 7. Rape—Sexual intercourse with his own wife below 15 years and other girl below 16 years without her consent is rape (S.375 I.P.C.). 8. Majority—A child is major on completion of 18 years but attains majority on completion of 21 years when under guardianship of Courts or wards. (S. 3, Indian Majority Act). 9. Evidence (witness)—A child of any age can give evidence if the Court is satisfied about his truthfulness (S.118 I.E.A). 10. Employment—A child of less than 14 years cannot be employed in a factory, mine or other hazardous employment. A person who has completed 15 years of age is allowed to work in a factory like an adult if certified by a doctor. 11. Kidnapping—It is taking away a person by illegal means. It is an offence to: • Kidnap a child with the intention of taking any movable property of a child less than 10 years (S. 369 I.P.C). • Kidnap a minor from lawful guardianship of less than 16 years boy and less than 18 years girl (S.361 I.P.C).
Identification • Kidnapping or maiming a minor for purpose of bagging. • To procure a girl for prostitution, if she is less than 18 years (S.366A I.P.C). • To import a girl to India from a foreign country for illicit intercourse, if she is less than 21 years (S. 366 I.P.C). • Kidnapping a minor for begging purposes.
SEX Criteria for Determination 1. Likely indicators of sex are outline of face, figure, clothing, habits etc. 2. Highly probable indicators are external sexual characteristics, breast, buttock etc. 3. Certain or stronger evidence are penis, testis, prostate etc. in males and vagin*, uterus, ovaries etc. in females. Medicolegal Importance The question of determination of sex arises in cases of (i) marriage (ii) divorce (iii) legitimacy (iv) impotence (v) rape and (vi) heirship. There are 46 chromosomes in a human being (male being XY and female being XX chromatin pattern).
105
bodies sex chromatin cannot be made out. The sex determination can be made from examination of specimen of buccal epitherial cells and saliva or hair follicles by the combined treatment of quinacrine dihydrocloride staining for Y-chromosome that is seen as bright fluroscent body in the nuclei of male cells and Fluroscent Feulgen reaction using Acriflavin Schiff reagent for X-chromosomes that is seen as a bright yellow spot in the nuclei. The quinacrine positive bodies in males range from 45-80%; 0-4% in females. With Feulgen reaction, fluorescent bodies are seen in 5070% cells in females and 0-20% cells in males. The Y-chromosomes can be detected in dental pulp tissue by using fluroscent dyes for about a year. F-bodies can be seen in 0-4% females and 30-70% in males. In addition to these sex can also be determine from bone marrow and amniotic fluid. 3. Biopsy: In intersex cases having unpredictable sexual morphological features, biopsy from the primary gonands namely testicl*s or ovaries can determine definitely as to whether the person is sexually active male or female or neither. CONCEALED SEX
Histological Examination 1. Barr and Bertram in 1949 and 1950 demonstrated the differences in nucleolus of the nerve cells. They found in females a body about 1 micron in diameter known as “Barr body” that appears as a small satellite to the large nucleolus in all types of nerve cells while in the males the nuclear satellite is seldom seen. They believed that this nucleolar satellite could be the product of the X chromosome. 2. Davidson and Smith in 1954 described the presence of drumstick appendage in the white cells of the females. He observed that six nuclear appendages were present in 300 neutrophils examined in case of females but in males no drumstick appendages were found even in 500 neutrophils examined. The former were known as chromatin positive and the latter as chromatin negative. In puterfied
The person dresses himself/herself similar to that of the opposite sex. The treatment to concealed sex lies in simply undressing the person. INTERSEX Intersex means intermingling of features of both sexes in varying degree in one individual. Though these cases are not presently in forensic practice, still one can diagnose them in life. They are intimately connected with sports, service, admission to school, medical science cases, inheritance, succession of property, of marriage, rape etc. Types Gonadal Agenesis There is lack of development of gonads or secondary sexual characters and nuclear sexing is negative. The chromosomes can be demonstrated
106
Textbook of Forensic Medicine and Toxicology
by microscopic examination but there is no sex chromosome. In addition morphological features of either sex are not developed during puberty. Gonadal Dysgenesis Gonads or sex organs are present but fail to develop during puberty. There are two types of medicolegally important syndromes. Turner’s syndrome Morphology is female, but there is no proper development of feminine features during puberty. Development of primary and secondary sexual features is not observed. Amenorrhoea, sterility, high urinary gonadotropin, short stature and webbed neck etc. are seen. Ovaries do not contain sufficient follicles. Nuclear sexing is positive. Sex chromosome is XO and the Total number of chromosome is 45 instead of 46. The cause is usually defective Polarization during cell division in the process of development of spermatozoa. Klinefelter’s syndrome In this condition, the anatomical structure is male but the nuclear sexing is female. The sex chromosomal pattern is XXY due to an extra chromosome. It is usually diagnosed when secondary sexual characters fail to develop during puberty. testicl*s are small and firm and non-functional. Azoospermia with a normal/small Penis and gynaecomastia are seen. There is scanty pubic hair, moustache and beard. Nuclear sexing is positive for a female. Sex chromosome pattern is XXY and the total is 47 instead of 46 due to non-polarization of sex during cell division. Sperms contain XY or XX chromosomes and only one of these goes to each sperm but in case of klinefelter’s syndrome both the sex chromosomes remain in the same sperm and leads to the XXY pattern. True Hermaphroditism or bisexuality The individual possesses two testicl*s or two ovaries or one testicl* or one ovary neither of which functions fully and properly. Hence contradictory secondary sexual features are present in the individual. Nuclear sexing is either positive XX type or negative XY (male type).
Pseudo Hermaphroditism Individual has contradictory features of both the sexes. Both groups are either of a male type or female. In male pseudo-hermaphroditism, the nuclear sex is XY but sex organs and features are that of a female due to testicl* feminisation. In female pseudo hermaphroditism, the nuclear sex is XX but sex organs and features are of a male due to adrenal hyperplasia. Determination of Sex from Bones General Features of Bones The female bones are usually smaller, thinner and lighter than bones of the males in adults whose bones are bigger thicker and massive. The bones in case of males have more prominent ridges and the processes are more marked compared to females. Also in males the shaft of bones have coarser surface and articular surfaces are wider. Compared to females where the shaft of long bones are smooth and articular surfaces are smooth and round. The male skeleton weighs about 4.5 kg while its 2.5 kg in females. While determining the sex from the bones the percentage of accuracy from independent skeletal part (as given by Krogman 1964) is: • Whole skeleton = 100% • Pelvis and skull = 98% • Pelvis alone = 95% • Skull alone = 92% • Skull and long bones = 96% • Pelvis and long bones = 98% • Long bones alone = 80-85% Pelvis alone is sufficient for determination of sex especially in adults in more than 90% of cases. In case of children and fetus even from the examination of the pelvis sex can be determined with fair accuracy. Even in adolescents’ greater sciatic notch is the single most important criteria from which sex can be determined. The sex differences in pelvis, skull, mandible, sacrum, clavicle, femur, humerus, sternum are given in Tables 6.8 to 6.15 and Figures 6.17 to 6.22.
Identification
107
Table 6.8: Differences between male and female skull Features
Male Skull
Female Skull
General appearance
Larger, heavier, massive, and surface is rough More capacious (10 % > females/ 1500-1550 cc) Muscle ridges are more marked and prominent over occipital and temporal areas Small Irregular Well marked and prominent More Prominent More Prominent More Prominent More Prominent Well marked and prominent. Facets are long are large. More deep Distinctly angulated Laterally arched, rough and large Larger and wider (U shaped) due to relative length of cheek, tooth and jaw
Lighter, smaller and surface is smooth
Capacity Architecture Frontal and parietal eminences Frontal surface Glabella Supraorbital ridges Zygomatic arches Mastoid processes Occipital protuberances Occipital condyles Digastric groove Fronto-nasal junction Cheek bones Palate
Orbits Forehead Nasal apertures Teeth
Smaller and square placed low down with round edges Steeper and less rounded Narrow and placed higher up Larger, lower first molars may have five cusps
Figure 6.17: Male and female skull
Less capacious (10% < males/13001400cc) Less marked Large Smooth Less marked and less prominent Less Prominent Less Prominent Less Prominent Less Prominent Less marked and prominent. Facets are small and broad. Less deep Smoothly curved Compressed, smooth and small Smaller and narrower (parabola shaped) due to relative length of cheek, tooth and jaw Larger and rounded placed higher up with sharp margins More Rounded and full Broad and placed lower down Smaller, lower first molars have four cusps
108
Textbook of Forensic Medicine and Toxicology Table 6.9: Differences between male and female mandible
Features
Male mandible
Female mandible
Size Chin Anatomical angle (between body and ramus) Height of symphysis menti Condyles Muscular impressions
Larger, thicker & heavier U or square & more prominent Less than 125o more prominent and everted Greater and Higher up Larger More prominent
Smaller, thinner & lighter V shaped &less prominent More obtuse, less prominent and inverted Smaller and shorter Smaller Less prominent
Table 6.10: Differences between male and female pelvis Features
Male pelvis
Female pelvis
General framework
Deep, funnel shaped. Massive and rough
True pelvis Pelvic brim Pelvic outlet Ilium
Narrow deep and funnel shaped Heart shaped Smaller Curve is more prominent, more sloped with less rounded margins More prominent Not widely separated Not prominent, narrow and shallow Wide and deep, diameter about 52 mm Higher and bigger in depth and narrow in width. Margins of pubic arch are everted and no parturition pits on the dorsal border. 70 o–75 o (acute) and subpubic arch is V shaped Smaller, deeper and narrower and less than right angle 4-5
Shallow, bowl shaped. Less massive and smooth Wide and shallow Circular Larger Curve is less prominent, less sloped with more rounded margins Less prominent Widely separated Prominent, broad and deep Small and narrow, diameter about 46 mm Lower, wider and rounded. Margins of pubic arch are not everted and parturition pits are present on the dorsal border children. 90 o (acute) and subpubic arch is U shaped Wider, larger and shallower and forming a right angle 5-6
Iliac crest Anterior superior iliac spine Pre auricular sulcus Acetabulum Symphysis pubis
Subpubic angle Greater sciatic notch Sciatic notch index = Width of sciatic notch
× 100
Depth of sciatic notch
Obturator foramen
Large, oval shaped with base upwards
Ischial tuberosity Pubis (body) Pubis (ramus) Pelvic index =
More or less inverted Narrow and triangular Is continuation of body
Small, triangular with the apex directed forwards Everted Broad and square Narrow appearance
More
Less
More
Less
AP diam. of pelvis
× 100
Transverse diam. of pelvis
Kell index = Surface area of acetabulum Surface area of ilium
× 100
Identification
Figure 6.18: Male and female mandible
Figure 6.19: Male and female pelvis
Figure 6.20: Female pelvis
Figure 6.21: Male pelvis
109
Table 6.11: Differences between male and female sacrum Features
Male sacrum
Female sacrum
General
Long and narrow, Sacrum promontory is well marked and anterior curvature is equally distributed along its length. curved in lower half. Large and extends upto 2.5-3 vertebral bodies Less movable 112
Shorter and wider with less prominent sacral promontory. Anterior curvature is straight in upper half and sharply
73-94
91-115
45
40.5
Sacroiliac articular surface Coccyx Sacral index = Breadth of base
Small and extends upto 2-2.5 vertebral bodies More movable 116
× 100
Anterior length
Ischio pubic index = Ischial length in mm
× 100
Pubic length in mm
Corporo basal index of sacrum = Breadth of 1st sacral vertebra Breadth of base of sacrum
× 100
110
Textbook of Forensic Medicine and Toxicology Table 6.12: Differences between male and female clavicle Features
Male clavicle
Female clavicle
Length
> 175 mm
< 103 mm
Circumference More
Less
Figure 6.22: Male and female Sacrum Table 6.13: Differences between male and female femur Features
Male femur
Female femur
Head
Larger and forms about 2/3rd of a sphere Forms obtuse angle (125° with the shaft) 47-49 mm
Small and forms less than 2/3rd of a sphere Almost right angle with the shaft 43-45 mm
74-89 mm 390 mm
67-76 mm 450 mm
Neck Vertical diameter of femoral head Bicondylar width Trochanteric oblique length
Table 6.14: Differences between male and female humerus Features
Male humerus
Female humerus
Average length Vertical diameter of head Transverse diameter Feature General features Curvature of radius
32.5 cm 48.7 mm 44.6 mm Male radius and ulna Larger, thicker and heavier Less curved
30 cm 41.5 mm 38.9 mm Female radius and ulna Smaller, thinner and lighter More curved
Table 6.15: Differences between male and female sternum Features
Male sternum
Female sternum
Body
Manubrium
Bigger, longer and more than twice the length of manubrium At the level of lower part of body of second thoracic vertebrae The combined midline length of manubrium and body = 149 mm Smaller
Shorter and less than twice the length of manubrium At the level of lower part of body of third thoracic vertebrae The combined midline length of manubrium and body = 149 mm Bigger
Sternal index =
46.2
54.3
Level of upper border Ashley’s rule of 149
Length of manubrium Length of body
× 100
Identification STATURE There is a progressive diminuation in stature as age advances, the annual diminuation being 0.06 cm. The stature diminishes during afternoon and evening by 11/2-2 cm. Body is said to increase in stature after death by about 2 cm due to loss of muscle tone, relaxation of joints and tensions of interventricular discs. To calculate stature of an individual, to the total length of entire skeleton 2½-4 cm are added for the thickness of soft parts. In calculating the stature from bones, more than one bone should be taken in to consideration and the long bones of lower limbs give a closer estimate than that of upper limbs. The highest corelation with stature is given by femur (r = 0.8) and tibia (r = 0.8) followed by humerus (r = 0.7) and radius (r = 0.7). A combination of bones is more reliable than a single bone in calculation of stature. For measuring the length of bones, sliding calipers can be used but Osteometric Board can be used that measures the length of the bone accurately. After measuring the length, to calculate the stature it is multiplied by multiplication factors as given by Pan (1924) for East Indians (Hindus). The multiplication factors are as follows: (i) humerus– 5.30 (ii) radius 6.90 (iii) ulna 6.30 (iv) femur 3.70 and (v) tibia and fibula (4.48). In case of dismembered or fragmented body, the stature can be calculated as: 1. Stature is equal to the length between the tip of one middle finger to that of the opposite when the arms are fully extended. 2. The length of one arm is taken and twice this length + 30 cm for two clavicle + 4 cm for sternum is equal to the total stature. 3. The length from vertex to symphysis pubis is roughly half of stature. 4. Length from sternal notch to symphysis pubis is measured and multiplied by 3.3, which gives the stature. 5. Length of forearm from tip of olecranon process to tip of middle finger equals 5/19 of the stature. 6. The height of head from top of head to tip of
111
chin (as verticle length) = 1/7th of the total stature. 7. The length of vertebral column is measured that equals 35/100 of the total height 8. Maximum length of foot is taken and divided by 0.15 that gives stature. The regression equations given by Trotter and Gleser, Dupurtuis and Hadden can also be used for calculating the stature.
RACE Race can be determined by: 1. Complexion: It has limited value as complexion varies from person to person even in the same race. Skin Colour is brown in Indians, fair in European while Negros are black. It is determined by melanin granules and melanocytes. Also skin colour changes during decomposition and burns etc. 2. Eyes: Eyes are dark in Indians though brown eyes are also found. Europeans have blue or grey colour. 3. Hair: Black, thin—Indians, Light Brown— reddish Europeans. Straight or weary— Mongolians, Indians and Europeans. Frizzy or wooly (arranged in tight spirals)—Negros. On histological examination, Mongoloid hairs are coarse and dark, circular on cross-section. Dense uniform pigmentation is seen with a dark medulla. Negros have hair that are elongated and oval in cross section with irregular distribution of dense pigment. Caucasian hair are oval or cuneiform with fine or coarse pigment. 4. Skeleton: The race can be devised from several indices such as 1. Cephalic index or index of breadth: It is calculated as maximum breadth of the skull divided by maximum length of the skull multiplied by 100. The length and breadth of skull are best measured by Sliding Calipers. In the absence of sliding calipers, the osteometric board can be used. The index varies in different races as shown in the table 6.16.
112
Textbook of Forensic Medicine and Toxicology
Table 6.16: Variations in cephalic index in different races Types of skull
Cephalic index
Dolichocephalic 70-75 (long headed) Mesati cephalic 75-80 (medium headed) Brachycephalic 80-85 (short headed)
Race Aryans, Negroes Europeans, Chinese Mangolians
Length of radius 2. Brachial Index =____________________________ × 100 Length of humerus (Radio humeral) Length of tibia 3. Crural Index = ________________________ × 100 Length of femur (Tibio-femoral) Length of humerus 4. Humero-femoral Index = _______________________ × 100 Length of femur
Age of Scars To ascertain the time elapsed since injury, the assessment of the age of scar is important. The time taken for the scar to develop depends upon the nature, site and size of the injury and also on supervening infection of the wound, the vascularity of the area and the age and sex of the individual. The scars at an early stage are red and sensitive due to blood supply from small capillaries and as blood supply gets obliterated the scar becomes shrunken, depressed, irregular and smaller in size with irregular and insensitive surface. The various stages of scar formation with the passage of time since the infliction of the injury are: Time since infliction of Injury
Characters of Scar
5-6 days
Reddish, soft, tender and sensitive scar with firm union of wound edges The scar is soft, pale and sensitive Soft, brownish or coppery reddish scar with no corrugation The scar is white, firm, tough, glistening and corrugated
SCARS End of 14 days
Identification from Scars The scar develops whenever there is injury to the dermis. It is a mass of fibrous tissue that is covered by epithelium. Incised, lacerated, penetrating and crushing injuries can cause the scars. The scars can be formed in burns, scalds, corrosive acid injuries, electricity and radiation in juries. All these result in disfiguration of the part. The scars are used to identify the person. The formation of scar and time required for its formation depends on the size, site, and nature of injury, whether the wound was infected, mode of healing, by first or second intention. In an incised wound with healing by first intention the reddish linear scar forms within 1014 days. The scar may form within 7-8 days when the wound heals with the formation of scab in superficial cuts. In a moderately infected area, the scar formation occurs in 2-3 weeks times. When the healing is by secondary intention, and when there is chronic suppuration with infection, the scar may take 4-6 weeks to form. In cases of burns, chemicals and electricity, the scar may form in several weeks to months even after grafting.
2-6 month After 6 months
The age of scar can be determined to be fresh, recent, old or late from the following features. Fresh scar (Within first few weeks)—Soft and sensitive or pale yellow ecchymosis around contusion or scab formation Recent (Few weeks-2-3months)—Brownish or copperish red, soft and not irregular Late (About 3-6months)—Similar to the scar of 2-3 months and usually shows no corrugation Old (More than 6months)—White, glistening, contracted and tough in consistency Examination of Scar While examining the scar, following points are to be noted: 1. The shape, size, direction of the scar. 2. The site of the scar. 3. Colour of the scar, whether reddish, brownish, copperish.
Identification 4. Surface whether it is irregular, thick, tough or firm in consistency and whether it is glistening or dull. 5. Whether it is tender or sensitive. 6. Whether is it freely mobile or fixed. 7. Evidence of marks of surgical interference from marks of stitches and incisions. Disappearance and Erasing of the Scar Superficial linear scars may disappear within a few years but scars resulting from large wounds, ulcers, skin diseases that involve whole thickness of skin are permanent. The scar if faint can be made prominent by rubbing or applying heat locally. The scar can be examined with a hand lens or under UV light. In the dead, the scar tissue can be examined microscopically by staining for reticuli and elastic tissue. The scar can be erased by excision and skin grafting. This may result in the formation of less obvious scar. If a person wants to efface the scar, he may get the part tattooed or may burn it but that in itself result in further scarring.
cates previous pregnancy. 5. Disfiguration caused on the face by scars resulting from assault, accident or vitriolage amounts to grievous hurt. EXAMINATION OF HAIR (TRICOLOGY) The hair can be examined by naked eye and hand lens as well as by simple microscopy with adequate photomicrography. Certain features like spatial configuration (curl, wave) and physical features such as softness, brittleness etc. are apparent only by naked eye and with hand lens examination. The examination of hair can provide information relating to the identification of the purpose and also it has evidentiary value. Anatomy of Hair Hair consists of a bulb or root and a shaft with distal termination of tip (Fig. 16.6). During the period of growth, the hair follicle lengthens and during its resting phase, the hair follicle shrinks, the hair ceases to grow and the
Medico-legal Importance of Scar 1. The scar helps in identification of an individual. 2. The age of the scar will tell us the time of infliction of injury. 3. The shape of the scar will give an idea about the nature of weapon or other causative agent. The scars from stab or punctured wounds are usually triangular and smaller than the causative weapon. In incised wounds and surgical incisions that have healed by first intention, the scar is linear and straight but if the wounds are infected, the scar is thick and wide. Scars from infected lacerated wounds, healing by second intention are irregular, thicker, broader and firmer. Scars from severe burns are prominent, irregular, thick and adherent. Vaccination scars are usually circular or oval, and slightly depressed. Scars resulting from corrosives, radiation burns are irregular and thickened. 4. Striae gravidarum, linea albicantes and old tears in the cervix and posterior commissure indi–
113
Figure 6.16: Parts of hair
114
Textbook of Forensic Medicine and Toxicology
hair bulb alters. This type of hair is readily shed and has shriveled, distorted bulb whereas the bulb of forcibly plucked actively growing hair is rounder and much of the follicle is pulled out of the skin with the bulb. Hair bulb: The bulb is formed within the follicle in the skin. To pluck a lock of healthily growing hair, considerable force is required. Hair shaft: The hair shaft is composed of keratinized mass of cortex that forms the bulk of the hair, which has an outer scaly covering or cuticle and a central core, medulla. Cuticle: The cuticle is a layer of thin, microscopic, non-pigmented scale-like plates, each attached at its lower end to the hair cortex. The thickness of cuticle layer depends upon the thickness of individual scales and the degree of overlapping occurs. Cuticle is usually thin and sometimes thick consisting of ten to twenty layers of scales. Cortex: The cortex forms most of the substance of a hair. It has abundant keratin that is responsible for the charring and acrid odour when the hair is burned. The cortex is responsible for the strength, the elasticity and the shape of the hair. The cortex is made up of closely set, longitudinally arranged, elongated cells with pointed ends and without nuclei. The fibrils within these cells may have granules on their surface. The cells are held together by cement. The hair when stretched is narrowed and pigment granules are separated in longitudinal direction. Continued stretching causes hair to break and untreated hair is resistant to deforming stresses. The cortex is pigmented, the degree of pigmentation varies from complete absence and sometimes quite intense. A large range of natural colors is present in natural hair of humans. Animal hair may show alternate bands of pigment. Granular pigment of hair is easily seen in hair mounted in an isorefractile medium. Transverse sections of hair enable the distribution of the granules to be determined in relation to the center and periphery of the cortex. The medulla: Many hairs also have a central, occasionally eccentric core that is hollow called
the medulla. The hair is so darkly pigmented occasionally so that it is difficult to visualize medulla. The medullary width is quite variable along the hair shaft and is expressed in relation to the diameter of the shaft. The tip: The tip of the hair is at its termination that is pointed and non-medullated. Repeated injuries cause the damage to the cuticle so that the exposed and unprotected cortex splits and frays. Forensic Importance of Hair Hair resists the destructive tendencies of adverse conditions such as exposure to gastric juice, prolonged drying, soaking and burial. The hair resists putrefaction for a long time and can be recovered from the graves many years after burial. For most forensic purposes, the durability of hair compare with most of the elastic tissues. The forensic importance of hair is to establish the identity of human remains. In addition, the hair is a source of establishing the association between a suspected person and a particular crime, or between a victim and a weapon or vehicle. The hair can be collected and fixed for transportation and storage by touching them with a sticky surface of transparent adhesive tape, and then pressing gently this tape to the glass slide. Isolated hair must be kept and labeled separately. When a sample of hair is submitted for examination, the following questions need to be answered from medico-legal point of view. 1. Is the sample hair or some other fiber? Few of the fibers can be burnt to note the source. Vegetable fibers burn readily without producing a disagreeable odour and leave sharply bent ends. Animal hair burn with difficulty, with odour of burnt feathers and show curved and rounded bead like ends. Human hair gets curled, blackish, brittle, shriveled, distorted and twisted. Human and animal hair consists of a root, cuticle, cortex and the medulla. Certain chemical tests with sulphuric acid and caustic soda can help in differentiating hair from the fiber. The
Identification
Figure 6.17: Microscopical appearance of cotton fibre
appearance of cotton fibres may be mistaken for hair that appears microscopically as shown in Figure 6.17. 2. Whether the hair of human or animal origin? Certain gross and microscopic findings help to differentiate the human and animal hair, are summarized in the Table 6.17. The microscopical appearance of human hair is showin in Figure 6.18. 3. If the hair is human, part of body, where it is derived from? The length of the hair, colour
115
Figure 6.18: Microscopical appearance of human hair
etc are noted to determine that which part of the body does it belong. • Scalp hairs are long, soft and taper towards the tip. They are circular on cross-section • Beard and moustache hair are straight, thick and triangular on cross-section • Axillary and pubic hairs are short, wavy and curly with split ends. They are oval on cross-section
Table 6.17: Differences between human and animal hair Features
Human hair
Animal hair
General appearance
Thin, fine and usually brown or black coloured Short, broad, and irregular margins are placed transversely. The pattern of cuticle is type VII of Moritz Well striated and broad; 4-10 times broader than medulla Continuous, narrow, fragmented or absent sometimes
Thick, coarse and may be different
Cuticle and cuticular scales Cortex Medulla Medullary index = Diameter of the medulla Diameter of hair shaft Deposition of pigment granules
Precipitin test
Less than 0.3 Concentrated towards periphery of the cortex and is usually light in the medulla and may not be continuous Specific to humans
Large with marked step like or wavy projections. The cuticle is other than type VII of Moritz Narrow, rarely more than twice or as broad as medulla Continuous, broader and always present
More than 0.5 (3.5) Heavy deposition in the medulla may be uniform, central or peripheral
Specific to animals
116
4.
5.
6.
7.
Textbook of Forensic Medicine and Toxicology
• Eyebrow, eyelashes and nostril hair are thick, straight, bristly, stiff and tapering. They are triangular and kidney shaped on cross-section. • Body hairs are soft, fine and flexible. They do not show pigment cells in cortex and the medulla is thin. • Downy hair of foetus or newborn lack medulla and have no pigment cells. Is the hair of male or female? The hairs in male are thick, coarse and dark compared to that in case of females. Beard and moustache are specific to males. Upper boarder of pubic hair is classically almost horizontal in the female and rises towards the umbilicus in the males. Some physiological and pathological conditions cause gross alterations of hair growth such as hirsuitism particularly in females. The Barr bodies can be detected in the hair bulb in about 70% of females and only about 7% of the males. The race of the person to whom hair belongs? The Indians have dark and fine hair; of Japanese and Chinese are dark, coarse and straight whereas those of Negroes are curly and wooly. What is the age of the person to whom the hair belongs? The age of the person can be deduced from the hair but within certain limits. The lanugo hairs of the newborn are fine, downy, soft and non-pigmented. These hair are non-medullated and cuticular scales have smooth and free edges. The hairs of an adult are coarser, pigmented and medullated having a complex cuticular pattern. Grey hairs are apparent after the third decade of life and are devoid of any pigment. Balding in man may begin in the second or third decade. In females, there is often loss of Axillary hair and increase of facial hair at menopause. Has the hair been dyed, bleached or is there any evidence of disease? The hair colour can be changed artificially by dyeing or
bleaching. To bleach dark hair, hydrogen peroxide is used and to render grey hair dark natural colourants such as henna, plant juices or hair dyes are used. People working in certain industries have their hair dyed automatically. Those in copper factories may have greenish hue in the hair, miners working with cobalt exhibit bluish tint. Bleached or coloured hairs are dry, brittle, lusterless and rough. The scalp is also coloured with the hair and the colouring is not uniform. The newly growing hair will be of the original colour. The hair colour is lighter in diseases such as kwashiorkor, malnutrition, and certain vitamin deficiencies. The use of hair dyes produce local dermatitis. 8. Was the hair pulled or did it fall naturally? If the hair has fallen naturally, the hair root is distorted and atrophied and the hair sheath is absent whereas when it forcibly extracted, the hair sheath is ruptured. In case of forcible extraction, the hair bulb is swollen, larger and irregular but when the hair has fallen naturally, the hair bulb has smooth, rounded end. 9. If there is presence of any injury to the hair and the nature of injury? Repeated injury to the tip of the hair damages the cuticle and the exposed cortex splits and frays. Blunt force injury and cutting hair by blunt scissors result in flattening and splitting of hair shaft. The hairs cut by a sharp weapon have a clean uniform cut surface. Hair when singed are swollen, fragile, curled and twisted. They emit a peculiar odour the carbon deposits can be detected. 10. Is there any relation with sexual assault? In rape and sodomy, the hair detected on the victim or undergarments of accused are important corroborative proof. Medicolegal Importance of Hair 1. Important clue is provided when the similar hair may be detected on the alleged weapon and on the body of alleged assailant.
Identification 2. The victim’s hair remains identifiable long after the commission of crime and provides valuable physical evidence. 3. In rape and sodomy, the hair detected on the body of the victim and underclothing of the suspected will provide valuable corroboration. In bestial*ty, the presence of animal hair in and around the genitalia, body and clothing of the accused is important evidence. 4. In road traffic accidents, presence of hair of the victim adhering to the car will provide valuable evidentiary proof. 5. The stains of mud on the hair are suggestive of road traffic accident in some muddy area or struggle in an open field. The pubic hair matted with seminal discharge may be suggestive of sexual offence. In asphyxial deaths, salivary stains are present sticking to beard and moustache. Bloodstains on the body hair suggest assault. 6. Many poisonings such as arsenic, thallium and lead can be detected from hairs. 7. In burns and close firearm injuries, hair shows singeing. 8. Age, sex, race and certain individual characters like bleaching, dyeing and waving of the hair can be deduced from examination that would help in individualization. 9. Nature of weapon whether sharp or blunt can be estimated from examination of hair. 10. Approximate time of death can be calculated from the growth of hair on the face. The growth rate is 0.4 mm per day. 11. Colour of the hair along with evidence of dirt, grease sticking to the hair may give an idea about the occupation of the person.
ANTHROPOMETRY (BERTILLION’S SYSTEM) In 1883, Alphonse Bertillon a French Law enforcement officer and biometric researcher created anthropometry, an identification system based on unchanging physical measurements that was the first scientific system police used to
117
identify criminals.He found that several physical features and the dimensions of certain bones or bony structures in the body remain practically constant throughout adult life. He concluded that these measurements can be used to distinguish a person from the other. This sytem is based on fourteen identical measurements, a standardised photographic portrait (frontal and profile), the classification of facial and body characteristics, and the notation of scars and tattoos. these were recorded on cards that were filed according to a complex method, so that they could be matched and retrieved. Bertillon’s sytem (called anthropometry, bertillonage, or signaletics) was adopted by police departments and correction systems in many jurisdictions in Europe and America Principle As the body measurements are not expected to change after 21-22 years (except stature). Thus this method is only applicable to adults after 21 years. Data to be recorded 1. Descriptive data such as hair, eyes, complexion, shape of nose, ears, chin, iris colour etc. 2. Bodily marks like moles, scar, tattoo etc. 3. Bodily measurements. • Height. • Stretch: Length of body from left shoulder to right middle finger when arm is raised. • Bust: Length of torso from head to seat, taken when seated. • Length of head: Crown to forehead. • Width of head: Temple to temple. • Length of right ear. • Length of left foot. • Length of left middle finger. • Length of left cubit: Elbow to tip of middle finger. • Width of cheeks. • Length of left little finger. 4. Photographs of front and right profile views of the head and face are also taken.
118
Textbook of Forensic Medicine and Toxicology
Disadvantages
Fundamental Principles of Fingerprinting
1. Photographs are not always reliable as there are chances of error when examined by the experts. 2. The measurements requires the use of instruments and trained operators. 3. The method is applicable only to adults. 4. Calculation errors can always be there. The method has now been replaced by fingerprint system (Dactylography).
First principle: Fingerprinting is an individual characteristic; no two fingers have been observed to possess identical ridge characteristic. Second principle: A fingerprint will remain unchanged during an individual’s lifetime. Though it is not possible to change one’s fingerprint, there has been no lack of effort on the part of criminals to obliterate them. If an injury reaches deeply enough in to the skin and damages dermal papillae, a permanent scar will form. For this to happen such a wound would have to penetrate 12mm beneath the skin’s surface. Presence of such permanent scars would serve as a new and additional characteristic for the purpose of identification. Third principle: Fingerprinting has general ridge characteristics that permit them to be systemically classified.
DACTYLOGRAPHY Dactylography is also known as Henry Galton system of identification. It is the study of fingerprints as a method of identification. The ultimate positive identification of the dead body presented in an unidentified state is a major goal of the medico-legal expert. There are many reasons to establish effective positive identification namely. To resolve the anxiety of the next of kin of a person missing and presumed dead. To settle the estate of the person missing and assumed dead. To establish the Corpus delicti. To allow the medicolegal official to release the body to the next of kin for burial. Since the turn of the century, fingerprints have been used as a very effective means of establishing identity of the individual. Introduction The skin on the palmer and planter surface is certainly wrinkled with narrow minute ridges that are known as friction ridges and is also completely free from hair and sebaceous glands. However there is profusion of sweat glands. The dermal carvings or fingerprints appear for the first time from the 12-16 week of intrauterine life and their formation gets completed by 24th week i.e., 6th month I.U. life. The ridge thus formed during the foetal period does not change the course of alignment throughout the life of the individual until destroyed by mutilation.
History of Fingerprinting In the BC era, fingerprints were used on pottery to indicate the make and brand. Clay slabs with fingerprints nearly 3000 years old have been found in Intan khanan and tomb in Egypt. Thumbprints were used as official seals or documents by Chinese emperors since 240BC. The work of Grew (1684) and Biloo (1685) are among the earliest scientific descriptions of dermatoglyphics. Purkinje’s contribution in 1823 is an important landmark because he classified the varieties of finger patterns systematically for the first. He pursued a treatise commenting upon diversity of ridge pattern on the tips of fingers and distinguished a variety of patterns of fingerprints. W.J. Herschel in 1858 began the first known official use of fingerprints in India on a large scale. He used it to prevent fraudulent collection of army pay accounts and for purposes of identity on other documents. Henry Faulds in 1880 wrote a comment on practical use of fingerprints for identification of criminals. Francis Galton began his observations around 1890 and published his book on fingerprints in
Identification 1892. He established the individuality and permanence of fingerprints and devised the first scientific method of classifying fingerprints. Juan Vucetich in 1891 installed fingerprint files as an official means of criminal identification. He based his system on the patterns identified by Galton. The first fingerprint bureau in the world was officially established in Calcutta in June 1897. In 1901, fingerprinting for criminal identification was officially introduced in England and Wales. Edward Richard Henry, IG of police in lower Bengal did extensive study on fingerprints to develop a register for classification of fingerprints. The system of Henry and Vucetich forms the basis of modern ten digit fingerprint identification. Importance of Fingerprinting 1. Identification of criminals whose fingerprints are found at the scene of crime. 2. Identification of fugitive through fingerprinting comparisons. 3. Assistance to prosecutors in presenting their cases in the light of defendants’ previous records. 4. Exchange of criminal identifying information with identification bureau of foreign countries in cases of mutual interest. 5. Assistance to probation or parole officers and to parole board for their enlightenment in decision making. 6. Imposition of more equitable sentences by the Courts. 7. Identification of persons and maintenance of identity records (service or criminal). 8. Identification of unknown deceased persons. 9. Identification of persons suffering from amnesia. 10.Recognition by the government of honored dead. 11. Identification of disaster work. 12. Prevention of hospital mistakes in the identification of infants. 13. Identification of missing persons.
119
14. Identification of licensing procedures for automobiles, firearms. 15. Identification of unconscious person 16. Problems of mistaken identity. 17. Establishing correct identity in cases of kidnapping. 18. Detection of bank forgeries. Classes of Fingerprints All fingerprints are divided in to three major classes on the basis of their general pattern (Fig. 6.19). These are: • Loops 60-70% (67%): Ridges start on one side then run parallely and end on the same side. May be medial (ulnar) loop or lateral (radial) loop. • Arches 5-10% (6-7%): Ridges start on one side and after a backward course end on the opposite side. • Whorls 30-35% (25%): Multiple circular or oval ridges one around another. • Composite 1-2%: Combination of more than one pattern. • Accidental: No specific ridge pattern. Characteristics of Fingerprints Each fingerprint being different from the other but all fingerprints have common characteristics among themselves, (Fig. 6.20) which are: 1. Pattern area: It is that part of a loop or whorl in which appears the core, deltas and ridges with which we are concerned in identifying 2. Type line: Are ridges that determine the pattern area of loops and whorls. Arches lack presence of type line 3. Delta or triradius: It is formed when a ridge bifurcates and the two arms of the bifurcating ridge diverge or when two adjacent ridges running side by side diverge causing an interspace within which the pattern lies. 4. Core: Core is the central portion of the pattern ant the type of core varies with the type of pattern. The three basic pattern types arch, loop and whorl are subdivided in to nine subtypes for the purpose of classification.
120
Textbook of Forensic Medicine and Toxicology
Figure 6.19: Various classes of fingerprints 6
Short Ridge
7
5 Bifurcation Dot Island or Enclosure
9
4 3 2 10
1 Ridge End
Figure 6.20: Characteristics of finger prints (1) Bifurcation (2) Dot (3) Dot (4) Bifurcation (5) Bifurcation (6) Ridge end (7) Short ridge (8) Island (9) Ridge end (10) Ridge end (11) Ridge end (12) Island (13) Short ridge
8
11
13
12
Identification Basic pattern Arch
Pattern type i. ii. i. ii. i. ii.
Plain Tented Loop Radial Ulnar Whorl Plain Central pocketed loop iii. Double loop -Lateral pocket loop -Twinned loop iv. Accidentals
Symbol
No. of deltas present
A T R U W C
Nil Nil One One Two Two
S S X
Two Two Two or more than two
Types of Fingerprints Obtained at The Scene The form of fingerprints obtained at a scene of crime may be classified under the following categories. • Visible prints: These are visible to the naked eye, they may be formed when a visible or coloured contaminants are present on the fingers of the perpetrator, it will leave a visible print, for example a blood print, an inked print, a colour print, a paint print, a dirt print. These visible prints are photographed directly for the purpose of comparison and maintenance of records. • Plastic prints: Formed when the fingers or the palm comes in contact with soft surface such as soap, butter,, wax, soft putty, tar, grease or freshly painted surface. Plastic prints should not be dusted with fingerprint powder and should not be photographed with the help of direct or side lighting. • Latent prints: Are such impressions not visible to the naked eye. Whenever the fingers or palm come in contact with any polished or smooth surface, they leave an invisible image on that surface of contact due to perspiration. This invisible image of fingers or palm is known as latent fingerprint. Sweat glands become more active when a person is nervous or excited and the hands perspire more than normal during this
121
state of mind. Thus a perpetrator of crime leaves behind invisible print impressions on whatever surface he touches during the act. The latent finger impressions then detected are converted to visible prints through fingerprint powders and chemical sprayer solutions so that they may be photographed, preserved and used for identification. Printing of Fingerprints Fingerprint impressions thus obtained are a reverse of actual pattern on the skin surface. The essential material needed for obtained fingerprints include Printer’s ink, Paper or card, Inking slab, Inking rubber or cotton pad, Benzene, Alcohol, Kerosene or gasoline and Soap. Fingerprint impressions can be obtained as: 1. Rolled impressions: By nail to nail rolling of fingers 2. Plain or dab prints: These are unrolled impressions obtained by direct contact For rolled prints, following precautions should be taken. (i) Hands should be properly wiped. (ii) Arm should be kept relaxed and not try to help in rolling the fingers. (iii) The rolling of the fingers and thumb should be in the following manner, the thumb should be rolled towards the subject’s body and the fingers are rolled away from the body that is thumb in and fingers out. (iv) Not too much ink should be used or excessive pressure applied on the fingers. (v) Unglazed papers are better for fingerprints. (vi) If a particular finger is missing or is so defective or deformed that it is not possible to obtain an impression, this fact should be specified in ink on the space allotted for that. (vii) Deformities on fingers like cut marks, scars shall be fully described and it should be noted whether they are temporary or permanent in nature. Fingerprints Classification System There are over fifty classification systems in use in different countries that are based on Galton, Henry and Vucetish systems. The famous ten digit classification systems and the single digit classification involve less famous features. Of
122
Textbook of Forensic Medicine and Toxicology
these systems the best known is the Battley system. The classification of fingerprint is a method through which the fingerprint impressions are transformed in to a formula to facilitate the recording and searching of the fingerprints. In the ten-digit system, it is analyzed under he following seven systems: 1. Primary classification system: Scores are allotted for presence of whorl pattern in different fingers of each hand as follows • Whorl in right thumb or = 16 scores right index finger • Whorl in right middle or = 8 scores for ring finger each place • Whorl in right little finger = 4 scores or left thumb • Whorl in left index or = 2 scores middle finger • Whorl in left ring or left = 1 score little finger • No scores for fingers where no whorls are present Scores are then R.T.+R.R.+L.T.+L.M.+L.L.+1 arranged as R.T.+R.M.+R.L.+L.I.+L.R.+1
• 1 is added for the purpose of calculation. • The total score of numerator is multiplied by denominator. 2. Major division system 3. Secondary classification system 4. Sub-secondary classification system 5. Second sub-secondary classification system 6. Final classification system 7. Key classification system (For the right thumb only). After the complete analysis of the seven systems, the complete Ten digit formula may be represented in the following manner for each fingerprint step for maintenance of records—Key, Major, Primary, Secondary, Sub-secondary, Second sub-secondary, and final
LATENT FINGERPRINTS Powdering and Lifting Latent Impressions A black or grey fingerprint powder is adequate in most places. Black powder should be used for light coloured and white objects and grey powder for black or dark coloured backgrounds. Among other powders, aluminium powder is used as a substitute for grey powder. The Dragon’s blood (a natural powder) may be employed on both dark and light coloured surfaces. A fluorescent type of powder is used for developing latent prints on multicoloured surfaces Magnetic brush and powders are used to increase the efficiency in development of latent prints. The magnetic brush marks with magnetic powders only, which are available in many colours (grey, black, red, yellow etc.). The two types of lifting medium employed in latent fingerprint work are: (i) Transparent cellulose tape in 1.5 or 2.0inch width rolls (ii) Opaque rubber lifter. Chemical Methods of Developing Latent Prints Perspiration consists of about 98% water with traces of salts like sodium, chloride, sulphates, phosphates, carbamates, lactic acid, fatty acid, glucose and urea. Chemical methods make use of the presence of chlorides, which will react with chemicals to produce visible prints. The following methods are used: • The Iodine method: Made visible by the absorption of iodine fumes that react with fatty acids and ridges of the print appear yellowish brown or brownish against the background, it is used for old prints. • Silver nitrate method: Sodium chloride reacts with silver nitrate to form silver chloride, which is an unstable white substance that darkens when exposed to light breaking in to silver and chlorine that appear reddish brown against background.
Identification • Ninhydrin method: Reacts to amino acids and gives purple reddish brown stains. • Osmium tetra-oxide method: It is used for recent prints. In the presence of fatty substance, osmium tetra-oxide is reduced to free osmium that is dark in colour. • Chem. Print method: Trade name in aerosol type container, used as spray. • Hydrofluoric method: On glass, waxy substance of the print itself repels the liquid. • Tannic acid method: Sets the albumin making the latent prints visible. • Osmic acid method: Osmic acid spray when exposed to light turns black. • Mercuric iodide method: Fumes of mercuric iodide are used. • Bromine method: Bromine vapours are used. • Reducing agents for developing prints: Organic reducing agents like amidol, pyrogallol or hydroquinone is used. • Fleming’s reagent method: Mixture of osmic acid, chromic acid and glacial acetic acid is exposed to diazine fast yellow dye that fluoresces in UV light. Factors making Satisfactory Fingerprinting of Dead Body Difficult Wrinkled skin of the finger pads resulting from immersion of the body in water; injection of air or various liquids in to fingerpads has been advocated If immersion is prolonged or decomposition is advanced or in some instances of radiant burns, the skin of the hands and fingers can be peeled away from the underlying tissue. Fingerprints can be made by inserting the technicians finger in to the ‘skin glove’ inking the area to be printed and rolling. Where the epidermis is absent, skin can be used for producing useful fingerprints. In dead bodies with contractures and with decomposing tissues, removal of the fingers from hands may permit more satisfactory printing.
123
Points of Comparison between Two Fingerprints (i) Ridge pattern, (ii) Ridge endings, (iii) Missing ridge, (iv) Gap in two ridges, (v) Ridge breaking, (vi) Ridge bifurcation, (vii) Ridge re-union, (viii) A dot in ridge gap, (ix) A stud in ridge, (x) An island formation, (xi) A lake formation, (xii) A dot in the lake, (xiii) Union of two ridges, (xiv) Starting of a new ridge in between two ridges, (xv) Presence of a scar, (xvi) Distance between delta and core, (xvii) Number of ridges between delta and core (xviii) Direction of any particular ridge. Points Necessary for Establishing Complete Identity Different countries have developed their minimum number of points for establishing complete identity of the fingerprints based on their personal practical experience for presentation before the Court. These are: France 16, Australia 12, Japan 12-14, Canada 10-16, Interpol 12, US 7-12, Spain 10-12, New zealand 8-12, Isreal 10-12. In India, Mahrashtra 12, Assam 7-12, Kerala 7, West Bengal 6, Madras 8-10, Bihar 7, Orissa 5-7, Central fingerprints Bureau (Calcutta) 9. In 1973, the first All India Forensic Science Congress held at Srinagar adopted a resolution stating that the minimum number of points for establishing the identity beyond doubt in case of fingerprint examination should be fixed at 8. However, if there are 6 or 7 points of identity a qualified opinion can be offered by the expert on his responsibility. The fingerprint experts of New Scotland Yard, London however recommended that at least 16 identical points should be established. Certain American experts are of the opinion that at least 12 identical points should be established. US, FBI is of the opinion that if there are 12 points of similarities in the two impressions, the identity is absolute.
124
Textbook of Forensic Medicine and Toxicology
Certain Indian experts are of the view that in partially blurred or smudged impressions, 3 identical points are sufficient to establish the identity. Supreme Court in 1978 upheld the opinion on 8 points. Under section 293 of Cr.P.C., the report of the Director of a fingerprint bureau is admissible as evidence without his physical presence in the Court.
when irradiated by a high kilovoltage monochromatic X-ray beam. For the proper functioning of electronographic technique, primary beam should be capable of causing the ejection of electrons and it must be so hom*ogenous and of such a short wavelength that it does not itself have a photographic effect.
Maintenance of Fingerprint Records
Here X-ray beam is first passed through a copper filter of 1 cm thickness. This was found to be the optimum thickness of copper necessary to remove all the soft wavelength components and render the beam practically hom*ogenous. The use of the emission electronographic method for the visualization of routine fingerprints is more advantageous. This method substitutes for the multiplicity of factors involved in the other techniques such as lights, lenses, focusing, positioning, black and grey powders, fluorescent substances, UV light etc. This is a routine procedure, which results in a well-defined print against a clear background. The pure metallic powders are admittedly, not so adherent to the fingerprint deposit as are the grey and black powders. They can, if necessary be brushed off and the normal police powders reapplied to the fingerprint deposit. The demonstration then carried out by the present methods. Thus there is never any danger or detriment to the fingerprint deposit by trying the electronographic method. If the normal police practice fails to satisfy in a particular case, the metallic element can be sieved over the already treated print. It will adhere to it and the electronographic method can be used. Method: To the fingerprint deposit, metallic powder is to be applied by sieving it through a 400-mesh sieve so that it drops in a free fall on to the suspected area. The excess powder is removed by blowing or tapping leaving the fingerprinting visualized against its background. Recording film should be mounted on the fingerprint and in intimate contact with it. If the object can be enclosed in a Cassette, it is placed in the cassette containing a layer of clear film.
Federal Bureau of Investigation (F.B.I.) USA maintains more than two crores of fingerprints. There is systemic maintenance of separate files for different types of prints. In 60% of the world population there is no whorl in any finger, so according to primary classification, the score is 1. On the basis of this scoring, 1,024 divisions are made called pigeon holes. Poroscopy Poroscopy was described by Locard. The ridges on the fingers and hands are studded with microscopic pores, formed by mouths of ducts of subepidermal sweat glands. Each millimeter of a ridge contains 9-18pores. These are permanent and immutable during life and vary in size, shape, position, extent and number over a given length of ridge in each individual. This method of examining pores is called Poroscopy and is useful when only fragments of fingerprints are available. ELECTRONOGRAPHY X-rays propagate themselves by a waveform motion just as does visible light. It was discovered by German physicist Plank that in some instances X-rays behave more as bullets or bundles called quanta. This means that X-rays are able to cause the ejection of electrons from their orbits round the nucleus of the atom and impart to these electrons a velocity which carries them away from the parent atom to become photoelectrons. This particular characteristic of X-rays can be use for a technique known as Electronography. Electronography is a method whereby metallic elements can be made to produce a recordable emission
Emission Electronography
Identification
125
The recording film is then placed with its emulsion surface in contact with the treated print. This is again covered with a layer of clear film. The cassette is then closed with cardboard packing to ensure intimate film object contact. The cassette with suitably selected filters on top is placed under the X-ray tube. An X-ray exposure is given and backgrounds are eliminated entirely and the palm prints stand out quite clearly. This technique can be applied to metallic objects also. In case of metallic objects, extremely differential results can be obtained. This is because finely powdered lead dust emits much more readily under the action of the primary beam than does the lead sheet.
1. 2. 3. 4. 5. 6.
GRENZ RAYS
FRONTAL SINUSES
Grenz ray unit is also extremely useful in many fingerprint investigations, especially when used in conjunction with Polaroid papers. It is simpler to use than Electronography and provides an immediate result. Its only application is to objects that can be penetrated by the beam and are of a fairly hom*ogenous structure.
Frontal sinuses can be found in over 95% of the population and they can be compared with finger prints. Like finger prints, sinus patterns are unique for the person, the structure is permanent and fixed. Unlike the finterprints and the bony sinuses can very rarely be altered by infection or injury. The frontal sinuses are classified based on: 1. Size of each frontal sinus. 2. Comparison between right and left frontal sinuses 3. Polar coordinate dimensions from frontal sinus prints. X-ray of the skull is taken in occipito-mental plane and the comparison is made to the line of frontal septum, upper border of the sinuses, partial septa and supraorbital.
FOOTPRINTS The offender at the scene of crime may also leave footprints. It can be of barefooted person or of the shoes. Small portion of footprint or shoe is sufficient for comparison. In case of shoe print, primary marking are caused by the make of shoes, soles and secondary markings are caused by changes due to usage. The footprints are used for identification of offenders and as well as of newborn children in hospitals. LIP PRINTS (CHEILOSCOPY) Lip prints can be found over wine glass, love letters, on private parts etc. Le moyne sunder (1950) pointed out that wrinkles and cracks of lips have certain individualistic characteristics like fingerprints. Japanese authors Kazuo suzuki and Yasuo tsuchihashi 1970 classified lipprints in the following ways:
Type I clear cut grooves running vertically. Type I’ vertical grooves but incomplete length. Type II branching. Type III intersected grooves. Type IV reticular. Type V other types or non-classifiable irregular prints.
NAIL STRIATIONS Striations over nails are said to be permanent but diseases destroying the nails can affect them. PALATOPRINTS Rugae present over the palate are also considered permanent and can be used for identification.
TATTOO MARKS Tattoo marks are fairly good for identification of both living and dead. It gives wide range of identification information about the persons. It tells us identity, mental makeup, social status, desires and inclinations of the person. Also they provide information about identification, nationality, religion, God, Goddess, occupation, name of person/relative/lovers, language, habits such as drug addiction etc. Flower,
126
Textbook of Forensic Medicine and Toxicology
obscene figure or an idol that is tattooed tells about the mental makeup of the person. Faded tattoo marks can be made visible by rubbing or by UV light and by burning. In dead bodies tattoo pigment may be found in regional lymph glands at autopsy. Artificial obliteration strongly suggests that the person is trying to conceal his identity. Tattoo in few cases may cause infection, sepsis, ulcers and keloid formation. Tattooing can be involuntary like by gunpowder or voluntary when they are produced by imprinting pigments of different colours in the dermis, by multiple puncture method mechanically or by electrical device. The pigment used in tattoing are: Carbon dust, Indian ink, Prussian blue, Vermillion/ lead tetroxide etc. The duration of tattoo is fairly permanent and can even stay for life if the pigment is put in the dermis or the covered parts of the body. They may fade if the pigments are placed in the subepithelial level or exposed parts due to sunlight, on those parts which undergo constant friction 8-10 years. They can be removed by surgical operation, local use of corrosive agents, electrolysis by dissolving the pigments and washing them away, by applying carbon dioxide snow and by inflicting deep burns over the area.
FORENSIC ODONTOLOGY It is the application of dentistry to forensic problems. It is important for: (i) Interpretation of bite marks (ii) Personal identification for establishing the individuality of the person especially in mass disasters. INTERPRETATION OF BITE MARKS Police may sometimes bring objects for examination like apple or piece of cheese. The unusual bite mark on the objects may be due to some dental abnormality. ‘Plastic’ marks on objects such as butter, cheese, lard, wax or chocolates are to be stored in refrigerator to prevent them from melting or flowing; they are not deep frozen as they may brittle and crack.
Fruits especially Apples are preserved in Campden solution (Meta bisulphate fluid) used for fruit bottling. Photographs are taken with film plane at right angles to the bite. Salivary traces should be swabbed. Bites are commonly seen in cases of : 1. Child abuse: In child abuse, the marks are seen anywhere on the body such as arms, hands, shoulders, cheeks, buttocks and trunk. Bites are examined whether the size of the mark is same as of adult dentition; if it is of small size, could be due to bite by the sibling and when it is of different size it could be an animal bite. 2. Sexual assault: Sexually oriented bites can be caused at any parts of the body namely Breasts, neck, shoulders, thighs, abdomen, pubis or vulva. 3. Police officers by the resisting offenders. 4. In sporting events like Football and wrestling. 5. In assaults anywhere on the body. Medicolegal Aspects of Bite Marks 1. Self inflicted: Self inflicted bite marks seen at accessible parts of the body such as shoulders or arms etc, usually seen in psychiatrics, teenage girls and old children. 2. Accidental at times resulting from falls on to the face and during fits; biting of tongue and lips will also be there. Nature of Bite Marks Bite mark comprise of a crop of punctate haemorrhages varying from small petechiae to large Ecchymoses merging in to a confluent central bruise. Front teeth cause bite marks from canine to canine with an invariable gap at either side representing the separation of upper and lower jaw. A circular or shallow oval is human bite and deep parabolic arch or U shaped is characteristic of an animal bite. Teeth may cause clear separate marks that run in to each other as continuous, intermittently broken lines. There may be abrasions, bruises and lacerations or a combination of all these.
Identification Suction petechiae without teeth marks in sexual assault are caused by human bites, have a sucking effect and due to the rupture of small venules petechial haemorrhages result. Identification from bite marks is possible if incisors and canines has some characteristic features. Bite Mark Investigation 1. Bite mark is photographed from different angles; from a directly perpendicular viewpoint with a plane of film at right angles to that of the lesion, with an accurate scale 2. Swabbing of saliva: To identify or exclude assailant; 80% of the people are ‘secretors’ who exude blood group substances in the saliva. Plain cotton wool swabs are rubbed on to the bite after moistening with water or saliva. These are then deep frozen and sent to serology laboratory 3. Impression of bite mark: Plastic substance is laid over the bite mark that hardens and produces permanent negative cast of the lesion. Plastic substance is made with a rubber or silicone based medium containing a catalytic hardener or Plaster of Paris (water based plaster). 4. Skin carrying the bite is removed and preserved in formalin for future examination; formalin causes shrinkage and distortion and makes tooth matching difficult. Matching the bite mark with the suspect’s dentition: 1. Full informed consent before examination of the suspect in writing to be taken 2. Oral consent with at least one witness, if not written to be taken 3. Dentition examined and points determined and recorded by diagram and writing 4. Photographs can be taken. The points to be noted in bite marks are: 1. Presence of full or partial denture; were they worn at the time of incidence? 2. Number of teeth in the upper and lower jaw.
127
3. Charting of missing teeth. 4. Estimate of bite overhang; whether there is an edge-to-edge occlusion or an undershoot projection of lower teeth. 5. Recording of any broken teeth or teeth with significant individual abnormalities are charted and described. 6. Any irregularity or marked variation in cutting edge profile of any front teeth. 7. Evaluation of size and prominence of any teeth especially canines and incisors. 8. Any developmental abnormalities are to be noted. 9. Recording of any abnormality in orientation of any tooth such as twisting (rotation) of anteroposterior tilting or double row of teeth; any gap or irregular spacing: (i) Six upper and six lower front teeth give the most information. (ii) Canines may provide particular help. (iii) Premolars and molars are rarely useful due to being posteriorly positioned in the jaw. DENTIFICATION OF THE DEAD FROM DENTITION The teeth helps in identification of the individual as no two sets of teeth are identical. This is particularly important in: 1. Disasters such as aviation accidents, marine accidents and air crashes in cases of mutilated or burned bodies. 2. To identify the unknown in accidents, suicides or homicides. Identification in mass disasters includes the: • General or reconstructive identity: This includes classification of the unknown by age, sex and race. • Comparative method: To confirm or exclude personal identity against antemortem dental records. General/Reconstructive Identity In fragmented bodies or skeletanised remains from jaw remnants and teeth, the following feature are easily recognized.
128
Textbook of Forensic Medicine and Toxicology
Sex of the Person There are certain differences in male and female dentition as given in Table 6.18. Table 6.18: Differences in male and female dentition Findings Size of upper central and lateral incisors Size and shape of the teeth
Mandibular first molar Pulp tissue from tooth (Fluorescent staining for intranuclear F body)
Males Different
Females Same
Less pointed and bigger, more in mandible Has a fifth cusp Absent
Mandibular teeth are more pointed and smaller Fifth cusp is absent Present
Race of the Person In civilized societies, first molar is the longest and third molar is smallest where in primitve races, first molar was smallest and third molar was longest in size. 1. ‘Shovel’ shaped upper central incisors is seen in Mongoloids. Posterior surface have a depression centrally with two marginal bars, causing the back of tooth to appear like a coal shovel with turned up edges. This is found in 91% of Chinese, Japanese and Tibetans; 84% Eskimos; 46% Palestinian Arabs, 90% Finns and rarely in Negroes and Australians aborigines. In White races, lateral incisors in upper jaw are smaller than the central especially in females; is less marked or absent in Negroid and mongoloids. 2. Long pointed canine roots are not seen in the mongoloids 3. Enamel pearls Are small nodules of enamel on the tooth surface, are frequent in mongoloids 4. Carbelli’s cusp Small nodules on lingual surface of maxillary molar is common in white races and in rare in others.
5. Taurodontism (Bull tooth) Are common in mongoloids; the pulp cavity of molars is wide and deep and the roots are fused and bent. 6. Congenital lack of third upper molar is common in Mongoloids. 7. Large teeth with more cusps in their molars even up to eight with two lingual cusps on Mandibular first premolars are common in Negroid races. Age of the Person 1. By eruption of deciduous and permanent teeth. 2. Gustafson’s criteria: • Occlusion attrition of the tip of the tooth • Secondary dentine deposition in the apex of pulp cavity. • Apical migration of attachment of periodontal membrane. • Increase in root transparency—Is best single criterion. • Root resorption. • Accumulation of cementum around the root. This method was later modified by Johanson; age can be calculated within + 5 years. 3. Comparative identification from the teeth by charting. Charting the Teeth: On the charts following are recorded: 1. Any extractions, recent or old from the condition of the socket. 2. Any fillings, number, position and composition. 3. Artificial teeth whether of gold, porcelain or stainless stain. 4. Prosthetic work in mouth such as bridge work or braces. 5. Any crowned teeth. 6. Any broken teeth. 7. Pathological conditions in teeth, jaws or gums 8. Congenital defects such as enamel pearls, carabelli’s cusps or ectopic teeth. 9. Malpositioned teeth that are rotated or tilted.
Identification 10. General state of care and hygiene like caries, plaque, tobacco staining, gingivitis etc. 11. Racial pointers such as shovel shaped upper central incisors and multi-cusped molars. Chart designation of teeth: In the middle of nineteenth century, the designation of teeth was based upon anatomical names such as upper and lower jaws, left and right in relation to midline. Latin names were used depending on the function of the teeth. There are various systems for charting of the teeth such as: 1. Zigmondy system: First system was given by Zigmondy in 1861. He numbered the permanent teeth with arabic numerals 1 to 8 from midline backwards. the quadrants were denoted by a line drawn between the central incisors bisected by a line separting the upper and lower teeth. The deciduos teeth were given Roman numerals I to V, individual teeth been denoted by the quadrant sign.
8 7 6 5 4 3 2 1 1 2 3 4 5 6 7 8 Right ____________________________________________________ Left 8 7 6 5 4 3 2 1 1 2 3 4 5 6 7 8
3. Universal (Cunningham) system: Cunningham in 1883 proposed that it would be simpler to avoid the quadrant symbols by using a straightforward numbering notation. Cunningham’s notation involved numbering the teeth 1 to 32 and lettering the deciduous teeth A to T, starting at the posterior upper right and continuing in a clock wise direction. In this system, the teeth are numbered from 1-16 from right to left in the upper jaw and 17-32 from left to right in lower jaw. The universal system followed by the international society of Forensic Odonotology. But it underwent a number of modifications in USA. 1 2 3 4 5 6 7 8 Right
1 2 3 4 5 6 7 8
__________________________________________________
8 7 6 5 4 3 2 1 V IV III II
I
1 2 3 4 5 6 7 8 I II III IV V
__________________________________________________
V IV III II
I
Permanent
Deciduous
I II III IV V
Every type of tooth had same designation so the angle of mandible was used to differentiate and the following numbers were given such as: 6 = upper right first molar; 3 = upper left canine and 2 = lower right lateral incisors etc. Disadvantages: This method could be not be easily adopted in the typewriters. As far as hand written system is concerned this system is very simple to use. 2. Palmer’s notation: This method was devised by dentist Palmar in 1870 and 1891 as
9 10 11 12 13 14 15 16
___________________________________________________
32 31 30 29 28 27 26 25
8 7 6 5 4 3 2 1
129
left
24 23 22 21 20 19 18 17
It is the best method of charting but the disadvantages are that it is difficult to learn and the risk of selecting the wrong number is great. 4. Haderup system: Haderup devised a notation published in 1902 which made use of the plus and minus sign and retaining the anatomical classification of single teeth as devised by Zsigmondy. To differentiate between the left and right sides the ‘+’ for the maxilla and ‘–’ for the mandible were placed in front of the number for the left side and behind for the right side, the sign thus being towards the midnight. For the deciduous teeth a zero was additonally placed in front of the number. This notation was adopted by the Scandinavian countries For permanent teeth, 8+ 7+ 6+ 5+ 4+ 3+ 2+ 1+
+1 +2 +3 +4 +5 +6 +7 +8
_____________________________________________________________________
8– 7– 6– 5– 4– 3– 2– 1–
–1 –2 –3 –4 –5 –6 –7 –8
130
Textbook of Forensic Medicine and Toxicology
For deciduous teeth, 05+ 04+ 03+ 02+ 01+
case should telegrams or telephone calls alone be relied upon. +01 +02 +03 +04 +05
_____________________________________________________________________
05– 04– 03– 02– 01–
–01 –02 –03 –04 –05
5. FDI Notation: A two digit notation capable of indicating tooth and quadrant was developmed. Each permanent and deciduous quadrant was designated by a separate number in a clock wise direction followed by Zsigmondy’s number at a meeting of the Federation Dentaire Internationale in Bucharest in 1971 this was adopted as the International Standard and was adopted subsequently by the American Dental Association, the International Standard Organizations, The International Association for Dental Research and the World Health Organization. From the Forensic Odontologist’s point of view the acceptance of this notation by Interpole for identification purposes was a significant step in International communication the the system is known as the FDI notation. For permanent teeth 18 17 16 15 14 13 12 11
21 22 23 24 25 26 27 28
48 47 46 45 44 43 42 41
31 32 33 34 35 36 37 38
For deciduous teeth 56 55 54 53 52 51
61 62 63 64 65 66
86 85 84 83 82 81
71 72 73 74 75 76
The disadvantage of this method are that teeth could be confused in the change over from one 2digit notation to another. Advantages of Dental Charting: The dental charting is better for forensic purposes involving telegrams or telephones. However in such cases, good photography is also necessary and in no
Medicolegal Importance of Dental Study 1. Identification of the individual: From the dental study, age, sex and race of the person can be identified as described before. Other factors for identification include: • The habits such as chewing tobacco are also helpful for identification. • Peculiarity in setting of the teeth may be familial and may help in identification. • The teeth resist decomposition so they are important for identification even for a long time after death as peculiarity of setting of teeth, evidence of any missing tooth or any artificial dentures help in proving the identity of the person. • Occupation can be known if there is anotch under tooth e.g. in case of tailors. 2. Grievous hurt: Fracture, Dislocation of tooth amounts to grievous hurt according to section 320 (7) I.P.C.. 3. Cause of death: The teeth resists putrefaction and the amount of deposition of heavy metals can be detected for a considerable period after death, special helpful in poisoning cases as well as in mass disaster. 4. In chronic phosphorus poisoning, evidence of phossy jaw and affection of teeth and gums are characteristic. 5. Bite mark over the articles or food help towards detection of the criminal. 6. Bite mark on private parts, breasts, cheeks, neck of a girl are suggestive of some sexual instinct. 7. Artificial dentures when dislodged can sometimes cause choking in the elderly. 8. Pink teeth: In putrefied bodies, near gum line, teeth are of pink colour. It is due to dentine being stained by haemoglobin products SUPERIMPOSITION It is the technique by which a particular skull recovered can be matched with the photograph. It
Identification is very helpful for identification. More recent photograph is better. Even photograph of lateral view can be used. Two negatives are prepared one of the person and the other of the skull. Appropriate magnification is done to achieve maximum alignment and where interpupillary distance of both exactly matches. It is a known fact that the interpupillary distance of a person never changes regardless of his age. The two negatives are then superimposed by keeping over each other and various points are compared. The canthus, the nasion, the nasal spine and lower border of nose and upper jaw, the supraorbital ridges, angle of jaw, external auditory meatus and the teeth etc. are compared and a photograph is taken which is analysed for similarities and dissimilarity to arrive at a conclusion. This test has more of negative value as it can definitely rule out a combination of a photo and a skull though only a possibility of a match can be established. Long Questions 1. What is identification? Discuss various points to establish the identity of a person. 2. Enumerate the points to identify a living person. Dicuss in detail Dactylography. 3. How you will proceed to determine the age of a person of 16 years? What is its medicolegal significance. 4. Discuss the medicolegal importance of age.
131
5. Discuss the role of dentition in age determination. 6. Discuss in detail the various aspects of forensic odontology and its application in identification of a person. 7. Discuss in detail the medico legal significance of dactylography. 8. What is the medicolegal importance of hair? Short Questions 1. 2. 3. 4. 5. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20.
Inter sex. Tattoo marks. Super imposition. Scar. Sutures of skull. Dactylography. Latent fingerprints. Poroscopy. Electronography. Tattoo marks. Klienfelter’s syndrome. Turner’s syndrome. Difference between temporary and permanent teeth. Difference between male and females skull. Difference between male and female mandible. Difference between male and female sacrum. Differentiate between animal and human hair.
132
Textbook of Forensic Medicine and Toxicology MULTIPLE CHOICE QUESTIONS
1. Identification means to determine the: A. Age of person B. Sex of person C. Height of person D. All of the above 2. Which of the following is the main part of corpus delicti: A. Identification of the dead body B. Identification of the weapon of offence C. Identification of clothing D. All of the above 3. Rule of Haase was formulated to calculate the: A. Age B. Sex C. Stature D. None of the above 4. Which of the following feature is not correct in a foetus of 7 months of intra uterine life: A. Testes are found close to kidneys B. Length is 35 cm C. Caecum is found in right iliac fossa D. Meconium is seen in whole of large intestine 5. The average length of a full term new born is: A. 40-45 cm B. 45-50 cm C. 50-53 cm D. 55-60 cm 6. In a child, first permanent tooth to erupt is: A. Central incisor B. First molar C. Canine D. Lateral incisor 7. Total number of teeth at the age of 8 years in females is: A. 12 B. 16 C. 20 D. 24 8. The anterior fontanelle usually closes between: A. 6-9 months B. 9-12 months C. 12-18 months D. 4-5 years 9. Maximum number of milk teeth in a child is: A. 16 B. 20 C. 24 D. 28 10. Temporary molars are replaced by permanent: A. Molars B. Premolars C. Canines D. Incisors 11. The permanent canine tooth erupts at: A. 9-11 years B. 10-12 years D. 12-14 years C. 11-12 years
1 A 12 C
2 D 13 D
3 A 14 B
4 C 15 A
5 C 16 A
6 B 17 C
12. Total number of teeth in females at age of 4 years: A. 16 B. 18 C. 20 D. 24 13. A boy has 20 permanent teeth and 8 temporary teeth. His age is likely to be: A. 9 yrs B. 10 yrs C. 11 yrs D. 12 yrs 14. Permanent second molar erupts at around….of age: A. 6 years B. 12 years C. 18 years D. 24 years 15. First permanent molar appears at age of: A. 6-7 yrs B. 7-9 yrs C. 9-11 yrs D. 11-15 yrs 16. To estimate the age of 16 years, following Xrays are advised: A. Elbow, hand, oblique view of jaw B. Wrist, pelvis, oblique views of jaw C. Knee, pelvis, skull D. Ankle, shoulder, pelvis 17. The appearance of center of ossification in case of olecranon is: A. 5 years B. 7 years C. 9 years D. 11 years 18. The different pieces of sternal body becomes a single bone at the age of: A. 16 years B. 20 years C. 25 years D. 30 years 19. The normal male skeleton weighs about: A. 2.5 kg B. 4.5 kg C. 6.5 kg D. 8.5 kg 20. The appearance of center of ossification in case of ischial tuberosity is: A. 12 years B. 16 years C. 18 years D. 20 years 21. X-ray of which of the following region is useful for the determination of age below 16 years of age: A. Lower end of femur B. Lower end of humerus C. Upper end of humerus D. Upper end of tibia
7 D 18 C
8 C 19 B
9 B 20 B
10 B 21 B
11 C
Identification 22. Age determination of an 18-year old on X-ray can be done from: A. Wrist and elbow B. Ankle and knee C. Knee and shoulder D. Shoulder alone 23. Angle of mandible is obtuse in: A. Edentulous person B. Females C. Person above 40 years of age D. Person above 60 years of age 24. Age estimation is best done by examination of: A. Pubic hair B. Dental X-ray C. X-ray of maxilla D. Eyes 25. Calcification in costochondral cartilage occurs at an age (years) of: A. 20-25 B. 35-50 C. 50-60 D. 70-80 26. Calcification in costal cartilage occurs at age of: A. 20-25 years B. 35-50 years C. 50-60 years D. 70-80 years 27. Xiphoid process unites with sternum at the age of: A. 25-30 years B. 40 years C. 16-24 years D. 60 years 28. Medial end of clavicle fuses at the age of: A. 12 years B. 14 years C. 16-18 years D. 18-22 years 29. Attainment of 16 years of age is diagnosed on X-ray of: A. Medial end of clavicle B. Knee C. Wrist D. Ankle E. Elbow 30. Angle of mandible is more obtuse in all except: A. Males B. Female C. Infancy D. Old age
22 C 13 D
23 A 14 B
4 C 15 A
5 C 16 A
6 B 17 C
7 D 18 C
133
31. Age of 21 years is important medico-legally in all except: A. To import a girl for illicit intercourse B. Marriage contract in boys C. If person is under protection of court D. To procure a girl for prostitution 32. In old age, the mental foramen opens: A. Near the lower margin B. Near the alveolar margin C. Midway between upper and lower margins D. None of the above 33. Best bone to assess age between 20-50 years: A. Skull B. Ribs C. Sternum D. Symphysis pubis 34. Hair usually start appearing at the pubic region in females at the age of: A. 11 years B. 13 years C. 15 years D. 16 years 35. Beard hair grows at the rate of: A. 0.3 mm per day B. 0.4 mm per day C. 0.5 mm per day D. 0.6 mm per day 36. The suture between the parietal bones is known as: A. Lambdoid suture B. Sagittal suture C. Coronal suture D. Metopic suture 37. Coronal suture completely fuses by the age of: A. 20 yrs B. 30 yrs C. 40 yrs. D. 45 yrs 38. Closure of all skull sutures indicates age more than: A. 40 years B. 50 years C. 60 years D. 70 years 39. Number of carpal bones ossified by 3 years of age are: A. 2 B. 3 C. 5 D. 7
8 C 19 B
9 B 20 B
10 B 21 B
11 C
12
134
Textbook of Forensic Medicine and Toxicology
40. Which of the following is the most reliable criteria to find out age by Gustafson’s method? A. Periodontosis B. Attrition C. Secondary dentine D. Root resorption E. Transparency 41. Age estimation from the physiological changes of teeth after 25 years is known as: A. Galton’s method B. Bertillon’s method C. Pearson’s formula D. Gustafson’s method 42. In Turner’s syndrome, the chromosomal pattern is: A. 46 XY B. 45 XO C. 47 XXY D. 48 XXY 43. The chromatin pattern in a female is: A. XX B. XO C. XY D. XXY 44. Sex Chromatin can be detected in: A. Monocytes B. Lymphocytes C. Neutrophils D. All of the above 45. Masculine or feminine characteristics most directly depends on: A. Genotype of somatic tissue B. Genotype of gonadal tissue C. Gonadotropin output D. Level of circulating sex hormones 46. In the buccal smears of females, the percentage of nuclei containing chromatin body ranges from: A. 0-4 B. 6-10 C. 12-16 D. More than 20 47. Karyotyping of foetus may be done from all of the following except: A. Lymphocyte B. Monocyte C. Amniocyte D. Fibroblast
1 A 12 C
2 D 13 D
3 A 14 B
4 C 15 A
5 C 16 A
6 B 17 C
48. For determination of sex, smear is taken from: A. Buccal mucosa B. vagin* C. Skin D. Nose 49. Sex can be determined by: A. Urinary epithelial cells B. Buccal mucosa epithelial cells and RBCs C. Dentine D. Bone marrow 50. Chromosomal defect is a feature amongst all of the following except: A. Inter Sex B. Concealed Sex C. Pseudo hermaphrodite D. True hermaphrodite 51. The chin in cases of male looks: A. Triangular B. Square C. Rounded D. Flattened 52. Skull of a male differs from that of a female by all of the following except: A. Capacity greater than 1500 c.c. B. Muscular markings over occiput are less marked C. Orbits are square D. Frontal eminence small 53. The cranial cavity volume of male skull as compared to female skull is more by: A. 100 ml B. 150 ml C. 200 ml D. 250 ml 54. The degree of accuracy in sexing adult skeletal remains from skull alone is: A. 50 percent B. 60 percent C. 70 percent D. 90 percent 55. All of the following are features of female pelvis which distinguish it from male pelvis except: A. Sub pubic angle 800 or more B. Wider greater sciatic notch C. Anterior part of iliac crest turned inwards D. Sacrum is short and wide 56. The obturator foramen in cases of females looks: A. Oval B. Rounded C. Triangular D. Square
7 D 18 C
8 C 19 B
9 B 20 B
10 B 21 B
11 C
Identification 57. The difference between a female pelvis and a male pelvis are all except: A. Subpubic angle 90° or more B. Wider greater sciatic notch C. Large obturator foramen D. Well marked preauricular sulcus 58. In male pelvis: A. Sub pubic angle is more than 900 B. Obturator foramen is oval C. Greater sciatic notch is larger and shallower D. Preauricular sulcus is well marked E. Ischiopubic rami is everted 59. Difference between female pelvis from a male are all except: A. Sub pubic angle 90° or more B. Wider greater sciatic notch C. Larger Obturator foramen D. Well marked Preauricular sulcus E. Female pelvis is lighter 60. The degree of accuracy is sexing adult skeletal remains from Pelvis alone is: A. 80% B. 85% C. 95% D. 98% 61. ‘Preauricular Sulcus’ is useful for: A. Age determination B. Sex determination C. Race determination D. Mode of death 62. A male clavicle differs from female clavicle by all except: A. Longer B. Broader C. Heavier D. More curved 63. Single best criteria to distinguish the female from male pelvis is: A. Shape of Obturator foramen B. Shape of ischial tuberosities C. Shape of acetabulum D. Shape of greater sciatic notch 64. Which of the following adult bone is most useful in determining sex: A. Skull B. Pelvis A. Femur D. Clavicle 65. 99% sex determination is by: A. Sacropubic angle B. Presacral sulcus
1 A 12 C
2 D 13 D
3 A 14 B
4 C 15 A
5 C 16 A
6 B 17 C
66.
67.
68.
69.
70.
71.
72.
73.
74.
75.
135
C. Iliosacral notch D. Obturator foramen E. Ischiopubic rami Ischiopubic index is used to determine: A. Age B. Sex C. Race D. Stature Height of the body can be deduced from the length of humerus by following equation: A. Humerus is 10 percent of height B. Humerus length is 50 percent of height C. Humerus length is 20 percent of height D. Humerus length is 2 percent of height Stature of a person is more at: A. Evening B. Night C. Mid-day D. Morning Cheiloscopy is used to identify the person from: A. Palato prints B. Lip prints C. Foot prints D. Finger prints The surest method of identification is: A. Cephalic Index B. Finger prints C. Handwriting D. All of the above The most common type of finger print is: A. Arch B. Whorl C. Loop D. Composite For the matching of fingerprints, the minimum points required is: A. 5 B. 10 C. 15 D. 20 Which of the following is the surest method of identification: A. Handwriting B. Speech C. Fingerprint D. Complexion and feature Majority of finger prints in Indians are: A. Loop B. Whorl C. Arch D. Composite Best method for identification of a person is: A. Dactylography B. Anthropometry C. Personal appearance after death D. Colour change of hair
7 D 18 C
8 C 19 B
9 B 20 B
10 B 21 B
11 C
136
Textbook of Forensic Medicine and Toxicology
76. Most specific and sensitive for identification is: A. Anthropometry B. Dactylography A. Skull D. Pelvis 77. Cephalic index of 80-85 is seen in: A. Pure Aryans B. Negroes C. Aborigines D. Mongolians 78. What would be the race of individual with the skull bone having following features— rounded nasal opening, horseshoe shaped palate, rounded orbit and cephalic index above 80: A. Negro B. Mongol C. European D. Aryans 79. Cephalic Index helps to determine the: A. Age B. Race C. Weight D. Sex 80. Human and animal hair are differentiated by: A. Scales and cuticle B. Medulla absent C. Both of the above D. None 81. Absent or fragmented medulla of hair is seen in all except: A. Mongols B. Negroid C. Caucasians D. Servocratarians
82. Which of the following feature of human hair distinguishes it from animal hair: A. Medulla is 1/3 of the shaft diameter B. Medulla and cortex have equal diameter C. Heavy continuous pigment in human hair D. Medulla has more than half of shaft diameter 83. Feature of human hair are all except: A. Cuticular scales are short and flattened B. Medulla is continuous and wide C. Cortex is thick and medulla is one third of shaft diameter D. Pigment in medulla is light and broken 84. Male and female hair can be differentiated by that female hair has: A. No medulla B. No bulb C. Is longer D. Sex chromatin is positive 85. Scar usually becomes pale at the age of: A. 1 week B. 2 week C. 3 week D. 4 week 86. For the erasure of tattoo marks, which of the following method is used: A. Laser beam B. Electrolysis C. Surgical method D. All of the above 87. Identification of the face using a skull X-ray is known as: A. Galton’s system B. Gustafson’s method C. Superimposition D. Locard’s Principle
7
Part 1—Forensic Medicine and Pathology
Artefacts Dorland’s Illustrated Medical Dictionary defines an artefact as any artificial product; any structure or feature that is not natural, but has been altered by processing. In Forensic Pathology, the artefact is any change caused or a feature introduced into a body after death that is likely to lead to misinterpretation of medicolegally significant antemortem findings. It is the duty of the pathologist to interpret the artefacts correctly. The misinterpretation may lead to: (i) wrong cause of death (ii) wrong manner of death (iii) undue suspicion of criminal offense (iv) halt in the investigation of a homicide and nondetection of murder (v) miscarriage of justice in civil suits (vi) unnecessary spending of time and effort as a result of misleading findings. The artefacts are divided in to two groups: 1. Artefacts introduced between death and autopsy. 2. Artefacts introduced during autopsy. ARTEFACTS INTRODUCED BETWEEN DEATH AND AUTOPSY Agonal Artefacts Regurgitation and aspiration of the gastric contents is a very common artefact seen in forensic practice. This may occur in natural deaths as a terminal event, from handling of the body or during resuscitation, this may result in physicians in wrongly giving aspiration of gastric contents as
cause of death. Resuscitation Artefacts The body may reveal injection marks, bruises and fractures etc. when the body is subjected to resuscitative attempts. The injection marks are usually seen in the cardiac region or on the extremities. The intracardiac injection may be associated with bruising of the heart and collection of some blood in the pericardium. The injection prick marks produced in the agonal period need to be differentiated from the marks of drug abuse. The defibrillator applied over the body produces ring like bruises over the chest. The ribs may sometimes be fractured from external cardiac massage but they do not show effusion of blood at the fracture site or in the intercostal muscles. Sometimes recent hemorrhages may be present in post mortem fractures, in such cases careful history of resuscitative measures is to be obtained. Evaluation of such fractures is of immense importance in deaths from violence particularly beatings and battered babies. Fat or bone marrow embolization is frequently associated with or without fractures of ribs or sternum with external cardiac massage. The positive pressure breathing apparatus used for resuscitation tend to leave the evidence of acute emphysema, occasionally with subpleural blebs, air in the mediastinum and even
138
Textbook of Forensic Medicine and Toxicology
tension pneumothorax. Embalming Artefacts The dimensions of the homicidal stab or gunshot wounds may be modified by the embalmer while trying to introduce the trochar through them. The multiple trochar holes may in a case of gunshot injuries may cause difficulties for the pathologist. Also the track of the weapon or the bullet may be disturbed, creating false tracks. The surgical alteration or suturing of gunshot wounds may complicate the situation. The embalming fluids may cause confusion for the forensic scientists when analyzing the viscera for drugs or chemicals. Embalming fluids generally contain formaldehyde, methyl alcohol amd sometimes other interfering compounds. Internment and Exhumation Artefacts In bodies interned for sometime and later exhumed, fungus growth is common at body orifices, eyes and site of open injuries. The underlying skin is discoloured simulating bruising. While performing autopsy on exhumed bodies, the agonal, resuscitative, embalming artefacts and those resulting from handling of the body after death should be borne in mind. Internment leads to the exposure of the body to the contaminants of the soil and draining water. Artefacts Related to Rigor Mortis and Hypostasis While handling the body the rigor may break resulting in false estimate of time of death. The onset or progress of rigor may be significantly affected by postmortem circ*mstances e.g. extreme heat or cold or antemortem conditions e.g. extreme hyperthermia due to widespread infections. Rigor of the heart causes the stiffening of the muscles and may simulate its concentric hypertrophy. The colour of the post mortem staining is usually purplish. Cherry red colouration may sometimes be seen in carbon monoxide poisoning. Pink hypostasis is a common finding in bodies exposed
to cold temperature in an open environment or in bodies refrigerated for sometime. Localized areas of hypostasis may resemble bruises. Decomposition Artefacts The decomposition of the body produces certain changes that may be mistakenly interpreted as pathological lesions. Advanced decomposition causes swelling of the lips, nose and eyelids, protrusion of the eyes, distension of the chest and abdomen and swelling of the extremities. These changes may lead to the false impression of the antemortem obesity. In decomposed bodies the presence of body fluids in the mouth and nose is a frequent finding. In the presence of pulmonary oedema, large quantities of such fluid may escape from the mouth and nose. This may lead to an erroneous conclusion that the person died of massive haemorrhage. Decomposition blebs are occasionally misinterpreted as vesications from burns. In a decomposed body, a deep groove may be seen around the neck if the deceased has been wearing a buttoned shirt or blouse at the time of death. These grooves often simulate ligature marks seen in strangulation cases. Even in nondecomposed bodies, bands or grooves of contact flattening in the skin of the neck of obese individual or of well nourished infants may be seen. The decomposed blood acquires a dark colour and produces appearance of congestion in the brain, lungs, right side of the heart and other parts of the body so that it becomes difficult to form the conclusion of death from asphyxia. The marks on the neck should be carefully interpreted. In some cases marked bluish discolouration of the loops of intestine is seen. This finding may be labeled by some pathologist as that of infarcted bowel. Correct interpretation of the finding of the air in the large veins and in the right side of the heart is of great importance in medicolegal autopsies. During life air may enter the systemic venous circulation during criminal abortions, craniotomy, urethroscopy, fallopian tube insufflation, pneumoperitoneum, aortography and intravenous
Artefacts infusions. In cases of air embolism following abortion, air bubbles are usually found in the cavity of the uterus and its wall, the uterine and adnexal veins, the inferior vena cava and right heart, the pulmonary arteries, the left heart and the systemic arteries. The presence of gas in the right side of the heart resulting from decomposition may resemble the findings in air embolism and it may be difficult to distinguish one from the other. The analysis of the gas that is collected from the heart and brought into contact with an alkaline pyrogallol solution turns brown in the presence of free oxygen, gives support to the diagnosis of antemortem air embolism. Gas produced by decomposition will not produce this colour change. Gunshot Wounds Artefacts During the hospital stay the victim of gunshot wound may sustain additional pseudogunshot wounds. The drainage holes in the chest or abdomen, such as embalmer’s trochar holes may be confused with the gunshot wounds. Surgical alteration or suturing of the wounds may lead to difficulty in evaluating the wound known as Kennedy phenomenon. In decomposed bodies these wounds may be greatly modified. Toxicological Artefacts Decomposition of the biological material often causes apparent alterations in the constituents of the tissue. It is generally known that the alcohol is produced postmortem because of putrefaction (enzymatic decomposition, especially of proteins, with the production of foul smelling compounds) of the tissues and the fact that many of the bacteria can produce alcohol. However it must be emphasized that the levels of alcohol generated by putrefaction are usually less than 100mg percent. If the levels are more than 100mg percent it should arouse the suspicion of alcohol ingestion prior to death. Decomposition is also known to cause an increase in the concentration of carboxyhaemoglobin in the blood; the increase
139
has been reported of 19-25% by various authors. Cyanide is produced by decomposition in toxicologically significant amounts; levels up to 10mg% have been found in three month old blood. Many substituted phenols (extremely poisonous compounds generally from coal tar) have been found in the decomposing tissues. The one that cause disturbing interference in the analysis of weak acid fractions are related to p-hydroxyphenyl derivatives. Combustion of the body tissues and other materials associated with the burned body produces several gases. Oslen and his colleagues investigated gases generated in experimental fires and demonstrated the presence of ammonia, carbon monoxide, hydrogen cyanide, hydrogen sulphide, nitrogen, oxides of nitrogen and sulphur dioxide. Combustible material like silk and wool produces high concentrations of several of these gases because their nitrogen content is high. Some of these gases may be detected in the body tissues and the results of toxicological analysis may raise false alarms. Cyanide levels in the blood of the burn victims were reported between 17220mg per 100ml. Miscellaneous Artefacts Fauna bites: The animal bites produce confusing changes but bears characteristic teeth marks. The rodent bites are commonly seen in bodies that are stored in a cold room. Drowned bodies may bear the marks of injuries produced by water creatures such as fishes, crabs and may simulate stab wounds. Postmortem haemorrhage: The finding of the extravasation of blood in the tissues or even pools of blood in the body cavities does not necessarily mean that the haemorrhage was from antemortem trauma. Under normal circ*mstances blood in the body remains in a fluid state for a time. During this time the postmortem injury may open a blood vessel and lead to postmortem haemorrhage. The significance of blood in the pleural cavities after death has been explained to be substantial
140
Textbook of Forensic Medicine and Toxicology
bleeding from wounds inflicted on the chest wall and the lung tissue. Flattening of the convolutions of brain: Flattening of the cerebral hemisphere is invariably seen in cases of oedema of the brain caused by pathological lesions. This flattening is generalized. However, regional flattening of the cerebral convolutions is a common postmortem artefact. The parts of the brain in contact with the cranium, particularly the dependent parts show flattening, the occipital lobes showing such flattening more frequently. The longer the body remains in such position and longer the time after death, the more marked is the flattening. To prevent additional artefactual flattening from contact with the container, the brains in order to be fixed should be suspended in 10 % formalin by a hook passed around the basilar arteries for a period of 3 weeks before dissection. Grooving of unci: It is widely accepted concept that the grooving of the uncus is an important accompaniment of genuine oedema of the brain from cerebral lesions. But this finding is an extremely common in normal brains at autopsy, and this artefact should not lead the pathologist to a misinterpretation. Discolouration of the liver: Blackish brown discolouration of the liver at the site of contact with the large bowel is fairly common. This is a postmortem change, the result of substances passing from the bowel to the liver and depositing sulfides in the adjacent liver tissue. Similarly bile also produces staining of the liver surface. ARTEFACTS INTRODUCED DURING AUTOPSY In the head one of the commonest artefacts is the introduction of air bubbles into the vessels at the top of the brain. In the majority of cases while the dura is being pulled in the sagittal line, air gains access to the blood vessels. Likewise postmortem introduction of air into the veins of the neck during the reflection of the skin is also very common. In cases of suspected air embolism following
attempts at criminal abortion, artefactual presence of air bubbles in the vessels of the brain and neck may initiate confusion; the diagnosis of air embolism may be erroneously entertained. While sawing of the vault of skull during the autopsy, partial sawing and the forceful pull of the cap sometimes leads to the fractures of the skull. In the already fractured skull, the antemortem fractures may be extended or additional fractures created. Postmortem tears of the midbrain may be caused during the removal of the brain from the cranium. Handling of the organs and incisions of the vessels during routine postmortem examinations often result in the extravasation of the blood into the tissues, particularly into the neck. Recognition of autopsy artefacts in cervical tissues is of special importance because they simulate antemortem bruises seen in cases of throttling and strangulation. Therefore dissection of the neck should be meticulous avoiding the artefacts from seepage of blood from the neck vessels. Toxicological Artefacts Some of the toxicological artefacts may be introduced during the autopsy caused by: Faulty Technique in Collecting Samples: Blood samples are sometimes drawn from the heart with a long needle and this may result in contamination of sample with gastric contents and tests particularly for alcohol may be misleading. In traumatic deaths such as those due to automobile accidents, the stomach may rupture and lead to the added likelihood of contamination. Also, alcohol is known to diffuse in significant amounts from the stomach to the pleural and pericardial cavities. During an attempt to draw blood from the heart, pericardial and pleural fluid may be withdrawn giving unreliable results. Faulty techniques in storage: Artefacts may be introduced by cutting the organs with instruments contaminated by stomach contents or by putting the samples of tissue in contaminated containers. It is a common practice to store
Artefacts portions of several organs in one container. Such a practice is apt to cause alterations in true levels of the poisons because the diffusion or drainage of the blood or fluid from one organ to another may lead to an altered concentration of the poison. Use of preservatives: The use of the preservatives can also add to the artefacts. It should be emphasized that preservatives such as EDTA (ethylene-diamine tetra-acetic acid), formalin, heparin and methanamine give a positive test for
141
methanol and these should not be used as anticoagulants for blood if an analysis for methanol is required. Long Questions 1. What do you mean by artefacts. Discuss the different artefacts that can be found during autopsy. 2. Discuss the artefacts produced between death and autopsy.
8
Part 1—Forensic Medicine and Pathology
Autopsy Procedures and Exhumation AUTOPSY Autopsy means examination of a body after death.In India, there is provision for a complete postmortem examination. Every cavity of the body should be examined. Even if the cause of death is evident, other areas and organs of the body to be examined to find out any contributory cause of death. Complete autopsy is necessary to corroborate the evidence of the eyewitnesses and the investigations done by investigating office since a poor autopsy can lead to miscarriage of justice. A qualified Registered Medical Practitioner should carry out the autopsy. He should himself dissect the body and examine the organs to find out the queries asked by the Investigation Officer, most frequently the cause of death. The Postmortem attendants and sweepers should be there to assist in the procedure. The term is synonymous with necropsy, thanatopsy and postmortem. The autopsy is of two types: (i) Medico legal autopsy (ii) Pathological autopsy. The Medicolegal autopsy is conducted in the Department of forensic medicine. The request comes either from the police or SDM who is the Investigation Officer of the case. The consent of the relatives is not required. The doctor conducts a full and complete postmortem to find out the cause of death and other relevant questions asked by the Investigating Officer.
The Pathological autopsy is done by the Department of Pathology and request comes from the relatives, who are the consenting party. In these cases the doctor conducts a partial autopsy of the organ or cavities where the pathology is suspected to find out the cause of death. The forensic autopsy differs from the pathological autopsy in its objectives as well as relevance. The forensic pathologist conducts the autopsy to determine the cause of death, manner of death (natural, accidental, suicidal or homicidal), the identity of the deceased if unknown and the time of death and/ or injury. The forensic autopsy may also involve collection of evidence from the body that can be subsequently be used to prove or disprove an individual’s guilt and confirm or deny his account of how the death occurred. The forensic autopsy involves not only the actual examination of the body at the autopsy table, but consideration of other aspects that the general pathologist does not consider part of the autopsy such as the crime scene, clothing and toxicological. The forensic pathologist should know the circ*mstances leading up to and surrounding the death prior to the autopsy. The history of the case should be obtained from the investigating police officer or the Sub-divisional magistrate. At times the relatives or the eye witness may give history. The scene of crime should when an opportunity arises be examined and documented either with
Autopsy Procedures and Exhumation diagrams or photographs or with both. The statements of the relatives and the witnesses at the scene should be recorded by the police and should be given to the pathologist. The body should be handled a very little at the scene. In cases of violent deaths, paper bags should be secured around the hands so that no trace evidence will be lost. Plastic bags should not to be used to cover the hands to avoid condensation in cold room and possible loss of trace evidence when it is moved to warm environment. The body should be wrapped in a clean, white sheet or plastic bag. The examination of clothing for blood stains and trace evidence and correlating the tears/ cuts on the clothing with bodily injuries is an important part of the autopsy. When fingerprints are to be taken for identification purposes, it should be done only after the examination of the hands. In all gunshot deaths and severely burnt bodies, X-rays should be undertaken. This is especially important in gunshot wounds in which the bullet appears to have exited. This is because the bullet may not have exited but rather only a piece of bullet or bone may have exited. This is common with the semi-jacketed ammunition in which the jacket may remain inside the body and lead core may exit. Aim and Objectives The aims and objectives of the postmortem are to: 1. Determine the identification in cases of unknown body. 2. Find out the cause of death. 3. Find out the manner of death whether suicidal, accidental or homicidal. 4. Find out the time since death. 5. In new born babies, determination of viability and cause of death. 6. Preserve the trace evidences and viscera when needed. 7. Reconstruct the accident scene from the examination of injuries as to nature and duration etc.
143
Permission for Autopsy A written request must come from the Police Officer, who is the investigation officer. At least the Police Officer of the rank of ASI should be the investigating officer. In cases of murder the Inspector is the investigating officer. In circ*mstances where the SHO/Inspector is busy and not available, he should get permission from the Deputy Commissioner to depute one junior officer for the same. The inspector should take the charge of the case once he is free. There are certain types of cases where the Magistrate holds an inquest and the request for autopsy should come from the Magistrate. Preparation for Autopsy 1. The Investigating Officer should fill the performa ‘Request for Postmortem’ and alongwith other inquest papers should submit the body in the mortuary. 2. Autopsy should be done without delay. 3. The I.O. and relatives whose names are written on inquest papers should identify the body. In cases of unknown bodies, the I.O. is directed to take the photographs and fingerprints of the body and the doctor should note at least five identification marks on the report. 4. Autopsy is conducted in a in the mortuary of a government hospital. At times the autopsy is carried out in the open space, or a covered area in emergency such as at the accident site in cases of mass disasters; air crash or train accident etc. 5. The mortuary should have good lightening, equipments, facility of cold storage and proper drainage system alongwith the manpower. 7. The Forensic Pathologist should take the history from I.O. and should carefully go through the inquest papers. 8. The autopsy is done during the daytime, because of difficulty in appreciating certain
144
Textbook of Forensic Medicine and Toxicology
colour changes in injuries and in jaundice etc. in artificial light. 9. No unauthorized persons should be present in the autopsy room. The I.O. may be allowed if required. 10. The autopsy is also carried out in a decomposed, mutilated, fragmented and skeletonized bodies as certain important information still may be found after examination. Procedure of Autopsy External Examination The external description should include the age, sex, race, physique, height, weight and nourishment. Congenital malformations, if present should be noted. A simple listing of the articles found on the body should be noted initially such as a short-sleeve white shirt, or a long-sleeve white shirt, unbuttoned down the front, or a blood stained white T-shirt. In a case of traumatic death with significant alterations of the garments due to trauma, the clothing should be described in further detail. One should then describe the degree and distribution of rigor mortis and postmortem staining. The colour of the eye, the hair and the appearance of the eyes should be noted. Any unusual appearance of the ears, nose, or face for example congenital malformations, scarring or severe acne should be recorded. Note the presence of teeth and or presence of any dental plates. The presence of vomitus in the nostrils and mouth should be noted. Any significant scars, tattoos, moles should be noted for the purpose of identification. If there is any evidence of disease, it should be recorded. All the old injuries should be noted. Evidence of recent medical and/ or surgical intervention should also be recorded. Evidence of injuries: All recent external as well as internal injuries, whether minor or major should be described along with the age of the lesions in this section, if possible. Gun shot wounds and to a degree stab wounds should be described under the separate sections of external and internal injuries.
In gunshot wounds, if possible each individual wound should be described in its entirety before going on to a second wound. The gunshot wound should be described on the body in inches or centimeters in relation to the top of the head or the sole of the foot and to the right or left of midline. It should then be described in regard to a local landmark, such as the nipple or the umbilicus. The features of the wound that make it an entrance and that determine at what range it was fired should be described, for example abrasion collar, soot or tattooing. Pertinent negatives should also be noted. Then, the course of the bullet through the body should be described. All organs perforated or penetrated by the missile should be noted. It is useful to give an overall description of the missile path through the body in relation to the planes of the body. If the bullet exits, the exit wound should be described in relation to the entrance. If the bullet is found, one should state where it was found, whether it is intact, deformed, or fragmented, whether it is jacketed, and the approximate caliber. A letter or number should be inscribed on the bullet. The bullet then should be placed in an envelop with the name of the victim, the date, postmortem, the location from which the bullet was recovered, the letter or number assigned to it and the name of the police station. To describe stab wounds, one should indicate whether the weapon was single or double edged, which edge of the wound is produced by the cutting edge of the knife, the exact dimensions, and an estimation of the depth of the wound track produced. In dozens of knife wounds, it may not be possible to handle each wound separately but it should be described in groups. Examination of clothing is to be done to locate the defects, whether they correspond to the injuries, the presence of trace evidence such as powder, soot, grease or car paint etc. Demonstration of Pneumothorax The various methods to demonstrate pneumothorax are: 1. The skin and subcutaneous tissue are first reflected from the chest wall, by sweeping cuts
Autopsy Procedures and Exhumation through the subcutaneous tissue over the chest wall angling the blade down towards the ribs, being careful not to open the pleural cavity. The intercostal soft tissues should not be punctured and neither the pleural space penetrated as this releases air from underlying pneumothorax. When reflection is completed to mid-axillary line, water is poured into the angle between subcutaneous tissue and the chest wall, and the intercostal tissue below the water line are pierced with the blade to detect an underlying pneumothorax, which may occur following trauma, in patients with chronic obstructive airway disease or asthma. If present, air bubbles will be seen rising through the water 2. Before giving any incisions over the body, a wide bore needle attached to a 50 ml syringe minus the plunger is introduced into the subcutaneous tissue over an intercostal space and the syringe is then filled with water. The needle is pushed slightly deeper to enter the pleural space and the water is observed for the presence of any air bubbles. The process can be repeated on the other side also. 3. The chest X-ray of the body to demonstrate pneumothorax can be undertaken. Demonstration of Air Embolism Whenever there is possibility of venous air embolism, the following steps should be performed 1. A plane X-ray of chest should be performed before eviscerating to demonstrate air embolism 2. The retina should be thoroughly examined with an ophthalmoscope for intravascular bubbles by moistening the cornea with isotonic saline to prevent interference from corneal opacity. 3. During dissection of the neck, the large neck veins should be carefully exposed but not opened before the heart is dissected in situ to avoid the confusion of air introduction during evisceration. 4. The abdomen is opened in the usual way to closely inspect the inferior vena cava for air bubbles in the lumen through its transparent wall.
145
5. The sternum is removed by dividing the ribs, being careful not to puncture the pericardial sac, and cutting through the sternum distal to the sternoclavicular joint. The internal mammary vessels should be clamped. The anterior pericardial sac is opened and external epicardial veins are inspected for evidence of intraluminal bubbles. The water is then introduced to fill the pericardial space. The right atrium and ventricle is incised covered in water and inspected for any air bubbles that escape. Alternatively, a water- filled syringe without the plunger is connected to a needle that is inserted into the right ventricle and the chamber of syringe is observed for air bubbles. When the presence of an air embolus is established the vena cava should be clamped and the thoracic and abdominal cavities flooded with water in an attempt to localize the source of embolism. Sometimes the intracardiac gas produced by postmortem bacterial activity may produce the appearance of a counterfeit air embolus. 6. Pyrogallol test: 4 ml of a 2% freshly prepared pyrogallol solution is collected into two 10 ml syringes. Four drops of 0.5M sodium hydroxide solution are added to the first syringe and the mixture should turn yellow in the presence of air. Gas is the aspirated from the right side of the heart; the needle is removed and replaced with a stopper. The syringe is then shaken and the mixture should turn brown, if air is present. In the absence the air, the solution will remain clear, indicating gas production by bacteria. The second syringe is used as a positive control by including a volume of air with the introduction of sodium hydroxide. This should also turn brown. The arterial air emboli are even more unusual and usually the result of traumatic injury such as thoracic trauma involving pulmonary veins or following air introduction during cardiopulmonary bypass. A much smaller volume of air is associated with such emboli and are much more difficult to demonstrate. Systemic emboli may be demonstrated by inspecting the intracranial
146
Textbook of Forensic Medicine and Toxicology
vessels of the meninges and circle of Willis and then examining under water after clamping the internal carotid and basilar arteries. Internal Examination In India due to provision of complete autopsy, the whole body is to be examined. The following types of incision are usually given depending upon the nature of the case, to open the body. The incisions given for autopsy (Fig. 8.1): 1. ‘I’ shaped incision: It extends from the chin straight down to the symphysis passing either on the left or right side of the umbilicus. The umbilicus is spared because of its dense fibrous tissue, which is difficult to stitch.
B C
A
Figure 8.1: Various incisions over the body: A = I shaped, B = modified Y shaped and C = Y shaped
2. ‘Y’ shaped incision: The incision starts at a point close to the acromial process on both sides. It extends down below the mammary line up to the xiphoid process from where it extends down up to symphysis pubis on either side of umbilicus. 3. Modified ‘Y’ shaped: An incision is made from suprasternal notch in midline up to symphysis pubis by the side of umbilicus. It extends from suprasternal notch to the middle of clavicle on both sides extending up to side of neck behind the ear till mastoid process. The choice of opening the skull or other body cavity depends upon the doctor doing the autopsy. The major organ systems as well as organ cavities are systemically described in this section. The various organ systems and body cavities to be described are the head, neck, thoracic, abdominal and pelvic cavity as well as the biliary tract, pancreas, adrenals, urinary tract, reproductive tract and musculoskeletal system when the need arises. Principles of Autopsy Dissection Techniques The autopsy techniques used in various centres and hospitals differ very little. Therefore the pathologist can depend on the method he masters best. Autopsy techniques may vary in the order in which the organs are removed, in the planes and lines of sectioning and most importantly in the method of removal of organs in the body. 1. R. Virchow’s technique: In this method organs are removed one by one. First the cranial cavity is exposed and from the back, the spinal cord, followed by the thoracic, cervical and abdominal organs. This method has been used most widely. The advantages of this technique that each organ can be studied in detail. However, the anatomico-pathological relationships of organs are not preserved thus cannot be studied. 2. C. Rokitansky’s technique: This technique involves in situ dissection in part combined with en block removal. This technique is commonly preferred whenever the pathologist wants to limit
Autopsy Procedures and Exhumation the spread of infection such as HIV, hepatitis B etc. The disadvantage of this method is that the organs cannot be studied in detail. 3. M. Letulle’s technique: In this method thoracic, cervical, abdominal and pelvic organs are removed en masse. But subsequently dissected as organ block. This technique is the best technique for routine inspection and preservation of connections between organ and organ systems. Also the body can be made available to the undertaker in less than 30 minutes without having to rush the dissection. The organ blocks can then be studied in detail. But the organ mass is often awkward to handle. 4. A. Ghon’s technique: In this method the thoracic, cervical, abdominal organs and the urogenital system are removed as organ blocks. But now a days the modification of this technique is used where the organs are removed enblock. The method of evisceration should be the one with which the pathologist is most comfortable that is removing thoracic and abdominal organ blocks prior to dissection or removing each organ in sequence. Many crucial observations can be made only during evisceration. All the organs should be weighed and a brief description of the organs with pertinent negatives should be recorded. With the pancreas, adrenals, and spleen, if there are no positive findings, use of the term ‘unremarkable’ as the sole description is acceptable. The term ‘normal’ should not be used as organs are rarely ‘normal’ whatever that is. The microscopic slides should be made when indicated. Samples of tissue from all major organs should be saved, but microscopic slides are often not needed in forensic cases, especially in trauma cases. The samples and viscera preserved for toxicological analyses should be noted. Finally, the opinion should be given describing briefly the cause of death in language as simple as possible. Detailed Examination of the Neck In asphyxial deaths, especially in hanging and strangulation, it is advisable to open the skull first
147
and brain is taken out to drain out the blood from the neck so that the neck structures can be examined in a relatively bloodless field thus avoiding artefactual haemorrhages. The chest organs can be removed prior to neck dissection avoiding injuring the neck veins. The modified Y-shaped incision will permit a thorough examination of the anterior neck organs and removal of the tongue. The primary midline (Ishaped) incision can be extended superiorly in one of the following ways; (i) a straight incision in front of the trachea, (ii) a bilateral extension of the primary midline incision along the anterior border of the clavicles to the skin in front of the acromion process and (iii) also a bilateral incision extending the primary again along the anterior border of the clavicles but moving superiorly towards the tragus along the lateral side of the neck, ending just behind the ears. If air embolism is a possibility, the neck dissection should be altered, being careful not to injure the large neck veins. The skin and superficial tissues of the neck should be reflected to expose the underlying structures by grasping and retracting the cut border of the skin using the fingers or non-toothed forceps and making gentle horizontal slices along the dermo-subcutaneous tissue plane. After retracting skin and muscles of the anterior chest, a pleural window should be created to detect pneumothorax by scraping the intercostals muscle off the external aspect of the parietal pleura. This should be done on both sides of the anterior aspect of the chest, usually near the third ribs. In cases of third and fourth degree burns, it is usually necessary to make a midline incision to the chin because the tissue is contracted and indurated. Dissection of anterior neck structures: Layerwise examination of the anterior neck structures is desirable in all cases, and is accompanied by sequential in situ photography in cases of suspected strangulation. The platysma muscle is inspected for evidence of bruising. The sternocleidomastoid muscles are left intact and the external jugular veins are then examined. The underlying neck muscles are then reflected in
148
Textbook of Forensic Medicine and Toxicology
layers. First the sternal head of the sternocleidomastoid muscles is divided from the manubrium and then the more lateral clavicular head is detached. These are reflected laterally and the suprahyoid and infrahyoid muscle groups are then examined being careful not to damage any adjacent vessels and produce a false impression of significant haemorrhage. The carotid sheath containing carotid arteries, internal jugular veins and the vagus nerve is exposed after the omohyoid is reflected. The contained structures are gently mobilized and inspected for evidence of haemorrhage. All the anterior neck tissues can now be separated dividing all the structures at the thoracic inlet or further dissection can follow removal of these structures with the thoracic contents. Dissection of posterior neck structures: Posterior neck dissection is necessary to rule out craniocervical derangement in cases of suspected suffocation in traffic accidents and is recommended in all infant deaths occurring outside the hospital. Layerwise examination of posterior neck structures is required for traffic fatalities in which there is sufficient trauma elsewhere to account for the death, or in which there is unexplained laceration of brainstem, or haemorrhage in the paravertebral fascia.The prevertebral fascia can be examined for evidence of traumatic injury, such as presence of crepitus. The fascia is then reflected from the underlying bone. The body is turned over and the superficial tissues including ligamentum nuchae is reflected from the occipital region inferiorly to the base of the neck, in order to expose the underlying soft tissue. Examination of the Heart The sternum is removed and then the pericardial blood clots, if present should be weighed. Normal hearts and most hearts with acquired disease can be excised separately. After removal of the blood clots, the heart is weighed. The heart may be of normal size or enlarged (cardiomegaly) due to hypertrophy or
dilatation, or both and can involve one or more chambers. The heart is normally conical shaped but it may be globoid or irregular, as with ventricular aneurysm and one or more chambers may be abnormal in shape. The endocardium is examined for evidence of fibrosis and any evidence of premortem thrombus. The colour of the subepicardial myocardium may be gray with an old infarct, pale with chronic anaemia, and mottled or haemorrhagic, with an acute infarct or rupture. Left ventricular consistency can be firm due to hypertrophy, fibrosis, amyloidosis, calcification or rigor mortis; or soft due to acute myocardial infarction, myocarditis, dilated cardiomyopathy or decomposition. Examination of myocardium: The myocardium is examined for fibrosis or recent infarct. The myocardial infarct is easily identifiable when it is of more than 12 hours. Between 12-24 hours, the infarct is dusky and shows hemorrhagic discolouration. At 1-4 days, the infarct is more obvious and shows a mottled yellow and red pattern. The infarct is more hom*ogenous and is at first yellow than white in colour after the passage of five days. The size of the infarct, its location, the extent whether it is sub-endocardial or transmural and its correlation with any arterial disease is to be noted. Evidence of ventricular hypertrophy: 1. Thickness of both ventricular walls at a point about one cm below atrio-ventricular valve is measured. However, any dilatation will mask the hypertrophy. The upper limits for thickness of ventricular wall is 1.5 cm for left ventricle, 0.5 cm for right ventricle and 0.2 cm for the atrial muscle. 2. Left ventricle and septal wall are separated from the right ventricle and then weighed and the ratio is obtained. Examination of valve: The circumference of the valve is measured with a ruler or the length of the string. The circumference of mitral valve is 8-10.5 (10 cm) and admits two fingers; tricuspid valve is 10-12.5 (12 cm); aortic valve is 6-8 cm (7.5 cm)
Autopsy Procedures and Exhumation and pulmonary valve is 7-9 cm (8.5 cm). The decrease in circumference denotes stenosis whereas increased circumference could be due to regurgitation and when the valves are incompetent. The abnormality in the measurement should always be accompanied by scarring, fusion or calcification of the valves otherwise little importance should be given to abnormal measurement. Evaluation of coronary arteries: Coronary arteries should be inspected for calcification and tortuosity. In subjects younger than 30 year, in which the cause of death is non-cardiac, the coronary arteries may be opened longitudinally. Otherwise, the vessels should be cut in crosssection at 3-5mm intervals. Calcified vessels that cannot be readily cut with a scalpel should be stripped off the heart and decalcified for at least 24 hour before cutting. To grade coronary obstruction, a four-point system is applied, by 25% increments of narrowing in cross sectional area. A grade-4 lesion indicates stenosis of at least 75% of the coronary artery and is considered as severe, whereas a grade-4 lesion of 90% represents critical stenosis. As a rule, grade-4 lesions should be documented microscopically. Depending on the number of major epicardial vessels with grade-4 lesions, a heart may have severe 1-vessel, 2-vessel, or 3-vessel disease, and its coexistence with grade-4 disease in the other three coronary arteries represents severe 4-vessel disease. Dissection of the Heart: Only two methods are practically used for routine diagnostic pathology, these are the inflow-outflow method and the short axis technique. 1. Inflow-outflow method or following the direction of blood flow: The technique is suitable primarily for normal hearts and the atrium is opened first on each of the side and then the ventricle is opened along its inflow and outflow tracts. The valves are cut between their commissures. Using scissors, the initial cut is made from the inferior vena cava to the right atrial appendage, sparing the superior vena cava with the region
149
of the sinus node. The right ventricular inflow tract is opened with a knife or scissors from the right atrium, through the posterior tricuspid leaflet, running parallel to and about 1 cm from the posterior ventricular septum. The outflow tract is opened in a similar fashion, about 1 cm from the anterior ventricular septum extending to through the pulmonary cusp and into the main pulmonary artery. The left atrium is opened with scissors between the right and left upper pulmonary veins and then between the upper and lower veins on each side. The incision can be extended into the left atrial appendage to assess for mural thrombus. The left ventricular inflow tract is opened with a long knife along the inferolateral aspect through the left atrial wall near its appendage, through the mid-portion of posterior mitral leaflet, between the two mitral papillary muscles and then through the apex. The outflow cut travels parallel to the anterior ventricular septum and about one cm from it. This curved cut is best accomplished with a scalpel, taking care not to cut into either the anterior mitral leaflet or the ventricular septum. Scissors can be used to extend the cut across the left aortic cusp and into the ascending aorta, to one side or other of the left coronary ostium. 2. Short axis or ventricular slicing method: This method is of choice to evaluate ischemic heart disease as well as any other cardiac condition as the slices expose the largest surface area of myocardium. They correspond to the short– axis plane produced clinically by the twodimensional echocardiography. The flat diaphragmatic surface of the heart is placed on a paper towel to prevent slippage and then cuts 1.0-1.5 cm thick are made with a sharp knife, parallel to the atrioventricular groove. One firm slice should be used, or two slices in the same direction, avoiding sawing motions that leave hesitation marks. Each slice is viewed from the apex towards the base. The basal third of the ventricle is left attached to the atria. The basal portion is then opened according to the inflow-outflow method.
150
Textbook of Forensic Medicine and Toxicology
3. Other tomographic methods of dissection of heart: For teaching purposes, the short-axis, long-axis and four chamber planes are ideally suited for demonstrating cardiac pathology. i. Long axis method: The plane for long-axis method is best demarcated with three straight pins before making the cut. The first pin is placed in the cardiac apex, the second in the right aortic sinus adjacent to the coronary ostium and the third near the mitral valve annulus, between the right and left pulmonary veins. The heart can then be cut along this plane, from the apex towards the base, passing through both the mitral and aortic valves. ii. Four-chamber method: In this method, the heart is divided into two portions, both of which show all four chambers. Using a long knife and beginning at the cardiac apex, a cut is extended through the acute margin of the right ventricle, the obtuse margin of the left ventricle and the ventricular septum. The upper half is then opened along the ventricular outflow tracts according to the inflow-outflow method. iii. Base of heart method: This method displays all four valves intact at the cardiac base and is ideal for demonstrating the relationships between the valves themselves and between the valves and adjacent coronary arteries and the atrioventricular conduction system. iv. The window method: This method is used for the preparation of dry museum specimens using paraffin or other material or plastination. Heart should be perfusion fixed. Windows of various sizes can be removed from the chambers or great vessels with scalpel. The tissue blocks can then be used for histologic study. v. Unrolling method: The technique is used for demonstrating opacified coronary arteries in a single plane. Following postmortem coronary angiography, the ventricular septum and free walls are unrolled by any
of the three techniques; Schlesinger technique, Lumb and Hardey technique and the Rodriguez and Reiner technique. But the latter is the simplest technique of the three. The unrolling method results in considerable mutilation of the heart and is best reserved for research purposes. vi. Partitioning method: Each ventricle is weighed separately for detailed assessment of ventricular hypertrophy. The epicardial fat and coronary vessels are stripped from the specimen then atria and great arteries are removed. Finally ventricular free walls are separated from the ventricular septum, the weight of each segment is now compared with the normal values. Biventricular hypertrophy may produce an abnormal ratio. Normal ratio of LV + S: RV is 2.3-3.3:1 In left ventricular hypertrophy, this ratio is more than 3.6:1 or left ventricle with septum is more than 225 gm whereas in right ventricular hypertrophy, the ratio is less than 2:1 or right ventricle is more than 80 Gms. vii. Examination of the conduction system: This conduction system is examined if pathology within the conduction system is suspected. It is largely a histological process and three tissue blocks containing SA node, AV node and AV bundles are made. Examination of the Lungs The lung is weighed prior to the dissection. The normal lung weighs 250-400 grams each but there is a considerable variation depending on the built and sex of the individual. The weight of the lung increases with severe cardiac failure or with diffuse lung pathology. The internal examination of lung can be done by: 1. Dissection of the airways: Airways are dissected using a pair of Scissors from the medial to the lateral including all the lobes and segments
Autopsy Procedures and Exhumation opening along the branches as they are documented. The airway caliber, mucosal surface and parenchymal appearance is examined for fibrosis, consolidation, tumours, scars or cavities. Old tuberculous cavities and fungal balls can be assessed. Chronic obstructive airway disease can be assessed by how peripherally airways can be opened. The examination of airways is of considerable importance in drowning, choking and burn deaths. 2. The pulmonary vessels can be dissected to look for the emboli and atheroma. 3. By horizontal slicing of the lung through each lobe with brain knife and to inspect the parenchyma for haemorrhages, abscesses and consolidations. Examination of Liver The liver varies in weight from 1300-1500 gms. The liver may be enlarged with inflammations and neoplasms and shrunken with cirrhosis. A series of parallel vertical slices 1-2 cm apart from one side to the other are made to examine the liver parenchyma for haemorrhages, lacerations or abscesses Examination of Brain in Adults Incision of scalp: First the head should be elevated using the head rest. The hair is then parted with a comb along an imaginary coronal plane connecting one mastoid over the other over the convexity. The incision is then given on one side just behind the ear lobe, as low as possible and is extended to a comparable level on the other side cutting whole thickness of the scalp using the scalpel blade (Fig. 8.2). The anterior and posterior halves of the scalp are then reflected forwards and backwards respectively by short undercutting of the scalp and using a dry towel draped over the scalp edges to facilitate further reflection. The anterior flap is reflected to above 12 cm above the supraorbital ridge. Removal of skull cap: The cranium is best opened using an oscillating saw within a protective device
151
Figure 8.2: Lines for removal of scalp
such as plastic bag for collection of dust. The temporalis muscle should be cut with a sharp knife clearing it from the path of blade of the saw. The frontal point of sawing should start approximately two finger breadths above the supraorbital ridge and then the head is turned to the opposite side and sawing extended to the temporal point that is at the top of ear in its natural position. Finally the occipital area that is approximately two finger breadths above the external occipital protuberance is sawed. The oscillating blade should be moved from side to side during cutting to avoid deep penetration in a given area. Ideally sawing should be stopped just short of cutting through the inner table of skull that can be further detached with mallet and chisel. A hand inserted between the skull and the dura helps the blunt separation of these while the other hand is pulling the skullcap. If the dura adheres too firmly to the skull, it can be incised along the lines of the sawing and the anterior attachment of the falx to the skull can be cut between the frontal lobes. The posterior portion of the falx can be cut from the inside after the skullcap is fully reflected. Leaving the dura and underlying leptomeninges intact allows viewing the brain with overlying cerebrospinal fluid still in subarachnoid space. To obtain this view, after removal of the skullcap, the dura must be cut with a pair of scissors along the line of sawing and then reflected. The dura is then peeled off the
152
Textbook of Forensic Medicine and Toxicology
skullcap. The superior sagittal sinus may be opened with a pair of scissors at this time. The dorsal dural flaps on both the sides can be removed easily from the brain by severing the bridging veins but in the presence of epidural or subdural haemorrhage or neoplasia, the dural flaps are left attached to the dorsal vein and can then be sectioned together (Fig. 8.3 and 8.4).
A
C
B
Figure 8.3: Methods of Removal of Skull cap
A
Removal of Brain in Adults The brain is removed by raising the frontal lobes gently and tearing the olfactory bulbs and tracts away from the cribriform plates. The optic nerves are then cut as they enter the optic foramina. Under its own weight, the brain is allowed to fall away from the floor of the anterior fossa, supported by the palm of the other hand. The pituitary stalk and internal carotid arteries are then cut as they enter the cranial cavity. Third, fourth, fifth and sixth cranial nerves and subdural communicating veins are also severed close to the base of skull. The attachment of tentorium along the petrous ridge is cut on either side with curved scissors while the brain is prevented from dropping backwards and causing stretch tears in cerebral peduncles. Now the VII, VIII, IX, X, XI and XII cranial nerves are cut and the vertebral arteries are severed with scissors as they emerge in cranial cavities. The cervical part of spinal cord is cut using curved scissors as caudally as possible and avoiding too oblique plane. The brain is reflected back further by using the support of hand to deliver the brain stem and cerebellum from the posterior fossa without causing excessive stretching at the rostral brain stem level. The brain is pulled away from the base of skull after cutting the lateral attachment of the tentorium to the petrous bone along with the pineal body. Fixation of the Brain
B C
D
Figure 8.4: Lines along which saw cuts are made for skull cap removal
The best routine fixative that allows the widest choice of stains for the nervous tissue is formalin, usually as a 10% solution. In fetuses and infants, the addition of acetic acid to the fixative solution appears to be helpful. It increases the specific gravity of the fixative and allows the brain to float in the solution; it also makes the tissue firmer without altering its histological characteristics. Fixation can be done by immersion and perfusion methods. For detailed anatomic studies, it is best to fix the brain specimen in a large amount of freshly prepared 10% formalin solution. The plastic buckets for holding 8 L can be used to suspend
Autopsy Procedures and Exhumation the brain to prevent distortion during fixation by passing a thread underneath the basilar artery in front of the pons. A thread can be passed under the internal carotid artery or middle cerebral arteries on both the sides, provided that no pathological lesions are suspected in these regions. Alternatively, the dorsal dura can be used as an anchoring point. However, suspension from blood vessels deforms the parenchyma less than dural suspension. The ends of the threads are tied to the attachments of the bucket handle, care being taken not to allow the specimen to touch the bottom or sides of the bucket. Formalin solution should be replaced within the first 24 hours but this is not mandatory if a large amount of fixative is used. If the fixative becomes bloody, is to be replaced with fresh solution that prevents undue discolouration of the specimen. About 10-14 days are required for satisfactory fixation. If the brain is dissected earlier, the central portion may remain pink. The brain can be perfused with fixative through the arterial stumps before further fixation by immersion. This shortens the fixation time and ensures adequate fixation of deeper portions of the brain. When it is necessary to dissect the brain at the time of autopsy, this preliminary fixation makes tissue further, facilitates dissection and decreases tissue wrinkling. For the perfusion, injection of 150ml of isotonic solution followed by 10% formalin manually with a syringe connected to a simple tubing system causes least problems.
153
The sections can then be made into primary slices of brain tissue to expose hidden but suspected lesions. The brainstem can be severed and cut into infratentorial structure and one horizontal cut through these structures is sufficient for preliminary examination. With fresh dissection of the brain, small lesions are easily missed and subtle lesions such as an early infarct can be overlooked. Every brain should be reexamined with new dissection after adequate fixation. Preliminary perfusion or cooling of the brain in a contoured support in refrigerator in about 30 minutes will increase the consistency of the brain and make regular dissection of the brain easier. The brain suspected of harbouring diffuse, roughly symmetric lesions as in cases of metabolic diseases or widespread infections may be bisected along the sagittal plane. One half may be submitted for chemical analysis or for microbiological examination while the other half is to be kept and later sections are taken for histological examination (Fig. 8.5).
A
Dissection of Fresh Brains In adults the examination of brain lesions in terms of anatomic correlations with clinical symptoms can be achieved when the brain is sectioned after adequate fixation. At times the brain must be dissected in fresh state when microbiological and chemical investigations are important or when immediate diagnosis is necessary. Three to four coronal cuts through cerebral hemispheres are given leaving anatomic structure basal ganglia and upper brainstem undisturbed (Fig. 8.5A). This reveals the presence of large lesions directly or indirectly by distortion of the ventricular system.
B +
C Figure 8.5: Coronal dissection methods for the cerebrum
154
Textbook of Forensic Medicine and Toxicology
Dissection of Fixed Brain
Pediatric Autopsy
The external surface of the brain is carefully examined and the arteries at the base may be exposed through the tears made into arachnoid membrane. The pathologic conditions like thrombosis, embolism or aneurysm are observed. After adequate external examination the next step is to separate the cerebellum and brain stem from the cerebral hemisphere. The brain is placed right side up that gives more stability to the specimen. The dissection may be carried out with the frontal lobes by slicing method. The preferred thickness is about 1 cm and each new cut surface is examined before a new cut is made. The slices are displayed on the autopsy table on the right side of the doctor. This corresponds to viewing one’s own brain from behind. There should be no overlapping of the slides displayed. The cerebellum can be dissected on the horizontal plane on planes perpendicular to the folial orientation, the latter method gives the best histological orientation of the structures. The brain stem is sectioned perpendicular to its axis (Fig. 8.6).
There are various pediatric autopsy techniques being used by the pathologists. The external examination particularly of the newborn is important. The pathologist should concentrate on the search for malformations such as cleft palate, choanal atresia, stenosis and atresia of the anus and vagin*. Face, ears and hands should be properly examined to look for characteristic changes in Down’s syndrome and renal agenesis. The placenta and umbilical cord must be studied in all these autopsies. The esophageal hiatus should be examined in situ. In this age group, the skull is often difficult to separate from the dura as in adults. Beneke’s technique is used to open the skull when the sutures are not closed and the skull bones are soft. After the scalp is reflected as in adults, the cranium and dura on both the sides are cut with blunt scissors starting at the lateral edge of the anterior fontanelle extending the incisions as shown in Figure 8.7 along the midline and the lateral sides of the skull. The midline strip about 1 cm wide containing the superior sagittal sinus and the falx is left and also an intact area in the temporal squama on either side, which serves as a hinge when the bone is reflected. This method usually results in damage to the brain. The damage can be minimized by B A
A
B
C
C
Figure 8.6: Dissection lines for brainstem and cerebellum
Figure 8.7: Method for opening skull in fetus and neonates
Autopsy Procedures and Exhumation infusion of 10% formalin in 70% alcohol through the neck arteries in an early stage of autopsy. In a modification of Beneke’s method, the skull is incised lightly along the sutures and at the fontanelles. The scalpel is then reversed and passed under the bones to separate it from underlying dura. The bone flaps are reflected after a small nick is made at the base in each of the bones. The dura is then cut as close to the base of skull as possible. This method protects the friable brain of the infant during its removal. The damage to the brain can further be minimized if the scalp and skull are opened and the falx sectioned with the body in a sitting position and infant’s head being supported by the assistant. The tentorium and vein of Galen are transected in this position by separating the parieto-occipital lobes. The tentorium is separated and the body is suspended upside down by the assistant, the brain being cut away from the base of the skull on both the sides in this position thus minimizing the movements of the brain and hence the damage. The brain is not touched during these procedures and when all the attachment are severed, it is allowed to fall free preferably in to the body of water, not on hard surface. In infants the whole chest cavity can be opened under water in order to demonstrate a pneumothorax. In infants and foetuses Letulle’s technique of en masse removal is the preferred technique in most cases so that certain rare malformations can be properly preserved for example pulmonary venous connections. Histological sections should be taken from lungs, liver, kidney, brain, thymus, placenta, umbilical cord and the free margin of falciform ligament. Routine Sampling of Toxicological Material The highest concentration of toxicological substances is found in dialysis and lavage fluids. The gastrointestinal tract is not the only route of entry of poisons in the body. Furthermore, if any significant period of 4-6 hours elapses from the time of ingestion until death or treatment, the
155
poison will have passed out of the stomach. The poison also could have been introduced to mask a homicide. Thus in all the cases a variety of tissues and fluids should be sampled for toxicological analysis. The knowledge of postmortem distribution of a toxic agent in different body fluids and tissues enables the forensic pathologist to distinguish inhalation poisoning from ingestion poisoning. Generally the viscera are preserved in rectified spirit except in poisoning by carbolic acid, alcohol, phosphorus, paraldehyde and acetic acid where it is preserved in saturated solution of common salt. Rectified spirit being costly and not easily available, all the viscera are routinely preserved in saturated solution of salt. Various types of samples that have to be preserved are: Tissue or fluid
Sample
Stomach
Stomach with all its contents (vomitus and gastric lavage fluid if available) Separately tied portions of intestinal tract with contents (about 30 cm of first part of intestine) 500 gms or whole organ with gallbladder One half of each kidney Half or whole organ 100 ml with preservative and 100 ml without preservative
Intestine
Liver Kidneys Spleen Blood
Blood, bile and urine should be kept refrigerated. Sodium fluoride may be added as a preservative when alcoholic intoxication is suspected (250mg/ 30ml of fluid). For longer storage periods toxicological material is best kept in deep freeze. Methods of preservation of various samples: Blood: After death the serous membrane of the stomach and intestine break down allowing the substance to migrate to the organs of the chest and abdomen as there is a false rise of the substance in the blood level. Ideally before autopsy about 50 ml of sterile blood should be collected from the peripheral (femoral, inguinal or subclavian) veins. After removal of the viscera again 10-15 ml of blood should be collected from these areas. No blood to be collected from the pleural and the peritoneal cavities. If the heart blood is
156
Textbook of Forensic Medicine and Toxicology
clotted, the vena cava or the aorta should be punctured. If peripheral blood cannot be obtained samples from the right and left sides of the heart should be collected separately. In cases of drowning 10 ml of blood is removed from each side of the heart for separate sodium, chloride or magnesium determinations. In barbiturate and ethanol poisoning, toxicological examination of portal vein blood may be of interest. Any anticoagulant other than heparin may be used. The blood should be preserved by adding 10 mg of sodium or potassium fluoride and 3 mg of potassium oxalate. CSF: It is usually collected by lumbar puncture or from the cisterna magna by inserting a long needle. This is to be done during internal examination. More than one blood free sample may be needed. Direct aspiration can be done from the lateral or third ventricle. Vitreous: Vitreous humour can be used for determination of alcohol and for other toxicological studies, particularly when other body fluids are not readily available. It can be withdrawn using fine needles through the outer canthus of the eye. 1 -2 ml can be taken from either eye. The tip of the needle should lie near the centre of the eyeball. Forceful aspiration must be avoided because it may detach retinal cells, which cloud the specimen and give spuriously high potassium values. The vitreous humour may be stored in a refrigerator at 4°C for upto 48 hours. Bile: Bile is best removed by puncturing the gallbladder in situ. Gastrointestinal tract: The stomach can be saved with its contents by placing ligatures around the lower end of esophagus and the upper end of duodenum. The organ is then opened to inspect the contents of the stomach and its walls. In poisoning with yellow phosphorus, the stomach has to be opened under nitrogen just before analysis. Several portions of the small and large intestine each about 60 cm long are tied by double ligatures. The separate portions are labeled and submitted unopened for toxicological examination.
Hair: Hair should be pulled from the scalp, not cut. A large sample of about 10 gm should be collected and tied in locks with cotton. This should be done in a manner that identifies the ends where the hair roots are. Skin: In suspected injections of poisonous substances the skin around the suspected site is excised at a radius of 2-4 cm from the injection site. If a poisonous substance might have been taken up by absorption, the skin is excised in an area where the absorption is thought to have occurred, and a distant preferably a contralateral area. Bone: In cases of subacute or chronic poisoning by heavy metals mostly arsenic, antimony and thallium about 10 cm of the shaft of femur to be preserved for analysis. Urine: Urine is best collected in a sterile needle and a syringe through the dome of the diaphragm. The sterilized wall is stretched between two hemostats and then punctured. Urine is of utmost importance for toxicological analysis. Every effort must be made to collect it. The urethra should be tied or clamped and the dome of bladder widely incised between hemostats, which then are used to hold the bladder open. Urine should be preserved in 50 ml bottles. Uterus: In deaths due to criminal abortion, uterus and appendages along with upper part of vagin* are preserved with any chemicals or foreign bodies found in the genital tract to be preserved separately. Heart: Heart should be preserved in cases of poisoning by cardiac poisons like strychnine and digitalis. Brain: Brain has to be preserved in poisoning from alkaloids, organophosphorus compounds and volatile organic poisons. Spinal cord should be preserved in strychnine poisoning. As a routine practice the stomach and intestine are preserved in one glass jar filled with saturated solution of common salt up to 3/4th of its volume. The second jar is used to preserve the liver, spleen and kidney. Blood is kept separately in a bottle.
Autopsy Procedures and Exhumation In another bottle the sample of the preservative is supplied. All the jars and bottles are sealed and kept in a wooden box which is finally sealed and handed over to the I.O. for onward transmission to the laboratory along with the sample seal. The polyethylene bags or containers can be used but the volatile poisons may diffuse through it. In cases where lungs have to be preserved for analysis like that of volatile poisons, nylon bags should be used and the blood should be kept in plastic capped tubes.
Laboratory Investigations Samples for histopathological examination: The internal organs like liver, lung, brain etc. are taken for histological examination. It is not being done routinely but if after gross examination some pathology is suspected then 1-2 mm thick tissue can be removed along with normal area. It is preserved in 10% formalin or 95% alcohol. The amount of preservative should be enough not to dry the tissues inside the container. Bacteriological examination: Blood should be kept in sterile containers using sterile syringe to collect the blood from the right ventricle. The samples from other organs must be collected by using sterile methods for culture of specific tissue. The surface is seared with a hot spatula and the area is punctured with a sterile instrument and the pulp is scraped. Smears: In deaths due to suspected malaria, the smears from cerebral cortex, spleen and liver may be stained and examined for malarial parasites. Bone marrow and ribs or sternum is used in cases of blood dyscrasias. Virological examination: A piece of the tissue is collected under sterile conditions and the sample is preserved in 80% glycerol in buffered saline or freezed for further examination. Second Autopsy There is no provision in Indian law to have a second autopsy. However, nowadays it is being conducted
157
either by the order of a district magistrate/senior police officer or by a order from the Court of law, though the instances are rare. Aim: (i) To find out the cause of death, when it can not be opined by the doctor who had conducted the First autopsy. (ii) When the relatives are not satisfied with the cause of death, they request to higher authorities for a second autopsy done. Procedure: Second autopsy usually done by a board of doctors, mostly three in number, from different institutions. In these circ*mstances, the body is usually buried which is to be taken out from the grave. If the body has been kept in the mortuary after the first postmortem, it should be removed to the place of the second postmortem. The board should obtain a request letter/ order of the competent authority along with the inquest papers. If possible the doctor who had conducted the first postmortem should be in the theatre, so that necessary clarification or collaborations can be obtained. The interpretation of the findings of an exhumed body, that has undergone the first autopsy is very difficult because of putrefactive changes and artefacts caused during burial/ exhumation, as well as the alterations made during the first autopsy. The findings should be written in detail irrespective of the fact that it correlates or contradicts with the findings during first autopsy. During the second autopsy some new facts may come up, that may help further investigations. If no new facts are discovered, the second autopsy will correlate the findings of the first autopsy and further doubt and allegations will come to an end. Negative Autopsy One of the important objectives of autopsy is to find out the cause of death as well as any contributory cause of death. Nevertheless, when the gross and microscopic findings fail to reveal any apparent cause of death, along with the examination of chemical analysis report and other relevant laboratory investigations, it is termed as negative autopsy. The rate of negative autopsy is
158
Textbook of Forensic Medicine and Toxicology
about 5-8% of all the autopsies. Even the best equipped centres of the World have more than 5% negative autopsy rate. The possible reasons are as follows: Inadequate history: In medicolegal autopsies, the doctors should take adequate history about the incidence. Particular references should be made about the signs and symptoms prior to death as deaths from vagal inhibition, epilepsy, laryngeal spasm, electrocution in water as well as hypersensitivity reactions may not show any external findings. Lack of proper external examination: Electrical burn marks should be looked especially for the exit wounds as they are most often missed by the pathologist due to lack of experience. In addition, the needle pricks in anaphylaxis are often missed. The concealed wounds may also be missed often. Improper internal examination: Faulty laboratory examination along with faulty toxicological analysis is also responsible for negative autopsies. The experience and capability of the doctors can be responsible for this. Insufficient histological examinations: Various microscopic lesions account for death, and are missed due to insufficient histological examination. Inadequate Pathologist’s training: Sudden, unexpected deaths with atherosclerotic narrowing of the coronary arteries without thrombosis or infarction may be a cause of death which is often missed by a hospital pathologist. Obscure Autopsy The autopsy is termed as obscure, as there is no definite or obscure cause of death. This type of autopsy is create a lot of confusion to the forensic experts. The causes of obscure autopsy are: 1. Concealed trauma: Concussion is a state of transient unconsciousness as a result of blunt force injury to head followed by amnesia and spontaneous recovery. Autopsy may not show
any change, but in some cases petechial hemorrhages are found. Even microscopic examination does not reveal any axonal injury up to 12 hours. Injury to the cervical spine causing fracture dislocation and injury to the spinal cord can cause instantaneous death without any obvious external injuries. 2. Cardiac lesions a. In blunt force injury to heart it may stop functioning without any visible signs. b. Cardiac arrest can occur during or immediately following heavy exercise in which there is increase in heart rate and systolic pressure with progressive ischemia and cardiac arrest. c. Cardiac arrythmias which, may be precipitated by emotional excitement can cause physiological asystole and may lead to death. 3. Reflex vagal inhibition: which can be due to pressure on neck following blows on the larynx, chest, abdomen and genital organs. When death is due to reflex vagal inhibition, there is hardly any findings at autopsy. It may occur during drowning, when the body is subjected to very cold temperature. Any manipulation of external auditory meatus may also lead to death due to vagal inhibition. Exhumation It is the lawful digging out of an already buried body from the grave. It is done both in civil and criminal cases. Also, if there is an allegation that the proper autopsy has not been done or the body has been disposed off without any autopsy and foul play is suspected, exhumation can be carried. Civil Cases (i) Accidental death claim (ii) Indurance (iii) Liability for medical negligence (iv) Workmans compensation claim (v) Inheritance and disputed identity cases. Criminal Cases (i) Deaths due to criminal abortion (ii) Homicide or suspected homicide when death
Autopsy Procedures and Exhumation has been labeled as otherwise (iii) Suspicious poisoning (ii) Criminal negligence Rules of exhumation: The written order is obtained from an Executive Magistrate. There is no time limit for exhumation in India. The magistrate along with police officer and medical officer should report at the spot. The spot of burial is to be identified correctly. This can be done with the help of relatives and other persons related with the disposal. Even the person who had made the coffin can be called to identify the coffin. Besides, the location of the grave from some fixed objects like road, tree etc. to be noted. If the map is available, it will be of help. The entries in the register should also be seen. The relatives are allowed to stay throughout the investigations (S.176(4) CrPC). Procedure: After correct identification of the spot, the area should be enclosed from the public. The exhumation is carried out in the early hours so that there is less public as well as the digging out work can be completed during day time. The identified grave then should be dug carefully up to the depth of 10-15 meters and condition of soil, water content and vegetable grown should be noted down. The grave is further dug up to coffin or corpse and photographs are taken. A sketch may be drawn about the position of coffin and body. At this point it should be identified by the relatives. The plastic sheet or a plank may be lowered down to the level of the corpse then it (corpse) is shifted to plank and taken out carefully to avoid artefacts. No disinfectant should be sprinkled on the body. In case of skeletonisation of the body, the grave is further dug and the skeleton is lifted to sheet/ plank. The soil to be searched for smaller objects like bullets, teeth, hyoid bone, metallic objects. If the body can not be transported or the mortuary is very far off then autopsy can be carried out at the spot. Any fluid and debris in the coffin should be collected. Injuries if present should be carefully noted. The injuries on soft parts may get distorted or disfigured due to decomposition thus care should
159
be taken to interpret them correctly. The possibility of artefacts during the process of digging should be excluded. In suspected poisoning, viscera should be kept for analysis. If organs are converted into mass, then loose masses to be preserved. If nothing is found then hair, soil, teeth and bones should be preserved. About ½ kg of earth to be collected from the top, sides, bottom of the body and kept in dry clean bottles for chemical analysis. A portion of coffin and burial cloths must be removed in order to exclude any possibility of contamination from external sources. Though, there is no time limit for exhumation in India. The period is restricted to 10 years in France whereas in Germany it is 30 years. BUNDLE OF BONES At times some skeletal remains may be recovered from an open land, ditches, rubbish dumps etc., or a skeleton may exhumed from a temporary grave, a burial ground, or even while new constructions. The bones should be listed and the photographs are preferably taken. The bones should be arranged in an anatomical position of articulation. If some earth, sand, dust etc is sticking to the bones, it is to be cleaned by brushing. General Examination of Bones: The bones are thoroughly examined as to whether the bones are dry, clean, brittle and whitish in colour with cartilages attached or whether they are moist and humid, yellowish or yellowish brown, with soft tissues still attached and cartilages adhering. The stage of putrefaction of soft tissues should also be noted (Fig. 8.8). Cleaning the Bones: The soft tissues can be separated by boiling in water containing sodium bicarbonate for about 6-12 hours and then brushing gently. Examination Proper: Whenever a skeletal remains or a single bone is brought for examination to the forensic expert, the following questions need to be answered:
160
Textbook of Forensic Medicine and Toxicology
Figure 8.8: Skeletanized remains
1. Whether they are actually bones: Sometimes pieces of stones may be mistaken by the Police officer for bones. For this, proper examination, looking for the protuberances, surfaces, borders etc. is necessary. 2. Whether the bones are human or animal? Human skull is commonly mistaken for that of the Chimpanzee, Gorilla or Monkey. The bones can be differentiated from that of an animal from the anatomical configurations. In an animal skull, glabella is more prominent, nasion is deeper, jaw is protruded and the cranium is small in size. In Human pelvis, iliac crest and upper border of symphysis pubis lie in the same plane whereas in animals they lie in different planes due to different postures while walking. Precipitin test being species specific would be helpful when the remnants of blood are still attached to the surface of bones. 3. Whether they belong to one or more than individuals: The bones are arranged in anatomical position and if all the bones fit properly and anatomically and there being no disparity between the bones of contralateral side or duplication and all bones belong to same age and sex it suggests that the bones are of same individual. 4. The race of the person to whom the bones belong? Race of the individual can be
known from cephalic index that is 70-75 when the skull is dolicocephalic in pure Aryans, 76-79 in mesaticephalic skull of Europeans and 80-84 in brachycephalic skull of mongoloids. The other indices used to determine race are (i) Brachial Index (ii) Crural Index (iii) Humero-femoral Index. 5. The sexing of bones gives definite results only after puberty. The sex of the person can be determined from the subjective and objective parameters. The subjective parameters include the examination of different bones determining the sex such as the pelvis, skull, long bones, mandible, sacrum, sternum, clavicle etc. When the bones are strong having rough surface, marked muscular marking and well marked prominences and tubercles they belong to males. The average weight of Indian male skeleton is about 4.5kg and in an average Indian female it is about 2.5kg. Children attain half the adult weight by about 12 years in case of boys and under 11 years in case of girls. The pelvis is the best bone used for the purposes of sexing; the accuracy for sexing from different bones according to Krogman is from pelvis (95-96%), skull (9092%), skull and pelvis (98-99%), long bones (80%). The objective indices for determining sex include: (i) Sciatic notch index (ii) Ischium pubic index (iii) Pelvic index (iv) Kell index 6. The age of the person to whom it belongs? The age of the person can be determined from the ossification and union of the bones state of dentition, closing of sutures, state of calcification of laryngeal cartilages, sternum and hyoid bone, condition of the symphyseal surfaces of the pubic bone, changes in the sacrum and mandible, extent of wear and tear in both the jaws with ageing and changes like bony lipping, osteoporotic and osteoarthritic changes. Epiphyseal union is about two years earlier in females compared to males. The age
Autopsy Procedures and Exhumation
7.
8.
9.
10.
changes after 25 years and in old age can be ascertained from the changes in the mandible, vertebra, pubic symphysis and internal bone structure. The stature of the individual: The stature is determined fairly accurately using the long bones such as femur, tibia, humerus or radius. The tibia being the best bone used for the purpose. Hepburn’s osteometric board is used for the purpose of measuring the lengths of long bones accurately. The length is then divided by the multiplication factors as devised by Pan and Nat. The stature can also be devised by using regression formulae devised by researchers such as Dupertuis and Hadden, Karl Pearson, Trotter and Gleser. Identifying features: The person identity can be established from the teeth, any congenital peculiarities, any bony disease or deformities such as caries, osteoarthritis, mal-united fracture, spinal deformities, supernumerary ribs and cervical ribs etc. when the skull is available, the superimposition technique can be used by comparing the skull with the photograph of the individual. Nature of injury: The bones should be examined as to whether they are any sharp cuts, or any fractures implying use of blunt weapon or from a vehicle or sometimes they are gnawed by animals when the soft tissues are attached. The charred and blackened bones are suggestive of burns. But in case of intense heat of fires, the bones turn to ashes and are so brittle as to turn to powder when touched. Superficial bones when burnt will show evidence of heat fractures, charring, and cracking, splintering and calcining whereas bones lying embedded amidst thick soft tissues will show molten or guttered condition. A bone when burnt in open fire will become white but when burnt in close fire is black or ash-grey. Time since death: The nature and circ*mstances of burial of the body modifies
161
the rate of decaying of the bone. If the bones are wet and humid, and have an offensive odour, they are recent. Bodies when exposed to open air gets skeletanised within seven to fourteen days. But when the bones loose their soft tissues, the decaying odour will be lost. Because of ground water seepage, the buried bones may show increase of decrease of mineral contents e.g. calcium phosphate, calcium carbonate etc. depending upon mineral rich content of soil. X-ray defraction studies may give an idea about the mineral content of the bone. Following putrefaction, the bones loose their organic constituents and thus become light and brittle, dark or dark brown in colour, such changes depend upon manner of burial (with or without coffin), the nature of soil of the grave, age of the individual etc.; usually the time taken for these to occur varies between 3 to 10 years. In case of burial in mass graves of in shallow graves without any coffin, putrefaction will occur very rapidly. Long buried bones may have chalky texture. Bone marrow and periosteum may persist in the bones for several months often after burial. Superficially buried bones may expand or crack within few years by repeated freezing or thawing. When burial is old, the cancellous bone at the metaphysis and epiphysis may get eroded by effects of weather. In case of fracture, the time may be judged with some accuracy by examining the callus by cutting it longitudinally. As globulin disappears rapidly, precipitin tests on 10 years old samples become negative. The Dating of Human Bones: Examination of the bones rarely, if ever, permits a precise estimate of the time interval since deposition in the ground. At the same time it is possible and important to decide whether they are ‘ancient’ or ‘modern’ bones that the interval is greater or lesser than 50 years. In recent years, a considerable amount of research
162
Textbook of Forensic Medicine and Toxicology
has been carried out in an attempt to increase the accuracy of dating skeletal remains. Some of these depend on sophisticated laboratory techniques, such as radiocarbon analysis, which are difficult and expensive to perform. Radio-carbon is essentially a tool for archeologists and its forensic use is limited because of the insignificant fall in the C-14 content of bones during the first century after death. This is the stumbling block for many physical and chemical methods for bone dating, as although old samples (in excess of 100-200 years) can fairly readily be differentiated from recent bones, discrimination between the dates of skeletal remains recent enough to be of interest to law enforcement agencies and coroners, is too poor to be of much practical use. The environmental conditions are more potent than age in causing progressive degeneration of the bone; even different parts of the same skeleton (and even opposite ends of the same long bone) may be quite different in their chemical and physical properties, if local changes in inhumation such as drainage, are marked. Bones in wet peaty soil may be decalcified and crumble within two decades, yet bones in dry gravel or sand may remain almost pristine for millennia. Naked eye appearances are very deceptive, but bones with remnants of periosteum, tags of ligament or soft tissue other than adipocere are likely to be less than 5 years old, unless kept in a dry protected place. A ‘soapy’ texture of the surface, from residual fat, also indicates a date of less than a few decades. The various laboratory test used for the purpose of dating human remains include the following but results of each test should be interpreted in the light of the others and with due regard to the macroscopic appearances and the fullest information of the place of concealment and any circ*mstantial evidence.
i. Nitrogen content: New bones contain 4.04.5 gm% of nitrogen, derived mostly from the collagenous stroma. After a variable interval following death, usually longer than 60-100 years, this declines. A value of 2.5gm% usually indicates an age of at least 350 years. ii. Amino-acid content: Amino acid content is estimated by autoanalyser after acid hydrolysis of the residual protein. Up to 20 acids may be found in bones less than a century old. They then decline in number and concentration. Earlier work using thin-layer chromatography suggested that praline and hydroxyproline (constituent of collagen) vanished by about 50 years, but the more sensitive modern methods of analysis do not confirm this. iii. Blood pigments: Blood remnants may be found up to a century using the most sensitive, though non-specific tests. As benzidine have carcinogenic activity, other tests such as phenolphthalein and leucomalachite green can detect blood only up to 5-10 years, using either bone dust or the periosteal surface as the test area. iv. Fluorescence: Fluorescence can be seen across the whole freshly sawn surface of a long bone under ultra-violet light for more than a century, but beyond this time, declining fluorescence is seen advancing from both the outer surface and the marrow cavity. The ‘sandwich’ of fluorescence progressively narrows during the first 50 years and may vanish with 300-500 years. v. Immunological activity: Eluted extracts of bone when tested against animal antihuman serum gives a visible antibodyantigen reaction, either in cross-over electrophoresis or by passing diffusion in gel. Early work suggested that this persisted for 5-10 years, but recent repetition of the tests indicated that it ceases within months of death.
Autopsy Procedures and Exhumation 11. Cause of death: Presence of depressed comminuted fracture, cut injury or bullet wounds in the skull, facture-dislocation of the vertebral column, facture of ribs, hyoid or any other limb bones etc. will be informative, pointing towards the cause and nature of death. Metallic poisons like Arsenic, Lead, Antimony, Mercury etc. can be detected in the bones long after death. Arsenic can be recovered even from examination of charred bony fragments. From the type and depth of cut in the bone the nature of the offending weapon can be made out. Examination of Mutilated Bodies and Fragmentary Remains Sometimes the mutilated bodies and fragmentary remains of the body such as one limb, part of trunk or only the head, a mass of soft tissue etc.is brought for examination by the investigating police officer. In such cases, not only the body parts mutilated but there are chances of disfiguring the face and dismembering the limbs to destroy the identity in order to hide the crime. The body may also get mutilated by the dogs, rats, jackals, vermins specially when left exposed in open places and also by the fishes when the body is recovered from the water, to such an extent that the body remains unrecognizable even by the nearrelatives. The assailants are also likely to also destroy finger tips for fingerprints, tattoo marks, scars, moles and also remove jewellery, clothing and other personal belongings to further make it difficult to the identify the person. The body may be burnt or incinerated. Also because of advanced decomposition, the soft tissue and viscera putrefy leaving behind the bare skeleton. The body parts may be deliberately dismembered after death and thrown off in rivers, canals, sewage holes. The body may be put in a vat of corrosive acids or alkalis to get it chemically destroyed as was in Acid bath murder case. The body parts may get mutilated into fragmentary remains beyond recognition in bomb explosions. The questions
163
listed below should be answered in detail while examining the fragmentary and mutilated body parts. 1. Whether the remains of human or animal origin? When the head, trunk or limbs are available, it is easy to specify them to be human or animal but when only soft tissue with no visceral organs is to be examined. The mass of soft tissue without any preservative should be sent to the forensic science laboratory for the precipitin or antiglobulin inhibition test that is a species specific test. 2. Whether the parts belong to one or different individuals? When the mutilated parts fit to each other snugly and anatomically with no disparity or duplication, bearing more or less the same skin colour etc, it can be said that all the parts are of the same individual. Bone from different skeletons can be differentiated, when they show different colour emissions on exposing them to short wave ultraviolet lamp. 3. Do the fragments belong to male or female? If the head or trunk is available, it may be easy to determine sex from the scalp hairs, beard, moustache, pubic hairs, external genitalia, breasts etc. it is known that prostrate and non-gravid resist putrefaction for a long period. In case of skeletal remains, the characteristic sex features in skull, pelvis, sacrum, femur etc. will be helpful. General configuration, remnants of cosmetics, jewelleries, clothing etc. will speak of characteristic feminine features. 4. The age of the person: The age can be ascertained from general development, teeth, ossification of bones, union of sutures, calcification of laryngeal cartilages, union of pieces of sternum and sacrum, changes in the symphyseal surface of pubic bone, osteoarthritic changes in the joints, colour of scalp, moustache and beard hair 5. Stature: The stature can be determined from the long bones, if any 6. Race: Race can be determined from the scalp hair, skin complexion, cephalic index
164
7.
8.
9.
10.
11.
Textbook of Forensic Medicine and Toxicology
and other anthropological features in the skull, vertebral column or other body parts. Establishing identity: The identity can be established from the finger print, tattoo marks, scars, moles, deformities, congenital abnormalities if any, dental study, recent or old fractures, personal belongings of the deceased if available. Any marks of habit or occupation: Occupational marks can help in determining the profession of the deceased. Manner of separation of parts: This can be determined by close examination of the margins of the dismembered parts to see, whether these had been cleanly cut, sawn, disarticulated by several strikes at different levels done haphazardly or gnawed through by animals. At times the face and other body parts may be defaced and disfigured to remove the identifying features purposefully. Meticulous examination can only help to differentiate the cut in bones by sharp weapons, or sawing of long bones by sharp weapons, for surgical amputation, from gnawing of dead bones by wild animals, showing no evidence of antemortem reaction. Time since death: The probable time since death can be ascertained from the conditions of the soft parts in relation to the stage of putrefaction Cause of death: It is easily determined in case of antemortem fatal injuries affecting large blood vessels, vital organs or body parts are there. Other causes are extensive antemortem burns, head injury with fracture of skull, fracture dislocation of cervical vertebra, fracture of hyoid bone or several bones. Sometimes bullet or its fragments and part of the weapon used are recovered from the body that points towards the nature of death. As the soft tissues decompose quickly, the injuries involving these tissues may be easily missed as in the case of neck
tissues when death has been caused by compression of neck. EMBALMING The treatment of the dead body with antiseptics and preservatives to prevent putrefaction is called embalming. Embalming causes coagulation of tissue proteins and they get fixed and hardened. It should be done as early as possible after death and for satisfactory results, preferably within 6 hours. The main constituents of embalming fluid are formalin, sodium borate, sodium citrate, sodium chloride, glycerin etc. dissolved in water. The fluid has to be forced into the arteries for diffusion to occur into the cells and tissues through the capillaries. It can be done by hand/foot pump, stirrup pump, bulb syringe, gravity injector and motorized injectors. The injection can be continuous or interrupted with a continous or interrupted drainage. Embalming is arterial when the fluid is injected in the arteries and then cavity embalming is done in which the fluid is injected in the body cavities. The vessel to be chosen for the arterial embalming should be preferably nearer to the heart for better results. A common method is the ‘six point’ injection system in which the carotids, axillary and the femoral arteries of both the sides are used for pumping the fluid for the different body regions. Long Questions 1. Discuss the general procedures to be followed for a medico legal autopsy. 2. What are the aims and objectives of doing the various types of autopsy? Short Question 1. 2. 4. 5.
Negative autopsy Obscure autopsy Preservation for viscera Exhumation.
Autopsy Procedures and Exhumation
165
MULTIPLE CHOICE QUESTIONS
1. The fluidity of blood after death is due to: A. Fat embolism B. Fibrinolytic enzymes C. Air embolism D. All of the above 2. The time limit for exhumation in India is: A. 10 years B. 20 years C. 30 years D. Unlimited 3. Which of the following is not a common incision technique for conducting autopsy? A. ‘I’ incision B. ‘Y’ incision C. Modified ‘Y’ incision D. ‘H’ incision 4. Which of the following methods involves removal of individual organs during autopsy? A. R. Virchow’s technique B. C. Rokitansky’s technique C. M. Letulle’s technique D. A. Ghon’s technique 5. After postmortem the body should be handed over to: A. Magistrate B. Patient’s relatives C. Local Inspector D. Coroner E. Investigating officer 6. During postmortem doctor is supposed to examine: A. All parts B. injured parts C. Parts requested by victims’ relatives D. Parts mentioned in the initial report 7. A sample to look for uric crystal (Gouty tophus) would be submitted to the pathology laboratory in:
1 B 11 B
2 D 12 C
3 D 13 B
4 A
5 B
6 A
8.
9.
10.
11.
A. Formalin B. Distilled water C. Alcohol D. Normal saline Sodium fluoride may be used for preservation of: A. Cyanide B. Arsenic C. Alcohol D. Urine Most commonly used preservative is: A. Formalin B. Distilled water C. H2SO4 D. Oxalic acid To preserve specimen, concentration of formalin used is: A. 1% B. 5% C. 10% D. 40% Preservative used for toxicological specimen: A. 20% formalin B. Saturated sodium chloride C. 20% alcohol D. 10% alcohol
12. Urine containing Bile salts, is preserved in: A. Formalin B. Rectified spirit C. Saturated sodium chloride solution D. Ethyl alcohol 13. ‘Rectified spirit’ is contraindicated as preservative in poisoning with: A. Phenol B. Paraldehyde C. Both of the above D. None of the above
7 A
8
C
9 A
10 C
9
Part 1—Forensic Medicine and Pathology
Crime Scene Investigation The objectives of crime scene investigation are: 1. To reconstruct the accident. 2. To ascertain the sequence of events. 3. To determine the mode of operation. 4. To disclose the motive. 5. To uncover the property that was stolen. 6. To find out what all the criminals may have done. 7. To recover physical evidence from the scene of crime. EVIDENCE Webster defined ‘evidence’ as something legally submitted to a competent authority as a means of ascertaining the truth of any alleged matter of fact under investigation before it. According to Section 3 I.E.A., evidence means and Includes: 1. All statements, which the court permits or requires to be made before it by witnesses, in relation to matters of fact under enquiry. 2. All documents produced for inspection by the courts. Types of Evidence Evidence is of two types: (i) Testimonial and (ii) Physical evidence that may vary from fiber to a building. 1. Physical evidence is very valuable as it can prove that a crime has been committed or establish key elements of a crime, e.g. in cases of alleged rape the victim’s torn clothing and
contusion over inner side of thigh are sufficient to prove a case of rape. 2. The evidence can place the suspect in contact with the victim or with the crime scene, such as in case of alleged bestial*ty. If the animal hair is found on the suspect’s clothes that can prove the contact with the animal. 3. The physical evidence can establish the identity of persons associated with the crime, e.g. the finger prints at the crime scene or over any articles present in the crime scene can pinpoint the identity of the criminals. 4. The evidence can exonerate the innocent, can corroborate the victims testimony,such as in a case of alleged rape, if the victim narrates the story alleging that the person lured her to an unknown place and after mixing some sedatives in the cold-drink which she drank and became unconscious was raped. On examination and susbsequent chemical analysis of the blood and urine, it has found that she was not given any sedatives. On repeated interrogation she told that she had given a false history as she was trying to falsely implicate the person. 5. A suspect confronted with physical evidence may make admissions or confess such as in a case of murder blood stained clothes were found in the accused possession. On grouping of the blood it has found to be matched with that of the victim after which the accused admitted the crime.
Crime Scene Investigation 6. It is more reliable than the eye witnesses. After several months of the crime when the eye witnesses are asked in the court of law to narrate the events, they give different versions to the same event but the physical evidences remains the same. 7. The Court’s decisions have made physical evidence more important and is expected in criminal cases by courts. As you know, the Court decisions depends more upon the physical evidences than that of the eye witnesses. In the recent years, more and more eye witnesses are turning hostile resulting in injustice during the trial. Collection and Preservation of Physical Evidences In any case of trial, the Court will require the proof that the evidence is collected at the crime scene is the same that are being produced in the Court for which the chain of custody is very important. Usually the evidences are kept in a container, tagged and identifying information are written over it such as: 1. Victim’s or suspect’s name, date and time of collection, case number and type of crime, brief description of the item, name of the person collecting the evidences and the name who has the custody of the item. 2. Storage of the physical evidences has a legal implications. It must be kept in a secured area prior to the transportation to the Court of law and no unauthorised person should have access to it. As a general rule, sufficient samples should be collected; as much as samples are available are to be collected. Control samples are also needed for the comparative study. The physical evidence should be handled as little as possible because too much handling may arbitrate the fingerprints, dislodge the minute evidences like hair, fibers etc. At times forceps, gloves and other instruments may be necessary to handle the evidences. Contamination is a great concern and to be avoided at any cost.
167
First Officer at the Scene Crime scenes are dynamic, rapidly changing and the first officer must be concerned with myriad of details. His actions or steps taken lead to a successful investigation /solution of crimes. The first officer’s most important duty is to prevent the destruction or diminished utility of potential evidence that may lead to the apprehension of criminal and solution of the crime. Nothing should be changed, destroyed, added or remove to or from the crime scene which may mislead investigators, though the general rule of protecting crime scene can not be applied to every case. It may not be possible to preserve the crime scene in certain crimes because of their locations e.g. when accident occurs on the road with heavy traffic on. Detailed and meticulous note taking should be adhered to. All movements should be calm and deliberate Errors committed at the scene of crime can never be rectified. Every effort should be undertaken to preserve the crime scene as Locard’s exchange principle states that whenever a body comes in contact with another there is an exchange of material between them. Recording the Time The time of examining the scene of crime should be recorded. Precise noting of the time is very important. The time at which the crime was committed, the first officer was called, his arrival at the scene etc. are very important. Track of time spent at the scene indicates the systemic way the things were done. Entering the Scene Proper Efforts should be made to observe the details and make notes on such points as doors, windows, lights, shades or shutters. Any odour like that of cigarette, smoke, gas, gun powder or perfume etc should be noted. Signs of activity like meal preparation, dishes in sink etc. date and time indicators like mail, newspaper, stopped clock, spoiled food and position of the articles to be noted
168
Textbook of Forensic Medicine and Toxicology
Nothing should be removed unless essential. Position of the body should be noted, alongwith sketches, photographs and videography. No one should use toilets, eat or drink anything at the scene. At times, it happens that the victim or relatives attempt to clear up the scene. Such persons would like to conceal something or want that the things should be in proper order. It is often possible to recover physical evidence on damaged items that have been thrown in the trash.
agencies but it partly depends upon the local custom. At most of the places, it is better for the investigating officer to arrive first and later the doctor should be called to the crime scene. Once the doctor is at the scene, he should first diagnose that the victim is dead. He alongwith the investigating team will collect the evidences, see the position of the body before transferring them to the mortuary. Examination of the scene is very important for the doctor as while doing the postmortem that can corelate between the two.
Protecting the Integrity of Scene
Diagnosis of Dead Persons
The scene should be protected from the public, other officers, press, family members and any other unauthorized access to be banned. For indoor crime scene, the door should be locked or the gate of the premises should be closed. While for the outdoor scene, one stringing rope or a commercially available tape should be used to cordon off the area. Vehicles and police barricades can act as physical barriers to intrusion by unauthorized people. Officers have to play a very active role in protecting the crime scene and extent of measures depends upon case to case. It is important to proect crime scene proper and paths of entry and exit by criminals. If it is a very large area then local trusted citizens can be of help to protect the area. The protective measures at the scene should be taken at the earliest thus preventing the destruction of valuable evidence. Injured persons at the scene have to be attended immediately. First aid has to be given even if valuable evidence is lost / destroyed. If first aid is not essential then detailed position, photographs and sketches should be made. Hands must be examined for hairs/fibers. Dying declaration should be obtained from the injured while on the way to the hospital. In the hospital clothing to be taken charge of.
Diagnosis of dead at the scene is important. The body should be touched and tested for circulation, respiration, light reflex, pupillary reaction and corneal reflex. Sketch or photograph of the stains etc should be taken and then the body is transferred to mortuary with identification tags. Each body should be sent in a separate bag.
ROLE OF FORENSIC PATHOLOGISTS
Crime Scene Search
At this point, the forensic pathologist should be called to the crime scene by the investigating
After collecting information about the crime scene, a quick survey should be done and actual crime
When a Suspect is Found at the Scene When a suspect is found at the scene then the duty of the officer is to protect the scene. When this is not possible leave the scene in charge of a civilian till other officers arrive. The suspect should be searched and removed from the location as he may try to destroy / change the evidence. Role of the First Officer before the Investigating Team Arrives 1. Writedown the name of the witnesses and other person who has entered the scene and who were at the scene before the arrival of the officer. 2. The basic facts to be established. 3. The suspect and the witnesses should be kept separated 4. The witnesses are instructed not to discuss anything with anybody. 5 The crime scene must be protected.
Crime Scene Investigation
Figure 9.1: Body found at the scene with smashing of head with heavy stone
169
scene search should be done. It can be done in the following ways (Fig.9.3): a. Spiral search method: In this method the search is started from a central point in the scene and then the single investigator walks in an outward spiral covering the whole area. b. Grid method: In this method the whole crime scene is divided into a grid and each of the grids are carefully searched for evidence. Multiple investigators can search the scene. c. Strip or line search: In this method a single investigator starts searching the scene from one end and covers the whole scene in straight lines returning from side to side. d. Quadrant or zone search: In this method the whole area is divided into quadrants and each of the quadrants are searched by one or more investigators. The quadrants can be further subdivided into more quadrants as per convenience. SPECIFIC CRIME SCENES Traffic Accidents Evaluation should be done with a request for ambulance, fire service, forensic experts and traffic control assistance. Tow truck service should be availed to remove the damaged vehicles. First aid must be provided to all the injured. Protecting the Scene The scene has to be protected by a patrol unit with flashing light warning and traffic flow should be arranged properly. Witness There are three ways to find out witnesses. One can ask “Did anyone see what happened” Or can say “I like to have witnesses to remain here.” One should watch the crowd while giving first aid. Teenagers and ladies are usually the best witnesses Evidences A sketch should be prepared or a photograph may be taken of the scene. Vehicle debris and broken glass etc should be collected.
Figure 9.2: Bleeding from the smashed head and face same as in figure
Vehicle Removal Tow truck driver is an important member. Vehicles should be removed one by one.
170
Textbook of Forensic Medicine and Toxicology 1
2
3
1
2
4
5
6
7
3
1
2
3
Figure 9.3: Various methods for searching the scene of crime
Crime Scene Investigation
Figure 9.4: Body found at the site showing decomposition changes
Figure 9.5: Body found lying on the bed early in the morning with no external injuries
Storage Report Drivers / passengers should be taken to hospital. Inventory of the vehicle should be maintained. Only engine key should go to avoid possible allegation of theft. Money and suitcase etc. should be sent with the victim. The roadways should be opened. Statements The passengers, drivers and public should be interviewed. Questions relevant to the accident must be asked. Statements of witnesses should be recorded. Identity of the witness should be recorded for future reference. To interview a child witness simple words and plain dress should be used rather than police dress. Arrests Drunken drivers should be arrested. Alcoholic testing should be done. Reporting Prepare a report and send it to higher authorities. Collection of Physical Evidence a. Skid marks: It should be identified by the type of mark, origin and termination. Measure with a steel tape and not by pacing. Attempt to
171
identify the skid marks with tyre of the vehicle. Measure the gaps, skips and deviations as they assist in locating the point of impact. If no skid marks are found write none. b. Graze marks: The length of grazing is to be measured and direction can be determined. Try to locate the point, grease, oil, water and residue around graze mark. These help in identifying the vehicle. c. Debris: Identify the type of debris and the location whether over the head lamp glass, radiator water and brake fluid etc. d. Vehicle parts: The bumpers, fenders, door handles, radio antennas etc. should be examined. Other Physical Evidences Examination of other physical evidence such as a suit case falling from the top of the vehicle or fall and breaking of the baggage while a pedestrian is crossing the road when hit by the car, all help in all these establishing the victim and reconstructing the scene of crime. Burns The burns can occur at any place. The room may be closed or open. The fire may be outside or any other place. Smell, cooking material, hair condition and sometimes bangles may be broken or weapons recovered from the scene. Pugilistic attitude and heat ruptures should be looked for. Hanging and Strangulation The points to be noted are height of suspension, the platform height, mark on resting points/ suspension / removal of the body. The pattern of knots and noose of certain type should be noted and whether the person can hang himself with it or not. Diagrams/sketches/photographs/ videography etc. should be done. Noose should be examined immediately and if it is cut, the pieces are to be recovered and analysed. The ground under and around the hanged person must be examined immediately. Knots in hanging case should never be undone/cut except while life saving
172
Textbook of Forensic Medicine and Toxicology Firearm In firearm cases, injuries and surroundings must be protected. Finding such as tattooing, blackening, singeing, condition of the clothes should be protected from rain while moving the body from the scene. Hands should be protected by wrapping in polythene and paper bags should be used for collection of evidence. Deaths by Poisoning
Figure 9.7: Body found at the site of crime with ligature in situ–ligature strangulation
Figure 9.6: Body found at the scene in a case of hanging showing ligature around the neck
measures are undertaken. A case of suicide at times gives a picture of homicide or a murder. On the other hand, there are cases of murder when the body has been hanged to simulate a case of suicidal hanging. In all such cases, it is important that the neck should be carefully examined along with other bodily injuries. The examination of circ*mstances where the crime has occurred is important such as noting whether the room was bolted from inside or not, other evidences of struggle at the scene.
In poisoning deaths, it is very rare for the investigating officer to find the presence of physical evidence at the crime scene that indicates the death was caused due to ingestion of some poisonous substance. Physical evidence located at the crime scene and will be noted on examination of the deceased may sometimes indicate poisoning. In case of death from poisoning the investigation of the scene and examination of witnesses will decide whether it is suicidal, homicidal or accidental. At the scene any vital clue in the form of tablets, powder, residues in bottles of medicines, wrappings, boxes, tubes, ampoules, vials and other containers if found should be preserved. All medicine bottles, tubes, syringes and needles including the empty ones should be preserved and sent for analyses to the forensic science lab. When food poisoning is suspected, the dishes should be collected and packed. Besides, food dishes and remains of food are packed in a clean glass jar that is well sealed. In cases of drug abuse when syringes are found at the scene they should be recovered preventing their contamination. The needle of the syringe is conveniently stuck in a cork to prevent it from breaking. The scene should also be searched for ampoules and vials. TEAMWORK Final element in crime scene investigation is teamwork. System was purposefully designed, so that, nobody can operate independently. No person is more important. Each person has vital role to play. Each must feel empowered to do what needs to be done for the sake of justice.
Crime Scene Investigation Long Questions
Short Questions
1. What are the objectives and usefullness of crime scene investigations? 2. Discuss the role of first officer at the crime scene. 3. What are the different findings in a crime scene?
1. Methods of crime scene search 2. Role of Forensic pathologist in crime scene. 3. Collection of evidences in crime scene.
MULTIPLE CHOICE QUESTIONS
1. Various methods of crime scene search are: A. Spiral search method B. Grid method
1 E
173
C. Strip method D. Zone method E. All of the above
10
Part 1—Forensic Medicine and Pathology
Anaesthetic and Surgical Deaths Anaesthetics are used for the management of pain in various surgical and operative procedures. Anaesthetics may in themselves result in various adverse effects and sometimes death of the patient. Various surgical procedures carry the risk of life for some of the patients. Anaesthesia may be the sole cause of death in itself and may be a contributory factor in some of the deaths. Every new technique can potentially form a new hazard that is why the lists of mishap that can occur through medical practice are unlimited. Deaths Associated with Surgical Operation 1. Those directly caused by the disease or injury for which the operation or anaesthetic was necessitated: In the advanced stage of some disease, the intervening surgical procedures may be undertaken to save the life of the patient. This procedure causes death of the patient but the disease from which the patient was suffering is given as cause of death. In cases when the patient dies on the operation table itself and is brought out dead from the theatre, the relatives may demand investigations into cause of death. In those cases where the patient is of trauma, and surgical operation is done, it is not possible to separate the relative contribution of the two to the cause of death. 2. Those caused by a disease or abnormality other than that for which the procedure was being carried out: When the death was caused by a disease other than that for which procedure was carried out and that was known to exist
before carrying out the surgical procedure, it is for the Pathologist to evaluate whether an operation is necessary. However, if clinicians did not suspect the disease and neither the facility of specialized diagnosis was available, the death is excusable. When common conditions such as hypertension, ischemic heart diseases etc. are present, they should be properly diagnosed and treated. In the aged and debilitated patients, who may be a poor risk for operation, account must be taken of the condition of their myocardium and lungs. 3. Surgical or diagnostic procedure mishap: Failure of surgical technique might be: i. Inadvertent in some unusually difficult operative circ*mstances or some anatomical abnormality. ii. Accidental due to failure of equipment iii. The result of error or incompetence on the part of the surgeon for which the surgeon can be sued. Deaths Associated with Anaesthesia Most fatalities are not related to the actual procedure but due to other factors. The fact that the death occurred during or soon after an anaesthetic by no means indicates that the anaesthetic played a significant part in the death. Anaesthetic deaths can be classified as: 1. Those occurring under anaesthesia, but not related to anaesthetic agent: These types of deaths can be due to: i. Death due to injury and disease that made the operation and anaesthetic necessary
Anaesthetic and Surgical Deaths ii. Deaths due to a disease other than that for which the operation was performed but about which the medical attendants knew before death. In this category, there is some contraindication to anaesthesia that surgeon and anaesthetist is aware of but there is presence of some other urgent injury or disease for which the operation is vital. In these cases, the risk of anaesthetic must be balanced against the risk of leaving the patient untreated. iii. Deaths due to a disease that is unknown at the time of operation. In an elective operation, a full clinical examination together with ancillary investigation should be made to detect any significant disease that might affect the patient during the operation. iv. Deaths may be due to surgical shock and exhaustion in cases where there is no preexisting disease. A poor risk patient because of the condition for which operation is being carried out is more likely to be affected. v. A surgical accident may occur under anaesthesia rarely by the inexperienced doctors under emergency situations. 2. Deaths as a result of administration of an anesthetic: i. Overdosage of an anaesthetic agent: The deaths that arise out of the overdosage of an anaesthetic agent are rare and usually result from ill-advised polypharmacy. To achieve Anaesthesia, the current trend is to achieve a light plane of unconsciousness with a barbiturate or a hypnotic, accompanied by the inhalation of nitrous oxide and oxygen along with small quantities of a liquid agent such as halothane. To achieve muscle relaxation, long acting muscle relaxants such as gallamine, tubocurarine or pancuronium that compete with acetylcholine at the motor end plate or short acting muscle relaxants such as succinylcholine,
175
decamethonium iodide, which depolarize the motor end plate rendering it unexcitable to acetylcholine, are used. Both the categories result in muscle paralysis. Overdosage with long acting muscle relaxants can be treated with neostigmine while overdosage with short acting agents such as succinyl choline can be overcome by the use of prolonged artificial respiration. Anaesthetic gases cause physical and psychological dependence and are commonly used by the medical personnel. ii. Anaesthetic misadventure: An anaesthetic misadventure or a critical incident is a human error or equipment failure that could have led, or did lead to an undesirable outcome, ranging from increased length of hospital stay to death when it is not discovered in time. The anaesthetic morbidity and mortality occur from the complications of anaesthetic procedure, failure of equipment and due to some human error such as emergencies, failure to perform a normal check, lack of skilled assistance, restricted access to patient, and inadequate supervision of the patient due to distraction, fatigue, inattention, boredom or anxiety. 3. The deaths that are the direct result of the administration of an anaesthetic can be due to i. Acute cardiovascular failure: This is the most common cause of sudden unexpected death due to the administration of general anaesthetic. Cardiac arrest is the usual way in which the mishap presents and it is often impossible to discover either clinically or at postmortem examination. Most cases occur under relatively light anaesthesia rather than deep unconsciousness and thus tend to occur either at the beginning or at the end of surgery. This can occur even in the hands of most experienced and careful anaesthetist.
176
Textbook of Forensic Medicine and Toxicology
Cardiac arrest appears to be mainly neurogenic in origin and can result from any form of irritation of the respiratory tract such as intubation or laryngoscopy. ii. Deaths due to respiratory failure: Hypoxia occurring during anaesthesia may be due to defects in the supply of oxygen from the anaesthetic machines, either from mechanical failure or from the inexpert manipulation by the anaesthetist. Respiratory failure can also occur due to an overdose of an anaesthetic depressing the respiratory center. Excess of premedication and the use of muscle relaxants also predisposes to respiratory failure, unless the appropriate anaesthetic procedures such as assisted respiration are carried out. Mechanical blockage in the air passage may lead to hypoxic respiratory failures due to laryngeal spasm. Regurgitation of stomach contents and other mechanical defects in the apparatus may cause hypoxia and respiratory failure. Laryngeal spasm, swabs, dentures or teeth in the airways and haemorrhage from the naso-pharynx may cause or contribute to hypoxia and unless appropriate posture is maintained after an anaesthetic, the tongue may obstruct the airway in the anaesthetized patient. iii. Recovery phase: During the recovery phase, hypoxia may follow anaesthetic hyperventilation. After a period of hyperventilation, the tissue carbon dioxide store being depleted, the body attempts to replenish them. The need for carbon dioxide elimination is diminished, and hyperventilation results which may prove fatal. The cause of impairment to ventilation may lie at the level of CNS, peripheral nerves, the myoneural junction or even at the level of upper or lower airways. iv. Postoperative problems: Adequate postoperative care must be undertaken
as medical practitioners will be responsible for any danger that befalls a patient due to his negligence a. Respiratory insufficiency: Respiratory insufficiency that occurs within 72 hours of the surgery is usually due to the preoperative pulmonary diseases. If it occurs after four to five days, it is due to atelectasis or pneumonia, peritonitis, pulmonary embolism or increase in energy required for breathing because of exertion. b. Aspiration: Aspiration of foreign material such as secretions, gastric contents, blood and food can contaminate the tracheobronchial tree. Aspiration of pus leads to multiple abscesses and that of gastric content may lead to irritation. As a result acute pulmonary oedema and chemical peritonitis may occur. c. Atelectasis: Atelectasis frequently occurs due to the misplacement of tracheal tube in to one of the bronchi or due to respiratory insufficiency. d. Pulmonary oedema: Pulmonary oedema may be the result of circulatory overload due to administration of excess blood, fluids or plasma expanders. e. Pneumothorax: Spontaneous pneumothorax may occur during operative procedures with inhalation of anaesthesia or due to rupture of an emphysematous bleb. Tension pneumothorax is dangerous as it displaces mediastinum and has a deleterious effect on the heart and blood vessels. f. Air embolism: Massive air embolism causes circulatory collapse by producing a frothy mixture of blood and air-bubbles within the heart chamber and causes immediate cessation of peripheral circulation.
Anaesthetic and Surgical Deaths v. Systemic toxicity of local anaesthetics: These are those adverse effects of the absorbed drug that affect the whole body. The blood shows high blood levels of these agents. There may be allergic reactions ranging from anaphylactic shock to dermatitis. They also depress medullary centers leading to apnoea and vascular collapse. Local anaesthetics may depress the myocardium directly resulting in hypotension. vi. Spinal anaesthesia: Spinal anesthesia causes two major types of neurologic complications namely myelopathy and arachnoiditis. vii. Deaths due to physical fault in the anaesthetic procedure: The failure of equipment leading to anaesthetic mishaps usually occurs in a small number of cases. Explosions are particularly common with cyclo-propane or ether. Flammable liquids can cause fires. The fatalities can occur from electric shock due to defects in monitoring equipments, defibrillators or diathermies in the operation theatre. Preventive Strategies to Combat Anaesthetic Complications 1. Training and supervision: The inexperience, inadequate training, inadequate knowledge about a new equipment or technique and even inadequate supervision by the seniors has been cited as a cause of error. To rectify these errors, regular in-house training of the anesthetists should be carried on. 2. Specific protocol development, more complete preoperative assessment and equipment and apparatus inspection: Preoperative assessment of patients and preoperative inspection of equipment and apparatus will prevent a number of critical incidents. 3. Additional monitoring instrumentation and equipment and human factors improvements:
177
Improved standardization or arrangement of drugs in the Anaesthesia workspace, and improvement in design of gas flow control knobs and breathing circuit scavenging connections are now mandated by the national standards for new apparatus. American Society of Anaesthesiologists has recommended the standards for basic patient monitoring such as electrocardiography, arterial blood pressure recorder, ventilator disconnection alarm and an oxygen analyzer. Besides these, the monitors that are encouraged but not mandatory include pulse oximetery, spirometry and capnography. Medicolegal Problems associated with Anaesthetic and Operative Deaths The main precipitating factors of negligence suits are failure of empathy and communication towards the patient and his relatives. To minimize the possibility of malpractice actions, the anaesthetists and surgeons should ensure the following 1. A proper physician patient relationship should be established. 2. In surgical procedures, the patient should be properly identified, the type of surgery to be performed, the side on which the surgery is to be performed is important. 3. Before carrying out surgery, an informed consent should be obtained from the patient in his own language, properly stating the detail of the procedure, the risks and disabilities associated with it. For anaesthesia, separate consent should be obtained. 4. Pre-anaesthetic check-up of the patient should be properly documented. 5. It is imperative to ascertain whether the anaesthetist has acquired the necessary skill to operate it by formal training. 6. Any preexisting natural disease such as the heart or lung disease should be properly evaluated before undertaking surgical procedures.
178
Textbook of Forensic Medicine and Toxicology
Autopsy Procedure in Anaesthetic and Operative Deaths Whenever deaths occur during or shortly after the performance of a surgical operation and general anaesthetic the pathologist must answer the following questions 1. Was the death due to the effects of the surgical procedure or anaesthetic or is it due to the natural disease for which operation was being carried out? 2. Would the patient have died at the time he had died, if he has not undergone through the anaesthesia or operation? 3. Was the surgery and anaesthesia vital to save the life of the patient? 4. Was there any defect in anaesthetic or surgical technique? 5. Was the patient suffering from any predisposing condition relating to the condition for which he was operated that made him more susceptible to death from anaesthetic or operative procedure? 6. Was the death due to some unsuspected natural disease directly unrelated to the disease for which surgery was being performed? i. Detailed hospital record of the patient, including full clinical and pre-anaesthetic check-up details are essential especially in anaesthetic deaths. ii. Surgical intervention and its sequelae like sepsis, haemorrhage, oedema etc. should be noted that frequently make examination of the operative site difficult. It is sometimes difficult to distinguish defects due to postmortem changes from abnormalities existing during life. It is common for the inexperienced pathologist to misdiagnose resuscitative artefacts. The finding of gastric contents in the airway at the autopsy should be cautiously interpreted. The agonal regurgitation of gastric contents in the air passages should not be misinterpreted.
iii. There are rare instances of surgical mishap, which may not be negligence if the operating conditions were difficult, include ligation of arteries and veins, ureters, bile ducts, perforation of large blood vessels. iv. A full clinical history along with the consultation with the surgeon, anaesthetist and other medical staff is necessary to arrive at the best possible opinion. Sometimes the cause of death is obscure even after the autopsy. v. Presence of pre-existing natural disease such as the heart disease, respiratory insufficiency due to the lung disease and their contribution to the cause of death must be evaluated. vi. In deaths occurring due to surgical shock and exhaustion, the pathologist must exclude or confirm surgical incompetence and also evaluate as far as possible the preexisting state of the patient. vii. If pneumothorax, air embolism or surgical emphysema is present, it should be clearly evaluated. viii. Surgical and anaesthetic devices such as airways, endotracheal tubes, needles, catheters etc. should not be removed prior to autopsy. ix. A radiograph that will show a ring of oedema of oesophageal mucosa at the level of the tube along with distention of stomach and intestines, in oesophageal intubation, can check position of the endotracheal tube. x. All the organs should be dissected and surgical sutures should be inspected. xi. Chloroform and halothane are hepatotoxic and chloroform may cause ventricular fibrillation sometimes. Halogenated hydrocarbons cause cardiac irritability. xii. The blood samples obtained prior to the death of the patient should be sent for analytical tests. xiii. Toxicological examination: For toxicological examination following samples should be collected:
Anaesthetic and Surgical Deaths • One lung sealed in nylon bag • Two grams of fat from mesentery • 100 grams of cerebrum • 100 grams of liver • 100 grams of kidney • 10 grams of skeletal muscle • Urine. In case of inhaled anesthetic specimens should be kept in containers of appropriate size to avoid empty space, are sealed and refrigerated or frozen. Alveolar air should be collected with needle and
179
syringe by puncturing the lung under water before the chest is opened. Long Questions 1. What are the causes of death on the operation table? What precautions you should take to avoid such deaths. 2. Discuss in detail the autopsy procedures in anaesthetic and operative death. And how do you preserve viscera in such cases.
11
Part 1—Forensic Medicine and Pathology
Sudden and Unexpected Deaths The medicolegal autopsy is conducted in cases of sudden and unexpected deaths, including apparently accidental death, primarily to establish cause of death. The definition of sudden death varies according to authority and convention. WHO defines sudden death as ‘death that is unknown or sudden and occurring within 24 hours from onset of symptoms’. However, some pathologists and clinician will only accept sudden death as the one occurring within one hour from the onset of illness. The unexpected nature of death is more important than its suddenness. Many unexpected deaths will be sudden those occurring immediately upon collapse or within minutes and there may be a delay of hours or even days without a diagnosis being clinically evident. In sudden deaths, the immediate cause is usually in the cardiovascular system. Causes of Sudden Death 1. 2. 3. 4. 5. 6.
Cardiovascular system Respiratory system CNS Alimentary system Genito-urinary system Miscellaneous
45-50% 10-15% 10-18% 6-8% 3-5% 5-10%
CARDIOVASCULAR SYSTEM In the cardiovascular, the causes of sudden death are: (i) Coronary atherosclerosis (ii) Hypertensive heart disease (iii) Aortic valve disease (iv) Coronary circulation anomalies (v) Coronary artery diseases-
polyarteritis (vi) Cardiomyopathic enlargement (vii) Congenital heart disease. Ischaemic heart disease is by far the most common cause of sudden death in Western Nations. The normal anatomy of heart and coronaries can be summarized. The normal weight of an adult heart varies between 275-300 gm and that of female between 225-250 gm. The atrial walls are 1-2 mm thick whereas right and left ventricular walls are 3-5 mm and 10-15 mm thick respectively. Blood Supply of Heart 1. The left coronary artery arises from the left aortic sinus and the main trunk after a short course of 1 cm or less is divided into (Fig. 11.1): i. Left interventricular (Anterior descending) branch: This courses down the interventricular septum to reach the apex of the heart and supplies anterior aspects of right and left ventricles and the anterior 2/3rds of I.V. septum at the apex of the heart. ii. Left circumflex branch: It follows left A-V sulcus to reach to back of heart. It supplies small portion of the lateral aspect of left ventricle extending slightly anteriorly and posteriorly. 2. The right coronary artery arises from right aortic sinus, passes behind the pulmonary trunk and follows the right A-V sulcus i. Right marginal branch: This branch is given off at the right border of heart and supplies the remaining anterior surface of right ventricle and posterior third of interventricular
Aorta
Left m ain
Anaesthetic and Surgical Deaths
Right
Right coronary artery
Left Circumcumflex
181
Left coronary artery Circumflex
Left Anterior descending Anterior descending branch Marginal branch Figure 11.1: Blood supply of heart
septum. ii. Posterior descending (interventricular) branch: The main part of right coronary artery continues at the back of the heart as posterior descending branch. Congenital Anomalies of Coronary Artery: Minor anomalies that usually involves the proximal coronary artery but the distal blood flow is normal. 1. “High take off”—location of the coronary ostia is 1 cm above the level of cusp margin. 2. Multiple coronary ostia. 3. Separate ostium in the right coronary sinus. 4. Third coronary artery arises from the noncoronary sinus. Frequency of Site of Fatal Coronary Stenosis with or without Thrombosis Coronary stenosis with or without thrombosis commonly involves first two cm of the origin of the vessel. The incidence of involvement of the branches is: 1. Anterior interventricular→45-64%. 2. Right main coronary→24-46%. 3. Left circumflex→3-10%. 4. Left main coronary→0-10%. 5. Right marginal and posterior interventricular branches are particularly immune.
Coronary Atherosclerosis Coronary atheroma may be focal, with irregular plaques. Every part of the major vessels must be examined at autopsy, with transverse cuts at no more than 3 mm intervals since few and localized atheromas may be present. Types of Occlusion 1. Simple atheroma: Plaques are often eccentric with a central pin hole leaving a crescentic or concentric residual lumen. 2. Ulcerative atheroma: This results due to breaking down of endothelium over atheromatous plaques. This is conductive to thrombus formation. 3. Subintimal haemorrhage: Sudden haemorrhage resulting from rupture of tiny vessels in the wall of a coronary artery. The hematoma thus formed forces the plaque inwards to further narrow or occlude the vessel lumina. 4. Coronary thrombosis: This occurs on an already stenosed plaque of atheroma with damaged endothelium. 5. Periarteritis Nodosa: This is pan inflammatory disease of arteries of unknown etiology that affects males around fourth decade involving mainly muscular arteries of heart and kidneys.
182
Textbook of Forensic Medicine and Toxicology
Sequelae of Coronary Occlusion 1. Sudden death: May occur at the time of occlusion or subsequently as a result of ventricular fibrillation due to damage to nodal tissue or conducting system or any other complication. 2. Myocardial infarction: Myocardial infarction occurs in the myocardium distal to a complete occlusion of coronary artery in the absence of an adequate collateral circulation 3. Rupture of the myocardium: The rupture of myocardium occurs in people over the age of 60 yrs. It usually occurs on the 2nd or 3rd day after infarction because at this time muscle wall is soft and necrotic. The cardiac rupture results in haemopericardium leading to cardiac tamponade and death. The rupture almost always involves left ventricular wall. 4. Myocardial fibrosis: Localized patches result from healed myocardial infarcts and are seen in areas of predilection of infarcts like distal interventricular septum, apex and the posterior wall. Diffuse fibrosis may arise from many causes like healed rheumatic carditis and are also seen in cases of long standing coronary stenosis, which are sufficient to produce focal infarcts. The fibrotic patches are also seen in hypertensive heart disease or hypertrophy due to aortic incompetence 5. Aneurysms: Aneurysm of the left ventricle may occur if a large full thickness plaque of fibrosis becomes stretched. Rupture of aneurysm is rare. 6. Mural thrombosis: Thrombosis very often develops over an infarct, which reaches the endocardial surface of ventricle due to adhesion of platelets and fibrin deposition. Thrombus always poses danger of emboli. 7. Pericariditis: Occurs in transmural infarcts involving epicardium. Ischemic heart disease is the most common cause of pericarditis. Myocardial Infarction An infarct is a localized area of ischaemic necrosis in an organ or tissue resulting from sudden reduction of the arterial supply or occasionally
venous drainage. Myocardial infarction occurs with factors predisposing to atherosclerosis like hypertension, cigarette smokers, Diabetes mellitus and familial hypercholesterolemia. Pathogenesis of Myocardial Infarction Myocardial infarction will occur in myocardium distal to complete occlusion of a coronary artery in the absence of an adequate collateral circulation. These are of the following types 1. Subendocardial infarction involves layers of muscle adjacent to lumen of infarction. 2. Intramural infarction: is less common and is usually seen as satellite areas to a more extensive infarct. 3. Transmural or full thickness infarction is of large extent and gives rise to both mural thrombi and pericarditis, involves most commonly lower part of I.V septum, apex and posterior wall of left ventricle. All transmural or full thickness infarcts involve: • Left ventricle with I/V septum—67-80%. • Right and left ventricular wall—15-30% of cases. • Isolated right ventricle—1-3% cases. • Isolated left atrial—Rarest of all. 4. Papillary muscle infarction: Involvement of papillary muscle of left ventricle are common especially posterior muscles which are susceptible to ischemia. Postmortem Demonstration of M.I. The autopsy demonstration of an early myocardial infarct have profound medicolegal implication. The age of an infarct is difficult to establish as the onset of clinical symptoms however dramatic, are often much later than the onset of the pathological lesion precipitated by a coronary occlusion. Gross Appearances It is generally impossible to detect MI by naked eye examination within the first 8 hours after coronary occlusion and in many cases, little or no change may be apparent up to 18 hours.
Anaesthetic and Surgical Deaths
183
This conventional method is very much helpful for the detection of early myocardial infarction. However, the main disadvantage is the time required for the preparation.
sections of muscle fibers known as cloudy swelling. At times it is a reversible phenomena. 4. Corrugation: Dead muscle fibers may be corrugated and they may be sharply angulated in the areas where there is severe bending of the fibers. 5. Granularity of the cell membrane: Granularity occurs at an early stage before the cells begin to disintegrate as a result of necrosis. Granularity is also seen as artefact in frozen sections but when found in paraffin sections it has got some significance unless there is advanced putrefaction. 6. Increase in Interstitial cells: Increase in numbers of cells occur quite early but may also appear late. Some time it does not appear at all. The increase is due to wandering macrophages and the cells which cannot be distinguished from fibroblast. Polymorphs never appear in an infarction before 24 hours. The above findings of early infarction goes on increasing as the time passes. There is increase in the necrosis of the cells with disintegration, heavy polymorph infiltration, filling of the interspaces with basophilic nuclear debris and marked vascular congestion and dilatation.
Haemotoxylin and Eosin Staining
Periodic Acid-Schiff Stain Technique
The paraffin embedded sections are stained with haemotoxylin and eosin and the following features are noted under microscope: 1. Eosinophilia: It is one of the most important features in the early stages not less than 6 hours of infarction. The cells are reddened and most of the cells are eosinophilic in nature along with the swelling as well as increased granularity at the same time. Eosinophilia is easily seen by the application of green filter. 2. Swelling of the Muscle fibres: The intercellular spaces are reduced due to edema of the cells. It may occur in the large masses and at times it may be patchy in nature. It is usually associated with some degree of increased eosinophilia. 3. Granularity of Cytoplasm: This may be found easily in both transverse and longitudinal
The main purpose of this technique is to detect glycogen and stains the necrotic myocardium purplish pink. The substance responsible is diastase-resistant and by histochemical analysis has been shown to be either a muco- or glycoprotein. It does not appear until 12 hours of onset of infarction. Thus it has very little value for the diagnosis.
On autopsy, the infarcted of the heart on cut section looks granular and dull instead of normal moist luster when cut by sharp knife. The infarcted area shows following features: 1. Oedema: There is swelling of infarcted area and coarsely fibrillar appearance of ventricle on cutting. The muscles seem separated with a grayish opaque sheen. 2. Colour: The colour of infarct is more pale than normal with a grayish opaque sheen. This changes to brownish purple darkening to reddish bluish Yellow after 24-48 hours of occlusion. 3. Tigroid appearance: The tigroid appearance that is alternate bands of red and pale areas is seen after 24 hours. 4. Fully developed infarct: A fully developed infarct is yellowish with reddish marginal zones of hyperemia and is gelatinous and than fibrous. Histological Methods
Phosphotungstic Acid-Haematoxylin Technique The above technique does not allow to detect the myocardial infarction earlier then the stains by haemotoxylin and eosin but it can demonstrate the cell death in a more clear way. The characteristic lesion is a break-up of the muscles striations, starting with a “sandy” appearance that progresses to a bizarre clumping and aggregation
184
Textbook of Forensic Medicine and Toxicology
of the muscle. This technique is superior to haematoxylin or eosin as the infarcted areas appear in a better way. Macro-enzyme Techniques During infarction, the metabolic changes in the cells occur before any morphological changes are demonstrable. One of these changes is loss of enzymes from the cells as a result the damaged fibers are enzymatically less active. The main enzyme dehydrogenases may be visualized by tracing their action in a suitable substrate by means of a colour indicator. The methods like tellurite reduction by Malic Acid Dehydrogenase and Nitro-BT method are found to be unsatisfactory because of the technical unreliability and the expense of reagent but the TTC method is of considerable practical use. Triphenyl Tetrazolium Chloride (TTC) Transverse slices of ventricles about 5 mm thick are cut with a knife during postmortem and incubated for one hour in the staining solution of 1% Triphenyl tetrazolium chloride in a phosphate buffer at pH 8. The maintenance of this pH is very important. If the solution is on the acid side of the neutrality, no deposition of the dye will form. Moreover, if the PH rises above 8.5 the reaction will be too rapid and formazan will be deposited over the whole surface of the heart slice. Normal heart muscle with active dehydrogenases acts on the TTC to produce a bright red formazan compound. After the reaction has been developed with 30 minutes, the slice may be fixed in formalin which retains its colors for several weeks when kept in the dark. The real contrast appears after proper fixation. The slice so obtained may be used at the direct evidence of infarction. The technique may be very simple but needs careful supervision with occasional agitation of the solution while incubating. Postmortem interval upto two days appears to have no deleterious affect on the reaction but the slices should not be exposed to the atmosphere before incubation.
Appearance of Myocardial Infarction with Appearance of MI with Time MI less than 6-12 hours old: • Unapparent on gross examination • Oedema • Slight pallor • Eosinophilia within 4-6 hours • Within 3-6 hours, histochemical techniques highlight necrotic area. • Increased cellularity (macrophages and lymphocytes) within 12 hours. MI > 18-24 hours old: • Inter fibrillar oedema deepens and cellular oedema subsides • Better demarcated pallor lesion • Eosinophilia with red line. • Tigroid appearance. MI 36 hours to 2-4 days: • Nuclei are hollow with marked polymorphic activity in 4 days. MI by 1st week: • Disintegrated muscle fibres • New capillaries and fibroblasts. By 2nd week: • Disintegrated macrophagic activity By 3rd week: • Removal of dead cells is complete • Collagen formation starts By 4-6 weeks: • Marked collagen formation (Table 11.1). Lesions Involving Myocardium 1. Hypertrophy of myocardium: Hypertrophy of myocardium may be associated with coronary ischemia. It can occur with hypertension, valvular disease, shunts and long standing pulmonary disease. Depending on the underlying cause either one or both the sides of the heart may be hypertrophied. It may be familial or sporadic. Interventricular septum is enlarged and bulges into both the ventricles producing a ridge beneath the aortic valve. Sudden death is common in the familial variety.
Anaesthetic and Surgical Deaths
185
Table 11.1: Gross and light microscopical findings in a myocardial infarct Age
Gross microscopy
Light microscopy
1 month
Yellow-tan core and irregular hyperemic red-brown border Yellow gray core and red brown border, depressed cut surface. Yellow gray core and red gray border, depressed cut surface Core becoming smaller, border becoming larger, grayer, firmer and less gelatinous, less depressed cut surface. Firm gray-white or red-gray scar, with scar retraction, variable wall thinning.
2. Neoplasm: Primary neoplasm such as rhabdomyoma are occasionally encountered. Secondary neoplasm are very rare. 3. Myocarditis: Myocarditis is inflammation of the heart muscle evidenced by exudative and proliferative cellular reaction. Acute purulent myocarditis can occur as a complication of septicemia and myocardial abscesses may be produced. This is seen sometime in death following severe burns with supervening infection with Pseudomonas aeruginosa. A pyogenic myocardial abscess as a cause of sudden unexpected death is quite unusual. 4. Alcoholic cardiomyopathy: Alcoholic cardiomyopathy may result from direct toxic effect on the myocardium, general nutritional deficiencies including vitamin deficiencies and Beri Beri heart disease. The toxic alcoholic cardiomyopathy is the most common. In alcoholic toxic cardiomyopathy, the heart is over weight with hypertrophy of both ventricles. Coronary arteries are free from atheroma. On microscopic examination left ventricular wall shows scattered fibrosis. 5. Miscellaneous conditions: Cardiac arrest may occur with no organic disease of the heart
apparent at the autopsy. A careful examination of deceased and family history can provide an evidence of preexisting disease or abnormality. A variety of minor and scarcely detectable insults to the myocardium can cause faults in the normal transmission of the heart and can cause sudden death. Sudden death can also sometimes occur in patients without any gross or microscopic abnormality of the heart who have a history of paroxysmal or sustained arrhythmia. Also in an apparently healthy young individual over exertion can cause sudden death but preexisting cardiac conditions should be excluded for the diagnosis. 6. Primary neurogenic shock or reflex vagal inhibition can cause cardiac arrest in the absence of any demonstrable cardiac lesion. Lesions Involving Pericardium Obliterated pericarditis following acute inflammatory changes can occur. Fibrinous pericarditis with blood stained fluid may result from infarction, rheumatic heart disease or uremia. These secondary effects may cause death.
186
Textbook of Forensic Medicine and Toxicology
Lesions Involving Endocardium Fibro-elastosis is commonly found as congenital abnormality causing death in infancy. The secondary form is associated with other congenital heart diseases. In the primary form the endocardium is thick and the changes are more diffuse. Death occurs from heart failure in first week of life in about 1/4th of the infants. Subendocardial hemorrhages are seen in cases of obstetric shock, arsenic poisoning, head injury and from infected blood transfusion. There may be severe drop in blood pressure accompanied by severe blood lesions. Valvular Lesions Congenital valvular lesions are most commonly associated with fusion of aortic or pulmonary cusps. This may be a site of valvulitis or calcification. Valvular disease may be accompanied by long-standing medical history, Mitral valve disease can be present undetected in life. It may be associated with ball valve thrombus in left auricle and some emboli may be found in kidney or spleen.
infection from hypoxia due to mechanical obstruction of air passage by pus in bronchopneumonia or acute purulent bronchitis superimposed upon chronic bronchitis. Acute respiratory obstruction of the larynx may be due to local neoplasm but may occur due to angioneurotic edema or inflammation arising locally. CENTRAL NERVOUS SYSTEM Subarachnoid hemorrhage Sudden and unexpected death due to diseases of central nervous system result from subarachnoid or intracerebral hemorrhage. Subarachnoid hemorrhage may be due to rupture of Berry aneurysm usually located on the circle of willis (Fig. 11.2) and sometimes on other cerebral arteries. These aneurysms are most commonly developmental resulting from congenital weakness of the vessel wall. Rupture of the vessel may be the result of atheromatous degeneration. Mycotic cerebral arterial aneurysm are due to damaged vessel wall by infected emboli as may arise in bacterial endocarditis. Subarachnoid hemorrhage Internal carotid artery
RESPIRATORY SYSTEM Sudden death due to respiratory tract disease in a healthy individual is rare. The main cause is hemoptysis in such cases. Death mainly results from haemorrhage or from inhalation of blood in to the lungs. Hemorrhages may result from neoplasm or inflammatory lesions of the nasopharynx, carcinoma of bronchus or esophagus infiltrating adjacent tissues. Inflammatory lesions such as tuberculous cavitation, lung abscess or bronchiectasis are less common causes. An aortic aneurysm may rupture into bronchus or esophagus. Spontaneous pneumothorax rarely causes death. It most commonly results from rupture of an emphysematous bulla. Respiratory tract infections may also result in sudden and unexpected death. However usually there is a period of some hours or a day or two preceding death. Death may result in respiratory tract
Anterior cerebral artery
Middle cerebral artery Circle of willis
Anterior communicating artery Posterior communicating artery
Basilar artery
Posterior cerebral artery
Vertebral artery
Figure 11.2: Circle of willis
Posterior inferior cerebellar artery
Anaesthetic and Surgical Deaths
187
may produce sudden collapse and rapid death. A transient rise in blood pressure for some relatively minor injury might contribute by causing damage in the already damaged tissue and by initiating the first split in the arterial wall resulting some time later in rupture. At autopsy, there is a massive collection of blood at the base of brain that is why it is difficult to locate the aneurysm. Multiple aneurysm may be present but are uncommon. Intracerebral Hemorrhage Intracerebral hemorrhage may be located in either internal capsule or in brain substance, in cerebellum or pons. It is commonly seen in capsular region and rarely immediately fatal. Death may occur after a few hours or the patient may partially recover and may later on collapse due to rupture into lateral ventricle. Sometimes intracerebral hemorrhage in capsular region resulting from cerebral artery aneurysm bursts and tears through the cerebral tissue and floods the subarachnoid tissue in the base of brain. Pontine Hemorrhages Primary pontine hemorrhages are usually single and involve hypothalamus. Secondary pontine hemorrhages may be associated with head injury and are of considerable medicolegal importance. Cerebral Thrombosis and Embolism Cerebral thrombosis and embolism may cause loss of consciousness and paresis. In cerebral embolism it is sudden and source of embolus is usually the left auricle in cases of auricular fibrillation, mitral stenosis, a valve or a mural thrombus. The embolus can originate from varying sites and the position of lesions are those supplied by cerebral arteries, basilar arteries and rarely carotid arteries. Spinal Cord Hemorrhages Spinal cord hemorrhages are uncommon and may be missed if spinal cord is not routinely examined.
Figure 11.3: Cerebral meningitis
Cerebral Tumours Cerebral tumours are incidental findings in small number of medicolegal autopsies. Mengiomata are the most common cerebral tumours. Rarely sudden death can occur from hemorrhage into neoplasm. The common tumour to cause hemorrhage is glioblastoma. Vascular tumours like hemangiomata may rarely bleed. Tumours themselves except meningiomata are not traumatic in origin. Sudden death is rarely of infective origin when occasionally cerebral abscess may rupture. Rapid death has been associated with meningitis (Fig. 11.3) – meningococcal, pneumococcal, influenza and tuberculous. Acute poliomyelitis and encephalitis may be fulminant, specially when brain stem is involved. Sudden death within hours of onset of symptoms may occur in malaria. Postmortem diagnosis depends on demonstration of malarial pigment in brain, spleen liver and kidney. The pigment must be distinguished from formalin pigment in tissues fixed for days or longer. Sudden death can also result from trypanosomiasis in which postmortem diagnosis is difficult as organisms are difficult to find in tissues. Nevertheless, the inflammation of brain and meninges with perivascular inflammatory reaction and large histiocytic cells (morula cells) are prominent. Sudden death can also occur in
188
Textbook of Forensic Medicine and Toxicology
an epileptic seizure frequently in status epilepticus from heart failure due to myocardial ischemia. Examination of brain may fail to reveal any lesion in idiopathic epilepsy. However, some evidence may be obtained from bite marks on the tongue and from the clothing for evidence of incontinence of urine and faeces. Organic diseases may precipitate epilepsy and evidence of cerebral tumours and cysticercosis should be looked for. ALIMENTARY SYSTEM The causes involving the gastrointestinal system that can be result in sudden death are: (i) haemorrhage into gastrointestinal tract resulting from peptic ulcer, esophageal varices (ii) perforation of ulcers such as peptic, typhoid (iii) strangulated hernia (iv) rupture of liver abscess (v) rupture of enlarged spleen as in malaria (vi) intestinal obstruction (vii) Twisting of the intestinal. GENITOURINARY SYSTEM The conditions involving genitourinary system that can be the cause of sudden death are (i) chronic
nephritis (ii) nephrolithiasis (iii) carcinoma of kidney and urinary bladder (iv) uterine haemorrhages (v) carcinoma of female genital tract eroding femoral vessels (vi) twisting of ovary, ovarian cyst or fibroid tumours. MISCELLANEOUS Many other conditions can be the cause of sudden and unexpected death such as (i) diabetes mellitus (ii) cerebral malaria (iii) vagal inhibition (iv) drug anaphylaxis (v) shock due to emotional excitement (vi) mismatched blood transfusions. Long Questions 1. Define sudden death. Discuss in detail the causes of sudden death due to cardiovascular disease. 2. Describe the anatomy of Heart and the diseases of heart that cause sudden death. 3. Draw a sketch of Circle of Willis. Describe in detail the disorders of central nervous system that cause sudden death.
MULTIPLE CHOICE QUESTIONS
1. The most common cause in sudden death involves: A. Cardiovascular system B. Respiratory system C. Nervous system D. Idiopathic
1 A
2 A
2. The most common site of fatal coronary stenosis is: A. Anterior interventricular B. Right main coronary C. Left circumflex D. Left main coronary
12
Part 1—Forensic Medicine and Pathology
Road Traffic Accidents Accidents occurring on the road between the vehicles or a vehicle with pedestrians. It accounts about 60 % of the total deaths. The most common for m of accident is between a vehicle with a pedestrian.
Human Factors
MECHANISM OF INJURY
Relating to road: Defective narrow roads, defective layout of cross roads and speed breakers, poor lighting, lack of familiarity. Relating to vehicle: Excessive speed, old, poorly maintained, large number of two or three wheelers, overcrowded buses, low driving standards. Bad weather, inadequate enforcement of existing laws, mixed tragic slow and fast moving, pedestrians, animals etc. Both the above factors lead to increased vulnerability and risk situation and lead to accidents. Prevention of accidents, measures to be devised. If accident is a disease, education is a vaccine. Safety education Belief that accidents are inevitable must be curbed. Safety education must begin with students, driver need to be trained for safe driving and proper maintenance of vehicles. Young people must be educated regarding risk factors, traffic rules, safety precautions and first aid.
The mechanism of road traffic accident is thoroughly studied by De’Haven. He has found that the severity of injury to a vehicle occupant is directly proportional to the degree of acceleration or deceleration force. The change of speed is the main culprit, rather than its absolute speed. The G formula is used to calculate the main force involved in an accident impact of deceleration force may be calculated from the following formula. V2 × 0.034 G = ________________ D
Where G = equal to force exerted by gravity V = velocity of the vehicle in miles / hour D = stopping distance in feet 0.034 is a mathematical conversion factor The injuries are caused to the occupants while they are inside the vehicle (Non ejection crash injury) or when thrown out of the vehicle (ejection crash injury) or both types of cases the nature, severity of injury vary. Primary Factors in Accidents These factors are the most important ones in the causation of the accident. The factors can be both human as well as environmental factors.
Age, sex, education, medical conditions, fatigue, psychological factors, lack of body protection. Environmental Factors
Non-ejection Crash Injuries Frontal impact is more common in road accidents, the occupant may also be exposed to lateral and rear impact collisions. During lateral impact, the force is of larger magnitude, for there is very little of the car structure to cushion the impact. In
190
Textbook of Forensic Medicine and Toxicology
general there is little difference in the frequency and locations of injury between rear seat and front seat passengers. Ejection Crash Injury Ejection is largely dependent on whether the door springs open at the time of crash. This occurs most commonly in roll over accidents. In ejection fatalities, one frequently sees severe multiple injuries, any one of which may be responsible for death. Head alone or in combination of chest and abdomen is injured in 2 out of 3 cases. Chest and abdomen alone or in combination is seen in more than half the cases. Fracture of ribs is seen in 2/ 3rd of cases. Non-ejection Crash Injuries Sitting position Front seat The front seat passengers are injured by the primary impact. The head, abdomen, knee and chest are injured in this impact. The head knee and the chest are injured as they hit the steering wheel and the dashboard of the car while the abdomen is injured by the seat belt. Seat belt injuries The injuries caused by the seat belt depend upon the type of belt present. Perforation of ileum, caecum and sigmoid colon is common due to compression of intra-abdominal viscera. Presence of abdominal wall contusion associated with paralytic ileus should raise a suspicion of significant intra-abdominal injury. Lap Belt Injury to the lumbar spine, Spleen, pancreas, uterus, urethra and iliac artery. Shoulder Restraints If shoulder restraints are used then various injuries occur such as fracture of the ribs, cervical spine, lumbar spine and sternum. Deep organ lesions of larynx, liver, spleen and kidney can be found..
Three Point Belts If three point seat belts are used it causes a pattern of injuries which includes fracture of ribs, sternum and clavicle. Abdominal injury leading to jejunal or duodenal perforation is seen. Contusions and abrasion in the chest, shoulder, neck and back amy also be seen underlying the position of the seat belt.. Ejection Crash Injury Ejection is 2nd only to the steering wheel as a major cause of injury. It depends upon whether the doors spring open at the time of crash. There are multiple injuries, the head alone or in combination with chest and abdomen alone or in combination with each other or with group. Fracture rib Laceration in liver Soft tissues and other abdominal viscera
66.6 % 33 % 50 %
Injuries caused by Vehicular Accidents • Primary impact injuries are the injuries caused to the first body part struck by the vehicle. • Secondary impact injuries are the ones caused by further impact by the vehicle. • Secondary injuries are caused by the impact with the ground. Injury to Pedestrians Both primary and secondary impact injury occur as the person is thrown to ground or may be crushed and run over. Bumper of the car causes injuries below the knee; the radiator hits the pelvis and the abdomen is hit by the fender. It has been found that the pedestrians sustain about 25 % cases fracture of legs while 40 % cases there is injury to chest and abdomen. The fracture of ribs and injury to heart and lungs are the commonest form of injuries. Bicycle When a person travels by a bicycle and is hit by a vehicle, fracture bones, severe soft tissue injuries and bicycle spoke injury, particularly in children.
Anaesthetic and Surgical Death Run over Accidents When a victim is run over the tire marks and grinding abrasion may be seen. Burning of the skin due to heat produced by sliding of the body, deep crushing of the body with rupture of internal organs may be found. Motorcyclist Usually occurs by running in front of a vehicle from one side to other. The cycle is hit and the person is thrown violently on the ground. At times they are thrown beneath a vehicle and crushed like any pedestrian. Helmet Egg shelled helmet may lead to fracture of spine or strangulation by the strap. Classical injury in motor cyclist and pillion passengers is fracture of skull usually from secondary impact on the ground. Crush Helmet This reduces friction of the head against the ground. It makes deceleration force less by allowing the protected head to skin across the ground rather than come to an abrupt halt. Temporal bone and parietal bone fracture, fracture of base of skull and contra coup injury to the brain are seen. Car Drivers Driver may impact the chest on the steering wheel or the upper abdomen on the wheel rim leading to fracture of the sternum, laceration to heart and splitting of the aorta. Lung roots may be pressed against the wheel rim and may crush the spine, liver, spleen or the kidney. Crush the throat by top of the steering wheel, split the head or face on a shattering windscreen. Asphyxia may result by inhalation of blood. Thrust the whole skull down on to cranial spine. Drivers or passengers may sustain 3 or 4 sliding forward off in seat and may also split one or both patellae or crush the knee joint. Fracture of femur or pelvis. If car overturns the person may be pinned to ground or crushed
191
leading to traumatic asphyxia. He may be burnt or get asphyxiated. Injuries to Vehicle Occupants These are important in identifying their positions in the vehicle at the time of accident including the driver and the persons in the front seat Dash board injuries Grazes or lacerations of the skin of knees from the impact with dashboard occurs. Also there may be fracture of leg bones. Investigation of Road Accidents Pattern of injury, role played by a concurrent natural disease, the crash as a possible method of self destruction (suicide) should be looked into. The crash as a possible method of making a homicide, role played by intoxicating drugs. The incidence of accidents caused by the natural death of a sober driver has been estimated to be less than 6 per 100,000 motor vehicle collision. The possibility must be kept in mind where bodily injury is minimal or absent and damage to the vehicle is limited. Hit and Run These cases requires very thorough investigation of the scene as well as clothing worn by the victim. Detection of patterned injuries, paint or metal fragments, grease, dirt or glass particles may provide the only evidence capable of leading to the identification of the responsible vehicle. Role of Alcohol and Drugs Driving under the influence of drugs or alcohol or both remains a major socio-economic problem in modern society. Drug use should be considered when drivers behavior is suggestive of alcohol consumption but tests of his blood or breath for alcohol are negative. This particular category of driver should be tested by standard methods of drug screening for barbiturates, amphetamines or other drugs that might explain the disorderly behavior. The alcohol intoxication contributes to a traffic fatality both by impairing judgment, coordination and vision before the accident and by interfering with the evaluation and interfere with
192
Textbook of Forensic Medicine and Toxicology
the treatment of injuries sustained at the time of crash. The most important investigation in road accidents is the determination of the degree of intoxication present. The concentration of blood alcohol should always be determined in the driver of a vehicle, in the pedestrian injured or killed in the accident in the passenger of the vehicle involved with accident. Suicide The imprint of the gas pedal pattern on the driver’s shoe sole and the absence of skid marks leading to the site of collision are believed by some to be suggestive of suicide, because they indicate that the driver was accelerating his vehicle at the time of impact. Purpose of Accident Injury Investigation To determine directly by detailed examination of the results of actual road accidents, the effects of different types and severities of vehicle collision upon the living human body. More accurate information relating to mechanisms of injury will be obtained resulting from impact of human body upon the vehicle interior (or in case of pedestrians, the vehicle exterior). Factors to be Investigated Include The pattern of injury and of death in various groups of road users. The time interval between accidents and death. The cause of injury in relation to specific parts of the vehicle. The direction in which force acts on the human body to produce injury. The levels of human tolerance to dynamic loads applied to different parts of the body. The effectiveness of various safety design features in terms of reduction in frequency and or severity or injury. Procedure of Accident Injury Investigation It is the same for all classes of road users whether they be vehicle occupants or pedestrians or motorcyclists. Research team is interdisciplinary and consists of medical scientists, engineers, professional photographers etc. and it requires cooperation of hospitals, police, garages, motoring
public etc. The standard procedure for investigation consists of: Medical interview and medical examination of injured persons. Follow up study of vehicles. Interview of police officers concerned with the accidents and other witnesses. Writing up the accident in detail. Analyses of results when number of accidents reaches and adequate level. Medical examination of casualties: • Undertaken usually in hospital • Patient’s informed consent is obtained • clinical and radiological findings are obtained • all injuries are classified according to their severity as minor, moderate, severe as per the road research laboratory leaflet issued in 1969 • exact site of injuries and nature recorded on diagrams. • Color photographic record made if possible • In case of fatalities, post mortem examination with details of all injuries, time elapsed between injury and death and an assessment of the cause or causes of death are recorded. • Enquiry into accident and examination of the vehicles it is necessary to reconstruct with reasonable accuracy the events of accident in relation to both the vehicle and occupant movement. • Whether using on the spot techniques or retrospective techniques, a three phase investigation of the accident circ*mstances is undertaken. • Reporting police officer and other witnesses are interviewed. • Accident site is examined. • Vehicles are subjected to careful scrutiny. Using Retrospective Techniques Certain basic data can be obtained from reporting officers regarding the accident which will include Directions in which various vehicles were traveling, Final positions of vehicle after the accident, Rough estimate of pre-accident speeds, Evidence of ejection or Trapping of occupants.
Anaesthetic and Surgical Death Examination of Scene It is useful for reconstruction of accident and for interpretation of wounds and the mode of dying. Dragging marks, which are superficial and extensive, suggest that the victim had been dragged and not ejected. Measurements of the leg fracture and other body injuries from the heel of the feet may help in identification of suspect vehicle in hit and run cases. The bumper fracture may be compared with the suspected car by measuring the height of bumper from the road. Diagrammatic representation of injuries is quite useful. All injuries cannot be interpreted but patterned injuries should primarily be considered. Specimens should be collected for alcohol, barbiturates, antihistaminic drugs, any foreign material like glass, paint or oil found on clothing, skin or the wound should be collected. The vehicle itself may give evidence of contact in the form of blood, flesh, hair, fragments of clothing, damage and signs of attempt to clean or repair. Reconstruction of the Crash Over interpretation of the post mortem findings is undesirable, since it must be remembered that it is usually impossible to attribute a specific causative mechanism to each and every injury on the victim’s body. Patterned injuries by virtue of their location are vital to the accident reconstruction for example the circular abrasion on the driver’s chest or face from the impact on the steering column or steering wheel or the impact of the head light on the thigh of a pedestrian struck by an automobile. It is advisable to collect blood and urine samples for alcohol in vehicular accidents. A driver who is not a property controlled diabetic or epileptic or suffers from cardiac disease is a potentially dangerous on the road. He is liable to unexpected impairment of consciousness. Also a driver who smokes more than 20 cigarettes in a day is considered to be living at a physiologic altitude of 8000 feet and impaired oxidation has striking effects on visual acuity at low levels of illumination.
193
PS = ½ MV2 P = deceleration force—this is the force acting on the person when brakes are applied and the speed of the vehicle starts decreasing. S = linear deceleration distance—this is the distance between the point when the brakes were first applied and the vehicle comes to a complete stop. M = mass of car V = velocity of the car at the time of applying the brakes. Promotion of Safety Measures Seat belts reduce the number of fatalities and nonfatal injuries by about 50%. It has been made compulsory for cars light trucks and similar vehicles. Safety helmets reduce the risk of head injury by about 30%. This reduces fatalities by about 40%. They prevent damage to scalp and skull fracture to a great extent. Full-face helmets are very popular among two wheeler riders. Leather Clothing and Boots Leather clothing reduces risk of extensive superficial soft tissue injury. Leather belts protect lower legs and feet. Children should remain seated when they are in vehicle. They should be prohibited to take front seats of cars. ‘Child locks’ should be present in the cars. Supreme court guidelines for school buses as safety measures are; • Foot boards to enter bus at lower levels. • Drivers with minimum of 5 years driving experience and with driving license. • Doors should be locked. • Parallel bars on windows. • A school teacher and a conductor is mandatory. • The bus should be painted clearly as school bus and in case of put buses should be clearly written as bus on school duty. • Spaces for bags behind seats. • Phone no. of school, name of school should be maintained in the bus. • First aid boxes.
194
Textbook of Forensic Medicine and Toxicology
Other features are use of door locks, proper vehicle design and use of laminated high penetration resistance windscreen glass. Alcohol and other drugs: Alcohol impairs driving ability and increases the risk of an accident as well as severity of its consequences. Alcohol is the direct cause of 30=50 % of road traffic accidents. Though the legal limit is 80 mg % but impairment can result at blood level of 50 mg % and accident risk increases in 50-80 mg % level. Drugs like barbiturate, amphetamines and cannabis impair driving ability. Primary Care Primary care includes planning, organization and management of trauma treatment and emergency care services for the trauma patient. Emergency care should begin at the accident site and anytime during transportation and should conclude in hospital emergency department. Elimination of Causative Factors Improvement of roads, imposition of speed limits, marking of danger points, reduction of electric voltage, provision of fireguards, increase of safety equipment in industries, safe storage of drugs, weapons, poisons. Accidentology deals with accident research and involves gathering precise information about extent, type and other causes of accidents, seeking ways to make environmentevaluating efficiency of content. Investigating new and better methods of altering human behavior. Accidents are a matter of chance, safety isn’t. So proper safety measure must be devised to minimize the chances of road traffic accidents. These can be broadly of three types. Primary preventive measures Primary preventive measures are devised to improve the driving condition and also to reduce the driving fatigue to avoid accidents. User Friendly Systems Electronic Power Steering: It uses less than half the power consumed by an ordinary power
assisted steering. It doesn’t suffer from losses of power assistance due to leakage. Electronic sensors in these provide varying levels of power assistance at different speeds for , better maneuverability and greater control. Electronically controlled and incorporates self diagnosis in case of any problems. Power brakes, roll control device, anti-lock brakes, brake assist, acceleration skid control, strengthened body shell, antiglare windscreens and glasses and mirrors, large vertical headlamps for enhanced visibility, good quality headlights for improved visibility and also high quality wide windscreen. Improved design of tail lights. Automatic transmission streamlined care structure and improved engine design for smooth and effortless pickup. Collapsible steering column: For total comfort full flat reclining front seats as well as reclining rear seats. Upright design, low side steps, high seats and wide opening doors for easy entry and exit. Better air-conditioning to reduce the fatigue of driving in temperate climates to minimize irritability arising out of heat and carbon monoxide emanating out. Various safety measure like child locks indoors, central locking of all 5 doors, Bernouli’s flaps on the undersurface of cars makes it to be driven sticking to the undersurface. Block shock absorbers, wide diameter shockers struts allow to drive smoothly over the worst roads. Wide tread tires ensure surest road grip and the safest drives. Better road designs for better safety and proper road lights to minimize accidents. Better traffic safety traffic lights and traffic signs should be visible from a distance and not be hidden behind a tree. Self diagnosing on board computers. The driver while driving should avoid talking on a cell phone. High volume music may divert attention. He should also avoid talking to the other occupants. New safety features being introduced include: • Lane departure warning system: This system warn drivers if they are about to leave a lane unintentionally • Adaptive cruise control: This system prevents the driver from getting too close to
Anaesthetic and Surgical Death the vehicle in front of them by applying brakes automatically if the distance is too little. • Pre crash warning: This system detects a possible collision and warns the driver. If the driver fails to react, the advanced versions of the system can activate the brakes and even turn the steering wheel. Secondary Preventive Measures These are to reduce fatalities if accident has occurred. Safety belts 1 or 2 point safety belt. It has a disadvantage of slipping out from the hold and causes whiplash injuries. 3 point safety belt. It is for a better hold. They avoid the impact of driver or other occupant to the front in case of sudden deceleration. The cars should have airbags and window bags. Injury over the dashboard on driver’s side reduces the injury in case of sudden impact. Collapsible steering column and energy absorbing steering column. High penetration resistant windscreen glass. Sturdy design of vehicle to absorb front and rear impact through crumple zones. Side impact beams and bars in front and rear door to take up the impact. Anti roll bars are net like pillar or strongholds in case of rolls during accidents and prevent the collapse of whole structure. Laminated windshields are designed to prevent the shredding of glass in case of impact and if it displaces then it gets stick to the place only. Fire proof paints, upholstery prevents fire from spreading. Helmets in case of two wheelers minimizes the impact to head in case of an accident. Tertiary Measures Enable speedy salvage, rescue in case of accidents: • Cellular. • Audio system. • Global positioning system. • Computers. Seat Belt Syndrome With abrupt deceleration, the set belt compresses the contents of the abdominal cavity the mus-
195
culature of abdominal cavity ruptures and often of left hemi diaphragm. Also shear forces lead to the bowel injury. Applied against adjacent structures, such forces cause bowel transaction, particularly near points of fixation, such as iliocaecal valve and the ligaments of trietz. Also fracture of lumbar spine results. Road Traffic Injuries Large varieties of injuries are sustained by persons involved in traffic accident and by detailed examination of these injuries it is possible to reconstruct the accident these may help in confirming or refuting the evidence of eyewitness. Further it may be possible to identify the hit and run accidents. In RTA, the following categories of people may receive/ sustain injuries. Injuries to Pedestrians Often the following pattern of injuries are seen: Primary Impact Injuries In these injuries, the part of body involved i.e. right or left side, front or back, will depend upon the position of person in relation to vehicles when struck i.e. whether crossing the road or waling with or against traffic. The injuries will be further modified as to whether both feet are on the ground or one is raised and the firmness or otherwise of either or both feet. The relative heights of various parts of the vehicle i.e. bumper, radiator, door handles etc. and the pattern of these parts of the vehicle if found on the body of person in the form of injuries, help in identification of vehicle. For reconstruction of accident, it is better to discuss injuries only in relation to one type of motor vehicle as the models keep on varying all over the world and from year to year (Figs 12.1 and 12.2). Secondary Impact Injuries Injuries caused if the victim strikes other objects such as the ground after falling from the vehicle. If the person is struck from behind with the feet fixed, primary impact will be on the back of legs and
196
Textbook of Forensic Medicine and Toxicology
Figure 12.1: Multiple abrasions over the shoulder in a case of road traffic accident
Figure 12.2: Abrasions over the forearm in a case of road traffic accident
fracture occurs if the feet are fixed. At the same time the buttocks and back will come in contact with the car and the person is pushed forward. It may cause fracture dislocation of lumbar or thoracic spine. If the person is struck from behind and feet slide forwards, the whole body may fall forwards and have a secondary impact of the head against the windshield, causing shattering of the wind shield and head injuries. Alternatively, the body may be thrown in to air or to one side with resultant secondary injuries from striking the ground i.e. on head and other parts of the body. If the person is facing the vehicle, he may receive intra abdominal injuries and injuries to the chest wall and thoracic
cage. The victim may get injured from the bumper over the front of legs resulting in fracture of both tibia (bumper fracture). Frequently bumper injuries are present at different levels on the two legs or absent on one leg which suggest that the person was walking or running when struck. An impact against a mudguard or headlamp may result in a fracture of pelvis or fracture dislocation of sacroiliac joint. If the person is struck on hip on its side, The initial impact will be against leg and produce bruises the other injuries will depend if the foot was fixed or sliding forwards. Additional injuries like bruising of elbow and fracture of ribs may occur from striking the different parts of the vehicle. Victim will then receive secondary injuries on striking the ground. In a glancing blow from the side of a car in cases where driver attempts to avoid a direct impact, injuries to projecting parts of body such as elbow, shoulder or hips may take place. Penetrating/ tearing wounds caused by protruding objects of the vehicle such as door handle etc may occur. When the vehicle travels at a greater speed, the pedestrian may be thrown height and fall on the vehicle roof and sometimes on the road behind the vehicle. In them the head is injured by direct impact with vehicle and by striking the road. Both impacts produce fracture involving almost all parts of the skull specially those with underlying extensive injuries of the brain. If the person is run over, Crush injuries will occur and its severity will depend on the weight of the vehicle and its clearance from the ground. The findings would be Tire marks and grinding abrasions. Skin avulsion, Burning of the skin due to heat produced by sliding of the body, Deep crushing of the trunk or limbs with rupture of internal organs Flattening deformities of the head, chest or pelvis. When a child is run over by a vehicle, fracture may not be produced due to elasticity of partly cartilaginous skeleton (Fig. 12.3). Injuries to the Driver Driver has the advantage of a momentary appreciation that an accident on steering wheel
Anaesthetic and Surgical Death
197
turns the occupants may be pinned and crushed or these may be serious injuries to heart lungs , liver, spleen or kidneys. Rarely occupants may be burnt or asphyxiated while in the interior of the car. Injuries to Motorcyclists or Scooter Riders
Figure 12.3: Crush injury over the leg
and thus avoids full impact on the chest or of the head against windshield. He may sustain sprains or fractures of the wrist or if he attempts to apply brakes. Fracture of femur or the pelvis takes place. Steering wheel impact type of injuries. Movement of the seat forwards and the steering wheel backwards may cause crush injuries i.e. fracture of ribs and sternum, splitting of aorta, crushing of heart, liver, spleen, kidneys etc. Imprints of brake or accelerator pedal designs on the sole of driver’s shoe may be found. Whiplash Injuries The driver and front seat passengers may split the head or face on a shattering wind screen and may even sustain a fracture dislocation of cervical vertebrae due to impact or jerk resulting in hyperextension / hyper flexion of neck causing fracture of the cervical vertebra at the level of C2C3 and C3-C4. Injuries from flying glasses are less common due to use of safety by laminated glasses but face may be cut or damaged by impact. The risk of front seat passengers is more to drivers or back seat passengers. Injuries to back seat passengers. They receive the injuries due to striking the side, or top of the vehicle or back of the front seat. Ejection injuries. The door may open sometimes and person may fall out. Traumatic asphyxia when vehicle over-
These in most of the cases are from being struck with a motor vehicle pattern of injuries will be of • Primary impact injuries of the leg. • Secondary impact injuries resulting from the contact with the vehicle. Secondary injuries will occur from striking the ground and on occasions being dragged with the vehicle. The same type of injuries are found in pillion passengers. Cervical fatal injury is fracture of skull usually from secondary impact with the ground. Temporoparietal fractures are common which usually extends across the base of skull through pituitary fossa. Crash helmet reduces friction of head against the ground and although the head injuries may be less, there will be other effects such as broken neck or fractured ribs or limbs with internal visceral injuries. Occasionally when helmet is pinned or crushed, the chin strap may be drawn upwards and cause strangulation. One type of injury peculiar to motorcyclists and scooter rider is collision with the rear of the truck when the vehicle will pass underneath the back but the head of rider impacts against the tailboard Injuries sustained by pedal cyclists If caused by an automobile Injuries may be similar to those sustained by a pedestrian except that the impact will be lower on the body or only against to some part of bicycle itself. The secondary injuries may be more severe due to greater distance to fall. Injuries due to running over may be present. Medicolegal Importance of Road Traffic Accident Most of the accidental deaths are caused by automobiles but it may be occasionally used to commit crime like Planned killing, Accident faked to conceal crime, victim killed by other means and thrown on the road, victim killed by other
198
Textbook of Forensic Medicine and Toxicology
means and dead body burnt in a car, Suicide with automobile is difficult to prove but following events may be useful. History of previous suicidal attempts and recent threat to commit suicide. History of depression recently or in the past or history of domestic quarrels or financial crisis, Evidence of speeding, Impact with a tree or bridge usually on the front of vehicle in its center, Single occupancy of the car, straightening of road, Absence of evidence of applying brakes, Suicidal note. Natural death at the wheel versus death from injuries. Natural disease like coronary artery disease may lead to an accident and sudden unexpected death of a driver. Driver suffering from uncontrolled diabetes or epilepsy is a potential danger on the road. In case of pedestrians. Cardiovascular diseases, cerebrovascular diseases, poor vision or impaired hearing may all lead to
accidents. In these cases only a complete autopsy can provide a right answer as to whether the persons died of accidental injuries or naturally. Sometimes death occurs after a considerable time lapse after seeing injuries and it is important to give opinion in such cases if the death was entirely natural or directly / indirectly related to injuries specially if injuries were minor. Long Question 1. What are the different patterns of injury seen in a pedisterian when hit by a car. Short Questions 1. 2. 3. 4.
Whiplash injury Seat belt syndrome Tail gating injury Rolling injuries
13
Part 1—Forensic Medicine and Pathology
Mechanical Injuries A wound is a break in natural continuity of any of the tissues of the living body. The question of examination of wounds arises in the Court of law. Mechanical injuries are the injuries that are caused to the body by physical violence. Classification of Injuries 1. Mechanical Injuries: (i) Those produced by blunt weapon: (a) Contusion (b) Abrasion (c) Laceration (ii) Those produced by sharp weapon: (a) Incised wound (b) Stab wound (iii) Firearm wounds (iv) Fractures. 2. Thermal Injuries: (i) Produced due to cold:(a) Local hypothermia (b) Frost bite (c) Trench foot (d) Immersion foot (e) General hypothermia (ii) Produced by local application of heat: (a) Burns (b) Scalds (iii) Produced by general application of heat: (a) Heat Hyperpyrexia (heat stroke) (b) Heat Exhaustion (c) Heat cramps 3. Chemical Injuries: (i) Corrosives (acids and alkalis) (ii) Irritants (weak acids and alkalis). 4. Injuries due to: (i) Electricity (ii) Lightning (iii) X-rays (iv) Radioactive substances. 5. Legally: (i) Simple injury (ii) Grievous hurt. 6. Depending on manner of death: (i) Suicidal (ii) Homicidal (iii) Accidental 7. Wounds can be: (i) Defense wounds (ii) Fabricated wounds 8. Wounds in relation to death: (i) Antemortem (ii) Postmortem. Mechanism of Wound Production Moritz has described in detail the mechanism of production of wound. According to him, wound is caused by a mechanical force, which may be
either: (i) Moving weapon (counterforce is provided by the inertia of the body) or (ii) Moving body (rigidity of some stationary object). Due to impact between the propelling force and counterforce, energy is transferred to the tissues of the body that causes a change in their state of rest or motion. Human body contains many complex tissues such as solidity, fluidity, elasticity, density etc that vary in their physical properties. Therefore, there is no uniform change or effect on the body. All the body tissues except the ones that contain gases are resistant to compression forces. Mechanical forces does not cause compression of the tissues but causes their displacement and deformation with the result that traction strains are produced in the affected tissues. Such strains may usually be due to forces causing simple elongation of the tissues. In addition, they may be due to other mechanisms such as bending, torsion or shearing that are more complex. Shear Strain: Shear strain is a strain, which is produced in a body by the forceful alteration of its shape but not volume. It causes stretch in direction parallel to the plane of contact. When tenacity of an organ exceeds, it ruptures and the bones fractures. Factors influencing nature and extent of wounds 1. Nature of the objects/instruments: i. Blow from pin pointed/sharp edged weapon: The force is concentrated over limited area resulting in incision or deep penetration. The hardness and friction of divided tissues resist passage of the instrument.
200 Textbook of Forensic Medicine and Toxicology ii. Blow from blunt objects: The force is dissipated over relatively large area so the damage caused to a unit of mass is less than when force is applied over a small area. A rapid transfer of energy over this small area is more likely to produce a wound than an equal amount over large area. The rapid transfer of energy is fatal than the slow transfer. 2. Amount of energy discharged: Kinetic energy is measured in a moving object by: K.E = ½mv2, where m = mass and v = velocity. An object with definite velocity and definite weight have a definite amount of energy. When the mass doubles, kinetic energy is also doubled. However, when velocity is doubled kinetic energy increases four times. This indicates that the velocity has far more influence on the energy compared to the mass of the object. 3. Conditions under which energy is discharged: Moving objects have energy due to their movement that is directly proportional to their mass and to the square of their velocity as explained above. When moving objects are stopped suddenly on an encounter with some stationary object, the energy is dissipated at the sites of resistance, which causes various types of injuries like abrasion, contusion, laceration or incised wounds. On the other hand, if the human body is moving and encounters a stationary object, similar injuries are produced. 4. Nature of the tissue affected: The tissue that encounters the resistance suffers damage depending on its type as well as nature. Bones being tough undergo fractures on infliction of injury while muscles develop hemorrhages due to rupture of blood vessels in them. Soft tissues also tend to have hemorrhages or may rupture on infliction of severe force especially in cases of large organs like liver. Even, mesenteries get torn by blunt injury to the abdomen.
painful swelling and is caused by crushing or tearing of subcutaneous tissue. There is no destruction of external surface in a contusion. Due to rupture of blood vessels, blood extravasates in to subcutaneous tissues and the margins are blurred. The size of a bruise varies from small pinhead sized to large collection of blood in the subcutaneous tissues. The more the force is used to inflict the injury, the more is the collection of blood and the bigger is the size of the resulting bruise (Figs 13.1 to 13.4).
Figure 13.1: Bluish bruise over the front of forearm
Figure 13.2: Bruise over the thigh
BLUNT FORCE INJURIES CONTUSIONS Contusions are a collection of blood into the tissues due to rupture of blood vessels, caused by blunt trauma. It can be caused in the skin or inner organs like liver, brain, kidney etc. It is a
Figure 13.3: Black eye—bluish black bruising
Mechanical Injury 201
Figure 13.4: Multiple abrasions and bruises over the thigh and abdomen
Factors modifying size and shape of bruise: 1. Condition and type of tissues: The softer the tissues, more easily they are likely to bruise. 2. Age: The persons who are old aged tend to bruise easily because of the loss of flesh and the age related cardiovascular changes in them. The children having a softer skin and delicate tissues also get easily bruised. 3. Sex: Women bruise more easily because of the delicate tissues and more of subcutaneous fat. 4. Colour of skin: Bruising is easily visible in fair skinned people compared to the dark skinned ones though the bruised area can be felt with palpation. In an embalmed body, the bruise becomes more prominent as the embalming fluid makes the skin lighter in colour and more of blood is forced into the damaged tissues and the embalming fluid makes a dark pigment complex. Photographs are quite helpful as they can highlight even those contusions, which are not clearly visible to the naked eye. 5. Natural disease:The appearance of a bruise varies with the various natural diseases such as:(i) Arteriosclerosis—Bruising may occur very easily even from slight coughing or exercise. (ii) Whooping cough—In children whooping cough causes violent bouts of cough, which may cause bruising without any direct external injury (iii) Conditions such as purpura, leukemia, hemophilia, vitamin C & K deficiency, phosphorous poisoning etc. lead to easy bruising and in purpura colour change is discernable without any swelling.
Antemortem and postmortem contusions: Signs of inflammation such as redness, pain, loss of function are the hallmark of antemortem bruising and in addition, extravasation of blood is present in case of antemortem injury. Colour changes can be seen only in case of antemortem injury. On microscopic examination, white blood cells are present in antemortem bruises and after about 12 hours rupture of red blood cells and the release of iron pigments occurs. A bruise has to be distinguished from postmortem lividity, congestion of organs and artificial bruise (Tables 13.1 to 13.3) Table 13.1: Differences between bruise and P.M. lividity Findings
Bruise
P.M. Lividity
Cause Cuticle Site Appearance Edges Cut Section
Blunt force Damaged Any part Elevated Ill-defined Clot cannot be washed Change of colours Lighter
Engorged vessels Not damaged Dependent part Not so Well defined Blood inside vessel, easily washed Bluish, no change No effect
Colour Pressure
Table 13.2: Differences between artificial and true bruise Findings
Artificial bruise True bruise
Cause Situation Colour Margins Shape Swelling Contents Itching Chemical test
Juice of plant Accessible parts Dark brown Well defined Irregular Not present Serum Present Positive
Blunt force Any part Change of colours Ill defined Shape of the weapon Slight swelling Blood Absent Negative
Table 13.3: Differences between bruise and congestion Findings Cause Colour Margins On dissection
Bruise Force Change Diffuse, ill-defined Extravasation of blood
Congestion Pathological condition No change. Well-defined Engorged vessels, blood inside
Medicolegal significance of bruise: 1. A bruise can be a simple injury. 2. When any vital organs are involved it may be a grievous hurt
202 Textbook of Forensic Medicine and Toxicology 3. Multiple bruises can also cause death 4. When the force is applied over the body by a weapon having definite patterns like belt, chain etc., it leaves a pattern simulating the size and shape of the object. This is called patterned bruise and is important from medicolegal point of view as from its examination, the type of weapon that has caused the injury can be known. This may connect the victim and the weapon and can indicate the nature of weapon. 5. Nature of weapon: The characteristics of bruise produced by different types of weapons/objects are:(i) Hammer, closed fist produces round bruise (ii) Rod, stick, and whip produces bruise in the form of two parallel linear hemorrhages (iii) In a broad and flat weapon like plank, the edges of plank may cause parallel lines separated by apparently normal tissue (iv) Ligature mark also forms a definite patterned bruise showing the pattern of woven, spiral ligature (v) Elliptical patterned bruise indicates teeth bite (vi) The tip of the shoe will also produce a definite patterned bruise (vii) Tyre tread marks in a road traffic accident produce the pattern of the tyre. 6. Age of a bruise: The age can be estimated by the characteristic colour changes that the bruise undergoes with the passage of time. These colour changes are due to breakdown of RBC’s and release of different pigments. These colour changes in a bruise are: Colour of bruise Red
Pigment Haemoglobin
Blue
Deoxygenated hemoglobin haemosiderin haemotoidin Bilirubin —
Bluish black to brown Greenish Yellow Completely disappears
Time Immediate (24 hours) 1-3 days 4 days 5-6 days 7-12 days 2 weeks
However, it is very difficult to estimate the exact age from the colour changes. Subconjunctival hemorrhages do not undergo the usual colour changes and becomes yellow from red. In old age and diseased it takes a longer time for the various colour changes
to appear. The colour changes are sustained during CO poisoning and remain bright red. III. From the examination of bruises, the degree of violence can be estimated and the character and manner of production of injuries can be ascertained as different types of violence produce different types of bruises. In deaths due to manual strangulation thumb and finger impression in the form of bruises are seen over the neck. In sexual assault cases, the bruises may be present over breasts, inner sides of thigh and genitalia. From the pattern of bruises over arms, it can be known if the arms were grasped by the assailant and also the relative position of the assailant; front or behind can be known. If bruising is present over shoulder blades, it indicates pressure on the body against ground or some other hard surface. IV. Delayed Bruising: The bruising at times does not appear immediately after the impact. This is due to the fact that the blood comes to the superficial layers after a delay of few hours or even days. This is known as delayed bruising and is commonly seen in abdomen, thigh etc.A deep bruise takes several hours to appear on the surface and very deep extravasations never appear on the surface. In casualty any injured person with no visible bruise should be advised to come after 24 hours to find delayed bruising. V. Shifting of the bruise: Bruising may not necessarily appear at the site of impact. The blood gravitates through the loose areolar tissue to appear at a different place at the lower area. A few examples of bruising at sites distant from the point of injury are as given below. • Anterior cranial fossa fracture causes bruising of the eyes and the eyelids become black. • Fracture of the base of skull leads to accumulation of blood behind the ears. • In case of an injury on calf muscle blood shifts in between the muscle planes to the ankles.
Mechanical Injury 203 ABRASION In an abrasion, there is damage of the superficial epithelial covering of skin/mucus membrane due to impact of hard surface or weapon. Mode of Production An impact causing friction between weapon and body surface is the commonest mode of production of an abrasion. Direction of force may be horizontal or tangential causing scratches or graze abrasions or it may be perpendicular when it causes an imprint or pressure abrasion. Features These are superficial injuries with denudation of the epithelium. Later on a scab of dried blood is formed at the site. Gradually the granulation tissue forms beneath the scab and wound healing occurs. Types 1. Linear or Scratches: These are caused by horizontal friction produced by pointed end of weapon. It is wider at the start and shows heaping of epithelium at the end. The features of linear abrasion depend on: (i) type of weapon (ii) direction of force and (iii) the relative position of victim and assailant. 2. Graze or sliding: These are produced by rubbing against a rough surface of an object or ground etc. Grazed abrasions are seen most commonly in vehicular accidents. It is wider and deeper at the beginning and there is thinning at the end. Heaping of epithelium is present and indicates the direction of the force. Its size and shape have no relation to the weapon. 3. Pressure: In this type of abrasion, the force is more or less perpendicular and its size and shape depends on the part of the weapon in contact. Examples include the ligature mark in hanging or strangulation and in throttling. Teeth bite marks are also pressure abrasions. 4. Imprint or patterned: They reproduce the pattern of weapon causing e.g, in vehicular accidents
patterned abrasion is caused by the impact by radiator grill, headlamp. In run over accidents, the tyre marks may also produce patterned abrasions (Figs 13.5 to 13.10). MedicolEgal Importance 1. They are usually simple injuries, as they do not leave a scar and usually abrasions are not dangerous to vital organs. 2. They can be self-inflicted for leveling false charges against enemies. 3. The type of weapon can be identified from the examining the abrasion 4. Time of assault can be estimated by estimating the age of an abrasion • Fresh – No scab • 8-12 hours – Reddish scab • 2-3 days – Brown scab • 4-5 days – Dark brown scab • 6 days – Black scab, starts falling 5. Nature of offence: In sexual offences, abrasion are found around breast, inner side of thighs whereas in asphyxial deaths such as throttling there are abrasions over the neck. 6. Postmortem abrasions are yellowish parchment like and may be caused during transport. 7. Type of weapon can be identified and matched with the injuries found on the person. LACERATED WOUND When the tissues gets crushed or stretched beyond the limits of their elasticity thus tearing off leading to the formation of lacerated wound. The lacerated wound is caused by a blunt trauma. Thus, it may be caused in falls, in accidents, and in blows to chest, abdomen, head etc. by blunt object. The lacerations can be divided into split, stretch, avulsion and cut lacerations. Split Lacerations This is the type of laceration, which occurs due to crushing of the skin between two hard objects and leading to splitting of the skin. It is usually found on the areas of the body, which have subcutaneous bones like scalp, shin of tibia and
204 Textbook of Forensic Medicine and Toxicology ulnar border of forearm. If these areas are hit with a hard object then it may crush the skin and the thin subcutaneous tissue and cause a split laceration. In these areas, the lacerated wounds may also appear clean cut and may simulate an incised wound. Such wounds are known as incised looking lacerated wounds. Even though they look like incised wounds but they are caused by blunt force on the areas where skin is closely adherent to bone and subcutaneous tissues is scanty like on the scalp, Jaw, pelvic bones (iliac crest) and eyebrows (Table 13.1). Stretch Lacerations
Figure13.6: Glazed abrasions
This type of lacerations are caused by excessive stretching of the skin beyond which it causes tear of the skin. It is usually seen in run over accidents or in cases where a body part may be caught in the some moving machinery. These type of lacerations if very extensive can cause a flap of loose skin and tissue. The flap can depict the direction of the force applied on the skin and can
Figure13.7: Abrasions over the forearm
Figure13.5: Multiple abrasions over the face
be useful in establishing the manner of the injury. Figure13.8: Abrasions over the shoulder
Avulsion This is the type of laceration in which there is separation of the skin from the underlying tissue. This is also caused in a similar manner as a
stretch laceration but the force involved is much more severe and the area involved is comparatively larger. It causes flaying of the tissue, which is a type of crush injury. The shearing or grinding force
Mechanical Injury 205 wound is less hemorrhagic as compared to an incised wound. Foreign matter may be present in the wound. Direction of the force can be established but the shape and size of the wound may not correspond to the instrument (Fig. 13.11). INCISED WOUNDS OR SLASH WOUNDS
Figure13.9: Abrasions over the heel
Figure13.10: Multiple abrasion over the thigh
produced by a weight is the reason behind this type of injury. Cut Laceration This is caused by a heavy sharp edged instrument, which causes a deep and wide cut over the body tissues. Characters of Lacerated Wound The margins of a lacerated wound are irregular with bruising present all around. The deeper tissues are unevenly divided and the hair bulbs are crushed rather than being cut. The lacerated
The incised wounds are produced by sharp cutting weapons like knives, dagger or a razor and blade etc. Some authors restrict the term incised wounds to wounds that are longer than they are deep but some include stab wounds under this category. An incised wound that is longer than its depth is referred to ‘cut’ or ‘slash. The knife, razor blade, sword, cleaver, panga, bottle or broken glass pieces may inflict such cuts that are typically seen in fights when the assailant strikes out with a sweeping action rather than the thrusting (Fig. 13.12). The force is delivered over a narrow area of the skin by a sharp edged weapon, which causes cutting of the skin. The edges are clear, well-defined and there is no bruising. Due to the elasticity of the skin, the width of the wound is greater than the edge of the weapon and the length is greater than the width and the depth. The length of an incised wound has got no relation to the cutting edge of the weapon. These wounds are spindle shaped as the skin retracts due to its elasticity more so in the middle of the wound. Gaping is more if underlying fibers are cut transversely or obliquely. Haemorrhage in an incised wound is more compared to a laceration or crush injury. The wound is deeper at the start as there is more pressure at that point than at the termination where it narrows down leaving only a superficial scratch which is known as tailing of the wound. The tailing of the wound can be evaluated for estimating the direction of the injury. When the weapon enters obliquely, then an oblique wound is created in which one flap is visible while the other one is undermined. This type of cut is known as a beveling cut. Chop Wounds
206 Textbook of Forensic Medicine and Toxicology Table 13.1: Difference between incised wound and lacerated wound S. No.
Incised wound
Lacerated wound
1. 2. 3. 4. 5. 6.
Any where in the body Edges are clean cut No bruising of margins Blood vessels, nerves clean cut Hair bulbs clean cut Bleeding more
Over bony prominences Lacerated Bruising present Crushed Crushed Bleeding less
These types of wounds are produced by a blow with a sharp cutting edge of a heavy weapon like an axe, basola etc. In this type of injury, the dimensions of the wound correspond to crosssections of penetrating blade. The margins are sharp with lacerated edges. Hesitational Cuts These are the cuts made by person with suicidal tendency. While attempting suicide these persons try to cut them to bleed to death. However, they hesitatingly make many superficial cuts before attempting a more deep cut. These hesitational cuts are typically multiple, superficial, parallel, uniform in depth and present on the accessible parts of the body. Incised wounds are less dangerous than stab wounds as the relative shallowness of the wounds is les likely to affect a vital organ. The arms and the face are the common targets. Since the brain and chest organs are well protected by the ribs and skull, it is only the abdomen that is the target for a swung blade. A broken drinking glass is also used as a weapon, it may be broken prior to the attack to produce exquisitely sharp edges. The glass can inflict deep wounds almost akin to a stab wound. Where a glass or bottle is used as a blunt object, it may shatter on impact with the victim’s head and the resulting injuries may be both blunt and incised.
Figure 13.11: Lacerated wound
manner and have a number of tentative cuts. If successful, there will be one or more deep incisions superimposed, which may destroy some of the previous shallow cuts. The classical description of the cut throat is of incisions starting high on the left side of the neck below the angle of
CUT THROAT WOUNDS Suicidal Cut Throat Wounds Cut throat wounds are commonly suicidal in
Figure 13.12: Multiple incised over the forearm
Mechanical Injury 207 jaw, which pass obliquely across the front of the neck to end at a lower level on the right. This assumes that the victim is right handed, the obliquity being reversed in a left-handed person. The cuts are said to be deeper at their origin, becoming shallower as they cross the throat, tailing off into surface cuts at the extremity but commonly the cuts show no variation at the either end. Most suicides raise their chin to provide a better access to the throat, so that the skin is stretched out when cut. This tends to cause straight-edged incisions, rather than the jagged cut that is seen when a knife is drawn over the loose skin. Throwing back the head moves the carotid bundle under the protection of the sternomastoid muscles and if cuts are confined to the centre of the front of the neck, only the larynx or trachea may be damaged, rather than large blood vessels. Homicidal Cut Throat Wounds Cut throat wounds are also homicidal in manner when there are no tentative cuts. The wound is more deep and is may be found any where on the neck. Usually there are findings of presence of ligature material and underlying ligature mark over the neck (Fig. 13.13). Cause of Death in Cut Throat Wounds Death from a cut throat deepens on the nature and extent of local damage to the neck. Sever haemorrhages from the jugular veins, or less often the carotid arteries, may lead to death from exsanguinations. If the larynx or trachea is opened, then even relatively minor haemorrhage from local vessels may cause blockage of airways by blood and clot, though many slashed air-passage victims survive. A rare cause of death is air-embolism, caused by aspiration into cut jugular veins while standing or sitting with the neck at a higher level than the thorax. Many suicides either use multiple methods of suicide or may sometimes abandon the pain of cut throat for some other mode such as poison, burns or fall from height.
STAB OR PUNCTURED WOUNDS A stab or punctured wound is a wound that is deeper than it is wide. Sharp pointed objects such as a knife, dagger, nails, needle, spear, arrow, screwdriver etc cause it. A stab wound can be produced by (i).Driving the object into the body or (ii) Falling against the object. A punctured wound is called penetrating wound when it enters the body cavity and once it passes through and through it is called a Perforating wound In a perforated wound, the entry is larger with inverted edges while the exit is smaller with everted edges. Though a stab wound may penetrate only the skin and subcutaneous tissue, more commonly fatal wounds are encountered in the practice of forensic medicine. Nature of Stabbing Weapon Most commonly, the knives are employed in producing a stab wound and their physical features are quite important in shaping the wound. The examination of the knife should include following: 1. Length, breadth and thickness of the blade of knife 2. Whether the knife is single edged or double edged 3. Whether the blade especially its extreme tip is sharp 4. In a single edged knife, the nature of the back edge 5. The face of the hilt guard adjacent to the blade 6. Is there any grooving, forking or serration of the blade 7. Note whether any foreign material sticking to the blade such as blood stains Besides the knife, certain knife like weapons are used for stabbing including scissors, chisels, razor blades, swords and even sharpened screwdrivers. In addition, larger cutting instruments such as axes, choppers, parangs, machetes, shears, hayknives have been used as stabbing weapons. Spiked instruments such as ice-picks, hayforks, case-openers cause a typical looking wound. Some of these weapons are exquisitely sharp and the wounds made by them exhibit extremely fine
208 Textbook of Forensic Medicine and Toxicology
Figure 13.13: Stab wounds over chest
Figure 13.13: Cut throat injury
divisions of the tissues. To razor and razor blades may be added surgical and craft knives, often with a disposable blade. Equally sharp is broken glass and sometimes porcelain. Both sheet glass and smashed glass utensils can provide edges that equal or exceed surgical scalpels in their cutting ability. Smashed china cups and mugs can also provide sharp cutting edges. Characteristics of Stab Wound By examining the characteristics of stab wound, the forensic expert cab provide opinion on (i) Dimensions of weapon (ii) Type of weapon (iii) The taper of the blade (iv) Movement of knife within the wound (v) Depth of the thrust (vi) Direction of thrust (vii) Amount of force used. Dimensions of the Weapon in Relation to Characteristic of Stab Wound The dimensions of the knife may be a vital part of investigation of a homicide when the weapon has been removed from the scene by the assailant. The examination of the suspected weapons recovered from the site, may indicate whether the dimensions are consistent with the injuries found on the body. For this purpose, the injuries found on the person of the victim should be thoroughly
Figure 13.13: Body showing multiple stab wounds on chest
examined under the following headings: 1. Length: Length of a stab wound is slightly less than width of the weapon due to elasticity of skin. It is measured to the nearest of a centimeters. In most instances, the wound will have gaped across the centre, to form a long ellipse. The extent of gaping will depend upon the anatomical situation, for example over joints or in the axilla or groin, and whether the axis of the stab is in line with or across the tension of Langer’s lines or underlying muscle bundles.
Mechanical Injury 209 The length of the wound should be again measured after opposing the edges that more accurately approximates the length when the blade was in situ. The length will be more if lateral movement of the weapon or the body occurs. When the knife is withdrawn the elasticity of the skin causes it to retract, making the woud smaller than when the blade was inside the body. 2. Breadth: The breadth is the second dimension on the surface of the body. 3. Depth: It is the length of the track and is the greatest dimension of the injury. In a patient, the injury should not be probed as there is danger of dislodging a clot causing more hemorrhage during life or it may cause a false track to be formed. Depth is equal to or less than the length of the blade producing it. Depth is greater on yielding surface such as anterior abdominal wall, rib cage and chest in young individuals. The depth of the wound and the force required depends on i. Nature of the weapon: A sharp, slender weapon will pass more easily through the body while a blunt pointed weapon will require more force to penetrate the body. ii. Part of the body: Soft body parts like abdomen can be pierced easily while parts with underlying bone like skull cannot be pierced and sustain only superficial cuts. iii. Age and bodily built of the injured: Healthy adults with muscular bodies are less likely to sustain deeper injuries while children who have softer skin can sustain deep penetrating injuries with small amount of force. To know the track of the wound it should not be probed with a metal probe, instead a pliable tubing should be used or a Radio opaque dye should be injected and then Xray is taken to reveal the complete track. A hard and stiff metallic probe may dislodge a loosely formed clot and cause excessive bleeding during life. 4. Margins: The margins of a stab wound are clean cut when produced with a sharper weapon. The
margins are irregular in case a blunt pointed weapon such as a screw driver is used. A hilt mark of the knife may be seen at the angles of the wound indicating that the full length of the weapon has entered 5. Shape: If both the angles of the wound are acute, it has been caused by a double-edged weapon. While if one angle is more acute than the other, the weapon is a single-edged. A stab wound that cuts the cleavage lines of Langer transversely or obliquely will gape. A stab wound that runs parallel to the cleavage lines will be slit like. Shape of the wound usually corresponds to the weapon used but it varies at different parts of the body. Single edged weapon may give a triangular or wedge shaped wound in which one angle is sharp and the other angle is blunt. But when the weapon enters parallel to the cleavage lines, even though single edged it can be produce wound with two acute angles. Because of initial penetration by the knifepoint, it first produces a dermal defect with sharp angles at each end. Double-edged weapon can cause elliptical, slit like wounds in which both angles are acute. Round object or a spear may cause a circular wound. A round blunt pointed object may cause a circular wound with ragged margins whereas square weapon causes cruciform injuries. Ice-pick or screw driver causes injuries like small bullet holes and two “A” or “V” shaped stab wounds can also be seen. In a homicidal stab wound, the knife may be pulled upwards and downwards during insertion or withdrawal and the length is more than the width of the blade. 5. Direction: In solid organs the track is better seen. The principal direction is noted first and then the others backwards and to the right. One external wound and two or more internal wounds may be caused. In a perforating wound entrance, track and exit indicates the direction of the wound. As far as the direction of the wound is concerned the pathologist should take care of the differences in the position of internal organs as measured at autopsy in a supine body
210 Textbook of Forensic Medicine and Toxicology compared with there position in the living body that is often in an upright position. In the chest and abdomen the relationship of the various organs varies with the stage of respiration. 6. Tapering of the blade: The wound size depends on the taper of the blade. If the taper blade is inserted to 4 cm, the length of the wound is that of the width of the blade whereas in case of blade showing tapering at 8 cm level, the wound will be correspondingly longer. When the blade edges become parallel the wound size will remain constant for further penetration of the knife. 7. Movement of the knife within the wound: When the knife is stabbed directly into the body and withdrawn along the same track then the size of the wound will indicate the minimum width of the blade at the maximum depth of penetration. A knife that is thrust into the body may itself move or the body may move against it before it is withdrawn. This relative movement may extend the wound in a linear fashion or there may twisting of the blade in the wound. In the latter case, the resulting skin incision may be V-shaped or is totally irregular. A single stab can also produce multiple skin wound such as stab over the arm that enters the superficial tissues and then reenters the chest wall. 8. Depth of the thirst: To assess the length of the weapon the depth of the stab wound is important. Certain point should be observed i. When the knife is driven inside the body upto the hilt, depth of the wound when measured at autopsy may be greater than the true length of the blade. This is quite common in the injuries on abdomen and rarely chest because the impact of stab may indent the chest or abdominal wall so that the tip of the knife penetrates tissues that apparently should have been out of the reach. This particularly happens when hiltguard of the weapon impinges on the skin. ii. Direction of thrust: Determination of the direction depends on the appearance of the skin wound and the track in deep tissues.
Where a knife penetrates the skin with the plane of the blade at appreciably less than a right angle to the surface, the wound is often undercut being shelved so that subcutaneous tissue is visible below one edge of the wound. Where the knife is plunged in obliquely but the plane of the blade remains perpendicular to the surface, no such shelving can be seen at the site of the wound though it may just be visible at the end of the wound. The track of the stab wound can further information on to the direction. Attempt have been made to delineate the track of the stab wound before dissection either by filling by the defects with the radio-opaque fluid before taking X-rays or by filling by the plastic or even metallic substance that will harden to form a cast. These method have a very little advantage over routine dissection method. 9. Estimation of the degree of force used in stabbing: The assessment of force used in the stabbing is subjective and cannot be quantified in any satisfactory way that is meningful to the court of law. i. This tissue most resistant to the knife penetration is the skin followed by muscle apart from the bone or calcified cartilage. ii. For skin penetration, the sharpness of extreme of knife is the most important factor. The cutting edge of the knife once the knife is penetrated has no significance. iii. In achieving penetration the speed of approach of knife is important as when a knife held against a skin and steadily pushed requires more force than the same knife launched against the skin like a dart. iv. It is difficult for the knife to penetrate a lax skin compared to a stretched skin. The chest warm is easy to penetrate to sharp knife as there is stretching of intercostal spaces. v. The thick of the palms and soles is tough to penetrate then the rest of the body. vi. When the knife penetrate skin rapidly as when the body falls or runs on to the blade,
Mechanical Injury 211 the knife does not need to be held rigidly in order to prevent it being pushed backwards. vii. Uncalcified cartilages such as costal cartilages are easily penetrated by sharp knife. Calcified rib and bone provide a resistant barrier but a forceful stab from strong, sharp knife can easily penetrate sternum, skull or rib. MedicolEgal Importance 1. The shape of the wound may indicate the type of weapon 2. The depth will indicate force of penetration as in homicidal injuries more force is used compared to suicide. 3. By the direction and dimensions the relative position of the victim and assailant can be known. 4. The age of injury can be evaluated. 5. The position and number of injuries can indicate whether it is homicidal, suicidal or accidental. 6. If broken fragment of the weapon is available it can identify the weapon (Tables 13.2 and 13.3). RAILWAY INJURIES Railway injuries are quite common in countries with many ‘level crossings’ where a public road crosses a railway track with either no barrier at all or with only a flimsy lifting pole. Few rail passengers are killed or injured in moving trains compared with accidents on railway property. Track workers may be run down and some may die from electrocution from overhead cables. The person to commit suicide lays himself in front of an approaching train. Decapitation is the most common injury with features of local tissue destruction, usually with grease, rust or other dirt soiling of the damaged area. In railway accidents the viscera should be analysed for alcohol and other drugs as suicides often employ multiple methods for committing suicide. Sometimes the individual is killed and the body is thrown over the railway track to mimic an accident but in such circ*mstances, the presence of coexistent injuries such as strangulation mark over the neck will be evident (Fig.
13.14). INJURY REPORT The patient in a medicolegal case should be examined by the doctor for preparation of medicolegal case report after receiving a written requisition from the investigating police officer. The preliminary details of the patient should be noted such as: 1. Name 2. Age, sex 3. Address 4. History 5. Brought by 6. Identified by 7. Identification marks: Two permanent identification marks preferably on exposed parts of the body that would help in identification of the victim in Court of law should be noted. 8. Consent: An informed consent of the patient should be recorded describing the procedure along with its risks and consequences. The doctor can be charged of assault if examination is attempted without prior consent. The consent should then be signed or the thumb impression applied by the patient in presence of a witness preferably third party. The signature of the witness should also be recorded. The injury report should describe the following in detail: 1. General physical examination noting the vitals of the patient as well as his systemic examination. 2. Examination proper that includes: i. Nature of each injury. ii. Size, shape and direction of the injury. iii. Part of the body on which injury is present (site). iv. Whether injury is simple or grievous. v. The type of weapon used. vi. Whether weapon is dangerous or not. 3. Opinion: The opinion should include the nature of injury whether it is simple or grievous, the time passed since the infliction of the injuries, the type of weapon producing it. In addition, if any investigations are mandatory such as radio-
212 Textbook of Forensic Medicine and Toxicology Tables 13.2 Findings
Suicide
Homicide
Position of wound Grouping No. of wounds Direction Severity Defense wounds Secondary injuries Weapon Clothes Motive
Accessible parts Arranged One In right handed persons, left to right Mostly superficial, 1-2 fatal Absent Absent Present Not damaged Domestic worries, disappointment in love
No fixed site, vital parts Irregular Multiple Any direction Mostly severe an extensive Present May be connected with fight Absent Damaged Revenge, robbery, sexual assault
Tables 13.3 Sl. No. Findings
Antemortem Injuries
Postmortem Injuries
1. 2. 3. 4.
Edge Hemorrhage Spurting Extravasation of blood
5. 6. 7.
Coagulation Vital reaction Enzyme
Swollen, everted, retracted, gaping Profuse Arterial flow, over clothing Staining of the edges of wound, by washing cannot be removed Firm and difficult to wash Swelling, reddening, and repair - Esterase, acid phosphates
Absent Slight, venous No spurting Not deeply stained, removed by washing Soft clot easily removed No such process No such reaction
logical examination in firearm cases, preservation of blood for grouping, examination of clothing should be mentioned in the report itself. Finally the report bears the signature of the doctor along with the date. Long Questions 1. Discuss in detail the injuries caused by a blunt weapon. Enumerate the differences between the various types of injuries and the age of the injuries. 4. How can you classify injuries? Discuss grievous hurt. How can you estimate the time of injuries? Short Questions 1. 2. 3. 4. 7.
Abrasion Contusion Laceration Stab wounds Ageing of a injury
Figure 13.14: Decapitation of head
Mechanical Injury 213
MULTIPLE CHOICE QUESTIONS
1. Colour of subconjunctival haemorrhages changes from red to: A. Blue B. Green C. Yellow D. Black
3. Sites notorious while looking for incised looking lacerated wounds are all except: A. Zygoma B. Skin C. Iliac chest D. Chest
2. Tentative cuts are seen in: A. Homicide B. Fall from height C. Suicides D. Accidents
4. The colour of postmortem abrasion is: A. Red B. Yellow C. Black D. Reddish-brown
1
2
214 Textbook of Forensic Medicine and Toxicology 5. The exact age of the abrasion can be assessed by: A. Histological method B. Histochemical method C. Naked eye examination D. None of the above 6. In cases of stab wounds: A. Depth is more than length and breadth B. Length is more than depth C. Breadth is more than length D. All dimensions are equal 7. The colour of the bruise becomes green on: A. 2nd day B. 3rd day C. 4th day D. 6th day 8. The depth of an incised wound is: A. Equal throughout B. Deeper at the beginning C. Deeper at the end D. Uneven throughout 9. Which of the following is not an example of pressure abrasion? A. Ligature mark in hanging B. Ligature mark in strangulation C. Finger nail marks D. Teeth bite
B. Force of penetration C. Relative position of assailant and victim D. Stretching of the tissues 14. Blunt force injury will produce incised looking wounds over: A. Forehead B. Mandible C. Skin of Tibia D. All of the above 15. Stretch laceration are caused due to: A. Run over vehicular accident B. Grinding force by a weight C. Injury of axe D. Pieces of glass 16. Blunt objects may cause: A. Contusion B. Laceration C. Abrasion D. All of the above 17. Defence wounds are found in cases of: A. Accidental injuries B. Homicidal injuries C. Suicidal injuries D. Self inflicted injuries 18. Grievous injury is: A. Disfiguration of face due to injury B. 14 days hospital stay C. 20 days hospital stay D. Permanent impairment of hearing.
10. A reddish scab is formed in an abrasion in about: A. 2-3 hours B. 6-8 hours C. 8-12 hours D. 12-24 hours
19. Lacerated would looks like incised wound at: A. Scrotum B. Thigh C. Bone with thin overlying tissue D. Abdomen
11. In an incised wound: A. Breadth is more than length B. Length is more than depth and breadth C. All are equal D. Depth is more than breadth
20. At 4th day, the colour of the bruise will be: A. Bluish-black B. Blue C. Green D. Yellow
12. Latent bruises can be detected by: A. Colour photography B. U-V light C. Oblique light D. Infra Red light 13. The direction of a stab wound indicates: A. Type of weapon
3 A
4 5
6 7
8 9
21. Margins of a clear incised wound adhere in: A. 6 hours B. 12 hours C. 18 hours D. 24 hours 22. Lacerated wound resembles incised wound on: A. Scalp B. Thigh C. Gluteal region
10 11 12 13 14 15 16 17
18
19
20
Mechanical Injury 215 D. Anterior abdominal wall
C. Histology
D. None of the above
23. Which of the following feature does not differentiates antemortem bruise from postmortem hypostasis? A. Variegated in colour B. Clearly defined margins C. Present anywhere in body D. Extravasated blood in surrounding tissues which cannot be easily washed away
31. Most dangerous wound is: A. Gun shot in head B. Stab wound abdomen C. Sucking wound in chest D. Fracture of femur
24. Lacerated wound looks like incised wound at: A. Forehead B. Scrotum C. Abdomen D. Thigh
33. The wound is antemortem if: A. Blood is clotted B. Spouting present C. Extravasation is present in edges and surrounding areas D. All of the above
25. Antemortem fractures differ postmortem fracture by: A. Effusion of blood B. Comminuted type C. No sign of injury over skin D. Lack of oedema
from
32. Greenish appearance of bruise is seen on: A. 3rd day B. 5th day C. 9th day D. 15th day
34. Avulsion is a type of: A. Chop wound B. Incised wound C. Laceration D. None of the above
26. Postmortem wound best differs from the antemortem wound by: A. Gapes on incising B. No clots C. Absence of erythema and cellular changes D. Stain can be removed by washing
35. ‘True bruise’ is distinguished from ‘artificial bruise’ by: A. Itching is present B. Present at accessible site C. Irregular shape with ill-defined margins D. Inflammatory reaction present at site of bruise
27. Tailing of wound indicates: A. Nature of weapon used B. Direction of force applied C. Whether suicidal or homicidal D. Is of no consequence
36. If there is bluish colour of a bruise, then the age of injury is: A. 1 day B. 2 days C. 5-6 days D. 14-28 days
28. Greenish discolouration of bruise is due to: A. Staphylococcus B. Streptococcus C. Klebsiella D. Hematoidin pigment 29. Which of the following statement is true about stab wound? A. Has entry and exit wound B. Breadth is maximum C. Depth is more than length & breadth D. Has irregular margins and broader than edge of weapon 30. Antemortem bruise is identified best by: A. Colour changes B. Bleeding
37. Postmortem fractures differ from antemortem fractures by all except: A. Absence of bleeding B. Absence of callus C. Absence of granulation at fracture site D. Laceration over skin 38. Colour of subconjunctival haemorrhages changes from red to: A. Blue C. Yellow
B. Green D. Black
39. Tentative cuts are seen in: A. Homicide A. Fall from height
216 Textbook of Forensic Medicine and Toxicology A. Suicides
A. Accidents
40. Sites notorious while looking for incised looking lacerated wounds are all except: A. Zygoma B. Skin C. Iliac chest D. Chest 41. The colour of postmortem abrasion is: A. Red B. Yellow C. Black D. Reddish-brown 42. In cases of stab wounds: A. Depth is more than length and breadth B. Length is more than depth C. Breadth is more than length D. All dimensions are equal 43. The colour of the bruise becomes green on: A. 2nd day B. 3rd day C. 4th day D. 6th day 44. The depth of an incised wound is: A. Equal throughout B. Deeper at the beginning C. Deeper at the end D. Uneven throughout 49. Which of the following is not an example of pressure abrasion? A. Ligature mark in hanging B. Ligature mark in strangulation C. Finger nail marks D. Teeth bite 50. A reddish scab is formed in an abrasion in about:
A. 2-3 hours C. 8-12 hours
B. 6-8 hours D. 12-24 hours
60. In an incised wound: A. Breadth is more than length B. Length is more than depth and breadth C. All are equal D. Depth is more than breadth 61. Latent bruises can be detected by: A. Colour photography B. U-V light C. Oblique light D. Infra Red light 62. The direction of a stab wound indicates: A. Type of weapon B. Force of penetration C. Relative position of assailant and victim D. Streching of the tissues 63. Blunt force injury will produce incised looking wounds over: A. Forehead B. Mandible C. Skin of Tibia D. All of the above 64. Stretch eaceration are caused due to: A. Run over vehicular accident B. Grinding force by a weight C. Injury of axe D. Pieces of glass 65. Blunt objects may cause: A. Contusion B. C. Abrasion D.
Laceration All of the above
66. Defence wounds are found in cases of: A. Accidental injuries B. Homicidal injuries C. Suicidal injuries D. Self inflicted injuries
15
Part 1—Forensic Medicine and Pathology
Regional Injuries HEAD INJURIES Anatomy of Scalp The scalp extends from the top of forehead in front to the superior nuchal line behind. Laterally it projects down to the zygomatic arch and external acoustic meatus. It consists of five layers: (i) skin (ii) subcutaneous tissue (iii) occipitofrontalis and its aponeurosis (iv) subaponeurotic areolar tissue and (v) pericranium (Figure 15.1). INJURIES TO SCALP The usual range of abrasion, contusions and laceration may be inflicted though a modifying
factor that is presence of brain, which may deflect a tangential blow or partly cushion a direct impact. In hair-covered areas, care must always be taken at autopsy to palpate the scalp in any case in which there is possibility of injury that otherwise be missed. When a lesion is found or suspected, the hair must be carefully shaved away to expose the scalp for further examination and photography. Bruising of Scalp Bruising may be difficult to detect until the hair has been removed. Marked swelling is a common feature of extensive bruising, as the liberated blood cannot extend downward because of the rigidity
Subcutaneous fibro-adipose tissue Epicranial aponeurosis
Emissary vein
Pericranium Diploic vein
Parietal bone Dura mater Arachnoid mater
Neuropial vein
Pia mater Falx cerebri
Superior sagittal sinus
Figure 15.1: Coronal section through scalp, skull and brain
Regional Injuries of underlying skull. In addition to frank bleeding beneath the scalp, marked oedema may occur after injury and the layers of the scalp may be greatly swollen and thickened by jellylike infiltration of tissue fluid. Bleeding under the scalp (Figure 15.2) may be mobile. A bruise under anterior scalp may slide downwards to appear in orbit. Similarly, a temporal bruise may later appear behind the ear. As with bruises elsewhere, those under the scalp may be obvious immediately after infliction or there appearance may be delayed either during life or as a postmortem appearance.
239
indication of the angle of blow. A major problem in scalp injuries is differentiation between incised wound and laceration. Close examination using a lens if necessary will show that this blunt laceration has (i) bruised margins, even though this zone may be narrow (ii) head hair crossing the wound are not cut (iii) fascial strands, hair bulb and perhaps small nerve and vessels are in the depth of wound. Scalp Injuries from Fall From the fall, the injuries usually involve th occipital protuberance, forehead or the parieto-temporal area and are not possible on the vertex even from a considerable height. Falls from standing position can occur if the person is drunk, in an assault and during some illness (fit/faint). Complications of Scalp Injuries 1. Deep bruise may take a longer time to appear and heal. 2. The infected lacerated wound may cause infection of superior sagittal sinus through the emissary veins. Black Eyes (Figs 15.3 and 15.4)
Figure 15.2: Effusion of blood underneath the scalp with diastatic fracture of skull
Laceration of Scalp Laceration of scalp bleeds profusely and dangerously and even fatal blood loss can occur from an extensive scalp injury. The injury that is most gross is avulsion of a large area of scalp. This may happen when hair is entangled in machinery while working in industries. Scalp injuries may bleed profusely even after death, especially if head is in dependent position. Severe blows from shaped object such as hammers or heavy tools may reproduce the profile of weapon totally or in part. A circular faced hammer may punch a circle but more often only an arc of circle is seen. In such cases, position of edges that digs in most deeply may give an
Black eye is also called periorbital hematoma and may be the result of 1. Direct violence: It may be associated with abrasion or laceration of upper cheek, eyebrow, nose or other part of the face. 2. Gravitational seepage: An injury to front of scalp and also on or above the eyebrow leads to gravitational seepage of blood beneath the scalp in to the eyelids. 3. Percolation of blood: This results from fracture of anterior cranial fossa of skull, is often a contrecoup injury caused by fall on to back of head leading to secondary fracture of paperthin bone of orbital roof. Anatomy of Skull Adult skull consists of two parallel, thin tables of compact bones; outer being twice thicker than
240
Textbook of Forensic Medicine and Toxicology be more than or equal to 15 mm. The frontal and parietal bones are about 6-10 mm in thickness. FRACTURES OF SKULL
Figure 15.3: Black eye in a case of head injury
Figure 15.4: Black eye with abrasion over the forehead
inner, separated by soft cancellous (spongy) bone containing bone marrow. The term ‘diploe’ is used to describe this cancellous bone within the flat bones of skull. The diploe starts forming at 4 years of age. Before this age, it is a thin compact and elastic bone. This zone is interrupted at suture lines and vanishes where the bone is particularly thin especially in floor of skull. Greater wing of sphenoid, petrous temporal, sagittal ridge, occipital protuberance and glabella are the strong parts of cranium. The thin areas are parietotemporal, lateral frontal and lateral occipital zones. The temporal bone is the thinnest with a thickness of 4 mm and occipital is thickest, in midline may
Fatal brain damage can occur even with an intact skull. Thin skull is less likely to be fractured as it is flexible and can return to normal after distortion like that of infants. It is rare for the skull fracture itself to be dangerous but the concomitant effect of transmitted force upon cranial contents makes it dangerous. The presence of skull fracture is an indication of the severity of force applied to the head. Postmortem and antemortem differentiation is difficult in the absence of soft tissue. The fracture of skull can occur either by direct or indirect violence. Direct violence: The forces act directly on the bone to produce a fracture such as: 1. Compression of foetus during forceps delivery or clinical use of a cranioclast. 2. Moving object like stone/bullet strikes the head. 3. Head crushed under wheels of a moving vehicle in road traffic accident. 4. Punch drunk—Due to repeated blows by boxers, the victim presents with findings that may be mistaken for drunkenness. Indirect violence: Here the forces act indirectly on the skull through some other structure, which receives primary impact such as 1. Fall on buttock from height transmits force through the vertebral column to occipital bone producing ring fracture 2. Blast explosions of face from below 3. Heavy blows on chin when the force is transmitted to skull with resulting fracture of base of skull. Mechanics of Skull Fracture Rowbotham has described direct and indirect injuries to skull. Direct injury to skull: Direct injuries can be due to local or general deformation such as: 1. Fractures due to local deformation (Struck hoop analogy): When skull receives a focal
Regional Injuries impact, there is momentary distortion of the shape of cranium. Infants skulls are more pliable and flexible and more liable for which more distortion occurs than the more rigid adult skulls. The area under the point of impact bends inwards, contents of skull being virtually incompressible, a compensatory distortion or bulging of other areas occurs called the struck hoop analogy. Skull is more susceptible to traction forces than the compression, so convexities fracture during distortion of ‘struck hoop’. When skull is deformed, compression occurs on the concavity of the curved bone and tension (tearing) forces on the convexity. If traction forces exceed the elastic threshold, fracture occurs. Thus inner table will fracture where skull is indented and outer table will fracture at the margins of deformed area. If forces are great enough, depressed comminuted fracture results. 2. Fractures due to general deformation: Skull is compressed like elastic sphere. When skull is deformed, compression occurs on the concavity of curved bone and tension (tearing) force on convexity. If tearing force exceeds the limit of elasticity, fracture results. The inner table will fracture where skull is indented and outer table will fracture at the margins of deformed area. If forces are great enough, comminuted fracture occurs. Indirect injury to skull: Here, the forces act away from the body that is chin, feet and buttocks resulting in skull fracture. This could result from: 1. Gurdijian gives the hypothesis for the purpose of linear fracture, which develops, in the areas of stress. When force is applied to the skull at a particular point, in bending of skull occurs at a point of impact and stress areas develop at places away from the point of impact and result in linear fracture, which may extend to join the point of impact. These stress areas may be primary, secondary or tertiary.
241
2. A heavy impact on the side of the top of head often leads to fracture of the vault running into base of skull usually across the floor of middle cranial fossa along the anterior margins of petrous temporal to enter the pituitary fossa. 3. Sometimes, fractures are initiated at a distance away from the point of impact due to compensatory deformation but running usually back towards the impact site. In major injuries, this fracture may often cross the floor of skull to form a hinge fracture. 4. A blow or fall onto the occiput may produce a fracture passing typically vertically or obliquely downward just to the side of midline of posterior fossa commonly reaching foramen magnum and causing ring fracture. 5. When severe local impact causes focal and general deformation, combination of depressed fracture and radial fracture lines may form a ‘spider web’ pattern. 6. Puppe’s rule—When two or more separate fractures occur from successive impacts and meet each other the later fracture (Y) will terminate at, that is not cross, the earlier fracture line (X) which naturally interrupts the cranial distortion which proceeds fracturing (Figure 15.5).
Y X
Figure 15.5: Puppe’s rule
242
Textbook of Forensic Medicine and Toxicology
Types of Skull Fracture I. Linear (fissured fracture): Linear fracture is commonly missed radiographically and is found at autopsy. The fracture is straight or curved lines often of considerable length. They either radiate out from a depressed zone or arise under or at a certain distance from impact area from bulging deformation. It usually involves either table of skull, sometimes both inner and outer. The fractures are common in weak unsupported areas like temporal, frontal, parietal and occipital. The fracture line may extend towards foramen magnum to the base of skull, across the supraorbital ridges or in to the floor of skull. In children and young adults a linear fracture may pass in to a suture line and causes a ‘diastasis’ or opening fracture of the weaker seam between the bones. The fracture is direct or ‘stepped’. It is also called ‘motorcyclist’s fracture (Figs 15.6 to 15.7). II. Diastasis (sutural fracture): It is a linear fracture, which in children and adults passes in to a suture line and cause diastasis or opening of weaker seam between sutures. The most commonly involved suture is sagittal and even the metopic suture may reopen. This type of fracture is common in child abuse syndrome. III. Ring fracture: Occurs in posterior cranial fossa and foramen magnum. It is most often caused by fall from height on to the feet. If kinetic energy of fall is not absorbed by fracture of legs, pelvis or spine, impact is transmitted up the cervical spine. This may be rammed in to the skull, carrying a circle of occipital bone with it. IV. Pond fracture: The pond fracture is shallow depressed fracture forming a concave ‘pond’. The fracture is more common in pliable bones of infants. Depression occurs in absence of fracture akin to distortion produced by squeezing a table tennis ball. V. Mosaic (spider web fracture, Fig. 15.8): A comminuted depressed fracture may also
Figure 15.6: Linear fracture
Figure 15.7: Linear fracture of skull
Figure 15.8: Comminuted fracture of base of skull showing spiderweb pattern
Regional Injuries have fissures radiating from it forming a spider web or mosaic pattern. This results when severe local impact causes focal and general deformation of the skull. VI. Depressed fracture (signature fracture): When the focal impact is severe, it causes outer table to be driven inwards and unless absorbed in the diploe, inner table will be intruded in to cranial cavity with all the dangers of direct damage to the contents. Sharp-edged weapons such as heavy knives and axes may cause this type of fracture. The deepest part of the depression will indicate where the weapon first struck, there may be ‘terracing’ of the margin (Fig. 15.9). VII. The presence of hair and scalp markedly cushions the effect of impact over the vault so that a far heavier impact is required to cause the same damage compared to base of skull.
Figure 15.9: Vault of skull showing depressed fracture
Force required for causing skull fracture 1. Tensile strength of adult skull is 100-150 psi and compressive strength varies from 5000 to 31000 psi. A force of about five foot-pounds can cause a simple fissured fracture of the skull. Falling to the ground from an erect posture develops at least 60 ft./lb and can easily produce skull fractures. A small stone or golf
243
ball weighing about 100 gms may cause a linear fracture or when thrown with moderate force against the temporal bone. 2. The adult head weighs 3-6 kgs averaging 4.5 kgs, when falling through about one meter so frontal area strikes hard surface, impact energy of about 35 ft/lb develops that can cause one to two linear or mosaic fracture. Great variations occur in this, the area of skull struck, the thickness of the skull, scalp and hair, direction of impact all affect the outcome. Complications of Fracture of Skull 1. Injury to brain: The fracture of the skull causes the injury to the brain that is dangerous to life. 2. Haemorrhage: If fracture passes through embedded meningeal artery haemorhage results that is fatal. 3. Traumatic epilepsy: Late effect of depressed fracture of skull is traumatic epilepsy that usually manifests as tonic or clonic fits, which may be difficult to differentiate from idiopathic epilepsy. Usually when fit starts one or two year after major head injury in otherwise fit individual then the diagnosis is easy. There is usually a depressed fracture impinging on underlying cortex often in parieto-temporal area. It is more common in open head injuries with infection. 4. Infections: Infections following skull fractures can be by (i) direct spread through compound fracture (ii) by spread from nasal cavity when fracture of cribriform plate is allowed communication to anterior fossa and (iii) by spread from fracture that involves a paranasal sinus such as frontal or ethmoid or from the mastoid air cells or middle ear cavity. TRAUMATIC INTRACRANIAL HAEMORRHAGES The intracranial haemorrhages are of the following types: Extradural haemorrhage Bleeding between inner surface of skull and duramater is least common of three types of brain
244
Textbook of Forensic Medicine and Toxicology
membrane haemorrhage. It is also known as epidural haemorrhage. According to Rowbotham, only 3% of head injuries have epidural haemorrhage. The dura is closely applied to the interior of the skull except in the posterior fossa, that extradural bleeding does not occur over the skull floor. Most extradural haemorrhage is associated with fractures of the skull. About 10% of extradural haemorrhage is associated with subdural haemorrhage. The usual site is unilateral in a parietotemporal area caused by the rupture of middle meningeal artery that run between the dura and the skull (Figs 15.10 and 15.12). Figure 15.12: Extradural hematoma in a case of road traffic accident
Figure 15.10: Extradural haemorrhage
Figure 15.11: Extradural haemorrhage underneath the depressed fracture of skull
Hume Adams suggests that a minimum volume of 35 ml is needed before clinical signs are apparent though other writers suggest 100 ml is usually the minimum associated with fatalities. Leakage of high-pressure arterial blood strips back the underlying dura with progressive accumulation of a hematoma. When bleeding is venous, the hematoma rarely reach a large size as pressure is insufficient to tear back much of dura. The clinical signs of a epidural haemorrhage are clinically those of a lucid or latent interval, as there may be recovery from the initial phase of concussion before. Typically the patient recovers consciousness from the initial trauma only to slip back into a progressively deepening coma. Sufficient blood accumulates to cause raised intracranial pressure and consequent relapse into unconsciousness. In Rowbotham’s series, the range of latent interval was from two hours to seven days, but most were apparent after 4 hours. Extradural hematomas are surgical emergencies that if not drained will produce uncinate herniation, tonsillar herniation, medullary compression, respiratory arrest and death rapidly. Heat Hematoma: This artefact mimics an extradural haemorrhage, when head has been exposed to severe external heat sufficient to burn the scalp and perhaps skull. Blood may be
Regional Injuries
245
extruded from diploe and venous sinuses into the extradural space to produce a ‘heat hematoma’. It contains about 100-120 ml of blood. This hematoma is brown and friable and adjacent brain shows hardening and discolouration from heat. The hematoma shows honey-coomb appearance and is pink in colour due to high levels of carboxyhaemoglobin. Level of carboxyhaemoglobin in the hematoma in cases of fire can give us the idea about whether the bleed is true extradural hematoma due to blunt force/surface impact or is heat hematoma. If level of carboxyhaemoglobin is same in both hematoma and blood, then it is probably heat hematoma. If there is, little or no carboxyhaemoglobin the bleed is due to head injury. Figure 15.13: Subdural haemorrhage
Subdural Haemorrhage Bleeding into relatively wide space between the dura and arachnoid membrane is much more common than extradural haemorrhage.It results from the rupture of the bridging veins that connect the venous system of the brain to the large intradural venous sinuses. Because the brain, in its bath of CSF, can move within the skull but the venous sinuses are fixed, the displacement of brain that occurs in trauma can tear some of these delicate veins at the point where they penetrate the dura. It is less often associated with fracture of skull. As subdural hematomas depend for their origin on movement of the brain rather than the direct application of force, they are the reflection of inertial rather than impact forces. Consequently, they occur most commonly where the freedom of movement is the greatest, that is over the convexities of the hemispheres (Figs 15.13 and 15.14). They are relatively uncommon where little relative movement is possible, such as the posterior fossa. Subdural haemorrhage can occur at any age but is common at extremes of lives. Subdural haemorrhage with long bone fracture is typical of child abuse as seen by Caffey. In old people, these haemorrhages exist in chronic form. The condition
Figure 15.14: Subdural haemorrhage with fracture of skull
is always due to trauma. In alcoholics and people with bleeding diathesis, minimal trauma can start the bleed. The lesion is traditionally classified in to acute, the subacute and the chronic. Acute subdural haemorrhage: The classical feature is presence of lucid (latent) interval. Since the bleeding in acute subdural haemorrhage is of venous origin and at lower pressure, onset of symptoms is delayed. The lesion is manifested by gradual decline in level of consciosness and focal signs rarely.
246
Textbook of Forensic Medicine and Toxicology
Chronic subdural haemorrhage: Older people and chronic alcoholics are commonly the victims of chronic subdural haemorrhage. In these patients, there is usually some atrophy of brain and consequent upon this, an increased range of movement of the brain within the skull. Thus there is a higher risk of rupturing the bridging veins and bilateral subdural hematomas may develop following slowly following an insignificant or unnoticed trauma. As they develop relatively slowly, the brain is able to accomodate to their mass effect. Thus these hematomas produce much greater cerebral distortion and herniation than acute subdural hematomas before symptoms and signs develop. Gross appearance of subdural haemorrhage varies with age. Recent lesions up to several weeks old are tan or brown with gelatinous membrane covering the surface. The contents are thick but liquid and may have area of redder more recent bleeding. An older hematoma up to months or even a year old is firmer with a tough membrane around both surfaces, resembling a rubber hot water filled with jelly or oil. The contents are liquid and may be brown or even straw coloured. Sometime variegation in colour is seen due to bleeds of different ages. Many subdural bleeds in old people are small and give rise to no neurological defects. Hence, the mere finding of such small lesion at autopsy should not be used to provide cause of death. The chronic hematoma may become large and press down on cerebral hemisphere sufficiently to dent or distort the surface. This may progress and give rise to sign of hippocampal and cerebellar tonsillar herniation and dangers to vital center in the brainstem. The chronic hematoma arises from the center lesion, which after an interval becomes sheathed in a capsule of connective tissue. The mechanism of enlargement is controversial; (i) one theory is repeated bleeding from new blood vessels that enter the mass as part of healing process and (ii) other theory involves osmosis, in which because the center of haemorrhage commonly liquefies forming haemorrhagic fluid that
osmotically attracts into it the CSF from outside the capsule. Dating of Subdural Haemorrhage Gross apperance: 1. Within few hours: Reaction to subdural bleeding begins within a few hours of onset, when cellular infiltration begins from dural surface. 2. A subdural hematoma gradually changes colour from dark red to brownish colour, first being apparent not before five days and sometimes not obvious for 10-12 days. 3. Discrete surface membrane becomes obvious by 2nd week. 4. Liquefaction of contents occurs after more than 3 weeks. 5. After one month, a firm capsule forming a cystic cavity containig a dark brown watery fluid is formed. Histological appearance: A delicate ‘neomembrane’ histologically composed of thin-walled capillaries and fibroblastic granulation tissue, grows from periphery to cover outer surface of the clot during next few days and weeks. If no further enlargement occurs, this capsule becomes more and more fibrous. According to Crompton the presence of a membrane firm, enough to be picked off with forceps makes subdural haemorrhage at least 12 days old. There are claims made for accurate dating of subdural hematomas by histological criteria given by Monro & Meritt. They are briefly summarized under Table 15.1. Subarachnoid Haemorrhage The third type of brain haemorrhage bleeding is even more common than subdural haemorrhage. It is usually associated with extradural or subdural haemorrhage, sometimes it can occur as pure lesions. It sometimes occurs as a result of natural disease especially ruptures of vascular malformation of several types. Appearance and mechanism of formation: The appearance of subdural haemorrhage caused by
Regional Injuries
247
Table 15.1: Histological dating of subdural hematoma Time
Histological appearance
With 36 hours By 4 days 5-8 days
Fibroblasts appear at margin of clot Neo-membrane adjacent to dura is few cell thick Membrane well established; fibroblast migrate from it into the clot. After 5 days, hemosiderin laden phagocytes are present which may be stained with Perl’s reaction Membrane 12 to 14 cell thick, visible to the naked eye after few days Strands of fibroblast subdivide the clot Membrane also present on the under surface of clot and outer neo-membrane is half to one third the thickeness of dura. Inner membrane is still only half thick. Membrane has lost many fibroblastic nuclei and becomes hyaline The membrane thick and fibrous resembling the dura
By 8 days By 11 days By 15 days
1-3 months 6-12 months
trauma varies greatly according to the nature and extent of injury. When it is secondary to laceration of the brain or extensive cortical contusions then its localization and severity depends upon primary injury. When it arises from a blunt impact, then position is not a good localizing sign. Blood in the subarachnoid space mixes with CSF, which dilutes it and makes it less ready to clot and allows more mobility. Hemolysis turns CSF into xanthochromatic yellow and within weeks, the blood is gone. There may be some residual brown or yellow staining of pia or arachnoid (Figs 15.15 and 15.16). Figure 15.16: Subarachnoid haemorrhage
Traumatic Intracerebral Haemorrhage
Figure 15.15: Subarachnoid haemorrhage of brain with petechial haemorrhages
Traumatic intracerebral haemorrhage is primarily occurring at the time of impact or soon afterwards; others are secondary and caused by changes in intracranial pressure. In the cerebral hemisphere, deep haemorrhage can be caused by coup or contrecoup mechanisms and may be situated anywhere in the hemisphere. They may rupture into ventricular system or through overlying cortex with resulting intracerebral haemorrhage. Whether a scalp injury (such as fall) was responsible for cerebral haemorrhage or whether sudden stroke caused by a natural cerebral haemorrhage resulted
248
Textbook of Forensic Medicine and Toxicology
Figure 15.17: Fourth ventricle bleed in a case of road traffic accident
in fall is to be answered during autopsy examination (Fig. 15.17). NON-TRAUMATIC INTRACRANIAL HAEMORRHAGE Spontaneous Subarachnoid Haemorrhage The hypertensive haemorrhages result from the rupture of microaneurysms called CharcotBouchard aneurysms that form at the bifurcations of small intraparenchymal arteries. Bursting destroys the aneurysm responsible for the haemorrhage and the adjacent brain tissue.These aneurysms are seen in increasing number in the arteries of the brain with age and length of history of hypertension. The major sites of hypertensive haemorrhages are the putamen (55%), lobar white matter (15%), thalamus (10%), pons (10%) and cerebellar cortex (10%). Bleeding into subaracnoid space is usually the result of rupture of an aneurysm or rarely an arteriovenous malformation. Aneurysms can be (i) Developmental (Berry, congenital) (ii) Arteriosclerotic (fusiform) (iii) Inflammatory (mycotic) and (iv) traumatic. Berry aneurysm are the most common variety accounting for 95% of the aneurysms that rupture.
Figure 15.18: Common sites of berry aneruysms in the circle of willis
They occur at the bifurcations of major cerebral arteries. The most common sites that account for about 85% of all ruptured berry aneurysms are (i) the junction of carotid and posterior communicating arteries (ii) the anterior communicating artery (iii) the major bifurcation of the middle cerebral artery in the Sylvian fissure. Remaining of the ruptures are in the posterior circulation. In about 20-30% of cases, there are multiple berry aneurysmal rupture (Fig. 15.18). Berry aneurysms are also called congenital anerysms but are not present at birth. They develop because there is a discontinuity in the smooth muscle of the media of the carina of arterial bifurcations. The areterial wall bulges out through the muscular defect to form a thin-walled sacular fundus, composed of only fibrous tissue in which there may be dditional local degeneration and calcification. Laminated blood clot and fibrin may be deposited on this attenuated wall. This insubstantial structure is like an inflated balloon, and ruptures in activities causing increase in intravascular pressure such as straining while defecation, lifting heavy weights and sexual
Regional Injuries intercourse. Mixed Subarachnoid and CNS Haemorrhages These mixed haemorrhages result from (i) arteriovenous malformations (ii) cavernous angiomas (iii) capillary telangiectasis. Medicolegal Importance of Brain Haemorrhage Ruptured berry aneurysm and trauma: Several variation of this exists. Most commonly, an assault is rapidly followed by signs of subarachnoid bleeding and subsequently death. When the blow to the head is hard then it is easy to prove that trauma led to the rupture of berry aneurysm, but when the blow is not so heavy then the evidence is not so convincing. The complicating factor is that most assault occurs in conditions when both the aggressor and victims are physically and emotionally active, so that adrenal response is likely to be present. Muscle tone, heart rate and blood pressure increases and it is likely that raised internal blood pressure in a weak aneurysm is a far more potent reason for rupture than a blow on the head. A second possibility is that already leaking aneurysm may have a rapidly developing neurological even behavioral abnormality that led him to conflict with another person or into dangerous physical position, such as fall or traffic accident. However, at autopsy, it may not be able to distinguish the sequence of events and the aneurysmal rupture may be blamed on the trauma instead of the reverse. Subarachnoid Haemorrhage and Alcohol: A high blood alcohol is said to facilitate bursting of an aneurysm because it dilates cerebral blood vessels and increases blood flow. The fibrous wall of an aneurysm is incapable of dilating; neither can major basal arteries do so to appreciate degree, as they possess little muscle. However, there is no evidence that alcohol is associated with completely natural subarachnoid haemorrhage
249
from a ruptured aneurysm, though intense physical activity such as sports or coitus certainly does predispose to rupture. Moreover alcohol increases the chance to fight producing trauma and leading to subarachnoid haemorrhage. Due to unsteady gait, there are always chances of fall. VERTEBROBASILAR ARTERY INJURY It has been recognized that blows to the side of the neck can give rise to fatal subarachnoid bleeding because of tearing or dissection of intrathecal course of vertebral artery allowing blood to track along the upper part of the vessel and enter the cranial cavity where the artery penetrates the dural membrane of the foramen magnum. Basilar artery and internal carotid artery can also give rise to the syndrome. The injury is manifested as skin bruising and bleeding into the deep neck muscles. Mechanism of vertebral artery trauma: The vertebral artery is injured due to (i) overstretching of atlanto-occipital membrane and (ii) impact on muscles overlying the transverse process of upper cervical vertebrae. The damage to the vertebral artery occurs at the following places: 1. In the canal within the first cervical vertebrae. 2. Just below the axis, in the space between transverse process of Axis and Atlas. 3. As it emerges from the exit of the canal in the Atlas. 4. Within the subarachnoid space in the foramen magnum. The most vulnerable points for trauma are (i) at the penetration of dura (ii) at exit from Atlas and transverse process and (iii) in osseous canal in Atlas. The demonstration of intracranial bleeding from the vertebrobasilar system is difficult since while removing the skull and brain at autopsy, the damage to vessels occurs causing artefactual bleeding. Autopsy findings: 1. When an external bruise is seen on the side of the neck in a case of fatal assault such as
250
2.
3.
4.
5.
6. 7.
8.
Textbook of Forensic Medicine and Toxicology
from a fist, shoe or blunt weapon, the possibility of vetebral artery injury should be borne in mind. When there are circ*mstantial evidences suggesting subarachnoid haemorrhage, vetebral artery damage should be suspected. Usually an external injury is absent but on dissection of neck, there is bruising of subcutaneous or deep tissues of neck. Radiographs of the anteroposterior and lateral view of the upper cervical region should be taken. These would reveal fracture of transverse process of the atlas vertebra, if rarely present. Before search for vetebral artery damage is made, brain should be examined for berry aneurysms or other vascular haemorrhages in cases of substantial subarachnoid haemorrhages. Postmortem angiograms can be taken, if facilities exist. When the facilities for radiography and angiogram do not exist, upper cervical region is dissected to search for vertebral artery damage. Upper cervical spine is exposed by a posterior approach by making spine free of muscles. The spine should be then sawn till fourth cervical vetebra. The block of bone is cut out of the floor of the posterior cranial fossa. This block is decalcified by prolonged immersion in 10% formic acid. After a week, lateral parts of transverse process can be shaved. The block is again decalcified for futher one week. The artery can now be exposed by shaving transverse processes.
HEAD INJURIES IN BOXERS Persons who indulge in boxing are at the risk of both acute and chronic damage to their brain. The acute injuries are less common but occur during or soon after fight itself. The most common lesion is a subdural haemorrhage. Extradural bleeding almost never occurs. Most attention has been paid to the chronic changes in boxer’s brain, which is very common and give rise to what is generally known as punch-
drunk syndrome. The length of time a boxer is involved in fighting is more important than number of serious traumatic events he has suffered. There are both anatomical and microscopic lesions. Grossly affected brain may show some cortical atrophy and slight hydrocephalus. Throughout the brain substance, there may be scars and patches of gliosis. These persons also suffer from development of an Alzheimers like condition, with neuro-fibrillatory tangles throughout cerebral cortex and brainstem though no senile plaques are present. CEREBRAL INJURIES The brain may be injured: 1. By direct intrusion by foreign object such as a penetrating weapon, either bullet or fragments of skull in a compound fracture. 2. By deformation of the brain in closed head injury. Rotatory movement is the main culprit in causing brain damage. No actual blow or fall need be suffered by the head to cause severe and even fatal brain damage. It is the change in velocity, either acceleration or deceleration with a rotational rather than solely axial element that leads to damage. Among the competing theories of brain damage are (i) rotational shear force theory (ii) pressure gradient theory (iii) the vibration theory (iv) transmitted wave force theory (v) brain displacement theory (vi) skull deformation theory (vii) theory of bony irregularities. Shear strain: Strain produced by applied forces, which causes or tend to cause adjoining parts of body to slide relatively or tend to cause adjoining parts of the body to slide relatively to each other in a direction parallel to their point of contact. Cerebral Lacerations and Contusions They are most often found in those areas of the brain where cortex is most likely to be exposed to irregularities in the internal profile of skull. The undersurface of the temporal lobes and the orbital surface of the frontal lobes suffer most often.
Regional Injuries Cerebral contusions: They occur where blunt trauma crushes or bruises brain tissue without rupturing the pia. The most common sites of contusions are either (i) directly related to the trauma, in which case they may be coup or contrecoup lesions or (ii) indirectly related, occuring at points where the brain as it moves, can strike the irregularities on the inner surface of the skull such as the lessr wing of the sphenoid, and the orbital ridges that produces contusions at the frontal and temporal poles and on the orbitofrontal gyri. Contusions usually affect only the crowns of the gyri, leaving the depths of the gyri intact, but there is often substantial attenuation of the underlying white matter that extends under adjacent intact cortex. In ischemia, cortical lesion is usually more extensive than the damage to white matter. Histologically, acute contusions show foci of haemorrhagic gray matter that is subsequently removed by macrophages leaving an irregular yellow-brown crater with a floor of reactive glial tissue and often some leptomeningeal fibrosis. Cerebral lacerations: These are tears in the brain tissue produced by more severe blunt trauma that is often accompanied by other damage such as fractures and local haemorrhage and necrosis. Resolution of lacerations is similar to that of contusions, except that it results in an irregular, yellow-brown gliotic scar that involves not only the cortex and meninges but also deeper structures. Coup and Contrecoup Damage Coup (blow impact) means injury that is located beneath the area of impact and results directly from impacting force. Contrecoup means that the lesion is present in an area opposite to the side of impact. The following practical points should be considered: 1. Sometimes only contrecoup lesion is there with no coup damage at all. 2. There need not be any fracture of skull, even in presence of coup and contrecoup lesion. 3. The most common sites for contrecoup injury is in the frontal lobes. It is often at the tips of
4.
5. 6.
7.
8.
9.
10.
251
frontal poles and may be symmetrical, if a fall on occiput has occurred. In temporal and parietal impacts, the contrecoup lesions are likely to be diametrically opposite on the contralateral surface of the brain. It is virtually unknown for a fall on the frontal region to produce occipital contrecoup. In a temporal impact, the contrecoup damage may not be on contralateral hemisphere but on opposite side of ipsilateral hemisphere from impact against the falx cerebri. The degree of contrecoup damage may be severe, sufficient to cause blood-filled cavitations in the deep cortex and underlying white matter especially in frontal lobes and tips of temporal lobes. With severe frontal contrecoup from a fall on occiput, the transmitted force may be sufficient to fracture the thin bone of the floor of anterior fossa. Such cracks in the roof of orbits may allow meningeal haemorrhage to seep into orbits and appear as black eyes. Though contrecoup contusion is classically caused by deceleration of a falling head, it can also occur when a fixed head is struck. Contrecoup lesions occur in the form of cortical contusions or lacerations.
Theories of Contre Coup Lesions The various theories for such type of injuries are: 1. Struck Hoop theory: Due to the elasticity of skull, the flattening of the skull result at the point of impact resulting in compression of skull so that skull assumes an ovoid shape shortly and thus damage is caused to the opposite side of the impact on brain. 2. Russell’s theory: Sudden displacement of brain towards impact site as the brain reacts as jelly mass and potential space is developed on opposite side, injuring the vessels and resulting in subdural and cortical injuries. 3. Gaggio’s pressure gradient theory: At the moment of impact, there is positive pressure
252
4.
5.
6.
7.
9.
Textbook of Forensic Medicine and Toxicology
on the side of impact and negative pressure on opposite side; this bursts the vessels on the other side. Holbourn shear strain theory (Rotational force theory): Contrecoup lesions are chiefly due to local distortion of blow that causes shear strains due to pulling apart of constituent particle of brain. When the moving head is suddenly decelerated by hitting a firm surface, contre coup injury results e.g. striking head on ground directing fall. The sudden arrest of head results in brain, which is still in motion striking the stationary skull. Rawling’s theory of bony irregularities: Irregular bony prominences particularly orbital and cribriform plate, lesser wings of sphenoid contuse or lacerate base of frontal lobes and tips of temporal lobe or lacerate base of frontal lobes and tips of temporal lobe sometimes with fracture of orbital plate. A blow at the front of head may damage inner and lower parts of back of brain by contact with the edges of tentorium leading to brain stem injury and pontine haemorrhage. Fall on the side of head producing contusion on the opposite side of the brain is due to formation of cavity or vacuum in cranial cavity on the opposite side of impact as brain lags behind the moving skull. The vacuum exerts a suction effect that damages the brain. Moritz radiating wave theory: Energy of impact in a hollow organ propagates by radiating waves along the meridional lines that damages as they leave the site of impact and converges as they approach the opposite side.
CONCUSSION It is a transient paralytic state due to head injury, which is of instantaneous onset, does not show any evidence of structural cerebral injury and is always followed by amnesia from actual moment of accident. There may be evidence of depressed medullary function. Rate of change of velocity of
head is important in producing concussion. It is extremely common and true concussion lasts for seconds or minutes. At autopsy, there is no macroscopic damage; though sometimes there is slight cerebral oedema and scattered nonspecific, petechial haemorrhages. Shear stresses are instrumental in causing neuronal damage. Concussion is followed by ‘post concussion’ state characterized by headache, unsteadiness and anxiety. Retrograde amnesia is almost inevitably associated with concussion and it may also be transient. Though commonly only of ‘minutes’ duration, it can extend to several days before head injury. However, there is often a later recovery of much the lost period, the memory of events immediately before the incident rarely return. The most acceptable hypothesis is ‘diffuse neuronal injury’. Histologically, extensive diffuse lesions are demonstrated as disruption of axon from shear and tensile strain, leading to bulbous and clubbed appearance. CEREBRAL OEDEMA Cerebral oedema leads to death because it compresses vital centers of brain. It may result from a local phenomenon around any laceration, contusion and infarct. Generalized cerebral oedema is common after head injury in children. Oedema is most common cause of raised intracranial pressure seen more often than localized space occupying such as hematoma and tumour. In cerebral oedema the amount of fluid in the brain mainly in the white matter increases and total weight of brain increases by 100 gms . Autopsy features of cerebral oedema: The weight of the brain is increased to more than 1450 gms. The dura is stretched and tense and the brain is bulging. The gyri are pale and flattened and there is thinning of grey matter. The sulci are filled and as a result, the cerebral surface is smooth. The cut surface is pale. In children, ventricles may be reduced to slits. Severe oedema causes large volumes of cerebral hemispheres to press down upon tentorium that herniates through midbrain opening. In addition, there are findings of uncal herniation.
Regional Injuries CHEST INJURIES The thoracic and abdominal viscera are most vulnerable to the penetrating injuries by the knife to the lower lateral wall of the thorax that may enter the pleural as well as the peritoneal cavity. The stab wounds of the heart may also involve the diaphragmatic and upper abdominal injuries. The stomach may often be penetrated. Injuries to the Chest Wall The integrity of the chest wall can be compromised either by severe mechanical failure of the rib cage or by the penetration of the pleural cavities. Rib fractures commonly occur but may embarrass respiration when they are multiple and thus prevent expansion of the thorax; their broken ends penetrate pleura and lungs or when the pleural and muscular pain limits respiratory effort. Flail Chest The flail chest occurs when there are multiple bilateral fractures of most of the ribs and also of sternum. The rigidity of rib cage is lost and attempts at expanding the thoracic volume during inspiration are impaired. The loose section is sucked inwards during inspiration, is called paradoxical respiration. In this condition dyspnoea, cyanosis and progressive hypoxia results that is incompatible with life. The flail chest is caused by: 1. Frontal impact in motor vehicular accidents where the victim is thrown against the steering wheel or fascia 2. In stamping accidents where the shod foot is applied violently to the supine body. In any substantial chest injury, broken rib ends may be displaced inwards, the jagged tips ripping the parietal and visceral pleura. This may cause a pneumothorax or haemothorax, or both with formation of bronchopleural fistula. Rib Fractures Rib fractures are most often seen in the anterior or posterior axillary lines caused by falls on to the
253
sides. The upper ribs are less often fractured, except by direct violence from kicking, heavy punching or traffic accidents. The fracture sites almost always show bleeding beneath the periosteum or the parietal pleura if the fractures occurred during life. Attempts at resuscitation especially external cardiac massage cause extensive rib fractures in about 40% of the cases. In infants, especially victims of child abuse, rib fractures are common. When an infant is squeezed from side to side, as when adult hands are clamped in each axilla or lower on the lateral sides of the chest, the hyperflexion can easily break ribs in their posterior segments usually near their necks. The ribs are levered against the transverse processes of the vertebrae by excessive anterior flexion, which explains the tendency to fracture in paravertebral gutter. Fresh fractures will be obvious both on radiography and autopsy. The sternum may be fractured by stamping or other frontal impacts, but far more force is necessary than with ribs. If posterior displacement of a fragment occurs, the underlying heart or great vessels may be severely damaged. Haemorrhage in the Chest Any injury to the chest wall or lung surface that breaches blood vessels and the pleura can lead to hemothorax. Intercostals and less commonly, mammary arteries can bleed into the pleural cavities but most massive haemorrhage comes from large vessels in the lung or mediastinum. The lung hilum can be torn or penetrated by stab wounds. Several litres of blood may accumulate in the chest, either as liquid or clot, or both (Fig.15.18). Death may occur from loss of circulating blood volume even if there is relatively little external bleeding. Many intrathoracic haemorrhages may be fatal with virtually no external blood loss. A knife that passes obliquely into the chest through intercostals muscles may puncture a great vessel or heart chamber allowing a fatal cardiac tamponade or hemothorax, yet the valve-like overlap of the tissues after withdrawal of the blade may seal up the external wound almost
254
Textbook of Forensic Medicine and Toxicology
Figure 15.18: Effusion of blood underneath the rib cage in injuries to chest wall
completely and prevent significant bleeding, especially as the blood inside the chest is not under any appreciable pressure. In a gunshot wound also, if the wound is uppermost after death, the bleeding can be virtually absent. Infections in the Chest Infection following a chest wound is uncommon in forensic practice as most deaths occur from haemorrhage within a relatively short time before infection sets in. Cellulitis, pleural inflammation and empyema may supervene due to use of some dirty weapon or clothing or some foreign material being carried in to the wound. Pneumothorax Pneumothorax are of three types: 1. Simple pneumothorax: Where a leakage through the pleura allows air to enter the pleural cavity but where the communication rapidly closes. The lung partly closes and the air is soon absorbed. If the communication remains open, then a bronchopleural fistula ensues with air in the pleural cavity, but is not under pressure. It will bubble out at autopsy when ‘water test’ is attempted. Radiology is the best to demonstrate this type of pneumothorax. 2. Tension pneumothorax: When the leak in the pleura or rarely the chest wall has valve-like
action, air is sucked into the pleural cavity at each inspiration, but cannot escape on expiration. This pumping action leads to a tension pneumothorax, which causes complete collapse of lung onto its hilum and a mediastinal shift to opposite side. This type can be demonstrated at autopsy by penetrating an intercostals space under water and also by radiological examination. 3. When an injury of the chest wall communicates with the pleural cavity, a sucking wound may form with direct passage of air from the exterior. This type is seen in military surgery and is complicated by haemorrhage and infection. A common traumatic cause of pneumothorax is a stab wound of the chest that allows direct communication with the exterior, though usually the layered skin and intercostals muscles closes the track when the weapon is withdrawn. Natural diseases such a ruptured emphysematous bulla, a tuberculous lesion at lung periphery or a tear at the site of fibrous pleural adhesion can also cause pneumothorax. Injuries to the Lungs The lung injuries can be of following types: Bruising of the Lungs: Bruising of the lungs can occur in open as well as closed injuries to the chest. The lungs can be contused at the site or opposite the site in any substantial impact to the chest. Deceleration injuries are seen in falls and traffic accidents commonly along the posterolateral surfaces where a vertical line of subpleural bruising occurs. The outline of the ribs may be imprinted in lines of contusion on the pleural surface of lungs. Severe bruising may cause subpleural blood blisters. In all severe chest injuries the central parts of the lungs may show bleeding with actual hematoma formation. Laceration of the lungs: Lacerations of the lungs can result in blunt injuries with detachment of lobes or parts of a lobe. The hilum may tear and the pulmonary ligament below the hilum is a frequent site of haemorrhage. Vessels in the hilum espe-
Regional Injuries cially pulmonary veins or those more peripherally, may be ripped, causing severe intrapleural or mediastinal haemorrhages. Penetrating Injuries of the Lungs: Penetrating injuries of the lungs are commonly produced by the knives. The wounds may penetrate lung parenchyma, large vessels or through and through causing severe damage to heart and great vessels. Blast Injuries to Lungs: Lungs are the most vulnerable organ to blast injuries. Injuries to the Heart The heart is vulnerable to both blunt and penetrating injuries. Penetrating Injuries to the Heart: A stab wound of chest that penetrates the heart is a common homicidal wound. Sometimes the sternum is penetrated by a forceful blow that reaches the underlying heart but most stab wounds enter via the intercostals spaces, or through a rib or costal cartilage. Rarely, an upward stab from the abdomen reaches under the costal margin to penetrate the diaphragm. The right ventricle is often injured by a stab wound as it presents the largest frontal area, but the anterior interventricular septum and the left ventricle are also vulnerable. A shallow stab wound may enter the myocardium and not reach the lumen of the ventricle. In such a case there may be little disability unless a coronary vessel is severed, which may either cause death from myocardial insufficiency, if a major artery is transected or cardiac tamponade. In the thin right ventricle the knife passes more often leading to copious bleeding in the pericardial sac even though the intraventricular pressure is relatively low because of the thin wall is unable to close the defect by muscle overlap and contraction. Whereas in the left ventricle, the contraction of the layered thick wall may partly or wholly seal the wound and there is slight bleeding. Cardiac tamponade can result if the drainage from the pericardial wound is less than the leakage from the ventricle. The wounds in the right ventricle are more dangerous than that in the left ventricle due
255
to absence of muscular self-sealing effect. The stab wounds of the heart are mainly through and through with knife entering one wall and emerging from the other. Blunt Injuries to the heart: The blunt injuries to the heart result in road traffic accidents fall from height and in stamping assaults. Multiple rib and sternal fractures result with or without flail chest. In a child due to pliable thorax, heart can be damaged in an intact rib cage. Fatal blunt damage to the heart may occur, without a mark on the skin or thorax or damage to rib cage. The cardiac injuries are usually seen on the front of the organ’ especially right ventricle. Rarely posterior bruising and laceration can occur if the heart is compressed against the thoracic spine as in stamping assaults and steering wheel impacts. In gross injuries such as aircraft crashes the whole heart may be avulsed from its root. Haemopericardium and Cardiac Tamponade Haemopericardium Haemopericadium or bleeding in to the pericardial sac may occur from the surface or the cavities of the heart, or from the intrapericardial segments of the roots of the great vessels’ particularly the aorta and the pulmonary artery. Haemopericardium may result from (i) ruptured myocardial infarct (ii) ruptured dissecting aneurysm of the aorta (iii) chest injury such as stab injury When the damage has been caused by the stab injury that has perforated the pericardial sac, bleeding can escape into the pleural cavities, mediastinum or even the abdomen when diaphragm has been perforated. Death usually occurs from haemorrhage. Cardiac Tamponade Cardiac tamponade is the condition when blood accumulates in the pericardial sac faster than it can escape, either because the bleeding rate exceeds the drainage or because the exit hole in the pericardium becomes blocked by blood clot. In cases where the bleeding is from a contusion
256
Textbook of Forensic Medicine and Toxicology
or laceration of heart, there is no escape route from the sac. When sufficient blood accumulates, the pressure in the pericardial sac increases and begins to prevent the passive filling of the atria during the diastole. The cardiac output falls, as does the systemic blood pressure and the venous pressure rises. If unrelieved the death will occur with collection of about 400-500 mL of blood Injuries to Great Vessels Injuries to Aorta Aorta is the most vulnerable vessel that suffers in injury in deceleration trauma from both road and air accidents and falls fro height. When the thorax is suddenly decelerated, the heart being relatively mobile in the chest, attempts to continue in the origin direction. This causes severe traction on the root of the heart with complete or partial rupture of the aorta in the descending part of its arch. In falls fro height, the lesion is the result of abdominal and thoracic viscera being forced caudally by the abrupt deceleration while landing on the feet or buttocks. Rupture commonly occurs almost constantly at a point 1.5 cm distal to the attachment of the ligamentum arteriosum. The lower thoracic aorta is closely bound to the anterior longitudinal ligament on the front of the dorsal spine, until it reaches the termination of the arch, where it curves forwards. This appears to be the weak point and transaction occurs at this level, sometimes so cleanly that it looks like a surgical incision. The tear is annular and at right angles to the axis of the aorta. Sometimes, there may be multiple parallel intimal tears near the main transaction, called the ‘ladder-rung tears’. In deceleration trauma, these incomplete tears, that affect the intima and media only, may be found without major transactions. Injuries to Pulmonary Artery The pulmonary artery may be damaged by depressed rib cage and sternal fractures in stamping assaults and steering wheel impact in vehicular accidents. The pulmonary artery and vein branches may also be damaged in the root of the
lung, where hilar tears are not uncommon. The great vessels are often involved in penetrating injuries, notably stab wounds. Stab of the upper part of the chest may pass directly into the arch of the aorta, especially on the right side of the sternum. Stabs that are too high or are directed too laterally puncture the chambers of the heart may penetrate the ascending aorta or pulmonary artery. If the wound is below the reflection of the pericardium, a haemopericardium and cardiac tamponade may result.
ABDOMINAL INJURIES Abdominal injuries can be of two types: 1. Open or penetrating injuries 2. Closed, non penetrating or blunt injuries. Closed/blunt injuries: These types of injuries usually result from increased abdominal pressure and cause dysfunction of chest and abdominal organs. They can occur in: • Road traffic vehicular accidents due to the impact of steering wheels was quite common when the use of safety belts or air bags was not popular or due to a carriage wheel passing over the abdomen. • Crush accidents that result from crushing between the two vehicles, crushing between a vehicle and a wall, railway accidents and industrial accidents. • Blow by blunt weapons or by kicking, stamping, heavy punching occurs in homicides, assaults and child abuse. The liver, spleen, intestine and mesentery are most vulnerable internal organs to be affected. • Fall from heights. Open/penetrating injuries: They may result from cutting or stabbing weapons, firearms, horns, and claws of animals or fall over sharp projecting object. These are dangerous injuries and death may occur without any injury to abdominal viscera sometimes. Sharp pointed weapon injuries to peritoneum, intestines or soft viscera may penetrate with slight force. The injuries may be fabricated for charge of assault such as superficial incised wounds. Homicidal injuries are the most common whereas suicidal stab wounds are
Regional Injuries rare, may result from the Japanese Hara-kiri method when the victim falls forwards on ceremonial sword and tries to disembowel himself. Intestines and mesentery are the major targets and are often involved in multiple wounds. Liver and spleen bleed extensively with resulting haemoperitoneum. Stomach is more commonly involved in chest stabs passing downwards through the diaphragm. Features of Abdominal Injuries 1. Bruising of abdominal wall: Bruising in muscle tissues without any external violence can occur in tetanus and strychnine poisoning whereas discrete bruising on abdominal skin may result from kicks that produces scuffed bruised abrasion if tangential unless protected by clothing and in cases of child abuse where fingertip/knuckle bruises from holding, forcibly gripping or lifting the child, on the side of the abdomen or along the maxillary lines of chest. Usually abdominal wall escapes gross injury by transmitting force of violence to more resistant organs inside the abdominal cavity, which gets injured due to protective clothing and owing to the large surface area of abdomen. Laceration of abdominal wall with protrusion of coils of intestine can result in run over accidents under the wheels. Blow on upper/central (epigastria region) of abdomen has an inhibitory action on the heart through reflex action on solar plexus. Bleeding may be subcutaneous from initial area of impact to more diffuse involving large area of abdomen. Injury to epigastric artery causes severe haemorrhage. Extensive bleeding into peritoneal cavity may result from rupture of the solid viscera or from bleeding from the mesenteric vessels. 2. Bruising or rupture of stomach: The stomach is less vulnerable than the intestines and are lacerated by heavy blows in upper abdomen when full of fluid or food or the penetrating injuries. 3. Intestines and mesentery: External bruising of the gut and vascular mesentery being crushed against the prominent lumbar vertebra
257
in the midline. Mesenteric lacerations occur in traffic accidents and assault. Bruising or tearing of central part of mesentery occurs while compression against the lumbar spine occurring towards the intestinal margins. Duodenum or jejunum is more vulnerable to transaction compressed against the spine especially in children from heavy blows to central or upper abdomen cutting through the third part of duodenum. Colon is rarely injured. The injuries to intestine and mesentery cause intractable bleeding. 4. Injuries of Liver: The rupture of liver results from the penetrating as well as non-penetrating injuries. The non-penetrating type of injuries may occur in abdominal trauma, fall from height, crush from wagon, and road traffic accidents from the impact of driver on rim/center of steering wheel or by unrestrained passenger being thrown against the face. The pedestrian can receive such injuries as primary impact from the vehicle or secondary damage by being thrown to the ground, external cardiac massage, sudden contraction of abdominal muscles such as during epileptic fits, lacerations by the fractured ends of ribs may perforate the diaphragm. In infants abdominal injuries may be found in child abuse syndrome and during breech delivery Penetrating injuries are usually stab injuries of the abdominal walls over the front, back or sides of lower part of chest. The liver is frequently injured due to its large size and weight, friable consistency and fixed and exposed position. The liver may be injured by forcible impact over the lower parts of right side of the chest, upper parts of right side of abdomen from the front, back and the sides. The right lobe of liver is injured five times more frequently than the left due to its size, and position. The convex surface and anterior margin gets involved. Anterior surface and inferior border is more commonly involved. Ruptures can vary from superficial linear tears on convex upper surface to oblique to anteroposterior and rarely transverse. The
258
Textbook of Forensic Medicine and Toxicology
tears are 1-2 inches deep and may pas through the entire substance of organs. There is complete transaction of organs when greater force is applied. There may be sub capsular tears or sub capsular dermatome. Liver is involved in 40% of multiple injuries. Lacerations may range from shallow splits confined to capsule to deep laceration separating right and left lobe of liver. In children, one lobe of liver may lie in peritoneal cavity, as it is more prone to being run over in road traffic accidents. According to Kindling et al, the lacerations along the line of falciform ligament occurs in drivers and passengers of automobiles due to severe compression causing bursting of organs; due to upward or downward displacement of liver. The satellite lacerations or fractures occur in pedestrians. The bruising of liver is usually localized to sub capsular dermatome and is common in new born due to complications of delivery. Penetrating injuries are caused with the help of knives by multiple thrusts; limited bleeding occurs and complete transpiration of organ may occur. The puncture of liver by needles while taking liver biopsy causes haemorrhages in diseased liver. The liver is more easily lacerated if enlarged and fatty as in alcoholics. The rupture of the liver cause haemorrhage and shock and immediate death occurs especially if portal vein or vena cava is injured. The liver abscess may rupture causing septic infection and if patient survives for long time, infarction results. The lacerations of liver can be of the following types: • Transcapsular over convex surface under the site of impact, the portal vein or inferior vena cava may be involved and profuse haemorrhage results. • Subcapsular over the convex surface under the site of impact. • Distortion can cause laceration over the superior or inferior surface. • Contracoup involving the posterior surface • Whole organ ruptures in vehicular accidents and gunshot injuries.
• Large subcapsular dermatome rupture after several days following muscular exertion or violence. • Fatal pulmonary embolus may result from liver tissue emboli. 5. Rupture of Spleen: Spleen is most vulnerable to injuries by blunt force and considerable crushing and grinding force is required like passing of carriage or motor car over the body; railway accident crushing, fall from height, foreign body piercing accidentally the pulp and by stabbing or cutting. Normal spleen may rupture by the broken ends of fractured ribs, severe kicks or blows by blunt weapon over lower part of right side of chest and in mechanical or industrial accidents. Enlarged spleen may weigh up to 2kgs, is 32.5 × 17.5 × 6.0cm, and is liable to rupture from fall or slight violence. Spontaneous rupture of spleen can occur during bouts of coughing, sneezing, vomiting or straining particularly if the spleen is abnormally mobile. When the spleen is diseased from malaria, infectious mononucleosis, kale azar and glandular fever it enlarges and is more friable and the incidence of rupture increases. It may also rupture spontaneously in pregnancy. The spleen can rupture due to compressive force resulting from laceration of the surface or whole of it and traction force that tearing spleen from pedicle and penetrating injuries. Concave or inner surface is the commonest site of rupture and death occurs from haemorrhage. The injuries may vary from the large lacerations of capsule most often on lateral surface running up to the hilum to multiple lacerations traversing the surface almost bisecting the organ; complete detachment from the hilum is uncommon. Subcapsular hematoma if capsule is intact and substance ruptured causes delayed death as capsule prevents excessive bleeding and is disrupted with sudden muscular exertion. PELVIC INJURIES In severe trauma, the pelvis undergoes various
Regional Injuries fractures as well as dislocations such as: 1. When there is application of great pressure to the front of abdomen or pubic area such as in run over by the wheel, the pelvis is splayed open, symphysis pubis seperates and one or both sacroiliac joints also dislocate. 2. When an impact occurs from the side, superior and inferior pubic ramus are fractured with dislocation of sacroiliac joint on the side of impact. 3. In circ*mstances of fall from height on to the feet, due to transmission of force up the legs, both the saccroiliac joints may dislocate and even one or both femoral head also may be driven in to acetabulum. When the hip joints remain intact, the pelvic girdle may fracture and sacroiliac joints may dislocate. 4. Due to a kick or heavy fall on to the base of spine, fracture of sacrum or coccyx may result. 5. Empty bladder is rarely injured in trauma but a full bladder gets injured from blows, kicks and other blunt trauma. Other pelvic organs are quite protected from blunt injuries. 6. Male urethra may be injured as aresult of direct trauma such as falling astride a solid objectlike a gate or being kicked in the crutch, due to being compressed against the undersurface of
the pubis. 7. External genitelia may suffer injuries especially scrotum is quite vulnerable to severe bruising resulting from kicks. Scrotum and vulva may suffer injuries from falling astride on objects and in vehicular accidents. Long Question 1. Discuss injuries caused by a blunt weapon impact to the head. Enumerate the differences between the various types of injuries and the age of the injuries in intracranial haemorrhages. Short Questions 1. Extra dural haemorrhage. 2. Sub dural haemorrhage. 3. Sub arachnoid haemorrhage. 4. Theories of head injury. 5. Contre coup injury. 6. Signature fracture. 7. Lucid interval. 8. Flail chest. 9. Injuries to spleen.
MULTIPLE CHOICE QUESTIONS
1. Pond’s fracture are seen in: A. Children B. Adolescents C. Young man D. Elderly
1 A
2 C
259
2. Contrecoup injury is seen in: A. Heart B. Lung C. Brain D. Kidney
16
Part 1—Forensic Medicine and Pathology
Explosion Injuries Explosions are uncommon and few doctors have much experience of them. Usually explosions occurs during work time but few notable explosions has occurred in the past affecting the civilians. For example in the Hulton disasters in 1911, 343 people died. Another disasters occurred in Taxas City during 1947 in which a ship loaded with ammonium nitrate fertilizers exploded at the dock filling 561 people and injuring 3000 people. But things have changed a lot now a days as terrorist activity in many parts of the world particularly the Ireland has added a new dimensions to the civilians explosions like that of bomb, latter bomb and car bombs. They have become a daily potential hazards in many countries. During explosion, explosive material is converted in to large gas volume and there is release of tremendous amount of energy. Pressures of 1000 tons/inch2 (150,000 atm) and the temperature of 3,000°C can be generated in an explosion. Effects of Explosion on the Individual 1. Those very near the seat of explosion are blown to pieces and scattered by force of explosion gases. 2. In those who are near enough for the skin to be in contact with explosion flame, flame burns are produced. 3. At greater distances, exposure to momentary heat radiation produces flash burns. 4. Persons can be injured by: • Shock wave that is the pressure wave spreading concentrically from the blast center.
• Air blast is the shock wave produced by the explosion in the air. • Post-blast wave also causes the damage. • Underwater blast is the pressure change occurring from explosion in water. • Solid blast: In underwater blast solid material like ship deck is forced against the body. 5. Person can be struck by the flying missiles propelled by the explosion. 6. The debris of building demolished by explosion can cause injuries. 7. The poisoning can occur by the fumes of the explosive material. Distruptive Affects of Blasts The persons in the immediate vicinity of the blasts are laterally blown into pieces. The small parts of the body may be scattered over a wide area. If someone is carrying the bomb or in cases of land mine explosions the victims is blown up. The body parts of the individuals who died as a results explosion should be collected by the trained persons otherwise mistakes are liable to be committed. The internal organs are less frequently found at the scene of explosion. In cases of small explosions, the limited body parts are blown up and in all cases the mangled remains are heavily soiled. When there is a blast in the civilian, the number of victims should be counted. Within 200 yards the areas must be searched for the parts that are usually scattered due to explosions. The parts thus recovered must be worst in water and carefully examined. The non human tissue must be identified and discarded, if it is not possible to
Fall from Height identify them tissue by naked eye examination then precipitation test can be done. The segregated parts will help to establish the number of victims. Pieces of scalp, skin, jaw, joints and hands etc. are put in separate heap. Thus skin must be kept according to the colour, likewise the hair to be segregated according to the colour length and texture. The joints to be marked whether they belong to left or the right side of the body. The sex can be determined from the genitalia, hair, and breast tissue. At times the help of the microscopic study will be required. From the above data the minimum number of the body will be counted but there is always is chance for more number of bodies. The identification of the bodies can be done by visual inspection after washing the parts recovered. The evidence of the lay people must be expected with caution because of the deformity of the skull or facial injuries may be a misleading factor. The clothing are to be identified by the relatives. The most important thing is taking the finger prints and matching with the records available specially in cases of the terrorist and criminals. In other cases the fingerprints will be matched with some article of use at home. The dentism and the denture found at the seen may also be recovered and matching to be done. Other points like the tattoo marks, scars and old factures are also helpful to identify the victims.
261
Figure 16.1: Burns over the back in a case of bomb explosion in a cinema hall
Figure 16.2: Burns over the back in a case of bomb explosion in a cinema hall
Effects of Flame and Radiant Heat The temperature rises to 3000°C and momentary flame contact causes burns (Figs 16.1 to 16.3). Radiated heat burns people outside this range. The burning effect of radiated heat depends on the total thermal energy received and the rate at which the energy is supplied. The rate of heat transfer depends on the duration of explosion. Thermal explosion received increases directly with the weight of the explosive and inversely with the square of distance from it. The flash burns produced effect an area perhaps the face or one side of limb and spares the area that are protected by the clothing and solid objects. Areas are dry
Figure 16.3: Burns over the sides in a case of bomb explosion in a cinema hall
262
Textbook of Forensic Medicine and Toxicology
and reddish brown or parchment like. The individual has to be with in feet of an ordinary bomb to sustain heat burns. Effects of Air Blast Shock wave spreads concentrically from the blast center in a round wave of very high pressure, the velocity of this shock wave soon decreases to about the speed of sound in air (1120 fps). It is many times faster near the explosion and as the distance from the explosion is increased the pressure component lasts longer. Blast wave can knock a person down, move objects and cause demolition of buildings. On the heels of the blast wave there are winds that can displace objects at considerable distances. Post blast wave can knock buildings down. Ground shock is a complex train of shock waves that is similar to earthquake. Biophysics of Air Blast Injury: Shock wave strikes the body surface and the part of it is deflected, a part reflected and the rest of it is absorbed. The shock wave passes through the hom*ogenous organs like heart and thigh and solid organs but does not damage them. The organs that contain air are very vulnerable e.g. in its passage through inhom*ogeneous lungs, there is considerable damping of wave achieved by the movements of lung tissue. Acceleration of parts of different density and compression and expansion of alveoli as pressure wave passes through them are thought to be among the causes of lung damage. Also the shredding and bursting effect that occurs when a pressure wave breaks out of liquid medium of lung tissue in to gaseous medium of the alveolus. Structural damage due to shock wave is confined to air/gas containing organs such as ears, lungs and segments of large bowel. Effects of air blast diminishes rapidly as the distance from the explosion increases. Tissue Damage Due to Air Blast The blast wave being a sound wave damages the ear and the damage depends on: (i) The intensity of the blast (ii) Its proximity to the source (iii) Orientation of axis of external auditory canal to
wave front (iv) Duration of exposure (v) Awareness of explosion (vi) Protection by any object. Effects of Air Blast on Ear 1. Hyperemia of intact tympanic membrane. 2. Punctate bruising of intact tympanic membrane. 3. Rupture of tympanic membrane at an overpressure of 5 psi, results in bleeding into middle ear. 4. Damage to the cochlea that is more frequent than tympanic membrane rupture. 5. Sudden severe deafness with period of recovery during which acuity for all frequencies is depressed. 6. Slight haemorrhage into scala tympani near round window. 7. Haemorrhage into basal coil of cochlea and in fundus of internal meatus. 8. Prominent symptoms are tinnitus, sensorineural and conductive deafness. Effects of Air Blast on Lung Lung lesions of the air blast are due to direct impact on the body wall of pressure component of shock wave. The severity of lung lesions vary from the size of explosive charge and becoming greater nearer the victim is to the explosion. The alveolar haemorrhages are due to tearing of alveolar septa and they arise in each lung immediately after explosion, if patient survives for few hours. Autopsy examination reveals Sub pleural haemorrhagic patches of purple red colour and of varying size. These haemorrhages are scattered at random, cross the lung surface in line of ribs and are grouped near anterior and costophrenic margins. Lung sections reveal discrete haemorrhages that are more central than peripheral and the rest of the lung tissue is patchily oedematous. On microscopic examination, alveoli contain haemorrhages and oedema fluid, the alveolar septa are not discernible and there is emphysematous dilatation of alveolar ducts. The haemorrhages are seen in the bronchioles and interstitial tissue. The pink staining fluid and red cells may be found
Fall from Height between epithelium and lamina propria is infiltrated by neutrophils. Direct blows by bomb fragments debris on chest bruise the lungs. Effects of Air Blast on Gastrointestinal Tract The injuries to GIT are inconstant. The haemorrhages beneath the peritoneum of gut, mesentery and omentum vary in size. They are usually seen as small punctate spots, over extensive areas of intestine. They extend circ*mstantially as annular bands occurring mainly over the ceacum, colon, small intestine and stomach. The stomach and small intestine are less frequently affected. There is no correlation between the abdominal haemorrhages and peak pressure or impulse of blast wave. Effects on Other Organs Other organs such as liver, kidney and spleen are uncommonly injured showing haemorrhages or rarely a laceration. No specific changes are seen in the brain. Zuckerman described haemorrhages around nerve roots of thoracic spine and posterior column of spinal cord and oedema around central canal. Clinical Effects of Air Blast The person receiving the blast is shocked, is pale, cyanotic and restless. The blood pressure falls, pulse is rapid and thready, there is chest pain, widespread crepts and haemoptysis. Blast (Shell) shock: The blast shock is psychogenic war neurosis and the symptoms of anxiety are produced. There is confusion, muscular and mental weakness, stammering and jerking, hysterical blindness, numbness and paralysis. Causes of Death 1. Suffocation: Death from suffocation occurs from extensive pulmonary haemorrhages in an hour of explosion and there is copious bloody froth in air passages. 2. Systemic air embolism is the result of air gaining the pulmonary veins after blast damage
263
to the lungs. In animals, air has been found in lethal quantities in coronary arteries, left chamber of heart and basal arteries of brain. Air embolism might account for those deaths that occur soon after explosion and no obvious pathologic changes can account for death. 3. Blast shock. Immersion Blast Immersion blast refers to blast effects of an explosion in water experienced in wartime by those who abandon the sinking ship. Injury can be expected within 150 feet of a 300 lb charge of TNT exploding at a depth of 50 ft. The physical changes are similar to those accompanying an explosion in air. Explosion converts the charge in to gas of a very high temperature and pressure, which expands pushing the surrounding water radically. Pressure of underwater explosion might be 1000 psi. The pressure waves pass through the solid tissues unimpeded. Injuries are found predominantly in GIT and less constantly in the lungs. Most of the lung injury is due to pressure transmitted from abdomen through the diaphragm. There is pain abdomen, abdominal rigidity and tenderness, occasional testicular pain, nausea, vomiting with blood and bloody diarrhoea. No external injury marks are seen over the trunk. Autopsy Findings 1. Haemorrhage: There is haemorrhage beneath the peritoneum, mesentery and intestinal mucosa. The submucosal haemorrhages account for blood found in the lumen of the gut, hemetemesis and malena. The haemorrhages are multiple and in majority are up to 3 cm in diameter and the intestinal walls are oedematous. 2. Perforations: The perforations are found in the small and large intestine are circular, half to one inch in diameter with prolapsed mucous membrane. They can occur anywhere but the anterior mesenteric border of ileum and outer side of ceacum are the sites of predilection. The gas filled bowel segments are vulnerable to pressure of more than 250 psi.
264
Textbook of Forensic Medicine and Toxicology
Solid Blast Solid blast refers to a wave of energy that spreads through a rigid structure when an explosion is detonated near it and people in contact with structure can be injured. Steel construction of tanks and warships conducts shock wave well and causes solid blast injury. An explosion beneath tank/ship causes initial movement of small displacement by very swift acceleration. Person standing in deck of ship could blow, bones can break and skin and subcutaneous tissue may burst causing compound fracture. The solid blast injuries are predominantly skeletal with fracture of calcaneum, lower end of tibia and fibula. The situation depends on subject’s position; those standing receive injuries to lower limbs and those seated in chair suffer from fracture of vertebral column. The skin of ankles and feet are bruised and lacerations of ankle and weight bearing surface of heel occurs. The knee joint may be dislocated and rarely fractured. The fractures of femur and pelvis occur rarely. Fracture of spine is more common and 9th thoracic or 4th lumbar vertebra are involved.
Figure 16.4: Triad of injuries in a case of AC blast of a compressor of AC
Flying Missiles Explosions injure and kill by means of solid material, which is propelled in all the directions. The material such as the fragmented containers of explosive, metal case of shell, hand grenade that is meant to expel missiles, missile casing designed to fragment into lethal shrapnel. In a nail bomb, large nails are bound round the stick. Other materials propelled by explosion are remains of explosive material and debris of surroundings namely earth, brick, plaster, wood and dust. Larger fragment penetrate deeply. The fragments accelerate more slowly than associated gases, lag behind blast in early stages and tend to be more damaging at a distance with kinetic energy of 1/2mv2.
Figure16.5: Blast injury over the neck due to blast of a compressor of AC
Injuries Resulting from Blast Common basic injury due to fragments of explosion is a triad of small lesions; bruises, abrasions and punctate lacerations intimately mixed on skin giving it a purplish colour (Figs 16.4 to 16.7).
Figure16.6: Blast injury over the neck and chest due to blast of a compressor of AC
Fall from Height
265
bomb in his lap or car receive injuries on the pelvis. The explosion at ground level produces more of leg injuries whereas explosion at the side have more of side injuries than other types of explosion. The fragments and debris of explosion may cause an eye injury. Injuries from Falling Masonry
Figure16.7: A triad of laceration, contusion and abrasion in a case of bomb blast
Abrasions and bruises are small 1-10 mm in diameter and puncture lacerations are up to 3 cm in diameter surrounded by an irregular zone of bruising and abrasion. Large lacerations due to larger fragments can perforate neck damaging carotid arteries or airways. Perforation of chest and abdomen results in internal organ injury. The dust propelled from the explosion is large in amount and when driven in to skin produces uniform tattooing and skin darkening. Fragments of minute size can penetrate soft tissues of the body quite deeply. The distribution and pattern of bruises, abrasion and punctate lacerations helps to determine relationship of victim to explosion. The severity, distribution and pattern of injuries can be compared. Those carrying a bomb have their arms, and midriff blown; the one carrying the
The demolished building by an explosion may lead to injuries caused by collapsing masonry. The body and clothes are soiled by dust from brick, cement or plaster. The cause of death in these cases is traumatic asphyxia and the findings are of purple discolouration of upper parts of body, patchily haemorrhages of skin and conjunctiva, oedema of conjunctiva and congestive haemorrhages of nose and ear. Poisoning by Fumes Toxic fumes are harmful in an enclosed space and mining accidents greater damp. Long Question 1. Describe the postmortem findings in cases of blast injuries. Short Questions 1. Blast lung. 2. Effects of air blast on ear. 3. Immersion blast.
MULTIPLE CHOICE QUESTIONS
1. Which of the following is most likely to be affected by shock waves in cases of explosion injuries? A. Liver B. Lungs C. Heart D. Kidneys
1 B
2 C
2. Triad of injuries are characteristic of: A. Vehicle accident B. Burns C. Explosions injuries D. Air craft accidents
17
Part 1—Forensic Medicine and Pathology
Fall from Height Fall is dropping down from a height of relatively high position by the force of gravity. International classification of diseases (ICD 9) gives a range of heights like slipping or stumbling through to the falls from the cliff. During fall the potential energy due to height is converted to kinetic energy under the influence of gravity. At impact some of the energy is imparted to the body resulting in injuries. Falls may occur at the ground level or from some height. FALLS AT GROUND LEVEL Causes of Fall 1. Mechanical: Due to slipping on polished surface or rugs or due to some faulty footwear. 2. Cardiovascular accidents. 3. Postural hypotension. 4. Intake of alcohol or hypotensive drugs. Injuries Resulting from Fall on Ground Level 1. Fractures: Femur (In old people, commonly), Cole’s fracture, Pot’s fracture, humeral fracture, pelvic fractures. 2. Internal organ injuries retroperitoneal haemorrhage resulting from pelvic fracture, rupture of liver and spleen, bruising of intestines. 3. Injury to head leading to subdural haemorrhage. Speculation arises as to whether femoral fracture has antedated the fall as this fracture can occur spontaneously due to bone rarefaction; poor blood supply.
FALL FROM HEIGHT The fall from height may vary from high rising building to ladder, chairs, tables or staircases. The falls are common in the middle aged from the windows or accidentally in children or suicidal in adults. Epidemiology of the Fall Age and sex distribution: Falls are more common in extremes of ages. The range extends from children falling from the cots through to elderly slipping on ice or at home. The falls in middle age persons are usually due to accidents related to work or suicidal. Females are more vulnerable to suicidal falls whereas males are more prone to falls in their late adulthood. Geographic distribution: Places near high rise buildings and high bridges are the preferred sites for suicidal attempts. For these sites considerable distances may be traveled to their chosen sites. Coexisting psychiatric conditions: Suicidal jumping makes a considerable proportion of those who die from fall in whom psychiatric conditions are common. More than 50% people have some preexisting psychiatric illness or heavy drug over dosage. In the elderly, coexisting medical problems also contribute to increased incidence of fall. Velocity of Fall For a fall on to the earth from a height, the acceleration is due to gravity ‘g’ and velocity ‘v’ after a fall from height ‘h’ is given V = ½gh
Fall from Height It is true for a fall in vacuum but in actual position, air drag, clothing, body surface area, human body flexibility and non-hom*ogenous mass distribution come in to play. The error may vary from 5-7% for jumps up to height of 23 meters. Factors influencing the pattern of injury 1. Height: A direct relationship exists between height fallen and survival. It is also correlated with the extent of injury as measured by Injury severity score. The height of fall of about 11 meters, results in pelvic damage and when the height is more than 15 meters, multiple rib fractures result. When a person falls or jumps from height, trajectory is downwards and outwards; the distance the body strikes the ground is variable. 2. Orientation: Orientation of body at point of impact is important in determining injury pattern and mortality. In majority of falls, vertical landing with feet first and the next common were with head first. In all falls, lower limbs were almost exclusively injured. In side impacts and in feet first impact, mainly upper limbs were injured due to secondary impact. 3. Surface impact: The surface on to which a body falls determines the pattern of deceleration and energy exchange. On a relatively yielding surface, such as a safety net, the energy is given up slowly, but on a relatively unyielding surface such as concrete, time of deceleration is shorter and hence the forces on the body are much great. 4. Deceleration: Quicker the body brought to rest, greater will be forces acting on it. It depends upon the weight of the body, surface of impact and energy dissipation i.e. bouncing back. Duration of deceleration is extremely short, in milliseconds. A fall onto concrete results in a very rapid onset of deceleration or a high jolt factor. At impact body comes to a halt, in doing this, it must give up the kinetic energy. The magnitude of kinetic energy and the way in which it is dissipated determines the changes
267
to body tissue. If certain tolerance limits are exceeded, injury results. The body turns and twists in an unpredictable manner during the fall. A person falling 15 meters, attains a speed of 17m/s. When falling from high building, the displaced air tends to act as the cushion, which drives the body from the wall. A simple fall can result in a body impact some distance from the foot of the building, not an evidence of push or deliberate jump. Injury Pattern from Fall The injuries due to fall from height can be direct or indirect. Direct Injuries These are immediately anatomically related to the point of impact. As a result of the injury resulting from direct impact due to impact on head, head is suddenly decelerated; brain tends to continue falling because of its momentum. Brain is suddenly pressured against the skull at the site of impact; a corresponding negative pressure is present on the opposite surface of brain. In more severe falls, the head is accelerated prior to impact and deformation of skull. It results in massive fracture often with laceration of scalp with extrusion of brain and vault and base fracture. Other injuries on various parts of head can be: 1. The top of the head: Injuries are severe and the character and extent will depend upon the surface or object against which impact takes place and they depend on the distance fallen. Other injuries such as fracture of spine, limbs or chest will usually be present. The point of impact against a hard flat surface e.g. concrete will be indicated by a bruised laceration overlying fissure fractures of skull following direction of lines of force Impact against blunt protruding object such as sharp corner of furniture will produce a localized depressed fracture of skull with comminuted or radiating fissure.
268
Textbook of Forensic Medicine and Toxicology
2. The side, back and front of head: These may occur from simple falls from erect position, the part of the head striking the ground depending upon the direction of fall. The usual injury is bruise situated just above and behind either ear with or without abrasion or laceration of scalp. On a flat surface, fissure fracture occurs parallel with the line of impact and usually run through the middle fossa in to pituitary fossa, sometimes to opposite side, anterior and posterior fossa may also be involved. Ring fracture of base of skull separates rim of foramen magnum from the rest of the base. It occurs in fall from height landing on feet or buttocks thus driving vertebral column in to skull. The leg bones (tibia) are sometimes driven through the side of the feet. The major blood vessels near their junction with the heart are severed. The inner lining of carotid arteries shows small horizontal tears. Heart may be driven through the pericardial sac and the diaphragm, may be burst and expose ventricle or may be torn from its pedicle. 3. Fall on the back of head: The inertia of brain produces a positive acceleration pressure over the fronto-orbital region and negative acceleration pressure over the occipital and cerebellar regions of brain. This pressure lasts until the deformation of skull at the site of impact reaches its maximum. Since with the onset of this deformation the brain becomes displaced towards opposite side, two positive forces act on the fronto-orbital cortex. At the site of impact, the positive force of deformation is diminished by the existing negative acceleration pressure that is why contrecoup contusions are formed in falls on head. The degree of acceleration does not depend on the height of fall. It may be greater and produce more damage in a fall from sitting position than from standing position. In fall from high buildings, brain and skull accelerate at the same rate; no acceleration pressures develop with in the skull prior to the impact i.e.
why skull may be totally fractured with minimal coup and contrecoup contusions. In a study, the variations of impact due to fall on the back of head were: • Fall on right parieto-occipital area resulted in contrecoup contusions on left temporal lobe. • Fall on cerebellar region with force of impact traveled forward causing contrecoup contusions in pons and in gyri. • Fall on lower surface of occipital region showed intermediary coup contusions in tegmentum of pons. Indirect Injuries From the forces transmitted through the body or from its deceleration.As a result of fall on feet, axial skeleton may break up at number of points and ring fracture results. Fractures of Skull Goonetilleke classified the pattern of skull fracture in fatalities into five groups: 1. Fracture of vault, including depressed fracture 2. Fracture at the level of brim of a hat 3. Fracture of the base only 4. Extensive fracture of the vault and base 5. Ring fracture at the rim of foramen magnum. The first four patterns of skull fracture are attributed to direct head impact, either primary or secondary. The ring fracture is associated with feet first and is attributed to indirect fracture, the deceleration force being transmitted up the spine to atlanto-occipital joint. The scalp can absorb 20 J of energy and 18-55 J forces can cause skull fracture. The extensive damage could be caused due to small increase in energy beyond that needed to produce linear fracture Injury to Brain A range of intracranial injury from the extradural, subdural and subdural bleed to brain laceration or contusion. It is clear from many reports that brain
Fall from Height injury may be present without skull and vice versa. Brain and skull injury offer the poorest correlation with height fallen but the severity of brain injury correlates well with probability of mortality. Other Injuries Resulting from Fall Rib fractures: The ribs are prone to fracture through direct force and break at the point of impact. Anterior impact produces indirect stress concentration at posterolateral angle of the rib, and laterally because of posterior curvature and caudal angle of ribs. Cardiac and pulmonary contusion and laceration: Cardiac contusion and laceration are frequently involved in extreme falls. Any chamber may be affected, the atria is more commonly injured in indirect injury without rib fracture. Pneumothorax and haemothorax are commonly associated with thoracic trauma. Pneumothorax in presence of rib fracture is explained by rupture of visceral pleura. Diaphragmatic injury: Diaphragmatic injuries are infrequent in falls related to deceleration. The mechanism involved is the relative upward movement of the abdominal contents, forced up against the diaphragm as a result of impact to abdomen or deceleration (feet first or head first) as abdominal contents oscillate up and down on impact. Abdominal viscera: Damage to sold viscera; the liver and spleen are common from fall from height in excess of 12-15 meters. Liver is more commonly involved than spleen with multiple laceration. These injuries are usually coincident with severe overlying trauma to bony thorax but in most cases indirect shear mechanism are involved. Medicolegal Aspects The death that occurs due to fall from height must be carefully evaluated. Majority of the cases are
269
either suicidal or accidental in nature but there may be allegations that the person was thrown/ pushed from high rise buildings. Therefore injuries over the body must be evaluated throughly while the intervening object to be kept in mind. 1. Suicidal: When the person commits suicide by jumping from the building, the body is usually found at a distance from the base line of the building. In these cases, usually the person lands on foot and he is expected to get injury involving both the feet alongwith the fractures, fracture of the pelvic bones that may be pushed upwards. Even at times, there may be fractures of base of skull (Ring fracture) due to transmission of force. 2. Accidental: In cases of accidental falls the body is found very close to base line unless there is rolling of the body on landing and usually there is injuries to the head, chest and abdomen. 3. Homicidal: On the other hand, if the person has been pushed or thrown from the building the body may be found a little bit away than that of the accidental fall though the injuries may be more or less similar to accidental fall. However, there may be defence wounds on the body during quarell or fight while the person is pushed down. The position of the body after the fall also depends on the weight of the body as well as the surface of landing. Autopsy Findings 1. Before deciding the nature of crime one has to visit the scene of crime and examine the location and height of the building, presence of any intervening objects, presence of boundry wall at the edge of the roof and the site and nature of injuries over the body. 2. While interpreting injuries over the body following factors should be considered: (i) Body orientation on forces of impact (ii) Distribution of forces of impact (iii) The age of the patient.
18
Part 1—Forensic Medicine and Pathology
Dysbarism and Barotrauma DYSBARISM Dysbarism consists of those disturbances in the body exclusive of hypoxia and air sickness that result from existence of a pressure differential between the total ambient barometric pressure and the total pressure of dissolved and free gases within the body tissues, fluids and cavities. Classification of Dysbarism Dysbarism has been classified by Adler as: 1. Those due to hyperbarism: Result from an excess gas pressure over that with in the body fluids, tissues and cavities are noted during the descent. 2. Hypobaric effects: Result from excess of gas pressure with in the body fluids, tissues and cavities over ambient gas pressure, are noted during ascent. Injuries From Hyperbarism (Barotrauma) Physical effects related to increase in atmospheric pressure are referred to as barotraumas. It occurs most frequently under water. The pressure of underwater environment is always greater than that of atmosphere. When pressure of air or gas in body cavity differs from surrounding tissues, problems of dysbarism arises. The failure to maintain equality of pressure between body and surroundings may be due to the: (i) Weakness of the individual himself (ii) Inadequacy of the protection available to him or his equipment (iii) Mishandling of the equipment by other people.
When an individual inhales a lungful of air and plunges in to aquatic environment, as he descends in to water, chest pressure increases with increasing depth and the volume of air in lungs is decreased as air pressure increases. At about 100 ft, the total respiratory volume may be reduced to residual volume and with increasing descent air in the lungs is at constant volume and pressure but pressure of pulmonary circulation and tissue wall continues to increase. Thus a pressure difference is created resulting in pulmonary oedema by fluid transfer from the alveolar capillaries into alveolar spaces leading to vessel rupture and haemorrhage, the air pressure increases than that of tissues that results in pulmonary tissue rupture and air escapes into interstitial tissue or pleural cavity or be drawn into circulation. High altitude decompression sickness has symptoms similar to those of Caisson disease but the two differs in circ*mstances of development and progression of the process. Syndromes of Barotraumas Pulmonary Barotraumas This can manifest as pneumothorax, interstitial emphysema and air embolism causing chest and abdominal pain, nose bleeding, haemoptysis, coughing and cyanosis. Immediate recompression is mandatory to shrink the embolism bubble mass. The clinical effects of air embolism depend upon the actual site namely, convulsions, visual changes, spastic/ flaccid paralysis, tingling in the
Dysbarism and Barotrauma limbs and vertigo. Barotalgia The second location where injury from barotraumas can occur is in middle ear where air pressure differs from that in the external ear and nasopharynx. If air pressure in middle ear cannot be kept in equilibrium with that of nasopharynx for example because of inflammation of eustachian tube, eardrum may bulge inwards resulting in stretching, pain, haemorrhage, and ultimately perforations. This occurs in sudden descents from high places such as mountains or in landing of an aircraft, and in diving. In diving this is more of a problem but acute pain prevents diver to go deep enough to produce the perforation in his ear. If an individual is wearing a tight fitting cap, air may be trapped in external canal. Barosinusitis and Barodontalgia Divers experience vertigo or dizziness under water and those with sinusitis or polyps of nasopharynx may experience a painful condition owing to pressure variations between surrounding tissue and sinuses. Small pockets of gas resulting from fermentation in the roots of teeth may shrink during compression and the space becomes occupied by blood or fluid with increased pressure and pain when the diver returns to the surface. Intestinal Complications As a result of increased volume of gaseous content of intestinal tract, continued fermentation may produce additional gas which will cause abdominal distension, discomfort and embarrassing flatulence upon return to the surface. Nitrogen Narcosis and Oxygen Poisoning Despite the chemically unreactive nature of some noble gases at certain pressures they display all typical properties of anesthetic agents. Nitrogen makes up about 79% of the air we breathe, produces euphoria followed by narcosis. With alcohol, the effect of nitrogen is greatly
271
enhanced. Usually upon release of pressure, excess nitrogen leaves tissues and recovery is complete. Helium is used in place of nitrogen in breathing mixtures which allows for deeper diving potentials. Hyperemia (Oxygen poisoning) The effects may result from prolonged exposure to low oxygen concentration or brief exposure to very high tensions (1500 mmHg). Acute oxygen poisoning is much more common danger in diving. Convulsions are reported if divers have breathed pure oxygen at a pressure of 4 atm. At depths greater than 25 ft pure oxygen is not currently used. Mechanism of oxygen poisoning includes an excessively high partial pressure of oxygen. In chronic oxygen poisoning, irritant effect on lung tissue from smaller excess pressure for a considerable time may be there. SCUBA Diving Fatalities SCUBA is a Self Contained Underwater Breathing Apparatus. The diver is supplied by one or more tanks strapped to his back, which enable him to remain submerged for indefinite periods of time Snorkeling: The hazards are similar to that of swimming. It refers to diving appratus that has mouth piece at one end and the other end of the tube remains above the surface of water unless the diver submerges, when the spherical float attached to it keeps the water from entering it. The diver holds his breath for the length of time he remains underwater. These fatalities are contributed by four basic groups of factors: 1. Panic in minor emergencies such as: (i) Loss of a mouth piece or face mask (ii) Entrapment in kelp or gill net (iii) Poor judgment in estimating distance from safety. 2. Improper use or maintenance of equipment: (i) Insufficient servicing (ii) Use of defective components (iii) Occasionally regulators are defective (iv) Water may be inhaled instead of air.
272
Textbook of Forensic Medicine and Toxicology
3. Acute alcoholism: Due to alcoholism, judgments are impaired and inhibitions are lost. 4. Organic diseases: Cardiovascular diseases especially severe coronary sclerosis. Hypoxia is associated with increased susceptibility to the effects of alcohol, impairment of coordination of muscular activity and decreased perception of depth and colour. Hazards of Scuba diving include drowning, barotraumas, bends (Caisson’s disease), acute pulmonary oedema, emphysema, pneumothorax and air embolism. In Scuba diving, frequently there is entrapment of air with in the lungs on rising from depths producing fatal or non-fatal extraalveolar air syndrome. Air escapes from alveoli and may result in interstitial emphysema, pneumothorax and air embolism. It is caused by disproportionate expansion of air containing alveoli compared to the adjacent fluid filled vascular changes during too rapid an ascent. Water Accident Investigation Team (WAIT) The medicolegal investigation technique for water accidents is developed by Noguchi. It consists of forensic pathologist and his medical or paramedical support team, diving expert (may be a medical officer who has sufficient experience in hyper baric medicine). The work of this team is coordinated by means of a liaison officer. Every scuba fatality should be thoroughly documented and investigated as to what happened, circ*mstances surrounding the death and what recommendations should be made to prevent such incidents. The training should be improved and licensing and maintenance of diving gear is important to prevent such fatalities. A coordinated effort should be made with active sports diving equipment manufacturers. Medicolegal Autopsy in Fatal Water Accidents including Scuba Deaths 1. Do not remove any mask or gear from the divers, as equipment should be examined for flaws such as absence of a weight belt.
2. Photograph the tank and send it to proper testing facility. 3. Leave wetsuit undisturbed until the autopsy begins. 4. Document the time of notification, arrival time and diving time. 5. Conversations with witnesses such as skipper, other divers and diving instructions are important. 6. Photograph the body in position in which it was found underwater (face down, face up) as soon as possible. 7. Note the condition of the body especially rigor mortis. 8. There should be minimum disturbance of the position of the remains, diving gear, wetsuit and safety equipments. 9. Transfer the body to the examining room without delay to prevent artefacts being increased by putrefaction. External examination: The external examination should be conducted from top of head to tips of toe without missing any surface of skin as: 1. Evidence of squeezing or pressure of skin. 2. Eyelid, conjunctiva, sclera, neck and thoracic wall should be examined for subcutaneous emphysema. 3. Radiological examination: X-ray of chest in standing position will indicate a fluid level in chest cavity or presence of pneumothorax or pneumomediastinum. Radiographs of knees will show nitrogen bubbles in the joint, indicating a long diving period. 4. In case of air embolism, air samples should be removed with a syringe lubricated by oil for gas chromatography and electron mass spectrometer analysis of gas components. >95% nitrogen indicates nitrogen narcosis (In case of massive air embolism from rupture of lungs, O2 to N2 ratio would be 20 : 80%). • While giving skin incisions, never overlook small air bubbles coming out from subcutaneous tissue. • Blood is generally fluid, not coagulated. • Heart need not be opened underwater.
Dysbarism and Barotrauma • It is more important to measure total amount of air in heart chambers to find out air embolism. 5. Stomach contents must be examined for presence of food, drugs or alcohol. Injuries Relating to Low Atmospheric Pressure (Hypobarism) The barometric or atmospheric pressure at sea level is above 760 mm Hg. This pressure is referred to as standard or 1atm if temperature is 0oC. The effects of hypobarism are related to its causation by: (i) Evolved gas types (ii) Trapped gas types. Evolved Gas Types Gases are evolved and form bubbles when with a rapid decrease in ambient pressure, tissues saturated with a dissolved gas may become supersaturated. Nitrogen is implicated in most of the cases but oxygen and carbon dioxide may also form and cause dysbarism. In the body nitrogen is transported in simple solution according to Henry’s law. It enters into and is removed from the body by establishment of equilibrium between nitrogen pressure in the alveolar air and venous blood and another between tissues and arterial blood. During an ascent, ambient nitrogen pressure is decreased and nitrogen transport is directed towards its removal from the lungs. Nitrogen in tissue, then being higher in pressure than that of arterial blood, is transported to blood then to alveolar air and is expired. As only a small amount of nitrogen can be transported by a given amount of blood, the rapid reduction in ambient pressure results in super saturation of the tissues with the resultant bubble formation. Nitrogen bubbles can form in any tissue including blood and are characterized by bends and chokes. Bends are joint pains caused by evolved gas bubbles with in the joints and Chokes are characterized by cough, chest pain and dyspnoea due to pulmonary evolved gas as
273
well as mediastinal emphysema from evolved gas bubbles. CNS symptoms are caused by evolved gas pressure on or in the brain as well as embolic phenomenon. CNS disturbances are produced due to evolved gas bubbles under the skin. Microcirculatory phenomenon are produced due to bubble pressure on nerves and blood vessels. Trapped Gas Types Gases may be trapped in hollow viscera, teeth or body cavities with resultant pain and possibility of ruptures. Gases may be trapped in sinuses, middle ear, teeth, joints, beneath skin, and intestinal tract. Factor Effecting Clinical Manifestations of Hypobarism 1. Age. 2. Obesity: Fatty tissue contains less blood than muscular tissues and nitrogen is five times as soluble in fat as in muscle. 3. Exercise, because of concomitant increase of tissue metabolic carbon dioxide. 4. Rate of ascent. 5. Attained altitude during ascent. 6. Increased tissue pressure of nitrogen prior to ascent. 7. Recent scuba diving: United States has adopted the ‘Rule of 12’ to cover the circ*mstances in which hypobarism occurs at lower altitudes; if individual has been Scuba diving for 12 hours. ‘No flight above 12,000 ft for 12 hours following a Scuba dive of 12 ft or more’. Physiological reason for this rule is that enough time must be allowed at sea level, breathing air to complete respiratory wash out of the excess nitrogen stored in the tissues during the dive. 8. Lower ambient temperature: Occurs with great frequency because of decreased nitrogen transport associated with peripheral vasoconstriction due to cold. 9. Total dissolved gas tension.
274
Textbook of Forensic Medicine and Toxicology
10. Previous injury: Bubbles tend to form at the sites of recent injuries 11. Repeated exposure: Having one such attack of dysbarism is prone to another episode
3.
Clinical Features 1. The Bends: Onset follows the ascent with a variable lag period. It includes joint symptoms, pain in muscles, long bones. The areas involved are first the knee then shoulder, elbow, wrist, hand and finger in decreasing order. The features are not serious and may be relieved in descent 2. The Chokes: Are characterized by substantial distress, nonproductive cough, respiratory distress, sense of apprehension and suffocation. The chokes are more serious than the bends. They result from bubble formation and accumulation in the pulmonary capillaries or from the effects of extravascular mediastinal bubbles exerting pressures on mediastinal contents and adjacent pulmonary tissue. It may be solitary manifestation of hypobarism and may accompany the bends. Chokes are found later than bends in the flight and become progressively disabling. Cough and substantial distress are markedly aggravated when an attempt is made to take deep breath resulting in decreased pulmonary ventilation, then hypoxia, syncope and collapse. Onset of chokes demands: (i) Prompt attention (ii) Return to normal pressure by way of descent to lower altitude (iii) Termination of
4.
5.
6.
flight of aircraft (iv) Removal from low pressure chambers. CNS involvement: Vision is disturbed and there is disturbance in orientation. This is related to bubble size and location of lodging in the arterioles and capillaries of the brain, indicate mandatory hospitalization. Skin manifestation: Are due to pressure on dermal nerve endings and sub dermal emphysema revealed by crepitation on palpation. Rapid and explosive decompression: They result from mechanical failure of aircraft pressurization system. Explosive decompression: Loss of pressure is less than a second in explosive decompression and more than a second in rapid decompression. The eardrums are ruptured in the absence of basal skull fractures. Microscopic examination of lungs will reveal presence of bone marrow emboli resulting from nonfatal injuries sustained before ground impact.
Long Question 1. Discuss injuries caused by exposure of humans to high pressure environment. Short Questions 1. 2. 3. 4.
Barotalgia Barodontalgia SCUBA Dysbarism.
19
Part 1—Forensic Medicine and Pathology
Thermal Injuries HYPERTHERMIC INJURIES Hyperthermia can cause systemic as well as localized injuries to the body. A delicate balance between heat loss and heat dissipation maintains thermal homeostasis. To maintain it both environmental and internal heat of the body are involved. Internal heat is generated by the oxidation of heat produced during rest that is the basal metabolism of the body. Environmental heat comes from the sun and its effects are influenced by: i. Moisture content of the air ii. By its wavelength iii. Spectral distribution iv. Absorption by ozone and dust v. Reflection and absorption by skin vi. Clothing worn by the individual Both the internal and environmental heat is measured in calories. A calorie represents the quantity of heat needed to raise a kilogram of water from 0o C to 1oC. Exogenous or No Febrile Hyperthermia The human body reacts to an environmental elevation of temperature by reducing thermo genesis and by increasing heat dispersion. Thermo genesis is decreased by reduction of metabolic rate to the minimal required for the vital functions and thermo dispersion is achieved by: (i) peripheral vasodilatation (ii) profuse sweating (iii) evaporation converting sweat to water vapour. All these factors are affected by the high humidity and lack of air movement.
The diseased states due to the effect of excessive heat are divided in to four categories in progressive order of severity: • Heat cramps • Heat exhaustion • Thermogenic anhydrous • Heat stroke. Heat Cramps (Boilers room, Miners cane cutters) The painful spasm of the voluntary muscles especially of the extremities and abdominal wall is produced during or after physical activity in a hot environment. The predisposing factors such as ill health and intake of alcohol result in depletion of salt that are the main causes of heat cramps. The cramps are severe, paroxysmal and affect the muscles of legs, arms and abdominal wall. Flushing of face and dilatation of pupil occurs. Administration of physiologic saline brings about dramatic relief. Prophylactically, salt tablets can be used to combat heat cramps. Heat Syncope Heat syncope is a circulatory phenomenon induced by posture and/or exercises. Heat Exhaustion Heat exhaustion results from dehydration and salt depletion producing the following symptoms: (i) intense thirst (ii) nausea, vomiting and headache. (iii) mental fogginess (iv) dizziness (v) irritability
276
Textbook of Forensic Medicine and Toxicology
(vi) incapability to work (vii) fainting (viii) peripheral vascular collapse (ix) sweating (x) temperature may or may not rise (xi) skin is not dry (xii) oliguria (xiii) death results from heart failure. Thermogenic Anhydrous Thermogenic anhydrous is also known as Desert syndrome or Anhydrite heat exhaustion. It occurred in some soldiers who were separated during the summer in American desert. The features are most likely that of heat exhaustion. After profuse generalised sweating for several days perspiration ceases suddenly in all parts of the body below the neck region and persists in face and neck. Eruption of prickly heat rash is seen known as miliria profunda. The condition is not uncommon in Bengali children, tanker personnel reforming from Persian Gulf. There is no suitable explanation for this. There is hyperkeratotic plugging of sweat glands leading to functional failure of sweat apparatus or a combination of both. Heat Stroke
2. Visceral haemorrhages and congestion in heart, liver, lungs and kidneys are present due to thrombocytopenia, decreased plasma fibrinogen concentration and decreased prothrombin levels causing hepatic damage. 3. Haemorrhage also occurs due to increased capillary fragility due to anoxia and circulatory collapse. 4. Patients who survive for more than 24 hours show lobar pneumonia, acute tubular necrosis, centrilobular necrosis, adrenal necrosis and haemorrhages. 5. Heart shows subendocardial haemorrhages, changes in the muscle fibers and the chambers are dilated. 6. Brain is congested and oedematous; convolutions are flattened and scattered patches are found in the walls of the third ventricle and floor of the fourth ventricle. 7. The cerebellar changes are more rapid and in the form of oedema of purkinje layer and swelling, degeneration and reduction of purkinje cells. 8. Those who survive longer show rarefaction of granular layer along with oedema of hypothalamic nuclei. 9. In the brain, the heat dissipation center (preoptic and supra-optic area) and the heat conservation and production center (occipitolateral portion of hypothalamus) are usually affected.
In heat stroke, there is complete absence of sweating and the body temperature is raised to 106°F or 41°C. In the environmental heat stress, absence of any other cause of pyrexia constitutes heat hyperpyrexia. Several workers have pointed out that heat stroke can occur at lower temperatures also. At a temperature of 32º C with 100%, humidity may lead to heat stroke. The features of heat stroke include hot and dry skin, increased depth of respiration, pulse is raised to 160-180/ min and there is severe asthenia. Cerebral deficit produces convulsions, delirium, stupor and coma. When there is hypotension, increased urea concentration and raised potassium levels then prognosis is bad. Urine shows proteins and casts. Serum iron and bilirubin levels are raised due to liver damage. SGOT is raised due to liver and muscle damage. The first 24 hours are critical and death usually occurs within a week.
The term systemic hypothermia is used to indicate cooling of the human body below 35oC (95oF). This occurs when the loss of heat exceeds the production.
Autopsy Findings of Hyperthermic Deaths
Causes of Hyporthermia
1. The autopsy findings in hyperthermic deaths are similar to those in cardiac failure.
1. Hypothermia caused by exposure to severe cold possibly with exhaustion called environmental
Medicolegal Aspects of hyperthermia 1. All hyperthermic deaths are accidental 2. Autopsy examination is done to rule out any other cause of death or contributory cause of death.
HYPOTHERMIC INJURIES
Fall from Height hypothermia depending on environmental factors. 2. Hypothermia under the influence of drugs and alcohol affecting the generation or conservation of body heat. 3. Hypothermia caused by climatic conditions with some disease affecting the body resistance. 4. Hypothermia ending fatally in connection with therapeutic procedure that has some medicolegal importance. Types of Hypothermia 1. Dry cold hypothermia 2. Immersion hypothermia Accidental Hypothermia It is produced during (i) hiking or skiing expeditions (ii) in ship wrecked, (iii) people falling in ice water or (iv) when there is insufficient heating facility in the room. Immersion Hypothermia In immersion hypothermia, the loss of heat is three times more than that due to exposure to dry cold air. Water conducts heat 25 times faster than dry air. Insulating air between skin and water is 1/ 10th than that of skin and air. Women endure cold water better than males due to body fat. Human body is able to retain body heat in water up to 22oC and below 16oC, survival time decreases sharply. Immersion hypothermia is more fatal as there is rapid loss of heat.
277
Clinical features in children: In children features produced are cold skin, redness of face, subcutaneous oedema, scleroma, muscular stiffness, feeble cry, unable to suck, cutaneous and mucosal lesions are uncommonly present. Convulsions are also seen in some cases. Clinical features in adults: In adults the features produced are red patches over the skin, pallor of skin, subcutaneous oedema of the face, stiffness of neck muscles, mental disorders, pulse is decreased and irregular with hypotension and respiration is slow. II. Laboratory Findings 1. E.C.G. is mandatory and following findings are discerned (i) occurrence of ‘J’ wave (ii) widening of QRS complex (iii) prolongation of PQ interval (iv) Inversion of ‘T’ wave. 2. Hyperglycemia. 3. Raised blood urea and lactic acid levels. 4. Haemoconcentration. 5. Serum amylase levels are increased. Causes of Death
Diagnosis of Hypothermia
The mechanism of death in hypothermia is: 1. Cessation of circulation preceded by ventricular fibrillation; the dangerous level of temperature for ventricular fibrillation is 26oC-30oC though people have survived at a much lower temperature. 2. There is decreased supply of oxygen to the central nervous system with resulting hypoxia of the brain cells.
I Clinical signs and symptoms
Autopsy Findings
Body temperature preferably oesophageal (rectal temperature is also satisfactory) should be taken. Clinically three phases are produced: 1. Body temperature is 37oC-32oC with shivering and vasoconstriction. 2. Body temperature is 32oC-24oC and body response to production of heat grossly disappears. 3. Body temperature is below 24oC, body cannot withstand the heat loss and general paralysis is produced.
1. Postmortem staining is red or pink due to antemortem binding of oxygen to haemoglobin and its postmortem diffusion through the skin. 2. Rarely the skin is white that is why hypothermic deaths are called the ‘white deaths’. 3. Spots of bluish discolouration are seen on the hands, elbows, and knees. They are minor frostbite lesions.
278
Textbook of Forensic Medicine and Toxicology
4. In the heart, there is dilatation of right atrium and ventricle and congestion of vena cava. 5. Trachea contains frothy and sanguineous fluid. 6. Lungs are congested, oedematous and shows haemorrhages. 7. Bronchopneumonia is a frequent complication. 8. Liver and spleen are congested. 9. Gastric mucosal erosions occur in 72% of cases. 10. Kidney shows acute tubular necrosis. 11. Fat deposition occurs in the cardiac and skeletal muscles and there is focal myocardial necrosis. 12. Viscera should be submitted for blood alcohol and toxicological analysis. 13. Histological examination of skin shows oedema and hyperemia of the dermis with occasional inflammatory cell infiltration. Treatment 1. Re-warming by warm water (40-42oC); but never rewarm the patient by exercise or intense dry heat or fire as it leads to gangrene. 2. The blisters should not be pricked. 3. Antibiotics should be given to combat infection. 4. Alcohol and tobacco is to be avoided as they hamper the peripheral blood flow. Local Cold Injuries 1. Chilblains (Acute perineo): Chilblains can be categorized as a first-degree frostbite. The skin is red or bluish as there is capillary congestion and mild inflammation. As a rule, complete recovery occurs without residual deficit. 2. Chronic perineo: Chronic perineo presents with reddish flat nodules in the skin, seen commonly in the women involving the lower limbs. There is ulceration, haemorrhages and scarring. These lesions become activated in the cold weather. The microscopic findings include skin atrophy, dermal fibrosis, panniculitis, angiitis, and sclerosis of arterial walls.
3. Cold panniculitis: This can be produced with local application of ice. There is inflammation and necrosis of the underlying adipose tissue. The children are most commonly affected because the fat of the children contains more saturated fatty acids than that of adults. The finding could be of interest in a battered baby syndrome as deliberate exposure of an infant to cold develops panniculitis. 4. Immersion foot and trench foot: Immersion foot and trench foot usually occurs at a temperature above 0 o C most commonly when the temperature is between 5-8oC. Wetness is an important contributory factor. There is necrosis of fingers and toes. Obliterating angiitis causes severe gangrene and loss of tissue. 5. Frostbite: Frostbite occurs due to exposure to dry cold as well as following immersion at temperature below 0oC (usually -2.5oC). It is commonly seen in mountaineering and polar expeditions. It is of superficial type when only the skin is affected and deep type when subcutaneous fat, muscles, nerves and bones are affected. Degrees of frostbite and their manifestations are given in table 19.1. Table 19.1: Degree of frostbite and their manifestations Degrees of frostbite
Features
First degree Second degree
Redness and oedema of skin Only epidermis is affected, there is blister formation Skin and subcutaneous tissue is necrosed Total loss of tissue in the exposed area including muscles and bone
Third degree Fourth degree
ELECTRICAL INJURIES Factors Influencing Electrical Injuries The factors are that affect production of electrical injuries and shock are: 1. Voltage or tension: Voltage is less important than the amperage or intensity. Low voltage (24 houtrs—Coarse fibrils. • >4 days—Small concentrated areas appeared. • >2 weeks—Solid areas predominated. • >1 month—Granular areas appeared among solid areas. • At 4 months—Only granular appearance. Platelets: Thrombosis has been recognized as an essential reaction to injury and was regarded by earlier writers as an unequivocal sign of antemortem infliction. Four stages are distinguished as platelet adherence, aggregation, degranulation and disruption. They are associated with formation of fibrin and platelet plug that is mixed fibrin red cell leukocyte mass and extension of thrombus. Agglutinated platelets arrest haemorrhage in normal skin by rapidly sealing the mouths of all cut vessels larger than capillaries. Elastic tissue: Haemotoxylin and eosin stains the elastic tissue; normal elastic fibers are pink and others are blue gray with pink granules. Toluidine stains as deep blue green and normal elastic fibers as colourless. From a microscopic examination of elastic fibers in skin, it is possible to differentiate between antemortem wounds where these are wave like and post mortem wounds when they are straight. Pigments: Phagocytosis of red corpuscles is well marked after 48 hours; formation of hemosiderin after 24 hours and formation hematoidin with in some 80 days. Disc electrophoresis: Distribution of esterases was compared using disc electrophoresis in the cathode area. Two of these fractions showed up more intensely in antemortem skin wounds compared with undamaged controls. No difference in the esterase pattern was distinguished in undamaged skin and postmortem wounds.
Biochemical Examination of Wounds Although enzyme histochemical methods have considerably shortened the indeterminable period after wounding but the study of last hour before death is very challenging. Histamine and serotonin (5-hydroxytryptamine) are vasoactive amines known to participate in an acute inflammatory process especially in the earliest phase after injury. The minimal increase of free histamine content occurs within in 20-30 minutes and of serotonin in 10 minutes of injury. These additives have been conducted in experimental investigations of skin injuries as well as autopsy materials. About 2 gm of injured skin sample is removed and an equal size of control sample is taken from neighbouring intact skin of the corpse. The subcutaneous fat is removed from the samples before further processing and the free histamine and serotonin in the wound samples are compared with those of control samples. Immunofluorescence Techniques Fibrin in certain tissue lesions does not stain by standard techniques in the generally accepted manner. Sections from these fibrin clots were shown to react specifically with fluorescent-labeled rabbit antihuman fibrin antibodies. Also fluorescent antibody method was used to demonstrate fibrin in leucocytes in areas of fibrin accumulation. Acute inflammatory cellular response to fibrin at ultra structural level by electron microscopy and by fluorescent microscopy using rhodamine antifibrinogen in experimental work on dogs was studied and was noted that fibrin is either a network of heavy interweaving strands with orange fluorescence or less intensely stained delicate fibers. Postmortem fibrin cannot be distinguished with any certainty on morphological grounds from vital fibrin. A large proportion of postmortem subcutaneous haemorrhages undergo fibrinolysis, which destroys the formed fibrin networks with a day of the haemorrhage. Therefore well preserved fibrin networks found at autopsy performed two to
Medicolegal Aspects of Injuries three days after death appear to point to the vital or agonal origin of a subcutaneous haemorrhage against its postmortem origin.
TORTURE The Webster dictionary defines torture as ‘anguish of body or mind; something that causes agony or pain, to punish, coerce or afford sad*stic pleasure. The oppression of the Nazi regimen during the second World War prompted the UNO to come out with Universal declaration of Human Rights (1948), followed by an International agreement of civil and political rights (1966) and a declaration on the protection of all persons from torture and other cruel, inhuman or degrading treatment or punishment (1975). In 1975, World Medical Association adopted a declaration called Declaration of Tokyo that defined torture as, ‘A deliberate, systemic or wanton infliction of physical or mental suffering by one or more persons acting alone or on the orders of any authority to force another person to yield information, to make a confession or for any other reason. This declaration clearly expressed that a doctor must in no way, for any reason take part in the practice of torture or other forms of cruel, inhuman or degrading procedures as the doctor’s role is to alleviate the distress of his fellow persons and no motive whether personal, collective or political shall prevail against this higher purpose. Though this definition is considered by many as the mot authoritative as far as doctors are concerned, it has few drawbacks, namely: 1. It is applicable only in content of detention and imprisonment and not in other situations where torture could take place. 2. There is no distinction as far as severity or aim of torture is concerned. 3. Unethical experimentation with human subjects has not been covered under this declaration. 4. It is implied that torture can be perpetrated only by others and not by self. No guidelines have been offered for self torture.
325
Classification of Torture 1. That done on the person by his consent. 2. That done by others (without consent) that can be further sub classified as that committed on an innocent person or on a person who is not innocent (criminals or terrorists). Reasons for Torture The reason for torturing a person varies from country to country and time to time depending on the availability of weapons, circ*mstances and the motive for the crime. In the earlier days, the basic purpose of the torture was to get information or confession; to spread terror in the society or a country; to destroy a personality; to take revenge and to get a testimony incriminating others. Types of Torture Torture can be physical or psychological. Types of Injuries in Torture Though virtually any type of injury can be inflicted deliberately to extract information, punish or degrade the victims, but the repetition of a particular injury, such as tram line bruises from beating, is suspicious. The following types of injuries are commonly produced in the victims of torture: 1. Beating is one of the most common forms of torture and can take various forms, varying both with the weapon used and the part of the body injured. The blows may be inflicted with a fist, foot, shoe or some weapons such as whip, a lathi, metal or wooden bars, clubs, batons, rifle butts or belts may be used. Many of these weapons produce a characteristic single or double edged linear bruise. The bruise may be line of confluent petechial haemorrhages or a continuous mark of red skin. The ‘tram line’ bruise is a double line of parallel marks with a pale unbruised zone between them, caused by the impact of a rectangular or circularsectioned object. The bruising may be intradermal, when it reproduces the pattern
326
Textbook of Forensic Medicine and Toxicology
of the weapon well. If a leather whip with, for example, plaited thongs is struck against the skin, the pattern may be imprinted clearly on the skin. Buckles on belts and other recognizable artefacts may occasionally be useful in identifying the weapon. Where the bruising is deeper, no such pattern is likely. The skin may be broken causing abrasions or lacerations and if full thickness is breached, healing will cause scars, which may even be recognizable as ‘tram lines’. Repeated beating leaves multiple overlapping and criss-crossing marks that have a generally similar orientation that indicates that the attacker stood in a relatively fixed position to the victim. The use of multithonged whip will leave a series of marks with same orientation as above. Back is the most common target but whipping and beating may be applied to the buttocks, thighs, front of chest, breasts and abdomen, lower legs, soles of feet and even perineum and genitals. Beating of the soles of feet with canes or rods (falanga) is extremely painful and debilitating a torture rooted in antiquity. The tough tissues and thick fascial planes of the foot do not readily reveal bruising, though it may be found on deep dissection in victims who have been killed by some other means. If injuries were inflicted months before the examination, little or nothing may be found unless the skin was broken, when scarring will have taken place. Sometimes however, faint red lines will be seen in pale skinned people and hyperpigmentation along the lines of injury in the dark-skinned. 2. Burns are also commonly caused as a means of torture and they may either may the actual cause of death or visible as recent or scarred evidence of previous torture. All kinds of burns may be suffered such as from molten rubber dripped onto victims from motor tyres suspended overhead, hot irons applied to the skin, ignited kerosene soaked
3.
4.
5.
6.
rags wrapped around the limbs and numerous burns from cigarettes passed on to the skin. The findings of burning motor tyre necklace and shadow areas indicating direction of contact where molten liquids have been dripped from above onto a bound victim may be seen on examination of the victim. Cutting and stabbing wounds are also quite common and may be caused by a variety of weapon but knives and bayonets are commonly used. The chest and upper arms are the favourite sites for infliction of injury. The old stab wounds from knives and bayonets may be recognizable as elliptical scars many months or years after the infliction. Blunt injuries and clubbing are quite common, either to cause death or as form of abuse. The head is the most common target, but the legs and knees are also often struck. Blows on the back and sides are neck may be from due to damage to vertebrobasilar artery. Suffocation and drowning are not commonly employed practices but non-fatal practices such as submarining (repeated dipping of the victim’s head under water or even in foul liquid such as sewage water) is a well-known method of abuse. Such practices may cause death from drowning or if the victim survives, pneumonia may develop. Partial suffocation by enveloping the head in an opaque plastic bag is more a means of disorientation than physical torture but may eventually prove fatal. Electrical torture is also quite commonly employed method of abuse. Either mains voltage of 110 or 240 volt is used, that can cause fatal cardiac arrhythmias and local burning. A magneto delivering high voltage is painful but not lethal and will not leave any significant marks over the skin owing to its low amperage. Electrical current may be applied anywhere on the body but the
Medicolegal Aspects of Injuries
7.
8.
9.
10.
genitals especially the penis and scrotum and the female nipples are the favoured sites. Injuries to ears may occur as a result of telefono (repeated slapping of the sides of head and ears by open palms of the assailant). Very rarely injuries to the inner ear and rupture of tympanic membrane may be demonstrated on autopsy. Suspension: In such cases abrasions, bruises and chafing marks may be found as ligature sites usually on legs, arms and sometimes genitals. It is a common method of torture. Shooting is a common means of execution or non-fatal punishment but not a method of torture. Knee-capping where opponents and suspected traitors are shot either through knee joint or lower thigh, perpetrated in Northern Ireland. Sexual abuse is commonly seen even multiple rapes in women that will leave some of the physical signs
Management of Torture Victims First and foremost is the diagnosis of torture by taking a proper history, complete examination including the general physical examination, examination of the injuries and proper investigation including the radiological examination and bone scintigraphy. The treatment of the victim is an important aspect by providing the physical and psychological treatment simultaneously and treating the victim and his family. The victim should not be reminded of torture and proper rehabilitation is necessary. Medico-legal and Ethical Aspects of Torture 1. Freedom from torture is among the human rights contained in the United Nations, Universal Declaration of Human Rights 2. Doctors are obliged by the Hippocratic Oath, not to use their professional knowledge in order to harm their patients. 3. Geneva Declaration of the World Medical Association reconfirmed this obligation and precludes any medical involvement in the
327
practice of torture. In spite of this the doctors are at the risk of being involved in the practice of torture directly or indirectly; 1. As a humanist citizen. 2. As a participant in the process of torture by coercion by society, government or terrorists, or sometimes unknowingly becoming a part of it and with his own desire. 3. As victims of torture themselves e.g., Chile, Turkey. Participation of Doctors in Torture The doctors can participate in torture in various ways, namely: 1. Evaluating the victim’s capacity to withstand torture 2. Supervising torture through provision of medical treatment, if complication occurs. 3. Providing professional knowledge and skills to the torturer. 4. Falsifying or deliberately omitting medical information when issuing health certificates, or autopsy reports. 5. Administering torture by directly participating in it. 6. Remaining silent in spite of the knowledge that abuse have taken place. The most vulnerable doctors are military doctors, police and prison doctors, those in Government jobs and forensic medicine specialists. These experiences led to the adoption of a special declaration on the doctor’s in torture at the World Medical Assembly in Tokyo in 1975, known as the ‘Tokyo Declaration’. These are 1. The doctor shall not countenance, condone or participate in the practice of torture or other forms of cruel in human or degrading procedures, whatever the offence of which the victim of such procedures is suspected, accused or guilty and whatever the victims’ belief or motives and in all situations including armed conflict and civil strife. 2. The doctor shall not provide any premises, instruments, substances or knowledge to
328
3.
4.
5.
6.
7.
Textbook of Forensic Medicine and Toxicology
facilitate the practice of torture or other forms of cruel, inhuman or degrading treatment or to diminish the ability of the victim to resist such treatment The doctor shall not be present during any procedure in which torture or other forms of cruel, inhuman or degrading treatment is used or threatened. A doctor must have completed clinical independence in deciding upon the case of a person for which he or she is medically responsible. The doctor shall in all circ*mstances be bound to alleviate the distress of the fellowmen and no motive whether personal, collective or political shall prevail against this higher purpose. Where a prisoner refuses nourishment and is considered by the doctor as capable of forming an unimpaired and rational judgment. Concerning the consequences of such voluntary refusal of nourishment he or she shall not be fed artificially. The decision as to capacity of the prisoner to form such a judgment should be confirmed by at least one other independent doctor, the consequences of the refusal of nourishment shall be explained by the doctor to the prisoner. The WMA will support and should encourage the international community, the national medical associations and the fellow doctors to support the doctor and his/her family in the face of threats or reprisals resulting from a refusal to condone the use of torture or other forms of cruel inhuman or degrading.
Statement by the International Union of Psychological Science (1976) ‘No psychologist in the exercise of his/her professional functions should accept instructions or motivations that are inspired by considerations that are foreign to the profession’. It requests beach member of society to make certain that it has enacted a code of ethics and to take those actions
required by its code against any member guilty of such abuses against human rights. Principles of Medical Ethics (United Nations 1982) relevant to the role of health personnel particularly physicians in the protection of prisoners and detainees against torture and other cruel, in human or degrading treatment and punishment as given by United Nations in 1982 are the following: 1. Health personnel particularly charged with the medical cases of prisoners and detainees have a duty to provide them with protection of their physical and mental health and standard as is afforded to those who are not detained or imprisoned. 2. It is a gross contravention of medical ethics as well as an offence under applicable international instruments for health personnel particularly physicians to engage actively or passively in acts which constitute participation in complicity in incitement to or attempts to commit torture or other cruel, in human or degrading treatment or punishment. 3. It is contravention of medical ethics for health personnel particularly physicians to be involved in any professional relationship with prisoners or detainees, the purpose of which is not solely to evaluate, protect or improve their physical and mental health 4. It is a contravention of medical ethics for health personnel particularly physicians i. To apply their knowledge and skills in order to assist in the interrogation of prisoners and detainees in a manner that may adversely affect the physical or mental health or condition of such prisoners or detainees and which is not in accordance with the relevant international instruments ii. To certify, or to participate in the certification of fitness of prisoners or detainees for any form of treatment or punishment that may adversely affect their physical or mental health and which is not in accordance with the relevant international
Medicolegal Aspects of Injuries instruments, or to participate in any way in the infliction of any such treatment or punishment which is not in accordance with the relevant international instruments 5. It is a contravention of medical ethics for health personnel particularly physicians to participate in any procedure for restraining a person or detainee unless such a procedure is determined in accordance with purely medical criteria as being necessary and for the protection of the physical or mental health or the safety of the prisoners or detainee himself of his fellow prisoners or detainees or of his guardians and it presents no hazard to his mental or physical health. 6. There may be no derogation from the foregoing principle on any ground whatsoever including public emergency. Declaration of Hawaii World Psychiatric Association (1983) The declaration states that “The psychiatrist must never use his professional possibilities to violate the dignity or human rights of any individual group”. If the patient or some third party demands actions contrary to scientific knowledge or ethical principles the psychiatric must refuse to cooperate. World Conference on Human Rights (1993) The conference stated that “Freedom from torture is a right which must be protected under all circ*mstances, including in times of internal or international disturbance or armed conflicts”. The Human Rights Act (1993) In the United States, the Human Rights Act has the principal aim to curb violation of any of the rights, including safety from torture of the individuals of this country. The victim of torture may either suffer from injuries or may die because of injuries and therefore such cases should be carefully and thoroughly
329
examined, reported to the police or the magistrate and treated. A proper examination may help in establishing or disproving the charge of torture both during the examination of injury and autopsy. S. 330 & 331 of the Indian Penal Code deals with crime and punishments of voluntarily causing hurt and grievous hurt for the purpose of extorting confession or any information which may lead to the detection of an offence or misconduct. The following are some of the steps taken to prevent torture 1. To abolish torture a campaign amongst the medical community against torture must be devised and how it is contrary to medical ethics. 2. Doctors should document evidence of torture and conduct autopsies in a fair manner and help the victims to obtain redress. It is the ethical obligation of all doctors to report cases of torture. 3. The medical association should issue official directive condemning and banning these practices and prescribe strict ethical rules and guidelines in this regard and strict measures should be taken for their violation 4. The law should be amended so that every accused person, on arrest should be medically examined and injuries of any on his person should be entered in to the record. 5. Training about torture, its consequences, treatment and rehabilitation of torture victims and medical ethics should form part of the medical curriculum especially at the undergraduate level. 6. Doctors involved in the cover-up operations should be made personally liable and preceded against section 166 of I.P.C.. The responsibility of filing such charges should be taken up by the Indian Medical Association. 7. State medical councils should be properly activated to enforce ethics within the profession.
330
Textbook of Forensic Medicine and Toxicology CUSTODIAL DEATHS
Custodial deaths are those occurring while a person is either in the custody of police or is an inmate of a prison. A meticulous autopsy is needed to confirm or dispel the allegations that an act of commission or omission on the part of custodians has led to, or contributed to, the death. It is sometimes helpful to the pathologist to visit the scene of the death, especially if it was caused by hanging or some form of mechanical trauma. Situations under which death may occur in custody: The death may occur during or soon after the arrest by the police officers during physical struggle, especially when the police officers are attempting to control or overpower the resisting offender. The offender may also threaten the police officers with a knife, gun or blunt weapon and the police have to subdue him either by sheer physical force, truncheons or riot sticks or by the use of firearms. The arrest of a drunken offender poses many problems. Causes of Deaths During Arrest 1. Traumatic asphyxia: When several policemen fall upon a resisting offender to overpower him. 2. Arm-locks or neck holds: Applied by police officers to resisting persons are other causes of deaths during arrest. The arm lock is applied either from behind or with the head of the offender tucked under the police officer’s arm against the waist. The dangers are compression of the front and sides of the neck and death can occur either from reflex cardiac arrest or cerebral ischemia during carotid compression or asphyxia from airway obstruction, though the latter is unlikely to be the sole mechanism. 3. Blunt injury may occur from the use of fist, arm or leg and by use of a weapon such as a truncheon, riot stick or pistol butt. Any type of blunt injury may be received. Head injuries may occur during a scuffle from falls either against the ground, or against a wall or other obstruction. A heavy punch in the face may cause nasopharyngeal bleeding that can block the air-
passages, especially in a person affected by alcohol. A blow on the sides of the neck can cause reflex cardiac arrest or a subarachnoid haemorrhage from vertebrobasialar vascular damage. A backward blow from the point of an elbow can be damaging, if it strikes the face, neck or abdomen. Kicking and stamping are unusual, but not uncommon in custodial deaths. A blow in the abdomen can be fatal if delivered with sufficient force. Though in an adult a fist blow is not very likely to cause serious damage, it can in a very younger person. The use of the elbow, knee or a head butt can deliver extreme force, especially from a fit, muscular police officer as well as from the offender. 4. Alcohol is a frequent cause of death in custody and also it is major factor in provoking aggression and violent resistance. When blood alcohol levels rise to above 350mg/100mL there is an increasing risk of coma and central respiratory depression. At lower blood alcohol levels there is still the risk of aspiration of vomitus and choking on gastric contents. At autopsy, this aspiration should be distinguished from the common agonal phenomenon. Where an otherwise healthy person dies with a high blood alcohol concentration in these circ*mstances, then gross blocking of the trachea and bronchi with vomit can be accepted as the cause of death. Alcohol also attributes to accidents during custody, especially head injuries resulting from falls on the ground, falls down steps and stairs. Falls onto a hard surface are often on the occiput and the frequent finding of frontal and temporal contrecoup brain damage at autopsy is good evidence of a deceleration injury rather than an assault with a weapon. Some falls may occur during custody or in transit from the site of arrest to the police station and the police is often blamed for allowing or causing the injury. Drugs such as amphetamine, cocaine or hallucinogen may also lead to physical damage. Drugs are commonly available within prisons and overdose and hypersensitivity deaths are occasionally seen.
Medicolegal Aspects of Injuries 5. Suicides in custody are quite common. Most police forces deprive the prisoner of any objects that could be used to hang himself in the cells such as belts, braces, cord or even bootlaces. In addition, the police cell may be specifically designed to avoid any convenient suspension points, such as bars, hooks, internal door handles. Nevertheless, prisoners regularly manage to find some means of killing themselves as hanging can be successfully accomplished by traction on the neck at low levels and need not occur at high suspension points, so prisoners have killed themselves by attaching ligatures to bed-heads, chairs and other unlikely objects in the cell. At autopsy homicidal hanging should be ruled out by the absence of signs of struggle and other injuries resulting in death.The person at times may be hanged after killing to simulate suicide. The situation is fully assessed preferably by a visit to the scene with the body at the site. 6. Deaths may occur from purely natural causes, usually of cardiovascular origin and no objective proof can be provided when the emotional and physical upset of being arrested and confinement may have affected the blood pressure and heart rate sufficiently, by an adrenaline response, to have precipitated an acute cardiac crisis in the presence of severe preexisting disease. The presence of diabetes, epilepsy, asthma or other diseases that can potentially cause sudden or unexpected death should be sought for by medical history and autopsy appearances. Investigations of Torture and Custodial Deaths 1. All deaths in custody should be examined with care to ensure that the guardians are cleared of any suspicion of ill-treatment. 2. The torture and custodial deaths are confirmed by circ*mstantial and corroborative evidence. 3. The victim is usually in detention in or some form of custody.
331
4. Such types of death are usually involved with the non-cooperating attitude of the authorities that are hostile to impartial injury. 5. The cases are handed over to the responsible authorities such as Red cross, Amnesty International, Physicians for human rights. 6. There is usually delay in the process before a victim is being brought for examination, the injuries may have healed and body may have decomposed. Body is sometimes disposed off early. 7. The causes of deaths in torture or custodial deaths may be sepsis, haemorrhage, internal organ injury and even sheer exhaustion. Recommendations of the National Human Rights Commission in custodial deaths and torture 1. The commission has required all District Magistrates/ Superintendents of the Police to report any instance of custodial death or rape directly to the commission within 24 hours of occurrence. Failure to send such reports, it has been emphasized would lead to a presumption by the commission that an effort was being made to suppress the occurrence. 2. The commission believes that the country must act deliberately and decisively to end custodial violence and signify to itself and to the World that it will not countenance brutality in custody. 3. The chairperson made clear that a permissive approach to the use of third degree methods in investigation led to serious violations of the right of the citizens of India and that it was wrong to believe that such practices were necessary for the successful investigation of cases and the matter continues to be pursued. 4. The commission is of the view that a recommendation should be made for the insertion of a Section 114(B) in the I.E.A.1872 to introduce a rebuttable presumption that
332
5.
6.
7.
8.
9.
10.
Textbook of Forensic Medicine and Toxicology
injuries sustained by a person in police custody may be presumed to have been caused by a police officer. The commission supports the recommendation of the Indian Law commission that section 197 Cr.P.C. to be amended to obviate the necessity of governmental sanction for the prosecution of police officer where a prima facie case has been established in an enquiry conducted by a session’s judge, of the commission of a custodial offence. The commission also endorses the view that there should be a mandatory enquiry by a session’s judge, in each case of custodial death, rape or grievous hurt. Commission believes that the arrested person being held in the custody is entitled, if he so requests to have a friend, relative or any other person who is known to him, or likely to take an interest in his welfare, to be informed that he has been arrested and told of where he has been detained. The compensation due to the next of kin of those who have died in custody should be the liability of not just the state government but of the offending police officials themselves. The commission gathered detailed information from all the states regarding the manner in which postmortem examination were being conducted, it was found to be substantial time gap between the PM examination and writing of the report; facilities in many mortuaries were abysmal and there is lack of trained and qualified personnel. The chairperson of the commission recommended all postmortem exami-
nation in respect of deaths in police or jail custody to be video-filmed and the cassettes sent to the commission together with the written reports of postmortem examination. Delhi Declaration on torture (Courtesy Justice MR V.S.Malinath NHRC, 1999) The symposium was held in Delhi that noted with concern that torture continues to be prevalent in many countries. Wars and situations of armed conflicts within and between states have in recent years given rise to the gravest human rights violations including torture. Health professional in many countries still find themselves under duress to condone or cover up torture in violation of their codes of ethics and the UN principles of medical ethics. The symposium urged the action to be taken at national level and the action to be taken by United Nations against torture. Long Questions 1. How can you classify injuries? Discuss grievous hurt. How can you estimate the time of injuries? 2. Discuss the autopsy findings in a case of death due to torture. Short Questions 1. Torture 2. NHRC guidelines for custodial deaths 3. Grievous hurt. 4. Simple injury 5. Section 44 I.P.C. 6. Falanga 7. Thromboembolism.
Medicolegal Aspects of Injuries
333
MULTIPLE CHOICE QUESTIONS
1. All of the following are grievous injury except: A. Tooth fall B. Avulsion of nail C. Facial injury D. Emasculation 2. All are grievous hurts except: A. Dislocated shoulder B. Incised wound on abdominal wall without peritoneal injury C. Nasal bone fracture D. Permanent disfigurement of face 3. Which of the following is a grievous injury? A. Extensive lacerated wound on the forehead B. 6 cm x 4 cm laceration present on the scalp C. 6 cm x 2 cm bruise present on extensor aspect of forearm D. Abrasion present at the back of trunk 4. Which of the following is a Grievous injury? A. Simple fracture of radius B. Sharp injury of abdomen without penetration of peritoneum C. Bruises over arms and back due to lathi D. Lacerated wound over the thigh with exposure of muscles 5. Which of the following is grievous injury? A. Fall of tooth B. 7 day’s absence from work C. Clean incised wound on face D. Lacerated wound scalp 6. A person beaten up but having no fracture or dislocation and is hospitalised for 20 days is considered grievously injured: A. Even if there is no other injury B. If during the twenty days he is in severe body pain or unable to follow his ordinary pursuits C. If during the first ten days he is in severe body pain but later on could follow his ordinary pursuits
1 B 9 D
2 B 10 B
3 A 11 D
4 A 12 A
5 A
6 B
D. Even if has sharp injury over abdomen without penetration of peritoneum 7. Which of the following indicates that the wound in a hospitalized woman typist hit by ‘lathis’ admitted for 20 days was grievous? A. She is not able to recognize B. Wound does not heal completely C. Incised wound over scalp D. She is not able to do her daily routines 8. Grievous injury is: A. Disfiguration of face due to injury B. 14 days hospital stay C. 20 days hospital stay D. Permanent impairment of hearing 9. Which of the following is a grievous injury under IPC section 320? A. Emasculation B. Privation of joint C. Fracture of bones D. All of the above 10. The exact age of the abrasion can be assessed by: A. Histological method B. Histochemical method C. Naked eye examination D. None of the above 11. Which of the following is not a feature of antemortem wounds? A. Copious haemorrhage B. Marks of spouting of blood are present C. Deep staining of edges & cellular tissue D. Wound edges are closely approximated E. Leucocytic infiltration along the margin of the wound with edema of wound margins 12. One of the following is Not a delayed cause of death from injury: A. Tetanus B. Fat Embolism C. Thromboembolism D. Air Embolism
7 D
8 A
24
Part 1—Forensic Medicine and Pathology
Asphyxial Deaths GORDON’S CLASSIFICATION OF DEATH Gordon in 1944 postulated that vital functions of the body depend upon the availability and utilization of oxygen by the body tissues and tissue anoxia finally leads to cardiac failure and death. It is a classification that lays stress on the pathogenesis in different forms of death of medicolegal importance. It is brought about in following four ways: 1. Anoxic Anoxia: Defective oxygenation of the blood in the lungs • By obstruction to air passage—suffocation, smothering, overlaying • By obstruction to the passage of air down to the respiratory tract—drowning, chocking, throttling, hanging and strangulation • Excessive compression of the chest and abdominal wall • Primary cessation of respiratory movements causing respiratory failure—in narcotic poisoning, electrical injury • Inhalation of carbon dioxide and carbon monoxide gases 2. Anaemic anoxia: Reduced oxygen carrying capacity of the blood—acute poisoning due to CO, Chlorates, nitrites 3. Histotoxic Anoxia: Depression in the oxidative process in the tissues—Hydrocyanic Acid poisoning 4. Stagnant Anoxia: Insufficient circulation of the blood in the tissue—Traumatic shock, heat stroke, acute Irritant and corrosive poisoning.
The term asphyxia is commonly applied to a variety of conditions in which interference with respiratory exchange occurs to a greater or lesser degree. Many of these conditions vary so greatly in their physiological mechanisms and in their pathological appearances, they present that the use of the term is best avoided, whenever possible. It is usual to divide the effects of asphyxia in to a number of stages: 1. Stage of inspiratory dyspnoea with deep and forceful respiration, cyanosis lasting for a minute or so. 2. Stage of expiratory dyspnoea with spasmodic efforts at expiration. During this stage, the consciousness is lost, pupils are dilated and blood Pressure is raised. 3. There is fall of blood pressure, pulse is increased and spontaneous defecation occurs. The erection of penis and ejacul*tion of sem*n may occur. 4. Respiratory movements cease except for terminal irregular occasional respiration. Heart continues to beat for 10-15 minutes. MECHANICAL ASPHYXIA Mechanical asphyxia is a term applied to circ*mstances in which mechanical interferences to the respiration occurs that either a. Impedes access of air to lungs, or b. Reduces blood supply to head and neck or c. Causes sudden cardiac arrest due to stimulation of carotid sinus resulting vagal reflex mechanism
Asphyxial deaths It is doubtful if there are any constant post mortem changes produced by the direct effect of anoxia upon the tissues except the appearance of cyanosis. There are abnormal appearances of respiratory obstruction in the form of local effects of the constricting agent, raised intravascular pressure and terminal heart failure. Classical Signs of Asphyxia The classical signs of asphyxia are nonspecific and can occur in deaths from other causes. 1. Cyanosis (Greek ‘dark blue’): Significance of cyanosis in a cadaver must be evaluated very critically. Cyanosis depends upon the absolute quantity of oxyhaemoglobin and reduced Hemoglobin in red cells. The normal pink colour of well-oxygenated blood may change to purple or blue when oxygen is lacking. Cutaneous cyanosis depends upon absolute amount of reduced haemoglobin, rather than amount of reduced oxy-hemoglobin. There must be at least 5 gm% of reduced hemoglobin before cyanosis becomes evident, irrespective of total amount of hemoglobin. In constriction of neck, cyanosis almost invariably follows congestion of face, as venous blood contains much reduced Hemoglobin. After perfusion to head and trunk, it is directed back to tissues and becomes bluer as blood accumulates. When the airway becomes blocked, then impaired oxygenation in the lungs leads to a diminution in the oxygen content of tissues, which leads to darkening of organs and tissues and accentuates the cyanosis of face. This depends upon complete or substantial obstruction of the airway or restriction of respiratory excursions of the chest. If the body is examined within few hours of death, presence of intense cyanosis is of some significance. The loss of oxygen of cadaveric blood is very variable, but certainly, after 24 hours the appearance of cyanosis may be due entirely to postmortem changes. Absence of cyanosis within few hours of death does not necessarily signify that cyanosis was not present at death.
335
Terminal cyanosis is common in many forms of death and its presence is seldom of much use in the diagnosis of respiratory obstruction. 2. Congestion: Visceral congestion is due to capillo-venous congestion and is the result of susceptibility of capillaries to hypoxia. This results in dilatation of capillaries with stasis of blood in the dilated capillaries and the venules. Systemic and pulmonary congestion and dilatation of right side heart are signs of asphyxial death. Their significance will be treated with greater reserve than the presence of cyanosis. There is considerable redistribution of blood in the cadaver under the influence of gravity and to some extent by rigor mortis. The effect of these factors also depends upon the fluidity of blood after death. Right ventricular dilatation and pulmonary congestion are common to many forms of death, by no means specific for death from interference with respiration. Conversely, when death is due to blockade of airway, one may fail to find this phenomenon. Furthermore, the size of heart chambers can alter with rigor mortis and so the amount of blood in the pulmonary circulation. Congestion immediately above a mark on the neck may be of great significance in the diagnosis of the cause of the mark. The time and force of infliction of pressure on the neck but general observation on capillo-venous congestion is of little value 3. Fluidity of blood; At one time, it was thought that fluid blood in the cadaver was an indication of asphyxia. The presence of fibrinolytic enzymes in the cadaver has been established, so fluidity depends upon fibrinolysin and the amount of fibrinolysin depends upon the rapidity of death rather than the nature. 4. Pulmonary edema: Some degree of pulmonary edema is common but not invariable in deaths associated with anoxia. It is debatable whether it is due to heart failure or increased capillary permeability. It has little or no value in the diagnosis of death due to respiratory obstruc-
336
Textbook of Forensic Medicine and Toxicology
tion. It is common in many modes of death. In anoxial deaths edema of anything more than a minor degree indicates that death has not been very rapid. Lungs should be weighed properly to know the extent of edema. 5. Pulmonary hemorrhages: Large submucosal hemorrhages in pharynx especially over the dorsum of cricoid due to direct trauma of this part against anterior surface of spine. Submucous venous plexus at this site is made of very large thin walled vessels and rupture of these vessels due to severe venous congestion. These haemorrhages are also found in variety of deaths unconnected with trauma. 6. Petechial hemorrhages:In the year 1866, Tardieu a French police surgeon described it and found beneath the pleura and pericardium. He was of the opinion that these hemorrhages were the pathogenesis of mechanical asphyxia. Later on, these hemorrhages were known as Tardieu’s spots. Injuries to the walls of the epithelium may result in the development of petechial haemorrhages (Fig. 23.1). Until 1944, Lime and Gordon questioned their significance as they had found it in many forms of death. In 1953 Gordon, Trevor and Trice also found it in secondary shock and natural cases. In 1955,
Gordon and Mansfield questioned their ante mortem origin as they commonly developed after death and were found during autopsy. In 1955, Shapiro again opined that some of these are spontaneous post mortem artefacts and disappeared in a short period. This disappearance was confirmed and depicted in the year 1981 by Zaini and Knight who considered them to diminish when intravenous pressure is reduced in major pulmonary vessels at autopsy. They found that it was difficult to distinguish between true and false petechiae by naked eye examination. Only one third of these haemorrhages are true and two thirds are false. These false hemorrhages were due to intra pleural venous channels air blisters, thickened pleural plaques and dust pigments. They are mostly unrelated to mechanical asphyxia. Tardieu spots develop from: i. Increased venous stasis causing congestion leading to increased pressure causing rupture of the vessels. ii. Increased permeability due to hypoxia. Tardieu spots are usually pinhead, but vary in size and shape. They may be scanty detectable under low magnification or may be numerous like measles rash involving the skin of the face and eyelids, beneath the conjunctiva etc. These are most prominent in the visceral pleura and epicardium. Examination for evidence of injury and severity should be done. Stasis Haemorrhages: These hemorrhages may be seen beneath the mucosa of larynx in the subglottic space and above the level of constriction of the ligature as in homicidal strangulation. venous stasis occurs leading to rupture of the capillaries. Differential Diagnosis of Petechial Haemorrhages
Figure 23.1: Petechial hemorrhages over the heart
1. Coronary deaths 2. In terminal stages of asphyxia. 3. Diseases: The hemorrhages found in diseases are small with greater distribution and more in number. Blood may reveal the underlying cause but laboratory findings may be misleading.
Asphyxial deaths
337
Classification of Asphyxial Deaths
Sudden Cardiac Arrest
1. Hanging i. Mode of hanging • Judicial • Sexual (Autoerotic) • Lynching (Homicidal hanging). ii. Manner of hanging • Suicidal hanging • Homicidal hanging • Accidental hanging iii. Position of noose • • Typical hanging • Atypical hanging iv. Position of feet • Complete hanging • Partial hanging – Partial standing – Sitting – Reclining (Kneeling position). 2. Strangulation i. Ligature strangulation ii. Manual strangulation (throttling) iii. Mugging iv. Garroting v. Bansdola vi. Palmer strangulation vii. Bend of knee/ elbow viii. Foot strangulation. 3. Suffocation i. Smothering • Overlaying • Burking ii. Gagging iii. Choking iv. Café Coronary v. Traumatic Asphyxia 4. Drowning i. Dry drowning ii. Wet drowning iii. Secondary drowning iv. Immersion syndrome.
There are cases where these findings like petechial haemorrhages, cyanosis, congestion etc. are present but death is rapid and diagnosed as sudden cardiac arrest like that in café coronary. In Knight’s experience, 50% of his cases where death occurred from mechanical asphyxia, cause was sudden cardiac arrest, as the cyanosis, haemorrhages or congestions were absent. These cases were deaths resulting from karate blows to the neck, mugging and some cases of drowning. Sudden death might occur due to cardiac arrest, accurate history of the circ*mstances of the death is important. Sudden collapse and loss of consciousness is the outstanding feature. Heartbeat or breathing may continue for 15-30 sec and there might be atrial fibrillation. An important factor is evidence of surprise, emotion, apprehension or fright. Alcoholic intoxication is commonly there. If no injury or slight injury is present over the body, the diagnosis of acute cardiac arrest is made.
HANGING Hanging is a form of asphyxial death, which is caused by the suspension of the body by a ligature that encircles the neck, the constricting force being the weight of the body. Asphyxia in hanging is secondary to compression or constriction of the neck structures by a noose or other constricting band tightened by the weight of the body. There may be either complete or incomplete (partial) suspension of the body Types of Hanging Complete hanging: This is the type of hanging when the constricting force is the weight of the body as the body is fully suspended in air. Partial (Incomplete) hanging: In this type of hanging, the constricting force is the weight of the head (about 5-6 Kg) and the lower part of the body such as toes, feet, knees or buttocks touches the ground (Fig. 23.2).
338
Textbook of Forensic Medicine and Toxicology the deepest. Ecchymosis and slight abrasion in the groove are rare. Ecchymosis alone has no significance but it is important to establish whether it is antemortem or postmortem Abrasions with haemorrhage are strongly suggestive of suspension taking place during life. Position of ligature mark: In 80% cases, ligature mark is present above the thyroid cartilage, in 15% at the level and in 5% it is present below the thyroid cartilage (common in partial hanging). The width of the groove is about or slightly less than the width of the ligature material. A definite pattern may be seen but when fresh, the ligature mark is less clear. After drying it becomes well marked (Figs 23.3 to 23.4). There may not be any visible mark due to beard, long hair, clothes intervening between the ligature material and the neck. Loop of soft material, towel, and scarf may
Figure 23.2: Partial hanging
Virtually all hangings are suicidal and in India, it is quite popular method of suicide more common amongst males. Ligature Mark On the neck, it will be a furrow (ligature mark). This furrow, as a rule, does not completely encircle the neck, but slants upwards, towards the knot, fading out at the point of suspension that is the knot. If the knot is under the chin, the site of the knot may be indicated by an abrasion or indentation beneath the chin. The clarity and configuration of the ligature mark depends upon the material used. The ligature mark produces a groove or furrow, which may be pale, yellowish or yellow brown and look like parchment due to drying of the abraded skin. It is usually inverted V shaped with the apex of the V at the knot. Impression of the knot may be found, depending upon its position. Along the edges of the depression, a thin line of congestion or haemorrhage will be seen above and below the groove at some point, usually
Figure 23.3: A case of hanging with ligature material in situ
Figure 23.4: A case of hanging same as fig. 23.3 with ligature mark
Asphyxial deaths not produce a ligature mark. In partial hanging there may be little mark or not at all. Decomposition obliterates ligature mark. It may disappear after several hours when the loop is removed. On microscopical examination, in case of antemortem hanging signs of vital reaction are present in the neck structures. The absence of vital reaction however does not exclude an antemortem hanging. The appearance of the furrow over the neck varies with the following factors: 1. Type of Ligature Material: In hanging, a simple slipknot type of noose is typically used. The noose is constructed from anything that is handy. Most common are ropes, electrical cords, wires, strings, belts, dupatta, sari, and any piece of cloth or any other material that is available at that moment. Even in jails or prisons, the convict may use his own clothes to hang. Occasionally to prevent change of mind, the individual may tie his hands. The usual point of suspension is the side of the neck, followed by the back or front. At the time of suspension, the noose typically slips above the larynx, catching under the chin. A rope will give a deep, well-demarcated, distinct furrow, often with a mirror image impression of the weave of the rope on the skin. This furrow initially has a pale yellow parchment appearance, with a congested rim. With time, the furrow dries out and becomes dark brown. If the ligature material is a soft material, the ligature mark may be poorly defined, pale and devoid of bruises and abrasions. In some cases, the lower margin of the grove (ligature mark) is pale with upper margin red due to postmortem congestion of vessels. A soft broad cloth such as a towel, dhoti or lungi may show no ligature mark over the neck. In majority of suicidal hangings, the ligature consists of a single loop and mark. If the noose is a belt, it will produce two parallel ligature marks, as the upper and lower edges of the belt will dig
339
Figure 23.5: A case of hanging showing V-shaped, brownish, parchmentised like ligature mark
into the skin. Less commonly, ligature consists of two loops (Fig. 23.5). This results in two furrows which may be parallel, overlap at points or follow two completely different paths, for example, one oblique and other horizontal. The two loops may pinch the skin between them, producing a haemorrhagic strip of skin. If a soft noose is used and the body is brought down by cutting the ligature shortly after death, no marks of ligature may be present on the skin. The groove will be narrow, deep and distinct when a thin and hard ligature is used. The mark becomes more prominent when it has been suspended for long. When the ligature is broad such as dupatta, strip of cloth, sari, the furrow will be broad and shallow. 2. Point of suspension: Usually, the ligature mark is deepest opposite the point of suspension. In addition, rarely there may be scratch abrasions above and below the ligature when the victim tries to undo the noose during terminal stages. 3. Type of hanging: When the hanging is complete, the ligature mark is more prominent while in partial hanging it is less prominent. 4. Tightness of ligature: When the ligature is tightly present around the neck, the mark is.
340
Textbook of Forensic Medicine and Toxicology
5. Time of suspension: The longer the body remains suspended the deeper is the ligature mark. 6. Position of the knot: The main force to the neck is applied, opposite to the point of suspension. When the knot is present over the occipital region (Typical hanging) the front of the neck shows a prominent ligature mark. 7. Slipping of ligature may cause a double impression of a single turn of ligature material. 8. Knot: Usually a simple slipknot is made to produce a running noose fixed by granny or reef knot. At times simple loop is used. It is placed either on sides or over occiput, but rarely under chin. Knot is higher than the ligature. Removal of the noose is done by cutting the noose away from the knot and ends are tied with string/wire. In most hangings, the face is pale and tongue is protruding and is black due to drying except in partially suspended individuals where the noose is tightened only by the weight of the head or the torso. In these instances while venous drainage is completely occluded, the blood supply of the vertebral arteries continues, in part producing congestion of the face and petechiae. Blood will pool in the dependent areas of the body, usually the forearms, hands and legs secondary to gravity. With time punctate haemorrhages, Tardieu spots due to hydrostatic rupture of the vessels will be seen. Prior to the removal of the noose from the neck, it should be described in detail as to the nature and composition, width, mode of application, location and type of knot. After removal of the noose, the ligature mark on the neck should be described in detail. One should describe the location of ligature mark over the neck in relation to anatomical landmark direction of the furrow as obliquely upward or horizontal, continuous or interrupted, its colour and dimensions and whether there is distinct imprint of the pattern of the ligature over the neck.
Causes of Death Death in hanging is due to compression of the blood vessels of the neck such that insufficient amount of oxygenated blood reaches the brain. Obstruction of the airway can also occur and is due to either compression of the trachea or, when the noose is above the larynx, elevation and posterior displacement of the tongue and floor of the mouth. Blockage or compression of the air passages is not necessary to cause death in hanging. A number of individuals have hanged themselves with the noose above the larynx and a permanent tracheostomy opening below. . As only a small amount of pressure is sufficient to occlude carotid arteries, quite commonly one can hang oneself in sitting, kneeling or lying down position. The weight of the head (10-12 lb) against a noose is sufficient to occlude the carotid arteries and cause death. Fracture of the neck plays virtually no role in nonjudicial hangings. It is extremely rare and is usually seen only in individuals with advanced degenerative diseases of cervical spine such as osteoarthritis, accompanying complete suspension of the body, a sudden drop, and frequently obesity or very old age Causes of Immediate Death In hanging immediate death can be caused by the following mechanisms. 1. Asphyxia: Ligature forces the root of tongue against the post wall of pharynx, and folds the epiglottis over the entrance of Larynx to block the airway. A weight of 15 Kg (33 lb) is required to compress the trachea to cause asphyxia. 2. Venous congestion: Jugular venous cerebral circulation can be stopped with a pressure of 2 Kg (4.4 lb) on the neck 3. Cerebral anemia: Carotid arteries require a pressure of 4-5 Kg (11 lb) to stop the flow of blood in them while vertebral arteries require 30 Kg (66 lb) of pressure 4. Reflex vagal inhibition: Vagal sheath or carotid bodies when compressed can get stimulated
Asphyxial deaths
341
and cause vagal inhibition of the heart causing it to stop. 5. Fracture dislocation of cervical vertebral, leading to injury to the spinal cord, as a result there is ascending edema that affects the vital centers in the medulla. Causes of Delayed Death In hanging delayed death occur due to the following reasons: 1. Aspiration pneumonia 2. Infections 3. Hypoxic encephalopathy 4. Edema of lungs 5. Encephalitis 6. Cerebral abscess.
Salivary mark
Figure 23.7: A case of hanging showing tongue clenched between teeth and salivary stain over the chest
Autopsy Findings External General Findings: Typical asphyxial signs are present in about 50-60% of all hangings. 1 Neck may be stretched and elongated and rarely may be severed from the body if the weight of the body is too heavy and the fall is from a greater height. 2 Head is bent opposite to the knot. 3 Face is usually pale but at times it may be congested and swollen. Swelling disappears when the ligature is cut down. 4 Petechiae on the skin and conjunctiva are present. 5 Signs of Asphyxia are more marked when the noose is high up in the throat. If only veins are obstructed there is engorgement of head and neck. The eyes protruded and firm due to congestion or may be closed and the pupil is dilated. The tongue is swollen, coming out between the lips (Fig. 23.7). Tip may be black due to drying and may be clenched between the teeth. There is dribbling of saliva from the angle of mouth, which is an indicator of antemortem hanging. The salivary stain may dribble over to the face, neck and sometimes chest (Figs 23.7 and 23.8).It is caused due to the stimulation of salivary glands by the ligature.
Figure 23.8: Salivary stains over the chest in hanging
6. Slight hemorrhage or bloody froth is sometimes seen caused by the congestion in the lungs and the pulmonary edema. In the head sometimes hemorrhages are present due to rupture of engorged vessels. In the middle ear hemorrhages may be seen due to rupture of the small blood vessels. The penis may show sem*n drops coming out of the urethral meatus. 7 Lower limbs show hypostasis (Figs 23.9 and 23.10) due to the prolonged hanging posture and are an indicator of the duration of hanging
342
Textbook of Forensic Medicine and Toxicology carefully interpreted whether they are self-induced, occurred during convulsive phase preceding death, produced when body was brought down, during attempted resuscitation, when the swinging body contacted other objects or were produced by a second party in a homicide.
Figure 23.9: Hypostasis in lower limb in a case of hanging
Differential Diagnosis of Ligature Mark 1. Skin folds on the neck of Infants simulate a ligature mark, especially after refrigeration of the body has caused coagulation of the subcutaneous fat. 2. Swelling of the neck due to decomposition and jewellery of the neck or clothing causing the ligature mark. Internal Findings
Figure 23.10: A case of hanging showing hypostasis over the forearm and and lower limbs
and later on seen on the back when the body is laid down. In few cases the post mortem petechial hemorrhage may be seen in the lower limbs. These hemorrhages are differentiated from the tardieu’s spots, being larger in size and bilaterally symmetrical. They are due to rupture of capillaries in lower limbs due to pressure of accumulated blood. Local Findings 1 Ligature mark over the neck. 2. Usually, except for the ligature mark, no other injuries are present over the body. However, when other injuries are present they should be
The dissection of neck structures should be ruled by two considerations. (i) Need for an extensive exposure and (ii) Necessity of avoiding artefacts from seepage of blood from the neck veins. The dissection of neck structures should be done in situ in a relatively blood free field after the cranial cavity, chest and abdomen is opened and the organs removed. Schrader (1940) drew attention to artefacts and recommended that neck should be drained of blood by removing the brain and dissecting heart followed by the dissection of neck structures done in situ. On examination of internal structures of the neck in 83 consecutive cases prospectively by DiMaio, no injuries (Fig. 23.11) were seen in more than 50% of the cases. Absence of petechiae in most hangings is because there is complete obstruction of the arterial system, so there is no pooling of blood in the head, no increased pressure and thus no petechiae. A dried rivulet of saliva often runs from a corner of the mouth down the chest. Besides this, blood tinged fluid may be present in the nostrils. The fractures of the hyoid bone and thyroid cartilage are considered antemortem when there is blood at the fracture site. Tissues under the mark are dry, white and glistening. Ecchymosis may be seen in the muscles. Neck muscles, the sterno-mastoid and
Asphyxial deaths
Figure 23.11: Neck structure
platysma are ruptured in about 10-15% cases if considerable violence is involved during hanging. Carotid Artery may show transverse tear in the intima. In long drop tears may be seen at different places. Vertebral artery may show rupture at place. Hyoid bone is fractured in 15-20% cases but it is rare below the age of 40 years due to elasticity of cartilage and the mobility of joints. It is more common above 40 years and usually found at the greater horn and junction of inner 2/3 and outer 1/3. Thyroid cartilage is fractured in about 40-45 % of the cases. Superior horn is fractured or the thyrohyoid ligament is torn. Visual inspection of the trachea reveals petechial haemorrhages over the epiglottis, trachea and larynx. Abdominal organs are congested and in the brain sub arachnoid effusions are commonly seen. Diagnosis of Antemortem Hanging 1. Presence of antemortem ligature mark with vital reaction. 2. Saliva dribbling mark from the angle of mouth. 3. Ecchymosis of larynx or epiglottis. 4. Extent of fracture of thyroid cartilage and hyoid bone. 5. Rupture of intima of carotid vessels. Medico Legal Aspects Hanging is most commonly suicidal but can be at times be accidental like in cases of sexual
343
asphyxias. Homicidal hanging is a very rare and is seen mostly in cases where the victim has been incapacitated by earlier assault or due to intoxication with alcohol etc. Judicial Hanging: Judicial hanging is the term used when convicted criminals are hanged. The person’s face is covered with a dark mask and he is made to stand over trapdoors that open downwards. The noose is put around the neck with the knot placed on the left side of the jaw, close to chin. A trapdoor is sprung and the prisoner falls a specific distance determined by his weight. The platform is at a height allowing for a fall of about 5 meters. If he falls an insufficient distance, he strangles rather than break his neck and if he falls too far he is decapitated. As the person falls there is a sudden jerk to the neck causing fracture dislocation at the 2nd to 3rd cervical vertebral level or sometimes at the atlanto occipital or atlantoaxial joint with transaction of the cord. In properly performed judicial hangings, the victim abruptly stops at the end of his fall when his head is jerked suddenly and violently backward, fracturing his spine. The neck is considerably lengthened and may be severed in some cases and the neck vessels are torn transversely. There is immediate unconsciousness leading to death though the heart may continue to bet for 8-20 minutes. In addition, there are muscular contractions of the facial muscles, twitching and convulsions of the limb and trunk, and violent respiratory movement of the chest. X-rays show bilateral fractures of either the pedicles or laminae of the arch of the 2nd, 3rd, or 4th cervical vertebra with dislocation of the 2nd or 3rd or 3rd or 4th cervical vertebra. Suicidal Hanging: Suicide is the most common mode of hanging. The person finds it as one of the easiest and surest methods of death. Hanging is known as painless mode of death. The person hangs himself with any long ligature material available that is tied to a ceiling fan, roof, window etc. There may be a fixed loop or a knot. Usually a suicide note may be found at the scene (Fig. 23.12) . The individual usually hangs himself in an isolated area and when hanged in his house, the room in such cases is bolted from inside.
344
Textbook of Forensic Medicine and Toxicology
Figure 23.12: Suicidal note in a case of hanging
Homicidal Hanging: Homicidal hanging is extremely rare. It can be a possibility in cases where the victim is a child, an unconscious person or a very frail person unable to defend himself. It would virtually be impossible for one of two healthy males, equally matched physically, to hang the other unless the victim was beaten unconscious or rendered helpless by alcohol or drugs. In the first instance, one would suspect homicide by virtue of the injuries on the victim. In the second scenario, or if the victim was rapidly subdued by two or more stronger assailants, there might not be any other marks on the body but for the noose mark or possible contusions of the arm inflicted while being forcibly restrained by the assailants. If there were also a marked disproportion in strength between the assailant and the victim such as an adult and a child, it would also be possible to hang the victim without any marks of violence. In addition, an individual might be first strangled with ligature and then hanged. In this case, the ligature mark over the neck would not have classic inverted V configuration of hanging. Although there are cases on record of suicidal hangings involving incomplete suspension, where the noose mark overlaid the larynx and was horizontal, not sweeping upward to the point of suspension in an inverted V configuration. To rule out any violence that might not be visible and to make sure that the individual was not drugged, in all alleged suicidal hangings, a complete toxicological screen
should be performed. If there are signs of violence then it may be homicidal in nature. Circ*mstantial evidence is of value in these cases. When an unruly mob hangs a person in public, it is called lynching. Accidental Hanging: Accidental hangings usually involve children who are playing while simulating judicial hanging get entangled in a rope. Boys playing in gardens while jumping from trees get their clothing caught in the branches and are accidentally hanged. Adults engaging in the practice of sexual asphyxia may be accidentally hanged. In addition, women may get their dupatta entangled in the cycle rickshaw and it may tighten around the neck sufficient to cause hanging. The chin may be suspended from the steering wheel of a vehicle. In cases of a fall from a staircase, a person may get his neck caught in the railing and hang. An intoxicated person may accidentally hang himself from the arm of a chair. Rarely an infant accidentally hang himself from a pacifier placed around his neck on a cord or are entangled in a toy placed above his crib. Crime Scene Examination Examination of the scene of crime is very important and has to be done carefully. The body should not be cut down so that proper photographic documentation can be made. The important points, which must be observed, include the posture of the body, any signs of violence in the area like disturbance of furniture etc. the noose should never be cut from the body but left intact for transport with the body to the morgue. The ligature material has to be examined carefully for the texture and the knot etc. When the noose is removed from the neck, the knot should not be untied. The noose should either be slipped off the head or cut opposite to the knot with the cut ends secure with the tape or string. The height from which the body is suspended should be measured and the platform that was possibly used by the victim must be noted. Sometimes when the ligature is broken, the body may be found lying on the ground. In such cases, the part of the noose around the neck should be properly secured and the other part that
Asphyxial deaths is left attached to the ceiling fan, hook or rod of window or doorknob should be removed and compared with the part around the neck. Critical Evaluation 1. At times when the person is attempting suicide and the first attempt fails he may fall down and sustain injury. The victim then tries a second attempt with another rope at another place and may be found with bleeding and injuries. The scene may also be disturbed in such cases with blood present at places. The injuries on the body of the person may be misinterpreted as struggle marks. Careful evaluation of the crime scene is required in such cases to arrive at a conclusion. 2. When a person hangs with a rope then it leaves its groove marks on the hook or beam, which is used to tie the rope. The groove mark has to be carefully observed for the pattern of the cord on it and must be matched with the width of the cord. If some clothing or hair comes in between, then the mark may not be visible. 3. Dead persons can show grooves on the neck which can be confused with hanging grooves. Such marks are caused by clothing like tight collar or a tight necklace etc. These marks disappear after decomposition while a ligature mark does not decompose as easily as there is little blood in the skin underneath leading to much reduced bacterial growth. 4. Murder by hanging is very rare and is usually possible in children, unconscious persons and those who are unable to defend themselves. 5. Persons who have committed suicide by hanging may show other injuries which in themselves could be fatal. 6. When the body is hanging free but there is no jumping point in the vicinity such as chair, table, step etc., there is every reason to suspect murder. In such cases scene must be examined for marks of climbing over trees and development of postmortem staining over the lower limbs. If staining is present on the back of a freely hanging body it signifies that person
345
has been killed first and then hanged. Wrinkles on the clothes may indicate that limbs were previously bent. 7. Presence of material evidence on the clothes such as leaves, twigs of plants, soil, dust that is not present at the scene of hanging must be noted. In addition the observations such as presence of blood, urine and saliva flowing in the wrong direction should arouse suspicion of crime. If the knots and noose present around the neck are such that it is not possible for the individual to make them should raise suspicion of crime. 8. In a right-handed person, knot is usually on the right side and any reversal should raise suspicion of homicide. 9. Autopsy rarely reveals whether the hanging is suicidal or homicidal. It is the duty of the Police Officer to correlate the course of events. SEXUAL ASPHYXIA (AUTOEROTIC ASPHYXIA) Sexual asphyxias are asphyxial deaths principally due to hanging in which the asphyxia is intentionally induced to enhance sexual arousal produced by masturbation. These individuals use transitory anoxia produced by the noose to intensify the sexual gratification produced by masturbation and the impaired circulation leads to impaired consciousness. The impaired consciousness causes hallucinations and feeling of erotic rapture. Degree of asphyxia is controlled by mechanical means and a failure of the mechanism accidentally may cause death. Such deaths are rare and the victim is virtually always male with a hom*osexual tendency in them. Abnormal sexual behaviour like masochism, transvestism may also be present. For hanging, the victim commonly uses a pad between ligature and neck. The weight of the body is used as control. The noose can be tightened by extending arms or legs, and then can be relaxed by flexing the limbs. Death may occur accidentally by a failure of the mechanism of neck constriction. The scene is usually the victim’s own house, and his bedroom or attic etc.
346
Textbook of Forensic Medicine and Toxicology
On examination of scene it is of incomplete hanging with his feet on the ground so that he can relieve pressure of the noose just by standing a little straighter. A stool or chair is found near hanging victim at the scene. the pattern of behaviour is repetitive and there are evidence of previous episodes such as old scars in the neck. The person is usually naked or partly naked. One of the partners to simulate a female body does padding of breasts. In addition, they like to wear female undergarments sometimes. At the scene, there may be erotic or p*rnographic photographs, literature, articles of female clothing, a mirror opposite the individual so he can observe his actions. can be found around the scene. Evidence of recent ejacul*tion must be looked for in the form of seminal stains. Sexual gratification may be obtained by electrical stimulation using a low voltage, to stimulate the genitalia. Addicts usually use plastic bags to inhale anaesthetics or narcotic vapours as an aid to intoxication. However, in the autoerotic practices, the victims use plastic bags to cover the head that induces partial anoxia accentuating sexual sensations. As a result, sometimes the victims may loose unconsciousness and die. Some individuals in order to obtain sexual gratification do inhalation of carbon tetra chloride, bichloro-ethane and other petroleum products (glue sniffing). To summarize, the scene in such a case should be examined for: 1. Evidence of abnormal sexual behaviour 2. Evidence of previous attempt 3. Evidence of padding between the ligature and the neck 4. No evidence of suicidal act such as absence of suicidal note etc STRANGULATION It is a form of asphyxia, which is caused by constriction of neck by a ligature without suspending the body. It is mainly of two types (i) Ligature strangulation and (ii) Manual strangulation. Nevertheless, the following types may also be encountered.
Classification 1. 2. 3. 4. 5. 6. 7.
Ligature Strangulation Throttling or manual strangulation Mugging Garroting Bansodala Palmar Strangulation Foot strangulation.
Medicolegal Aspects 1. Whether death is due to strangulation? This can be asertained from the general features of asphyxia mainly on the head and neck that are strongly presumptive of strangulation deaths., the ligature mark around the neck, internal findings in the neck, circ*mstantial evidence. The manner of death can be: Homicidal: It is a common form of murder and is seen in adult women usually combined with sexual acts. Single turn of ligature with one or more knots, at the front or sides of neck is usually found. If two or more knots are present with each turn of ligature then homicide is almost certain. Abrasions are usually seen due to movement of the ligature in the neck during struggle by the victim. Evidence of struggle may be absent in cases like that of weak and frail individuals especially children or when the victim is attacked suddenly or made unconscious earlier by trauma or drugs. Strangulation should be taken as homicidal unless otherwise proved. The observations which can prove to be of value in establishing the nature of the injury include ownership of ligature and the possession of the ligature material with the suspected person. Unusual ligatures may indicate a particular occupation of the assailant. Looseness of the ligature or missing ligature is a near definite sign of homicidal strangulation. If the mark does not correspond with the ligature material recovered, it is also indicative of homicidal strangulation. Circ*mstantial evidence is of value in deciding doubtful cases.
Asphyxial deaths Accidental: Children may accidentally get entangled in ropes during play. An infant may be strangled with a string attached to a log-tied to the crib. Intoxicated persons may get accidentally strangulated by their necktie, scarf or collar etc. In industry, belts, ropes and parts of clothing may be caught in rollers or parts of moving machinery and cause strangulation. Umbilical cord inside the uterus may also accidentally strangulate the foetus. Suicidal: various methods for tightening the ligature are employed by the victims. Number of knots, tightness, method of knotting should be considered. The ligature material can be used like a tourniquet by the victim. A person can have one or two knots before consciousness is lost. Some arrangement is always made to keep the ligature tight. A cord may be tied around and twisted by stick working as a lever. When consciousness is lost, the grip is released, but ligature will not become loose, as it gets arrested against the shoulder or chin. When a running noose is applied to neck, a weight is attached to the free end of the rope at the end of the bed on which the patient is lying. Signs of venous congestion are very well marked above the ligature and very prominent at the root of the tongue due to slow tightening of ligature and no draining of postmortem blood. Injuries are less marked on the body of the person as less force is used. No signs of struggle are seen. Ligature is found in situ. Application of ligature with several turns whether closed with half knot or complete knot is consistent with suicide. Single turn of a broad ligature of rough cloth, closed with a half knot also indicates suicide. Opinion is given based on the ligature material recovered, the way it was tightened, no marks of violence on the body and the surrounding environment. Pseudo Strangulation In persons having short neck, depression mark similar to ligature mark is produced after death
347
due to the fold of skin. Even in infants and children with short neck, similar marks are produced after death called Pseudo Ligature marks. LIGATURE STRANGULATION In ligature strangulation, the pressure on the neck is applied by a constricting band that is tightened by a force other than the body weight. This is the type of strangulation in which a ligature material is used to compress the neck and the assailant applies the constricting force without suspending the body. Usually a U shaped ligature is pulled around the neck from behind though multiple turns of the ligature material are often used. Virtually all cases of ligature strangulation are homicides, suicides and accidents are rare. Females are predominantly involved. Ligature Mark The ligature used in ligature strangulation may range from electrical cords, ropes, telephone cords, sheets and neckties. The appearance of the ligature depends on the nature of ligature, amount of resistance offered by the victim and the amount of force used by the assailants. When the ligature used is soft material, the ligature mark may be faint, barely visible or even absent in children or incapacitated adults. When a very thin in ligature is used, the mark appears as deep mark and encircling the neck. Facial Findings The face and neck above the ligature mark are markedly congested with confluent petechial haemorrhages in the sclera and conjunctivae. Fine petechial haemorrhages over the face especially in periorbital area are seen. The findings of congested face, congestion, petechiae and haemorrhages in the sclera (Figs 23.13 and 23.14) in ligature strangulation are due to the fact that unlike hanging there is no complete occlusion of the neck vessels. The blood continues to enter the head from vertical arteries. This results in increase intravascular pressure, congestion and rupture of vessel.
348
Textbook of Forensic Medicine and Toxicology moderate then it may cause only the compression of the veins leading to venous congestion. Vagal nerves can get stimulated and cause depression of the heart to cause death. Fracture dislocation of the cervical vertebrae is a very rare finding but may happen in case of thin and frail person who is attacked by a very strong assailant. Postmortem Appearances External findings: the ligature mark is usually a well-defined depressed mark present at the middle or lower part of the neck (Figs 23.15 and 23.16). The mark may encircle the neck fully but is most prominent at the front and the sides of the neck. It is usually transverse but may be oblique if the
Figure 23.13: Congestion of sclera in a case of petechiae in a case of manual strangulation
Figure 23.15: Ligature mark over the neck in a case of strangulation Figure 23.14: Subconjunctival haemorrhage in a case of ligature strangulation
Causes of Death Death in these cases is due to asphyxia, cerebral anoxia, vagal inhibition and fracture dislocation of cervical vertebrae. By far the most common cause is asphyxia caused due to elevation of the larynx and tongue, which closes the airway at the pharyngeal level. If extreme pressure is applied by the assailant then the trachea or the larynx itself may be blocked and cause asphyxia. Cerebral anoxia is caused by compression of the blood vessels in the neck and if the pressure is
Figure 23.16: Ligature mark in in a case of ligature strangulation
Asphyxial deaths victim has been dragged by the assailant for some distance. Internal findings: Hemorrhages are found in the muscles and soft tissues underneath the ligature mark. If severe force is used carotid artery tear may be present. Fracture of Hyoid bone and thyroid cartilage may be seen. Hyoid fracture is seen in inward compression fracture, which can be bilateral while outward compression such as in hanging gives rise to antero-posterior compression fracture of the greater horn at the junction with the body. Avulsion fracture may be seen in due to muscular over activity without there being direct injury to the hyoid bone. Called traction ‘Tug’ fractures. The differences in findings between hanging and ligature strangulation are enumerated in Table 23.1. MANUAL STRANGULATION (THROTTLING) It is asphyxia produced by compression of the neck. The mechanism of death is occlusion of
the blood vessels supplying blood to the brain. Occlusion of airway probably plays a minor role in causing death. Virtually all manual strangulations are homicide. Suicidal Throttling: Suicide by throttling is impossible as when the pressure by the victim’s own hands is sustained for a sufficient time to cause unconsciousness, the hands relax and the victim recovers. Accidental Throttling: The application of one or both the hands to another person’s throat can cause sudden death from vagal inhibition. This may occur in unintentional circ*mstances brought on by touching, grasping and demonstration of affection such as during intercourse, or during physiological experiments. This is theoretically possible but highly improbable and suspicious. The mechanism of death in this case would be an arrythmia produced by stimulation of the carotid sinuses. The carotid sinus is a focal area of enlargement of the common carotid artery at the point it bifurcates in to the external and internal
Table Difference in findings in hanging and strangulation Features Ligature mark: i. Shape ii. complete or incomplete iii. Level of thyroid iv. Base Abrasions and ecchymoses at the edge of ligature Bruising of neck muscles Subcutaneous tissue Hyoid bone fracture Carotid Artery damage Thyroid cartilage fracture Fracture of larynx & Trachea Facial congestion and petechiae Protrusion of tongue Asphyxial signs Bleeding from nose, mouth & ear Salivary stains Neck Lungs Subpleural hemorrhage sem*n discharge Bullous lesions of lungs
349
Hanging
Strangulation
• Oblique -Incomplete -Above or over thyroid -Hard, pale and parchment like Uncommon
-Transverse -Complete -Below -Soft and reddish Quite common
Not very common White, hard, glistening Very common May be seen Rare Rare Pale Less common Less marked Less common Present Stretched or elongated No bulking Less common Common Not present
Very common Ecchymosed under the mark Less common Rare Common May be found Marked with petechiae More common More marked More common Absent Not stretched or elongated Congested and oedematous More common Not very common Present
350
Textbook of Forensic Medicine and Toxicology
carotid arteries. The compression or stimulation of the carotid sinuses causes an increase in blood pressure in these sinuses with resultant bradycardia, vasodilation and hypotension. Pressure on the common carotid artery below the sinuses reduces blood pressure within the sinuses by reducing the amount of blood flowing into it. This mimics hypotension or decreased blood supply from haemorrhage and shock causing tachycardia, vasoconstriction and hypertension. This explains the fact that why in some cases of throttling if the hands are lower down over the neck there is tachycardia, vasoconstriction and rise in blood pressure Homicidal Throttling: Death resulting from asphyxia consequent upon manual strangulation raises the suspicion of homicide. This method is employed when the victim is an infant, a child, or woman. Healthy adults can be throttled only when they are under the influence of drugs or other intoxicants, are stunned or the attack is sudden. Throttling is a common method of infanticide. Postmortem Findings External Findings The situation and extent of bruise on the neck will depend upon the relative positions of the assailant and victim, manner of grasping the neck and degree of pressure. Bruises are produced by tips and pads of fingers, are oval or round and of the size of digits (1.5-2 cm). The size may be altered due to bleeding underneath the skin. The grip can be produced by right hand with thumb on right side of neck and fingers on left side and vice versa. Finger marks may be present obliquely, separately or clustered together (Fig. 23.17). Both hands are commonly used with the thumb of one hand and finger of other hand present over both sides. Strangulation is easier for assailants with big hands on victims with small necks. Signs of struggle or bruises may be found anywhere, not definite to say whether the attack was from behind or from the front. Bruises may go for the usual colour change. When fingertips are deeply pressed, nails produce crescentic marks on the skin. During grip
Figure 23.17: External findings on neck in manual strangulation
thumb exerts more pressure than the other fingers. Two types of abrasions may be seen. When nails skid down the skin parallel, linear lines for several centimeters may be seen. In other cases regularly curved, comma like, disk like or straight 1.5 cm in length and few mm width. Many scratches are produced by the victim while trying to pull away from the assailant’s hand. As most victims are females, usually having long nails, scratches are more severe than those of assailants. Parallel lines in vertical direction are seen in such cases. The nail marks are more marked when the skin is dry. Internal Findings 1. Hemorrhages are found in the muscles underneath the ligature mark (Fig. 23.18). Carotid artery tear may be present. 2. Fracture of Hyoid bone is very common especially in the elderly. Thyroid cartilage may also be fractured in many cases. Hyoid fracture is seen in inward compression fracture, which can be bilateral 3. If death was due to throttling then suicidal mode of death is not possible. Homicidal or accidental possibility has to be ruled out. Sudden application of one or both hands on the other person’s throat out to affection can also cause death.
Asphyxial deaths
Figure 23.18: Internal findings in neck in manual strangulation
BANSODOLA Strong bamboo or stick is put in front of neck and another one at the back of neck. Both ends are tied and squeezed, from front of chest and back to cause death. It interferes with respiration, and causes fracture of ribs etc. GARROTING In this the victim is attacked from behind without warning, the throat may either be grasped by hand or a ligature which is quickly tightened, by twisting it, with a lever causing sudden onset of consciousness and collapse leading to death. In one of the refined methods of garroting, a spike was used behind a clamp, which penetrated the spine and caused the death of the person. It was a mode of execution in Spain and Turkey. MUGGING Strangulation is caused by holding the neck of the victim in the bend of the elbow. Pressure is exerted either on the front of larynx or at the sides of neck by forearm or arm. Marks in the neck may be minimal in such cases. Fractures of hyoid bone Various types of fractures of hyoid bone may be seen in asphyxial deaths such as
351
1. Inward compression fracture in which the greater horns of hyoid are compressed inwards causing fracture of the bone with tear of its periosteum on the outer side and not on inner side displacing the posterior fragment inwards. It is seen in manual strangulation. This type of fracture can occur on both the sides. 2. Outward compression (antero-posterior compression) fracture in which hyoid bone is driven backwards, when divergence of greater horns is increased, causing fracture with outward displacement of posterior small fragment. As a result, the periosteum on inner side of fracture only is torn when the fragment can be easily moved outwards but inner movement is limited to normal position only. Either this type of fracture can occur in the greater horn at its junction with the body or it may be bilateral. This type of fracture is seen in hanging and ligature strangulation. 3. Avulsion fracture that occurs due to muscular over activity without there being direct injury to the hyoid bone. This type of fracture is also called traction ‘tug’ fracture. This occurs as a result of traction on thyro-hyoid ligament either by downward or lateral movement of the thyroid cartilage from antero-posterior or lateral compression or when direct pressure is exerted between the hyoid and thyroid by the pressing fingers.
SUFFOCATION The term suffocation is usually regarded as synonymous with asphyxia. However, the term is restricted to a group of circ*mstances except drowning in which asphyxia produced by causes other than constriction of the neck by a ligature, hands, or a stranglehold. This includes closing the external respiratory orifices either by hand or by other means or blocking up the cavities of nose and mouth by introduction of a foreign substance, mud, paper clothes etc. The following types of suffocation is usually seen: 1. Smothering 2. Overlying
352
Textbook of Forensic Medicine and Toxicology
3. Burking 4. Choking 5. Gagging 6. Traumatic Asphyxia 7. Suffocation due to irrespirable gases. In all these forms of suffocation, the asphyxial symptoms and signs are severe since death is usually the result of slow asphyxia, often taking 2-5 minutes to kill. Usually the external signs of asphyxia such as cyanosis of the face and petechial haemorrhages of the facial skin, conjunctiva is common. However, there may not be any external injury at all. Alternatively, these injuries may be slight and can escape the eyes of the most experienced examiner.
even assailants hand that is gently applied. 2. There are scratch abrasions, finger nail marks, laceration of soft parts of victim’s face (Fig. 23.19). 3. There may be bruising and laceration of lips, gums and tongue (Fig. 23.20). 4. Pressure marks on the face can rarely be distinguished from postmortem postural changes, where circumoral and circumnasal pallor is caused merely by passive pressure of the dependent head after death, preventing the gravitational hypostasis from entering these areas. Even when the head is found supine,
SMOTHERING Smothering refers to the death resulting from mechanical occlusion of the mouth and nose that prevents breathing. The smothering agent is usually a fabric, an impervious sheet or a hand, though occasionally a mobile solid such as sand, mud, grain or flour may be responsible for blocking the air-passages. In smothering, death may occur either by the occluding substance pressing down upon the facial orifices, or by the passive weight of the head pressing the nose and mouth into the occlusion. Deliberate homicide is seen usually in the old, the debilitated and in infants. It is extremely difficult to prove homicide from the objective findings. The smothering of babies whether intentional or accidental is not so rare in India compared to western world. However, in these cases, the findings are not significant as the classical signs of asphyxia such as congestion, cyanosis and facial and conjunctival petechiae are not commonly present. Since intrathoracic petechial haemorrhages are common in sudden infant death syndrome, these cannot be accepted in isolation as evidence of suffocation.
Figure 23.19: Contused abrasions in and around the lips in a new born in case of smothering
External Findings 1. No external signs are there when the obstruction is by some soft material such as bedclothing, pillow, cushion, mother’s breast or
Figure 23.20: Contused laceration over the inner sides of lips in a case of smothering
Asphyxial deaths variation in colour is still common on the face, with contrasting white and pink patches, which usually change as the postmortem interval lengthens. 5. Unless there are bruises or abrasions on the cheeks, around the mouth, lips or lesions within the lips or mouth, it is dangerous to over interpret mere colour variations from alterations for blood in the facial capillary bed, which is usually a postmortem phenomenon. Medicolegal Aspects Suicidal smothering: This can occur in mental patients or prisoners. Suicide is practicable merely by burying the face in a flock mattress or even it would appear by lying against the bed clothing to obstruct the nose and mouth, especially when drunk. The death by cutthroat may occasionally terminate by smothering. If the trachea is completely severed, the lower end is likely to be drawn down within the thorax by the weight of the heart and lungs; if the soft parts then close over the wound, they can obstruct the trachea and the victim is smothered. Accidental smothering: The circ*mstances of accidental smothering vary according to the age of the victim. The bedclothes covering the nostrils and mouth of the infant infants during first month of life especially premature. Suffocation of the infant is also possible when it turns on its face in its cot and buries his face in a soft pillow or mattress. Accidental smothering in children and young adults may be predisposed to by an epileptic fit. Another variety of accidental smothering likely to involve children in an airtight place or one in which ventilation is negligible such as disused refrigerator. Accidental smothering of adults by precipitation into a quantity of finely divided, solid materials such as flour, sand, coal-dust, cinders, grain or feathers may occur in the course of their occupation. Besides, smothering may occur subject to epileptic or epileptiform fits. Accidental smothering may occur outdoors when the victim, in the course of an epileptic fit or under the influence of drinks or drugs, falls face down into mud, snow or thick grass.
353
Homicidal smothering: homicide of an adult by smothering is possible when there is a gross disparity between the assailant and the victim or else when the victim is helpless by virtue of his age, ill health or incapacity from drink or drugs or when stunned by a blow. It is a common mode of infanticide. Usually infant’s mouth and nostrils are closed by means of hand, or even a plaster. Usually the assailant uses far more force than is necessary to kill and consequently finger-marks in the form of scratches and bruises are found over the victim’s face. CHOKING It is a form of asphyxia caused by an obstruction within the air passage. It is almost always accidental and is usually due to inhalation of a foreign body, but it can be caused by the inhalation of the products of disease or by anatomical changes due to disease. The usual mechanism of asphyxia in choking is simple mechanical obstruction. However, occasionally the entry of foreign material may cause sudden death from vagal inhibition (Café-coronary). Causes of Choking 1. Inhalation of foreign body into the glottis such as bolus of meat, potato, button, coins, marbles, corns, fish, screws, pins or artificial dentures. 2. Inhalation of vomited material in an unconscious, when intoxicated, during anaesthesia or epileptic fits. 3. Belching out of milk by infants and young children may be aspirated into the air passages 4. Inhalation of products of disease or violence such as blood or pus while haemoptysis in Tuberculosis, rupture of an aortic aneurysm in air passages, or due to flooding of air passages with pus and necrotic debris in a lung abscess. 5. Anatomical changes due to disease such as a bronchial growth, laryngeal oedema and tumours, pharyngeal abscess, angioneurotic oedema.
354
Textbook of Forensic Medicine and Toxicology
6. In conditions such as poliomyelitis or bulbar palsy, accidental inhalation of food occurs due to disturbance in swallowing mechanism. Mechanism The usual mechanism of asphyxia in choking is mechanical obstruction but the entry of foreign body may cause sudden death from vagal inhibition. Causes of Death 1. Asphyxia is most common 2. Vagal inhibition: There are cases where the immediate result of choking is vagal inhibition and sudden death. The diagnosis is difficult due to absence of overt signs especially in an infant with small quantity of foreign material in the respiratory passages. The diagnosis is simple when a massive foreign body causes the obstruction but even when the foreign body is small, yet the cause of death seems to be vagal inhibition. Sudden death can occur when there is flooding of postnasal space with regurgitated food or even when minute particles are exposed to the vocal cords. The surgical procedures on larynx with light anaesthesia may cause sudden death from vagal inhibition. 3. Laryngeal spasm: This occurs due to entry of an irritating foreign material in the air passages. This is likely if acid gastric juice alone suddenly enters the air passages. Medicolegal Aspects Death by choking is commonly an accident but occasionally it may be homicidal. Accidental Choking It is very common and is seen in very, young, elderly, psychiatric patients when the ability to chew or shallow is impaired. It may commonly occur during a meal when food is accidentally inhaled while the person is laughing or crying or even when someone unexpectedly slaps the person of the back.
Suicidal Choking Suicide by choking is quite rare but may be seen in mentally ill patients or prisoners who do not have access to other methods of committing suicide. Homicidal Choking Choking is an uncommon and rare mode of committing homicide. However, the literature suggests that cases are on record where murders have been committed by choking the victim. Choking due to regurgitation of food may occur during rape or violent sexual intercourse. Autopsy Findings 1. Presence of impacted foreign body in the air passages. 2. Regurgitated food particles such as vomitus, milk etc may be found mixed with mucus in trachea, bronchi and lower bronchioles. 3. All organs are congested. CAFÉ-CORONARY A condition where a healthy and grossly intoxicated person, suddenly turns blue, coughs violently, then collapses and dies. Death appears to be due to sudden heart attack. However, at autopsy one may find some food material or piece of meat obstructing the larynx. Clinical signs of choking are absent, as there is a high blood alcohol content, which anaesthetizes the gag reflex. As the person vomits, the vomited matter may be inhaled leading to choking. Infants often regurgitate clotted milk after a meal in to larynx and children may often place coins, small stone in the larynx. Rubber balloons may also be accidentally ingested by children. And may get stuck in the pharynx or glottis. Suffocation may be caused by some diseases like diphtheria, Infectious mononucleosis, Haemoptysis in pulmonary tuberculosis. Larynx and bronchial growths may cause hemorrhage in to trachea
Asphyxial deaths Insect bites and drug reaction Larynx edema leading to death Blow to the front of the neck may cause swelling of the mucosa, edema, haemorrhage and death may occur due to reflex vagal inhibition. TRAUMATIC (CRUSH) ASPHYXIA This is the name given to those kinds of asphyxia, which are caused due to mechanical fixation of the chest so that normal movements of chest wall are prevented. This occurs when a large weight falls onto or presses down on an individual’s chest or upper abdomen. The most common form of traumatic asphyxia encountered is while repairing a car the jack slips and the vehicles falls on top of the individual. Great force is necessary to compress the chest and so this type of asphyxia is seen in cases like multiple deaths during stampede (chest is compressed and respiratory movements prevented by stampeding people piling on the top of each other—Riot crush or ‘human pile’ deaths), hotel fire, and lane crowd in an enclosed place, building collapse and in coalmines. Traumatic asphyxia is usually accidental in manner. Postmortem Findings There is deep red or purplish black discolouration of the skin of head, neck and upper trunk with numerous petechiae and ecchymoses in these areas, petechiae of the sclera, conjunctiva and periorbital skin and retinal haemorrhages. There is intense cyanosis of deep purple or purple-red colour cyanosis above the level of compression usually to the level of third rib. Haemorrhage is seen in the tissues around the site of compression whereas below the level of compression, skin is pale and mild cyanosis may be seen. Areas of pallor are seen at the level of collar of the shirt, folds or creases of garments. Internally, there is often no evidence of trauma in spite of the heavy weight on the chest. In addition, fracture of ribs may be present. If the patient recovers, the purple colour gradually disappears in 10-14 days without the usual colour changes. Individuals who survive
355
an episode of traumatic asphyxia usually make an uneventful recovery, though occasionally there is some permanent visual impairment due to retinal haemorrhage. Due to compression of chest, retrograde displacement of blood from superior vena cava into subclavian veins and veins of head and neck occurs leading to the cyanosis and congestion. Valves in the subclavian veins prevent spread of hydrostatic force to the veins of the upper limb and displacement of blood in to the valveless veins of the head and neck causes the rupture of distal venules and capillaries. As a result there is formation of numerous arterial haemorrhages into eyelid and conjunctiva with oedema of conjunctiva and bleeding from nose and ears. Internal organs are congested and petechial haemorrhages may be found in the pleura and pericardium. The abnormal purple red colour may persist for several days. in addition there may be presence of fractures of ribs. POSITIONAL ASPHYXIA Positional asphyxia is virtually always an accident and is associated with alcohol or drug intoxication. An individual becomes intoxicated and falls into a restricted area, where because of his position of his body, he cannot move out of that area or position and there is restriction on his ability to breathe. There is usually marked congestion, cyanosis and petechiae. Positional asphyxia occurs if an individual falls down a well and is wedged between the walls. Every time he exhales, he slips farther and farther down the well preventing inhalation OVERLAYING This form of asphyxia is a combination of mechanical asphyxia and smothering. It is seen most commonly when an infant is put to bed with one r more adults. During the night, one of the adult inadvertently rolls on to or otherwise crushes and asphyxiates the infant by compressing the chest thus preventing respiratory movement and occluding the nose and mouth with bedding or
356
Textbook of Forensic Medicine and Toxicology
the body of the adult. Later on the adult rolls off the child. The next morning the child is found dead without any evidence of trauma. These deaths are often thought to be due to SIDS. The autopsy findings are nonspecific and are few fine petechiae over the face but not over the sclera or conjunctiva. The history of an adult sleeping with the child is important to differentiate such deaths from the ‘cot deaths’. In England under the Children and Young Persons Act, 1933, it is a criminal offence to share bed by a person of the age of sixteen years or more with an infant in an intoxicated state and the child dies of suffocation.. When individuals are buried in loose earth or sand (cave-ins) or in grain silos, they die as a result of occlusion of the nose and mouth along with immobilization of the chest and abdomen by external pressure sufficient to prevent respiratory movement. Autopsy Findings 1 Presence of petechial haemorrhages beneath the conjunctiva, epicardium and pleura. 2 Evidence of contact flattening of face and nose may or may not be there. This is suggestive of infant being laid on the face at the time of or after death. 3 Blood tinged froth from mouth and nostrils that may stain the bed clothing. 4 Absence of injury marks over the body. BURKING Burking is a form of mechanical asphyxia plus smothering that is homicidal in nature. Burke and Hare were murderers during the 1820s in Edinburgh who supplied dead bodies for anatomical dissection to the medical schools. They first started out as ‘resurrectionists’ but later on decided to eliminate the chore of digging up bodies. Instead, they would go straight to the source and would invite the individual to their house and intoxicate him. According to Hare, who turned King’s evidence, Burke would kneel or sit on the chest, covering the mouth and nostrils with his hand thus producing a combination of traumatic asphyxia and smothering. External injury was
absent and for Hare, the precise mechanism of asphyxia might not have been discovered. There was some bleeding into the tissues around the cervical spine but it was concluded that the injury occurred shortly after death. Burke later confessed to sixteen of such murders, which were committed for gain. SUFFOCATION FROM IRRESPIRABLE GASES Deaths from suffocating gases are due not to the toxic nature of the gases, but rather to displacement of oxygen from the atmosphere. Carbon dioxide and methane are two most commonly encountered suffocating gases. Both are essentially nontoxic and odourless and are found in sewers and mines. Methane is the principal constituent of the natural gas (94-96%). Reduction of atmospheric oxygen to less than 25% of normal displacement of oxygen by inert gases such as carbon dioxide and methane produces unconsciousness in seconds and death in a matter of minutes. The cause of death can be determined from the circ*mstantial evidences as there are no specific autopsy findings. If death is prolonged, the individuals appear cyanotic with petechial haemorrhages of the epicardium and visceral pleura. Petechiae are frequently absent in rapid anoxic deaths. Toxicological analysis for methane can be done. When is detected in blood being nontoxic death cannot be attributed to it. however, it suggests that the individual was exposed to an atmosphere containing methane. As far as presence of carbon dioxide is concerned, it is a normal constituent of blood.
DROWNING Drowning is a form of asphyxia due to aspiration of fluid in to air passages caused by submersion in water or other fluid. Complete submersion is not necessary for drowning to occur. Our knowledge of the events that take place in the drowning victim is by no means complete. It is primarily derived from animal experiments and to some extent from the observations on human
Asphyxial deaths where drowning was witnessed and reported. Submersion is usually followed by a panicky struggle to reach the surface. When energy reserves are exhausted, the struggle subsides and actual drowning begins. When a person falls in to water and sinks it is partly due to specific gravity of the body and partly due to force of fall. On sudden immersion in to cold water, he may take a deep inhalation of water due to reflex from stimulation of the skin. The person may hold his breath for a varying period and then inhale carbon dioxide to stimulate the respiration center. As a result, inhalation of water may occur. He then cries to help that leads to inhalation of more water causing coughing and air is expelled out. If cerebral asphyxia will continue then death occurs in 3-10 minutes. Several phases are recognized in the drowning process: • Breath holding lasts for a variable length of time until carbon dioxide accumulation in blood and tissues reaches a level at which stimulation of the respiratory center in brain leads to inevitable inhalation of large volumes of water. • Swallowing of water, coughing, vomiting and progressive loss of consciousness follow in rapid succession. Escape of air remaining in the lungs and replaced by water leads to next phase. • Profound unconsciousness and convulsions associated with gasping precede respiratory standstill, which is followed by failure of heart, irreversible changes in the brain and death supervene within a very short time. Types of Drowning Drowning is of following four types: 1. Wet drowning: In this type of drowning, more water goes to lungs. 2. Dry drowning: In this type of drowning, no water enters into the lungs and death occurs by laryngeal spasm. 3. Secondary drowning: It is post immersion syndrome and is also called near drowning. Death
357
occurs after several episodes of resuscitation due to electrolytic disturbances such as metabolic acidosis. Lungs show haemorrhages and atelectasis. Myocardial anoxia may occur and may cause delayed heart failure. 4. Immersion Syndrome (Hydrocution): Death in immersion syndrome is due to cardiac arrest as a result of vagal inhibition. It is produced by (i) cold water stimulation by water striking the epigastrium and (ii) by cold water entering the ear drums, mucosa of pharynx or Larynx. Alcohol increases such effects due to general vasodilatation. Pathophysiology of Drowning Pulmonary alveolar lining is semi permeable and if water enters the alveoli, exchange of water takes place through the alveoli. The extent and direction depends upon the gradient between the osmotic pressure of blood and the water. Drowning in Fresh Water or Brackish Water In fresh water (NaCl content is 0.6%), water passes rapidly from the lungs to the blood, haemolysis and dilution of blood and volume increases 2.5 liters or more. Because of low salt content of these waters (brackish water has approximately 0.5% salinity), precipitous absorption in to the circulation takes place. This results in hemolysis and dilution of blood constituents associated with an abrupt violent increase in blood volumeFresh water alters or denatures the protective surfactant, which lines the alveolar wall. Loss of or inactivation of pulmonary surfactant and alveolar collapse decrease lung compliances causing severe ventilation perfusion mismatch up to 75% of the blood perfusion non-ventilated areas. When water is inhaled, vagal reflexes cause increased peripheral air way resistance with pulmonary vasoconstriction, pulmonary hypertension and increase in lung compliance and ventilation perfusion and increased Na+ and K+ concentration in serum leading to over burdening of heart causing pulmonary edema. The heart is rapidly overburdened by this increased load and pulmonary edema becomes manifest.
358
Textbook of Forensic Medicine and Toxicology
Arrhythmias of heart beat, which culminate in ventricular fibrillation leads to death within 35minutes from the start of submersion In heart, there is hypoxia with decreased Na+ and K+ causing cardiac arrhythmias in the form of ventricular fibrillation and tachycardia and haemodilution leads to haemolysis causing haemoglobinemia and haemoglobinuria. Drowning in Sea Water In sea water (NaCl content is 3%) due to high concentration, water is drawn from the blood in the lung tissue causing severe pulmonary edema, hypernatremia and haemoconcentration. In contrast to fresh water, seawater is strongly salty (usually over 3.0% NaCl conc.). Due to this high salinity, fluids are drawn from blood in to lung tissue causing severe pulmonary oedema. At the same time, there is an attempt to re establish osmotic balance, salts from sea water in the lungs pass to the blood stream with slow death from Asphyxia. Death occurs in 4-8 minutes. Overall, death may occur by asphyxia, ventricular fibrillation, cerebral anoxia, injuries caused during drowning, vagal inhibition and laryngeal spasm. Saltwater drowning usually lasts longer and hence is likely to be more amenable to resuscitation than drowning in fresh water. The different mechanisms in freshwater versus saltwater drowning has significant implications with respect to blood alcohol concentration of the victim. In freshwater drowning dilution of blood may be expected to cause a decrease in the alcohol level, whereas in saltwater drowning a slight increase occurs. Diagnosis of Drowning Drowning is mostly accidental. In a relatively small number of cases, it is suicidal. In some cases, death in the water is due to natural causes, such as heart attack or cerebral haemorrhge during bathing or swimming. Disposal of victim of a homicide to simulate drowning is rare yet because of such possibility, distinction between changes due to drowning and those resulting from post-
mortem immersion of the body is of prime importance. There is no reliable test permitting an equivocal diagnosis of drowning that are available. Thus, the central question in the case of a body recovered from water is whether the individual was alive at the time he entered the water. The scene, the circ*mstances surrounding the incident with all available background information, the deceased’s clothing all play a significant role for example the finding of an alcoholic floating in water 20ft below the cliff with his zip open suggests that he had been urinating before he fell. The rare instance of hand clutching weeds concludes that the deceased may have struggled to stay on surface. The presence of water in the lungs and stomach of a drowning victim is of no real significance. Water may well reach these organs after death. At autopsy, the lungs of a drowning victim commonly resemble those seen in cases of atherosclerotic heart disease. Drowning in the bathtub occurs only if unconsciousness is brought down by disease (epilepsy, or heart disease) or after consumption of alcohol or drugs. Accidental drowning in the swimming pool sometimes results from jumping off the diving board. Impact of the forehead on the floor of pool may cause hyperextension of the head and loss of consciousness with subsequent inhalation of water. Common autopsy findings in these cases consist of hemorrhage in the deep neck muscles in the region of cervical 1 & 2 vertebra with or without vertebral fractures. There are cases seen in which young healthy individuals while engaged in underwater swimming died by sudden drowning. A plausible explanation to that is that usually a diver hyperventilate before entering the water, the over breathing followed by exercise under water cause fall in arterial oxygen tension to a level at which consciousness is lost and water is inhaled. Abundant foam is usually noted extruding from mouth and nostrils of a drowning victim. This foam may not be apparent when the body is recovered from water, but it
Asphyxial deaths appears when pressure is applied to the chest. The foam is produced by mixture of air, mucous and water in presence of respiratory movements. Hence, the presence of foam in the airway indicates beyond doubt that the victim was alive at the time of submersion frequently the foam is bloodstained, not as a result of injury to the chest, but due to the tears of the lung tissue by increased pressure within the lungs, which is part of drowning process. When decomposition sets in foam is rapidly changed to a foul smelling, brown somewhat bubbly fluid. Drowning cases with relatively dry lungs are occasionally observed. Heart action continues in drowning after cessation of respiration, this is sufficient to absorb the water from the lungs in to the bloodstream and as no significant amount of water reaches the alveoli after inhalation is stopped and the same can be seen when resuscitative measures are started immediately. Spot like hemorrhages in the lungs especially under the pleura are often noted in drowning. These hemorrhages result from over distension of the lungs by drowning liquid, hemolysis and dilution accounts for their pink appearance. An occasional small haemorrhage may be seen in the conjunctiva but multiple pinpoint hemorrhages as seen in strangulation or hanging do not occur in drowning. Hemorrhage in middle ear and mastoid air cell are occasionally encountered in persons recovered from water. However, this is not specific for drowning, as it can also be seen due to pressure change as in underwater diving or from extreme congestion as seen in other types of asphyxia deaths or heart failure. Wrinkling of skin of hands and feet seen in individuals recovered from water is frequently referred to as washerwoman’s skin. It is not associated with the process of drowning but is due to prolonged immersion. It cannot be used to determine the length of time the body was in water. After a certain time depending on the temperature of water and the length of immersion, the superficial layers of skin peel like a glove, including the nails. In cold water, several days may elapse,
359
while in warm water several hours may suffice. The glove may be used for fingerprint for identification. In second-degree burns and in decomposition, peeling of skin from hands and feet occurs in similar fashion. The microscopic findings in the lungs in drowning are not characteristic, yet they differ to some extent depending on whether drowning occurred in fresh water or in seawater. Differences in Lungs in Fresh Water and Sea Water Drowning In freshwater drowning, the lungs are overdistended, alveolar walls are torn and structures in the way of the inundating fluid are disrupted. This picture is referred to as ‘aqueous emphysema’ and the intraalveolar hemorrhage leading to pinkish or red staining of foam in the airway. In seawater drowning, the architecture of lungs is often better preserved and aqueous emphysema is less pronounced. Laboratory Diagnosis of Drowning • Carrara in 1902 established disproportionate dilution of left heart blood in freshwater versus saltwater based on specific gravity, and freezing point. Also there is difference in electrical activity between the two sides but no definite findings were given. • In 1903, Placzela emphasized the diagnostic value of the specific gravity method. • In 1921, Gettler published a test for drowning from right and left heart chambers, a difference of 25mg/100ml between the chlorides concentrations of the two sides of the heart indicated that the death was due to drowning. In freshwater drowning the chloride level in the blood in the left side of the heart was lower than in the right side; the reverse situation was noted in saltwater drowning. Positive is seen in seawater drowning due to hemoconcentration and negative in fresh water drowning due to hemodilution. • In 1944, Mortiz suggested magnesium as being reliable than chlorides particularly for
360
Textbook of Forensic Medicine and Toxicology
seawater drowning. proposed that plasma concentration of magnesium differed between the left and right side of heart due to absorption of the ion from the drowning water especially if it is seawater. • In 1955, Freimuth et al using specific gravity of heart plasma, concluded that negative differences between the left and right side may be obtained either in drowning or non drowning cases, while positive values usually indicates that the death was caused by means other than drowning. There are considerable doubts about the reliability of these chemical tests. • In 1941, Incze published the findings of Diatoms in the lungs and systemic circulation of individuals recovered from water as a diagnostic test for drowning. The portal of entry of diatoms in to bloodstream was believed to be via lungs through microscopic tears of alveolar walls that occur in the process of forceful water inhalation. • In 1963, the value of this method was questioned by recovery of diatoms in the liver and in other organs of individuals who had died of cause other than drowning. These diatoms may have been absorbed through GI tract when the water containing diatoms was drunk. • Quantitative assays of peroxidase in animal lungs yielded value close to 800units in freshwater drowning and 6400units in saltwater drowning. Postmortem Findings in Drowning Deaths A body in water will sink unless air trapped among the clothes keeps it afloat. The body will resurface when gas is formed because of putrefaction. Putrefaction in water proceeds at a considerably slower rate than in the air but once the body is removed from water, postmortem changes progress far more rapidly than is usual under the same prevailing environmental conditions. Putrefaction is slower in seawater compared to freshwater because high salinity retards bacterial
growth. The time until reappearance of the body depends on the temperature of water. It may take two to three days in summer and weeks or months in winter. While the body is underwater, it is subject to injuries by wildlife or by drifting along the ground. These injuries be recognized and be distinguished from injuries sustained during life. A victim of drowning tends to bleed more readily and more blood oozes from a wound of such an individual. Postmortem lividity is difficult to recognize in a body recovered from water due to swelling and loss of translucency of the upper layer of the skin, the skin becomes waterlogged if immersion is prolonged. Algae grow on the exposed part giving prolonged green or black colour to those areas. Adipocere formation is common in victims of submersion. Caisson disease: It occurs in underwater diving when the diver remains underwater for prolonged period at great depths due to change of ambient pressure cause formation of bubbles in his blood and tissues if the ascent is too fast. At autopsy, the finding consistent of foci of ischemic necrosis especially in brain, lungs show haemorrhage, edema, atelectasis and areas of emphysema. Signs of Immersion 1. Maceration of skin begins with minutes in warm water, such as death in bath tub, but in cold water is visible after variable time; the minimum probably being 4-5hours. The first sign t0ends to be on areas with an appreciable keratin layer such as fingertips, palms, back of hands and then soles where the surface becomes wrinkled, pale and sodden, the so called ‘washer women’s skin’. After some days in warmer water and up to several weeks in cold, the thick keratin of hands and feet becomes detached and eventually peels off in ‘glove and stocking’ fashion. The nails and hair becomes loosened at the same time. 2. Cutis anserina or goose flesh: It is a common finding in immersed bodies but is related to cold water than warm water. The erector pilae
Asphyxial deaths muscles attached to each hair follicle can contract in any type of death and cause a generalized dimpling of skin. 3. The distribution of postmortem hypostasis: It is usual for most corpses to float or hang in water with uppermost and the head and limbs hanging down but water movement often roll the body constantly unless in a placid lake. Other corpses may float upon the back and gravitational staining of the skin may therefore be in any pattern if the body is subject to frequent change of posture. 4. Estimation of duration of immersion: This is another difficult problem and one that is often too dogmatically answered by doctor with insufficient experience to appreciate the potential error. The overriding variable factor is water temperature that has most common effect on decomposition. When a body falls in to water in average temperature climate the following is an approximate guide to timing: i. If no wrinkling of finger pads is present, less than few hours. ii. Wrinkled fingers, palm and feet progressively from half a day to three days. iii. Early decomposition often first in the dependent head and neck, abdomen and thighs is 4-10 days. iv. Bloating of face, abdomen with marbling of veins, peeling of epidermis on hands and feet is 2-4 weeks. v. Gross skin shedding, muscle loss with skeletal exposure, partial liquefaction in 1-2 months. These times may be reduced or exceeded by wide margin according to animal predation, climatic changes and bodily built. Other Signs of Drowning During the autopsy at times it poses problems as findings are minimal, obscure or completely absent. In such cases, the cause of death may be given as (i) Consistent with drowning or as (ii) Cause cannot be given.
361
External 1. Clothing is wet and skin is wet, cold and clammy and pale due to vasoconstriction. 2. Post mortem staining is pink due to oxygenation, may be dusky and cyanotic. 3. Head, neck and face, upper part of chest and upper arm show postmortem staining. 4. Cyanosis may or may not be there. 5. Conjunctiva is congested and petechial haemorrhages may be present. 6. Pupils may be dilated and the tongue is swollen and protruded. 7. Rigor mortis appears early, when violent struggle takes place before death. 8. The froth is fine, leathery, tenacious and white or mixed with blood over mouth and nostrils into pulmonary bleeding and is more on pressing the chest. Inhalation of water irritates the mucosa, membrane and stimulates the secretion of mucous. Air with mucous and water creates a churning effect and causes the froth. Fine bubbles don’t easily collapse when touched with the points of a knife. It may project as a small balloon or mushroom like mass or a cured horn from the mouth and nostrils. The froth may not be there in dry drowning. 9. Cutis anserina or goose skin: Skin has granular and puckered appearance due to spasm of erection fibers and the muscles attached to hair follicles. It can occur in living in cold weather and it may occur in submersion of body in cold water of the death during molecular death. Retraction of scrotum and penis occurs. 10. Cadaveric spasm: Presence of weeds, ground and grass. It indicates the person was alive when drowned. Damaged nails and abraded fingers may be present due to struggle. 11. Washerwoman’s hand: Soddening of the skin due to absorption of water into its outer layer. First in fingertips, then in 2-4 hours it spreads
362
Textbook of Forensic Medicine and Toxicology
to palm and back of the hand in 24 hours. Similar changes are seen in the foot. If shoes are there, it takes twice as long. Skin is bleached, wrinkled and sodden and then turns white in colour. Internal Internally lungs show the main features. Macroscopically they are voluminous, completely covering the pericardial sac and bulge out of the chest when the sternum is removed. Passive collapse, which usually occurs in death, does not occur due to the fact that edema fluid blocks the bronchi. Due to distension rib impression on surface of lungs is seen and when they are removed and kept on a table they don’t collapse. On cut section they may appear dry, but large amount of water, sometimes foamy, ooze from the surface on squeezing. If lungs are left alone, water will start to trickle from the surface and it will slowly collapse because of increased pressure during forced expirations, alveolar walls may have ruptured, producing hemorrhages, when located subpleurally called paultauf’s hemorrhages. They are shining, pale bluish and may be minute or 3-5 cm in diameter. 1. Paltauff’s haemorrhages: Paultaff’s haemorrhages are usually present in the lower lobes of the lungs. They may be seen on the anterior surface and interlobar surfaces of lungs. They are red or grey patches and they may be seen on the surface due to paultaff’s haemorrhages and interstitial emphysema. They may however be absent. This condition of the lung is called ‘Emphysema aquosum’ and ‘trockenes oedema’. This drowning lung is fairly characteristic but not pathognomic. Active respiratory movements were a prerequisite for the drowning water to reach all the peripheral parts of lungs. After death, also water could not reach the lungs by hydrostatic pressure when the body is submerged but the amount of water would be small and it would gravitate only the lower parts of the lungs. Therefore, hydrostatic lung cannot simulate drowning lung. Muller, Reh and Eisele,
using high pressure chamber or lowering the body in normal water shows that hydrostatic lung may develop that cannot be distinguished from drowning lung. Thus drowning lung was developed by putting the body 3 meters deep for 65 hours (death is due to hanging) and even 2 meters depth for 20 hours may produce drowning lung. Therefore, Reh was of the opinion that drowning lung is diagnostic for drowning only if the (i) Body has remained floating on or very near the surface (ii) Drowning lung with frothy fluid over mouth and nostrils should not leave any doubt about the diagnosis of drowning. 2. Microscopic findings of drowning lung: The microscopic findings after haematoxylin and eosin staining does not yield much about the diagnosis. Following stages are encountered: Stage 1: Thickness of the alveolar wall (normally 2-3 times the capillary width) is reduced to capillary width. Capillary appear round or oval like a chain. Partial fiber ruptures that may be observed. Stage 2: Alveolar are more distended and capillaries lie separately. Fiber rupture is more marked. Stage 3: Maximal distension of alveolar walls. Capillaries appear thread like only occasional lumina are observed. Distinct intraseptal fiber rupture is there. Stage 4: This stage is seldom seen and may involve only scattered alveoli. There is complete rupture of alveolar walls and retraction of the fiber like a corkscrew. Differential diagnoses of drowning lung: i. Aspiration of blood. ii. Capillary bronchitis. iii. Fatal Asthmatic attack. iv. Hypoxia for strangulation and throttling. v. Chronic emphysema. In hydrostatic lung, reticular fibers show different picture. The fibers do not withstand hydrostatic pressure. Therefore, the fibers show coarse rupture and fragmentation. No stage of 2 and 3 of drowning lung.
Asphyxial deaths 3. Water in Stomach and duodenum: Water is present in the stomach and duodenum. Much amount of water may be swallowed which passes in to the duodenum. It does not enter into the stomach after death as a result of the hydrostatic pressure. If a body is kept at a depth of 15 meters for 65 hours then no water enters the stomach. So it is very vital sign that the person entered the water when he was alive and no significant sign of drowning. The fallacy is that the deceased might have drank water prior to death or taken beverages before drowning in water. Therefore, absence of water proves nothing. 4. Froth in air passages: The positive signs of drowning as opposed to mere immersion are scanty and not specific. The most useful is which in fresh bodies, often exudes through the mouth and nostrils. The froth is oedema fluid from the lungs and consists of proteinaceous exudates and surfactant mixed with the water of the drowning medium. It is usually white but may be pink or red-tinged because of slight admixture with blood from intrapulmonary bleeding. The froth extends in to trachea, main bronchi and smaller air passages. Differential diagnosis of Froth in drowning: i. Strangulation. ii. Acute Pulmonary edema. iii. Electrical shock. iv. Epilepsy. v. Opium poisoning. vi. Putrefaction. 5. Over-inflation of lungs: Apart from generalized water logging, the lungs may be markedly over inflated, filling the thoracic cavity when the sternum is removed. The texture is rather pale and crepitant, superficially resembling that in asthma. The older name for this condition is ‘emphysema aquosum’. In drowning on the lateral surfaces of the lungs impression of the ribs, leaving visible and palpable grooves after removal of the organs from the thorax. 6. Other organs: There are no reliable autopsy changes in drowning. The heart and great veins
363
have often been said to be ‘dilated and engorged’ with fluid blood especially the right side but this is a nonspecific finding. The stomach may contain watery fluid or even foreign materials from the water such as slit, weed or sand but this cannot be accepted as positive aid in the diagnosis. Haemorrhage in to middle ear has been postulated as a positive sign of drowning, but this is non-specific and occurs due to change in hydrostatic pressure as depth increases or due to congestion. Diatoms and Diagnosis of Drowning In 1941 Incze demonstrated that, diatoms could enter the systemic circulation via the lungs during drowning. All waters, fresh or salt water contain microscopic plants, the algae. The algae do not grow or grow only in small numbers in heavily polluted waters. Such water may also contain particulate matter characteristic for local pollution but have the algae are considered. Revenstrof in 1904 was the first to attempt to use diatom as a test for drowning. The basic premise is that when a living person is drowned in water containing diatoms, many diatoms will penetrate the alveolar walls and be carried to distant organs such as brain, kidneys, liver and bone marrow. After autopsy, samples of these organs can be digested with strong acid to dissolve soft tissue, thus leaving the highly resistant diatom to be identified under microscope. When a dead body is deposited in water or when death in the water is not due to drowning then although diatom may reach lungs by passive percolation, the absence beating heart prevents circulation of diatoms to distant organs. The great advantage of the diatom test, if it were reliable would be a positive diagnosis of drowning could be made even in the frequently putrefied bodies that are removed. There are two main types—green algae and diatoms that are supplied with a delicate and beautiful heat and acid resistant siliceous shell, which is unicellular. Cell wall is usually strongly impregnated with silica and contain chlorophyll and diatoms a brown pigment. Diatom secretes
364
Textbook of Forensic Medicine and Toxicology
Figure 23.21: Diatoms
hard siliceous outer box like skeleton called frustule. They resist heat and acid and vary in size from 2 microns to 1 mm though most of them are 10-80 microns in size and 10 microns in width. Diatoms upto the size of 60 microns can enter the pulmonary circulation during drowning. They vary from place to place and there is seasonal variation in the same place. They occur in cultivated soils and surface of moist rocks. Large numbers of free-floating diatoms are found in seawater and fresh water. Their shape is circular, triangular, oval, linear or rectangular (Fig. 23.21). They can be demonstrated by the following: Direct microscopic examination: This is only used in the examination of the lungs. Water is squeezed out of the lungs and centrifuged and the sediment is examined. Microscopic examination of tissue sections: Optically empty sections are prepared and quantitative analysis is done. Chemical digestion: The tissue is prepared with acids where by all organic matter is digested, but the siliceous shells of the diatoms are well preserved. Incineration: Organic matter is destroyed with heat in an oven (Fig. 23.22).
Principle of diatoms: The drowning fluid and the particles in it i.e. diatoms and planktons pass from the ruptured alveolar wall into the lymph channels and pulmonary veins and left side of heart. Only in living body the diatoms are found in bone marrow, brain, liver and skeletal muscle etc. its also found in bile and urine etc. bone marrow is highly suitable and reliable after cutting the bone the marrow is curetted from the gutter. There can be situations where the diatoms may be absent even though the person is known to have drowned or they are present without drowning. • Seasonal variation: a person may have drowned when the water is almost devoid of diatoms so no diatoms are found. • A person may eat raw fruits or vegetables, which have been in contact with soil diatoms and shellfish, which feed on diatoms and show diatoms in the body. • Large amounts of diatoms are found in materials used for manufacturing of buildings like cement, paint, paper, insulators etc. the atmosphere near the plants providing such material is highly polluted and the person might have inhaled and may have such diatoms in his body. • Certain dusting powders contain diatoms, which may have been inhaled by the person and are found in his body. • Diatoms are ubiquitous, being present in soil, water supplies and in the air. • They can also penetrate the intestinal lining and gain access to the bloodstream and hence any body tissues. • Certain food, notably shellfish contains vast quantities of diatoms that may enter the circulation. According to Henday, following two requirements to be fulfilled: 1. All the species recovered from the organs of the body must be present in the samples of water in the place of submersion.
Asphyxial deaths
Lungs
Diatoms in water
Heart via circulation to
365
Bones and Visceral Organs
Figure 23.22: Transmission of Diatoms
2. They must be present in approximately the same proportion in the organ as in the sample from the place of submersion. Histological Changes in Drowning Much of the work has been done to confirm histologically the genuineness of ‘emphysema aquosum’ in both fresh and decayed bodies, but the dilation and rupture of the terminal air space can occur not only as a result of drowning but of passive immersion in water deeper than 4m. Dilatation of the alveoli, thinning of the walls and compression of the capillaries are easy to obscure but the significance is ambiguous. The number of macrophages in the alveoli adjusted to the size of the alveoli where distended was studied by Betz, who carried a diagnostic usefulness of the method as long as no autolytic changes are present. Haffner has used the weight of spleen as a diagnostic marker in drowning compared with other modes of asphyxia about an 18% reduction in weights and spleen-liver ratios were recorded. The skin changes in maceration are also well recorded. Long Questions 1. Define asphyxia. Discuss the various types of hanging and the autopsy findings in a case of hanging.
2. Classify asphyxia. Discuss the types of homicidal asphyxia with the autopsy findings in manual strangulation. 3. Discuss the various types of drowning withth the autopsy findings in fresh water drowning. Short Questions 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16.
Hanging Strangulation Bansdola Sexual asphyxia Dry drowning Diatoms Judicial hanging Cafe coronary Gettler’s test Suffocation Throttling Mugging Garroting Burking Paultauf’s hemorrhages Differences between fresh water and sea water drowning
366
Textbook of Forensic Medicine and Toxicology MULTIPLE CHOICE QUESTIONS
1. Hyoid fracture is common in: A. Hanging B. Strangulation C. Throttling D. Choking 231. At autopsy, a body is found to have copious fine leathery froth in mouth & nostrils which increased on pressure over chest. Death was likely due to: A. Epilepsy B. Hanging C. Drowning D. Opium poisoning 232. Gettler’s test is done for death by: A. Drowning B. Hanging C. Bums D. Phosphorus poisoning 233. Feature indicative of ante mortem drowning is: A. Cutis anserina B. Rigor mortis C. Washerwoman’s feet D. Grass and weeds grasped in the hand 234. Best indicator of ante mortem drowning is: A. Froth in mouth and nostrils B. Cutis anserina C. Washerwoman’s hand D. Water in nose 235. Paltauff’s haemorrhages may be seen in: A. Hanging B. Drowning C. Strangulation D. Carbon Monoxide poisoning
vascularity of lung: A. Hypoxia causes vasodilatation B. Distended capillaries in lower lobe C. Increased perfusion of apical lobe D. Pulmonary resistance is half of the systemic vascular resistance 238. Fine leathery froth that emanates from the nostrils on chest compression is diagnostic of death due to: A. Drowning B. Hanging C. Morphine poisoning D. Strangulation 239. In judicial hanging fracture of vertebral column is seen between: A. C1 and C2 B. C2 and C3 C. C4 and C5 D. C5 and C6 240. Most important sign of death due to strangulation is: A. Signs of asphyxia present B. Fracture of hyoid bone C. Horizontal ligature mark with ecchymoses round the edges D. Fracture dislocation of cervical vertebrae 241. Which of the following is characteristic feature of strangulation: A. Fracture of thyroid cartilage is present B. Fracture of cricoid cartilage is present C. Fracture dislocation of cervical vertebrae D. Extravasation of blood under the ligature mark and rupture of neck muscles 242. Ante mortem hanging is best indicated by: A. Dilated pupil B. Protruded tongue C. Patechial haemorrhages with congested face D. Oblique ligature mark which does not completely encircle the neck
236. Goose skin or cutis anserina seen in: A. Drowning B. Lightening C. Strangulation D. Fire arm injury 237. Which of the following is not true regarding
1 B 9 D
2 B 10 B
3 A 11 D
4 A 12 A
5 A
6 B
7 D
8 A
Asphyxial deaths
367
243. Which of the following is not true about fresh water drowning: A. Hyperkalemia B. Hypovolemia C. Haemolysis D. Ventricular fibrillation
251. Most reliable evidence of death due to drowning is: A. Froth in mouth and nostrils B. Water is stomach C. Voluminous oedematous lungs D. Weeds and grass firmly grasped in hand
244. In strangulation there is: A. External signs of asphyxia are not well marked B. Neck muscles rupture is common C. Fracture dislocation of cervical vertebrae D. All of the above
252. Ante mortem drowning is best demonstrated by: A. Cyanosis B. Diatoms in stomach and lungs C. Froth in mouth and nostrils D. Washerwoman’s skin
245. Surest sign of death from hanging is: A. Signs of asphyxia well marked B. Dribbling of saliva from angle of mouth C. Bleeding from nose & mouth D. Neck stretched & elongated
253. Presence of fine white leathery froth in mouth and nostrils is seen in: A. Hanging B. Bums C. Scalds D. Drowning
246. Diagnostic feature of ante mortem hanging is: A. Dribbling of saliva B. Ligature mark C. Hyoid fracture D. Incontinence of urine 247. Dry drowning is: A. Due to sudden laryngeal spasm B. Due to sudden immersion in cold causing cardiac arrest C. Occurs in dry well D. Same as wet drowning 248. Fracture of hyoid bone occurs in: A. Drowning B. Hanging C. Strangulation D. Traumatic asphyxia 249. Diatoms in bone marrow are seen in death due to: A. Drowning B. Electrocution C. Asphyxia D. Strangulation 250. Dry drowning is: A. Water does not enter larynx due to laryngospasm B. It is common than wet drowning C. Common in bronchial asthma D. If resuscitated patient does not have pleasant recollection
254. Tardieu’s spots are seen in death due to: A. Haemorrhage B. Vasovagal shock C. Brain tumor D. Obstruction of respiratory passages 255. Drowning is absent if there is no: A. Froth in mouth and nostrils B. Fracture hyoid bone C. Cutis anserina D. Water and diatoms in lungs and stomach 256. In strangulation, there is: A. External signs of asphyxia are not well marked B. Injury to neck muscles is rare C. Subcutaneous tissue under the mark is white, hard and glistening D. Abrasion and ecchymoses round about edges of ligature mark 257. ‘Cutis anserina’ or ‘goose flesh’ is seen in death due to: A. Criminal abortion B. hanging C. Drowning D. Strangulation 258. Burking is smothering and: A. Throttling B. Strangulation C. Gagging D. Traumatic asphyxia
368
Textbook of Forensic Medicine and Toxicology
259. Seen in drowning are following except: A. Weeds in stomach and lung B. Wet heavy, lungs C. Frothing from mouth D. Miosis 260. Diatom test is to determine death due to: A. Drowning B. Strangulation C. Hanging D. Bums 261. Hanging causes large amount of injury to: A. Vertebral artery B. Carotid artery C. Trachea D. Oesophagus 262. In child drowning, most common consistent feature after taking out from pond is: A. Water in lungs alveoli B. Patechial haemorrhages C. Washer woman skin D. Cyanosis 263. Which of the following is diagnostic of drowning: A. Froth in the nostrils B. Cutis anserina C. Water in the stomach D. Mud in the respiratory passages 264. The type of hanging with haemorrhages on the dependent parts of legs is seen in: A. Partial hanging B. continued postmortem hanging C. Judicial hanging D. Accidental hanging 265. Ligature mark is: A. Laceration B. Abrasion C. Ecchymoses D. Potential margin 266. Tardieu’s spots are seen in: A. Drowning B. Electrocution C. Mechanical asphyxia D. Corrosive acid poisoning 267. In death due to hanging: A. Trachea is obstructed by a weight of 5 kg B. Usually the vertebra to get fractured is C3 C. Abduction fracture of hyoid may be seen
D. All are true 268. Ligature strangulation is also called: A. Mugging B. Gagging C. Garroting D. Throttling 269. Café-coronary refers to: A. Myocardial infarction in cafeteria B. Myocardial infarction due to intake of large amount of coffee C. Choking D. Strangulation 270. Hydrocution refers to: A. Electrocution in water B. Vasovagal arrest due to stimulation by cold water C. Touching live with wet hands D. All of the above 271. Emphysematous bullae are seen in lungs in case of: A. Drowning B. Electrocution C. Strangulation D. RTA 272. ‘Intimal tears of carotid’ are usually seen in: A. Ligature strangulation B. Mugging C. Judicial hanging D. Partial hanging 273. Which of the following postmortem findings suggest that the person was conscious and alive at the time of falling into water? A. Emphysema aquosum B. Edema aquosum C. Washerwoman’s hand D. Postmortem staining o the face and shoulders 274. Beveling of inner table of skull suggests: A. Stab wound B. Wound of firearm entry C. Wound of exit of firearm D. Penetrating wound 275. Le facies sympathiec is seen: A. At the side of knot in hanging B. Usually in strangulation C. Opposite the side of knot in hanging D. Also in drowning E. Any of the above
25
Part 1—Forensic Medicine and Pathology
Infanticide Infanticide is unlawful killing of a newborn child below the age of one year. It was a recognized practice in many primitive communities. This problem persists throughout the world and took place for a variety of reasons in the past. It does not include death during labour by craniotomy or decapitation. Motives of Infanticide Uncivilized societies: The motives in uncivilized societies could be 1. The basic motive is survival of the fittest with destruction of those suffering from malformation and females being of less potential value to the community are killed. 2. Some newborns are killed due to tribal superstitions due to the question of being unlucky such as twin births, foetus that have teeth at birth and those with leg presentations. 3. Due to the age long desire for strength and fertility some communities believe that destruction and eating the first newborn child added strength to those who devoured it. Civilized societies: The motives in civilized societies are usually 1. To get rid of illegitimate children. 2. To get rid of child when mother is widow or unmarried. 3. When the parents belong to socially and economically weaker section of the society.
Laws in Relation to Infanticide The infanticide law differs in different countries but its evolution in England is of particular interest. Until 1922, the unlawful killing of newborn was murder, no matter by whom it is done. This made no allowance for the fact that the effects of delivery may temporarily disturb the balance of the mother’s mind and she would not then be responsible if, at that time, her act or omission led to the destruction of her child. 1. The Infanticide Act (1922): It was passed that made provision of the act of infanticide being committed by the mother with disturbed mental balance under the effects of delivery. This was applicable only to England (not applicable to Ireland or Scotland). This Act also did not take into account lactation and no age limitation was defined. In 1926, this Act was re-enacted and defined the age limit that is the child under 12 months. There are some points that should be stressed i. It is only the mother who can be charged with the offence. ii. The child must be borne alive (of course be viable) iii. It must have been killed. iv. There must be evidence to establish that the mother is suffering from the disease of the mind for the reason mentioned. The Act clearly says that it is applicable only to the mother and anyone else including the
370
Textbook of Forensic Medicine and Toxicology
husband will be charged with Murder or Manslaughter. 2. Infanticide Act 1938: Section I enacts that “ Where a woman by any willful act or omission causes the death of her child being a child under the age of 12 months, but at the time of the act or omission the balance of her mind was disturbed by reason of her not having fully recovered from the effect of giving birth to the child or by reason of the effect of lactation consequent upon the birth of the child, then, notwithstanding that the circ*mstance were such that but for this Act the offence would have amounted to murder.” She if guilty of the felony of infanticide and may be dealt with and punished as if she had committed manslaughter. This Act talks of the ‘balance of mind was disturbed at the time of the act’. This being a broader term needs to be proved by the doctor who is conducting her obstetrical check-up and the psychiatrist. In pursuance of Section 60 “Offence against the Persons Act, 1861” for which the child is deemed to have been recently born, if it has been born within 12 months before its death. In every case of infanticide, legal presumption is that the child is born dead, and the onus of proving that the child was born alive rests on the crown. There is no need to produce the body and it is not necessary to prove that the child has been viable. 3. Infant Life (Preservation) Act 1929: The law was amended with regard to the destruction of children at or before labour. This Act defined the crime of child destruction “ Any person who, with intent to destroy the life of a child capable of being born alive, by any willful act causes a child to die before it has an existence independent of its mother, shall be guilty of felony, to wit of child destruction and shall be liable on conviction thereof on indictment to imprisonment for life. Thus, this offence cannot be committed during the earlier stages of pregnancy. The criteria to be fulfilled or the purpose of this Act
i. The woman must be pregnant for a period of 28th weeks or more. ii. There shall be prima facie proof that she was at that time pregnant of a child capable of being born alive. This Act provides that if the person is not guilty of offence of murder, manslaughter or infanticide, he can be charged to be guilty of child destruction. 4. Criminal law of England: According to this law, a child is considered to be born alive when it is completely born external to the mother irrespective of the attachment or severance of the cord. Hence, according to the English Law destruction of an infant before its complete birth has taken place is not homicide. Nevertheless, the definition held by Indian law is more correct and appropriate. It constitutes live birth, even if any part of a living child has been brought forth external to the mother, though the child may not have breathed or completely born. 5. Laws in India: The law in India draws no distinction between the murder of the newborn and that of any other individual as the provisions of the law that apply to homicide also apply to infanticide. Hence, according to Indian law, killing of an infant before any part of it is born is not homicide, but destruction of an infant after any part of it is has been brought forth external to the mother, but before its complete birth constitutes homicide. Therefore, the definition of infanticide could be applied not only to the mother but also to the father. Legal bearing is same as culpable homicide except that the law presumes child is born dead. It is for the prosecution to prove that the child is born alive and died from criminal violence. The crime is usually committed at the time or within few minutes or hours after the birth of the child. Signs consistent with a precipitate or difficult labour are impossible to find if more than 3 weeks have passed after delivery. However, immediately after delivery extragenital and genital signs can be discerned. In such cases, the Medical Officer is required to examine the woman.
Infanticide Examination of the Woman It should include: (i) Time interval between delivery and examination (ii) Mental status that is heneral demeanor and emotional state (iii) Signs of recent delivery. Points in Relation to Infanticide 1. Is the body of the child found that of a viable child? 2. Is the body of that child of the person accused? 3. Was the child still born or dead born? 4. Was the child born alive? 5. If born alive, how long survived? 6. What was the cause of death? Is the Child Viable? Viability means capability of having a separate existence after birth by virtue of certain degree of development. It should be explained that unless the child born has reached a stage of development, which is consistent with the possibility of a live birth, the charge of infanticide or child destruction would not be preferred against mother. In law, a foetus which has not attended a completion of 7th month of intra-uterine life is said to be incapable of maintaining a separate existence and therefore non-viable. Where it can be shown that the child was premature, there is a strong presumption of still-birth or death from prematurity shortly after live-birth. Presumption of law: if the child shows evidence of less than 7th month failed to leave by reason of immaturity. On the other hand, if there is any evidence that the foetus has lived after birth; charge of infanticide will apply. Viability need not be proved, but in doubtful cases, it is improbable that
371
the child had a separate existence. The Court sometimes requires to know whether the infant had attained the 28th week of gestation at the date on which the pregnancy terminated. The opinion is based on not a single criterion but upon several parameters. i. General condition of the foetus: Its plumpness that is fullness or fatness of the body and absence of apparent disease or malformation ii. Weight of the foetus: In multiple births, the weight of each of the infants is appreciably less than that of a single birth at the same stage of gestation. The female foetus is 100gm less in weight than the male foetus. iii. Crown-heel length of the foetus: It has been established that there is a close relationship between age and height of the foetus. To calculate age from height, crown-heel length is the best criteria (Table 24.1) Features of 6 months fetus: The height of foetus is 30 cms and weight is 2 lb. The skin is wrinkled and fat is absent. Eyelids are adherent and membrana pupillaris exists. The eyebrow and eyelashes start forming. The testicl*s are close to the kidney and the meconium is present in upper part of large intestine. In addition, ossification for all the four divisions of sternum is present. Features of 6 months fetus : The height is 35 cm and weight is 2½-3 lb. the eyelids are separated and eyelashes are present. The membrana pupillaris disappears. The nails are thicker and they do not reach at the end of fingers. Meconium present in whole of the large intestine. The testicl*s present in external inguinal ring and there is appearance of center of ossification for talus.
Table 24.1: Weight and length of the foetus in relation to age Age
Weight
Crown-heel length
28 32 36 40
2½-3lb (1.1-1.3 kg) 3½-4lb (1.6-1.8 kg) About 5lb (2.2 kg) 6-7lb (2.7-3.2 kg)
35cm 40cm 45cm 50cm
weeks weeks weeks weeks
372
Textbook of Forensic Medicine and Toxicology
Is the Body of the Child of the Person Accused? Proof on this point is most usually established for the evidence of persons with whom the suspected woman has more or less intimately associated in work or social life. At times careful examination by the police of the wrappings, which envelop the body of a child, may throw some light on the identity of the mother. Was the Child Still Born or Dead Born? A distinction must be drawn between still born and dead born. Stillborn fetus is defined as one, which has issued forth from the mother after 28th week of pregnancy and did not at anytime after being completely expelled breathed or show any other signs of life. This definition poses some problems in the English law. For example should the mother, whilst one foot of the child is still in the vagin*, strangle it or kill it by some other means, even if it has cried since the delivery of the head, she is not guilty of offence, because the child by definition a still birth, not being completely expelled. Cases have occurred that have been acquitted. From practical point of view it is highly unlikely that a woman who does not know the law would invent the story of incomplete expulsion, hence if she volunteers it in her original statement, it is difficult to repute. In other aspect, in cases of unidentified children, it is slightly impossible for the pathologist even if he finds evidence of breathing to say that it had a separate existence. Dead born child: The fetus had died in the uterus and may show one of the following signs after it is completely born: 1. Rigor mortis at delivery 2. Maceration: Maceration is a process of aseptic autolysis and is the usual change. If the foetus remains in the uterus for 3-4 days surrounded with liquor amnii, but exclusion of air. It is not seen if the foetus is born within 24 hours after death. If air enters, then putrefaction
will set in. Macerated baby is soft, flaccid and flattens out when placed on a surface level. It has a sweet, disagreeable odour; skin is red or purple. i. The earliest sign is slippage of skin that is seen within 12 hours of death of child inside the uterus. ii. If there is presence of gas in great vessels (Aorta), it indicates fetal death. iii. Large blebs filled with serous fluid are present. iv. Epidermis is easily peeled off leaving a moist and greasy area. v. The tissues are oedematous, abdomen is distended, and serous cavities are filled with serous turbid fluid. vi. Soft parts are readily detachable from the bone. vii. There is abnormal mobility of the joints and the small bones are separated. viii. All the viscera is softened except lungs and uterus which are unchanged for a long time. ix. Spalding’s sign: Spalding sign is loss of alignment and overlapping of the bones of the cranial vault due to shrinkage of brain. It develops earlier in vertex presentation. It can be detached within a few days of death of the foetus but often takes much longer time like 2-3 weeks. x. Mummification: Mummification is dried up and shriveled appearance due to deficient blood supply and scanty liquor amnii; no air enters in the uterus. Was the Child Born Alive? Separate existence and live birth are the two terms that are not synonymous with each other. The principal requirement of legal birth is that the child had or was capable of having a separate existence independent of its mother. In cases of child destruction, it is required to be proved that that the child was capable of being born alive. The pregnancy must have reached the 28th weeks or over and that the child was viable.
Infanticide Further, it must be proved that a willful act caused its death before it had an existence independent of its mother. Viability is the crux of matters of child destruction. Infanticide requires proof that the child has had a separate existence; it had lived after complete extrusion of its body from that of his mother. The viability need not be proved. However, when the viability is doubtful, it is improbable that the child had a separate existence. External examination: A separate existence requires complete extrusion from the body of the mother but does not include the severance of the cord and detachment of the placenta. In accidental tear of the umbilical cord, the break is usually close to one of its attachments, either near the placenta or the navel of the infant. At the naval end of placenta little haemorrhage is unlikely to cause death. According to Morris and Hunt (1966), the cord can be easily broken by the hands, a force of 5 kg is required. The ends of the cord should be examined at a low magnification by placing two portions in water or on a board and their ends are then gently spread out. Gross irregularities suggest tearing whereas a linear break with regular margin is indicative of separation by cutting. A blunt instrument can also produce a ragged line of separation. In addition, the tear can resemble superficially a clean-cut division of the cord. If the body has decomposed or there is severe drying, no opinion can be formed on the mode of severance of the cord. Internal Examination: It may provide strong evidence of a separate existence. If extraneous material, which could enter only after complete extrusion of the infant, is present either in the air passage or digestive tract. 1. Extraneous material can enter the air passage for a limited distance after death but its entry in to intrapulmonary bronchi is resisted by air in the lungs. Therefore, for material to be demonstrated in secondary bronchi or beyond, it must have been inhaled. It excludes contamination and milking of the material, downwards from trachea and
373
bronchi by compression of the infant’s body. The examination must avoid these artefacts and thoracic contents should be removed by ‘no touch technique’. The thoracic viscera is placed on a clean slab or dish. The bronchial contents should be obtained by a clean pipette or syringe. Specimen obtained (material) must be compared with the source of extraneous material; soil or sand and proof obtained that the two samples are identical. 2. Extraneous material may enter in to the oesophagus, stomach and pass beyond even in to small intestine during life but unlikely to reach up to the stomach after death. A sample of extraneous material must be compared with the probable source. The demonstration of food e.g., milk in infant’s stomach is suggestive of live birth. Examination of Respiratory system The Aeration of Lungs This is based upon the expansion of the alveoli by postnatal breathing and is ascertained by inspection. However, it does not take into consideration the phenomenon of partial aeration or the fact that the child may cry in utero or breathe after expulsion of the head and before complete expulsion. Proof of breathing is not proof of live birth. There are illustrations of authentic cases in literature where breathing can occur before complete delivery. In addition, breathing is by no means rare while the head of the child is still in the vagin* and in the uterus itself (Clouston1933). About 130 cases have been recorded out of which 122 are authentic. Earliest cases of Lebarius (1596) alleges that the child’s cry could be heard from a distance. Ryter (1943) reviewed the literature relating to vagitus uterinus. Vagitus uterinus and vagitus vagin*lis is the hearing of the cry while the foetus is in the uterus or vagin* respectively. This is due to rupture of the membranes resulting in entry of air in the lungs and the stimulation of the baby. Other signs like movements of the limbs, muscle twitching etc.
374
Textbook of Forensic Medicine and Toxicology
Gross examination of lungs: When the lungs are generally distended, soft and crepitant they have been aerated out. Osborn (1953) disproved the belief that size of lungs has any relation to aeration. He has disproved the former belief that small solid lungs are indicative of stillbirth. The lungs fill the thorax in at least three-quarters of all cases whether the child is born alive or not. Osborn also demonstrated that lungs may fail to expand due to bilateral pneumothorax with surgical emphysema, a result of artificial respiration. The presence of Tardieu’s spots of asphyxia and evidence of bronchopneumonia are not evident of live birth as they may be seen in the still-born. Occasionally sub-pleural interstitial emphysema may be seen and may represent attempted resuscitation by mouth-to-mouth respiration after
birth. (Table 24.2) Hydrostatic test: Scheyer first noted hydrostatic test in 1683. The basis of the test is that, even with compression, if the alveoli are compressed they will still contain some air if aerated at all. It is because on breathing the lung volume is increased. The specific gravity of lungs 1040 to 1050 diminishes to 940 after respiration. The test involves the determination of the buoyancy of lungs. The test depends upon the ratio of the specific gravity of the lungs to that of water as a lung containing air is lighter than water and therefore it floats. The lungs should be removed at autopsy with the bronchi, trachea and larynx intact. This ‘pluck’ is then placed in water, and if it floats, the test is positive. Finally, each lung is cut into 15-20 fragments which are again tested,
Table 24.2: Differences in findings in respiratory system before and after aeration Features
Before respiration
After respiration
Shape of the chest
Flat, circumference is 1-2 cm less than the abdomen at the umbilical level. At the level of 4th rib Fills pleural cavities in 75% cases. Sharp Dense, firm, non-crepitant and liver like.
Expands, arch shaped or drum shaped.
*Position of the diaphragm **Changes in the lungs of the cases Margins ***Consistency
At the level of 6th-7th rib. Fills pleural cavities in 75% of the volume Rounded Soft, spongy, elastic and crepitant
****Colour and expansion of air sacs
Uniformly reddish brown, bluish or deep violet according to the degree of anoxia. On pressing little froth-less blood comes out
Air sacs are distended with air and expanded raised slightly above the surface. Polygonal areas on the surface—mosaic appearance. On cut section, frothy blood comes out. As blood becomes aerated, mottled or marbled appearances
Blood in the lungs
The circulation is not increased
The circulation is twice after respiration.
*****Weight of the lungs i. Fodere’s test or Static test: Lungs are ligated across hila and separated ii. Ploucquet’s test
30-40 gm
60-70gm
1/70th of the body weight
1/35th of the body weight
*Abdomen should be opened before the thorax. Position of diaphragm is affected by decomposition. **It’s not true that the lungs are not expanded in the stillborn. ***The lungs are crepitant in artificial respiration and putrefaction also. ****In artificially inflated lungs, mottling is absent and on cut section little blood with no froth comes out. *****Both the tests result due to increased circulation and the weight of the lungs is not constant.
Infanticide and if they float the test is positive (this should exclude irregular and partial aeration). The pieces are then squeezed between thumb and index finger under the surface of water so that air bubbles comes out. If it still floats, then it is wrapped in piece of cloth and squeezed by putting a weight. If these pieces are still floating that means there is presence of residual air that indicates that respiration has been established. Before performing this test, a piece f liver that serves as control is allowed to dropped in water and if the liver also floats the test is of no use. Fallacies of hydrostatic test: 1. Expanded lungs may sink due to: i. Diseases such as acute pulmonary oedema, pneumonia and congenital syphilis ii. Atelectasis (non expansion) • Air not reaching the alveoli due to feeble respiration. • Complete absorption of air from the lungs by blood if circulation continued after respiration has been stopped or a state of asphyxia. • More air being expelled from the lungs during expiration due to recoil of lung tissue. • Obstruction by alveolar duct membrane. iii. Drowning: When birth occurs in a toilet bowl or in to a bucket containing water, the foetus may die due to drowning. 2. Unexpanded lungs may float: i. Putrefactive gases: Foetal lungs are resistant to putrefaction due to less blood. Soft, greenish air bubbles of different sizes that shift by pressure sink in water. ii. Artificial inflation: In conditions of mouth-tomouth respiration and blowing air by a tube, the lungs are inflated partially and stomach contains air. iii. Alcoholic fixation. 3. Hydrostatic test is not necessary, if i. Foetus is A. Testify in court B. Enter a contract of marriage C. Manage his own property D. None of the above Feigned insanity is A. Gradual in onset B. Without any motive C. Insomnia is absent D. Has dry and cracked lips and skin In real insanity all are present except A. The person has dirty and filthy habits B. Has a vacant expression C. Signs and symptoms are uniformly present D. Resents frequent medical esamination All the following are true about psychosis except: A. It is a reaction to stressful circ*mstances B. Empathy is absent C. The person looses touch with reality D. Insight is present
8
35
Part 1—Forensic Medicine and Pathology
Starvation Deaths Starvation is a state that occurs from withholding the food or administration of unbalanced food. Starvation can be acute or chronic. The acute starvation occurs from the sudden and complete stoppage of food but chronic starvation occurs from the gradual intake of deficient food. The starvation deaths may be intentional or accidental and even homicidal. The usual causes are famine, neglect on the part of the guardians or parents, willful refusal to take food like in case of hunger strike, the passengers during shipwreck or landslides if they are stranded and there is deficient supply of food. Clinical Features Acute starvation The sign and symptoms usually appear after 1216 hours of stoppage of food. There is a hungry feeling followed by epigastric pain, which is relieved by pressure. The absorption of subcutaneous fat starts after 5-6 days resulting in general emaciation. Therefore, the eyes are sunken, pupils are mildly dilated, the cheeks sink and the body prominences become more visible. The lips are dry and cracking is present, the tongue is coated and the person feels thirsty. There is salivation, voice becomes weak, the skin is dry becomes rough and pigmented at places. After a weeks time the muscles become weak. On physical examination the pulse becomes slow, the temperature is subnormal and constipation is the usual feature. The urine becomes scanty and evidences of acidosis are found. As time passes the body is
reduced to a skeleton, the thoracic cage becomes more prominent. The loss of 40-45% of body weight is fatal. In these cases the intellect remains clear. But in some cases the person experiences delusions, and at times hallucinations. Chronic Starvation The features of chronic starvation are: 1. The patient complains of hunger pains relieved by pressure, he becomes lethargic and there is disorientation. There is oliguria. 2. Evidence of pigmentation and the patient becomes anemic 3. Subnormal temperature leading to hypothermia 4. Edema of the feet and limbs 5. There is risk of infection like diarrhea, dysentery 6. The death occurs due to exertion, cardiac failure and chronic absorption. Fatal Period The fatal period if food is completely withdrawn then death occurs in 7-10 days. If the food alone is withdrawn death may prolong 8-10 weeks or even more. If there is complete starvation without intake of both food and water then death occurs in 10-12 days. If water is continued then death may occur in 6-8 weeks or more. 80-90% body fat should be lost along with 20-25% body weight should be lost for death to occur. However the following factors may modify the fatal period. 1. The young and the old die earlier than the adults 2. The females they tolerate starvation for a longer period than the males.
Starvation Deaths
515
3. Fatty and healthy people tolerate better than the weak. 4. Persons with active physical exertion die earlier
empty. In wasting diseases the gall bladder is empty in contrast to death due to starvation.
Cause of Death
The diagnosis of starvation is done on the basis of history and other general findings. But at the same time one has to exclude the wasting diseases like malignant diseases Addison’s disease, diabetes mellitus, tuberculosis, even pernicious anemia and sometimes chronic diarrhea. So in the absence of above diseases diagnosis is usually made in favour of starvation.
Death occurs from exhaustion, circulatory failure due to brown atrophy of the heart or intercurrent infection. Postmortem Appearance All organs and tissues show changes similar to premature senility. There is extreme emaciation and a reduction in the size and weight of all organs except brain. The brain can become soft and pale. Muscles get atrophied and become dark in colour as the muscle fibers loose the striations due to granular degenerations. The fat of orbits and female breast is the last to go. Fat is absent from the subcutaneous tissues and almost completely lost from the mesenteries. Subepicardial fat is replaced by a gelatinous material. In acute starvation subcutaneous body fat is not lost completely. In children, the skeleton shows spinal curve, rickets and dental defects. In adults progressive demineralization and osteomalacia are seen. Stress fractures may be present and the skin is lusterless and looses its elasticity. The face becomes pale. Ascites may be present in some cases. Hairs are also dry and lusterless and the nails are dry and brittle. The lungs are pale and collapsed and exude very little blood on cutting. The stomach and intestine are atrophied and are stained with bile. The spleen is shrunken and the gall bladder is distended with bile. The kidneys show atrophy of the nephron. Blood volume is reduced, and there is severe anemia. The urinary bladder is also
Medicolegal Aspects
Suicidal: Some persons have to voluntarily starve for the purpose of fulfillment of their grievances. At times the lunatics and hysterical women may refuse to take food. Rarely fasting is undertaken to attract the public attention. Right to life is guaranteed under article 21 of the constitution of India, which does not include the right to die. So forcible feeding of these persons are lawful. Homicidal: The victim is usually an infant or an aged person. At times the lunatics or mentally deranged persons also deprived of their food resulting in chronic starvation and finally death. Accidental: Accidental starvations may occur during famine or being trapped in landslides or shipwreck. There is failure to provide food due to ignorance of the people. Certain diseases produces stricture of the esophagus resulting in intake of insufficient food. Long Question 1. Define starvation. What are the postmortem findings in a death due to starvation?
MULTIPLE CHOICE QUESTION 1. In acute starvation: A. Feeling of hunger lasts around 10 hours B. If both water and food are withheld death occurs by 6-8 weeks
1 D
C. Both are true D. Both are false
36
Part 2—Forensic Toxicology
General Toxicology Historical Perspectives The use of poisons dates back as far as spiritual and mythological beliefs have been recorded. Perhaps the first accounts deciphered are from the Sumerians of Mesopotamia, the modern day Iraq. Here there are associations of poisons with ‘Gula’ who was regarded as a spirit or ‘the mistress of charms and spells’. This dates back to around 4500BC and tabulated accounts of her have been found from about 1400 BC. Even in Greek mythology there is reference to poison, although no apparent citation to specific poisons used exists. An example is that of Medea, one of the children of the sun. She became the wife of Aqueus, king of Athens. Aqeus’ son Theseus, returned to Athens to claim his rights and Medea, according to myth, resented this and vainly attempted to poison Theseus with a poisoned goblet. Records of Egyptian knowledge can be dated about 300BC. Menes, the earliest recorded Egyptian king studied the properties of poisonous plants. Detailed accounts at this time were not recorded as it was forbidden to reveal any secrets taught in the temples. Exposing these mysteries carried the penalty of death. There is however sufficient evidence from various papyri that the Egyptians were conversant with antimony, arsenic, copper, lead opium and mandrake etc. also the Egyptians were probably the first to master distillation and discovered how to extract a powerful poison from peach kernels. A translation by Duteuil on a payrus in Louvre shows the earliest recording of a preparation of a substance for lethal purposes. Today this extract is known as prussic acid (cyanide). Also peach kernels contain ‘cyanogenic glycosides’ that release toxic substances
in the presence of water. The ancient Greeks knew of arsenic in the form of realgar and orpiment, metals such as lead, mercury, copper, silver and gold and some of their properties. Amongst vegetable poisons, the Greeks chiefly employed Hemlock, for suicidal purposes and as State poison as a form of capital punishment. Socrates was found guilty of corrupting the youth of Athens with his philosophical teachings and in 402BC was made to drink the State poison that is Hemlock. The knowledge of poisons appears to have been more general among Eastern races. The Persians were very interested in the art of poisoning (405359BC) Queen Parysatis supposedly poisoned her daughter-in-law, Statira by means of a poisoned knife. Poisoning at the dinner tables was certainly not uncommon, especially in ancient Roman times. The Chinese around 246BC adopted a custom, which still exists today is the Chou Ritual. They used 5 poisons of which four are known; cinnabar (mercury), realgar (arsenic), green vitriol (copper sulphate) and loadstone. They are burnt together and the fumes are used on a bunch of features that is to be used externally. Now, the people started looking towards methods of prevention of fatal effects of the poisonous substances. Mithridates, the King of Pontos (Turkey) around 114-63 BC studied the subject of antidotes extensively. He tested various poisons on condemned criminals. During these ancient times, poisons were essentially viewed as ‘mysterious’ substances, and were poorly understood. Even in the relatively unscientific world of medieval Europe, there was a remarkable amount of knowledge about the effects, uses and treat-
General Toxicology 517 ments of poisonings. Poisoning was a popular subject of fiction along with the academic texts published on this subject. The monks often wrote these, as monasteries were the main seats of learning in a largely illiterate population. Magister Santes de Ardoynis wrote ‘The Book of Venoms’ in 1424 that had comprehensive account of poisons known at that time. Many of the poisons such as arsenic, atropine, opium, cyanide, strychnine and heavy metals were described in the treatises. Poisons and their effects were being studied predominantly to create a more virulent effect by the 14th and 15th centuries. Italian alchemists realized that combinations of known poisons could create a more potent effect. By the 17th century, poisoning had become such an art that there were schools in both Venice and Rome. By 1589, even a publication was made on the art of poisoning. The most notorious poisoner of the 17th century, a woman named Toffana had a recipe named ‘Aqua Toffana’ that aided the murder of over 600 people, usually husbands. In Rome in 1659, a society of women was formed in secret; meeting regularly and the members were issued with the poison they required and the instructions for its use. In the latter part of the 16th century, the popularity of homicidal poisoning spread from Italy to France, where those practicing criminal poisoning became known as the ‘French School of Poisoners’. In 1625, Louis XIV decided to limit the sale of poisons and passed a decree forbidding apothecaries to sell arsenic, sublimate or any other poisonous drugs except to persons known to them, and required purchasers to sign a register stating why they needed the substance. At this time Catherine Deshayes, a famous poisoner sold poison to many women wishing to rid themselves of their husbands. During the late 18th century, an important case of poisoning in Britain was that of Sir Theodosius Boughton, whose body was exhumed and found to be impregnated with what appeared to be arsenic. Mathieu Orfila is considered to be the father of toxicology, having given the subject its first formal treatment in 1813 in his Trait des poisons, also called Toxicologie generate. The late 19th century is often associated with poisoning epidemic. To try to improve the
way in which poisoners were caught and convicted the science of toxicology became increasingly important in the field of forensic medicine. However, as science progressed throughout the 19th century, so did poison detection (tests for arsenic—Marsh test in 1836 and the Riensch test in 1841) and the science of toxicology grew in importance and reliability. During the 20th century, the source, preparation and administration of poisons were stripped down; each process became cleaner, more attenuated and intellectually mastered. Poisoning in the 20th century grew massively because the man was evolving and discovering new things. Industry, agriculture, petro-chemistry, chemical warfare and pharmacology are but a few areas where hugely toxic agents were being put to use, often without the knowledge of their possible effects on life. Due to toxicological studies, many formerly hazardous occupations are now controlled and present minimal risk. For example, exposure to substances such as lead, mercury and aniline is now strictly controlled. Pharmacological disasters such as the use of thalidomide as a sedative during pregnancy in the 1960s, led to the development of teratology and a greater understanding of potential in-utero poisons. Arsenic remained a favourite for homicides in early part of the century. Cyanide too was popular around the middle of the century. The poison found a niche during the Second World War, and was used in liquid form as a suicidal tool for tortured agents of the resistance. Homicidally, cyanide enjoyed a resurgence of popularity in the latter half of the 20th century, with most of the poison secreted in food, drink and pharmaceutical products. Ricin, called the political poison of the 20th century became famous in the UK as a result of the ‘Umbrella assassination’ of Georgi Markov in 1978, who died several days after he was stabbed by the point of the umbrella. At autopsy it was found that at the site of injury a device containing Ricin was implanted. Thallium, a true 20th century poison is found in pest control substances. It kills by disrupting the sodium potassium ATPase pump and thus causes cell depolarization. In ancient India, women to get rid of their oppressive husbands used aconite, arsenic and
518 Textbook of Forensic Medicine and Toxicology opium. When we have a look at the history of ancient India, the literature describes various instances of poisoning. These include the description in Mahabharata of Bhim Sen being poisoned by Duryodhana. In India, poisonous substances are used to commit suicide, or homicide. It can also be accidental more commonly in the Children who may ingest the poison in lieu of the sweets. However, suicidal and homicidal poisoning is quite common in this country compared to the west. These days the use of the chemicals for domestic and industrial purposes accounts for an increase in number of accidental poisonings. The use of quack remedies for a quick relief and the injudicious use of Ayurvedic and desi medicines also result in accidental poisoning very often. Poisoning is the fourth most common cause of accidents in children. Children less than 5 years of age and adolescent are prone to poisoning. Accidental ingestions are most common in children less than 5 years old. The pattern of misuse of substances is changing these days with increase in number of intake of pesticides and insecticides that is easily available. In India the most common agents for poisoning are the pesticides such as the organophosphates, carbamates and pyrethroids etc. Besides the pesticides, sedatives, corrosives and alcohol are also commonly used. Also plant toxins are rarely used in the rural India. In the north India, aluminium phosphide is most commonly used to commit suicide as it does not have any antidote and is highly fatal. Poisoning is the fourth most common cause of accidents in children. Children less than 5 years of age and adolescent are prone to poisoning. The problem of illnesses and deaths is getting worse with the emergence of new drugs and chemicals. The properties, mechanism of action, lethal dose, detection and management of various poisonings will be discussed in the next few chapters. Forensic Toxicology Forensic toxicology deals with medico-legal aspects of the harmful effects of the chemicals on the human beings. It combines the basics of toxicological principles with analytical chemistry.
Toxicology Toxicology is the science dealing with the toxicity of substances. The word toxicology is derived from the Greek word ‘Toxon’ that refers to a bow used for shooting arrows. The word ‘toxeuma’ meant an arrow, and ‘toxicos’ is consigned to such a poison that in ancient times was often used on tips of arrows to produce a more lethal weapon. The substance inflicting toxic effect can be any drug, or any organic or chemical substance in the environment. Toxicology deals with the properties, actions, toxicity, lethal dose, symptoms, mechanisms, diagnosis, estimation and treatment of the poisonous substances. Toxinology Toxinology is the specialized area of toxicology that deals specifically with biological toxins, such as venoms or poisonous plants. Poison A poison is a solid, liquid or gaseous substance, which if introduced in to the living body, or brought in contact with any part produces ill effects or death by its local, systemic or both types of action. This definition is unsatisfactory as a substance in particular dose causes beneficial effects whereas in the same dose it can cause the toxic effects. Drugs that are used for the treatment of diseases in higher doses will produce toxicity. As Paracelsus, the father of modern toxicology said, “All things are poison and nothing is without poison. It is the dose that determines the poison”. Thus every drug is potentially a poison when used erratically. Paracelsus, the 16th century toxicologist was the first person to explain the dose response relationship of toxic substances. In Indian law, there is no definition of ‘poison’ and the various expressions are for it. In biology, poisons are substances that cause injury, illness or death of organisms usually by a chemical reaction or other activity on the molecular scale. Some poisons are also toxins, usually referring to naturally produced substances that kill rapidly in small quantities such as bacterial proteins that cause botulism and tetanus. Animal toxins that
General Toxicology 519 are delivered subcutaneously (e.g. by sting or bite) are called venom. A poisonous organism is one that is harmful to consume but a venomous organism uses poison to defend itself while still alive. A single organism can be both venomous and poisonous. Deliberate application of poison has throughout the ages been used as a method of homicide, suicide and execution. As a method of execution, the poison can be administered as ingested, as the ancient Athenians did, breathed, such as carbon monoxide or hydrogen cyanide or taken intravenously. Many substances are regarded as poisons are toxic only indirectly such as methyl alcohol, which is not poisonous itself, but is chemically converted to toxic compound formaldehyde in the liver. Many drugs are made toxic in the liver, and the genetic variability of certain liver enzymes makes the toxicity of certain compounds differ between one individual and the next. Exposure to radioactive substances can produce radiation poisoning. LD50—It is the dose of a toxic substance that kills 50% of a test population (typically rats or other surrogates when the test concerns human toxicity) Types of Poisoning The poisoning can be acute, subacute or chronic. Acute poisoning: In acute poisoning, whatever amount of poison is taken and the toxicity is manifested immediately Chronic poisoning: Small amount of poison are repeatedly administered for a long period producing the toxic effects. The substances commonly causing chronic poisoning are metallic poisons, opium, antimony etc. Subacute poisoning: In this the poisoning manifests between the acute and the subacute types of toxicity. Mechanism of Action of Various Poisons Some of the poisons on contact cause absorption and rapid death or impairment of function. The compounds acting on nervous system paralyze within seconds or less, include both biologically derived neurotoxins and so-called nerve gases, which may be synthesized for warfare or industry. Inhaled or ingested cyanide is used as method of
execution on US. Gas chambers almost instantly starves the body of energy by poisoning mitochondria and synthesis of ATP. Intravenous injection of an unnaturally high concentration of potassium chloride, such as in the execution of prisoners in parts of the United States, quickly stops the heart by eliminating the cell potential necessary for muscle contraction. Such rapid reactions are often called acute poisoning. A poison may also act slowly known as chronic poisoning and is most common for poisons that accumulate such as lead, mercury, copper etc. Factors Modifying the Actions of Poisons There are a number of factors that modify the actions of poisons: Quantity: The toxic effects of a poison vary with its quantity. Every drug is a poison when taken in a large quantity. But sometimes when a drug is ingested in a large quantity, it may induce vomiting and is rapidly eliminated leading to reduced toxicity. This occurs in alcohol and copper sulphate poisoning. Route of administration: The severity and rapidity of action depends on the route of administration or intake of the poison. Inhaled poisons are rapidly fatal compared to the parenteral poisons whereas ingested poisons are less severe and act slowly compared to that taken subcutaneously or intramuscularly. The poisons are more effective when taken on an empty stomach. Age and state of the body: Children, old, weak and diseased are more susceptible to the effect of the poison compared to the adults, healthy and stout persons. Idiosyncrasy: Idiosyncrasy is allergic or anaphylactic response to a substance in which even a drug that is otherwise safe produces toxic effect. This effect can be produced by a large number of substances. A substance that is being used therapeutically may produce toxic effects. This can be due to anaphylaxis, idiosyncrasy or from the over dosage of the drug. Tolerance: When a person uses some substance continuously, he is liable to tolerate larger than
520 Textbook of Forensic Medicine and Toxicology normal dose of that substance. This commonly occurs in an alcoholic who can tolerate larger than normal amount of morphine and related drugs. Cumulative action: When a poison that is excreted may accumulate and produce toxicity when given in repeated doses for a long time. Manner of Poisoning a. Homicidal poisoning is the administration of poisonous substance by a person to kill another. b. Suicidal poisoning is the intake of some poisonous substance by the individual himself for self-killing. c. Accidental poisoning generally takes place due to the storage of poisonous and non-poisonous substances at the same place. The injudicious use of the magic remedies and lovephilters can also result in accidental poisoning. The characteristics of ideal suicidal and homicidal poison are described: Characteristics Suicidal
Homicidal
Availability Cost Colour, taste and odour
Easy and free Low in cost Tasteless or with pleasant taste
Not so Not so Colourless, tasteless and odourless
Solubility with food and drink
Present
Present
Signs and symptoms
Should not be Resemble some there or very few natural disease
Onset of action Antidote
Quick onset Should not be available
Slow onset Should not be available
Toxicity Diagnosis from chemical tests
Highly toxic Difficult
Highly toxic Difficult
Death
Painless
Definite
Postmortem changes
May be produced
Nil
Common compounds used for the purpose
Aluminium phosphide, pesticides such as organophosphates and carbamates, barbiturates, potassium cyanide and copper sulphate and oxalic acid
Arsenic, antimony, aconite, thallium, organophosphorus compounds, strychnine, potassium cyanide.
CLASSIFICATION OF POISONS I. Corrosives A. Strong acids: • Inorganic or mineral acids—Sulphuric acid, nitric acid and hydrochloric acid. • Organic acids—Carbolic acid, Oxalic acid, acetic acid and salicylic acid. B. Strong alkalis: • Hydrates • Carbonates of sodium and potassium. C. Metallic salts: • Zinc chloride • Potassium chloride • Ferric chloride. II. Irritants A. Inorganic: • Metallic—Arsenic, lead, mercury, copper, zinc, thallium etc. • Non metallic—Phosphorus, chlorine, bromine, iodine. B. Organic: • Vegetable poisons—Castor oil seeds, croton oil, madar, semicarpus anacardium, calotropis, capsicum, aloes, Abrus precatorius • Animal—Cantharides, snake venom, insects, scorpion, spiders etc. C. Mechanical: Powdered glass, diamond dust, chopped hair etc. III. Neurotoxic A. Cerebral: • Somniferous—Opium, barbiturates • Inebriants—Alcohol, Ether and chloroform • Deliriant—Dhatura, Belladonna, Cannabis, Hyocyamus, Cocaine. B. Spinal—Nux vomica and gelsemium. C. Peripheral—Curare, Conium. IV. Cardiotoxic Aconite, Quinine, Digitalis, oleander, nicotine and hydrocyanic acid. V. Asphyxiants These are poisonous irrespirable gases such as carbon dioxide, carbon monoxide, hydrogen
General Toxicology 521 sulphide and coal gas. This category also includes the cyanides. VI. Miscellaneous A. Food poisons—Food borne botulism etc. B. Agaro-chemicals: • Pesticides and insecticides—Organophosphates, carbamates and organo chlorine compounds. • Bipyridal herbicides—Paraquats and diquat • Chlorophenoxy herbicides—Bromoxynil, ioxynil. • Rodenticides—Zinc phosphide, Strychnine sulphate, Sodium monofluoroacetate, Floroacetamide. • Fumigants—Aluminium phosphide, ethylene dibromide.
C. Domestic and commercial poisons: • Petroleum distillates—Kerosene, Petrol mineral oil • Disinfectants, detergents and cleansing agents. D. Drugs of abuse—Alcohol, Tobacco, Cannabis, Cocaine and opium derivatives, sedatives and hypnotics E. Chemical and biological warfare agents. Common Household Poisons and Their Treatment The common household poisons along with the symptoms and signs of their poisoning (Table 35.1).
Table 35.1 Preparation
Poisonous substance
Symptoms and signs
Management
Moth balls
Naphthalene
Nausea, vomiting, pain abdomen, albuminuria and hematuria, pulmonary oedema and coma
Stomach wash, soda bicarbonate, i.v. fluids. oxygen &artificial respiration
Baby powder
Boric acid
Nausea, vomiting, diarrhoea, convulsions, respiratory depression
Stomach wash, oxygen and artificial respiration
Insecticide spray
DDT/ organophosphorus compounds
Nausea, vomiting, tremors, convulsions, coma
Stomach wash, paraldehyde, oxygen and artificial respiration
Chalk
Arsenic, copper and lead in coloured chalks
Nausea, vomiting, pain abdomen, symptoms of metallic poisoning
Stomach wash and treatment of metallic poisoning
Fireworks
Arsenic, mercury, lead and phosphorus
Burns
Burns to be treated
Cosmetics (nail Potassium hydroxide, enamel, and thinners) barium sulphate, acetone, methyl salicylates and denatured spirit
Nausea, vomiting, burning in stomach
Stomach wash
Baking powder
Tartaric acid
Nausea, vomiting, burning pain abdomen,
Immediate soda bicarb to neutralize the acid
Baking soda
Sodium carbonate
Nausea, vomiting, abdominal distension
Vinegar
Crockery washing substance
Sodium and sodium polyphosphates
Variable symptoms depending on the substance
Symptomatic treatment
Match box and sticks
Silicates, antimony, phosphorus and potassium chlorate
Antimony and phosphorus poisoning
Treat symptoms of poisoning
Rat poison
Zinc phosphide
Nausea, hematuria,
Stomach wash, Inj. vitamin K i.m.,
Grain preservative
Aluminium phosphide
bleeding
oxygen and artificial respiration
522 Textbook of Forensic Medicine and Toxicology DUTIES OF MEDICAL PRACTITIONER IN A CASE OF POISONING The duties of medical practitioner are both legal and professional. Professional Duties Legal Duties of the Doctor 1. In all cases of suspected or confirmed poisonings the attending doctor should record all the findings in a medicolegal case report and inform the nearest police. 2. If the homicidal poisoning is suspected by the doctor, the Police officer should be informed (S. 39 CrPC). If the doctor fails to report the matter to the police, he will be held culpable under section 176 I.P.C. 3. The attending physician should collect, preserve and seal the evidence related to the case of poisoning such as the gastric lavage fluid, vomitus, faeces and urine etc. for onward transmission to the Forensic Science laboratory for chemical analysis. If the doctor deliberately fails to do so he is liable to be punished under section 201 I.P.C. 4. In all the cases of poisoning whether suicidal or homicidal, it is the duty of the attending physician to divulge to the police whatever information he has. Withholding the information or providing wrong information makes the doctor liable to be punished under section 202 and 193 I.P.C. 5. In case of poisoned patient on the verge of dying it is the duty of the attending doctor to record dying declaration if the magistrate is not available at that time. Even when the magistrate is recording the statement of such a patient, the doctor should examine the patient in regards to his consciousness and whether there is clear faculty of thought and judgment or not (compos mentis). 6. In cases that are brought dead to the hospital or the patient has died during the course of treatment, the doctor should not issue death certificate but instead send the body for autopsy examination.
7. In cases of food poisoning, the doctor should collect the contaminated food and sent it to the forensic science lab for chemical analysis. It is the duty of the doctor to report such cases to public health officials. TREATMENT IN POISONING CASES A. Stabilise the Patient It is very important to stabilise the patient first of all and to treat the most imminent danger to life immediately. B. Removal of the poisoning material from the system (Decontamination) • In cases of inhaled poisons, the individual should be shifted to fresh air and artificial ventilation should be started. • In cases of injected poisons from bite or an injection, a ligature should be tied to prevent it from further reaching the circulation. The ligature is loosened for one minute after every ten minutes to prevent gangrene formation. • In contact poisons affecting the skin, mucous membrane, any wound or introduced in the uterus or vagin* they should be irrigated with water and neutralized by application of suitable chemical. The poisons are most commonly ingested orally. Depending on the time lapsed after ingestion; much of the poison lying unabsorbed in the stomach should be removed. In all ingested poisons the guidelines to treatment are: 1. The stomach should be emptied by gastric lavage or emesis but emetics are avoided in corrosive intake. 2. Appropriate antidote should be given to neutralize the poisonous compound even despite gastric lavage and emesis as some poisons are secreted again in stomach after having been absorbed. 3. Aid elimination of poison by the intestines and kidneys of what has been absorbed. 4. Symptomatic treatment. 5. Egg whites are useful in most poisonings and tannin is antidotal to all alkaloids.
General Toxicology 523 In ingested poisons, the methods of decontamination are: (i) Gastric lavage (ii) Emesis (iii) Catharsis (iv) Administration of activated charcoal (v) Whole bowel irrigation. Stomach Wash (Gastric Lavage) Gastric lavage is indicated in patients who present within three hours of ingestion of poison. The stomach wash can also be carried in the presence of gastric secretions, delayed gastric emptying or in case of ingestion of sustained release medications. Gastric lavage beyond 6-12 hours is recommended in ingestion of salicylates, tricylics, carbamazepine and barbiturates. Gastric Lavage Tube: For gastric lavage, a soft rubber tube with a funnel at its one end known as Ewald or Boas tube is most commonly used. In adults an ordinary, soft, non-collapsible tube with 36-40 French size having one cm diameter and 1½ mts length is used. In children with 22-28 French size (Ryle’s tube) diameters should be used. The tube should have an attached glass funnel at one end and the other end should be rounded with lateral openings. There is a mark at a distance of 50cm from its rounded end. A suction bulb is placed at the mid of to tube to pump out stomach contents. Procedure for Stomach Wash Before performing stomach wash, the patient should be lying in a left lateral position or in a prone position with head hanging over the edge of the bed and the face is positioned downwards so the mouth is at a lower level than the larynx and chances of aspiration of fluid are eliminated. The gastric lavage tube is gently passed in to the stomach through the mouth by lubricating with glycerin or Vaseline jelly up to a distance of 50cm in adults and 25cm in children. The position of the tube in stomach can be checked by stethoscope or putting the upper end in a cut of water, if the lower end in the trachea, air bubbles will come out. For carrying out stomach wash, initially 250300mL of warm (35oC) saline or plain water is passed through the funnel held high up. In children, instead of water 10-15mL/kg body weight of warm
saline is used as in them there are chances of inducing hyponatremia and water intoxication. The stomach contents can be siphoned by the use of suction bulb. The first sample of stomach wash should be preserved for chemical analysis. Then stomach is carried out with chemical agents specific to the poisons. In certain specific poisonings, instead of plain water or normal saline, other solutions can be used that are specific for particular poisons. These solutions are: 1. Potassium permanganate (1:5000 or 1:10,000) is used as gastric lavage fluid in various oxidizable poisons e.g., alkaloids, salicylates. 2. Sodium bicarbonate (5%). 3. Tannic acid (4%). 4. Sodium thiosulfate (25%) can be used in cyanides and 5. Calcium gluconate is used for oxalates. 6. 1:2 Castor oil and warm water solution is to be used for carbolic acid and phenolic group of poisons. 7. Desferrioxamine (2 gm in 1 liter of water) is used for iron poisoning. In cases where potassium permanganate (a powerful oxidising agent) is used as gastric lavage fluid, the gastric lavage is continued till the colour of lavage fluid is colourless, odourless and no particulate matter is visible. At this time, a small quantity of fluid containing specific antidote or 1 gm/kg body wt. of the suspension of activated charcoal and/or an ionic cathartic is left in the stomach. Complications of Gastric Lavage 1. 2. 3. 4.
Laryngeal spasm. Aspiration pneumonitis. Perforation of stomach or oesophagus. Sinus bradycardia and ST elevation on ECG.
Contraindication of Gastric Lavage The contraindication for stomach wash are absolute and relative. Absolute contraindication: 1. Corrosive poisoning except Carbolic acid as there is danger of perforation. 2. Convalescent poisons.
524 Textbook of Forensic Medicine and Toxicology 3. Comatose patient as there is risk of aspiration 4. Volatile poisons due to the risk of inhalation. 5. If the patient is hypothermic. Relative contraindication: 1. If the patient is suffering from alimentary tract diseases like oesophageal varices. 2. Comatose patients. 3. Ingestion of alkali. 4. Advanced pregnancy. 5. Any haemorrhagic diathesis. 6. Any history of recent surgical operation. Emesis The emesis should be avoided as there is danger of aspiration of stomach contents in an unconscious patient. The easiest way to induce vomiting is by tickling the fauces. Also vomiting can be produced by the use of emetics of which ipecac is the most effective whereas mustard powder and warm saline can give rise to complications. Also Apomorphine and zinc sulphate are no longer used. These emetics are: i. Warm saline water comprising of 2tsf salt in 200mL of water. ii. Mustard powder 15 gms in 200mL of water iii. Zinc sulphate 1-2gms in 200mL of water iv. Apomorphine 3-6mg I.M. is the most potent and immediately acting emetic as it produces copious vomiting within 3-4 minutes. Apomorphine causes severe narcosis that is why it should not be used in comatose patients. If it is used, Naloxone hydrochloride, 5-10 mg i.m. should be administered that will counteract narcosis. v. Ipecacuanha powder 1-2gm or 30mL (15mL in children) of ipecac syrup causes vomiting with satisfactory results in a poisoned patient. It is derived from the root of Cephalis ipecacuanha and C. acuminata. The active principles are cephaline, emetine and traces of psychotropine and it causes activation of peripheral sensory receptors in the GIT and also stimulates the chemoreceptor trigger zone and vomiting center in the medulla thus causing vomiting. The contraindication of emesis are:
Absolute Contraindication 1. 2. 3. 4. 5.
Pregnancy. Heart disease. Haemorrhagic diathesis. Cardiotoxic poison ingestion. In infants and old patients.
Relative Contraindication 1. During convulsions. 2. Ingestion of convalescent poison such as strychnine. 3. Ingestion of strong acids and alkalis due to the chances of perforation. 4. Ingestion of kerosene oil as there are chances of aspiration pneumonitis. 5. Comatose or unconscious patients. 6. Foreign body ingestion. 7. Impaired gag reflex. 8. Poison that causes emesis. 9. Ingestion of petroleum distillates or drugs causing altered mental status. Complications of Emesis 1. Features of cardiotoxicity such as bradycardia, atrial fibrillation and myocarditis. 2. Aspiration pneumonitis. 3. Oesophageal tears may be caused due to protracted vomiting. C. Administration of Antidotes An antidote is defined as a remedy to counteract or neutralize the effects of a poison. In various poisonings antidotes are used to counteract the pathophysiology produced by a toxin. According to the mode of action antidotes are classified as: Mechanical or Physical Antidotes The mechanical antidotes counteract the effect of poison mechanically preventing their absorption without inactivating the damaging action of the poisons. These are of the following types Adsorbent like activated charcoal: Activated charcoal is a fine, black, odourless and tasteless type of amorphous carbon prepared by destructive
General Toxicology 525 distillation of materials such as burning wood, coconut shell, bone, sucrose, or rice starch that have much higher surface area than charcoal followed by treatment with an activating agent such as steam, carbon dioxide etc. The large surface area of activated charcoal confers a great adsorptive capacity to this material. Each gram of activated charcoal works out to a surface area of 1000 m2. Activated charcoal strongly adsorbs aromatic substances such as acetaminophen, salicylates, barbiturates and tricyclic antidepressants thus reducing their absorption from the gastrointestinal tract. Most inorganic substances are poorly absorbed by activated charcoal. The dose is 1gm/kg body weight (50-100 gm in adults and 10-30 gm in children) after making a suspension in 4-8 times the water. 4-8 gms of activated charcoal acts mechanically by absorbing and also retains in its pores organic poisons and mineral poisons to a less degree. The side effects are vomiting, diarrhoea, constipation, pulmonary aspiration and Intestinal obstruction. The contraindication of the use of activated charcoal are ileus, small bowel obstruction and when there is history of caustic or petroleum distillate ingestion. Demulcents: Demulcents produce protective coating over the mucous membrane of stomach to protect it from the action of poison. These are milk, egg white, starch, milk of magnesia and aluminium hydroxide gel. Bulky foods like Bananas, boiled rice or potatoes allow smaller amount of poison to be available to the stomach mucosa for absorption as they are admixed with the poison itself. The bulky foods are commonly used in ingestion of glass powder as these particles are embedded in them and prevent damage to the stomach mucosa. Diluents such as water, milk or other similar drinks that dilute the poison and delay their absorption. Chemical Antidotes The chemical antidotes disintegrate and inactivate poisons by undergoing chemical reactions along with the poisons and forming harmless or insoluble compounds. These are:
i. Weak non-carbonate alkalis: In corrosive acid poisonings, weak non-carbonate alkalis act as neutralizers. Strong alkalis are avoided as they can cause further damage the stomach. Non-carbonate alkalis are preferred as carbonate alkalis react with acids to produce carbon dioxide gas that inflates the stomach and may get ruptured. ii. Weak vegetable acids: In corrosive alkali poisoning, weak vegetable acids like citric acid, and acetic acid (vinegar, lemon juice) may be used. For arsenic poisoning, freshly prepared solution of ferric oxide can be used as it forms non-absorbable ferric arsenate. iii. Albumen: It is used for mercury poisoning as it precipitates Mercuric chloride. iv. Copper sulphate is antidote for phosphorus v. Potassium permanganate is an oxidizing agent use in poisoning with oxidizable substances like cyanides, phosphorus, atropine and other alkaloids. A dilute 1:5,000 or 1:10,000 solution of potassium permanganate is used in any poisonings such as aluminium phosphide, opium derivatives, insecticides, nicotine, cyanides, hydrocyanic acid atropine and strychnine etc. vi. Tincture iodine or Lugol’s iodine in a solution of 15 drops in half a glass of water precipitates lead, mercury, silver, alkaloids and strychnine. vii. Tannic acid (4%) or strong tea or 1 tsf of tannic acid dissolved in water is used to precipitate metals like lead, mercury, nickel, zinc, copper, aluminium, cobalt and silver; strychnine, nicotine, cocaine etc. Physiological Antidote The physiological antidote acts on the tissues and various systems of the body and produce signs and symptoms opposite to the signs and symptoms produced by the poison. They are basically of use when some of the poison has already been absorbed in to the circulation. They antagonize the effects produced by the poisonous substance. These are like Atropine for organophosphorus compounds, physostigmine, and neostigmine for
526 Textbook of Forensic Medicine and Toxicology Dhatura and barbiturate for strychnine. The different types of antidotes for various poisons are listed below: Poisons
Antidotes
Acetaminophen Anticholinergics (Datura fastuosa) Carbon monoxide Anticholiestrases (Organophosphorus compounds) Cyanide
N-acetylcysteine Physostigmine
Ethylene glycol Heavy metal poisoning
Iron Methanol Methaemoglobinemia Opioid Arsenic compounds Copper compounds
Oxygen Atropine sulphate, Pralidoxime chloride (2-PAM) Amyl nitrite, sodium nitrite and thiosulphate Ethanol Chelators, calcium disodium edentate (EDTA), dimercaprol (BAL), penicillamine and 2,3-dimercaptosuccinic acid (DMSA) Desferroxamine Ethanol Methylene blue Naloxone hydrochloride Ferric oxide Potassium ferrocyanide
Universal Antidote Universal antidote comprises of: 1. Activated powdered charcoal—2 parts by weight 2. Magnesium oxide—2 parts by weight 3. Tannic acid—1 part by weight 15 gms of this powdered mixture should be added to half a glass of warm water before consumption. The use of universal antidote is obsolete now-a-days but this can definitely used as a first-aid measure at homes.
used as war gas. This compound is used in heavy metal poisoning especially arsenic, mercury, lead, antimony, gold and thallium and also to some extent against copper, bismuth etc. Mechanism of action: Heavy metal ions have a great affinity for sulphydryl (SH) radicals in the cells and tissue enzymes and they combine with them by displacing hydrogen, thereby depriving the body of certain tissue enzymes whose activity depend upon the SH groups. The thiol (SH) group of B.A.L. will combine with the heavy metals in the system and will dislodge them from their combination with the sulphydryl radicals in the tissue enzymes and thus sparing the tissue from its toxic effects. Dimercaprol forms a rather stable compound with the heavy metal and gets excreted out of the body mainly in urine without causing any damage to the liver, kidneys etc. Dose of B.A.L is 3-4mg/kg body weight that is to be administered deep intramuscularly within first 4 hours of poisoning. The ampoule of B.A.L (100mg/mL) contains 2ml of 10% compound in Arachis or peanut oil with 20% benzyl benzoate solution. The injection must be given 4 hourly for first 2 days and then thrice daily for 10 days. Contraindications: Administration of Dimercaprol is absolutely contraindicated in cadmium poisoning (forms a nephrotoxic compound with cadmium) and any pre-existing liver disease. Also it is relatively contraindicated in any kidney disease.
Chelating agents inactivate a metallic ion with the formation of an inner ring structure in the molecule, when the metallic ion becomes the member of the ring. The chelating agents will form no-toxic stable soluble compounds with calcium and other heavy metals like arsenic, lead, mercury, copper, zinc, nickel, cobalt, manganese etc.
Side effects: The side effects of administration of Dimercaprol appear when it is administered in a dose more than 3.5mg/kg body weight. 1. Anorexia, nausea and vomiting. 2. Excessive salivation or lachrymation. 3. Generalized aches and pains. 4. Hyperthermia. 5. Feeling of constriction of chest. 6. Burning of eyes and throat. 7. Fall of blood pressure.
British Anti-lewisite (B.A.L)Dimercaptopropanol
E.D.T.A (Ethylene Diamine Tetra-acetic Acid)
B.A.L. was originally used as an antidote for Lewisite, a vesicant containing arsenic that was
E.D.T.A forms readily soluble, practically nonionized and nontoxic compound with heavy
Chelating Agents
General Toxicology 527 metals. It is a useful antidote for those heavy metals that have an affinity for calcium. Mechanism of action: When lead, zinc, manganese, cadmium, iron and copper form compounds with edetate, calcium cannot displace them. Calcium disodium EDTA chelates extracellular lead in soft tissues as well as in bones. In practice, edentate is given in the form of calcium disodium versenate to prevent rapid removal of calcium from the body. In the presence of lead, this chelating agent readily exchanges calcium for lead and thus detoxification and excretion of lead is done. The chelating agent renders lead water soluble, nontoxic, non-ionized and non-metabolized to get excreted intact in the urine. Edetate does not get metabolized in the body like Dimercaprol and is poorly absorbed by the gut. Calcium disodium versenate is the best known chelating agent against inorganic lead intoxication but not so effective in tetraethyl lead poisoning. It is used principally against lead intoxication but can also be used in copper, zinc and nickel poisoning. It is less effective in manganese, iron, cadmium and radio-active elements poisoning. It is superior to both BAL in the treatment of arsenic and mercury. Dose: 5 mL ampoule of 20% calcium edetate is dissolved in normal saline or 5% saline dextrose (250-500mL) solution. It is administered by slow I.V. drip. The concentration should not exceed 3% and the drip should not take less than two hours to complete. The usual dosage is 50-70mgm/ kg per day and in adults 1gm can be given I.V. Twice daily for five days. This should be repeated again after a gap of three days. E.D.T.A. should not be given orally as lead will get chelated in the G.I.T. and more of it will be absorbed. Side effects: 1. Thrombophlebitis from administration of strong solution. 2. Lower-nephron nephrosis. 3. Hypersensitivity to the agent. 4. Fever, headache, generalized malaise and fatigability. 5. Nausea, vertigo and vomiting. 6. Hypotension.
Contraindication: The only contraindication is raised intracranial pressure when fluids are to be restricted. Penicillamine (Cuprimine) Penicillamine is the product of hydrolysis of penicillin. It acts as a chelating agent because of possessing stable SH groups. It is advantageous to use this compound against poisoning due to lead, copper, mercury and zinc preparations, as it can be used orally and continuously for a long time without producing any major toxicity. It is also useful in treating Wilson’s disease (hepatolenticular degeneration) resulting from disorders of copper metabolism and cystinuria. Dose: It is given 0.5 gm orally half an hour before meals four times a day for a period of 8-10 days. Pyridoxine 25-50mgm/day can be given to counteract symptoms of pyridoxine deficiency. Side effects: The side effects of Penicillamine therapy are rare and are more pronounced when the patient is suffering from copper storage disease, cystinuria or scleroderma for a long period. 1. Hypersensitivity reactions in the form of skin rashes and nephrotoxicity 2. Optic neuritis resulting from pyridoxine deficiency. 3. Leucopenia, thrombocytopenia and agranulocytosis. Desferrioxamine Mesylate or Deferoxamine Desferrioxamine is a water soluble compound that has a great affinity for ferric ion. This acts as chelating agent against iron intoxication especially in case of acute poisoning through its role in accelerating removal of iron from the body in case of haemochromatosis cannot be challenged. It removes iron from ferritin, hemosiderin, a little from transferring but not from haemoglobin and cytochromes. Dose: It can be given orally, intramuscularly as well as intravenously: Orally: 8-10gms dissolved in 80-100mL of distilled water Intramuscularly: 1gm initially to be followed by 0.5gms twice or thrice daily
528 Textbook of Forensic Medicine and Toxicology Intravenously: 1-2gm in 5% of 500 mL of dextrose saline solution; not more than 15mg/kg body wt per hour or 80mgm/kg in 24 hours should be administered. D. Elimination of Poison by Excretion When more then 6-8 hours have elapsed after ingestion of the poison, the absorbed poison should be eliminated by excretory channels that are kidneys. In barbiturate and salicylates poisoning, this is the only treatment. Diuretics like chlorothizide, mannitol or furosemide are commonly used drugs. Fluid balance is to be maintained by IV fluid infusion. Peritoneal dialysis and exchange transfusion is done in small children in poisonings due to barbiturates, salicylates and iron. Hemodialysis is employed for removing barbiturates, salicylates, bromides, boric acid and thio-cyanates. The methods employed for the purpose are: Catharsis Cathartics reduce the transit time of the poisonous substance in the G.I.T but their efficacy in reducing the mortality or morbidity is not established. The cathartics are: Saline cathartics: These cathartics alter the physico-chemical forces within the intestinal lumen leading to osmotic retention of fluid which activates motility reflexes and enhances expulsion. The dose of recommended cathartics is: • Magnesium citrate—4mL/kg. • Magnesium sulphate—30gm (250mg/kg in children). • Sodium sulphate—30.gm (250mg/kg in children) in copious amount of water. The high dosage magnesium cathartics can result in hypermagnesemia. Saccharide cathartics: Sorbitol (D-glucitol), 50 mL of 70% solution is the cathartic of choice in adults because of better efficacy than saline cathartics but in children there is risk of hypernatremia. E. Symptomatic Treatment The patient should be treated for the symptoms accompanied with good nursing care under
constant supervision of the physician. Respiratory tract infection is commonly encountered more common in older patients who have been unconscious for hours and in whom gastric lavage was done. In such cases, routine antibiotic prophylaxis should be given. Dehydration, anuria, convulsions, circulatory collapse hepatic and renal failure should be taken care of. Fluid balance to be maintained by I.V. fluid infusion and I.V. mannitol should be administered to combat renal failure. BP and pulse rate should be maintained continuously. The airways should be protected and artificial respiration with oxygen inhalation to be given. Diagnosis of Poisoning in the Living 1. Symptoms appearing suddenly in a healthy person. 2. The symptoms appear uniformly and rapidly increase in severity. 3. When several persons are affected at the same time like food poisoning. 4. Detection of poison in the food. In such cases the following material should be collected: i. Stomach wash fluid. ii. Blood with sodium fluoride as preservative. iii. Urine with sodium fluoride as preservative. iv. Faeces. Diagnosis of Poisoning in the Dead 1. Postmortem appearances: Clothes and external surface of the body should be looked for stains of poison, vomitus and faeces etc. The dark brownish or black stains of lips and cheeks occurs in Sulphuric acid poisoning, yellowish brown stains appear in Nitric acid poisoning and grayish white stains in carbolic acid poisoning. 2. Colour of postmortem staining: The colour of postmortem staining depends on the poison ingested; Yellow coloured hypostasis develops in Phosphorus, Copper and Cherry red discolouration occurs in CO poisoning. 3. Odour from the body cavity: Many poisons have a characteristic smell that is peculiar to that particular poison.
General Toxicology 529 Type of poison
Characteristic smell
External Examination
Cyanides
Bitter almonds
Carbolic acid
Hospital disinfectant (soap like)
Alcohol
Acetone-apple like
Chloral hydrate & paraldehyde
Acrid-pear like
Aluminium phosphide & zinc phosphides
Fishy, phosphene like
Carbon monoxide
Coal gas
1. Postmortem staining: Normal colour of postmortem staining is coppery red or purple. It is: • Pink in CO poisoning, hydro cyanic acid poisoning, and in burns. • Purple or violet in asphyxia deaths. • Coffee brown in Potassium chlorate poisoning. • Dark brown in phosphorus poisoning. 2. Odour from the body: No disinfectants should be used as they may mask the smell. On opening the body the characteristic smell of poisons like HCN, Carbolic acid, Alcohol, ether, chloroform and opium can be felt. 3. Examination of the natural orifices: In the natural orifices the evidence of corrosive changes over the mouth, lips and tongue can be seen. They may be discoloured yellow in HCN poisoning. 4. Injection marks: This is particularly important in injectable poisons. 5. Colour of the skin: The skin may be discoloured yellow or jaundiced in phosphorus or acute copper poisoning.
Organophosphates
Garlicky
Hydrogen sulphide & N-acetyl cysteine
Rotten eggs
Ethanol, Chloroform & Nitrites
Sweet or fruity
4. Natural orifices: The discharges from natural orifices are characteristic of some of the poisons. 5. Injection marks over the body should be noted in some injectable poisons. 6. Evidence of marks of violence may be seen in homicidal deaths. The bodies that are poisoned are not readily decomposed. Postmortem Examination in a Case of Poisoning Aims: 1. To identify the type of poison. 2. To find out time since death. 3. To find out cause of death. 4. To find out the manner of death whether suicide, accident or homicide. 5. In infants to find out whether it is a live birth and viability. Diagnosis: The diagnosis in a case of poisoning should be made from postmortem appearances. The autopsy surgeon should read the inquest papers and the information relating to the poisoning should be gathered from the relatives about: (i) Quantity and quality of poison consumed (ii) Time of onset of symptoms after taking the poison (iii) Duration of illness (iv) Treatment given. Very often the information is inadequate so it is quite a difficult task when the bodies are decomposed or has ingested corrosive or irritant poisons. For this a thorough examination is to be carried out along with the histopathological examination and chemical analysis of viscera.
Internal Findings 1. All the organs must be examined and contents preserved for chemical analysis. 2. Any peculiar smell should be noted. 3. Mouth and throat should be examined for erosions or staining. 4. Upper respiratory tract should be particularly examined in cases of poisoning with volatile irritants or there may be presence of inhaled poisonous matter. 5. The mucous membrane of the stomach and gastro-intestinal tract should thoroughly be examined for the following signs of corrosive and irritant poisoning: i. Colour of the mucous membrane of stomach: The normal mucous membrane of the stomach is pale and white. Irritant poisons cause patchy redness of the mucous membrane at the cardiac end and greater curvature of the stomach but rarely of the pyloric end. Due to the irritant action of the
530 Textbook of Forensic Medicine and Toxicology poison, there may be small haemorrhagic areas along with mucous secretion. Redness of the mucosa of the posterior wall may also be found after death. In a case, gastric redness was detected after nineteen months of Arsenic poisoning and in another case twenty-one months after exhumation. The mucous membrane is velvety in appearance in Arsenic poisoning and is covered with viscid secretion that is blood stained. Redness of mucous membrane of stomach encountered in asphyxial deaths is due to generalized venous congestion. The hyperemia of stomach occurring in some of the diseased states is uniform in distribution. The colour of stomach walls may be discoloured due to the bile, fruit juice or food ingested that is uniform in distribution with no signs of inflammation. The mucous membrane may be red or hyperemic: • When the deceased had died during the process of digestion. • Asphyxial deaths when there is generalized venous congestion. • When the mucous membrane is exposed to oxygen. • In diseased states like chronic gastritis or gastric ulcer, the redness is uniformly spread and the ridges are usually not involved. • In deaths from poisoning, the redness is patchy; more marked at the cardiac end and greater curvature and also involves the mucosal ridges.The colour of stomach walls may be discoloured due to the bile, fruit juice or food ingested that is uniform in distribution with no signs of inflammation.In various poisonings, the colour of the walls of the stomach may be: Type of poisoning
Colour of stomach walls
Ferrous sulphate Amytal Soneryl Mercury Oxalic acid Nitric acid Copper sulphate
Green coloured Blue coloured Pink coloured Slate coloured Black coloured Yellow coloured Bluish green coloured
ii. Softening: Corrosive acids, alkalis and irritants cause softening of greater curvature and cardiac end of stomach as they damage the superficial epithelium. In diseased states such as peptic ulcer or malignancy this softening is uniform and limited to stomach whereas in putrefaction, the softening starts at the dependent parts and involves all the layers of stomach wall and inflammatory signs are absent. Carbolic acid causes hardening and shrinkage of mucous membrane. iii. Ulcers: Ulcers due to corrosives or irritant poisons are present on the greater curvature, have thin, friable margins and surrounded by signs of inflammation. The mucosa is soft and hyperemic. The ulcers due to disease or malignancy are seen on the lesser curvature with their well- defined punched out margins that are thickened and indurated. Gastric ulcer involves the lesser curvature, has sharply defined, thickened and indurated edges and redness in the neighbourhood of the ulcer. But the redness in the irritant poisoning is diffuse and extends to duodenum and small intestine. In chronic ulcer due to disease, aperture is oval or rounded and the margins are punched out. There is no charring and chronic adhesions to other organs are present. Rarely both the ulcers will look similar. After death, autodigestion by gastric juices occurs that appears near cardiac end, is large, irregular with rough edges and no inflammation or charring is there. iv. Perforation: The perforation of stomach may be found in strong acid such as sulphuric acid poisoning. The stomach is usually black in colour with extensively damaged mucosa. The aperture is large with irregular edge and the coats are lacerated through which acid escapes to the peritoneal cavity causing acute peritonitis. In a chronic gastric ulcer when perforation occurs, it looks either oval or round with a punched out appearance with indurated margin. In rare instances it may cause autolysis at the cardiac end of stomach without any peritonitis.
General Toxicology 531 v. Stomach contents: The contents of the stomach should be thoroughly examined for traces of poison and also for any distinguishable odour. All the organs of the body should be thoroughly examined for the signs of diseases to rule out diseased states leading to the death of the patient. Sometimes abortifacient drugs are introduce through the vagin*l route for which the vagin* and whole of the female genital tract be examined. Chemical Analysis in Poisoning An important proof of poisoning is the detection of poisons in the excreta, blood and viscera. The finding of the poison in the food, medicines act as a corroborative but not a conclusive proof. The medical practitioner must preserve all the viscera and get it sealed in his presence for onward transmission to the police officer who will forward it to the Forensic science lab for chemical analysis. Defence lawyer’s argument: If the poison is present in the stomach, it might have been introduced after death. The argument is useless if the poison is found in the viscera and preserved in a clean container to avoid contamination. It is not necessary to lay stress on the amount of poison in the analysis, except that: • Poison might have been taken as a medicine. • Poison is used on a regular basis habitually. • It is a natural constituent of the body. • It is a normal constituent of food. • It is produced during decomposition. It is possible that a person may die from the effects of the poison but none is found after death. When the poison has not been detected, the judge should the symptoms, postmortem report and oral evidence. The viscera along with certain body fluids should be collected, preserved and sent to the Forensic Science laboratory for chemical analysis by the forensic pathologist. The presence of poisons should be demonstrated by standardized analytical methods. The preservative for the viscera is rectified spirit or saturated saline solution. The blood can be preserved in potassium oxalate or sodium fluoride and urine should also be preserved
with sodium fluoride. The viscera that is preserved routinely should include the following: Viscera
Quantity
Preservative
Stomach with its contents
Whole of the stomach with entire contents
Saturated saline or rectified spirit
Small intestine with contents
Up to 30 cm with –do– 100 gms of contents.
Liver with gall bladder
500 gm
–do–
Kidney
–do–
Spleen
One half of each or whole Whole
Blood
10-20 ml
Potassium oxalate or sodium fluoride
Urine
30-50 ml
Sodium fluoride
–do–
About 10-20 ml of blood should be taken in a glass bottle from the femoral vein and should not be taken from the abdominal or pleural cavity, with potassium fluoride or sodium fluoride as preservative in suspected alcohol poisoning. About 30-50 ml of urine should be kept with sodium fluoride as preservative. Most of the poisons are ingested, so stomach and intestines are preserved. As they pass through the liver, it is also preserved and kidney being the organ of excretion and finally it is excreted in urine. Points to be followed while preserving the viscera: 1. The viscera are preserved in saturated solution of common salt or rectified spirit. Rectified spirit is not to be used in poisonings due to Alcohol, Acetic acid, Phenol, Phosphorus and paraldehyde where saturated solution of sodium chloride is used. Formaldehyde should not be used as a preservative because it makes extraction of poisons difficult. 2. Stomach and intestine are kept together in a glass jar and in another jar pieces of liver, kidney and spleen are preserved. Blood and urine are preserved separately in two glass bottles. Rubber inserts should not be used as it extracts some poisons like chloroform and phenols.
532 Textbook of Forensic Medicine and Toxicology 3. Quantity of preservative should be equal to the bulk of the organ. 4. Only two-thirds of the bottle should be filled allowing space for decomposition gases. 5. Bottles should be properly sealed. 6. Bottles should be well labeled bearing the name of the deceased, PM no., date and name of the police station. 7. Sample of the preservative used that is 100ml of spirit or 25gm of sodium chloride should be sent to the lab to rule out contamination. 8. A Copy of the postmortem report should also be sent along with the viscera. 9. A sample of seal should be sent along with the viscera. 10. Viscera along with the sample of preservative and sample of seal should be handed over to the police. Poisonings where special viscera is to be preserved: 1. Heart is preserved in Strychnine poisoning. 2. Brain is preserved in Strychnine and Organophosphorus poisoning. 3. Spinal cord is preserved in Strychnine poisoning. 4. Lungs are preserved in gaseous poisoning, Alcohol and Chloroform poisonings. 5. Skin with subcutaneous tissue is preserved in deaths resulting from injectable poisons, drugs of abuse and deaths from snakebite. In all these types of poisonings, control site should also be preserved. Failure to Detect Poison on Chemical Analysis of the Viscera Failure to detect poison occurs many a times in forensic practice in an alleged case of poisoning, in spite of circ*mstantial evidences are pointing towards the poisoning. The poisonous substance may not be detectable due to some of the following reasons. 1. Some individuals may be unusually susceptible to the deleterious effect of the poisonous substance 2. The whole of the poison has already been eliminated from the stomach and intestines by
vomiting or other means such as purging and if absorption had occurred it got detoxified, neutralized, conjugated and finally eliminated by the kidneys etc. 3. The chemical analysis may be faulty due to submission of wrong, insufficient or decomposed material for analysis whereas sometimes faulty techniques used in the lab or inexperienced technical staff resulting in improper evaluation of the death or the quantity of poison is below detection limits. 4. Some of the alkaloids, toxins of Clostridium and Salmonella and chemicals like LSD-25 cannot be detected by chemical analysis. 5. There may be uneven distribution of absorbed poison in various organs depending on the type of poison and mode of administration e.g. when a poison is injected intravenously the blood levels are higher than liver levels. Analytical Techniques in Medical Toxicology The analytical techniques for the detection of poisons, drugs and various chemicals are more dependable and satisfactory than the usual chemical and biochemical methods. The common analytical techniques employed in toxicological analysis are: I. Spectrophotometric: It is based on the absorbance or transmission of light from a colour reaction at a specific wavelength. It include the following techniques: (i) Calorimetric (ii) Fluorimetric (iii) Automation. II. Chromatographic: It is based on the migration of compound on adsorbent (solid phase) by a mobile phase. It includes: • Thin layer chromatography (TLC). • Gas liquid chromatography (GLC). • High pressure liquid chromatography (HPLC). • Gas liquid mass spectrometry (GL-MS). III. Competitive binding assay or immunoreactive assay: • Radioimmunoassay (RIA). • Enzyme immunoassay (EIA). • Fluorescent Polarization immunoassay (FPIA). • Immunotubidimetric assay.
General Toxicology 533 Samples to be Collected for Various Analytical Procedures i. Blood for recently used drugs. ii. Serum or plasma sample for protein bound drugs. iii. 24 hours urine sample for free drug analysis. iv. Random urine sample for drugs with a longer half life. Important Points to be Remembered • The sensitivity and specificity of the technique determines its utility. • The target of drug testing is either the parent drug or its metabolite. • The urine and blood are analyzed usually but urine contains 1000 times more drug than the blood so it is the preferred sample. • Blood is useful to identify recently used drugs • The cut off value is also critical in determining if a drug test is to be reported as positive or negative. • False negatives are far more common than false positives. Comprehensive drug testing is very important mainly for psychiatrists in arriving at precise evaluation and appropriate treatment plan for a drug addict. Diagnosis of polydrug abuse is not possible of which the psychiatrists and forensic toxicologists are now more aware of and are therefore interested in laboratory testing of body fluids for various drugs of abuse. Thin Layer Chromatography (TLC) Thin layer chromatography is used as a broad spectrum screen for detection of drugs of abuse. It is most inexpensive technique and does not require any sophisticated instruments. The results of this technique are only qualitative and cannot be quantified. Its major drawback is that it has a low sensitivity (1000-2000 mg/mL) and low specificity. TLC relies on a reproducible migration pattern by the drug on a thin layer adsorbent such as silica gel coated glass plates. The characterization of a particular drug is achieved by colour reactions produced by spraying the plates with colour complexing reagents. The patient’s sample
is spotted along with other known drugs on a TLC plate which is put in a solvent chamber. The solvent is dried and sprayed with various complexing reagents. The coloured spots of various known drugs are compared with unknown patient’s sample. The location of spot is identified by an Rf number =
Distance traveled by a drug Distance traveled by solvent from the origin, where sample was spotted
The spots in the TLC plates can be visualized by UV or fluorescent light. TLC method was designed to detect high dose of a drug, recent drug abuse and toxic levels of drugs. It is a good test for an emergency where drugs taken are not known and presence or absence of a drug is necessary to start the specific treatment. The TLC results are not generally admissible as forensic evidence. In this technique, it must be understood that whether the sample is positive or negative depends upon the concentration of drug in a sample or the sensitivity of cut-off value of the assay. Often the cut-off value is set high to avoid false positives especially for legal purposes. False positive results are quite unusual by TLC but they can be confirmed with a more specific test. The low level of substances is not easily determined by this method. Gas Liquid Chromatography(GLC) Gas liquid chromatography separates molecules by the use of a glass or metal tube that is packed with material of a particular polarity. The sample of drug is vaporized at the injection site and carried through the column by a steady flow of gas. The column terminates at detector that permits recording and quantification. The time from injection till a response is observed at the recorder or integrator, referred to as Retention time (RT). Identical compounds travel through column at the same speed because their interaction with packing material is same. The drug of abuse in patient’s sample (urine/blood) is extracted and purified before it is injected on to the column. Retention time of patient’s sample is compared with RT of known drugs of abuse, processed under similar conditions. If the two are identical, the sample is
534 Textbook of Forensic Medicine and Toxicology confirmed with that particular drug of abuse. GLC is significantly more specific and sensitive than TLC and some drugs are detected better with GLC. High Pressure Liquid Chromatography (HPLC) High pressure liquid chromatography is similar to GLC but it uses liquid rather than gas to propel the sample through the column in HPLC. Some drugs are better chromatographed on HPLC e.g., tricyclic antidepressants and Benzodiazepines. HPLC is more specific and sensitive than TLC. Gas Chromatography-mass Spectrometry (GC-MS) Gas chromatography-mass spectrometry analyzes a drug according to its fragmentation pattern. Weaker bonds of molecules are broken under stress to produce a fragmentation pattern. A perfect match with a fragmentation pattern in a computer library is considered an absolute confirmation of the drug and is referred to as ‘fingerprinting’ of molecules. GC-MS is 100-1000 times more sensitive, specific, more reliable and most definitive forensic quality procedure that the TLC system. Being expensive, it is impractical for screening but vital for confirmation of drug presence and identity which is specific for medicolegal cases. Radioimmunoassay and Enzyme Immunoassay (RIA and EIA) They operate on the principle of antigen antibody interactions. The drugs of interest are compelled to large molecules and then injected into rabbits or sheep to produce antibodies against the drug. The immunologic methods used for detection employ antibodies against specific drug and competing drug molecules that are tagged enzymatically or that possess radioactivity. Immunoassay reliability depends on how specific and sensitive the antibodies are to a given compound. This is important because cross reacting compounds can result in false positives or falsely elevated results. That is why competitive binding assays are deemed to have much lower specificity than chromatographic techniques. Enzyme Multiplied Immunoassay Technique (EMIT) is the most widely used EIA methodology. It utilizes the
enzyme glucose-6 phosphate dehydrogenase (G6PDH) as the active tag. The assay is based on the catalytic reduction of NAD→NADH, which is measured spectrometrically at 340 nm. EMIT procedures are less sensitive and specific in cannabinoids that the RIA but EMIT is quite popular and commonly used because no extraction or centrifugation is required and system levels itself to easy automation. EIA screens yielding positives should always be confirmed by alternative methods GC-MS. Prevention of Poisoning The poisonings usually results due to lack of proper storage places in the house. Various accidental poisonings can be avoided when the following precautions are taken: 1. The medicines and chemicals should be stored out of reach and site of children and at a considerable height and preferably locked and separately from other household products. 2. The medicines, chemicals and household products should not be transferred and be kept in their original, labeled containers. 3. The medicines should be stored in child resistant packs and all the medicines and chemicals etc. should be properly labeled. 4. Before consuming the label with its directions for use should be properly read. 5. Empty containers of liquid medications, chemicals and household products should be rinsed with water before throwing. 6. Always protect skin and eyes while spraying insecticides with maintenance of adequate ventilation. POISON INFORMATION CENTRES The incidence of poisoning has increased markedly during the last decade but has received attention of public professionals and authorities quite recently. Poison information centre is a specialized unit that provides information on poisoning to the community. The main functions of such a centre are: 1. Provision of toxicological information. 2. Advice on the management of poisoning cases 3. Training to the professional and paraprofessionals on first-aid, management and prevention of poisoning.
General Toxicology 535 4. It also provides toxicological laboratory services 5. In developing contingency plans for chemical disaster with other responsible bodies. 6. The center responds to chemical disasters. 7. The center carries out epidemiological and experimental studies to find out the toxic risks and mechanisms. National Poison Information Centre, Delhi In India, National poisons information centre was established in 1995 at department of pharmacology, All India Institute of Medical Sciences, New Delhi. The center provides information on poisoning management. It holds teaching and training program on poisoning prevention and management. It also plays an important role in developing contingency plans for chemical disasters and conducts research related to antidotes, environmental and biological monitoring of the chemicals and toxico*kinetics. The centre provides information on management and treatment protocols of various poisonings all over the country. The centre provides round the clock service all 365 days of the year. Besides this, the center has the backup of latest literature on poisoning. The Poison Information Consultant after taking an exact history and the relevant details about the product consumed will provide the precise and concise information on the product involved, likely signs and symptoms, pre-hospital treatment, supportive and symptomatic care, antidotal therapy including dosage and availability. Also the entire information is recorded in a specific Performa for evaluation of data and further follow-up. The Poison Information Centre also conducts studies on the pattern of poisoning in a particular area and developing a prevention programme. National Poison Information Centre has readymade information cards covering the signs and symptoms, prehospital and hospital management protocols including therapeutic drugs and antidote dosing schedule on Organophosphates, Carbamates, Organochlorines, Aluminium phosphide, Ethylene dibromide, Pyrethroid, Rodenticides, Corrosives, Tricyclic antidepressants, Benzodiazepines, Phenytoin, Methyl alcohol, Carbon monoxide, Paracetamol, Opioids, Datura, Yellow Oleander, Scorpion sting,
Copper sulphate and Cyanide. Various poisoning manuals and books are available at the centre. The Centre is also in the process of setting up a National Antidote Bank that will stock all essential antidotes. In India, besides this centre, there are Poison information centres at Ahmedabad, Cochin and Chennai. Western Australian Poisons Information Centre This centre serves more than half of the area of Australia including Western Australia, South Australia, the Northern Territory, the Australian Capital Territory and a small region of western New South Wales. The centre provides telephonic consultation to medical professionals and the general public in cases of acute and chronic poisonings. The centre provides toxicological advice on the management of exposures to prescription and nonprescription pharmaceuticals, household and industrial chemicals, plants, animals, pesticides and other agricultural products. The centre also conducts formal training in clinical toxicology and toxinology for all its staff members. The centre also undergoes many research activities. The American Association of Poison Control Centres It is a nationwide organization of poison centres and interested individuals with the objectives: 1. To provide a forum for poison centres and interested individuals to promote the reduction of morbidity and mortality from poisonings through public and professional education and scientific research. 2. To set voluntary standards for poison center operations. The activities of this centre include: i. Certification of regional poison centers and poison centre personnel. ii. Interaction with private and governmental agencies whose activities influence poisoning and poison centers. iii. Development of public and professional education programs and materials. iv. Collection and analysis of national poisoning data.
536 Textbook of Forensic Medicine and Toxicology The association also grants awards and research fellowships. Victorian Poisons Information Centre This centre is located at the Royal Children’s Hospital, Melbourne. The centre provides timely and safe information in cases of poisonings and suspected poisonings. Telephonic advice is provided on first-aid treatment of poisonings or suspected poisonings with or without referral to the hospital. To the health professionals information is given about formulations of products and management of poisoned patients. National Poisons Information Service, UK This centre also responds to queries relating to toxic exposures to drugs and chemicals. The queries from doctors and other healthcare professional are answered. The NPIS on-line database, Toxbase is available for consultation. LAWS IN RELATION TO THE POISON Indian Statutes on Drugs Many legal acts controlling and regulating the manufacture, sale, distribution and possession of drugs and poisons are passed in India. These include the following: The Opium Act 1857 This Act was the earliest enactment concerned with the issue of licenses for cultivation of poppy, the delivery of produce to the officers of the central government at the established rates, fixing the limits of issuing licenses from time to time within which licenses can be issued and fixation from time to time of prices to be paid for the opium produced in respect of which it ensured. The Opium Act 1858 This Act was enacted to regulate the possession, transport, export, import, and sale of opium. The primary aim was protection of public welfare by preserving health, eliminating undesirable moral and social effects, commonly associated with the indiscriminate use of this drug.
The Poisons Act, 1919 The Poisons act was passed in 1919 and it prohibits the import of any specified poison except when it is according to the conditions of license and regulates the grant of licenses. It also regulates the possession for sale and the sale of any specified poison. The Act was amended in 1958. The Act followed the Opium Act 1878 as an important drug legislation touching dangerous drugs. The Dangerous Drugs Act 1930 This Act was enacted in pursuance of the obligation undertaken by the Government of India to ratify the Geneva Dangerous Drugs Convention 1925, for the suppression of illegal traffic in and abuse of dangerous drugs, especially cocaine and morphine. With that object it provided for the exercise of control by the Central government over the cultivation of dangerous drugs; production and supply of opium and opium derivatives; manufacture of or manufactured drugs like cocaine, methadone, morphine and other narcotic substances, medicinal opium; export, import and transshipment of dangerous drug. It deals mainly with opium, Indian hemp and coca leaves. The Drugs and Cosmetics Act, 1940 The drugs and cosmetics Act deals with the import, manufacture, sell, stock or exhibit for sale, and distribution of proprietary medicine. Every patent or proprietary medicine should display on the label of the container either the true formula or list of ingredients contained. The Act was amended by the Drugs Act 1964 to include Ayurvedic, Siddha and Unani Drugs. The Drugs Act 1940 The Drugs Act 1940 regulates the import, manufacture, distribution and sale of the following drugs in India: • Patent or proprietary medicines. • Vaccines and sera, toxins, toxoids, antitoxins, antigens and other biological products of such nature.
General Toxicology 537 • Vitamins, hormones and analogous products • The drugs meant for use of humans and animals and those used in the treatment, mitigation or prevention of a disease. The Drugs Act 1940 was amended by the Drugs Act 1955. The Drugs (control) Act 1950 This Act seeks to control the sale, supply and distribution of drugs. It provides for the fixation of maximum prices chargeable, the maximum quantity which may at any time be possessed by the dealer or producer, the maximum quantity which may in any one transaction be sold to any person. It also includes the issue of cash memo for sale, markings of prices and exhibiting list of prices and stocks, etc. The Drugs and Magic Remedies Act 1954 This Act prohibits the advertisem*nts of magic remedies for: 1. The procurement of miscarriage or prevention of conception in women 2. Improvement and maintenance of the capacity of sexual pleasure 3. To correct menstrual disorders 4. For the diagnosis, cure, mitigation, treatment or prevention of any disease, disorder or condition specified in the Schedule to the Act or the rules The Act also specifies the exceptions to these advertisem*nts. The Narcotic Drugs and Psychotropic Substances Act 1985 This Act repeals the Opium Act 1857, The Opium Act 1878 and the Dangerous Drugs Act 1930. The Act shall extend to whole of India. The object of the Act is to consolidate and amend the law relating to narcotic drugs, make stringent provisions for the control and regulation of operations relating to narcotic drugs and psychotropic substances and make provisions for matters connected therewith. The Act defines Narcotic drug, psychotropic substance, medicinal cannabis, opium, opium derivatives, opium poppy, poppy straw, poppy straw concentrate, cannabis (hemp), canna-
bis plant, coca derivative, coca leaf, manufacture, production, preparation and addict etc. Narcotic drug: It is defined as meaning coca leaf, cannabis (hemp), opium, poppy straw and includes all manufactured drugs: Manufactured drug: It means: 1. All coca derivatives, medicinal cannabis, opium derivatives and poppy straw concentrate. 2. Any other narcotic substance or preparation that the Central government declares to be a manufactured drug. Psychotropic substance: It means any substance, natural or synthetic, or any natural material or any salt or preparation of such substance or material included in the list of psychotropic substances specified in the schedule. Addict: It means a person addicted to any narcotic drug or psychotropic substance. Small quantity: It means such quantity as may be specified by the Central government in the official Gazette. The burden of proving that it was intended for personal consumption shall lie on the person found in possession of the drug or psychotropic substance. The small quantities as specified in the central govt. in the official gazette given in the table below: Drug
Quantity
Heroin Cocaine Hashish/Charas Opium Ganja
5 grams 2 grams 100 grams 25 grams 1 Kg
Offences and penalties: Chapter IV of the Act defines offences and penalties under the Act. The Act provides punishment with rigorous imprisonment which shall not be less than 10 years but which may extend to 20 years with fine which shall not be less than one lakh rupees but which may extend to two lakh rupees for the following contravention. The Court may for the reasons recorded in the judgment impose a fine exceeding two lakh rupees. The contraventions for which such punishment is contemplated, may be of any rule or order made or condition of a licence granted thereunder relating to poppy straw, coca plant and coca leaves, prepared opium, opium poppy and
538 Textbook of Forensic Medicine and Toxicology opium, cannabis plant and cannabis, manufacture dugs and preparations, psychotropic substances, embezzlement of opium by cultivator, illegal import or export or transshipment of narcotic drugs and psychotropic substances, external dealings in narcotic drugs and psychotropic substances in contravention of S.12 (S.24), allowing premises etc. to be used for the commission of an offence punishable under the Act (S.26). LAWS IN RELATION TO POISONING IN THE INDIAN PENAL CODE Section 284 I.P.C: Negligent conduct with respect to poisonous substance: Whoever does, with any poisonous substance, any act in a manner so rash or negligent as to endanger human life, or to be likely to cause hurt or injury to any person, or knowingly or negligently omits to take such order with any poisonous substance in his possession as is sufficient to guard against any probable danger to human life from such poisonous substance, shall be punished with imprisonment of either description for a term which may extend to six months, or with fine which may extend to one thousand rupees, or with both. Section 299 I.P.C: Culpable homicide: Whoever causes death by doing an act with the intention of causing death, or with the intention of causing such bodily injury as is likely to cause death, or with the knowledge that he is likely by such an act to cause death, commits the offence of culpable homicide. Hence if A administers a substance to B with such intent or knowledge and thereby causes B’s death, A may be convicted under this section of the offence of committing culpable homicide, irrespective of whether the substance administered may or may not strictly be called a poison. For it is the intent which suffices to constitute a crime, irrespective of the dose or even the nature of substance. Section 304A I.P.C: Causing death by negligence: Whoever causes the death of any person by doing any rash or negligent act not amounting to culpable homicide, shall be punished with imprisonment of either description for a term
which may extend to two years, or with fine, or with both. Section 324 I.P.C: Voluntarily causing hurt by dangerous weapon or means: Whoever, except in the case provided by Section 334, voluntarily causes hurt by means of any instrument for shooting, stabbing, or cutting, or any instrument which, used as a weapon of offence, is likely to cause death, or by means of fire or any heated substance, or by means of any poison or any corrosive substance, or by means of any explosive substance, or by means of any substance, which is deleterious to the human body to inhale, to swallow or to receive into the blood, or by means of any animal, shall be punished with imprisonment of either description for a term which may extend to three years, or with fine, or with both. Section 326 I.P.C: Voluntarily causing grievous hurt by dangerous weapons or means: Whoever, except in the case provided for by the Section 335, voluntarily causes grievous hurt by means of any instrument for shooting’ stabbing, or cutting, or any instrument which used as a weapon of offence, is likely to cause death, or by means of fire or any heated substance, or by means of any poison or any corrosive substance, or by means of any explosive substance, or by means of any substance, which is deleterious to the human body to inhale, to swallow or to receive into the blood, or by means of any animal, shall be punished with imprisonment of either description for a term which may extend to ten years and shall also be liable to fine. Section 328 I.P.C: Causing hurt by means of poison, etc., with intent to commit an offence: Whoever administers to or causes to be taken by any person any poison or any stupefying, intoxicating or unwholesome drug, or other thing with intent to cause hurt to such person, or with intent to commit or to facilitate the commission of an offence or knowing it to be likely that he will thereby cause hurt, shall be punished with imprisonment of either description for a term which may extend to ten years, and shall also be liable to fine.
37
Part 2—Forensic Toxicology
Corrosive Poisons Corrosives are the poison that fixes, destroys and causes erosion of the surface coming in its contact. Some organic acids like oxalic and carbolic acid act as corrosives in concentrated form as do carbonates of sodium and potassium. Certain metallic salts e.g. sodium chloride, potassium cyanide, ferric chloride, chromates and bichromates of alkalis also act as corrosives. Classification 1. Strong acids: A. Inorganic or Mineral: (i) Sulphuric acid (ii) Hydrochloric acid (iii) Nitric acid. B. Organic (i) Carbolic acid (ii) Oxalic acid (iii) Acetyl salicylic acid 2. Acid like corrosives: (i) Dimethyl sulphate (ii) Diethyl sulphate (iii) Ozone, atmospheric oxidants (iv) Sulphur dioxide 3. Alkalis: (i) Sodium hydroxide (ii) Potassium hydroxide (iii) Sodium carbonate (iv) Potassium carbonate (v) Ammonia 4. Phosphates such as polyphosphates. Mode of Action The mode of action of inorganic or mineral acids like sulphuric acid, hydrochloric acid and the nitric acid are: 1. Causes only local action but no remote effects on the system. 2. In concentrated form, they cause corrosion and destruction of the tissue 3. Extracts the water from the tissues. 4. Fixes, destroys and erodes the tissues. 5. Converts Haemoglobin in to Haematin. 6. Causes coagulation necrosis by precipitation of proteins.
7. The mucosa of the Oesophagus is relatively resistant to the acids. 8. Mucous membrane of stomach especially pyloric region is very susceptible and in this region necrosis commonly occurs. 9. Complications develops from 3 weeks to 3 months of ingestion of the substance.. 10. Corrosives act as irritant and when well diluted act as stimulant. General Principles of Treatment 1. The stomach wash should not be given as there are chances of perforation of stomach. However Levin tube can be used for stomach wash within half an hour of ingestion of poison. The tube should be passed softly and with due care avoiding the risk of perforation of stomach and oesophagus. 2. Emesis is to be avoided as there is risk of perforation of already thinned out stomach and oesophagus 3. Acids should be immediately diluted and neutralized by drinking plenty of water containing a tablespoonful of calcium oxide, magnesium oxide or aluminium hydroxide gel. If these are not available then Demulcents like vegetable oil, soap solution, milk, limewater or white of an egg should be followed by Barley water and olive oil. 4. Bismuth subcarbonate 30gm should be given. 5. Morphine 15 mg i.m or i.v or Meperidine HCL 50-150mg orally or i.v should be given for pain. 6. 10mL of 10% Calcium gluconate should be given intravenously
540 Textbook of Forensic Medicine and Toxicology 7. Blood transfusion can be given if needed. 8. Tracheostomy can be performed if oedema of glottis is present. 9. Oxygen inhalation and artificial respiration can be given, if necessary. 10. Corticosteroids should be administered to prevent oesophageal strictures. 11. To prevent formation of strictures later on, ½ inch mercury filled bougie should be passed daily. 12. In case of skin burns, wash with large quantities of water or apply paste of sodium bicarbonate. 13. Eye burns are treated symptomatically after irrigating with water for 10-15minutes. 14. Use of strong alkalis such as carbonates and bicarbonates of sodium and potassium should be avoided as they produce CO2 and can cause distension and perforation. Causes of Death I. Death occurring within few hours can be due to shock or spasm or oedema of glottis II. Within 24hrs, death results from perforation of stomach leading to peritonitis and shock. III. Within first week the death may result from septic absorption IV. After months or years due to exhaustion and malnutrition due to oesophageal or pyloric stricture or incurable dyspepsia due to destruction of coats of mucous membrane of the stomach. SULPHURIC ACID (OIL OF VITRIOL) Properties • Pure Sulphuric acid is colourless with no fumes and it chars, and blackens the skin. • Commercial Sulphuric acid is dark or brown in colour due to the addition of impurities like lead sulphate, arsenic or nitric acid. • Nordhausen acid or H2S2O7 (pyrosulphuric acid) is stronger; brown, oily and fuming liquid used in the manufacture of indigo. • Sulphate of indigo is 1: 10 (H2S2O7) • Sulphuric acid is chiefly used for preparing chlorine, for dissolving metal, for cleansing
drains, for medicinal purposes, and to remove fur from kettles Signs and Symptoms of Sulphuric Acid Poisoning Immediately after swallowing are: 1. Intense burning pain in mouth, throat, oesophagus and up to the stomach. 2. Dribbling of acid mixed with saliva on the angles of mouth and chin causing corrosion and brownish discolouration of skin over angles of mouth, chin and over the chest 3. Frothy eructation, retching and vomiting; vomited matter is acid, contains blood, mucous and shreds of mucous membrane 4. Oral cavity: Mucosa of mouth and lips are softened, excoriated, corrugated and covered with dirty white necrotic membrane that assumes brownish black discolouration. The oral cavity is full of secretions consisting of saliva, blood, mucous making speech and swallowing difficult and may even result in death from asphyxia. 5. The tongue is swollen, excoriated and discoloured with white coating that becomes dark later on. It may get disorganized in to a shapeless, pulpy mass 6. The teeth are dead chalky white deprived of polish 7. Lips are swollen, excoriated, brown or black streaks resulting from the action of acid running from the angle of mouth to the chin and chest 8. Intense thirst and an attempt to drink water brings vomiting that leads to dehydration. Along with vomiting, there is extreme dysphagia 9. Voice is hoarse and husky and speech is painful and difficult due to the inflammation of epiglottis, uvula etc. 10. Breathing is difficult and noisy due to swollen and inflamed fauces and tender abdomen 11. Asphyxia may result from glottic oedema or aspiration of regurgitated acid contents 12. Bowels are constipated with marked tenesmus and straining during defecation.
Corrosive Poisons 541 13. Urine is scanty or suppressed with pain during micturition. 14. General condition of collapse like cold, clammy skin, decreased Blood Pressure and increased pulse may be there. 15. Mind remains calm until the end. 16. Cold clammy skin, feeble pulse and difficult respiration, convulsions and death in 12-24 hours 17. Complications in the form of mediastinitis or peritonitis from perforation of oesophagus or stomach and stricture of oesophagus may develop within a few weeks Acid burns: These are full thickness burns that have well defined edges and tend to heal slowly with scar formation.
Figure: 36.1: Mucosa of stomach as seen in sulphuric acid poisoning
Autopsy Findings Postmortem findings depend upon the quantity and strength of acid and the time of survival. A. External findings: Evidence of acid corrosion and chemical burns with brownish black parchment like and corroded spots are seen over chin, cheek, neck and chest resulting from trickling of the acid. Excoriation of lips, corrosion of mucosa of mouth and tongue, chalky-white teeth are characteristic. Mucous membrane of mouth, tongue and lips shows brown or brownish black corroded spots with necrosis that are grayish white initially but changes to brownish black and leathery. When taken by spoon, lips and mouth escape injury. B. Internal findings 1. The changes produced from corrosive poisoning are limited to the upper digestive tract and respiratory system. 2. The mucous membrane of oesophagus is inflamed, swollen by oedema and severe interstitial haemorrhage is present even when corrosion is absent. The perforation is rare 3. The mucous membrane of stomach is inflammed, oedematous blackened with peppery feel. 4. Peritoneal cavity is filled with black grumous acidic liquid containing mostly altered blood
5.
6. 7.
8. 9. 10.
from escape of the acidic stomach contents into peritoneal cavity following perforation of stomach (Fig. 36.1). The greater part of the stomach is converted in to soft, boggy, black mass that readily disintegrates on touching. The mucosal ridges are more damaged than intervening furrows. The mucosa on stripping shows intense congestion and inflammation underneath. The perforated stomach has softened walls and edges of rupture looking black and irregular. The small intestine especially duodenum shows evidence of irritation. As a result of perforation of oesophagus or stomach, the thoracic and abdominal viscera is blackened and corroded by acid with features of chemical peritonitis. Corrosion and severe inflammation of larynx and trachea may be found. Oesophageal strictures in delayed deaths. If patient survives longer fatty degeneration and toxic swelling of liver and kidney may be seen.
Diagnosis 1. Haemoconcentration in red blood cells is noticed. 2. Diffuse mottling of lung fields on X-ray when there is inhalation of acid vapour.
542 Textbook of Forensic Medicine and Toxicology 3. Chemical tests i. When sulphuric acid is mixed with barium nitrate or chloride, white precipitate of barium sulphate is produced. ii. Strong sulphuric acid chars organic matter. Medicolegal Aspects (i) Accidental as it is mistaken for glycerine or castor oil (ii) Mostly it is employed for suicidal purposes due to its easy availability (iii) Not used for homicidal purposes (iv) Acts as an abortifacient when injected in to vagin* (v) Employed for the purposes of vitriolage causing grievous hurt (vi) Cases are there when acid is thrown on the private parts, out of jealousy in extramarital affairs. Vitriolage or Vitriol Throwing Vitriolage is throwing of strong sulphuric acid, concentrated mineral acid, corrosive alkalis, carbolic acid, or the juice of marking nut over the face or body of the victim for the purpose of disfiguring the face, destroying the vision for causing injury on the body or even destroying the clothing of the victim. Malicious persons do this when they have a hatred or enemity to the victim. Some people use old electric bulb filled with acid to carry out their motive. Local effects: (i) There is severe burning pain and corrosion of the tissues with formation of brownish black burned areas that later on leave a permanent scar. (ii) The stains on skin and cloth are yellowish when nitric acid is used but blackish when sulphuric acid is used. (iii) Blindness may result if eyes are involved. (iv) Extensive disfiguring injuries are caused on the face. (v) Death may occur from shock, toxaemia or infection from severe chemical burns inflicted on the skin. The burns are penetrating, painless and the acid devitalizes the tissues and predisposes to infection. Slow repair and formation of scar tissue with contracture occurs. Treatment 1. Wash with plenty of water or soap solution. 2. Apply magnesium oxide or carbonate as thick paste.
3. Cover the raw surface with tannic acid jelly or soframycin or penicillin tulle gauze dressing. 4. Wash the eyes with plenty of water and irrigate with 5 gm of sodium bicarbonate and one ounce of water. Subsequently few drops of castor or olive oil are to be dropped in to eye. The corneal ulcers are treated with atropine ointment, hydrocortisone and antibiotics. Medicolegal Aspsects (i) Blindness amounts to grievous injury (ii) Scar tissue formation also amounts to grievous injury (iii) Vitriolage amounts to dangerous injury. NITRIC ACID— HNO3 (AQUA FORTIS) Pure nitric acid is colourless, clear liquid gives fumes when exposed to air. It has a peculiar chocking odour. A powerful oxidizing agent dissolves all metals except gold and platinum. It destroys organic matters with formation of xanthoproteic acid that imparts deep yellow colour to the affected tissues. Signs and Symptoms The signs and symptoms produced by ingestion of concentrated nitric acid are similar to those of sulphuric acid but since it has tendency to char the tissues, perforation of stomach does not occur. 1. Lips, tongue and mucous membrane of mouth are soft. Initially it is white then yellow due to formation of xanthoproteic acid. 2. The clothing is also stained yellow due to xanthoproteic reaction 3. Teeth and clothes are yellow stained. 4. Abdomen is more distended and tender due to formation of large quantities of gas by direct action of acids on the organic matter of stomach. 5. Violent vomiting occurs and the vomitus is yellowish brown containing altered blood. 6. Gaseous eructations are more frequent and distressing. 7. Oliguria and anuria occurs and albumin and casts are seen in the urine. 8. As nitric acid like hydrochloric acid but unlike sulphuric acid is volatile and gives fumes at
Corrosive Poisons 543 room temperatures, the effects produced by the inhalation of fumes are: (i) Irritation of the eyes with lachrymation and sneezing (ii) Photophobia (iii) Burning in the throat (iv) Cough (v) Feeling of constriction in the chest. (vi) Dyspnea—The death may occur immediately from suffocation due to oedema of glottis or later on from pulmonary oedema or bronchopneumonia. Fatal period→12-24 hrs Fatal dose→10-15 ml. Tests for Nitric Acid i. When Ammonia water is added to the yellow stains, it turns to yellow. ii. When iodide and ammonia is added to the yellow stains, the stains disappear. iii. When bile and ammonia is added to the yellow stains, there is no change iv. If strong solution of ferrous sulphate and Sulphuric acid is added to a solution containing nitric acid, a brown ring is formed at the junction between the two. The test is for the presence of nitrates. Autopsy findings 1. Postmortem appearances are similar to those of sulphuric acid but tissues are stained yellow. 2. Oesophagus and stomach are not stained yellow but is brown or brownish black due to the formation of acid haematin. 3. Perforation is not so common. 4. If the death is from inhalation of fumes then the respiratory passages are congested; lungs are congested and oedematous and the lining membrane of right auricle may show inflammatory changes. Medicolegal Aspects (i) Mostly accidental or suicidal (ii) rarely homicidal. HYDROCHLORIC ACID (HCL) Pure Hydrochloric acid is colourless and fuming liquid with strong pungent irritating odour. The strong solution gives fumes even at ordinary air and temperatures. When the solution is ingested, its liberated gas is also inhaled. It is a natural
constituent of the fluids of stomach and bowel. It is used for preparing chlorine, for dissolving metal, for cleaning drains, to remove fur from kettles and as medicine. Muriatic acid is the solution of hydrochloric acid gas in water having yellow colour and fumes strongly in damp air. It is used commercially and is less destructive than sulphuric and nitric acids. HCL does not stain the skin and mucous membrane but stains dark clothes reddish brown. Since it is volatile, it readily affects the Respiratory tract mucosa. Signs and Symptoms 1 Hydrochloric acid is less active than the other two acids hence symptoms are much milder. 2. It does not corrode or damage the skin. 3. It readily destroys the mucous membrane. 4. Mucous membrane is gray or gray white changing to brown or black. 5. Inhalation of fumes causes: (i) Irritation of the air passages (ii) Spasm of glottis (iii) Symptoms of suffocation (iv) Cough, Dyspnea and cyanosis. Chronic Poisoning Constant exposure to fumes produces chronic poisoning. The symptoms and signs of chronic poisoning are: (i) Coryza (ii) Conjunctivitis (iii) Corneal ulcer (iv) Pharyngitis (v) Bronchitis (vi) Inflammation of gums (vii) Loosening of teeth. Fatal dose→15-20 ml Fatal period→18-24 hours. Autopsy Findings 1. The findings are the same as that of sulphuric acid poisoning but there is less tendency to charring and tissue destruction. 2. Oral cavity and oesophageal mucous membrane is ashy grey in colour but may get blackened, swollen and hardened if the acid is concentrated. 3. The stomach contains brownish acidic fluid and mucosa is corroded and grayish white in colour 4. Perforation is rare. Chemical tests: On addition of silver nitrate to a solution of hydrochloric acid, a white precipitate of silver chloride is formed.
544 Textbook of Forensic Medicine and Toxicology Medicolegal Aspects (i) Mostly suicidal poisoning is common (ii) There are a few cases of accidental poisoning (iii) It is very rarely homicidal (iv) It is rarely injected in to the vagin* to produce abortion and it causes atresia of the vagin* (vi) It is used for erasing writing; attempts for forgery may be there. CARBOLIC ACID This is hydroxy benzene obtained from coal tar oil by fractional distillation. Pure carbolic acid has colourless, prismatic needle shaped crystals with burning sweetish taste. It turns pink and liquefies when exposed to air. It has carbolic smell, is slightly soluble in water and freely soluble in glycerine, ether and alcohol. It is used as an antiseptic and disinfectant agent. Commercial carbolic acid is dark brown liquid containing several impurities chiefly cresol. Carbolic acid and its derivatives are commonly used as disinfectants, antiseptics, germicides, caustics and preservatives kept in cupboards and almirahs. Lysol is as dangerous as phenol, which is used in the manufacture of explosives, fertilizers, textile, rubber, plastics, dyes, drugs and in preservations of vaccines etc. Significance of change in colour: It serves as a warning of toxic properties of acid when use as an antiseptic on the wounds Poisoning by carbolic acid is known as Carbolism. Absorption: It is readily absorbed from gastrointestinal tract, respiratory tract, rectum, vagin*, serous cavities, wounds and skin. Elimination: Phenol is converted in to hydroquinone and pyrocatechol in the body before it is eliminated in the urine. Only traces are excreted in lungs and it is partly detoxified in the liver. Complete elimination occurs by 36-48 hours Fatal dose→10-15 gm Fatal period→3-4 hours.
2. Carbolic acid has a great penetrating power as it coagulates protein but does not occur in chemical combination with them. 3. When applied to the skin, it produces burning sensation, numbness, and anaesthesia due to its action on the nerve endings. 4. It produces a white opaque eschar, which falls off in a few days and leaves a brown stain that may persist for several weeks. 5. It causes irritation and necrosis of the mucous membrane that may slough and get inflamed. 6. In small doses, it stimulates respiratory centre and methemoglobinemia can occur following poisoning with hydroquinone. Signs and Symptoms
Mode of Action
The signs and symptoms arise immediately after swallowing the acid (i) Burning sensation in the mouth and throat. (ii) Mucous membrane of the mouth and lips is hard and white (iii) Rapid absorption of acid in to the blood stream is soon followed by giddiness insensibility and coma (iv) Face is pale and cyanosed (v) Pupils are constricted (vi) Temperature is decreased (vii) Pulse is increased, feeble and thready (viii) Respiration is slow and laboured (ix) Smell of carbolic acid is present in the breath (x) Convulsions and lockjaw may be present. (xi)Carboluria: Urine is scanty and suppressed, when passed there is normal or greenish hue that becomes dark or olive green on exposure to air due to oxidation of pyrocatechol and hydroquinone in air that are the oxidation products of carbolic acid. Phenol is partly oxidized; partly unchanged that is excreted in the urine; partly free and partly unstable combination with Sulphuric acid and glucoronic acid (xii) Oochronosis: The hydroquinone and pyrocatechol may cause pigmentation in the cornea and venous complexes. and various cartilages , it is seen in chronic poisoning. It is normal associated with alkaptonuria and gets deposited in cartilage.
1. Carbolic acid acts locally as a corrosive and systemically as narcotic, induces sleep and drowsiness.
Causes of death: (i) Syncope (ii) Asphyxia due to respiratory failure, oedema of glottis and complications such as pneumonia.
Corrosive Poisons 545 Treatment 1. Emetics at times fail due to anaesthetic effect 2. Stomach wash: The tube is passed carefully and the wash is done with plenty of warm water along with charcoal, olive oil, castor oil, magnesium or sodium sulphate. The combination with phenol of these substances forms a harmless compound. The soap solution or 10% glycerine can also be used, until the washing are clear and odourless. Then 2 ounce of castor oil or liquid paraffin is left in the stomach. 3. Demulcents such as milk and white of an egg are given. 4. To combat circulatory collapse, i.v. Saline containing 7gm/litre of sodium bicarbonate is administered. Sodium bicarbonate also helps to dilute carbolic acid content of blood and it promotes excretion by promoting the flow of urine. 5. Oxygen inhalation and artificial respiration when needed. Autopsy Findings External findings 1. Dark brown excoriations may be seen at the angle of mouth and chin. 2. Signs of splashing may be present on the other body parts. 3. Tongue is white or swollen. 4. Smell of phenol comes from the mouth. 5. Mucous membrane of mouth is corrugated, sodden and white or ash gray small submucosal haemorrhages may be seen. Internal findings 1. Oesophageal mucosa is tough, white gray, corrugated and arranged in longitudinal folds. 2. Stomach mucosal folds are swollen and covered with opaque gray or brown mucous membrane with a leathery feel (Fig. 36.2). The intervening furrows are less damaged and the mucosa is often dark red, partly separated and necrotic with severe congestion of underlying mucosa. The stomach may contain reddish fluid
Figure: 36.2: Mucosa of stomach as seen in carbolic acid
3. 4. 5. 6. 7.
mixed with mucus and shreds of epithelium emitting odour of phenol. Duodenum and upper part of small intestine shows changes similar to the stomach. Liver and spleen are in the form of white, hardened patch when in contact with stomach. Kidney is inflamed and shows haemorrhagic spots. Lungs are congested and oedematous. Brain is congested and at times oedematous.
Medicolegal Aspects (i) Used for suicidal purposes (ii) Accidental poisoning results from its medicinal use and when it is introduced in to vagin* for abortion. Application of phenol preparations on wounds, ulcers, abraded skin, injections into abscess cavity, rectum, vagin* or uterus can also result in accidental poisoning (iii) Due to its peculiar phenolic odour and taste, it is rarely is it used for homicidal purposes. OXALIC ACID (ACID OF SUGAR AND SALT OF SORREL) Oxalic acid is colourless, transparent and prismatic crystals resembling magnesium sulphate. It is an organic corrosive acid. It is prepared from sugar by oxidation with nitric acid or by heating sodium or potassium formate. The differences
546 Textbook of Forensic Medicine and Toxicology between oxalic acid and magnesium sulphate are summarized in the table below: Difference in oxalic acid and magnesium sulphate Features
Oxalic acid
Magnesium sulphate
Taste
Sour and acid
Reaction
Strongly acid, pH0.8mg/litre is suggestive of chronic lead poisoning.
Metallic Poisons 553 • • • • •
5pg/dL—indicates exposure. >30pg/dL—there is a need to find the source. >60pg/dL—de-leading agents should be given. >80pg/dL—there is a risk of Encephalopathy >100pg/dL—should be treated as emergency.
Urine Levels 1. In a 24-hour urine sample, an excretion of more than 0.08 mg/litre is significant. On examination of urine: • Coproporphyrin level more than 0.15 mg/ 24hrs are suggestive of lead exposure. • δ- Amino-levulenic acid >6 mg/L has some lead effects. • δ-Amino-levulenic acid >19 mg/L leads to lead poisoning. 2. Glycosuria, haematuria, proteinuria occurs. 3. The urinary excretion of more than 1 mg of lead/ mg of calcium edetate at 25 mg/kg but not exceeding a total of one gram. Spinal fluid: Spinal fluid analysis should be avoided unless it is quite essential. The pressure is raised with increased proteins and pleocytosis. X-Ray findings: Radiological examination shows transverse bands of increased density at the growing i.e., metaphyseal ends of the bones in the children 2-5 years old mainly. Multiple bands suggest repeated episodes of exposure. Abdominal X-ray shows opaque particles at the recto-sigmoid area. Autopsy Findings (i) Blue line on the gums at their junction with the teeth (ii) Fatty degeneration of paralysed limbs (iii) Stomach and intestine show ulceration and haemorrhages and the walls are contracted (iv) Liver and kidneys are contracted and show granular degeneration (v) Heart is hypertrophied and shows atheromatous changes. Treatment 1. Remove the individual from the source of exposure. 2. Potassium or sodium iodide 1-2 gm thrice daily for 5-7days to assist in the elimination of lead by the kidneys.
3. Sodium bicarbonate 20-30 G/day for 4-5 doses leads to transformation of tri-basic lead phosphate to soluble dibasic phosphate and carbonic acid is liberated. 4. De-leading may be carried out. 5. EDTA, Penicillamine or B.A.L. is given i.m. for 7-10 days; 18 mg/kg/24 hrs for 2 days then 12 mg/kg/24 hrs for third day and 6 mg/kg/24 hrs for next 2 days. 6. Saline purgatives can be administered 7. In lead encephalopathy, EDTA is given. Prophylactic Treatment in Chronic Poisoning (i) Adequate exhaust ventilation in factories (ii) Personal cleaners (iii) The worker should take a diet rich in calories and plenty of milk (iv) Water containing minute quantities of H2SO4 (v) Saline purgatives should be given (vi) Periodical medical examination of the staff working in lead factories. Medicolegal Aspects Metallic forms not poisonous, but when acted upon by secretions of the intestine and may act as a poison after being absorbed in to the system as a salt: 1. Chronic lead poisoning is regarded as one of the industrial diseases. 2. Compounds of lead are poisonous provided they are in a condition fit for absorption. In the absence of air, pure water has no action on lead, but in the presence of air, it is slightly soluble and lead hydroxide is formed. 3. Acute lead poisoning is very rare, when it occurs, recovery usually occurs. 4. In chronic poisoning, workers are referred to medical practitioners under ‘Workman’s compensation Act 1923. Children get compensation, if death occurs. 5. Homicide by lead is rare as very few cases are reported when lead acetate is mixed with beer. 6. Accidental poisoning occurs by use of Litharge (Mudrasang)—lead monoxide as a remedy for syphilis by quacks. 7. Used criminally as abortifacient, the paste used on abortion stick contains red lead or lead tetra oxide.
554 Textbook of Forensic Medicine and Toxicology 8. Cattle poison: Red lead alone or when mixed with Arsenic is used as a cattle poison. 9. It is used as to adulterate snuff (powdered tobacco or medicine sniffed through the nostrils) to improve its colour. 10. Lead is normally present in all human tissue, deposited in the bones, nail, tooth and hair and very poorly in lead. No lead is found in ovary but is present in the testes. It has got no affinity for fetal tissues. Accidental poisoning occurs in the children by eating pica, old paint, plaster; feeding bottles made of glass contain lead, lead nipple shields, toys, and street dirt. Also the cosmetics like face powders, hair dyes used by the mothers secreted in the milk can cause accidental poisoning in the children.
ARSENIC Arsenic is a metallic poison known since ancient times. The Greeks knew it as early as 500BC and Hippocrates used it as an external remedy for ulcers, although there is no record of it being used as a poison this early. An eight-century Arab alchemist Jabir ibn Hayyen was the first to obtain white arsenic by heating realgar. It is thought that it was around this time when criminals first employed arsenic as a poison. Before white arsenic was known, most of the poisons used had a distinguishing taste, smell or colour but arsenic has very little smell or taste so it is undetectable by the victim. It is the common environmental toxicant and is found in soil, water and air. It ranks 20th in elemental abundance in earth’s crust and 12th in the human body. Properties of Arsenic Arsenic is element 33 in the periodic table and is classically considered a heavy metal. It exists in 3 allotropic forms and in several ionic forms. Environmental arsenic exists mainly as sulphide complexes realgar (As2S2), Orpiment (As2S3) and iron pyrites. On heating of these ores, arsenic sublimes and oxidizes to form arsenic trioxide (As2O3) a fine granular white powder also known as white arsenic. Arsine gas (AsH3) is another
arsenic compound, formed by the hydrolysis of metal arsenides and by the reduction of metals of arsenic compounds in acidic solutions. The main source of Arsenic is Arsenopyrites, realgar (Arsenic di-sulphide, As2S2) orpiment (Arsenic trisulphide, As2S3) and Arsenolite (Arsenic trioxide, As2O3). It is usually obtained as a by-product from smelting of copper, lead, zinc and ether. Natural Sources of Arsenic The average daily intake of arsenic in adults is 0.5-0.1mg. Arsenic is a widely distributed element and is found in: (i) Rocks and soil in concentrations of less than 1ppm (ii) Hot spring mineral waters (iii) Drinking water supply (iv) Sea-water contains 2-5mg/L (v) Plant and plant products (vi) Vegetables, fruits and grains (vii) Seafood (Fish, Shellfish, crabs and Dover-sole) and meats. Marine organisms particularly shellfish may contain large amounts of well-absorbed trimethylated organoarsenic, arsenobentaine that exerts no known toxic effects when ingested by mammals and is excreted unchanged in the urine (viii) Poultry and meat products: Arsenilic acid has been used as a food additive for poultry and other livestock to promote growth and weight gain. The poisoning may result from regular consumption of such products but at times accidental poisoning of livestock has occurred. There are instances of Beef or cattle being poisoned by ingestion of field grass that has been previously sprayed by herbicides. The interaction of Arsenicals with bacteria is thought to account for the changes in the oxidation state and chemical form of arsenic. Industrial Sources of Arsenic Arsenic is used primarily in the production of glass and semiconductors, in wood and hide preservation, as an additive to metal alloys to increase hardening and heat resistance. In the past Arsenic was used as weed killer, rodenticide, in chemical warfare and in the production of pigments and enamels. Arsenic may be introduced in to the environment through (i) Industrial process such as smelting of other metals (ii) Application of arsenical
Metallic Poisons 555 pesticides and herbicides (iii) Generation of power from coal (iv) Geothermal sources (v) Coal and combustion of coal. In the metallic form Arsenic is not poisonous as it is insoluble in water and cannot be absorbed from alimentary tract, but when it is oxidized by exposure to air becomes poisonous. But some workers believe that the metallic form may undergo oxidation in the GIT producing symptoms. Compounds of Arsenic The compounds of arsenic are organic as well as inorganic. The inorganic compounds are Arsenate (AS5+) and Arsenite (AS3+) 1. Arsenious oxide or Arsenious tri-oxide (AS2O3): It is a heavy metal with a specific gravity 3.669. Its curious property is that it floats in water as a white film and is soluble in spirit. It is found as impurity in iron ores, mineral acids. Also found in soils, mineral water and coal smoke. It is widely used in: (i) Calico-printing (ii) Taxidermy (preparing, mounting skin of animals) (iii) Preparation of artificial flowers (iv) Wall papers preparation (v) Preservation of timber and skin against Ants (vi) Used by Hakims and Vaidhs to treat Rheumatism, skin diseases, syphilis and impotence. 2. Copper Arsenite (Scheel’s green, Paris green) 3. Red Arsenic (Arsenic disulphide) 4. Yellow Arsenic (Arsenic trisulphide) 5. Arsine gas (AsH 3 )—is hemolytic and nephrotoxic. Organo-chemicals Many organo-chemicals ranging in toxicity from the war gas Lewisite to lead additives such as Arsenilic acid. In general their toxicity is similar to that of inorganic ones. These are: (i) Cacodylic acid (ii) Sodium cacodylate (iii) Atoxyl (iv) Salvarsan (v) Neo salvarsan. Pharmaco*kinetics and General Toxicity of Arsenicals Arsenic can be inhaled and absorbed through the skin or through GI tract after ingestion. After a very small dose of arsenic (like that experienced
daily by most people) most of the absorbed inorganic arsenic undergoes methylation, mainly in liver to monomethylarsonic acid and dimethylarsinic acid, which are excreted along with residual inorganic arsenic in the urine. However, if the dose of arsenic is very large, the elimination half-life is prolonged. Once absorbed, arsenic rapidly combines with the globin portion of haemoglobin and therefore localizes in the blood. There is minimal penetration of the blood-brain barrier and within 24 hours arsenic redistributes itself to the liver, kidney, spleen, lung and GI tract, with lesser accumulation in muscle and nervous tissue. Once in the tissues, arsenic exerts its toxic effect through several mechanisms, the most significant of which is the reversible combination with sulphydryl groups. Arsenic blocks the Krebs cycle and interrupt oxidative phosphorylation thus resulting in a marked depletion of cellular ATP and eventually death of the metabolizing cell. Arsenic also inhibits the transformation of thiamine in to acetyl CoA and succinyl-CoA resulting in the features of thiamine deficiency. Arsenolysis is a major form of toxicity in which the arsenic anions can substitute for phosphate in many reactions. Arsenic is capable of inhibiting oxidative phosphorylation through two different mechanisms 2-4 weeks after ingestion, arsenic is incorporated into hair, nails and skin as it binds to the sulphydryl groups of keratin. Four weeks after ingestion, arsenic begins to localize in the bone where it substitutes for phosphate. Organic Arsenicals are more rapidly excreted than the inorganic form. Pentavalent forms are cleared faster than trivalent form. The toxicity is related to: i. How fast it is excreted from the system? The inorganic forms are more toxic than the organic forms and the trivalent forms are more toxic than the pentavalent forms depending on their rapidity of excretion. ii. To what degree it may accumulate in the tissues? Pentavalent forms are accumulated more rapidly than the trivalent forms which is approximately the reverse order of excretion.
556 Textbook of Forensic Medicine and Toxicology Arsine gas (AsH3) causes rapid haemolysis and renal damage may persist for years following single acute poisoning. Arsenite is absorbed from GIT and retained in high levels in the tissues. The poisoning due to Arsenic compounds can be acute, subacute and chronic. Acute Arsenic Poisoning The acute arsenic poisoning results from the: (i) Oral ingestion (ii) Inhalation of arsenic gas (iii) Rubbing in to the skin (iv) Introduction in to rectum or vagin*. Arsenic poisoning is usually the result of accidental or suicidal ingestion of insecticides; (Paris green) that is copper arsenite or calcium or lead arsenate. Pesticide containing arsenic is freshest source of poisoning The toxic symptoms of acute arsenic poisoning depends upon individual susceptibility. Orchardists can ingest 6.8 mg /day without any signs and symptoms but arsenic trioxide as low as 30 mg has been found fatal. This extraordinary degree of tolerance to ingestion of arsenic could be due to blockage of absorption, alteration in its distribution to tissues, enhanced or accelerated transformation of arsenite to less toxic arsenate, and decreased reduction of arsenate to arsenite by peripheral tissues. Fatal dose→The fatal dose of arsenic trioxide is 180 mg but the dose depends on the compound ingested, its physical form and the inherent tolerance of the patient to arsenic Fatal period→Fatal period for arsenic poisoning is 12-48 hours but can be fatal even within 2-3 hours. Mechanism or Action The mechanism of toxicity of all arsenic compounds is the same. Once in the tissues, arsenic exerts its toxic effect through several mechanisms such as: (i) Reversible combination with sulphydryl groups (ii) Reacts with SH group in tissue proteins (iii) Interferes with number of enzyme system essential for cellular metabolism (iv) Capillary poison, dilates capillary (v) Fatty degeneration of liver
(vi) Hyperemia and haemorrhages in the intestine (vii) Renal tubular necrosis (viii) Peripheral nerves show disintegration of axis cylinder (axonal neuropathy) with fragmentation and resorption of myelin. Signs and Symptoms Acute Poisoning The symptoms of acute intoxication usually occur within 30 minutes of exposure: 1. Initially the patient experiences a metallic taste in the mouth and slight garlicky odour in the breath along with xerostomia (dry mouth) and dysphagia. 2. This is followed abruptly by severe nausea and vomiting, colicky abdominal pain and profuse diarrhoea (bloody in some cases) with rice water stools, due to vasodilation with transudation of fluid into the bowel lumen in addition to mucosal vesicle formation and sloughing leading to increased peristalsis. 3. Generalised vasodilation caused by capillary damage results in transudation of plasma and severe hypovolemia. 4. If the dose of arsenic ingested is large, cyanosis, cold clammy extremities, hypoxic encephalopathy, convulsions and acute tubular necrosis may occur following shock. 5. Hyperpyrexia and acute haemolysis may also occur. 6. If the ingested dose is smaller, the patient will have severe headache, vertigo, periorbital oedema, skeletal muscle cramping and evidence of renal damage manifested as oliguria, proteinuria, and haematuria. 7. If death does not occur in the first few hours from shock, the patient may die a few days later from acute hepatic or renal failure. 9. Cardiac manifestations include acute cardiomyopathy, subendocardial haemorrhages, and ECG changes (prolonged QT interval and non-specific ST-T changes). The cardiac symptoms are due to decreased cardiac output due to hypovolaemia and direct toxic effect on the cardiac muscle.
Metallic Poisons 557 10. Arsenic has a predilection for keratin that is why the concentration is higher in hair and nails. 11. Death from acute arsenic poisoning is usually caused by irreversible circulatory insufficiency. When the dose is not large enough to kill the patient, a number of secondary effects can be seen 2-4 weeks after ingestion of the poison. These include hair loss, Mee’s lines (white transverse lines seen on the nail plate up to a year after arsenic intoxication), sensorimotor peripheral neuropathy (may develop within a few hours of ingestion but usually seen 2-8 weeks after exposure), skin changes (as in chronic poisoning) and possible chronic renal failure. The signs and symptoms start within half an hour but may be delayed for several hours when it is given in rectum, vagin* or skin. The dilatation of capillaries is responsible for most of the symptom: (i) Burning pain and throat constriction (ii) Stomach pain which may increase on pressure (iii) Increased salivation (iv) Intense thirst (v) Vomiting that is projectile, dark brown or yellow in colour and contains stomach contents, blood and mucus (vi) Purging, tenesmus, pain and irritation about anus. The stools are dark coloured and bloody and later on are colourless, odourless and watery resembling rice water (vii) Due to capillary transudation of plasma following rupture of vesicles under intestinal mucosa (viii) Cramps in the calf muscles (ix) Restlessness (x) The patient is dehydrated (xi) Skin is cold and clammy (xii) Face is pale and anxious (xiii) Eyes are shrunken (xiv) Pulse is irregular and quick (xv) Respiration is laboured (xvi) Hypoxia, convulsions and coma precede death (xvii) Cirrhosis and ascites results from the therapeutic doses of Flower’s solution (1% Arsenious trioxide) (xviii) Due to direct action on the myocardium the ECG shows T-wave inversion and persistent prolongation of QT interval (xix) Arsine dust: When arsine dust is inhaled, it causes cough with frothy sputum, pulmonary oedema, cyanosis, breathlessness, corneal ulcer and conjunctivitis.
Table 37.1: Differential diagnosis of acute arsenic poisoning Findings
Arsenic poisoning Cholera
Pain in throat Present before vomiting Purging Follows vomiting Vomitus Consists of mucous bile and blood Stools High coloured, discharged with straining and tenesmus Voice conNot affected junctivitis Inflamed
Present after vomiting Precedes vomiting Watery Rice water and involuntary
Peculiar and rough Not inflamed
Narcotic form produces mainly CNS symptoms such as: (i) Giddiness (ii) Precordial distress (iii) Tenderness of muscles (iv) Delirium (v) Dilated pupils and complete paralysis of muscles at times. Unusual symptoms such as (i) Convulsions (ii) Lockjaw (iii) Raised temperature (iv) Loss of speech and memory (v) Joint pains can also be produced. Arsine Gas Arsine gas acts as a poison to haemoglobin of red blood cells and causes haemolysis. It most commonly produces haemoglobinurea and anaemia. The other symptoms produced as a result of poisoning due to arsine gas Jaundice, dark red urine, heart failure, delirium and coma. Subacute Poisoning Subacute poisoning results when the compounds of arsenic are given in small doses at repeated intervals. The signs and symptoms that are produced are dysphagia, cough, foul smelling tongue that is dry and congested, the motions are bloody. Chronic Arsenic Poisoning This is much more insidious and the diagnosis is often difficult to establish. The earliest cutaneous manifestation is persistent erythematous flushing caused by cutaneous capillary dilation. Hyperkeratosis then occurs with desquamation of the palms and soles, brittle nails with Mee’s lines, patchy of diffuse alopecia (hair loss) and oedema
558 Textbook of Forensic Medicine and Toxicology of the face, periorbital region, or ankles from localised transudation of intravascular fluid. Bowen’s disease is a long-term complication of chronic arsenic intake and often indicates that systemic neoplastic processes are occurring. Haematologic abnormalities include normochromic and normocytic anaemia caused partly by haemolysis, leukopenia and thrombocytopenia and mild eosinophilia. Karyorrhexis is normally seen and manifested by bizarre nuclear forms seen on bone marrow examination. Interference with folate metabolism may lead to a megaloblastic picture. Neuropathy is the hallmark of arsenic poisoning. It is usually a symmetrical sensorimotor polyneuropathy, often resembling Guillain-Barre syndrome. The predominant clinical features of neuropathy are paresthesia, numbness, and pain, particularly of the soles of the feet. Eventually, muscular atrophy (possibly even paralysis) and ataxia are seen. Encephalopathy may be seen in some cases, presenting as severe headache, personality disturbance, convulsions or coma. Other features of chronic arsenic poisoning are nausea, vomiting, diarrhoea and irritability. Patients who recover from the acute form of poisoning develop (i) Skin and mucosal changes (ii) Peripheral neuropathy (iii) Linear pigmentation in the fingers (iv) Cutaneous manifestations appear within 1-4 weeks and consist of dry, diffuse and scaly desquamation with hyperpigmentation over the trunk and extremities and hyperkeratosis of palm and soles (v) Mucosal surfaces also show signs of irritation like conjunctivitis, photophobia and pharyngitis (vi) After 5 weeks, transverse white streaks 1-2mm width appears above base of each fingernail called Mees line. Those who have more than one exposure may show double line, several millimeters apart (vii) After 1-3 weeks, features of peripheral neuropathy like decreased sensations of touch, pain and temperature appear in a symmetrical fashion. There is ‘glove and stocking’ distribution. There is distal weakness resulting in wrist drop, unable to walk, distal reflexes are decreased and atrophy of muscles. Laboratory Findings Diagnosis Definitive diagnosis of arsenic poisoning is difficult
because of the natural presence of trace amounts of arsenic in the body and because, due to the multi systemic toxicity of arsenic, the clinical manifestations vary widely so both acute and chronic poisoning simulate many other diseases and be overlooked in the differential diagnosis. Diagnosis is often particularly difficult in homicidal poisoning attempts because the patient will not usually know that he/she has ingested arsenic. Arsenic poisoning is usually diagnosed with a urine test for arsenic since monomethylarsine and dimethylarsine are present in the urine 24 hours after ingestion and arsenic ions are present very shortly after ingestion (useful for diagnosis of acute poisoning). A urinary excretion of arsenic >200 mg/24 hr is regarded as indicative of exposure to a potentially toxic amount of arsenic. The gastric contents can also be screened for arsenic and, if it is very soon after ingestion a blood test will also reveal arsenic. Analysis of body tissues, nails and hair is important in diagnosis of chronic arsenic ingestion. Colorimetry, polarography, atomic absorption spectroscopy and neutron activation analysis are effective methods for arsenic detection. Hair and nail samples containing >3ppm or 100mg or arsenic per 100g of specimen are diagnostic of arsenic poisoning. Analysis of hair is often used many years after death to determine the cause of death. This is how the true cause of death (chronic arsenic poisoning) of Napoleon Bonaparte was determined 140 years after he died (Weider, 1999). i. Urine: Normal value of arsenic is 0.010.06mg/litre of urine and it may be even upto 0.2 mg/litre. Most patients with exposure having more than 0.1 mg/litre, upto 1mg/litre of urine. Proteinuria, casts and albuminuria are there. ii. Blood: The normal blood level is 100mg/litre. There is moderate anaemia and leucopenia 2000-5000 mm3 except Arsine poisoning causes leukocytosis and mild eosinophilia. iii. Liver function tests: There is failure to excrete bilirubin, decreased metabolism of protein, serum alkaline phosphatase and bilirubin is raised, urobilinogen in the urine iv. CSF is normal.
Metallic Poisons 559 v. Hair: In normal persons, average concentration is 0.05/100 gm of hair but more than 1mg/100 gm indicates poisoning. As arsenic is widely distributed in nature, their presence may not always indicate of the poisoning. Treatment 1. Empty stomach by emetics, tartar emetics should not be used; copper sulphate also should not be used as it leads to the formation of copper arsenite. 2. Stomach wash should be done with freshly prepared solution of ferric oxide in table spoonful doses suspended in water; with arsenious acid it forms ferric arsenite that is a harmless and insoluble salt. Ferric chloride (45 ml) and sodium carbonate or magnesium oxide (15 gm) in half glass of water, strained through muslin is used for the lavage. The following reaction occurs FeCl3 + MgOFe2O3 + MgCl2 3. For gastric lavage, 1% sodium thiosulphate in water is helpful. 4. Dialysed iron may be used as a substitute. 5. 10% solution of sodium thiosulphate as 7½ gm I.V. injection but it is of doubtful value. 6. British Anti Lewsite (B.A.L.) is administered 4 hrly for 2 days, 6 hrly for 1 day and total dose 12 hrly afterwards; total dose is 2.53mg/kg body wt. The duration of B.A.L. depends upon (i) Clinical state and (ii) Response of the patient. B.A.L. is to be stopped if side effects like nausea, vomiting, burning sensation in the mouth, tachycardia, hypotension, constriction in the throat appear. 7. To know when the chelation is to be stopped, 24 hr urine sample is to be collected and if Arsenic levels fall below 50 mg/24 hrs, it should be stopped for 5 days and then started again so that the tissue arsenic is mobilized and ready for chelation. 8. Oral Penicillamine 100 mg/kg body wt in four divided doses is given in 24 hrs for 4-8 days after initial 12-48 hrs of B.A.L. therapy. 9. Demulcents such as ghee and barley water are given.
10. Castor oil or magnesium sulphate is administered to diminish intestinal absorption of arsenic. 11. Morphine is given to relieve pain. 12. Saline is administered intravenously for dehydration and enuresis. 13. To relieve cramps, massage is employed. 14. Body temperature is to be maintained. Treatment of Poisoning by Arsine Gas (i) Patient to be taken to fresh air (ii) Oxygen inhalation to be started (iii) Exchange transfusion should be undertaken (iv) Haemodialysis (v) Alkaline drinks. All of the above methods help to eliminate arsine from the blood. B.A.L. is not effective in arsenic gas poisoning. Autopsy Findings 1. Rigor mortis lasts longer. 2. General shrunken appearance due to dehydration. 3. Eyeballs are shrunken. 4. Cyanosis of hands and feet is there. 5. Jaundice is also present. 6. Mucous membrane of mouth and pharynx is inflamed and ulcerated. 7. Stomach is the main organ to be inflamed; food particles are mixed with arsenic embedded in the mucous. The inner wall of the stomach is swollen, congested and tinged with streaks of blood and arsenic. On scraping the mucous membrane is congested and inflamed and is brownish red or scarlet in colour. There is petechial haemorrhages. The inflammation is more marked in the greater curvature and the cardiac end. Ulceration, gangrene and perforation have been rarely reported. 8. Small intestine is flabby and contains large flakes of mucous with little faecal matter, submucosal haemorrhages are present and the epithelium is flabby and oedematous. 9. Large intestine contains seromucous and the intestinal glands are swollen and enlarged. 10. Lungs are congested, oedematous and show subpleural ecchymosis.
560 Textbook of Forensic Medicine and Toxicology 11. Caecum and rectum are inflamed and the mucous membrane is flabby. 12. Liver, spleen and kidney is enlarged and congested and shows fatty infiltration and degeneration. 13. Heart contains coagulated blood and ecchymosis of the endocardium and muscles of the left ventricle is there. 14. Brain is congested and ventricles are full of serum. Autopsy Findings in Arsine Gas Poisoning (i) Skin is dirty yellow in colour (ii) Mucous membrane of stomach and intestine is yellow and inflamed (iii) Liver is small or enlarged and shows fatty degeneration (iv) Spleen shows evidence of destruction of blood and deposition of blood pigment throughout the organ (vi) Kidney is enlarged, congested and shows tubular necrosis (vii) Lungs are congested and oedematous. Chronic Arsenic Poisoning Chronic arsenic poisoning results from: (i) Chronic repetitive inhalation of arsine gas (ii) Chronic repetitive ingestion. Chronic poisoning usually results from the: 1. Persons engaged in the occupation of: (i) Smeltering that is extraction of metals from ore by melting (ii) Refining of ores (iii) Manufacture of weed killers, insecticides, paints, dyes and cosmetics. 2. Persons who ingest it as medicine for long periods. 3. May follow the acute poisoning after recovery. Chronic poisoning consists of the following stages: First stage: The following symptoms are produced in the first stage: (i) Loss of weight (ii) Loss of appetite and salivation (iii) Colicky pain and constipation (iv) Vomiting and diarrhoea (v) Gums are red and soft (vi) Tongue is coated, is thin white silvery and furred (vii) Oedema of eyelids and ankles (vii) Temperature and pulse is raised. Second stage: In the second stage of chronic poisoning following symptoms are produced: (i) Cutaneous eruptions (ii) Catarrh of larynx and
bronchial tube (iii) Dryness and itching of skin (iv) Voice is hoarse and husky (v) Photophobia and conjunctivitis (vi) Running nose and coryza (vii) Cough with bloody expectoration (viii) Liver is enlarged and cirrhotic (ix) Kidneys are damaged (x) Prominent changes are produced in the skin: • Generalized or localized, rain drop type of pigmentation of the skin involving the covered parts of the body such as flexors, nipples, lower abdomen, temples and eyelids. This can be differentiated from Addison’s disease as mucous membrane of the mouth is spared. • Epithelial hyperplasia, discrete multiple wart like keratosis on the palm, soles, head and trunk (Basal cell carcinoma—Bowen’s disease) • Epitheliomata are present in 20% of the cases. • Nails are brittle with linear pigmentation. • Hairs are dry and fall off. • Painless perforation of the nasal septum. Third stage: (i) Sensory symptoms are predominantly present such as headache, tingling, numbness and hyperaesthesia of the skin (ii) Tenderness and muscle cramps (iii) Circ*mscribed oedema of eyelids and ankles (iv) Knee jerk is usually lost (v) Impotence is commonly present (vi) There is evidence of bone marrow depression and aplastic oedema. Fourth stage: (i) Peripheral neuritis with glove and stocking type of anaesthesia; there is decreased pain, temperature and touch sensation (ii) Muscular atrophy of extensor muscles resulting in wrist drop and foot drop (iii) Muscular weakness (vi) Ataxia (v) Cramps (vi) Tremors and general emaciation (vii) Anaemia and dysuria (viii) Death is due to failure of heart muscles. Differential diagnosis: Chronic arsenic poisoning is to be differentiated from alcoholic neuritis. In the former the symptoms and signs are produced more rapidly. Are widespread and there is no glycosuria whereas in alcoholic neuritis glycosuria is positive. Treatment 1. Remove the patient from source of poison. 2. B.A.L. is to be given 6 hourly for 2-3 days and then once daily.
Metallic Poisons 561 3. Vitamin B1 injection for peripheral neuritis. 4. Improve general health.
8. It has the power of retarding decomposition and it does not disappear with decomposition.
Medicolegal Aspects
Postmortem imbibitions of arsenic: When there is a criminal charge of arsenic poisoning, the defence may take the plea that Arsenic was introduced after death and postmortem imbibition occurred in the tissues. The doctor can defend it by replying that it takes an anatomical course, more on the left side. Signs of inflammation and ulceration of stomach will be absent in case of postmortem imbibition of arsenic.
1. It is an ideal homicidal poisoning, used for frequently in India; can be mixed with sweets, bread, cooked vegetable, drinks, milk, pan and cigarettes. Mass homicidal poisoning simulates cholera. It is tasteless, odourless, easily available and small doses are required for homicide. In western countries, small doses are given for a prolonged period that simulates gastroenteritis to conceal the crime. The disadvantages of being used as a homicidal poison are: (i) Can be detected even in the charred bodies (ii) It delays putrefaction (iii) Can be detected in decomposed bodies (iv) Can be found in bones, hair even years after the poisoning. 2. It is used on abortion sticks as paste or ointment. 3. It is used as a cattle poison, is mixed with water in the well. 4. Is used for suicidal purposes. 5. The poisoning can result accidentally due to its improper medicinal use when it is applied locally as a cure for impotence, poisoning can result from its application on the abraded skin, when it is accidentally mixed with food or drinks, when used as vagin*l pessaries, and when it is mistaken for baking powder or soda. Beer drinkers in Lanceshire country in 1900 developed chronic arsenic poisoning and peripheral neuritis was produced. Arsenophagists: Arsenophagists use the drug as a habit for impotency 6. By dividing hair in small successive lengths from the root upwards and analyzing them separately, one may get the important information regarding the time that has elapsed since the administration of arsenic. Arsenic starts depositing in the hair after 15 days. If the length of hair is 1 cm that is equal to 25 days. By neutron activation analysis, the relation between ingested arsenic and arsenic content of the hair can be known. 7. Arsenic is excreted in the stomach and intestine after absorption, even when administered by routes other than mouth.
Exhumed body: Arsenic cannot percolate in the cadaver from the soil, as it is an insoluble form of salt. The nails and hair will have a higher concentration from the soil. The soil is to be kept for chemical analysis.
MERCURY Mercury is known as quick silver, a liquid metal with bright silvery luster that is volatile at room temperature. We ingest some amount of mercury along with our diet; 5-20 mg is taken along with the foodstuffs daily. The tolerable weekly intake of mercury per person is 300 mg out of which not more than 200 mg should be methyl mercury. It is not a normal constituent of the human body. Normal levels in unexposed individuals: • 0-8mg/100ml of blood. • 0.6-1.6μg per 100ml of urine. • 5-150μg per 100gm may be found in liver and kidney. Deadening of mercury: Mercury is converted in to a dull gray powder (contains 33% of mercury): (i) When it is shaken with oil (ii) Triturated with sugar, chalk (iii) Used for ointment purposes. Uses of Compounds of Mercury Have a wide range of use: 1. Inorganic salts: (i) Calomel cathartic—Mercurous chloride, used as purgative (ii) Mercurial ointment (iii) vagin*l creams (iv) Fingerprint powders (v) Amalgam (dental filling) (vi) Vermilion (Mercury sulphate).
562 Textbook of Forensic Medicine and Toxicology 2. Organic salts (Methyl and ethyl mercury: compounds) are an industrial waste and are used in manufacture of: (i) Thermometer (ii) Barometer (iii) Electrical industry (iv) Drug manufacturing (v) Persons working in mercury mining , hatters and furriers (vi) In agriculture as fungicide. Medicolegal Points of Importance 1. Pure metallic mercury is not considered poisonous, as it is not absorbed by the gastric juice. 1-2 pounds of liquid metal is taken to cure constipation but has no harmful effects. In exceptional cases, mercury may undergo chemical change and acts as a poison. 2. Few cases of mercury embolism are reported while the blood is collected from arteritis under the mercury seal. 3. When injected subcutaneously, local abscess formation occurs. 4. The mercurial vapours cause poisoning; 0.5mg/m3 causes poisoning. 5. When it is rubbed on to the skin, is absorbed and poisoning occurs. There is a reported incidence of the death of three persons when they applied mercury ointment for itching. 6. Amalgams used for curing carious tooth sometimes cause poisoning. 7. Mercuric salts are more poisonous than Mercurous salts. Trivalent salts are more poisonous than the bivalent salts. 8. Mercuric chloride causes accidental poisoning when it is widely used as: (i) Disinfectant and antiseptic causes accidental poisoning (ii) Contraceptive vagin*l tablets (iii) For antisyphilitic treatment. 9. Phenyl mercuric acetate jelly leads to poisoning when used as a contraceptive. 10. Mercuric chloride (Calomel) is poorly absorbed and has a low solubility; used in teething powders, causes pink disease in infants 11. Mercuric sulphide (vermilion) is not absorbed through the skin, is nonpoisonous. 12. It is eliminated through the saliva, urine, faeces, milk and perspiration 13. By neutron activation analysis, it is found that the maximum amount of mercury in the
human tissues is in the kidney, nails, scalp hair and skin. 14. Mercury may be detected in the bone in acute poisoning. 15. Mercury is often used as a medicine; hence detection in small quantity in the viscera does not contraindicate the death from other causes. 16. Mercury is not a constituent of human body; hence its presence indicates that it must have been introduced in to the system. 5-150 mg/100 gm is normally present in the tissues like liver and kidney. Compounds of Mercury 1. Mercuric oxide, HgO (Sipichand). 2. Mercuric chloride (corrosive sublimate); has (i) Antiseptic properties (ii) Largely used as medicine, taxidermy (iii) Violent poison. 3. Mercuric iodide (Red iodide of mercury). 4. Mercuric cyanide, is poisonous. 5. Mercuric nitrate. 6. Mercuric sulphide (Vermilion), is not poisonous 7. Mercuric sulphate. 8. Mercurochrome: contains 25-28% of mercury, discolours readily in water and the toxic effects develop after prolonged use. 9. Organic compounds are: (i) Ethyl and methyl mercury (ii) Thiomerin sodium (iii) Neptal. Poisoning results from both organic and inorganic salts; the organic compounds produce irreversible effects and booth the compounds affect CNS. Methyl mercury is more poisonous than the inorganic salts. Acute Mercury Poisoning This poisoning is mostly due to corrosive sublimate, mercuric chloride. The signs and symptoms start immediately after swallowing the poison, and rarely they are delayed for half an hour (i) Acrid metallic taste in the mouth (ii) Feeling of constriction or chocking sensation (iii) Hoarseness of voice (iv) There is difficulty in breathing (v) Mouth and tongue are corroded and swollen with graywhite coating (vi) Hot, burning pain in the mouth, stomach and abdomen (vii) Stools are blood stained (viii) Urine is suppressed and scanty,
Metallic Poisons 563 contains blood and albumin; is accompanied by necrosis of renal tubules and damage to glomeruli (ix) Pulse is quick, small and irregular; there is circulatory collapse (x) Thrombocytopenia and Bone marrow depression (xi) When vapours are inhaled, the following signs and symptoms are produced: salivation, gingivitis and loosening of teeth (xii) When injected intravenously, it produces: dyspnea, cyanosis, hypotension and convulsions (xiii) Death may be due to anaphylactic shock or ventricular fibrillation. Diagnosis Acute mercury poisoning is to be differentiated from arsenic poisoning from the following features: (i) The symptoms are produced sooner (ii) Acrid taste in the mouth (iii) Constriction of the throat is more marked (iv) Vomitus more often contains blood and mucous (v) Kidneys are more affected (vi) Urine contains >500μg. Fatal dose→15gm; 2gm is the smallest recorded dose Fatal period→3-5days Treatment 1. Stomach wash with warm water and magnesium carbonate. 2. With albumen such as egg albumin, skimmed milk or vegetable gluten, albuminate of mercury is formed (is insoluble in water but soluble in excess of albumin); is digested and absorbed in the stomach. 3. Demulcent drinks are given to protect the stomach wall. 4. Activated charcoal and water absorb mercury salts. Add magnesium sulphate that has increased absorptive power and hastens the removal. 5. B.A.L. is to be given in the dose of: • 3.5 mg/kg 4 hourly for 2 days • 2.5 mg/kg 6 hourly for 1 day • 2.5 mg/kg twice daily according to the severity. 6. Penicillamine is given 250mg 4 times a day orally. 7. Sodium formaldehyde sulphoxylate is the chemical antidote that reduces the prechloride
to metallic mercury. 5-10% sulphoxylate and 5% sodium bicarbonate is used for stomach wash of which 200ml should be left in the stomach.. This is beneficial if given in first half an hour. If colitis has developed, high colonic lavage as 1:1000 solution is to be given. 8. For diuresis 5-10% glucose is used in normal saline. Chronic Mercury Poisoning 1. Workers may get poisoned due to the vapours or dust. 2. When small doses are taken for prolonged period. 3. When used for external application as an ointment. The signs and symptoms of chronic mercury poisoning start at a blood level of 100mg/ml. The daily urinary excretion is more than 300mg. The following signs and symptoms are produced: (i) Nausea, vomiting and diarrhoea (ii) Indigestion, dyspepsia and colicky abdominal pain (iii) Excessive salivation with swollen and painful salivary glands (iv) Foul smelling breathing (v) Inflamed and ulcerated gums with brownish blue line (vi) Loosening of teeth (vii) Necrosis of jaw; should be differentiated from phosphorus poisoning. Mercuria lentis: A brownish reflex from the anterior lens capsule of both the eyes is seen when observed in slit lamp in persons exposed to mercury vapours for some years. It is bilateral and has no effect on the visual acuity. Erythematous, eczematous (watery and weeping) papular type of skin lesions mostly in the hands and feet accompanied with thickening of skin are produced. Mercurial Tremors (Hatter’s shake or glass blower’s shake): These are coarse tremors that are detected early by writing and they involves the fingers, muscles of tongue, face, arms and legs; are excited by voluntary movements and are absent during sleep. There is incoordination of movements, increased deep reflexes, paresis of limbs and peripheral neuritis. The tremors should be differentiated from thyrotoxicosis in which there is presence of fine tremors, exophthalmos, raised pulse and goiter
564 Textbook of Forensic Medicine and Toxicology Mental symptoms (Erethism): Erethism develops in the mirror-manufacturing firms, these include shyness, timidity, irritability, loss of confidence, mental depression, loss of memory, insomnia, hallucinations and delusions that are features of insanity Treatment 1. Removal of the individual from the source of exposure. 2. Plenty of milk should be given. 3. Mouth wash by borax. 4. Saline purgative to be given. 5. Sodium thiosulphate i.v. to be used. 6. B.A.L.—one course of B.A.L. to be administered. 7. Symptomatic treatment for paralysis. 8. Prophylactic treatment including proper ventilation and periodic medical check up. Autopsy Findings 1. If taken in concentrated form, appearances similar to corrosive poisoning will be present. 2. Signs of irritant poisoning will be there. 3. Mucous membrane of lips, mouth, pharynx and Oesophagus will be grayish white. 4. Stomach contents are coagulated, albuminous with mucous and blood. 5. Mucous membrane is eroded, inflamed and covered with grayish deposit of mercury or black deposits of mercury sulphide. 6. There is great softening of the walls so great care must be taken during post mortem examination to remove it; perforation is rare. 7. Caecum, colon and rectum are inflamed, ulcerated and gangrenous, if alive for sometime. 8. Liver is congested with cloudy swelling. 9. Spleen is congested. 10. Kidneys are congested, there is necrosis of tubules and deposition of lime. 11. Heart shows fatty degeneration. 12. Postmortem lesions are found in the alimentary canal even when applied on the skin or absorbed from the vagin* or uterus.
COPPER Copper is also known as ‘Tamba’. Metallic copper is not poisonous but some of its salts have a medicolegal importance. All salts of copper are poisonous. Copper alloyed with other metals when given in fine powdered state acts as a poison. 1. Copper is a normal constituent of the body and is found in traces in urine, faeces, blood, tissue fluids and liver. It is also detectable in minute amount in various food materials such as potatoes, spinach, beans, spinach, fruits and mineral water. The normal dietary intake of copper is about 3mg/day. In Wilson’s’ disease there is increased absorption of copper in the system due to congenital defect in ceruloplasmin formation. All copper salts are powerful inhibitors of various enzyme systems. 2. Elimination of copper from the body: Copper is eliminated more through faeces and bile than through urine. It is also excreted in saliva, milk in utero from the mother to the foetus. Copper Sulphate (Blue vitriol, CuSO4, 5H2O, Nila tutiya) It occurs as large blue crystals, freely soluble in water having metallic taste. On heating upto 100oC, it loses its water of crystallization and becomes white with a blue tint and at 220oC it becomes completely white. On standing, it draws moisture and again becomes blue, as it is hygroscopic. Copper sulphate is used as astringent in small doses; as an emetic in slightly large doses and an irritant in larger doses. Uses of copper sulphate: (i) It is used as an algaecide (ii) It is also used by bookbinders and straw-hat makers (iii) Is a constituent of Fehling’s solution I (iv) It was used for removal of excess granulation tissue in wounds (v) To impart rich green colour and for preservation of fruits and vegetables but their dose should not exceed 50mg/ kg. But the toxic effects does not result from their use as copper salts are converted into albuminate of copper, which is a harmless substance (vi) In bakeries for fermentation of dough to make breads
Metallic Poisons 565 in winters (vii) It is commonly used as an emetic in various poisonings except arsenic where it will form cupric arsenite or acetoarsenite of copper and produce toxicity (viii) It is used as an antidote in phosphorus poisoning where it forms cupric phosphide—A non-toxic substance. Copper subacetate (Verdigris or Zangal): Copper sulphate is a bluish green salt formed by the action of vegetable acids on improperly tinned copper cooking vessels. It is used as medicine for external use and is used in arts and industry. The signs and symptoms of verdigris poisoning are similar to that of copper sulphate poisoning. Copper Sulphate Poisoning Fatal dose→15-30 gms but small repeated doses are more fatal compared to single large dose Fatal period→1-3 days Acute Copper Sulphate Poisoning Signs and symptoms Signs and symptoms appear within 15-30 minutes of the ingestion of the poisonous substance: (i) Metallic taste in mouth and sense of constriction in throat (ii) Burning pain in the mouth, throat, oesophagus and up to the stomach (iii) Repeated, violent and profuse vomiting; the vomitus is bluish or greenish blue in colour that becomes bluer on addition of ammonium hydroxide. The colour of vomitus will not change if it is bilious (iv) Intense thirst, salivation, nausea and gaseous eructations (v) The gums and tongue are stained bluish (vi) Repeated diarrhoea with liquid, brown motions that is accompanied with tenesmus and colicky abdominal pain (vii) Oliguria, anuria and albuminuria leads to uraemia (viii) Hemolytic tendencies due to increased concentration of copper in the erythrocytes, resulting in hemetemesis and malena (ix) Jaundice may develop (x) Muscular cramps, paralysis of limbs, convulsions, dyspnoea, quick, weak and feeble pulse, fall of blood pressure, cold clammy skin and coma and death occurs in 1-3 days (xi) Liver biopsy shows centrilobular necrosis and biliary stasis.
Chemical test: Ammonium hydroxide gives a greenish blue precipitate with substances containing copper salts; this precipitate is soluble in excess of ammonium hydroxide solution giving a deep blue colouration Treatment 1. No emetics as copper sulphate causes emesis 2. Gastric lavage using 1% freshly prepared potassium ferrocyanide that acts as an antidote. It changes copper sulphate in to insoluble cupric ferrocyanide. 3. Demulcents like milk and egg albumen convert copper sulphate in to insoluble cupric albuminate. 4. To maintain fluid and electrolyte imbalance infuse 5% intravenous dextrose saline with vitamin C and amino acids. 5. Morphine is given to allay pain. 6. As chelating agent, Penicillamine 2 gm in divided doses is given orally for 5-7 days or parenterally 30 mg/kg body wt. or B.A.L. as 300mg i.m stat and then 150 mg 4hourly for next 6-7 days or until recovery. 7. Calcium E.D.T.A. is also given as an antidote Autopsy Findings (i) The skin is yellow due to jaundice (ii) Greenish blue froth comes out of the mouth and nostrils (iii) The mucous membrane of mouth, oesophagus, stomach and intestines will be inflamed, congested, swollen and excoriated and bluish green or bluish stained (iv) Stomach contents are stained greenish blue or blue (v) There is rectal perforation sometimes (vi) Liver is enlarged, congested, soft and greasy showing features of fatty infiltration degeneration (vii) Kidneys are congested and features of tubular degeneration with deposition of copper. Chronic Copper Sulphate Poisoning Chronic copper sulphate poisoning results from: (i) Preservation and cooking of food in unclean copper utensils may result in poisoning as it is
566 Textbook of Forensic Medicine and Toxicology contaminated with verdigris (ii) The chronic consumption of fruits and vegetables preserved and coloured with copper sulphate (iii) Inhalation of copper dust or absorption through skin by workers in copper industry (iv) Brass-founder’s ague (Metal fumes fever)—Inhalation of fumes of copper and zinc in workers engaged in smelting grassan alloy of copper and zinc results in this condition. Signs and Symptoms (i) Styptic metallic copper taste in tongue and mouth with a bluish-green or purple line on the gums at its junction with the teeth (ii) Lassitude, giddiness and headache (iii) Nausea, vomiting, indigestion and dyspepsia (iv) Occasional diarrhoea with colicky abdominal pain (v) Laryngitis and bronchitis (vi) Peripheral neuritis (vii) Anemia and slight jaundice (viii) Muscular weakness with atrophy may lead to paralysis (ix) Hair may be brownish golden in clolour (x) Features of renal and hepatic damage are prominent (xi) Conjunctivitis and corneal ulceration occur due to contact with copper dust (xii) Dermatitis due to skin contamination with copper salts. Treatment 1. Patient should be removed to fresh air. 2. Correction of dyspepsia. 3. Copper utensils used for cooking should be very clean and well-tinned. 4. E.D.T.A, Penicillamine should be given. 5. Nutritious diet with multivitamins and intravenous fluids to be given. Autopsy Findings (i) Fatty degeneration, necrosis of liver cells and haematochromatosis (ii) Degeneration and cloudy swelling of kidney.
the compound is used for homicidal purposes (ii) Rarely used for cattle poisoning (iii) Accidental poisoning can occur from contamination of food stored or cooked in copper utensils due to formation of verdigris and eating fruits and vegetables preserved in copper sulphate (iv) Used on the abortion sticks to procure abortion.
IRON Iron is a normal constituent of the body and is eliminated in faeces and urine. It is present in the food we take and in various multivitamin syrups, tablets, tonics and capsules. The salts of ferrous such as ferrous sulphate and ferrous carbonate are easily absorbed whereas ferric salts are not absorbed. The poisoning may results from ingestion of iron preparation available in the market by children in lieu of sweets. Teenagers and young females can also suffer from iron poisoning after a long period of treatment for anemia, in pregnancy or during postpartum period with these preparations. All iron preparations are dangerous except for ferrous gluconate. Ferrous sulphate: It occurs as greenish crystals soluble in water and is used in industry for making blue black ink and dyes. Ferric chloride: It is water soluble and a powerful irritant, forms triferriperchlor that produces sloughing endometritis and even peritonitis when applied locally in vagin* and uterus. Mechanism of action: In dilute forms, the iron preparations act as astringent and corrosive in concentrated for leading to corrosion or perforation of gastric mucosa. It causes increased capillary permeability and inhibition of mitochondrial function. They may cause stricture formation. Fatal dose→20 -30 gm, Variable (24-48 hours). Signs and Symptoms
Medicolegal Aspects (i) Copper salts especially copper sulphate are not commonly used for suicidal purposes due to its blue or bluish-green colour, being self-emetic, strong metallic taste and big lethal dose. However,
The signs and symptoms are described in three stages: Stage I: (i) Metallic taste in mouth (ii) Nausea and vomiting and epigastric pain (iii) Hemetemesis, diarrhoea with black stools (iv) Severe gastro-
Metallic Poisons 567 intestinal haemorrhage results in shock followed by convulsions and coma, peripheral circulatory failure and death (v) Iron released from the tablet or solution will exert its necrotizing effects on gastrointestinal tract mucosa and the unbound iron will soon get absorbed to produce systemic manifestations Stage II: The phase may last for days and with improvement of signs and symptoms, the patient may recover in mild cases of poisoning. In severe cases:(i) Frequent black, offensive stools are passed (ii) Severe headache, confusion, delirium occurs (iii) Convulsions, photophobia, dimness of vision and loss of consciousness develops (iv) Respiration is deep and circulatory collapse can occur. Stage III: (i) Recurrence of shock and development of hepatic failure (ii) Features of acute hepatic necrosis with jaundice progresses to hepatic coma and death (This results from release of iron from reticuloendothelial system). If patient survives for 3-4 days, recovery is the rule (iii) Pyloric obstruction is a late complication. Diagnosis: (i) Iron levels in blood and gastric aspirate (ii) Urine for bilirubin, bile salts and urobilinogen (iii) Liver function tests and tests for rise in aminotransferases and prothrombin time should be carried out. Chemical test: Ammonium sulphide when mixed with ferric or ferrous salts gives black precipitate that is soluble in dilute hydrochloric acid.
Treatment 1. Immediately wash stomach with 1% sodium bicarbonate solution or 5-15% disodium phosphate solution. 2. Desferrioxamine (1gm of Desferrioxamine chelates 85 mg of iron) is the most active antidote against iron poisoning. It is introduced in stomach in the dose of 5 gm dissolved in 100 mL of distilled water through stomach tube and be left out. Desferrioxamine 1 gm in 5 mL of distilled water can be given i.m and further 500 mg in 12-24 hours depending upon the serum iron estimation. Intravenously maximum of 60-80 mg/kg in 24 hours can be infused. 3. Cathartics can be given to evacuate bowel in the absence of perforation. 4. Shock and acidosis to be treated. 5. Symptomatic and supportive treatment. Autopsy Findings (i) Evidence of congestion, inflammation and corrosion of gastrointestinal tract (ii) Liver will show hepatic necrotic changes (iii) Kidney will show renal tubular necrosis. Medicolegal Aspects 1. Ferric chloride is rarely given to intoxicated persons for homicidal purposes 2. Accidental poisoning occurs in children commonly who ingest it in lieu of sweets 3. Locally in the genital tract to procure abortion.
568 Textbook of Forensic Medicine and Toxicology
39
Part 2—Forensic Toxicology
Irritant Poisons ORGANIC IRRITANT POISONS ABRUS PRECATORIUS (INDIAN LIQUORICE OR RATTI) The plant grows throughout India and all parts of the plant are poisonous but the seeds are particularly used for the purpose of poisoning. The seeds of Ratti are 1/3 inches long and ¼ inches broad and are of the size of small pea. Usually the seeds are red coloured, egg shaped having a black spot on one end but it may be of white, black, or yellow colour (Fig. 38.1). Ratti seeds are used as decorative ornaments. The seeds are tasteless and odourless. The active principle is Abrin that is a toxalbumin similar to ricin and its action resembles the viperine snakebite. Besides this, it contains some poisonous proteins such as: (i) Abrussic acid ( fat splitting enzyme) (ii) Abrin (nitrogenous compound) (iii) Ureases (iv) Haemagglutinin (v) Abraline (glucoside) (vi) Glycyrrhizin present in root, stems and leaves
ends about 2.5cm long and 90-120mg by weight. The needles are then hardened by drying in the sun and then fitted to the holes of a bamboo pole. These needles are stabbed on the buttock of the animal, implanting the needles but detaching the handle. At the site of inoculation of ‘sui’, there will be inflammation, oedema or necrosis with oozing of haemorrhagic fluid from the puncture site similar to the viper bite. The animal stops eating food for 3-4days, will be unable to move or stand. It will become apathetic and will develop convulsions before it gets comatosed. The collapse soon sets in and the animal dies by 48-96 hours later. The signs and symptoms simulate snakebite. When the ‘suis’ are stabbed in the human body, there will be painful swelling with ecchymosis at or about the site of injection. The inflammation sets up and necrosis begins soon. The patient suffers from headache, nausea, vomiting, vertigo, drowsiness and apathy. There is increasing prostration, dyspnoea, quick, weak, irregular and feeble pulse, and cold clammy skin. The blood pressure falls, oliguria, haemorrhagic manifestations and lately uremia may set in. Death occurs from 3-5 days from cardiac failure. Signs and Symptoms
Figure 38.1: Ratti seeds
Preparation of ‘Suis’ or ‘Sutari’ The seeds are first soaked in water, decorticated and made into a paste mixed with opium, onion, datura, little oil or water. The paste is then shaped in the form of small, sharp needles with pointed
The ingestion of intact ‘Ratti’ seeds does not result in poisoning. Powdered seeds are boiled with milk and are used as a nerve toxin but when taken uncooked it acts as severe gastrointestinal irritant causing vomiting and diarrhoea. Abrin is slightly inactivated by gastric juice when crushed seeds are swallowed and it loses all its poisonous properties when boiled:
Irritant Poisons 569 1. Extracts of seeds when injected under the skin of an animal cause inflammation, oedema and necrosis. 2. In human beings, ingestion of crushed seeds results in: (i) Nausea and vomiting (ii) Vertigo, tinnitus and giddiness (iii) Cold clammy skin and fall of blood pressure (iv) Irregular pulse and laboured breathing (v) Convulsions, haemolysis, oliguria (vi) Death occurs from cardiac failure. Fatal dose→90 -120mg (½ to 1 crushed seed) Fatal period→3-5 days rarely even 24 hours. Treatment 1. Gastric lavage and emesis is carried out. 2. Locally the part containing ‘sui’ should be excised in both humans and animals. 3. Sodium bicarbonate 10 gm orally per day helps in maintaining alkalinity of urine and prevents agglutination of red cells and blocking of renal tubules with haemoglobin G. 4. Antiabrin, an antiserum that is prepared by injecting abrin in rabbits, is to be administered. 5. A mixture of dilute hydrochloric acid and pepsin is to be give orally. 6. Symptomatic treatment. Autopsy Findings (i) Inflammatory oedema and necrosis at the site of injection (ii) Sometimes fragments of ‘suis’ are found at the site of injection (iii) Gastrointestinal tract is congested and haemorrhagic (iv) Petechial haemorrhages are seen in the skin, pleura, pericardium as well as peritoneum (v) The visceral organs are congested. Medicolegal Aspects (i) It is a mainly a cattle poison (ii) ‘Suis’ are made by mixing with Datura, Opium, Onion and Spirit and used for poisoning the cattle and also for homicidal purposes (iii) The seeds act as an abortifacient preventing conception (iv) The application of powdered seeds on to the eye by malingerers to produce conjunctivitis (v) The paste made from the powder of Ratti seeds is used as an arrow poison and also as an aphrodisiac.
SEMECARPUS ANACARDIUM (MARKING NUT, BHILAWA) The plant of marking nut is found all over India and the fruit of this plant is called marking nut (Bhilawan). The fruit is black, heart-shaped, having a rough projection at the base. It has a hard black rind, which contains a thick pericarp. This pericarp or fleshy pulp contains brownish oily acrid juice turns black when mixed with the lime and exposed to air used by washerman for marking cotton clothing and linen. That is why, it is known as marking nut. The juice mixed with the melted butter is used as a remedy for syphilis. The active principles are: (i) Semicarpol—0.1% (ii) Bhilawanol—15-17% (iii) Non-volatile corrosive residue—18% (iv) Fatty oils and tannic acids. Symptoms and Signs On external application: (i) When applied externally, it causes irritation and itching. (ii) When it is applied to the scrotum, it causes fever, haematuria, and painful micturition. (iii) Blisters are painful, black and raised containing acrid serum (iv) The acrid serum causes eczematous eruption of the contact area of skin (v) Blisters resemble bruises and may get infected and ulcerate (vi) The blisters are also associated with fever, Dysuria, haematuria and painful defecation. (vii) It is possible to detect poison from the serum from the blisters. Table 38.1: Differences between true and false bruise Features
True bruise
False bruise
Swelling and redness Ecchymosis Contents Itching Fingers
Present Present Blood Not present No marks over the fingers Negative
Not present Not present Serum Present Fingers may show marks due to the juice Positive for the vegetable poison
Chemical analysis
When ingested (i) Intense, painful irritation with blister formation locally in the mouth, tongue and throat (ii) Gastroenteritis with nausea and vomiting (iii) Tachycardia
570 Textbook of Forensic Medicine and Toxicology (iv) Quick weak pulse and hypotension (v) Pupils are dilated (vi) Cyanosis and dyspnoea (vii) Delirium and areflexia (viii) Collapse, coma and death occurs within 12-24 hours. Fatal dose→5 gm Fatal period→ Uncertain, usually 12-24 hours Treatment 1. External application: Washing with lukewarm water with some antiseptic and application of antibiotic cream or ointment, if infected 2. When ingested: Stomach wash with plain water; Demulscent drinks; analgesics for pain and symptomatic measures to be employed. Autopsy Findings (i) Fatty degeneration of the liver (ii) Blisters in the mouth, throat and even stomach Medicolegal Aspects (i) Accidental poisoning occurs when Vaids administer the juice of Semecarpus anacardium for the treatment of pain or for treating paralysis (ii) Homicidal poisoning is rare (iii) It is criminally introduced in to the vagin* as a punishment for infidelity (iv) The juice of marking nut is applied on the skin for the false charge of bruise (v) It is applied on to the uterus for criminal abortion (vi) It is sometimes applied on to the eyes by malingerers to produce ophthalmia. RICINUS COMMUNIS (CASTOR OIL PLANT OR ARANDI) History and Background Ricinus communis or the Castor oil plant is cultivated in southern United States and also grows as a weed and ornamental plant (Fig. 38.2). It is native to tropical Africa but has naturalised sub-tropical and temperate areas as well. The whole plant is poisonous, containing the heterodimeric ribosome inhibiting protein ricin that reaches the highest level in the seeds. It consists of a water-soluble glycoprotein, Toxalbumin that causes agglutination, cell destruction and haemolysis. Its residue contains the toxin, ricin. The seeds also contain purgative oil, the triglyceride of ricinoleic acid. In the tropics, eating a single
Figure 38.2: Plant of Ricinus communis
seed for the purgative effect is a widespread custom. The seeds have been used in folk medicine against many diseases for centuries. They appeared in classical Greek medicine and are described in the Sanskrit work on medicine, Sushruta Ayurveda from the 6th century BC. The oil is used for lubrication in the motor industry and is still being used as a laxative. The dust of this plant causes irritation of the eyes, nose and throat that causes asthma, allergy and dermatitis. Each fruit of Ricinus communis contains three mottled seeds, 5-15mm long, that are red grey or polished brown in colour. The poison is more effective when injected than when taken by mouth as it is destroyed by digestive enzymes. The plant also contains compounds which may elicit anaphylactic reactions. Because of this, ingestion of any dose of Ricinus communis can be fatal within minutes. Ricin has been known as a poison for years, usually through livestock deaths. The cattle may eat fruit or in our country, malicious neighbours are said to have administered extract of castor bean to their neighbour’s cattle using a metal nail or ‘Suis’. In Nigeria the beans are eaten as a food after careful preparation as heat inactivates the toxin, but in East Africa, unwanted children in the past have been murdered by adding castor beans to their food. The seeds of castor are commonly mistaken for that of croton but can be clearly distinguished on close inspection (Table 38.1) Fatal dose→The fatal dose is 1mg/kg or 8-10 crushed seeds in adults and 2-3 seeds in children. As lots of ricin is destroyed in the gastrointestinal tract, it is much more potent when administered parenterally. A dose of 2 millionths of the body weight may prove fatal. Fatal period→2-24 hours
Irritant Poisons 571 Table 38.1: Differences between castor and croton seeds (Figs 38.3 and 38.4) Features
Castor seeds
Croton seeds
Appearance
Grayish with brown patches
Size Cross section Transverse striae
1.25 cm long and 0.85 cm broad Lumen is circular Cells show ribbed appearance due to fine, transverse striae
Dark brown or brownish gray shell which on scrapping becomes black 1.2 cm long and 0.82 cm broad Lumen is slit like with radiating creases No transverse striae and no ribbed appearance
Figure 38.3: Castor seeds
Figure 38.4: Croton seeds
Signs and Symptoms Toxic effects of Ricin have a latent period and take 2-24 hours to develop. After ingestion: The symptoms are: (i) Burning pain in the abdomen (ii) Vomiting and diarrhea often with blood (iii) Haemorrhages occur in intestines, mesenteries and omentum (iv) A diffuse nephritis and multiple necroses occur in liver and kidneys (v) Within several days there is severe dehydration, oliguria, thirst, burning throat, headache and patient may die of hypovolaemic shock (vi) The body temperature decreases before death and the patient often undergo a characteristic shivering (vii) Consciousness remains till the end (viii) Death occurs due to exhaustion or cramps. When administered parenterally: Ricin is twice as toxic as cobra venom and is probably the most toxic parenteral substance in the plant kingdom. After parenteral administration, the patient may present with fever, leucocytosis and then hypotension and hypothermia. It primarily targets the liver and the kidneys. Treatment Measures should be undertaken to prevent absorption after ingestion of the poison as there
is no specific antidote for Ricin: (i) Stomach wash using potassium permanganate should the carried out (ii) Syrup of ipecac and activated charcoal should be administered (iii) Stimulants should be given (iv) Intravenous glucose saline to be administered for dehydration (v) Sodium bicarbonate (vi) Supportive care including blood transfusion to combat blood loss (vii) The patient should be constantly monitored for hypoglycemia, haemolysis and hypovolaemia. Medicolegal Aspects (i) The poisoning is usually accidental when is taken by children by mistake (ii) It is also given mixed in food for criminal intent (iii) The powder when instilled in to the eyes causes conjunctivitis (iv) The castor oil is non poisonous and is used as purgative (v) The triglyceride of ricinoleic acid may act as an irritant poison (vi) It is used to make ‘Suis’ and injected in to the buttock of the animal. Autopsy Findings (i) There is congestion of stomach, intestine and other visceral organs (ii) Inflammation and hemorrhages in the stomach, intestines, mesenteries and omentum are identifiable (iii) There is softening of the organs (iv) Fragments of seeds may be recovered from the stomach (v) There are findings of hepatic and renal necrosis. CROTON TIGLIUM (JAMALGOTA OR NAEPALA) The plant grows all over India and the seeds as well as oil expressed from the seed and the root of the plant are highly poisonous. The seeds are 0.65 × 0.85 cm in size, grayish white in colour with a white oily kernel having some longitudinal
572 Textbook of Forensic Medicine and Toxicology lines over the surface. Croton oil is vesicating agent, has brown colour and disagreeable odour and contains crotonoleic acid, methyl crotonic acid, crotonol and other fatty acid. The oil does not contain crotin that is left out in the croton seed cake on expression of the oil. When applied on the skin, it causes burning, redness, vesication and suppuration. When the seeds are swallowed, they cause irritation of the gastro-intestinal tract. Croton seeds are poisonous to fish and a case is reported where croton oil was used to poison fishes at Midnapur, West Bengal.
Medicolegal Aspects
Active Principles
The Calotropis plant is found all over India in two varieties; Calotropis gigantea and Calotropis procera. The dried root freed from its outer cortical layer is called Madar. Its constituents are Madaralbum, a crystalline colourless substance; Madarfluavil, an amber coloured viscid substance and Mudarine, gelatinizes on heating.
The active principles of seeds of Croton tiglium is: (i) Crotin a toxalbumin is less poisonous than Ricin (ii) Crotonaside is a glycoside. Signs and Symptoms It is a gastrointestinal irritant and produces symptoms similar to Ricin poisoning (i) Severe hot burning pain in mouth, throat and abdomen (ii) Salivation, nausea, copious vomiting (iii) Frequent watery stools mixed with blood and mucus accompanied with gripping pain abdomen, anal irritation and tenesmus (iv) Features of dehydration are prominent (v) Quick weak pulse, shallow respiration and vertigo (vi) Circulatory collapse and death (vii) Being toxalbumin, it produces agglutination of red cells causing hemolysis, jaundice, pain in renal angles, haemoglobinuria (viii) The blocking of renal tubules leads to oliguria, anuria and uremia and resulting renal failure accounts for delayed deaths (ix) On application to skin, it produces burning, redness and vesication. The vesicles may suppurate resulting in scarring on healing. On contact with eyes will produce conjunctivitis and corneal ulcer. Fatal period→4-6hours to days. Autopsy Findings (i) Gastrointestinal tract mucosa shows erosion, inflammation and congestion (ii) Liver, and spleen are congested (iii) Kidneys may show cloudy swelling and tubular necrosis (iv) In rare cases, the findings are negative.
(i) Poisoning results from eating seeds or inhaling dusts (ii) Accidental poisoning results from overdosage of croton oil that is used as purgative or administered after mixing with food (iii) It is rarely suicidal (iv) Used for homicidal purposes by boiling the root and adding to food (v) Root of the plant is commonly used as abortifacient (vi) It is used as an arrow poison CALOTROPIS PROCERA AND GIGANTEA (MADAR OR AKDO) (Fig. 38.5)
Figure 38.5: Calotropis procera
Active principles: (i) Uscharin (ii) Calotoxin (iii) Calotropin (cardiac glycoside) (iv) Calactin. Uses: (i) The flowers are dried and powdered and used as digestive, carminative and tonic (ii) The dried leaves are used as purgative in small doses; applied locally it relieves headache and in large doses act as an emetic (iii) The tincture prepared from bark or root may be used in dysentery (iv) The acrid milky juice may be used as an emetic, purgative, vesicant and also for treatment of chronic skin diseases (v) The dried bark is used by vaids as an expectorant, emetic and purgative; bark may also be utilized for making madar or ushar fibres (vi) Madar juice or the powdered bark or root of the plant may be used by tanners as a depilatory; this imparts yellow colouration to the skin and destroys offensive odour of fresh leather (vii) The
Irritant Poisons 573 plant may also be used for treatment of impotence, asthma, syphilis, gonorrhoea and elephantiasis. Medicolegal Aspects (i) Madar juice is commonly used as an abortifacient either taken by the mouth or applied locally into the uterus by abortion stick, either alone or in the form of paste with lead oxide or arsenic preparation (ii) Madar juice may be used for the purpose of homicide, suicide or infanticide; for infanticide, the madar juice may often be given by mouth mixing it with milk and water (iii) Madar juice is commonly used as a cattle poison, when a cloth or rag smeared with the juice is either given with fodder or introduced into anal or vagin*l canal of the animal (iv) The root of calotropis procera is reputed to be strongly poisonous to cobras and other poisonous snakes, who cannot stand its smell. Hence, snake charmers may carry it to control freshly caught cobras (v) When used with snuff, powdered madar root may cause death (vi) The juice can often be used to produce artificial bruises (vii) It may also be used as arrow poison. CAPSICUM ANNUM (LAL MIRCH, CHILLIES) Capsicum fruits or seeds are extensively used in India as a condiment, in preparation of curries, chutneys etc. They have pungent acrid odour and taste, which lasts for a long time; may be used as stomachic and carminative. Chilli seed is approximately 0.30 cm (1/8") long and 0.20 cm (1/10") wide; they resemble very much dhatura seeds (Figs 38.6 and 38.7).
Differences between chilli and dhatura seeds Features
Chilli Seeds
Size Shape Surface
Smaller in size Round Smooth
Colour Smell Taste Convex Border On section
Dhatura Seeds
Larger in size Kindney Finely pitted or reticulated Yellowish Brownish Pungent Odourless Pungent Bitter Single-edged Double-edged The embryo lies The embryo lies embedded in the embedded in the fleshy albumen white oily albumen and curved and curved inwards outwards
Active principles: (i) Capsicin (ii) Capsaicin Signs and symptoms: (i) Burning sensation in mouth (ii) Profuse salivation, thirst and difficulty in swallowing (iii) Pain in abdomen and constipation (iv) Burning sensation around the anus during passing stool (v) Nausea and vomiting (vi) Irritation and vesication on the skin, when applied locally (vii) Burning, lacrymation and chemosis, when applied to eyes (viii) Burning, lacrymation, coryza and cough, due to fumes of burned chillis. Fatal Dose→Low toxicity Fatal Period→Fatality is unknown. Treatment (i) No specific treatment (ii) Stomach wash with plain water (iii) Cathartics should be given (iv) Irrigation of eyes with plenty of cold water or sterile normal saline and application of eye drops, in case of eye contamination (v) Skin contamination should be treated with plenty of water and an emollient cream locally. Medicolegal Aspects
A
B Figure 38.6: Red chillis
Figure 38.6: (A) Dhatura and (B) chillis Seeds
1. Chilly powder may be thrown into the eyes to rob or steal valuables, money etc. from the persons by burglars and robbers specially from the bank counters 2. It can also be used to stupefy and disable a person to facilitate commission of crime 3. Chilli powder may be used for the purpose of torture to extract money or to extort confession of guilt, when it is introduced into the nostrils,
574 Textbook of Forensic Medicine and Toxicology eyes, vagin* or urethra or rubbed over the breasts of females, burnt under the nose or when head is covered by nose-bags containing chilly powder. 4. Burning of chilly seeds may at times be done by superstitious people to scare away devils and ghosts. PLUMBAGO ROSEA, PLUMBAGO ZEYLANICA OR LAL CHITRA OR CHITRA They grow as two types, Plumbago rosea (red flowers) and Plumbago zeylanica (white flowers) all over India. Active principles: The active principles is plumbagin contained in the roots and other parts of the plants. It is a highly acrid crystalline glycoside, the non-alkaloidal active principle. Plumbagin is powerful irritant and in small doses it stimulates contractions of heart, intestine and uterus. In large doses, it produces respiratory failure. Fatal dose and Fatal period→Uncertain. Signs and Symptoms On external application of crushed roots and twigs of plants in the form of paste causes swelling, redness and inflammation and blister formation. Ingestion of crushed roots in large doses causes: (i) Burning pain in mouth, throat and stomach with vomiting (ii) Intense thirst and diarrhea (iii) Convulsion (iv) Uterine contractions leading to abortion (v) Collapse and death from cardio respiratory failure. Treatment 1. In case of local application of paste or abortion stick, it should be removed and vagin*l douching with warm water and an antiseptic solution. 2. In case of ingestion, stomach wash with plain warm water, demulcents, stimulants, analeptics to combat shock and collapse. Autopsy Findings (i) Inflammation and injury in vagin*, cervix and uterus when used as an abortifacient (ii) Gastrointestinal irritation with congestion of all internal viscera (Fig. 38.7).
Figure 38.7: Congestion and haemorrhagic gastritis in irritant poisoning
Medicolegal Aspects (i) The crushed roots of plumbago are used to procure abortion. The quacks used crushed roots as birth control pills (ii) It is less commonly used for homicidal purposes (iii) The paste or milky juice of crushed stems or leaves is applied to the skin to form reddish brown artificial bruise (iv) The powdered leaves and roots may be used in the treatment of leprosy, scabies and influenza etc. ERGOT Ergot is dried sclerotium of the parasitic fungus claviceps purpurea that grows on cereals like wheat, rye, oat, barley and bazra etc. in wet seasons and ill-drained soils. The spores of ergot contaminate the grains through insects or wind. The spores then replace the grain and form dark purplish bodies larger than the original grain. These diseased grains when collected, dried and powdered constitutes ergot for the market. Alkaloids of Ergot These are grouped into: 1. Amino-acid alkaloids that comprises of: (a) Ergotoxine (mixture of ergocrystine, ergocornine and ergocryptine) (b) Ergotamine (c) Ergosine. 2. Lysergic acid and amino-alkaloids that comprises of: (a) Lysergic acid (b) Lysergic and diethyl-amide (c) Ergonovine (ergometrine) (d) Methyl ergonovine (e) Methysergide. Ergotoxine: It promotes contraction of pregnant uterus in last months of pregnancy but no or little effects are there on the uterus in other periods. It also produces gangrene by causing vasoconstriction. Ergometrine: It is an active ecbolic and it causes prolonged uterine contraction especially
Irritant Poisons 575 on post-parturial uterus. It does not usually produced gangrene. Lysergic acid and amino-alkaloids: They cause stimulation of central nervous system. Ergot acts on smooth muscles of intestine, uterus and arterioles and it is commonly used in obstetrics for its ecbolic action. It is also used in the treatment of migraine, as abortifacient and in veterinary practice. Fatal Dose→1-2 grams Fatal Period→The death does not occur from single large dose but when small or medicinal doses are given for a long time. The fatal period is usually one day but death may be delayed for several days. Signs and Symptoms Acute poisoning: The signs and symptoms of acute poisoning are: (i) Dryness and irritation of throat with intense thirst (ii) Nausea and vomiting (iii) Pain abdomen and diarrhoea (iv) Vertigo, giddiness and dizziness (v) Tightness and sense of constriction in chest (vi) Disturbance of speech and vision (vii) Tingling of hands and feet with feeling of numbness and coldness (viii) Muscular weakness and cramps in muscles (ix) Body temperature falls with hypoglycemia and suppressed urine (x) There may be abortion or bleeding from uterus (xi) Epistaxis, haemetemesis and haematuria may occur (xii) Convulsions and confusion leading to stupor and coma and finally death results from cardio-respiratory failure (xiii) In survivors, the extremities may develop gangrene. Chronic Poisoning (Ergotism): Ergotism develops in those taking medicinal preparation of ergot or consumption of flour contaminated with ergot for a long time. The patients with focal sepsis and hepatic damage are more sensitive to ergot alkaloids. Signs and symptoms may present in convulsive or gangrenous form. Convulsive form: This form is presumed to occur with consumption of flour containing about 10% of ergot and is associated with vitamin A deficiency. The patient presents with (i) Tingling and itching (ii) Feeling of numbness in hands and feet and pain on walking (iii) Sensation of insects
crawling under the skin (iv) Drowsiness and giddiness (v) Dimness of vision and fixed dilated pupil (vi) Loss of hearing and ataxia (vii) Loss of arterial pulsation and finally tonic or clonic convulsive seizures (viii) Paralysis of sensory nerves and maniac depressive psychosis (ix) Death results from asphyxia due to spasm of respiratory muscles. Gangrenous form: This form occurs with consumption of flour containing more than 10% of ergot. The following signs and symptoms are produced (i) Pain in the limbs with feeling of hot and cold sensation (ii) Tingling and numbness in fingers and toes resulting from vasospasm of arterioles (iii) Swelling of limbs and feet with red patches and blisters (iv) Loss of sensation of the part followed by gangrene formation from vasospasm and vasoconstriction with obliteration of the lumen of small blood vessels (v) The gangrene is of dry affecting fingers, toes and limbs that become cold to touch and dark in colour. The gangrene may extent upto elbow or knee and may affect the nose, ears or even intestines with formation of ulcers Treatment In case of acute poisoning: (i) Stomach wash with plain warm water, tannic acid or activated charcoal (ii) Purgatives or enema can be given (iii) Vasodilators such as amylnitrite can be given orally or parenterally (iv) The convulsion should be treated (v) Heparin should be given i.m for hypercoagulability of blood In case of chronic poisoning: (i) The patient should be removed from the source of poisoning (ii) Sodium nicotinate 140 mg i.v. to counteract the vasoconstrictive affect of ergotamine (iii) Gangrene to be treated by amputation (v) Nitrites and papaverine 100-150 mg orally or parenterally to restore circulation in incipient gangrene. Autopsy Findings (i) Gastrointestinal tract will be congested with inflammatory changes (ii) All the visceral organs will be congested (iii) Gangrene of toes and fingers is evident (iv) Small blood vessels will show
576 Textbook of Forensic Medicine and Toxicology evidence of intimal degeneration Medicolegal Aspects 1. Acute ergot poisoning may result from over dose of ergot preparations to cause abortion. 2. The use of ergot preparations for a long time can result in ergotism CANTHARIDES (SPANISH FLY) The dried beetle Cantharis vesicatoria, known as ‘Spanish fly’ contains a vesicant, cantharidin. Contact of either the live or the dried beetle with the skin results in immediate burning with vesication. Besides this, other beetles causing similar pictures include Epicauta cinerea (blister beetle) and members of genus Paederus. The compound is used as an aphrodisiac in both humans and cattle. Signs and Symptoms A. The ingestion results in: (i) Burning sensation and vesication in mouth (ii) Nausea, vomiting and bloody diarrhoea (iii) Circulatory collapse (iv) Coma, convulsions and death. B. Local application on genitals results in: (i) Intense haemorrhagic cystitis and urethritis with resulting priapism (ii) An intense pelvic congestion leading to abortion and priapism (iii) The onset of oliguria, haematuria and finally anuria heralds the appearance of several renal involvements Fatal dose→10-120 mg. Treatment 1. Gastric lavage to be carried 2. Supportive and symptomatic treatment. Autopsy Findings (i) The forewings of the beetle may be found in the gastrointestinal tract (ii) Vesication of mouth and oesophagus may or may not be present (iii) Intense congestion and haemorrhage of the gastrointestinal tract (iv) Urinary bladder may be haemorrhagic (v) Haemorrhagic toxic nephritis in patient who survive longer
SNAKES
Snakes belong to the class Reptila, order squamata, and sub-order Serpentes. The snakes are found all over the world except New Zealand, Ireland and in Arctic lands. Of the 2500-3000 species of snakes distributed world-wide, about 500 are poisonous to Humans. There are 238 species of snakes in India out of which only 52 are poisonous. Of these 52 poisonous species majority of bites and consequent mortality is attributable to 5 species viz. Ophiophagus hannah (king cobra), Naja Naja (common cobra), Daboia rusellii (Russell’s viper), Bungarus caeruleus (krait) and Echis carinatae (saw-scaled viper). In India, deaths as a result snake-biting are mainly accidental in nature. It has been reported that in most developing countries, up to 80% of individuals bitten by snakes first consult traditional practitioners before visiting a medical centre. It is reported that there were about 200,000 bites and 15,000 deaths in India due to snake bite poisoning as far back as 1954. In Sri Lanka, the overall annual mortality from a single venomous species ranges from 5.6 per 100,000 to as high as 18 per 100,000 in some areas. Myanmar seems to have the highest mortality in Asia and 70% snakebites are by Russell’s viper. However, this may only reflect a better reporting system prevalent in that country. Maharashtra, one of the states of India with the highest incidence, reported 70 bites per 100,000 population and mortality of 2.4 per 100,000 per year. The other states with a large number of snakebite cases include West Bengal, Tamil Nadu, Uttar Pradesh and Kerala. General Characteristics of Snakes A snake is a reptile without limbs and has a short tail. Vent is the opening in the rear part of the body for intestinal and genitourinary system. The part behind the vent is the tail that is flat in sea snakes and round in land snakes. The body of snakes is covered with scales. On the head, there are two eyes, two nostrils but no external ear. The eyes are covered with transparent scale bearing no eyelids and the pupils are round or vertical. All snakes are cold-blooded creatures with carnivorous habits. They use sharp teeth and strong
Irritant Poisons 577 muscles to catch the prey. The lower jaw comprises of two bones, in front joined by an elastic ligament and it does not properly articulate with the upper jaw. The mouth of the snake is easily distensible allowing it to swallow even large animals as a whole. Their pointed and backwardly teeth are found on both jaws and palate. The upper marginal teeth get modified to form fangs. A new fang will appear in place of a broken one within 46 weeks. The fangs are solid in nonpoisonous snakes but are grooved or channeled in poisonous ones for transport of venom from the poison glands to which they are connected through ducts. In poisonous snakes, parotid glands situated behind and below the eyes, one on each side secreting toxic saliva, and act as poison glands. The fangs of elapid snakes and sea snakes are short, fixed and grooved while those of vipers are long, movable and canalized. The tongue of the snake is forked at the tip and it acts as a sense organ for its search for food, other sex or enemy. Because of the shape of the body, the paired organs are laid one behind another. Poisonous snakes have only one right lung. The snake moults its skin several times a year throughout its life to keep oneself active. The snakes move by gliding motion. Some snakes lay eggs, others give birth to young ones. Several species of egg layers such as pythons, cobras and water snakes have been found to stay with the eggs until hatching. The King cobra is the only snake in the world that
builds nest. In India the snakes range from the giant reticulated python (Python reticulates) that grows to 10 meters, to the tiny worm snake (Typhina bramina) which grows just 10 cm, and often mistaken for a worm. The King Cobra (Ophiophagus Hannah), the largest venomous snake in the world, which grows to 5 meters in India, is ‘ophiphagus’ that is they eat only snakes, mostly the ubiquitous rat snake and sea snakes eat fish. Differences between poisonous and nonpoisonous snakes: There are certain physical characteristics that help to distinguish between the venomous and non-venomous snakes. Of these there are the belly scales that can be seen after turning the snake with belly upwards. The other distinguishable features are the size of head scales, fangs, appearance of tail, the teeth bite mark over the body of the victim and the habits of the snake whether they are nocturnal or diurnal (Table 38.2). VENOMOUS SNAKES There are more than 52 species of venomous snakes in India of which there are four important types of snakes. These are King cobra, Krait (Bungarus Russell), Russell’s viper (Vipera Russell) and the saw-scaled viper (Echis carinatus). Each of these snakes is easily distinguishable, though it is easy to confuse them with other harmless species. The venomous snakes are
Table 38.1: Differences between venomous and non-venomous snakes (Figs 38.8 to 38.10) Features Belly scales • Size • Distribution
•
Size of head scales
• • • •
Fangs Tail Habits Teeth-bite marks
Venomous snake
Non-venomous snake
Large They cover the entire breadth of the belly. Some non poisonous snakes may also possess such scales similar to those on the back or may be moderately large. Usually small as in vipers except in pit vipers, Cobras or coral snakes and Kraits where they are large Are hollow like hypodermic needles Compressed Usually nocturnal Two fang marks are left at the site of bite usually with or without marks of other teeth. Usually they have two long teeth or fangs
Small Never cover the entire breadth of the belly
Usually large
Short and solid Not markedly compressed May be nocturnal or diurnal Two fang marks are left at the site of bite and a number of several small teeth marks
578 Textbook of Forensic Medicine and Toxicology
B
A
C Figure 38.10: Large heads sales of non venomous snakes
Figure 38.8: Large belly scales of venomous snakes with varioatus such as in (A) Belly scales small like those on the back as in (B) or moderately large but not covering the entire breadth of belly as in (C)
Figure 38.9: Small head scales of venomous snakes e.g. Russel viper
classified in to three families based on the type of poison secreted.
scales (plates) on the head. They differ in having more advanced venom delivery systems than the venomous Colubrids. Elapids have fangs that are effectively tubular in that the fangs contain grooves that are enclosed by an infolding of the edges. The fangs are in the front of the mouth rather than the rear as is seen in venomous Colubrids. The Elapidae contains some of the world’s most dangerous snakes including: (i) Common cobras (Naja naja) (ii) King cobra (Naja hanna) (iii) Kraits: Kraits are bluish black in colour, shiny with transverse thin white cross bands, which may be very faint or sometimes even absent. They are subdivided into (a) Common Krait (Chitti) and (b) Banded Krait (Sankhini) (iv) Mambas (Dendroaspis) (v) Sea snakes (Hydophinae and Laticaudinae) (vi) Coral snakes In cobras and the coral snakes the third labial head scale touches the eye and nasal shields.
I. Elapidae or Colubridae that secrete Neurotoxic poisons Colubridae (Colubrid Snakes) The colubrine snakes lay eggs. Their oval heads covered by large scales are nearly of the same girth as of their neck that is indistinct and the pupils are circular. Their anteriorly situated fangs are short, fixed and grooved, thus they cannot effectively bite through the clothing and inject a complete lethal dose. The Colubrid snakes are sometimes referred to as “typical snakes”. They comprise the largest family by far with over 2000 species worldwide. Most are medium sized snakes, and all lack a pelvic girdle and have no vestigial hind limbs and whose left lung is either absent or greatly reduced. Most species are considered members of two large subfamilies, Colubrine and Natricinae which are distinguished by the presence (Natricinae) or absence (Colubrinae) of spines on the lumbar vertebrae. The colubrines are subdivided into Elapidae or land snakes, viperidae and hydrophidae or sea snakes. Elapidae (Cobras and Coral snakes) The cobra family is thought to have evolved from Colubrid snakes and many appear very similar in appearance with long, slender bodies and large
II. Viperidae that secrete Vasculotoxic poisons The viperines are viviparous that is they give birth to young ones. The vipers are generally considered to be the most advanced family of snakes since they possess a very sophisticated venom delivery system. Large movable and tubular fangs are placed in the front of the mouth and they are hinged, allowing them to be folded back when not in use. The vipers can bite through the clothes
Irritant Poisons 579 and inject the venom. Their triangular heads are covered with numerous small scales and their eyes have vertically elliptical pupils. All the viperine species are poisonous. The viperine snakes have following subfamilies: (i) Saw scaled viper (ii) Pit viper (iii) Russell’s vipers.
is usually jet black but can also be brownish to greenish and sometimes yellow. The tail scales are entirely present in their proximal ends but divided in the distal ends (Fig. 38.11 to 38.13). Common Krait (Bangarus caeruleus)
III. Hydrophidae or Sea-Snakes that secrete Myotoxic poisons There are about twenty types of sea snakes found in India and all are venomous. They have small heads, small eyes and a flat tail that helps in swimming. Their valved nostrils are situated on the top of the snout for free breathing. The belly plates are not broad and have dull trabeculated scales on their back. The poison glands are delicate with short fangs that are situated posteriorly. Their bodies are greenish black, dark black or bluish black in colour. Common Cobra (Naja naja, Nag, Gokhurra) Common cobra is seen throughout India, Sri Lanka and Burma. These are 1.5-2 meters long. The cobra varies in colour from cream to black, though generally it is brown. The hood may have the typical spectacle or monocle marking on its underside, which are two dark round spots and at times only one spot surrounded by an ellipse. The characteristic hood of the cobra is visible only when it raises its head while in danger, enraged or about to strike. The underside of the hood also bears three dark bands on the central part and a white band in an area where hood touches the body. The divided tail shield helps in identifying a cobra when hood is not visible. The maxillary bone extends beyond the palate and the poison fangs are followed by one or two small teeth. King Cobra (Naja bangarus, Raj Nag or Daras) The King cobra is found the hills and forests of South India, Orissa, Assam and the Himalayas. It is bigger in size compared to the common cobra and its length is usually 2.5-4.5 meters. The head is flat with a hood but no spectacle mark on it. It
Figure 38.11: Cobra and Figure 38.12: Hood of its belly scales cobra showing spectacle mark Nasal shield Nostril Mental shield
1
Eye
Eye shield
2
3 Figure 38.13: In Cobra head scales are large and third labial touches the eye and nasal shields with round pupil
The common krait is found throughout India and is known by the names of Chitti (Calcutta), Kawriya (Punjab), Maniyar (Maharashtra). They are nocturnal and their habitat is near dwelling houses. The size may be 1.5 meters long and are usually steel black in colour. They bear single or double narrow bands across their back that extends from below the head up to the tip of tail. The belly is creamy white in colour. Their head are oval with one enlarged central row of hexagonal scales on the back. The undersurface of the mouth has only four infralabials-the fourth is the largest and there are bands or half rings across the back. The third labial scale does not touch the nose and eye. The tail is round
580 Textbook of Forensic Medicine and Toxicology with tail scales that are entirely placed and not divided. Banded Krait These snakes vary in length from 2.5 to 3.5 mts, longer, bigger and stouter than common krait. It bears alternate jet black and yellow bands across its back, hence the name. It has a black mark on its neck spreading up to the eyes. It is deadly poisonous snake (Figs 38.14 and 38.16). Rat Snake (Zamenis mucosus, Dhamana
Figure 38.14: Central hexagonal scales on the middle of the back of krait Mental shield
1
2
3
4
Figure 38.15: Fourth infralabial in krait is the largest (View is from below)
The coral snakes are relatively small snakes that spend most of their time underground and are found in hilly areas. Their size may be up to 1.5 mts (3ft) and their primary food is other snakes. The bellies are pinkcoral coloured and the tail is round. Despite their small size and small fangs, their venom is extremely toxic. Pit vipers (Crotalidae) Pit vipers have a pair of heat sensing pits located on the head between each eye and nostril. The pit helps in detecting warm blooded prey in the dark. They are usually 2-4 feet (30-100 cm) in length and are found in the hills. These snakes are seldom fatal to humans. Their body is flat and broad and triangular head. They are found in hilly areas with their distinct green or sometimes yellow color (Fig. 38.17). Russel’s viper (Chandra Bora or Daboia) Russel’s vipers are heavy bodied snakes with narrow necks, triangular heads and three longitudinal regular chain-like pattern or rows on the back. The scales are quite rough and the overall colour is yellowish and brown. It is found throughout India in the plains. It is 1-1.5 m long and is stouter than any other poisonous snake. Head scales are small and the nostrils are bigger than any other Indian snake. The tail is short with divided shields and the belly scales are broad. It makes a loud hissing sound before striking the enemy (Fig. 38.18). Saw-scaled Viper
Figure 38.16: Banded krait
Samp)
Figure 38.17: Pit viper
They may look like a cobra but do not have a hood, spectacle mark or monocle mark on its head. They are 5-6ft in length with large nostrils. Figure 38.18: Russels viper
Coral Snakes
Irritant Poisons 581 (Phoorsa or Echis carinata) The saw-scaled viper is the smallest of these four types of snake, growing to just a foot, it is brownish with white marking and has a triangular head typical of the vipers The scales on the head are small and that on the body are broad having serrated edges. It makes a peculiar rustling sound while moving because of its saw-like scales on the body (Fig. 38.19). Differences between Cobras and Vipers
Figure 38.19: Saw scaled viper Features
Cobras
Vipers
Body Head
Long and cylindrical Small & seldom broader than body, same width as neck, covered with large scales Has 2 poison fangs and other teeth Round pupil Grooved, short & fixed Round Neurotoxic Oviparous
Short and stout Larger & broader than body, wider than neck, triangular and covered with small scales
Upper jaw Eyes Fangs Tail Venom Parity
Only poison fangs Vertical pupil Canalized, long & mobile Tapered Haemotoxic Viviparous
SNAKE VENOM The snake venom is the secretion of the racemose salivary glands that is a modification of the parotid salivary gland of other vertebrates, and is usually situated on each side of the head below and behind the eye, invested in a muscular sheath. It is provided with large alveoli in which the venom is stored before being conveyed by a duct to the base of the channelled or tubular fang through which it is ejected. Snake venom is poisonous only when it
is injected but is not absorbed by the stomach mucosa when ingested. The blood of animal bitten by snakes will be poisonous and lethal when injected into the human body. The Vipers furnish examples of the most highly developed poison apparatus, although inferior to some in its toxic effects, the poison gland is very large and in intimate relation with the masseter or temporal muscle, consisting of two bands, the superior arising from behind the eye, the inferior extending from the gland to the mandible. When the snake bites, the jaws close up, causing the gland to be powerfully wrung, and the poison pressed out into the duct. From the anterior extremity of the gland the duct passes, below the eye and above the maxillary bone, where it makes a bend, to the basal orifice of the poison fang, which is ensheathed in a thick fold of mucous membrane, the vagin* dentis. By means of the movable maxillary bone hinged to the prefrontal, and connected with the transverse bone which is pushed forward by muscles set in action by the opening of the mouth, the tubular fang is erected and the poison discharged through the distal orifice in which it terminates. The Proteroglyphous Colubrids: The poison fangs are not tubular, but only channelled and open along the anterior surface. As the maxillary bone in these snakes is more or less elongate, and not or but slightly movable vertically, the poison duct runs above the latter, making a bend only at its anterior extremity, and the transverse bone has not the same action on the erection of the fangs. Otherwise the mechanism is the same. The Opisthoglyphous Colubrids: The grooved teeth are situated at the posterior extremity of the maxilla and a small posterior portion of the upper labial or salivary gland is converted into a poisonsecreting organ. This is distinguished by a light yellow colour, provided with a duct larger than any of those of the labial gland, and proceeding inward and downward to the base of the grooved fang. The duct is not in direct connection with the groove, but the two communicate through the mediation of the cavity enclosed by the folds of mucous membrane surrounding the tooth, and united in front.
582 Textbook of Forensic Medicine and Toxicology The reserve or successional teeth, which are always present just behind or on the side of the functional fang of all venomous snakes, are in no way connected with the duct until called upon to replace a fang that has been lost. When biting, a Viperid snake merely strikes, discharging the venom the moment the fangs penetrate the skin, and then immediately leaves go. A Proteroglyph or Opisthoglyph Colubrid, on the contrary, closes its jaws like a dog on the part bitten, often holding on firmly for a considerable time. The poison, which is mostly a clear limpid fluid of a pale straw or amber colour, more rarely greenish, sometimes with a certain amount of suspended matter, is exhausted after several bites, and the glands have to recuperate. The venom retains its poisonous properties for several years in dried state. The Cobra venom is slightly viscous and when exposed to sun it becomes a little turbid. The venom of Russel’s viper is usually white or yellow. It must be added that the poison can be ejected otherwise than by a bite, as in the so-called Spitting Snakes of when irritated are in the habit of shooting poison from the mouth, at a distance of 4 to 8 feet. In all probability, the poison escapes from the sheath of mucous membrane surrounding the base of the fangs, and is mixed with ordinary saliva, the membranes of the mouth perhaps acting as lips, in which case the term “spitting” would not be incorrect. The spitting, which may take place three or four times in succession, has been observed to be preceded by some chewing movements of the jaws. If reaching the eye, the poisonous fluid causes severe inflammation of the cornea and conjunctiva, but no more serious results if washed away at once. Snakes emerging out from hibernation after winter usually give fatal bite. Nocturnal bites are more serious than those occurring during the day. Less venom will be injected if the fangs are broken or if the snake had bitten a prey previously. The vipers give a strong and complete bite whereas in cobra bite the transfer of venom is not complete. Bite on limbs and adipose tissue is less dangerous than those on the trunk, face or scalp.
It is noteworthy that the size of the poison fangs is in no relation to the virulence of the venom. The comparatively innocent Indo-Malay Lachesis alluded to above have enormous fangs, whilst the smallest fangs are found in the most justly dreaded of all snakes, the Hydrophids. Venoms of different species of poisonous snakes varies in the toxicity, composition and antigenic structure. It is basically a mixture of one or more of the toxic substances, toxalbumins and enzymes in varying proportions such as: 1. Proteolytic enzymes or proteolysins: It causes liberation of histamine from the damaged muscular endothelium leading to dissolution of walls of blood vessels with extravasation of blood in the tissue space, also causes digestion of tissue proteins and peptides and produces marked tissue destruction. 2. Fibrin ferments or fibrinolysin thromboplastin enhancing the coagulation process. 3. Neurotoxins (mainly in elapidae venom) producing curare like effect causing paralysis especially of respiratory center 4. Cholinestrase (mainly in elapidae venom) causing hydrolysis of acetylcholine to choline and acetic acid thus causes impairment of neuromuscular transmission. 5. Haemolysin (mainly in viper venom) causing widespread hemolysis in presence of lecithinase. 6. Cytolysin (mainly in viprine venom) causing lysis of cell structures of blood and tissues. 7. Agglutinins causing agglutination of red blood cells. 8. Phosphatidases produce haemolysis and toxic effects on heart and circulation with haemorrhage from lungs. 9. Proteinases have trypsin like action, causing tissue damage. It produces anticoagulant effect from destruction of fibrinogen. It also catalyses the conversion of prothrombin to thrombin thus producing coagulant effect. 10. Phospholipase A, B, C, D acts as catalyst in hydrolysis of lipids. By destroying phospholipids in nervous tissues, it alters neuromuscular conduction. It also helps in
Irritant Poisons 583 penetration of neurotoxin in to nervous tissue. 11. Hyaluronidase helps in rapid spreading of the venom from the local site of bite and thereby quick absorption. It is present in all snake venoms. 12. Ribonuclease and deoxyribonulease helps in rapid spreading of the venom from the local site of bite and thereby quick absorption. It is present in all venoms. 13. Ophi-oxidase helps in autolysis and early onset of venom kile hyaluronidase. 14. Protease causes dissolution of vascular wall and help in spreading of red blood cells and serum in the tissues. 15. Lecithinases acts on the lipid layer of the cells causing increasing fragility and permeability leading to cell destruction. 16. It also contains enzymes such as: Acetylcholine, 5-Hydroxytryptamine, 5-nucleaotidase, endonucleases, transaminases, NAD nucleosidase, phosphodiesterase, ATP, acid phosphatase, phosphom*onoesterase. The Colubrine Venom The effect of the poison of Proteroglyphous Colubrids (Hydrophids, Cobras, Bungarus, Elaps, Pseudechis, Notechis, Acanthophis) is mainly on the nervous system, respiratory paralysis being quickly produced by bringing the poison into contact with the central nervous mechanism which controls respiration; the pain and local swelling which follow a bite are not usually severe. The colubrine venom is predominantly neurotoxic and is primarily toxic for respiratory and cardiac centres. It also has some toxic effects on the cardiovascular system. The cobra venom produces muscular paralysis involving firstly the muscles of the mouth, throat and lastly muscles of respiration, seat the action of venom being upon the motor nerve cells, the action resembling curare. It consists of: (i) Neurotoxin (ii) Cholinesterase (iii) Proteases (iv) Phosphotidases (v) Hyaluronidase (vi) Ribonuclease (vii) Thromboplastin (viii) Fibrinolysin (ix) Proteolysin (x) Cardiotoxin (xi) Phospholipase A. Cobra venom produces convulsions and para-
lysis, while krait venom produces only muscular paralysis. The Viperine Venom The viperine venom is predominantly hemolytic and hemotoxic. It produces cytolysis of cells of vascular endothelium; causes lysis of red cells and other tissue cells and coagulation disorders. It consists of: (i) Proteases (ii) Hyaluronidase (iii) Haemorrhagin (iv) Haemolysin (v) Leucolysin (vi) Lecithinase (vii) Cytolysin (viii) Thromboplastin (ix) Phospholipase A (x) Proteinases. Viper poison (Vipera, Echis, Lachesis, Crotalus) acts more on the vascular system, bringing about coagulation of the blood and clotting of the pulmonary arteries; its action on the nervous system is not great, no individual group of nerve-cells appears to be picked out, and the effect upon respiration is not so direct; the influence upon the circulation explains the great depression which is a symptom of Viperine poisoning. The pain of the wound is severe, and is speedily followed by swelling and discoloration. There will be haemorrhage from the site of bite, associated with the necrosis of renal tubules, convulsions from intra-cerebral haemorrhage. Locally, there will be severe swelling of the bitten part, with oozing of blood and spreading cellulitis. Blood from such patients fails to clot even on addition of thrombin, because of the very low level of fibrinogen. The oozing of blood and serum is very much pronounced in case of viper bite than in cobra bite. Absence of oozing will indicate that the venom has not been injected into the wound. A Cobra can inject about 40 times the fatal dose in a single bite. The amount of dried venom produced in a single bite is: • In Viperine bite—150-200 mg • In Cobra bite—200-250 mg • In Krait bite—20 mg • In Saw-scaled viper—4.5-5 mg Fatal doses of various bites are: (i) Dried cobra venom—12-15 mg (ii) Dried viper venom—15-20 mg (iii) Dried krait venom—5-6 mg (iv) Dried Sawscaled viper venom—8 mg.
584 Textbook of Forensic Medicine and Toxicology Fatal Period→The death may occur instantaneously from neurogenic shock resulting from fright otherwise the fatal period is: (i) In colubrine bite—1/2-24 hours (ii) In viperine bite—2-4 days. Signs and Symptoms of (Ophitoxaemia) 1. Psychological trauma: The most common and earliest symptom following snake bite (poisonous or non poisonous) is fright, particularly of rapid and unpleasant death. Owing to fright, a victim attempts ‘flight’ which unfortunately results in enhanced systemic absorption of venom. These emotional manifestations develop extremely rapidly (almost instantaneous) and may produce psychological shock and even death. Fear may cause also transient pallor, sweating and vomiting. 2. Local manifestations: With the possible exception of the psychological trauma of being bitten, local changes are the earliest manifestations of snake bites. Features are noted within 6-8 minutes but may have onset up to 30 minutes (i) Local burning pain with radiation and tenderness and the development of a small reddish wheal are the first to occur (ii) This is followed by oedema, swelling and appearance of bullae all of which can progress quite rapidly and extensively even involving the trunk (iii) Tingling and numbness over the tongue, mouth and scalp and paraesthesias around the wound occur mostly in viper bites (iv) Local bleeding including petechial and/or purpuric rash is also seen most commonly with viperine bites (v) The local area of bite may become devascularized with features of necrosis predisposing to onset of gangrenous changes (vi) Secondary infection including tetanus and gas gangrene may also result. 3. Systemic manifestations: Regional lymphadenopathy has been reported as an early and reliable sign of systemic poisoning. The time onset of poisoning is similar in different species. Cobra produces symptoms as early as 5 minutes or as late as 10 hours after the bite. Vipers take slightly longer - the mean duration of onset being 20 minutes. However, symptoms may be delayed for several hours. Sea snake
bites almost always produce myotoxic features within 2 hours so that they are reliably excluded if no symptoms are evident within this period. Other systemic manifestations depend upon the pathophysiological changes induced by the venom of that particular species. As mentioned previously, based on the predominant constituents of venom of a particular species, snakes were loosely classified as neurotoxic (notably cobras and kraits), hemorrhagic (vipers) and myotoxic (sea snakes). However it is now well recognized that such a strict categorization is not valid as each species can result in any kind of manifestations. Features of neurotoxicity: Neurotoxic features are a result of selective d-tubocurarine like neuro-muscular blockade which results in flaccid paralysis of muscles. Cobra venom is however 15-40 times more potent than tubocurarine (i) Ptosis is the earliest neuroparalytic manifestation followed closely by opthalmoplegia (ii) Paralysis then progresses to involve muscles of palate, jaw, tongue, larynx, neck and muscles of deglutition-but not strictly in that order (iii) Generally muscles innervated by cranial nerves are involved earlier. However, pupils are reactive to light till terminal stages (iv) Muscles of chest are involved relatively late with diaphragm being the most resistant. This accounts for the respiratory paralysis, which is often terminal (v) Reflex activity is generally not affected in ophitoxaemia and deep tendon jerks are preserved till late stages (vi) Onset of coma is variable, however several cases of cobra bite progress to coma within 2 hours of bite (vii) Symptoms that portend paralysis include repeated vomiting, blurred vision, paraesthesiae around the mouth, hyperacusis, headache, dizziness, vertigo and signs of autonomic hyperactivity. Features of cardiotoxicity: Cardiotoxicity occurs in about 25% viperine bites (i) There are fluctuations in rate, rhythm and blood pressure in the form of tachycardia, hypotension and ECG changes (ii) In addition, sudden cardiac standstill may also occur owing to hyperkalemic arrest (iii) Non dyselectrolytemic
Irritant Poisons 585 acute myocardial infarction has also been reported. Tetanic contraction of heart following a large dose of cobra venom has been documented. There is a single case report of non-bacterial thrombotic endocarditis following viper bite. Myalgic features are the most common presentation of bites by sea snakes. Muscle necrosis may also result in myoglobinuria. Hemostatic Defects: Snake venoms cause haemostatic defects by a number of different mechanisms. Some cause activation of intravascular coagulation and result in consumption coagulopathy. Notable in this group is Daboia russelli which has procoagulant activating factors V and X. Certain other venoms cause defibrinogenation by activating endogenous fibrinolytic system. Besides direct effects on the coagulation cascade, venoms also can cause qualitative and quantitative defects in platelet function. In India and Sri Lanka, Russell’s viper envenomation is often associated with massive intravascular haemolysis. Haematological changes, both local as well as systemic are some of the most common features of snake bite poisoning (i) Bleeding may occur from multiple sites including gums, GIT (haematemesis and melaena), urinary tract, injection sites and even as multiple petechiae and purpurae (ii) Even subarachnoid haemorrhages, subdural haemor-
rhages and extradural hematoma have also been reported (iii) Almost every species of snake can cause renal failure. It is fairly common following Russell’s viper bite and is a major cause of death In a series of 40 viper bites, renal failure was documented in about a third. The extent of renal abnormality in them correlated well with the degree of coagulation defect; however in a majority renal defects persisted for several days after the coagulation abnormalities normalised: suggesting that multiple factors are involved in venom induced ARF. Rarer Systemic Manifestations: These include (i) Hypopituitarism (ii) Bilateral thalamic haematoma (iii) Hysterical paralysis. (Table 38.3) 4. Delayed manifestations of snake bite: The delayed onset of signs and symptoms of snake bite is rare but definitely occurs in the form of bleeding manifestations including brain haemorrhages up to one week after the bite. Some patients develop compartment syndromes several weeks after the bite. The possible explanation for delayed bleeding is that local blebs constitute a venom depot, which is suddenly released into the blood stream, especially when the wound is handled surgically. Laboratory Diagnosis in Ophitoxaemia The laboratory serves rather poorly in the diagnosis of snakebite but laboratory tests are useful for
Table 38.3: Comparative features of clinical manifestations of Colubrine and Viperine bites Features
Colubrine bite
Viperine bite
Onset of signs and symptoms Development of gangrene Feeling of intoxication Gait Speech and power of deglutition Involvement of tongue and larynx
Within 10-20 min Early, wet type Marked Staggering Lost Are paralysed with trickling of saliva from mouth Normal Slow, weak and laboured Not affected Not present From respiratory paralysis
Within second to 10 min. Slower onset, dry type Not marked Not so but features of general paralysis Not so Not affected, salivation is absent
Pupils Respiration Blood coagulability Haemorrhagic manifestations Death
Dilated, not reacting to light Quick and laboured Completely deranged Most important feature When rapid, due to pulmonary thrombosis; when slow, from toxic action of venom on heart and blood
586 Textbook of Forensic Medicine and Toxicology monitoring, prognosticating victims of Ophitoxaemia, as well as determining stages of intervention i. Enzyme linked immunoabsorbent assay (ELISA): ELISA studies which are now available to identify the species involved, based on antigens in the venom. These tests are expensive and not freely available-hence of limited value; except for epidemiological study. ii. Blood changes include anaemia, leucocytosis and thrombocytopenia iii. Peripheral smear may show evidence of haemolysis, particularly in viperine bites. iv. Deranged coagulant activity manifested by prolonged clotting time and prothrombin time may also be evident. The quality of clot formed may be a better indicator of coagulation capability than the actual time required for formation, since clot lysis has been observed in several patients who had normal clotting time. Hypofibrinogenemia may also be evident. v. Among the metabolic changes, hyperkalaemia and hypoxemia with respiratory acidosis, especially with neuroparalysis may be present. vi. Urine examination could reveal haematuria, proteinuria, haemoglobinuria or myoglobinuria. vii. In cases of acute renal failure, all features of azotemia are also present. viii. CSF haemorrhage has been documented in a minority of victims. ix. ECG changes are generally non-specific and include alterations in rhythm (predominantly bradycardia) and atrioventricular block with ST segment elevation or depression. In addition, cases who develop hyperkalaemia manifest typical changes of this dyselectrolytaemia. x. Serum cholesterol levels correlates negatively with severity of envenomation. xi. Recently EEG changes have been noted in up to 96% of patients bitten by snakes; starting within hours of the bite. Interestingly none of them showed any clinical features suggestive of encephalopathy. These abnormal EEG patterns were picked up mainly in the temporal lobes.
Management of Ophitoxaemia First aid for snakebite 1. The bite should not be washed as traces of venom that are left on the skin can be used to identify the snake, and therefore the type of antivenom that should be used if required. 2. Incising and sucking: Venom is injected deeply so there is no benefit in cutting or sucking the bite. It was formerly believed and therefore advocated that incision over the bite drains out venom. However, it has now been established from animal experiments that systemic venom absorption starts almost instantly; this form of ‘therapy’ is therefore being questioned. Some experts suggest that longitudinal incisions within fifteen minutes of the bite may be beneficial. 3. The most effective first aid for snakebite is the pressure-immobilization technique. The principle is to minimise the movement of the venom around the body until the victim is in a hospital by applying a firm bandage (or suitable alternative) to the bitten area and limb, and to immobilise the victim. When applied properly, this method can trap the venom in the bitten area for many hours. The victim might not suffer any effects of the venom until the compression is released, which is done in hospital where antivenom can be administered if required. The tourniquet should be tight enough to occlude the lymphatics, but not venous drainage; though some also prefer to occlude the veins. Enough space to allow one finger between the limb and bandage is most appropriate. Should the limb become edematous, the tourniquet should be advanced proximally. Tourniquets should never be left in place too long for fear of distal avascular necrosis. 4. In the case of Viper bites, tourniquets are also a risk. The Viper’s venom contains procoagulant enzymes which cause the blood to clot. In the small space below the tourniquet the venom has a greater chance of causing a clot. When the tourniquet is released the clot will rapidly enter the body and can cause embolism and death.
Irritant Poisons 587 5. The majority of the Indian venomous snakes have venom that contains toxins that do serious local damage at the bite site. This is true of all vipers and the Cobras. This toxin breaks down tissue and destroys it. Confining this toxin in a smaller area, by use of compression techniques creates a greater risk of serious local damage. 6. Most physicians are in disagreement with regard to nature, duration and even necessity of first aid. Russell advises minimal wastage of time with first-aid measures which often end up doing more harm than good. In a recent report from Brazil, two cases were reported to have increased local envenoming subsequent to a tourniquet. 7. Cleansing the wound: Reid has advised that the wound site be minimally handled. Most authors recommend saline cleaning and sterile dressing. Some however advise that the wound be left open. 8. There is disagreement over the use of drugs as part of first-aid care. It has been suggested that NSAIDS particularly aspirin may be beneficial to relieve local pain. Russell however dissuades use of analgesic and in particular aspirin for fear of precipitating bleeding. In Reid’s experience, pain relief with placebo was as effective as NSAID. Codeine may be useful in some cases. Similarly, there are proponents as well as opponents for use of sedatives Specific Therapy—Antivenins Antivenins are prepared by immunizing horses with venom from poisonous snakes and extracting the serum and purifying it. Antivenoms or antivenins may be species specific (monovalent) or effective against several species (polyvalent). Monovalent antivenom is ideal, but the cost and non-availability, besides the difficulty of accurately identifying the offending species—makes its use less common. Indications for use: There are specific indications for use of antivenom. Not every bite, even if by poisonous species merits its use. This caution against the empirical use of antivenom is due to the risk of hypersensitivity reactions. Therefore,
antivenin is indicated only if: I. Serious manifestations of envenomation are evident viz coma, neurotoxicity, hypotension, shock, bleeding, DIC, acute renal failure, rhabdomyolysis and ECG changes. II. In the absence of these systemic manifestations, swelling involving more than half the affected limb, extensive bruising or blistering and progression of the local lesions within 30-60 minutes are other indications. Dose: Despite widespread use of antivenom, there are virtually no clinical trials to determine the ideal dose. Conventionally: (i) 50 ml is infused for mild manifestations like local swelling with or without lymphadenopathy, purpura or ecchymosis (ii) Moderate envenomation defined by presence of coagulation defects or bradycardia or mild systemic manifestations, merits the use of 100 ml (iii) 150 ml is infused in severe cases, which includes rapid progression of systemic features, Disseminated Intravascular Coagulation, encephalopathy and paralysis. Administration: The freeze-dried powder is reconstituted with 10 ml of distilled water or saline or dextrose. A test dose is administered on one forearm with 0.02 ml of 1:10 solution intradermally. Similar volume of saline in the other forearm serves as control. Appearance of erythema or wheal greater than 10 mm within 30 min is taken as a positive test. In this event, desensitization is advised starting with 0.01 ml of 1:100 solution and increasing concentration gradually at intervals of 15 minutes till 1.0 ml s.c. can be given by 2 hours. Infusion is started at 20 ml/kg per hour initially and slowed down later. Antivenom is administered by the intravenous route and not at local bitten area. Besides this, systemic administration of antivenom has been shown to be effective at the local site as well. Therefore, most experts do not advise local injection of antivenin. Efficacy of intramuscular administration of antivenom followed by standard hospital management has also been evaluated and a definite reduction in the number of patients with systemic envenomation, complications and mortality from Russell’s viper toxemia has been noted.
588 Textbook of Forensic Medicine and Toxicology Timing: There is no consensus as to the outer limit of time of administration of antivenom. Best effects are observed within four hours of bite. It has been noted to be effective in symptomatic patients even when administered up to 48 hours after bite. Reports suggest that antivenom is efficacious even 6-7 days after the bite. It is obvious that when indicated, antivenom must be administered as early as possible and data showing efficacy with delayed administration is based on use in settings where patients present late. Response: Response to infusion of antivenom is often dramatic with comatose patients sitting up and talking coherently within minutes of administration. Normalization of blood pressure is another early response. Within 15 to 30 minutes, bleeding stops though coagulation disturbances may take up to 6 hours to normalize. Neurotoxicity improves from the first 30 minutes but may require 24 to 48 hours for full recovery. If response to antivenom is not satisfactory, use of additional doses is advocated. However, no studies establishing an upper limit are available Infusion may be discontinued when satisfactory clinical improvement occurs even if recommended dose has not been completed. In experimental settings, normalization of clotting time has been taken as end-point for therapy. Side effects: Hypersensitivity reactions including the full range of anaphylactic reactions may occur in 3-4% of cases, usually within 10 to 180 minutes after starting infusion. These usually respond to conventional management including adrenaline, anti-histamines and corticosteroids. Availability: Several antivenom preparations are available internationally. In India, polyvalent antivenom prepared by C.R.I., Kasauli is effective against the 4 most common species. Antivenom produced at the Haffkine Corporation, Parel includes more species as well. This is about 10 times as expensive as the former. The WHO has designated the Liverpool School of Tropical Medicine as the international collaborating centre for antivenom production and/or testing.
Supportive Therapy 1. In cases of bleeding, replacement with fresh whole blood is ideal. Fresh frozen plasma and fibrinogen are not recommended. 2. Volume expanders including plasma and blood are recommended in shock, but not crystalloids. 3. Persistent shock may require inotrope support under Central Ventilation P monitoring. 4. Early mechanical ventilation is advocated in respiratory failure though dramatic responses have also been observed with edrophonium followed by neostigmine. 5. Cases of acute renal failure generally respond to conservative management. 6. Occasionally peritoneal dialysis may be necessary. 7. In cases of Disseminated Intravascular Coagulation, use of heparin should be weighed against risk of bleeding hence caution is to be taken.. 8. Routine antibiotic therapy is not necessary though most Indian authors recommend use of broad-spectrum antibiotics. Chloramphenicol has been claimed to be useful as a post bite antibiotic even when used orally since it is active against most of the aerobic and anaerobic bacteria present in the mouths of snakes. Alternatives include cotrimoxazole, flouroquinolones with or without metronidazole or clindamycin for anaerobic cover. A study of the organisms isolated from the mouth of the Malayan pit vipers suggests that crystalline penicillin with gentamicin would also be appropriate antibiotic cover following snakebite. 9. Recent studies have reported the beneficial effects of intravenous immunoglobulin (IVlg) in ophitoxaemia. There are suggestions that its administration may improve coagulopathy, though its effect on neurotoxicity is questionable. A pilot study indicates that IVIg with antivenom eliminates the need to repeat antivenom for envenomations associated with coagulopathy.
Irritant Poisons 589 10. A compound extracted from the Indian medicinal plant Hemidesmus indicus R (2hydroxy-4 methoxy benzoic acid has been noted to have potent anti-inflammatory, antipyretic and anti-oxidant properties, particularly against Russell’s viper venom. These experiments suggest that chemical antagonists from herbs hold promise in the management of ophitoxaemia; particularly when used in the presence of antivenom. 11. Injection of tetanus toxoid is necessary. 12. Early surgical debridement is generally beneficial though fasciotomy is usually more harmful than useful. 13. There is no role for steroid therapy in acute snakebite. Although it delays the appearance of necrosis, it does not lessen the severity of outcome. Autopsy Findings Findings in a colubrine snakebite: (i) The puncture marks of fangs are usually 1.2cm (½") deep and are well visible by hand lens with oozing of serum, blisters and necrosis at the site of bite (ii) Blood remains fluid showing features of hemolysis (iii) Froth in mouth and nostrils (iv) Features of asphyxia are prominently seen (v) Microscopically, the nervous tissue will show changes in Nissl’s granules, fragmentation of reticulum of the nerve cells, opacity, fragmentation and swelling of the nuclei. Cells of medulla shows acute granular degeneration. Findings in a viperine snakebite: (i) Puncture marks are usually 2.5cm (1”) deep with swelling, extravasation of blood, inflammation, cellulitis and discolouration in and around it (ii) Blood-tinged serum oozes out of the punctured marks (iii) Blood is fluid with purplish tinge (iv) Evidence of haemorrhages from G.I.T, respiratory and urinary tract is there (v) Petechial haemorrhages in pleura, pericardium and substance of kidney, liver, lungs and brain with congestion of these organs (vi) Haemorrhage in the endocardium of left ventricle, interventricular septum and papillary muscles (vii) Regional lymphadenopathy is there.
Medicolegal Aspects (i) Always occurs accidentally (ii) Suicide is unknown except by Cleopatra (iii) Homicides, rarely allegations of snake being thrown into the enemy’s place but cannot be proved without circ*mstantial evidences (iv) Cattle poisoning does occur by placing snake and banana in an earthen pot and irritating snake by firing it. The cobra bites the banana injecting the venom into it. The fruit is taken out and smeared into a rag that will be injected into rectum of the animal by bamboo stick.
SCORPIONS Scorpions are poisonous insects that have a fleshy segment body with four pair of legs, a pair of claws and a tail. The posterior segment is long and bulbous and contains the venom gland and a hollow sting at the end of the tail in its last joint. The sting communicates with the venom gland by means of a duct. The stings inject venom in the injury produced by it. The adult scorpion are 2-20 cm long and big, black coloured are more dangerous that the small, brown ones. The scorpion’s bites are always accidental as they live in cracks and holes in the houses. Scorpion Venom Scorpion venom is a clear and colourless toxalbumin that is more toxic than the snake venom. The small quantity of venom is injected. The scorpion venom consists of a neurotoxin (acts on the preganglionic and postganglionic nerve terminals and muscle endplates), haemolysins, agglutinins, haemorrhagins, proteinases, phospholipase A, leucocytolysin, coagulins, cholesterin and lecithin. Signs and symptoms: (i) Site of bite is having a red wheal with a hole in the centre and severe burning pain radiates from the site. The area is swollen, red and oedematous (ii) Increased temperature with chills and headache (iii) There is feeling of giddiness and fainting (iv) Excessive sweating and salivation (v) Muscular cramps and convulsions followed by unconsciousness (vi) Paresis and
590 Textbook of Forensic Medicine and Toxicology muscular weakness persist for a week (vii) Death occurs in children from pulmonary oedema and respiratory depression and it is rare in adults. Treatment 1. Application of tourniquet or pressure bandage above the site of bite and incising and washing the bitten area with weak solution of potassium permanganate, borax or ammonia. The tourniquet should be loosened for 1-2 minutes after every 10-15 minutes. 2. Local infiltration of 5% cocaine, or lignocaine solution in and around the bite relieves pain 3. To treat shock, 5% of 500 ml of dextrose saline should be give I.V. along with glucocorticoids i.m. 4. Calcium gluconate 10ml of 10% solution should be given intravenously to combat muscular cramps. 5. To prevent pulmonary oedema, atropine sulphate should be administered.
BEES, WASPS AND ANTS 1. Produce a painful local reaction, which recedes with time. 2. An allergic phenomenon produced by them may kill the patient because of prior sensitization. 3. The number of stings may be so great or the patient is so young as to kill with primary toxicity. Signs and symptoms: (i) Nausea, vomiting (ii) Thoracic oppression (iii) Cardiac irregularities (iv) Pulmonary oedema (v) Nephrosis (vi) Cyanosis, coma, convulsions and death. The fatalities may result a short while after the infliction of stings Fire Ants This insect Solenopsis saevissima richteri causes an immediate and very painful local reaction in the form of vesicles and swelling. The insect inserts its stinger number of times and as a result, number of sensitization occurs to its bite. The systemic reaction can also be produced in sensitized persons that can be febrile and allergic.
INORGANIC IRRITANT POISONS PHOSPHORUS Phosphorus is a non-metallic, hepatotoxic and protoplastic irritant type of poison. It exists in two forms; red phosphorus and white phosphorus. Of the two, red is not poisonous but white phosphorus is a deadly one. White/yellow phosphorus: White phosphorus occurs in the form of white, waxy, translucent and pliably soft sticks. It is insoluble in water, somewhat soluble in alcohol and ether and readily soluble in carbon disulphide. On exposure to air, it slowly oxidizes or ‘phosphorescences’—Phosphorescence is the condition of white phosphorus, when it emits white fumes of phosphorus trioxide, which is luminous in the dark giving strong garlic odour. At 34°C, it ignites in the air emitting greenish-white flame, hence it is to be preserved under water or kerosene oil. It should not be handled even by wet finger as even the body heat can cause ignition. Red phosphorus: Red phosphorus is prepared by heating white phosphorus at 240o-250oC in an atmosphere with nitrogen or carbon dioxide gases. It occurs ordinarily as violet red solid mass that is odourless, tasteless, is insoluble in carbon disulphide, and does not luminescence in the dark (Table 38.5). Uses of Yellow Phosphorus 1. It is used in the preparation of vermin pastes that contain arsenic, fluor, oil, sugar, some colouring agents mixed with 1-4% conc. of yellow phosphorus 2. In manufacture of gunpowder, fireworks, and incendiary ammunitions and for creating smoke screens during warfare. 3. In various chemical and fertilizer industries. Medicolegal Aspects 1. Phosphorus is not commonly used for homicidal purposes due to its characteristic garlicky odour, taste, luminosity in the dark makes for its easy detection. But it acts as a god homicidal poison as phosphorus containing rat poison mixed with strong tea is not easily detectable.
Irritant Poisons 591 Table 38.5: Differences between red and yellow phosphorus Properties
Red phosphorus
Yellow phosphorus
Colour Appearance Taste and odour Luminosity in dark Solubility in carbon disulphide Exposure to air
Violet-red or reddish brown Amorphous, solid mass Tasteless, odourless Non-luminous Soluble Does not phosphorescenses, non fuming Non-toxic Not so
Originally white, turns to yellow on exposure Waxy, translucent and soft pliable sticks Garlicky taste and odour Luminous Insoluble Phosphorescenses
Toxicity Ignition in air
Besides, there is delay in onset of clinical features and post mortem findings simulate that caused by hepatotoxic drugs and diseases. 2. Vermin pastes, rat killers containing phosphorus are commonly used for suicidal purposes. 3. Accidental poisoning can occur in children as they may ingest rat-poison. The poisoning can also occur from fragments of projectiles containing yellow phosphorus, inhaling hydrogen phosphide gas produced in ship holds from cargo and inhaling the gas evolved from ferrosilicon used in steel industry. 4. Arson using phosphorus is done in villages when moist cow-dung and yellow phosphorus are mixed together and thrown over thatched cottage-roof that when dries in sun catches fire from phosphorescent phosphorus Fatal dose: Adults—60-120 mg Children—10-25 mg Fatal period: Upto 24 hours (4-10 hours) Mechanism of Action (i) Locally it acts as an irritant (ii) On absorption, it remains in the blood in elemental form for a day or two, then gets oxidized into hypophosphorus and phosphorus acid when it acts as hepatotoxic, protoplasmic poison disturbing the normal cell metabolism by affecting cellular oxidation (iii) It produces widespread fatty infiltration with degeneration of different organs especially the liver and cells of cerebral cortex (iv) It also causes tissue destruction by interfering with carbohydrate, fat and protein metabolism especially by deposition of fat in the liver at the cost of glycogen (v) Chronic absorption of phosphorus leads to bone formation in the epiphyseal cartilage and in the bone marrow
Highly toxic Possible
and Haversian canal thus impairing blood circulation in bones. This leads to necrosis and sequestration of bones with or without spontaneous fractures. Acute Phosphorus Poisoning Signs and Symptoms The signs and symptoms of acute phosphorus poisoning usually appear within a few minutes and sometimes may be delayed for up to 6 hours. First stage: (i) Garlic like taste in mouth and smell in breath that is luminous in the dark (ii) Sense of warmth with burning pain in mouth and throat radiating down to oesophagus, stomach and finally all over the abdomen (iii) Intense uncontrollable and non-quenchable thirst with frequent gastric eructations and patient drinks lots of water trying to quench his thirst (iv) Copious vomiting occurs that is frequent, profuse and persisting; has garlicky odour, luminous in the dark, bile stained and even blood tinged in later stages (v) Painful throat as a result of repeated retching and vomiting (vi) Diarrhoea though uncommon is in the form of dark, offensive, and phosphorescent motions usually preceded by colicky pain (vii) Abdomen is tender and distended with epigastric discomfort (viii) Hypoglycemia may result (ix) Cardiac and respiratory depression, cold clammy skin, hypothermia occurs (x) Delirium is followed by convulsion, collapse, coma and death occurring within 12-24 hours of ingestion of poison (xi) Patient usually does not die in Ist stage but he enters IInd stage by 36-48 hours when signs and symptoms reduce in intensity and vitals improve
592 Textbook of Forensic Medicine and Toxicology Second stage:This is a stage of apparent improvement of signs and symptoms that may last for 24days. There may be little pain in the abdomen with occasional vomiting and purging, malaise and headache. Third stage: (i) Vomiting and diarrhoea reappear and is more intense and distressing and contains mucous and blood (ii) Abdomen distended with severe abdominal pain (iii) Jaundice sets in and deepens quickly (iv) Liver is enlarged, soft and tender (v) Skin becomes cold, respiration laboured and pulse is feeble (vi) Haemorrhages in the form of epistaxis, haematemesis, haematuria, malena and menorrhagia are commonly seen (vii) Petechial haemorrhages over the mucous membranes (viii) Blood urea is usually raised (ix) Urine is scanty, high coloured, contains blood, ammonia, casts, albumen, free fat globules, excess of lactic acid, bile and some amino acids like leucine, tyrosine and cysteine (x) Headache, restlessness, insomnia may be seen (xi) Tinnitus and vertigo are usually present (xii) Impaired vision, cramps, muscle twitchings and even paralysis, delirium and frequent priapism may also develop (xiii) Features of increasing hepatic and renal insufficiency followed by hypoglycemia, quick weak and irregular pulse, fall of BP, pulmonary oedema, dyspnoea, cyanosis, oliguria, even anuria, subnormal temperature progressing to death (xiv) Yellow phosphorus produces usually second or third degree burns that are slowly healing and are surrounded by blisters on the skin. Treatment 1. Stomach wash using 0.5% potassium permanganate solution that oxidizes phosphorus into harmless phosphoric acid and phosphates itself changing into manganese dioxide. 2. Stomach wash using 0,1% copper sulphate solution or 250mg of copper sulphate in a glass of water may be given by mouth every 5 minutes until free emesis starts. Copper sulphate also acts as an antidote as it is reduced by phosphorus and is precipitated as copper phosphide forming a coating over
3. 4. 5.
6.
7.
8. 9. 10.
11.
12.
the phosphorus particles thus rendering them inert. Hydrogen peroxide 2% solution can also be used as gastric lavage fluid. Activated charcoal also helps in adsorbing the poison. Oils, fats, milk etc. should not be given to the patient as they help in dissolving phosphorus and promotes its absorption. Liquid paraffin retards absorption of phosphorus and hastens its elimination but castor oil should not be used. Bowels should be thoroughly washed using potassium permanganates and purgatives especially magnesium and sodium sulphate. Glucose and alkaline drinks by mouth in plenty to protect liver. High carbohydrate and low protein and fat diet should be given. To combat shock and dehydration plenty of glucose saline (500 ml of 5%) fluids and 10 ml of 10% calcium gluconate should be administered intravenously. Symptomatic treatment such as non-narcotic analgesics for pain, multivitamins especially injections of vitamin K should be given. Locally, skin can be irrigated with 1% copper sulphate solution in water for at least 10 minutes.
Autopsy Findings The post mortem findings will depend on the period of survival: Death within first 24 hours: (i) Slight icteric tinge of the skin (ii) Mucous membranes of pharynx, oesophagus, stomach and intestines shows signs of inflammation, redness, ulceration and corrosion (iii) Stomach is contracted and mucosa is inflamed, softened, yellowish green with garlicky odour that luminesce in dark Death after 24-48 hours: (i) Skin will look jaundiced (ii) Petechial haemorrhages under the skin and over serous and submucous surfaces of the lungs, brain, leptomeninges, uterus and kidney (iii) Garlicky odour from the body (iv) Mucosa of stomach and intestine is yellow or yellowish green
Irritant Poisons 593 with evidence of inflammation, softening, corrosion and haemorrhagic. This is also luminous in the dark (v) Liver is usually enlarged though it may be normal or contracted also. It is lemon yellow with doughy, soft and greasy consistency. A moderate pressure will allow the pressing finger to sink deep down in to the liver substance, which will be easily friable. Small haemorrhagic spots are seen on the glisson’s capsule and in liver substance. Evidence of fatty degeneration, cellular necrosis, fibrosis, cellular infiltration is there. Evidence of accumulation of fat in Kupffer’s cell is the earliest manifestation of necrobiosis the liver undergoes in phosphorus poisoning (Table 38.6) (vi) Heart is soft, flabby and dilated with evidence of fatty degeneration and subendocardial haemorrhages (vii) Kidneys may be filled with cellular debris, fatty casts, albumen etc. and are enlarged, soft, greasy, yellow with petechial haemorrhages and fatty degeneration. Although phosphorus is readily oxidized in air, it may de detected in unoxidised form in dead body several days after death, even when the body is in an advanced state of decomposition. This may be explained by the fact that reducing gases that are formed during decomposition protects phosphorus from oxidation. Phosphorus occurs in combination with food articles, in tissue and body fluids mainly as phosphates. Hence, detection of phosphate has little medicolegal importance; but when detected in elementary form in the body, it is taken to be sufficient to have produced phosphorus poisoning as it does not occur in free form in nature. Chronic Phosphorus Poisoning Chronic phosphorus poisoning usually occurs due to inhalation of fumes of white phosphorus
amongst those employed in manufacture of fire works and some ammunitions where phosphorus is being used, inhalation of phosphorated hydrogen in preparation of acetylene gas from carbide and also from escape of the gas from ferrosilicon results in poisoning. It is also seen in workers in matchbox and sticks factory. Signs and symptoms: The symptoms and signs usually develop after working for weeks, months or even years in these factories: (i) Nausea, vomiting, garlicky smelling eructation’s and purging (ii) Generalized wasting, weakness, lassitude, emaciation and joint pain (iii) Abdominal discomfort and pain (iv) Anaemia, jaundice, shallow complexion (v) Tracheitis and bronchitis (vi) Phossy jaw—It is osteomyelitis and periostitis of jaw due to chronic phosphorus poisoning associated with necrosis of the alveolar part of jawbone along with the sloughing of gums and loosening or falling of teeth. At first, there is history of toothache, swelling of jaw, loosening of teeth, sloughing of gums, necrosis and sequestration of mandible with multiple foul-smelling pus discharging sinuses. Phosphorus mainly attacks the lower jaw through carious or decayed teeth or through interspaced between the missing teeth adjoining the raw surface. Treatment 1. Prophylactic measures such as cleanliness and ventilation of factories; oral hygiene of workers regularly that is washing mouths with soda bicarb solution and extraction or filling up of carious tooth should be followed. 2. If necrosis of mandible occurs surgical intervention is undertaken.
Table 38.6: Difference in liver in yellow phosphorus poisoning and yellow atrophy of liver Morphology of liver Yellow phosphorus poisoning
Yellow atrophy of liver
Size Consistency Colour Greasiness Microscopic features of liver substance
Contracted with wrinkling of glisson’s capsule Leathery Dirty yellow Soft & greasy to touch Extensive cellular necrosis
Usually enlarged, normal or even contracted Doughy and soft Uniformly yellow Greasy to touch & fingers dips easily Extensive fatty infiltration with degeneration, cellular necrosis and haemorrhages
594 Textbook of Forensic Medicine and Toxicology IODINE Iodine occurs in the form of bluish black, soft, scaly crystals that have a metallic sheen and unpleasant taste. It is freely soluble in water, the solubility increasing in presence of iodide. Idiosyncrasy is more common than bromide. It is very commonly used household antiseptic and potassium iodide is largely used as medicine. Mechanism of Action It acts as corrosive and coagulates cellular protein causing necrosis. The iodine vapours are irritant to respiratory passages. Iodine is converted to iodide in the body. The normal iodide content of the blood is 2-5 mg/100 ml. The prognosis is good if the patient survives for 48 hours after ingestion of the poison. Fatal dose→2-4 gm (in solid form) and Two drachms of tincture iodine. Signs and symptoms: (i) Burning pain in mouth radiates to throat, oesophagus, stomach and abdomen (ii) Increased thirst, nausea, vomiting, salivation and purging (iii) The lips and angles of mouth are stained brown; the vomitus and faeces are stained dark brown or blue mixed with blood smelling of iodine (iv) Urine is scanty or suppressed and reddish brown containing albumen; painful micturition (v) Headache, muscle cramps, giddiness (vi) Cold clammy skin and fall of BP (vii) Respiratory depression, quick weak pulse (viii) Delirium and collapse (ix) Consciousness is retained till the end (x) Iodides may cause enlargement of salivary glands and lymph nodes (xi) Application of iodine to skin causes weeping eruptions, with raised temperature in sensitive individuals (xii) Injection of compound of iodine may cause sudden fatal collapse due to idiosyncrasy (xiii) Inhalation of iodine vapours results in glottic oedema and death from asphyxia. Chronic Iodine Poisoning (Iodism) It results from chronic use of potassium iodide in large doses as medicine. The clinical features are in the form of frontal headache, running nose, sneezing, watering from eyes, conjunctivitis, bronchitis, parotitis, excessive salivation, nausea, vomi-
ting and diarrhoea associated with oedema of face and eyelids that clears up once the medication is discontinued. Treatment (i) Gastric lavage using 5% sodium thiosulphate solution or water containing soluble starch and albumen (ii) Emetics should be given (iii) Demulcents as barley water, egg albumen, milk, alkaline drinks and castor oils should be given (iv) Shock and dehydration to be treated with 5% dextrose saline drip i.v with mephentin and other analeptics to maintain BP (v) Glucocorticoids and antihistaminics in repeated doses help in allaying oedema. Tracheostomy to be performed to relieve glottic oedema (vi) 5% Sodium thiosulphate 100-150mL orally helps to reduce free iodine to non-toxic iodides (vii) fluid and electrolyte balance should be maintained (viii) in chronic poisoning discontinue the drug and give large doses of Sodium bicarbonate or sodium chloride with fluids to hasten recovery. Autopsy Findings (i) The face and eyes are swollen and there is evidence of glottic oedema (ii) Mucosa of gastrointestinal tract is stained yellow or brown, is congested, inflamed and excoriated at places. Also the stomach contents are turned blue due to inter-reaction of iodine with starchy food (iii) Lungs are congested and oedematous (iv) Heart and liver shows fatty change (v) Kidneys may show glomerular and tubular necrosis (vi) Brain is usually congested and oedematous Medicolegal Aspects 1. Accidental poisoning is common in children from accidental drinking of tincture iodine, betadaine etc.or when an alcoholic solution when excessively used for external application. 2. Suicidal and homicidal poisoning is rare. CHLORINE Chlorine is a greenish yellow gas having an unpleasant irritating odour even when diluted. It is largely used in industry as bleaching agent and disinfectant
Irritant Poisons 595 Fatal dose→Exposure to air containing 1/1000 chlorine for 5 minutes is fatal by causing acute pulmonary oedema. Fatal period→Inhalation of pure chlorine gas results in death within 12-24 hours. Signs and Symptoms (i) Inhalation causes intense irritation of respiratory passages, throat and eyes causing dry harsh painful violent cough with yellowish expectoration, intense watering eyes and coryza (ii) Headache, nausea and vomiting, abdominal pain occur (iii) Tachypnoea, extreme dyspnoea, palpitation and pyrexia results (iv) In extreme cases, glottic oedema, asphyxia, intense cyanosis, tachycardia occurs (v) Unconsciousness soon supervene and death results from acute respiratory or cardiac failure (vi) Chronic exposure to chlorine vapours shows features of anemia, cachexia, dyspepsia, chronic bronchitis and emphysema. Treatment 1. Patient to be removed to fresh air immediately 2. Oxygen inhalation, artificial respiration and suction of frothy fluid from air passages 3. 5% dextrose saline drip with sodium bicarbonate to combat dehydration and shock 4. Treatment of pulmonary oedema, acidosis etc. should be ensued 5. As a prophylactic measure the respirator masks soaked in sodium bicarbonate solution and sodium hyposulphite and goggles for eyes should be used Autopsy Findings (i) The respiratory tract mucosa shows intense congestion (ii) Lungs are congested, oedematous exuding frothy, tenacious blood-stained fluid and showing areas of patchy haemorrhages and collapse (iii) Stomach and intestines are congested (iv) Heart is also enlarged (v) Odour of chlorine from the ventricles of brain that is congested (vi) All organs are congested. Medicolegal Aspects Poisoning is usually accidental by chlorine and its compounds especially bleaching powder in
industry. Use of chlorine gas in Ist World war caused numerous causalities BROMINE Bromine is a dark reddish brown liquid that volatalises at ordinary temperatures giving out irritating fumes of unpleasant odour. Compounds of bromine displace chlorides from the plasma and cells; thereby will cause depression of central nervous system hence are not commonly used in medicine as sedatives. They are also used as anticonvulsant agents. Children may get more readily affected from bromide poisoning than adults. The poison gets rapidly eliminated in the urine, saliva, sweat and milk. Fatal dose→Uncertain; 20-30gms of sodium or potassium bromide can cause alarming symptoms causes alarming symptoms. Fatal period→One ounce of undiluted bromine causes death in about 7 days. Signs and Symptoms (i) Intense burning sensation in mouth, throat, oesophagus and stomach (ii) Intense thirst and excessive salivation (iii) Nausea and vomiting, gaseous eructations, dysphagia and diarrhoea (iv) Inhalation of Bromine fumes causes acute bronchial catarrh, irritating cough, running nose and watering from eyes and intense chest constriction (v) Oedema of glottis, pulmonary oedema develops with death from suffocation Chronic Poisoning (Bromism) Long continued use of bromides in large doses as medicines result in bromism, especially when the blood level reaches >50 mg%. persons with low sodium level are more prone to bromism apart from those who are sensitive to these preparations Signs and Symptoms (i) Bromide acne vulgaris’ with popular or pustular skin eruptions on the face, shoulders and upper part of chest (ii) Headache, coryza, watering eyes (iii) Swelling of face and eyelids (iv) Indigestion with loss of appetite, constipation, furred tongue, foul breath (v) Tremors, muscular weakness,
596 Textbook of Forensic Medicine and Toxicology staggering gait, loss of memory, slurred speech (vi) Features of bromide psychosis such as confusion of ideas, delirium, delusions or hallucinations, loss of sexual ability with mental depression and drowsiness (vii) Stupor and coma may result Treatment (i) Patient to be removed to fresh air (ii) Stomach wash with plain water containing starch or albumen (iii) Emesis to be induced (iv) Artificial respiration and oxygen inhalation (v) Tracheostomy to relieve oedema of glottis (vi) Sodium chloride 12gm flavoured with fruit juice is given every 6 hours orally until bromide level falls below 50mg% (vii) 5% Dextrose saline drip to be given i.v. that helps in excretion of bromides (viii) Diuretics like frusemide or chlorthiazide help in excretion (ix) Analeptics to treat shock and collapse. Autopsy Findings (i) Mucous membrane and skin bears dark brown parchment like stains (ii) Gastrointestinal tract is congested with inflammation (iii) There are features of pneumonia and pulmonary oedema (iv) All organs are congested. Medicolegal Aspects 1. Accidental poisoning occur in those sensitive to bromides preparations. It was used in Ist World War when bromide vapours were used as asphyxiating and lacrymating agents. 2. Used commonly for homicidal purposes.
MECHANICAL IRRITANT POISONS The irritant mechanical poisons act mechanically to cause local irritation of the gastro-intestinal tract when ingested. These are powdered glass, pins, needles, nails, diamond powder, and chopped human and animal hairs. POWDERED GLASS The powdered glass and diamond dust does not act as poison as they are not absorbed in the blood but they do act mechanically causing irritation of the gastrointestinal tract. Their fatal periods as well as fatal doses are uncertain. The faint shadow of glass particles on X ray due to presence of radio opaque silica helps in diagnosis Signs and Symptoms (i) Burning pain in mouth, throat, stomach and intestines (ii) Nausea, vomiting and constipation (iii) Rarely diarrhoea with tenesmus and bloody stools occur (iv) Death may result from shock following perforation of stomach or intestines by sharp glass fragments. Treatment (i) Bulky foods such as rice, porridge should be given (ii) Purgatives and cathartics should be given (iii) Big pieces of banana when swallowed as a whole envelops the glass fragments within itself (iv) Symptomatic treatment.
40
Part 2—Forensic Toxicology
Neurotic Poisons DELIRIANT POISONS The Deliriant poisons are Dhatura, Cannabis and Belladonna. DATURA FASTUOSA The flowers and fruits are supposed to have been blessed by Lord Shiva and are known as Shivashekhara. It exists in two varieties: (i) Datura Alba—‘Safed’ or white flowers (ii) Datura Niger— Kala datun with black or deep purple flowers. Both the varieties grow in waste places all over India. The fruits are spherical with sharp spines— Thorn apple (Fig. 38) and contains yellowish brown seeds. Dhatura stramonium grows at high altitudes in the Himalayas. Two other varieties that are commonly met with are: (i) Dhatura atrox and (ii) Dhatura metal. All parts of the plant are poisonous but the fruit and seeds are most poisonous.
Figure 39.1: Dhatura plant with its fruit
Active Principles The active principles are: (i) Hyoscine (ii) Hyoscyamine (iii) Traces of atropine. It has been suggested that atropine does not exist as such but is a racemic form of Hyoscyamine that is converted to atropine during the process of extraction. The
seeds of Dhatura seeds may be mistaken for capsicum seeds but the differences do exist. Signs and Symptoms (i) Contact with the leaves and flowers cause dermatitis in sensitive patients (ii) When the seeds are ingested, the symptoms appear within half an hour (iii) At times vomiting occurs immediately after taking the seeds when crushed due to gastric irritation (iv) Bitter taste and dryness of mouth and throat (v) Burning pain in the stomach (vi) Dysphagia and difficulty in talking (vii) Headache followed by giddiness (viii) Staggering gait and incoordination of muscles (ix) Flushing of face (x) Dry and hot skin with rise in body temperature to 107-108 oF (xi) Pupils are dilated; there is photophobia (xii) There is loss of accommodation for near vision (xiii) The conjunctiva is red and injected (xiv) There is inability to pass urine (xv) Drowsiness (xvi) At times scarlentiniform rashes or exfoliation of skin are seen over most of the body (xvii) Pulse is full and bounding, later on it is weak, irregular and intermittent (xviii) Respiration is increased (xix) Muscle tone and deep reflexes are increased; muscular spasm is present at times (xx) Delirium is restless and purposeless. He is silent or mutters indistinct or inaudible words, but usually he is noisy, tries to run up away from his bed, picks bed clothes, tries to pull imaginary threads from the tips of his fingers, threads imaginary needles— pin rolling movements (xxi) Dreadful hallucination of sight and hearing is present (xxii) Delusions are present. The signs and symptoms of acute Dhatura poisoning can be summarized by 10 D’s: (i)
598 Textbook of Forensic Medicine and Toxicology Dysphagia (ii) Delusions (iii) Dermatitis (iv) Delirium (v) Drowsiness (vi) Dry skin, mucous membrane (vii) Dilated pupil (viii) Dreadful hallucinations (ix) Dysuria (x) Dysarthria. The signs and symptoms can also be remembered as: (i) Hot as a hare—increased temperature (ii) Blind as a bat—disturbed vision (iii) Dry as a bone—intense thirst (iv) Mad as a hen—mental symptoms (Delirium, hallucination, delusion, restlessness) (v) Red as a beet—flushing of the face As intoxication advances, this excitement phase passes off in 1-2 hours, deep coma or sleep ensues that may end in death from respiratory paralysis. Patient may stay ill for 2-3 days but definite improvement occurs in 24 hours. The cases that improve develop secondary delirium as stupor passes away. They remember nothing about the illness and are surprised to find themselves in the hospital. Fatal dose→4 fruits; 100 seeds or 0.5-1 gm Fatal period→24hours. Treatment (i) Emetics can be used (ii) Stomach wash using 5% tannic acid or a weak solution of potassium permanganate (iii) Enema should be given using sodium sulphate as purgative (iv) Prostigmine 0.51mg subcutaneously as single dose is more effective and less toxic (v) Physostigmine 0.5mg i.v or i.m 1-2 hourly to relieve both cerebral as well as peripheral manifestations, it crosses the blood brain barrier (vi) Pilocarpine nitrate 5 mg is given subcutaneously as a single dose and repeated after two hours. It has no central action (vii) Morphine is contraindicated, though it is physiological antidote (viii) Short acting Barbiturates can be given for convulsions (ix) Sponging to relieve high temp. (x) Artificial respiration and oxygen inhalation. Autopsy Findings (i) The postmortem findings are not characteristic but signs of asphyxia are there (ii) Seeds or their fragments may be found in the stomach or intestine (iii) Stomach may show slight inflammation (iv) Lungs are congested and oedematous (v) All the organs are congested.
Medicolegal Aspects 1. Dhatura is used mostly for criminal purposes. It is used to stupefy travelers for the purpose of robbery, rape and theft by: (i) Seeds that are mixed with rice, dal, coffee and sweets (ii) Seeds and leaves are mixed with tobacco or ganja and smoked in Chillum (pipe) (iii) A decoction (boiling to extract the essence) of seeds is added to liquor to enhance its intoxicating property. 2. Accidental poisoning can result: (i) When children and adults eat raw Dhatura fruits (ii) The seeds may be mistaken for capsicum seeds. (iii) Seeds have an aphrodisiac property. (iv) Juice of Dhatura leaves is used to treat rheumatism and applied for pain and inflammation. (v) Vaids and Hakims use Dhatura as medicine. (vi) Medicated ghee is prepared with ghee for local application. 3. Active principle is excreted unchanged in urine immediately after administration for 10-12hours. Urine should be preserved for analysis. 4. Dhatura seeds resist putrefaction for a long time but mydriatic principle contained in them is destroyed by putrefaction. Can be chemically detected even after a long time. 5. Dhatura is sometimes used for homicidal purposes. In 1921, the wife gave Dhatura seeds to her husband in the food. 6. Is used as an abortifacient, in a case a man administered Dhatura powder to a woman to produce abortion but she died 3 hours later. 7. Medicinal use of Dhatura: (i) Dried leaves mixed with Cannabis in the form of Cigarettes are used for the treatment of Asthma; the smoke is antispasmodic (ii) Tinctures have been used for application on the wounds— belladonna tinctures (iii) Dhatura leaves are used to treat some types of fever. Differential Diagnosis of Dhatura Poisoning (i) Poisoning by Hashish (ii) Opium poisoning; differentiated by pinpoint pupil and slow respiration (iii) Cerebral haemorrhage is differentiated by the presence of hypertension and CSF is diagnostic.
Neurotic Poisons 599 CANNABIS INDICA OR SATIVA
Effects Produced by the Small Doses
The plant Cannabis indica or sativa grows all over India but its cultivation is restricted due to the monopoly of the state government. Female plant is tall about 16-18 feet and has more darker and luxuriant leaf foliage than male plant (Fig. 39.2). It yields sticky amorphous resin, cannabinone, which consists of cannabinols (C12H26O2), a colourless oily liquid, cannabidiol, cannabinolic acid and Tetrahydrocannabinol.
(i) Sense of well being (Euphoria) (ii) Loss of inhibitions (iii) Tendency to talk and laugh (iv) Impairment of coordination and balance (v) Loss of concentration (vi) Increased appetite (vii) Increased pulse and heart rate (viii) Reddened eyes (ix) Then the person passes to calm state of mind and sleepiness that lasts for 2-3hours after smoking (x) There can be hangover, drowsiness and poor coordination for several hours. Effects produced by Large Doses
Figure 39.2: Cannabis sativa plant
Medical Applications of the Drug (i) THC appears to control nausea, vomiting, and lack of appetite in cancer patients receiving chemotherapy when other drugs such as antiemetics fail (ii) Used as antidepressants for cancer patients (iii) Antidepressants for cancer patients (iv) Marijuana dilates bronchioles but it is usually not given in asthma (v) THC in small doses acts as anticonvulsant; in large doses, it causes convulsions (vi) Workers have found that the topical application on the skin and mucous membrane has antibiotic activity (vii) It dilates the vessels of iris that leads to increased intraocular pressure and glaucoma. Effects of Cannabis The effects of cannabis depends upon: (i) Amount of Cannabis (ii) Route of intake, whether smoked or eaten (iii) Body size, weight and health of the person (iv) Tolerance and dependence (v) Individual’s mood (vi) Circ*mstances under which it is taken whether to reduce stress or with others in a social setting.
(i)Confusion (ii) Restlessness (iii)Excitement (iv) Hallucination (v) Anxiety or panic. Sometimes inexperienced Cannabis user can hallucinate in small doses. Cannabis also affects and impairs short-term memory, logical thinking, motor skills and ability to perform driving. Tetrahydrocannabinol (THC) Tetrahydrocannabinol is the active principle of Cannabis indica (Marijuana). For time immemorial it has been the most popular recreational and ritualistic intoxicant All parts of the male and female plant contain active principles. Tetrahydrocannabinol (THC) is absorbed in to the blood stream through the walls of the lungs, when smoked and through the walls of stomach or intestine when ingested. The blood stream carries THC in to the brain that produces the ‘high’ effects of the drug. It exerts quicker action through inhalation. The Tetra hydrocannabinols, are labile compounds that may change when exposed to U-V light or acid. The typical psychological effects are due to them. The following are the forms in which it is used: Bhang (Siddhi, Patti or Sabji) is formed of the dried leaves and flowering or fruiting shoots. It is used as an infusion in the form of beverage. It is prepared by rubbing on a stone and black pepper, dried leaves and sugar is added to form pill or bolus. The water is added and it is drunk after it is strained through the muslin cloth. People of Northern India consume this drink at festivals like Holi especially at some of the places like Varanasi.
600 Textbook of Forensic Medicine and Toxicology It is the mildest form containing about 15% of the active principle. Bhang is usually intoxicated to produce cheerful mood for dancing and singing. It acts as an appetizer so the individual consumes more food and he also seeks sexual enjoyment. The intoxication lasts for 3 days resulting in sleep. Fresh bhang is highly intoxicating and narcotic. Bhang that is kept for 2-3years is mildly intoxicating and pleasure giving. Majun: It is sweet meat of confection prepared from bhang after treating with sugar flow, milk and butter. It has an agreeable odour and sweet taste and sold in the market in small lozenge shaped pieces. It increases appetite and sexual desire. The person feels happy and quite contented as if he belongs to Raja’s family and he has all what he wants. Sometimes Dhatura is mixed with Majun. Ganja: It is prepared from the flowering tops of female plant. Has rusty green colour and characteristic odour and its active principle is 15-25%. About 20-30 grains are rubbed with little water on palm till it becomes sticky and then mixed with tobacco and smoked in a pipe (chillum). The person on smoking feels heavy and lazy. Also conjunctiva gets suffused and tachycardia and hypotension is produced. The person indulges in pleasant reveries though he is able to discharge ordinary duties. Sadhus, faqirs and poor labourers, cut leaves and flowering tops of American hemp plant Cannabis Americana or Marijuana and rolled them in to cigarettes with their hands and then smoke them. These cigarettes are called ‘reefers’ or ‘pot’. A good quality cigarette contains 500 mg of marihuana that is effective after 15 minutes of smoking and produces benign ergosyntonic experience. Charas or Hashish: Is of dark green or brown colour and commonly known as Hashish. It is a concentrated resin exuding from leaves and stem of the plant that grows in hilly areas, 6-8 thousand feet above the sea level. It has 25-40% active principle and is smoked with tobacco in a pipe or hookah. It is most potent of all the forms. Hashish oil: It is an extract of cannabis and is thick, oily liquid spread on a tip of paper of cigarette. It is smoked and is strongest of all the prepara-
tions of Cannabis. Unlike alcohol it is always taken in a company. It produces the effects such as fleeting, brief and pass rapidly. Signs and Symptoms They appear soon after smoking ganja or Charas and after half an hour after swallowing bhang. Hen taken in small doses, effects are slight and then patient becomes pleased with himself. He becomes talkative, cheerful though rarely violent or aggressive. There are two stages: 1. Stage of inebriation: Person becomes dreamy or semiconscious. There are realistic visions of erotic nature. He sees nude beautiful females dancing before him, playing music, and singing amorphous songs. The higher faculties are depressed, he may laugh, sing or make purposeless movements. Judgment in relation to time and space is lost and sensation of pain is lessened. It hampers the psyche motor activity (physical coordination, quick reaction time and visual perception) headed for driving and operating machinery. Interferes with immediate memory, arithmetic problem solving and thinking in general. Frightful hallucinations are there at 300-480ìg/kg oral and 200-250ìg/kg of THC. He is delirious, has homicidal tendency or a fear of death. Symptoms vary with the dose and personality of the user. 2. Stage of narcosis: 0.5-1mg/kg as single oral dose produces giddiness and ataxia. Speech may be confused and rambling. Tingling and numbness of skin occurs and in severe cases general anaesthesia and muscular weakness develops. The victim becomes drowsy and passes in to deep sleep and wakes with lassitude and impaired mental function. Recovery occurs in about 6 hours. In extreme rare cases death is due to respiratory failure. Fatal dose→ 1000-2000mg or 30 mg/kg Charas 2 gm Ganja 8 gm Bhang 10 gm/kg Fatal period→Cannabis is very rarely fatal and the period of fatality varies from 12 hrs to several days.
Neurotic Poisons 601 Treatment (i) Stomach wash to be done (ii) Purgatives should be administered (iii) Oxygen inhalation and artificial respiration to be given (iv) Symptomatic treatment.
4.
Autopsy Findings (i) The postmortem findings are not characteristic (ii) Only signs of asphyxia are present (iii) Its necessary to preserve urine (iv) Microscopic examination of the ingested material: The suspected material is placed on a slide and one drop of oil potassium hydroxide is added, covered with cover slip and examined under the microscope,. Morphological features of hair of the THC derivatives should be studied distinctly; ganja hair are smooth and Charas hair are wavy or warty.
5.
6.
Chronic Poisoning Regular users develop features of intoxication and may experience some physical, mental or social problems. There is an: (i) Increased risk of bronchitis, lung cancer and respiratory diseases associated with smoking (ii) There is a change of motivation: The person feels that they begin to loose energy after the drink. Their performance at the place of work suffers. When cannabis is stopped, the symptoms disappear (iii) Decreased concentration, memory and learning abilities— Toxic psychosis (iv) Interference with sexual and hormone production—Impotency, gynecomastia, low sperm count and irregular menstrual cycle (v) THC is soluble in fatty tissue, can be deposited in fatty tissue including brain then gradually can be realized in to blood stream (vi) Insanity, hallucination, delusion of persecution. Medicolegal Aspects 1. Poisoning by Bhang is mostly accidental. Majun and Charas are used as stupefying poisons. Cannabis can be used for homicidal purposes; there are cases where it has been used to kill the other person. 2. To steady nerves before committing crime. 3. Run amok: After its intake, the person first kills a person or persons against whom they have entertained fancied or real enmity then
7.
kills anybody who comes in their way until homicidal tendency lasts. Then usually he may commit suicide or surrender before the police. Cannabis and other drugs: Marijuana and alcohol when used together are more effective and dangerous than when it is used alone. There is no evidence as to the use of Cannabis automatically leading to the use of other drugs. Cannabis and pregnancy: There is not much information about the effect of THC in an unborn child but experiments on animals do show some abnormal developments and behaviour in the offspring. Cannabis and the Law: Cannabis is a banned drug and the punishment for cultivation of plant and ganja illegally is imprisonment of 5 years and fine of Rs 50,000. For other products the punishment can be vary from 10-20 years with fine of 1-2 lakhs. The small quantity for personal use of Hashish and Charas is 5gms and for Ganja it is 500 gms. Exceeding this quantity will be liable to punishment of six months and fine or both. Cannabis and driving: While driving intake of Cannabis affects motor and coordination skills along with the vision, perception of time and space. There are increased chances of vehicular accidents.
COCAINE Cocaine is also commonly known by the names of co*ke, Snow, White lady and Cadillac etc. It is an alkaloid derived from the leaves of the tropical shrub coca-tree, (Erythroxylon coca and E novogranatense) These trees grow well in Central and South America, Mexico, Indonesia East Indies and India. The leaves are traditionally chewed in many countries such as South America to allay fatigue. Purified cocaine first became commercially available in 1884. Cocaine acts as a good surface anaesthetic and it was introduced as first local anaesthetic for use as ocular anaesthetic. Cocaine along with heroin and its associated drugs forms the core of the hard-drug problem from which fatalities may result. In areas where cocaine use is common, a significant proportion of fetal deaths are associated with this narcotic. In a
602 Textbook of Forensic Medicine and Toxicology series reported in New York by Morild and Stajic, toxicology revealed cocaine in 64 out of 103 fetal deaths. The study also suggested that cocaine causes an increased incidence of fetal deaths, abortion and abruptio placentae. Many a times, the smugglers have died due to bursting of packets of cocaine in their gastrointestinal tract resulting in a massive overdosage. The leaves of coca plant (Erythroxylon coca) contain about 0.5-1% cocaine. Cocaine, methylbenzoyl ecgonine may be synthetically prepared. Routes of Administration (i) Orally, it is rapidly destroyed (ii) Injection (iii) Snuffing via nasal and oral mucous membranes when it is rapidly absorbed and causes cerebral stimulation followed by depression (iv) Inhalation of freebase cocaine produces almost immediate absorption and a rapid onset of effects. Various forms Used for Abuse 1. Cocaine hydrochloride: It is water soluble and is typically used for injection or snorting but in not well suited for smoking as it is largely destroyed by heat of burning. The hydrochloride salt can be converted to the freebase form by treatment with alkali and extraction with organic solvents. 2. Cocaine sulfate (coca paste, pasta basica, basuca) is a crude intermediate product, usually contaminated with solvents is used for smoking. 3. Crack: Crude form of freebase cocaine may be obtained by heating the cocaine with sodium bicarbonate to yield ‘crack’, a hard white mass that is freebase plus impurities but without hydrochloride moiety. When smoked, this material gives off a cracking sound, hence the name. 4. Speedball: Sometimes cocaine abusers simultaneously inject intravenously a mixture of an opiate, such as heroin called speedball. This mixture is especially euphorigenic. . Mode of Action Cocaine acts as a CNS stimulant and local anaesthetic with potent vasoconstrictor properties.
It stimulates the vagal centre, vasomotor centre, vomiting centre and temperature regulating centre. It blocks uptake of noradrenaline and adrenaline in to adrenergic nerve endings producing sympathomimetic effects. The reinforcing effects of cocaine are related to effects on dopaminergic neurons in the mesolimbic system. Metabolism The half life of a single dose of cocaine in the blood is only about 30-90 minutes. It is hydrolyzed by butyrylcolinestrase (plasma pseudocholinesterase) and the liver esterase into inactive metabolites, mostly benzoylecgonine and ecgonine methylester. With repeated high dosages, cocaine or its metabolites may accumulate in the body compartments such as fat and central nervous system from where it is then slowly released. Consequently, using sensitive techniques, cocaine may be detectable in the urine of heavy users for a couple of weeks. Metabolites can also be detected in blood, saliva, sweat and hair. Blood and saliva provide a better index of current concentrations, whereas urine provides a longer window of opportunity for detecting use over the previous few days. Use in Conjunction with Other Drugs Drugs such as cannabis, ethanol, sedatives and hypnotics are frequently taken with cocaine to reduce its unpleasant effects. Use with alcohol: Alcohol is most commonly used along with cocaine as it modulates both the ‘cocaine high’ and ‘dysphoria’ associated with abrupt disappearance of cocaine’s effects. The concurrent use of cocaine and alcohol may result in the accumulation of a distinct metabolite, cocaethylene. Cocaethylene; Cocaethylene is an active metabolite and produces changes in the cardiovascular functions as that produced by cocaine alone. It produces long lasting effects than cocaine itself and also accounts for the enhancement of subjective effects as well as toxic symptoms when the two are used simultaneously.
Neurotic Poisons 603 Fatal Dose
Chronic Intoxication
As little as 20-50 mg when applied to nasal mucosa has caused deaths but even a gram when taken orally does not result in death. Chronic users of cocaine develop tolerance and habituation that is why it is difficult to estimate dangerous dose levels. Intravenous doses are of 100 mg and a lethal dose is ten times this dose, though there are chances that far larger doses can be tolerated by habitual users. Absorption through the nasal mucosa is less effective and larger doses are to be used to obtain the same effect as that produced by the intravenous route.
It is also known as Cocainism/cocainophagia/ cocainomania. Cocaine is usually abused by upper classes of society to enhance self-image or improve professional performance. There is a tendency for compulsive use of the drug though classical physical dependence is uncommon. Psychic dependence is common with chronic use of the drug and the euphoria following injection is short-lived, perhaps only for 15-20 minutes. Immediately upon intake there is: 1. Euphoria (rush) followed about an hour or so later by rebound depression (crash). To avoid unpleasant effects of rebound depression, the person feels compelled to take the drug again 2. It can also induce a toxic delirium and a more persistent toxic psychotic disorder characterized by: (i) Suspiciousness (ii) Paranoia (iii) Visual and tactile hallucinations such as hallucinations of bugs (cocaine bugs) and worms crawling under the skin (formication/ magnan’s symptoms) (iv) Loss of insight. 3. Chronic intake of cocaine in males causes impotence and gynaecomastia and in females menstrual disorders including amenorrhoea, galactorrhoea and infertility. 4. In pregnant woman with cocaine abuse there is incidence of abortion, abruption placentae and cerebrovascular diseases in mother. In the foetus also incidence of congenital malformations. The smoking of ‘crack’ results in production of ‘crack babies’. 5. Rarely, ulceration and perforation of the nasal septum occurs in chronic ‘snorters’.
Acute Intoxication Cocaine users develop the signs and symptoms of intoxication during the course of single binge and a hyperadrenergic state is produced. Stage of euphoria: This stage is accompanied with (i) Increased suspiciousness and hypervigilance (ii) Anxiety, hyperactivity and talkativeness (iii) Grandiosity and excitement. Signs and symptoms resulting from central stimulation: (i) Increased sense of well-being with increased power of endurance (ii) Tachycardia and ventricular arrhythmias (iii) Changes in blood pressure (iv) Pupillary dilatation (v) Perspiration and chills (vi) Hallucinations especially tactile (vii) Judgment is impaired but insight into drug induced nature of the hallucination is usually retained (viii) Dyspnea. Stage of depression: (i) Loss of reflexes (ii) Paralysis of muscles (iii) Coma and tonic-clonic seizures (iv) Circulatory and respiratory failure (v) Sudden death may follow i.v injection, smoking and snorting due to cardiac arrhythmias and cardiopulmonary arrest (vi) Complications such as pulmonary oedema after intravenous injection of freebase cocaine and pneumomediastinum and pneumothorax may occur after sniffing. Causes of death: (i) Cocaine overdose or hypersensitivity (ii) Sudden cardiac arrest in first time users.
Treatment (i) To control seizures, intravenous diazepam 0.5mg/kg may be given (ii) Propranolol 0.5-1 mg I.V. for ventricular arrhythmias (iii) To treat psychosis, haloperidol should be given (iv) Treatment of chronic cocaine abuse requires combined efforts of primary care physicians, psychiatrists and psycho-social workers. Autopsy Findings 1. There are no specific autopsy features.
604 Textbook of Forensic Medicine and Toxicology 2. Findings of hypoxia are evident. 3. Oral ingestion results in findings of gastric ischemia. 4. The diluents such as quinine, mannitol and other bitter flavouring agents used to ‘cut’ the drug for illegal sale may be found at injection sites, the regional lymph nodes, in the lungs and in other organs. 5. Particles of cocaine can be seen in the form of microemboli. 6. Adulterants used with cocaine are same as that in heroin such as talc, starch, quinine, lactose and dextrose. Quinine was used as diluent to treat falciparum as malaria transmission was quite common among amongst needle and syringe sharers. 7. Formation of foreign body granulomas in the lungs when cocaine mixed with talc or starch is used intravenously. This is due to filtering out of the undissolved components in the pulmonary capillary bed. 8. Evidence of cerebral haemorrhage is found at autopsy. These haemorrhages are the result of hypertension when blood pressure rises to over 300 mm Hg. 9. Complication of the use of septic methods of injections: (i) infections HIV and Hepatitis (ii) endocarditis affecting the right heart valves (iii) phlebitis and distant embolic abscesses. 10. Nasal swabs, one from each nostril should be taken and sent for analysis along with an unused cotton wool swab as control. 11. Samples to be preserved: (i) swab from each
nostril using a plain cotton swab along with another swab used as control (ii) Routine viscera and blood sample for cocaine levels (iii) Sample of urine as cocaine metabolites can be detected for varying lengths of time in urine depending on the dose of cocaine and sensitivity of the assay. The metabolite is generally detectable in the urine for 24-72 hours after brief periods of use. (iv) Injection prick site along with control sites. 12. According to Baselt, blood levels in fatal cases range from 1-21 mg/L with a mean of 5.2mg/L. Medicolegal Aspects 1. Accidental cases occur from the addiction, hypodermic, urethral, vagin*l or rectal injections 2. The drug is locally applied on penis as it is believed to be an aphrodisiac. Prostitutes sometimes inject cocaine solution into vagin* to produce local constriction. Cocaine is also instilled in the urethra 3. Chronic users may develop metal derangements who may get involved in crimes, of which there are three categories: (i) Psychopharmacological effects (ii) Economic compulsion (violent crimes committed to obtain money for drugs) (iii) Systemic violence (associated with business methods and lifestyle of drug dealers). 4. Cocaine induces states of paranoid and aggressive behaviour. 5. Protracted cocaine abuse may cause paranoid ideation and visual and auditory hallucinations, a state resembling alcoholic hallucinations.
41
Part 2—Forensic Toxicology
CNS Depressants The term ‘alcohol’ always means ethyl alcohol. Alcohols are organic substances bearing ‘OH’ groups. Only human beings in the form of various alcoholic drinks consume ethyl alcohol. Methyl alcohol is not fit for human consumption and is found as a impurity in a number of cheap alcoholic drinks. The chemical formula for ethyl alcohol (ethanol) isC2H5OH. Its specific gravity is 0.79 that is 1 ml of alcohol weighs 0.79 gm. Type of alcohol
Percentage of alcohol
Absolute alcohol Rectified spirit Denatured alcohol or industrial spirit
99.95% 90% 95% alcohol + 5% wood naphtha.
Proof spirit is one that at 10.5°C weighs exactly 12/13 part of an equal measure of distilled water. The weaker spirits are known as ‘Under proof’ and stronger spirits are called ‘Over proof’. Alcoholic drinks contain alcohol with water and congeners (organic acids and esters). Wine and brandy have methyl alcohol as congeners. The percentage of alcohol in various drinks is given below: Products of alcohol
Alcohol by volume
Rum Whisky, Gin, Brandy Port, Sherry Wine Beers Arrack (Liquor distilled from palm rice, sugar or jaggery)
50-60% 40-45% 16-20% 10-15% 4-8% 40-50%
Absorption Alcohol is absorbed 20% through the empty stomach and 80% through the small intestine to
the blood. From the blood, the alcohol goes to liver where it is damaged by a specific enzyme at a constant rate. Blood alcohol reaches the lungs through the venous circulation and through the arterial side of the heart in to all the organs and tissues of the body mainly the brain. In brain, it interferes with the normal brain functions such as judgment and coordination of muscle movements. The blood concentration is influenced by many factors. Only the concentration of alcohol in the blood influences the behaviour. The amount in stomach and intestine indicates only the ingestion and has no effects as such. After death, alcohol in the stomach may diffuse in to the blood and tissues. This results in higher blood level than actually existed during life, if the blood sample is taken from the part in to which post mortem diffusion has taken place. In reference to absorption of alcohol, certain points need to be elaborated: 1. Absorption is slower in the stomach than intestine. 2. Absorption is faster in empty stomach than when it contains food. 3. Food affects the absorption by delaying the emptying time of the stomach:(i) Fatty foods, proteins and starch delay the absorption (ii) Milk has similar effect i.e., it delays absorption (iii) Food prevents 10-20% of the ingested alcohol from being absorbed. 4. Diluted form of alcohol is absorbed slowly than the concentrated form 5. The type of beverage also affects the rate of absorption. Whisky is absorbed rapidly and its complete absorption occurs within 1-3
606 Textbook of Forensic Medicine and Toxicology
6.
7.
8. 9.
10. 11.
12.
hours. Then there is equilibrium between blood and tissue concentrations of alcohol. After 15 minutes of drink, the level of alcohol in arterial blood may be 40-60% higher than peripheral venous blood and may persist during the first hour. However, after absorption is complete alcohol levels in venous blood is slightly higher than the arterial blood. Therefore, the blood samples should be taken after equilibrium is reached. The absorption of alcohol depends on habituation and tolerance of the individual as habituated heavy drinkers tend to absorb alcohol more rapidly. Emotional state of the person affects the contraction of the stomach resulting in rapid emptying time and the rate of absorption. Drugs like Benzedrine and atropine slows the absorption and retards the emptying time. The age of the person also has an effect on the absorption as it occurs less rapidly in younger (24 hours No poison is found in the food. Cl. tetani bacillus can be demonstrated
43
Part 2—Forensic Toxicology
Cardiac Poisons Cardiac poisons have mainly actions on the heart, either directly on the musculature or through its nerve supply. Oleander, nicotine, digitalis and aconite belong to this group NICOTIANA TABACUM (TOBACCO) Nicotine is a colourless, hygroscopic liquid alkaloid. It was first given to Columbus by Native Americans that subsequently spread to Europe. However, the use of cigarettes is a modern phenomenon throughout the world. Uses: Preparations of nicotine are extensively used in agriculture and horticulture for fumigating and spraying, as insecticides, fumigants, vermin paste, worm-powder, sheep dip etc. The dried leaves of the plant Solanaceae comprise of the tobacco used for smoking. These leaves of tobacco (tambaku) contain 1-8% of nicotine and are used in the form of smoking, snuff and for chewing. They are used for the preparation of cigars, cigarettes, bidis and powdered tobacco is used as a snuff. The tobacco is also consumed by mixing with lime alone (khaini) or with lime and betel. Active principles: All parts of the plant are poisonous except its ripe seeds. The leaves contain two active principles as toxic alkaloids; Nicotine and Nicotianine. Nicotine is very toxic and exists in all parts of the plant, in combination with malic acid and citric acid. It first stimulates the vagus nerve then depresses autonomic, central and spinal nervous system. In small doses, it contracts the pupil but in larger doses, it causes dilatation. The poisoning occurs in persons employed in tobacco extraction, processing or spraying of insecticides containing nicotine.
Absorption and excretion: Concentrated liquid nicotine is exceedingly dangerous. However, tobacco is much less poisonous than would be expected from its nicotine content when smoked. Most of the nicotine is burned and when ingested in the form of tobacco, it is poorly absorbed from the stomach. Nicotine poisoning can occur from ingestion or application over skin and by inhalation. Nicotine in the cigarettes is rapidly absorbed through the arterial circulation to reach the central nervous system directly and the effect occurs within a few minutes. About 85-90% is metabolized in the liver, but some amount is metabolized in the kidneys and lungs. It has a half-life of about 2 hours. Mechanism of action:(i) Nicotine binds to nicotinic receptors, which are present mainly on the CNS, spinal cord and neuromuscular junctions (ii) It also binds to autonomic nervous system and adrenal medulla. It first stimulates the vagus nerve, and then depresses the autonomic, central and spinal nervous system (iii) In small doses, it contracts pupil but in larger doses, it causes dilatation. Acute Poisoning: Following signs and symptoms are produced in acute poisoning: (i) Burning acid sensations in the stomach (ii) Salivation, nausea and vomiting and diarrhoea (iii) Headache, Giddiness, numbness and faintness (iv) Muscular weakness and tremors (v) Cold and clammy skin (vi) Hearing and vision may be affected (v) Cardiovascular manifestations include, slow pulse at first and then rapid, Blood Pressure is raised and arrythmias also develop (viii) Pupils are first contracted then dilated (ix) Respiration is at first rapid then slow (x) Sometimes delirium and
Cardiac Poisons 629 convulsions may occur (xi) Death occurs due to respiratory failure. Chronic poisoning: (i) Chronic poisoning is produced in heavy smokers and persons working in tobacco factories (ii) Respiratory system is mainly affected; chronic cough, bronchitis and laryngitis are produced due to irritation of pyridine bases (iii) Pulmonary emphysema is quite common in smokers and smoking may lead to lung cancer. The incidence of following diseases are more in smokers: (i) Coronary heart disease (ii) Oral cancer is directly related to smoking (iii) Hyperacidity and peptic ulcer are produced (iv) Dermatitis may be produced from dust and juice of tobacco leaves (vi) Optic atrophy is also commonly observed in the smokers (vi) Hypertension, extrasystoles and ventricular fibrillation are frequent in the smokers (vii) Thromboangiitis obliterans may be present. Fatal dose→60-100 mg of nicotine 15-30 gm of crude tobacco Fatal period→5-15 minutes. Treatment (i) Gastric lavage with weak solution of potassium permanganate or warm water containing finely powdered charcoal or weak tannic acid solution. (ii) Saline purgation to be given by mouth (iii) In mild to moderate cases, inj atropine sulphate 1-2 mg i.m. and hexamethonium chloride 25-50ng s.c to counteract peripheral autonomic disturbance and it also acts as a respiratory stimulant (iv) Mecylamine (inversine) is the specific antidote. As it is only antidote in tablet form, is of little value if patient is vomiting (v) Vasodilators like nitrites, methacholine can be given for amblyopia(vi) Oxygen inhalation and artificial respiration is recommended. As nicotine is completely excreted from the body within 16 hours thereafter, there is no danger to life. Autopsy Findings (i) Odour of tobacco and its leaves from the stomach contents (ii) Mucous membrane of stomach and intestines is congested and haemorrhagic due to caustic action of nicotine (iii) All the organs are
congested and oedematous (iv) Nicotine resists putrefaction so it can be recovered from the viscera for a long time after death. Medicolegal Aspects 1. Accidental poisoning is quite common due to its extensive use and usually occurs under the following circ*mstances: (i) Tobacco is used in different ways like smoking, chewing, swallowing or by decoction. It is also widely used in agricultural and horticultural work (ii) Accidental toxicity occurs when tobacco is applied as a poultice for ulcers or from mucous membranes when used as enema (iii) Oral tobacco use can lead to gum diseases and oral cancer (iv) Poisoning is usually accidental resulting from excessive smoking (v) Application of leaves or juice to the wound or abraded surface may lead to the absorption of the poison (vi) Drinking hookah water and Cheroots in water are applied over the axilla (vii) Malingering by soldiers to avoid duty, they soak the leaves in water and place in axilla with the bandage. 2. Suicidal and homicidal poisoning is rare. DIGITALIS PURPUREA The plant is cultivated in whole of Jammu and Kashmir of India and throughout the World. The entire plant of digitalis purpurea is toxic. Only leaves are used for medicinal purposes. Active principles: The active principles in the form of glycosides are present in the leaves, roots and seeds of the plant. There are about more than thirty glycosides out of which only four are important. Of this digitalin, digitoxin and digitalein are cardiac stimulants whereas digitonin is cardiac depressant. The poisoning by digitalis is mostly accidental as it is used in different types of cardiac diseases and over doses do occur. Mode of action: The main action of the poison is on the heart due to its glycosides content. In the heart: (i) It prolongs the period of systole in cardiac cycle (ii) It regulates the rhythm of the heart by depressing both excitability and conductivity (iii) It shortens the period of diastole (iv) It causes rise of blood pressure (v) In toxic doses, there is increa-
630 Textbook of Forensic Medicine and Toxicology sed excitability of the heart with development of extra-systole, ultimately toxic arrythmias and bradycardia develops leading to heart failure. Signs and Symptoms The poison first acts on the gastro intestinal tract then the cardiovascular system. The signs and symptoms produced are: (i) Gastrointestinal tract: Anorexia, thirst, nausea, vomiting, abdominal pain, watery diarrhoea, vertigo and fatigue are produced (ii) Cardiovascular system: Extrasystoles, pulsus bigeminus and heart block (iii) Respiration is slow and sighing, pupils are dilated and visual derangements are there (iv) Central nervous system: Headache, neuromuscular disorders, confusion, disorientation, drowsiness, delirium and hallucinations are present (v) Death is due to ventricular fibrillation.
(viii) Lignocaine 100 mg i.v. to be given for arrythmias (ix) Potassium salts are administered to reduce extrasystoles (x) Electrolyte imbalance should be corrected using IV fluids Autopsy Findings (i) Fragments of leaves of digitalis may be found in the stomach (ii) Mucous membrane of stomach is congested and inflamed (iii) All organs are congested. Medicolegal Aspects (i) Poisoning occurs due to intake of overdose of medicinal preparation accidentally (ii) It is also sometimes used for homicidal purposes (iii) Digitalis being a cumulative poison, accidental death may occur in susceptible persons. ACONITE (Mitha bish, Mitha zahar, Bikh)
Tests for the Glycosides The glycosides can be extracted from the acidified organic matter. When these glycosides are treated with strong sulphuric acid, the reactions of all three are different: (i) Digitoxin will give green colour, which does not change with bromine (ii) Digitalin gives yellow colour that soon changes to brick red and to violet red on addition of bromine water (iii) Digitonin produces red colour and the colour intensifies with addition of bromine water Fatal dose→ Digitalis—2-3 gm Digoxin—5 mg Digitalin—15-20 mg Powdered leaves—2.5 gm Fatal period→ 24 hours. Treatment (i) Stomach wash using tannic acid and activated charcoal to be given (ii) Bowels should be evacuated (iii) Atropine 0.6mg i.v. is given for bradycardia that can be repeated (iv) Quinidine sulphate 0.2gm is given 4-6hourly (v) Lignocaine 50mg i.v is given for ventricular tachycardia (vi) Digoxin specific antibody fragments (Fab) are given in the dose of 0.4-0.8 mg i.v. slowly (vii) Phenytoin 50 mg i.v / min, can be given upto 1gm followed by 300 mg daily for ventricular fibrillation
The term aconite is derived either from greek akonitus or from the greek city “acona”. Few suggest that the word aconite has come from the hill of aconitus. The plant Aconite is grown in garden for its showy flowers in the Himalayan ranges in India. Aconitum napellus belongs to the family Ranunculaciae. All parts of nearly all the varieties of the plant are poisonous but the root is chiefly used as poison. There are several species of aconite out of which aconitum ferox and aconitum napellus are commonly used as poison. They are also known as Monk’s hood, Blue Rocket, Bear’s foot Mitha zeher, Bish and Bikh etc. The dry root is conical and shows scars of broken rootlets. The upper end of it is usually about 2 cms thick and has a length of usually 8-10 cms. The root is dark brown in colour (Fig. 42.1) that on cut section is whitish and starchy, which, on exposure to air, turns pink. It has to be differen-
Figure 42.1: Root of aconite
Cardiac Poisons 631 tiated from horseradish root that is long, cylindrical and yellowish white externally and whitish internally that does not change in colour on exposure to air and it has a pungent taste. It has no odour but is sweetish in taste hence the name Mitha Bish.On chewing tingling and numbness in the tongue, lips and mouth is felt.
Tests for diagnosis: Paper chromatography and ultraviolet spectrophotometry helps in analyzing the poison. Fatal dose→1-2 gm of root; 2-5 mg of aconitine. Fatal period→1-5 hours.
Mode of action: The poison first stimulates the sensory nerve endings, producing tingling sensation then paralyzing them causing numbness. It produces similar effect on the motor and secretory nerve endings, the centres of the medulla and cord, while the higher centres are always left out. The alkaloids depresses the myocardium, smooth muscles and skeletal muscles. Its depressant effect on motor ganglia and cardiac muscles produces heart block. Temperature falls gradually due to its action on thermogenic centre.
(i) Stomach wash with tannic acid or milk (ii) Maintain body heat (iii) Atropine sulphate 1mg i.v is given for bradycardia (iv) Oxygen inhalation and artificial respiration to be given.
Elimination: Aconite is mainly excreted in urine, but traces are excreted in bile, saliva and sweat
Medicolegal Aspects
Active principles: The alkaloids isolated from the different varieties of the Aconite are: (i) From Aconite napellus (a) Aconitine (Acetyl-benzoylaconine) (b) Picraconitine (Benzoyl-aconine) (c) Aconine (ii) From Aconite ferox (a) Pseudoaconitine (Veratroyl-aconine) (iii) From Aconite charmanthum (a) Indaconitine (iv) From Aconite spicatum (a) Bikhaconitine Of all these alkaloids obtained from the Indian varieties of the aconite plant, pseudoaconitine is the most toxic, Indaconitine and Bikhaconitine are less toxic than pseudo-aconitine but a bit more poisonous than Aconitine
NERIUM ODORUM (White oleander, Sweet scented oleander or Kaner)
Signs and Symptoms The symptoms of aconite poisoning start immediately after its consumption: (i) Bitter taste in the mouth (ii) Burning pain in the abdomen (iii) Nausea, vomiting and salivation (iv) Diarrhoea is rare (v) Pupils alternately dilate and contract which is known as hippus, but at a later stage, they remain dilated. The diplopia is also present (vi) Pulse is slow and irregular (vii) Temperature is subnormal (viii) Consciousness usually remains clear till the end (ix) Death results from ventricular fibrillation.
Treatment
Autopsy Findings (i) Bronchial tree contains froth and mucous (ii) Mucous membrane of stomach and small intestine may be congested (iii) All organs are congested (iv) It is extremely unstable and is destroyed by putrefaction.
(i) As aconite is largely used as medicine, accidental poisoning is common (ii) It may be mistaken for Horse radish shoe (iii) It is given with betel leaf to mask its taste (iv) It is added with liquor to increase its intoxicating effect (v) It is used as arrow poison in hilly areas.
The plant grows wildly all over the country. It is also grown in gardens for its beautiful pink and white flowers (Fig. 42.2). The plant has lanceolate leaves and bears two folllicled fruit that contains numerous seed. All parts of the plant are poisonous Uses: (i) Powdered roots are used for the treatment of venereal diseases, epilepsy, malaria, skin diseases and menstrual disorders by the quacks (ii) The powdered roots are also applied as paste to treat ulcerations and cancerous growths (iii) Decoction of the leaves may be applied to reduce swelling of body. Active principles: The active principles are several cardiac glycosides known as (i) Nerin (ii) Oleandrin and (iii) Karabin
632 Textbook of Forensic Medicine and Toxicology cardiac arrhythmias, phenytoin 100-200mg orally or 100 mg i.v every 5 minutes until they are reverted (vi) Symptomatic treatment for maintenance of circulatory collapse. Autopsy Findings (i) Stomach and intestinal mucosa is congested (ii) All the chambers of heart distended with blood (iii) All organs are congested (iv) Subendocardial haemorrhages are pathognomic (v) The poison resists heat so it can even be detected in burnt human remains. Figure 42.2: Nerium odorum plant
Fatal Dose→
Powdered root—15G-20 G Neriodorin and karabin—150 mg
Signs and Symptoms 1. On ingestion: (i) Peculiar taste in mouth (ii) Nausea, vomiting and profuse salivation (iii) Difficulty in deglutition and articulation (iv) Acute pain in epigastrium associated with diarrhoea (v) Fibrillary twitchings of muscles of upper limbs followed by tetanoid convulsion occurs. It affects nearly all muscles of the body, but may be unilateral. It is accompanied by lock-jaw (vi) Pulse rate is slow, weak and feeble in late stages (vii) Fall of blood pressure and cardiac arrythmias development respiration is hurried and stertorous with dilated pupil (viii) Exhaustion and drowsiness leading to insensibility, collapse and coma (ix) Death occurs from heart failure. 2. On inhalation of the smoke from burning plant: (i) Cough, frothy salivation and dysphagia (ii) Fibrillary twitching of muscles (iii) Pulse is slow, weak and feeble (iv) Blood pressure is low and respiration is hurried and stertorous. Treatment (i) Stomach wash using weak solution of potassium permanganate or tannic acid (ii) Vomiting and diarrhoea should be controlled (iii) Morphine or pethidine 5mg i.m for sedation that will control spasm (iv) Absolute bed rest is a must (v) To treat
Chemical Tests Keller’s test gives green colour appearing slowly in the acetic acid layer and crimson colour in the sulphuric acid layer when nerium extract obtained by Stass-Otto process is added. Medicolegal Aspects (i) Accidental poisoning can occur from ingestion of powdered root or decoction for treatment or when used as a love-potion (ii) The powdered roots, decoction of leaves or paste of the fruit may be ingested for committing suicide (iii) Cases are on record when it has been used or homicidal purposes (iv) It is commonly used as cattle poison; the paste of powdered root is smeared on a rag that is pushed into anal canal of the animal. It is also mixed with the cattle fodder (v) The paste is commonly smeared on the abortion stick to be used as an abortifacient CERBERA THEVETIA (Thevetia nerifolia or yellow oleander) The plant is also known by the names of Bastard oleander, Pila kaner etc. it belongs to N.O. Apocynaceae, alike Nerium odorum and is widely cultivated in gardens in India. The plant has linear lanceolate leaves and bears yellow coloured bellhaped flowers. The fruit is globular in shape, green and contains a single pale-brown nut that is triangular in shape with a deep grove along the edge, having two cells (kernels), each enclosing a pale yellow cotyledon. All parts of the plant are highly poisonous
Cardiac Poisons 633 Uses: The powdered bark of the plant may be used as an antipyretic like Cinchona in the dose of 125mg; in little bigger dose, it acts as an emetic and purgative and in further bigger dose, it is toxic. Active principles: The milky juice from nearly all parts of the plant gives out the active principle the are cardiac glycosides. Of these thevetin and thevetoxin can be recovered from the kernels of seeds: (i) Cerberine—It is a neurotoxic acts like strychnine (ii) Thevetin—It is a powerful cardiac toxin (iii) Thevetoxin—Action is similar to digitalis (iv) Nerifolin—Action is similar to digitalis. →Uncertain but death can occur in Fatal dose→ adults by 8-10 seeds and children by1-2 seeds. →Uncertain but usually 2-3 hours. Fatal period→ Signs and Symptoms (i) Burning sensation in the mouth with feeling of dryness (ii) Tingling and numbness of mouth, tongue and throat (iii) Headache, dizziness and faintness (iv) Dilated pupils with indistinct vision (v) Loss of muscular power and have fainting fits (vi) Nausea, vomiting and loose frequent motions due to the irritant action on bowel (vii) Depressant action on cardiac muscles causes slow and irregular pulse rate (viii) In late stages, pulse is weak, feeble, irregular with fall of blood pressure and heart block (ix) Respiration hurried and stertorous (x) Tetanic convulsions may occur (xi) Collapse, Coma and death from peripheral circulatory failure. Treatment (i) Stomach wash using weak solution of potassium permanganate or tannic acid followed by animal charcoal suspended in water (ii) Barbiturates to control convulsions (iii) Stimulants, analeptics, digitalis, I.V dextrose saline, noradrenaline and corticosteroids to counteracting cardiac failure (iv) To treat cardiac arrhythmias, phenytoin 100200mg orally or 100 mg i.v every 5 minutes until they are reverted (vi) Symptomatic treatment for maintenance of peripheral circulatory collapse. Autopsy Findings (i) Stomach and upper intestinal mucosa is congested (ii) The fragments of seeds may be
recovered from the stomach contents (iii) All organs are congested (iv) Subendocardial haemorrhages are characteristic Chemical Tests As cerberine is easily destroyed by hydrolysis with dilute hydrochloric acid and gastrointestinal secretions, it is rarely detected in the viscera on chemical analysis. Thevetin is resistant to such destruction and is available for extraction in poisoning by yellow oleander. Thevetin contained in the acid ether extract obtained by subjecting the viscera of suspected yellow oleander poisoning to Stas-Otto procedure can be recognized by: 1. Keller’s test—When the ether extract is dissolved in 1 mL of glacial acetic acid containing 5% ferric sulphate and this solution is put over a mixture of 100 parts of concentrated sulphuric acid and 1 part of ferric sulphate, blue colour appears on acetic acid layer and mauve colour on the sulphuric acid layer. 2. When portions of any part of yellow oleander is boiled with dilute hydrochloric acid, a blue colour develops and bluish colour also appears when alcoholic extract of the seed is warmed with dilute hydrochloric acid, this may disappear on adding potassium permanganate solution. Medicolegal Aspects (i) Accidental poisoning can occur from ingestion of powdered root or decoction for treatment and common in children (ii) The powdered roots, decoction of leaves or paste of the fruit may be ingested for committing suicide (iii) It is not used for homicidal purpose. It is commonly used as cattle poison that is given mixed with the cattle fodder (iv) The paste is commonly smeared on the abortion stick to be used as an abortifacient. The powdered root or seeds are taken after mixing with food or drink to cause abortion CERBERA ODALLAM (Dabur or Dakur) This plant closely resembles that of Cerbera thevetia that grows wild in the swams and the creeks of the seacoasts of India. The plant has a dark, fleshy lanceolate leaves similar to jasmine
634 Textbook of Forensic Medicine and Toxicology and the fruit resembles unripe mango contains a single oval white seed that is flat and oval, has two cotyledons (kernels) that appears bluish when dry. Milky juice exudes out from all parts of the plant. The kernels yield a non-poisonous oil that is used for burning. Active principles: The kernel contains a glycoside cerberine and alkaloid –Cerebroside that has digitalis like action. Fatal dose→Kernel of one fruit. Fatal period→About 1-2 days. Signs and Symptoms They appear within one hour of ingestion. Initially gastrointestinal symptoms appear followed by cardiac toxicity: (i) Violent vomiting and diarrhoea. (ii) Irregular respiration (iii) General paralysis and collapse (iv) Death results from heart failure (v) ECG changes—Sinus bradycardia, S.A. node block, atrial and ventricular fibrillation. Treatment (i) Mainly symptomatic treatment (ii) Stomach wash using weak solution of potassium permanganate or tannic acid followed by animal charcoal suspended in water (iii) Injection atropine sulphate 0.5mg i.v is to be given and repeated if needed (iv) Hyperkalemia should be corrected (v) Barbiturates to control convulsions (vi) Stimulants, analeptics, digitalis, I.V. dextrose saline, noradrenaline and corticosteroids to counteracting cardiac failure (vii) To treat cardiac arrhythmias, phenytoin 100-200 mg orally or 100 mg I.V every 5 minutes until they are reverted. Autopsy Findings The autopsy findings are non-specific. Chemical test: The extract is treated with boiling dilute hydrochloric acid and cerebrine will form a bluish or bluish green colour. HYDROCYANIC ACID (Cyanogen, Prussic acid) Hydrocyanic acid is a vegetable acid that is widely distributed in nature in many fruits and leaves. Here it exists in the form of harmless glucoside
known as amygdalin, which, coexist with the enzyme emulsion in the kernels of various fruits such as peaches, plums, apricots, bitter almonds, Bamboo shoots, certain oil seeds and beans and leaves of cherry laurel and bitter almonds. The emulsion can readily hydrolyse amygdalin in presence of water to form hydrocyanic acid, glucose and benzaldehyde. It is present in the leaves of Cherry laurel in the strength of .08-0.1% and 10% in oil of bitter almonds. Several people suffer from the effects of hydrocyanic acid poisoning after eating handful of bitter almonds. Liquid hydrocyanic acid when pure, is a highly volatile colourless liquid having a peculiar odour of bitter almonds or peach-kernels. The hydrocyanic acid is usually obtained by distilling potassium cyanide or potassium ferrocyanide with dilute sulphuric acid. Hydrocyanic acid is decomposed in neutral or alkaline solution with formation of ammonia. It rapidly decomposes when exposed to air and light The odour of hydrocyanic acid is that of bitter almonds and all persons cannot smell hydrocyanic acid gas as the ability to do so is a sex-linked trait and when a person is habituated to the smell for few minute, it disappears and again he has to come to fresh air, then only he can smell it. Uses of Cyanide: (i) Potassium, sodium or silver cyanides are used in the industry for (i) Metallurgy (ii) Photography (iii) Electroplating (iv) As spray to destroy blight (v) Fumigation of ships (ii) Sodium cyanide is extensively used in: (i) Metallurgy (ii) Electroplating (iii) Case hardening of steel and iron (iv) Tanning (v) Manufacturing of dyes (iii) Calcium cyanide is used for (i) Mining industry (ii) As a source of hydrocyanic acid (iii) Fertilizer (iv) Preparation of basic chemicals for plastics (iv) Hydrocyanic acid is used for (i) Photography (ii) Electroplating (iii) Agriculture and horticulture for spraying citrus trees (iv) Fumigation of rooms, ship-holds to free them from bugs, lice and vermins (v) For metal cleaning of, refining of ores and production of synthetic rubber (v) Flowering agent (i) Crude oil of bitter almond—2-10% HCN (ii) Cherry laurel water 0.1 HCN that looses strength on storing. The hydrocyanic acid gas is capable
Cardiac Poisons 635 of being absorbed by the skin, when it is moist with perspiration as the poison is readily soluble in water. It is too dangerous to remain too long in a high concentration of the gas in the atmosphere even when wearing a respirator. The hydrocyanic gas is used for fumigating premises and ship-holds Mode of action: (i) Inhibits the action of cytochrome oxidase, carbonic anhydrase and other enzyme systems as a result the cells are unable to utilize oxygen by dissociating it from the oxyhaemoglobin of the red cells. Tissue anoxia or histotoxic anoxia results even with normal oxygen content in blood that accounts for bright red colour of the venous blood. (ii) There is an interference with the intracellular oxidative process in the tissues (iii) Death is due to histotoxic or cytotoxic anoxia although the blood may contain normal oxygen. Absorption and Excretion Cyanide gas is absorbed rapidly from the respiratory system and the acid and salts from the stomach. The acid is also absorbed through the skin. Absorption is delayed when cyanide is taken on a full stomach or with much wine. Cyanide when ingested, in contact with hydrochloric and gastric juice leads to the formation of hydrocyanic acid and chloride. Therefore, it has been suggested that achlorhydric patients cannot be poisoned. It cannot be held not true as the water in the gastric juice and tissues can cause hydrolysis, and leads to liberation hydrocyanic acid. Signs and Symptoms Signs and symptoms develop most rapidly when gas is inhaled and the action is instantaneous. Massive doses produce sudden loss of consciousness and the death due to respiratory failure. When large doses are inhaled, symptoms start immediately that is within 1-2 minutes. Voluntary acts are possible like walking and throwing some articles. On ingestion by mouth, the symptoms produced from cyanide poisoning may be delayed up to 15-20 minutes until the liberation of hydro-
cyanic acid by the action of gastric juice on salts of cyanide. Double cyanides—Potassium Ferro cyanide and ferricyanide are practically non toxic, but they give off hydrocyanic acid in certain conditions. They are toxic when they are taken with the acids. Potassium and sodium cyanide has a corrosive action on the mouth, throat and stomach: (i) Burning taste and feeling of constriction in the mouth and throat (ii) Nausea and vomiting (iii) Excessive salivation and blood stained froth from the mouth (iv) Anxiety and confusion (v) Headache, vertigo and giddiness (vi) Initially Hyperpnoea and Dyspnea is present caused by stimulation of the chemoreceptors and the respiratory center, then respiration becomes rapid, slow and irregular with short, inspiration and long expiration (vii) Smell of bitter almonds in breath and vomitus (viii) In early stages, blood pressure is increased and heart rate is decreased. Later on pulse is rapid, weak and irregular (ix) There is sense of constriction in the chest (x) Unconsciousness and violent convulsion; paralysis follows the convulsive state (xi) Opisthotonus and trismus may develop (xii) Involuntary micturition and defecation (xiii) Skin is covered with sweat and is brick red in colour (xiv) Eyes are glassy and prominent; pupils are dilated and non-reactive to light (xv) Inhalation of gases produces (a) Sense of constriction in throat and chest (b) Dizziness and vertigo (c) Insensibility and death from respiratory failure (d) Epigastric pain and vomiting (xvi) Death is due to respiratory failure Fatal dose→HCN—50-60 mg. KCN and NaCN—200-300 mg. Air concentration 1:500 causes immediate death. Fatal period→HCN—2-3 minutes. KCN and NaCN—half an hour. Treatment Treatment should be started immediately without losing any time. To reverse cyanide cytochrome combination, haemoglobin is converted in to methaemoglobin by the action of nitrites: • Cytochrome oxidase + NaCN®cytochrome oxidase cyanide
636 Textbook of Forensic Medicine and Toxicology • Sodium Nitrate + Hb→Methhaemoglobin • Methhemoglobin + NaCN® Cyanmethhemoglobin (non toxic). (i) Break 0.2cc ampoule of Amyl nitrite in a handkerchief and hold over the patient’s nose for 15-30minutes until sodium nitrite is given (ii) 0.3gm of 3% sodium nitrite and 10ml of sterile water is given intravenously over2-3 minutes (iii) Through some needle 25gm of sodium thiosulphate in 50% solution is given i.v, over 10 minutes. It converts cyanide to thiocyanate that is non-toxic. Repeat the nitrite thiocyanate injection after one hour if necessary (iv) Gastric lavage by 3% hydrogen peroxide, Sodium thiosulphate (5-10%) and Potassium permanganate (1:5000) of which, 200ml is left in the stomach (v) Methylene blue is an antidote; 50 ml of 1% aqueous solution is used. It converts haemoglobin to methaemoglobin that combines with free cyanide, which is non-toxic and is removed from the circulation (vi) Cobalt salts such as cobalt acetate is given 100 mg i.v, and cobalt edetate 600 mg (vii) Para amino propiophenon (PAPP): It converts haemoglobin to methaemoglobin (viii) Artificial respiration (ix) In delayed cases, a mixture of ferric and ferrous sulphate with potassium carbonate is the chemical antidote to form Prussian blue (x) Maintain clear airway (xi) Symptomatic treatment. Therapy with amyl nitrate: Amyl nitrate converts a portion of the hemoglobin’s iron from ferrous iron to ferric iron, converting the hemoglobin into methemoglobin. Cyanide is more strongly drawn to methemoglobin than to the cytochrome oxidase of the cells, effectively pulling the cyanide off the cells and onto the methemoglobin. Once bound with the cyanide, the methemoglobin becomes cyanmethemoglobin. Therapy with nitrites is not innocuous. The doses given to an adult can potentially cause a fatal methemoglobinemia in children or may cause profound hypotension. Treatment of children affected with cyanide intoxication must be individualized and is based upon their body weight and hemoglobin concentration.
Alternative management protocols in other countries: 1. The United States standard cyanide antidote kit: It uses a small inhaled dose of amyl nitrite followed by intravenous sodium nitrite. 2. In U.S.A, the next part of the cyanide antidote kit is sodium thiosulfate, which is administered intravenously. The sodium thiosulfate and cyanmethemoglobin become thiocyanate, releasing the hemoglobin, and the thiocyanate is excreted by the kidneys. 3. In France, hydroxycobalamin (a form of vitamin B12) is used that combines with cyanides to form the harmless vitamin B12a cyanocobalamin. Cyanocobalamin is eliminated through the urine. Hydroxycobalamin works both within the intravascular space and within the cells to combat cyanide intoxication. This contrasts with methemoglobin, which acts only within the vascular space as an antidote. 4. Administration of sodium thiosulfate improves the ability of the hydroxycobalamin to detoxify cyanide poisoning. This treatment is considered so effective and innocuous that it is administered routinely in Paris to victims of smoke inhalation to detoxify any associated cyanide intoxication. However it is relatively expensive and not universally available. 5. 4-Dimethylaminophenol (4-DMAP) has been proposed in Germany as a more rapid antidote than nitrites and with reportedly lower toxicity. It is used currently by the German military and by the civilian population. In humans, intravenous injection of 3 mg/kg of 4-DMAP will produce 35 percent methemoglobin levels within 1 minute. 6. Cobalt salt have also been demonstrated as effective in binding cyanide. One current cobaltbased antidote available in Europe is dicobaltEDTA, sold as Kelocyanor. This agent chelates cyanide as the cobalticyanide. This drug provides an antidote effect more quickly than formation of methemoglobin, but a clear superiority to methemoglobin formation has not been demonstrated. Cobalt complexes are quite
Cardiac Poisons 637 toxic, and there have been accidents reported in the UK where patients have been given dicobalt-EDTA by mistake based on a false diagnoses of cyanide poisoning. Autopsy findings (i) Rigor mortis starts early and lasts longer (ii) Eyes are bright, glistening, and prominent with dilated pupils (iii) Jaws are firmly closed (iv) Froth is coming from the mouth (v) Post mortem staining is of cherry red colour due to the formation of cyanmethaemoglobin, tissues cannot take up oxygen and oxygen remains in the cells as oxyhaemoglobin; asphyxia occurs in the presence of oxygen (vi) On opening the body, the odour of cyanide can be felt from the stomach contents and other organs (vii) Brain is to be opened first as the odour is well marked here (viii) Trachea contains blood stained froth (ix) All the visceral organs are congested (x) Lungs are oedematous (xi) CNS shows degenerative changes (xii) Potassium and sodium cyanide cause corrosion of the mouth (xiii) Gastric mucosa is crimson red in colour that changes to rusty brown due to the formation of acid Haematin (xiv) Blood is cherry red coloured due to formation of cyanmethaemoglobin. Spectroscopic Examination of Blood The spectroscopic examination of cyanides resembles that of reduced haemoglobin with a thick band between the lines D and E. Chronic Cyanide Poisoning Chronic poisoning may occur by continued inhalation of low concentration of cyanide gas for a long period; the symptoms are those of suboxia including cachexia, mental disturbance, visual defects, such as scrotomata, optic atrophy and psychosis.
Judicial Execution The condemned or prisoner person is strapped to a chain in a closed room and several cyanide eggs are dropped in to a pan of strong acid that leads to liberation of cyanide gas. Unconsciousness takes place very rapidly though heart continues to beat for 10-15 minutes then death occurs. Medicolegal Aspects (i) Commonly used for the purpose of suicide, as it is quick acting and only a small dose is fatal. (ii) Oil of bitter almonds (2-10% HCN) and cherry laurel is used as flavouring agent (iii) Causes of accidental poisoning: (a) Inhalation of cyanide vapours used as fumigating agent causes accidental poisoning (b) May be ingested in accidentally in lieu of some medicine (c) It may be accidental to the workers employed in the industry (iv) It is rarely used for homicidal purposes (v) Putrefaction produces 1/10th of the cyanide poison (vi) Cyanide is destroyed by embalming (vii) It is present in fire victims in very small amount (viii) Cattle poisoning results by eating jawar, kadvi, or alsi plants. Growing plants, flowers, and seeds contain maximum hydrogen cyanide. One pound of flower is fatal to a bullock—cyanogenic glucoside (ix) On keeping it for a long time harmless carbonate may be formed by the action of atmospheric carbon dioxide and moisture on potassium cyanide and potassium formate. The nitrite forms methaemoglobin that reacts with hydrogen cyanide and allows the enzyme to function. The sodium thiosulphate helped by the enzyme Rhodenase inactivates the cyanide by converting it in to non-toxic thiocyanate. Methylene blue converts the haemoglobin of the blood in to methaemoglobin, which combines with free cyanide there by removing it forms, the reaction.
44
Part 2—Forensic Toxicology
Drug Abuse DRUG In 1969, WHO Committee on Drug dependence defined drug as “A substance that when taken in to a living organism, may modify one aspect of its function”. As this definition included water and air also, certain modifications were made in the definition. These are: (i) Drug in the broadest sense is any chemical entity or mixture of entities other than those required for the maintenance of normal health, the administration of which alters the biological function and bodily structure (ii) Second level of definition could then specify the users to which these entities are put that is the drugs used for the treatment or alleviation of disease known as medications, therapeutic agents (iii) Third level of definition: One may differentiate chemical entities based on bodily system or function on which they exert their most marked or obvious affects e.g. Diuretics, CNS Stimulants etc. (iv) The main concern is about the possible adverse effects on health or social function e.g. psycho-active drugs, Anti histaminics. Use, Abuse and Misuse: Abuse and misuse are unsatisfactory concepts because these terms involve value judgment, they are impossible to define in such a way that they are appropriate for different drugs in different situations. Drug Abuse 1969 WHO Expert Committee defined drug abuse as “Persistent or sporadic excessive drug use inconsistent with or unrelated to acceptable medical practice”. Further attempts to achieve a comprehensive definition of abuse have been considered depend-
ing on the medical need, individual and social harm and the degree of tolerance by the community. Drug abuse refers to the use usually by selfadministration of any drug in a manner that deviates from the approved medical or social pattern within a given culture. In some cultures, some drugs/substances are not considered against the society and so may not be against the legal system of the country. Use of medically prescribed drugs e.g. barbiturates to induce sleep is permissible but if it is used to induce euphoria (when not medically indicated); it is called drug abuse e.g. opiates can be taken when prescribed medically for the relief of pain but not solely for its euphoric effect. When people continue to take these drugs in the absence of disease, intensity of dependence varies from mild desire to the compulsion to use the drug is called drug abuse. Clinicians and research workers can often manage without using the terms such as unsanctioned, hazardous, dysfunctional or harmful use as they are concerned more about the effects of drugs and their route of administration. Nevertheless, if such terms are to be used then following concepts may be useful (i) Unsanctioned use— Use of a drug, not approved by a society or a group within that society, it implies that we accept disapproval as a fact (ii) Hazardous use—Use of a drug that will probably lead too harmful consequences, for the users either to dysfunction or to harm e.g. smoking 10-15 cigarettes per day may not be accompanied by any harm, but we know it to be hazardous (iii) Dysfunctional use—Use of a drug that is heading to impair psychological or social functioning such as loss of job, marital problems etc. (iv) Harmful use—Use of a drug that
Drug Abuse 639 is known to have caused tissue damage on mental illness, in a particular person. Drug addiction: Drug addiction is a state of periodic or chronic intoxication, produced by repeated consumption of a drug, which is harmful to the individual and to society such as Heroin, alcohol, cannabis, Hashish, barbiturates, opiates, cocaine, amphetamine, LSD, Mandrax and bromides. Of these, Heroin is the most dangerous. Drug habituation: A condition resulting from the continued consumption of a drug, which does not cause much harm to the individual or to the society though there is psychological and emotional dependency on the drug. These are Caffeine, Nicotine etc. Table 3.1: Differences between drug addiction and drug habituation Features
Addiction
1. Compulsion
Present
Desire
2. Dose 3. Dependence
Increased tendency Psychical & Psychological Characteristic
No such Some degree of Psychological Mild or nil
Individual and society
Only to the Individual
4. Withdrawal symptoms 5. Harm
Habituation
Causes of Drug Abuse: The drug abusers start with a smaller dose but gradually increase the dose and frequency of intake until they develop tolerance. The abusers use the drug due to many reasons such as: (i) To get respite temporarily from various physical or mental ailments (ii) For the purpose of recreation and relaxation (iii) For better performance (iv) For controlling feelings of anger or distress and to get relief from chronic tension (v) For performing spiritual exercises e.g. LSD and Methaquolone (vi) For alleged aphrodisiac properties (vii) To get relief from frustration in life, love or sex (viii) Just out of curiosity. Types of persons exposed: The persons likely to be exposed to drug abuse are: (i) Neurotic or mentally imbalanced subjects (ii) Persons in habit of taking risks and having rebellious nature (iii) Individuals with sexual promiscuity
Magnitude of problem of drug abuse: Drug abuse is a worldwide phenomenon because of its harmful effects on the health and morale of the individual and society at large. Misuse of drugs have become part of the modern life in order to obtain kicks, thrills, excitement and escaping from day to day problems of life. United States has described the threat of drug abuse as a menace to which no country feels immune. Of late, many cases of forgery of prescription, criminal activities following ingestion of drug, antisocial activities of teenagers, illicit trafficking of the drugs and their abuse is going on but only few are caught and reported. The trafficking of drugs is done in many countries such as Myanmar, China and Thailand (Golden triangle) that fall along the eastern side of the region and Pakistan, Afghanistan, Iran and India (Golden crescent) that fall on the western side. One third of the total Heroin seized is from India. Addiction to narcotics especially Heroin is important cause of committing crime. 50-80% of the street crimes committed in big cities of US are committed by addicts. These include the crimes of robbery, house breaking, borrowing and begging to keep heroin flowing in their veins (can even sell their property). The addicts call heroin by the names of ‘our heroin’ and ‘white queen’. Besides heroin amphetamines, cocaine and barbiturates are also prevalent among the addicts. The drug addicts are involved in causing sexual offences, forgery, cheating, and vehicular accidents. Demographic studies: The students both male as well as females are given Marijuana called ‘Reefers’ by their classmates free of cost. Later on when this person becomes habituated, these addicts start selling the drug at a higher price. Drug addicts indulge in polygamy and sexual intercourse in groups under the effect of marijuana or LSD. Devotees of marijuana call it social drug and are under the theory ‘make love and not wars’ ‘Hippies’ share their quota of drugs with the students. A survey conducted by Tata Institute of Social science revealed that most of the students taking drugs belong to the upper class and those of effluent stream are more inclined. The addicts belong usually to 10-20 years age group and males
640 Textbook of Forensic Medicine and Toxicology are more prone. Drug abuse is more common in bright and brilliant students’ particularly professional college students. In urban areas, narcotic drugs and psychotropic substances are commonly abused whereas in rural areas mainly Charas, Ganja and country liquor is consumed. Classification of Drugs of Abuse The abuse of narcotic as well as non-narcotic drugs is quite common and the non-narcotic drugs are commonly referred to as soft drugs to distinguish them from the narcotics or the hard drugs. The drugs of abuse are classified as: (i) Hypnotics such as Barbiturates (called ‘sleepers’ or ‘goof balls’ by drug abusers) (ii) Stimulants are commonly used by drug addicts and the tolerance to these drugs develops slowly but can be acquired to the massive doses. These are Amphetamines (called ‘Purple Hurts’, ‘Black bombers’, ‘pep pills’ or ‘desk), Benzedine, and Ephedrine (iii) Antidepressants—Tricyclic antidepressants and MAO inhibitors (iv) Hallucinogens drugs such as Cannabis, Mescaline, Cocaine, Lysergic, LSD, Phencyclidine, Methaquolone (Mandrax) and various hydrocarbon preparations (v) Sedatives as well as hypnotic and tranquilizers—Benzodiazepines (vi) Narcotics such as opium and its derivative (pethidine and heroin) (vii) Alcohol and alcohol containing beverages (viii) Deliriants. The action of all these drugs overlap to a certain extent that is those substances acting as central nervous system stimulants can impair consciousness when taken in sufficient quantity whereas those that depress the CNS may arouse and cause loss of inhibitions before exerting their depressant action. Routes of Administration The route of administration depends predominantly on the nature of substance and the intensity of action desired. The possible routes are: (i) Orally– This route is commonly employed the absorption from the gastrointestinal tract is relatively slow and the impact of the drug on the brain is muted unless large quantities of the drug are taken (ii) Inhalation—The method is also quite commonly employed as there is increase in the speed of
absorption. This method is commonly employed for inhaling nicotine from tobacco and charas (iii) Snorting—This route is not commonly employed except in cocaine. Cocaine is commonly dissolved and the solution sniffed up in the nostrils where a part of it is absorbed (iv) Injection—This methods is the fastest method of getting the desired affect as high concentration of the drug is absorbed through the brain. Two methods are commonly employed; Skin-popping is injection via subcutaneous route and mainlining is injection via intravenous route. Besides this injection is also taken intramuscularly. Rapid I.V. injection of an opioids produces warm flushing of skin and sensation in the lower abdomen described by addicts similar in intensity to sexual org*sm that lasts for 45-50 second and is described as ‘rush’, ‘thrill’ or ‘kick’. Fatal Results of Drug Abuse The hazards of drug abuse are: Overdosage of the drug: The overdosage of the drug commonly occurs accidentally, intravenous injection carries the highest risk of accidental overdosage, and when it occurs, the drug cannot be retrieved. When the supply of high quality drug is less, the drug pushers may cut (dilute) the drugs that are sold on the streets in order to experience the ‘kick’ or ‘rush’, they tend to increase the dose. Toxicity due to contaminants: The substances such as talc are commonly used to cut the drugs in order to reduce the cost. These are used by the drug addicts while preparing the drug for injection. The abuser may develop pulmonary granulomas due to these contaminants and other toxicity e.g. quinine. Infections: Infections such as Hepatitis B, HIV, bacterial abscesses, thrombophlebitis, endocarditis and moniliasis may result from the use of contaminated needles, sharing of needles following other unhygienic practices. Gangrene: Gangrene may result from inadvertent intra-arterial injections. Anaphylactic reaction: The drugs of abuse are likely to cause hypersensitivity reactions
Drug Abuse 641 Risks of body packing and body stuffing: For smuggling of the drugs, the individuals (swallowers) make small packets of the drugs and swallow them that can later on be recovered from the vomitus or faeces. The individuals (stuffers) may also insert the packets of drugs into their vagin* or rectum. Drug preparations that are financially lucrative such as high quality cannabis, cocaine, heroin, and morphine are smuggled in this way. There exists a risk of overdosage with these practices as the packets may burst and get absorbed through the gastrointestinal, vagin*l or rectal mucosa. The body packer is at risk of acute intestinal obstruction as the drugs are commonly wrapped in aluminium foils, cellophane paper or condom etc. in such cases, abdominal radiographs help in revealing the physical characteristics of the wrapping material together with the nature of the drug contained therein. This helps the physician in deciding the protocol of management.
hypotension is also present in cases. There is development of withdrawal symptoms with maximum intensity within 2-3 days of withdrawal (iii) Cocaine type—In this type of dependence there is desire to continue taking the drug but there is no tolerance. Psychological dependence is present and there are no withdrawal symptoms (iv) Cannabis type—In this type also there is no tolerance and there are no withdrawal symptoms. There is no desire to increase the drug dose also (v) Amphetamine type—This type may be combined with barbiturates. There is increased desire to take the drug and there is a tendency to increase the dose. Tolerance and psychic dependence is present. No abstinence syndrome is seen and continuous use may lead to toxic psychosis.
Drug Dependence
Withdrawal symptoms: These are the symptoms, which are seen due to sudden stoppage of the regular supply of drugs. Usually the symptoms start within 6-8 hours following stoppage of drug but may be delayed depending on the type of drug. The intensity of withdrawal symptoms depend upon the dose and type of drug, duration of addiction and whether the drug has been withdrawn suddenly or gradually
According to WHO recommendations of 1964, drug addiction and drug habituation should be substituted by the term ‘drug dependence’ meaning deviation from normal social behaviour of the patient under the influence of drugs. Addicts initially use the drug for some disease but gradually they develop the habit and become dependent on it as they find the drug an easy cure for the various diseases. They may also use the drug for their narcotic effect. Types of dependence: WHO has recognized five types of dependence (i) Morphine type—In this type of dependence there is an overpowering craving for the drug, which tends to increase with time. There is tendency to increase the drug. Tolerance & cross-tolerance is seen in this type of dependence. The drugs are usually taken by intramuscular, intravenous route or by sniffing. Withdrawal symptoms develop if the drug is withdrawn over a period of hours. Death may result from arrythmias (ii) Barbiturate type—There is a strong desire to continue taking the drug. Tolerance develops to high doses of the drug. Crosstolerance is seen in this type also and postural
Acute signs and symptoms: (i) Loss of weight and appetite (ii) Unsteady gait (iii) Tremors (iv) Reddening of eyes (v) Puffiness of eyes (vi) Slurring of speech (vii) Impairment of memory and concentration.
Early symptoms: (i) Chilliness (ii) Sensation of cold (iii) Uneasiness (iv) Rhinorrhoea (v) Yawning. Late symptoms: (i) Respiration: rapid and laboured (ii) Loose skin (iii) Lachrymation (iv) Gross tremors (v) Dilated pupil (vi) Anorexia. Third stage: Final stage of sleep lasting for 8-16 hours is seen and on awakening all the previous symptoms become intense. Other symptoms produced are: (i) Fever (ii) Tachypnoea (iii) Hypertension (iv) Pain and cramps in legs (v) Perspiration (vi) Diarrhoea & vomiting In new borne: Newborns of addicted mothers develop withdrawal symptoms within 1-56 hours of birth in the form of hyperactivity, convulsions and twitching.
642 Textbook of Forensic Medicine and Toxicology Causes of deaths in drug abuse Most of the drug addicts die as result of complications of drug administration such as: (i) Infection and septicemia (ii) Endocarditis (iii) Hepatitis (iv) Tetanus (v) Pulmonary and cerebral abscess (vi) AIDS complications (vii) Suicidal tendency from overdose of drugs during withdrawal of certain drugs particularly amphetamine (viii) Person may die due to electrocution, fall resulting in head injury or fall in water (drowning) under the effect of drugs (ix) Accidental aspiration of food, vomitus or artificial dentures resulting in choking. Autopsy Findings External: (i) The person is emaciated with a shabby appearance with lots of tattoos and scars over the body. (ii) The fingertips may be stained with different types of drugs used (iii) IV drug addicts known as main-liners show typical linear needle prick and scar marks usually over veins of cubital fossa, forearms, dorsum of hands, lower extremities, neck, and dorsal vein of penis (iv) S.C heroin drug users known as skin-poppers develop typical depressed, circular, atrophic scars and ulcers (v) The superficial veins in hands and legs and rarely in scalp, penis and popliteal area may be thrombosed due to the injections (vi) Punctate areas of tattooing are seen along the needle tracks due to deposition of carbonaceous material along the needle track (vii) Various recent and old injection sites may show zones of inflammation and perivenous fibrosis (viii) Multiple recent as well as scars of old healed abscesses may be seen (ix) Habitual inhalation of cocaine or heroin by snorting & snuffing may lead to perforation of nasal septum. Internal: (i) The gastro intestinal tract may still contain pills or capsules if they have been ingested recently. Active filler material like starch, talc or cellulose may be seen adherent to the gastric mucosa (ii) Microscopic examination of the various scars often shows foreign material like fibres of cloth, talc or dirt particles in the scar (iii) On repeated i.m and i.v injections, there is abscess formation in the muscle and at injections sites near the veins. The skin, subcutaneous tissue, muscle and vein surrounding the area of recent
injections along with the control from opposite side should be preserved in normal saline for chemical analysis (iv) Hepatic lymphadenopathy is a very common finding. The lymph nodes in the porta hepatis are enlarged and microscopically show non-specific hyperplasia (v) There is non-specific pulmonary edema, bronchopneumonia and aspiration of gastric contents. Froth is present in the upper respiratory tract and may be present over the nose and mouth (vi) Pulmonary hypertension with right ventricular hypertrophy may be present due to presence of extensive microcrystalline pulmonary emboli (vii) The lungs appear congested and edematous (viii) IgM and IgG concentration is increased in the spleen and lymph nodes indicating acute and chronic antigenic stimulation. Treatment (i) Chlorpromazine/promethazine is given in 5% dextrose 8 hourly along with vitamin B complex (ii) For the treatment of pain proxyvan is given (iii) To treat insomnia, alprazolam or nitrazepam can be given (iv) After 3 days, Methadone, Naloxone, Naltrioxone can be given (v) By 2-3 week, the dose of Heroin is reduced gradually (vi) At the end of 3 week the drug is totally stopped and all other drugs tapered. Treatment of addiction: (i) Steps to guide abuser to come back to a sober way of life (ii) Gradual withdrawal of drugs (iii) Use of others drugs (iv) Keep a careful watch to avoid obtaining secrete supply of drugs (v) Person should be removed to an institution (vi) Administration of drugs like: Sedative, Benzedrine and hyoscine is beneficial (vii) Group and individual psychotherapy with counselling about bad affects of drugs on the patients and society (viii) Diverting the mind of the person by engaging physically/mentally in vocational courses (ix) Improving general health to the person with adequate nutrition and food (x) Symptomatic treatment. HALLUCINOGENS (Psychedelics) Hallucinogens are psychotomimetics, psychotogen, psychedelics or psychodysleptics. These are drugs that causes excitation of central nervous
Drug Abuse 643 system characterized by (i) Hallucination (ii) Mood changes (iii) Anxiety (iv) Sensory distortion (v) Delusion (vi) Depersonalization (vii) Increased pulse rate, temperature and Blood pressure (viii) Dilatation of pupil (ix) Psychic dependence and (x) Depressive or suicidal psychosis. Since prehistoric times man has used many natural products having hallucinogenic property. However, a number of synthetic compounds have also been formed. These are: (i) LSD (Lysergic Acid Diethyl amide) (ii) Mescaline (iii) Psilocybin and (iv) Phencyclidine. There is individual variation in response to these drugs but autonomic and perceptual reactions are prominent.
Signs of symptoms: Small doses of 20-25μg produces (i) Pupillary dilatation (ii)Increased blood pressure (iii) Hypereflexia (iv)Tremors (v) Muscle weakness.
Signs and symptoms: (i) Hallucinogens produce a dream like state with disorientation, loss of contact with reality (ii) There is distortion of visual perception such as swaying of the field of vision, objects appear distorted similar to images in a curved mirror and faces may appear grotesque. There is an awareness of intense luminosity of colour and on closing eyes colourful images appear to surge (iii) There is alteration of time sense and music appears tangible (iv) Ability to concentrate is impaired (v) Ataxia is not a prominent feature (vi) The person feels relaxed and is extremely happy; may sometimes laugh uncontrollably or become sad or weep (vii) With higher doses, panic reactions and sinking sensations are common.
Lysergic Acid Diethylamide (LSD)
Tolerance and dependence: Tolerance is readily induced by hallucinogenic drugs and cross tolerance has also been demonstrated. Physical dependence does not occur but psychological dependence varying from mild (occasional trips) to marked (compulsive abuse) does occur. Medicolegal aspects: Few of the hallucinogenic drugs are primary causes of death but some may lead to traumatic deaths because of the abnormal behaviour of the person who is under their influence. Lysergide It is psychomimetic, semisynthetic derivative of Ergot that acts at multiple sites in the central nervous system from the cortex to spinal cord.
Large doses produces (i) Dizziness (ii) Drowsiness (iii) Euphoria (iv) Colours may be heard (v) Sounds are visualized (vi) Time is passed to pass slowly (vii) Psychological dependence may develop (viii) Serious depression and (ix) paranoid behaviour. Treatment: (i) Antianxiety drugs should be given (ii) Barbiturates to be given (iii) It is better to talk to the patient.
It is also known by the names of Acid, microdot, purple haze, white lightning etc. LSD has derived its name from the German ‘lyserge saure diethlyamid’. It is the most powerful hallucinogen known to man. It is one of the indole alkaloid derivative; others being psilocybin and psilocin that is contained in the Mexican mushroom (Psilocybe mexicana). LSD was synthesized by Hofmann in 1938 who was working on the chemistry of ergot alkaloids and himself experienced its hallucinogenic effects. The properties of LSD were known in 1943. The discovery of psychedelic effects of LSD in 1947 led to an epidemic of LSD abuse during the 1960s. It is the most potent psychedelic and doses as low as 25-50 μg may induce profound psychological and physiological effects. The action of LSD may persist for 12-18 hours even though the half life of the drug is only 3 hours. Abrupt abstinence following continued use does not produce withdrawal signs and symptoms. The use of LSD for therapeutic purposes should be undertaken only with great caution. Signs and symptoms: LSD causes alteration in consciousness; there is dream like state and sense of unreality. Easily induces laughter and crying. There are visual and tactile hallucinations (i) Within minutes of oral administration of LSD, following symptoms are produced (i) Tachycardia (ii) Hypertension (iii) Pupillary dilatation (iv) Tremors and (hypereflexia) (ii) Within half an hour of oral
644 Textbook of Forensic Medicine and Toxicology intake, following symptoms are produced (i) Bizarre and conflicting perceptual and mood changes (ii) Visual illusions (iii) Synthesias (iv) Extreme lability of mood (iii) Time seems to pass very slowly (iv) Behaviour becomes disturbed with paranoid delusions (v) Flashbacks in which effects of LSD may be reexperienced without further exposure to the drug for several years (vi) Bad trip: It is a medical emergency associated with use of LSD consisting of panic episode and that may persist for 24 hours. Dose: (i) 1-3 μg/kg produces moderate effect and duration of action is 1-56 hours (ii) 20-100 μg produces the effect (iii) 14 mg is Fatal dose. Treatment: (i) Supportive measures (ii) Anxiolytic drugs in small doses (iii) Chloropromazine counteracts the effects of LSD. Medicolegal aspects: Individual intoxicated with LSD rarely present for medical help. The drug was most popular with the hippies in the West in the 1960s. The deaths are commonly attributed to the bizarre behaviour induced by the drug that can result in accidental and suicidal deaths. Suicidal and homicidal tendency occurs. The persons explore their own feelings. Mescaline Mescaline is a phenylalkyl amine that was isolated in 1896 from Mexican ‘Peyote cactus” Lohophora Williamsi growing in the deserts of Central America. Of the four alkaloids, alkaloids mescaline is most important. The extracts are used as an intoxicating drink called ‘Mescal buttons’. 3-15mg/kg produces the moderate effects and duration of action is 1-56 hours 200mg of Mescaline Sulphate produces intoxicating effects. This is the oldest known drug with a primary hallucinogenic action. Signs and symptoms: (i) Dilated pupil (ii) Static tremors (iii) Sweating (iv) Increased pulse rate (v) Visual hallucinations (vi) Disorientation of speech and time (vii) Other effects such as (i) Insomnia (ii) Vertigo and (iii) Headache are also produced (viii) Large doses produce symptoms of poisoning such as (i) nausea (ii) vomiting (iii)bloody diarrhoea
and shallow breathing (iv) BP is low and death is due to respiratory failure Phencyclidine Phencyclidine is also known by pseudonyms as Angel dust, Peace pill, Hog, Goon, Rocket fuel, Cadillac, Super grass etc. Phencyclidine (PCP) was developed for use as a anaesthetic in the late 1970s but was abandoned quickly because of an unacceptably high incidence of postoperative psychotic reactions. PCP (1-phenylcyclohexyl piperidine) is easily synthesized and several variants exist. It is usually smoked in combination with tobacco and less frequently with marijuana but it may also be ingested or injected. Phencyclidine binds to inotropic n-methyl-d-aspartate (NMDA) receptors in the nervous system, blocking ion current through these channels. The most common street preparation, angel dust, is a white granular powder that contains 50-100% of the drug. Signs and symptoms: 1. Pleasurable effects: (i) Initial euphoria and a feeling of dissociation (ii) Numbness (iii) Perceptual distortion (iv) Visual hallucinations. 2. Users may show: (i) Horizontal or vertical nystagmus (ii) Flushing (iii) Diaphoresis (iv) Hyperacusis. 3. Behavioural changes: (i) Distortions of body images (ii) Disorganization of thinking (iv) Feelings of estrangement. 4. Higher doses of PCP (5-10mg) may be complicated by: (i) Hypersalivation (ii) Profuse sweating (iii) Generalized seizures (iv) Prolonged psychotic reactions (v) Dystonias (vi) Hypoglycemia (vii) Rhabdomyolysis and acute renal failure. Diagnosis: (i) Determination of phencyclidine levels in the urine as PCP is excreted in the urine for a long time after ingestion and autopsy samples may also be positive for up to a week (ii) The levels of PCP in the serum are also diagnostic but CSF concentrations may be three to four times higher than those in the serum and may take much longer time to clear. Treatment: (i) Gastric lavage is helpful in achieving excretion of PCP from the body and gastric suction may be of some value by removing PCP secre-
Drug Abuse 645 ted in gastric juice and preventing its re-absorption (ii) Oral diazepam is preferred but chlorpromazine can be given if hypertension is there (iii) Diaphenhydramine i.m has been reported to abolish acute dystonic reactions (iv) Acidification of urine enhances renal elimination (v) Supportive measures including treatment of coma, convulsions and respiratory depression. Medicolegal aspects: (i) It is commonly smoked by sprinkling on parsley or marijuana leaves and the intoxication can result from this as cases have been reported in children who are in the same room with adult smokers (ii) It is sometimes use as an adulterant in expensive drugs of abuse such as cocaine (iii) Addiction may lead to violent behaviour, psychosis, suicidal and homicidal behaviour. TRICYCLIC ANTIDEPRESSANTS Tricyclic antidepressants and benzodiazepines, the ubiquitous sedatives and hypnotics are the major causes of clinical problems with drugs which depress the central nervous system. Imipramine was found during clinical trial in 1958 to selectively benefit depressed but not agitated psychotics. Tricyclics include (i) Imipramine (ii) Amitryptaline (iii) Nortriptyline (iv) Trimipramine (v) Doxepin (vi) Dothiepin, and (vii) Clomipramine. Mode of action: Tricyclic antidepressants have complex actions which account for the diverse nature of the features seen after overdosage. They inhibit the active uptake of biogenic amines noradrenaline (produces antidepressant action), 5hydroxytryptamine (produces antidepressant and sedative action) and dopamine (produces stimulant action) into their respective neurons. They however differ markedly in their selectivity and potency for the different amines. They are also potent anticholinergic and antiarrythmic activity. Signs and symptoms: Features of poisoning usually appear within an hour or so after an overdose and usually reaches maximum intensity in 4-12 hours. The features are: (i) Anticholinergic symptoms: (i) dry mouth (ii) constipation (iii) Epigastric distress (iv) Urinary retention (v) Dilated pupil and blurred vision and (vi) Palpitations are
produced Peculiar clumsy feeling (ii) Tiredness and light headedness (iii) Drowsiness and sleepiness (iv) Difficulty in concentrating (v) Unsteady gait (vi) Increased reflexes and extensor planter responses (vii) Tachycardia is due to anticholinergic and noradrenaline potentiating actions (viii) Postural hypotension is due to inhibition of cardiovascular reflexes (ix) ECG changes: T wave suppression or inversion is the most common consistent change (x) Arrhythmias occur due to interference with intraventricular conduction, combination of noradrenaline potentiating and acetylcholine blocking actions and direct myocardial depression that are major causes of death. Tolerance and dependence: Tolerance to the anticholinergic and hypotensive effects develop gradually, though antidepressant action is sustained. Psychological dependence on these drugs is rare as their acute effects are not pleasant. There is some evidence of physical dependence occurring when high doses have been used for long periods. Withdrawal symptoms: Withdrawal symptoms do occur on discontinuation of the drug that is why gradual withdrawal of these drugs should be done. The features such as malaise, chills, muscle pain may occur on discontinuation of the drug. Treatment: (i) Gastric lavage with administration of activated charcoal (ii) Supportive measures such as adequate oxygen inhalation and control of convulsions (iii) Correction of acidosis by bicarbonate infusion intravenously (iv) Physostigmine 0.5-2mg i.v. should be given to reverse the anticholinergic effects (v) To treat arrhythmias, propranolol or phenytoin should be used (vi) Diazepam may be injected intravenously to control delirium with auditory and visual hallucinations as well as convulsion that occur during recovery phase. AMPHETAMINES Amphetamines were first synthesized in 1887 but began to be therapeutically used only since 1930s. Amphetamines are drugs of abuse and are capable of producing but little or no physical dependence. Because of its abuse potential, its therapeutic administration is greatly restricted today.
646 Textbook of Forensic Medicine and Toxicology Ecstasy (methylenedioxymeth-amphetamine), was developed in 1914 and was used in as a conscious altering agent in psychotherapy. Mode of action: Amphetamines predominantly stimulate the central nervous system and maximum selectivity is exhibited by Dextroamphetamine and methamphetamine, which in the usual doses produce few peripheral effects. They also cause stimulation of respiratory system especially when it is depressed. They inhibit hypothalamic feeding centre and also have a weak anticonvulsant, analgesic and antiemetics actions. Derivative of amphetamines: The derivatives of amphetamine are (i) Methamphetamine, (ii) Dextroamphetamine, (iii) Fenfluramine, (iv) Phentermine, (v) Mephentermine, (vi) Methyl phenidate, and (vii) Synthetic amphetamines (‘Designer drugs’)—Methylenedioxymeth-amphetamine (MDA or ‘Love drug’) and Methylenedioxyethamphetamine (MDEA or ‘Ecstasy’). Signs and symptoms: (i) Alertness and increased concentration (ii) Initial euphoria and more extrovert behaviour (iii) Increased talkativeness with rapid speech (iv) Increased work capacity with allaying of fatigue (v) Improvement of athletic performance initially followed by further deterioration (vi) Stimulation of reticular activating system causing wakefulness and postponement of sleep deprivation induced physical (vii) Hunger is suppressed (viii) Tremors (ix) Pupils are dilated (x) Tachycardia and hypertension are not so significant (xi) High doses produces euphoria, marked excitement, that may progress to metal confusion, delirium, hallucinations and an acute psychotic state (xii) Peripheral component of toxicity include vasomotor effects, palpitation, arrhythmias, vomiting, abdominal cramps and vascular collapse (xiii) Death is uncommon and is usually preceded by convulsions and coma. Autopsy findings: (i) No specific findings (ii) Cerebral or subarachnoid haemorrhage from induced hypertension may be produced. Treatment: (i) Chlorpromazine should be used for
sedation (ii) β-adrenergic blockers are used to antagonize the peripheral sympathomimetic actions of amphetamines (iii) Acidification of urine helps in increased renal elimination of methamphetamine (iv) Supportive measures. Medicolegal aspects: (i) Acute overdosage is not so common (ii) Amphetamine abusers are generally teenagers seeking thrill or kick which is obtained on rapid i.v. injection and designer drugs are commonly abused by youngsters during parties (iii) Amphetamine abuse is also seen in athletes who use it to enhance their athletic ability and Amphetamine is one of the drugs included in the ‘dope test’ for athletes. BENZODIAZEPINES The benzodiazepines are one of the most important groups of psychotropic drugs. They are widely used as tranquilizers, sedatives and hypnotics. They include the following compounds: (i) Chlordiazepoxide (ii) Diazepam (iii) Temazepam (iv) Lorazepam (v) Triazolam (vi) Bromazepam (vii) Clonazepam (viii) Desmethyldiazepam (ix) Medazepam (x) Prazepam. Signs and symptoms: Benzodiazepines are one of the safe drugs when their overdosage occurs alone. Cases have been reported when as many as 70 tablets of any of them are unlikely to produce any thing more than mild effect in most adults. Many benzodiazepines have active metabolites that account for their prolonged sedative effects. Benzodiazepines potentiate the effects of other CNS depressants, particularly alcohol, tricyclic antidepressants and barbiturates. Flurazepam is most likely to produce significant CNS depression. The signs and symptoms that are produced are: (i) Drowsiness (ii) Dizziness (iii) Ataxia and slurred speech (iv) Respiratory depression (v) Hypotension and coma. Treatment: (i) Supportive measures (ii) Gastric lavage is doubtful (iii) Flumazenil, specific benzodiazepine antagonist in the dose of 0.5 mg i.v over 30secs and further 0.5mg over next 30secs can be repeated, if necessary.
45
Part 2—Forensic Toxicology
Asphyxiants Classification of Asphyxiant Gases Henderson and Haggard divided asphyxiant gases in to five groups: (i) Irritants: The gases in this group infiltrates the air passages or lungs or both and produces inflammatory changes, such as smoke, ammonia, formaldehyde and chlorine (ii) Chemical asphyxiants: These are gases that by combining with haemoglobin or by acting on some tissue constituents prevent oxygen from reaching the tissues, or from using it. These are hydrocyanic acid and carbon monoxide; produce histotoxic anoxia (iii) Simple asphyxiants: These are inert gases which, when breathed in high concentration act mechanically by excluding oxygen. These are carbon dioxide and nitrous oxide (iv) Volatile drugs: Have little or no irritant effect after absorption; they act as an anaesthetic agent or toxic to the liver, kidney etc. (v) Systemic poison: These are insecticides, arsine gas etc. CARBON MONOXIDE POISONING Sources of carbon monoxide gas: (i) Carbon monoxide is prepared by the decomposition of organic substances such as oxalic acids and formic acids by means of sulphuric acid (ii) Where there is incomplete combustion of carbonaceous material on carbon, carbon monoxide is produced (iii) It is found in the gaseous products from charcoal fires, salamanders, refineries, blast furnaces, limekilns, gas engines, water heaters, gas refrigerators and burning houses (iv) It is also generated up to 8% in Gunpowder, Dynamite explosion and coalmine explosion (v) In coal gas it is present in 4-10% (vi) When blown in to red-hot coal, it is 3040% (vii) In diesel engines, exhaust gas of motorcars and trucks, it is 7-13% that is represented
as 1% of carboxyhaemoglobin (viii) In city dwellers and smokers there is 3-5% of carboxyhaemoglobin (ix) The CO produced per minute by 20-horse power motorcar is approximately 1 cubic foot that is enough to render the atmosphere of small closed garage (10 × 20) feet poisonous in less than 10 minutes. Properties: Carbon monoxide is colourless, tasteless and lighter than air with a garlicky odour. It is a highly poisonous gas that is absorbed in to the lungs and combines with haemoglobin of the RBC in the blood and forms a stable compound carboxyhaemoglobin. The affinity of haemoglobin for Carbon monoxide is 240 times more than that of oxygen. Mechanism of action: Since Carbon monoxide has 200-300 times greater affinity for haemoglobin than oxygen, it displaces oxygen for haemoglobin and forms a stable compound known as carboxyhaemoglobin. It reduces oxygen content of blood and then of tissues. Since carboxyhaemoglobin does not take part in oxygen transport, symptoms of oxygen deprivation will follow inhalation of the carbon monoxide gas. Carbon monoxide acts as a chemical asphyxiant and it has a direct toxic effect on the myocardium. Since the main action of carbon monoxide is oxygen deprivation and not a toxic manifestation due to the carbon monoxide alone, the important factor is not the level of carboxyhaemoglobin in the blood but the percentage of the haemoglobin that is prevented from carrying oxygen. Normally after somatic death, cells near the capillaries continue to function by extracting oxygen from oxyhaemoglobin and cause blue staining. Nevertheless, in CO poisoning this cannot
648 Textbook of Forensic Medicine and Toxicology occur because the cells cannot break carboxyhaemoglobin compound. In potent cellular poisons such as cyanide, fluroacetate and freezing break the metabolism of cells so fast that they cannot extract oxygen from oxyhaemoglobin. In these cases, blood under the skin and tissues will remain cherry red due to oxyhaemoglobin. Some people are in a metabolic state in which they can withstand the oxygen lack better than the others are. This is the reason why some persons may recover and live with a level of carbon monoxide that would be lethal to others. It must be taken into consideration also that patients with anemia, coronary artery sclerosis and pulmonary disease are much less able to tolerate oxygen lack. Medicolegal Aspects (i) Carbon monoxide poisoning is mostly accidental. The diseased, drugged and drunk persons are involved more in the poisoning. The poisoning usually occurs in ill ventilated rooms where incomplete combustion of wood or coal occurring and the persons’ sense of smell and hearing are impaired. It can also occur in dwellings with faulty fittings with leaky gas pipes and taps. In small garages people die from the gas from the motor exhausts. The poisoning can also result in narrow streets where there is dense traffic. Some sexual deviants may also be poisoned when they inhale coal gas. In suspected cases of poisoning air samples should be taken for analyses of Carbon monoxide. In deaths due to fire >50% concentration is of carboxyhaemoglobin. In some victims with blood carboxyhaemoglobin concentration of 15-20%, the symptoms similar to drunkenness are produced (ii) Sometimes Carbon monoxide poisoning may be confused with vehicular accidents (iii) The presence of occasional bullous lesions similar to the 3rd degree burns on the body is diagnostic of CO poisoning (iv) The tendency of the dying person to become wild may cause an impression of violent quarrel, can cause an erroneous suspicion of murder (v) Carbon monoxide poisoning is suicidal mostly in western countries when the room is closed after placing the fire; in the garage the exhaust fumes are inhaled through a pipe or sometimes the gas is inhaled through the gas taps. It is sometimes associate
with suicidal pacts, e.g., the mother ends life along with her children (vi) The poisoning is very rarely homicidal unless drink, drugs or disease incapacitates the person when a gas tap is opened when the person is sleeping in the bedroom (vii) Carbon monoxide with chlorine leads to the formation of carbonyl chloride—phosphene that is war gas (viii) Putrefaction has a little effect on the carboxyhaemoglobin as it is extremely stable, may be detected in the blood after several days even up to seven months after death. Types of Poisoning The Carbon monoxide poisoning can be: 1. Acute poisoning: The acute poisoning is further divided depending on the percentage of carboxyhemoglobin in the blood. The percentage of CoHb is 10-30 % (mild poisoning), 3040% (moderate poisoning) and severe (>40%). 2. Chronic poisoning: The toxicity depends upon (i) Concentration (ii) Duration of exposure (iii) General health of the person. Signs and Symptoms The signs and symptoms run parallel to the percentage of saturation of CO in the blood. The effects produced are those of suboxia.The symptoms are not noticeable until 20% saturation of haemoglobin occurs. The central nervous system is the first to be affected. (1) When the gas is inhaled in concentrated form: (i) Sudden weakness and dizziness is followed by coma and death due to respiratory failure (ii) Pale or cyanosed appearance (iii) Colour of the skin is cherry red due to carboxyhaemoglobin; the colour is characteristic of the poisoning but its absence by no means excludes it (iv) Coma may last for 3-5 days, sometimes even longer so bronchopneumonia and oedema of the lungs occur. (2) When the gas is inhaled in dilute form: (i) Tightness of the forehead (ii) Dizziness (iii) Agitation (iv) Muscular weakness (v) Emotional instability and confusion (vi) Lethargy (vii) Slurred speech (viii) Dilated and fixed pupil (ix) Coma (x) Sudden apnea and death (xi) In some cases rapid and feeble pulse, low BP and tremors are seen (xii) Myocardial ischemia, infarction and arrhythmias have also been reported. ECG findings
Asphyxiants 649 are suggestive of Prolonged PR interval, A-V block, Bundle branch block, Prolonged QT interval and ST depression (xiii) Liver is enlarged (xiii) There is tendency to bleed resulting in retinal haemorrhages and papilloedema (xiv) increased sweating (xv) Glycosuria and albuminuria is there. (3) When recovered after prolonged illness: Due to hypoxic changes in the brain, nervous and mental symptoms are produced, that are (i) Cerebral haemorrhage (ii) Encephalitis (iii) Optic neuritis (iv) Retrograde amnesia (v) Mental confusion. (4) There is formation of bulla in CO poisoning, these are discrete and isolated, contains thick and cellular fluid with an inflammatory ring around them. The bullous eruptions can be localized by external pressure and are produced due to sudden hypoxia. (5) The presence of other diseases like respiratory diseases or severe anaemia with barbiturate etc reduces the lethal concentration of the Carbon monoxide. (6) Physical activity during the exposure increases the rate of saturation; children saturate their blood more rapidly due to increased rate of respiration. (7) Depending on the concentration of carboxyhaemoglobin in the blood, following signs and symptoms are produced (Table 44.1). Diagnosis of Carbon monoxide poisoning: (i) Presence of smell of utility gas on the victim’s clothing (ii) Exposure is fairly sudden (iii) Face is livid or sweaty (vi) Cherry red colouration of skin (v) Blood is highly saturated with CO (vi) No anaemia (vii) Cyanosis is present (viii) Cheynestroke breathing in comatose patients (ix) In mild cases, little involvement of the cardiovascular system with raised pulse and Blood Pressure (x) In severe cases, low BP; thready and irregular
pulse with extrasystoles (xi) Heart dilates rapidly after exposure and death is due to acute circulatory failure (xii) Pupils are dilated, loss of light reflex occurs late, and other reflexes are decreased (xiii) In deep coma extensor planter response is there, limb reflexes and muscle tone are lost (xiv) There is hyperpyrexia and neurological involvement (xv) In the urine glycosuria and albuminuria occurs (xvi) Bullous eruptions on the skin are seen on the pressure areas (xvii) On spectroscopic examination of blood, the line that is nearer to ‘D’ is half of the other and is unchanged after the addition of ammonium sulphate. Concentration of carbon monoxide in the air: In the atmosphere: (i) 0.01%→safe limit (ii) 0.020.05%→produces toxic symptoms (iii) 0.25-3.0 or 3.33%→is fatal to an adult within 4 hours. Chronic Carbon Monoxide Poisoning This results from the intermittent exposure to the gas in the workers of automobile workshops, gas houses, and steel plant blast furnaces and in the persons staying in ill ventilated rooms for a long time. The following signs and symptoms are produced: (i) Dull frontal headache (ii) Nausea and vomiting (iii) Digestive disturbances (iv) Palpitations (v) Dyspnea (vi) Loss of memory (vii) Anaemia (viii) Visual disturbances (ix) Ataxia (x) Tachycardia (xi) Hepatomegaly (xii) Skin lesions (xiii) Angina (xiv) Mental symptoms (xv) Polycythemia. Treatment 1. Prophylactic: The industry and domestic plants should be properly installed and well
Table 44.1: Signs and symptoms produced depending on % saturation of Carboxyhaemoglobin CoHb level in % saturation 80%
Signs and symptoms No appreciable symptoms Breathlessness on moderate exertion, mild headache & tightness across forehead Throbbing headache, irritability, emotional instability, defective memory, rapid fatigue and lethargy Severe headache, nausea & vomiting, dizziness and confusion and dimness of vision Increasing confusion, hallucinations, severe ataxia like a drunk and rapid respiratory collapse Syncope and coma with convulsions, tachycardia, and tachypnoea Coma is increased with incontinence of urine and feces Prolonged coma, weak thready pulse, absent reflexes and convulsions Rapid death from respiratory arrest
650 Textbook of Forensic Medicine and Toxicology maintained. Adequate ventilation should be maintained and special masks should be used, 2. Therapeutic: (i) Removal of the patient to fresh air (ii) Clearing of the airway by suction (iii) Mouth to mouth respiration should be given (iv) 100% Oxygen inhalation can be employed through the mask for greater dissociation of carboxyhaemoglobin. Some advocate the use of 5%CO2 and 95% O2 (v) In serious cases, 0.5-1% adrenaline sulphate and 5ml of 25% solution Should be given intravenously for half to one hour and repeated (vi) Antibiotics should be given to combat infection (vii) Dehydration should be corrected (viii) In cases of acute heart failure, i.v digoxin to be given (ix) CSF pressure taken by lumbar puncture, if elevated then 500 ml of 10% mannitol i.v and furosemide to be given to relieve cerebral oedema (x) The body should be kept warm by hot water bottles and blankets (xi) In cases of severe collapse: (a) Normal saline should be administered subcutaneously (b) Hypothermia or exchange transfusion may be helpful (c) If cerebral oedema is there, 500 mL of 20% mannitol and corticosteroids should be administered (d) Procaine hydrochloride 500mg in 500ml of 5% dextrose i.v once a day should be given for 7days (e) Cytochrome C should be administered intravenously (f) Patient should be kept in a chamber filled with hyperbaric oxygen at two atmospheric pressure; the oxygen dissolved in the plasma is raised from 0.25 to 3.8-vol% and rate of dissociation of CO for haemoglobin is greatly increased. The disadvantages of hyperbaric oxygen are oxygen poisoning, pulmonary oedema and haemorrhages (g) After the breathing is established, tea and coffee is given and antibiotics. A man when brought to normal oxygen atmosphere, the carboxyhaemoglobin level reduces to half in 4 hours and with 100% oxygen inhalation, the carboxyhaemoglobin concentration reduces to half in just 40 minutes. Prognosis: (i) A close watch should be kept on the complications like renal failure, gangrene,
pulmonary oedema and progressive paralysis due to hypoxia and local pressure (ii) The neurological sequel is well known but may leave residual disability after 20-30 days (iii) If the degree and duration of hypoxia has damaged vital centers, the period of coma may be prolonged but may be followed by complete or partial recovery (iv) Muscle rigidity and increased tone of limbs in severe poisoning (v) Persons more than 60 years of age and coma for 24 hours usually succumb to its effects (vi) Repeated exposure may lead to polycythemia. Autopsy Findings External findings: (i) Bright red colour of the lips, and fingertips (ii) Postmortem staining is cherry red in colour; to be differentiated from cold exposure and cyanide poisoning (iii) Fine froth is present at mouth and nostrils (iv) Muscle necrosis and skin blebs are present. Internal findings: (i) Blood is cherry red and fluid (ii) Mucous membrane is red in colour (iii) Hyperemia is general and serous effusions are common (iv) Lungs are congested and oedematous, consolidations may be present (v) Heart shows haemorrhages and necrotic changes (vi) Brain has serous effusions in the ventricles, punctiform haemorrhages in the white matter and softening in the cerebral cortex, globus pallidus and corpus striatum. The bilateral symmetrical necrosis of ventricular nuclei is present. Brain is oedematous (vii) Renal failure is the pathological evidence. CARBON DIOXIDE POISONING The carbon dioxide intoxication usually results from the physiological disturbances. The gas may disperse slowly if ventilation is poor. The carbon dioxide gas may also be: (i) Formed during fermentation reactions (ii) Found also in grain bins, caves, ships’ holds and in fires (iii) Released from water in wells by changes in atmospheric pressure (iv) Released from some fire extinguishers (v) Released from dry ice. Features of hypoxia are prominent in carbon dioxide poisoning.
46
Part 2—Forensic Toxicology
Biological and Chemical Warfare Agents Chemical Warfare Chemical warfare is warfare (and associated military operations) using the toxic properties of chemical substances to kill, injure or incapacitate an enemy. They are also used in civilian conditions to disperse unruly mobes. Chemical warfare is different from the use of conventional weapons or nuclear weapons because the destructive effects of chemical weapons are not primarily due to any explosive force. The use of nonliving toxic products produced by living organisms (e.g., toxins such as botulinum toxin, ricin or saxitoxin) is considered chemical warfare under the provisions of the Chemical Weapons Convention. Under this Convention, any toxic chemical, regardless of its origin, is considered as a chemical weapon unless it is used for purposes that are not prohibited. Biological warfare: The offensive use of living organisms (such as anthrax) is considered to be biological warfare rather than chemical warfare. Chemical weapon agents: A chemical used in warfare is called a chemical weapon agent (CWA). About 70 different chemicals have been used or stockpiled as chemical weapon agents during the 20th century. These agents may be in liquid, gas or solid form. Liquid agents are generally designed to evaporate quickly; such liquids are said to be volatile or have a high vapor pressure. Many chemical agents are made volatile so they can be dispersed over a large region quickly. Chemical weapons are classified as weapons of mass destruction by the United Nations, and their production and stockpiling was outlawed by
the Chemical Weapons Convention of 1993. Under the Convention, chemicals that are toxic enough to be used as chemical weapons, or may be used to manufacture such chemicals, are divided into three groups according to their purpose and treatment: Schedule 1: Have few, if any, legitimate uses. These may only be produced or used for research, medical, pharmaceutical or protective purposes (mustard gas, lewisite). Schedule 2: Have no large-scale industrial uses, but may have legitimate small-scale uses (dimethyl methylphosphonate, a precursor to sarin). Schedule 3: Have legitimate industrial uses (phosgene, chloropicrin). The earliest target of chemical weapon agent research was not toxicity, but development of agents that can affect a target through the skin and clothing, rendering protective gas masks useless. In July 1917, the Germans first employed mustard gas, the first agent that circumvented gas masks. Mustard gas easily penetrates leather and fabric to inflict painful burns on the skin. Classes of chemical weapon agents: Chemical weapon agents are organized into several categories according to the manner in which they affect the human body. The names and number of categories varies slightly from source to source, but in general, types of chemical weapon agents are as follows. There are other chemicals used militarily that are not technically considered to be chemical weapon agents, such as: 1. Defoliants that destroy vegetation, but are not immediately toxic to human beings. (Agent
652 Textbook of Forensic Medicine and Toxicology Orange, for instance, used by the United States in Vietnam, contained dioxins and is known for its long-term cancer effects and for causing genetic damage leading to serious birth deformities.) 2. Incendiary or explosive chemicals (such as napalm, extensively used by the United States in Vietnam, or dynamite) because their destructive effects are primarily due to fire or explosive force, and not direct chemical action. 3. Biological warfare agents that includes the viruses, bacteria, or other organisms. Chemical weapon agents are also divided into lethal and incapacitating categories. A substance is classified as incapacitating if less than 1/100 of the lethal dose causes incapacitation, e.g., through nausea or visual problems. The distinction between lethal and incapacitating substances is not fixed, but relies on a statistical average called the LD50. Although crude chemical warfare has been employed in many parts of the world for thousands of years, modern chemical warfare began during World War I. Initially, only well-known commercially available chemicals and their variants were used. These included chlorine and phosgene gas. The methods of dispersing these agents during battle were relatively unrefined and inefficient. Use of Poison Gas in World War I The French were the first to use chemical weapons during the First World War, using tear gas. The first full-scale deployment of chemical weapon agents was during World War I, originating in the Second Battle of Ypres, April 22, 1915, when the Germans attacked French, Canadian and Algerian troops with chlorine gas. Chemical Warfare in World War II During World War II, chemical warfare was revolutionized by Nazi Germany’s accidental discovery of the nerve agents tabun, sarin and soman. The Japanese used mustard gas and the recentlydeveloped blister agent Lewisite against Chinese troops. During these attacks, the Japanese also employed biological warfare by intentionally spreading cholera, dysentery, typhoid, bubonic plague, and anthrax.
Developments by the Western Governments In 1952 the U.S. Army patented a process for the “Preparation of Toxic Ricin”, publishing a method of producing this powerful toxin. Also in 1952, researchers in Porton Down, England, invented the VX nerve agent but soon abandoned the project. In 1958 the British government traded their VX technology with the United States in exchange for information on thermonuclear weapons; by 1961 the U.S. was producing large amounts of VX and performing its own nerve agent research. This research produced at least three more agents; the four agents (VE, VG, VM, VX) are collectively known as the “V-Series” class of nerve agents. Classification of the Warfare Agents Poisons used as war gases can be classified according to their primary physiological actions as: Lung irritants (Asphyxiants or choking gases): (i) Chlorine (ii) Phosgene (iii) Chloropicrin (iv) Diphosgene. Lacrimators (Tear gases): (i) Chloroacetophenon (C.A.P) (ii) Bromo-benzyl cyanide (B.B.C.) (iii) Ethyl-iodo-acetate (K.S.K). Vesicants (Blister gases): (i) Mustard gas (ii) Lewisite. Sternutators (Nasal irritants or vomiting gases): (i) Diphenyl-chlorarsine (D.A.) (ii) Diphenyl-aminechlorarsine (D.M.) (iii) Diphenyl-cyan-arsine (D.C.). Paralysants (Nerve poisons): (i) Carbon monoxide (ii) Hydrocyanic acid (iii) Hydrogen sulphide. Nerve gases: These are toxic chemicals having acetylcholine like action. Lung Irritants These are irritant gases that exert their main action on the pulmonary alveoli through the upper respiratory passage. Of these, chlorine and phosgene are the gases that are kept liquid under pressure. Chlorine has bleaching powder like smell whereas phosgene has musty odour. These can be released from tanks, gas shells and canisters. Chloropicrin is a yellowish oily liquid having flypaper like odour and Diphosgene is also an oily liquid with smell of phosgene. Bothe phosgene
Biological and Chemical Warfare Agents 653
47
Part 2—Forensic Toxicology
Agrochemical Poisons Various pests, fungi, weeds and rodents cause much harm to the production and storage of food grains. A large number of pesticides including insecticides, rodenticides, herbicides and fungicides are available in the market. They enable the farmers to control their crops, from being destroyed by insects, diseases and weeds. As a result, though the yields of food crops have reached new high levels but their extensive use by the agriculturists has resulted in poisoning of human beings and domestic animals.
Since the growth of undesirable herbs and weeds in the field yields low production, the herbicides or weed killers are used to protect the field. These are: (i) Sulphuric acid (1%); is a corrosive acid (ii) Sodium chlorate; is irritant (iii) Potassium cyanide; causes tissue anoxia (iv) Paraquat.
Thallium (d) Phosphorus (ii) Organic compounds (a) Fluoro-acetate (iii) Convulsants (a) Strychnine (iv) Anticoagulant (a) Warfarin. Insecticides are further classified according to their toxicity as: 1. Virtually Harmless (i) Pheno-oxalic acid (ii) Copper oxide—fungicide (iii) Lime sulphur— orchard fungicide (iv) Petroleum washes— orchard insecticide 2. Comparatively Harmless (i) Sulphuric acid 20%—weed killer (ii) Sodium chlorate—mass herbicide 3. Mildly toxic (25-60gm) (i) Chlorinated hydrocarbons (ii) DDT (iii) Gammaxene (iv) Aldrin, dieldrin: used to control flies, louse, tick and as an agricultural insecticide. 4. Moderately toxic (10-25 gm) (i) Diazinon 5. Highly toxic (i) Sodium arsenite (ii) Lead and calcium arsenate (iii) Organic polyphosphates (iv) Organophosphorus compounds which include (a) HETP (Hexa Ethyl tetra phosphate) (b) TEPP (Tetra Ethyl pyro phosphate) (c) Parathion.
Insecticides
ORGANOPHOSPHORUS COMPOUNDS
Insecticides are the compounds that are employed for killing insects, are classified as: (1) Organophosphorus compounds (i) Alkyl phosphates (ii) Aryl phosphates 2. Halogenated hydrocarbons (i) Aldrine (ii) Endrine (iii) DDT 3. Miscellaneous compounds: (i) Mercurial salts (ii) Arsenic salts 4. Rodenticidal (i) Inorganic compounds (a) Aluminium phosphide (b) Zinc phosphide (c)
Historical considerations: The first organophosphate insecticide was tetraethyl pyrophosphate (TEPP) and it was developed in Germany as a substitute for nicotine, which was in short supply in the country during World War II and in 1944, Parathion was synthesized. They are extensively used as agricultural insecticides being affective against a wide range of insects and pests. Nevertheless, a number of these compounds have proved to be more toxic to human beings, than to the insects and rodents.
Fungicidal Fungicides preserve the seeds for seedling purposes. These are mainly mercurial compounds Herbicidal or Weed Killers
656 Textbook of Forensic Medicine and Toxicology Mode of Action Organophosphates cause some degree of irritation to mucous membrane. They are primarily nerve poisons affecting both autonomic and central nervous system. On autonomic nervous system, it exerts parasympathomimetic action by inactivating cholinesterase. Therefore, both muscarinic and nicotinic action of acetylcholine is increased. It causes depression of central nervous system Acetylcholine is recognized as mediator of impulses of autonomic ganglia. It is present in an inactive form that bounds loosely with a protein or lipoprotein. Acetylcholine as chemical transmitter plays a vital role to propagate nerve impulse across the synapses of peripheral and central nervous system. Traces of acetylcholine are produced at the myoneural junctions and synapses of the ganglions. On stimulation of the nerve, acetylcholine is set free and diffuses down the nerve fibers. These same nerve fibers contain an enzyme Choline acetylase that is capable of synthesizing acetylcholine with great rapidity. Free acetylcholine is unstable and gets spontaneously hydrolysed to Choline and acetic acid, the hydrolysis getting accelerated by the enzyme, acetylcholinesterase present in the plasma, cell membrane or cytoplasm of many cells of the body. In blood and nerve tissue, cholinesterase inactivates acetylcholine after its liberation as shown below: Acetylcholine ⎯⎯⎯⎯⎯⎯→Acetic acid + Choline Ach esterase
Cholinesterases are of two types namely true cholinesterase that is present in blood cells and central nervous system whereas plasma and white matter of brain contains pseudocholinesterase. Usually true cholinesterase inactivates acetylcholine but when excess of acetylcholine escapes in the blood, plasma or pseudocholinestrase also plays a role. Cholinesterases are most effective in the presence of small amount of acetylcholine. Organophosphorus compounds inactivate acetylcholinesterase by the process of phosphorylation to facilitate the action of acetylcholine. This occurs first at the plasma level then at the cellular level of brain. As a result, there is
accumulation of acetylcholine at the nerve endings resulting in interference at the passage of nerve impulses across the myoneural junctions and synapses of autonomic ganglions. As such, these compounds are known as Cholinesterase inhibitors. Hence, the action of organophosphorus will simulate actions of physostigmine, acetylcholine, Pilocarpine and muscarine. A drop in the activity of cholinesterase to 25-30% of the normal value will be characterized by signs and symptoms compounded as: (i) Muscarinic like effect on the parasympathetic system affecting the postganglionic cholinergic nerve fibres (ii) Nicotinic like actions followed by paralysis of preganglionic sympathetic fibres and somatic motor nerves (iii) Effect on central nervous system with stimulation followed by depression (iv) Porphyrinuria leading to shedding of red tears; Chromadocryorrhoea due to accumulation of porphyrin in the lachrymal gland. The organophosphorus compounds may cause: 1. Irreversible inhibition of cholinesterase due to: (i) Direct action—TEPP (ii) Delayed action—Parathion and Malathion 2. Reversible inhibition of cholinesterase: (i) Carbamates (a) Carbaryl (b) Mactacil Organophosphorus compounds are divided mainly in two groups: i. Alkyl phosphate (a) TEPP—Tetra ethyl pyrophosphate (b) HETP—Hexa ethyl pyrophosphate (c) Dimefox (d) Malathion (e) Sulfotepp (f) Systox ii. Aryl phosphates (a) Parathion (b) Paraoxon (c) Chlorothion (d) Methyl parathion (e) Diazion (f) Methyl umbeliferone Routes of Absorption (i) Absorption through intact skin (ii) Respiratory system by inhalation (iii) Gastrointestinal tract by ingestion (iv) Circulatory system by intra muscular and intravenous route. Signs and Symptoms 1. Muscarinic like effects: Muscarinic receptors for acetylcholine are found primarily in the smooth muscles, the heart, and exocrine glands. The muscarinic like effects produced by the organophosphorus compounds are: (i)
Agrochemical Poisons 657 Tightness in the chest (ii) Wheezing respiration (Expiration due to bronchoconstriction) (iii) Increased bronchial secretion (iv) Increased salivation (v) Increased sweating (vi) Tone and peristalsis is increased (vii) Nausea, vomiting and abdominal cramps (viii) Diarrhoea (ix) Tenesmus and involuntary defecation (x) Bradycardia and heart block (xi) Frequent and involuntary urination due to constriction of smooth muscles of bladder (xii) Constriction of pupil causing miosis 2. Nicotinic like symptoms: Nicotinic signs and symptoms result from the accumulation of acetylcholine at the endings of motor nerves to skeletal muscle and autonomic ganglia. The effects include: (i) Easy fatigability and mild weakness followed by involuntary twitching, fasciculation and cramps (ii) Muscles of respiration are affected leading to Dyspnea and cyanosis. Nicotinic action at autonomic ganglia masks the muscarinic effects, thus: (iii) Tachycardia is produced instead of bradycardia (iv) Pallor (v) Blood pressure is raised (vi) Hyperglycemia (vii) Cardiac arrhythmias (viii) Pulmonary oedema. 3. Accumulation of acetylcholine in central nervous system (i) Anxiety, tension and confusion (ii) Restlessness, insomnia and headache (iii) Irritability and neurosis (iv) Excessive dreaming and nightmares (v) Slurred speech and tremors (vi) Ataxia and convulsion (vii) Depression of respiratory and circulatory centers (viii) Coma leading to death. Fatal Dose TEPP is most toxic whereas HETP is the least toxic comparatively as 5 mg i.m or 25 mg taken orally of TEPP produces toxic symptoms. The fatal dose of various organophosphorus compounds are: • TEPP→50mg i.m or 100mg oral • Parathion→80mg i.m. or 100-175mg oral • HETP→160mg i.m. or 350 mg oral • OMPA→ 80 mg i.m. or 175 mg oral • Malathion & Diazinon (Tik20)→1gm oral.
Fatal Period→In fatal doses symptoms start within half an hour and death occurs within three hours. In non-fatal cases, effects last for 36 hours and fade off in 48-72 hours to 3 weeks. Blood cholinesterase level drops to 22-28% that is up to 50% of the normal value. Normal value is 77-142 units in red blood cells that is more appropriate than the plasma levels of 41-140 units. About 3% of the population suffers from congenital cholinesterase deficiency and the level decreases in patients with severe liver disease. Diagnosis 1. Cholinesterase level in blood: As organophosphates inhibit cholinesterase activity, level of cholinesterase should be estimated in the blood. The normal level of cholinesterase is about 40 - 142 in red cells and 90- 140 in the plasma. In organophosphorus poisoning, the cholinesterase activity of blood and plasma falls by 25- 85 % of its normal value. Periodic measurements of blood cholinesterase level helps in detection of poisoning because marked depression of cholinesterase activity of blood occurs, before the symptoms become evident. Normally the symptoms may not appear until the level of cholinesterase falls by 20% or less. Five ml of heparinised blood should be collected for estimating level of cholinesterase in blood. 2. The cholinesterase level in the motor end plate: The cholinesterase level can be demonstrated histochemically in muscles kept at room temperature for 1–2 days and up to several months when kept at 4o C. The cholinesterase activity at the myoneural junction is not affected by embalming the body or if the tissue is fixed by formalin or acetone up to 24 hours. 3. Test by atropine: When 2 mg of atropine is given intravenously, there are signs of atropinisation in a normal individual, while in a case of organophosphorus poisoning it will have no effect. Treatment 1. Removal the patient from the source of exposure.
658 Textbook of Forensic Medicine and Toxicology 2. Strip off contaminated clothing 3. Wash all parts with soap and water under the shower bath. 4. Give life supporting measures such as oxygen inhalation 5. Gastric lavage with 2% potassium permanganate 6. Purgatives like sodium or magnesium 30gm orally 7. Dehydration and shock must be treated 8. Diazepam intravenously should be given to control convulsions 9. Morphine and aminophylline are not to be given 10. Exchange transfusion: It takes 2-3months for complete recovery after exchange transfusion. Blood cholesterol level should be checked every 15days 11. Atropine sulphate is the readily available best-known antidote against all organophosphorus compounds. It inactivates acetylcholine, arrests muscarinic and other effects but not the nicotinic action. Atropine sulphate, 2-4mg is given I.V or I.M in adults and 0.05 mg/kg in children. The dose is to be repeated as 2-4mg i.m. every 20-30 minutes until full atropinization is achieved. Then the dose has to be decreased and given less frequently. The repetition of dose of atropine depends upon severity of case: • In mild cases, 2-4mg i.m/i.v. initially that is to be repeated after 20 minutes as 2mg and then repeated again. • In moderate cases, 2-4mg i.m/i.v. that is to be repeated after 10 minutes interval. • In severe cases, 4-6 mg i.m/i.v. that is to be repeated after 3-10 minutes interval and then 50 mg is administered in 24 hours. • Usually 40-50 mg may be required during first 24hours and 12 mg may be given safely in the first 6 hours. Signs of Atropinization (i) Flushing of face (ii) Dry mouth and dry, warm skin (iii) Blurring of vision (iv) Dilatation of pupil (v) Rapid and
irregular pulse (vi) Loss of neuromuscular coordination Precautions while Atropinization: (i) Adequate oxygen therapy should be given simultaneously to prevent myocardial infarction (ii) The drug should be withdrawn judiciously there may be rapid development of pulmonary oedema and respiratory (iii) Atropine is ineffective against autonomic ganglionic actions of acetylcholine and peripheral neuromuscular paralysis (iv) To combat overdosage of atropine, physostigmine salicylate should be administered in the dose as given below: • In adults, 1-2 mg i.m/iv; to be repeated up to a total of 6 mg. • In children, 0.5 mg i.m/iv; to be repeated up to a total of 2 mg. The dose of atropine should be reduced when oximes are given together. 12. Specific Reactivator Oximes: Relief of muscle weakness in particular respiratory paralysis can be achieved with certain Oximes, which can reactivate the cholinesterase by reversing the phosphate ester bond formed at the enzyme active site (Cholinesterases and organic phosphates are bound by phosphate bond). They should be used within 24 hours. They are superior to atropine but are not to be administered in Carbamate poisoning: i. PAM (Pralidoxime chloride): Protopam chloride is to be given 1gm I.V. over a period of 2 minutes or in 250 mL of normal saline infusion for 20-30 minutes that is to be repeated after 8-12 hours. In children 25-50 mg i.m or i.v/kg, body weight is to be given within 2 minutes or as an infusion for 20-30 minutes ii. P2AM (Pyridine-2-aldoxime methiodide) can be given as 50 mg/kg in one litre of normal saline slowly to be followed by another litre of same infusion over a period of 12 hours. iii. DAM (Diacetyl monoxime) can be given as 2 gm in one litre of normal saline slowly
Agrochemical Poisons 659 iv. P 2 S (Pyridine-2-aldoxime methane sulfonate) in the dose of 1-2 gm in adults and 25-50mg/kg in children. The dose is to be repeated every 12 hours. Adverse Reactions of Specific Reactivator Oximes: (i) When given intravenously, it produces tachycardia and muscular rigidity (ii) When given intramuscularly, conjunctival hyperemia is produced (iii) When given orally nausea, vomiting and diarrhoea may result. Autopsy Findings (i) Findings of asphyxia such as congestion of face and cyanosis of lips, nails and mucous membranes is present (ii) At times blood-tinged froth is found over the nostrils and mouth (iii) Smell of kerosene may be present on opening the oesophagus and stomach (iv) The mucosa of stomach is congested and submucosal petechial hemorrhages are present (v) Frothy fluid at times tinged with blood may be found in the trachea and bronchi (vi) The lungs show congestion and gross edema and submucosal hemorrhages (vii) The brain shows petechial hemorrhages, is congested and oedematous and the meninges are dilated. Prophylaxis from Organophosphorus Poisoning (i) The body should be properly protected while spraying in the fields with aprons, gloves and masks (ii) The agriculturist should not spray for more than 2-4hours a day and should not work for more than 6-7 successive days (iii) He should not eat, drink, chew or smoke while spraying (iv) After the operation, the face, hands, feet, eyes should be washed thoroughly with soap and water (v) Even the spraying machines, tanks or containers and hoses should be washed after each operation (vi) When the worker is suffering from upper respiratory tract infection, he should restrain from spraying Medicolegal Aspects (i) Accidental poisoning usually during manufacturing, spraying or dusting in the field and when mixed with other food stuffs. In the Kerala food poisoning tragedy in 1958, about 100 people died
due to inadvertent stocking of foodstuffs and parathion (ii) Less frequently used as homicidal poison (iii) Most commonly used for suicidal purposes next to barbiturates due to their easy availability, quick action, are cheap and can be easily purchased for domestic use. PARAQUAT POISONING Uses: Paraquat is an herbicide that is sprayed on unwanted weeds and other vegetation before planting crops. It is absorbed by the foliage and rapidly kills the plant, but is inactivated when in contact with the soil, so cannot harm the seeds or young plants that are placed in the same ground a short time later. Properties: Paraquat and the Diquat are both dipyridyl compounds and paraquat is 1 : 1 dimethyl 4 : 4 bipyridium. It is produced commercially as a brownish concentrated liquid of the dichloride salt at 10-30% strength. Both are water soluble herbicides supplied in 20-25% concentration in bulk to the farmers and horticulturists. Its is marketed under the trade name gamaxone or weedol. Toxicity: (i) Ingestion most commonly (ii)Inhalation through spraying of liquid stored in soft drink bottles (iii) Skin contamination. Fatal dose→4 mg/kg Fatal period→3-5 days. Signs and Symptoms (i) Paraquat is irritant to epithelial tissues in concentrated form and causes erosion of the mucous membrane of the lips, mouth, pharynx and oesophagus (ii) The lungs are usually affected because of aspiration of irritating liquid while regurgitation or swallowing (iii) Renal failure may develop within 2-3 days (iv) Death is due to failure of vital organs like liver, kidney. At times oesophageal perforation occurs resulting in mediastinitis. Laboratory Findings (i) Elevation of blood urea, serum alkaline phosphatases and bilirubin are characteristic of kidney and liver damage (ii) Serum trypsin inhibitor gets depressed indicating extent of damage to lungs.
660 Textbook of Forensic Medicine and Toxicology Treatment (i) Stomach wash using 4-7% bentonite-magma solution and repeated with caution and some of it is left in the stomach (ii) Activated charcoal should be given orally (iii) No known antidote (iv) Forced diuresis as early as possible to prevent renal damage (v) Hemodialysis to remove any poison left after forced diuresis (vi) Glucocorticoids for progressive lung proliferative lesions (vii) Supportive therapy (viii) Fullers earth or 7 % bentonite should be given. Autopsy Findings (i) Centrilobular necrosis of the liver with giant mitochondria and crystalline inclusion bodies are seen on electron microscopy (ii) Diffuse tubular damage of the kidneys (iii) Proliferative damage to the lungs is characteristic lesion of paraquat poisoning. When paraquat reaches the distal air spaces, diffuse pulmonary oedema and haemorrhages occur. Ulceration of mouth and lips may be present. Medicolegal Aspects (i) Suicidal by deliberate self ingestion of the liquid (ii) Accidental resulting from ingestion. CHLORINATED HYDROCARBON INSECTICIDES D.D.T (Chlorophenothane) is the most commonly used chlorinated hydrocarbon insecticide in agriculture and public health. The commonly used agents are Endrin, Aldrin, Chlordane, Dieldrin, Lindane (Gammexene), Methoxychlor, Toxaphene and D.D.D (Dichloro-diphenyl-dichloroethane). Even though some of the compounds individually exhibit differences in chemical configuration and physiological actions, from chemical standpoint, their effects on human beings are essentially the same and hence can be described in a group. Poisoning by Endrin is more common than D.D.T in rural India. D.D.T (Dichloro-diphenyl-trichloroethane) Properties: D.D.T is white crystalline powder with faint aromatic odour. It is insoluble in water but
soluble in kerosene, vegetable oil and other organic solvents. While dusting as powder, it is to be diluted to 10% with powdered chalk or kaolin. It can be used as spray in 5% solution diluted with suitable solvents. Uses: D.D.T acts as both insecticide and parasiticide to kill mosquitoes, flies, bed-bugs, lice, arthropods and other insects. They usually become resistant to D.D.T later on. Routes of Absorption: In pure solid form, it does not get absorbed through skin but when it is dissolved in kerosene oil or other solvents, it gets easily absorbed through the gastrointestinal tract, skin and lungs. A 2% solution of D.D.T acts as poison to human beings and its solution in fatty acids increase the toxicity. D.D.T powder is safe for dusting animals. Mode of action: (i) It first stimulates then depresses the cerebellum and motor cortex (ii) It sensitizes the myocardium to the action of catecholamines, so that injection of epinephrine may induce ventricular fibrillation (iii) It depresses adrenal cortex causing irritation and sensitization of the skin (iv) Locally it acts as an irritant, when swallowed (v) Chronic exposure causes liver necrosis, degeneration of renal tubules, myocardium and voluntary muscles Fatal Dose • D.D.T.→30 gm or 0.5gm/kg • Lindane→15 gm • Chlordane→30 gm • Methoxychlor→350 gm. Acute Poisoning The signs and symptoms develop within half an hour of ingestion of the poison: (i) Salivation, nausea, vomiting and abdominal pain (ii) Apprehension, hyperexcitability, restlessness, nervousness (iii) Tinnitus and vertigo (iv) Blurred vision with twitching of eyelids that is followed by muscular tremors, first affecting the head and neck, then involving the extremities (v) Tonic clonic convulsions are characteristic of D.D.T, Aldrin, dieldrin and lindane poisoning (vi) Generalised epileptiform convulsion occur in toxaphene poisoning (vii)
Agrochemical Poisons 661 Rarely muscular weakness, ataxia, incoordination, numbness and paralysis may occur (viii) Pulmonary oedema, respiratory distress, Fall of B.P, delirium and unconsciousness, coma and collapse (ix) Death occurs from respiratory failure. Chronic Poisoning After absorption, these insecticides gets accumulated in body fat and concentration gradually falls over several months. The workers with history of many months of exposure having more than 648 ppm of D.D.T in their fat suffer from chronic poisoning. The signs and symptoms are: (i) Anorexia, nausea and vomiting (ii) Cachexia, loss of weight, anemia (iii) Anxiety, headache, hyperirritability (iv) Blurred vision (v) Tremors, convulsions and coma (vi) Liver moderately enlarged. Treatment (i) Immediate gastric lavage with 0.2% potassium permanganate (ii) Emetics should be given (iii) No known antidote of D.D.T (iv) Cathartics, fats or oils should be avoided as they promote absorption (v) Atropine sulphate should be administered (vi) Oxygen inhalation and artificial respiration (vii) To control muscular twitching, tremors and convulsion, Thiopentone sodium 100-250mg i.v followed by i.m injection of 100mg of Phenobarbital sodium (viii) Calcium gluconate 10mL of 10% with glucose i.v and calcium lactate orally are beneficial (ix) Adrenaline, epinephrine should not be used as they induce ventricular fibrillation. Morphine is also avoided (x) For skin contamination, thorough washing with soap and water (xi) In chronic poisonings, the patient should be removed from the site of exposure and given low fat, high protein & carbohydrate die. The treatment is symptomatic. Autopsy Findings (i) Stomach contents may smell of kerosene and are blood-stained (ii) Mucosa of stomach and intestines is congested and haemorrhagic (iii) The liver is enlarged with fatty degeneration (iv) The lungs are congested and oedematous (v) Spleen, brain and kidneys are congested.
ENDRIN Properties: Endrin is the most toxic of all the chlorinated hydrocarbons. It is 12-15 times more toxic than D.D.T and 3 times more toxic than Aldrin and dieldrin. It is insoluble in water, sparingly soluble in alcohol and freely soluble in aromatic hydrocarbons and fats. It remains stable for months or years. Uses: Several preparations containing endrin are sold in the market in 20-25% concentration mixed with petroleum hydrocarbon. They all smell like kerosene. Endrin is also known as plant penicillin as it is a popular pesticide against insect pests of cotton, paddy, sugarcane and tobacco. It is used as spray in solutions, or as dust mixed with some other inert powders. It is marketed under the trade name Endox DR - 50 Trafdrine and Endrex. Absorption: Endrin is not absorbed through intact skin in dry powder state and poorly absorbed from the gastrointestinal tract mucosa but when it is dissolved in oil it gets freely absorbed from skin as well as mucous membrane Fatal dose→5-6gms Fatal period→Usually 1-2 hrs (1-2 days rarely) Mode of action: (i) Has no effect on cholinesterases (ii) It is neurotoxic primarily acting on central nervous system, causing respiratory failure. Signs and Symptoms (i) Salivation, nausea, vomiting and abdominal discomfort (ii) Apprehension, hyperexcitability, restlessness, nervousness, incoordination and ataxia followed by mental confusion and delirium (iii) Profuse frothing at mouth and nostrils (iv) Tonic clonic convulsions (v) Unconsciousness, coma and collapse and death from respiratory failure Diagnosis: to diagnose, chemical examination of blood and subcutaneous fat is undertaken Treatment (i) Immediate gastric lavage with 0.2% potassium permanganate (ii) Emetics should be given (iii) There is no known antidote of endrin (iv) Cathartics, fats or oils should be avoided as they promote
662 Textbook of Forensic Medicine and Toxicology absorption (v) Atropine sulphate should be administered (vi) Oxygen inhalation and artificial respiration (vii) To control convulsions, Thiopentone sodium 100-250mg i.v. followed by i.m injection of 100mg of Phenobarbital sodium should be given (viii) Calcium gluconate 10mL of 10% with glucose I.V. and calcium lactate orally are beneficial (ix) Adrenaline, epinephrine should not be used as they induce ventricular fibrillation. Morphine is also avoided (x) For skin contamination, thorough washing with soap and water (xi) In chronic poisonings, the patient should be removed from the site of exposure and given low fat, high protein and carbohydrate diet. The treatment is entirely symptomatic. Autopsy Findings (i) Congestion of face (ii) Cyanosis of lips and fingertips (iii) Conjunctiva is congested and pupils are dilated (iv) Blood stained frothy fluid discharge smelling of kerosene coming out of mouth and nostrils (v) Gastrointestinal tract is congested and stomach contents are bloodstained smell of kerosene is present (vi) Respiratory tract mucosa is congested, oedematous containing bloodstained frothy fluid mixed with mucus (vii) Lungs are congested and oedematous with subpleural ecchymotic patches (viii) Evidence of hepatic and renal tubular degeneration (ix) Blood remains fluid and dark for long (x) Subpericardial and subendocardial haemorrhages are seen (xi) Endrin resists putrefaction for a long time that is why it is be detected in the viscera for long after death. Medicolegal Aspects (i) For homicidal purposes, it may be given mixed with sweets, food and alcohol to mask its smell (ii) Suicidal use is quite common inspite of its unpleasant smell and painful death (iii) Accidental poisoning occurs commonly from skin contamination while spraying. NAPHTHALENE (TAR, CAMPHOR, C10H8) Properties: It occurs as large white crystalline plaques from coal tar distillation having a char-
acteristic odour. It is insoluble in water but freely soluble in ether, chloroform, alcohol and oils. It sublimes at ordinary temperatures. Uses: (i) It is used commercially as moth repellant, wool preservative and as deodorant in lavatories (ii) It is also used in the manufacture of indigo and azo dyes (iii) Chlorinated naphthalene is used for giving insulated coating on electrical wires and other electrical equipments. Mode of action: It produces haemolysis, causing blockade of renal tubules by precipitated haemoglobin and may cause hepatic necrosis. Only the patients with deficiency of glucose-6-phosphatedehydrogenase in the red cells resulting in low level of reduced glutathione and increased susceptibility to hemolysis by the metabolites of naphtha– lene. In children below 6 years absorption occurs quickly. Fatal dose→2 gm Fatal period→few hours to 2-3 days. Signs and Symptoms On ingestion of naphthalene: (i) Nausea, vomiting, diarrhoea, abdominal pain and hepatomegaly (ii) Burning micturition, pain in loin and hypogastrium, oliguria and haematuria (iii) Urine is dark brown containing albumin, casts and haemoglobin (iv) Acute nephritis, haemolytic anemia, jaundice and optic atrophy are characteristic features (v) Profuse sweating (vi) Headache, excitement, delirium, muscular twitchings and staggering gait (vii) Cyanosis, tachycardia and drowsiness resulting in coma, collapse and death (viii) Anemia and leucocytosis on hematological examination. On inhalation of naphthalene vapours: (i) Headache, malaise and tinnitus (ii) Photophobia, conjunctivitis, retina and choroid plexus are affected (iii) Nausea, vomiting (iv) Anemia and jaundice (v) Severe hyperthermia due to the formation of naphthylamine Contamination of skin: (i) Dermatitis with scaling-weeping-crusting of skin and pruritis (ii) Conjunctivitis (iii) Headache (iv) Anemia, jaundice and hematuria
Agrochemical Poisons 663 Treatment (i) Stomach wash with warm water to be followed by one ounce of saturated solution of magnesium sulphate (ii) Oily and fatty preparations should be avoided as dissolve the poison (iii) Whole blood transfusion followed by sodium bicarbonate 15gm orally every 4 hours or exchange transfusion will be helpful in nervous complications (iv) 5% Dextrose saline i.v for anuria (v) Glucocorticoids should be administered as they prevent naphthalene hemolysis (vi) Diet rich in proteins, carbohydrates and vitamins but poor in fat to be given. Autopsy Findings (i) Skin is pale and yellow due to anemia and jaundice (ii) Gastrointestinal tract mucosa is inflamed, congested and tinged yellow (iii) Larynx and trachea contains blood stained froth (iv) Kidneys are congested (v) Liver is enlarged and congested and showing features of fatty degeneration. Medicolegal Aspects (i) Accidental poisoning is common in children as they ingest naphthalene balls and in adults resulting from inhalation of naphthalene vapours due to heavy dusting of bed clothes (ii) Very few cases of suicide using naphthalene balls have been reported (iii) Homicidal poisoning is also quite rare. ALUMINIUM PHOSPHIDE Aluminium phosphide tablets are marketed under the names of ‘Celphos, ‘Alphos’ or ‘Sulphas’. It is known as the agent of sure death. A single grayish green tablet weighs 3gm mixed with urea and ammonium carbonate. Each tablet releases 1 gm of phosphine gas (PH3) Fatal dose→4-5 gm (1-3 tablets) Fatal period→12-36 hours. Mechanism of action: On exposure to air and moisture, the aluminium phosphide tablets releases phosphine gas ALP + 3H2O→Al (OH)3 + PH3 (Phosphene) Uses: Aluminium phosphide is widely used as fumigant to destroy grain insects and rodents. The tablets are removed from airtight containers and mixed with grains that on contact with moisture
and air, liberates phosphine and thus fumigates the grains. Signs and Symptoms Phosphine when inhaled by human beings results in severe pulmonary oedema. Due to the release of phosphine gas in contact with moisture, symptoms of severe gastrointestinal tract irritation are produced that cause cardiovascular collapse and death. The aluminium phosphide poisoning has a high mortality. The signs and symptoms produced because of aluminium phosphide poisoning are: (i) Nausea, vomiting and burning pain in the epigastrium: (i) Garlicky (fishy) odour from breath (ii) Intense thirst and diarrhoea (iii) Tightness in the chest and dyspnoea (iv) Excitement and agitation (v) ECG abnormalities—Sinus tachycardia, bradycardia and heart block) (vi) Oliguria (vii) Arrythmias (viii) Hypocalcaemia tetany, convulsions and coma (ix) Shock (xi) Hypotension (xii) Myocardial damage (xiii) Cold clammy skin with respiratory distress in terminal stages (xiv) Rarely muscular wasting, bleeding diathesis, cardiac complications like pericarditis, congestive cardiac failure (xv) Death occurs due to cardiac failure Chemical tests: The patient is asked to breath on a piece of filter paper in the form of mass impregnated with 0.1 N silver nitrate solution for a period of 5-10 minutes. If the paper is blackened, it indicates presence of phosphine in breath as silver nitrate is reduced to silver on exposure to phosphine. Management (i) There is no specific antidote of aluminium phosphide (ii) Early stomach wash using 3-5% sodium bicarbonate, 1% copper sulphate, 1% potassium permanganate or mineral oil should be carried. All these compounds convert it to phosphate within half an hour. Recent studies advocate not to carry out stomach wash because in contact of moisture, the remaining aluminium phosphide in the stomach is converted in to phosphine (iii) Magnesium sulphate is given i.m, or I.V. to correct arrythmias as 3gm bolus followed
664 Textbook of Forensic Medicine and Toxicology by an infusion of 6gm for 24 hours for a period of 5-7 days (iv) Calcium salt is given intravenously (v) Steroids are administered to combat pulmonary oedema (vi) Low dose dopamine infusion to be given (vii) Antibiotics are given to treat infection (viii) To combat metabolic acidosis, sodium bicarbonate 50mEq is given ever 15 minutes until arterial bicarbonate level increases above 15mmol/ L (ix) Oxygen inhalation and artificial respiration to maintain respiratory distress. Distribution of magnesium in the body: In adults, 2000 meq of magnesium is present in the body, of which 60% is concentrated in the bones and 40% in the soft tissue. The Plasma concentration of magnesium is 1.5-2.2meq/lt and 4-8meq/day is excreted through the kidney in to urine, milk, saliva and gastrointestinal tract. In cardiovascular system high concentration of magnesium of about 10-15meq/litre produces symptoms similar to hyper alkalinity in where conduction time is increased and PR interval and QRS complex is lengthened. More than 15meq/ litre of magnesium causes cardiac arrest. Hypermagnesemia due to renal insufficiency results from the decreased excretion of magnesium. The manifestation starts at 12-15meq/litre level resulting in respiratory paralysis. The above concentrations can vary independently and deficit in one compartment may not be accompanied by a significant change in the other.
Plasma concentration and muscle biopsy is required to diagnose magnesium deficiency, but exchange of magnesium does not occur between bone, plasma and intracellular components. In patients with the renal failure the administration of magnesium is of little value as there is risk of hypermagnesemia. Incidence of deaths from Aluminium Phosphide poisoning: There is a drastic increase in mortality from aluminium phosphide poisoning especially in Haryana, Punjab, Uttar Pradesh and Rajasthan since the last 20-25 years. In 1989, 14 cases are reported of which 4 are accidental deaths and 10 suicidal. In 1990, 9 cases were reported of which 6 are suicidal and 3 accidental. In 1991, 12 cases were reported of which 6 are accidental, 4, suicidal, and 2 homicidal deaths. Autopsy Findings (i) Cyanosis is present (ii) In few cases, froth over the mouth and nostrils are present (iii) On opening the body, fishy or garlicky smell of phosphine gas is present (iv) All the internal organs are congested and showing evidence of petechial haemorrhages (v) Lungs are congested and oedematous; In a study, pulmonary oedema is well established in 30 cases resulting from irritation from the phosphine gas.
48
Part 2—Forensic Toxicology
Organic Solvents Organic compounds used in industry or at home may result in death from their careless use for improper purposes. Environmental exposure occurs from improper disposal and leakage from toxic dump sites resulting in contamination of drinking water. The various compounds are: (i) Gasoline (ii) Lighter fluids (iii) Aerosol sprays (iv) Spot removers (v) Paint removers (vi) Floor/ tile cleaners. The compounds such as anaesthetic agents, solvents and fluorohydrocarbons are used as propellants in aerosol products. SOLVENT ABUSE Solvent abuse is deliberately inhaling a variety of substances especially organic solvents that results in symptoms similar to alcoholic intoxication The distortion of consciousness, euphoria (sometimes of erotic nature), distortion of perception and actual hallucinations are produced. Predominantly males of 14-22 years to beyond the either end or solitary users are commonly involved. Most common substance inhaled was toluene-based adhesive that is why it is also called ‘Glue sniffing’ Common Method of Solvent Abuse 1. A solvent or chemical is taken in a plastic bag; the open end is placed against the nose and mouth and air re-breathed. The warm air results in vaporization of solvent, enters tidal air stream and absorbed through pulmonary membranes into blood. 2. The inhalant is placed on the hanky and inhaled directly as pad over nose and mouth. Gaseous substances (butane or propane) are taken from
either a large cylinder used for camping, heating or cooking or from small ampoule cylinders sold for refilling gas cigarette lighters are introduced into mouth or nose. 3. They may be used directly from pressurized aerosol cans or pain relieving sprays. They can be derived from tins, jerry cans and petrol filters of motor vehicles. Fire extinguishers contain an organic bromine derivatives that when inhaled sensitizes the myocardium to catecholamines. Various Compounds Used For Solvent Abuse I. Aliphatic Hydrocarbons C1-C4 Aliphatic hydrocarbons: Straight chain hydrocarbons with 150mg/kg or >10g in an adult) is taken, it causes serious toxicity. Fatality is common with doses >250mg/ kg. Paracetamol is a potent liver poison, as a small portion is converted by the liver enzyme ‘P450’ (microsomal mixed function oxidase) into a toxic compound, probably N-acetyl-p-benzoquinone. Normally glutathione and other sulphydryl compounds detoxify this substance, but in overdose, these are exhausted and the toxic agent causes a profound centrilobular necrosis. The plasma halflife is a guide to hepatotoxicity; it is dangerous to have a half-life of more than two hours at a level of 300mg/L at four hours after ingestion. Typical blood levels in overdoses when at least 10-15gm
668 Textbook of Forensic Medicine and Toxicology has been taken are 100-400mg/L, with an average around 250 and the urine may contain 150-800mg/ L. All the levels depend on dose and survival time. Mechanism of Toxicity N-acetyl-benzoquinone-imine is a highly reactive arylating minor metabolite of Paracetamol, which is detoxified by conjugation with glutathione. When a very large dose is taken, hepatic glutathione is depleted and this metabolite binds covalently to proteins in liver cells and renal tubules causing necrosis. Toxicity thus shows a threshold phenomenon, manifesting only when the glutathione is depleted to a critical point. In chronic alcoholics, even 5-6gm/day taken for a few days can cause hepatotoxicity. Paracetamol is not recommended in premature infants that are of less than 2 kg for fear of hepatotoxicity. Signs and Symptoms Early manifestations: (i) Nausea, vomiting and abdominal pain (ii) Tenderness of liver (iii) No impairment of consciousness After 12-18 hours: (i) Centrilobular hepatic necrosis (ii) Renal tubular necrosis (iii) Hypoglycemia progressing to coma (iv) Fulminating hepatic failure and death may occur when plasma levels are above the level of 200μg/mL at 4 hours and 30μg/mL at 15 hours. Treatment Treatment should be started as early as possible as it is practically ineffective if started 16 hours or more after Paracetamol ingestion: (i) Gastric lavage and induction of vomiting (ii) Activated charcoal given orally or through the tube (iii) Nacetylcysteine 150 mg/kg should be infused intravenously over 15 minutes followed by the same dose over the next 20 hours. Alternatively, 75 mg/ kg may be given orally every 4-6 hours for 2-3 days. It replenishes the glutathione stores of liver and prevents binding of the toxic metabolite to other cellular constituents.
Autopsy Findings (i) Nothing specific is in the gastrointestinal tract (ii) In massive overdoses, death may result from depression of central nervous system (iii) Most deaths are delayed for 2-4 days when liver failure develops; the liver may be enlarged but is often < 1500 gms. It is pale yellow to tan coloured and centrilobular necrosis is visible microscopically (iv) Renal tubular necrosis may be seen (v) Myocardial fibril damage may be visible histologically. INSULIN POISONING Medicolegal Aspects Death from parenteral administration is insulin is quite common. Fatal insulin toxicity can be accidental, suicidal and even homicidal. Accidental fatalities are mostly medical errors resulting from misreading the label on the box or ampoule. Suicide insulin is also quite common. Insulin is inactive orally and has to be given parenterally for its hypoglycemic action. Autopsy Findings 1. Peripheral blood samples, skin, and underlying tissue from the injection as well as control site should be preserved. The needle marks are usually not evident at autopsy unless a small vessel has been damaged. The samples should be either frozen or kept in refrigerator. 2. Frozen serum separated from red cells should be sent for analysis. 3. Porcine or bovine insulin can be detected as such but immunoassay of the insulin itself, measuring C-peptide, produced on a one-toone basis by the pancreas assists in distinguishing endogenous from exogenous insulin. 4. Attempting to prove insulin-induced hypoglycemia by measuring glucose levels in human post-mortem fluids is impracticable, due to the unreliability of such estimations after death. 5. Very low vitreous humour glucose levels suggest hypoglycemia but not well acceptable.
50
Part 2—Forensic Toxicology
Food Poisoning Food poisoning or the food borne illness includes all the illnesses resulting from ingestion of food containing bacterial products, toxins, viruses, prions or parasites or acute gastroenteritis due to bacterial infection of food or drink. The contamination may result from improper handling, preparation or storage of food. Food borne illness can also result by adding pesticides or medicines to food or by accidentally consuming naturally poisonous substances like poisonous mushrooms or fish. Contact between food and pests, especially rodents, flies and co*ckroaches is a further cause of contamination of food. The WHO defines it as ‘diseases, usually either infectious or toxic in nature, caused by agents that enter the body through the ingestion of food.’ Ptomaines: An early theory on the causes of food poisoning involved the ptomaines that are alkaloidal bodies are formed as a result of bacterial decomposition of protein in decaying animal or vegetable protein. These alkaloidal bodies when formed in the dead tissues are called ‘cadaveric alkaloids’. These are not bacterial poisons and do not cause food poisoning but are formed only when food becomes too disagreeable to eat. The ptomaines are usually nonpoisonous except for neurine and mydalein that are produced in traces 5-7 days after death. The signs and symptoms produced resemble that of atropine poisoning. Leucomaines: These are alkaloids that are secreted by living cells during metabolism that are toxic when injected but harmless when they are ingested. While some poisonous alkaloids are the cause of poisoning, the discovery of bacteria left the ptomaine theory obsolete
Causes and Incidence of Food Poisoning (i) Poisoning due to bacteria and toxins (ii) Poisoning of vegetable origin (natural food poisons): (a) Lathyrus sativus (b) Poisonous mushrooms (c) Ryes, Oats, Barley etc. (d) Poisonous berry such as Atropa belladonna (e) Argemone mexicana (f) Cotton seeds (g) Groundnuts (h) Cabbage (i) Soyabeans (j) Sweet clover (iii) Poisons of animal origin (a) Poisonous fish (b) Mussel (iv) Chemicals that are added intentionally (a) Flavouring agents in processed form (b) Colouring agents (c) Preservatives (d) Extraction of fat by solvents like hydrocarbons (e) Accidentally added such as pesticides and insecticides (f) Products of food processing such as smoking of fleshy food (g) Radionuclides. Incidence: (i) Chemical—28.4% (ii) Staphylococcal—21.4% (iii) Salmonella—17.4% (iv) C.botulinum—10.4% (v) Parasitic—8% (vi) C. perfrigens—7.5% (vii) Other bacterial—4% (viii) Viral— 3%. Infectious dose: The infectious dose is the amount of agent that must be consumed to give rise to symptoms of food poisoning. The infective dose varies according to the causative agent and the victim’s age and generalized health. In Salmonella food poisoning, as few as 15-20 cells may suffice. BACTERIAL FOOD POISONING Bacterial infection is the most common cause of food poisoning. The symptoms are delayed for 12-36 hours after consumption of contaminated food. Bacterial food poisoning is divided in to two groups: (i) Infection type: The pathogenic orga-
670 Textbook of Forensic Medicine and Toxicology Table 49.1: Difference between infection and toxin types of bacterial food poisoning Features
Infection type
Toxin type
Causative organisms
1. Salmonella group (i) S.enteritidis (ii) S.typhimurium (iii) S.cholerasuis (iv) S.paratyphi 2. Shigella sonnei 3. Proteus, E.coli, Sterptococci, Sh flexneri are also involved Ingestion of contaminated, uncooked or imperfectly cooked food
1. Staphylococcus toxin 2. Botulinum toxin 3. Bacillus cereus
Type of food ingested
nisms in food multiplies in the body (ii) Toxin type: Ingestion of poisonous substances that are formed in the food due to bacterial proliferation (Table 49.1. The common bacterial foodborne pathogens are Aeromonas, Bacillus, Brucell, Campylobacter, Corynebacterium, Coxiella burnetii, E. coli, Listeria, Salmonella, Shigella, Streptococcus, Vibrio cholera, Vibrio parahaemolyticus and Yersinia enterocoiltica. The incubation period of various food poisonings (Table 49.2). Table 49.2: Incubation periods of food poisoning caused by various organisms Causative organism
Incubation period
C. botulinum
2 hrs-several days (12-36 hrs) 8-20 hrs 12-48 hrs 10 days or less to 14 days or more 1-6 hrs (24-48 hrs)
C. perfrigens Salmonella except S.typhi S.typhi causing typhoid fever Staphylococcus aureus
Some foodborne illnesses are caused by exotoxins that are secreted by the cell as the bacterium grows. Exotoxins can produce illness even when the microbes that produced them have been killed. Symptoms typically appear after 1-6 hours depending on the amount of toxin ingested. These are caused by Clostridium botulinum, Clostridium perfringens and Staphylococcus aureus. Clostridial food Poisoning Clostridium is gram positive, anaerobic, spore forming bacilli that are responsible for three major diseases namely tetanus (Cl.tetani), gas gangrene (Cl perfringes, Cl septicum, Cl novyi, Cl histolyticus & Cl fallax), food poisoning (Cl botulinum & Cl perfringens type A & C and acute colitis (Cl
Ingestion of:(i) Preformed toxin in prepared (canned and preserved) food (ii) Imperfectly or undercooked food such as cheese, meat, fish, and eggs
difficile). Infant botulism is produced by ingestion of contaminated honey. Clostridium perfringens food poisoning:The organism is a square ended gram positive, nonmotile rod that is fastidious anaerobe. It is an important cause of gas gangrene. The incidence is more often reported at restaurants and public gatherings. The organism is found in soil and is a normal inhabitant of intestinal tract of man and animals. It has been isolated from meat, poultry and fish purchased from the market. The organism is heat resistant and if the meat is left unrefrigerated the level rises to hazardous concentrations. The organism grows in a food is improperly refrigerated after initial cooking. Clostridium botulinum toxin: Cl botulinum elaborates powerful exotoxin that is produced intracellularly and released only on the death and autolysis of the organism. This is the most powerful toxin known to humans. The lethal dose for humans is just 1-2 mg or 1 picogram/kg. It is basically a neurotoxin that acts slowly taking several hours to kill. The food contaminated by the toxin can be rendered safe by pressure cooking or boiling for 20 minutes. The spores resist boiling at 100o C even for several hours. Mode of action: Botulinium toxin enters preganglionic nerve terminals by endocytosis and binds rapidly and irreversibly to the cell membrane. It inhibits calcium dependent exocytosis preventing the release of Acetyl choline that results in presynaptic blockade and interference with cholinergic transmission at all acetylcholine dependent synapses in peripheral nervous system. The toxin has no effect on the central nervous system or on
Food Poisoning 671 axonal conduction system. Food borne botulism: This type of botulism occurs when Cl. botulinum multiplies in food such as Sausages, tinned meat, fish and fruits and vegetables infected with soil contamination, as Cl. botulinum is normally present in the soil. The incidence of food borne botulism in: (i) Canned food is 2% (ii) Restaurant food is 4% (iii) Family home canning is more than 90%. It produces a powerful exotoxin and is caused in humans by its distinct strains type A, B, E and rarely F. The food contaminated by type A, B & E strains looks and smells abnormal due to the action of proteolytic enzymes and that contaminated by type E strain is normal in appearance and odour. The initial phase is so subtle as to go unnoticed or misdiagnosed. The clinical features are: (i) Vomiting, thirst and abdominal pain (ii) There may be constipation (iii) Ptosis, difficulty in visual accommodation, mydriasis and diplopia (due to ocular paresis) (iv) Dysphonia and dysphagia (v) Bilaterally symmetrical descending motor paralysis beginning with abducens or oculomotor nerve palsy and progressing to respiratory insufficiency (vi) Urinary retention (vii) Mental status, sensorium, reflexes, body temperature and pulse are usually normal. Wound botulism: It is a rare life threatening complication of trauma. It occurs after spores of Cl. botulinum have germinated in a wound and the produced botulinum toxin results in flaccid paralysis. It may also result from fatal intravenous drug abuse. Cocaine and Heroin when injected subcutaneously result in wound botulism. Deep wounds crush injury and compound fracture treated with open reduction predisposes to wound botulism. The incubation period is 4-18 hours and the clinical features are: (i) Fever associated with sinusitis, abscess and tissue infection acts as a focus of infection (ii) There is absence of gastrointestinal manifestations (iii) Cranial nerve palsies result in ptosis, diplopia, poor accommodation, ophthalmoplegia, dysphagia, Dysphonia and dysarthria (iv) Flaccid paralysis (v) Shortness of breath (vi) Respiratory failure.
Infant botulism: This type of botulism results from the ingestion of Cl botulinum organism with subsequent in vivo production of the toxin followed by absorption form the gastrointestinal tract. Bacterial growth associated with breast-feeding may favour Bifibobacterium development instead of bacteria known to inhibit Cl botulinum i.e. Coliforms, Enterococcus and Bacteroides species. Honey is the most common food source contaminated with Cl botulinum spores. The clinical features produced are: (i) Feeding difficulties (ii) Constipation (iii) Feeble crying (iv) ‘Flobby’ baby with decreased muscle tone particularly of neck and limbs (v) Loss of facial grimacing (vi) Ophthalmoplegia (vii) Diminished gag reflex (viii) Dysphagia (ix) Poor anal sphincter tone (x) Respiratory failure. Diagnosis: The diagnosis is made from: (i) History of ingestion of canned food, vegetables, fruits and honey is there (ii) Clinical features (iii) Laboratory analysis of sample of blood, stool, vomitus, gastric contents and suspected food item, which are tested for Cl botulinum and botulinum toxin (iv) Tensilon test : Tensilon (edrophonium) is a rapid acting anticholinestrase used to differentiate botulism from myasthenia gravis. 10mg of the drug is injected slowly intravenously, 1-2 mg at first followed by rest of it by next 5 minutes. The muscle strength in myasthenia will improve with in ½-1 minute and last for about 5 minutes and there will be no or little improvement in botulism (v) Electromyography: In all forms of botulism, EMG pattern is characterized by brief, small, abundant motor unit action potential. The motor nerve conduction velocity is normal. Treatment 1. All patients should be hospitalized. 2. Respiratory status should be monitored for vital capacity, peak expiratory flow rate, negative inspiratory force, pulse oximetry ad gas reflex. The moment signs of bulbar palsy occur; intubation or tracheotomy should be done. 3. Evacuate GIT of spores and toxins with the help of activated charcoal, emetics, gastric lavage and catharsis-Sorbitol.
672 Textbook of Forensic Medicine and Toxicology 4. Botulinum antitoxin: Trivalent botulinum antitoxin is available in 10mL vial containing: (i) 7500 IU of type A (ii) 5500 IU of type B (iii) 8500 IU of type E produced by horses immunized against botulinum toxin and then defibrinated, digested and dialyzed and prepared as a 20% protein antitoxin. Equine globulin preparation is available in the west since 1960s but not yet produced in India. One vial is administered by slow i.v. as a 1:10 vol/vol dilution in 0.9% saline, and intramuscular dose of single vial and then after 2-4 hours again i.v. dose is administered. The antitoxin is not administered in infant botulism. It has got serious side effects such as anaphylaxis and serum sickness. It has a lack of effect on toxin producing organisms in the gut. 5. Guanidine: Its use is controversial as its efficacy is low and there is high incidence of adverse effects. If found appropriate, the dose is 15-40 mg/kg/day orally until EMG improvement occurs at least in ocular muscles. 6. Human derived Botulism Immune Globulin (BIG): It is used to treat infant botulism. It is a pentavalent (types A, B, C, D & E) immune globulins harvested by plasmapheresis from donors who received multiple immunizations with pentavalent botulinum toxoid. It avoids the use of foreign equine protein, thereby eliminating the risk of hypersensitivity reactions. 7. Supportive measures: These include the nutritional supplementations as oral feeds are contraindicated unless there is intact gag reflex and respiratory supportive measures. Prevention of Botulism (i) Improperly preserved home canned food should be avoided especially the green beans, Asparagus and peppers (ii) The food should be pressure cooked at >100°C for 10 minutes that kills spores (iii) Jams and jellies can be consumed, as they do not contain Cl botulinum due to their high sugar content (iv) Cooked food should not be kept at temperatures of 4°-6°C for more than four hours (v) Boiling the food before eating destroys the toxin (vi) Food pH should be maintained to less than 0.5; NaCl should be more than 3.5% and nitrites
level should also be sufficiently high (vii) Acidifying agents like citric and phosphoric acids are used while canning low acid food like mushrooms, beets, beans, corns and olives etc. Medicolegal Aspects The poisoning is commonly accidental and in literature, there is no incidence of use of botulinum toxin as homicide. Its incidence is more common in western countries and recently in Iran, Russia and Japan. It is quite rare in developing countries like India due to non-popularity of preserved and canned food. Autopsy Findings (i) The visceral organs and meninges are congested (ii) The mucosa of gastrointestinal tract is congested, swollen and haemorrhagic (iii) Microscopically fatty degeneration of the liver can be seen. Viruses Viral infections make up perhaps one third of cases of food poisoning in developed countries. They are usually of intermediate (1-3 days) incubation period, cause illnesses which are selflimited in otherwise healthy individuals, and are similar to the bacterial forms described above. The viruses that commonly cause food poisoning are: (i) Norovirus (formerly Norwalk virus) (ii) Rotavirus (iii) Hepatitis A is distinguished from other viral causes by its prolonged (2-6 week) incubation period and its ability to spread beyond the stomach and intestines, into the liver. It often induces jaundice, or yellowing of the skin, and rarely leads to chronic liver dysfunction (iv) Hepatitis E. Parasites Most foodborne parasites are zoonoses and are caused by: (i) Platyhelminthes (Taenia saginata & Taenia solium) (ii) Fasciola hepatica (iii) Nematode (Ascaris lumbricoides, Trichinella spiralis and Trichuris trichiura) (iv) Protozoa (Acanthamoeba and other free-living amoebae , Cryptosporidium parvum, Entamoeba histolytica, Giardia lamblia, Sarcocystis hominis, Sarcocystis suihominis) (v)
Food Poisoning 673 Toxoplasma gondii. Prevention of Food Poisoning 1. In a final product, it must be important to know the origin of the ingredients (originating farm, identification of the harvesting or of the animal) and where and when it was processed. 2. Respect of hygiene procedures maintenance of “cold chain” 3. There should be power of control and law enforcement of the veterinarians. 4. At home, the prevention mainly consists of: (i) Separating foods while preparing and storing to prevent cross contamination. (i.e. clean cutting boards, utensils, and hands after handling meat and before cutting vegetables, etc.) Wash hands and/or gloves before handling ready-toeat foods (ii) The respect of the food storage (hot foods hot and cold foods cold) and food preservation methods (especially refrigeration), and checking the expiration date (iii) Washing the hands before preparing the meal and before eating (iv) Washing the fresh fruits and vegetables with clear water, especially when not cooked (e.g. fruits, salads) Scrub firm fruits and vegetables with a brush to clean (v) Washing the dishes after use (vi) Keeping the kitchen and cooking utensils clean. (vii) Bacteria need warmth, moisture, food and time to grow. The presence, or absence, of oxygen, salt, sugar and acidity are also important factors for growth. In the right conditions, one bacterium can multiply using binary fission to become four million in eight hours. Since bacteria can be neither smelled nor seen, the best way to ensure that food is safe is to follow principles of good food hygiene. This includes not allowing raw or partially cooked food to touch dishes, utensils, hands or work surfaces previously used to handle even properly cooked or ready to eat food (viii) High salt, high sugar or high acid levels keep bacteria from growing, which is why salted meats, jam, and pickled vegetables are traditional preserved foods (ix) The most frequent causes of bacterial foodborne illnesses are cross-contamination and inadequate temperature control. Therefore control of these two
matters is especially important (x) Thoroughly cooking food until it is piping hot, i.e. above 70 °C (158 °F) will quickly kill virtually all bacteria, parasites or viruses, except for Clostridium botulinum and Clostridium perfringens, which produces a heat-resistant spore that survives temperatures up to 100 °C (212 °F). Once cooked, hot foods should be kept at temperatures out of the danger zone. Temperatures above 63 °C (145 °F) stop microbial growth (xi) Cold foods should also be kept colder than the danger zone, below 5 °C (41 °F). However, Listeria monocytogens and Yersinia enterocolitica can both grow at refrigerator temperatures.
POISONOUS FOODS POISONOUS MUSHROOMS The Amanita genus of mushroom that is Amanita phalloides, Amanita muscaria and Amanita pantherina are responsible for most cases of mushroom poisoning. These are Amanita Phylloides Poisoning This specie of mushroom is very toxic even after cooking. The onset of symptoms is slow and the prognosis grave. The mushroom is responsible for majority of deaths in cases of mushroom poisoning. The toxic constituents are peptides. Signs and symptoms: The signs and symptoms vary with the passage of time after ingestion of mushroom: (i) After 8-12 hours of ingestion (a) nausea (b) vomiting (c) diarrhoea and dysentery (d) intense thirst (ii) Within 24 hours of onset: (a) circulatory collapse (b) restlessness (c) twitching (d) delirium proceeding to coma (iii) After 3-4 days (a) hepatic damage (b) renal damage (c) death after 2-4 days. Treatment: (i) Gastric lavage (ii) Saline cathartics (iii) Symptomatic Medicolegal aspects: (i) Mainly accidental poisoning (ii) The mushrooms have been rarely used for homicidal purposes. Autopsy findings: (i) Extensive fatty infiltration of the liver (ii) Renal tubular necrosis (iii) Haemor-
674 Textbook of Forensic Medicine and Toxicology rhages in gastrointestinal tract (iv) Renal and hepatic haemorrhages (v) Basal ganglia necrosis. Amanita Muscaria and Amanita Pantheria Poisoning Both these mushrooms contain muscarine and give rise to a syndrome resembling that seen in pilocarpine poisoning Signs and symptoms: They appear within a short time of ingestion of the mushroom: (i) Profuse salivation (ii) Perspiration (iii) Severe nausea, vomiting (iv) Watery diarrhoea (v) Pupil is miotic with no reaction to light (vi) Muscular twitching may be present (vii) Sensorium is usually clear (viii) Maniac excitement or hallucinations may be present occasionally more common with A. pantheria than A.muscaria (ix) In fatal cases death may occur within a few hours. Autopsy findings: (i) Congestion of all visceral organs(ii) Findings suggestive of effects of hypoxia. TOXIC HONEY The Bees have little selection in the type of nectar, which they transport back to the hive to make honey, as it requires about 17,000 bee-loads to make 1kg of honey, the stand of poisonous plants must be rather great for enough of the toxic material to get in to the honey. The most common type of toxic honey is that from the laurels or rhododendrons. The following plants have been thought to be present in large enough plantings to cause production of toxic honey: (i) The laurels: Sheep laurel (Kalmia angustifolia), Mountain laurel (K. latifolia), Swamp laurel (K. polifolia), Great laurel (Rhododendron maximum), Black laurel (Leucothoe davisiae), Dog laurel (L.catesbaei) (ii) Rhododendron (Rhododendron species): California rose bay (R. californicum) and Rose bay (R. catawbiense) (iii) Bog rosemary (Andromeda glaucophylla) (iv) Jasmine (Gelsemium sempervirens) (v) Soapberry (Sapindus drumondii) (vi) Indian hemp (Cannabis indica) (vii) Oleander (Nerium odorum) (viii) Black locust (A androsaemifolium) & Clammy locust (R.viscosa) (ix) Lily of the valley (Convallaria majalis) (x) Death campus (Zygadenus) (xi) California buckeye
(Aesculus californican) and Horse chestnut (A. hippocastanum) (xii) Dogbane (Apocyanum cannabinum). Signs and symptoms: (i) Are of the toxic material in the honey? (ii) Tingling of fingers (iii) Vomiting and diarrhoea (iv) Inability to stand (v) Features of mania. FISH POISONING Poisoning by ingestion of fish may result from bacterial growth in partially decomposed fish or by the presence in certain fishes of a neurotoxin. The neurotoxin is present in the whole fish but is concentrated in the ovaries, testes and liver. This is particularly marked during spawning. The syndrome is called ‘ichthyotoxicosis’ or ‘ciguatera’ Signs and symptoms: The signs and symptoms begin within 10-30 minutes following ingestion of the fish: (i) Burning of the throat (ii) Nausea, vomiting and pain abdomen (iii) Ascending motor and sensory paralysis (iv) Mydriasis (v) Hypotension and bradycardia (vi) Respiratory difficulties (vii) Conduction disturbances (viii) Syncope and death resulting from respiratory failure. Treatment: (i) Gastric lavage (ii) Symptomatic treatment (iii) Cerebral depressants should be avoided. Venomous Fish 1. Some fishes cause poisonous wounds with their spines either while trying to get the fish off a hook or out of net. These fishes are commonly Plutosus and Paraplutosus. They cause painful wound with swelling and redness. The patient is treated with morphine and prevention of secondary infection. 2. One genus of fish, the Muraena (eel) inflicts poisonous bite producing local symptoms of pain to general symptoms of coma, respiratory failure and death 3. The stingrays’ fishes are most important, the tail has a series of barbs which close down for the thrust into the victim, flesh and then swing open to make the exit very painful. These fishes are fat and lie in the sand and mud at the bottom of water and attack with the poison tail or string
Food Poisoning 675 when disturbed or frightened. The tail is cut out to remove it from the victim’s body. Intense pain is produced and paralysis and other systemic manifestations may develop. Marked abdominal pain with cramps is produced. Respiratory difficulty, delirium and circulatory collapse progress until death ensues. In cases that recover, the necrosis of sting site occur and sloughing and healing may be delayed.
of people from low socio-economic strata. Continuous consumption of this pulse in quantities more than 30% of the total diet for more than six months results in a condition called Lathyrism. When mixed with three times its weight of wheat, the grain becomes apparently harmless but when cooked alone, it acts as a poison. The pulse loses 90% of its toxic amino acid when it is steeped in hot water or parboiled
Coelenterate Urtication
Lathyrism
This group of invertebrates includes jellyfish, corals, Portuguese man of war and medusae and is present in waters in great numbers. Especially dangerous is the Rhizostoma sp. that causes severe fatigue and depression along with others symptoms. This group of fish’s causes release of an urticating fluid that contains several toxic fractions; a neurotoxin, a primary irritant, a haemotoxin and an anaphylactic principle. It causes intense burning pain and irritation, severe abdominal pain, muscular cramps, convulsions and respiratory depression. The treatment is symptomatic.
Lathyrism is a condition characterized by features of paralytic manifestations due to the presence of a neurotoxin 1% BOAA [B (N) Oxalyl amino-LAlanine], a free water soluble amino acid in the seed cotyledons. This neurotoxin has predilection for pyramidal tract.
Both mussels and clams contain neurotoxins during certain months. These are heat stable and not destroyed by cooking. The shellfish contains poisonous plankton ingested as food. Intoxication has been reported with two species of Gonyaulax catanella, these dinoflagellates in larger numbers impart a reddish tinge to the water and luminosity at night.
Signs and symptoms: (i) The patient suffers from severe agonizing pain in the calf muscles and limbs that are paralyzed (ii) There is weakness in the legs with difficulty in sitting and getting up (iii) The patient later on finds difficult to walk with spastic gait characterized by walk on tip-toes (iv) Complete spastics paraplegia of lower limbs occurs in late stages and patient can just crawl (v) The motor nerves of the muscles of trunk, upper limbs and sphincters are spared (vi) There will be no atrophy or loss of muscle tone and no reaction of degeneration (vii) The knee jerks will be increased, ankle clonus well marked and extensor planter reflex (viii) There are no sensory changes and no loss of consciousness (ix) There is usually no involvement of bladder and rectum unless the lumbar segment gets affected.
Signs and symptoms: The signs and symptoms appear within 10-20 minutes after ingestion of shellfish: (i) Nausea and vomiting (ii) Burning paraesthesiae of the hands and feet (iii) Numbness of lips and tongue (iv) Ataxia (v) Extreme mydriasis (vi) Convulsive seizures (v) Death from respiratory failure 2-12 hours later.
Treatment: (i) No specific treatment (ii) The pulse should be excluded from the diet and if it is necessary to consume, it should never exceed 25% of the total amount of cereals and pulses consumed per day (iii) The diet rich in vitamin A, carotene and other vitamins should be given (iv) Physiotherapy for muscular and neurological involvement.
Shellfish Poisoning
Treatment: (i) Gastric lavage (ii) Symptomatic. LATHYRUS SATIVUS (Keshari Dal) Keshari dal grows under extreme conditions of drought in several parts of India. It is a staple diet
ARGEMONE MEXICANA The plant Argemone mexicana grows widely all over India in winters at the same time when mustard plants are growing. The seeds are commonly con-
676 Textbook of Forensic Medicine and Toxicology fused with the mustard seeds and are deliberately or accidentally mixed with mustard seeds. Mustard oil is widely used for cooking purposes in Bengal, Assam, Maharashtra, Orissa and Bihar and is often adulterated with the oil of Argemone mexicana. The plant has thistle like, sessile and spiny leaves and yellow flowers. The seeds of argemone are dark brown, globular, smaller than the mustard seeds and are covered by regular minute projections and depressions. The seeds on pressing burst with a sound giving out argemone oil whereas mustard seeds on pressing burst without any sound and give out mustard oil. All parts of this plant are poisonous and seeds being more poisonous. The plant contains two alkaloids—berberine and protopine, whereas oil extracted from the seeds contains—sanguinarine and dihydrosanguinarine, the former being more toxic. The adulteration of mustard oil with the oil of Argemone mexicana causes Epidemic dropsy and glaucoma. The symptoms usually break out in an epidemic form amongst the consumers of adulterated oil (Fig. 49.1). Signs and symptoms: The symptoms appear gradually on consumption of the adulterated oil: (i) Loss of appetite, nausea, vomiting, dyspepsia and diarrhoea (ii) Oedema of legs and generalized anasarca (iii) Fall of blood pressure, quick weak pulse, dyspnoea with features of myocardial damage (iv) Breathlessness on slight exertion (v) Enlarged, tender liver (vi) Subcutaneous telengiectasis or hemangiomas due to peripheral vasodilatation (vii) Small fleshy dark red growths may be noticeable on various body parts and also
Figure 49.1: Agremone mexicana
on the mucosa of cheek, gums, tongue and nose (viii) Tingling and hyperaesthesia with diminished or even absent jerks (ix) About 1/10th of the cases develop glaucoma with dimness of vision and raised intraocular pressure (x) The application of adulterated oil on scalp causes burning and fall of hairs (xi) Death results from heart failure. Tests for Argemone To the edible oil mix equal volumes of nitric acid, the development of crimson colour indicates presence of argemone oil Treatment: (i) The adulterated oil should be discarded and sent for analysis (ii) Mainly symptomatic treatment should be undertaken (iii) Supportive treatment to combat heart damage in the form of digitalis, diuretics and prednisolone (iv) Good nutritious diet with multiminerals and multivitamins especially B complex group should be administered.
