Essentials of Forensic Medicine and Toxicology, 1st Edition [1 ed.] 8131254577, 9788131254578

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TE

AINA

Essentials of

Forensic Medicine

&Toxicology S.Chand

ELS4158594.

ELSEVIER

ABBREVIATIONS Td

Jd

Increased Decreased Lead(s) to/results into More than or equal to Less than or equal to

Micrometer Airway, breathing and circulation ABC Acetylcholine Ach Allow natural death AND Anterior superior iliac spine ASIS Associated with a/w Blood alcohol concentration BAC BBB Blood-brain barrier Body weight BW Chaudhary Charan Singh University CCU Continuous medical education CME Central nervous system CNS Carbon monoxide CO COHb Carboxyhaemoglobin COI Constitution of India Criminal Procedure Code, 1973 CrPC CVS Cardiovascular system Differential diagnosis D/D DIC Disseminated intravascular coagulation DMC Delhi Medical Council DNR Do not resuscitate DU Delhi University D/W Difference between um

EDH EUL FD

FP FSL

FPs

GA

h Hb HR HSR

MR

ICP IEA

IHD

IM IPC

Extradural haemorrhage Extrauterine life Fatal dose Fatal period Forensic Science Laboratory Finger prints General anaestheticCS

Hour/Hours Haemoglobin Heart rate Hyper sensitivity reaction Indian Council of Medical Research Intracranial pressure Indian Evidence Act, 1872 Ischaemic heart disease Intramuscular Indian Penal Code, 1860

IUL IVC 1/V JJB

LAMA LBW LMP LOC LQ LTI

MCI mg% MI MIP MLC MLI MLR MOA

nm NREM N/V OD OIC OT POCSO POTA PSIS PVS

RMP RTA

Intrauterine life Inferior vena cava Intravenous Juvenile Justice Board Left against medical advice Low birth weight Last menstrual period Loss of consciousness

Long question Left thumb impression Medical Council of India milligram percent) = mg/dL (milligram per decilitre) = mg per 100 mL Myocardial infarction Mentally ill person Medicolegal case Medicolegal importance Mediclolegal case report Mechanism of action

Nanometer Nonrapid eye movement Nausea and vomiting Once a day

Officer-in-charge Operation theatre Protection of Children from Sexual Offences Act Prevention of Terrorism Act Posterior superior iliac spine Persistent vegetative state Registered Medical Practitioner Road trafic accident

WMA

Subarachnoid haemorrhage Subdural haemorrhage Sudden infant death syndrome State Medical Council Short note Solution Superior vena cava Terrorists and Disruptive Activities Act Total body surface area Tricyclic antidepressants World Medical Association

ww-I and II

World War-first and second

SAH

SDH SIDS SMC SN

Sol SVC

TADA TBSA TCAs

ABBREVIATIONS

PUNISHMENTS P

I,

or F (Rs 10) or both: Punishment is mprisonment for 4 years or fine of Rs 10 or both. P 1, + F: Punishment is 'imprisonment for life =

with'fine.

P=110 rm +F: Punishment is 'imprisonment for 10 years which may extend to lifec' with fine. RI + F: Punishment is 'rigorous imprison-

P

ment' with fine.

Punishment is 'rigorous inmpris. onment extending from 6 months to 2 years. P

smenths-2 years

CONTENTS Preface, vii

Acknowledgements, Abbreviations, xi

SECTION 1

7

ix

Introduction to Forensic Medicine

Procedures 3 Medical Jurisprudence 3A Code of Medical Ethics, Medical Councils, Acts, Medical Records and Professional Misconduct 3B Consent 3C Medical Negligence 4 Medicolegal Autopsy (Postmortem Examination) 5 Identification 5A Identification, Age, Race, Sex and Stature 5B Forensic Osteology 5C Forensic Odontology 5D Dactylography (Fingerprinting) and Other Prints 2 Legal

9

3 5 22

22 33 37 49 56

56 75 85

93 97

of

Identification: Forensic Trichology, Marks and Deformities, Anthropometry, Superimposition and Biometric methods

6 Thanatology 6A Death and Its Causes 6B Sudden Death and Unexpected Death 6C Euthanasia

Postmortem Changes 7 Injuries 7A Medicolegal Aspects of Injuries 7B Mechanical Injuries 7C Regional Injuries 7D Thermal Injuries 6D

8

Forensic Medicine

5E DNA Fingerprinting 5F Miscellaneous Methods

Firearm Injury Miscellaneous injuries (electrical injurics and lightning) Mechanical Asphyxia Sexual Jurisprudence 9A Impotence and Sterility 9B Virginity, Pregnancy, Delivery and Legitimacy 9C Abortion 9D Infanticide 9E Sexual Offences and Sexual Perversions Blood Stains Forensic Psychiatry Miscellaneous Topics 12A Anaesthetic and Surgical Deaths 12B Torture and Custodial Deaths 12C Recent Methods of Interrogation 12D Fall From Height 12E Trauma and Disease 12F Medicolegal Importance of AIDS/HIV 12G Starvation Deaths 7P

101 106

106 113

115 117 135

135 144 163 180

10 11

12

191

207 211

232

232

238 247 253

263 282 289 306

306 308 310 312 313

314 315

SECTIONII Forensic Toxicology 13 General Aspects of Forensic Toxicology 14 Corrosive Poisons 15 Inorganic Irritant Poisons 16 Organic Irritant Poisons 17 Poisons Acting on Nervous System 17A CNS Depressants 17B Deliriants 17C Spinal and Peripheral Nerve Poisons

18 Cardiac Poisons 19 Asphyxiants 20 Agricultural Poisons 21 Drug Abuse 22 Miscellaneous Poisons

319 336 342 355 368

368 381

389 394 398 404

410 417

xiii

xiv

CONTENTS

SECTION I

Practicals

SECTION IV Appendix

MA Specimens

423

(For Spotting and Grand Viva) IB Injury Examination Report IIC Age Estimation Report IIID Grand Viva in Forensic Medicine IIIE Grand Viva in Forensic Toxicology (Except Specimens)

423 446 455 465 483

483

Weights and Measurements 2 Important Sections in CrPC, IPC and Sample Papers 1

Index

491 IEA

492 496 499

1 Introduction to Forensic Medicine INTRODUCTION TO FORENSIC MEDICINE The

term forensic has come from the Latin word which means of the forun' or

esis

ia.

'court of

In ancient timmes, 1n Rome, forum was the civic and legal matters meeting place whe were discussed by the conmpetent authorities.

Forensic medicine: It deals with the application of medical knowledge to aid in administration of justice; it also deals with the medical aspects of law It is used by legal authorities to solve legal problems.

Medical jurisprudence (Latn, Juris = law; prudentia= knowledge): It deals with the legal aspects of medicine, that is, the legal principles that guide the medical personnel. It includes legal rights, privileges, duties and obligations of a medical practitioner, doctor-patient relationship, consent, medical negligence, serious professional misconducts, medical ethics and so on. Forensic science: It deals with the application of scientific knowledge (e.g. physics, chemistry, biology, etc.) for the purpose of law and administration of justice. The laboratory established to carry out scientific examination and evaluation of evidence for legal purpose is known as the forensic science laboratory (FSL).

HISTORY OF FORENSIC MEDICINE

Imhotep (2980-2900 BC): He is considered as the nrstmedicolegal expert. He was the chiet justice and chief physician to Pharaoh Zoster, the king of Egypt. Hippocrates (460-377 BC): The father of western nedicine, Hippocrates was born and practised medicine in the island of Kos in Greece. He

discussed the lethality of wounds. Hippocrates was the first to write the code of medical ethics. Orfila (1787-1853, France): He is considered as the founder and father of modern toxicology as he introduced precise chemical methods into toxicology.

First autopsy: (1) Outside India-Bartolomeo da

Varignana (AD 1302) performed the first medicolegal autopsy in Bologna, Italy. Then in AD 1562, Ambroise Paré performed an autopsy in France on the dead body of King Henry II. (2) In India-Dr Edward Bulkley (1693) performed the first medicolegal autopsy in Chennai on the dead body of Mr Wheeler. Dr Hamilton (1725) performed the first autopsy in Kolkata.

CRIME SCENE INVESTIGATION Crime scene: It includes the actual location where the crime was committed. The investigation of a crime scene done by authorities to help in administration of justice is known as crime scene inves-

tigation. Evidence: Anything which helps to support truth is evidence. Anything which is in the form of an identifiable object is physical evidence, for example, hair, blood stains and so on. When physical evidence is present in very tiny quantities, it is known as trace evidence. Trace evidence can be thought as evidence occurring in such small amounts that it can be transferred (or exchanged) between two surfaces (or persons or bodies) without being noticed. The evidence is collected from crime scene and then preserved and transported to laboratory or court. It is very important to maintain the chain of custody of evidence Locard's principle of exchange [SN-1]

3

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Forensic Medicine

QUESTIONS-ANSWERS SN-1: Locard's principle Edmond Locard (1877-1966), a French crimiDrnalist and in forensic

pioneer science, described a principle popularly known as Locard's exchange principle. This principle constitutes the basis of the concept of trace evidence and all crime detection. It states that 'Every contact leaves a trace. It means when any two objects come into contact, there is always a transfer of material from each object onto the other. In crime scene investigation, Locard's principle has a very important role. The perpetrator after committing crime leaves the crime scene after destroying the evidence. But it is the principle of nature that when a perpetrator touches something dur ing crime, he leaves some evidence which is either not visible to him or which he is not aware of. The evidence left at crime scene may be grossly visible

to the naked eye (e.g. blood) or it may be invisible (e.g. sweat, epithelial cells, saliva, semen, finger. prints, etc.). Nowadays, criminals are more aware about the scientific investigation of crime, so the criminal after mmitting crime tries to destroy the evidence, but modern techniques recently developed in the field of forensic science can detect trace evidence at microscopic level.

Examples: Rape: The semen is transferred to the female genitals, but vaginal cells are transferred to the penis. 2) Homicide: Blood of the victim sticks to the dagger and the dagger leaves its metallic traces at the wound. 3) Fingerprints: The perpetrator touches a glass by his hands to leave his fingerprint patterns. 4) Shoe marks: A criminal after committing crime runs away but leaves his footprints on soil. The soil sticks to the sole of his shoes. 1)

,

Legal Procedures INDIAN LEGAL SYSTEM The Indian legal system was founded by the Colonial British, and after independence it was adopted by India after making some amendments. The criminal justice in India

governed by the Constitution of India (COI), CrPC, IPC, IEA and various categories of criminal courts' (c.g. Supreme Court, High Court, Session Court and so on) is

criminal justice. Criminal Procedure Code, 1973 (CrPC): provides themechanism for punishment of offences against thesubstantivecriminallaw. It prescribes the proce dures to be followed by the police in criminal cases, forexample police duties in arresting.offenders, dealingwith absconders. in production of documents and investigating offences. It classifies courts and deals with actual procedure in trial, appeals, references, revisions and transfer of criminal cases, Indian Penal Code, 1860 (IPC): It classifies all possible crimes and prescribes punishments for them. Chapter XVI is the largest chapter in IPC, which contains 78 sections [S.299-S.377]; it describes offences affecting the human body, which include some of the important sections relevant to medical practitioners. Indian Evidence Act, 1872 (TEA): It deals with law of evidence and prescribes rules regarding procedures for tendering evidence in a court of law. which conduct trials and help in

It

TYPES OF COURTS OF LAW IN INDIA Ihere are two types of courts: civil courts and criminal courts. Civil courts: They dealonly with civil matters, for examPle, land and property (eg. landlord/tenant disputes), Industrial, financial, administrative, family matters (e.g. avorce), etc. Examples include consumer protection 1orum, tribunals and family courts. The punishment 8ven by these courts is in the form of compensation. Conduct money is paid to witnesses for attending court.

Criminal courts: They deal with criminal offences codified in IPC, for example, murder, rape, theft, robbery, etc. and award punishment in the form of imprisonment or sometimes death penalty with or without fine. Examples include Supreme Court, High Court, Session Court and Magistrate Court. Conduct money is not paid to witnesses for attending the court but they can get TA/DA. Supreme Court (SC): It is the highest court of the

country situated in New Delhi.The Supreme Court has been establishedunder Article 124 of COL It is presided over by the Chief_Justice of India who appointed by the President of India. Article 145 is empowers SC to frame its own rules for regulating thepractice and procedure of the court as and when required (with the approval of the President). High Court (HC): It is the highest court of a state usually located in thecapital of every state. Ithas been established under Article 214 of COL. It is presided over bythe Chief lustice of State whois appointed by the President of India. Some states share a comn mon HC for example, (1) Guwahati HC caters for all seven states in the North East (Arunachal Pradesh, ASsam Manipur Meghalaya, Mizoram, Nagaland and Tripura), (2) Mumbai HC caters for the states of Maharastra, Goa, Union Territories of Dadra and Nagar Haveli and Daman and Diu. Session Court (or District courts): It is the high: est court of a district located at district headquar ters, It is presided over by a "District Session ludge DS) appointed by High Court. High Court may LSO appont additional session judge and asSIstanE Session_judge, to exercise_ jurisdiction in a court or Session,DSI is also knownas district judge whenhe when he presiles over a civil case, and session judge case, Fast track courts havE presicles over a griminal are Courts. They

Session of additional cases and tor ne established to reduce long pending

ne_statuS

speedy disposal of cases.

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Forensic Medicine

Magistrate Courts are specialised in law 1) Judicial magistrate: They are empow(i.e. have LLB and LLM degree) and types. ered to deliver judgment. They are of thrce metropoli(a) Chiefjudicial magistrate (CJM): In tan cities, CJM is known as Chief Metropolitan Magistrate. (b) First-class judicial magistrate: In metropolitan cities, first-class judicial nagistrate is known as Metropolitan Magistrate (c) Second-class judicial magistrate. 2) Executive magistrate: They are administrative officials appointed either through a civil service examination or through promotion. So, they may have LLB degree but most often do not. They are not authorised to deliver judgment because their duties are of executive nature. They do not give any punishment. Examples, District Magistrate (DM), Additional District Magistrate (ADM), Subdivisional Magistrate (SDM), Collector, Tahsildar.

Powers of Various Criminal Courts [SN-1]

First information report (FIR): FIR is the first information report about the commission of a'cognisable offence, given either by the victim or any other person to the police. It is recorded in writing in FIR register by the officer-in-charge of a police station [S.154, CrPC)

INQUEST [SN-2] Inquest: It is an inquiry by legal authorities into the cause of death in cases of sudden, unnatural and suspicious deaths. Types of inquest are shown in Table 2.2

TABLE 2.2 Types of Inquest [Mnemonic: Prime Minister Chief Ministerl Police Inquest

Magistrate Inquest ISN-3]

Coroner's Inquest

It

It is

It is

conducted by police

OFFENCE AND FIR Offence is defined as 'any act or omission made punishable by law for the time being in force. Depending on the nature and gravity of an offence, it may be classified as cognisable and noncognisable (Table 2.1).

TABLE 2.1 Cognisable Offences Versus Noncognisable Offences Cognisable Offences

Noncognisable Offences

These are offences of such These are offences not of such nature and such nature and such gravity that gravity as is cognisable immediate arrest of the offences and thus the offender is necessary and police officer firstly has thus the police officer may warrant. to take warrant from arrest without are magistrate to arrest offences serious These These are minor offences and so the punishment and so the punishment for for these offences is more offences is less than than that of noncognisablethese that of cognisable offences. offences. Examples: Murder, sexual offences, sexual

harassment, voyeurism, stalking, dowry death, Kidnapping,etc. An FIR can be filed only in the case of cognisable

offences

Examples: Adultery, bigamy, bribery, causing miscarriage, etc.

Here, the police will not file an FIR but it will register the complaint in the dally dlary report/register (DDR).

[SN-4]

conducted

conducted

by

by

magistrate.

Coroner

Medical Examiner System [SN-5] It is

conducted by 'medical

examiner

SUMMONS [SN-6] Summons (or subpoena): t is a written document issued by the court, compeling the attendance of a witness in the court of law, to depose evidence, at a particular date and time and purpose under penalty.

Conduct money [SN-7] Warrant: If a witness fails to attend the court due to some reason (e.g. illness, emergency and so on), he should convey the message to the court and then the next date of hearing will be issued to him. If the witness has no valid reason for not attending the court, a warrant for his arrest may be issued to secure presence of the witness.

WITNESS [SN-8] Witness: A person who provides evidence about a fact in the cort of law under oath is known as witness. Types of witness (Table 2.3): There are three types of witness: common witness, expert witness and hostile witness.

CHAPTER 2

TABLE 2.3

Vpes of WitneS

Common

[SN-9]

Witness A

common

person wno has or actualy seen observed the facts narrates and he in facts those

box the witness common is a witness. He is not allowed to draw conclusions from his observations.

Expert Witness A

Hostile Witness

[SN-10]

person who

person who purposefully makes statements contrary to the fact or has some interest or motive for concealing truth. A

is skilled in a

particular field (e.g. law, science or art) and

who provides evidence about a fact in the court of law under oath is known as expert witness.

Perjury ISN-11)

Wilfully giving

false evidence under oath.

PROCEDURE IN COURT When a witness appears in court, starts in the following sequence.

the court procedure

) Oath taking [SN-12]: Before giving evidence in the court, the witness has to take oath because it is presumed that after taking oath, witness will speak the truth. 2) Recording of evidence (i.e. examination of a witness in the court): According to S.138, IEA, the order of examination in the court of law is in the following sequence. A.

Examination-in-Chief [SN-13]

then

B.

Cross-examination [SN-14]

C.

Reexamination

D.

then

Questions put by the court (note: The court can ask any question any time during the pro-

cedure.) Summary trial [S.260-265, CrPC]: It means short and rapid trials avoiding the regular lengthy procedure. Summary trial aims at speedy/quick disposal

offences. A summary minor De

case is one which can of at once. In summary trial, of imprisonment for a term more than months can be imposed by the magistrate. tried and disposed

ence

Frocedure of criminal trial: The proceedings of Estigation by the police in criminal offences are magistrate of that area. All offences Punishable with death, imprisonment of life or prisonment for >2 years are tried as warrant cases. l other cases are tried as summons cases.

E udicial

Legal Procedur

According to S.226 of CrPC, public prosecutor (PP) tries to prove, on the basis of witnesses and evidence, that the arrested person is an offender (accused) in the concerned case. If Magistrate finds that there is no specific ground (witness or evidence) to take any legal action against the accused then he can release the accused IS. 227, CrPC|.

If

Session Court finds that arrested person is an offender, then court charges the accused [S.228, CrPC). Session Court gives a charge sheet, recites it, and asks him whether he admits his guilt or not. If Session Court finds (thinks) that the case does not deserve to be heard, then the court sends (hand-over) the case to the CJM. According to S.229 of CrPC, if accused confesses his guilt, then court punishes him, but if he refuses his guilt, then the court does not admit him as an offender under S.229 of CrPC but gives another date of hearing for statement of witnesses. According to S.231 of CrPC, court proceeds with the testimony (statement) of witnesses on the fixed date of hearing. The PP sums-up [presents the point (contents)] the case before the court and the accused or the counsel of accused shall be entitled to reply. If the counsel of accused raises any questions regarding the case, then PP answers those questions. After that, a final argument takes place between counsels of both parties. On the basis of this argument and the witnesses and evidence, the judge gives his decision (judgement) regarding the case.

EVIDENCE Evidence: 'Anything which is presented in the court to support the truth' or 'anything presented in support of an assertion' is called evidence. According to S.3 of IEA, evidence is of two types: 1) Oral evidence: It means 'all statements (oral or verbal) which the court permits or requires to de made before it by witnesses, in relation to matters of fact under inquiry. 2) Documentary evidence: It means 'all documents for the including electronic records produced inspection of the court. 'acquisition Classification of evidence on the basis of

of evidence': directlyY the witness had When evidence: Direct senses, it A) his felt it by any of Seen the crime or had

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Forensic Medicine

is called direct evidence. Example, a street saw a murder in the street.

vendor

(B) Indirect: Witness did not directly see the crime.

may be of two 1)

2) Evidence given by a witness in a previous judicial proceeding is admissible in a subsequent judicial proceeding when the witness is dead or can't be foun or is incapable of giving evidence [S.33, IEAJ. 3) Expert opinion expressed in a treatise: Expert opinions printed in standard text. books are accepted as evidence without oral evidence of the author [S.60, IEA]. 4) Deposition of a mental witness taken in

It

typeCS:

Circumstantial cvidence: The witness

dicd

not see actual crime; but some related act observed

by him indicates strongly the comnmision of crime. For example, W committed murder of 13 C saw 'A'with knife in hand just bcfore the murder. Here, since 'C' did not see the murder with his eyes; the evidence of C is a circumstantial evidence. If'C had actually seen the murder with his own eyes, it would have been direct evidence.

2) Hearsay evidence: The witnes

only heard about the crime from someonc. Example, 'A told that B had told him that he has seen 'C while committing the crime. Here 'B' can give direct evidence as he has seen C committing the crime; however, the evidence of 'A will be hearsay evidence. Generally, hearsay evidence is not admissible in court. Classification of evidence on the basis of 'presentation in the court': 1) Oral evidence (testimony): All statements (oral or verbal) which the court permits or requires to be made before it by witnesses, in relation to matters of fact under inquiry [S.3, IEA]. Oral evidence must be direct i.e. it must be evidence of an eyewitness [S.60, IEA]. In other words, a person must have himself seen or heard something or perceived by some other sense. Oral evidence is more important than documentary evidence because it permits cross-examination. Documentary evidence is accepted by the court only after oral testimony by the person concerned. Oral evidence by a dumb witness is possible if in the open court, he tries to do so by writing by signs, or by an interpreter |[S.119, IEA]. Exceptions to oral evidence: Documentary evi dence is accepted in the court only on oral testimony (i.e. oral evidence). But in some cases, documentary evidence is accepted in the court without y oral testimony. These exceptions to oral evidence are: 1) Statements of relevant facts made by a peris son who dead (i.e. dying declaration) or can't be found or is incapable of giving evidence (S.32, IEA].

lower court: Evidence of a doctor recorded and attested by a Magistrate in the presence of accused who had an opportunity to cross examine the witness, may be accepted as evidence in a higher court [S.291, CrPC]. 5) Reports of certain government scientific experts e.g. (A) Chemical examiner, (B) Chief controller of explosives, (C) Director of Finger Print Bureau or Director of Haffkeine Insti tute of Mumbai, (D) Director, Deputy direc tor or Assistant director of Central or State FSL, (E) Serologist [S.293(4), CrPC]. The court may however summon and examine any such expert if it thinks fit [S.293(2), CrPC]. 6) Public records: Birth certificates, Death certificates, Marriage certificates. 7) Hospital records: Routine entries eg. date & time of admission, discharge, vitals (e.g. pulse, temperature, urine output, etc), etc. 2) Documentary evidence: All documents produced before the court is called documentary evidence. These may be (1) primary evidence (i.e. original document itself produced for inspection by the court) and (2) secondary evidence (i.e. the documents, which are not original, e.g., certified copies, photocopies and so on). Documentary evidence related to medical field are known as medical documents. Medical documents include (1) medical certificates, (2) medicolegal case (MLC) reports, (3) dying declaration [SN-16] and (4) dying deposition [SN-17].

MEDICAL CERTIFICATES wwww

They

are the simplest form of documentary evience, issued by a registered medical practitioner (RMP) at the request of the patient. Examples: sickness certificate, fitness certificate, disability certificate, unsoundness of mind certificate, age certificate, death certificate.

accepted in the court of law as a piece of eviaccepted It is the RMP who has issucd it may be dence Even l testify the consummoncd to the court of law to it cross-examineeded, oath; certificate on entsof due care take done. So, RMP must nation can be certificates. skill in issuing such

and

signing false certificates: This is punctor can be S.193, IPC and the ishable under and fine. The atwarded 7 ycars of imprisonment such ertificates will also be punatient using similar punishment. ished under S.198, 1PC with

Issuing or

(DC) Death Certificate

Death ,According to Registration of Birth and registered be are to all births and deaths Act, 1969, throughout India. must inspect the body Before issuing DC, a doctor person is dead. and satisfy himself that the the patient during his last Ifa doctor has attended illness, he must issue DC without charging any fee [S.10(3), RBD Act, 1969]. The Brodrick Committee says that a doctor should not be allowed to issue a DC unless he has attended the deceased at least once during the 7 days preceding death. If the doctor refuses to issue a DC even if the aforementioned conditions are satistied, he will be charged Rs 50 [S.23(3), RBD Act]. A doctor cannot refuse or delay issue of DC. But ome situations, such as the following, he must refuse to issue DC and inform police: (1) when he is not sure about the cause of death, (2) there is suspicion of foul play, that is, doubtful cases, (3) death by Violent and unnatural cause, drugs, poisoning, etc. Relative of deceased may plead, persuade, presSurise, offer a price and at times even threaten the doctor to issue a false certificate. WHO ([nternational) format of DC is in two parts. Part I: There are three subsections for the Sequence of events leading to death. (a). Immediate cause of death: The disease or condition directly leading to death. It should not be the mode of death. 'Car

diopulmonary arrest or cardiorespiraory arrest or "cardiac arrest or caraiac Talure or heart failure' or asphyxia are Commonly seen written in death certificates as immediate cause of death, which 1S wrong. These terms are actually the modes of death. It is well known to all medical practitioners that every one dies

cardiopulmonary arrest or cardiac failure. It should be a discase, injury or complication, which caused death. I(b). Antecedent cause (or intermediate cause of death): The morbid condition that caused the immediate cause of death. I(c). Antecedent cause (or underlying cause of death): The basic pathological condition present before the aforementioned two causes [i.e. I(a) and I(b)] and leading to the aforementioned two causes. So, I(a) must be caused due to I(b), and I(a) and/or I(b) must be caused due to I(c). Underlying cause of death is the disease, which initiated the train of morbid events leading directly to death. Features of part I: If the sequence of events in part I comprised more than three stages, extra lines may be added in part I. Most recent condition has to be written in the top line and the earliest (i.e. the condition of

that started the sequence of events between normal health and death) in the last. Part II: Contributory cause: The condition, which contributes to death but not directly related to the disease or condition causingit. should represent a distinct in part Conditions sequence so that each condition may be regarded as being the consequence of the condition entered imme diately below it. Where a condition does not seem to fit into such a sequence, it may belong to part II. Examples: A patient dies from myocardial infarction (MI) due to coronary artery disease (CAD). Immediate cause of death is MI; write it in part I(a). Anteced ent cause of death is CAD; write it in part I(b). 2) A patient died from cerebral haemorrhage due to hypertension. He had a history of diabetes. Inmediate cause of death is cerebral haemorrhage; Is Write it in part l{a). Antecedent cause of death nypertension; write it in part 1(6). Contributory cause of death is diabetes; write it in part l days after 3) A man of 65 died of peritonitis a few pertoration. e noperation for duodenal duocdenal ulcerations. had a history of chronic death is peritonitis; Here immediate cause of pertora is duodenal antecedent cause of death chronic is cause of death contributory tion and duodenal ulceration.

I

10

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Forensic Medicine

MEDICOLEGAL CASE AND MEDICOLEGAL CASE REPORT (in Medicolegal case (MLC): If an attending doctor casualty or OPD) after taking history and examining the the case patient suspects foul play or has doubts about and/or thinks that some investigations by law enforcing agencies are essential so as to fix responsibility regardIt ing the case, the case is regarded as medicolegal case. MLC is left to the doctor's judgment to label the case as whether patient agrees or not. Sometimes, the patient or relative may request or conmpel a doctor not to make MLCbut the doctor has to be firm with his own decision. Medicolegal case report (MLR): This includes the legal documents prepared by a doctor at the request of some investigating authority, for example, police, magistrate. It is made on both living and dead patients. Examples are (1) injury report, postmortem report, vaginal swab report in case of sexual offences, etc. Who can make MLC ?: A government as well as a private practitioner can make MLC. It is very common for private hospitals and private practitioners to avoid MLC cases; they generally refer doubtful cases to government hospitals. If condition of such a patient is serious and he dies on the way to hospital, the private practitioner as well as the private hospital can be sued

under S.304A. Following cases are labelled as MLC and the police must be informed: (1) injury cases, (2) poisoning, (3) burns, (4) sexual assault, (5) brought dead cases, (6) brought unconscious, (7) road traffic accidents (RTA), (8) fall from height, (9) factory accidents, (10) death in OT during MTP, criminal abortion, delivery or other surgical procedures, (11) suspected homicide or suicide. Precautions while preparing MLC 1) Consent for examination: If a patient is not arrested, consent is required. the purpose of medicolegal examination, For consent can be given by any person of sound mind and >12 years of age. If the person is unconscious or insane or Cross examination in the

court of law

is in

Reexamination

After examination-in-chiet, the crosS-examination is the next procedure. The lawyer of the opposite party, that is defence lawyer examines the witness.

Main objectives of cross-examination: 1)

to elicit facts favourable to the

cross-examining

party 2) to test the accuracy of the facts told by witness, 3) to find out the weak points in the case, and

discredit the witness and prove that the report given is not correct and is a biased one. cross-examination, the defence lawyer will try to weaken the evidence given by the witness in the examination-in-chief. He will elicit points favourable to the defence side and for this, he will try to establish that the evidence given by the witness was conflicting and contradictory. So, the witness must be very careful in answering questions during cross-examination. Leading questions are allowed in cross-examination [SN-15]. 4) to

In

SN-15: Leading

question

Leading question [S.141, IEA]: Any question suggesting the answer, which the person putting it wIshes or expects to receive. In simple language, t is a question, which suggests the answer by itselt, unat 15, the answer lies implied in the question itsel. answer is expected as simply either 'yes' or'no. he Leading questions are asked during 'cross-examination' (S.143, IEA].

Legal

Procedures

Leading question for an expert witness Examples: (c.g. doctor) may be as follows. Q.1: Did you carry out postmortem examination? Q.2: Did you find a 4 cm laceration on the forehead? Q.3: Was the length of knife 10 cm? are not allowed in examination-in-chief They and reexamination [S.143, IEAJ. In 'chief examination, the leading questions may be asked uncler two conditions: 1) if the court permits to ask leading question, or 2) when the witness is declared 'hostile' by the court. are leading questions asked? To test the Why truthfulness, skill and character of the witness. So, witness must be very careful in answering the questions.

SN-16: Dying declaration Dying declaration [S.32(1), IEA] is a written or verbal statement of a person who is dying as a result of some unlawful act. If he dies, the document containing the statement is produced in the court as a dying declaration. It is followed in India, that is, dying declaration is legally accepted in the courts of law in India. It is a type of hearsay evidence. Dying declaration is considered legally relevant because it is commonly believed that a dying person always speaks the truth. Who can record dying declaration? If possible, it should be written by the dying person himself and then signed by him. If impossible, it can be recorded by the following. 1) Executive magistrate: The dying declaration recorded by executive magistrate is preferred and has more importance as compared to that recorded by doctor or police officer or any other

person. 2) Other persons, for example, doctor, police ofncer or even any lay person (like Panchayat head declaration but or relative) can record dying It should be in s evidential value will be less. should sign the presence of two witnesses who dying declaration.

Role 1)

of doctor: Stabilise the patient.

SECTIONT

the police wil

1)

and then 2) Inform the police magistrate to record inform the arca executive

dying declaration. if the life of patient 3) Write the dying declaration delay in the arrival is in danger or there is much of magistrate. state4) Compos mentis: Before recording the ment, the doctor first has to certify that patient is in perfect mental condition (i.e. compos mentis) to make a declaration. The doctor should be there throughout the declaration to check the mental condition of the patient. 5) Signature Magistrate signs the written declaration on the paper and then the doctor signs. The Signature by' the doctor signifies that the patient was in a sound state of mind and was well oriented in time, space and person while the statement was being recorded.

Procedure:

If

posible, it should be written by the dying

person himself and then signed by him. If not possible, it should preferably be video recorded. Record word to word: Dying declaration should be recorded in declarant's own words without any alteration of terms or phrases. If he is unable to speak, the signs and gestures are recorded. No oath and no leading question: The oath is not administered while recording dying declaration because of the belief that dying person tells the truth. Léading questions should not be put. Reading out and signature. If the statement is written by declarant himself, it should be signed by him with date and time. If the statement is recorded by any other person, it should be read out to the declarant and if he agrees, his signature or thumb impressions are taken. It is also signed by the magistrate, the doctor and the witness. Send declaration to magistrate: When the declaration is recorded by a person other than the magistrate, the declaration is sent to the magistrate in a sealed cover, The person recording the declaration will have to give evidence in the court to prove it. .FIR lodged by dying person to police is valid dying declaration. The person recording dying declaration should be present in the court to certify the fact. declaration is not admissible under two Dying conditions:

In

Ifthe person survives after makino.

dying laration, the dying declarat de Then he is called to the court dence. The oral evidence givento give c by this by attending the court has more impoperson as compared to the dying declaration record carlier. The dying declaration recorded earle acts as corroborative evidence. If the dying person is not in a soundstate mind as certified by the doctor. Western countries, the concept of dying depo sition |SN-17] is followed. Difference between dying declaration and dying deposition [D/W-24].

SN-17: Dying deposition Dying deposition: It is a statement of a person on oath, who is dying as a result of some unla ful act; it is recorded by magistrate in presence of accused or his lawyer. is followed in Western countries, for example It United States, where there is a provision for the court to be brought to the dying person, that is magistrate comes to the bedside. Here in addition to the magistrate, accused and his lawyer are alsa present. Rest of the procedure is exactly the same s in the court. This is called dying deposition; anda it is a full-fledged court procedure at the bedside, t is also known as 'court by the bedside. In India, the procedure of dying declaration (n0t dying deposition) is followed in which the stale some ment of a person, who is dying as a result of a

unlawful act, is recorded [either written or veru (oral)]. If he dies, the statement is produced in u court as a dying declaration). magiStrde oath is administered and then The records the evidence. in Inus Unlike dying declaration, which is followed dying deposition is recorded always by a magistr victim S-examine the The lawyer is allowed to erossand so leading questions are also allowed. retains t the victim survives, the dying deposition the its value. If we compare both the statements,with dying deposition has more value compared the dying declaration. Dying deposition is not followed in Inda. and dying declaration and between dying ilference deposition [D/W-24].

CHAPTER 2

SN-18: Exhumation

identification

autopsy when the first autopsy report is doubtful or has not been done properly. 3) When the body has been disposed off without any autopsy and then after disposal, foul play is 2) For second

Suspected.

determine cause of death, time since death, manner of death and to establish identity.

4) To

Prerequisites:

Writfen order of a first class magistrate.

C.

Supervision of magistrate: The digging out of buried dead body has to be done under thesupervision of magistrate. The police officer and medical officer also have to be at the spot, Early in the morning: Procedure of exhumation should be started early in the morning to

avoid publicexposure D.

Screening of the area: The area should be screened off from the public.

DW-19: Police

TABLE 2.5 Sr. No.

Identify the spot of buriat: The spot of burial has to be identified with the help of relatives and other persons related with the disposal. Besides, the location of the grave from some fixed objects such as road, tree, etc. is to be noted. E. Photography and sketching. Photographs are taken from very beginning of the procedure till cnd. Sketches may be drawn aboutthe position of coffin and body. Digging out of body: (1) Removal of earth in layers, (2) lifting out of bodycarefully to avoid artifacts, (3) identification of body by relatives, (4) noting the condition of soil and water, (5) collection of soil-about % kg of soil should be collected from above, lateral sides and below the body for chemical analysis in suspected poisoning. The soil from the control site should also be colleçted. If the jintermenthas Been recent, autopsy Autopsy: should be conducted either in the open near thee graveyard but screened off from the public, or at the mortuary. Injuries must be noted and interpreted correctly. Preservation of viscera in suspected poisoning: is If nothing found, then hair, soil, teeth and bones should be preserved. About % kg of soil should also be collected from the top, sides, bottom of the body and kept in dry clean bottles for toxicological analysis. E.

Exhumation S.176{3), CrPC): It is the lawful digging out of an already buried body from the grave. (Latin ex= Out ot, humus= ground). Scenario in world: In India, the bodics are mainly disposed of by cremation (i.e. burning), so exhumation is rarcly done in India. In Western coun tries, dead bodies are buried for disposal, so exhumation is more common. Purposes:

B.

Time limit: Though there is no time limit for exhumation in India, the period is restricted to 10 years inFrance and 30 years in Germany.

inquest and magistrate inquest (Table 2.5)

Difference Between Police Inquest and Magistrate Inquest

Features

Police Inquest [S.174, CrPC

Conducted

t

in cases

is done in those

cases where a person

committed suicide, or has 2. has been killed by another man/animal machinery, or 3. has been killed in an accident,or 4. has died in suspicious circumstances.

Investigating officer

Palice officer above the rank of head constable (HC), that is, SI

Warrant

Can not issue

Fine/Punishment Exhumation

Value

Legal Procedures

Can not impose Can not allow Inferior

Magistrate Inquest [S.176, CrPC]

the following cases: Dowry death 2. Death during police firing or poliço cdstody or prison or interrogation 3. Death in reformatories, borstal sckod, psychiatrjc hospital 4. Exhumation It is done in

1.

DM/SDM Can issuJe Can impose Can allow

Superior

SECTIONI

Forensic Medicine

D/W-20: Coroner's court and TABLE 2.6

St. No. 1

.

5.

Court Difference Between Coroner's Court andMagistrate

Presided by coroner

'court of inquiry

deaths Coroner enquires into sudden, suspicious, unnatural jurisdiction within his Accused need not be present during trial

punishment Coroner has no power to impose fine or give if Coroner can punish a person for contempt, committed within the premises of his court

D/W-21: Common

TABLE 2.7 St. No.

2.

5

Magistrate Court

Coroner's Court It is a

3.

magistrate court (Table 2.6)

Presided by magistrate It is a

'court of trial'

Magistrate enquires dowry deaths, exhumation, deaths police firing/prison/custody

Accused should be present during trial

Magistrate can impose fine and give punishment Magistrate can punish whether the offence is committed within or outside the premises of court

witness and expert witness (Table 2.7)

Difference Between Common Witness and Expert Witness

Common Witness

Expert Witness

Legally defined in S.118, IEA

Legally defined in S.45, IEA

A

in

common person who has actually seen or observed perceived the facts and narrates those facts in the witness box is a common witness

An expert witness is a person who is skilled in a particular field (e.g. law, science or art) and he is capable of drawing a conclusion on the facts observed by him or by others

He is not allowed to draw conclusion from his observation

He can

He can not express opinion on the observations made by others

He can

Responsibility is less

High

DW-22: Examination-in-chief and cross-examination (Table 2.8) TABLE 2.8 Sr. No.

Difference Between Examination-in-Chief and Cross-Examination

Examination-in-Chief In

the order of sequence described in S.138, IEA, it is the first examination ofa witness in the court of law

The witness is examined by the lawyer of the party that

has called him

3

Cross-Examination the order described in S.138, IEA, it is the second examination of a witness in the court of law; it means the examination-in-chief is followed by cross examination

1. In

2. Here

the lawyer of the opposite party, that, is the lawyer of the accused (defence lawyer) examines the

witness Leading questions must not be asked in chief examination; however, they can be asked in chief-examination only a) if the court permits, or b) when the court suspects that the witness is a hostlle

witness

3. Leading questions' are asked in

IS.143, IEAI

cross-examination

Legal Procedures

CHAPTER 2

21

Dw-23: Oral evidence and documentary evidence (Table 2.9)

2.9 Difference Between Oral Evidence and Documentary Evidence

TABLE St. No.

Oral Evidence

Documentary Evidence

oral/verbal statements under oath made before the court Types of oral evidence: Direct, indirect and hearsay

All

All

evidencee

More important because examination

it

permits cross

documents including electronic records produced for the inspection of the court

Verities of docurnentary evidence: Medical certificate, death certificate, medicolegal case (MLC) report, dying declaration, dying deposition

Less impor tant

D/W-24: Dying

declaration and dying deposition (Table 2.10)

TABLE 2.10

Difference Between Dying Declaration and Dying Depositíon

St. No.

Dying Declaration

Dying Deposition

Followed in India

Followed

merely the recording of a statement of a dying person It can be recorded by a magistrate or doctor or

It is a

It is

police officer or Panchayat head or relative The accused and his lawyer need not be present

in

Western countries, for example United States

ful-fledged court procedure at the bedside, so aiso known as court by the bedside'

Recorded always by a magistrate.

The accused and his lawyer have to be present

Oath: Not administered

Oath: Has to be administered

Cross-examination: Not allowed

Allowed

Leading questions: Not allowed

Allowed

the victim survives, it loses its value and is not admissible in the court of law but it acts as corroborative evidence

f the victim survives,

If

Less

value

More value

it

retains its value

Medical Jurisprudence Chapter 3A Code of Medical Ethics, Medical Councils, Acts, Medical Records and Professional Misconduct INTRODUCTION amananmanmoa

dence

law; pruin relalaw of study

jurisprudence (Latin juris

Medical =

knowledge): It is the

=

Regulations 2002 (amended and then notified on 2009). The text of the code is actually prescribed in two parts: the declaration and the code proper. Declaration of Helsinki (1964) prescribes ethical principles for human experimentation.

tion to medical practice. Medical ethics: It means moral principles (code of conducts) which should guide the members of the medical profession in course of their practiceDUTIES OF A DOCTOR of medicine and their dealings with patients and Duties and Responsibilities of Physician other members of the profession. Medical etiin General quette means sense of courtesy and mutual respect (1) He should be pure in character and modest and which should govern the conduct and relationship pleasing in personality. He should be among the members of the medical profession. dedicated to is earliest known code provide service to humanity and he should uphold Hippocratic oath: It (4th-5th century BC), the modern version of the dignity and honour of his profession. (2) He which is the Declaration of Geneva, 1948. should maintain good medical practice by continCode of Medical Ethics, 1949: International uously improving his medical knowledge and skills. World Medical Association (in 1949) adapted cer(3) He should participate. in.continuing medical edutain codes of medical ethics (solely based upon cation (CME) for at least 30 h every 5 years. (4) He Declaration of Geneva), popularly known as Intershould bea member of medical societies and should national Code of Medical Ethics. attendtheir meetings.(5) He should maintain medof Medical las Ethics Code enumerated by Medical records for a period of 3 years fronm_ the date of ical Council of India (MCI)] in India: It is a set commencement of treatment. He should maintain a of regulations to maintain the professional conregister of medical certificates issued. (6) He should duct and etiquette among the members of a sysdisplay his MCI/State Medical Council (SMC) reg tem of medicine. It has eight chapters. In S.20A, istration number almost everywhere, for example, Indian Medical Council Act, 1956, MCI brings in clinic, on prescriptions, money slips, certiicates out regulations relating to the professional con and so on. (7) He should use generic names of drugs, duct, etiquette and ethics for registered medical not brand names. (8) He should employ only qual practitiopners (BMPs), but these regulations have ified medical and paramedical personnels to attend been now presented in Indian Medical Council patients. (9) He should announce fees before starting (Professional Conduct, Etiquette and Ethics) treatment. 22

CHAPTER 3

Their Patients

Duties of Physicians to exercis a reasonable degree of skill and 1) Duty to knowledge. (2) Duty to tell about the prognosis of to give legible prescription and discase. (3) Duty aboo the dosage and timing of proper instruction drugs. (4) Duty to warn the patient about side effects

to warn paticnt as well as closely of drugs. (5) Duty related people in case the paticnt is suffering from secrecy [SN-1]. infectious disease. (6) Protessional emergency (7) Duty to immediately respond to any (S)

Therapeutic privilege lplease refer to Chapter

3B, SN-3].

Duties of Physician in Consultation should be avoided. (2) (1) Unnecesary consultation Consultant should be punctual for consultation. (3) Patient should be reterred to consultant with case summary. (4) Fees and other charges should be displayed on the board of his room and in visiting room. des(5) Prescription letter should contain name and

a

1gnation.

Duties of Physician

Towards Professional

Coworkers Consultation fees should never be taken. It is professional courtesy and a doctor should consider it a pleasure and privilege to render service to all fellow doctors and their family dependents. (2) An RMP should never criticise his coworkers in front of patient. (3) The doctor should always help his fellow coworkers, especially in professional matters. (4) When a doctor requests his coworker to take over his patients temporarily during his absence, the coworker should agree only if he has the capacity to discharge the additional responsibility. (1)

Duties of Physician

Towards State

should cooperate with_authorities in the administration of sanitary or public health laws and Tegulations. (2) During epidemic, (a) a doctor should not.abandon his duty for fear of contracting disease himself, (b) a doctor is bound to bring every case of mmunicable disease under his care_to the notice Opublic health authority. (3) The police should be about medicolegal cases brought to him. (4) births and deaths should be brought to the notice of authorities. (5) The physician should respond to emergen military service when required.(6) A med ical practitioner bound to treat or proVide medical Is (1) He

med

Medical Jurisprudence

aid to persons wounded or sick in the armed forces, ship-wrecked persons, prisoners of war or civilians of cnemy nationality without any discrimination based On sex, race, religion or nationality. (7) Privileged

communication

|SN-2].

RIGHTS AND PRIVILEGES OFA DOCTOR (1) A doctor has right to choose his patient except in emergency. A doctor can refuse a patient (a) if patient is unable to pay doctor's fees and (b) if the condition of the patient does not belong to the pro-

fessional specialisation of the doctor. The right to choose patients does not apply in case of emergency. The doctor must attend every patient in emergency even if he is not able to pay fees. After the management of the case, the doctor can demand fees from the patient. It is the right of the doctor to recover fees from his patient. If the patient denies paying doctor's fees, the doctor can sue the patient in the civil court for recovery of his fees. (2) He has the right to prac tice medicine and prescribe medicines. (3) The doctor has the right to possess or prescribe drugs listed in the Dangerous Drug Act. (4) He has the right to add professional titles to his name (i.e. doctor) and qualifications after his name (e.g. MBBS, MD). (5) The doctor has the right to give evidence as an expert in the court. (6) He has the right to issue medical certificates. (7) The doctor has the right for appoint ment to any public or government hospital.

DUTIES, RIGHTS AND PRIVILEGES OF PATIENTS

Duties of Patient (1) He should furnish the doctor with complete infor mation about the facts and circumstances of his ilness. (2) He should strictly follow the instructions ot the doctor. (3) He should pay reasonable fees to the doctor. (4) lt a patient wishes to take second constt tion/opinion, he has to inform the first doctor.

Rights and Privileges of a Patient

facilities and emer (1) Right to access to healthcare social or age, sex, religion, regardless of services gCncy his own doctor Right to choose from another (2) status. cOnomic opinion Right to seek second during consultation privacy doctor. (4) Right to have complain and redressal of treatnnent. (5) Right to

Cly.3) Or

SECTIONT

Forensic Medicine

with dignity, with grievances. (6) Right to be treated discrimination. (7) Right of care and respect without about confidentiality. (8) Right to get information treatment, alternatives, his diagnosis, investigation, to refuse complications and sIde ettects. (9) Right Right to (10) treatment. any diagnostic procedure or access his medical records.

UNETHICAL ACTS Advertising: (a) A physician should not use an unusually large signboard. The contents of his signboard should be title, name and qualification. Signboard should not be affixed on a chenmist shop, tree or in places where he does not reside or work. (b) Prescription paper should contain title, name, qualification, address, registration number and telephone number. (c) Consultation fees should be clearly exhibited in consulting room or waiting room. (d) A physician should not publish in press the reports of cases treated by him. (e) A physician can announce in press, his starting of practice, interruption or restarting after a long interval, a change of his address, temporary absence from duty and so on. 2. A physician may patent surgical instruments/medicines/procedures. But it shall be unethical if the benefits of such patents/copyrights are not made available in situations where the interests of large population are involved. 3. Running an open shop for dispensing of drugs and appliances by physicians is unethical. 4. Dichotomy (fee-splitting), that is the practice of sharing (e.g. offering, giving or receiving) fees for the referral of a patient with professional coworkers, is also unethical. 5. All drugs prescribed should always carry a proprietary formula and clear name. Prescribing a secret remedy of which he does not know the composition, the manutacture or promotion of their use is unethical. 6. Physician should not aid or abet torture. 7. Practicing euthanasia is unethical. 8. Code of conduct for doctors and professional association of doctors in their relationship with pharmaceutical and allied health sector industry: Doctors should not take any gifts or mone-" tary grants or avail any facility or seek any type of hospitality from any pharmaceutical companies. A 1.

physician may carry out, participate in, or work in rescarch projects funded by pharmaceutical and allied healthcare industries. Doctors must main tain professional autonomy.

PROFESSIONAL MISCONDUCT (INFAMOUS CONDUCT) [SN-3] MEDICAL COUNCIL OF INDIA (MCIY CI is the statutory body tor establishing and maintaining uniform standards of medical education and recognition of medical qualifications

It grants registration to medical practitioners and monitors medical practice in India. It was established in 1934 under Indian Medical Council Act 1933. In 1956, this Act was repealed and a new Act, known as Indian Medical Council Act, 1956, was enacted. Functions of MCI include (1) maintenance of a medical register, (2) formulation of medical uniform standard of medical education, (3) recog nition of medical qualifications, (4) registration, (5) warning notice, (6) appeal against disciplinary action, (7) CME programmes and (8) formulation of code of medical ethics. NITI Aayog has recommended the replacement of MCI (IMCAct, 1956) with National Medical Commission (NMC), and thus National Medical Com mission Bill, 2017, has been drafted. Indian government dissolved MCI and replaced it with seven-member Board of Governors (BoG) by bringing an ordinance [Indian Medical Council (Amendment) Ordinance 2018] dated 26 September 2018. The BoG has been appointed initially for a period of 1 year, and will be the sole decision-making body till the NMC Bill, 2017-meant to replace the MCl-is cleared in Parliament. A similar BoG was also appointed in May 2010.

NATIONAL MEDICAL COMMISSION (NMC) NMC shall consist of total5 persons: a chair person, 1#ex officio members, 21 part-time mem bers anedan-ex-efficio member secretary. A person who is aggrieved by any decision of NM may preter an appeal to the Central Government against such decision within 30 days.

CHAPTER 3

and functions of NMC: (1) To lay dowvn policies for (1) maintaininga high quality and high standards in medical education, (ii) regulating medical institutions, medical researches and medical professionals; (2) to assess the requirements in health care, for example, human resources, infrastructure; (3) to nmake necessary regulations for the proper functioning of the Commission, the Autonomous Boards and the State Medical Councils; (4) to ensure compliance by the State Medical Councils; (5) to ensure observance of professional ethics in medical profession. Medical Advisory Council (MAC): It shall be the primary platform through which the states and union territories nmay put forward their concerns before the NMC. MAC shall advise the NMC on the measures to maintain the minimum standards in medical education, training and research. National Eigibiity-cum-Entrance Test and Examination (NEETE): There shall be a uniform NEET for admission to UG medical education in all medical institutions There shall be a uniform National Licentiate Examination (NLE) tor the studentsgraduating from medical institutions for granting hcense to practise medicine. Only the person enrolled in the State Register or the National Register shall be allowed to practise medicine and shall be entitled to sign or authenticatea medical certificat¢. Any person who contravenes shall be punished with fine of Rs 1-5 lakhs.

Powers

Autonomous Boards Autonomous boards, which have been constituted, are (1) UG-MEB (Undergraduate Medical Education Board), (2) PG-MEB (Postgraduate Medical Education Board), (3) MARB (Medical Assessment and Rating Board) and (4) EMRB (Ethics and Medical Registration Board). A person who is aggrieved by any decision o an autonomous board may prefer an appeal to the

Commission against such decision within 60 days. Functions of UG-MEB: (1) To grant recognition to a medical qualification at the UG level; (2) to deter

ne standards of medical education at the UG level develop

competency-based dynamic curricuthe UG.level and (ii) for primary medicine Community medicine to ensure health care; Irame guidelines for setting up of medical institutione tutions for mparting UG courses; (4) to determine dards and norms for infrastructure, faculty and

at

Medical Jurisprudence

quality of education in medical institutions; (5) to facilitate development and training of faculty members teaching UG courses; (6) to specify norms for compulsory annual disclosures, electronically or otherwise, by medical institutions, in respect to their functions. Functions of PG-MEB: Almost same functions as that of UG-MEB, but these functions are at the PG and super-speciality levels. Functions of MARB: (1) To carry out inspections of medical institutions for their assessment and rating (2) to grant permission for the establishment of a new medical institution; (3) to determine the procedure for assessing and rating medical institutions for their compliance with the standards laid down by the UG-MEB or PG-MEB; (4) to make available on its website the assessment and ratings of medical institutions at regular intervals; (5) to impose monetary penalty against a medical institution for failure to maintain the minimum standards specified by the UG-MEB or PG-MEB. Functions of EMRB: (1) To maintain a National Register: It should contain name, address and all recogg nised qualifications possessed by a licensed medical practitioner. It shall be a public document, and it shall be made available to the public by placing it on the website of EMRB. EMRB shall ensure electronic synchronisation of National Register and State Register in such a manner that any change in one register is automatically reflected in the other registers (2) to regulate professional conduct and promote medical ethics.

State Medical Council If a doctor is aggrieved by any action taken by SMC, he may prefer an appeal to the EMRB. If he is aggrieved by the decision of EMRB, he may prefer an appeal to the Commission within 60 days of decision. If he is aggrieved by the decision of the

the Commission, he may prefer an appeal to the entra Government within 30 days of the decision.

SOME IMPORTANT ACTS (Care and Protection

(3)Juvenile Justice

of Children) Act, 2015 and chilconflict with law in children

addresses

dren in need of care

and protection.

Medicine SECTIONI Forensic

It

'child' as defines juvenile' or

a

below person bclow

years of age. law [S.2(13)] means 'a Child in conflict with offence have conmitted an child who is alleged to ageas on the date of commisand was 18 ycars of sion of such offence. 18

consists first class judicial magisof three persons: One magistrate) with 2 years trate (or metropolitan workers at least one of experience and two social For every district, of whom should be a woman. there will be one or more JJBs. Action against the offender:law is apprehended by conflict with Ifa child insuch child shall be placed under the the police, charge of Special Juvenile Police Unit or Child Welfare Police Officer, who shall produce the child before JJB within 24 h of apprehending the child. The child shall not be placed in a police lockup or jail. of age is aPpreIf any person of 18-21 yearsoffence when he hended for committing an 18 years, then, such perwas below the age of a as shall be treated child during the proson

Juvenile

If

Justice Board ()]B) |S.4]:

It

cess of inquiry.

any person of >21 years of age is apprehended for committing any serious or heinous offence when he was between the age of 16 and 18 years, then he shall be tried as an adult.

Punishment:

If the age of child is 18 valid consent for an valid consent for an act not likely act 'not intended to intended or not known to be cause death done in to cause death or grievous hurt faith for person's good Example: Ram and Shyan (both

benefit

>18 years of age) agree to fence with each other for

amusement. This agreement implies consent of each to suffer any harm which in the course of such fencing may be caused

Example: Surgical operation done by a surgeon with consent in good faith for the benefit of patient

without foul play; if Ram, while playing hurts Shyam, Ram commits no offence. It means Ram will not be responsible for his act because Shyam (a major being>18 years) is able to give a valid consent and he gave Consent to suffer any harm in this amusement

In

this section, the age has been mentioned (i.e. 18 years)

TABLE 3B.2

In

this section, the age has not been mentioned

S.89, IPC Versus S.92, IPC S.92,

S.89, IPC

IPCc

Any act done in good A child of 99% probability of doctor being guilty. Otherwise accused per SOn will be presumed to be innocent.

at

Medical Jurisprudence

Punishment

well as fine.

for doctor: Imprisonment as

Classification of cases

of criminal

negli-

gence: 1) When 'no injury' occurs due to negligence: Since there is no damage, the patient cannot claim compensation in civil court or consumer court. But patient can still go to criminal court where according to S.336, IPC, the negligent doctor will be punished with P = I, mnh Or F (Rs 250) or both. For examnple: A doctor conducts a deliv-

ery under influence of alcohol but fortunately the delivery occurs safely. Later the patient becomes aware of the fact and she goes to civil court to ask for monetary compensation. Will she get compensation? No, because delivery was safe and there was no damage. Still she has another option. She can go to criminal court where the doctor will be punished according to S.336, IPC. 2) When 'injury' occurs due to negligence: a) When hur is caused to the patient due to negligence of doctor: The doctor will be punished according to S.337, IPC with P = I month Or F (Rs 500) or both. For example, a doctor gives penicillin injection without testing sensitivity and the patient develops anaphylaxis. By treatment, the anaphylaxis was controlled by the doctor. Although the patient is alright now, he can stil sue the doctor according to S.337, IPC. b) When grievous hurt is caused to the patient due to negligence of doctor: The doctor will be punished according F (Rs 1000) to S.338, IPC with I,.or years or both. For example, a doctor ampu

tates a wrong leg. negligence 3) When 'death' occurs due to punished according The doctor will be example, a doctor to S.304A, IPC. For testing8 injection without anagives penicillin develops patient sensitivity and the patient The relatives of phylaxis and dies. according to S.304A, doctor can sue the IPC.

SECTIONT

Precautions

Forensic Medicine

against negligence:

A

no complaint will be entertained [S.24A,Co

doctor should

be very careful while treating a paticnt because a slight mistake done by the doctor can be a cause of negligence and the patient who suffered damage can suce the doctor; thus the doctor should kecp some important points in his mind and take some precautions to avoid these consequences [Mnemonic TEST-TLC For MI]. 1) Take informed consent. 2) Examination of a female patient should be done in the presence of a third party which should be a female, for example, female nurse. 3) Sensitive tests should be done before injecting some drugs which are likely to produce anaphylaxis, for example, penicillin. 4) Tetanus injection has to be given in every case of injury which is bleeding. 5) Telephone: Do not prescribe drugs on telephone. 6) Labour: Do not leave the patient unattended during labour. 7) Confirm a diagnosis by proper investigations. 8) Frequently check the conditions of the equipment. 9) Maintain accurate medical records. 10)

sumer Protection Act, 1986). It means that if

3)

4)

5)

6)

Inform police if death occurs during anaesthe-

7) 8)

sia or during operation.

Discuss the defences that a physician can take when he gets a Suit of medical negligence.What are different forums where action can be taken against a negligent doctor, and discuss the penalties awarded by these forums LO-2:

Defences against medical negligence [Mnemonic New Low Cost PCM, Now Vanishes RMP] 1) No duty owed towards the patient: The doctor did not agree to treat the patient; therefore, no duty exists. 2) Law of limitation: It prescribes the time-limit for different suits within which an aggrieved person can approach the court for redress or justice. For example, in relation to Consumer Protection Act, a complaint has to be filed by an aggrieved patient within 2 years from the date of cause of action (i.e. negligence). After 2 years,

65 9)

patient brings the claim tothe consumer forum after 2 years of alleged negligence, that person cannot claim compensation and the doctor can use the concept of law of limitation' as a defenca

Calculated risk doctrine: If a physician chooses for his patient a course of treatment which is potentially dangerous to life, yet has a proven record of saving the lives of patients in

scveral cases, the doctor is said to have taken a calculated risk. If the patient suffers any harm due to such a procedure, the doctor would be protected by the calculated risk doctrine. Patient negligence: When only the patient is negligent, the doctor can take a defence of patient negligence. Contributory negligence: It is not necessary that only the doctor is negligent; patient may also be negligent. When the negligence of the doctor is combined with the negligence of the patient, the doctor can take this defence. Medical maloccurance [SN-4] and Medical misadventures [SN-5]. Novus actus interveniens [SN-6]. Volenti non fit injuria (voluntary assumption of risk in the United States): In Latin, it means to a willing person, injury is not done. The doc tor explained the risks of a particular treatment to a patient and clearly warned him. The patient willingly consented for that treatment even after doctor's warning. If injury occurs to the patient the doctor will not be responsible and the patient will not be able to bring a claim against the doc tor. In a sense, the patient consented to waive all claims for damages. For this, the doctor must show that an informed consent had been taken and all side effects had been explained clearly to the patient. The doctor can use the concept ot volenti fit non injuria' as a defence. For exampls patient sustains radiation burns during ther apy and he had earlier been explained about the risks; he cannot claim damages. Res Judicata (or Doctrine of Double Jeop

ardy): According to S.300, CrPC, person once convicted or acquitted cannot be tried for tne same offence 10) Medical indemnity insurance: Insurance companies have been providing 'Medical

ag

CHAPTER 3

Indemnity Insurance (MI) to doctors since 1991 in India. The company provides compensation amount to the paticnt when doctor is charged with medical negligence. It works like other life insurances. When a manulac1) Product Liability |SN-7|: a delective medical product (c.g. supplics turer instrument, medicines), that detfective product is used inadvertently by the doctor on a patient and the patient sustains injury, then the manufacturer is held responsible for the injury sustained by the patient. Different forums where action can be take [SN-8] against a negligent doctor

SN-3:

When

Contributory negligence the negligence of the patient simultane contributes to the negligence of the doctor

ously to cause harm, it is called contributory negligence. Patient's negligence + Doctor's negligence = Con-

tributory negligence Example: Doctor applied a tight plaster cast on patient's leg (i.e. the doctor is negligent). As a result, the patient developed numbness in his toes but he did not inform the doctor (i.e. the patient is also negligent). Consequently, the patient suffered permanent injury. Here, both the doctor as well as patient are negligent, so this is a case of contributory negligence. The patient

contributes his negligence when he not provide proper history to the doctor, or (2) refuses to take up the suggested advice, or (3) does not follow treatment prescribed by the doctor, or (4) leaves the hospital without doctor's advice (LAMA) (5) fails or to seek further medical treatment if signs and symptoms persist. Contributory negligence is a good defence for the Physician only in the case of civil negligence; it has no place in criminal negligence. The burden of proof lies with the doctor. Doctrine of comparative negligence: The quanO Injury caused by the patien's negligence and the doctor's negligence is decided by the court and accordin the ompensation is awarded. Suppose, atient's negligence contributes 70% of his injury and doctor's negligence 30%, then the patient would entitled only to 30% of the mpensation. Exceptions (1) does

or

of contributory negligence

1)

Medical Jurisprudence

Last clear chance doctrine: If the doctor fails to prevent damage resulting from the negligent act of the patient, even after getting sufficient clear time, he cannot plead contributory negligence in civil cases. For example, a doctor prescribes a drug to the patient, but fails to inform the patient about the side effects (the doctor is negligent). The patient develops rashes, but does not inform the doctor (the patient is also negligent). The patient visits the doctor on next appointment date. The doctor sees rashes and yet does not change the drug. The patient suffers injury later. He sues the doctor. The doctor takes the plea of contributory

negligence. The patient can say that the doctor had the last clear chance to avoid injury, because on the patient's subsequent visit, the doctor had seen the rashes and yet did nothing. 2) Avoidable consequence rule: A negligent act of thé patient aggravates the damage already caused by the negligent act of the doctor. The damage could have been avoided if the patient was not negligent afterwards. In such cases, the patient cannot plead contributory negligence in civil cases. For example, a patient with a gaping lacerated wound approaches the doctor. The doctor does not apply bandage and antibiotics to the wound (the doctor is negligent). He however advises the patient not to allow the wound to get contaminated. The patient at home thinks that applying cow dung would heal his wound faster and he applies cow dung. Later, his wound gets infected. During this period, he does not contact the doctor (the patient is negligent). When the condition of the patient got worse, he visits the doctor the next week to get his wound examined again. Here, both the patient and doctor are negligent and normally the com pensation should have been shared between the doctor and patient, but since the patient aggravated his own injury by doing something which pay Was avoidable, the doctor does not have to any compensation.

SN-4: Medical maloccurrence God) (inevitable accidents; Act of

are many biolog maloccurrence: There Medical body which cannot human the Ical variations in

44

SECTIONI

Forensic Medicine

always be explained. Every hunman being responds differently to different drugs as well as different give treatment modalities. A doctor always tries to improve best care and attention to his patient to occahis health or to save his life. But on certain given sions, despite all proper care and attention fails to by doctor during treatment, the patient reacrespond properly or may suffer from adverse severe injurics tions of the drug which may lcad to is as mediknown or permanent deformities. This biocal maloccurrence and it is duc to unexpected logical variations in the human being. to Since the doctor gives best care and attention said his patient during treatment, he cannot be responsible for to be negligent; he is not actually these medical maloccurrence cases. Therefore, the injured person does not get monetary compensation in every mishap or accident which results in injury, if the doctor is careful in the selection of the

drug and has taken appropriate measures to overcome undesirable foreseeable effects. Medical maloccurrence can be a defence for a doctor against medical negligence. Examples of medical malocurrence: (1) Breaking of a needle during intramuscular injection due to sudden muscular spasm. (2) Damage to recurrent laryngeal nerve during thyroidectomy.

SN-5: Medical misadventure

(therapeutic misadventures) Medical misadventure: It is the occurrence of some unexpected and unforeseeable dangerous mishap or accident or disaster with the patient due to use of some drugs or procedures. An injury or death of the individual occurs due to some inadvertent or unintentional act by a doctor or his agent or hospital. Types:

(i.e. during treatment): a effect of particular drug which It is the harmful is known to have adverse reactions but finding no

Therapeutic misadventure

other alternatives and taking into consideration all pros and cons, the drug was used to treat a diseased condition. Diagnostic misadventure (i.e. during diagnostic procedure): For example, the harmful etfect of dyes.

Experimental misadventure (i.e. when the patient agrees to become a subject in an experimental study).

It is a known fact that almost every therapeui. drug and every therapeutic and diagnostic procedu can cause death. A doctor is not liable for inir ries resulting from adverse reaction to a drug, however the ignorance of the possibility of an adverse reaction tion o the drug amounts to negligence.

Doctor must warn the patient about the possibility of side cffects of a drug. Examples of therapeutic misadventures: Severe hypersensitivity reaction or anaphylaxis with penicillin, aspirin and so on. Barium enema may cause traumatic rupture of rectum resulting in chemical peritonitis. A burn caused by a hot water bottle. Thyroid cancer with I131 therapy. Breast cancer by prolonged use of diethylstilbe strol. Prevention: 1) Prior to prescribing a drug, a doctor should (1) ask the patient about the history of hypersensitivity reaction, (2) know the adverse effects of drug, (3) prescribe the drug having lesser side effects and (4) tell the patient about the possible side

effects

2) Doctor should be well prepared (i.e. well equipped with life-saving measures) to treat the adverse

effects of a drug if they occur. 3) Sensitivity tests should be done before injecting certain drugs which are likely to cause anaphylaxis.

SN-6: Novus actus interveniens Novus actus interveniens in Latin, means 'new or unrelated intervening act. It is sometimes referred to as an act of God. A person is responsible not only for his actions but also for the logical consequences of these actions. At times, some new unexpected and unforeseen happening (i.e. new act) occurs which breaks the continuity of events. It means a new act breaks the causal connection between doctor's negligence and subsequent new unexpected and unforeseen damage/injury. This new unexpected and unfore seen event relieves the negligent doctor from by responsibility of the damage/injury suffered the patient. Most of such interventions are of medical natur but sometimes they may be related to natural disasters (e.g. accident or earthquake).

E

CHAPTER 3

ample: A patient of myocardial infarction (M1) treated by a doctor in OPD for a long Was being he calls the doctor and says eriod. One night peri cst pain. Doctor does is having severe h e that calls him again Paticnt seriosly. not take him continues to ignore him. the doctor and again but A fer 2 h, the wife of patient calls and informs the cOndition of her husband is the doctor that ambulance. The worsening. The doctor sends an hospital after to ambulance returning quickly the patient receiving the patient, overturns, and in the accident. The wife sues the doctor. is killed was the negthis case, ignorance by the doctor In

as not the cause of

ligent act but this negligence death. The cause of death was the was

accident which

completely unexpected and unforeseen act.

act which had no relation proximate cause of death. the The accident (i.e. neW intervening act) breaks chain of causation. Here the doctor can take the defence of doctrine of novus actus interveniens. novus MLI: Doctors frequently use the doctrine of actus interveniens as a detence to protect themselves from the consequences of negligent acts committed by them. There are some circumst: aces where the victim dies of novus actus interveniens and the doctor gets into trouble, though the injury caused by him was not serious enough to have caused death of the victim. This new intervening with negligence is the

SN-7:

Product liability

Product liability: When a manufacturer supplies a defective medical product (e.g. instruments, medICines or prosthetics), and that defective product 1S used inadvertently by the doctor on a patient and consequently the patient sustains injury, then tne manufacturer is held responsible for the injury Sustained by the patient, that is manufacturer is able. This is known as product liability. The docOr may or may not be liable. Duties of manufacturer:|It is the duty of the manacturer to give information in the package insert 4rding indications, dosage, route of adminisration, side effects, ontraindications, precautions and so on. Vhen

the manufacturer is liable: Usually, the facturer is liable, unless the doctor used the nstrument incorrectly. Moreover, if the drugs are

Medical Jurisprudence

4

found to be adulterated, contaminated or dosage has been printed incorrect, the manufacturer is liable.

Duties of doctor: It is the duty of the doctor to provide such information to the patient. Manufacturer has no duty to ensure that such information in the package insert reach the patient. When the doctor is liable: (1) If it is proved that the instrument was functioning satisfactorily in previous operations, (2) if the instrument is incorrectly used or mishandled by the doctor due to lack of knowledge about the instrument, (3) if the instrument was not sent for servicing to the manufacturer for a long time and no request was sent for the same purpose, (4) if the doctor knew the dangerous side effects of the drug and he could have used a safer substitute, yet he prescribed the same dangerous drug for no specific reasaon and (5) if the manufacturer has provided information in package insert but doctor did not convey it to the

patient. manufacturer nor doctor liable: When Neither is danger unexpected, unknown or unforeseeable, for example, medical misadventure. Who can suethe manufacturer? Buyer (e.g. hospital owner), user (e.g. doctor) or the person who sustained injury (e.g. patient). Who can be sued? The person who suffers injury can sue anyone in the chain of sale/supply, that is, manufacturer, distributors, sellers, hospital or doctor.

SN-8:Vicarious liability (Vicarious responsibility) Vicarious

liability (or vicarious responsibility)

means lHability of an employer for the negliget act of his employee. It implies that an employer 1s responsible not only for his own negligence but also for the negligence of his employees so long it scope or Occurs within the reasonable course and their employment. principle It is based on the Latin principle 'the is, let the superior of respondeat superior, that answer or "let the be responsible' or let the master means submistake'. Vicarious Superior reply to the stituted. oftheship' known as Captain also is doctrine This doctrine.

SECTIONI

Conditions

Forensic Medicine

to be met for doctrine of vicarious lia-

bility: 1) There must be an employer-employce relationship. 2) The negligent conduct of employee must have occurred within the scope of his employnent. 3) It should have occurred while on the job.

Examples:

a) A doctor leaves a swab (or sponge or forceps) in

the body of a patient after operation. Doctor is responsible for damage to the patient although it is the duty or responsibility of the theatre nursing sister to count all articles used during operation. So for the nistake of nursing sister (an employee), the doctor (employer) is responsible. b) Doctors are well known for their illegible handWriting on the prescription card. When he

Writes illegible prescription, the pharmacies may dispense wrong drug in wrong dosage. Here, the doctor is vicariously liable.

SN-9: Res ipsa loquitur Res ipsa loquitur: Ordinarily, if a patient alleges a doctor to be negligent, the patient has to prove negligence of the doctor. However in certain cases, the medical negligence is so obvious and gross that the patient does not have to prove anything, that is, the fact speaks for itself. This is known as the Doctrine of res ipsa loquitur (Latin, res ipsa

loquitur means the thing or fact speaks for itself). In other words, the patient is not obliged to prove negligence in the case where the rule of res ipsa loquitur applies. Here, the doctor has to prove that he was not negligent. Components: 1) The injury/wrong would not have ordinarily occurred without the negligence of the defen dant (doctor). 2) The doctor (defendant) had full exclusive control over the treatment or injury producing instrument' which produced the injury. 3) The patient (plaintiff) must not contribute to his own injury, that is, the patient not guilty of contributing negligence. in cases of negligence, the patient Normally requires the expert testimony of a doctor in order to prove that the required standard of care had not been taken. In case of res ipsa loquitur, the patient

docs not have to produce the testimony of any expert, because a laymen with common sense can say that the doctor was negligent.

Examples:

Removal of wrong limb or wrong organ. 2) Failure to remove swab or instruments (ea scissor or forceps) from the abdomen/chest aft 1)

operation.

3) Failure to give TT injection in a case of bleedino

4) 5) 6) 7) 8) 9)

injury. Transfusing mismatched blood. Causing burns from careless use of hot water bottles or X-ray therapy. Breaking needle while injecting but not inform. ing the patient about it. Giving medicines in overdoses. Careless administration of poisonous medicines. Loss of function of a hand from prolonged

splinting. This doctrine is applied to both civil as well as criminal negligence. This doctrine can be applied against several defendants (i.e. doctors). Doctrine of common knowledge: It states that when negligence is of such nature that even a layman with ordinary common knowledge having no technical expertise can appreciate it, then evidence a medical expert to prove negligence is not required. Usually in medical negligence cases, expert tes timony by competent and qualified doctors s required. But according to the doctrine of common knowledge, expert testimony is not required in cases of res ipsa loquitur. Calculated risk doctrine: It is an exception ot rs ipsa loquitur. If a physician chooses for his patient a course of treatment which is potentialy danger the lives Ous to life, yet has a proven record of saving of the patients in several cases, the doctor is saxdany have takena calculated risk. If the patient suffers e harm due to such a procedure, the doctor would protected by the calculated risk doctrine. toos In other words, the doctor is not liable if he n a reasonable and calculated risk to save the su of a patient and in the process, the patient fered injury. at impose liability, a plaintiff must show t To meu doctor's decision was below the certified mu ical standard at that time. The doctor prove that the line of treatment he chose

CHAPTER 3

medically acceptable procedure and had unavoidable risks. a

an

SN-10: Consumer (COPRA= CPA)

.

Protection Act, 1986

introduco to protect the interest COPRA was consunme atnd for settlement of consumer of the disputes. National mission, On appeal April 1992,the decided that the Commission Kerala State from Consumer medical services be covered under CPA). = Act (COPRA

In

Protection 1995, the Supreme Court (Justice . On 13 November in a landmark decision (Indian Bal Krishna Erade), V. P. Shantha), upheld Medical Association versus (done on payment basis as that the medical services covered under COPRA. well as done free of cost) are

that a patient (consumer) can make a complaint to a redressal forum in respect to defecdoctor. tive service given by the lodging comCentres (i.e. redressal agencies) for plaint: A complaint can be lodged at any of the following centres (Table 3C.4)

of the Act: If any person is aggrieved by an order made by National Commission, he can appeal to Supreme Court within a period of 30 days from the date of order. Penalty: aPor noncompliance of any order by these commissions, a person shall be punished with imprisonment ranging from month to 3 years. a Where a complaint is frivolous, the complaint is dismissed and complainant is ordered to pay cost to oPposite party not exceeding Rs 10,000. Apprehensions in medical profession 1) This Act will totally disturb doctor-patient relationship. 2) Medical practitioners will opt for Defensive Medical Practice' [SN-12]. 3) The insurance companies have been providing8 MIr to the doctors since 1991 in India. aS.23

This means

Procedure of complaint: oLimitation period for complaint: Complaint

has to be filed within 2 years from the date of cause of action. After 2 years, no complaint will be entertained |S.24A]. District forum shall refer a copy of such complaint to the opposite party within 21 days, directing him to reply (ie. give his version of the case) within a period of 30 days. Notices can be served through fax. There is no court fee (even if the compensation is in crores of rupees). e is expected to be decided in 90 days (maxmum in 150 days). However, no limit has been laid down by the Act.

DLE 3C.4 Features Level

Headed

by Juisdiction

Medical Jurisprudence

SN-11: Defensive medicine Defensive medicine is one where the doctor advises

each and every laboratory test or radiological examination of the patient to avoid charge of negligence in future. According to CPA, 1986, doctors and hospitals are liable for any act of medical negligence and they can be sued for compensation under CPA. There is apprehension in medical professionals hat CPA will totally disturb doctor-patient relationship and there are chances of misuse. Thus, medical practitioners will opt for defensive medical practice, that is,: 1) Doctors will recommend diagnostic test or treatment that is more than that which is

required by the patient. 2) Doctors (especially general practitioners and new graduates) will be more evasive of their responsibilities towards their patients.

Consumer Disputes Redressal Agencies State Commission (i.e, State Consumer Dispute Redressal

District Forum (i.e. District Consumer Dispute Redressa

Commission)

Forum)

At district level,

thatis, situated

each district of the state

District judge

Rs 20L

in

State level, that is, situated the capital of each state

AT

Judge of High Court Rs

20-1

Cr

in

National

National Commission (i.e. Redressal Consumer Dispute

Commission) At national Delhi

Judge of >Rs

1

Cr

level; situated in

Supreme Court

ew

48

SECTIONI

Forensic Medicine

3) They will reter more number of cascs to specialists. 4) They will advise extensive laboratory investigations, which will make their position comparatively safe without improvement of clinical

mind/expericnce. 5) Physicians will avoid treating high-risk patients in order to reduce their exposure to lawsuits. 6) Doctors will order unnecessary CTs, MRls and biopsies and prescribe more antibiotics than medically indicated. 7) The doctors will opt for MII. Term 'indemnity means reimbursement to compensate. It works exactly like life insurance schemes. In MII plan, the insurance conmpanies can provide needful help to a doctor to pay the compensation amount to the patient when legally imposed to pay penalty for the confirmed charges of medical negligence. Physician is always advised to take up MII to safeguard his interest against any possible suit of negligence.

If

doctors adopt defensive medicine,

it bece

quite costlier to the patient, making the treatm much costlier beyond the reach of many. Moreo the patient will be exposed to the risks involved in the procedures prescribed by the doctors.

D/W-12: Civil negligence and criminal negligence (Table 3C.2)

DW-13: Professional misconduct and professional negligence (Table 3C.3)

conduct and medical negligence (Table 3C.4): D/W-14: 1Infamous

Same as the difference between professional miscon

duct and professional negligence

4 Medicolegal Autopsy (Postmortem Examination) INTRODUCTIONAND 0BJECTIVESS self, opis = view) means examination of a ody after death. It is also known as necropsy (necros= death, opis = view), thanatopsy examination (thanatos = death) or postmortem (post= after, mortem = death). Autopsy

(auto

=

Objectives

identity when not known, that is, in cases of unknown body. (2) To find out the cause of death (natural or unnatural). (3) To find out the manner of death, whether suicidal, accidental or homicidal.(4) To find out the time since death. (5) In new born babies, to determine viability and cause of (1) To establish

death. (6) To collect and preserve evidence, for example, gross evidences and trace evidences. (7) To col lect and preserve viscera for chemical analysis. (8) To

reconstruct the accident scene from the examination of injuries as to nature and duration, etc of accident.

PROCEDURE OF AUTOPSY

Prerequisite Investigation officer (IO) comes to

mortuary and to perform autopsy. For form and then along with his inguest report and MLC if any, he provides all doc uments to the doctor. The doctor takes history about the case and checks whether the IO has written down ne same facts as he has stated. Then he proceeds to conduct autopsy. Tequests the available doctor this, he fills a request

External Examination

C

doctor notes down all points on paper, which he

external

examination. (1) Clothing: number, tears, stains; ockets should be checked to collect evidences, for example, drugs of abuse, medication, identitycard etc.; trace evidences, for example, hair, fibres, etc. should be collected; jewellery should colour,designs,

es,

be collected. The clothing must be dried, packed, scaled, labelled and handed over to the escorting police personnel. (2) General body features: body weight, length, built and nourishment, sex, complexion. (3) Postmortem changes: rigor mortis, rectal temperature, postmortem hypostasis, putrefaction, maggots. (4) Deformities, identification marks (e.g. tattoos, moles, scars, amputation and so on), circumcision, diseases, etc. (5) Skin: rash, petechiae, colour, oedema. (6) Face: cyanosis, pallor, petechiae; mouth-protrusion and/or biting of tongue, injuries or marks of cor rosion on lips, gums, teeth; eyes: condition of eyelids, conjunctivae, eyeball softening, colour of sclera, papillary size and opacity, lens. (7) Neck: ligature mark, abrasions (e.g. nails marks), bruises, lacerations, etc. (8) Thorax: injuries, signs of pregnancy on breasts. (9) Abdomen: distension, stria gravidarum, linea nigra. (10) External genitalia: size, position and diseases of testes or penis. (11) Extremities: fractures and dislocations; hands should be examined for defence wounds, electrical marks, any material grasped in clenched hands; fingernails should be checked to get any evi dence, for example, blood, mud, etc. (12) Natural orifices (eg. nose, mouth, ears, vagina, urethra, anus): any discharge; (13) Injuries: size, shape, site (in relation to two external anatomical landmarks), direction (vertical or horizontal), colour, margin or edge, duration; body should be examined for concealed puncture wounds; injuries should be drawn in diagrams.

Internal Examination open three major cavities, that is, skull, thorax and abdomen, but the question is which cavity has to be opened first (Table 4.1). We have to

Incisionss

the body cavities The different incisions for opening are as follows (Fig. 4.1): from chin 1) 1-shaped incision: It extends physis pubis (i.e. ymphysis to down phiysis menti) straight 49

SECTIONI Forensic Medicine

5

TABLE 4.1

Which Cavity has to be Opened First?

which 'Chest and Abdomen' are Opened Fire

Situations in which 'Skul' is Opened First

Situations

Hanging and strangulation: To appreciate neck injuries clearly, we want bloodless field and this is achieved by opening skull first which drains out blood 2) Poisoning, for ewample, alcohol, carbolic acid, organophosphorus compounds. The smel of poisons is best appreciated before odorous gases from abdomen are released

Head injuries: To appreciate head injuries clearly, we want bloodless field and this is attained by pening chest and abdomen first which drains out blood 2) Stab or blunt trauma to the chest or abdomen 3) In foetuses or newborns to note the actual position of diaphragm to differentiate live birth from stillbirth

1)

Otherwise general rule

is

in

1)

abdomen that the head should be opened first, then chest and

Acromian

Chin

process

Mastoid

process

Suprasternal notch

Xiphoid

process

-shaped

Modified Y-shaped

Y-shaped

Fig. 4.1 Types of incisions for opening of thoracic and abdominal cavity

pubis) avoiding the umbilicus. The umbilicus is avoided while giving an incisión. Why? Answer: Dense fibrous tissue in umbilicus is difficult to penetrate with the needle when body is stitched after autopsy. 2) Y-shaped incision: Acromion process on both sides Anterior axillary folds > Curve down Xiphoid process (in midbelow the breast line) > Pubis. 3) Modified Y-shaped incisíon: It is given for dissection of neck. From mastoid process on both sides to suprasternal notch, it should proceed down to pubis.

EXAMINATION OF HEAD (SKULL AND BRAIN)

Method of Removal of Brain ( Make a bone-deep incision along_the vertexof thescalp joining both mastoid processes,Nowretlect theflaps of scalp isreflected anteriorly as well as pos teriorly as much as

possible. Note contusion in thescalp or temporalis muscle or (i) (lii) ihe fracture

on both of skull. Then remove temporalis muscle cap exposes

sides. (2) Sawing and removing of skull the dura. Note any extradural haemorrhage (EDH. 3) Cut dura from its extremeperipherv: then hold it tightly: cut falx cerebri and then pull gently from frontto back. Examine arachnoid,subdural haemor: rhage (SDH) and subarachnoid haemorrhage (SAHL. Measure the weight and volume of SDH and its pres: Sureeffects on brain. SDH can bewashed under run: ning water whereas SAH cannot be washed.H remove brain,insert lefthand fingers between front lobes and skull and draw them backwards. Now cu the structures visible, for example, nerves and ve sels. tentorium and at last spinal cord with yertebg arteries. Remove the brain with cerebellum with0s SLuPport of both hands. (5) Examine the remainus Venoussinuses forantemortem thrombiz pull out duraattached with theskull bone af cranialfossaea CXamine for any fracture at the base of skull

Examination of Brain Measure the weight ofbrain. Examinefor any oeden Ilattening

of convolutions)_or shrinkage. Exan

CHAPTER 4

Medicolegal Autopsy (Postmortem Examination)

Wilis for any aneurys arteriosclerosis or of study the brain may need fixalism. For better all,. sep109 formalin for 2-3 wecks. First of tionin from the cercbrum. cerebellum and brains sliced coronal planeat cm is in ebrum

a

Usually

by this knife. Now examine the pleural cavity before complete removal of sternum or blood/fluid/pus or

adhesions.

Dissection of Lungs

may be cut through intervals brain knite but it structureS. We may note anyplanetostudy various punctuate acmorrhages or petechialhaemorrlhages natter. Cerebellun is dissected in horizonn whiteso that dentate nucleus can be seen clearly plane tal mm at intervals perpendicBrainstem canbesliced 5 can be visualised haemorrhage to Pontine ulat its axis. removed the case of head inury Spinal cord is not L

Tie the bronchi of both sides and then separate both lungs. Note petechial haemorrhages on pleura. With the help of scissors, cut open from large to small airways in all lobes. Lungs may be cut horizontally into slices. Lung parenchyma is squeezed to see frothy fluid, pus or any fluid.

Dissection of Heart (Table 4.2) DExternal examination: Adhesions,

in

routinely,

EXAMINATION OF NECK incision is used to dissect the neck and thus expose the wide area at the front and sides of the neck especially in hanging and strangulation. Layer-wise dissection of neck is carried out to inspect the structures of neck. Following layers have to be dissected in stepwise fashion: (1) platysma, (2) sternodeidomastoid, (3)(a) omohyoid, (b) digastric, (4) sternohyoid and (5) sternothyroid and thyrohyoid. Modified Y-shaped

Note the followings: (1) haemorrhages into the-softtissues, (2) fractures of hyoid bone and thyroid caf-

tilage and (3)

injury to carotid arteries and musclesy

EXAMINATION OF CHEST

Dissection of Chest

NGC.N7DS Dele..

:2a

ROH!

Dissection starts from the I-shaped incision. The skin and muscles of the chest are dissected sidewise up to

midaxillary line, down to Over the clavicles. Note any

the costal margin and up fracture of ribs or sternum asociated with extravasation of blood. Now with the o cartilage knife, pcostochondral cut the costal cartilage close to junctions from second rib downwards. Also, disarticulate sternoclavicular joints of both sides TABLE Wall

4.2

Thickness

Leftventricle Rightventricle Atria

Measurements of Heart Weight= 300 10-15 mm (1.5 cm) 3-5 mm (0.5 cm) 1-3 mm (0.3 cm)

pericarditis,

discolouration of underlying infarct, aneurysms. Before cutting, palpate pulmonary arteries and SVC/IVC for thrombus/embolus. Subendocardial haemorrhages (or Sheehan's haemorrhages): These are flame-shaped confluent haemorrhages seen in left ventricle on the left side of interventricular septum and on the opposing papillary muscles. They are seen in haemorrhagic shock, head injury and cerebral oedema, death due to ectopic pregnancy or ruptured uterus, antemortem or postpartum haemorrhage and arsenic or oleander poisoning. Methods of dissection in different situations Ischaemic heart disease: Examination of cor onaries-in younger subjects (K30 years), in whom the cause of death is noncardiac, the coronary arteries may be opened longi tudinally. Otherwise, cut in cross-section at 3-5 mm interval. Calcified vessel that cannot be cut readily, should be stripped off the heart and decalcified for at least 24 h before cutting. Grading of coronary obstruction (Table 4.3). SAN (SA node): Present just below the summit (highest point) of right atrium, at the Junction of SVC and crest of right atrial appendages.

and 250 g (Female) Valves Circumference (Male and Female)

g (Male)

Tricuspid valve Mitral valve Pulmonary valve Aortic valve

10.5)

12 cm (11.5 and and 8.5) 10 cm (9.5 6.2)

and 8.5 cm (66 and 6.3) 1.5 cm (6.7

SECTIONI

TABLE 4.3 Obstruction

Forensic Medicine

Grading of Coronary

Grading

Stenosis

Grade

0%

Grade 2

25%

Grade 3

50%

Grade 4

275 (75% severe; 90% is critical stenosis)

AVN (AV node): Situated between the opening

of coronary sinus and medial leaflet of tricuspid valve (in triangle of Koch). Assessment of ventricular hypertrophy: Total heart weight is the best gross indicator of cardiac hypertrophy. There are two methods to assess ventricular hypertrophy: (1) by measuring ventricular thickness and (2) Fulton's technique.

PRESERVATION OF VISCERA Preservation of viscera is done in following circumstances: (1) suspected poisoning/intoxication, (2) when unusual smel, colour or an unidentifiable material is detected in stomach contents, (3) drug abuse, (4) anaphylactic deaths, (5) advanced decomposition, (6) accidental deaths involving driver of a vehicle (RTA, road traffic accident) or machine operator, (7) cause of death not found after autopsy and (8) when IO requires such as a part of investigation.

What is Preserved? Stomach and its contents. 2) Intestine: Upper part (30 cm) of small intestine and its contents. In infants, whole intestine. 1)

3) Liver: 500 g along with gall bladder; whole in

infants. 4) Kidney: Half of each (as one may be dysfunctional). When one is present whole of it. Both kidneys in children. 5) Spleen: Half. 6) Blood (50 mL): Central luminal blood (any chamber of heart, intrapericardial thoracic aorta, pulmonary artery, vena cava) is preferred to cavity blood (haemothorax/pericardium/peritoneal, pooled blood left in cavity after removal of heart and lungs). Peripheral blood (femoral vein, subclavian vein) is preferred in TCAs poisoning. In

cocaine poisoning, the blood is collected as soon possible in order to inhibit postmortem hydroly.is of cocaine. 7) Urine (50 ml.): Urine is aspirated with a syrino ringe through the dome of bladder after the peritor cavity is opened. If bladder is near empty, it can be sccurcd by haemostats before incising the dome to facilitate aspiration of the bladder lumen under direct vision. Toxicologists often prefer urine as a specimen for EMIT (enzyme-multiplied immune technique) and ELISA drug screening. Use of NaF as a preser. vative is optional, because immunoassays detect cocaine metabolites rather than parent cocaine. In certain cases, preserve the following: (1) brain

4.

(100gofcerebrum/cerebellum)-strychnine,organo-

phosphates, opiates, CO, cyanide, barbiturates anaesthetics, volatile organic poisons; (2) spinal cord (entire length)-strychnine and gelsemium; (4) vitreous humour-MCA (3) CSF-alcohol; (alcohol-morphine-cocaine), TCAs, chloroform; (5) heart cardiac poisons (digitalis, aconite, nicotina, quinine, Nerium", Cerebra"), strychnine; (6) lung (one lung)-alcohol, chloroform, HCN, gaseous poisons; (7) bile-opiates, alcohol, barbiturates, cocaine, methadone, narcotics; (8) skin (a radius of 2-4 cm from injection site)-take the skin of injection site (morphine-heroin--cocaine-insulin are injected locally in skin) or where absorption of poison may have occurred for corrosive poisons; (9) hair (20-30)-chronic heavy metal (arsenic) poisoning and chronic drug abuse; (10) nail; (11) bone (10 cm of shaft of femur)-arsenic, antimony, thalium, radium; (12) fat (10 g) (abdominal/perinephric) pesticides and insecticides; (13) muscle-if internd organs are badly putrefied, thigh muscle (3 x3 cm) is usually well preserved and can be analysed. ln embalmed body, the skeletal muscle from the buttock is the best and (14) uterus-in criminal abortion.

Preservatives I. Saturated NaCl solution: It is the most comn preservative used in lndia because it is cheap an easily available. It is indicated in all poisoning caseo

oi except corrosives (acids or alkalis), vegetative po sons (aconite) and mercuric chloride. Corrosi should be preserved in rectified spirit. 2. Rectified spirit: It is the best or ideal preservan for preservation of viscera but is less commony used because it is costly and highly volatile. It

6.

1-

CHAPTER4

Medicolegal

sons excespt alcohol, erosene, dicated in most acid, formic acid, acetic carbo ether chloroform, paraldehy chloral hydrate. phosphorus, cid. Anticoagulant (sodium or polassium fluoride) ibitor) is added to blood, urine, 3. enzynme inhib (an vitreous humour when alcohol is to be CSF and 1 ml of blood). estimated 10 mg uoride in Fluoride is also dded to samples for analysisof Fluoride inhibits both cocaine, cyanide and CO. esterases (wlhich hydrohacterial growth and serum

. 5.

6.

Embalming (SN-4]

LIST OF IMPORTANT QUESTIONS

FOR EXAMINATION SHORT NOTES (SN)

postmortem). citrate/1 mL of Sodium citrate (3 mg of sodium ethylene glycol blood): In poisoning by Oxalic acid,

2. Obscure autopsy 3. Various techniques

and CO.

4. Embalming

yse cocaine

100 mg For urine: 1 mLof concentrated HCl or added to 10 mL thymol or sodium fluoride is

of of

1.

Negative autopsy

urine. Preservatives are not necessary (1) when viscera (2) when sample can can be analysed within 24 h; is.bone, be kept in refrigerator; (3) when sample

and (4) when lungs are preserved for detecting inhaled poison. Viscera should not be preserved in formaldehyde because extraction of poison, especially nonvolahair, nails

7.

Autopsy (Postmortem Examination)

compounds, becomes difficult.

tile organic

Containers One litre capacity, wide-mouthed, glass/polyethylene containers. Rubber inserts should not be used under caps because it can extract certain poisons (e.g. chloroform, phenol) from the contents. Glass containers should be cleaned with dichromate solution (or sul-

phuric acid-chromate solution), ringed with distilled water and dried. During transport, they may break. Since volatile

poisons may diffuse through plastic

polyethylene) containers, nylon bags are used when lungs or other tissues are to be preserved for analysis ot

ANSWERS

SN-1: Negative autopsy autopsy which fails to reveal a cause of death An with gros, microscopic (histological and microbiological), immunological, serological, radiological and toxicological analysis. Rate: 596-8% of all autopsies are found to be negative autopsy. Even the best-equipped centres of the world have > 5%% negative autopsy rate.

Reasons of negative autopsy 1) Inadequate history about signs and symptoms prior to death: Vagal inhibition, laryngeal spasm in drowning, epilepsy, status epilepticus, electrocution in water, HSR. 2) Inadequate: (1) External examination-exit wound in electrical burn, needle pricks in anaphylaxis, snakebite, insect stinging and (2) internal examination-air embolism, pneu-

vo1atile substances.

able and should

Preservation

Polyethylene containers are perme not be used for volatile poisons.

of removal of organs at autopsy

3)

and Dispatch of Viscera

mothorax. Insufficient: (1) Laboratory examination histological serum levels of electrolytes, (2)

have stomach ana

examination-consolidation or carcinoma of toxicological examination-alco-

0.5-1cm or ey can be mixed a grinder so that they in are well preserv (3) of the capacity Only two-third ofbottle

hol, opium, etc. inadequate (collec4) Samples: (1) wrong and preservation of samples) and samples hon of and (2) exchange of samples.

Two containers-one should intestine kidneys.

toavoid

with contents, other should have liver and (2) Liver and kidneys are cut into pieces of

should be

bursting

areformed.

filled with viscera and preserv bottle if gases of decomposition

of

ung and (3)

doctor/pathologist. Wrong labelling. of training Inadequate 6) 5)

SECTIONI

Forensic Medicine

SN-2: Obscure autopsy An autopsy done meticulously, properly and perfectly by an expert, but where no definite (i.e. obscure) cause of death was found is callcd obscure autopsy. It is most commonly found in the cases of young acdults. It creates a lot of confusion to forensic experts. N Causes: Usually unexplainable. AGCCE 1) Natural diseasc: Obscure morbid anatomy: lntramyocardial small vessel abnormalities of ventricular septum (prominent medial and fibrointimal thickening-intimal humps, with variable degree of Poor blood flow Inadeluminal stenosis quate perfusion> Arrhythmias Sudden death. Threats/bad causes: Emotional/stress arrest Cardiac death. Sudden news

Paroxysmal fibrillation. (status epilepticus): Postictal respi Epilepsy Death. Cardiac arrhythmias ratory failure induced by disorganised neural discharges of seizures.

Ted Asthma (status asthmaticus) Co, Metabolicacidosis> Death. During/immediately after exer Exercise cise Progressive T in SBP and HR but DBP is affected very little, ed peripheral Primary cardiac arrest. Levresistance els of catacholamines Ts 10 times with ischaemia->Arrhythmia -> Sudden death. 2) Biochemical disturbance: Uraemia, diabetes, K* deficiency, anaemic anoxia, porphyria. 3) Endocrine dysfunction: Adrenal insufficiency, thyrotoxicosis or myxoedema. 4) Cardiac lesions: (1) Acute rheumatoid cardiSudden cardiac death. Diagnosis: Aschoff's tis bodies; (2) acute toxic myocarditis of diphtheSudden cardiac death; (3) acute oclusion of ria coronary artery (due to thrombosis or h/ge within the wall of artery) and (4) cardiac arrhythmiasprecipitated by emotional excitement and physio logical asystole.

5) Concealed trauma: Cerebral concussion, self-induced neck injury. The blunt force injury/contusion of the chest/heart stops functioning without any visible signs. 6) Poisoning and anaesthetic overdose: Strychnine,

cobra bite, ricinus communis, datura, narcotic poisoning (e.g. heroin, BZD, barbiturates, alcohol).

SN-3: Various techniques of removal of organs

at autopsy

Virchow's technique: Most commonly performed techniquc. Organs removed one by one. lirst of all, the cranial cavity, then spinal cord from back, then thoracic, cervical and abdomi. nal organs are opened. Advantage: Each organ can be studied in detai however, the anatomicopathologic relation ships of organs are not preserved. 2) Rokitansky's technique: It involves 'in-situ dissection is commonly preferred when the pathologist It wants to limit the spread of infection (e.g. HIV Hepatitis B) and usually when there is lot of pus in cavities. Organs cannot be studied in Disadvantage: detail. 3) Ghon's technique: It involves 'en-block removal' (=organ block) Thoracic, cervical, abdominal and urogenital organs are removed as organ blocks (en-block removal). 4) Letulle's technique: involves 'en-masse removal (ie. all organs It of a particular cavity are removed intact as a mass). Thoracic, cervical, abdominal and pelvic organs are removed en-masse, but subsequently dissected as organ block. It is the best technique for routine inspection and preservation of connections between organ and organ system. requires less time but awkward to handes It thus, it requires more experience to dissect 1)

SN-4: Embalming

the procedure

in which the dead body treated with chemicals to avoid putrefactions preserves the dead body for a long tinme. For anatomical dissections; for puu Purpose: lic display at a funeral; to transport to a dista place. erIt should be done immediately after death, pree ably within 6 h of death. It inhibits decompositio for many months.

It

is

CHAPTER 4

Medicolegal Autopsy (Postmortem Examination)

ABLE 4.4 Composition of a Typical TABLE Embalming Fluid St. No.

.

3.

Class of

Ingredient Chemical

Quantity

Preservative and germicide

Formalin

1.5

Buffer

600 9

Buffer 2

Sodium borate Sodium chloride

Wetting agent

Glycerine

600 mL

Anticoagulant

Sodium citrate

1

Composition of

a

typical

fixed, (2) blood is converted into a brownish mass and (3) proteins are coagulated. Embalming fluid used should be 15% of the body weight with 2% formaldehyde content. When embalming fluid is injected into the body through arterial route, it is called arterial embalming. When cmbalming fluid is directly injected into the body cavities, it is called cavity embalming. Usually, cavity embalming is done as a supplement to arterial embalming. Only cavity embalming is done when there is severe mutilation of the body and the arterial vessels are damaged. Some poisons (e.g. cyanide) are destroyed by the formaldehyde of the embalming fluid.

L

800 g

embalming fluid

(Table 4.4).

Apparatus used for the purpose of embalming are (1) bulb syringe, (2) gravity injector and (3)

Medicolegal importance: 1) Relatives must sign an informed consent form in which the details of the procedure must be written. 2) Embalming report form must be filled up afterT completion ot embalming procedure. 3) Interpretation of injuries or disease becomes difficult. 4) If any embalmed body comes to mortuary for autopsy, some amount of vitreous or muscle tissue must be collected.

motorised injector.

Methods of arterial injection: (1) Discontinuous

injection and drainage is the best method, (2) continuous injection with disrupted drainage, (3) alternate injection and drainage and (4) continuous injection and drainage is the most satisfactory method. Changes which occur due to embalming: (1) Organs are bleached and hardened; tissues are

T

ldentification Chapter 5A ldentification, Age, Race, Sex and Stature INTRODUCTION Identification: Determination of the individuality of a person, live or dead, is known as identification. It is done by recognising certain features or characteristics that are unique to that person.

Types of ldentification

2) Dead persons, for example, recently dead person. decomposed body, burnt body, mutilated bodies (e.g. in mass disasters like air crash, earthquakes,

etc.). Identification of dead is carried out by a medical person. 3) If only a part of the body is found, for example, limb, skeleton or bone, then also help of medical person is taken. Identification is also needed in: (1) Civil matters: insurance, pension, disputed sex, marriage and missing person and (2) Criminal matters: assault, murder and rape.

Complete (or absolute) identification: When there is 1006 surety about the identity of a person, it is known as complete or absolute identification. Here there is no doubt regarding the identity. For example, dactylography (fingerprinting) is the only (In Latin, Corpus means by which absolute identification can be madeCorpus Delicti Delicti Body of Offence) because fingerprints (FPs) of no two individuals are same. FPs are not same even in identical twins. It means body of offence or 'the essence of crime' or 2) Partial (or incomplete) identification: When there 'the facts of a criminal offence (e.g. homicide) which is less than 100% surety about the identification proves the commission of a crime. In a case of hom is cide, corpus delicti includes not only the dead body of of a person, it known as partial or incomplete identification. Here there is still doubt regarding the victim, but also other factors which are conclusive the identity. Only certain features of the person of death by foul play. Those factors include weapon are known, for example, age, race, sex and stature, of offence (e.g. a knife) or bullet found at the crime* while others remain unknown. scene; clothing showing the marks of weapon; dra ing and photographs of the deceased showing fata Identification is Required in the Following: injury, etc. The main purpose of corpus delicti is to establish the identity of the dead body (of victim). 1) Living persons: Identification of the living is usually carried out by police. It can be done in followCriteria Used for ldentification ing cases: (1) impersonation, that is, a situation in They are given in Table 5A.1. which a person pretends to be another person for the purpose of fraud; (ii) identification in court of AGE law, a person is identified in the court by the docis tor who has examined him earlier; (ii) mix-up of and dead Methods age living of in estimation newborn babies in hospitals and (iv) absconding solexplained in Table 5A.2 and in different ages is give diers and criminals.

1)

56

in Table 5A.3.

CHAPTER 5

Griteria Used for

ABLE 5A.1 Identification

(Mnemonic: Best Friend Pays Money) Age, Hace, Sex, Stature Big four parameteS: Forensic 2) Osteology (bones) Odontology (teeth and bite marks) Trichology (hair) 3) Prints

Finger prints (dactylography) and other prints, for example, poroscopy, p prints (cheiloscopy), palato prints, foot prints, ear prints, nose prints DNA fingerprinting

4)

Miscellaneous methods: Marks (scars, moles, tattoo marks, birth marks, occupational marks) and deformities

Anthropometry Superimposition Biometric methods (e.g. frontal sinus prints)

Religion Special characteristics, for example, physical characteristics (e.g. complexion, facial features,

deformities, personal belongings) and behavioural characteristics (e.g. Speech and voice, hand writing, manner and habits, memory and education, gait)

TABLE 5A.2 Methods of Age Estimation in Living and Dead

n

In Living

Teeth: Eruption Bones: X-rays (ossification centres)

Secondary sexual characteristics: Tanner's staging

Miscellaneous features,

Dead

Teeth: Gustafson's method and Boyde's method Bones: Skull (cranial sutures closure),mandible, ribs, symphysis pubis, sacrum Age of foetus

for example,

1) General

development

2) Arcus sanilis

TABLE 5A.3

Methods of Age Estimation in Different Ages In

From Birth to 25 Years of Age

lUL

Rule of Hasse

Dentition

ISN-2]

Rule of Morrison

(temporary and permanent)

Ossification of bonesS

(epiphyseal

IUL, intrauterine

life

union)

After 25 Years of Age

Gustafson's

method Miles method

Aspartic acid

racemisation

ldentificatioon

57

Methods of age estimation in intrauterine life (age estimation of foetus) is given in Table 5A.4.

Age of a foetus can be estimated by two methods or rules; one is rule of Hasse [SN-2] and the other is

rule of Morrison [SN-2]. Various important findings in foctus of various ages have been tabulated in Table 5A.4.

Age Estimation in Living Individuals by X-Ray Examination: Age of Appearance of Epiphyseal Centres and Their Fusion to the

Shaft

Introduction: There are four parts of

a long bone diaphysis, metaphysis, epiphyseal plate and epiphysis. Initially, the skeletal framework in the body is cartilaginous but with time some ossification centres (OC) appear. The ossification of a bone starts from these centres and most of the bones ossify with increasing age. OCs may be primary or secondary (Table 5A.5).

A. Upper limbs

Humerus (Fig. 5A.1A) Upper end: There are three OCs which appear at upper end of humerus. The OC for head of humerus appears at 1 year of age, OC for greater tuberosity appears at 3 years of age and OC for lesser tuberosity appears at 5 years of age. All three OCs fuse together at 6 years of age to form conjoint epiphysis. Then this conjoint epiphysis fuses with metaphysis at 17 (17-18) years of age (Table 5A.6). Lower end: There are four OCs which appear at lower end of humerus. The OC for medial epicondyle appears at 5-6 years of age, OC for lateral end appears at 10-12 years of age (1.e. double the age of OC for medial epicondyle), OC for capitulum appears at 1 year of age and OC for trochlea appears at 10 years of age (Tro10). Lateral three centres chlea> T> Ten trochlea) (i.e. lateral epicondyle, capitulum and at fuse together to form 'conjoint epiphysIS epiphysis 14 years of age and then this 'conjoint of age. Medial fuses with metaphysis at 15 years 166 alone at years shaft the fuses with epicondyle of age (Table 5A.7). two OCs 1B): There are

DRadius and ulna (Fig. 5A.for ulna.

OC for upper OCs age and OC tor lor radius and two years of 5 upper appears at end of radius of age. OC for for years 2 OC lower end appears at years of age and

chd of ulna

appears at 9

58

SECTIONI

TABLE 5A.4 Age

Forensic Medicine

Month-Wise Development of Foetus

Length

(Months) (cm)

Weight

Ossification Centrees

Features

2.5-5 9

Clavicle: two primary centres

Eyes

appear the shaft between 4th and 5th week of IUL, and both fuse at 45th day Long bone shafts in

2

22

10 g

4

as two dark spots and mouth as a cleft

n Four limb buds: four bud-like of formation of limbs

processes

mark the beginning

Anus as dark

spot webbed feet and Hands embryo can be recognised as of human; the week, 8th At human appearance demarcated from limbs, mouth and nose

Placenta starts forming

3 9

3

42

30 g

120 g

16

Sacral vertebra 1-3rd

nSex bud appears, but sex organs (penis and clitoris) not distinguishable Pupillary membrane (membrana pupilaris) appears Fingers and toes well developed; nails appear as a membrane Neck and palate forms Heart: four-chambered

Sacrum (lower sacral vertebrae); ear ossIcles

Sex can be differentiated Lanugo hair (first exhibited between 3 and Pupillary membrane becomes visible Brain convolutions begin to develop Meconium found in duodenum

OSsity

4 months)

Quickening 52

400 g

25

6 x5 30

800

7 x5=35

1.5 kg

Calcaneum and ischium

Manubrium sternii and 1st segment of sternum

g

Talus

Sternum piece)

(2nd and 3rd

Light hair appears over scalp; downy lanugo hair over whole body; nails distinct and soft

Vernix caseosa appears and covers the skin Meconiunm found in beginning of large intestine Germinal centres of permanent teeth appear in jaw Scalp hair appreciable Eyelashes and eyebrows appear Gall bladder contains bile Testes close to the kidneys Pupillary membrane disappears; eyelids open Scalp hair 1 cm long; lanugo hair greatest Meconium in whole of the large intestine Left testis at external and right testis at internal

inguin

I ring

in right iliac fossa; valvulae conniventes start appearing9 Brain convolutions formed; grey matter not formed

Caecum

MLI:

8x5

40

9x 5 45

9

10

10

x5

2.5 kg

7

Scalp

2 kg

Lower end of femur

50 2.5-5 kg Upper end of tibia; cuboid

months (28 weeks) is the age of viability hair 1.5 cm long; lanugo hair clisappears from face

Nails reach finger tips but not toe tips Left testis in scrotum; right at external inguinal ring Meconium reaches the rectum Cerebral convolutions well developed Posterior fontanelle closes Scalp hair 2-4 cm long; lanugo hair around shoulders onily Both testes in sorotum; scrotunm shows wrinkling Vernix caseosa in joint flexures, armpit Umbilicus midway between symphysis pubis and xiphister Head circumference, 33 cm Anterior fontanelle, 4 x 2.5 cm Lanugo hair present only on the shoulders Umbilicus situated between pubis and xiphisternum Grey matter begins to form

CHAPTER 5

TABLE Primary

Identification

A.5 Types of Ossification Centres

Ossification Centre

Secondary Ossification Centre

start ossifying Itis development prenatal appears during ltusually bone developing central part of each in the in the occur centres primary long bones, the Indiaphysis bones, irregular the in (or shaft) and of body occur in the usualy primary centres the first area of a bone to

It

is the area of ossification that appears after the primary Ossification centre Most of them appear during the postnatal (except for distal femur and proxirnal tibia, which appear during foetal development or at 9 months) and adolescent yearss In long bones, the secondary centres appear in the

the bone only one Most bones (e.g. all long bones) have bones, irregular such some centre but primary as the hip bone and vertebrae, have multiple primary

epiphyses

Most

bones have more than one secondary

centre

ossificatioon

centres

(A)

1

At 6

These three centres fuse together to form conjoint epiphysis'

3

3 5

At 17 Conjoint epiphysis fuses with the shaft At 15epiphysis Conjoint fuses with the shaft

At 16

Centre for medial epicondyle fuses separately with the shaft

At 14

10-12

5-6

(Lateral epicondyle)

(Medial

epicondyle)

C= (B)

1

T=

Lateral three centres fuse together to form

coinjoint epiphysis'

10

(C)

-9

Base of 1st metacarpal

3 -17

Heads of 2nd, 3rd, 4th and

5th

metacarpal

Bases of 2nd, 3rd, 4th and 5th proximal phalanges

Bases

2-18

318

of middle and terminal

phalanges

2-

and their fusion in humerus and ppearance of ossification centres (C) ation the bones of hand Centres and their fusion in radius, ulna and

(B)

age of appeardln

of

SECTIONI

Forensic Medicine

TABLE 5A.8 Ossification in Radius

TABLE 5A.6 Ossification in Upper End of Humerus Age of

Appearance

of Epiphyseal

Centres (Years)

Part Head of humerus

Greater

Lesser tuberosity

Epiphyseal Centres

Pat

3 5

Fusion With Metaphysis

(Years) Ulna Radius

Part

of Humerus three centres fuse

together to form conjoint epiphysis' at 6th year of age, and then this 'conjoint epiphysis' fuses with metaphysis at 17 (17-18) years of age

tuberosity

E

Age of Appearance of

Fusion With Metaphysis of Upper All

1

and Ulna

(Years)

Upper end

5

16 (16-17)

Lower end

2

18 (18-19)

TABLE 5A.7 Ossification in Lower End of Humerus Age of Appearance of Epiphyseal

Part Medial epicondyle

Trapezoid Capitate

Fusion With Metaphysis of Lower

Hamate

Centres (Years) Part of Humerus Lateral three centres 5-6

(i.e. lateral epicondyle, capitulum and trochlea) fuse together to form conjoint epiphysis at 14 years of age and then this conjoint epiphysis fuses with metaphysis at 15 years of age Medial epicondyle fuses with the shaft alone at 16 years of age

Lateral 10-12 epicondyle

Capitulum Trochlea

Trapezium

10

Pissiform

Scaphoid

Lunate

Triquetral

Fig. 5A.2 Carpal bones seen on X-ray of hand

lower end appears at 6 years of age. OCs of upper end of radius and upper end of ulna fuse with their respective metaphyses at 16 (16-17) years of age. Similarly, OCs of lower end of radius and

lower end of ulna fuse with their respective metaphyses at 18 (18-19) years of age (Table 5A.8). o Hand bones (Fig. 5A.18) 1) Carpals: First of all, we need to remema ber the name of all eight carpal bones in sequence (Figs 5A.2 and 5A.3). Proximal

row (lateral to medial) includes Scaphod, row Lunate, Triquetral, Pissiform. Distal

Lower end or radius

2 years

18 years

Base of 1st metacarpel

3 years

17 years

Lower end of ulna [6 years

18 years]

Heads of 2nd, 3rd, 4th and 5th metacarpels 2 years>18 years Bases of 2nd, 3rd, 4th and 5th proximal phalanges Bases of middle and terminal phalanges 3 years 18 years]

Fig. 5A.3 Age of appearance of ossification centres and their fusion the bones of wrist joint and hand

in

CHAPTER 5

(lateral to medial) includes Trapeziu, Trapezoid, Capitates, Hamate. pissiform is the We need to remember that appear, to that is, at 11 (10last carpal bone appearance of all 12) years of age. The age ot carpal bones is in years, except capitate and hamate which appear in months (Table 5A,9). 1st metacarpal, the OCs 1) Metacarpals: In appear in base and not head. In 2nd to 5th metacarpals, the OCs appear in heads and not bases. The OCs in base of Ist metacarpal appearat 3 years of age and fuse with its metaphyses at 17 years of age. The OCs in the heads of 2nd to 5th metacarpals appear at 2 years of age and fuse with their respective metaphyses at 18 years of age (Table 5A.10). 2) Phalanges: The OCs appear in the bases of all phalanges (proximal, middle and distal) and not in heads. OCs in base of 2nd to 5th proximal phalanges appear at 2 years of age and fuse with their respective metaphyses at 18 years of age. OCs to 5th middle and distal in base of 2nd phalanges appear at 3 years of age and

TABLE 5A.10

Ossification in

Metacarpals

of Epiphyseal Centres (Years)

Part Base (proximal end) of 1st metacarpal Heads (distal ends) of 2nd to 5th metacarpals

Ossification in

Phalanges

(Proximal End)

Bones

1.

18

Middle and terminal phalanx

3

18

TABLE 5A 12 Ossification in Clavicle

One secondary centre

a

(10-12) ie. last carpal bone to appea

11

5.Trapezium

6.Trapezoid 7.Capitate

8. Hamate

2

months of

lUL

3 months of IUL Order of Appearance of Carpal Bones Capitate 2 months of IUL (.e, Triquetral Lunate

andTrepazoid

caphoid

Pissiform

D

earliest

carpal bone to appear)

Hamate

and Trapezium

months of JUL 3 years 4 years 5 years 11 years (10-12) (i.e, last carpal bone to appear 3

Age of Appearance of Epiphyseal

Centres 4-5th week of 10-20 years

IUL

Fusion With

Metaphysis 45th day 20-22 years

(at medial end)

3. Triquetral 4. Pissiform

Metaphysis

(Years)

2

Scaphoid

2.Lunate

Fusion With

Age of Appearance of Epiphyseal Centres (Years)

Proximal phalanx

Age of Appearance of Centres (Years)

Carpals

17

2

TABLE 5A.11 Part: Base

(Years)

3

Two primary centres

Ossification in Carpal

Fusion With Metaphysis

Age of Appearance

Centres TABLE 5A.9

Identification

fuse with their respective metaphyses at 18 years of age (Table 5A.11). Clavicle: There is one primary centre at medial end and two secondary centres in clavicle. The two secondary centres appear at 4-5th week of IUL and fuse with metaphysis at 45th day of IUL. One primary centre appears at 18-19 years of age and fuses with the metaphysis at 20-22 years of age (Table 5A.12). Scapula: It ossifies from two primary and seven secondary centres (Table 5A.13 and Fig. 5A.4): primary "Primary centres (total two): First by scapula centre appears in the body of centre Bth week of IUL and second primary lite. ot year appears itn coracoids process by 1st There are two

Secondary centres (total seven): acromion, two for corasecondary centres for inferior border, one for vertebral for coids, one infraglenoid tubercle. for one and angle

OECION

TABLE 5A.13

Scapula

Parts

Meaicine

rorenSIC

Ossification of 4

Fusion at 17|

Age of Appearance of Epiphyseal Centres

-14

Fusion With

Metaphysis (Years)

(Years)

Two centres for inner border

14-15

Acromion process Coracoid

14-15

17-18

Subcoracoid Infraglenoid tubercle

16

17

17-18

15

All

epiphyses

of scapula join t he bone by 20 years of age

14-15

9 months (i.e. at birth)

Fusion at 10K Coracid process (1

years) years)(15 Acromion process (14-15 years)

(17-18 years)

(17-18 years) -

Infraglenoid

tubercle (14-15 years)

Fusion at 16

Innerborder

(14-15 years) (17-18 years)

Fig. 5A.4 Age of appearance of ossification centres and their fusion in the scapula B.

Lower limbs

DFemur(Fig. 5A.5)

D

Upper end: There are three OCs at upper end of femur; one for head which appears at 1 year of age, one for greater trochanter which appears at 4 years of age and one for lesser trochanter which appears at 14 years of age. All fuse with metaphysis at 17 (17-18) year of age. No conjoint epiphysis is formed here as seen in upper end of humerus (Table 5A.14). Lower end: There is only one OC at lower end of femur and this is common for both condyles. It appears at 9 months of IUL (or at birth) (Fig. 5A.4) and fuses with metaphysis at l8 (1819) years of age (Table 5A.15 and Fig. 5A.6). Tibia Tibia and fibula (Fig. 5A.5): There are two OCs for tibia and two OCs for fibula. OC for upper

1

Fig. 5A.5 Age of appearance of ossification cent res and their fusion in the bones of lower limb

TABLE 5A.14 End of Femur Parts

Ossification at Upper

Age of Appearance of Epiphyseal Centres (Years)

Head Greater trochanter 4 Lesser trochanter 14

Fusion With Metaphysis of Upper Part of

Femur (Years 17 (17-18)

IUL (0r end of tibia appears at 9 months of i ) birth) and OC for lower end appears at rs of age. OC for upper end of fibula appe Deas appr 4years of age and OC for lower end tibia a at i year of age. OCs of upper end ofrespecu upper end of fibula fuse with their

CHAPTER 5

ABLE 5A. 15

End

of Femur

Ossification at Lower

Bones

Age of Appearance of Epiphyseal

Centres

Part

TABLE 5A. 17

months of

Only one common9 (at birth) centre for both condyles

Fusion With Metaphysis of Lower Part of

Femur

IUL

18 (18-19) Years

Bones

-

ldentification

Ossificationin Tarsal Age of Appearance

Cuboid Navicular Talus

9-10 months of lUL (at birth) 3 Years 7 months of lUL 5 months of lUL

Calcaneum Cuneiform

Lateral: 1 Year Middle: 3 Years Medial: 2 Years

TABLE 5A.18 Ossification

ofPelvis

Part liac crest

14

13

Ossification centre at the lower end of at autopsy in a 9-month-old foetus seen femur metaphyses at 18 (18-19) years of age. Similarly, OCs of lower end of tibia and lower end of fibula fuse with their respective metaphyses at 16 (16-17) years of age (Table 5A.16). Foot (tarsal bones) (Table 5A.17. C.Pelvis (Table 5A.18 and Fig. 5A.7): OCs for iliac Crest appear at 14 years of age and fuse with shaft at 8-21 years ofage. OCs for ischial tuberosity appear at 14years of age and fuse with shaft at 20 years of age. iradiate cartilage is the Y-shaped epiphyseal plate between ilium, ischium and pubis in acetabulum of hip bone. Actually, three bones (i.e. ilium, ischium

Parts Upper Lower

end

Tibia

Fibula

(Years)

9 months of IUL

4

18 (18-19)

1

1

16 (16-17)

(at birth)

end

male.

D.

Fusion With Metaphysis

1st three segments: 3rd month of IUL Last two segments: 4th month of lUL

Fusion (Years) 18-21 20

Ossification of intervertebral discs between five pieces of sacrum starts from below upwards and is completed by 20-25 years

and pubis) start to ossify towards the acetabulum and when almost all these bones are ossified, there remains a Y-shaped portion of non-ossified cartilage in the acetabulum. This Y-shaped portion of non-ossified cartilage is called triradiate cartilage. Ultimately, ossification occurs in this triradiate cartilage and in this way, triradiate cartilage disappears at the age of 15 years and these three bones The comfuse together to form a single hip bone. cartilage in the plete disappearance of triradiate female than in pelvic bone occurs 2 years earlier in

Ossification inTibia

Age of Appearance of Epiphyseal Centres (Years)

14

tuberosity Triradiate cartilage

Fig. 5A.6

5A.16

Centres (Years)

Ischial

Sacrum

ALE and Fibula

Age of Appearance of Epiphyseal

5A.8): OC of ster

Sternum: ('Table 5A.19 and Fig. ossifies from num:Appearance and fusion; sternum secondary centres and one SIX Centres (five primary xiphoid. for

is only centre). Secondary centre E. Skull (Table 5A.20). 5A.21). centres) (Table age. (six bone Hyoid years of ossify at 3 G. Patella begins to

SECTIONI

Forensic Medicine

TAE

liac crest

1418-21

Triradius cartilage

Pubis

13>15

14-20D

Ischium

16->20

Fig. 5A.7 Age of appearance hip bone and sacrum

Stemum Parts of

Stemum

Age of Appearance of Epiphyseal

Centres

Ossification of intervetebral discs between five pieces of sacrum begins at 20 years and starts from below upwards and is completed by 25 years. of ossification centres and their fusion in

1st segment 2nd segment 3rd segment

months of IUL 7 months of lUL 7 months of IUL 10 months of IUL 5

Fusion of

Segments Manubrium and 1st

months of lUL

Manubrium

Xiphoid

Last two segments: months of IUL

Ossificationin

5

4th segment

S.GenN

4

Ischio-pubicramus

TABLE 5A.19

First three segments: 3 months of IUL

segment: 60-70 1st and 2nd: 25 (15-25) 2nd and 3rd: 20 (15-25)

3rd and 4th: 15 4th and xiphoid: 40

3years

Ske

TABLE 5A.20 Age of Closure of

Fontanelles and Sutures Fontanelles

Age of Closure

Anterior fontanelle (bregma)

Within 2 years (18-24 months) after birth

Posterior fontanelle (lambda)

Within 2 months after birth

Mastoid fontanelles

Shortly after birth

Old age (60-70 years)

5 months (IUL)-

25 years

7 months (IUL)-

20 years

7 months (UL)10 months (1UL)-

15 years 40 years

pers as

(i.e. two posterolateral fontanelles)

Sphenoidal fontanelles i.e. two anterolateral fontanelles)

race

6 months

m ane

Age of Closure (Years)

SuturesS 5 months (IUL)-

10

Metopic suture Coronal suture Saggital suture Lambdoid suture Asterion Pterion Masto-occipital suture

3

40

SE Sex

40

Ph

45

bre

50

an-

65

se

80 Ca

3 years

Fig.5A.8 Age of appearance of ossification centres in sternum and their fusion

Medicolegal Importance of Age It is explained in [SN-3]

RACE Humans have been categorised racially into Cau casoids, Mongoloids and Negroids; the race of a

In

TABLE 5A.21 Bone

Ossification in Hyoid

Parts of Bone

Age of Appearance Towards the end of (just before birth)

Two centres appear in the body

At birth

total 2) One centre appears in each lesser cornua (total 2)

At puberty

G D

of Centre

One centre appears in each greater cornua (total 2)

It

lUL

O

CHAPTER 5

TABLE

Identification

5A.22 Features in Different Races

Features

Caucasoids

Example

Europeans

Skin

White

Eyes

Blue

Black-brown

Narrow (NI< 70)

Black

Medium

Broad (Nl> 85)

Light golden colour, wavy with oval cross

Dark coloured, straight With round cross section

Dark coloured, wooly

Prognathism

75-80 (mesaticephalic) Least common

Orbits

Triangular

70-75 (dolichocephalic) Most common Square

9.

Nasal aperture

10.

Palate

Narrow Triangular

Cusp of Carabelli

Present

80-85 (brachycephalic) Common Rounded Medium Rounded Absent

No. S.General features

Nose nasal index =

nose wath of of height

Hair

nose

x1 00

Mongoloids

section

Chinese, Japanese and Mongols

Africans

Yellow

Black (NI = 70-85)

Skeletal features

6 8.

Cephalic index

person can be determined by general features as well as skeletal features (Table 5A.22). Nowadays, pure races are not seen commonly. Indians are a highly mixed race (Caucasoids + Negroids) with brown skin

and black/brown eyes.

SEX Sex can be determined by the following methods: Physical (morphological) characteristics,

(1) for example, breast, external genitalia, gonads, Adam's apple and facial features; (2) microscopic examination: sex chromatin (or nuclear sexing), gonadal biopsy; 3) DNA profiling; (4) skeletal remains; (5) radiological investigation and (6) hormonal analysis.

Intersex

with kidney-shaped cross section

Broad

Rectangular

Absent

In 'gender identity disorder, a male child identifies himself to be a female and a female child identifies herself to be a male. Also the person suffers from distracting and uncomfortable feeling known as gender dysphoria because there is a mismatch between their biological sex and gender identity. These persons having gender identity disorder are known as 'transgenders. Transman (Female to male' (FTM)) is a transgender person who was assigned female at birth but whose gender identity is that of a man. Transwoman ('male to female' (MTF)) is a person who was assigned male at birth but whose gender identity is that ofa woman.

Nuclear Sexing It is explained in [SN-6].

tis explained in [SN-5]. Gender Identity

Negroids

Disorders

It isnow known as gender dysphoria' according to SM-V: At birth, a child is identified either as male or a female earance of his genitalia.This on the basis of appea is the biological sex assigned to the child at birth. When the child grows, the male child idenifies himself as aa male and a female child identifies herself as a fem female. This is known as gender identity

Concealed Sex It is explained in [SN-7].

Sexual Characteristics

gencharacteristics include external vulva sexual Tary in male and (SSCS) example, penis and testes lor characteristics ala, sexual Secondary puberty, for n temales. appear during which features axillary) and nclude the pubic, facial, (e.g. CXample, breasts, hair

SECTION

I

Forensic Medicine

larynx. For the purpose of identification, SSCs are not very helpful because they give very vague idea about sex the age. James Tanner developed formal stages of ual development in puberty called sexual maturity

rating.

STATURE

Introduction When the skeleton is incomplete or severely disintegrated, the stature may be calculated by applying mathematical formula to the length of long bones. Long bones must be measured by osteometric board only. Different international formulae are available for stature calculation. There is no standard formula for Indians as stature varies from state to state. There are some Indian formulae which can be used for different states in India. Errors remain between 1.5 and 2" (3.8-5 cm) if stature is calculated from Trotter and Gleser's formula in different parts of India.

Some Facts (1) There is a progressive diminution in stature as age advances; the rate being 0.6 mm/year. (2) Stature ds in evening by 1.5-2 cm. (3) Stature 1s on lying down by 1.5-2 cm. (4) Stature Ts after death by about 2 cmn due to loss of muscle tone, relaxation of joints and tensions of intervertebral discs.

Stature Estimation from Bone

If

whole skeleton

is available,

stature = length of entire skeleton + 2.5-4 cm (for soft tissues). If only long bones are available, some international (e.g. Karl Pearson; Trotter and Gleser) as well as Indian formulae (e.g. Pan, Nat, Singh and Soha, Siddiqui and Shah) are available. Karl Pearson's regression formula (1899): It is the most commonly used method to determine stature from long bones. Example: From femur,the formula (in males) for stature = 81.306 + 1.88 x femur length and in females, stature = 72.884 + 1.945x femur length. Trotter and Gleser's formula (1952, 1958): Stat ure = (bone length x multiplication/fixed factor) +constant factor + (2.5-4) cm). Example: For femur, the formula for stature = (femur lengthx 2.38) + 61.41.

bones versus dry bones: (1) Wet bones: Wet slightly longer than dry bones. (2) When bon length is measured in wet state, deduct 7 mm from femur, 5 mm from tibia and humerus and 3 mm from radius to get the lengths in dry state. (3) In the skull, all measured dimensions are reduced by 1%-2% by drying. (4) In vertebral column, total length is rcduced by 2.7% by drying. bones of lower limb give a closer estimate Long than that of upper limb to calculate stature. The highest correlation with stature is given by femur and tibia followed by humerus and radius.

Stature Estimation in Case of Mutilated/ Fragmented/Dismembered Body Stature = distance between tips of middle fingers of both hands when arms are fully outstretched. 2) Stature = [(length of one arm) x 2] + 30 cm (for two clavicles) + 4 cm (for sternum). 3) Stature = (length from vertex to symphysis pubis) X 2 or (length from pubic symphysis to heel) X 2. 4) Stature = height of head (from top of head to tip of chin) X 7. 5) Stature = height of skull x 8. 6) Stature = length from suprasternal notch to symphysis pubis x 3.3. 7) Stature = length of forearm from tip of olecranon process to tip of middle finger x 19/5. 8) Stature = length of vertebral column X 100/35. 9) Stature = length from symphysis menti to mandibular angle X 16. 10) Stature = length of foot x 100/15. So stature can be calculated from foot print. 11) Rule of thumb: Humerus is 20%, femur is 270 tibia 22% and spine 35% of the individual's height in lifetime. 1)

IMPORTANT QUESTIONS FOR EXAMINATION LONG QUESTIONS (LO) 1.

What is iclentification? Bnumerate various criterh used for identification in the living. How wo you proceed to estimate the age of a person o 18 years of age who is accused of thett? Discus radiologica the findings of physical, dental and

CHAPTER 5

vamination, you would expect in this person. Discuss indetail the medicolegal importance of age. SHORT NOTES

(SN)

(or Hasse's rule) [CCU 2014] Medicolegal importance of age [CCU 2003, 2009 Medicolegal importance of 18 years of age

lasse 2. Rule of 3. 4.

5. 6. 7.

Intersex [CCU 2003, 20091 Nuclear sexing Concealed sex

MEDICOLEGAL IMPORTANCE (MLI) an intersex (V. Imp) 9. The person is 12 years of age 10. The person is 14 years of age 11. The person is 16 years of age 12. The boy is 18 years of age 13. The girl is 18 years of age 14. The person is 21 years of agge 8. Person is

DIFFERENCE BETWEEN (DW) 15.

Turner and Klinefelter syndrome

ANSWERS LO-1:What is identification? Enumerate various criteria used foridentification in the living. How Would you proceed to estimate the age of a person of 18 years of age who is accused of theft? Discuss thefindings of physical, dental and radiological examination, you Woula expect in this person. Discuss in etail the medicolegal importance

of age

ldentification Determination of the individuality of a person, live or deadis known as identification.

Identification

Criteria Used for Identification

They are given in Table 5A.1.

Estimation of the Age of a Person of 18 Years

Physical features: Pubic and axillary hair are well grown. Beard and moustache are present. Genitalia have adult appearance in both sexes. Breast is fully developed in females. Voice is hoarse in males. Adam's apple is more prominent in males. Dental features: a All teeth in the mouth are permanent. Teeth present are incisors, canines, premolars and molars; the dental formula being 2-1-2-2 (i.e. two incisors, one canine, two premolars and two molars) or 2-1-2-3. Total number of teeth may vary from 28 to 32. The reason is that the last molars (i.e. wisdom teeth) erupts at the age of 17-25 years and sometimes may not erupt at all. Hence, presence of all the four 3rd molars indicates that the subject is over 18 years of age. After eruption of 2nd permanent molars at 12 years, the body of mandible increases in length and the ramus of mandible grows and moves behind, so a space is created behind 2nd permanent molar (M-2) for 3rd permanent molar. It is known as spacing of jaw. While examining teeth, the space behind 2nd permanent molar is to be felt. If space is present, examine whether it is hard to feel or not. A tooth may be partially erupted. Radiological features: Lower ends of radius and ulna (i.e. at wrist fused joint): The epiphyses of radius and ulna with their respective shafts. knee joint): The o Lower end of femur (i.e. at with its epiphysis of lower end of femur fused shafts.

knee

(i.e. at ends of tibia and fibula fused tibia and fibula joint): The epiphyses of with their respective shatts. be fused. metacarpals: lliac crest may or may not 2nd to 5th of ends) (distal Heads metacarpals are O 5th to 2nd The epiphyses of respective shafts middle and fused with their proximal, (proximal end) of epiphyses fused with Base phalanges: Their terminal shafts. their respective

Upper

SECTIONI

Forensic Medicine

trochanter and lesser trochanter may or nmay not be fused witlh shaft.

Epiphyses

of head, greater

Medicolegal Importance of

18

Years of Age

Please refer to [SN-4].

SN-2: Rule of Hasse (or Hasse's rule) and rule of Morrison determine the age of foctus in uterus, tlhere are two rules: Rule of Hasse and Rule of Morrison. Hasse's rule is applicable only up to 5 months of intrauterine life while Morrison's rule is applied from 6 months of intrauterine life onwards (Table 5A.23). Rule of Hasse: is a rule to calculate the intrauterine age of It foetus, but it is applicable only up to 5 months of intrauterine life (or when crown-heel length (CHL) is 25 cm). The age of foetus (in months) is equal to the square root of the CHL (in centimetres). Rule of Morrison is a rule to calculate the intrauterine agé of It foetus, but it is applicable from 6 months of intrauterine life onwards (or when CHL is >25 cm). The age of foetus (in months) is equal to CHL (in centimetres) divided by 5. Medicolegal importance: In the case of foeticide or infanticide, these rules help to estimate age by measuring the lengths of the newborn child.

To

SN-3: Medicolegal importance of age 7 yearsofagc: Nothing is an offence when done By child of 18 years of age can give consent for surgery. According to S.11, Indian Contract Act (1872), only a child of > 18 years can enter into a valid contract and the surgi cal operation is a contract between doctor and patient. If he is 78

of shaft 80 with condyles (degrees)

>4.8

83.3

86.49

86.2

Lo femur (F) Lof IH+ 100 70.4 Lof [F+ T]

Inter membral index Humerofemoral index

67.27

70.3

71.11

72.4

Lof

Lof

x100

69

H100 F

L Length;T= Tibia; F

Femur: H= Humerus;

R

Radius

Tibia (1) Age: Appearance of OCs in X-rays (Chapter 5A). (2) Sex: The difference between male and female tibia (Table 5B.17). (3) Race: From crural index and intermembral index. (4) Stature: Multiplication factor varies usually from 4.18 to 4.49 because of variation

of people of different population.

Fibula (1) Age can be determined from appearance of OC in X-rays. (2) Sex: Difference between male fibula and female fibula (Table 5B.18). (3) Stature: Multiplication factor varies usually from 4.43 to 4.55 because of

variation of people of different population.

OTHER B0NES

Clavicle (1) Age can be determined from appearance of OC in X-rays (Chapter 5A). (B) Stature of individual = length

TABLE 5B.17 Difference Between Male Tibia and FemaleTibia No. Features

Male Tibia

1

General

Heavier and rough

2

Length (cm) Mid-shaft circumference

3730

472

Angulation

Head diameter (vertical) (cm

index

(European) Indian groids

of

tibia

Crural

Ne

Caucasoids

Calculated as L

S,

(collodiaphyseal angle) (degrees) Bicondylar width

Races

Smaller, 18 years after taking risk with his own consent suf fers death.

Injury Likely to Cause Death Versus Injury Sufficient to Cause Death Injury likely' to cause death belongs to the defini tion of culpable homicide [S.299, IPC] and injury sufficient to cause death belongs to the definition of murder S.300, IPC). It is the degree of probability of death which makes

the difference. The injury likely to cause death means that it is not just a possibility, but is probable. Injury 'sufficient to cause death means death will be the most probable result of injury in ordinary course.

3) Histochemical methods or enzyme histochemistry SN-5]

INJURY REPORT

Consent for examination: If the patient is not arrested, consent is required. For the purpose o medicolegal examination, consent can be gue by any person of sound mind of >12 years o age. If the person is unconscious or insane SI2 years, the consent can be obtained fromn the guardian. Signature or left thumb impression (it illuter e) of patient as well as witness must be taken.

ness may be the police officer who brought

If

request by using reasonably necessary toree

A-ra

take

torm

After

C

been C onthe

Deal The

bodypo

ha

tne

patient.

patient denies, then under S.53, CrPC. medicolegal examination of accused can done on police (not below the rank ot

kept

Subs

Precautions

AGE OF WOUND OR INJURY Age of wound or injury can be determined by (1) Gross changes in a wound due to healing (2) Histopathological changes (Table 7A.3)

OUS

Injury report is a type of medicolegal document or certificate (MLC). It is usually prepared by the first attending medical officer (emergency/casualty MO) in a case of injury. I.

Ca

HORTT be SI)

Gtevs

O

CHAPTER 7 MLC: It is Ieft to the doc as ML 2. label the case as MILC, whether pa udgment to es or not. The patient or relatives may compel a but doctor has to stand by make doctor.not to i decision. ision. If loctor delays in labelling a case as his own labelled at any later date and time. MLC, it can be so nformation to police: Police must be informed as 3. possible. early as in duplicate and both 4. MLC reports must be made 'medicolegal case'. Original cOpies must be marked handed over to police and his signature must cOpy is copy, that is, doctor's copy. be taken on the other Doctor's copy is retained in medicolegal register. reports (e.g. X-rays/CT requisition 5. Investigation marked slip, lab reports slips and so on) must be medicolegal case and then handed over to the police. They should never be given to patient.

Labelling the case

What is More Important, Treatment or Completion of Injury Report? It

depends on seriousness of the patient. Injury report

can be

completed after the emergency treatment.

Case Where the Doctor Has to Give Opinion (1) If the nature of injury

to Wait

(simple, dangerous or griev-

ous) is not immediately apparent, the patient must be kept under observation and (2) if investigations (e.g.

X-ray/CT or blood) have been sent for and it would take a long time for the results to be collected, the doctor may have to wait to give opinion.

Subsequent Opinion After observation period is over and all reports have been collected, the subsequent opinion is given based on the new findings.

f Death Occurs During Treatment The police must be informed immediately and the Dody handed

over to police only, not relatives

IMPORTANT QUESTIONS SHORT NOTES

.Grievous hurt

(SN)

[DU 20061 [CCU 2004, 2005, 2009,

2011] 2. S.320, IPC [CCU 2012]

139

Emasculation 4. Dowry death 5. Enzyne histochemistry 3.

DIFFERENCE BETWEEN (D/W) 6. Antemortem wounds and postmortem wounds

CCU 2003

7. Suicidal

wound versus homicidal wound [DU 2004]

ANSWERS

SN-1: Grievous hurt Grievous hurt [S.320, IPC): GH is hurt of more serious nature. Physician's opinion in his report about injury as simple or grievous is to guide the investigating officer only. Actually, the court will decide whether the hurt is simple or grievous. According to S.320,, IPC, the definition of GH includes eight clauses. Only the following kinds of hurt are designated as grievous (Table 7A.4): [Mnemonic Eat 3 Pears Daily: Purely Free Advice for 20 days] 1. Emasculation [SN-3] 2. Permanent privation of sight of either eye or comIt means permanent loss (partial eye. The either plete) of sight or vision of loss of sight may be partial or complete, but it has to be permanent. Permanent does not mean that it is incurable. Surgical interference is not taken into account.

TABLE 7A.4

Grievous Hurt

LMnemonic: Eat 3 Pears Daily: Purely Free Advice for 20 days 1)

2) 3) 4)

EXAMINATION

FOR

Injuries

Emasculation Permanent privation of "'sight of either eye Permanent privation of 'hearing' of either ear Privatlon of any member or joint of the power Destruction (or permanent impairing) of any member or joint or tace Permanent disfiguration of head

6Fracture/Dislocatlon of a bone or tooth 8)

which causes endangers life or (2) days in severe Any hurt (1) which 20 of the spaceordinary pursuits be during follow his the sufferer to unable to

bodily pain, or

140

SECTIONI

Forensic Medicine

Gabbar Singh causes a scratch abrasion on Viru's cornea. The corneal

Example:

leaves abrasion heals completely but permanent scar due to which Viru is not able to see clearly, that is, Viru suffers froom partial loss of vision. Since Gabbar Singh has caused permanent privation of sight of one eye, he has caused GH. After that, Gabbar Singh offers for corneal transplantation and Viru agrees. After corneal transplantation, Viru is now able to see very clearly. Here, Gabbar Singh is still guilty of causing GH. Permanent privation of hearing of either ear There is permanent loss of sense of hearing, that is, permanent deafness. Loss of hearing may be partial orcomplete but has to he permanent. Permanent does not mean that it is incurable. it

3.

a

Examples:

teacher slaps a student. The tympanic membrane of student ruptures and he cannot hear. The teacher has caused GH. 2) A quack inserts a stick to clean X's ear and he punctures tympanic membrane. The quack has caused GH. 3) Gabbar Singh cuts an ear of Ramu. It is not GH because hearing is not impaired. It falls under two clauses, that is, Clause 4 because ear is a member; Clause 6 because 1) A

it disfigures face/head. is less serious than injury classified It under Clause 2 as it only deprives a man of use of his auricular organ; it does not disfigure him.

4. Privation of any member or joint

Privation ofany member or joint means loss of member, for example, by cutting. 'Member means an organ or limb of a person per-

forming a distinct function. It includes eyes, ears, nostrils, mouth, hands, feet, etc. Joint means place where 22 bones and muscles join. Their privation must involve permanent stiffness so that the person is unable to perform normal function. Examples: (1) cutting of a finger is GH; (2) trimming of nail is not GH because it can regrow, but if nail is evulsed from base, it is GH because it cannot regrow; (3) mutilation of body parts is GH.

Punishment provided by code depends upon

the nature of member or joint (arm > fin. ger) lost. 5. Destruction (or permanent impairing) of the powers of any member or joint human body can discharge its normal A functions properly when it can use its limbs and joints freely and effectively, without any hindrance. Deprivation of this power, because of permanent impairment of func. tion of any limb or joint will render the sub. ject crippled and unable to do his normal function. Here, there is permanent impair. ment of the use of any limb or joint without causing its total destruction, so there is life long crippling. Classical example: a foot was paralysed due to the injury in LS-spine. It is GH. 6. Permanent disfiguration of head or face Abrasion: Since an abrasion usually involves only epidermis, it heals without scarring and so it is a simple injury. It does not matter whether the abrasion is on the face or other parts of the body. Laceration on any part of body may or may not be GH, but on face, a lacerationis GH because it heals with scarring and so disfigures face. Examples: (1) Cutting nostrils or ears and (2) causing laceration (and so scar) on the face of young girl or an actress is GH because it disfigures face. In the case of an old woman, the laceration (and so scar) caused on her face is also GH. According to law [i.e. clause (6) of S.320, IPC], it does not matter whether permanent disfiguration of face affects the life or career of a person or not. 7. Fracture/dislocation of a bone or tooth Causing fracture is GH. (Fracture includes any type of fractures, even cut on a bones hairline fracture, fracture of outer table or inner table of skull, gutter fracture, etc.). Causing dislocation of any joint, for example, shoulder joint or elbow joint is GH. Practure or dislocation of any tooth (tem porary or permanent) is GH. If a tooth 15 already loose in socket, then making it fAa is GH. 8. Any hurt (1) which 'endangers life', or (2 which causes the sufferer to be during tne

$.32 SN=

SN EE

ing

Iti ne Th

ua

to

Itca TAB Direct

Ctouse

me sic

Reme

CHAPTER 7

severe bodily pain, or (3) spaceof 20 days in lhis ordinary pursuits. nable to follow which endangers life: Compound D Any hurt of skull, rupture of an internal

puberty causes impotency in most cases but in a few cases, erectile function may be retained because sexual behaviour is partly a learned phenomenon. Suppose 'X' cuts away testes of' Y but 'Y retains penetrating power, it means X is not guilty under Clause but is guilty under Clause 4. 2) Cutting away of a permanently flaccid penis does not fall under Clause 1 but under Clause4. To bring the case under this clause, the impotency caused must be 'permanen.

fracture a large blood vessel, stalb organ, injury of squcezing tesinjury on chest or abdomen, dangerous mjuries are grievous, tes, etc. Al are not dangerous. but all grievous injuries

2)

continuous. sufferer to be Any hurt which causes the unable to follow his ordinary pursuits for day-to-day 20 days. Ordinary pursuits means personal acts of an individual (e.g. taking food, taking bath, wearing clothes, combing hair).

3)

SN-2: S.320, IPC IPC defines grievous hurt. Please refer to SN-1] on grievous hurt.

S.320,

SN-3:

Emasculation

Emasculation means loss of masculine power. (Masculine power means penetrating power during sexual

intercourse).

Itis a type of grievous hurt. in Clause 1 of S.320, IPC.

This

It has been mentioned

the only clause which is almost confined to males only because masculine power is confined to males only.

It

is

can be caused in two ways

ABLE Direct 1)

(Table 7A.5)

7A.5 Causes of Emasculation

Castration (i.e. removal Of

1

causes the sufferer/victim

Any hurt which severe bodily pain for a period off to be in in the lhospital for 20 days 20 days. Mere stay need not be will not constitute GH. 20 days

testes) or squeezing

testes 2) Amputation (i.e. cutting

Indirect 1) Injury to

testis

2) Injury to LS-region

spineImpotence

o

of penis)

SN-4: Dowry death Sections related with dowry death are: S.304 and S.498 of IPC and S.113 and S.113B of IEA. Dowry death [S.304B, IPC}: This is death of a woman by any burn or bodily injury or which occurs otherwise than under normal circumstances within 7 years of her marriage and it is shown that she was subjected to cruelty or harassment by her husband or his relative for dowry. If any one of these two components is absent, it is not dowry death. Punishment: Such husband or his relative shall be deemed to have caused her death and will be punishedwith P =1, ar1,i.e. imprisonment for 7 years which may extend to imprisonment for life). According to S.498A of IPC, if the husband or his relative treats the woman with cruelty, he will be + F (i.e. imprisoned for up punished with P = I,,ar, 3years to 3 years with fine). S.113A of IEA: If death of the woman occurs by suicide and the two components of dowry death are present, the court shall presume abatement of suicide by husband or relative. S.113B of IEA: When the question is whether a person has committed dowry death of a woman and it is shown that just betfore her death such woman had been subjected by such person to cruelty or harassment for dowry, the court shall preSume that such person caused dowry death.

SN-5: Enzyme histochemistry

Clause

1isjust about emasculation. Since penis is a nember, Clause 4 already covers emasculatio.

Classical

examples:

1) Removal

of estes before puberty causes impoency in all cases. Removal of testes alter

Injuries

It

is a

in tiSSues. technique to demonstrate enzyme in demonstrated can be

Enzymes histopathological changes Wounds before any become visible.

Principle:

142

SECTIONI

Forensic Medicine

Peripheral zone

0.1-0.3 mm]

Central zone [0.2-0.5 mm

Wound

Epidermis

Dermis

Fig. 7A.1 Histochemical changes in an antemortem

wound

Take damaged skin tissue: 2 g of skin. Also take control skin. Tissue is frozen and treated with suitable reagent. Development of a specific colour indicates the presence of a particular enzyme. Precautions: (1) Skin tissues should not be treated with formalin as it would destroy the enzyme. (2) Application of antiseptic agent does not affect these reactions. Histochemical changes in an antemortem wound (Fig. 7A.1): Immediately after a wound is produced, two zones can be demonstrated around it. 1) Central zone (0.2-0.5 mm wide): The enzymatic activity decreases in central zone. 2) Peripheral zone (0.1-0.3 mm wide): The enzymatic activity increases in peripheral zone.

TABLE 7A.7 Sr. No. Features

5. 6.

Sr. No. Age of Wound

Vasoactive Amines (Enzymes)

1

10

2.

30 min

3

1h

4

2h

Serotonin, calpain, cathepsin Histamine ATPase and esterase Aminopeptidase

5.

4h 8h

Acid phosphatase Alkaline phosphatase

6.

Technique:

2.

TABLE 7A.6 AgeEstimation ofWound by Enzyme Histochemistry min

Age estimation of wound by enzyme histochemistry (Table 7A.6) wounds do not show these changes. Postmortem Enzyme histochemistry is less useful in cachexia and senility as the ability of tissues to produce reparative enzymes is decreased. In contusions, the damage is more diffuse and there are no definite zones.

D/W-6: Antemortem and postmortem wounds (Table 7A.7) D/W-7: Suicidal wounds and homicidal wounds (Table 7A.8

Difference Between Antemortem Wound and Postmortem Wound

Haemorrhage Source of haemorrhage Signs of spurting on body, clothes, floor and walls Coagulation Extravasation of blood Staining of wound edge

Antemortem Wound Copious Arterial

Present Firmly coagulated blood

Present Present and resists washing with water

Wound age

Everted, gaping, retracted, swollen

8.

Vital reaction

9.

10

Infection Histological examination

Present Present

11

Histochemical examination

Infiltration by leucocytes, macrophages, fibroblasts; formation of new capillaries Increased enzymatic activity

Postmortem Wound Slight or absent Venous

Absent No clotting or soft clot

Absent Absent;

stained rarely, it can be easily washed with water Do es not gape, edges are closely if

approximated Absent Absent No such findings

No enzymatic activity

CHAPTER 7 TABLI Sr.No.

Features Wounds

Direction 3

Severity Hesitation marks 6.

8

14

7A.8 Difference Between Suicidal Wounds and Homicidal Wounds Target area

5.

Injuries

Defence wounds Weapon at crime scene

Clothes

Circumstances

Suicidal Wounds

Usually incised or stab

Accessible parts only, for example, neck, wrist, left side of chest From left to right and above downwards (in a right-handed person) Mostly superficial, one or two deep wounds Present Absent Usually present (may be firmly grasped by cadaveric spasm)

Homicidal Wounds Stab, lacerated, incised No fixed site, head, chest and abdomen Any direction

Mostly severe and extensive

Absent May be present

absent; in rare instances, a criminal may put weapon in the hand of the victim so as to mimic suicide Not damaged as they are removed May be damaged Closed room bolted from inside. Crime scene Crime scene is usually disturbed usually undisturbed Usually

144

SECTIONI

Forensic Medicine

Chapter 7B Mechanical Injuries INTRODUCTION For the common pcople, the term 'injury' means a physical injury (e.g. bruise, cut, laceration and so on) inflicted by a wveapon and causing pain. Usu ally the term 'injury refers to 'mechanical injury. The injuries produced by mechanical force are known as mechanical injuries. Classification ofmechanical injuries (Table 7B.1) 1) By blunt weapons: They result in four types of injuries-abrasion, contusion, laceration and fractures. These injuries are caused by sudden forceful impact of blunt weapons. 2) By sharp edged weapons: They result in two types of injuries a) Incised wound: When sharp edged weapons are used in a swiping manner, they result in incised wounds. b) Stab wound: When sharp edged weapons are used in a thrusting manner, they result in stab wound. 3) Firearm injuries: Discussed in Chapter 7E.

By Blunt Weapons By'Sharp'Weapons By Firearm

4) Fracture

Incised wound 2) Stab wound 1)

Entry

7B.2

Abrasions Produced Tangential' Force

Types of Abrasions by

1) Scratch (linear)

2) Grazes (sliding/glancing)

Wound

Exit wound Injuries to the tissues in the way

of bullet or pellets

ABRASIONS DAbrasion: It is a type of mechanical injury in which

o

a

TABLE

TABLE 7B.1 Classification of MechanicalInjuries 1) Abrasion 2) Contusion 3) Laceration

o

bleeding does not occur when abrasion involve only cpidermis. On other hand, since dermis vascular, bleeding occurs when abrasion involves epidermis along with dermal papillae. Healing of an abrasion: Since pure abrasion involves only epidermis, it never bleeds and thus it heals without formation of any scar. When an abrasion involves epidermis along with dermal papillae, it bleeds and thus heals with formation of scar. An abrasion starts to heal from periphery by new growth of epithelial cells. It is difficult to interpret an abrasion on a wet skin but becomes more prominent (i.e. becomes dark brown) after the skin dries. Due to this reason, in a drowning case, the body must be allowed to dry before inspection. Types of abrasions (Table 7B.2): According to the force used, there are two categories of abrasions, abrasions produced by 'tangential' force and abrasions produced by perpendicular force.

the most superficial layer of the skin (i.e. epidermal layer and/or tips of dermal papillae) is damaged. It is the most superficial of injuries. Bleeding in an abrasion: Since epidermis is avas cular (i.e. has no blood vessels in its thickncss),

Abrasions Produced by Perpendicular' Force 1) Pressure (crushing9 2) Imprint limpact) 3) Patterned (both of

aforementioned may be patterned)

IMnemonic Save Ganja, Put

In Pursel

Scratch (linear) abrasions are the linear injuries caused by snal pass* pointed olbjects (e.g. thorn, pin or neede ng tangentially and superficially across skin. sig These have appreciable length but no cant width. d ot opithelial tags are found at the terminal che Such type of abrasion, which thus indicat direction of movement of the weapon.

They

mpr

CHAPTER 7

or gliding, scraping or (Fig. 7B.1) glancing or brush) abrasions

caused by tangential sliding movement broad or wider rough surlace against skin. of itudinal parallel lines. multiple They show These are widerat the starting point and naro rower at the end. occur by the person being They frequently dragged at rough roadsides in road traffic accibody, for example, dents (RTA). Some foreign dirt, grit or gravel may be found sticking to the abrasion which can indicate the surface where the person was dragged. Sometimes during dragging, the great friction generates heat and the grazed area appears like burn injury. The term 'brush burn' or 'gravel rash' is used for such graze abrasions. The direction of graze abrasion can be determined by observing 'heaped up epidermis' (or epithelial tags) at the end of this abrasion; the start of the abrasion being clean. They are

Pressure (Crushing) Abrasions

14

Example, radiator grille mark, tyre marks, shoe sole marks, recoil muzzle impression in tight contact rifled wound.

Grazes (sliding

o

Injuries

Patterned Abrasions Thesc abrasions are produced when a weapon with a patterned surface strikes the skin or the body falls against a patterned surface. Here, the pattern of the object or surface is reproduced on the skin. o Both pressure' abrasions as well as imprint' abrasions may be patterned. o Example, motor tyre, cycle chain, whip marks, muzzle of a firearm, shoe sole, bite mark, ligature mark. Weapon can be identified from the pattern of the abrasion. Contused abrasion versus abraded contusion: When abrasion as well as contusion are found at the same place, there may be two situations (a) when abrasion is more prominent as compared to contusion, it is called contused abrasion (Fig. 7B.3); (b) when contusion is more prominent as compared to abrasion, it is called abraded contusion. o

o

oThey are produced by the crushing of epithelium when a relatively small force is applied perpendicularly over a small area of the skin continuously for a long period of time (Fig. 7B,2). o Example: Ligature mark in hanging and strangulation, teeth bite marks. lmprint (Impact or

They

Contact) Abrasions

are produced by crushing of epithelium when a relatively large force is suddenly applied

perpendicularly over the skin for a 'very short period' of time.

Fig.7B.1

A)

scratch (linear) brasions.

(B)

Fig. 7B.2 Ligature mark in hanging, a type of pres-

sure abrasion

graze (sliding) abrasions

46

SECTIONI

Forensic Medicine Since a pure abrasion olves only epidermis, the is scar not formed. Hence, abrasions are ally considered as 'simple injuries because they heal without formation of any scar. If the injury involves dermal papillae, bleeding occurs and later on, after healing, it would result in superficial scarring

5)

A

Fabricated abrasions: A person can inflict abrasion injury on himself in order to level falea charges against enemies.

6)

ig. 7B.3 Patterned contused abrasion

tuary or (2) erosions produced by ants, that is, ant bite. Antemortem abrasions versus Postmortem abrasions (Table 7B.3).

Fingernail marks and teeth bite marks:

Fingernail marks may be either 'scratch' (linear) abrasion or 'pressure (crushing) abrasions. These may be curved or straight. They may be parallel linear scratches if the fingers are dragged down the skin. Teeth bite marks are 'pressure' (or crushing) abrasions. Various colour changes in abrasion are as follows: Fresh: Reddish 1 day: Reddish scab days: Reddish-brown scab 2-3 days: Dark brown scab 4-5 6 days: Black scab dries and shrinks (i.e. starts falling) >7 days: Scab and completely falls off 2 weeks: Completely healed without scar formation An abrasion is a 'simple injury. Since an abrasion usually involves only epidermis, it heals without formation ofany scar; that is why an abrasion is usually considered as 'simple injury'. Usualy those injuries which involve both epidermis as well as dermis form scar and are not considered simple. o In histology of abrasion, reticulum fibres are seen at 8 days and collagen fibres at 9-10 days. o Medicolegal importance (MLI) of abrasion: 1) Type of weapon' can be identified from the examination of the abrasion. 2) 'Direction of force' used to inflict abrasion can be determined by observing 'heaped up epidermis' (or 'epithelial tags) which is present at the end of this abrasion. 3) Time of assault' can be estimated by determining the age of abrasion by various colbur changes 4) 'Simple injuries': Usually those injuries which involve both epidermis as well as dermis form scar.

Postmortem abrasions: These can be caused by (1) manual handling during transport to mor.

TABLE 7B.3 Difference Between Antemortem Abrasions and Postmortem Abrasions [D/W-11] Sr.

Antemortem

No. Abrasions

Site: Anywhere on

the body 2.

Show colour changes during life

3.

4

5

.

It

may be of any

Postmortem

Abrasions Usually on the bony prominences

Do not show colour changes

after death Yellowish parchment like

colour according to the time since injury Exudation: More; Less; scab often lies slightly Scab slightly raised below the level of skin Cause may be Cause may be 1) Manual handling during according to the transport to mortuary type of abrasions 2) Ant bite

Microscopic: Vital reaction and congestton seen

9)

Not seen

CON

Contu tissues trauma

thetiss

Bruis Avioler

effusio external

Whe Erosions produced by ants: Ants eat the SkI" anu of moist parts (eyes, ears, groins, scrotum, and armpit) after death and produce whit Iik 1sh or brownish erosions which may look ay antemortem abrasions as they become also have They do not show vital reaction; they irregular margins (Table 7B.4). abrasio 8) Nature of offence: In sexual offences, the inne are found at and around breast and at (thro Side of thighs. In manual strangulation nails a thng), scratch mark abrasions due to 7)

seen over the neck.

itintact is

15usu bruise neous

) Int diat

due scale

2 and Subc than

CHAPTER 7

Between

TABLE 7B.4 Difference [D/W-12] AbrasionandAnt Bite Marks Ant Bite Marks Abrasion Features Sr. No. Moist parts, Anywhere Site

for example, around eyelids, nostrils, mouth, groin,

scrotum, armpit, ears

and anus

Reddish

Pale

Antemortem or postmortem

Antemortem

Postmortem

Examination by hand lens may reveal

Heaped up epidermis at one end

Crescent

Present

Absent Absent

Colour 3.

Vital

reaction

Signs of healing May be present

9)

shaped ant bite marks

Correlation with the scene of crime: Presence of foreign material (e.g. dirt, sand, mud and so on) in an abrasion may connect the injuries with the scene of crime.

CONTUSIONS (OR BRUISES) Contusion: The extravasation of blood into the soft

tissues due to rupture of blood vessels

caused by blunt

trauma is called contusion. The blood is collected in the tissue outside the blood vessels.

Bruise vs. Contusion A violent

blunt force impact causes extravasation or effusion of blood in soft tissues. It may become visible externally or may not become visible externally. When it becomes visible externally, that is, when it is observed by naked eyes through the overlying intact skin as bluish-purple discolouration and 1S usually associated with swelling, it is known as DrUise. Bruise may occur in dermis or in subcutaneous tissues or deeper tissues (e.g. muscles). 1) Intradermal bruise: This bruise lies in immediate subepidermal layer. It is usually produced Caue to violent impact by the blunt surface of a ght flattened weapon, for example, metallic Scale, whip, etc. This bruise is usually patterned and so has sharply defined margins. 4) Subcutaneous bruise: Since this bruise is deeper than intradermal bruise and is produced usually

Injuries

147

fatty layer, its edges are ill defined. It is the most common type of bruise and is commonly seen in a scuffle. 3) Deep bruise: This type of bruise occurs either in superficial muscles or muscular facial planes. Since it is deeper than the aforementioned two types, it may take hours to 2 days to appear at the surface and due to this reason, this type is also known as delayed bruise and the phenomenon delayed bruising. Therefore, keeping this fact in mind, it is very important to reexamine the person 1-2 days

after first examination. *When it never becomes superficially visible, it is known as contusion. It occurs due to the rupture of blood vessels in the deep muscles or visceral organs, for example, liver, kidney, spleen, muscles, heart, etc. It can be observed at autopsy after incising muscles or opening the body cavities. Both terms 'bruise and 'contusion' are often interchangeably used. However, bruise denotes injury noted superficially on the body surface and associated with swelling of involved area. Contusion denotes injury to the deeper muscles or internal organs. At autopsy, a bruise can be examined without incision but contusions require incision for examination.

Factors Influencing Bruise 1) Age: Bruises

elderly.

are easily produced in children and

2) Sex: Bruises are easily produced in women because

of presence of more delicate tissues and more sub-

cutaneous fat. 3) Size of body: Bruises are more easily produced in obese people as compared to lean people. 4) Colour of skin: Bruises are more clearly seen in fair skinned people as compared to dark skinned people. In dark skinned people, bruises are better felt than seen. 5) Site and type of tissues involved: Soft, lax and vas Cular tissues (e.g. scrotum, face, eyelids) develop large bruises with minimum blunt force trauma. Bruises of scalp are better felt than seen. In athletes, muscle tone. bruising is much less because of good People taking aspirin bruise easily. develop easily in persons o) Natural disease: Bruises chronic alcoholism), Suffering from cirrhosis (due to

SECTIONI

148

Forensic Medicine

haemophilia, scurvy, vitamin K or prothrombin deficiency, bleeding diathcsis, leukaemia, ctc. 7) Ectopic or migratory bruise 1SN-1]: When extravasated blood at the point of impact by a blunt weapon tracks down duc to gravity along the fascial planes or between muscular layers and reappears at a site below the injured site, it is known as ectopic or migratory bruise.

Age Changes in a Bruise The age ofa bruisc can be estimated by colour changes histological changes. In a living person, the bruise heals by the destruc-

as well as

tion and removal of extravasated blood. With time, the bruise undergoes colour changes; the colour changes starts from periphery and extends inwards. The rate of colour change is quite vari able, not only between persons, but in the same person. Bruises of same age may show different colour and this variation does not necessarily mean that there have been multiple episodes of injury. Colour changes in a bruise: Fresh: Reddish days: Bluish black/purple 1-3 days: Brownish (due to the presence of 4 haemosiderin')-RBCs disintegrate by haemolysis and the haemoglobin is broken down into haemosiderin days: Greenish (due to the presence of 5-6 haematoidin')-because haemosiderin is converted into haematoidin. days: Yellow (due to the presence 7-10 of

bilirubin')-because haematoidin is converted

into bilirubin. Normal skin colour. A bruise heals completely in 2 weeks without leaving a perma2 weeks:

nent scar. Factors Affecting Colour Changes in Bruise in Living Persons Depth of bruise: A deeply situated bruise takes a longer time to appear externally. It is also faint.

Environmental lighting Overlying skin colour: A bruise in a fair individual is more clearly visible as compared to that in

dark pigmented individual. Age of the person: Bruise in children change colour rapidly because of fast healing. a

In

CO poisoning, fresh bruise may be bright

in colour.

MLI of

reä

Bruise

of bruise: The time since infliction of injury (i.e. bruise) can be estimated by the colour changes in the bruisc; this date and time can be correlated with the date and time alleged by the history of the

1) Age

individual. 2) In battered baby syndrome, a. Bruises of different ages can be seen at a particular time. b. Six penny bruises: These are multiple smalI bruises produced by pressure of fingertips. 3) The interpretation of the age of bruise by its colour is very difficult because of great variations in healing 4) Subconjunctival haemorrhage does not show similar colour changes as normal bruises show because haemoglobin in the conjunctival vessels is kept oxygenated by air. 5) A medical officer should reexamine the patient after 24 h as by this time, the bruises are clearly

visible. 6) A bruise should be differentiated from postmor tem hypostasis (Chapter 6D, Table 6D.2). 7) Artificial bruise: These are falsified bruises pro-

duced by rubbing some irritant substances (e.g calotropis, semicarpus, plumbago) on the skin. Such bruises are actually discolourations which look like true bruises. These falsified artihcial bruises should be differentiated from true bruises (Table 7B.5). Artificial bruises are produced to bring a false charge of assault against an enemy or a talse charge of torture against policemen. These are also produced by malingers to go on

leave.

8) Postmortem bruises: Bruises which appear ater death are called postmortem bruises. They may be causecl by antemortem or postnmortenn nyury trauma, tne

Suppose death occurs soon after blunt bruise appears after death. The blood comes ou from blood vessels passively due to gravity. Ine pigment from haemolysed blood then dittuses locally to stain on the surface. Putrefactive gast may also push blood from damaged blood vesseb Postmortem bruise should be differentiated tro an antemortem bruise (Table 7B.6).

LAC

a

Me On

SO

tore

he

mic

CHAPTER 7

Injuries

149

D BetweenTrue Bruise and Artificial Bruise [D/W-13) TABLE 7B.5 Difference TABLE 7B.5

True Bruise

Trait Sr.No.

Anywhere

Site

Shape

Atypical colour changes Usually round

Margins

Not well defined, diffuse and

Colour

irregular No vesicles

Redness and inflammation Contents

9.

0.

Juice of marking nut, Calotropis or Plumbago rosea Exposed accessible parts Dark brown

Trauma

Causes

8.

Artificial Bruise

Itching

Vesicles

Chemical analysis

Seen in the site Extravasated blood Absent Absent Chemical negative

7B.6 Difference Between Antemortem Bruise and Postmortem TABLE

Bruise [D/w-14]

Antemortem Bruise (Contusion) St. No. Swelling: Present

Damage to epithelium:

Postmortem Bruise

(Contusion) Absent Absent

Present Coagulation: Present

Extravasation of blood:

Present Colour changes:

Present

Margins: It merges with

surrounding areas

Absent Absent Absent Sharply demarcated

LACERATION

Laceration (Latin, lacerare = to tear): It is a form of mechanical injury characterised by a tear of skin, mucous membrane, muscle or internal organs caused by blunt force

impact.

Mechanism: Lacerations are caused ons (e.g. hammer,

by blunt weapP

iron rod, cricket bat, hockey and So on). The blunt force may be either shearing 1orce or crushingforce. During blunt force impact, the tissues get stretched or crushed beyond the limits of their elasticity produce to laceration. Characteristics of lacerations: Irregular uneven

margins ADrasion and bruise may be found around the WOund and so accordingly the laceration may be called abraded laceration contused

laceration. and 1SSue bridges (or bridging fibres) are the hallmark of lacerated wounds. They are found in the

Irregular Well defined and regular covered with small vesicles

Seen

in

the surrounding skin

Acrid serum

Present Finger tips and other parts of the body due to scratching Chemical positive

depth of a lacerated wound. Bridging may also be found in the laceration of internal organs. Why are bridging fibres found in lacerated wound, and not in incised wound? Because the blunt weapon causing lacerated wound may crush but does not cut all tissues in the depth of the wound and so some strong and hard tissues (eg. blood vessels, elastic fibres and nerves) remain intact, which appear as bridging fibres. The sharp weapon causing the incised wound cuts all tissues coming in the way in the depth of wound. Hair bulbs in the skin around a laceration may be crushed but not cut as in incised wound. Hair, epidermal tags and foreign material are usually present in the wound. Haemorrhage is less in laceration as compared to incised wound because in laceration, the blood vessels are crushed and torn irregularly (they can even retract) and the blood clots readily. But there is an exception where haemorrhage is more in laceration as compared to incised wound and that is scalp laceration. Actually, in scalp, there is copious flow of blood; here the temporal artery is firmly bound and is unable to retract. Types of lacerations: 1) Split laceration: When blunt force is applied over any bony prominence (e.g. scalp, forechin, tip ot nead, eyebrows, zygomatic process, it results shin), shoulder, back of elbow, ASIS, the sites, Actually, at these in a split laceration. with minimum Skin directly overlies a bone tissues and muscles amount of subcutaneous

D

SECTIONI Forensic Medicine

and any blunt force impact at these sites causes linear splitting of tissues. Since this linear splitting (i.e. split laceration) appcars clean cut and looks like an incised wound, it is also known as 'incised looking lacerated wound' [SN-2]. Close inspection with magnifying lens is helpful to differentiate an 'incised-looking lacerated wound' from a true incised wound. An 'incised looking lacerated wound' reveals contused edges and the presence of tissiue bridging. On microScopic examination of hair root, the hair bulbs in the skin around an 'incised looking lacerated wound' may be crushed but not cut as seen in a true incised wound. 2) Tear laceration: When an object (relatively

blunt hard narrow) hits the skin and the skin is pulled in opposite direction, it causes tear laceration, for example, car door handle, radiator mascot.

3) Stretch laceration: When blunt force applied

on the body overstretches the skin and subcutaneous tissues, it results in stretch laceration. Examples: a glancing kick by foot. Moreover, in RTA, stretch lacerations can be caused in the region of groin when pressure is applied over the thigh stretching the skin towards the knee. It is also seen when two ends of fractured bone stretches the skin and subcutaneous tissues beyond their limit. 4) Avulsion laceration: It is commonly seen in run over cases by vehicles in RTA. It is produced by the rolling or grinding movement of the car

wheel which involves a shearing force delivered at an oblique angle to detach the skin and subcutaneous tissues over a larger area. This is known as flaying. Amputation injuries of the limbs are a type of avulsion injury. A large area of the skin separates (avulses) from its underlying tissues and is lost, that is, the wound is devoid of any overlying skin. 5) Cut laceration (chop wounds or slash wounds): It is caused by a heavy cuting weapon, for example, axe, chopper, hatchet, etc. Since the edges of the weapon are heavy and not sharp, they crush and bruise the margins of the wound

too. MLI: (1) Lacerations are usually accidental or homicidal, rarely suicidal. (2) Patterned laceration: The type of laceration may suggest the shape

of the blunt weapon. (3) The foreign matteri the wound can give clues about the weapon used. lor example, the paint on the vehicle may he transferred into the laceration. (4) Bagh nukh (tiger claws) is a metallic claw like weapon which fits over the knuckles and is concealed under and

against the palm.

INCISED WOUNDS Incised wound (Latin incidere = to cut into): It is a clean-cut wound caused by sharp edged weapons, for example, blade, razor, knife, scalpel, broken glass. An incised wound is longer than its depth due to swipe action. Dimensions (Fig. 7B.4): 1) Shape: Spindle shaped due to greater retraction of edges in the centre. Gaping is maximum if underlying elastic fibres in the skin (i.e. Langer's line) or the muscle fibres are cut transversely and minimum if elastic fibres or muscle fibres are cut longitudinally. 2) Margins/Edges: Clean cut, well defined and everted. At certain sites where the skin is wrinkled (e.g. scrotum), the margins may be irregular and inverted. The incised wound produced over wrinkled skin may appear as lacerated wound due to irregularity of the edges of wound. These wounds are known as lacerated looking incised wound [SN-3]. 3) Angles: The ends of incised wound are known as angles. 4) Length: The distance between two oppo site angles is the length. The length of incised wound is greater than its width and depth. 5) Width: The widest measurement between two margins is its width. The width of incised weapon. wound is greater than the width of the knile 6) Depth: More pressure is applied on the at the beginning of the incised wound. Due to at the this reason, the incised wound is deeper beginning

b

M

TAS

Inte

Length Head

end WIdth

Angle

Depth

Margins Angle

Fig. 78.4 Dimensions of an incised wound

Tailing Unir

l

CHAPTER 7 Injuries

Features: 1)

No abrasions and gins and no tissue

contusions are seen on marbridging secn in the depth of

wound. tail ofthe woun More pressure is 2) Head and applied on the knite at the beginning of the incised wound. Due to this reason, the incised wound is deeper at the beginning. This deeper end of the wound is known as 'hcad of the wound'. After passing through some distance, the wound gradually becomes more shallow towards the tail because as the assailant draws is gradually the knife away from the head, it withdrawn. Finally, as the knife leaves the tissue, the depth is so less that only the skin is

cut to produce a scratch. This portion where the epithelium alone is cut is known as tail of

the wound' and this phenomenon is known as

TABLE 7B:8 Dating of an Incised Wound Gros: s

Duration Findings Fresh

Haemorrhage in an incised wound is more as compared to that in lacerated wound because in incised wound, the blood vessels are cut cleanly. Bevelling cut [SN-4]: If the blade of the weapon enters obliquely, it creates a bevelled wound. Cut throat wounds: Suicidal cut-throat wounds and homicidal cut-throat wounds [D/W-20]. Healing of an incised wound can occur either by primary intention or 'secondary intention 3)

(Table 7B.7).

Dating of an incised wound (Table 7B.8). Manner of injury a) Suicidal: While attempting suicide, the victim hesitantly makes many superficial cuts before

TABLE 7B.7 Healing by Primary Intention vs. Healing by

Intention

Healing by'primary intention When healing

occurs uninfected wounds in

nflammatory reaction, Lessintense Scaring: Less

Secondary

Margins red, swollen and

12 h

adherent Scab of dried

24h

clot

2-3 days

4-6 days 7days

Microscopic Findings Capillary dilatation, margination and emigration of neutrophils Reactive changes in tissue histiocytes

Reactive changes in fibroblasts; Monocytes appear in exudate Epithelium begins to grow at edges. A continuous layer of endothelial cells cover the Surtace Vascularised granulation tissue formation (fibroblasts)

New fibrils

Scar formation

attempting a final fatal deeper cut. These cuts are known as hesitation cuts or tentative cuts

SN-5].

b) Homicidal: The wounds are usually multiple, fatal and may be on areas inaccessible to victim himself. If incised wounds are present on face and genitals, it is suggestive of homicidal. Defence wounds [SN-6]: The wounds sustained by a person in an attempt to protect himself from blows or in an attempt to grasp the weapon of offence are known as defence wounds. *Glasgow smile (also known as Chelsea smile or Cheshire grin): Small cuts are made by a sharp weapon on the corners of a victim s mouth; then the victim is beaten or stabbed until the muscles in the face contract, causing the cuts to extend up to the ears. It leaves a scar in the shape of a smile. The practice is said to have originated in Glasgow, Scotland but became popular with English street

Healing by 'secondary

intention

When healing occurs in infected wounds More intense, much granular tissue is formed More

Red with

clotted blood

tailing of the wound'. Tailing of the wound indicates the direction in which the force was applied. The tail of the incised wound does not show bleeding as the epithelium is less vascular.

151

C)

gangs (especially anmong the Chelsea Headhunters, a London-based hooligan firm, among whom it is known as a 'Chelsea grin or Chelsea smile'). lt can Accidental: Commonly seen at the hands. cutting fruit/vegetaOccur in home (e.g. during professions, in certain Dles by knife) as well as pathologists, surgeons butchers, example, lor and so on.

SECTIONI

152

Forensic Medicine

d) Fabricated wounds (or

fictitious wounds or

forged wounds) [SN-7] MLI:

ofthe weapon, sharp-edged. that 2) It can give an idea about the direction of force applied. 3) Relative position of assailant and victim can be determined. 4) Age of injury can be determined. 5) Fatality: Incised wounds are rarely fatal because they seldom penetrate deeply enough to damage large blood vessels. However, incised wounds over the neck or wrist can prove fatal because major blood vessels lie superficially in those areas. 6) Manner of injury: As described earlier. 7) Difference between incised wounds and lacerated wounds (Table 7B.9). 8) Incised wound should be differentiated from incised looking lacerated wound (Table 7B.10). 1) It

helps to determine the nature

TABLE 7B.10

Incised Wound and lncised Looking Lacerated Wounds [D/W-16] Sr.

is

TABLE 7B.9 Difference Between Incised Wounds and Lacerated Wounds [D/W-15] Sr. No.

.

2.

3.

.

Features Caused by Appearance

Abrasion around wound Bruising around wound

Structures in the depth of

Incised

Wounds Sharp weapon

Lacerated

Wounds

Blunt weapon

Smooth, even, Iregular clean cut, linear/spindle shaped Absent May be present

Absent

Present

Cleanly cut

Bridging fibres (consisting of nerves, blood vessels or

wound

Difference Between

No.

Features

1.

Caused by Site

3.

Abrasion around wound Bruise around

Incised Wound

Incised Looking

LaceratedWound

Sharp weapon Blunt weapon Anywhere on Shin, forehead, the body scalp

Absent

May be present

Absent

Present

Edges of wound

Clean cut

Haemorrhage

Irregular (on hand lens examination)

Profuse Absent

May be present

Absent

Usually present

wound

6

7

Associated underlying

Less

fracture

8.

Foreign bodies e.g. soil, dust, iron rust)

STAB WOUNDS wound is one whose depth is more than its length. The word 'stab' means to wound or to pierce with a pointed weapon (Fig. 7B.5). is caused by penetration of a long weapon It through its narrow pointed end into the depth of the body. The pointed end of the weapon may be sharp (eg, dagger, knife, arrow, spear, scissor, broken glass, forks, pens, nail, pins, needle) or blunt (e.g. cricket stump, screw driver, iron rod, wooden stake and so on). A stab

Connective tissue Haemorrhage

fibres) present

Profuse Slight (except spurting may scalp where the be seen haemorrhage is profuse)

Hair bulbs in skin Cleanly cut

Bones Foreign bodies e.g, soil, dust, iron rust)

May be cut

Absent

Crushed or torn May be fractured Usually present

Fig. 78.5 Stab wound in lower part of front o neck

CHAP IER

delivered along the long may be caused of the weapon. A stab wound a axis weajpon into the ways: (1) By thrusting in body and (2) the body may be pressed depth ofthe instrunment. ainst or falls against the again 7B.11): Classification (Table Mechanics: The

,

TABLE 7B.11 Wounds

rce

is

Classification of Stab

on Weapons of Penetration Based 1) Incised stab wound wound 1) Punctured 2) Lacerated stab wound wound 2) Penetrating Based on Depth

3)

Perforating wound

Punctured wounds: It is a stab wound caused by pins, needles, syringe, therapeutic injection, snakebite. Concealed puncture wounds: Homicidal needle punctures are frequently inflicted at unusual sites to hide their locations, for example, nape of neck, axilla, fornix of upper eyelids, inner canthus of eye, nostrils, ear, underfold of female breast, vagina, rectum. Needle punctures

method of infanticide through frontanelle. Preservation of tissue for chemical analysis: In case of deaths due to therapeutic injections, drug addiction or snakebite, the tissue around punctured wound should be excised and are a common

sent frozen for chemical analysis.

Penetrating wounds: The weapon enters into a body cavity (e.g. thoracic, abdomen, skull), thus producing only one wound, that is, entry wound. Perforating wounds: The weapon enters the body from one side and comes out from another side, thus producing two wounds, that is, one entry wound and one exit wound. The entry wound is arger and inverted. Exit wound is smaller (due to tapering of the blade) and everted. nape of stab wound: Normally the wound is slit shaped with two acute angles. Stab wounds which run parallel to the cleavage lines of Langer produce a narrow, slit-shaped wound with minimum gaping. The width and thickness of the blade can be determined with considerable accuracy. e stab wounds which cut through the lhnes OTLanger transversely will gape. The gaping,e. wIdth of wound) is maximum when the long

/

Injurlees

axis of stab wound is at right angle to the lines of Langer and in this case, the shape is spindle shaped or oval. Sharp-edged weapon: This produces a stab wound and its shape depends upon the weapon, whether it is single- or double-edged. 1) Single-edged weapon (e.g. knife): It produces a wound having one sharp angle and one blunt (or rounded or squared off angle). The sharply acute angle is produced by the sharp edge of the weapon and the blunt (or rounded or squared off) angle is produced by the blunt edge of the weapon. Sometimnes, the blunt angle may have a small split in the skin such that the wound looks like a fish and the blunt angle appears like the tail of a fish. This type of stab wound is sometimes known as fishtail wound' and the phenomenon is known as 'fishtailing. 2) Double-edged weapon (e.g. dagger): lt pro duces slit like, elliptical or spindle shaped wound with two sharp acute angles. Shape of stab wounds versus cross-section of the penetrating end of weapon: (1) Icepick Round; (2) Scissor (closed)> shaped; (3) Fork of 3-4 wounds depending upon the Cluster number ofprongs on the fork and (4) Screw driver > Slit like stab with squared ends and abraded margins. Margins of stab wound: case of sharp-edged weapon (e.g. knife, In dagger): Margins are clean cut (incised stab wound). If the weapon has hilt, there may be an abrasion outside the wound but near any one end or both ends. case of pointed weapon (e.g. cricket stump, In lacscrew driver, pencil, iron rod): Margins are erated and contused (lacerated stab wound). is Length of stab wound: Length of stab wound normally less than the width of weapon. Reason-congaping ot traction of severed elastic fibres leads to know the corwound and so length decreases. To wound must the rect widlth of weapon, the edges of increased length new be brought together, and the weapon. gives the original width of the than the thickness It is more Width ofstab wound: of the blade due to gaping. Depth is the greatest wound: Depth of stalb stab wound. In a living patient dimension of a

Z

154

SECTIONI Forensic Medicine

emergency, never introduce a probe in a stab wound to measure its depth bccause it may disturb a loose clot and may lead to fatal haemorrhage. But in OT, depth of the wound can be determined during its repair. Depth of stab wound depends upon following factors: Knife fully thrust on an unyiclding surface (e.g. chest wall): Depth of wound = Length of the blade of knife. fully thrust on a yiclding surface Knife (e.g. abdomen, breast, buttocks): Depth of wound Length of the blade of knife because the force of thrust pushes the yielding surface inwards. Sharpness of tip of knife: Sharper the tip, more is depth. Resistance offered by bone > calcified cartiin

PEDESTRIAN INJURIES [SN-9J The injuries sustained by a person walking or stand. ing on the ground by a vehicle are known as pedes. trian injuries.

SOME IMPORTANT TERMS

Harakiri

(Seppuku): It is a form of Japanese ritual suicide'. It was used either voluntarily by a samurai (Japanese warrior) to die with honour rather than fall into the hands of their enemies or as a form of capital punishment for samurai who had committed serious offences. The victim inflicts a single large abdominal stab with a short sword into the left side of abdomen (or falls upon ceremonial sword), drawing the blade across to the right side, turning it upwards producing an L-shaped cut and then pulling out intestines. Sudden evisceration of abdominal organs causes immediate collapse and death. Overkill: Infliction of multiple and massive injuries

lage>skin Clothing resist the penetration of blade. Stretched skin is easier to penetrate than lax skin. Direction

of stab wound: If the weapon was penetrated at an angle, then bevelled margin may be visible on one side and undermining on the other

by exceeding the extent necessary to kill the victim. Langer's lines: The lines of tension or eleavage within the skin due to the natural orientation of collagen and elastic fibres in skin.

side. MLI: 1) Concealed

punctured wound: It suggests homi cidal nature. 2) Shape of wound: It suggests type of weapon. 3) Depth of wound: It indicates the amount of force used. More depth favours homicidal nature. 4) Direction of wound: It indicates the relative position of the victim and assailant. 5) Manner of production (i.e. homicidal, suicidal or accidental) may be determined. 6) Multiplicity of wounds: More number of wounds indicate greater intention to kill, for example, in case of revenge. 7) Age of wound can indicate the time of infliction of injury. 8) Foreign material may be inserted into the wound, for example, paint, soil. It may relate the wound with a weapon and crime scene. Chop wounds |SN-8J: Large deep gaping wounds caused by a blow with moderately sharp cutting edge of a fairly heavy weapon (eg. axe, chopper, hatchet, sword, meat cleaver, butcher's knife) applied with a significant degree of force.

LIST OF IMPORTANT QUESTIONS FOR EXAMINATION

SHORT NOTES (SN) 1.

Migratory bruise

2. Incised looking lacerated wound 3. Lacerated looking incised wound

4. Bevelling cuts

5. Hesitation cuts [CCU 2014] 6. Defence wounds 7. Fabricated wounds 8. Chop wounds [DU 2005|

9. Pedestrian injury 10.

Patterned injuries [DU 2008]

DIFFERENCE BETWEEN (D/W br I1. Antemortem abrasions and postmortem a 12.

sions Abrasion and ant bite marks [DU 2003

CHAPTER 7

bruise and false (artificial) bruise |CCU 3. 2014]1 2009, Antemortenm bruise and postmortem bruise 14. DU 2007] CCU 2004, [CCUJ Incisea wounds and lacerated wounds 15. 2009] 2004, 2005, Inciscd wound and incised looking lacerated wound (CCU 2012] True

17.

18. 19.

20.

and defence wounds Defence wounds and hesitation wounds Postmortem staining (lividity) and contusion Self-inftlicted

(bruise) Suicidal cut throat and homicidal cut 2001, 2006] ICCU 2010]

throat [DU

ANSWERS SN-1:

Migratory bruise (or shifting

bruise or ectopic bruise)

Migratory bruise (also known as ectopic bruise or percolated bruise): When extravasated blood at the point of impact by a blunt weapon tracks down due to gravity along the fascial planes or between muscular layers and reappears at a site below the injured site, it is known as migratory bruise. Most bruises are located in the subcutaneous tissues above the deep fascia. These bruises are known as superficial bruises. They are easily and fairly visible.

Some bruises are located below deep fascia. These bruises are known as deep bruises. The deep bruises: 1) may take a long time to become visible at the point of impact (delayed bruising); or 2) may not become visible at the point of impact but remain localised; or 3) may not become visible at the point of impact but the extravasated blood at the site of injury racks down (under the influence of gravity) along the fascial or muscular planes and collects at a site below the injured site where superfiClally it reappears as a bruise. This type of bruise which appears at a different site from the actual Site of impact is known as migratory or shilt ing or ectopic bruise. t is clear that the site of bruise does not necessariy indicate the site violence. of Examples of migratory bruise:

Injuries

55

Spectacle haematoma (racoon eye): In case of impact due to blunt weapon on the forehead or front of head, the extravasated blood in spite of accumulating at the site of impact gravitates down through 4th layer of scalp (i.e. loose areolar tissues) and collects around the eyes. In this casc, racoon eye is an example of "migratory bruise because the bruise migrates from the site of impact (i.e. forehead) to the eyelids. 2) Mastoid ecchymosis (battle's sign): It is the bruise behind the car. It is scen in the fracture of middle cranial fossa of the base of the skull. Battle's sign occurs as a result of extravasation of blood along the path of the posterior auricular artery. The sign is named after William Henry Battle. 3) Fracture of jaw. Bruise appears in neck 4) Fracture of pelvis: Bruise appears in thigh. 5) Fracture of femur: Bruise appears on lower outer aspect of thigh. 6) Blunt injury to upper part of thigh: Bruise appears above knee. 7) Blunt injury on the calf: Bruise appears around ankle. MLI: The pain is maximum at the site of injury and it may be mild or absent at the site of migratory bruise. Since migratory bruise may take a long time to appear superficially, it is also known as 'delayed bruise. Therefore, the victim should be reexamined after 24 h of first examination. 1)

SN-2: Incised looking lacerated

wound looking lacerated wound: When blunt force is applied to an area of the body where the skin directly overlies a bone with minimumn amount of subcutaneous tissues, it may cause the linear splitting of tissues. This linear splitmay look ting of tissues may appear clean cut; lacerated a like an incised wound but it is actually looking lacerwound, so it is known as 'incised ated wound'. is a type of split laceration. It often at shin and These wounds are seen most at scalp, eyebrows forehead but may also be seen iliac crest and forearm, chin, ulnar border of

Incised

knee.

156

SECTIONI

Forensic Medicine -

With naked eyes, these wounds look like clean cut incised wound but on close examination witlh hand lens, the edges of the wound are irregular. Moreover, bruising of the adjacent scanty soft tis-

lacerated wound due to irregularity of the edges of wound. These wounds are called lacerated lookin incised wounds. Sites: Scrotum and elbow. A hand lens examination can differentiate it frOm a laccrated wound. The margins are clean cut and bruising of the adjacent skin is absent.

sues may be seen. MLI: These types of wounds (which are actually lacerated wounds) may be wrongly interpreted as incised wounds by an inexperienced doctor in casualty at the time of preparing medicolegal case (MLC) report. Moreover, at the time of autopsy, an inexperienced pathologist may wrongly interpret. In the court of law at the time of giving evidence, the doctor as an expert witness has to give explanation tor this type of mistake and he may be cross-examined. The wrong interpretation and so the wrong opinion of the doctor can change the true facts about the weapon of offence.

SN-4: Bevelling cuts Bevelling

cut (Fig. 7B.6): If the blade of the weapon enters the body tissues obliquely (i.e. the striking angle of the sharp edge of the weapon is not perpendicular), it creates a bevelled cut/wound. The interior of the wound has a slanting base and a

slanting ro00f. The edge of the slanting roof which makes an angle 90° with the surface is known as bevelled edge. The subcutaneous tissue of the bevelled edge is generally visible and

SN-3: Lacerated looking incised

wound Lacerated looking incised wound: Incised wound produced over wrinkled skin may appear as

Weapon strikes

obliquely i.e. 1500 g (4) flattening o EY nd teration of sulci. Gyri are pale. Cerebral surface and corrugated. Cut surface is pale and espechildren, the ventricles may be reduced to slits y the swelling of adjacent white matter; (5) uncal groov gyrus is swollen; (7) cerebellar tonppocampal herniation and (8) idline shift if oedema is U/L. is the most common an extracellular

th

in

T65

INJURY TO SPINAL CORD

JURYTO

IN

Injuries

Railway Spine [SN-16]

Whiplash Injury [SN-17 INJURY TO CHEST AND HEART Flail chest or 'stove-in' chest: When multiple rib fractures occur in a localised area, the area of the chest around the fractures moves inwards on inspiration but again returns to the previous position on expira tion. It interferes with respiratory exchange and may cause dyspnoea. At least three successive ribs must be fractured at two points to cause flail chest. Stab wounds of heart may be fatal. (1) When left ventricle is pierced, the thick muscle wall may restrict the bleeding, allowing time for surgical management. (2) When right ventricle is pierced, the thin muscle wall may not restrict the bleeding effectively. Due to this reason, stab to the right ventricle is more fatal as compared to stab to left ventricle. Here, the blood escapes the stab wound of right ventricle rapidly and cause haemopericardium and consequently cardiac tamponade. Accumulation of around 150-500 mL of blood in pericardial cavity can increase intrapericardial pressure which is enough to interfere with the ventricular contractility and cause death. The right ventricle is most often wounded because it lies towards the front of the chest. Cardiac tamponade presents with three signs (Beck's triad): (1) Low arte rial blood pressure; (2) increased central venous pressure and (3) distant heart sounds. Cardiac concussion (or commotion cordis): It means sudden cardiac death following a blunt trauma to the chest. It occurs in sports activities and if the impact occurs during early ventricular repolarisation, that is, 15-30 ms before the peak of T-wave.

INJURY TO ABDOMEN *

Injuries to the abdomen may be nonpenetrating (closed) or penetrating (open). These injuries 1) Nonpenetrating (closed) injuries: caused by is intact. It is OCcur when peritoneum fall from example, in RTA, weapblunt force trauma, for or kick) by blunt in atfected height and assault (blow abdominal organ common organs Ons. Most is solid visceral nonpenetrating injuries

166

SECTIONI

Forensic Medicine

which in order of frequency are spleen (first), liver (second), kidneys and pancreas. 2) Penetrating (open) injuries: These injuries occur when peritoneum is pierced or torn. Most com-

mon abdominal organ alfected in penetrating injuries is hollow visceral organs which in order of frequency are small intestine, large intestine and stomach. Laceration of spleen produces rapid and profuse haemorrhage, whereas laceration of liver produces slow but considerable bleeding over a period of time. Spleen: Spleen is the most common abdominal organ to be injured in blunt abdominal trauma. Liver: Liver is the second most common abdominal organ to be injured in blunt abdominal trauma.

LIST OF IMPORTANT QUESTIONS FOR EXAMINATION

LONG QUESTION (LO) 1.

Enumerate various injuries caused by blunt force trauma to the head. Discuss the pathophysiology and medicolegal aspects of intracranial haemorrhages.

SHORT NOTES(SN) 2. Racoon's eye (or racoon sign) 3. Fractures of skull [CCU 2010] 4. Gutter fracture of skull [DU 2003] 5. Basilar skull fractures 6. Puppe's rule

20. Skull shows ring fracture 21. Person has signature fracture 22. Head shows counter-coop injuries

DIFFERENCE BETWEEN (DW) 23. Heat haematoma and extradural haematoma 24. Drunkenness and concussion 25. Traumatic intracerebral haemorrhage and spon.

taneous cerebral haemorrhage

26. Extradural haemorrhage (EDH), subdural haem-

orrhage (SDH) and subarachnoid haemorrhage (SAH)

9. Subdural haematoma

10. Subarachnoid haemorrhage 11. Circle of Willis 12. Berry aneurysm 13. Intracerebral haematoma 14. Concussion of brain [DU 2007 15. Contrecoup injury 16. Railway spine 17. Whiplash injury [DU 2007

MEDICOLEGAL IMPORTANCE (MLI) 18. Extradural haematoma is present 19. Skull shows depressed fracture

2

ANSWERS

Enumerate various injuries caused by blunt force trauma to the head. Discussthe pathophysiology and medicolegal aspects of intracranial haemorrhagesS. LO-1:

)

Various Injuries Caused by Blunt Force Trauma to the Head 1) 2)

3) 4) 5) 6)

7. Extradural haematoma 8. Lucid interval

M

Scalp injuries-abrasions, contusions, lacerations Facial injuries Skull fractures Meningeal injuries Intracranial haemorrhages Brain injuries: cerebral contusions, cerebral lacer ations, cerebral concussion, diffuse axonal injur (DAI)

Types of intracranial haemorrhages 1)

Epidural (or extradural)

haemorrhage

(EDFU

SN-71

2) Subdural haemorrhage (SDH) [SN-9| 3) Subarachnoid haenmorrhage (SAH) |SN-10| haemorthage 4) Parenchymatous (intracerebral)

SN-13

5) Intraventricular

haemorrhage: When haemot

rhage present in the ventricles of the brain, It 3 IS known as intraventricular haemorrhage. or usually arterial in origin. It may be traumatic is

1t

nontraumatic in origin. The nontraumatic pathological causes are (1) rupture of A-V m formation in the wall of ventricle, (2) rupture o

CHAPTER 7

aneurysm of posterior communicati

Berry bleedingg into anterior portion of tenmartery and lateral ventriclk or (3) rupture of

of

poral horn aneurysm of basilar artery through the floor Berry ventricle. of3rd MLI Negligence: f doctor does

not tak proper history interthe patient (who is in a lucid patient, the of discharged by the doctor. After reachyah may be may again become unconscious, may ing home, he be deteriorate and die. The issue of negligence can raised against the doctor. aneurysm: Alcohol is a vaso2) Alcohol and berry fibrous dilator and it dilates cerebral arteries. The wall of an aneurysm is incapable of dilating, and so the high blood pressure facilitates bursting of berry aneurysm through thin, weak and inelastic walls. Alcohol also results in aggressive behaviour and increases the chance of conflict and fight producing trauma which ultimately may lead to rup1)

ture. 3)

Intense physical activities (e.g. sports, coitus, straining while defecation and so on) predispose to bursting of berry aneurysm to cause SAH.

SN-2:

Racoon eye (or racoon sign)

Racoon eye: It is the dark black/bluish/purplish discolouration of the tissues (eyelids) around the eyes. It is also known as periorbital haematoma or spectacle haematoma or black eye or racoon eyes or panda eyes. Since it is a sign of blunt injury to the head, it is also known as racoon sign. Racoon (Procyon lotor) is a bear-like mammal native to North America which has black marks around the eyes making it appear as though the animal has on black spectacles.

Causes of black eyes:

Bhunt impact on forehead: In case of impact due to blunt weapon on the forehead or front of head, the extravasated blood, in spite of accumulating at the site of impact, gravitates down through 4th layer of scalp (i.e. loose areolar tissues) and collects around the eyes. In this case, racoon eye is an example of migratory bruise ecause the bruise migrates from the site of impact (i.e. forehead) to the eyelids. 2) Direct blunt impact to the eye.

Injuri

67

3) Fracture of anterior cranial fossa of the base of

skull. The blood leaks from fracture site and tracks along fascial planes into periorbital tissues. Raccoon eyes may be bilateral or unilateral. MLI: Black eyes do not show up for several hours after injury, so the black eyes that are visible immediately after trauma are more likely the result of direct facial trauma (i.e. eye injury), for example, due to a punch and it excludes the fracture of anterior cranial fossa.

SN-3: Fractures of skull

Fractures ofskull can occur by

Direct violence: The force acts directly on the skull bone to produce a fracture. Examples: head in motion striking an object, for example, in road traffic accident; crushing of head under the wheel of a heavy vehicle; compression of foetus during forceps delivery. 2) Indirect violence: The force act indirectly on the skull through some other structure which receive primary impact. For example, ring frac ture in fall on feet and buttock. Types of skull fractures (Fig. 7C.2) [Mnemonic: Love can do problem, girls please be serious] 1) Linear (fissured) fracture: It is the most common type of fracture. Linear fracture is a 1)

straight or curved fracture line on the skull. It usually involves either table of skull, but sometimes involves both inner and outer tables. A linear fracture on temporoparietal region may rupture a branch of middle meningeal artery to cause epidural haemorrhage. 2) Comminuted fracture: In this kind of fracture, bone is broken into several pieces of different sizes. It is seen in fall from height. Depressed fracture: A small portion of a frac tured bone is driven inwards in depressed fractures. They are caused by blows from heavy for examWeapon with a small striking surface, etc. ple, stone, axe, chopper, hammer, FracturesalasignaSignaturefractures (or shape of the depressed ture): Sometimes the and resembles the corresponds bone weapon; part of surface of the striking Shape of the has left its sigthe weapon if depressed appears as lt This type of fractures skul. the nature on known as 'signature fracture is also

168

Forensic Medicine

SECTIONI

1.

Linear (Fissured)

2. Comminuted

3. Depressed

6a. Basilar (Hinge)

6b. Basilar (Ring)

4.

Pond fracture

Gutter fracture

Skull

5. Gutter fracture

Fig.7C.2 Types

ofskull fractures

(or fractures a la signature). The weapon of

offence can be identified by observing the signature fracture. Spider web' (mosaic) fracture: Sometimes a depressed fracture occurs with multiple linear fractures radiating out of it. It resembles with spider web so it is also called 'spider web (mosaic) fracture. 4) Pond (indented) fracture: It is a simple dent (i.e. a concave depression) of the skull. It is just like a dent created by thumb and fingers in a ping pong ball. It occurs only in the skulls of infants because the skulls of infants are elastic like a ping-pong ball. Fractures occur only in the outer table around the periphery of the dent; the inner table is not fractured. This fracture occurs by obstetric forceps blade or a blow from a blunt object. 5) Gutter fracture [SN-4] 6) Perforating fracture: The cull is perforated either by a sharp pointed weapon or a rifled bullet. It creates a hole in the skull involving both outer and inner table, The shape and size of the hole may correspond with the dimensions weapon. of

7. Sutural (Diastatic)

7) Basilar skull fractures 8) Sutural (diastatic) fracture: The cranial bones are separated at a suture line due to trauma. In other words, the fracture line runs along a suture. It is most common in young persons because of nonunion of sutures.

SN-4: Gutter fracture fracture: It is a type of skull fracture which part of the thickness of skull bone removed so as to form a gutter or furrow in the bone. Usually, the outer table of skull is partially removed but it also involve inner table. "Appearance: A long, narrow furrow or groove lKe depression in the skull. Most commonly, it is produced by a Gutter in

1S

i

High-velocity glancing bullet from a rifled firearm 2) Tangential strike by the sharp edge ofa swora. Itis usually accompanied by comminuted depressed fracture of inner table of skull; the released frag ments cause injury to the meninges and brain. MLI: Even fracture which involves the outer ta of skull is considered as grievous hurt [S.320, IP 1)

C A

CHAPTER 7

skull fractures

SN-5: Basilar fractures that skull fractures are linear skull Basilar base of skul More force is required ur in the the base ofsskull as compared cause ractures at to areas of the skull. to other .Classification 1: Fractures of base of skull may be: A.

means a fracture which Hinge fracture: lt parts, divides the entire base of skull into two It may be

thus creating a hinge. at the base of 1) Transversc. It is the fracture skull which runs transversely; it splits the skull into two halves, anterior half and posterior half. Most commonly, the hinge frac-

ture extends from one petrous bony ridge through sella turcica (i.e. pituitary fossa) to the opposite petrous ridge. It is the most common type of hinge fracture and is also known as motorcyclist's fracture. 2) Longitudinal: It divides the skull into two halves, right half and left half. BRing fracture: It is a type of fissured fracture which occurs in the form of a ring around (usually 3-5 cm outside) the foramen magnum in the basal part of occipital bone in posterior cranial fossa. It is caused by fall from height on to the feet or buttocks. If the kinetic energy of fall is not absorbed by fracture of legs, pel vis or spine, the impact is transmitted through the cervical spine to the basal part of occipital bone around the foramen magnum; in this way, ring fracture is created. It also occurs if there 1S a heavy blow (or fall of heavy load) over the vertex. A forceful blow over the chin in traffic accident may produce ring fracture. Ring fracture is very rare.

Classification 2: A. Fracture of 'anterior cranial fossa': It occurs mostly due to an impact in front of the head. A heavy blow on the chin may also transmit the impact through maxilla to the base of skull and so results in fracture of cribriform plate of ethmoid. inical features are (1) CSF rhinorrhoea, that is CSF coming from nose; (2) EpistaxIs 1.e. blood coming from nose); (3) Anosmia (loss of ability to smell) and (4) Raccoon's S1gn, that is, the dark purplish discolouration

B.

Injuries

169

around the eyes following the fracture of the anterior cranial fossa of the skull base. Fracture of 'middle cranial fossa': It occurs due to the direct impact behind the

car or crush injuries of head (i.e. side by side compression). Clinical features are (1) Otorrhoea or CSF otorrhoca, that is CSF coming out from ear, (2) Haemotympanum, that is, blood coming out from ear), (3)) Cranial nerve (VIlth and VIIIth) palsy. C. Fracture of 'posterior cranial fossa': It is due to the direct impact of the back of head on the ground. An important sign is Battle's sign, that is the bruising over the mastoid process as a result of extravasation of blood in the fracture of posterior cranial fossa.

SN-6: Puppe's rule Puppe's rule: 'A fracture line resulting from blunt force trauma to the skull never crosses the preexisting fracture line'. In other words, 'a fracture line resulting from the second injury will not cross the fracture line resulting from the first injury'. Or 'the second fracture line is arrested when it meets the first fracture line' (Fig. 7C.3). Explanation: Suppose after first blunt force injury, a fracture line 'A' is formed on the skull. After 2nd blunt force injury, a second fracture line 'B' is formed. According to Puppe's rule, the 2nd fracture line B caused by second injury disappears when it meets the lst fracture line 'A caused by first injury, that is, in a sense second fracture line B never crosses lst fracture line 'A'. 1st fracture caused

by 1st impact

2nd fracture caused by 2nd impact

Fig. 7C.3 Puppe's rule

SECTION

170

I

Forensic Medicine

the rule was given by Puppe (1930s) in context with fractures due to blunt force trauma to the skull. This rule was devised to assist forensic interpretation when there is more than one fracture from more than one blunt force injuries. Madea and Staak in 1988 devcloped this rule in relation to multiple firearm (bullet) injuries to the skull. The fracture line produced by the impact of a bullet stops at preexisting fracture of the skull. So Puppe's rule regarding how to determine the sequence of multiple blunt-force injuries of the skull can also be applied directly to determine the sequence of gunshot wounds of the skull. It can

Originally

determine the sequence of shots when several bullets have struck the cranium. Puppe's rule is concerned with multiple linear fractures of skull and helps to determine the chronological order in which the fractures occurred one by one. Although multiple firearm (bullet) wounds of the skull are much more difficult to analyse than wounds from blunt force weapon, the pattern of radial fracture lines sometimes allows the determination of the sequence of the shots.

SN-7:Extradural haemorrhage (or epidural haemorrhage) Extradural

(or epidural) haemorrhage: The

potential space between skull and dura is called extradural or epidural space and the haemorrhage in this space is called extradural or epidural haemorrhage (EDH) (Fig. 7C.4 and 7C.5).

Skull fracture

Fig. 7C.5 EDH seen at autopsy

T HE

Cause:

Trauma

is

the most common cause of EDH. It occurs due to the rupture of branch a of

the middle meningeal artery (usually posterior branch) by associated linear fracture of the skul. Most EDHs are associated with fractures of skul. EDH may occur in the torn venous sinuses in which case there need not be a fracture. Frequency: EDH is the least common of the three types of brain membrane haemorrhages, that is, SAH most common) >SDH > EDH (least common). Lucid interval is seen in only about 35% cases or EDH. During this interval, a suficient quantity of blood may accumulate to cause raised intracranial pressure and consequent relapse into unconscious: ness. Site: EDH is usually unilateral in 'parietotempor

area'. at EDH shows limitation due to dural attachments suture lines.

the interot Mechanism: Dura is closely applied to ocrur at tne of the skull at the base, so EDH does not space betwe

Epidural space.

base. In the vault, there is a potential be sepurileu bone and dura and here the dura can presure: from the interior of skull by arterial blood blood to cause Mininmum volunme of accunmulated

Dura materMiddle meningeal artery is tornby linear fracture of skull

fatality: 100 ml.. eud MLI of EDH: ot hea a victim 1) lssue of negligence: Suppose to the hosple njury (with EDH) is brought conscious. On arrival, he is tound to be or exanmine history tor does not take proper by be discharged t properly, the patient may

t

Epidural haemorrhage (EDH)

Fig. 7C.4 Extradural haemorrhage

(EDH)

D

SN

Luc nsa

Afte uncc

beco

tor a the nCO

luc

CHAPTER 7 nmay be the lucid Actually, Actually, the patient from doctor. his transient recovering ntervnl after may again he home, reaching nCuSsion. After condition may deteunconscious; his become die. The issue of1negligence can be

in

riorate and

raised against

drunkenness: the victim is brought state and the history is 2) It doctor in concusi to victim nmay be discharged by the nknown, the drunkenness. may think it a case of doctor who in a case of death autopsy, heat haCmatoma 3) At EDH burn may be confused with due to

(Table 7C.1).

TABLE 7C.1 Difference Between Heat Haematoma Haematoma and Extradural St No. Features Cause

Heat

Haematoma

Extradural

Haematoma

Trauma: Blunt force trauma results in rupture (longitudinal of middle venous sinuses meningeal and diploic veins)

Heat: Heat results in rupture of blood vessels

artery 2.

Skull fracture

May be present

3.

Position

Usually bilateral

4.

Appearance

Cherry red colour with honeycomb

Usually present Usually unilateral

Reddish purple

appearance

5. 6.

Consistency

Soft, friable Presence of CO Yes on chemical

Firm

No

analysis

SN-8: Lucid

Unconsciousness

(2)

Patient again becomes unconscious

Consciousness

Unconsciousnesss

(Lucid interval)

the doctor.

mimics

DW23

Palient becomes conscious

Injuries

Head trauma

Concussion-> Unconsclousness

Enlarged EDH pressescortex

Blooding in epidural spaco begins

Fig. 7C.6 Lucid interval in head injury

During lucid interval, continuous bleeding occurs in extradural space which causes the haematoma to expand beyond the extent to which the body can compensate for. So, there is a rise in intracranial pressure which damages brain tissues. Because a patient may have a lucid interval, any significant head trauma is_regarded as a medical

emergency and receives emergency medical treat ment even if the patient is conscious. Delayed cerebral oedema, a veryseriousand potentially fatal condition in which the brain swells dramatically, may follow a lucid interval that occurs after minor head trauma. MLI:

a

person during the period of lucid interval is responsiblefor all actions. If he commits a criminal açt, he will be held responsible for that act. 2) Ifa patient in lucid interval (due to head injury) approaches doctor and the doctor without examining him properly discharges him, the doctor may be sued for negligence if the patient dies due to complications. 1) A

a

SN-9: Subdural haemorrhage (SDH)

interval

Lucid

interval is seen in cases of head injury and insanity. It is explained in Fig. 7C.6. After head injury, a normal person may become

unconscious. After a variable time, the person Decomes coonscious. This consciousness persists r period of, time after which the condition of the patient deteriora and he again becomes unconscious. This 'period of consciousness Ween two phases of 'unconsciousness' is callea lucid interval. is especially indicative of an EDHL dinterval (extradural/epidural haematoma).

Subdural haemorrhage: The space between dura and arachnoid is called subdural space and subdural the haemorrhage in this space is called clots haemorrhage (SDH). When collected blood called subdural and torms a large firm mass, it is haematonma (Fig. 7C.7). (so it is never Cause: SDH is always due to traunma fracture ot with spontaneous) but not associated the skull. "bridging by rupture of caused is lt the Mechanisn: veins) that traverse communicating dural and (or vessels Vems the cortical Subcdural space between or capilkary SDH is venous of blood Sinuses. So, the and not arterial.

172

SECTIONI

Forensic Medicine

Skull Dural venous sinus

Skull

Dura mater

-Dura mater

Arachnoid mater

Arachnoid

Pla maler Ruptured bridging vein

Subdural haemorrhage

Brain

(SDH)

Cortical vessel

-

Fig. 7C.7 Subdural haemorrhage (SDH)

Frequency:

Out of the three brain membrane haemorrhages, SDH is more common than EDH, that is, SAH (most common) SDH> EDH (least common). SDH is most common at both extremes of life (i.e. childhood as well as old age). Lucid interval may be seen in 30% cases of SDH. Site: Frontotemporal region. Classification ofSDH: Three types A. Acute SDH: It is due to the rupture of bridging veins (or 'communicating veins') that traverse the subdural space between the cortical vessels and dural sinuses. So, the blood of SDH is venous or capillary and not arterial. B. Subacute SDH C. Chronic SDH: It is most common in infants ( 60years). The clotted blood is encased by outer (i.e. dural) and inner (i.e. arachnoidal) neo-membranes.

MLI:E 1)

In Caffey's syndrome, SDH is often associated with long bone fractures.

2) Confusion with 'subdural hygroma': When arachnoid membrane is torn, CSF may pass from subarachnoid space into the subdural space. This collection of CSF in subdural space

called subdural hygroma. 3) Age of SDH can be correlated with the events prior to death. is

SN-10: Subarachnoid haemorrhage (SAH)

Subarachnoid

haemorrhage: The space between

arachnoid and the haemorrhage in this space is called sub arachnoid haemorrhage (SAH) (Fig. 7C.8). SAH (most common) > SDH> EDH Frequency: (least common). SAH is the most common of the three types of brain membrane haemorrhages

and pia is called subarachnoid space

mater

Subarachnoid

haemorhage Pia mater

Brain

Fig. 7C.8 Subarachnoid haemorrhage (SAH)

Subarachnoid space contains CSF and blood ves of brain (including circle of Willis at the base of brain). Causes and types: 1) Traumatic ( head injury): First most common cause of SAH. 2) Nontraumatic (i.e. spontaneous): Second most common cause of SAH. It includes: a) Spontaneous rupture of berry aneurysm in the circle of Willis. b) A-V malformation c) Extension/leaking of a primary intracerebral haemorrhage into subarachnoid space. Rupture of berry aneurysm: Most unruptured berry aneurysms are completely asymptomatic for a long time but on rupture, the clinical features are sels

as follows:

1) Sudden severe

excruciating headache (usually

generalised). 2) Sudden transient loss of consciousness (due to Sudden rise of intracranial pressure) or altered sensorium. 3) Neck stiffness, vomiting and photophobia. Diagnosis: Noncontrast CT scan, lumber puncture Differential diagnosis: Bacterial meningitis Features at autopsy: The SAH can be seen atthe sur face of brain under transparent arachnoid menibrnc SAH can be distinguished from SDH by pournng water on the brain. The SDH will wash away und gently running water, whereas SAH does not wash ot.

MLI:

or

) SAH can be produced during the removal brain at autopsy. lt nmay cause suspicion. " 2) Alcolhol and berry aneurysm: Alcohol 5 Vasoclilator and it dilates cerebral arteries ncupa The ibrous wall of an aneurysm is pressure ble of dilating, and so the high blood

CHAPTER 7

aneurysm through wall. Alcohol also inelast weak and thin, aggressive ehaviour and increases the rcsults in conflict and fight producing trauma chan of may lead to rujpture. which ultimately physical ctivities (e.g. sports, coitus, Intense 3)straining while cfecation and so on) predispose bursting of berry ancurysm to cause SAH. burst bursting of berry facilitates tes

to

SN-11: Circle

of Willis

(circulus arteriosus)

It 1s a large arterial anastomosis , Circle of Willis: a circle or ring present in the subin the form of

arachnoid space within the interpeduncular cisthe optic tern at the base of the brain surrounding

chiasma, intfundibulum (1.e.

pituitary stalk) and

mammillary bodies.

main source of blood supply to the brain. Structure: It is formed by two systems: 1) Internal carotid system: The right and left internal carotid arteries (ICA) arise from the right and left common carotid arteries (CCA), respectively. The internal carotid artery at each side divides and terminates into anterior cere bral artery, middle cerebral artery and posterior communicating artery.

It

is the

Injuries

2) Vertebrobasilar system: The right and left ver-

tebral arteries ascend through the foramina transversaria of upper six cervical vertebrae, enter the cranial cavity through foramen magnum and then ultimately unite at lower border of pons to form basilar artery in midline. Then this basilar artery divides at upper border of pons into right and left posterior cerebral arteries. MLI [SN-12]

SN-12: Berry aneurysm Berry (saccular) aneurysm: It is a sac-like (or balloon like) bulge in a cerebral blood vessel, which is berry-shaped having a very small neck and a large dome. (Note: Aneurysm [Latin aneurysma = dilatation] is an abnormal local dilatation in the wall of a blood vessel, usually an artery, due to a defect, disease, or injury). It is the most common form of cerebral aneurysm. Berry aneurysm is the most common cause of massive subarachnoid haemorrhage. It is also the most common cause of all spontaneous haemorrhages. Sites (Fig. 7C.9): Berry aneurysm occurs in the arteries of circle of Willis, often located at or near the bifurcation of arteries. About 85% of berry

Berry aneurysm Anterior communicating artery

Ant. cerebral artery

Middle cerebral artery

Internal carotid-

artery

Post. communicatingartery

-Post. cerebral artery Superior cerebellar artery

Basillar artery

Pontine branches Labrynthine branch Ant. inf. cerebellar artery

-Post.

inf.

cerebellar artery

-Ant. spinal artery Vertebral artery ig.

7C.9

173

circle of willis Important sites of berry aneurysms at the

SECTIONI

174

Forensic Medicine

aneurysms occur in anterior circulation. The most frequent location in decreasing order is as follows: 1) 'Anterior comimunicating artery: "Anterior cere bral artery junction 2) Posterior comnunicating artery: "Internal carotid artery': junction 3) Middle cerebral artery bifurcation 4) Internal carotid artery bifurcation 5) Basilar artery 6) Intervertebral artery (least common) In other words, most common sites are the anterior communicating artery (35%), internal carotid artery (309%), middle cerebral artery (22%) and finally basilar artery.

Pathology:

Berry aneurysm is the result of developmental weakness of tunica media in vessel wall. It is never congenital, so it is never seen in neonates and children. It develops during the course of

life through the developmental weakness of

media. aneurysm occurs when there is (1) collagen deficiency in the "internal elastic lamina Internal elastic lamina disappears; (2) thinning of the 'tunica media because smooth muscles are replaced by connective tissue.

Berry

Then

tunica intima' protrudes through the

defect in the internal elastic lamina and tunica media to produce the aneurismal sac but the tunica adventitia remains intact. Hence, the balloon like bulging consists of only tunica intima and tunica adventitia. The fibrous wall (i.e. tunica adventitia) of an aneurysm is inelastic and incapable of dilating, so the high blood pressure facilitates bursting of berry aneurysm through thin, weak and inelastic walls. Risk factors for berry aneurysm: Alcohol, smoking, hypertension, trauma, infection. Clinical features of Unruptured aneurysm: Most unruptured berry aneurysms are completely asymptomatic for a long time. Occasionally, a progressively enlargng unruptured aneurysm may produce mass/ pressure effects, for example, 3rd and 6th cr. nerve palsy, bilateral temporal hemianopsia, pain in eye.

Ruptured aneurysm: (1) Sudden severe excruciating headache (usually generalised); (2)

Sudden transient loss ot consciousness (d. sudden rise of intracranial (due pre ssure) to or altered sensorium and (3) neck stiffness and vomie miting, Features at autopsy: Massive blood noid space at the undersurface od in subarad of brain. MLI of berry aneurysm: Rupture of berry aneurysm may be traumatic or nontraumatic (i.e. spon. ntaneous). 1) Trauma and berry aneurysm: Emotional stress may lead to sudden rise in blood pressure to cause rupture of aneurysm in a weak berry aneurysm. During a conílict/fight, the adrenal response (increased catecholamine) leads to high BP and increased heart rate. An already leaking aneu rysm may irritate meninges which may lead to neurological and behavioural abnormality, this ultimately may lead him to conflict with another person or fall or cause a traffic accident. 2) Alcohol and berry aneurysm: Alcohol is a vasodilator and dilates cerebral arteries. The fibrous wall of an aneurysm is incapable of dilating, and so the high blood pressure facilitates burst ing of berry aneurysm through thin, weak and inelastic wall. Alcohol also results in aggressive behaviour and increases the chance of contilict and fight producing trauma which ultimately may lead to rupture. 3) Intense physical activities (e.g. sports, coitus, straining while defecation and so on) predis pose to bursting of berry aneurysm. 4) Drugs (e.g. cocaine) may predispose to burst

ing

SN-13: Intracerebral haematoma Intracerebral

haemorrhage: The haemorthag

which occurs within the parenchyma of brain (L Within brain tissue) is called intracerebral haemor rhage. is the most common type of intracranal ne It orrhage. Causes: It may be traumatie or nontraumat injuriet 1) Traumatic: It appears along with other bra1. for example, contusion and laceration ot ca 2) Nontraumatic: The most common hypertension' (i.e. hypertensive haemorrn haemor Most common site of hyperten ive puta rhage is "basal ganglia' (especially 55%), thalamus (15%), white matter

CHAPTER 7

cerebellum (109%). Most Com109%) and Pon in renchymatous (cereartery involved mon is branch nticulostriate haemorrhage bral) artery' which supplies putamiddle cerebral of outerglobus pallidus, etc. men, The clinical features occur while nical features: and stressed. They include atient is awake the headachc. vomiting and Contralateral basal ganglia is involved:

TABLE 7C.2

Sr.

It

Signs. 2)

Concussion resembles drunkenness. The victim may be discharged by the doctor who may think it a case of drunkenness. The victim may be held in custody by police officer (Table 7C.2).

Dilated, contracted

Contracted

coma

Pulse Respiration

Memory

Retention of urine Rapid and bounding Slow and feeble Shallow, Sigh, puffs, irregular, slow eructates Confused, Retrograde disoriented amnesia Quite, retracted, Uncooperative, abusive, talkative curled up in bed,

photophobia

8

Urine/blood

Examination is helpful

History of

Consumption of alcohol. Smell of alcohol present

Retention of urine History of head injury with features of concussion

3) The person may pretend to be sufifering from

concussion after an accident or assault to claim compensation.

SN-15: Contrecoup injury

3) Confusion

Concussion may cause death without any gross

Pupils

Behaviour

seconds to few minutes) or 2) Retrograde amnesia (i.e. memory loss), that is, the person may forget everything for a few minutes or

MLI:

Pale, cold, sweating

4

6.

Clinical syndrome includes: 1) Sudden transient loss of consciousness (for few

vomiting. Mechanism: Concussion results from acceleration/deceleration of head. Rotational force is the key in concussion. Punches in boxing deliver more rotational force to the head. "Violent head movement causes shearing and stretching of nerve fibres and axonal damage. Postconcussion syndrome (PCS): Concussion may be followed by symptoms such as headaches, anxiety, dizziness, fatigue, memory and attention problems, sleep problems, and irritability.

Flushed, congested, warm

Urine/blood Examination is helpful

5

Concussion

Skin

3.

Concussion of brain

(disorientation), disturbance of Vvision, headache, contracted pupils, nausea and

Drunkenness

in

Concussion (Latin, concutere= to shake violently): It is a clinical syndrome seen immediately after head injury and is characterised by temporary cerebral1 dysfunction' (or transient impairment of neural functions). is also known as mild traumatic brain injury (mTBI).

)

No. Featuress

2

hemiparesis.

SN-14:

Difference Between

Drunkenness and Concussion (D/W-24]

When

is involved: Contralateral hemi. When thalamus paresis, downward and inward deviation of eyes with unequal pupil with loss of light reflex.

175

Injuries

a

Coup and contrecoup injuries: The injury which occurs immediately beneath the area of impact and results directly from impacting force is known = blow). The injury presas 'coup' injury (coup ent in an area opposite to the site of impact is known as 'contrecoup' injury (contre = opposite coup = blow) (Fig. 7C.10).

Coup

injury is caused when

The head is fixed (i.e. person standing still) and there is a violent impact on the head. A blow to the head pushes the head in the direction of the blow, the skull also moves in that direction At but the brain lags behind for a short while. the at skull this moment, the brain strikes the injury. So, it is Site of impact and causes coup lt is more considered as an acceleration injury. head. common with blunt force blows to the hard strikes a stationary a 2) The head falls and concrete floor. When Surtace, for example, 1)

176

SECTIONI

Forensic Medicine

Moving. blunt weapon, for example

hammer,

Coup injury

Countrecoup

Fall

injury

stone Point of

impact

Coup injury Static head

Falling/moving

head

Ground Point of impact

Fig. 7C.10 Mechanism of coup and contrecoup injury of the brain

a

moving head strikes a hard stationary object, the moving skull comes to a sudden stop but the moving brain moves on and strikes the skull to cause coup injuries. For example, when a person falls on occiput, the coup injury occurs at occipital lobes of the brain; in the same way, similar coup injuries occurs in other regions also. Contrecoup injury (as per struck hoop theory): When moving head strikes a stationary hard surface during a fall, the skull flattens at the point of impact due to its elasticity. This flattening causes compression of skull as a result of which pressure is increased and the underlying brain just beneath the site of impact is compressed to cause coup injury. Simultaneously, the region of the skull opposite to the site of impact will bulge outward to accommodate the deformation. It creates vacuum due to negative pressure which causes tension and shear strain which tries to pull apart the tissues of the brain to cause contrecoup injury. Contrecoup injury is considered as a decelera-

tion injury.

It is rare in children of It increases blood TlOw to the skin and extremities, making a persOn

eel warm, while increasing heat loss Lowers the core temperature. It results in consumption of

more and more alcohol to keep oneself warm. 6) Cold stiffening must be differentiated from rigor mortis (Table 7D.2).

3.

4.

Crepitation on manipulation of joints

Present (due to breakdown

Followed by

Cold stiffening is followed by rigor mortis

Absent

of frozen synovial fluid) Rigor mortis is followed by

decomposition

SYSTEMIC HEAT DISORDERS Heat cramps: Severe painful voluntary muscle spasms (especially those of extremities and abdominal wall). It results from doing prolonged heavy exercise, heavy sweating and drinking excessive water in extreme heat. It is caused by loss of salt in sweating. Treatment is salty drink. Heat syncope: A person collapses. Reason: Intense peripheral vasodilatation leads to peripheral pooling and hypotension. Management is placing the head low and feet in an elevated position. Heat exhaustion: Prolonged physical exertion Severe sweating> Dehydration (water +salt). Management is rehydration with water and salt. Heat stroke [SN-2] DRY HEAT BURNS Some facts: In an adult, the total body surface area or skin surface is about 1.6- 1.9 m'. Pure cotton fabrics ignite easier and burn faster than other types of fabrics (e.g. nylon, wool, polyester), so produce more severe burns. Close fitting garments are safer than loose garments. In a case of burn, subcutaneous fat further aids ignition. Lowest temperature that produces burn tor 3 s is 44 °C for 5 h. A temperature of 60 °C only °C will can cause burn. A temperature of about 1000 completely incinerate the body in about h. I

Classification of Heat Burns A. B.

7D.)

Pathological classification: (Table Clinical classification: partial: (1) Superficial deeppartial: ) Partial thickness burns: dermis and (2) Burns up to papillary reticular dermis. of parts deeper dermis Durns up to Burns involving burns: 2) Full thickness and beyond.

SECTIONI

182

Forensic Medicine

TABLE 7D.3 Differentiypes of classifications of Burms Depth of Damage 1.

Erythema

A. Dupuytren's Classification 1

2. Vesication

2

B. Hebra's Classification

degree

1

degree

(i.e. Dupuytren

degree degree

+

degree) 2 degree (i.e. Dupuytren 3 degree + 4 degree)

3. Damage to superficial skin

3 degree

4. Damage to whole skin

4 degree

5. Damage to

5 degree

3

6 degree

(.e. Dupuytren 4 degree+

6. Damage to bones

Classification

Epidermal

2

muscles

C.Wilso Ison's

degree

Dermoepidermal

Deep

5 degree) Note: Dupuytren divided burns into 6 degrees but they were merged into 3 degreed by Hebra. Wilson named first-deareo Hebra as epidermal, second degree Hebra as dermoepidermal and third ee degree Hebra as deep.

Wilson's Classification 1)

Epidermal burns (i.e. dupuytren 1 + 2 degree): Only epidermis is destroyed. Characterised by erythema (i.e. red hyperemic skin) and vesication (i.e. blisters). Erythema results from capillary dilatation and transudation of fluid into tissues and is associated with swelling. Blister results when fluid accumulates at dermoepidermal junction below epidermis. A blister or bulla is covered by a white avascular epidermis and is bordered by a hyperemic zone. Blister is filled with a fluid containing protein and chloride. Ifthe blister bursts, it leaves a pink or bright red raw surface.

Very painful.

Singeing of hair is present. Completely heals without scarring. 2) Dermoepidermal burns (i.e. Dupuytren 3 + 4 degree): Full thickness of skin is destroyed. Epidermis is coagulated or charred. There is a central shrivelled and depressed zone of necrotic tissue which is surrounded by first-degree burns or a zone of hyperaemia. The central necrosis sloughs off within a week and epidermis grows in from the margins. These burns are the most painful type of burns because the free nerve endings (nociceptors, C-fibres) responsible for pain are exposed. Heal with scarring. The contraction ofscar tissue may cause disfiguration or impaired function. 3) Deep burns (i.e. Dupuytren 5 + 6 degree): They include destruction of skin, subcutaneous tissues, muscles and bones. "The burnt parts are completely charred. Burns are painless because free nerve end ings (nociceptors, C-fibres) responsible for pain are destroyed.

Rule of Nines [SN-3] Wallace rule of nines is used to calculate the percentage of total body surface area (TBSA) that has been burnt. Lund and Browder chart is used for individuals of

20%%

of TBSA is involved, the marked fluid loss

results in shock. In Indian scenario, if 250% of TBSA is involved, the prognosis is fatal.

Superficial Burns vs. Deep Burns Superficial burns are associated with more pain and so cause neurogenic shock. Deep burns are associated with less pain and since fluid loss is more, it causes hypovolemic shock as well; healing is delayed leading to many complications.

Fatal Period Most deaths from burn injuries occur within 24-4S h and cause of death is shock. After this period, death occurs due to toxaemia within 4-5 days.

Management of a Case of Burn First aid: Cold water bath immediately. Hospitalise in a burn ward. 2) ABC: Endotracheal tube may be required in case ot laryngeal oedema (in flame burns). 3) Pluid resuscitation: It may be required in children with > 10% TBSA burns and in adults with TBSA to prevent hypovolemic shock. The thu Biven is Ringer lactate (RL) or Hartmann solutio or fres frozen plasnua (FFP). In children, dextrose alsohas to be given as a maintenance dose. Perk Iand fornmula is used to calculate the amount o 1)

CHAPTER 7 in case

of burn. Amount of fluid (in

wrinkles of face. These areas appear as light fair lincar spots on a black face. Actually, the burning person has severe pain and makes tight facial gestures; the soot and smoke is not allowed at the base of wrinkles. Heat stiffening or heat rigor: Due to application of heat, coagulation and denaturation of muscle proteins occur which leads to the contraction and stiffness of muscles. The dead body attains a peculiar posture similar too a boxer

fluid quired (in kg) x Burn first 24 h =4X Body weight ml) in with half of this total given in first 8 h. arca (96) The amount of uid needed in first 24 Example: weighing 60 kg with a 40% case of a patient in the (4 X 60 x 40)= 9600 ml. Half will be TBSA burn 1h

h after mL) has to be given in first 8 ic. 4800 remaining half (i.e. 4800 mL) has to injury and the in next 16 h. begiven killers: Opioids (e.g. IV morphine) 4) Pain (a) Clean the wound with antisep5) Care of wound: application of silver sulphadiazine tics; (b) topical (c) daily dressing. on burn surface and

antibiotics: To Tetanus injection and systemic prevent septicaemia. poisoning; 7) Miscellaneous: (a) Management of CO (b) monitoring of vitals (temperature, pulse, respiration, BP) and urine output (by inserting Foley's catheter) and (c) nutrition and antioxidant therapy. Ryle's tube should be passed to do cold stomach wash and to instill antacids to treat Curling's

(pugilist). This peculiar posture is known as pugilistic attitude. Pugilistic attitude [SN-4] or boxing attitude or defence attitude: This is a posture attained by a dead body in a case of death due to burn. Difference between heat stiffening and cold stiffening (Table 7D.4).

6)

ulcers.

TABLE 7D.4 Difference Between Heat Stiffening and Cold Stiffening [DN-111 Sr. No. Features

Causes of Death in a Case of Flame Burns

Cause

deposition over some areas may lead to blackening. The burns may appear in the shape of ornaments (by close contact of heated orna ment) or burn may be absent in areas of skin in tight contact with clothing. The skin detaches as a glove. Body may be completely charred. Tattoo marks become visible after removing superficial layer of skin. Hair is singed or completely burnt. Face: Face swollen, distorted, tongue protrudes. Two findings on face that signify that the person was alive when burnt are 1) Froth at mouth and nose. Actually, heat irritates lungs to develop pulmonary oedema. It indicates that the person was breathing while the fire was in progress. 4) Crow's feet. Absence of burns and soot deposits in the corners of eyes and at the base of

Heat Stiffening Cold Stiffening Intense heat (in

[LO-1]

Postmortem Appearance Externalappearance: There may be smell of kerosene or petrol. Burnt areas have a patchy distribution and appear reddened, blistered or charred. Soot

Injuries

2.

Body

3

Mechanism

Cold

burning)

Very hot

Very cold

Muscle protein Solidification of Coagulation at body fats and °C >50 muscles at Increased pressure of steam inside skull > Separation of ununited sutures or bursting of skull. (2) The skull bone dries and contracts. It involves only the outer table of the skull. There is no displacement of bones. Usually, it is seen on either side of the skull above temples. Such fracture consists of several lines radiating from a common centre. 3) Hyoid bone may get fractured on gentle manipulation.

TABLE 7D.6 Sr. No. Features 1.

Skull fracture

4. 5.

Appearance

6.

Consistenc

8.

10.

5)

Respiratory system: Hot smoke ot particles or carbon particles) (along with

the victim, so respiratory passages is inhaledby trom mouth to bronchioles may be congested and ocdema tous. Lungs congested and ocdematous. Sot in terminal bronchioles: Presence of soot (ie carbon particles) below vocal cords, that is in trachea, bronchi and terminal bronchioles prove that the person was breathing during fire and suggests antemortem nature of burns. On histological examination, if carbon particles are found in terminal bronchioles, it is an absolute proof that the person was breathing during fire. So, trachea should be incised before eviscera tion for the presence of soot. 6) GIT: Soot may also be found in oesophagus and stomach. It suggests the act of swallowing soot during fire, that is, ante-mortem nature of burns. Curling's ulcer: A burnt patient can devel acute stress ulcers (or acute peptic ulcers) in duodenum (especially first part). Mecha nism: Stress and reduced plasma volume Mucosal ischaemia Mucosal cell necrosis 7)

Sloughing ofmucosa> Ulcer. Carbon monoxide (CO) in blood: In

deaths

due to burns, blood CO level is > 10% (may be up to 80%). CO may be absent in blood due to rapid death, for example, in an explosion. Blood is cherry red.

Difference Between Heat Haematoma and Extradural Haematoma (D/N-13

Cause

Fracture line Position

4) Although internal organs are served, they may be cooked. usually wellpre

Adjacent brain shows Presence of CO (carbon monoxide) on chemical analysis Soot in respiratory tract

Carboxyhaemoglobin in blood

Heat Haematoma

Heat: Heat results in rupture of blood vessels (longitudinal venous sinuses and diploic veins) May be present

Extradural Haematoma Mechanical trauma (blunt force impact): Trauma results in uptue of middlle meningeal artery Usually present

Need not cross middle meningeal artery Usually bilateral

Crosses

Cherry red colour with 'honeycomb appearance Soft, friable Heat effects Yes

Firm

Usually present; it is usually indiocative of death from suffocation following antemortem burns Usually present

Usually unilateral

Reddish purple Injury No

Not present

Absent

CHAPTER 7

The clothes and metallic articles preserved to establish

Prese rvation: removed and have to be identity.

ML Identification of ceased: It is difficult to iden1) tify a body when it is completely burnt, but following points may be helpful: (1) metallic objects worn, for example rings, bracelets, keys and so on; (2) age can be determined by examining teeth and

identifed by examining prostate or nulliparous uterus because they are well protected in the pelvis even at very high temperature. 2) Whether the burns áre accidental, suicidal or homicidal: (1) Accidental burns are common among children and elderly persons. Accidental bursting of kerosene stove in rural areas of India occurs quite often. (2) Suicidal burns are very common among Indian women. After pouring kerosene oil, they set fire to themselves. (3) Homicidal burns are also very common in India and the main reason is dowry. The husband or relatives of husband pour kerosene oil on the woman and set fire. Such death (dowry death, S.304B of IPC), very frequently, is claimed to be accidental. 3) Whether the burns are antemortem or postmor(3) sex can be

tem (Table 7D.7) 4) Age

of burns: (1) Immediate-redness; (2)

1-2 h-vesication; (3) 12-24 h-exudates begin to dry; (4) 2-3 days-crust formation and pus

formation; (5) 5 days-superficial slough separation; (6) 15 days-deep slough separation; (7) 15

days-granulation tissue appears and (8) many of cicatrix anddeformity.

weeks: formation

TABLE 7D.7

Sr. No.

Features

.

.

185

MOIST HEAT BURNS (SCALDS) The

injuries caused from application of moist heat are known as scalds. The moist heat may be any boiling liquid (e.g. water, milk, oil and so on) or hot steam. They are caused by splashing of hot liquid. For Cxample, bursting of pressure cookers in kitchen, splashing of liquids from cooking utensils, slipping while carrying hot water to take bath, etc. Water at 70 °C can cause full thickness scalds of the skin in one second of contact. Scalds are severe at the site of initial contact with the liquid. As the liquid trickles down the body, the degree of scalding also progressively diminishes.

Pathology: 1) Degree

of scalds: (1) Erythema; (2) blister and (3) necrosis of dermis 2) Redness (erythema) appears immediately and then within a few minutes, blisters are formed. There is a hyperaemic zone around blisters. Blisters are formed due to increased permeability of capillaries. The blisters are filled with a fluid which contains WBCs and RBCs. 3) Removal of the skin of blisters leaves a pink, raw surface which if left open becomes brownish, dry and hardened. 4) Scalds may produce soddening and bleaching but are not associated with singeing, blackening or charring. 5) Scalds are not as deep as flash burns because of cooling of liquid due to evaporation. appearance: The clothes are wet but intact. PM Streaks of liquid run downwards from the main

Difference Between Antemortem Burns and Postmortem Burns [D/W.14|

Blisters

3

Injuries

Line of redness around blister Vital reaction

Enzymatic activity (by histochemistry) Signs of healing and repair (e.g. granulation tissue) Infection

Soot particles in respiratory tract CO (or carboxy-Hb) in blood

Antemortem Burns Postmortem Burns True: Contains serous fluid with False: Contains air/gases due to postmortem

Present Present

changes; if fluid is present, it has very little protein (albumin) but without chlorides and polymorphs Base is dry, hard and yellow Absent Absent Absent Absent

Present Present Present

Absent Absent Absent

proteins (albumin), chlorides and polymorphs. Base is red, inflamed and swollen Present Present

SECTIONI

186

Forensic Medicine

area causing lines of blisters. The scalds usually have sharply demarcated margins which correspond to the extent of fluid contact. Cause of death: Immediate causes may be (1) shock and (2) fluid and electrolytic imbalance. Delayed cause is secondary infection. MLI: 1) Scalds ate mostly accidental, very rarely suicidal. 2) Sometimes hot liquid (e.g. oil) may be thrown intentionally on the victim to injure him. If faace is disfigured, it is considered as grievous hurt 3)

4)

5) 6) 7)

S.320, IPC] Scars of scalds cause less contraction and less disfigurement. Clothes soak the hot liquid and so prolong the contact time with the liquid and cause more damage. Moist heat burns should be differentiated from dry heat burns (Table 7D.8). Antemortem scalds must be differentiated from postmortem scalds (Table 7D.9). The scalds have to be differentiated from burns (Table 7D.10).

LIST OF IMPORTANT QUESTIONS FOR EXAMINATION LONG QUESTIONS (L0) -

1.

Classify thermal injuries. Discuss various causes of death in a case of flame burns.

SHORT NOTES (SN) 2. Heat stroke 3. Rule

TABLE 7D 8 Difference Between Dry Heat Burms and IMoist Heat Bums [D/W-151 Sr.

No.

Sr. No. Features Cause 3.

Site Splashing

9 10.

Moist Heat

Bums

Cause

Flame, heated body or Steam or liquid radiations (e.g. X-rays)

2.

Site

At or above the site of

At or below the site of contact

Skin

Dry, wrinkled, may be charred (black)

Sodden, bleached

Vesicles

At the circumference of

Over the burnt area

3.

. 5.

Splashing

contact Absent

Present

Charring

burnt area May be present

Absent

Singeing

Present

Absent

Scar

Thick, contracted

Thin, less contracted

Clothes

Burnt

Wet, not burnt

TABLE 7D.9 Difference Between Antemortem Scalds and Postmortem Scalds [D/w-16 s Postmortem Antemortem

No. 2.

Features

Scalds

Blisters (vesicles)

Present

Usually absent

Scalds

Flame or any heated solid object At or above the site of contact

Steam or hot liquid

Absent

Present Sodden and bleached

contact At or below the site of

Charring

Blackish, dry. shrivelled or charred May be present

Singeing of hair

Present

Scar Clothes Crime scene

Absent Absent

Thick and contracted

Thick but

Soot particles in upper respiratory tract

May be present More fatal

Fatality

Scalds

Content of blister Albumen protein Gas, air Line of redness Absent Present around the blister

Difference Between Burns and Scalds [D/W-171 Burns

Skin

8.

Dry Heat

Features Burns

1.

3. TABLE 7D.10

of nine [CCU 2010]

less contracted

Burnt Wet (i.e. not burnt) There may be burning (with charring) of nearby No burning of nearby obye objects

Absent Less fatal

CHAPTER Pugilistic attituc

4.

Heat

5.

[CCU 2004, 2009, 012, 2014]

1)

haematoma

IMPORTANCE (MLI)

MEDICOLEGAL

shows pugilistic attitude presence of heat hacma-

The dead body shows The dead body

6. 7.

toma that the body was burnt alive Autopsy revealed present in trachea on autopsy Soot particles are

8.

9.

DIFFERENCE BETWEEN

(D/W)

mortis cold stiffening 11. Heat stiffening and lacerated wounds 12. Heat rupture and haematoma 13. Heat haematonma and extradural DU 2008] [DU 2011] 14. Antemortem and postmortem burns CCU 2003, 2005, 2009, 2011, 2012] 2006] 15. Dry heat burn and moist heat burn [DU 16. Antemortem scalds and postmortem scalds Cold stiffening and rigor

10.

17.

Burns and scalds [DU 2001, 2007]

ANSWERSS

L0-1: Classify thermalinjuries.

Discuss various causes of death in a case of flame burns? Classification of Thermal Injuries

(Table 7D.1)

Causes of Death in a Case of Flame Burns Immediate (i.e. within 24 h) 1) Primary (neurogenic) shock due to severe pain 2)

and fear. Asphyxia:

a) Suffocation

3)

due to inhalation of smoke and carbon monoxide. Burning of plastic material produces HCN gas and oxidesof nitrogen. Burning of wood/silk produces NH, HCN, H,S and oxides of sulphur. D) Traumatic asphyxia due to fall of heavy objects (e.g. beam, roof, wall and so on). Accidents (e.g. jumping/fall from window of height) occur in an attempt to escape Irom a

burning house.

Late 2)

3)

4) 5)

6) 7)

8)

7 Injuries

187

(i.e. after 24 h) Secondary (hypovolemic) shock due to fluid loss from the surface of burns within first 48 h. Toxaemia: Absorption of various metabolites and toxic substances (e.g. smoke, cyanide and so on) ocurs from burnt tissues into the blood. Septicaemia (sepsis) occurs 4-5 days or longer after burning. Meningitis, peritonitis, pericarditis, etc. occur. Pulmonary oedema Renal failure (due to acute tubular necrosis) and biochemical disturbances, for example, hypokalaemia. Anaemia and hypoproteinaemia Marjolin's ulcer: The malignant transformation of a burn scar (Marjolin's ulcer) years after recovery. Others: Curlings ulcers, gangrene, tetanus,

SN-2: Heat stroke (sun stroke) Heat stroke: It is a type of systemic hyperthermic injury in which there is complete absence of sweating and the temperature is raised to 41 °C (106 °F). Mechanism: Thermoregulating mechanism is lost. It usually occurs in persons undergoing hard work in open fields under conditions of high temperature with lack of acclimatisation. It may present in two forms: 1) An acute form with sudden onset without any

prodromal symptoms. 2) A gradual onset form with definite prodromal

symptoms, for example, headache, nausea, vomiting, dizziness, weakness in legs, excessive desire to micturate. The victim may become unconscious and fall on ground. Skin is dry and hot, flushed face, increased depth of respiration, high pulse rate (160-180/ min), hypotension. Renal and hepatic failure may occur. Pupil dilate initially but constrict (pinpoint) delirium, in later stage. CNS features: convulsions, stupor, coma. Treatment: It is a medical emergency requiring hospitalisation. (i.e. By passive cooling ) Lower the temperature: area/shade and then move the person to a cooler cooling (i.e. cold remove the clothes) or activeimmersion in cold compress, water bath, cold bathtub). or intravenous. 2) Hydration: Oral

188

Forensic Medicine

SECTIONI

findings: Features are same as in cardiac failure. (1) Postmortem caloricity, that is, the body temperature is high even after death. (2) Rigor mortis sets in early and passes off carly. (3) Putrefaction is rapid. (4) Visceral congestion and haemorrhages, subendocardial hacmorrhages in heart, brain is congested and oedematous. Medicolegal aspects: 1) Suspended animation: In case of sunstroke, the person may pass into a stage of suspended animation. So, resuscitation has to be considered before pronouncement of death. 2) Workmen's Compensation Act: Unfavourable working conditions at working place leading to hyperthermia in an employee can attract provisions of Workmen's Compensation Act. 3) Death due to hyperthermia is usually accidental. But it may be created artificially by drugs (malignant hyperthermia by general anaesthesia).

Autopsy

SN-3: Rule of nines

of nines is the simplest and most easily remembered method to estimate percentage of total body surface area (TBSA) that has been burnt. It was given by Alexender Wallace in 1951 and thatt is why it is also known as Wallace rule of nines. This rule is applicable only for adults. In children, the Lund and Browder chart' is considered the most accurate in measuring the percentage of burns and is widely used in everyday clinical practice. The reason is that the surface area in children is different from adults. According to rule of nines, the body is divided into 11 anatomical regions and each region represents 9% of total body surface. Remaining 1% area is perineum (Table 7D.11) (Fig. 7D.1). Rule of Nines

Head and Neck Upper limbs Chest

Abdomen Lower limb: Right

Lower limb: Left

Fig. 7D.1 Rule of

Uses 1)

9

9

9

9+

9

nines applied in a case of burn

of rule of nines: Rapid rough assessment of burnt

area in

emer gency. 2) Prognosis: Rule of nines also helps to know the prognosis in case of burn injury. Actually, prognosis depends on the percentage of burnt area. If 250% of TBSA has been burnt, the prognosis is fatal. 3) Treatment plan: Rule of nines is very important to calculate the amount of fluid to be given a burnt person. The Perkland formula is used to calculate the amount of fluid required in case of burn. Amount of fluid (in mL) in first 24h=4x Bodyweight (in kg) X Burn area(%) Half of this total amount of fluid has to be given in first 8 h and remaining half in next 16 h. 4) At autopsy: Rule of nines is routinely used at the time of autopsy to assess the burnt area. t

Rule

TABLE 7D.11 Regions

9

9

Body Surface Burnt (in %) 9 9 (Right)+ 9 (Left)

9 (Front)+ 9 (Back) 9 (Front)+ 9 (Back) 9 (Front)+9 (Back) 9

(Front)9(Back)

Perineum (External genitalia)

1

Total

19x

11)+1 100

SN-4: Pugilistic attitude (or boxer's attitude)

Pugilistic attitude (pugilist means a boxer): This is

a posture attained by a dead body ina case of death due to burn (Fig. 7D.2). Since this posture is similar to the posture adopted by a boxer in defence during fight, it is known

boxer's attitude or defence attitude. known as fencing attitude. as

It is also

It occurs due to (1) coagulation o protein in the muscles and (2) dehydration and contraction of muscles due to excessive heat. case of death due to burn, the flexor muscieo In (being bulkier than the extensors) contract m flexion. Hea So that the body attains a position of are flexe is slightly extended. Upper extremities on and are placed in front

Mechanism:

at shoulders and elbows metacarpophalange body. Fingers are flexed at

CHAPTER 7

Injuries

189

The brain is shrunken, firm and yellow to brown due to cooking and the dura is leathery. Heat haematoma should be differentiated from extradural haematoma because heat haematoma resembles a traumatic extradural haematoma (Table 7D.6).

MLI-6: The

dead body shows pugilistic attitude the person died due to burn injury. It It means is not strongly suggestive Fig. 7D.2

Pugilistic attitude in a case of burn

and interphalangeal joints to result in clawing of the fingers. Lower extremities are flexed at hips and knees and are placed high up. Rigor mortis does not appear in such muscles. Putrefaction is delayed because heat destroys

microorganisms and autolytic enzymes. This attitude can occur when death is due to burn or when a dead body in molecular phase is burnt. Similar type of attitude of the body can be seen in gas stifening but will be associated with other fea tures of putrefaction.

SN-5: Heat

haematoma

Heat haematoma: In case of death due to extensive flame burn injuries, the exposure of skull to tremendous heat leads to charring of skull. Beneath this charring, a haematoma may develop in extradural space.

of antemortem nature of burn because it may also develop when a dead body in molecular phase is burnt. Due to heat, coagulation and denaturation of muscle proteins occur which leads to the contraction and stiffness of muscles. The dead body attains a peculiar posture similar to a boxer (pugilist) known as pugilistic attitude. It should be differentiated from cold stiffening and rigor mortis.

MLI-7:The dead body shows

presence of heat haematoma

It means the haematoma was caused due to heat, not blunt force trauma to the head. Intense heat produces bubbles of steam in the accumulated blood to give rise to 'honeycomb appearance' and so it becomes soft and friable. It should be differentiated from extradural haematoma.

Mechanism of formation: Heat evaporates water of the blood inside blood vessels (longitudinal venous sinuses and diploic veins)> Rupture of blood vessels> Accumulation of blood and coagulation Heat haematoma.

DIstribution is related to the charring of skull but most common site is parietotemporal region. Appearance:

It

is

1.5

mm-1.5 cm thick, soft, friable, choc-

olate coloured clot of blood. If blood contains CO, its colour is pink. t contains up to about 120 mL of blood. Intense heat produces bubbles of steam in the accumulated blood to give rise to 'honeycomb ppearance' and so it becomes soft and friable. part of brain adjacent to heat haematoma shows discolouration and hardening from the heat.

ne

MLI-8: Autopsy

was burnt alive

reveals that the body

clues at autopsy which indicates that body was burnt alive are as follows. ) Burn wounds: Line of redness present. Base of blisters is red, inflamed and swollen. 2) Froth at mouth and nose. Actually, heat irritates It indiungs to develop pulmonary oedema.wvhile the cates that the person was breathing fire was in progress. absent soot deposits are wrin3) Crow's feet: Burns and of base eyes and at the in the corners of fair linas areas appear lightburning These face. kles of face. Actually, the facial car spots on a black and makes tight person has severe pain

Some

190

SECTIONI

Forensic Medicine

allowed is gestures and the soot and smoke not at the base of wrinkles. 4) Curling's ulcer may be present in duodenum. 5) Cherry red blood indicates the presence of carbon monoxide in blood.

Carbon particles in terminal bronchioles and/ or oesophagus and stomach. the victim is a lady who was married within last 7 ycars, it will be presumed to be a case of dowry death [S.304B of IPC] until proved. The magistrate will conduct inquest. 6)

If

MLI-9: Soot

particles are present in

trachea on autopsy

lf

soot particles are present in trachea (i.e. below vocal cords), it mneans the person was breathing during the fire and suggests antemortem nature of burns.

DW-10: Cold stiffening and rigor mortis (Table 7D.2) D/W-11: Heat stiffening and cold stiffening (Table 7D.4)

D/W-12: Heat rupture and lacerated wounds (Table 7D.5)

DW-13: Heat haematoma and extradural haematoma (Table 7D.6) D/W-14: Antemortem and postmortem burns (Table 7D.7) D/W-15: Dry heat burn and moist heat burn (Table 7D.8)

DW-16: Antemortem scalds and postmortem scalds (Table 7D.9) D/W-17: Burns and scalds (Table 7D.10)

CHAPTER 7

91

Injuries

Chapter 7E Firearm Injury INTRODUCTION

study of fircarms and discharge of a ammunition along with the effects of problenms arising from their use. A firearm and the the air; this projectile firearm propels a projectile into a hits target. Forensic ballisafter travelling in the air It is the Forensic ballistics:

three subdivisions: ballistics: The 1) Internal (or proximal or interior) deals with the branch of forensic ballistics which mechanics of the firearm and the study of motion of the projectile within the firearm from the moment of ignition until it leaves the barrel. 2) External (or intermediate or exterior or transitional) ballistics: The branch of forensic ballistics which deals with the projectile motion/behaviour after it leaves the barrel of the firearm. tics has

Terminal ballistics: The branch of forensic ballistics which deals with the study of (1) the behaviour of projectile when it hits target, that is, what happens to the projectile and (2) the impact of projectile on the target, that is, what happens to the target. Wound ballistics is a type of terminal ballistics which deals with the study of effects of projectile on hitting living tissues, that is, the injuries produced. Firearm: A firearm is a mechanical device which pro pels a projectile (i.e. bullet or shots) forcefully by the expansile torce of the gases generated by combustion of an explosive (i.e. propellant or gunpowder). The projectile is propelled at a high velocity to hit a target. Ammunition: Objects which are either fired (e.g. cartridges) to propel projectile(s) to hit target or which are thrown (e.g. bombs, grenades) to cause explosion. Cartridge: A cartridge is a complete round of ammunition. It consists of a case which contains the follow ingthreethings: 3)

Detonator

2)

(or priming mixture): It is a mixture Present in a metal cup called primer or primer cup and is used to ignite the propellant. It consists of three components, Barium nitrate, Lead styphnate and peroxide and Tetrazene.

Propellant(orgunpowder): It is an explosive which s Situated in close proximity to the primer. It 1s

ignited/burnt by a spark in the primer the projectile (Table 7E.1).

to propel

TABLE 7E.1 TVpes of Propellant

e.

Gunpowder)

Black Powder Composition A) Potassium nitrate (75%): Oxidiser 2) Charcoal (15%: Fuel 3) Sulphur (10%): Fuel+a binding agent. It decreases the

a

Smokeless Powder 1.

Single base: Nitrocellulose

2. Double base: Nitrocellu-

lose+Nitroglycerine 3. Triple base: Nitrocellulose

+Nitroglycerine + Nitroguanidine

ignition temperature

but inçreases the speed of combustion 1g of powder yields 280 cc of gas (CO, CO, N H HS, CH,) Use: Only in muzzle oading firearms, country made firearms and blank

o1gof nitrocellulose yields 950 cc of gas

cartridges

Combination of aforementioned two, that is, semismokeless powder Black powder (80%) + Smokeless powder (20%). Not used so much

part of cartridge which is propelled by a firearm through its barrel to hit target. It may be multiple pallets/shots in case of shotgun cartridge and a bullet in case of rifled

3) Projectile: It is the

cartridge. Muzzle velocity vs. Striking velocity: The speed at which a projectile leaves the muzzle of a firearm 1s known as muzzle velocity. A projectile attains maxmuzimum velocity when it leaves the muzzle. So, Zle velocity is the maximum velocity of a projectile of the attained during its movement. The velocity as strKing projectile at the point of impact is known

velocity. up to whicn Effective range ofa firearm: The distance the projectile(s) ofa fiearm can harni.distance up to firearm: The CTminal range of a a fiearm can travel wnlch the projectile(s) of

192

SECTIONI

Forensic Medicine

GENERAL MAKE UP OF FIREARM firearm has three main parts: barrel, action and grip. nmetallic tube through 1) Barrel:It is the long hollow which bullet travels and comes out. Its recar/proximal end (i.e. breech end) is closed and the front/ distal end (i.e. muzzle end) is open. The most proximal part of the barrel at the brech end is the widest part of the barrel which accommodates car-

A

known as chamber. The part of the barrel which connects chamber to the long distal part of barrel is known as taper. The taper is known as chamber cone in smooth bore firearms and leed in rifled firearms. The backside of the chamber has a metal plate known as breech plate which has a central hole to give entry to the firing pin. Bore: It is the interior or the hollow portion of a barrel through which the bullet travels. The open end (mouth) of the bore of the barrel is known as muzzle. The firearms in which bore is smooth are known as smooth bore firearms (or shotguns) and the firearms in which bore is rifled are known as rifled bore firearms (or rifled firearms). When speaking of the bore of a shotgun', it not only refers to the inside of the barrel, it also refers to the Size of the bore, that is diameter of the bore. When we refer to a shotgun as being a *12 bore' -we are speaking of the size of the bore of the barrel. ) Action: It is the part of a firearm between the barrel and grip where all mechanical movements occur. The firing mechanism (also known as breech action) consists of the moving parts, for example, (1) trigger protected by trigger guard, present at the base of action; (2) hammer/striker (3) bolt or block: It lies at the proximal part of barrel and can be opened to introduce cartridge; it can then be closed and locked; (4) spring and (5) firing pin. The processes occurring through firing mechanism are loading of bullet, triggering, strike of firing pin on primer, propulsion of projectile(s) and in case of rifled firearms (except revolver), the ejection of empty cartridge. ) Grip/butt: The wooden part at which the firearm tridge. It is

15

gripped firmly.

CLASSIFICATION OF FIREARMS The inner aspect (i.e. interior) of the barrel may be smooth or may be rifled and typhus accordingly;

TABLE 7E.2 Classification of Firearm Weapons [La-1] Smooth Boro Forearms (slhotguns) Rifled Firearms A.

On tho basis of length of barrol: 1) Long barrelled (e.g. musket) 2) Short barrelled B. On the basis of number of barrels 1) Single barrelled 2) Double barrelled 3) Multiple

barrelled C. On the

loading

basis of

A. B.

barrel) = Rifles 1) Carbine

2) Assault rifles, for example, AK-47, AK-56, SLR, INSAS

3) Machine guns, for example, LMG (light machine gun), HMG (heavy machine gun) C. On the basis of firing

mechanism

1) Muzzle loader

2) Breach loader D. On

basis of interior of barrel 1) Cylinder bore

2) Choke bore

Hand arms (short

barrel)=Pistol and revolver Shoulder arms (long

D.

1) Bolt action 2) Pump action 3) Lever action

Miscellaneous 1) Single action 2) Double action

3) Automatic 4) Semiautomatic

the firearms are classified as smooth bore forearmms (shotguns) or rifled firearms (rifles) (Table 7E.2) (Fig. 7E.1).

SMOOTH BORE FIREARMS Introduction: A smooth bore firearm

is one whose barrel is smooth from inside. It fires multiple pellets. It is used to shoot small moving targets (e.g. birds.

rabbit) which change their direction unpredictably. Shotguns: They are smooth bored long barrelled (5572 cm) firearms which fires several spherical pellets (shots). Some may fire slug. Range: < 30 m. Muzzle velocity: 250-300 m/s. Effective range: 3040 m. Most common is 12 bore (others are 16 and 20 bore). It can be openecd on hinge for insertion and extraction or cartridge cases. Choking [SN-3]1 Shotgun cartridge (Fig. 7E.2): It is a complete round of ammunition of a shotgun and is 5-7 cm long. l consists of case, detonator, propellant and shot/pellels. of cardboard cy

structure: lt consists 1s inder; most often, it is of red/green colour. It covered at distal end by retaining cardboard disc. Towards the base, some region of the cartriuge cOvered by a thin brass covering called brass hea base with a rim which provides strength to the base of cartridge. In the centre of the rim at the

External

7

CHAPTER

Injuries

193

Three parts of a firearm

( Barrel

0

Two

Action

parts of barrel

Breech/rear end

Muzzle end

(open enddof barel)

Interiorof bamel

-Central hole in the breech plate

Bullet

(bore

May be Smooth or Rifled Smooth bore)(Rifled bore) firearms

Grip/Butt

Proximal part

Distal part

Muzzle-f)

V

Taper

Chamber

for firing pin

firearms

Land (elevation) Calibre

Calibre (bore/gauge)

Fig. 7E.1 Parts

(the distance between to opposite lands) Groove (depression)

of a firearm and internal structure of the barrel Primer without indent

Cardboard cylinder

Brass head-

Propellant

RimBase of brass head

Fig. 7E.2

Wad

Shot/pellets

Primer with

indent

Shotgun cartridge, its parts and contents

of cartridge, the

primer can be seen as a central

depressed circular

Internal

area.

structure: There are three main compart ments from above towards the base separated from cach other by cardboards. These are (1) pellets (shots); (2) felt wad; (3) propellant and (4) detonator in primer. 1) Fellets (shot): These are spherical balls made up of lead. Pellets used in smooth bore firearms are collectively known as Shotgun slug is

shot.

large projectile (weight 10-30 g), made up of lead and often used for hunting. Slugs have greater range than pellets. 2) Felt wad: It is disc shaped or cup shaped cushIt contains 10n made up of felt or cork or plastic. firing. It after 8rease wlhich lubricates the bore from fusing prevents the heat from gunpowder as a piston also acts or distorting the pellets. It thus, preventing completely, and seals the bore from escaping. the expending gases a single

SECTION

194

I

Forensic Medicine grooves inside a bolt make the nut turn s grooves insi a rifle weapon make the around. e bullet revolve. After coming out from muzzle, the bullet revolyes around its own axis at 3000 revolutions/s. This revolution stabilises the bullet and gives it better penetrat. ing power (gyroscopic effect). Rifle (Fig. 7E.3): It is a long barrelled rifled firearm designed to be fired from the shoulder. Muzzle velocity is 500-1500 m/s. Examples of rifled firearm are revolver, pistol and rifles. Rifling [SN-4] Revolver (Fig. 7E.4): It is a short-barrelled rifled firearm which has a revolving cylinder containing multiple (usually six) chambers. These chambers accommodate rifled cartridges for firing. The chamber rotates or revolves after each shot to bring the next shot opposite the barrel. The revolver allows the user to fire multiple rounds without reloading. When a cartridge is fired, the empty cartridge remains in the chamber. Pistol (Fig. 7E.4): It is a short-barrelled rifled firearm in which the cartridges are contained in a vertical

Propellant (gunpowder): Propellant is an explosive material that is ignited/burnt by a spark generated in the primer to propel pellets/shots. 4) Detonator (or priming mixture): lt is a mixture present in a metal cup called primer or primer cup which is used to ignite the propellant. 3)

Other Types of Smooth Bore Firearms muzzle loading smooth bore firearm designed for use by infantry. Airguns: It fires projectiles by means of compressed air or other gas in contrast to other firearms which use a propellant charge. Paradox gun: It is a smooth bore firearm whose muzzle end is rifled for 2-3 in. (i.e. 5-7 cm). It is intended to be used as both a rifle and shotgun. Since the barrels of shotguns are smooth, a rifled shotgun is thus a paradox. Countrymade (orimprovised) firearms: These are firearms illegally made by unskilled or semiskilled personnel. Example is 'desi katta' (also known as tamancha). It is an ideal weapon for criminals in India as it is very cheap. It was designed first in western Uttar Pardesh. Unorthodox guns: The firearm weapons which cannot be classified into a particular category of weapon. For example, captive bolt pistol, stud guns, pen guns, zip guns, walking stick guns and

Musket:

sO

It is a

Bore of the Barrel

on.

Lands

Grooves

RIFLED FIREARMS

Introduction: A rifled firearm

is a firearm which has spiral grooves (i.e. riflings) inside its barrel. Just as the

Rear sight

Revolving Cylinder

Hammer Cylinder release Grip-

Fig. 7E.3 Rifling of the bore of the barrel

Barrel

Rear sight

Foresight

- Muzzle-

Hammer

EE

-Frame Trigger. th

-Grip

Trigger guardMagazlne

release

Revolver Fig.7E.4 Parts of revolver and pistol

Plstol

Magazine well to accomodate magazine

CHAPTER 7

within the butt. When

a

cartridge

is

magazine place empty cartrid is cjected om the ejection fired, the automatically inserted the next cartridge is port andchamber. The magazine can have 6-10 carinto the tridges. wlhen a Revolver vs. pistol: ln a case of revolver, empty cartridge renains in tlhe cartridge is fired, the when a cartridge is chamber but in a case of pistol, is cjected and falls on ground. fired, the empty cartridge cartridge is found at the crime scene by If this empty investigation authority, it becomes very casy to conwas pistol, not revolver. So, clude that the weapon used weapon can be identified by forensic examithe type of crime scene. nation of the cartridge case found at the by killers favoured is nmore Due to this reason, revolver (Table 7E.3). than pistol. D/W: revolver and pistol

Difference Between Revolver and Pistol St. No. Features Pistol Revolver TABLE 7E.3

Muzzle velocity

180-410 m/s

Effective range

100-150 m

3.

lerminal range

4.

Empty cartridge after

200 m Remains in the chamber Chambers of

firing

Cartridges present in

400 m/s 200 m 400 m Ejected Magazine

revolving cylinder

6

Base Number of maximum cartridges loaded at one time

Rimless Less (usually 6) More

Rifled firearm cartridge (Fig. 7E.5 and 7E.10): It is a complete round of ammunition of a rifled firearm. It consists of case, detonator, propellant and bullet.

Primer

without indent

a

er-cup, which is used to ignite the propellant. Primary missile vs. secondary missile: Sometimes a bullet strikes a bone and breaks the bone into fragments. These fragments attain sufficient velocity and penetrate soft tissues. In this case, the bullet is known as primary missile and the fragments of bone are known as secondary missiles. Bullet embolism: This happens when a bullet enters a large blood vessel and is carried to another site by the blood. It is usually associated with small calibre, low velocity bullet.

MECHANISM OF DISCHARGE OF PROJECTILE (Fig. 7E.6) moves torWhen trigger is pressed, the hammer tip of the firing wards and it strikes firing pin. The

Metal

case

Base Rifled

cartridge Fig. 7E.5 Rifled

Base of cartridge

cartridge, its parts and contents

Empty cartrldge metal cases

Propellant

with

indent

195

External structure: It consists of metal case usually made up of brass (70% Cu+ 30% Zn). The bullet fits in the apex (i.e. upper end) of the case. At the base of cartridge, there is a rim. At the centre of the base of the cartridge, there is a central depressed circular area known as primer which contains priming mixture (i.c. detonator). The bullet is held in the cartridge case either by a groove called cannelure or by indentation of cartridge case. Internal structure: There are three main compart ments from above towards the base 1) Bullet: It is made up of lead with varying amount of antimony added to provide hardness. The tip of bullet is known as nose. The calibre of a bullet is its cross-sectional diameter. 2) Propellant (gunpowder): It is an explosive material that is ignited/burnt by a spark generated in the primer to propel bullet. 3) Detonator (priming mixture): It is a mixture present in a metal cup called primer or prim

Bullet-

Primer

Injuries

Bullet

SECTION

196

I

Forensic Medicine

Metal case

Vent or flash hole

Primer

Block with

Anvil

central hole

Hammer

Bullet

Firing

Propellant (gun powder)

Fig.7E.6 Mechanism of discharge of bullet

pin moves forwards through the hole in the block and hits the central recess at the base of cartridge. The central recess is the base of the primer. The blow of firing pin on primer suddenly crushes the priming mixture against the anvil. This sudden crushing is a type of friction which produces heat. This heat ignites the priming mixture. The spark passes out from the primer through the vent/flash hole and sets fire to the propellant (gunpowder). Suddenly, a large amount of gas is produced under high pressure which causes the metal case to swell outwards; the bullet gets free from the hold of metal case and the bullet is forced/pushed forwards to pass out the barrel. Products of firing (Fig. 7E.7): (1) flame; (2) smoke; (3) powder particles (burnt, partially burnt and Flame

Burning, scorching9

Priming mixture

Rifles

3 inch (7.5 cm) 6 inch (15 cm) 12 inch (30 cm)

Trigger

unburnt); (4) highly compressed hot

FIREARM WOUNDS

Introduction The

firearm wounds may be either (1) penetrating that is, the bullet enters a body but does not exit or (2) perforating that is, the bulet enters a body and also exits, so there is entry wound as well as exit wound Some visible characteristics of firearm wounds: muzzle/recoil impression, fouling, dirt/grease collar, abrasion collar, blackening, tattooing/stippling Muzzle/recoil impression: In a tight contact sho, the impression of the muzzle with or without the

Smoke

Blackening

Powder

Bullet

Tattoolng

Wound Dirt collar (inner) Abrasion collar (outer)

6 inch (15 cm) 12 inch (30 cm) 24 Inch (60 cm)

Shotguns Fig. 7E.7 Products of firing of a gun and their ranges

gas; (5) frag-

ments of metal or cartridge and (6) grease.

singeing Hand arms

pin

12-18 Inch (30-45 cm) 24-36 inch (60-90 cm) 48-72 inch (120-180 cm)

CHAPTER 7 impression

of foresight may

be scen on the skin in.

contused abraClassically, a muzzle mpression form of a ring althoug the ring may sion in the when the incomplete. It is seen most frequently he area overlying shallowly placed bone, shot is in the (front/back). It example, head, shin and chest for pressure of (1) due to hrm mechanical is formed extensive and (2) rapid muzzle over the skin and expansion of gases lifting the skin is a

subcutaneous

muzzle. forcefully up against the entry wound vs. Firearm exit

Firearm

wound

D/W-10

Wounds From Smooth Bore Firearms Shotgun entry wound [LQ-1] uncommon espeShotgun exit wounds: These are cially when they involve the chest and abdomen. The reason is low kinetic energy of pellets (because of low mass and low velocity). They are seen (1) when there is welding of shot, (2) in contact wounds or (3) the region is neck or any extremity (upper/lower limb). No singeing, blackening or tattooing is seen. Appearance: (1) serrated, irregular laceration with everted margins; (2) sometimes, the pellets accumulate immediately beneath the skin opposite the wound of entrance after they have travelled through the body and have been trapped by the skin. They can be observed as raised nodules in the skin and can be easily palpated.

Wounds From Rifled Firearms [LO-2] AUTOPSY IN A CASE OF FIREARM WOUNDS 1)

Examination and preservation of clothing

Remove clothing layer by layer. Record the number and location of bullet holes. A single bullet may produce several holes due to presence of folds. Clothes should be dried before packing. They have to be preserved in clean brown paper or plastic bags and sent to FSL.

2) Send

the body for X-ray if needed: It is done to bullet. 3) Examination and preservation of wounds: a) Inspection of wounds (injuries): Photography should be done. (1) Location: Exact location of wound should be described in relation to its alstance from a fixed anatomical landmark. (2) locate the position of

Injuries

197

Size.(3) Shape: round, oval, star shaped, etc. (4) Abrasion collar: The width of abrasion collar should be measured from all sides of a wound to know the direction of fire. (5) Blackening and/or tattooing. (6) Muzzle imprint. (7) Skin around the wounds should be cut out including at least 2.5 cm of the skin around and 5 mm bencath the wound. They should be packed in rectified spirit, labelled and sent to FSL. b) Cutting of skin around wound

c)Track of wound d) Examination of bullets/pellets in situ and ex situ: abel all bullets with relationship to wounds. Remove the bullets from the body with bare hands to avoid scratches due to forceps or seizures. Describe the bullet whether intact, deformed or fragmented. All bullets should be weighed and their calibre should be measured. They should be dried and not washed because washing removes the powder residue. In case of shotgun injury, there is no need to recover all pellets, only a few pellets can be recovered from the body to send to FSL. 4) Description of firearm if recovered at the crime scene 5) Collection, preservation, marking and dispatch of exhibits

VERY INTERESTING MEDICOLEGAL

QUESTIONS REGARDING FIREARMS Q.1:Is the injury caused by the discharge of firearm? Ans. Look for (1) entry wound and exit wound along with corresponding holes in clothes; (2) muzzle impression near entry wound; (3) abrasion collar, blackening and tattooing; (4) tract of bullet and (5) bullet/pellets in the wound. Q.2: What kind of weapon fired the shot?

Ans. (1) By studying the cartridge case found at the bullet, crime scene. (2) By characteristics on the crime characteristics. for example, primary and secondary Q.3: From what distance was the shot fired? imprint, burning Ans. (1) By presence of muzzle Spread ot pelsngeng. blackening and tattooing. (2) lets. was the shot fired? Q.4: From which direction wound and position of entry the Look for Ans. (1) direction of the track of the for Look Cxit wound. (2) body. the wound inside the

198

SECTIONI

Forensic Medicine

Q.5: Did the suspect fire the gun? Ans. By detecting gun shoot residue (GSR) on the

hand of the suspect.

Q.6: Is it possible to identify the victim/assailant

from a recovered bullet? Ans. Yes, by (1) DNA typing on tissues recovered from the surface of bullet. (2) Fingerprints on the surface of fired cartridge case. Q.7: How long did the victim survive? Ans. It depends on the cause of death, for example, injury to a vital organ, shock, haemorrhage, septic complication. Q.8: How much activity could the victim perform following the injury? Ans. It depends upon the site of injury and the organ involved. If brain stem, motor area or cervical cord is destroyed, the death is instantaneous. Wounds of auricles are most rapidly fatal, followed by wounds of right ventricle; the wounds of left ventricle are least rapidly fatal. Q.9:Is it a case of suicide, accident or homicide? Ans. Most contact shotgun wounds of the head are suicidal in nature. The person tends to use his domninant hand to press the trigger, steadying the muzzle against the head with his nondominant hand. The powder soot may be collected on the nondominant hand. The sites of preference for suicides are temple (60%) > Centre of forehead > roof of mouth > midline behind the chin> front of chest> abdomen. Q.10: Can a single bullet produce multiple wounds of exit? Ans. Yes, in two cases: (1) Ifthebullet after entering the body splits up into few pieces and those pieces come out the body separately or (2) If the bullet strikes a bone and the fragments of that bone come out of the body separately. Here, bullet is primary missile and the bone fragments are secondary missiles Q.11: Can there be multiple wounds of entry and exit from a single shot? Ans. Yes, it may be seen in reentry wounds. For example, (1) Case 1: The bullet passes through arm and chest. Here, four wounds (two entry and two exit) are caused by a single bullet. (2) Case 2: The victim may be sitting in an unusual position, for example, upper limbs and lower limbs flexed. The bullet passing through chest, thigh and leg produces six wounds (three entry and three exit). Q.12: Is it possible that entry wound is present but the bullet is not found in the body?

Ans. Yes, the bullet may enter the stomach from where it may be vomited out or passed out in stool. The b let may also enter Windpipe and may be coughed up. Q.13:Is it possible that a bullet after entering thebod is found at a distant site without any complications Ans. Yes, through bullet embolisation. A small light bullet entering the IVC may be carried up to the right atrium and then to right ventricle where it may stay

permanently. Q.14:What is Kennedy phenomenon? Ans. It states that 'when interpretation of firearm wounds (entry and exit) becomes difficult at autopsy as a result of their surgical alteration (e.g. debridement and suturing)', it is known as Kennedy phenomenon as it actually happened in John F. Kennedy case. John F. Kennedy was the 35th president of the United States. He was assassinated by Lee Harvey Oswald in November 1963.

LIST OF IMPORTANT QUESTIONS FOR EXAMINATION LONG QUESTION (LQ) Classify firearms. Draw a labelled diagram of a shotgun cartridge. Discuss the appearance of entry wound caused by a smooth bored firearm at different ranges. 2. Draw a labelled diagram of a rifled cartridge. Discuss the appearance of entry wound caused by a rifled firearm at different ranges. 1.

SHORT NOTES (SN 3.

Choking

4. Rifling 5. Types of bullet [CCU 2014] 6. Ricochet bullet [CCU 2004] 7. Puppe's rule

8. Abrasion collar 9. Tattooing

DIFFERENCE BETWEEN

(D/W)

Entry and exit wounds of rifled firearm |DO 2006, 2008| |CCU 2009, 2010, 2012 I1. Cartridge of shotgun and rifled firearm 12. Suicidal and homicicdal firearm wounds 13. Contact shot and distant shot of rifled firearm T0.

CHAPTER 7

ANSWERS

Draw a 10-1: Classify firearms. shotgun labelled diagram of a cartridge. Discuss the appearance of entrance wound caused by a smooth bored firearm at diferent ranges. Classification of Firearms (Table 7E.2)

Smoke 30

Flame Powder particles (burnt or unbrunt) Card

XI

Metallic

Primer

If muzzle is (1) pressed firmly: soiling and burning is absent and (2) if it is not pressed firmly (or is loosened by recoil): flame, gas and soot may escape sideways and soil the adjoining area. interposes between muzzle and skin, If clothing soot will be found on the clothing also. Skin is lifted forcibly against the muzzle due to expansion of gases. As the gases are blasted within the wounds, the subcutaneous and deeper tissues show severe disruption. Felt wad from cartridge will be found in the depth of wound. It gives clue to the type of cartridge used. Back spatter: In contact shot, the negative pres sure created in the barrel may suck blood, hair, tissues and cloth fibres several centimetres back inside the barrel. Wound track appears bright red/pink (or chery red) due to CO (carbon monoxide). Wound on bony prominence (e.g. skul) is cru-

Felt wad

Percussion cap

Fig.7E.8 Shotgun cartridge

Appearance of Entrance Wound (Fig. 7E.9) Caused by a Smooth Bored Firearm at Different Ranges: In

case of smooth bored firearm, the range is classified as A. Contact and near B. Closerange:

D

of shot-

skin.

rimAnvil

2 m

impression (recoil abrasion): it is due to firm mechanical pressure of muzzle against

-Propellant (powder charge)

Vent (flash hole)

60-90 cm

Muzzle

Lead shots or pallets

Cardboard disc

45 cm

2-5 m Fig. 7E.9 Ranges of different components gun

Retaining cardboard disc

cylinder

cm

Wad

Labelled Diagram of a Shotgun Cartridge (Figure 7E.8)

Cardboard-

199

Injuries

contact range Up to lm C. Short range to intermediate range: 1-4 m D. Distant (long) range: >4 m Contact and near contact range: The wound is single, usually round, equal to the diameter of bore of the shotgun. The wound is Single because the shot (i.e. the group of pellets) enters as a mass.

a

ciate/stellate. Usually shotgun projectiles (i.e. pellets, slugs) wounds are do not exit out of the body so exit rare. Close range (Up to 1 m) The wound is single, round/oval. m, the 30 cm and Rat hole wound: Between rim of the wound is irregular. blackening and tattooWithin 30 cm, singeing, by flame; singeing ofhair occurs soot and (1) occurs: 1ng and occurs by smoke blackening tattooing (3) (2) by wiping and removed can be 1

SECTIONT

200

Forensic

viedicine

occurs by unburnt and partially burnt powder granules, not by lead pellets.

Wound track appears bright red/pink (or cherry

o

o

red) due to CO (carbon monoxide). Felt wad or plastic cups from cartridge may be found in the depth of wound. Short range to intermediate range (1-4 m): Minimal distance at which shot mass begins to spread is extremely variable. It is 2 m for cylinder bore shotguns and 4 m for full choke bore shotguns. Wad may be found in the wound (because the range of wad is 2-5 m), which can be used to determine bore of the gun. Distant (long) range (>4 m) At a distance of 4 m, the shot spreads widely and so all individual pellets penetrate separately. There is no central wound/hole. Wad may be found in the wound (because the range of wad is 2-5 m) which can be used to determine bore of the gun.

L0-2:

Drawa labelled diagram ofa rifled cartridge. Discuss the appearance of entry wound caused by a riiled cartridge at different ranges. Labelled Diagram of Rifled Cartridge Fig. 7E.10)

Jacket (Cu,

Ni

or Sn) -

Bullet

-Propellant -

Anvil

Metallic cartridge

case

(of

brass)

-Primer (a metallic cup which contains priming mixture) Priming mixture (detonator)

Fig. 7E.10 Rifled cartridge

A.

Contact shot

Hard contact over head Blowback phenomenon: All contents of the discharge (e.g. bullet, flame, gases. powder and metallic particles) enter into the skull through scalp. In this case, the skull bone offers some resistance, so amount of gases may be reverted some backward and laterally under the scalp. The expansion of gases between skull and scalp tends to blast out around the muzzle and

so creates a large, irregular, cruciate or star shaped entry wound with everted and rag ged margins. This is known as blowback phenomenon. Since carbon monoxide (CO) present in the

discharge also enters into the soft tissues, it combines with haemoglobin and myoglobin to impart pinkish colouration to the tissues in the interior of whole track.

Muzzle impression may be present around the wound.

Ricochet bullet [SN-6]: Sometimes, a bullet entering the cranial cavity has insuficient energy to make its exit from the other side and it may ricochet inside the skull to cause more brain damage. This bullet is known as ricochet bullet. Puppe's rule [SN-7]:The fracture lines produced by the impact of a bullet stops at preexisting fractures of the skull. Hard contact at sites other than head: Since there is no resistance offered as seen in the aforementioned case, all contents of the discharge enter into the track taken by bulet in soft tissues; so the entry wound is circular. is little or no external evidence There

Cannelure Vent (flash hole)

Appearance of Entry Wound Caused bya by Rifled Cartridge at Different Ranges a

burning, singeing. blackening or tattoong but burning, blackening and powder grans are found in the depth of wound. In this case also, the carbon monoxide (C

present in the discharge enters into the sol issues to give pinkish colour to tissues whole track. impression may be present arouna Muzzle the wound.

CHAPTER 7

(within

range of flame or muzzle

the shot B.tosei.e. cm): blast, 5-8 wound is small,

Bore of barrel in a shotgun

circular, with

inverted Entry margins. lacerated contused classical features of a discharge are possible andevident at such range: (1) Evidence of burnblackening and tattooing ing (with singeing), seen around entry wound. (2) Grease/dirt colzone and abrasion collar is found on the inner zone. lar (SN-S] is found on outer From inside outwards, the four rings formed are as follows: 1) Dirt (grease) collar = Bullet wipe soiling 2) Abrasion collar/ring [SN-8]: It surrounds the dirt collar.

Choke bore

.All

Blackening (smudging or smoke soiling or soot soiling): It is due to deposition of powder soot (i.e. carbon) produced by the combustion of gunpowder. It can easily be wiped off the skin by a wet cloth. 4) Tattooing or stippling or peppering [SN-9]: It is due to embedding of burnt, semiburnt and unburnt powder particles in the superficial layers of the skin. Fouling: It means the tiny lesions around the entry wound caused by fragments of metal expelled either from the surface of bullet or from the interior of barrel. These metallic fragments arise by the friction between the bullet and the rifling of the barrel. They cannot be wiped off from the skin. C. Near shot (short/medium/intermediate range shot) (outside the range of flame or muzzle blast but within the range of powder deposition, i.e. 30-60 cm). Entry wound is small, circular, with inverted lacerated margins. No evidence of burning or singeing. Grease/dirt collar is found on the inner zone and abrasion collar is found on outer zone. Tattooing present. D. Distant shot (outside the range of > 50 cm in case of handguns, >75 cm in case of rifles): Entry wound is smaller than the bullet, circular, with inverted lacerated margins. No evidence of burning, singeing, blackening and tattooing. Exit wound will be larger than the entry wound. 3)

201

Injuries

Terminal (distal) end constricted

Cylinder bore Terminal (distal) end is not constricted ****.

***

*****i

::..

*********

....

*****

*

****

***.

*****

:*

..**e*s**!***.... ** *

Maxinum dispersion

Minimum dispersion

KA

Fig. 7E.11 Effects of choking in the barrefoCAL

LIBRARY

SN-3: Choking|

Acc.

No..oS3

E ar7 Dala.23..:23.

to-nmechaical The term 'choking is used in relation asphyxia and in firearms. Chokingin relation to firearms will be discussed here. o Choking: Terminal 7-10 cm of the bore of the barrel near the muzzle end is slightly constricted in some shotguns. This constriction of the bore near the muzzle end in a shotgun is known as choking (Fig. 7E.11). aTypes of shotguns on the basis of constriction of bore near muzzle end: a) Choke bore: When 7-10 cm of the bore near muzzle end is constricted in a shotgun, the shotgun is known as choke bore shotgun. b) Cylinder bore: When entire barrel from breech to muzzle is of same diameter (i.e. the bore is cylindrical) in a shotgun, the shotgun is known as cylinder bore shotgun. aType of choke according to the shape a) Standard choke: Terminal7-10 cm of the barrel is constricted. b) Cone choke: Whole length tapers to form the cone. a Degree of choking (Table 7E.4): According to m constriction, the degrees of choking are given maxT'able 7E.4 Full (maximum) choking means dis imum constriction and so causes minimum cylinder persion of pallets. Open (or improved or it causes maxibore) means no choking at all and mum dispersion. metallic choke Polychokes: Nowadays, readymade and having varying screwed tubes of different diameters available which are are choking degrees of barrel. over the muzzle end of the

a

202

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Forensic Medicine

TABLE7E.4 Degree of Choking Constriction

Sr.

No.

Degree

of

Choking

Full (maximum)

4 13 quarter h (Half 4 (Quarter

2.

4.

Open (or cylinder bore)

o

In Inches In Millimetres 0.04 0.03 0.02

0.75 0.50

0.01

0.25

0

0

Functions of choking: 1)

It decreases the spread of shots pallets, that is, causes minimum dispersion of pallets. 2) It increases the explosive force. 3) It increases the velocity of shot pallets. 4) It increases the range of shot pallets.

SN-4: Rifling Rifling:

The interior (i.e. internal surface) of the wall of the barrel is cut longitudinally into a series of parallel shallow spiral grooves from the breech end to the muzzle end. These grooves are known as rifling. The firearm weapons which have rifling in their barrel are known as rifled firearms. For example, pistol, revolver, carbine, assault rifles (e-g. AK-47, AK-56, SLR, INSAS), machine guns, for example, light machine guns (LMG), heavy machine guns (HMG). Land and grooves: The elevated areas are called lands and the depressed areas are called grooves. Total number of grooves and lands in a barrel may vary from 2 to 20 but most common is 6. Calibre (or gauge):'The distance between two diametrically opposite lands across the bore is known as calibre. Twist and twist rate: The turning of spiral grooves is known as twist. It can be either right (clockwise) or left (anticlockwise). The distance of barrel in which a groove completes a full revolution is known as twist rate. For example, 1:10 inches mean I turn in 10 inches. A shorter distance means a faster twist and it imparts a high spin rate to the bullet. Pitch: The angle at which the rifling is cut in the barrel is known as pitch. Helixometer: It is an instrument to examine the interior of barrel. It can also measure twist within a barrel.

of rifling gives spin (rotatory motion) to the bullet

Functions 1) It

in

its long axis (gyroscopic etfect) and therefore.

imparts stability. 2) It prevents the bullet from wobbling in air, so gives straight course. 3) It incrcases the power of penetration. 4) It increases accuracy and provides longer range. Rifled firearms are more lethal as compared to smooth bore firearms. MLI: Rifling gives the bullet a signature marking that is unique to that group of weapons. It is known as primary marking which can reveal the manufacturer of the gun.

SN-5: Types of bullet Types of bullet [Mnemonic drift-gystt] Dumdum bullet: It is a jacketed, 0.303 centrefire rifle bullet. It is a special type of expanding (mushroom) bullet which expands (like mushroom) on impact to produce a more serious wound. 2) Ricochet bullet [SN-6]. 3) Incendiary (explosive) bullet: It catches fire on hitting the target due to the presence of phosphorus. If an incendiary bullet is present in the body, the use of USG or microwave diagnostic techniques must be avoided as they can cause the bullet to explode. The wound produced is larger than usual. General surgeons and pathologists should wear goggles and use long handled instruments to manipulate this bullet. Removed bullet should be handled with long rubber-covered forceps and kept in a padded container to protect it from excess impacts, vibration and heat. 4) Frangible bullet: It is a bullet which fragments on impact and completely disintegrates, so its recovery and matching is very difficult. 5) Tracer bullet: It is a bullet in which a pyrotech nic charge present at the base burns very brightly during its flight. It makes the trajectory (i.e. path) of projectile visible to the naked eyes; moreover, the whole scene becomes visible, so the shooter can aim correctly. 6) Glazer bullet: lt is a bullet which consists of a copper jacket containing nmany lead pallets rather than a solid lead core. The tip is nonjacketed but closed with a plastic ball. On hitting the target, the lead pallets come out to produce

CHAPTER 7

to the wounds produced

Sometimes a bullet enters the Souvenir bulle not cause fatality; it is retained body but does bullet which body for a long time. This in the without time a long in the body for is present called souvenir producing harmful cffects is

bullet. bullet (piggy back bullet): Tandem 9) Tandem bullet) (tanbullet (also known as piggy back a rifled When other): dem = one behind the in weapon is fired, the bullet sometimes get stuck the muzzle. the barrel and fails to come out from bullet hits second the When the gun is fired again, forces the first the first bullet from behind and one forwards. So, in this way, two bullets come out

projectile called tandem bullet. 10) Tumbling bullet: A bullet that tumbles, that is, rotates end-on-end during its motion. 11) Others: (1) Mushroom (expanding) bullet: It is a bullet which expands (like mushroom) on impact to produce more serious wound. Example is dumdum bullet. (2) Crime bullet is the bullet recovered from the body of the victim. Test bullet is the bullet that is fired from the suspect firearmby forensic scientist to compare the marking on this bullet with that of crime bullet. as a single

SN-6:

Ricochet bullet

Ricochet

bullet: The bullet which strikes intervening object first, rebounds (glances), get deflected or deviated and then hits the object aimed at, is known as ricochet bullet. Path ofa ricochet bullet in completely unexpected.

(A)

Inner tangential at

entrance side

(B)

Inner tangential at contralateral side

ig.7E.13 Types of internal ricochet

203

Roof (intervening object)

wounds simi shotgun pellets. bullet travelling in irregular Yawning bullet: A travelling nose-on. 7) fashion instead of 8)

Injuries

Bullet fired at roof

Bullet hitting the body

Fig. 7E.12 External ricocheting

Ricocheting is more common with (1) inferior (old unused) firearm, (2) low-velocity than high velocity bullet, (3) round nose bullets than flat nosed, and (4) jacketed bullets than unjacketed bullets; (5) it is also common with 0.22 lead bullets. The critical impact angle for ricochet for hard surface is 10-30 degrees. The bullet ricochets off at an angle smaller than the critical impact angle. Ricocheting may be external or internal. External ricocheting (Fig. 7E.12): The bullet strikes some external surface (e.g. roof) and then hits the body. Most bullets on striking a hard surface break up or penetrate the surface. When the bullet hits a hard, flat surface, it may be deformed, and the wound produced is large irregularly oval (keyhole appearance), triangular or cruciate with irregular abraded margin. The bullet lies in the wound nose facing outwards. may contain chips of paint, soil/mud, fibres It or fragments from intervening objects. ricocheting, the bullet loses gyrating After movement, so abrasion collar, burning, blackening and tattooing are absent. Internal ricocheting (Fig. 7E.13): It occurs in skull (most common), chest or pelvic cavity.

(C)

Slngle rlcochet

(D)

Double ricochet

204

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Forensic Medicine

Sometimes after passing through the skull at one side, there is not enough energy left in the bullet to penetrate the dura and so it may move along the epidural space. Sometimes after passing through the skull and brain, there is not enough energy left in the bullet to penetrate the skull again at the opposite side. So, it may rebound/ricochet from inner table of the skull of opposite side like a billiard ball producing a second track or even third track. It more commonly occurs if the bullet hits the inner table of the skull at an acute angle. The bullet may move along the dura and cause a shallow wound track along the surface of the brain. In single ricochet, the bullet rebounds once; while in double ricochet, the bullet rebounds twice. In autopsy, when the straight line joining the wound of entrance and the resting bullet does not have any wound, it means internal ricochet had ocurred. So, it can be said that bullets which do not exit the head are retained in the cranial cavity and show internal ricochet. MLI: In the case of external ricocheting, if the bullet hits a person and that person is killed, the accused may try to defend himself by claiming that he merely fired at the roof to threaten the deceased. The accused may be charged under S.304A of IPC. Crime scene investigation may be done to see the damage in the roof.

SN-7: Puppe's rule

Puppe's

rule states that 'a fracture line resulting from a blunt force trauma to the skull never crosses a preexistingfracture line', In other words, 'a fracture line resulting from the second injury will not cross the fracture line resulting from the first injury. Or "the second Jracture line is arrested when it meets the first fracture line (Fig. 7E.14). Originally, the rule was given by Puppe (1930s) in context with fractures due to blunt force trauma to the skull. This rule was devised to assist forensic interpretation when there is more than one frac ture from more than one blunt force injuries. Later on, Madea and Staak (1988) developed this rule in relation to bullet injuries.

1st fracture caused by 1st impact

2nd fracture caused by 2nd impact

Puppe's rule: The second fracture line 'B' never crosses the first (pre-existing) fracture line 'A'.

Fig. 7E.14 Puppe's rule: the second fracture line never crosses the first (i.e. Preexisting) fracture line

Puppe's rule is concerned with multiple linear frac

tures of skull and it helps to determine the chronological order in which the fractures occurred one by one. Explanation: Suppose after first blunt force injury, a fracture line *1' is formed on the skull. After 2nd blunt force injury, a second fracture line 2' is formed. According to Puppe's rule, the fracture line caused by 2nd injury, that is, 2' disappears when it meets the 1st fracture line 1, that is, in a sense, the 2nd fracture line 2 never crosses the 1st fracture line 2. This rule has also been applied in relation to multiple firearm (bullet) injury to the skull. The fracture lines produced by the impact of a bullet stops at preexisting fractures of the skull. So, Puppe's rule regarding how to determine the sequence of multiple blunt-torce injuries of the skull can also be applied directly to determine the sequence of gunshot wounds ot the skull. It can determine the sequence of shots when several bullets have struck at the craniun. Although multiple firearm (bullet) wounds ot the skull are much nmore difticult to analyse than wounds from blunt-force weapon, the pattern of radial fracture lines sometimes allows the determnation of the sequence of the shots.

SN-8: Abrasion collar Abrasion

collar: lt is the abrasion of the skin caused by the bullet around entry wound.

CHAPTER 7 1. Dirt

(grease) collar=

bullet wipe soiling

O

-2.Abrasion (abraded

Central

wound/hole

contused) collar

3. Blackening ('smudging' or 'smoke soiling' or 'soot soiling) 4. Tattooing ('stippling' or

peppering9) Fig. 7E.15

Bullet entry wound

from inside outthe entry wards, four rings are formed around is one of them. wound (Fig. 7E. 15). Abrasion collar (grease) collar. Abrasion collar surrounds the dirt abrasion collar. Some contusion is also present in Mechanism: As the gyrating bullet strikes the skin, skin surface; it first indents and then stretches the then, at last, it penetrates the tense area of skin. Both the rubbing of the gyrating bullet against the inverted skin epidermis and the heat are responsible for causing abrasion collar. The width of the abrasion collar depends upon 1) Calibre of the weapon, 2) Angle at which bullet strikes the skin surface: A bullet striking the skin surface perpendicularly will produce a concentric rings a bullet striking at an oblique angle, will produce an eccentric zone with the wider zone on the side from which the bullet came. Colour: Fresh abrasion collar is reddish but as it dries, it becomes reddish brown or dark brown. case .In the

of rified weapons,

205

Injuries

SN-9:Tattooing Tattooing Numerous reddish-brown punctate abrasions surrounding the wound of entrance in case of firearm injury. is due to embedding of burnt, semiburnt and It unburnt powder particles in the superficial layers of the skin. They are seen within the range ofpowder deposition, that is within 30-45 cm in case of hand arms, 60-90 cm in case of rifles and 120-180 cm in case

of shotguns distribution of tattooing around the entry The

wound may be either symmetrical or eccentric, depending upon the angle of the gun. is an antemortem phenomenon and indicates It that the individual was alive when shot. It cannot be wiped away. If the person was dead before being shot, they would be moist grey or yellow. The greater the range, the larger and less dense the

If

powder tattooing. the person survives, these marks heal completely. MLI: The size and density of the powder tattoo pattern around the entry wound can be used to determine the range at which the weapon was discharged.

DW-10: Entry and exit wound of a rifled firearm (Table 7E.5)

MLI:

Abrasion collar is the proof of an entrance wound. 2) Its distribution around the margin of the 1)

wound can indicate the direction of fire. a) Ifbullet strikes perpendicular to the body surface, the abrasion ring is circular and uniform. b) If the weapon has been discharged obliquely, the abrasion collar is elliptical in shape and Its longer axis points towards the direction of approach of bullet. 3) Abrasion collar may be absent, for example, high velocity centrifire rifle bullets may not show abrasion ring but may show small splits/tears.

D/W-11: Cartridge of shotgun and

rifled firearm (Table 7E.6) D/W-12: Suicidal and homicidal

firearm wounds (Table 7E.7) D/W-13: Contact shot and distant 7E.8) of rifled firearm (Table

shot

206

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Forensic Medicine

TABLE 7E.5 Difference Between Entry Wound and ExitWound Sr. No. Features

Entry Wound

Size

Smaller than the diameter of bullet except contact wound Inverted

Edges

6. 8.

10

1

Abrasion and grease collar Blackening and tattooing Burning with singeing of hair Bleeding Fat extrusion Cherry red (bright pink) colour of tissues due to carboxyhaemoglobin Lead (metal) ring around the wound Fibres/clothes Chemical tests

TABLE 7E.6 Sr.No. Features

Present

Present Present Smooth bore firearm Multiple small wounds (tattooing)

Crime scene

3. 4.

6.

Rifled Cartridge Smaller Metallic bullet Metallic

Absent Absent in

distant range or one large wound

in

contact/

Rifled firearm Only one

Difference Between Suicidal, Homicidal and Accidental Firearm Wounds Suicidal Homicidal Accidental

Range Direction Number of wounds Firearm residue on hand Weapon at the crime scene Cadeveric spasm

Victims Suicide note

Sr. No. Features

Absent Not so Negative

Larger Lead shots/pallets Only the base is metallic

Site of entry wound

TABLE 7E.8

near discharge

Seen on X-ray May be turned in Positive for lead and carbon monoxide

close range.

10.

in

Shotgun Cartridge

Firing weapon Wound caused

9.

Absent Absent Absent More May be present Absent

May be present May be present

Less Absent May be present

Larger Everted

Difference Between Shotgun Cartidge and Rifled Cartridge

Size Projectile Cartridge case Wad Cardboard disc

TABLE 7E.7 Sr.No. Features

Exit Wound

Head: side of temple, forehead or under the chin Chest: over the heart Contact or close Upward or backward Usually one

Present Present May be present with weapon found firmly grasped in the hand Usually in his own house Usually males May be present

Any part

Any part

Any range Usually upward Usually multiple

Any direction

Close

Absent Absent Absent

One Present Present Absent

Any place; evidence of struggle

In marriage and

and disturbed scene present Any sex Absent

parties Usually males

Absent

Difference Between Contact Shot and Distant Shot of Rifled Firearms Contact Shot

contact with skin

Range

In

Number of woundss Shape of wound

Single Circular

Blackening Tattooing Singeing of hair Burning (scorching)

Present Present Present Present

Distant Shot >4m Multiple Multiple pallet hole injuries

Absent Absent Absent Absent

CHAPTER 7

Injuries

207

Chapter 7F Miscellarned AMiscellaneous injuries (electrical injuries and lightning) ELECTROCUTION Electrocution means

death caused by clectricity.

Autopsy eatures mark: The entry mark, if present at autopsy, A. Entry diagnostic finding of electrocution. is the most exclude death Absence of electric mark does not from electrocution. [SN-1]: The 1) Endogenous burn (orjoule.burn) is point where the current enters the body usually characterised by the presence of an electrical mark known as endogenous burn or Joule burn. It occurs when the electrical source is touched or grasped firmly. Joule burn is also known as endogenous burn because the heat causing burn was produced internally, that is, in tissues. 2) Exogenous burn: It is known as exogenous burn because the source of heat is outside the body. It occurs when there is a gap between body and the electrical source. In this condition, the electric arc jumps from electrical source towards the body. An electric arc has a tendency to jump up to a certain distance (e.g. 1,000 V can jump up to few mm; 5,000 V up to 1 cm; 20,000 V up to 5 cm; 40,000 V up to 12 cm and 100 kV up to 35 cm). It may be of two types: a) Spark burn: It is due to loose contact with electrical source. b) Flash burns: It is typically caused by high voltage current (e.g. high-tension wire). It is characterised by 'crocodile skin in which there are multiple, hard, brownish nodules on the body. Actually, high-voltage current creates very high temperature near the skin and so the keratin of the skin melts over multiple areas to form these nodules which resemble the skin of crocodile. D.Exit mark: Splits in skin, or sometimes lacerations. Burns and perforations of clothing or shoes. MLI of

Electrical Injuries

usually accidental. (2) Suspended animation may occur after getting a current

Manner of death

is

The person should be resuscitated immediately. (3) Judicial clectrocution (electric chair) is a method of imparting death penalty in the United States. (4) If a pregnant woman receives an electric shock at workplace and consequently her abortion occurs, she can demand compensation. (5) During electroconvulsive therapy (ECT), a person may sustain fracture; he may sue the doctor for negligence. Example, Bolam case. (6) Electric crematorium is used for disposal of a dead body.

LIGHTNING Lightning: It is the visible zigzag flash of light which appears in the sky during a thunderstorm due to discharge of electricity between clouds. It is often followed by a loud noise called thunder. Persons struck by lightning have a better chance of survival, so immediate resuscitation must be done.

Postmortem Features A. External features:

The clothes may be torn or burnt. Metallic objects (e.g. coins, necklace) may be found molten (distorted) or magnetised. Plastic objects may be completely molten and distorted. caused Exogenous burns: The surface burns arevictim's if by external heat. They may occur wearing was clothing is ignited or if the victim example for or carrying any metallic article, rings, coins, necklace. may be (1) inear burns DEndogenous burns:They skin) or (2) punc(in moist creases and folds of burns (or Filigree tate burns or (3) arborescent [SN-2, 3|. flower) trac burns or Lichtenberg's effect: Lacerations or blast to due Lesions may becongested tures. (1) CNS: Brainhaemorrhages. (2) features: Internal B. Intracranial oedematous. lungs congested. and Cardiopulmonary: respiratory: tympanic memcataract, perforated Others: (3)

Wearing:

brane,

SECTIONI

208

Forensic Medicine

MLI (1) Death due to lightning is always accidental. It can help differentiate a natural death from homicide. (2)

this peculiar feature, immediate Ifanybody recognises may save the life the victim.

of

resuscitation

IMPORTANT QUESTIONS FOR EXAMINATIONS SHORT NOTES (SN) 1.

Joule burn

2. Filigree

burns

3. Arborescent burns/markings [DU 2011)

DIFFERENCE BETWEEN (D/W) 4. Skin lesions in

lightning and electrocution

MEDICOLEGAL IMPORTANCE (MLI) Arborescent markings are present on the body 6. The deceased has joule burn 5.

ANSWERRS

SN-1: Joule burn (or endogenous burn or electrical mark) Joule burn: The

point where the electric current enters the body is usually characterised by the presence of an electrical mark. This electrical entry mark is known as endogenous burn or Joule burn. is very specific and diagnostic It to contact with electricity.

Mechanism of production: Electric energy is con-

verted into heat energy in tissues and this heat causes a localised thermal burn called Joule burn. The fluid in the skin and subcutaneous tissues boil and the steam thus generated bursts throughout the skin. Joule burn is also known as endogenous burn because the heat causing was burn produced internally, that is in tissues. The presence of Joule mark is not in itself a proof of electrocution because such marks can be produced after death(excluding a zone of hyperaemia) but there are two features which are found in the

case of antemortem wound (not postmortem wound) and these are (1) vital reaction and (2)

HSP-70 (heat shock protein).

Chracteristics oflesion: Chaky white,or yellow

peupstat,

Crater: Round or oval shallow crater withn a raised ridge of skin around it. Floor of the crater is pale and lined by a flattened skin. 2) Areola: There is an areola of pallor or blanched skin at the periphery of the lesion. This areola of blanched skin is because of local vasoconstriction (especially arteriolar spasm) from the direct effects of the current on vessel wall musculature. This pallor survives after death and is a useful indicator of electric damage. 3) Hyperaemia: There may be mild hyperaemia (or erythema) of the intact skin immediately beyond the pallor. When the contact is prolonged, it may be brown, charred or even a circular hole penetrating deep into the tissues even up to bone simulating bullet wound. 4) Metallisation: When the current passes from a metal conductor into the body, the metal is volatised, and the particles of that metal are embedded in the skin. This is known as metallisation and it is a very peculiar characteristic of contact with electricity because it is not possible to induce metallisation in the skin by a metallic conductor without current; even hot metal or flame cannot induce it. Metallisation may provide the fade colour 1)

to the electric mark, for example, the colour is reddish brown in case of copper, brownish black in case of iron, and silvery grey in case ot aluminium. They persist for few weeks it the person survives. Metallisation can be demonstrated by acroreaction test, histochemcal methods, scanning electron microscope (SEM), spectroscopy, stereonmicroscopy, etc. It can be detected on the skin even when no current marks are evident. Metallisation can be demonstrated only on entry wound, not exit wound. It can be anywhere on the body but are usuau lound on the exposed parts of body and more commonly on the palmer aspect of hand especially the tips of index fingers and thumb. Histology: (1) Epidermal separation > Microblis ters.(2) Palisading and streaming of nuclei: Nucie

CHAPTER 7

epidermal cells are tretched, clongated and angles to the dermis. (3) Electric placed at right that is, cells are separated (vacuolatid channels space or slits. (4) Coagulation necrosis. to create elongation of basal layer. (6) Nuclear (5) Nuclear follicle. elongation of hair possible to proctuce changes in the skin It is also glowing or resembling an electric imark by applying a here metallisation will intense hot wire to the skin but absent and so acrorcaction test will be negative.

of

be

SN-2: Filigree burns (arborescent markings or Lichtenberg's flower or lightning mark or Keraunographic markings) Filigree burns: These are the characteristic fern like (arborescent) pattern on the body produced by the lightning flash (i.e. due to an electrical discharge from the cloud to the earth). Appearance (Fig. 7F. 1): They are superficial, thin, irregular (or tortuous or dendritic) red markings in the skin which resemble the branches of an inverted tree. They indicate the path taken by discharge and they generally follow the long axis of the body towards the ground. Incidence: They are seen in only 25% cases of lightning strike. Usual sites: Shoulders, front and back of chest, abdomen and flanks. Appearance: They appear within 1 h of lightning and disappear within 1-2 days if person survives.

Injuries

209

Histopathology:

Filigree burns are actually not burns, so there are no pathological changes in the epidermis or dermis. Oedema may develop in the soft tissues at the point of entry wound in those who survive. It is due to paralysis of capillaries and the lymphatic vessels. Mcchanism: There are several theories regarding

the mechanism 1) High current breaks down RBCs along its path and the escaped haemoglobin stains the surrounding tissues. The path of the current is not along the blood vessels (or may rarely be along the blood vessels), so the arborescent markings do not correspond to the blood vessels. 2) Current flows along superficial blood vessels and nerves. 3) Current follows the moist creases and folds of skin. 4) There is copper deposition in dermis 5) Electron showers are present eliciting an inflammatory response in the skin. Cause of death: Cardiopulmonary arrest due to passage of current is the most common cause. Other evidences to support death due to lightning: (1) A history of thunderstorm in the locality. (2) Vegetations (trees) in the vicinity of the scene of death may be found damaged (e.g. broken tree or its ranches broken and its leaves scorched). House may be damaged. (3) Some metallic articles (eg. coins, rings, keys, watches, nail cutter and so on) may be found fused together (or even magnetised) in the vicinity of the body due to tremendous heat produced by the electrical discharge. (4) The clothes of the victim may be torn, and his shoe may be burst open.

MLI:

1) These are pathognomonic of lightning strike, that is, these characteristic markings can occur only in lightning strike. So, death is accidental. It can help

differentiate a natural death from homicide. 2) Ifanybody recognises this peculiar feature, immevictim. diate resuscitation may save the life of the

SIN-3:

Arborescent burns/markIngs

Arborescent markings mean Fig.7F1 Filigree buirns or arborescent markings

filigree burn |SN-2

lightning D/W-4: Skin lesions in electrocution (Table 7E1)

and

SECTIONI

210

Forensic Medicine

TABLE 7F.1 Difference Between Skin Lesions in Lightning and Electrocution

[D/W-4]

Skin Lesion in

Sr.

No. Features 1.

2.

3.

4.

Lightning

Skin Lesion in

Electrocution Joule burn

Pathognomonic Arborescent burns or filigree burn feature True nature of They are not true They are true burn; there are burn burn no pathological changes in the epidermis or dermis Crater Absent Present formation Metallisation Absent Present

5.

Site

6.

Appearance

Shoulders, front Usually hands and back of chest, abdomen and flanks Within 1 h of Immediately

7

Disappearance

Within 1-2 days if

lightning

8.

Acroreaction test

person survives Negative

after current Very late

Positive

MLI-5:

Arborescent markings are present on the body Please

referto [SN-2]

MLI-6:The deceased has joule burn

If

deceased has Joule burn, it means most probably death was caused due to electric current. Joule burn is a mark of electric entry and is very specific and diagnostic to contact with electricity. Most of the cases are accidental, very rarely are they homicidal.

8 Mechanical Asphyxia AND ANOXIA ASPHYXIA, HYPOXIA Asphyxia

=

not, pulse-less-ness' but in splryzein = pulse) mcans denotes 'exclusion common use, the term asphyxia' relevance of asphyxia of air from lungs. The usual 'mechanical asphyxia. Here, in forensic context is in passage some type of mechanical interference to the of air into the respiratory tract occurs and it may lead a to death (asphyxial death) if interference extends for longer period (Table 8.1). (Greck, a Etymologically, the term 'asphyxia'

Hypoxia Versus Anoxia Inadequate supply of 0, at tissue level is known as hypoxia'but the complete absence of O, at tissue level is known as 'anoxia. The O, saturation of arterial blood is less than the normal value. Anoxia has been classified as 1)

Anoxic anoxia: Prevention of 0, from reaching the lungs. It includes all types of mechanical asphyxia,

TABLE 8.1 Hanging

sUspension of the body 1) Complete

2) Partial DOn the basis of "position of

knot

1) Typical

2) Atypical

On the basis of 'manner of

2)

Postmortem

and opium). 2) Stagnant anoxia: Impaired circulation > Lack of

transport of oxygenated blood to the tissues, for example. CHF (congestive heart failure), shock and heat stroke. 3) Histotoxic anoxia: o, is freely available in blood but cannot be utilised by the tissues, for example, cyanide.

4) Anaemic anoxia: Low haemoglobin (Hb) content

Inability of the blood to carry sufficient O, to the tissues, for example, anaemia, CO poisoning, sulpha-Hb, met-Hb.

Classical Signs of Asphyxia These signs of asphyxia are no more considered pathognomonic of asphyxia because they are also found very commonly in other conditions.

Classification of Mechanical Asphyxia

DOn the basis of 'degree of

hanging' 1) Suicidal 2) Homicidal 3) Accidental 4) Judicial DIn relation to death 1) Antemortem

for example, hanging, strangulation, suffocation and drowning. It also includes high altitude, lung diseases, paralysis of respiratory centre (e.g. electric shock) or respiratory muscles (e.g. Gelsemium

hanging hanging

Strangulation 1) Ligature

2) Manual

3) Garrotting

4) Palmer 5) Bansdola 6) Mugging

IMnemonic: Love Makes Girls Pretty and Boys

Muscular

Suffocation 1) Smothering 2) Gagging 3) Chokin9 4) Traumatic asphyxia 5) Wedging 6) Positional asphyxia 7) Overlaying 8) Burking9 [Mnemonic: Smart Gils

Drowning 1) Typical (wet)

Freshwater Seawater

2) Atypical (dry) 3) Immersion syndrome

(hydrocution) 4) Near drowning 5) Secondary drowning

drowning 6) Shallow water

Crack The Wonderful Personalitles Of Boys]

211

212

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Forensic Medicine

Decreased O, > Increased Cyanosis: Hypoxia reduced Hb>Cyanosis, that is, bluish discolouration of body, for example, nail, lips, tongue and ear lobes. There must be at least 5 gof reduced Hb per 100 mL blood before cyanosis becomes evident. 2) Congestion: Pressure around neck -> Obstructed venous return from head and neck > Increased venous pressure Congestion. 3) Petechial haemorrhages (Tardieu's spots): They are well-defined, round, pin-point to pin-head sized (i.e. 0.1-2 mm), dark-red coloured spots. They are found in those parts where capillaries are least supported, for example, conjunctiva, face, subpleural surface of lungs, heart and its pericardium, meninges. Increased intravenous pressure > Rupture of thin-walled capillaries and venules -> Tardieu's spots. They are not pathognomonic of asphyxia but their absence does not exclude asphyxia. 4) Oedema (general and pulmonary): Hypoxia -> Increased capillary permeability > Leakage of fluid into soft tissues Oedema. 1)

5) Dilatation of right chamber of heart. 6) Increased fluidity of heart: Hypoxia leads to release of fibrinolysins which increase the fluidity

of blood.

HANGING

Hanging It is a form of asphyxial death caused by suspension of body by a ligature tied around the neck; the constricting force is the weight of the body (in complete hanging) or weight of other parts of the body (in partial hanging).

Types of Hanging A. On the basis of'degree of suspension of the body'

(Fig. 8.1)

Complete hanging: The body is completely suspended in the air (i.e. the feet do not touch the ground). The constricting force is the weight of the body. 2) Partial (incomplete) hanging: The body is partially suspended, that is, any of the lower parts of the body (e.g. feet, toes, knees or buttocks) touch

1)

the ground. The constricting force is only a part The body may be in partial of the body weight. standing, sitting. reclining or kneeling position. B. According to the position of knot (Fig. 8.2)

Complete hanging

Partial hanging

Fig. 8.1 Complete and partial hanging

Typical hanging

Atypical hanging

Fig. 8.2 Typical and atypical hanging

Typical hanging: A type of hanging when the knot of the ligature material is placed centrally at occiput (i.e. the point of suspension is over the centre of occiput). 2) Atypical hanging: A type of hanging in which the knot is placed at any other position apart from occiput. C. On the basis of manner of hangin8 1) Suicidal: Most common type. 2) Homicidal: It is uncommon. 3) Accidental: It can occur while at work or dur ing play. In sexual (autoerotic) asphyxia, accidental hanging occurs commonly. 4) Judicial hanging lSN-6]. D. In relation to death: Antemortem hanging and postmortem hanging. 1)

Ligature Material Used in Hanging

are The materials most commonly used by the victim scar rope, wire (electric or cable), belt, dhoti/sari, dupatta and so on. The knot may be either a simple slipknot (most common) or fixed/granny knot. Usual sites of knot around the neck of the victim are occiput, Types of mastoid or mandibular angle and below chin.

CHAPTER 8

or fixed noose. 'To noose may be either running n00se away from the noose remove ligature material, cut the tie the cut ends of the noose with a thrcad. knot and then

Constricting Force Required to Occlude 8.2) Different Structures of Neck (Table TABLE 8.2 Constricting Force Required Structures of Neck to Occlude Different Force (kg) Structure Jugular veins

Effect Cerebral venous congestion

Carotid artery

Cessation of blood supply

15

Trachea

Obstruction to respiration

30

Vertebral arteries

Cessation of blood supply to brain

to brain

Causes of Death in Hanging Immediate: (i) Asphyxia due to occlusion of trachea, (i) venous congestion due to obstruction of jugular veins, (ii) cerebral ischaemia due to occlusion of blood vessels of neck, (iv) reflex vagal inhibition of heart due to pressure over carotid bodies and (v) (A)

Mechanical Asphyxia

213

fracture dislocation of cervical vertebrae in judicial hanging. (B) Delayed: (i) aspiration pneumonia, (ii) pulmonary ocdema, (ii) infection and septicacmia, (iv) hypoxic encephalopathy and brain abscess and (v) laryngcal ocdema.

Postmortem Findings in a Case of Hanging [LQ-1

Other Important Topics Related to Hanging a

Near hanging [IQ-2] Lynching [SN-7]

asphyxia (sexual asphyxia): When Autoerotic a person intentionally develops a state of partial asphyxia in his own body by any means to enhance sexual arousal, it is known as autoerotic asphyxia. Methods used by the victim may be hanging or suffocation by plastic bags or manual pressure on carotid vessels. Death is usually accidental (not suicidal) and results from the failure of safety pre cautions employed by the victim. Postmortem suspension: A person is first killed and then suspended by tying a ligature around his neck to simulate suicide. It should be differentiated from antemortem hanging. (Table 8.3)

Difference Between Antemortem Hanging and Postmortenm Hanging

TABLE 8.3 [D/W-22]

Sr. No.

10.

12.

13

Postmortem Hanging (Postmortem Suspension)

Signs of asphyxia

Present

Absent

Ligature mark

Dried, parchmentised

Not such

Subcutane US tissues underneath ligature mark

White, hard, glistening

Not such

Salivary stain

Present

Absent

La facie

sympathetique

Present (rarely)

Absent

Drag marks on the body

Absent

May be present

Protrusion of tongue Rope fibres in the hand of the victim Faecal, urinary or seminal discharge

Present

Absent

Present

Absent

Present

Absent

PM (postmortem) staining

Present

Absent

Present

ligature mark

11.

Antemortem Hanging

FeatureS

above

PM staining on hands, legs, (glove and stocking type)

Cause of death

Asphyxia due to hanging

dead body is hanged soon after death, the distribution if of staining is same as in antemortem hanging; distribution is hanged after 8 h, there no such on Asphyxia due to throttling. poisoning and so

Suicide note

Present

Absent

soles

If

214

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Forensic Medicine

STRANGULATION Strangulation: It is a form of asphyxia which is caused by constriction of neck by a ligature without suspending the body. So in strangulation, the constricting force is anything other than the weight of the body.

by a rope. The other ends when forcefully brought together, squeeze the neck uMugging: It is strangulationto cause death. caused by holding neck of the victim the in_the bend of the elbow.The attack is made from behind.

Classification of Strangulation According to the Type of Ligature

Postmortem Findings in a Case of Strangulation, that is,

Mnemonic Love Makes Girls Pretty and Boys Mus

cular:

Ligature strangulation: It is the classical, most common type of strangulation in which ligature material (e.g. rope, wire or cloth) is used to constrict the neck. The word 'strangulation' usually refers to ligature strangulation. It may be homicidal or accidental. Accidental strangulation usually occurs when one end of the scarf or chunni of a woman travelling on an autorickshaw or a bike is suddenly pulled by the moving wheel and the loop of the chunni around the neck constricts theneck. o Manual strangulation (throttling) [LQ-4]: It is the strangulation caused by human hands. Death is mainly caused by occlusion ofblood vessels. Homicidal throttling is a most common form and is indicated by multiple number of bruises and fingernail marks over neck. Most common victims are weak individuals, for example, children, woman, old, sick and so on. When the victim is young and healthy, the signs of struggle are more marked and are present on both the victim as well as accused. o Garrotting: The victim is attacked from behind without warning. The assailant throws a loop of a ligature around the neck of the victim and quickly tightens it by twisting it with a lever. It results in sudden loss of consciousness and collapse. Palmer strangulätion (a combination of smothering and strangulation): One palm (eg. left one) is placed horizontally across the mouth and nostrils, and other palm (e.g. right one) is placed perpendicular across the first hand in such a way that its heel presses uponthe front of neck. o Bansdola: It is a form of strangulation in which the neck is compressed in between two bamboos to kill the victim. A strong wooden (bamboo) rod is placed in front of the neck and other one behind theneck. One ends of these rods is tied together o

[LO-3]

Ligature Strangulation

SUFFOCATION Suffocation: It is a form of asphyxia in which the air entry into the lungs is prevented by means other than the constriction of neck and drowning.

Classification of Suffocation Mnemonic: Smart Girls Crack the Wonderful sonalities of Boys]

Per-

Smothering It is a type of asphyxia caused by mechanical obstruction of external respiratory orifices (i.e. nose and mouth) by any means (e.g. hand, pillow or fabric). Smothering may be (A) Accidental smothering: It may occur in following situations-i) when a person accidently falls in mud or sand, (ü) when children put plastic bags over their heads while playing, (ii) an infant may be killed by suffocation due to overlaying and (iv) in autoeroticasphyxia.

(B) Homicidal smothering-It may be possible

by pressing the external orifices with a pillow especially in weak individuals, for example, infants, children, old or intoxicated. (C) Suicidal smothering-It is very rare. The mentally retarded per son may cover his head by a polythene bag.

Postmortem findings: Cyanosis of tace with pale area around mouth and nose. Nose may be tlattened with fractured nasal septum. Lips may show contusions/lacerations on either side. Some abraSions, scratches or contusions may be present on the_facc. Face may be congested with petechal

haemorrhages.

Gagging type of asphyxia caused by pushing a g8 material (e.g. paper balls, piece of cloth and so on) into the mouth, sufficiently deep to block the phar moutt, ynx. When the gag material remains in the It is a

CHAPTER 8

initially may remain patent through nose

the airway to constant foreign body irritation, but later on duc mucous secretions are relcased in excess. saliva and abSorbs these secretions and swells The gag nmaterial MoreOver, ocdema of pharincreasc its size. uD to contribute together to factors All these ynx develops. pharynx. the obstruction of cause complete

Choking (SN-8] asphyxia causcd by an obstruction It is a form of at or just below the air passages (especially

within

to be differentiatecd

vocal cords). Choking has [SN-9] (Table S.4) from café coronary

Traumatic Asphyxia [SN-10]

Mechanical Asphyxia

example Jack-knife position in which victim's thighs and knees arc driven against his own chest.

Overlaying traumatic asphyxia caused by mother sleeping on the top of an infant. During slecp, the mother rolls over the infant and infant dies cither due to smothering or traumatic asphyxia or both. It is accidental death by smothering and lor

Burking method of homicidal killing by two simultaneously used methods of asphyxia, that is 'smothering and 'traumatic asphyxia. The term 'Burking was coined after William Burk and William Hare (1820s) who used to kill their victims by this method. It is a

Wedging

narrow means compression of the body within which space. The chest wall movements are prevented leads to asphyxia. It

DROWNING

Positional (or Postural) Asphyxia

It is a type of asphyxial death due to submersion of body in water or any liquid medium preventing entry of air in the lungs. Complete submersion of the body is not necessary to constitute drowning because drowning can occur in very shallow water when only

form of asphyxia caused due to abnormal position of body. The abdominal organs press upon the diaphragm and so expansion of chest is prevented, for It is a

TABLE 8.4

the mouth and nostrils are submerged.

Difference Between Choking and Café Coronary [D/W-261

Sr.

No.

Features

Choking

Café Coronary

Definition and

Accidental mechanical obstruction within the air passages (especially at or just below vocal cords)

Café Coronary is the sudden death due to obstruction of upper airwvays by a bolus of food

Usually children and very old

Usually old, obese, grossly intoxicated (e.g. drunken) person

mechanism 2.

Age

3.

It is

Any foreign object

Large bolus of food

4.

Alcoholism

Usually no

Yes

Gag reflex

Present

6.

Absent

Violent coughing

Present

Management

Absent

7

8

Cause of death

9

Signs of asphyxia

10.

5

11.

due to

In

most of the cases, Heimlich manoeuvre is successful

Heimlich manoeuvre less successful

Mechanical asphyxia

Reflex vagal inhibition of heart

Often absent

Time taken by death after obstruction

Present, for example, congestion cyanosis, petechiae and so on

3-5 min

Sudden and rapid

On chemical analysis of blood

Normal

AlCohol or other intoxicating in blood

substances are usually detected

SECTIONI

216

Forensic Medicine

Classification of Drowning on the Basis of Entry of Water into the Lungs Wet (or typical) drowning [SN-11]. Dry (or atypical) drowning [SN-16]. Immersion syndrome (lhydrocution): When death ocurs from cardiac arrest due to reflex vagal inhibition subsequent to immersion in water or any liquid, it is known as 'immersion syndrome' or "hydrocution. It may be caused by (1) fright or terror, (2) sudden and unexpected fall in water (especially water striking against the epigastrium), (3) sudden entry of cold water into the ear canal or nasopharynx and (4) alcohol. 4) Near drowning and secondary drowning: If the person dies during or within 24 h of drowningepisode, it is simply called 'drowning. If the victim survives the drowning episode for>24 h, it is known as near drowning. The use of the term 'near drowning continues if he survives. If he dies after 24 h due to some complications, then it is known as secondary drowning. 5) Shallow water drowning: An unconscious per son (e.g. under influence of alcohol or any drug), or an epileptic or any person rendered unconscious due to head injury may get drowned in any place where there is little amount of water (i.e. depth of water is a few inches), for example, pit, ditch, drain and so on and the mouth and nose of the victim come in direct contact of water. 1) 2) 3)

TABLE

8.5

The incrcased amount of CO, in blood stim lates respiratory centres and so the vicious cycle inhalation of water, bf coughing and again inhalation water continues. Inhaled of water irritates the and bronchial mucosal trachesl glands to secrete tenacious mucous. The violent respiratory efforts (i.e. force. ful inspiration and the coughing during expiration) churn the water already inhaled with air with mucous (along with surfactants) of respiratory tract to form froth. This froth prevents entry of air into the respiratory passages. Cadaveric spasm may occur (clenched hands with mud or weeds).

Wet Drowning Versus Dry Drowning (Table 8.5)

Near Drowning If the victim survives the drowning episode, it is known as near drowning. The person may be in a state of 'suspended animation' and immediate CPR (cardiopulmonary resuscitation) may save him. Mud or any weed from the mouth and nostrils of the vic-

tim must be removed immediately. To remove water from the upper respiratory tract, his face must be turned downwards with the head at the lower level than the rest of his body. Treatment: Oxygen (100%), surfactant therapy, electrolytic balance and antibiotics. Defibrillation in case of ventricular fibrillation.

Difference Between Wet Drowning and Dry Drowning [D/W-29]

Sr. No. Features 1.

Formation of Froth

Definition

Wet (Typical) Drowning It is a type of drowning in which 'water or fluid

Dry (Atypical) Drownin9 type of drowning in which the 'water or fluid does not enter the lungs" but death Occurs immediately

It is a

enters the lungs'

2.

Cause of death

Heart failure

O.

Signs of

Present

4.

Lungs

asphyxia

Frothing at mouth and nostrils

Voluminous, bulky, water logged and over inflated, filling the chest cavity and overlapping the heart; it bulges out of chest when sternum is removed; Surface may show pale grey appearance and

indentationofribs Fine, leathery, tenaclous and white or mixed

with blood

1)

Laryngeal spasm inhibition of heart due to syndrome) (immersion submersion

2) Reflex vagal

May be present (e.g. laryngeal spasm) May not be present (e.g. vagal inhibition of heart Trachea may contain very little amount of water Lungs are usually dry, that is, do not

contain water

No frothin0

CHAPTER 8

IMPORTANT QUESTIONS FOR EXAMINATION LONG QUESTIONS 1.

down sigins, symptoms, treatment and postmortem findings in a case ot hanging. [CCU

2011). asphyxial deaths. Discuss the 3. Classify mechanical 'strangulation. a PM findings in case of asphyxial deaths. Discuss the 4. Classify mechanical a PM findings in case of 'manual strangulation.

mechanical asphyxial deaths. Describe postmortem findings in a case of drowning or a body recovered from a well.

5. Classify

6. Judicial hanging 7. Lynching 8. Choking 9. Café coronary [CCU 2009, 2014] 10. Traumatic asphyxia [CCU 2004] 11. Wet drowning 12. Freshwater drowning 13. Seawater drowning [CCU 2009] 14. Diatoms [CCU 2003, 2004] 15. Diatoms test [CCU 2005] 16. Dry drowning

MEDICOLEGAL IMPORTANCE Diatoms are present in bone marrow Death is due to café coronary 19. Death is due to traumatic asphyxia 20. Death is from secondary drowning 21. Death was due to manual 17. 18.

strangulation

BETWEEN

Antemortem hanging

25. Hanging

and postmortem hanging

and strangulation [CCU 2004, 2010, 2011,2014]

24. Ligature mark

2002, 2008)

ANSWERS LO-1: Classify

mechanical asphyxial

deaths. Discuss the PM findings in a

case of 'hanging

Classification of mechanical asphyxial deaths (Table 8.1)

POSTMORTEM FINDINGS IN A CASE OF HANGING

External Features

SHORT NOTES

DIFFERENTIATE

217

27. Freshwater and seawater drowning {DU 2002] 28. Antemortem and postmortem drowning |DU 2004, 2006| 29. Wet and dry drowning

Classify mechanical asphyxial deaths. Discuss the "hanging PM findings in a case of

2. Write

22.

Mechanical Asphyxia

in hanging and strangulation |Du

25. Facial findings in hanging and 26. Choking

and café coronary

strangulation

Classical signs of asphyxia in typical hanging are less marked as compared to strangulation. and face: (1) Head is inclined to the side Head opposite to the knot. (2) Face is usually pale but may be swollen or congested. (3) Eyes are protruded. (4) Petechial haemorrhages due to asphyxia, known as Tardieu's spots which are pinpoint to pinhead size, are present on the skin and conjunctiva. (5) Bleeding from nose, mouth and ears. (6) Tongue is protruded, black/ brown, caught between teeth. (7) Salivary stain (due to dribbling from mouth) is the surest sign

of antemortem hanging. It is formed by running out of saliva through any one angle of mouth. (8) La facie sympathetique: In a case of hanging, sometimes, the knot presses on cervical sympathetic ganglia, the eye on the same side remains open and its pupil dilated. It is an antemortem phenomenon. Ligature material may be present around neck with a knot. Its colour, length, width, position, material, pattern, and number of turns, must be noted. Neck is stretched and elongated. Ligature mark in a case of hanging: It is a type of 'pressure abrasion' due to cotinued pressure by ligature on the neck. It may or may not be 'patterned' according to the pattern of ligature material. is usually seen as a furrow or groove in the It is skin. It is deeper in complete hanging and

218

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Forensic Medicine

much shallower in partial (incomplete) hanging. The ligature mark may be absent or indis tinct if ligature material is broad and soft (e.g. scarf, sari). Initially, it is soft and pale but as the skin dries up, it becomes hard (parchment-like) and dark brown. is obliquely present around the neck. 1lt does It not completely encircle the neck. Ligature mark in typical hanging (i.e. when the knot is present at the occiput). It is obliqucly present around the neck. It does not completely encircle the neck (Fig. 8.3). At the front and sides of neck: In typical hanging, usually, it runs from midpoint of neck outwards, backwards and upwards from either side of neck to reach behind the neck and then disappears. At front of neck, ligature mark is situated above thyroid cartilage (in 80% cases), at the level of thyroid (in 15% cases) and below the level of thyroid (in 5% cases). At the back of head: In typical hanging, the ligature material is pulled upwards and away by the vertical part of ligature material. So the ligature mark is absent at the back. If we look at the back of the head, the ligature mark at both sides of neck appears to run medi ally and upwards and at some point disappears.

Medicolegal importance of ligature mark: 1) Vital reaction, that is, a thin line of congestion or haemorrhage along the edges of the groove. It is strongly suggestive of antemortem strangulation. 2) Ligature mark may also indicate the nature of ligature material. The patterned ligature mark

At front of neck

Fig. 8.3 Ligature mark

in hanging

At

caused by a patterned ligature material, f example, rope. 3) Fibres of ligature material athough invisible are always present at the ligature mark. They can stripped of with a sticking be tape and then examined under microscope. The ibres must match with the ligature material found at is

the crime scene.

Others:

a. Hypostasis is seen in most dependent the body in hanging position. lower parts of In limbs, it is present on legs, feet and soles. In upper limbs,

it is present on forearms and hands. seen on penis and under the surface

It is also

of breasts.

b. Involuntary discharge of faeces and urine less common in hanging as

is

compared to strangulation, but involuntary discharge of seminal fluid is more common in hanging as compared tu strangulation.

Internal Features Tissues underneath ligature mark: Usually the tissues underneath the ligature mark are dry, white and glistening 2) Subcutaneous tissues and muscles: May show haemorrhages. 3) Fractures of hyoid bone and thyroid cartilage are 1)

rare.

bone fracture: Found in only 15%-20% cases. It is outward (i.e. antero-posterior) compression fracture in which the periosteum is rupP tured on the inner side of the bone. Site is the junction of inner two-third and outer one-third. Thyroid cartilage fracture: Rare but if present,

Hyoid

they are of superior horns.

4) Amusat's sign: Multiple transverse tears (lacerations) in the intimal layer of the carotid artery seen in cases of hanging. Mostly unilateral. Most

sldes of neck

At back of neck

CHAPTER 8 frequent mechanisim of these tears is the combi nation of forced compression of the artery and its

5)

6)

longitudinal stretching. Simon's bleedings/hacmorrhages: At autopsy, in hanging, the bleeding between a casc of complete anterior longitudinal igament and intervertebral ot lumbar spine is known as discs in the region Simon's hacmorrhages. They are caused by overstretching of the spine becaisc of Irce suspension

of the body. lungs and All internal organs (e.g. brain, heart, Tardicu's spots abdominal organs) congested. heart. and present on lungs

Write down signs, symptoms, treatment and postmortem findings in a case of hanging. LO-2:

form of asphyxial death which is caused by suspension of body by a ligature tied around the neck; the constricting force is the weight of the body. Near hanging: When a person survives the hanging incident, it is known as near hanging. The person hangs himself but within a very short period of suspension, either igature material breaks or he is brought down by someone. If he is treated in the hospital, he may survive.A person who survives the hanging incident shows the following signs and symptoms Signs and symptoms: a. Immediate: The person may be conscious or unconscious. He may have residual effects of partial asphyxia, for example, drowsiness, dementia, amnesia, mental confusion, dilated pupils, blurring of vision, hyperthermia, amnesia, convulsions, hemiplegia and parotitis. Other features may be like ringing in ears. There may be a ligature mark around the neck. b. Delayed: (1) aspiration pneumonia, (2) emphysema, (3) ARDS (adult respiratory distress syndrome), (4) oedema: laryngeal oedema, puimonary oedema and cerebral oedema, (5) infections and (6) hypoxic encephalopathy and infarction due to cerebral hypoxia. Treatment: The patient should be admitted in ICU (intensive care unit). The condition of the patient should be assessed by Glasgow Coma Cale (GCS). Mortality and morbidity is high.

Hanging:

It is a

1)

2)

3)

Mechanical Asphyxia

219

Ligature must be cut immediately if not removed by attendants. ABC: Airway, breathing and circulation. Endotracheal intubation may be required. Tracheostomy may be required. Assisted ventilation may be required. The neck has to be stabilised by cervical collar because, very rarely, there may be a fracture in cervical spine. Sedation may be required in case of convulsions. Nutrition by IV route.

4) 5) 6) Prophylactic antibiotics. 7) Fluids are restricted because of cerebral oedema. 8) Symptomatic treatment. Causes of death in cases of near hanging (1) aspiration pneumonia, (2) hypoxic encephalopathy, (3) infection and septicaemia, (4) pulmonary

oedema, (5) laryngeal oedema and (6) cerebral infarction and abscess. findings in a case of hanging [LQ-1]. Postmortem

Classify mechanical asphyxial deaths. Discuss the PM findings in a case of 'strangulation. LO-3:

Classification of mechanical asphyxial deaths (Table 8.1)

Postmortem Findings in a Case of Strangulation

ternal Features Head

and face: Markedly congested with petechial

haemorrhages. Bleeding from nose/ears. Eyes are prominent with subconjunctival haemorrhages pupils are dilated. Tongue protrusion is more marked as compared to hanging. Neck:The ligature may be present around the neck. Ligature mark shows following features (Fig. 8.4): 1) It is a type of 'pressure abrasion' due to continued pressure by ligature on the neck. It is a well-defined groove. 2) Usually, it is reddish, soft and less depressed in the skin. 3) It is transversely/horizontally present around was the neck but may be oblique if the victim dragged by ligature. neck. It may be inter4) It completely encircles the victim's fingers rupted at the front (due to

220

SECTIONI

Forensic Medicine

At front of neck

Fig. 8.4 Ligature mark In strangulation

At sides of neck

attempting to remove ligature) or back (due to long hairs in females or clothes in either sex). 5) In most cases, it is situated below thyroid cartilage.

6) Petechial

haemorrhages are common around ligature marks. 7) There may be multiple abrasions around ligature mark. They may be vertical, irregular or crescentic. These may be due to cither assailant's fingernails (in case of throttling) or victim's own fngernails (in an attempt to remove ligature). Others: (1) involuntary discharge of faeces and urine is more conmmon as compared to hanging, but involuntary discharge of seminal fluid is less common as compared to hanging and (2) evidence of struggles-abrasions and contusions on differ ent parts of body.

Internal Features (1) Tissues underneath ligature mark: usually the tissues underneath the ligature mark show haemorrhages. (2) Subcutaneous tissues and muscles: they may show haemorrhages. (3) Fractures: hyoid bone fracture is rare. Thyroid cartilage fracture may be present. (4) All organs are congested. Lungs are congested and oedematous with subpleural petechial haemorrhages. Brain shows petechial haemorrhages in white matter.

LO-4:

Classify mechanical asphyxial

deaths. Discuss the PM findinggs

in a case of manualstrangulation mechanical asphyxial deaths Classification of (Table 8.1)

At back of neck

Postmortem Findings in a Case of Manual Strangulation Manual strangulation human hands.

is

the strangulation caused by

External Features Head and face: Congested with petechial haemor rhages. Eyes are prominent with subconjunctival haemorrhages. Tongue is protruded.

Neck:

Bruises: Usually the bruises on neck are irregular because of struggle, but in a typical ideal situation, the bruises may be oval or round, 1.5-2 cm in size. Tips of thumb produce more prominent bruises as compared to other fingers. Presence and extent of fingertip bruising and nail scratch abrasions depend upon relative position of victim and assailant, manner of grasping the neck and degree of pressure applied. In case grip is from right hand from front, there is one mark (thumb impression) on right side of neck and four marks (finger tips) on left side of neck. In another case, if grip is from left hand from front, there is one mark thumb impression) on left side of neck and four marks (finger tips) on right side of neck. 2) Abrasions: They may be produced either by (1) assailant's fingernails-erescentic abrasions (curved, comma-like) and horizontal abrasions (multiple linear, parallel, horizontal and closely placed) or (2) victim's fingernails: vertical abrasions. (1) involuntary discharge of faeces and Others: urine and(2) evidence of struggles-abrasions and contusions on different parts of body. 1)

CHAPTER 8

Internal Features underneath ligature mark: Usually the 1) Tissues tissues underncath orrhages.

the ligature mark show hacm-

tissues, 2) Subcutaneous muscles other cles and 3)

sternocleidomastoid musmay show hacmorrhages.

Fractures

most common in throthanging and ligature tling as compared to strangulation. lt occurs in 30%-50% cases of is inward (i.e. throttling. Most conmmon type lateral) compression fracture in which periosside of the bone. teum is torn on the outer Extravasation of blood is also present at and

Hyoid bonefracturc is

around the fracture site. Thyroid cartilage fracture: The fracture of supeone) is much rior horns/cornuae (usually right laminae. more common than the fracture of 15% 4) Carotid arteries may show intimal tears in cases.

organs are congested. Lungs are congested and oedematous with subpleural petechial haemorrhages. Brain shows petechial haemorrhages in

5) All

white matter.

Classify mechanical asphyxial deaths. Describe postmortem findings in a case of drowning or a body recovered from a well. LO-5:

Classification of mechanical asphyxial deaths: Please refer to [LO-1] Postmortem findings in a case of drowning or a body recovered from a well: Please refer to (SN-12]

SN-6: Judicial

hanging

Judicial hanging: It is a type of capital punishment (or death penalty) inflicted upon a person by judiauthorities as a punishment for an offence.

cial

Position ofjudicialhanging in Indian law: S.354(5)

of CrPC deals with judicial hanging: "When any

person is sentenced to death, the sentence shall direct that he be hanged by the neck till he is dead.

Procedure of judicial hanging: Head and face of otfender is covered with a black mask, and then he is made to stand on a platform with trap doors which open downwards when a.bolt is drawn. A

Mechanical Asphyxia

strong noose (made up of rope) is placed around the neck with the knot at the side of neck. The length of the rope is kept more than his height (i.e. 10-15 ft.). By mechanical device, the trap doors are suddenly opened and the person is made to drop to full length of the rope. This causes sudden stoppage of the moving body at the end of its fall. It causes the head to jerk violently against the body weight. of knot in judicial hanging: At the side Position of neck (under the ear or angle of jaw) preferably at left side. Knot may be placed just below the chin in midline; this method has been the most efficient method of execution because death occurs rapidly. Cause of death in judicial hanging: Injury to spinal cord in the neck due to fracture and dislocation of upper cervical vertebrae. Fracture in judicial hanging occurs most commonly at C2-3 level, less commonly at C3-4 level. Bilateral fractures of either the pedicel or the laminae of the arch of second, third or fourth cervical vertebrae occur (Hangman's fracture).

With proper judicial hanging, there is rupture of brainstem between pons and medulla. It results in instantaneous and irreversible loss of consciousness (due to destruction of reticular formation) and in irreversible apnoea (due to destruction of the region of respiratory centre). But heartbeats and respiratory movement may continue up to 10-15 min until hypoxia causes arrest. Asphyxial signs are not seen in properly performed judicial hanging.

SN-7: Lynching It is a type of homicidal killing in which an angry mob (i.e. a large crowd of people) kills an offender in public often by hanging, without a legal trial. The usual methods used to kill an offender are hanging, burning, beating and so on. was common in North America where black It rapists used to be lynched by the anigry white mob. The term 'Lynch's Law' (and subsequently 'lynch law' and lynching) apparently originated during Lynch, the American Revolution when Charles extralea Virginia justice of the peace, ordered Americans who gal punishment for Tory acts by George. remained loyal to the British and King

Lynching:

SECTIONI

Inquest

in a case of

Forensic Medicine

lynching is done by police (i.e.

police inquest). The cause of death in lynching is asphyxia when person is hanged. Postmortem examination: In case of hanging, the features are of asphyxia. The body may show various injuries inflicted by the mob, for example, contusions, abrasions, fractures and so on. MLI: Lynching is considered murder. The persons belonging to a mob committing lynching are punished according to S.302, IPC.

Autopsy

findings: Features of asphyxia.

Foreia-

eign body may be found in larynx, trachea or bronchi Respiratory passage may be congested and th at site of blockage, it may be oedematous. is usually accidental, MLI: (1) especially children. It may be suicidal (e-g. in psychiatric patients) and very rarely homicidal. (2) Chokino ng should be differentiated from café coronary.

t

SN-9: Café coronary Café

SN-8: Choking Choking

is a term which relates to two offences:

one is related to smooth bore firearm and the other is related to asphyxia. Choking: It is a form of asphyxia (suffocation) caused by an obstruction within the air passages (especially at or just below vocal cords). Foreign bodies that may cause choking are balloon, button, battery, coin, seed, toffee, candies, hairpin, pen cap, dentures, fish bone, piece of meat, round worm and so on. Choking occurs in the following circumstances: 1) Person whose power to masticate or swallow is impaired, for example, very old, psychiatric patient or sick. 2) Ingestion of food while laughing or crying or even talking and also in drunken state. 3) Medical reasons, for example, (1) choking on vomit or regurgitated food can occur during anaesthesia; (2) choking by gauge piece can occur during operation; (3) choking by natural diseases, for example, diphtheria, pharyngeal abscess and so on and (4) choking by laryngeal mucosal swelling can occur in drug reactions and insect bite. Management: Heimlich's manoeuvre is the first aid procedure used for management of choking and can be life saving if the condition is detected immediately. The rescuer stands behind the patient and by his fist (made by interlinked fingers of both hands) exerts upward and backward thrust in the epigastric region of the patient. It expels any foreign object obstructing the upper airway. Cause of death in choking is usually mechanical asphyxia. The foreign body may irritate mucosa to cause vagal inhibition of heartor laryngeal spasm to cause death

coronary: It is a condition in which a healthy person who begins a meal suddenly collapses and dies without any further distress. Sudden death due to obstruction of upper airways by a bolus of food is known popularly as café coronary. The term 'café coronary' is a misnomer: The term café coronary French café = coffee or coffee house; Latin corona = that which encircles, that is, coronary arteries] was given by Dr Roger Haugen (1963). The term 'café coronary' was initially applied to the cases attributed to heart attack (i.e. myocardial infarction). Actually, it has nothing to do with a coronary occlusion, that is, a person in this condition does not die from coronary occlusion or heart attack. Mechanism: Usually, a very large bolus of meat or cheese stimulates'recurrent laryngeal nerve (a branch of vagus) to inhibit heart Cardiac arrest. A large bolus of food may also dilate oesophagus Bronchospasm and Through vagus nerve bradycardia > Cardiac arrest. Cause of death is 'reflex vagal inhibition of heart (not mechanical asphyxia/choking). In some cases of choking, death is very rapid and the reason reflex vagal inhibition of heart.

factors: Old age (inadequate mastication due to poor dentition/denture), drugs (alcohol, sedatives and anti-Parkinsonism), dis eases (e.g. Alzheimer's disease, Parkinson's disease and stroke) and mental retardation. Typical history: A healthy but grossly intoxicated individual (especially old and obese), sitting in a restaurant or cafe, who begins a meal in a hurry suddenly turns blue, coughs violently and then dies. The suddenness and rapidity of death suggests an acute heart attack, thus, the name cafe coronary.

Predisposing

CHAPTER 8

.

reflex

and consumption, already cough In alcohol a bolus of food is So if suppressed. gag reflex are impacted in the larynx, the person may be unablec

The bolus may continue to irritate larv vagal inhibition of heart. geal mucosa to cause to cough.

Postmortem findings: chewed food (bolus) may 1) A large piece of poorly entrance of the larynx. be found obstructing the choking/asplhyxia are often absent 2) Signs of to vagal inhibibecause death is instant due choking may tion. Sometimes, the symptoms of vagal inhibi occur first, then death occurs from asphyxia may be present. tion; here the signs of Management: Heimlich's nmanoeuvre can be life is detected immediately. saving if the condition and by his The rescuer stands behind the patient both hands) fist (made by interlinked fingers of the exerts pressure in the epigastric region of patient. It expels any foreign object obstructing the upper airway.

SN-10: Traumatic

asphyxia

form of violent asphyxia due to mechanical fixation of chest due to either heavy pressure on the chest or forceful compression of the chest preventing respiratory

Traumatic asphyxia: It

is

a

movements. Causes: (1) in riot crush or stampede (human pile death); (2) fall of vehicle on the car mechanic due to slipping of jack; (3) fall of a machinery on the person; (4) falling of big stone or heavy tree (e.g.in landslides, earthquakes); (5) person buried under rubble of collapsed building and (6) constriction by a python snake.

Postmortem

examination:

External: There

is a very

clear line of demarca-

tion at the level of compression. Above the level of compression (i.e. over face, neck,

shoulder and upper part of chest): The ret-

rograde displacement of blood from SVC (supe rior vena cava) into the subclavian veins and the veins of head and neck leads to (1) face, lips and Scalp being swollen; (2)) cyanosis, congestion and purple discolouration body with

of the

multiple

petechial haemorrhagic spots may be present; and (3) ears and

nose may bleed.

Below the level of compression, the body is pale or mildly cyanosed,

Mechanical Asphyxia

Internal: Fractures of ribs, sternum or verte brae. Brain is congested. Right side of heart is markedly distended. Contusions and/or lacerations may be present on lungs or heart. paticnt recovers, the purple discolouration gradIf ually disappears in 1-2 weeks. (1) It is mostly accidental, for example, in MLI: riot crush/stampede (human pile death), restraint asphyxia (by policeman), fall of vehicle on the car mechanic due to slipping of jack, falling of big stone or heavy tree (e.g. in landslides, earthquakes) or constriction by a python snake. (2) It may be homicidal and rarely suicidal. (3) It is a component of burking.

SN-11: Wet drowning Wet drowning: It is a type of drowning which occurs due to inhalation of water into the lungs. Since this form of drowning is the most common form of drowning, it is also known as typical drowning. Treatment of a case of near drowning: The person may be in a state of 'suspended animation' and immediate resuscitation may save him. 1) First aid: (a) Mud or any weed must be immediately removed from the mouth and nostrils of the victim; (b) water must be removed from upper respiratory tract, and face turned downwards with the head at the lower level than the rest of his body; (c) resuscitation and (d) hypothermia must be avoided. 2) In hospital: oxygen (100%), electrolytic balance and antibiotics. Any injury if present must be treated. Cause of death in wet drowning: Asphyxia, head injury, exhaustion, hypothermia, ventricular fibrillation and apoplexy. Types of wet drowning: 1) Fresh water drowning: Hypervolaemia, hyperkalemia (i.e. excess potassium), hyponatraemia (i.e. sodium deficit), hypoxaemia and metabolic acidosis lead to ventricular fibrillation Death. 2) Sea water drowning: Hypovolaemia, hypernatraemia and hypoxaemia lead to heart failure

Death. Postmortem

examination:

External Features

pupils Cyanotic, conjunctiva congested, protruded and froth dilated, tongue swollen and

Face:

SECTIONI

Forensic Medicine

mouth. Appearance of froth: fine, white, leathery, tenacious, mushroom-like mass at nostrils or mouth. On wiping, the froth reappears, especially when chest is compressed. The colour may be blood stained due to intrapulmonary bleeding. The bubbles do not readily collapse when touched with the point of a knife. 2) Cutis anserina (Latin cutis = skin, anser = goosc) also known as goose skin or goose flesh: In a case of drowning, the skin may show a granular and puck ered appearance like an orange peel. It may be an antemortem phenomenon or a postmortem phe nomenon. In case of antemortem phenomenon, it develops due to contraction of erector pilorum muscle of the skin when cold water comes in contact with skin. In case of postmortem phenomenon, it can occur when dead body is immersed in water soon after death while the muscles are still irritable, that is, before molecular death. It can be due to the rigor mortis of erector pilorum muscle of skin. 3) Washerman's hands and feet: The skin appears just like the skin of washerman, that is, bleached (white), sodden, thickened and wrinkled. It is due to the absorption of water into the outer layers of the skin. It is merely a sign of immersion and not a sign of antemortem drowning. Exact calculation of time of drowning is not possible. It is seen early in warm water as compared to cold water. But average durations are as follows: h: Wrinkling and soddening of fingertips 2-4

4-8

at nose and

TABLE 8.6 Sr. No. 2.

3.

.

24

h: Bleaching of epidermis h: Wrinkling, soddening and bleachingn

entire hand 48 h: Peeling of cuticle from

palm and sole days: Skin can be peeled off like a glove 4) Cadaveric spasm: The grass, gravel, sand, mud o weeds or any aquatic vegetation may be held firmy in clenched hands due to cadaveric spasm. It is a vital proof of antemortem drowning. a 5) Rigor mortis or putrefaction 6) Hypostasis: In standing water, hypostasis may be present at head, neck, front of chest and hands and feet, whereas in running water, it may not develop because of constant change in body's position.

3-4

Internal Features Trachea and bronchi: Full of froth and water. 2) Lungs: Congested or pale. Paltauf's haemorrhage: Rupture of alveolar walls produces haemorrhages just below pleura. They are multiple, shining pale pink or bluish red, up to 3-5 cm in diameter, subpleural haemorrhage of lungs, seen in 50% of wet drowning cases. Their absence does not exclude drowning but their presence confirms it. Most common sites are lower lobes of lungs but may be interlobular surfaces or anterior surfaces of lungs. Emphysema aquosum and oedema aquosu. These are the two characteristic conditions of lungs in wet drowning (Table 8.6) 1)

Diference Between Emphysema Aquosum and Oedema Aquosum

Features

Emphysema Aquosum

Oedema Aquosum

Seen when the victim is

Live and conscious

Live and unconscious

Violent respiratory efforts Entry of water

Present

Absent

The water enters the lungs actively with each violent respiratory effort

The water enters the lungs passively with each inspiration

Yes

No

Yes (in excess)

No or very less

Relatively less (because of constant coughing and spasm of air passages)

in

4

Churning of wate with mucous

6.

Froths Amount of water in lungs in air

passage

excess (because of absent cough reflex, water enters with each inspiration)

Lungs at autopsy

Voluminous, bulky, water logged and over inflated, filling the chest cavity and overlapping the heart; it bulges out of chest when sternum is removed; indentation of ribs On cut section: emphysematous, watery, frothy,blood-stained fluid oozes out

Simply over distended with water (oedema aquosum)

Aveolar wal

Ruptured due to violent efforts at breathing

Intact

CHAPTER 8

seen in postmortem is immersed for 20 h drowning if the dead body 2 m. The water enters the lungs at a depth of water is prescnt passively. At autopsy, minimal traclhea, bronchi and lungs. without froth in inhalaheart is dilated because after of side Right 3) stops and the water, pulmonary circulation tion of side of heart. is cxerted into the right back pressure 4) Water in water in threc Stomach: Stomach contains If the compodrowning. fourth cases of wet stomach is same as that of sition of water in antemortem drowning medium, it confirms indicates peristaldrowning. Water in intestine phenomenon. tic movement, a vital contains water due to Middle ear: Middle ear the water enters violent efforts at inhalation; eustachian tube. into middle ear through

Hydrostatic luig:

Paranasal

It

is

sinus: Paranasal sinus contains

Diatom Test

Diatoms are microscopic unicellular algac present A in water. Femur is the best sample for diatom test. negative diatom test does not rule out the possibility of drowning, as it could be a case of dry drowning.

SN-12: Freshwater drowning The water on this earth can been divided into two types: 1) Freshwater: The water of ponds, lakes, canals, rivers and so on is known as freshwater, and it contains very low concentration of salt. 2) Seawater: It contains high concentration of salt. as Freshwater (0.6% NaCI) is relatively hypotonic very well compared to blood (0.9% NaCI). We know that water always flows from hypotonic solution (i.e. freshwater in lungs) to hypertonic solution (i.e. blood in the body) due to osmosis.

drowning episode, when freshwater (0.6% NaCl) is inhaled into the lungs, it is rapidly absorbed (by osmosis) through alveolar membrane leads to into the blood plasma (0.9% NaCI). It hypervolaemia and haemodilution (Fig. 8.5).

During

water.

5)

Mechanical Asphyxia

is fluid, size Others: Brain is oedematous, blood all organs are and weight of spleen is decreased and congested. Fresh water (0.6% NaCi) Hypotonic

Blood (0.9%)

Relatively hypertonic

Fresh water

(0.6%)

Fresh water in blood

Haemodilution

Hypervolaemia (increased blood volume)

Overloads the heart

Hyponatraemia (also decreased Mgt and C)

RBC Swell and burt to release

Ventricular fibrillationK* into

Hb into circulation

(hyperkaemla)

Hb appears in urine

circulation

Heart failure

(haemoglobinuria

Death

Fig. 8.5 Pathophysiology of

freshwater drowning

SECTIONI

Forensic Medicine

from the plasma, the freshwater enters red blood cells (RBCs) (0.9% NaCl) due to osmosis and so RBCs swell and then burst to cause haemolysis which leads

Now

hacmoglobinuria, hyperkalemia (because all potassium comes out of RBCs) and hyponatraemia (i.c. sodium deficit). Freshwater also denatures the protective surfactant which leads to pulmonary oedema (with transuda tion of protein-rich fluid into the alveolar spaces). Hypoxia and metabolic acidosis also develops. Hypervolaemia, hyperkalemia, hyponatraemia, hypoxaemia and metabolic acidosis lead to ven tricular fibrillation Death. Fatal period: 4 min in freshwater (8-12 min in seawater). to haemoglobinemia,

very well that water always flows from hypotoni. solution (i.e. blood plasma) to hypertonic solution (i.e. seawater in lungs) due to osmosis. seawater (23% NaCI) is inhaled into When the lungs, due to its hypertonicity (i.e. high Nac concentration), the water is drawn from the c. culation into alveoli by osmosis leading to (1) hypovolaemia and haemoconcentration (with crenation) and hypernatraemia and (2) severe pulmonary oedema (Fig. 8.6). Simultaneously, in an attempt to re-establish osmotic balance, the seawater from the lungs also enters the circulation. So Na" level increases in plasma which leads to bradycardia. Hypovolaemia hypernatraemia and hypoxaemia Heart failure

Death.

Fatal period: 8-12 min in seawater.

SN-13: Seawater drowning pathophysiology in seawater drowning is reverse to that of freshwater drowning. Seawater (23% NaC) is relatively hypertonic as compared to blood (0.9% NaCl). We know

The

SN-14: Diatoms Diatoms (Fig. 8.7): They are microscopic (2 um-2 mm) unicellular algae (phylum

Sea water (> 3% NaCI) Hypertonic

Blood (0.9%) Relatively hypertonic

Sea water

Water

(>3%)

in

Pulmonary oedema Hypovolaemia

blood

Haemoconcentration

Hypernatraemia

Heart failure Death

Fig. 8.6 Pathophysiology of seawater drowning

RBCcontract (crenation)

CHAPTER 8

Mechanical Asphyxia

rectangular piece of bone is removed with knife. Some marrow is taken. b. Soft tissues, for example, brain, liver or kidney are taken, washed with distilled watera I cm piece is cut from deeper tissues. cmX 2) Reference water samples: Taken from the sus1Pected site of drowning Procedure of diatom test (Fig. 8.8): 1) 5 g of bone marrow (or soft tissues) is put in test tube. Sufficient quantity of H,SO, (con centrated) is added. It is left at room tempera ture for 1-2 days or boil ed for 10-15 min. All organic tissues are dissolved but not diatoms. Only the supernatant fluid is collected. 2) Centrifugation: The supernatant fluid collected above is centrifuged. After this, the supernatant acid is poured off. Distilled water is then filled process is in the tube and again poured off. The repeated 2-3 times to dilute the acid. 3) Microscopic examination: The deposit settled at the base of tube is examined under the microscope. If they match those recovered from the is removed. A

a

1

O

Fig. 8.7

microscope Diatoms seen under

Bacillariophyceae) of various shapes and sizes as well as freshwater. that live in seawater up of silica and is cell wall is very hard, made

The

known as frustule. acid because of silica They are resistant to heat and wall.

there is seasonal They vary trom place to place and

variation at the same place. The water along with diat In antemortem drowning: efforts rupture oms enters the lungs. Violent respiratory size cross different the alveolar walls. The diatoms of

the ruptured alveolar walls but only the diatoms of size Discard Yellow transparent fluid

Bone marrow Centrifugation

SN-15: Diatom test

Supernatant>Discard

Diatoms are microscopic unicellular algae present

Centrifuged deposit

in water.

Djatoms

Microscopy

test is conducted to know whether death

is dueto drowning

or

not.

Samples for diatomstest: 1) Tissues: a.

Bone marrow of long bones (e.g. Jemur, sternum and humerus) is most useful, highly reliable and least contaminated. The bone is

Washed in distilled water. The

periosteum

Fig. 8.8 Diatom test

SECTIONI

Forensic Medicine

Controversies: Diatoms are also present in air and drinking water. They enter the body during life. So diatoms are present in bone marrow and organs of normal individuals also. MLI: (1) Diatom test is not conducted routinely. (2) It is important when only bones or isolated parts are recovered from water. (3) When the body is putrefied, diatoms test is usefil because diatoms resist putrefaction (4) A negative diatom test does not rule out the possibility of drowning as it could be a case of dry drowning.

SN-16: Dry drowning

Dry

drowning (also known as 'atypical' drowning): It is a type of drowning in which the water or fluid does not enter the lungs' and death occurs immediately. Since this form of drowning is less

common, it is also known as atypical drowning. Cause of death in dry drowning: (1) laryngeal spasm or (2) reflex vagal inhibition of heart or (3) submersion of unconscious (i.e. shallow water drowning). Incidence: About 10%-15% of all drowning cases are of dry drowning. Dry drowning due to laryngeal spasm: The sudden entry of water into the larynx causes sudden violent laryngeal spasm that prevents entry of water into the respiratory passage. So water does not enter the lungs and death occurs due to asphyxia. is commonly seen in children; adults It under the influence of alcohol or sedatives. Autopsy findings: Signs of asphyxia present. Trachea may contain very little amount of water. Lungs are usually dry, that is, they do not contain water. Dry drowning due to reflex vagal inhibition of heart (immersion syndrome or hydrocution): Immersion in liquid leads to sudden reflex vagal inhibition of heart Sudden death. Causes: Cold water stimulates the nerve endings at body surface or mucosal surfaces, for example, ear drums, nasal passage, pharynx and lar ynx. Water may also strike the epigastrium > Vagal inhibition of heart. Diving into water feet first also may lead to vagal inhibition of heart.

Aggravating factors: Alcohol, emotional sion.

Autopsy findings:

Signs of asphyxia abses Lungs are dry, that is, ent. they do not contai Ain water.

MLI-17: Diatoms are marroN

present in bone

Diatoms

are present in bone marrow: means that the death was due to 'wet drowning It Controversial issue. Diatoms are also present in air and drinking water. They enter the body during life. So diatoms are present in bone marrow and also in organs of normal individuals. A negative diatom test does not rule out the possibility of drowning, as it could be a case of dry drowning. Diatom test is conducted to rule out drowning when any bone or organ is found in a water source. It is also done to differentiate antemortem drowning from postmortem drowning. In postmortem drowning, the diatoms are usually not present in bone marrow.

MLI-18: Death is due to café coronary

(very important) [SN-9

MLI-19: Death is due to traumatic

asphyxia [SN-10] MLI-20: Death is from secondary

drowning

is from secondary drowning: It means Death that the drowning person had been brought out of water and had been saved, but after a period (>24 h) of relative well being, he dies. If the victim is brought out of water within a very short period of submersion, he can be saved. If the victim survives the drowning episode, it is known

CHAPTER 8 a period (>24 h) of near drowning. lf after is known as secondit relative well being, he dies, drowning. ary secondary drowning nmost common cause of Theposthypoxic encephalopathy but other causes is metabolic acibe electrolytic imbalance and

as

may dosis.

have been accirarely would it have dental or suicidal in nature; been homicidal.

episode would MLI: Thedrowning

are marks of abrasions and bruises (e.g. nail marks) on the neck. On autopsy, features of asphyxia are present on the fac. Subcutaneous tissues and the muscles of the neck show haemorrhages. Fracture of hyoid bone and thyroid cartilage is also present. assailant is punished for murder according to The S.302, IPC.

There

D/W-22: Antemortem hanging and postmortem hanging (Table 8.3)

MLI-21: Death is due to manual strangulation

manual strangulation: It means The assailant killed the case is homicidal in nature. the victim the victim by strangulating the neck of

.Death

is due to

by using his hands.

TABLE 8.7 Sr. No.

3.

Mechanical Asphyxia

D/W-23: Hanging and strangulation (Table 8.7)

Difference Between Hanging and Strangulation [D/W-23]

Features

Hanging9

Strangulation_

Ligature mark

A. Oblique

A. Transverse

B.

Incomplete C. Above thyroid cartilage D. Hard, parchment-ike

B. Complete C. Below thyroid cartilage D. Soft, reddish

Abrasions and bruises around ligature mark

Absent

Present (due to struggle)

Subcutaneous issues underneath ligature

White, hard, glistening

Haemorrhages

Signs of asphyxia, for example

Less common

More common

Salivary stain

Present

Absent

Fracture of hyoid bone

More common

Less common in ligature strangulation (but most common in manual strangulation)

Less common

More common

Less common

More common

More common

Less common

Mostly suicidal

Mostly homicidal

mark

A. Petechial

haemorrhages

B.

Bleeding from nose, mouth and ear C. Protrusion of tongue

Fracture of Thyroid cartilage, larynx and

. 10.

11.

Discharge of faeces

trachea

and urine

Discharge of semen Manner of death

Method of capital

punishment

Yes, nanging is a method of capital punishment in India (i.e. judicial

hanging)

a No, strangulation is not method punishment in India

of capital

230

SECTION

1

Forensic Medicine

DW-24: Ligature mark in hanging and strangulation (Table 8.8)

DW-26: Choking and café coronary (Table 8.4)

DW-25: Facial findings in hanging and strangulation (Table 8.9)

D/W-27: Freshwater and seawater drowning (Table 8.10)

TABLE 8.8 Sr. No.

Difference Between Ligature Marks in Hanging

Ligature Mark in Hanging

Ligature Mark in Strangulation

Obligue

Transverse

Incomplete (i.e.

it

does not comletely ercirtie the neck)

3.

Above thyroid cartilage

4.

Base is hard and parchrnerit-like Abrasions and bruises around ligature mark

5.

6

Complete fi.e. it completely encircles the neck) Belcw thyroid cartilage Saft. reddish

atsent

Subcutaneous tissue underneath the igeture mark white, hard, glistening Bruising of neck muscles: less Oormmon

Present (due to struggle) Haemorrhages More common

TABLE 8.9

Difference Between Facial Findings in Hanging

Sr.No

Facial Findings in Hanging

Congested

Petechial haemonhages (ardieru's spotsl. iens cormmocn Bleeding from nose, cas, mouth iess common

More common

Protrusion of tongue: less comman

More comnon

Salivary stain: present

ADsent

La Tacie

TABLE 8.10 No.

1

sympathetique: may De presen

More common

Absent

Difference Between Freshwater Drowning and Seawater Drowning Freshwater Drowning It

occurs

in

freshwater (0.6%

D/Wz

Seawater Drowning NaCt)

it cCCurs in

Features in blood Hypervolaemia and haemodilution

3.

and Strangulation [D/W-251

Facial Findings in Strangulation

Pale

Sr.

and Strangulation [D/W-24

Ryponatraemia: SOdium deticit to lead to ventncular iibrillation

seawater (>3% NaC)

Hypovolaemia and haemoconcentration Hypernatraemia: due to raised sodium level in plasma leads to bradycardia

Features in lungs Water content: less 5.

6.

More Ballooned but heavy (due to oedema)

Size and weight: balooned but light Colour: pinkish

Purplish or bluish

Consistency: emphysematous

Soft. jelly+ike

Shape

ater removal

from body: retained,

On cut section: crepitus

do not collapse

heard, litle froth, no fluid Cause of death ventricular fibrilation

Not retained, tends to flaten out No crepitus, copious froth, fluid

Pulmonary oedema

CHAPTER 8

W-28: Antemortem and

drowning (Table 8.11)

E

8.11

[D/W-28] Sr.

No.

postmortem

Mechanical Asphyxia

D/W-29: Wet and dry drowning (Table 8.5)

Difference Between Antemortem Drowning and Postmortem Drowning Features

Antemortem Drowning

Postmortem Drowning

Signs of asphyxia

Present

Absent

Present

Absent

Present

Absent

Present

Absent

Froth at nmouth and

nose

Cadaveric spasm

Water

in lungs

Gettler's test

+ve

Diatoms test

+ve

-Ve

Hands tied behind the back

May be

No

-ve

231

9 Sexual Jurisprudence Chapter 9A Impotence and Sterility IMPOTENCE

STERILITY

Impotence: It is defined as 'inability of a person to perform sexual intercourse. Although a male as well as a female can be impotent, the term impotence is generally referred to 'male impotence. Impotence in females is also known as female sexual dysfunction and it means inability of a female to take part in satisfactory sexual intercourse. Impotence in males: It means 'persistent inability of a male to achieve or maintain penile erection for sat isfactory sexual intercourse or persistent inability ofa male to achieve or maintain penile erection sufficient to conclude coitus to orgasm and ejaculation. Not achievng sexual gratification is an ingredient of this definition because the male is not performing satisfactory sexual intercourse. This definition has two components: (1) erectile component, that is problem in erection and maintaining erection. The term 'erectile dysfunction' includes only erectile component and is defined as inability of a male to achieve or maintain penile erection for sexual intercourse. (2) Ejaculatory component, that is ejaculatory problem. Ejaculation problems may be: (a) failure to ejaculate (i.c. impotentia ejaculandi) or (b) premature ejaculation (i.e. ejeculatio praecox) or (c) ejaculation without orgasm (i.e. orgasmic anhedonia). It means that 'impotence is a broad term which also includes 'erectile dysfunction' as well as ejaculatory problems. Since erectile dysfunction is the main and major culprit to cause impotence, the term impotence usually means erectile dysfunction.

Sterility: Sterility in general means inability to procre ate. For males, sterility means failure to impregnat? or 'inability of male to beget children' and for females, sterility means failure to conceive or inability of

232

females to conceive children. A person can be sterile without being impotent and can be impotent with out being sterile. Sterility is not a ground for voidable marriage, but impotence is a ground for voidable marriage under S.12 of Hindu Marriage Act, 1955. Sterilisation: It is a procedure to make a person sterile, without interfering with the potency. It includes (1) surgical methods, for example, vasectomy and orchidectomy in males, and tubal ligation and hysterectomy in females. (2) Chemical castration: Administration of anti-androgens, for example, cyproterone which decreases libido and sexual activity. Its use is usually restricted to rapists, child molesters and other sexual ottenders. Its effects are reversible.

SOME IMPORTANT POINTS AND DEFINITIONS (or 'vera copula'): It includes erection (erectio) and penetration (intromossio) but generally it means penetration after marriage. peneIn the case of marriage, a single act of full tration (penile-vaginal) results in consummation of marriage, even without mutual orgasm or emis sion of semen.

Consummation

CHAPTER 9

hoc (Latin, quoad hoc = with Impotence quoad this): 1It is also known as 'selecti impo respect to man is impotent with a particutence. It neans a others. (c.g. wife) but not with

woman sexual desire. Libido means frigidity = cold): It is regarded Frigidity (Latincounterpart in females wherein a Jar

desire and she fails to respond

female have no sex stimulation. to sexual

. Satyriasis:

A statee in

scxual desire

which

.Nymphomania: A state cessive seual desire.

a

in which

female has

Aptavira: A female who is capable of taking part sexual intercourse. Non-aptavira: A fenmale who is

CAUSES OF IMPOTENCE AND STERILITY IN MALES

male has cxcessive a

in

not capable of tak-

ing part in sexual intercourse. Aptoe viris: It is a way by which

immature girls are made fit for sexual intercourse. For this the sholapith is inserted into the vagina and the girl is allowed to sit in water. Sholapith acts as a sponge, soaks water and dilates the vagina. The size of sholapith is increased gradually for further dilatation. Hymen is often torn by this method. Fecundatio ab extra: Conception is possible without penetration of the vagina by the penis. It is due to the deposition of semen on the vulva. The sperms travel up from vulva to fertilise ovum. If an impotent person, who has never had even a single act of penetration with his wife (i.e. consumma tion of marriage has not occurred) deposits semen on vulva which results in pregnancy, the marriage will not be said to be consummated; it can still be annulled on the grounds of impotency. Thus birth of a child is not a conclusive evidence that the marriage has been consummated. Causes of impotence: (1) psychogenic cause: is the most important cause of impotence. Sudden overnight development of impotence in a male Suggests psychogenic cause. (2) Organic causes eg neurogenic and vascular): gradual failure of Sexual function over a period of time suggests OTganic cause. If spontaneous REM sleep erections during are absent, suggests it Purpose of organic caus marriage: The marriage Detween man is a cOnurac and woman which union. Marriage implies the sexual summation. also mear implicit right of conThere are two o purposes of marriage:

233

one is sexual gratification and the other is procreation. Baxter versus Baxter (1947) was the first case where House of Lords held that the procreation of children was not the sole purpose of marriage. That is why the sterility is not a ground for divorce, but impotence is.

I

as impoten

Sexual Jurisprudence

A. Age:

The power of coittus starts earlier than the power of procreation. The power of coitus starts at the onset of puberty (i.e. at 13-14 years of age) and so a boy is considered sexually potent at the age of puberty. After 1-2 years of this, the power of procreation starts (i.e. at 14-15 years). 2) The power of procreation ceases earlier than the power of coitus. It is because of obliteration of canal of epididymis or vas deferens with advancing age. Towards the end of life, both powers decrease. B. Congenital anomalies: (1) Penis: Absent (or rudimentary) penis, hypospadias and epispadias. (2) Testes: Absence and cryptorchidism. C. Local diseases: (1) Penis: Phimosis, paraphimosis, elephantiasis, balanitis, balanoposthitis, ulcers (of syphilis, TB and gonorrhoea) and malignancy. (2) Testes: Acute orchitis, hydrocoele, scrotal hernia, elephantiasis, syphilis/TB/gonorrhoea/mumps, seminoma and carcinoma. (3) Trauma or surgery, for example, amputation of penis and removal of testes. 1)

D. General diseases: 1)

Acute illness with high fever: Malaria, typhoid, pneumonia and meningitis. 2) Chronic illness: TB, CH, hemi-/paraplasia, tabes dorsalis, transverse myelitis, syringomyelia, schizophrenia and manic depressive psychosis. 3) Endocrine factors: Diabetes mellitus, Addison's disease, hypopituitarism and thyrotoxicosis. 4) Trauma to head (ocripital region) and spinal cord (DL-LS region). E. Drugs for long term use: Alcohol, tobacco, cannabis, cocaine and barbiturate. E

G.

Chronic lead/arsenic poisoning.

Exposure to X-rays may lead to temporary azoo-

spermia.

234

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Forensic Medicine

H. Psychic causes: They are the most common cause of impotence explained as follows: 1) Fear (of inconmpetence or of inability to complete

sexual act), anxiety, absence of desire, excessive passion and sexual desire, habit of excessive masturbation or sexual overindulgence, disgust of the act and dislike of partner. 2) Impotence quoad hoc (Sclective impotence): A man is impotent with a particular woman (e.g. wife) but not with others. 3) Frigidity of constitutions: It is a state of natural impotence in which some healthy, young, well-built individual have no sex urge or desire. 4) Bridal night impotence: It is the sudden temporary impotence developed in a newly married male in first night of marriage. The penis may not erect or may partially erect and a slight penetration may lead to premature ejaculation.

EXAMINATION OF A MALE IN CASE nE

IMPOTENCY

Prerequisite:

(1) Obtain the order of

court police: The person is examined only when ast by court/police in alleged rape case. (2) Identis cation: Identification of the male is to be done h. a close relative. At least two identification mart should be mentioned. A recent photograph should be attached duly signed by doctor. (3) Obtain con. sent: Informed consent of accused, duly attested by the witness with time, date and address should be obtained. History: (1) Sexual history; (2) medical historv for example, previous illness, smoking, obesity, diabetes, nocturnal tumescence, peripheral neuropathy and medication; (3) surgical history, for example, prostatectomy and (4) psychological history, for example, fear, anxiety, depression and phobias. CAUSES OFIMPOTENCE AND STERILITYExamination: (1) General physical examination: Pulse, BP and secondary sexual characteristics. (2) IN FEMALES Systemic examination: CNS, CVS, respiratory and A. Age: The puberty starts at abdominal. (3) Local examination: (a) Penis: Con13-14 years of age in females in India. A female is sterile before genital deformity, phimosis, etc. Bulbocavernosus puberty and after menopause. reflex is done to detect adequate nerve sensation B. Congenital diseases: Absence (or atresia) of in the penis. The doctor squeezes the glans of the vagina, adhesions of labias, imperforated penis which immediately causes the anus to conhymen and Turner syndrome. tract if nerve function is intact. (b) Testes: Size, C. Local diseases: Adhesions developed hydrocoele, absence, etc. (due to vaginal diphtheria/ulcers), tumours of vagina, vulval Investigations: (1) Blood levels of HbAlc, ipelephantiasis, LGV, TB, gonorrhoea ids, thyroid, FSH and testosterone. (2) Intraand bacterial infections. cavernosal injection of vasoactive substance (eg D. General diseases: DM/TB/CHB, transverse myeliPapaverine or PGE1) to produce erection and use tis and Ca-breast. of pornographic videos. (3) Cavernoso-grapny E. Drugs: Since a woman is a passive agent, she will (4) Nocturnal penile tumescence: Normally a man not become impotent by abuse or overindulgence has five to six erections during REM sleep. Absence of drug. But impotency in a woman is of erections indicates defect in nerve functions or active in nature (due to vaginismus: reflex spastic blood spasm). supply in penis. It may be useful in diteren F. Chronic lead poisoning. tiating psychogenic causes from organic causes. G. Exposure to X-ray leads to sterility. Duplex USG: To check the atherosclerosis or cal" H. Psychic factors, for example, disgust of the act, cification inside the penile vasculature. (6) Penile morbid fear of getting hurt, emotional disturbance biothesiometry. (7) Others, for exanple, penile and sense of guilt with mental trauma from prearteriography and spongiosography. vious act. Vaginismus is a psychogenic cause of Opinion in case of male: Forensic expert gv impotence in females. It is a condition in women opinion whether the person examined is capabie in which any attempt to sexual intercourse results of performing sexual intercourse or not. in severe painful spasmodic contraction of the When everything is normal, the opinion is given muscles of vaginal outlet. in negative form: "There is nothing to suggest

a

CHAPTER 9 is incapable of performing sexthat the person intercourse'. ual per. abnormal, the opinion can be: The When of performing the son xamincd is not capable Iwrite cause/disof sexual intercourse because

ease here)

female examined inion in case of a female: The taking part in sexual act (aptavira) is capable of ot taking part in sexual act or she is not capable (non-aptavira).

MEDICOLEGAL IMPORTANCE OF

IMPOTENCE AND STERILITY

In

charges of sexual offences, impotence defence. put forward as a plea of

is

often

(1) Question of impotence and sterility arises in discivil cases, for example, marriage, adoption, damages puted paternity and legitimacy, claims for when loss of sexual function is a result of assault/ accident and blacknmailing and defamation cases; (2) criminal cases, for example, rape and unnatural sexual offences and when an injured person thinks that he has become impotent and can be due to wounds/injuries inflicted by others and (3) both civil as well as criminal case, for example, adultery. Marriage versus impotence and sterility: impotence is present at the time of marriage: (1) According to S.12 of Hindu Marriage Act, such type of marriage is voidable. It means if the affected party brings a suit in the court for nullity, the marriage is dissolved. If no such suit is brought before court, the marriage may continue. (2) According to S.24 of Special Marriage Act, such type of marriage is void. The impotence should be imcurable for a successful suit of nullity. If impotence is curable, nullity would not be granted. Marriage is neither null and void, nor voidable, nor can divorce be obtained in remaining three cases: (1) If impotence develops after marriage, (2) if sterility is present at the time of marriage and (3) if sterility develops after marriage.

A. If

B.

IMPORTANT QUESTIONS FOR EXAMINATION SHORT NOTES 1. Artificial

(SN)

insemination

2. Surrogacy

Sexual Jurisprudence

DIFFERENCE BETWEEN (DW) 3. Artificial

insemination homologous (AIH) and artificial insemination donor (AID)

ANSWERS

SN-1: Artificial insemination It is the artificial introduction of Introduction: scmen into the reproductive tract of a female so as to result in pregnancy. It is done when female can not conceive through sexual intercourse with her husband. It may be intracervical, or intrauterine, or less commonly intrafallopian (i.e. sperms are put near the mouth of fallopian tube), intraperitoneal (i.e. sperms are put near the ovaries) or intravaginal. a Types and indications of AI: 1) AIH (AI-homologous/husband): Semen of husband is artificially inseminated into genital tract of a woman. Indications: (1) Hus band is impotent due to any cause (e.g. hypo/ epispadias), (2) husband is dead and his semen was harvested after death, (3) when husband is being treated for cancer with radiotherapy/ chemotherapy and (4) unfavourable cervical factors: (a) cervical mucus too thick and sticky;s or not enough to allow sperms to move easily or not compatible with sperms, (b) cervical stenosis and (c) persistent cervicitis. 2) AID: Semen of donor (i.e. some person other than husband) is artifhcially inseminated into genital tract of a woman. Indications: (1) Husband is sterile, (2) husband is suffering from HIV or hepatitis B or hereditary disease, (3) Rh incompatibility and (4) woman is allergic to husband's spernm 3) AIHD (AI-homologous and donor) (Pooled donor): Semen of the husband is mixed with semen of donor to bring the sperm count to normal. Now there is a possibility that husband's sperm would fertilise ovum. Indications: Husband is oligozoospermic.

Precautions: 1) Donor should be of 22 and 23) is the commonest cause, (2) low implantation of zygote, 3) defects in placenta or embryo and (4) disease of placenta and decidua. 5. Maternal: (1) Cervicouterine factors usuaily cause second trimester abortion and these include cervical incompetence,

abortion: Infection of the uterine contents at around the time of abortion.

Septic

THERAPEUTIC (OR JUSTIFIABLE OR LEGAL) ABORTION

NATURAL ABORTION (OR

o

tive spontaneous abortions.

congenital

It is the abortion which is done in good faith by qualified personnel to save the life of the woman. It is done according to the provisions of Medical Termination of Pregnancy (MTP) Act, 1971.

Methods to procure therapeutic abortion: They are categorised as methods for first trimester and methods for second trimester. Methods for first trimester: 1) Medical methods: Mifepristone (RU-486) 1s followed by Misoprostol. This regimen (accordeffective up to 7 weeks of pregnancy 1971) with success rate ing to MTP Act,

90%-95%. (a) to Prerequisite: (1) USG must be done which nmust confirm duration of pregnancy

SECTIONI

248

Forensic Medicine

exclude ectopic (i.c. be 25 cm) (in

CHL in cm

CHL is 40 cm, the age of foetus

2.

months)

is

40/5=8 months If age of foetus is 6 months, its length is = 6 30 cm

x5

VIABILITY Viability: It is the capability having a separate exisof tence after birth by virtue of certain degree of development.

Age of Viability

ne age of viability in India has been

46

What Events Occur at the Age of Viability? 1)

CHILD AGE OF THE

TABLE 9D.1

not been defined in the law. It means in India, if a foctus is born at or after 28 weeks (i.e. 7 months), it is capable to survive outside and it can be saved by modern medical facilities available. The age of viability in England has been considered as 24 weeks (i.e. 6 months) of gestation. It means in England, a foetus born at or after 24 weeks (i.e.6 months) is capable to survive outside and it can be saved by modern medical facilities available in England.

considered as weeks (i.e. 7 months) of gestation although it hasS

Pulmonary surfactants: In pulmonary alveoli, the type lI alveolar epithelial cells (also known as'pneumocytes, which occupy only 5%-10% of alveolar surface) start synthesising the surfactants' at 20th week of gestation. At 26th week, these cells begin to release surfactants by exocytosis of lamellar bod-

ies. Although at 28th week, the surfactants are well

developed so that a child can survive outside, but the quantity of surfactants reaches peak at 35th week. (Note: Surfactants decrease the surface tension caused by water molecules in alveoli and thus alveoli are able to expand. Deficiency of surfactants increased surface (e.g. in premature babies) the alveoli are collapsed (i.e. atelectatension hypoxaemia, CO, retention and acidosis sis) endothelial and pulmonary hypoperfusion epithelial damage > plasma leaks into alveoli > fibrin and necrotic cells > hyaline membrane. This condition is known as hyaline membrane disease (HMD), also known as infant respiratory distress syndrome (IRDS). For prevention of HMD, antenatal steroids are given to mother 48-72 h before delivery. For its treatment, surfactants are given h of locally through trachea of infant within 24

birth).

of viabil2) Ossification centres appearing at the age and third piece ity (i.e. at 28 weeks): Talus, second

of sternum. 3) Features of foetus at the age of viability:

cm disappears; eyelids open b. Pupillary membrane longest cm long: lanugo hair C. Scalp hair is the large intestine d. Meconium in whole of

4.

weight=1.5 kg,length= 35 1

254

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Forensic Medicine

testis at erternal and right testis at internal7 inguinal ring Caccum in right iliac fossa; valvulae conniventes

e. Left f.

start appearing convolutions formed; grey nnatter not formed.

g. Brain

STILLBORN (STILLBIRTH) AND DEAD BORN (DEAD BIRTH)

Stillborn Foetus A foetus which was born after 28th weck (24th week in UK) of pregnancy but did not breathe or show any sign of lite after being completely expelled. The child

was alive in uterus just before the start of labour pains but dies in birth canal during the process of birth, for example, by aspiration or strangulation by cord. Causes of stillbirth are: (1) Prematurity; (2) anoxia of premature foetus; (3) birth trauma; (4) congenital defects; (5) prolonged labour; (6) toxaemia of pregnancy and (7) Rh-incompatibility (i.e. erythroblasto sis foetalis).

Dead Born Foetus Foetus had already died in uterus and that died foetus

was expelled out. A dead born foetus may show five signs: (1) Rigor mortis at delivery; (2) putrefaction occurs ifair enters the uterus; (3) maceration occurs if air does not enter uterus; (4) mummification: occurs

o

a

when blood supply is deficient or liquor amnii is scanty or when no air enters into the uterus and (5) adipocere. Radiological signs of a dead born foetus (mnemonic Robotic Surgery Delivers Healthy Child). Kobert's sign: Gas in great vessels, for example, heart and aorta. It is the first radiological sign in a dead born foetus. 2) Spalding's sign: Overriding of foetal skull bones. It appears 2 days after death. It occurs due to shrinkage of cerebrum after intrauterine death. 3) Deuel's halo sign: Separation of subcutaneous fat of the foetal scalp from the cranial bones. 4) Hyperflexion of spine 5) Crowding of ribs

Maceration: It is a process of 'aseptic autolysis which occurs in a dead foetus inside uterus. It develops if the foetus dies and remains in uterus for 3-4 days surrounded with liquor amnii (i.e.

with intact amniotic membrane) e) withexclusion

of air.

Mechanism of maceration: After

adeah the cell membranes start to break down: cytoplasm containing ytic enzymes andthe (e.g.glyco lytic, proteolytic and lipolytic) is released these disintegrating cells into extracellularfrom ca space. These enzymes cause autolysis (or autodio tion) of other cells and tissues. Since auto occurs without any microbial (bacterial) olysis act ity, it is completely an aseptic chemical proces Signs of maceration: (1) Slippage ofskin isthe earliest sign (within 12 h of death). (2) Sti blebs (fluid-filled bullae) appear at 24 h. Epi dermis can be easily separated from underlyina dermis leaving red, moist and shiny areas. (3) In 48 h: Body is soft, flaccid and flattens out when kept on flat surface. Soft parts are easily detach able from bones abnormal mobility of joints. (4) After 3 days: Oedema. Umbilical cord is red smooth and soft. Viscera is softened and loss morpholo8Y. (5) At last, dehydration results in shrinkage of foetus. Grading of maceration: Genest grading and Pauli's stages. Medicolegal importance: Time since death can be estimated. If a foetus dies in uterus and is stll in the uterus, the 'radiological' signs can help in estimation of time since death. If it is delivered, then at autopsy, we can estimate time since death by postmortem changes which occured in uterus. foetal

Difference Between Stillborn and Dead Bom It is explained in Table 9D.2.

LIVEBIRTH According to S.2(d) of Registration of Births anu Deaths Act (1968), live birth means 'the comp te expulsion of foetus from its mother, irrespectve the duration of pregnancy, which after such exp sion, breathes or shows any other evidence of lite. Du, according to Indian Criminal law, the definition live birth is something different.

Legal Definition of Live Birth in India

erit Even if any part of foetus comes outside, whether breathed or not, it is considered live birth in

h

E 9D.2 Difference Between Stillborn Foetus and Dead Born Foetus [D/w-111 TABLE Stillbom Foetus (Stillbirth) Dead Born Foetus (Dead Birth) No. Features

S.

Period of gestation

Death of foetus

Seen

in

Signs

Causes

>28 weeks The child was alive in uterus just before the start of labour pains but dies during the process of birth legitimate and immature male children in primiparae Prolonged labour, for example, severe moulding of head and caput succedaneum 1) Prematurity

Foetus had already died in uterus and so the dead foetus was expelled out Not so Rigor mortis, maceration,

mummification,

etcC.

Congenital anomaly, ABO and Rh incompatibility

2) Anoxia of premature foetus 3) Birth trauma 4) Congenital defects 5)

Any

Prolonged labour

6) Toxaemia of pregnancy 7) Rh incompatibility (erythroblastosis foetalis)

of S.299, IPC]. For example, suppose live birth whether the one foot comes out, it means foetus breathed or not. The causing of death of such child may amount to culpable homicide and punishment has been prescribed in S.304 of India Penal Code (IPC). The causing of death of child in the mother's womb is not homicide, it will be considered as foeticide. Punishment for foeticide has been prescribed in S.312, 313 and 316 of IPC. Explanation

3

Legal Definition of Live Birth in

England

When whole foetus comes outside completely, irrespective of the attachment or severance of the cord, then it is considered live birth in England. For example, when whole foetus comes outside, then it is considered as live birth, it does not matter whether umbilical cord is attached or cut. Here destruction of intant before its complete birth is not homicide, but destruction of infant after complete birth is homicide.

Evidence of Life Any sign of life after complete birth of a as proof of live

child is accepted birth, for example, crying, sneezing yawning, movement of limbs. The muscle twitching 1S not safe to take as evidence of life as muscles may twitch for some time after death. After birth the intant Cries (it involves breathing) and it is quite usual and normal. But sometimes, breathing and crying occus Defore complete birth. When membranes rupture an r enters into the uterus or vagina, the foetus maytak reath and may cry. When the head of foetus is inside uterus and it cries, then the cry is called vagitus

uterinus. When the head is inside the vagina, the cry is called vagitus vaginalis. So obviously, the proof of breathing is not always the proof of live birth.

Signs of Live Birth (Demonstrated at Autopsy) of chest: Before respiration, the chest is flat with circumference 1-2 cm less than the abdomen at umbilical level. After respiration, the chest is expanded and arched or drum shaped. Position of diaphragm: Before respiration, the diaphragm is at higher level (4-5th rib) but after respiration, the diaphragm is at lower level (6-7th rib). To note the level of diaphragm, first of all open the abdomen and note the highest point of diaphragm.

A. Shape

B.

C. Lungs: Unrespired lungs must be differentiated

from respired lungs (Table 9D.3). Hydrostatic (Raygat's) test is explained in [SN-3]. D. Signs of struggle to breathe: Dark fluid blood due to increased CO,, cyanosed expanded lungs, Tardieu's spots (on pericardium, pleura and thymus) in both live birth and stillbirth, pulmonary oedema and ascitis. E. Other signs of live birth depending on the time of survival: 1)

Contents of stomach: Air in GIT (Breslau's second life test

= stom-

ach bowel test): Remove stomach and intesend tine intact after tying ligature at each respiration and put in water. They float if The surhas occurred, otherwise they sink. follows: as vival period can be calculated

256

SECTIONI

TABLE 9D.3 S. No. Features

Forensic Medicine

Difference Between Lungs Before Respiration and After Respiration Before Respiration (Unrespired Lungs) Level of 4-5th rib Small, collapsed near the hilum Dense, firm, non-crepitant, liverlike Reddish brown, bluish or deep violet

Position of diaphragm Lung volume

3.

Consistency

4.

Colour

5.

Weight (both lungs) -

6.

according to degree of anoxia

Fodor's test Ploucquet's test

gravity of water

=

1.

2.

3

70 g (just double) 1/35th of body weight

1/70th of body weight 1.04-1.05

0.94

1000)

Gas in stomach (immediately after birth), small intestine (2 h), colon (6h) and rectum (12 h). Saliva, amniotic fluid, blood, milk, meconium, mucus and mucins. 2) Changes in middle ear (Wredin's test): Before birth, the middle ear contains gelatinous embryonic connective tissue. With respiration, the sphincter at the pharyngeal end of eustachian tube relaxes and the air replaces that gelatinous connective tissue in a few hours to 5 weeks. It is ot at all reliable.

TABLE 9D.4 S. No. Features

3) Blood: Nucleated RBCs disappear by 24 h. HbF is reduced to 7%-89% by 3rd month of life and disappears completely by 6th month of life. 4) Meconium: It is completely expelled from GIT within 24-48 h. In anoxia and breech presentation, it is completely expelled from GIT before

birth.

5) Cephalhaematoma versus caput succedaneum: It is explained in Table 9D.4 and Fig. 9D.1. 6) Skin colour changes from bright red to darker, then brick red and then yellow. It becomes nor mal by 7th day.

Difference Between Cephalhaematoma and Caput Succedaneum [D/W-131

Mechanism

Cephalhaematoma

Caput Succedaneum

Swelling due to localised collection of blood deep to scalp between periosteum and bones of skull Rupture of a small diploic or emissary vein due to mechanical trauma, for example, forceps delivery

Swelling due to stagnation of fluid between the skin and glea Long contact of head over the dilated cervix; rigid cervical ring presses the Scalp and interference with venous return

Situation

Unilateral (usually right one)

May be bilateral, over the presenting part of the head in vertex position

Cross suture line

Never crosses suture line (i.e. it is limited by suture) and is limited to periosteal sheath of parietal bone

Crosses suture line

Cause

egte

Content

Blood

6.

Size

Smaller

7

Occurrence

Rare

8.

Development

Never present at birth but gradually develops 1-2 days after birth

Disappearance

Disappears in 6-8 weeks by absorption of blood

10.

Larger, fills pleural cavity Soft, spongy, elastic, crepitant Red/pink, mottled or marbled

appearance

35 g

Hydrostatic (Raygat's) test, that is specific gravity test (Specific

After Respiration (Respired Lungsl 6-7th rib

3

Felation toneonatalNeonatal jaundice may become worse due to extra jaundice load of blood plgments

Serosanguineous

fluid

Larger Common Present at birth, it means it develops before birth an It starts disappearing soon after birth completely disappears within 7 days with Neonatal jaundice has no relation

CHAPTER 9

Sexual Jurisprudence

Cephalohaematoma Blood collects between skull and periosteum -It does not cross sutures SkinGlea Periosteum

Suture

Scalp-

Parietal bones

Parietal bones of skull

of skull

(A)

Cephalhaematoma and

2 h: blood Changes in umbilical cord: (1) In clots; (2) in 12-24 h (1 day): cord shrinks and dries: (3) in 36-48 h (2 days): inflammatory day ring forms at base of stump; (4) in 2-3rd (3 days): cord shrivels and mummifies; (5) in 5-6th day: cord falls off leaving a raw area and (6) in 10-12 day: heals and leaves the scar. 8) Changes in circulatory structures is given in 7)

Table 9D.5.

CAUSES OF INFANT DEATH Natural: Prematurity, birth trauma, neonatal infection, congenital malformation, AB0 and Rh incompatibility.

Unnatural: (1) Accidental: (a) perinatak injury to mother, prolonged labour, prolapsed cord or cord around neck and death of mother and (b) postnatak Sufocation and precipitate labour. (2). Criminal: (a)

act of commission: strangulation/smothering/drownng, poisoning, head injury, twisting of neck and burning and (b) act of omission: failure to clear respiratory passage, failure to tie cord after cutting, failure to protect the child heat/cold and failure to feed.

IMPORTANT MEDICOLEGAL POINTS RELATED TO INFANTICIDE lf

(B) Caput succedaneum

Cephalohaematoma Fig. 9D.1 (A)

any person does

an act with intent (to prevent cHita or (to cause it to die after birth), will be punished [S.315, IPC]: P = I,. or F or both Abandonment of child (S.317, IPC]: parents or If 8uardian of a child NL) + a) If a police officer commits rape within the limits of his jurisdiction, or in the premises of any police station or on a woman in his custody. b) If a public servant takes advantage of his official position and commits rape on a woman under his custody. c) If any member of armed force commits rape. d) If the staff member in jail or remand home or institution for children/women commits rape in such places.

e) If the staff of a

hospital commits rape in that hospital. f) Ifa relative, guardian or teacher commits rape. g) Rape during communal or sectarian violence. h) Rape on a woman knowing her to be pregnant. i) [Omitted as per Criminal law (amendment) Act, 2018]. )Rape on a woman incapable of giving consent k) If any person in a position of control or dominance over a woman commits rape on such woman. 1) Rape on a woman suffering from mental and

physical disability. m)If any person while committing rape causes grievous bodily harm, disfigures, maims or endangers her life. n) It any person commits rape repeatedly on the same woman. 3) Whoever commits rape on a woman of NL) or death. (Mnemonic A = Aruna Shanbaug case in which she was suffering from PVS and then she died.)

S.376AB: Committing

rape on a Woman NL) +E. (Mnemonic D =Delhi Damini (Nirbhaya) gang rape case) S.376DA, IPC: Gang rapeofa woman purple colour. These tests are sensitive but not specific for semen due to presence of SAP in other body tissues. Other sources containing signifcant lower level of SAP are other body fluids (eg. vaginal secretions, RBCs), animals semen and vegetables (e.g. cauliflowers, ginger, clover

and turnips). specific antigen (PSA): A glyeoprotein, Prostatic derived from prostatic epithelial cells. It is found only in males (in seminal fluid, urine and blood) not in temales. Also found in seminal fluid, mae urine, breast milk, amniotic fluid and blood but its concentration is much more in semen. Ther between 1s no significant difference of PSA levels vasectomised and non-vasectomised individuals It can be found in vagina up to maximum of abou

2 days.

Its concentration fluid. i is double in sperm than any other body in st quite stable and the test gives a +ve result 6 months. It is also found in ol as as

Creatine

phosphokinase (CPK):

about old etinal tissues, tor example, brain, muscles and ic photoreceptor cells.

Immunological tests:

tory

ejacula Mab 4E6: The epithelial cells of to binds duct secrete an antigen 4E6 which is tected detc Surface of spermatozoa. This antigen iantiby monoclonal antibody (Mab 4E6). antihuman-spern ecitie 2) Monoclonal mouse vesicle-sp seminal detects (MHS-5) body seminal vesIc antigen (SVSA), produced in 1)

CHAPTER 9

examination: ion: It is a confirmatory ry oMicroscopic senen. The sperms are scen motile(i wet test tor (in dry specimen). specimen) or non-motile specimen: Remove semen by a moist swab 1) Wet it on a glass slide. Put a drop of and then touch saline on it. Examine under 1microscope normal sal At room temperature, motility perfor motility. 3 h, 50% are motile for 8h and sists for about h. In living persons, 1motile sperms 10% for 24 may be seen up to 6h atter ejaculation into the may be seen maxivagina. Complete sperms which they disintegrate. mum up to 3 days after on fabrics): Put a few drops 2) Dry specimen (e.g. dry speciof 1% HCl or 3% acetic acid on the is fresh and wait men and wait for 1h it stain for 4 h if stain is old. Then rub the moistened

Sexual Jurisprudence

281

portion of fabric on a slide. Dry in air. Fix it for min in methyl or ethyl alcohol. Then staining is done by any one of the following methods: a. Christmas tree stain: This stain consists of two dyes: nuclear fast red dye (it stains nucleus red) and picroindigocarmine (stains other cells, c.g. epithelial cells green). b. Methylene blue for 30 min and counterstained with eosin for 2 min. c. Haematoxylin for 2-5 min and counterstained with eosin for 3 min. Only posterior 1/3rd of head (containing nucleus) and the tail is stained by eosin deep red or pink. The anterior 2/3rd part of head (acrosome) is faintly stained or even not stained.

10 Blood Stains EXAMINATION OF BLOOD STAINS If a stain is found at the crime scene and it looks like blood in appearance and consistency, then the following basic questions come into mind: (A) Whether the stain is of 'blood' or 'something else'? There are different varieties of stains that resemble the blood stains and may confuse us. They are: (1) Rust stain of iron weapon/instrument; (2) vegetable stains: Mulberry, blackberry, tobacco, pan juice; (3) synthetic dye; (4) mineral stains; (5) miscellaneous stains: Spots of resins, grease, paints, coal tar on fabrics look like an old blood stains. To differentiate blood stain from other stains, there are screening (colour) tests as well as confirmatory tests [Table 10.1]. (B) Whether the blood is

of 'human origin' or 'non -human origin'? (i.e. determination of species origin): When it is confirmed by confirmatory tests that the stain is blood, the next question is whether that blood belongs to human or animal.

Thus to know this fact, serological tests are conducted, for example (1) immunological tests; (2) isoenzyme methods, for example, lactate dehydrogenase, peroxidases, esterases, etc.; (3) DNA tests. (C) What is the 'age' of blood stain? Fresh stain on light coloured cloth appears bright red, moist and sticky. In 24 h, it turns reddish brown. After 24 h, it turns dark brown and black. (D) Whether it is 'arterial' or 'venous'? Arterial blood stain: (1) Recently shed arterial blood is bright red; (2) arterial bleeding has a sprouting effect. Venous blood stain: (1) Recently shed venous blood is dark red; (2) venous bleeding occurs passively. (E) Whether it is 'ante-mortem' or postmortem'? Ante-mortem origin of bloodstain: Coagulation occurs with partly solidification and separation of serum. Clot can be taken out en masse from

282

the spot. After removal of clot, the staineduSually retains the impression of fibrinous net. work owing to the process of clot formation.On stretching, the clot can be separated in scales due to presence of fibrin. Postmortem origin of blood stain: Postmortem solidification occurs without proper coagulation change. Clot cannot be taken out en masse from the spot. After removal of clot, the stained area oes not retain the impression fibrinous net of work. On stretching, the clot becomes powder.

(F) What is the 'source of blood'?: Stomach and gas tric bleeding is chocolate coloured due to presence of acid haematin. And is acidic in reaction. Nasal bleeding has blood mixed with mucous and hair. Haemoptysis results into bright red (being oxygenated in lungs) and frothy (due to churning effect with inspired and expired air) and is alkaline in reaction. Menstrual blood is dark-coloured. foul-smelling fluid blood, often with endome trial debris t vaginal epithelial cells and is acdic in reaction. Blood from abortion is dark clote blood with endometrial and placental debris witn some foetal remnants. (G) What is the 'sex' of the individual? (i.e. sexing o blood stain): By Leishman staining. (H) Blood group identification of the stain.

ABO BLOOD GROUP SYSTEM RBC membrane contains 'antigens' (also kno antiagglutinogens) which in the presene ofsuitable utim bodies' (also known as agglutinins) cause aK tion' (i.e. clumping). Antigens (= Agglutinogens) (Ags): These (e and B) are carbolydrates present on the RBC n brane, They first appear in sixth week of 1UL, be dletected even before birth, their strength go and increasing after birth, till about 3 years of ag

o

Sac

RR

CHAPTER 10

Tests to Differentiate TABLE 10.1 Other Stains from Stains Blood Screening

(Colour) Tests

(SN-1

(Mnemonic: Boys Only

Like

Pretty Girls]

stains:

visible blood For test Benzidine (Adler's) 1.

2. 3.

Microscopic test 2. Microchemical (crystal) 1.

tests

Leuconmalachite green

test

Orthotolidine (Kohn Kelly)

(a)

and

(b)

test

Phenolphthalein (Kastle-Meyer) test Guaiacum test

5. blood For invisible

1.

Confimatory Tests [SN-3]

Haemochromogen

crystal (Takayama) test Haemin crystal (Teichmann) test

3. Spectroscopic test 4. Electrophoretic test 5. 6.

B3

galactosamine, galactose,, N-acetyl glucosamine, galactose, and fucose (Figs. 10.1 and 10.2). Addition of N-acetyl galactosamine to galactose, creates A antigen, that is blood group A. Addition of a galactose molecule to galactose, produces B antigen, that is blood group B. Addition of both N-acetyl galactosamine and galactose to galactose, produces both A and B antigens, that is blood group AB. " When neither N-acetyl galactosamine nor galactose is added to galactose,, no antigens are formed and so the blood group is O.

Immunoelectrophoretic

test

stains Luminol test

Blood Stains

Chromatographic test

RBC

RBC

N-Acetylgalactosamine

L-Fucose is added at the terminal galactose molecule (i.e. at Galactose-2) by enzyme

Galactose-1N-Acetylglucosamine

Galactose-2

thereafter they remain unchanged. Child's blood late group may not be set in its true ABO type until as as1 year after birth.

Antibodies (= Agglutinins) (Abs): These (i.e. Anti-A and Anti-B) are globulins of IgM type, so cannot cross placenta. They appear on 10th day after birth, rise to peak at 10 years and then decline. H gene locus: It is a gene on chromosome no. 19q, which is responsible for the expression of H substance. It encodes fucosyl transferase enzyme which adds fucose at terminal galactose (i.e.

galactose,) molecule of oligosaccharide chain surface of RBC. the on The addition of fucose to this oligosaccharide chain produces the H antigen (= H substance) on the surface

3

Fucosyl transferase

L-Fucose Ollgosaccharide chain at the surface of RBC

It consists of

a

chain of N-acety

H-antigen or

H-substance

Variants

HH

Fig. 10.1 Formation of

H

hh

Hh

substance

RBC

Gene A

Gene B (at chromosome no. 9)

(at chromosome no. 9) N-acetyl-galactosaminy transferase N-Acetylgalactosamine

of RBCs.

Individuals with homozygous dominant (HH) or heterozygous co-dominant (Hh) genes show phenoypic expression of H substance. Since H substance s the precursor of ABO antigens, so in these people, ABO blood group system is expressed. nalyiduals with homozygous recessive (hh) do not Snow any phenotypic expression of H substance ana so, ABO blood group system is These people not expressea. are very rare and are called as Bombay phenotype. H substance (H antigen): saccharide) del se ant It is a carbohydrate (oligosequence RBC membrane. linked mainly to proteins of the

H-gene

(at chromosome no. 19q13.3)

Galactosyl

transferase

Galactose

3

Blood group

Blood group

Fig. 10.2 Formation of ABO blood groups

Genetics of ABO System are The genes that determine the A and B phenotypes a found on the chromosome 9q and are expressed in Mendelian co-dominant manner. The gene products enzyare glycosyl transferases, which confer the antigenic specific matic capability of attaching the carbohydrates.

SECTIONI

TABLE 10.2

Forensic Medicine Secretors or Group-specific Substances [SN-41

Blood Groups andTheir

Coresponding Antigens and Antibodies Antigen

'Antibody' (Agglutinin)

Blood Group

Agglutinogen)

Aor A

A

B

B or B

B

a for Anti-A

th A and

AB

O or

O

B

No antigen

Bombay Phenotype (SN-5]

MEDICOLEGAL IMPORTANCE 0F BLOOn GROUPS

(or Anti-B)

Civil Importance Disputed paternity: (1) When the child is born in lawful wedlock and the husband denies that he is the father of the child and seeks divorce on this ground. (2) Blackmailing: When a child is born out of lawful wedlock and the mother accuses a certain man as the father of the child but the man denies the accusation. (3) Suits for maintenance of illegit-

No antibody

Both a (or Anti-A) and B

(or Anti-B)

A encodes N-acetyl galactosanninyl-transferase which adds an N-acetyl galactosamine to galactose, of H substance. Gene B encodes galactosyl-transferase which adds a galactose to the galactose, of H substance.

Gene

imate children. Disputed maternity: (1) When two women claim the same child. (2) Allegation of interchange of a child with another in the maternity home or hos pital. (3) In kidnapping, when the woman who has kidnapped the child claims to be the mother. She may name a friend as alleged father. (4) In case of suppositious child, when a woman pretends pregnancy and delivery. In case of a suppositious child, as for a true one. Divorce and nulity of marriage, for example, in

Landsteiner's Law (1900) 1) If an 'antigen' (= Agglutinogen) is present on the membrane of RBCs of a person, the corresponding'antibody' (= Agglutinin) must be absent from plasma.

2) If an antigen' (= Agglutinogen) is absent in RBCs of a person, the corresponding 'antibody

So,

= Agglutinin) must be present in plasma.

full description of blood group is B. AB A Op [Table 10.2]. Note:This law is not applicable for Rh system.

Inheritance of ABO System The genes that determine the A and B phenotypes are found on the chromosome 9q and are expressed in a Mendelian co-dominant manner. The six genotypes (i.e. AA, AO, BB, BO, AB, OO) produce four phenotypes (i.e. blood groups A, B, AB and O). Please see Table 10.3.

TABLE 10.3 Genotypes (Six in Mumber)

intersex cases.

Criminal Importance In

case of homicide: In case of murder and assault, it may establish link (1) between the offence, offended and offender; (2) between offence and offensive agent. In case of sexual assault: In case of sexual assault, for example, rape, it may establish link between victim and accused. In case of criminal abortion, delivery.

AB0 Blood Group Syster Phenotypes (Blood

Antigens (Agglutinogens) in RBC Membrane

Antibodies (Agglutinin) in Plasma

A (or Ap)

A

Anti-B (or

lor B

B

Group) (Four in Number)

B

AB

A

and

None

B

Distribution India

)

21

Anti-A (or a)

39

None Both Anti-A (or a) and Anti-B (or B)

31

%

Britain

CHAPTER 10

IMPORTANT QUESTIONS FOR EXAMINATION

SHORT NOTES

It

2) 3) 4)

(SN)

Screening tests for blood 2014] Benzidine test |CCU

Confirmatory tests for blood stains group-specific subGroup-secretor sutbstance or

stances phenotype 5) Bombay

ANSWERS

SN-1:

Screening tests for blood stains blood stains are given in

Screening (colour) tests for Table 10.1.

Principle for colour tests: Peroxidase enzyme present in RBCs acts on hydrogen peroxide (H,O,) used in test to liberate 0, which acts on the reagent to change its colour to blue. Such activity is a common property of all haemoproteins, for example, haemoglobin, myoglobin, cytochrome and catalase. Actually, haemoglobin in the presence of H,0, acts as a peroxidase enzyme. Here,

haem part of the haemoglobin catalyses the breakdown of H,O, As H,O, breaks down to O, and HO, the O, oxidises the reagent to give a colour (Fig. 10.3).

aiftar

2H,02 Peroxidase activity of Hb in RBC

O2

2H0

+

Oxidatio

Reagent---

(colourless base)

>

Reagent

(blue-coloured salt)

ig.10.3 Basic principle of colour tests for blood stains Benzidine

Test [SN-2] Leucomalachite

Green Test rinciple and drawbacks are same as of benzidine test.

uses

a 1% solution in

acetic acid

0-Toluidine

Princi test.

40% aqueous solution and gives bluish green

(Kohn

285

uses 1% solution in 40% alcohol and gives a blu ish green colour.

Phenolphthalein (Kastle-Meyer) Test Principle is same as in benzidine test. stains

1)

Blood Stains

colour.

o

and Kelly) Test

and drawbacks are

same as of benzidine

Phenolphthalein is an acid-base indicator. It consists of reduced Phenolphthalein (phenolphthalin) in alkaline solution which is oxidised by peroxide in the presence of Hb in blood. The reaction shows phenolphthalein (colourless in alkaline solution) being oxidised to phenolphthalein (pink in alkaline solution).

Procedure: A drop of saturated solution of phenolphthalein in glacial acetic acid (GAA) is added to the sample. After a few seconds, a drop of H,0, is added. Pink/purple colour is suggestive of blood. More specific for blood but less sensitive as compared to benzidine test. Guaiacum Test. Guaiacum is used as a reagent and the colour change is deep blue. Luminol Test. It is essentially a crime scene test and is more of a screening nature than confirmatory test. It is used when blood stains are rendered invisible by washing of the crime scene (in an attempt to obliterate the stains). Principle Luminol (3-aminophthalic acid hydrazide), a colourless substance, when sprayed on a suspected area, would make the entire area glow in the dark if blood is present. Mechanism: It reacts with iron (Fe) of haemoglobin which leads to the luminescence revealing the location of blood.

Procedure 1) Activation of luminol: Luminol must first be activated with an oxidant (usually a solution of H,O, and a hydroxide salt in water is used as the activator). In the presence of a catalyst (e.g. the iron compounds found in human haemoglobin) the hydrogen peroxide is decomposed to form oxygen and water. H,O,0, +H. luminol and activa2) Spray of the solution (of investigation. tor) throughout the area under lasting forabout 30s. Result The blue coloured glowfairly dark room. Detecting the glow requires a Drawbacks trigchemiluminescence can also be 1) Luminol alloys), copper-containing gered by copper (or and certain compounds of Co and Fe Some

286

SECTIONI

Forensic Medicine

bleaches. If a crime scene is thoroughly cleaned with a bleach solution, the residual bleach will cause the entire crime scene to produce the typical blue glow, elfectively camouflaging any organic evidence, such as blood. 2) Luminol also reacts with urine, faccal matter and animal blood to give the same result. 3) KMnO, and hydrated sodium hypochlorite also give +ve luminol reaction.

horseradish, potato, turnip, onion, tomato ,Cab. bage, dandelion root, etc.), in body fluid fluids pus, saliva, mucous, CSH, bone marroy (e brain, intestine, milk) and in animal juicee 3) Bacteria. 4) Animal blood gives the same result. Benzicdine is a known carcinogen, so seldom today. Nowadays, it is only of historical value. used

SN-3: Confirmatory tests for blood SN-2: Benzidine test (Adler's test)

Introduction:

It is a screening (colour) test for

blood stains. This test tells whether a particular stain (which resembles blood) found at crime scene is blood or other material. Principle: It is based upon the presence of enzyme peroxidase in RBCs. Peroxidase present in RBCs acts on hydrogen peroxide (H,O,) used in test to liberate 0, which acts on the reagent to change its colour to blue. Peroxidase activity is a common property of all haemoproteins, for example, haemoglobin, myoglobin, cytochrome (in granulocytes and monocytes) and catalase (liver, kidneys). Haemoglobin in the presence of H,0, acts as a peroxidase. Here, haem part of haemoglobin catalyses the breakdown of H,O,. As H,O, breaks down to O, and H,O, another substance in the reaction mixture is oxidised producinga colour change (Fig. 10.3). Procedure: A drop of saturated benzidine solution (10% benzidine in GAA) and a drop of H,O, are poured on the stain, dark-blue colour. It is the best preliminary test for blood. It has been used probably more extensively than any other test for presumptive identification of blood. Although this test is highly sensitive to minute traces of Hb and its derivatives (+ve with 1 in 10 lac dilution), it is not specific to blood. Negative test is of more value as it rules out blood, that is it indicates absence of blood in the stain but +ve test suggests that further steps should be taken to confirm the nature of the stain because false +ve reaction is given by: 1) Chemical oxidants and catalysts, for example, Cu and Ni salts, rust, paint, formalin, KMnO K-dichromate, some bleaches, hypochlorite, iodine, lead oxides and vitamin C, etc. 2) Peroxidase present in plant sources (e.g. apple, apricot, beans, blackberry, Jerusalem, artichoke,

stains Confirmatory tests for blood stains [Table 10.

Microscopic Test Microscopy reveals RBCs. In mammals, RBCs are

circular, biconcave and non-nucleated except that of camels (oval, biconvex, but non-nucleated). In fishes, amphibians, reptiles and birds, RBCs are oval, biconvex and nucleated. Staining of extract with Leishman stain reveals WBCs which may help to know the sex of the origin of blood by counting Davidson's bodies in the polymorphs.

Microchemical (Crystal) Test These tests are based on the property of haem (iron) to form characteristic coloured crystals (seen under microscope) with certain reagent

Haemochromogen Crystal (Takayama) Test Place a small piece of suspected material on a glass sice Add 2-4 drops of Takayama reagent (10% NaOH) 3 mL pyridine 3 mL, glucose 3 mlL, distilled water / m

Cover with a coverslip Slight warming ofslide (hastens the reaction After 1-6 min Microscopy

Pink feathery rhomboidal crystals' of haemochromogen or reduced alkaline haeli arranged in clusters Note: The result is -ve if crystals are not formea in 30 min. The test gives good results even wi old stains. It is delicate and more reliable. Takayau reagent should be stored in dark place in amber coloured botle. It will retain efficacy for 1-2 mont

a

P

ree

CHAPTER 10

(Teichmann) test: Haemin crystal ted material on a glass piece of Place a small slide Add a small

crystal of Naci and 2-3

drops of GAA

Cover with a coverslip

Heat over a small flame to evaporate the acid

Cooling

Microscopy (high power) red (dak

brownish/brownislh black)

Faint yellowish or rhombic crystals of haemin

arranged single or

in

haematin chloride clusters'

If Confimation of nature of crystals: a drop of are given by haemin H.0 is added, bubbles of gas

est

crystals.

Principle:'Haemoglobin' is converted into 'haematin chloride' (i.e. Ferriprotoporphyrin) in presence of halogen (e.g. NaCl).

-ve results may be obtained in both tests if extract is contaminated with some chemi cals; (2) stain is very old or decomposed or rusted (3) salt is added in excess; (4) reagents are very old/ defective; (5) moisture in acid; (6) overheating False

(1) stain

ad

Egas

Spectroscopic Test. 1It is most delicate and more reliable test for both recent and old blood stains. Here a very less quantity (i.e. 3 years.

Insanity and custody of minor children: Children need more of mother's care and love during this period, hence should not be separated from each other during this time. So in the suits of divorce, courtesy of law usually allows the custody of the child to vest with the mother, but the father is also allowed to visit the children periodically. If the mother, however, remarries, then the father may get back the custody of the children. 8) Guardianship: An MIP is not considered as a legal guardian of a minor. 9) Transfer of property: An MIP is not competent to transfer the property. 10) Adoption: According to Hindu Adoption and Maintenance Act, 1956, any Hindu male who is of sound mind and is not minor can adopt a child with the consent of his wite provided that his wife is of sound mind. Any Hindu female who is of sound mind and is not minor and is married can adopt a child. Any MIP cannot adopt a child. Government service: An MIP can enter into a government service. Criminal responsibility of MIP [SN-14]: ProISions as to accused persons of unsound mina 1ave been incorporated in S.328-339 of CrPC 7)

SOME IMPORTANT

TERMS

Abreaction: Reviving and bringing into consciousness, SOme

forgotten or other

traua

Forensic Psychiatry

293

experiences or repressed emotions from subconscious level by catharsis. Affect is the external expression of internal emotional content. Anhedonia: Inability to experience pleasure in previously pleasurable activities. A neurodevelopmental disorder charAutism: acterised by impaired social interaction, social communication and restricted and repetitive behaviour. Catalepsy: Maintains posture for a long time into which it is placed. Abrupt loss of muscle tone without Cataplexy: impairment of consciousness. Often seen in narcolepsy. |Greek, catharsis =purificationor Catharsis cleansing'1: The emotional release or discharge of tension. Mental process of knowing and Cognition: becoming aware. Compos mentis: Of sound mind. Confabulation: A false memory that the patient

believes to be true. The false answers are given by amnesia patients without a deliberate attempt to mislead. It is seen in Korsakoff's psychosis. Confabulation is different from lying and it may be very difficult to differentiate from it. of Empathy: Ability to experience the feelings persons another person or understanding another condition from their perspective. Fugue: A state of altered awareness during which his life, an individual forgets part or whole of leaves home and wanders. It may occur in hysteria, depressive illness, schizophrenia and epilepsy. between a Mental health: It is a state of balance a state ot person and the surrounding world; co-existence a harmony between oneself and others; other peobetween realities of the self and that of ple and that of environment. emotional state ot an Mood refers to an internal individual. buying. Oniomania: Compulsive Disorders caused disorders: mental Organic abnormalities of brain structures or by clirectly by neurophysiology, tor or chemistry brain alteration dementia. example, delirium and repetition of words Persistent Perseveration: feature of schizoA known relevance. their

beyond phrenia.

SECTIONI

Forensic Medicine

Phobia:

a

An excessive or irrational fear of particular object or situation, for example, acrophobia (abnormal fear of height), agoraphobia (open spaces), algoplhobia (pain), claustrophobia (closed Spaces), mysophobia (dirt), nccrophobia (dead bodies), 1yctoplhobin (darkness), thanatophobia (death), sitoplhobia (eating) and social phobin (social activities or public performance). Verbigeration: Senscless repetition of same worcds or phrases over and over again.

IMPORTANT QUESTIONS FOR EXAMINATION

SHORT NOTES (SN) 1.

Delusion [DU 2008] [CCU 2004, 2011, 2012, 2014,

2017]

2. Illusion 3. Hallucinations [DU 2010] [CCU 2009, 2010, 2015] 4. Impulse [DU 2007] [CCU 2016] 5. Delirium

6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17.

Delirium tremens [CCU 2015] Manic depressive psychosis [CCU 2014] Somnambulism Automatism Obsession and obsessive compulsive disorder Lucid interval [DU 2010] [CCU2010, 2011] Oligophrenia Testamentary capacity [DU 2007] [CCU 2009] Criminal responsibility of a mentally ill person McNaughten's rule [CCU 2005, 2010] Section 84, IPC [CCU 2004, 2010] Doctrine of diminished responsibility

DIFFERENCE BETWEEN (D/W) 20. True and feigned insanity [DU 2002, 2004, 2011] CCU 2003, 2009, 2011, 2012, 2014] 21. Delusion and hallucination 22. Lucid interval of head injury and insanity

23. Psychosis and neurosis

MEDICOLEGAL IMPORTANCE (MLI) 24. Person is having hallucinations 25. Person is in lucid interval 26. A person is feigning insanity |CCU 2010

ANSWERS

SN-1: Delusion Itis 'False belief in something () which is c notasact, (2) wlhich persists even after its falsity has been el demonstrated and (3) which is not ordinaril shared by other members of the patiepts ypciocultural. and education group. Types: (MnemoniPretty Girls Love'Indian Style Romance In Nepal) 1. Delusion of Persécution (or delusion of ara. ara noia): It is the most common type of delusion. The person thinks that the people around him are trying to kill him. is seen in paranoid schizophrenia, dementia It and depression. Delusions of persecution and grandeur are often present together in the same person. McNaughten was suffering from delusion of persecution (paranoid schizophrenia). 2. Delusion of Grandeur: A person imagines himself to be very rich. although in reality he is pauper (poor). He thinks himself to be a king or god or saint or great per sonality (e.g. prime minister or president of country), but actually he is a common man. He is convinced that he has a great talent, or special religious power, or a special relationship With a prominent person. It is seen in delirium tremens. 3. Delusion of Love (erotomanic delusion) (Cleram bault's syndrome): (usually female) believes that a person One of higher socioeconomic status is in love witn him or her. The person tries to get close wn the person through telephone calls, letters, gts visits and so on. A lemale erotomanic may claim that the dottor or teacher showed strong erotic feelings towats

PEILIANG

her.

It

n

remely

believed to occur most often ext sexually frustrated (eg. married) individuals. Delusion of love can occur in paranoid schi is

phrenia, organic mental disorders and bip mood disorders. and 4. Delusion of Influencef The person believes. ctions complains that his thoughts, feelings and a SOme are being influenced and controlled by

CHAPTER

5.

agency, for example, radio hypnotism, outside so on. telepathy andhypochondrial) delusions: The perSomat (or belicves that there is something wrong with his son is healthy. The following sub-

although he found: types are Ekbom's syndromc): a Delusional infestation (or fecls parasites crawling, biting or The person burning. jumping on his body caising itching or fecls body foul person Delusional halitosis: The b) in his body. odour or foul breath c)Delusional dysmorphophobia (or beauty hypochondria): Although any part of body can delusion is usube the focus of concern, yet the ally centred on facial features and the person feels an ugly nose, ear and so on. Woman's concern may be the unusual shape and size of her breasts. Man's concern may be with penile size, shape or its deviation. Delusion of Reference: The person believes that everyone is looking at him or talking about him; or the radio and TV are referring to him; or newspapers are wTiting about him. Delusion of Infidelity (jealousy): A man thinks that his wife is unfaithful to him, whereas in reality she is chaste. It is also known as Othello syndrome. The person searches his/her spouse's belongings to confirm the truth. If the spouse confesses to soothe the patient, the matters only become worse and may lead to divorce. Delusion of Nihilistic: The person feels he does not exist or that there is no world. is It also known as Cotard's syndrome. body,

6.

7.

dat

8.

Medicolegal 1)

importance:

Delusion is often taken as defence in

law.

4) Delusion is

the court

of

never an isolated disorder, but is

merely an indication

of deep seated, widespread sorder. For this reason, person cannot be held ully

responsible for his antisocial act. )lendency to commit suicide and homicide may be present. 4) A will made

by a person, who is suffering from n any way not related with the disposal of property. SN-2: 1

usion, may be valid if the delusion is

lusion

lusion: False interpre pretation of external object has real existence isknowt as illusion.

which

11

Forensic Psychiatry

295

For example, a dog at night may look like a lion, or a rope as a snake, or a tree as a ghost and so on. A sane person also has illusion but he is able to correct the illusion; however, an insane person cannot correct his falsity. Illusions can occur in insanity or intoxicated states.

Medicolegal importance: A person ble for his act.

is

not responsi

SN-3: Hallucination o

o

Hallucination: It is 'false sense of perception without any external stimulus (or object) to pro

duce it. It occurs in schizophrenia, temporal lobe lesions, drugs (e.g. LSD, mescaline, small doses of alcohol and cannabis), uraemia, high fever and so on. Types of hallucinations (Mnemonic 5 senses,ie. Auditory, Visual, Gustatory, Olfactory, Tactile +3 more, i.e. Psychomotor [kinaesthetic], Nonpathological, Synesthesia). 1) Auditory hallucinations: It is most common type of hallucination. The person hears voices or noises, and imagines that someone is speaking to him when no one is present. is common in paranoid schizophrenia. It (Note: McNaughten was suffering from paranoid schiZOphrenia and had auditory hallucinations.) Frequently auditory and visual hallucina tions are experienced together. Command hallucinations: In these hallucinations, the patient is ordered by hallucinatory voices to do unwanted and undesirable act like suicide or homicide. 2) Visual hallucinations: The person may see something which in reality does not exist, such as God, ghost, attacking animals and so on. It is common in schizophrenia. 3) Gustatory hallucinations: The person feels is no tastes (e.g. sweet, sour or salt) when there sertood in the mouth. lt occurs in uncinate epilepsy). Zures (or temporal lobe person perceives 4) Olfactory hallucinations: A Smells but there is none. called form5)Tactile/haptic hallucinations (also insects or imagines that Ications): A person underneath the skin, although crawling are mice hallucinations are types of there are none. These

96

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seen in cocaine abuse and so also called 'cocaine

bugs. 6) Psychomotor/kinaesthetic hallucinations: The person feels the movement of some part of tlhe

body, although there is none. 7) Non-pathological: (1) Hypna-gogic, that is false sensory perceptions occurring while falling asleep. (2) Hypna-pompic, that is false sensory

perceptions occur while awakening from sleep. 8) Synesthesia: A stimulus perceived by sensory organ other than the one that should actually perceive it, for example, visualising music, hearing different colours and so on. Medicolegal importance: Hallucinations may be pleasant or unpleasant. In unpleasant hallucinations, the person may commit suicide or homicide. The person is not responsible for his acts.

SN-4: Impulse Impulse: It is a sudden and irresistible urge compelling a person to perform some action without motive or forethought. A sane person can control impulse, but an insane person cannot control. Types: 1) Kleptomania: An irresistible desire to steal small articles of little value. 2) Pyromania: To set fire to things. 3) Mutilomania: A desire to maim animals. 4) Dipsomania: An excessive desire to drink alco hol. 5) Sexual impulses: A form of sexual perversions by abnormal means to obtain gratification. 6) Suicidal or ho: icidal impulse. oMedicolegal importance: In India, the person is criminally responsible because he knows very well what he is doing. But in more advanced 'irresistible impulse tes an accused person is not criminally responsible even if he knows the nature and quality of his act and knows that it is wrong, if he is incapable of restraining himself from committing the act, because the free agency of his will has been destroyed by mental disease. It is not followed in India. It is also known as New Hampshire doctrine.

SN-5: Delirium a

A disorder of consciousness generally produced by a transient disturbance of brain tissue functions

impaired orientation, critical faculty blunted/lost,

thought content is irrelevant/incoherent. : commonest organic mental disorder seen in s cal practice.

Features: 1) Clouding of consciousnesS: Decreased a aware ness of surroundings and decreased abili y to respond to environmental stimuli. 2) Disorientation in time, place and person. 3) Decreased attention span and distractibility 4) Illusions and hallucinations (most commonl ny visual) present. 5) Impairment of retention of new memories Remote memories normal. 6) Sleep-wake cycle is usually disturbed. Insomnia at night but drowsiness in daytime. 7) Sun downing: 1The symptoms become worse in evening. 8) Waxing and waning: The periods of complete clarity may be mixed with the periods of confusion. 9) Psychomotor disturbances: Hyperactivity and agitation. 10) Speech and thought disturbances. 11) Motor symptoms: Flapping tremors, arphologia or flocculation (i.e. picking movement at cover sheets and clothes). a Causes: (1) Medical conditions, for example, high fever; (2) head injury and (3) poisoning, for exam ple, datura. o Medicolegal importance 1) Delirium is less often associated with hallucina tions and delusions. 2) Person is not responsible for his act. 3) Will made in delirium is not valid. 4) A person may become impulsive and and may commit suicide.

viole

SN-6: Delirium tremens It

precipitat an acute episode of deliriumpre 5% by alcohol withdrawal. It is seen in only typl patients with alcohol withdrawal and Occurs 34 days after the last drink. is

Signs and symptoms: CNS: Agitation, coarse muscular tren

alluci-

tongue and hands, confusion, delirium, ntd tactile), diso nation (auditory, visual and men tion in time and place, insomnia, Ic restlessness, seizures and uncontrollable

CHAPTER

Pupils dilated, increased temperature Generaaeral: seizures, arrhoea, achycardia and tac due to hypnoea. occurs in -15% cases due to carDeath arrhythmia with hypokalemia, fat emboli diac

hyperpyrexia, dehydration, hypotension respiratory failure. o

and

Management: Benzodiazepines are the DOC. Diazepam 1) Drugs: 5 min. Rectal paraldehyde 10 mlL 5 mg iv every every 30 min. (NS and DNS). 2) Supportive: Fluid Medicolegalimportance: The person has a tendency to commit suicide, homicide and violent assault. He can danmage property also. Immediate restraint is done according to .81, IPC because there is no provision in Mental Health Act, 1987.

SN-7: Manic

depressive psychosis

term 'manic depressive psychosis' (MDP) was coined by psychiatrist Emil Kraepelin (1856

The

1926).

disorder (= bipolar affective disorder) was previously known as MDP. It is characterised by unpredictable swings in mood from mania (or bypomania) to depression. There may be the alternate periods of elevated mood and periods of depression. According to the severity, the elevated mood is known as mania and hypomania (a milder

Bipolar

form of mania). At the most severe level of mania, the manic individuals can experience much distorted beliefs about the world known A depressive'

o

episode. Types:

as psychosis. episode commonly follows a 'manic

Bipolar I disorder: There

may be two situations.

There are only the episodes of mania. To be

4

D

included in this category, there should be at least one manic episode. There are the episodes of mania and episodes of

depression.

Bipolar II disorder. Thereare the episodes of hypomania and episodes of depression. To be included tnis category, there should be at least one hypo* manic episode and one depressive episode MDP is a kind of bipolar mood disorder where the primary disturbance is in affect (i.e. od)

11

Forensic Psychiatry

297

from which all other symptoms arise. The mood varies between extreme poles of mania (i.e. cheerfulness) and depression (i.e. sadness). When two components, that is mania and depression, are present in a person at different periods of his life, the condition is called MDP. It means the attack of mania remains for a considerable time, and then it is followed by the attack of depression which also remains for a considerable time.

Manic

The

phase: patient

optimistic (i.e. thinks positive), full of self-confidence and has a general feeling of well-being. Mood is elated. Conversation reflects characteristic flight of ideas, that is no sequence. Attention is fleeting and there is high degree of distractibility. Delusion of grandeur present. Sleep is disturbed. Intake of food is reduced. Medicolegal importance of manic phase Offences like petty theft, deception and drunken misbehaviour are committed. A person with manic disorder seems to be in lucid interval during depressive phase. If he kills during manic phase, he may get benefit of S.84, IPC. Depressive phase: The patient looks tired, self-concerned. Sadness is reflected in his posture, movements and facial expression. Feels guilty. There is change in the history of the behaviour. He avoids friends and social activities. Whole mental activity may be reduced to lead in to stuporous stage. Loss of appetite and libido. There is early morning waking and sleep 1s not freshening. Medicolegal importance of depressive phase: first Suicide or suicidal attempt is otten the Someillness. and last symptom of depressive with delusions times there are hypochondrial esppecially homicidal tendency to kill relatives,tendency is Suicidal dependent young children. present is

SN-8: Somnambulism

person (known as which the in low/ disorder sleep in a state of lt is a sleep the from Sleep walker) arises

SECTIONI

Forensic Medicine

dissociated consciousness and performs activities as if he is awake. It most often occurs during stage 3 or 4 of deep NREM sleep (early in the night, i.e. first third of the night, i.e. between 11 p.m. and a.m.). Mostly there is one episode of sleep walking in a night (Pig. 11.1). I

Light sleep

Awake

Somnambulism REM sleep Occurs

Stage

n

Depth Stage 2

sleep

Stage

3

Deep sleep

Stage NREM sleep

(S-sleep)

4 REM sleeep

(D-sleep)

Stages of sleep and somnambulism: NREM (non-rapid eye movement) sleep consists of four stages (stages 1-4). Somnambulism occurs in stages 3 and 4 of NREM sleep.

Fig. 11.1 Phases of sleep and somnambulism

It

is a state

of dissociative consciousness; the mental faculties are partially active. Sleepwalking may last as little as 30 s or as long as 30 min. Most episodes last for less than 10 min. Sleepwalking may include simply sitting up and appearing awake while actually asleep, getting up and walking around, or complex activities such as moving furniture, going to the bathroom, dressing and undressing and similar activities. Some people can even drive a car while actually asleep. Such persons (mostly between the age of 5 and 12 years) are well adjusted in life and are socially well behaved and not aggressive. Medicolegal importance: 1) A sleep walker may commit a crime (homicide or suicide), or meet with an accident and even solve a difficult problem, but he has no recollection of the events. In some cases the events of one fit are remembered in another subsequent fit. 2) During this period, crimes are not wilful or premeditated. Such persons, when they commit a crime, are not held criminally responsible for

the act done during this period. The person can get the benefit of S.84, IPC if he can show he was not aware of the act.

SN-9: Automatism conduct that is performed by a person consciousness is impaired to such an extent whose that is not fully aware of his actions. nere may he There beno consciousness at all of the actions in question A

on, or there may be awareness that falls below level the normal consciousness. It is mechanical, repetitive, apparently purposefi and complex behaviour that iS not conscious con. trolled and for which there is amnesia later. Classification: (1) Insane automatism-associated with psychiatric disorder and (2) sane automa tism-not associated with psychiatric disorder. Aetiology: Cerebral disease, hypoglycaemia, hyg terical states, epilepsy, sleep walking (i.e. somnambulism), toxic (drug) and trauma (e.g. concussion, posttraumatic automatism). Drug automatism: There is a tendency to takea drug (sleeping pills) over and over again, forgetting each time that one has already taken the dose Repetitive intake of a drug because of drug-in duced drowsiness and anterograde amnesia leads to a cumulative overdose. In anterograde amnesia, there is loss of memory for events occurring tor ward in time. The victim keeps taking pills aill e dies. Most common drugs responsible are barbirl rates (most common cause) and benzodiazepines (especially midazolam). The manner of death s accidental. Medicolegal importance: 1) The concept of automatism is very vague t unsatisfactory. The Indian law has no spe provision for automatism. He can get the bene aware fit of S.84, IPC if he can show he was nota of the act. 2) In cases of life insurance claims, the cka drus settled for accident, not for suicide. Sincevictum automatism is accident, not suicide, the ion. party can claim for monetary compensu

SN-10: 0bsession (and obsessive

compulsive disorder, OCD) Introduction: A sane person can

arin

step

twice an wl

ular act (e.g. locking the door) the act after verification. But sometinnes may continue to repeat such particular yP (or again and again despite being well awar

M of SOu

Mes

Can

cate

Ocr

CHAPTER 11

about s) about conscious)

act, and also ther the repetition of the

affected person genthe act. The desire.to stop as irrational/sensehas recognises his obsession rther distressed by this erally become furth may and ess realisation. has two compoof OCD: An OCD Compeobsession and compulsion. nents, is a single 'thought Obsession: An obsession ) all efforts to and persIsts despite that recurs perconfront it. This recurrent and or ignore cannot be eliminated from consistent thought or reasoning. The patient sciousness by logic that this aware, and knows very well is fully act is senseless. So thought leading to a specific that cona obsession is actually just thought' person's a tinuously preoccupies or intrudes usually sexual or mind. Pure obsession includes aggressive thoughts. (either rituals or 2) Compulsion: Certain acts' behaviours) which are repeated again and again due to an obsession are called compulsions. The aim of the compulsive act is preventing and neutralising the distress or fear arising out of obsession. An MIP may not sleep and may spend whole night by repeating compulsive acts.

pure 'obsesmost of the cases obsession is associated with compulsion. When 'obsession' is associated with 'compulsion, OCD: Although a person may have sion' or pure 'compulsive acts, yet in

the combination is called

Examples of OCD: 1)

Forensic Psychiatry

OCD.

Washers: It is the most common type of OCD. Here the obsession is of contamination with dust and germs, whereas compulsion is washing hands again and again. The

person may also take bath repeatedly many times a day; may even wash clothes or bathroom repeatedly. 2) Checkers: The person repeatedly checks whether the door has been locked or not; kitchen gas has been switched off or not; money has been counted correctly or not. Medicolegal importance: Obsession is a disorder Ot mind that is borderline between sanity (menta Soundness) and insanity (mental unsoundness). Mentally sound person can have obsessions but can correct it. Depression ciatea is very commonly asso ciated with OCD and approximately OCD 50% of the patients have major depressive episodes. In

3 Manic phase

Depressive

phase

Manic phase

(Lucid interval) Person ls responsible for all acts

Fig. 11.2 Lucid interval in a case of insanity lar disorder)

(bipo-

extreme form of OCD, the person may commit suicide.

SN-11: Lucid interval It is seen in two cases: Head injury (in Chapter 7C) and insanity. Lucid interval during insanity (Fig. 11.2): Lucid interval is that space of time between two episodes of mental illness in which all the signs and symptoms of mental illness completely disappear, the person has clarity of mind, and he is able to judge and foresee the consequences of his acts. In simple language, the space of time between two episodes of mental illness during which a person behaves normal is known as lucid interval. occurs in bipolar disorders. In bipolar disorIt ders, lucid interval occurs between two subsequent attacks of mania, that is the depressive phase corresponds to lucid interval. Medicolegal importance: The person is legally responsible for his all civil acts and criminal acts

done during lucid interval.

SN-12: Oligophrenia Oligophrenia: It is another name of mental subnormality or mental retardation. It is said to be present when intelligence quotient (1Q) is fall in BP. 3) Cardiac arrhythmia due to electrolytic distur bance. 4) Diminished myocardial contractility.

306

B.

Respiratory causes 1) Respiratory (airway) obstruction by (1) soft tissues of mouth and pharynx (due to loss of

protective reflexes and general anaesthesia); (2) laryngeal spasm (due to laryngeal irritation); (3) secretions, blood, denture, swabs, vomiting (in emergency surgery when the patient is full stomach) and (4) wrongly placed endotrachea tube. 2) Aspiration of gastric contents: In light phas may of GA, the oropharyngeal manipulation leads provoke active vomiting, but it seldom to serious aspiration because laryngeal protec tive reflex is still intact. During deep anaesthe Sia, laryngeal protective reflex is lost passive regurgitation occurs which is a more serious event because it leads to airway obstruction anu bronchopneumonia. 5)

Pneumothorax: Positive pressure

ventilauon

converts a simple pneumothorax to tensio cause pneumothorax. Use of nitrous oxide will nay a pneumothorax to expand rapidly and contribute to hypoxia and death.

Respiratory depression due to overdose anaesthetic agents- hypoxia. due t 5) Equipment failure: Failure of O, supply misconnection. Empty 0, cylinders. C. Other causes opy or 1) Vagal inhibition of heart while laryngosceo intubation. Usc* 2) F'aulty use of anaesthetic drugs and 4)

relaxants 3) Malignant hyperthermia.

Procedure and Finding. in a Case Anaesthe and Operative Death

Autopsy

of

odour: Because inhalational anaesthetic

Note the specific odour. has ld be should

started with devices in situ. into the body are Devices attached to or inserted needles, chest tube, wound airwa IV cannulae, on. Autopsy pathologist should drains and so devices in situ to know here open cavities with the other end was reaching, for example, intuhation device may be found in oesophagus, thoracic drain pipe may be puncturing lungs and

Autopsy

so on.

is, wound and Site of surgical intervention, that surgical sutures (healthy or infected?). Surgical error, for example, ligation of a wrong blood vessel, ureter or bile duct.

CHAPTER 12 MiscellaneousTopics

Artefacts,

for example, sutures from stomach and intestines may appear to have broken down; however, it may be due to autolytic changes. Visceral organs (e.g. heart, kidneys, liver, spleen) show hypoxic changes.

Brain: 1)

Hypoxic changes are seen in hippocampal gyrus and cerebellum. 2) Leukoencephalopathy of cerebral hemispheres. 3) Demyelination and obliteration of axons in white mater and the infarction of basal ganglia. Check for common causes of intraoperative deaths: (A) Detectable-aspiration (ofregurgitated material), embolism, anaphylaxis, retained instruments, internal haemorrhage and peritonitis. (B) Undetectable-cardiac arrhythmias, fall in BP, laryngeal spasm and vagal inhibition of heart.

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Chapter 12B Torture and Custodial Deaths TORTURE The deliberate, systematic, 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' (According to the declaration of Tokyo, 1975). Reasons for torture may be (1) to obtain confession; (2) to take revenge; (3) for interrogation and obtaining information; (4) to spread terror in society/country and (5) to destroy the personality of individuals. Torture medicine is one of the recent branches of medicine dealing with various aspects of torture from the medical point of view.

Types of Torture Beating on (1) anywhere on body; (2) soles of feet (Falanga/kalaka/Bastinado); (3) ears by palms (el telephone) and (4) abdomen while lying on a table with upper half of body unsupported (el quirofano). 2) Suspension by (1) wrists (la bandera); (2) ankles (murcielago); (3) arms or neck and (4) head down from a horizontal pole placed under the knees with the wrists bound to the ankles (Parrot's perch, Jack, Pau de arara). 3) Forced posture: (1) Prolonged standing (el planton); (2) forced straddling of a bar (sawhorse, el

1)

cabellate). 4) Thermal torture (heat torture and cold torture). 5) Electrical torture (cattle prod): (1) La picana current is applied to sensitive parts, for example, nipples, tongue, penis and so on; (2) La parillaelectric shocks are given while the victim is tied to a metal bed frame. 6) Asphyxial/near-suffocation torture: (1) Forced immersion of head in water often contaminatecd (wet submarine, pileta, Latina); (2) tying of a plastic bag over the head (dry submarine). 7) Chepuwa: Both legs/thighs are tightly clamped with bamboo.

8) Others: (1) Roller torture; (2) pulling oro

of nails/hairs/tongue/teeth/ th/breasts; (3) twisting mutilat disfiguration by cutting, acids and so on: tant torture: Tiger balm of Rajkot; (5) sexual ture; (6) pharmacological torture; (7) dehydrait tion and (8) animal bites.

Management of Torture Victim (A) Treatment (1) Avoid, as far as possible, to remind the patient

the procedure of torture'. (2) Treatment should be both physical and ps chological, and both should be provided simultaneously. (3) Treatment should include not only the victim but also his family. (4) Personal social service should be a part of treatment. (B) Rehabilitation

Ethical and Legal Aspects of Torture According to both Hippocratic Oath and Decla tion of Geneva, doctors are obliged not to use ther professional knowledge in order to harm ther in the patients and prohibit medical involvement practice of torture. (1945: Universal Declarations of Hunman Rights tortur Article 5 says No one shall be subjected to or to cruel, inhumane or degrading treatient

punishment.

(1) 10s World Medical Association (WMA): Maltu 2) declaration, 1976 talks about torture: ( declaration, 1991 talks about hunger strike Act, 199 The Protection of Human Rights constitutiol Was enacted to provide for the (NHR ommission National Human Right in >talc State Human Right Commissions protec enkations Human Right Courts for better human rights. NHRC has given recomnei in custodial deaths and torture. rtur tort about deal IPC S.339 of S.330, S.331 and

SHO

SN Fa Be-

It for Re-

Fa

lov

(1

(2

CHAPTER 12

IMPORTANT QUESTIONS FOR

EXAMINATION

NOTES (SN)

SHORT

SN-1: Falanga

"Bastinado'): knowT as Falaka' or .Falanga (also feet with canes or rods is on the soles of Beating falanga. known as

It

is a

type of physica

interrogation. It reasons. for many police

torture commonly used in can be used by perpetrator

Reasons forfalanga: (2)

obtain confession, to take revenge,

(3)

for interrogation and

(1) to

obtaining information, (4) to spread terror in soiety/country, and (5) to destroy the personality of individuals. Falanga is preferred by perpetrator due to the following reasons:

Extremely painful because there is clustering of nerve endings in the feet. (2) The injuries in soles take long time to heal (1)

because soles are

the weight-bearing region.

Miscellaneous Topics

309

(3) Due to the thickness of soles, the injuries are not visible. Injury caused: Deep bruising occurs by repeated beating with blunt weapons, for example, canes or rods.

Management of the victim of falanga: It is quite casy to diagnose a torture victim by proper history and general physical examination. (1) Avoid, as far as possible, to remind the patient the procedure of torture. (2) Treatment should be both physical and psychological, and both should be provided simultaneously. (3) Psychological treatment should include not only the victim but also his family. (4) Rehabilitation. Autopsy: Deep dissection of the soles is necessary to reveal bruising. Other injuries may be present on body. Medicolegal aspects: Falanga is a type of torture and is punishable under S.330 of IPC (i.e. Voluntary causing hurt to extort confession) by P=I +F.

310

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Forensic Medicine

Chapter 12C Recent Methods of Interrogation Court of India in 2010 has opined that all

INTERROGATION method used by police for getting information from a suspect/witness/victim after a crime has been conmitted.

A

IMPORTANT QUESTIONS FOR EXAMINATION

3)

SHORT NOTES (SN)

SN-1: Narcoanalysis (or narco test) Narcoanalysis is interrogation of a suspect by investigating agencies after inducing narcosis to obtain information. Principle: A subject by his conscious imagination can voluntarily decide to tell a lie. In narcoanalysis, the subjec's capacity of conscious imagination is neutralised by making him semiconscious (i.e. narcosis). In semiconscious state, all his inhibitions are lost; he becomes relaxed and may speak truth. His answers are supposed to be specific and restricted to facts he is already aware of. Term Truth serum' has beèn used to describe a variety of drugs that are used in narcoanalysis. This term is a misnomer in two ways: first, the drugs used are not serums, and second, the truthfulness is not guaranteed. Team that conducts narcoanalysis consists of three persons: (1) the physician certifies the fitness of the person before and after the test. (2) The anaesthetist controls the depth of anaesthesia by giving drugs. (3) The psychologist interacts with the person. Most common drugs used as truth serum are (1) barbiturates, for example, thiopentone sodium and sodium amytak, (2) ethanol and (3) anti-allergics, for example, scopolamine (hyoscine). Medicolegal aspects 1) The test is conducted in government hospital after a court order is passed and the consent of the subject is also required. 2) The use of narcoanalysis is illegal in India. Article 20(3) of the Constitution of India says No person accused of any offence shall be compelled to be a witness against himself. Supreme

4) 5) 6)

three tests (i.e. narcoanalysis, polygraph and RE violate the right against self-incrimina:A nation that is constitutionally protected under Ari Artice 20(3), so the test cannot be forced upon subject. S.161(2), CrPC states that a person ay can not be bound to answer questions whichen xpoe him to a criminal charge' According to the International law and Declara. tion of Tokyo, forced use of truth drugs is co. sidered as a form of torture. The use of narcoanalysis is scientifically and lezal valid in the evaluation of psychiatric patients. The excess dose of (or hypersensitivity reactions to) truth drugs may cause sudden death. There are chances of large number of false neg atives. u

SN-2: Truth serumn Term Truth serum' has been used to describe a variety of drugs that are used in narcoanalysis [SN-}

SN-3: Polygraph Polygraph

is also known as lie detector. It is a device which simultaneously records severl physiological parameters, for example, blood pres

sure (BP), heart rate (HR), respiratory rate (RK and electric conductance of skin, while a series ' questions are being asked in an attempt to detect ie and Principle: When a person lies, he gets nervous iviy develops fear/anxiety >Ted sympathene Td BR, Td HR, Td RRand Tdsweating. StressSweating (especially on fingertips)->Td conductnuy (i.e. electrodermal activity). The two galvl plates are attached to two of the subject's finger. plates measure skin's ability to conduct electrici nevusy If a person is asked a question and simultan these physiological parameters are being monitorle the investigator would knowwhen he isspeaki Procedure: pre 1) Pretest interview: Polygraph starts th a inte test interview to gain some preliminary ntro co mation which will later be used for questions (CQ).

t

wior

CHAPTER 12

Explanation of test: The tester explains how 2) the polygraph is supposed to work. It has test can. detect lies and it is phasised that this answer truthfully. inmportant to rery different types of questions are Following three alternate: (1) these qucstions may asked and relevant questions questions; (2) irrelevant (IR) is realhy"interested' in these ques(RQ): the testator probable lic control questions (CQ): 4)

tions (3) lie about. that most people will the questions physiological (1) Result and interpretation: than those to CO, responses to RQ are greater

If

physiological person is lying. (2) If those to RQ, responses to CQ are greater than guilty. In this situation, it means person is 'not it means

posttest interview. Medicolegal importance there may be a

Propranolol (a beta blocker): It is an anti-anxstressful iety drug. Many people take it in acute situations, for example, examination, public appearance and so on. If a suspect is on antihypertensive treatment and has already taken propranolol without the notice of tester, the symptoms of anxiety will not appear and so above-mentioned physiological parameters will be within normal limit. Polygraph test is also a stressful situation and a suspect having sufficient knowledge aboutthe propranolol may take it before the test without the notice of tester. 2) NHRC on 12 November 1999 had published Guidelines Relating to Administration of Polygraph Test (Lie Detector) on an accused: Lie detector test should be administered with the consent of accused. If accused agrees for the test, he should be given access to a lawyer. Consent should be recorded before a Judicial Magistrate. The recording of the test shall be done in a hospital in the presence of a lawyer. 1)

ea

2.KTE

SN-4;

Brain fingerprinting

Drain fingerprinting

is

also known as

map

brain ping or P300 test and it was developed by a neurol o851, Dr. Lawrence

Itisa

neuroscience

Farwell (1919-95).

cificinformation technique sed to determine spe inasubject'sb (regarding a crime) already stored It detects the presence or absence of inf rmation and not theguilt or innocence per se. based

nat

on the electrical activity of the brain, record. It does es nou require the

is EEG

not

Miscellaneous Topics

311

subject to give verbal responses to questions or stimuli. Principle: ERP or P300 is an electrical signal emitted from an individual's brain 300 ms after showing a familiar stimulus. It means if the subject is shown a familiar image, his EEG would show ERP/ P300. If the subject is shown unfamiliar image, his EEG would not show ERP/P30o. Procedure: A headband with electronic sensors is placed on the shaven scalp of the subject and connected to the EEG apparatus. Then the subject is shown stimuli consisting of sounds, words, phrases or pictures on a computer screen. If suspect had prior knowledge of any Results: event (e.g. a crime), then he would respond to the stimuli provided to him. If the subject has killed the victim with a weapon, then his brain would recognise the scene of crime and weapon. His EEG would show memory-related P300 waves. Originally, the technique used the P300 brain response. Later, Farwell used MERMER (Memory and Encoding Related Multifaceted Electroencephalographic Response) which includes the P300 and additional features.

SN-5: P300 (or Event-Related Potential [ERP]): ERP or P300 is an electrical signal emitted from an individual's brain 300 ms after showing a familiar stimulus. P300 is used in the brain fingerprinting, a tool of interrogation. Principle:If a subject has committed a crime, the crime-related information would be stored in his brain. If any crime-related information is presented to the subject on a computer screen, his brain would recognise that information, although he may consciously deny the information. The EEG response to that information is known as ERP, also known as P300. delay These ERPs are known as P300 because between stimulus and response is 300 ms. weapon, Ifa suspect has killed another person witha would him, his brain and it the weapon is shown to P300. r'ecognise it and his EEG would show familiar image, means if th subject is shown a It is ERP/P300. If the subject show would EEG his EEG would not show shown unfamiliar image, his P300 waves are genERP/P300. The gist is that the the has connection with subject the erated only if picture or sound. Stimulus, for example,

P300

SECTIONI

Forensic Medicine

Chapter 12D Fall From Height 3) Fracture of pelvis and vertebr column. 4) Upward forceful acute displacemenr

FALL FROM HEIGHT It deals with the dropping down from a height of relatively high position by the force of gravity. It may OCcur at ground level or from some height.

IMPORTANT QUESTIONS FOR EXAMINATION LO-1: Classify

injuries. Discuss in detail the pattern of injuries in fall from height case. How will you differentiate between suicidal, homicidal and accidental fall. [DU 2009] Classification Table 7A.1]

of injuries [refer Chapter 7,

Pattern

of injuries in a fall from height case: A. Direct injuries: Immediately anatomically related to the point of impact. For example, 1) Fall on head: Direct contact of head on hard flat concrete surface results into bruised laceration overlying comminuted fractures of skull along with cerebral damage (i.e. craniocerebral damage).

2) Fall on both feet resulting into fractures

bf abdominal organs may lead to i. Injuries to thoracic organs: Diaphragmat. injury and cardiac injury. Atria th are most common region of heart injured indirect injury without rib fracture. i Aorth may rupture at the junction of aortic arch and descending thoracic aorta. Pulmonary trunk may be lacerated. ii. Lacerations of liver and spleen. .Difference between suicidal, homicidal and acci. dental fall (Table 12D.1)

M

TABLE 12D.1 Difference Between Suicidal, Homicidal and Accidental Fall Sr.

No. Features

1.Incidence 2.

Body found

Suicidal

Homicidal

Accidental

Fall

Fall

Fall

Most common

Less

Most

Common

At a distance Near the

from baseline of

baseline of building

building

3.

of

the bones of lower limbs. 3) Fall on chest resulting into rib fractures most commonly seen at posterolateral angle of the rib. 4) Horizontal fall on a divider may result into spinal fractures. B. Indirect injuries: Caused by the transmission of force through the body or from its deceleration. For example, 1) 'Ring fracture' at the base of skull which occurs in fall landing on feet or buttocks, thus driving vertebral column into the skull. 2) Comminuted fracture at the base of skull with associated injuries to brain stem and inferior surface of brain.

TR

Orientation of body during fall

The person lands on both feet

common

Near the baseline building

Not specific Not specitc

4.

Fractures of Present lower limbs

Rare

Hare

5

Fracture of

Common

Common

skull

Less Common

(e.g. ring

SHC

fracture at the base

of skull) 6.

Multiple injuries due to fight

Absent

Present

Hesitation

May be

Absent

Cuts 8.

present

Suicidal note May be

Present

Absent

Absent

Absent Absent

CHAPTER 12 Miscellaneous Topics

313

Chapter 12E Trauma and Disease either predispose to a natural discase or natural disease. ggravate an already existing

Trauma may may

TRAUMA AND

NEOPLASIA

postulates. Each postulate must be fulfilled before trauma may be legally said to have caused malignant disease.

Criteria:

MALIGNANCY

Previous integrity of the part affected must be proved. It means the part developing the malignant disease must have been normal prior to trauma. 2) Undeniable and adequate trauma must be proven. It means the trauma must be sufficient to cause tissue disruption. 3) The disease must develop in the exact location of injury. 4) The tumour must develop within a reasonable amount of time after sustaining trauma. This period is usually from 3 weeks to 3 years after injury. 5) There must be a positive (i.e. pathologic as well as microscopic) diagnosis of the presence and nature of the tumour. The tumour must be of dissame histologic type, as the cells that were rupted. Medicolegal importance Compen(1) Compensation (under Workman's sation Act). (2) Insurance. 1)

may occasionaly cause cancer. James in 1935 established a relaEwing, a US pathologist, The postutionship between trauma and neoplasia. as Ewing's postulates. lates given by him are known a malignant . A single traumatic event 1iever produces tissue. Repeated minor tumour in previously normal cause neoplasia. trauma (irritation) is more likely to

Trauma

the repeated irritation stimulates cellular proliferation which ultimately leads to neoplasia. Cancer develops in (1) chronically irritated skin, for example, chronic sinus tract of chronic osteomyelitis; (2) scarred skin (by burns andX-ray burns).After burns, the untreated or long-standing non-healing wounds may lead to chronic ulceration which may undergo malignant transformation (squamous cell carcinoma) to cause Marjolin's ulcer. (3) Chronically inflamed lesions, for example, varicose ulcer. Trauma can affect a preexisting tumour in two ways: (1) either it accelerates growth or (2) it disseminates (metastasises) the tumour cells more quickly. Actually,

IMPORTANT QUESTIONS FOR EXAMINATION SHORT NOTES (SN)

SN-1: Ewing's

James Ewing

ncoplasia', and had given criteria called Ewing's

postulates

(a US pathologist, 1935) had

CStablished a relationship

between 'trauma

and

314

SECTION

I

Forensic Medicine

Chapter 12F Medicolegal Importance of AIDS/HIV A.

Duties of doctors: Professional secrecy (confidentiality): In case of HIV-positive patient, a doctor must maintain confidentiality, but he can reveal his HIV-positive

status to the other medical and paramedical fellow working for that patient for safety purposes. Also, doctor can reveal the HIV-positive status to the spouse. If the patient is going to be married, doctor can reveal HIV status to the prospective partner. Surgery of an HIV-infected patient: Use full face mask with protective spectacles. Use fully waterproof disposable gowns. Wear boots. Wear double gloves (a larger sized glove inside is more comfortable). Laparoscopic procedures are safer. Careful screening of blood before transfusion. Use double gloves during blood sample collection. Autopsy of an HIV-infected patient: Use double gloves (if chain mail or Kevlar gloves not available). If there is a cut on finder, dip immediately in sodium hypochlorite solution. Use full face mask with protective spectacles. Use fully waterproof disposable gowns. Wear rubber gum boots of knee length. Wear double gloves (a larger sized glove inside is more comfortable). Used instruments should be washed in glutaraldehyde solution (e.g.cidex plus) and then dipped for 20 min. Soiled cotton and gauze are collected in a double plastic bag and then sent for incineration. B. Rights of HIV-positive patient: According to Article 21 of Constitution of India, the HIV-positive persons have the right to life and personal liberty, and right to privacy. They cannot be discriminated in jobs, schools and so on. They cannot be isolated or quarantined on the basis of their HIV status.

C.

Marriage or sexual intercourse:

S.269.

'Negligent' act likely to spread of disease dangerous to life: Example, infcti suppose an HIV-positive person does not know HIV-positive status, or if he knows his status, he does not know the route of spread of HIV and he marries a woman or performs sex with a woman. If the intection is transmitted the to woman, he will be punished with imprison ment for 6 months or with fine or with both. S.270. Malignant act likely to spread infectionoi disease dangerous to life Example, an HIV-pos itive person knows his HIV-positive status rerr well, in spite of that he marries a woman or per forms sex with woman without informinghe of his status. If the infection is transmitted to the woman, he will be punished with imprison ment for 2 years or with fine or with both. An HIV-positive person has no right to marr If an HIV-positive person marries with the other person, the marriage shall be considera invalid. D. Divorce: If a person gets HIV infection ater mar ony riage, the other person can get divorce n disease spouse has been suffering from venereal a communicable form, for example, AIDS, syphils S.5(V) of Hindu Marriage Act]. E. National Policy on HIV/AIDS and the Worn Labor dnd of Work is issued by the Ministry of Employment, Government of India. HIV/AIDS (Prevention and Control) Bil Rs ot ommends 2 years of imprisonment and nina10,000 for those spreading hatred and discrin tion against HIV patients.

.

CHAPTER 12 Miscellaneous Topics

Chapter 12G Starvation Deaths ults from the depristate which ation: It is a food. I1 regular.and constant supply of vation of chronic. or be acute starvation: It occurs when supply of food I 1) Acute completely withheld as in mines and suddenly is religious landslides, or hunger strikes or or store is utilised, then fats rituals. Initially glycogen As the starvation progresses, the and lastly proteins. FFAs and ketone bodies increases plasma level of in urine. Feeling of hunand then can be detected 48 h. After that epigastric pain ger lasts for about buccal fat is appears. Eyes sunken, pupils dilated, 5 days of starvation, genlast to disappear. After subcutaneous eral emaciation and absorption of fat begin to occur. Weight loss of >30% of body weight is life threatening, but weight loss of 40% of body weight is fatal. 2)

the supply of withheld as in incompletely gradually and famines. The emaciation is more marked. Death occurs after a prolonged period from some infection (eg. pneumonia, TB, meningitis) because starvation leads to hypoprotenemia which further decreases the immunity. It may be dry or wet. Dry cases of chronic starvation are characterised by extreme emaciation, fatigue, mental apathy, gener aised cyanosis and mild pedal oedema. Wet cases of chronic starvation are characterised by Ascius, pleural effusion, watery diarrhoea, generalised Chronic starvation:It occurs when food is

oedema and fever.

ratal period: Death usually occurs when (1) 80% of body fat' is lost; (2) 40% of 'body weight' is lost and

20%% of 'body proteins' is lost. If water (with or nout food) withdrawal, death occurs in 2-3 weeks. Only food withdrawal (but water allowed), death Occurs in 3-8 weeks. Newborn without food and Water may survive for 10 days. stmortem dings in a death due to starvation: 1) General:

A) Disagreeable (8) Oed

ma:

ankles. C)Pace pale.

offensive odour. Under eyelids, cheek, chin, arouna

Ascitis in 10% cases.

(E) Loss of subcutaneous fats: Fats of female breast and orbit are spared till late. Subepicardial fats become and ARE replaced by a watery gelatinous material. Total absence of fat throughout the body is not seen in wasting disease, for example, TB, diabetes. (F) Emaciation is extreme and it gives rise to sunken eyes and cheeks, more prominent bony prominences. Prominent ribs with intercostal concavities. Supraclavicular fossae sunken. Abdomen concave and scaphoid. Limbs thin. 2) Rigor mortis sets early and disappears early. 3) Muscles are atrophied and darker due to increase

in 'lipochrome'. 4) All organs atrophied and contracted: The size and weight of all organs are reduced except 'brain. 5) GIT atrophy. Walls of intestine appear like tissue paper with mucosal atrophy. 6) Gall bladder distended (because there is no food in duodenumdue to which there is no CCK and so there is no contraction of gall bladder. The bile is filled and accumulated inside gall bladder to cause

distention). 7) Urinary bladder empty. Opinion: Before giving opinion,

essential to example, for exclude diseases which cause weight loss, malignancy, Addison's disease, diabetes mellitus, progressive muscular atrophy, TB, pernicious anaemia is 'starvaand chronic diarrhoea. The cause of death tion. Dehydration, intercurrent infection and hypothermia may contribute to death. it is

Medicolegal aspects

Suicide 1)

= Hunger strike

exhibition or A person fasts for purpose of strike) till he public attention (e.g. hunger demands. A jail docgets the solution of his force-feed the political tor is often requested to his life. If the doctor prisoner in order to save prissave the life ot for acting in good faith to forcefully, he may be sued feecds him may oner and he force [S.350, IPC) imprisonment Lusing criminal with 3 months of be punished Constitution of India Since S.352 of IPC).

316

SECTIONI Forensic Medicine

(Article 21) includes 'right to life, not 'right to die, the arrest and forcible teeding of person going on hunger strike is lawful. It means doctor can force-feed a prisoner on the request by higher jail authorities. The criteria to advise forced feeding are (1) loss of weight and (2) acidosis with ketone bodies in urine. 2) WMAhas given guidelines in its Declarations of Tokyo and Declaration of Malta. These Declarations respecting the autonomy of the patient suggest that the doctor should not force-feed

in the case of hunger strike, but the feedin allowed when the patient has lapsed into com oma. Homicide: The starvation may be caused inten tionally and the victims are intant, older person mentally ill person, paralysed persons or illegiti.

mate children. Accidents, for example, during famine, or being trapped in pits/mines/landslides. As per Article 21 of Constitution of India, it is the duty and responsibility of the government to provide food to the citizens.

II

SECTION ForenSIC loxiCology 13.

14. 15. 16. 17.

17A.

General Aspects of Forensic Toxicology, 319 Corrosive Poisons, 336

Inorganic Irritant Poisons, 342 Organic Irritant Poisons, 355 Poisons Acting on Nervous System, 368 CNS Depressants, 368

17B. Deliriants, 381 17C. Spinal and Peripheral Nerve

18. 19. 20.

21. 22.

Poisons, 389 Cardiac Poisons, 394 Asphyxiants, 398 Agricultural Poisons, 404 Drug Abuse, 410 Miscellaneous Poisons, 417

317

13 General Aspects of Forensic Toxicology INTRODUCTION Toxicology

medical science which deals with The branch of to their sources, properties, the poison in relation mechanism of action, fatal dose, signs and symptoxicity, diagnosis and treatment is toms produced, (Greek, toxikon = arrow poiknown as toxicology is often referred to sons). Paracelsus (1493-1541) toxicology. Mathieu Orfila (1787as the father of 1853) is considered the father of modern toxicology.

Poison Versus Toxin Versus Venom Versus Medicine Poison is any substance either

from a chemical source (e.g. arsenic, lead and so on) or a biological source (e.g. poisonous fish, i.e. fish whichh is poisonous on consumption) which if taken in any amount, by any route, produces harmful effects i.e. disease, deformity or death) over the body. Poisons are absorbed either by skin or by GIT mucosa, so accordingly poisons are harmful when touched or consumed. Study of poisons is known as toxicology. Toxin is a type of poison produced by a biological source, for example, bacteria (> Bacterial toxins,e-g. botulinum toxin), fungi (Mycotoxins), algae (> Phycotoxins), plants (- Phytotoxins, e.g. abrin and ricin) and animals ( Zootoxins, e.g. snake venom). They are small molecules (peptides or proteins). Toxin is very harmful and is active at very low concentrations. Study of toxins is known

Clinical Toxicology

of toxicology which deals with diagnosis and management of poisoning in humans. Example: In casualty or emergency department of a hospital, the doctors diagnose and manage a case of It is

the branch

poisoning.

Forensic Toxicology It is the branch of toxicology which deals with the medicolegal aspects of the harmful effects of poisons on humans. Example: In second year MBBS, the medical students read and understand forensic toxicology. In casualty or emergency department, the doctor preServes gastric lavage (GL) and prepares MLC (medcolegal case) in a case of poisoning. In mortuary,% 1orensic pathologists conduct autopsy in a case of polOnng and preserve viscera and other specimen (e.g. 8Astric contents, blood, urine and so on) for chemical analysis.

Analytical

Toxicology

ection and measurement of poisons

tissue

in lbiological specimens. Example: The GL preserved by the

and the viscera (and other speciby forensic pathologist in mortuary are sent to FSL for chemical analysis.

mene

asualty mens) preserved

as toxinology.

.

Venom is a variety of toxins produced by some organisms and injected into other organism by bite (e.g. snake and spider) or sting (e.g. honey bees, wasps, scorpion and venomous hsh) to pro0duce harmful effects. save lite, Ifa substance is given with the intention to the intention it is medicine, but if it is given with Almost anything to cause bodily harm, it is poison. Paracelsus, the is a potential poison. According to venenum). dose makes the poison' (dosis facit

CLASSIFICATION OF POISONS (TABLE

13.1

Corrosives Inorganic/mineral acids(hydrochloric Strong acids: (1) HCI acid), H,SO, (sulphurie 319

A.

32

SECTION I

TABLE

13.1

Forensic Toxicology

Classification of Poisons Systemic Poisons IV.

I.

Corosives l. Irritants

A. Acids B. Alkalis

A. Inorganic

A. Cerebral

Metallic

Nonmetallic

B.

Organic

Plants Animal

1.

B.

Spinal Spinal

(neurotic) CNS

1.

stimulants

lants 2. Spinal depres-

2. CNS

de

pressants

Somnifer ous

C. Poripheral

stimu-

sants

Poisons

Affecting Organs

1. Neurotoxic

V. Asphyxiants VI. Others

poisonso,o2,MaS

A. Cardiac B. Hepatotoxic C. Nephrotoxic D. Toxic to lungs,

skin, etc.

A.

arbons

B. Agrochemi cals C. Domestic poisons D. Food poisoning

Inebriants

S

3. Deliriants

acid), HNO, (nitric acid) and others acids, for example, boric, chromic and phosphoric acid. (2) Organic acids-carbolic, oxalic, salicylic, acetic, formic, citric, tartaric and picric. B. Strong alkalis: NaOH (caustic soda), KOH (caustic potash), Na,cO, (sodium carbonate), KCO, (potassium carbonate), KMnO, (potassium permanganate) and H_0, (hydrogen peroxide). II. Irritants A. Inorganic: (1) Metallic-Mercury, Arsenic, Lead, Iron, Copper (e-g. CuSO,) and Others, for example, thallium, cadmium, lithium, cobalt, manganese and zinc. (2) Nonmetallic-phosphorus, halogen and formaldehyde. B. Organic: (1) Plant irritants-Abrus (ratti), Ricinus (castor), Croton, Semecarpus anacardium, Capsicum, Calotropis and Plumbago. (2) Animal irritants-cantharides, snake venom, arthropods (e.g. insects, scorpions, centipedes, bees, wasps, ants and spiders) and others, for example, jelly fish, venomous fish and lizards. C. Mechanical: Powdered glass, diamond dust, chopped hair and nails. III. Neurotoxic poisons A. Cerebral (neurotic): (1) CNS stimulantsamphetamines, tricyclic antidepressants, cocaine and (2) CNS depressants-(a) inebriants: alcohols, sedatives-hypnotics (e.g. bar-

biturates, benzodiazepines, chloral bydrate, paraldehyde and potassium bromide), general anaesthetics (chloroform and ether) and (b) somniferous poisons (narcotics): opium

and its derivatives, for example, opiates and opioids. B. Spinal: (1) Spinal stimulant (Strychnos) and (2) spinal depressant (Gelsemium). C. Peripheral: Curare and hemlock. IV. Poisons affecting organs A. Cardiac poisons: Digitalis, nicotine, aconite, oleander, quinine and cyanide. B. Hepatotoxic: Liver necrosis (phosphorus, chloroform and CCI) and fatty liver (ethanol, arsenic, ferrous sulphate and CCl). C. Nephrotoxic: Necrosis of PCT (mercuric chloride, CCl, carbolic acid, cresol and cantharides) or necrosis of DCT (amphotericin, cisplatin and glycols). V. Asphyxiants: CO,, CO, H,S and cyanide. VI. Others: (A) hydrocarbons-kerosene petr way diesel, grease, tar, turpentine oil, parafhn benzene, naphthalene balls, chloroform, etc (B) agrochemical poisons-organophospno rus compounds, carbamates, paraquat, 21n phosphide, aluminium phosphide, strychnine etc. and (C) domestic poisons-striking/igning pou Surtace of safety matches (red phosphortus, dered glass, sand particles and glue), matchsts

head (potassium chlorate, antimony sulpts powdered glass or coarse sand particles),HC (10% polish remover (acetone), Harpio (trans Good Knight/Mortein liquid vaporiser Juthrin), Odomos cream (diethyl benzamile Out coil (transallethrin), Hit spray (transale kha KE or imiprothrin + cypermethrin), Laxman nover remo (deltamethrin and cypermethrin), ink (sodium hypochlorite), etc.

CHAPTER 13

13.2 pifference BetweenHomicidalPolsoning and Suicidal Poisoning

TABLE

No.eature

St.

Homicidal Poisoning

symptoms signs and

Onset of Characteristics of noison consumed

IMPORTANT CONCEPTS

Poisoning (Table 13.2)

Nature of (1) Acidcntal (2) Suicidal

(3) Homicidal

ldeal Homicidal

Poison Versus ldeal

Suicidal Poison (Table 13.3). Fulminant poisoning: A single massive dose (i.e. more than fatal dose) of a poison causes death very rapidly without any symptoms. Acute poisoning: A single excessive dose (i.e. less than massive dose or equal to fatal dose) of a poi-

symptoms.

TABLE 13.3 St.

No. Feature

Alurniniurn phosphide, opium, barbiturates

Common

3) Subacute poisoning: It occurs gradually over some time, taking more time as compared to acute poisoning. The poison is taken repeatedly in small amount but over a short period of time, for example, drug automatism. 4) Chronic poisoning: A very minute amount of poison is taken over a long period of time, for example, occupational poisoning (e.g. chronic lead

plumbism). Many times the poison (e.g. arsenic) may be given to the victim in his diet over a long period of time. 5) Secondary poisoning: Poisoning that results when one organism ingests (or comes into contact with) another organism that has been poisoned. Examples: (1) Minamata Bay disaster and (2) the doctor or any other staff can get secondary exposure to poisons . during treatment of organophosphorus poisoning

poisoning

Poisoning

son causes

Depression, low self-esteem More prorminent

Rare

Suspicion

2)

Definition

L.

Characteristics

in The poison characteristics of which are favour of accused in committing homicide Colourless, odourless, tasteless, soluble

3.

Cost

Cheap and easily available

Symptoms

Should resemble a natural disease and should appear late after administration to avoid suspicion

Onset of signs and symptoms

Should be very slow

Toxicity

Highly toxic with short fatal period

and fatal period

Antidote

Should not be available

Detectability

Should not be detectable

Dis

DIsappearance after death

Postmortem Example

=

Difference Between ldeal Homicidal Poison and ldeal Suicidal Poison IdealSuicidal Poison Ideal Homicidal Poison

1

10.

Not such characteristics

Arsenic, thallium, lead

Poisons used

1)

Very quick, causes painless death

Less prominent

Postmortem signs

Types of

Suicidal Poisoning

Very slow, resemble a natural disease Colourless, odourless, tasteless, soluble

Jealousy, revenge

Cause

sOME

General Aspects of ForensicToxicology

signs

Should disappear No postmortem signs KC Arsenic, thallium, aconíte, insulin,

in The poison characteristics of which are suicide favour of the person committing

Does not matter Does not matter Should cause an easy, painless and quick death Should be very quick fatal period Highly toxic with very short

Does not matter Does not matter Does not matter Does not matter phosphide barbiturates, aluminum Opium,

2

SECTION

II

ForensicToxicology

Arrow Poisons The poisons used at the tip of arrow or dart for hunting or to kill animals. Plant source: Curare, strychnine, Abrus, aconite and Calotropis. Animal sources: Batrachotoxin, tetrodotoxin, diamphidia and Gila monster. Medicolegal importance: (1) Death may occur accidentally cither during preparation of the arrow poison or hunting. (2) Can be used for honmicidal purpose. (3) They have becn used in warfare.

Stupefying Poisons The substances which are used to stun a victim or put the victim into a state of little or no sensibility (i.e. drowsy and unconscious). Stupefying nmeans to cause (someone) to become confused or unable to think clearly. They are used by the criminals for the purpose of robbery, kidnapping, rape, etc. during travel, for example, in bus, train and railway station. The cases have been seen especially near festivals. The stupefying agent is usually mixed with food (c.g. chat and laddoo) or drink (e.g. sattu, fruit juice, tea and coffee). Stupefying poisons are Datura, Cannabis and Chloral hydrate.

Cattle Poisons Poisons used to kill attle. For example Abrus, aconite, strychnine, oleander, zinc phosphide, organophosphorus, etc.

Ordeal Poison It is a poison which is supposed to prove or disprove the innocence or guilt of a suspect. It was practiced in past and the ordeal poison used to be given to a suspect acCused of a crime. If he died, he was considered to be guilty but if he survived, he was considered innocent. Due to strong belief, the innocent people suspected of an offence used to subject themselves to the test. Common ordeal poisons are calabar bean (Physostigma venenosum), ordeal tree (Cerbera odollam), Cerbera tanghin, Croton seeds.

viperine snake venom. Each toxalbumin is d a consisting of two units (A and B) held togethe. disulphide bond. Unit A is the actual toxin and it cleaves N-glycosicdic bond in 28S ribosomal RNA. Unit R which lectin part binds to the cell surface. A few ev examples of toxalbumin are ricin (in Ricinus commu nunis), crotin (in Croton tiglium) and abrin (in Abruspreca torius).

Aphrodisiacs In Greek, Aphrodite is the Greek goddess of love. Suh. stances that are considered to increase sexual desire are known as aphrodisiacs. Examples: (1) poisonone substances (e.g. cantharides, cocaine, Cannabis, arse. nic, strychnine and opium); (2) foods (e.g. Ginkgo biloba, ginseng. yohimbe, oysters, watermelon, chocolates, spicy chilli peppers and (3) drugs (e.g. sildenafil.

phenylethylamine and arginine)

Coma Cocktail In a poisoned comatose patient where the identity of poison is not known, the coma cocktail (i.e. a combination of three substances) is given via I/V. It con sists of dextrose (100 mL of 50% solution), naloxone (2 mg) and thiamine (vitamin B,) (100 mg). It is given with the apprehension that these patients are the vie tims of opiates, alcohol or any other hypoglycaemic agent poisoning. Even if the patient is not sufiering from poisoning, it will not cause any harm.

Toxicity Rating for Humans (70 kg Body Weight) (Table 13.4)

TABLE 13.4 Toxicity Rating for Humans 70kg Body Weight) Rating/Class 5.

Toxalbumin It is the toxic plant protein (orphytotoxin) which resembles a bacterial toxin (tetanus, cholera, botulinum and diphtheria) in its action and inhibits protein synthesis by inactivating ribosomes. It is antigenic in nature and is capable of producing antibody when administered into the body. It causes agglutination and lysis of RBCs. The properties of toxalbumin are similar to those of

2

Dose

Supertoxic

Rs 5000) and penalty for manufacture and sale of spurious

drugs is P

1s,+ F (>Rs 5000). and Cosmetics Rules, 1945: It contains 25 schedules (A to Y). Schedule H contains non-OTC Le.non-over the counter) drugs. These are the drugs cannot be purchased over the counter without ch Eprescription of qualified doctor. It means they sold only on prescription. They must be labelled with the symbol Rx and a arning 'Schedule H warning:To be sold by retail on the prescription of aRegistered Medical titioner only, Also thhere must be a red ertical line on the left side of the container =

he Drugs

e

6. 7. 8.

9. 10.

11.

2012, 2014] 12. Legal duties of doctor in case of poisoning 13. Postmortem examination in a suspected death due to poison [CCU 2003] 14. Preservation of viscera in a case of suspected poisoning [CCU 2003]

DIFFERENTIATE BETWEEN

(D/W)

homicidal poison and ideal suicidal poison 16. Chemical antidote and physiological antidote 17. Suicidal and homicidal poisoning 15. Ideal

ANSWERS SN-1: Duties of a doctor or medical practitioner in case of poisoning

a

IPCsections1 related dix 3 for IPC sectic with poisons: Please see Appen326 and tions S.272, 273, 274, 275, 284, 324, 328.

poisoning General line of treatment of a suspected case of acute poisoning [CCU 2011] Method of removal of unabsorbed poisons from GIT Gastric Lavage [CCU 2014 Stomach wash tube [CCU 201] Method of removal of absorbed poisons from the body Antidotes [CCU 2003, 2010] Activated charcoal Chelating agents [DU 2005, 2006] [CCU 2014] British anti-Lewisite (BAL) Universal antidote [CCU 2003, 2004, 2005, 2009,

ot a doctor in case There are two types of duties of legal cduties. poisoning, professional duties and

Professional (medical) Duties It

[SN-2

a case of poisoning includes the treatment in

Legal Duties [SN-12]

formalities in It includes legal

a case

of poisoning.

SECTION I

Forensic Toxicology

SN-2: General line of treatment of a suspected case of acute poisoning 1)

Dialysis:

Some toxins can be removed tively by dialysis, for example, efec. nobarbital, salicylates, lithiummethanol Haemodialysis is more etfective and quinine,. than De

Stabilisation of patient (immediatc resuscitative measures): ABCD

neal dialysis.

A(= Airway): Chin lift or jaw thrust, clean airway

Haemoperfusion: The blood passes through throne

of secretions or vomitus.

external filtering device that contains an charcoal a or synthetic resin that adsorbs poison. Others: For example exchange transfusion purging and diaphoretics (i.e. drugs whirh increase sweating, e.g. alcohol, antipyretics and pilocarpine).

B(= Breathing): Maintain adequate tidal volume,

give oxygen. C (= Circulation): Maintenance of circulation, for example, check pulse (radial, femoral and carotid), ECG. Secure IV access for 1/V fluid administration. Be ready for CPR. D= Depression of CNS): Turn the unconscious patient to one side. Assess the level of consciousness by GCS (Glasgow coma scale). 2) Removal of unabsorbed poison from the body: Contact poison: Remove clothes and jewellery. Wash the affected part (skin or eyes) with water Inhaled poison (CO, H,S): Remove the patient into fresh air. Give oxygen. Injected poisons (snake/insect bite, scorpion sting and drug abuse): Remove sting in case of bee, wasp, scorpion and centipede sting. Adrenalin injection around injected area. Apply ice locally. Treat allergy and anaphylactic shock. Ingested poison: Do emesis, GL, whole bowel irrigation and catharsis (by sorbitol). GL is done to remove unabsorbed poison from the stomach. It is indicated in patients who present within 4 h of ingestion. A soft rubber tube called GL tube (also called stomach wash tube or Ewald tube or Boas tube) is used most commonly for stomach wash. 3) Removal of absorbed poison from the body: Urine alkalinisation: Normally the urine is slightly acidic (pH 6-6.5). In urine alkalinisation, the urine is made alkaline by the use of sodium bicarbonate. It is used for the poisoning with salicylates, barbiturates (e.g. phenobarbitone), lithium, etc. Urine acidification: To make urine more acidic (i.e. to decrease pH), ascorbic acid or ammo nium chloride 1-2 g every 4-6h is given l/V. It is done in the poisoning with MAP-CQ (i.e. methadone, amphetamine, phencyclidine, cocaine

and quinine).

perito-

4) Administration of antidotes: Antidotes neutralie the effect of poison. 5) Symptomatic treatment: Give fever.

paracetamol

for

6) Follow-up.

SN-3: Method of removal of unabsorbed poisons from GIT Methods of removal of unabsorbed poisons

from

GIT:

Emesis: It should be avoided especially in unconscious patient because there is danger of aspiration of stomach contents. Emetics used most commonly are ipecacuanha, apomorphine (G-6 mg IIM injection), warm saline water (200 mL) with salt (2 tsf) or mustard powder. When nothing s available, emesis can be used. 2) GL with appropriate antidote (mechanical or chemical) [SN-4]. 3) Catharsis: A cathartic is a substance that act erates defecation. This is in contrast to a laxatve which is a substance which eases defecation, ally by softening faeces. It is possible for substance to be both a laxative and a cathartic. nd Sorbitol, magnesium citrate Examples: sodium sulphate. present, they are no longer routinely rec At mended for the management of poisoningentire 4) Whole bowel irrigation: It fushes out thetrolyte GIT in 5 h. For this, polyethylene glyco-erh avage solution (PEG-ELS) at 2 L/h (1n dren 0.5 L/h) is given via nasogastrie teusual lt is huum) the patient has to sit on a toilet seat. It reserved wlhen the ingested poison (e-g nd is not adsorbed by activated charcoal; or Sus ested been Ing release or enteric coated drugs have 1)

:

CHAPTER 13

5)

for example, cocaine has been drug, son illegal transport. or body 1packers for ed by opic/surgical removal: It is used when the End ingested som cocaine packets or m

has

are chances of

bowel

obstruction.

lavage

SN-4: Gastric (also nown as stomach wash). Gastric Lavage present within 2-3 h indicated in patients who

It

is

ingestion.

of Contraindications of GL (Table 13.8). time can we do GL? Up to

2-3 h, we ,Up to what an do GL. After 3 h, none or very little poison GL is not useful. But in remains in the stomach, so 3 h may be useful, for certain poisonings, GL after example: 1) Poisons which cause pylor1c

spasm or reduce

anticholinergic, morphine and tricyclic antidepressants). These drugs delay gastric emptying and so a good amount of poison can be recovered after several hours GIT motility (e.g.

2)

of ingestion. Poisons which clunnp to forma mass and stick tob the wall of stomach (e.g. salicylates).

TABLE 13.8 Gastric Lavage

Contraindications of

Absolute

e. gastric lavage must not be done under any of

Relative gastric lavage should not be done normally, but may be done after taking

(1.e.

the tollowing poisonings due

to risk of perforation)

1. Corosive poisoning except carbolic Note: In case of

acid):

organic

acids (e.g. oxalic

acid and the gastric lavage can be done

aceic acid),

2. Sharp

and pointed

materal ingestion

precautions) 1.

Poisonings Volatile poisoning Kerosene poisoning c) Convulsant (e.g. strychnine) poisoning d) Alkali ingestion a) b)

2. Medical conditions: a) Coma or unconscious

patient Hypothermia c) Oesophageal varices d) Haemorrhagic diathesis ) Cardiac arrhythmias 1) Advanced pregnancy g) History of recent Surgical operation b)

General Aspects of ForensicToxicology

GLtube

27

used most commonly for stomach wash. Nowadays, in most of the hospitals, the GL is done by Rylc's tube (especially in children). is

Proccdure: Position

of the patient:

Lying in a left lateral

position or prone position with head hanging over the edge of the bed and the face downwards so that the mouth is at the lower level than the larynx and so the chances of aspiration of fluid are less. Insertion oftube: GL tube is gently passed into the stomach through the mouth by lubricating with glycerine or Vaseline jelly up to a distance of 50 cm in adults and 25 cm in children. To check the position of the inserted distal end of the tube whether it lies in the stomach or in the lung, we can put the bell of the stethoscope on the chest. If on pressing suction bulb, we hear the gargling sound of air, it means it is inside the stomach otherwise it lies inside the lung. Alternatively to check the position of tube, put the upper (funnel) end of the tube in water. If the air bubbles come out, the tube lies in trachea. Hold the funnel high up and pour 250 ml of warm saline or plain water into it. In children, use warm saline instead of water because there are chances of inducing hyponatraemia and water intoxication. The first sample of stomach wash should be preserved for chemical analy sis. Then stomach wash is carried out with the appropriate antidotes (mechanical or physical) specific to the poison. to stoP GL: The KMNO, solution Indication (pink in colour) when introduced into the stomach through GL tube oxidises the poison and itself get reduced to colourless compound. So initially, the returning GL fluid is colourless due to reaction between poison and KMNO, but when no more tluid poison remains in the stomach, the returning solution). At is of pink colour (i.e. it is KMNO, colour, this stage when returning fluid is of pink we should stop Gl.. circucase of poisons showing enterohepatic In remember two (e.g. morphine and heroin),

lation

things

of KMNO, or amount some GL doing ) After stomach be left in the activated charcoal must secreted in to poison which is to neutralise the on. the stomach later

SECTIONII Forensic Toxicology

SN-6: Methods of removal of absorbed poisons from the body

2) GL has to be done even if the poison was admin-

istered parenterally. Complications of GL: Laryngeal spasm, aspiration

pneumonitis, perforation of stomach or oesopha gus and sinus bradycardia. Medicolegal importance: 1) Faihure to do GL by the doctor may amount to negligence by the treating doctor. 2) Failure to preserve contents of GL is an offence and is punishable under S.201 of 1PC.

SN-5: Stomach wash tube (GL tube) Stomach

wash tube (also known

as GL tube or

Ewald tube or Boas tube) is a soft rubber tube used most commonly for stomach wash in case of

poisoning (Fig. 13.1). Size: It is available in different sizes and the size is measured in F scale (i.e. French scale; 1 F = 0.3 mm). It is 1.5 m long; 1 cm diameter. Size of 40 F is used for adults and size of 24 F for toddlers. Parts: Proximal end has a funnel and distal end is rounded having lateral openings. Suction bulb is at the middle of the tube to pump out stomach contents. A mouth gag is present near to the suction pump. There is a mark at a distance of 50 cm from its rounded distal end. The distal end is rounded and contains lateral openings. Nowadays GL tube has been replaced by levacuator. In children, Ryle's tube has been used at the place of GL tube. Use: GL is done in case of ingested poisoning. Funnel at proximal end

Rubber tube

-Suction bulb -Mouth gag

-Mark of 50 cm Distal end with lateral openings

Fig. 13.1 Stomach wash tube

alkalinisation: Normally the urine is slight. acidic (pH6-6.5). In urine alkalinisa the uri is made alkaline by the use of sodium bicarbonas It is used for the poisoning with salicylates, barhi turates (e.g. phenobarbitone), lithium, etc. Urine acidification: To make urine more acidi (i.c. to decrease pH), ascorbic acid or ammo nium chloride 1-2 g every 4-6 h is given 1/V, done in the poisoning with MAP-CQ (i.e. meth. adone, amphetamine, phencyclidine, cocaine and Urine

i

quinine).

Dialysis:

Some toxins can be removed effectively by dialysis, for example, methanol, phenobarbital, salicylates, lithium and quinine. Haemodialysis is more effective than peritoneal dialysis. The blood passes through an Haemoperfusion: external filtering device that contains charcoal or a synthetic resin that adsorbs poison.

Others:

exchange transfusion, purging and diaphoretics (i.e. drugs which increase sweating, e.g. alcohol, antipyretics and pilocarpine).

SN-7: Antidotes Antidote:

It is a substance used to counteract the

effect of a poison.

Classification

(Table 13.9).

according to

mode of action

Mechanical (or physical) antidotes: It either neutralises poisons mechanically in GIT without destroying the poison or prevents their absorption. Adsorbents, for example, activated charcoal adsorbs poisons on to their surface. Dose 50-100 g mixed in 250 mL of water. Demulcents prevent systemic absorption by torming a protective coating over gast stric mucosa. 2. Chemical antidotes neutralise the poison c enmically within GIT to form harmless or insoluuble compounds. Potassium permanganinate (KMn InO,) (1:5000): It oxidises poisons and in the process reduced itself (i.e. loses its pink colour). 1 he stomach wash is continued till the solle coming out of stomach is pink in colour is used preferably in poisoning with alka 1.

CHAPTER 13

Mechanical

2. Chemical

1. Physical Activated orAdsorbents:

1.

1

charcoal Aluminium Demulcents: magnesium 2.

IMgrOH),

hydrovide magnesia),

5.

4

=

1nilk

of

magnesium oxide

white, MoO), egg milk Diluents: Bulky food

fats, milk

KMnO, (potassium petmanganate)

2. CusO, 3. Tannic acid (or strong tea) 4. Albunmen 5. Weak alkalis

6. Weak vegetables acids 7. Lugol's (tincture) iodine

3.

3.

Physiological

(or Pharmacological) Atropine 2.

Physostigmine and neostigmine 3. Naloxone 4. Nacetyl cysteine 5. Barbiturates 6. Oxirnes

8. Common salt

mixture of

sal antidote is a charcoal (two parts) Activated powdered

2.

329

of ntidotes According to Mode Classification C of Action

TABLE13.9

hydroxide,

General Aspects of ForensicToxicologyy

4. Chelating Agents 1.

British anti-Lewisite

2. British anti-Lewisite analogues

(dirnercaptosuccinic acid and dimercaptopropane sulphonate) 3. Ethylenediarninetetraacetic acid calcium disodium edetate) 4. Penicillarnine (Cuprimine) 5. Desferrioxamine

idotes (two physical antidotes and one chemical antidote)

Magnesium oxide (one part) Tannic acid (one part)

atropine, strychnine and opium), barbiturates, cyanide and phosphorus. Copper sulphate (CuSO,) in phosphorus poisoning but not used nowadays. Tannic acid (4%) or strong tea precipitates alkaloids (e.g. strychnine), lead, mercury and copper. (e.g.

Albumen (egg white) is given in mercuric chloride (HgCl,) and copper poisoning. Weak acids: Vinegar and lemon juice. Weak alkalis: Avoid sodium carbonate and sodium bicarbonate to neutralise acids because excessive release of CO, may cause perforation of weakened stomach wall.

incture iodine (or Lugol's íodine) precipitates alkaloids, lead

and mercury. Common salt: In silver nitrate poisoning. 3. Physiological (or pharmacological) antidotes act at the target cells by producing pharmacoOg Ical effects exactly opposite to those produced by poisons. They are used after some of the poison is 2bsorbed into the circulation. Examples: hlropine and oximes (e.g. pralidoxime or 2-PAM) for organophosphates.

Naloxone

for morphine. Diazepam for strychnine.

Amyl nitrite for cyanide. acetyl cysteine for acetaminophen (paraceta mol).

Anti-sna

venom for snakebite poisoning are the chemicals which form com inactivateth molecules with metaliions and te them. x

4. Chelating

agents g agen' thesoluble

BAL also called dimercaprol: It is given as an antidote in poisonings by Mercury, Arsenic, Lead, Antimony, Bismuth, Copper and Gold Mnemonic MALA-BCG]. CaNa EDTA [calcium disodium edetate (i.e. ethylenediaminetetraacetic acid)] is most commonly used in lead po1s0ning D-Penicillamine (or Cuprimine) is used for poisoning with Mercury, Lead and Copper [Mnemonic: MLC]. Desferrioxamine is used in acute iron poison-

ing.

DMSA (dimercaptosuccinic acid) and DMPS (dimercaptopropane sulphonate) are used in poisoning by Mercury, Lead and Arsenic [Mnemonic MLA].

SN-8: Activated charcoal charcoal is a form of carbon (odourless, an tasteless and fine black powder) that is used as effective antidote for ingested poisons. mechanical/physical has been classified as a It the nmode of antidote (adsorbent) according to

Activated

action.

charcoal adsorbs and thus the in sulbstances toxic binds toxic substances inhibits their absorption. It them until they exit holds on to to its surface and defecation. lt is estimated to up the body through poisonous substances

Mechanism of action: Activated lumen of GIT

reduce absorption to 60%.

of

SECTION

lI

Forensic Toxicology

Microporosity: I is a fine, black, odourless powder that has been processed to make it highly porous. The very high degree of microporosity increases the surface area available for adsorption of poisons. Preparation: It is most commonly prepared by the destructive distillation (i.e. heating in absence of air) of carbonaceous substances, for example, coconut shels, nutshells, wood, bone, pulp, starch, lactose, sucrose, etc. If market preparation is not available, the charcoal may be prepared by burning and then grinding cgg albumen or bread toast. Dose: For adults: 50-100 g mixed in 250 ml. of water; for children: g/kg body weight. of administration: It is given after GL that Method is do GL before administering activated charcoal. After GL, administer the prepared solution of activated charcoal through GL tube. It can be given orally if the patient is able to drink. Activated charcoal is effective in following poisonings: Surychnine, opiates, antidepressants, barbiturates, benzodiazepines, amphetamines, atropine, digitalis, etc. Multiple dose activated charcoal is the administration of 50 g of activated charcoal every 6 h for 3 days. It is indicated for those drugs which after absorption in GIT are again secreted into the lumen of GIT. Universal antidote: The universal antidote was supposed to be effective against every poison. It consisted of three components. Activated powdered charcoal (two parts), magnesium oxide (one part) and tannic acid (one part). The mixture is ineffective and no longer used; activated charcoal is nowadays considered to be medicine's most powerful adsorbent. 1

SN-9: Chelating agents Chelating agents (Latin chela = claw of a lolbster): The chemicals which form the soluble complex molecules with toxic metal ions and inactivate them. Chelating agents hold the metal as if in a claw.

Chelating agent + Metal ion (loxic)

>Chelate (Nontoxic complex molecule) The process of gripping metal jons by chelating agents is called chelation. The hallmark of chelation is the formation of'chelate ring'. The resulting

soluble complex molecules formed in th e proc of chelation are known as elates. Thechelate metal ions cannot enter living cells and are rapidly excreted from the body. Chemistry of chelating agents: A chelatina agent is a multidentate ligand that the molecule of a chelating agent can form several bonds to Single metal ion. Chelating agents are used as antidotes in heavy metal poisonings. Characteristics of an ideal chelating agent: ( Minimal toxicity of chelating agent as well a chelate. (2) High affinity for toxic metals but loe for essential metals. (3) Kapid elimination of toric metal in urine. Examples: (1) BAL also called dimercaprol (2) BAL analogues (DMSA and DMPS); (3) EDTA (CaNa_EDTA) (ethylenediaminetetraacetie acid calcium disodium edetate); (4) D-penicilamine (or Cuprimine) and (5) desferrioxamine. BAL: It is given as an antidote in poisonings by Mercury, Arsenic, Lead, Antimony, Bismuth, Cop per and Gold [Mnemonic: MALA-BCG]. It is given by I/M route, not I/V route because if given I/N.it causes fat embolism due to the presence of peamut oil in the preparation. DMSA (dimercaptosuccinic acid = succimer) and DMPS: Used in poisoning by Mercury, Lead and Arsenic [Mnemonic MLA]. DMSA is very effectve if used with EDTA. Dose of DMSA: 10 mg/kg D for 5 days then BD for 14 days. Advantages of DMSA and DMPS over BAL and EDTA is less toxic then BAL, so sonieant DMSA substituted for BAL when patient's condine mproves. DMPS is less effective than DAISA (I/M aDMSA can be orally administered [BAL route) and EDTA (1/V route) DMSA is less toxic than BAL and EDIA. 0DMSA can be used in G6PD deticieney: to the does not redistribute mercury DMSA brain as BAL does. ron can be coadministered with DMSA tra* It does not decrease the level of essent elements, for example, zinc. EDTA (CaNa,EDTA): Use: Lead and arsenic poison (also for nickel! d per, cobalt, cacdmium, iron, mercury and

CHAPTER 13

combines with lead to form a hich is excreted in soluble copound inary lead excretion EDTA increases

echanism: It urine.

50-fold. in a concentration Given by 1/V infusion Dose: it over 24 h in NS/DNS. By 1/M route,

25-to

f0.5%

causes pai Available in 5 mlL

ampoule containing 1000 ng EDTA). mlL = 200 mg of EDTA (so cach of disease. Contraindicated in renal and hepatic

Cuprimine):

D-Penicillamine (or with MLC (MercurY used in poisoning lt is Wilson's disease. Lead and Copper) and metabolite of penicillin but having no It is a allergy antibiotic properties. The people having penicillin may display hypersensitive reacto

tion to it. Only the D-isomer

1s

used because

General Aspects of ForensicToxicology

example, mercury and arsenic have a great affinity for-SH groups. Preparation: BAL is available as a yellow, viscous, oily liquid with a disagrecable sulphurous odour. A 3 mL ampoule contains: (1) 100 mg/mL of BAL; (2) 700 mg/ml. of peanut (Arachis) oil: It stabilises BAL and (3) 200 mg/ml of benzy benzoate-it makes BAL miscible with oil. Route of administration: It must be given by I/M route not by I/V route. It must be injected deep I/M in gluteal region. I/V injection causes fat embolism' due to the presence of peanut oil. Dose: 3 mg/kg every 4 h and then twice daily for 10 days.

Contraindications: 1)

-isomer

produces optic neuritis by inhibiting the action

2)

of pyridoxine. Dose: 30 mg/kg BW (maximum 2 g/day) in four divided doses orally for 7 days. N-acetyl-D-penicillamine is another penicillin metabolite which is useful in mercury poison-

3)

ing.

Deferoxamine: is used in acute iron poisoning. Dose is 6 g in 24 h orally or I/V. Production: Microorganisms, for example, bacteria (actinobacteria Streptomyces pilosus) and

It

secrete small

iron-chelating compounds (Greek: iron carrier). These SIderophores sequester iron (Fe) from their surrounding for their own use. Deferoxamine is a type of siderophore. Siderophores are amongst the strongest binders to Fe3+ known. Because 0r this property, they have been used in metal chelation frungi

called siderophores

therapy.

SN-10: BAL BAL(British

(British anti-Lewisite)

anti-Lewisite, also called dimercapro

isachelating agent

used as an antidote in several metal poisonings. cations of BAL: Poisoning by Mercury, Arsenic, ad,Antimony, Bismuth, Copper and Gold. Mnemonic: MALA-BCG). heavy

Mechanism ofaction of urated Tated thiaction BAL:!BAL has two unsatofBAL: thiol

(-SH) SH) groups. groups. Heavy metals, for

331

4) 5)

Cadmium poisoning: BAL increases the uptake of cadmium (a nephrotoxic poison) in kidneys, thus increasing its nephrotoxicity. Iron poisoning: BAL reacts with iron to form BAL-iron complexes which cause severe vomiting. Organic mercury (e.g. methyl mercury): BAL causes redistribution of organic mercury to the brain and increases its toxicity. Hepatic dysfunctions. Peanut allergy: Because BAL contains peanut oil.

Precautions: 1) Since BAL-metal chelates dissociate in acidic urine, so before giving BAL, the urine should be alkalinised. 2) Use with caution in G6PD deficiency because BAL causes haemolysis. 3) BAL may cause deficiency of essential metals

such as zinc.

effects: Vomiting, increased BP, tachycardia, tingling and burning sensation, sweat-

Adverse

effects, ing, headache, etc. To avoid these adverse anti-histamines should be given 30 min betore the injection of BAL.

SN-11: Universal antidote antidotes

antidote is a mixture of threeantidote): one chemical (two physical antidotes and charcoal (two parts): ) Activated powdered Adsorbs alkaloids. milk of magnesia (MgO) or oxide 2) Magnesium Neutralises acids. part): (one I(Mg(OH),I

Universal

332

SECTION

Il

Forensic Toxicology

3) Tannic acid (one part): Precipitates alkaloids,

glycosides and metals. When the exact nature ofpoison consumed in not known, then the universal antidote may be used. All three components neutralise the actions of many poisons. The mixture is incffective and no longer used; nowadays, activated charcoal is useful and effective. Activated charcoal is nowadays considered to be medicinc's most powerful adsorbent. Apparently, the magnesium oxide and/or tannic acid component of 'universal antidote' interferes with the adsorptive activity of activated charcoal. Tannic acid was also found to be hepatotoxic.

SN-12: Legal duties of doctor in a case of poisoning 1)

Inform police: In all cases of suspected poisoning i.e. homicidal, suicidal or accidental), the doctor

has to inform the police. If a doctor does not inform the police, he may be punished with imprisonment for 6 months or fine (Rs 1000) or both [S.176, IPC|. If a doctor provides false evidence' during judicial proceeding, he may be punished with imprisonment for 7 years with fine [S.193 of IPC]. If patient dies from poisoning, the doctor should not issue the death certificate but should inform the police. 2) General: Inform and consult senior doctor. The doctor should administer himself the medicine and food to the patient. Do not allow any suspected person to be with the patient. Maintain detailed record of the condition and treatment of the patient. 3) Collection of evidence: The doctor should collect, preserve and seal the related evidences, for example, GL fluid, vomitus, blood, urine and faeces, clothes/bed sheet soiled with vomitus/faeces/urine or any half empty bottle of poison for the purpose of chemical analysis in FSL. If the doctor does not collect and preserve evidence, the punishment for him is imprisonment for I month or fine (Rs 500) or both [S.201 of IPC]. 4) Prepare MLC report: The doctor should record all the findings to prepare a MLC report and then he should provide one copy of MLC report to the police.

5) 6)

Opinion regarding the case can be given venaf after the of chemical analysis report. recipt In casc of food soning: The doctor sho

collect the sample of contaminated food f for purpose of chemical analysis in FSL and (2) he doctor has to report such casesto thepublic hea

authorities. 7) Arrangement for dying declaration: If a pa just about to die, doctor should arrange for record. ing dying declaration. For recording dying decla ration, the doctor has to call the Magistrate and then in the presence of Magistrate, the doctor has to examine the patient and certify that the patient is mentally fit in regards to consciousness, thought and judgment (compos mentis). In the absence of Magistrate, doctor should take dying declaration himself. 8) Send the body for postmortem examination: Ifa body is 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 postmortem examination.

SN-13: Postmortem examination in a suspected death due to poisoning

Prerequisite history. A farmer most commonly s Occupational poisoned by organophosphates. The autopsy surgeon can also ask the police about any evidence (e.g. empty vials) recovered from tne crime

scene.

2

External Examination Look for constriction or dilatation of pupil changes Lips and oral cavity: Look for any mucosal or remnants of poison. Stains: Look stains of poison, vomit or tueeca the clothes and any part of the body uucous Colour changes in corroded skin and m membrane (Table 13.10). Natural orifices: Look for poisonous materlhe 13.11 Postmortem staining stasis) (Table colour of hypostasis nmay indicate the type ou Skin: Look for injury, injection marks, ny atosis and pigmentation (in chronic arse soning), jaundice (in phosphorus and pot chlorate poisoning), etc.

1) Eyes:

2) 3)

4) 5) 6) 7)

e

CHAPTER 13

Coroded Skin 3.10 Colour ofPoisonings in and Mucous Membrane

TABLE

Coroded Skin

Colour of Membrane Mucous

and Brown'yellow Greyishblack

Greyish white

Reddish brown Bluish white

General Aspects of Forensic Toxicology

TABLE 13.13 Colour of Gastric Mucosa seen in Various Poisonings Colour

of Gastric Mucosa

Seen in Poisoning

Poisoning

Black

H,SO,

Nitric acid

Blue

Sulphuric and hydrochloric acid

Copper sulphate

Yellow

HNO,

Carbolic acid

Green

Ferrous sulphate

Hydrofluoric acid

Buff white

Carbolic acid

Mercuric chloride

White particles

Arsenic

HCI

Zinc chloride

Whitish

Colour of Hypostasis in

13.11

3) Stomach:

Bluish green

HS

a) Smell of poison may also indicate the poisoning. b) Contents: The poisonous material, for example, tablets, seeds, leaves, etc.

Bright pink

Hypothermia

c) Hyperaemia of mucous membrane.

Bright red

HCN

TABLE

PoisoningsS Poisoning

Colour of Hypostasis

CO

Chery red

CO

Deep blue

Opiates

Black

of the poison may be noted before opening the body as some stains of the poison or some stains of the vomitus may be present on the external surface of the body.

Smell: The smell

8)

Internal Examination In any case of poisoning, the skull should be opened first to note the smell. If other cavity 15 opened first, the smell of that particular poison may be masked (Table 13.12). Mouth, throat and oesophagus: Look for any inflammation, erosion or staining.

1) Smell:

4)

TABLE

13.12

in Poisonings Smell

Bitter almond

Kerosene Garlic

Burnt rope

Rotten egg

Musty odour

rotten

fish)

Different Types of Smell

Poisoning Cyanide

Organophosphates Arsenic, phosphorus, organophosphates

Cannabis (marihuana)

Dimercaptosuccinic acid, H,S, disulfiram,

Nacetylcysteine Aluminum phosphide and Zinc phosphide

d) Gastric mucosa: The mucous membrane is congested and haemorrhagic (Table 13.13). e) Softening: It is seen in alkali corrosives poisoning. f) Ulcers: Along the lesser curvature of stomach, there are some longitudinal mucosal folds through which liquids travel easily from oesophagus into duodenum. This ribbon like passage of folds is known as 'Magenstrasse (in German, it means stomach street). In case of corrosives (i.e. acids and alkalis) which are mostly liquids, the ulceration is usually found along the lesser curvature. To examine these ulcerations, the stomach must be opened by a scissor along the greater curvature. These ulcerations are seen up to pylorus. Ulceration beyond pylorus is due to natural disease (e.g. chronic gastric ulcer) and not due to corrosives. g) Perforation: Although perforation is seen in all corrosives (acids as well alkalis), it is most commonly seen in sulphuric acid poisoning. On corinternal examination, a perforation due to from rosive poisoning has to be difkerentiated autolysis the perforation due to postmortem (Table 13.14). duodenum is usualy 4) Intestines: Perkoration of caused by alkalis. nay cause liver necro 5) Liver: Hepatotoxic poisons liver and CCl,), fatty Sas (phhosphorus, chloroform sulphate and CC). (ethanol, arsenic, ferrous of poisons cause necrosis Nephrotoxic Riclneys: cresol 6) CCl,, carbolic acid, PCT (mercuric chloride,

Difference Between Perforation due to Corrosive and Perforation dues to

TABLE 13.14

Postmortem Autolysis

Perforation due to

Sr.

No.

2

Perforation due to Corrosive

Feature Site

Seen at places where corrosive came in contact, for example, ips, oral cavity, tongue, oesophagus, stomach, intestines

Surrounding mucous

Inlamed

membrane Peritonitis

and cantharides) or DCT (amphotericin, cisplatin and. glycols); cantharidin poisoning causes par enchymatous degeneration. 7) Respiratory tract: Corrosives may cause oedema of glottis and congestion and desquamation of mucosa of trachea and bronchi. 8) Heart: Subendocardial haemorrhages in left ventricles are seen in poisoning with phosphorus, arsenic, antimony and viper bite.

a

o

Indications: It

is

case

done in following circum-

stances: 1) Suspected poisoning/intoxication. 2) When unusual smell, colour or an unidentifiable material is detected in stomach contents. 3) Drug abuse 4) Anaphylactic deaths. 5) Advanced decomposition. 6) Accidental deaths involving driver of a vehicle (RTA) or machine operator. 7) Cause of death not found after autopsy. 8) When IO requests (as a part of investigation). What is preserved? In routine 1) Stomach and its contents. 2) Upper part (30 cm) of small intestine and its contents. In infants whole intestine has to be preserved. 3) Liver-500 g along with gall bladder. In infants, whole liver has to be preserved. 4) Kidney-half of each kidney (as one may be dysfunctional). When one kidney is present, the whole kidney has to be preserved. Both kidneys are preserved in children. 5)

Spleen-half.

especially at cardiac end Not inflamed, but softened and gelatinous

Absent

Present

SN-14: Preservation of viscera in of suspected poisoning

Postmortem Autolysis It is seen only in stomach

6) Blood (50 mL)--central luminal blood any

chamber of heart, intra-pericardial, thoracic aorta, pulmonary artery and vena cava) is preferred to cavity blood (haemothorax or haemopericardium or peritoneal blood, pooled blood left in cavity after removal of heart and lungs). 7) Urine (50 mL)-urine is aspirated with a syringe through the dome of bladder after the peritoneal cavity is opened. In certain cases preserve the following: 1) Brain (100 g of cerebrum/cerebellum) strychnine, organophosphates, opiates, CO0 cyanide, barbiturates anaesthetics and volatile organic poisons. 2) Spinal cord (entire length)--strychnine and Gelsemium.

CSF-alcohol. (alcohol-mor Vitreous humour-MCA phine-cocaine), TCAs and chloroform. 5) Heart-cardiac poisons (Digitalis, Aconitum Nicotina, quinine, Nerium" and Cerbra') and

3) 4)

strychnine. 6) Lung (one lung)-alcohol, chloroform, HCN and gaseous poisons. 7) Bile-opiates, alcohol, barbiturates, cocains

methadone and narcotics. 8) Skin (a radius of2-4 cm from injection site take the skin of injection site (morphineoin-cocaine-insulin are injected localy have skin) or where absorption of poison may Occurred or corrosive poisons. 9) Hair (20-30)-chronic heavy metal arsenic) poisoning and chronic drug abuse. 10) Nail-chronic heavy metal (arsenic)posoning. antiC, (10 cm of shaft of femur)-arsenia Bone mony, thallium and radium.

CHAPTER 13

(abdominal/perinephric)-pesti-

a

(10 g) 12) Fat insecticides. cides and solution of comPreservative ives: (1) Saturated usec preservative in Most commonly salt: mon should not be used in corrosive poiIndia. It be used in Rectified spirit: It shou

soning. (2) poisoning. (3) For blood: For 10 ml. corros 1oride (enzyme sodium fluo blood, use 100 mg of oxalate (anticoaginhibitor) + 30 mg potassium ulant).

TABLE

General Aspects of ForensicToxicology

2335

D/W-15: Ideal homicidal poison and ideal suicidal poison (Table 13.2)

D/W-16: Chemical antidote and physiological antidote (Table 13.15) D/W-17: Suicidal poisoning and homicidal poisoning (Table 13.3)

physiological antidote 13.15 Difference between chemical antidote and

Sr. No. Feature Mechanism of

Chemical Antidote It

neutralises the poison chemically within the GIT

action

Physiological Antidote It

acts at the target cell by producing pharmacological effects exactly opposite to those produced by poison

Examples

KMnO CusO,, albumin, tannic acid, etc.

Atropine, physostigmine, strychnine, barbiturates, etc.

Use

Used frequently

Use is limited

Used

Before absorption of poison in gastrointestinal tract

After poison has been absorbed

Principle

They do not

Fatal dose

Veryhigh

act on the principle or antagonism

in

circulation

They act on the principle of antagonism Low

14 CorrosiIVe Poisons Corrosives or corrosive poisons are those substances which corrode and destroy tissues through direct chemical action. They almost always act locally and have few systemic effects. Classification (Table 14.1).

TABLE 14.1 Classificationof Corrosives [LO-1] Strong Acids

Strong Alkalis

Inorganic (mineral) acids H,SO, (sulphuric acid) HCI (hydrochioric acid) HNO, (nitric acid) Others: boric, chromic and phosphoric acid Organic acids Carbolic, oxalic, salicylic, acetic, formic, citric, tartaric and picric acid

NaOH (caustic soda)

(caustic potash) Na,CO, (sodium KOH

carbonate)

KCO,(potassium carbonate)

KMnO, (potassium

permanganate) H,O, hydrogen peroxide

Facts Common to CorrosivesS They fix, corrode and destroy the tissues. Exothermic reaction occurs during which they extract water from tissue. Cause necrosis (coagulative necrosis by acids and liquefactive necrosis by alkalis). Convert haemoglobin into haematin. Stricture formation occurs both in acid and alkali ingestion but is more common in alkali > acid.

Important Features of Three Most Common Acids (Table 14.2).

TABLE 14.2 Important Features of Three Most Common Acids

Features Fuming/ non-fuming Perforation of

stomach Fatal dose Fatal period

336

H,SO

HNO,

Poisoning

Poisoning

Non-fuming

Fuming

Most common

Less

5-10 mL 12-24 h

10-15 mL 12-24 h

commonn

HCI

Poisonin9 Fuming

Least common 15-20 mL 18-36 h

INGESTION OF ACIDS

Acids

cause significant injury at pH Decreased visual 1t is

acuity. 5.

Death is due to respiratory paralysis and cardiac

arrest

Treatment 1)

Prussian blue (potassium ferric-hexacyanoferrate): Dose-250 mg/kg/day orally via a nasogastric tube in 2-4 divided doses. Why given? Thallium undergoes enterohepatic circulation. Prussian blue given orally, traps thallium secreted in the bile, and excretes in to faeces. Since thallium causes severe constipation by intestinal stasis, 50 mL mannitol (15%) needs to be administered along with Prus-

sian blue. 2) Gastric lavage with 1% KI and activated charcoal. 3) Saline purgative to increase faecal excretion.

PHOSPHORUS

Chemistry Phosphorus (Greek, phos = light, phorus = bearingli

a nonmetallic, irritant poison and there are two variet. ies, white and red (Table 15.6). Compounds: organa.

phosphates, aluminium phosphide, zinc phosphide

Fatal Dose It is 60-120 mg

2-8 days.

of white phosphorus. Fatal period

Mechanism of Action Locally phosphorus oxidises and injures tissues to cause both chemical and thermal burns. White phosphorus is a 'protoplasmic' poison (i.e. affects cellular oxidation) Hepatotoxic, nephrotoxic and cardotoxic.

Pharmacokinetics Phosphorus is absorbed rapidly when stomach contains fatty food so fatty substances should not be given during management of acute poisoning.

Fulminant Poisoning

Massive intake (>1 g) of phosphorus results u occ minant poisoning. Peripheral vascular collapse in

Death.

TABLE 15.6 Difference Between VWhite Phosphorus and Red Phosphorus [D/w-19 White/Yellow Phosphorus Red Phosphorus Features 1.

Appearance

Originally white translucent waxy crystals. yellow on exposure to light

It

turns

Reddish brown, amorphous solid mass

Garlic

Odourless and tasteless

3. Toxicity

Highly toxic

Nontoxic

4. Luminescence

Glows in dark (i.e. luminous

5. On exposure to air

Gives white fumes

No fumes

6. Uses

Tracer bullet and incendiary bombs, rodenticides e.g. aluminium phosphide and zinc phosphide), fertilisers

The striking

2. Odour and

taste

in

dark)

Does not glow (i.e. nonluminous) onsists

surface of safety match box powdered glass, sa phosphorus, of red particles and glue

Inorganic Acute

t

Poisonin Phosphorus Poisoning

of phosphorus. (duc to local irritant action on GIT: st stage taste and smellin breath. Burning pain ic-like stoma > lntense thirst-> mouth,ithroat and in odour and garlic diarrhoca. mitus miting, dark. Fumes may evolve from the Juminous in (smokystool drome). Phosphorus in stool stool form phosphocombines with atmospheric 0, to

dosc of 0.1-1 occurs with a

g

in

pentoxide.

rus stage Sccond 2)

(dormant phase of 2-3 days): Signs symptoms of irst stage subside in intensity, and is marked improvement of signs and that is, there days. The patient wants to SVTmptoms for next 2-3

discharged. home but he should not be After secThird stage (due to absorbed poison): recovery, the symptoms of ond stage of apparent severity. the first stage reappear with increased Flapping tremors of hands (i.e. asterixis), bleeding tendency (due to prothrombin deficiency), priapism, convulsions. Organs affected are: (1) hepatic failure-initially liver is enlarged due to fatty go

3)

degeneration (i.e. necrobiosis) but later on liver is shrunken due to necrosis (acute yellow atrophy, AYA). In AYA, the liver is half the normal size, has a marbled colour with alternating red and yellow areas. Jaundice and pruritis. A mousy odour of breath (Foetor hepaticus). Finally, hepatic encephalopathy: (2) renal failure and (3) CNS damage

encephalopathy, Cause of death is

convulsions, delirium, shock.

Autopsy Findings

Preservation of Viscera

Stomach and intestines should be tied at both ends before preservation. Viscera must be preserved in urated NaCl solution and not in spirit because satluminosity is lost. Viscera must be opened under nitrogen just before analysis.

Chronic Poisoning It results from long-term occupational exposure to the fumes of phosphorus pentoxide. Bristowe (1862) described a condition called Phossy jaw (or Glass jaw) SN-12] due to chronic phosphorus poisoning.

Medicolegal Importance (1) Homicidal poisoning: rare because of strong gar licky odour and luminescence. (2) Suicidal poisoning was also in records in earlier days of Luciter matches. The match heads were used to be soaked in brandy and ingested. (3) Accidental poisoning can occur in children by using rat paste (e-g. Ratol containing 3% phosphorus) which is similar to toothpaste. (4) Phosphorus can be detected in putrefied body.

coma.

IMPORTANT QUESTIONS FOR EXAMINATIONSS

hypocalcaemia and hypoprothrom-

Managemet of Acute Phosphorus Poisoning Avoid direct contact with the patient as phosphorus an get absorbed through skin. The phosphorus pres n patient's clothing may ignite spontaneousiy. Gastric lavage 4 with KMnO, solution (1:5000) which phosphorus into less toxic phosphoric acid and phosphate.

IN saline.

iruitjuice.

347

(1) Stomach contains luminous material with odour. Gastric mucosa garlic is yellowish or greenish with haemorrhagic white erosions. (2) Heart: subendocardial hacmorrhage. (3) Liver: fatty, enlarged yellow. and

Investigation Hypoglycaemia, binemia.

Irritant Poisons

(3) N-acetyl cysteine. (4) For shock:

(5) For

hepatic failure alkaline drinks and

hydrate Patient is kept on high protein and carbodietbut low fat. (6) Glucose (for hypoglycae-

na,calcium

gluconate (for hypocalcaemia), vitamin hypoprothrombinemia), )Forrrenal vitamins C and B, failure.

K (for

nodialysis.

LONG QUESTIONS (LQ) 1.

manifestaClassify poisons. Discuss the clinical postmortions, investigation, management and poisoning tem findings in a case of 'acute arsenic

[CCU 2012]. Describe clinical tea2. Classity irritant poisons. management, tures, laboratory investigations, medicolegaal significance postmortem findings and 2014). 2004, 2007] |CCU [DU CLP. case a of in

SHORT NOTES (SN) 3.

Plumbism

CLP 4. Clinical features of (lead line) 5. Burtonian line

I

348

SECTION

ForensicToxicology

6. Basophilic stippling (punctate basophilia) 7. Hydrargyrism (chronic mercury poisoning)

8. 9. 10. 11. 12. 13.

Acrodynia Hatter's shake Mercuria lentis Erethism Phossy jaw [CCU 2014] Metal Fume Fever

MEDICOLEGAL IMPORTANCE (MLI) 14. Person is suffering from plumbism. 15. A patient showed blue line on gums [CCU 2010). 16. Burtonian lines are present in a person. 17. A person is suffering from erethism.

DIFFERENCE BETWEEN (D/W) 18. Acute arsenic poisoning and cholera (very important) [DU 2002] [CCU 2010, 2011,2014]. 19. White phosphorus and red phosphorus.

ANSWERS LO-1: Classify poisons. Discuss the

clinical manifestations, investigation, management and postmortem findingss in a case of acute arsenic poisoning

Classification of Poisons (Table 13.1) Acute Arsenic Poisoning Clinical Features Signs and symptoms start within 30 min of ingestion. Most of the symptoms are due to capillary dilatation. Fulminant (narcotic) type of acute poisoning: It occurs if massive dose (3-5 g) in ingested, or if stomach is empty. Here, GIT symptoms are not prominent, even if present, they are minimal. Usually, signs and symptoms supervene within 5-10 min of ingestion of the poison. Gastroenteritic form of acute poisoning: Common form of acute poisoning, and resembles bacterial food poisoning.

Metallic

taste, increased salivation, garlic odour in breath, dysphagia, irritation/burning pain in throat spreading to abdomen and intense thirst.

Vomiting:

Profuse, projectile, dark brown.

presence of blood.and mucous due n dueto to ca transudation of plasma following apillary rupture of mucosal vesicles. Purging: Stool expelled frequentlyand ino tarily. Initially stool is bloody but later bec ecomes colourless and watery resembling rice water (rice watery stool). Pain, tenesmus and irritation around anus. Colicky abdominal pain: Burning pain allover the abdomen becomes acute and intense fire is burning inside tummy. Slight pressute on the abdomen will be violentdy resented: nd patient refuses to be examined. CVS features: Exhaustion from pain and rapid fluid loss from loose motion Extreme prostration, collapse, week/feeble pulse, sunken eyes, cold extremities, subnormal temperature, decreased BP, cyanosis. Arrhythmias, acute cardiomyopathy,

subendocardial haemorrhage. Renal: Painful micturition, oliguria and uremia. CNS: Convulsions, tremors and formication. Liver: Fatty degeneration.

3)

5)C 6)

Post

Investigation. ECG: QT prolongation, ST depres sion, T wave flattening. Serum arsenic: >0.9 umol/L

Management 1) Elimination: Emetics (apomorphine

injection,

gastric lavage with warm water and milk.

2) Antidotes:

BAL

(2,3-Dimercaptopropanol=Dimercapro Modern antidote of choice. Kept in 20% benzyl benzoate solution gne Arachis (peanut/groundnut) oil, so I/M, not I/V. weg Dose in severe cases is 3 mg/kg body /M injection in gluteal region 4 hourlydays first 2 days, then 6 hourly for next * reco then BD for next 6 days, until full (Table 15.7).

TABLE 15.7 Dose of BAL in Sever Acute Arsenic Poisoning 3 mg/kg Bo Weight l/M Injection in Gluteal Regio 4 hourly

for first 2 days

6 hourly

for next 4 days Tor next 6 days, until

12 hourly (BD)

3

ve imp

full recovE

CHAPTER 15 nild cases: 2.5 mg/kg body weight Dose in mild OD until full recovery. hourly for 2 days, then AL: Nausea, vomiting, effects of BAL

Inorganic Irritant Poisons

8Classification of Irritant Poisons

Side

vation,

lachrymation,

tin-

anorexia, numbness of extremities, generagling and increased BP, fever, lised body pain, slightly Before tachycardia, covulsions and coma. a dose of barbiturate and using BAL give ephedrinc hydrochloride 50 mg orally to these side effects.

avoid

3)

C6)

injection. Continued nasogastric is re-secreted in gastric

secretion because arsenic tract. It has been detected ingestion. in GIT 7 days after 5) Cathertics, for example, castor oil and MgSO 4)

T

1/N injection Sodium thiosulphate D-Penicillamine and sodium thiosulphate 1/V

Whole bowel

irrigation.

erun

eyes due to dehydration. CyanoExternally: Sunken sis (or jaundice). Early and longer lasting rigor mortis. Delayed putrefaction (because of antibacterial activity of arsenic and partly due to dehydration). Internally: 1) Stomach: A mass of sticky mucous containing arsenic particles cover the mucosa. Mucosa is swollen oedematous, bright red, desquamated, especially in pyloric region. Erosions and

ulcerations are seen. Congestion

and inflamma-

tion is most marked at the crest of rugae at the greater curvature, posterior part and the cardiac end of stomach. Lines

of redness present along

the walls. Red velvety appearance (multiple petechiae are seen scattered over mucosa).

organs are congested and enlarged. Lungs with subpleural ecchymoses. Brain oedematous with patchy necrosis or haemOrrhagic encephalitis. Meninges are congested. Heart: Subendocardial 4) Al

are congested

of ventricles.

petechial haemorrhages

0-2,Classify

irritant poisons. Describe clinical nvestigations, features, laboratory

management, postfindings and medicolegal portance poisoning in a case of chronic lead mortem

(Tables 15.1 and 16.1)

Clinical Features of Chronic Lead Poisoning SN-4] Laboratory Diagnosis 1) Blood: (1) Reference blood lead level in adult 10 ug%. In adults, symptoms can occur at levels above 40 ug%, but are more likely to occur only above 50-60 Hg%. (2) Erythrocyte protoporphyrin >35 ug%. (3) Free erythrocyte protoporphyrin is increased. (4) Basoplilic stippled RBCs. 2) Urine: Contains albumin, sugar, blood, copropor phyrin Il1, delta-ALA and lead. 3) X-ray: Dense transverse bands at growing ends of bones (just underneath the metaphyseal plates) around the wrists and knees on the X-ray.

Management. (1) Removal from the source of poi-

Postmortem Findings

ICR

349

soning, for example, if CLP is due to occupational exposure, switch to another job. (2) Chelation by BAL and CaNa, EDTA. (3) Calcium gluconate for abdominal colic. (4) Folic acid, pyridoxine, thiamine and parathormone. (5) Diet poor in calcium.

Postmortem Findings. (1) Lead line (or Burtonian lead line) on gums. (2) Brain: Pale and oedematous. (3) Heart hypertrophied. (4) Liver and kidneys contracted. (5) Muscles fatty degeneration.

Medicolegal Importance. (1) Donors with CLP have

increased seminal lead levels and have lower fertility rates. Even a healthy woman if impregnated by a man suffering from CLP is likely to abort. (2) Drug abusers: CLP in drug abusers also has been seen because lead is usually adulterated in drugs of abuse. (3) Occupational disease: since CLP is an occupational disease, an occuemployer is liable to pay compensation in case ot bullet: pational disease due to lead. (4) CLP by souvenir cause sometimes a bullet enters the body but does not time. long latality, and it is retained in the body for a ettects show ill The person survives, usually does not lead component causes of the retained bullet but theencephalopathy is usually CLP (5) Cause of death: lead brain damage. Irreversible and causes permanent

SN-3: Plumbism

(LQ-2, lead poisoning chronic means Plumbism

SN-4.

350

SECTIONII Forensic Toxicology

SN-4: Clinical features of CLP Clinical Features of CLP (Table 15.8): [Mnemonic: FLARE

4) Lead encephalopathy: It is most commo dren and is seen almost in all cases of CLp Most commonly seen in poisoning by TE lead).

(tetraethyl

It

TABLE 15.8 Clinical Features of Chronic Lead Poisoning (Mnemonic:

ible.

Mechanism: Leacd combines with SH-radicalsf

Facial pallor 2. Lead Lead line (i.e. Burtonian line) 1.

Lead palsy Lead encephalopathy

Lead osteopathy 3. Anaemia with basophilic stippling + Abdominal colic and Constipation 4. Retinal stippling 5. Effects on: Reproductive system (abortion, impotence and sterlity). cVs (hypertension), kidney (nephritis)

ad getting absorbed from sucking Crayons, coloured pencils and so on. It is usuallyirreve is

FLARE)

occurs at blood lead level >0.08 mg'%

MAO (monoamine oxidase) enzyme and inac. tivates it. Features In children-personality changes

10

mental retardation, restlessness, iritability insomnia, convulsions, delirium, hallucinations and coma. 5) Lead osteopathy: In children, lead is deposited beyond the epiphysis of growing long bones and it is detected by X-ray. Deposition of lead is promoted by calcium and vitamin D. Arthralgia present with deep-seated boring pain in bones and major joints. 6) Anaemia with basophilic stippling: Anaemia: Initially microcytic and hypochrom but later on normocytic and normochromic. t occurs at lead level of 70-80 mg% of bloo Causes of anaemia are: 1) Impaired synthesis of haem from protoperd-ALA phyrin, and porphobilinogen from (delta-amino-levulinic acid). It is dueo inhibition of d-ALA dehydrogenase. loss of 2) Increased fragility of RBCs due to intracellular K which is due to increas leads o permeability of cell membrane. It decreased survival time of RBCs. Basophilic stippling (punctate basophilna is

Facial pallor: It is earliest (first) and most conclusive sign of CLP. It is due to vasospasm (i.e. constriction of capillaries), particularly around the mouth. It is independent of the degree of anaemia. 2) Lead line (or Burtonian line) [SN-5]. 3) Lead palsy: It is a late and uncommon (310% cases) phenomenon, seen most commonly in males as compared to females and especially in adults. Lead-induced peripheral neuropathy (demyelination) leads to increased nerve conduction time and subsequent paralysis of muscles (purely a motor type of paralysis). Following conditions arise: (1) wrist drop-all extensors of wrist are affected except supinator longus or brachioradialis; (2) foot drop-all extensors of feet are affected except tibialis anterior and (3) other features are tremors, hyperaesthesia, numbness and cramps. Lead palsy affects those muscle groups, which are most liable to strain and fatigue. Lead palsy is often preceded by pain in large joints, tremors, cramps, numbness and hyper aesthesia which get increased by voluntary movements. may OCCur on treatment, with slow Recovery progress (taking> l year). Mechanism: It is due to-(1) toxic action of lead in anterior horn cells of spinal cord and (2) interference with phospho-creatinine metabolism. 1)

RBCs SN-6].

ualls

Abdominal colicand constipation: Colic ustu synipo symptom and it is often the tirst eraly lt genc vexsek that arouses suspicion of plumbisnn. altects intestine, ureters, uterus and blood sever The pain is sudden, nocturnal, very few h modic and intermittent (lasts for a During umbilicus. felt usually around contracted and abdominal wall gets rigid and forward benlh relieved by heavy pressure or by disc, 8) Retinal Stippling: Acdjacent to optic ojpht 7)

is

ae

o

ng greyish

lead particles are seen on

SCopic examination.

t

SN

CHAPTER 15

9)

EMects on:

Sterility and impotence Reproductive system:St sexes. In females: Menstrual disorders in both nenorrhoca and men1orrhanenorrhoea, dysmes

abnormalities.

abortion and foetal Hypertension. CVS: Nephritis, glycosuria, hacnnaRemai system: albuminuria and gout. turia, manitestations: General weakness/ General exhaustio11, headache, vertigo and eia),

10)

fatigue, carly

hair loss.

SN-5: Burtonian

line (or lead line)

very imporCLP. It is the bluish black discoloutant feature of occurs on the edge of ration of gums which always teeth. gum at its junction with

It Burtonian line (or lead line):

is a

the

in upper jaw. It is seen in only about 50%-70% cases of CLP It is especialy with poor dental hygiene (dirty or car-

usually seen

ious teeth).

deposited and appears within a week of exposure of lead. It is not seen in edentulous person (i.e. one without teeth).

It

is

Mechanism of development of lead line: In people with poor dental hygiene, the decomposition of food in mouth leads to the formation of H,S (hydrogen sulphide). H,S so developed reacts with tne lead in tissues to form black PbS (lead sulphide). The subepithelial deposition of black PbS (lead sulphide) granules leads to the formation of lead line. Ihe line disappears in $3 weeks if: (1) the mouth IS kept clean or (2) the carious teeth are removed Or (3) patient is removed from the occupation or the place of exposure. LA: If a worker ease due to

contracts any occupational dis-

lead, the employer is liable for compenSation [S.3, Workmen's Compensation Act, 1923

It

due to (1) condensation of iron-containing RNA ncar mitochondria and (2) clustered

ribosomes. Other features of RBCs associated with basophilic stippling are anaemia, anisocytosis, poikilocytosis, reticulocytosis and nucleated RBCs. MLI: Basophilic stippling when found associated with other clinical and laboratory features of CLP the employer is liable for compensation [S.3, Workmen's Compensation Act, 1923).

SN-7: Hydrargyrism (or chronic

mercury poisoning)

Hydrargyrism

(Latin, Hydragyrus (Hg) = mercury) means chronic mercury poisoning. Clinical features [Mnemonic: ATM-Easy Money-

Machine.

Acrodynia (pink disease): Hands and feet become puffy, pinkish painful, paraesthetic with peeling of skin. Redness, vesication and desquamation of peripheral parts of limbs (palm, fingers, soles and toes). 2) Tremors (also known as mercurial tremors or Danbury's tremors or Hatter's shake or Glassblower's shake): It is the classical feature of chronic mercury poisoning. Tremors occur first in hands (shabby and shaky hand writing), then progress to lips and tongue (stamnmering and hesitation in speech), then in arms and legs (staggering gait). 3) Mercuria lentis: A peculiar eye change due to exposure to the vapours of mercury. Brownish deposit of mercury through the cornea on ante rior capsule of lens. erethism 4) Erythism (also known as mercurial etfects psychological or mad hatter): The are known as of chronic mercury poisoning manmercurial erythism. lt is seen in mirror 1)

shyness/ firms. Anxiety/depression, uhcturing irritability/hallucinations/delusions,

timidity, (manic depressive suicidal nmelancholia, MDP insomnia/loss of psychosis = mad hatter) and memory in kidney.

Basophilic stippling (punctate basophilia) (punctate basophilia): It is very peculiar featur of RBCssseen in CLP Many discrete loured, pinhead sized spots found dark blue in the toplasm of RBCs.

351

is

SN-6:

asophilicstippling

Inorganic Irritant Poisons

5)

glomerulonephritis Membranous into converted in the blood Mercury is rapidly Renal tubular damage mercuric ions (Hg*')> urine). (hyaline and fatty

casts in

352

SECTION

II

Forensic Toxicology

organic Minimata disease (1956): A type of mercurial (methyl mercury) poisoning due Minamata Bay of to eating of poisoned fish in Japan. It resulted into CNS features. lines 7) Blue line on gums (similar to Burtonian's in lead poisoning). Management of hydrargyrism or chronic mercury poisoning. 1) Removal of paticnt from further exposure. 2) Demulcents. 3) Chelation therapy in chronic mercury poisonBAL 1ng is same as in acute mercury poisoning. 6)

followed by DMSA. BAL: Chelating agent of choice. Route deep I/M. 5 mg/kg every 4 h for 2 days, then 2.5 mg/kg every 6 h for 2 days, then 2.5 mg/kg every 12 h is

for 7 days. DMSA: After following the above mentioned BAL regimen, when the patient is able to take oral medication, replace BAL with DMSA at (10 mg/kg TDS for 5 days) followed by (10 mg/ kg BD for 14 days). Medicolegal importance: 1) Criminal abortion: HgCl, has been used for criminal abortion. 2) If thermometer bulb is broken accidentally in the mouth, it will cause no harm because metallic mercury is not poisonous if ingested. 3) Dentistry: Metallic mercury is used in dental amalgam. 4) Sindoor used by women in Indian culture contains mercuric chloride and lead tetroxide.

SN-8: Acrodynia Acrodynia (or pink disease or Swift disease): It is thought to be an idiosyncratic hypersensitivity reaction particularly seen in children in chronic mercury poisoning (mercurous chloride in teething powder). Its onset is insidious with anorexia, insomnia, sweat ing, generalised body/skin rash and photophobia. Hands and feet become pully, pinkish painful, paraesthetic with peeling of skin. Teeth may shed. Redness, vesication and desquamation of peripheral parts of limbs (palm, fingers, soles and toes), This condition can develop by chronic exposure of any form of mercury.

SN-9: Hatter's shake shake: It is also known as 'Glasshin. sblower's tremors 'mercurial or shake' or 'Danbury's trem Den in 19th century, thepeople Hatter's shake: Because working in hat-manufacturing factories (hatte used to remove fur from pelts by using mercu nitrate. Glassblower's shake: Because they are common in people working in glasS-blowing or hat industri is the classical and most consistent manifesta. It tion of chronic mercury poisoning.

Hatter's

Characteristics oftremors:

types of tremors are seen: (1) resting trem. ors (i.e. occurring at rest) and (2) intentionad tremors (i.e. more excited by purposeful voluntary movements) are absent during sleep. 2) Tremors ocur first in hands (shabby and shaky hand writing), then progress to lips and tongue (stammering and hesitation in speech), then in arms and legs (staggering gait). 3) Tremor is moderately coarse (more coarse than thyrotoxicosis) and is interspersed by jerky movements. Patient then becomes unable to dress himself and write or walk properly. any actv Lastly, the person is unable to carry out ity. This most severe form is known as 'concussion mercurialis' where no activity is possible. 1) Two

SN-10: Mercuria lentis Mercuria lentis: It is a peculiar eye change duc mercur long-term exposure to the vapours of mercury throu" There is a brownish deposition of the cornea on anterior capsule of lens. Dro "On slit lamp examination, there is 'malt reflex' from anterior lens capsule. acun is bilateral and has no effect on visual It vapou "Avoid further exposure to the mercury

SN-11: Erythism

py

'neun Erythism (or nnercurial ethism): The oisoning chiatric effects' seen in chronic mercury oisoning lt is occupational chronic mercury vohed

among hat makers whose felting work prolonged exposure to mercury vapours.

CHAPTER 15 known as 'madIhatter alsomanulacturing firms.

because

it is

seen

SN-13: Metal Fume Fever (Monday

Itis mirror

morning fever = smelter's shake = Brazier's disease = brass chills)

features:Mncmonic: DR ANISHA is Depression, Rough temper, AnxiSLIM), hat is, Irritability, Shyness, HallucinaNervou ety; tions/delusions Anorexia, Suicidal melancholia, memory, Insomnia, MDP Loss of move the patient from the site of Managem hygicne. Saline purgatives, maintain oral exposure. Sal DMSA). (BAL and Chelation therapy Clinical

It

jaw): It is the Phossy jaw (or Glass Jaw or Lucifer

sequestration and osteomyelitis of the lower jaw near the decayed tooth. seen in chronic phosphorus poisoning and It is also if bisphosphonates are used for long term. The epidemic of phossy jaw osteonecrosis was linked to yellow phosphorous, the key ingredient in 'strike-anywhere matches. In match-making factories, workers were exposed to heated fumes containing yellow phosphorus. Clinical features: (1) It affects preferably lower jaw near the decayed tooth. (2) Pain in teeth with swelling of jaw. (3) Multiple sinuses, discharging foul Smelling pus. (4) Mandible bone may be exposed after loosening of teeth. There may be complete mandibular sloughing with facial disfiguration. (5) There is persistent and slow progression of Osteonecrosis and it has a tendency to become infected. osteonecrosis,

TEJAE

Mechanism.

Chronic

yellow phosphorous

poisoning In phosphorus is converted into Disphosphonates. In osteoblasts, these bisphos phonatesinhibittheenzymefarnesylsynthetaseApoptosis Osteonecrosis. the body, yellow

51sphosphonate

drugs (e.g, alendronate ana

Pamidronate)

are usually used for treatment OSteoporosis. Their side effect is osteonecrosis

of the jaw, popularly called bisphososteonecra (BRON)). ecrosis of the jaw nonate-related

MLl:

Phossy

though rare

MLI-14: Person is suffering from

nowaday

if a worker develops jaw due to long-term long-term exp oSphorus, exposure to yellow

tion

the employer

.3, Workmen's

is liable for compensaCompen ensation Act, 1923].

is an

acute 'flu-like (or influenza-like) illness caused by the repeated inhalation of fumes produced when zinc or other metals (e.g. copper, iron, manganese, chromium, ferrous, cobalt, nickel, cadmium, lead, antimony, silver, aluminium and so on) are heated above their melting point. It was first described by Potssier in 1822. It is also known as 'Monday morning fever or "brass chills or brazier's disease Cause: The white fumes of zinc oxide (ZnO) are produced when Zn is heated above its melting point. Inhalation of these white fumes causes the MFF Seen in: It is seen in industrial workers who are exposed to welding, galvanising, metal refining, electroplating, alloy making, smelting and so on. Symptoms: A flu-like (or influenza-like) illness, for example, fever (low grade), chills, frontal headache, nausea, sweating, thirst, chest discomfort, low-back pain, joint pain, dry cough, myalgia, tachycardia, weakness, fatigue and so on. An attack usually subsides after 6-12 h but may last up to 24 h after the stoppage of exposure to the fumes of zinc oxide (ZnO). Laboratory diagnosis: (1) Transient leucocyto sis is typical of MFF and resolves usually within 24-48 h. (2) Chest X-ray may show transient ill-defined opacities. Treatment: (1) removal from the exposure sites (2) oxygen; (3) paracetamol for fever and pain and (4) chelation therapy in heavy exposure. Differential diagnosis: These clinical features of MFF are similar to other two conditions: (1) influenza or common cold and (2)) polymer fume fever due to inhalation of gases produced by burning ot polytetrafluoroethylene (Teflon).

SN-12: Phossy jaw

to

Inorganic Irritant Poisons

plumbism

f

means

from plumbism, it a patient is suffering 'Chronic Lead Poisoning.

he

is

suffering from

354

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ForensicToxicology

MLI-16: Burtonian lines are present in a person

Gums

Upper teeth

Blue line or lead line or Burtonian line

[MLI-15.

Poor dental hygiene

MLI-17: A person is suffering

from erethism Fig. 15.1 Blue line on gums

It

Since CLP is an occupational discase, an employer Is liable to pay compensation in case of occupational disease due to lead.

MLI [LQ-2]

MLI-15: A patient showed blue

line on gums

Blue line on gums (Fig. 15.1) is also known as lead line or Burtonian line. It indicates plumbism or CLP. Since CLP is an occupational disease, an employer is liable to pay compensation in case of occupational disease due to lead.

means he is having and showing'neuropsychiat. ric manifestations of "chronic mercury poison. ning. It is an occupational disease. Management: Remove the patient from the site of exposure. Saline purgatives, maintain oral hygiene. Chelation therapy (BAL and DMSA).

D/W-18: Arsenic poisoning and cholera (Table 15.9)

DW-19: White phosphorus and red phosphorus (Table 15.6)

TABLE 15.9 Difference Between Arsenic Poisoning and Cholera [D/W-18] Sr. No. Features

3.

8

Arsenic Poisoning

Cholera

Sequence of symptoms

Pain in throat Vomiting

Vomitus

Contains mucous, bile and blood

Does not contain mucous, bile and icc sO is watery

Stool

Dark coloured, bloody but later on rice watery

passed Hice watery without blood; jet continuous involuntary

Tenesmus and anal iritation/pain

Present

Absent

Voice

Not affected

Rough and whistling

Conjunctiva

Inflamed

Not inflamed

Laboratory investigation

Arsenic in stool

Vibrio cholerae

Number of victim

Generally one

cholera) Many (in an outbreak of

Manner

Suicidal, homicidal or accidental

Accidental

Purging

PurgingVomiting

Pain in thioar

in a

16 Organic Irritant Poisons The

irritant major organic

poisons are listed elow

(Table 16. 1).

TABLE

16.1 Organic Irritant Poisons

Vegetable

Animal Organic Irritants

Organic Imitants Abrus precatonus (ratti) Ricinus communis (castor)

Croton tiglium

Semecarpus anacaroiurm Capsicum (chilli)

Calotropis madar) Plumbago (chitra)

Cantharides Snake venom

Arthropods (i.e. insects), for example, insects, scorpions, centipedes, bees, wasps ants and spiders Others: Jelly fish, venomous fish and lizards

Abrus precatorius (RATTI, INDIAN LIQUORICE,

JEQUIRITY AND

ROSARY PEA) It

an organic irritant (vegetable) poison. Ratti is a seed of a plant, Abrus precatorius. It was is

raditionally used in India as a standard weight by

jewellers.

Ratti

seeds: Oval, 8 mm X 6 mm, red colourea a black spot at one end. The seeds may be w 01aly black; or white with black spot. The weight of a ratti seed is about 105-120 mg. ACTve

principle: Abrin (a toxalbumin, similar to

Pne

snake venom), abrine (an amin0 acid) abralin (a glucoside) and abric acid. Only 1-2 crushed seeds. Seeds if ingested as a whole will pas out of the gut intact without any harmful effect. Seeeds when boiled lose their poiSonou activity, so after proper cooking the secus be consumed with food. It is more toxic by subcutaneous 1route as compareo to oral route

FP:3-5 days. Mechanism of

action of abrin: Abrin is a protein which consists of two chains, A and B, linked together by a disulphide bond. The B chain binds to the surface of the cell. Then the whole toxin enters the cell by endocytosis. In cytosol, the A chain inactivates the ribosomes Stops protein synthesis. The action of ratti poisoning resembles with the action of viperine bite.

Clinical

features:

1) Locally

applied into eyes > Conjunctivitis. Treatment is washing with running water. 2) Ingestion: Nausea/vomiting, gastric irritation, haemorrhagic gastritis, abdominal pain and bloody diarrhoea. Pupils are constricted, cold perspiration, weakness, trembling of hands and convulsions. Management: (1) Patient should be admitted in hospital as severe symptoms can develop after several days of ingestion. (2) Gastric lavage or induce emesis. Activated charcoal. (3) Sodium bicarbonalkaate (NaHCO,) 10g orally per day to maintain RBCs. linity of urine. It prevents agglutination of (4) Anti-abrin antibodies have no role in manage-

ment.

of death: Cardiac failure. ingestion: GasAutopsy features: (1) In case of

Cause

Organs are congested tric mucosa is congested. injection of sui, and haenmorrhagic. (2) In case of ecchymoses, intlampainful swelling ancd oedema, tluid and necrosis mation, oozing of haemorrhagic wound consists of The around the site of puncture. fragments of the neetwo needle prick marks, the tound in the wound. cdlle along with sui nmay be (SN-1};:(2)arrow poison-the The MLI:(1) sui/sutari (3) malingering: and used is persons powdered seed been used by has seeds to powder of ratti produce conjunctivitis to jawans especially army

355

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Forensic Toxicology

obtain medical leaves in situations where getting leaves is difficult. Unilateral conjunctivitis indicates suspicion.

Ricinus communis (CASTOR/ARANDI) It

is an organic

irritant poison. In Latin, °Ricinus means 'tick (i.e. the skin of castor seed looks like a tick) and 'communis means 'common. Castor fruit: Green coloured, spiny, size about 2 cm X 1.5 cm X 1.5 cm. The fruit is a three-lobed capsule and each capsule contains single seed so each fruit contains three seeds. Castor seeds are of two types: (1) larger seeds (around

2 cm

x

x

cm) are red with brown blotches and (2) smaller seeds (around l cm x 0.75 cm X 0.5 cm) are gray with brown spots/mottling and resemble with Croton tiglium in size and shape. are two confusions: There 1) The castor'frui' is confused with 'Datura fruit' (because both fruits have spikes) (Table 16.2). 1.5 cm

1

TABLE 16.2 Difference Between Castor (Ricinus) Fruit and Datura Fruit Castor (Ricinus) Fruit Castor fruit is smaller in size and present in

clusters No sepals present at the base of the fruit Fruit is trilobed on

external appearance One fruit contains three seeds

Datura Fruit Datura fruit

is larger in SIze and not present in

clusters

A calyx

(fused sepals) persists at the base of fruit Fruit is almost spherical or Ovoid

One fruit contains about 400-500 seeds

2) The castor 'seeds' are confused with 'croton seeds' because of same size and appearance (Table 16.3).

Active principle: Ricin (a toxalbumin). Mechanism of action: Same as that of abrin

About 8-10 crushed seeds or 6 FD: of ricin. If intact seeds are swallowed, they wil will not poisoning because hard coa of seed cau revents absorption. After cooking, the seeds become become poisonous. Note: Castor oil is not poisonousnon and it is used as a purgative in constipation. Reason. that ricin is present only in the seed press cake, not the oil. FP:3-5 days. Clinical features: Nausea, vomiting and violent purging with straining and bloody diarrhoea Dehydration> Hypotension. Abdominal pain, liver and renal failure. Management: (1) There is no antidote, so treatment is mainly supportive; (2) IV fluids and vasopressors; (3) gastric lavage, demulcents and (4) whole bowel irrigation. Medicolegal importance: 1) Ricin is probably the most toxic substance in the plant kingdom. Its toxicity ratingis6. 2) Ricin is twice as toxic as cobra venom. Similarity between 'ricin' and 'cobra venom is that both are organic irritant poisons. 3) Ricin and bioterrorism: The US Centers for Disease Control and Prevention (CDC) classfied potential biologic threats into three categories: category A (first highest priority), category B (second highest priority) and category been (third highest priority). The 'ricin' has kept in category B. 4) Homicide: Rarely used. One famous exampie umbrella assassination. to ee 5) Malingering: Powder of seeds applied produces conjunctivitis.

Croton tiglium an organic irritant poison. ln Greek, k means 'tick. ariety smaller a of size equal the to almost are "Seeds I of castor seeds, that is around cm X 0.70 0.5 cm. tono cro Active principle: Crotin (a toxalbunmin), cid crotonic acid, methyl crotonic acid (or tig FP crotonoleic acid and crotonoside. ot drops) (20 mL 1-2 Four seeds or FD: 6 h-3 days. It

TABLE 16.3 Difference Between Castor (Ricinus) Seeds and Croton Seeds Castor (Rcinus) Seeds Dark brown with irregular patches/strips of different colours (white, black, yellow and brown) longitudinally present Shiny (glossy) polished

Croton Seeds

Dark brown with Irregular

patches of diferent colours (black, yellow and brown)

Appear dull

is

CHAPTER 16

cake as well as croton oil are p seedpress croton principles. Both because these contain active onous disagreeable odour. Croton oil has vomiting, symptoms: Nausca,

burning diarrhoea, hot prostration,collapse and stomach, vertigo,

symptomatic.

linternal organs are congested.

features: , Autopsy (1) Accidental

much common

poisoning is homicidal; (2) abortifacient-oil than suicidal or (4) in Ayurveda, oil is and root; (3) arrow poison; used and (5) ordeal poison.

MLI:

Semecarpus anacardium (MARKING NUT OR DHOBI NUT OR BHILWA)

It CODrd

is an organic iritant poison. Fruit: The fruit is called marking nut or dhobi nut because it looks like a nut and it is used by washermen (dhobis) for marking cotton clothing and linen. For this purpose, the fruit is dipped in limewater and then the juice of the fruit is obtained by SCratching the pericarp.

Fruit is about 1 in. (2-3 cm) long, ovoid or heart shaped. The pericarp of the fruit contains a bitter, rritant juice (i.e. brown oily resinous fluid), which turns black on exposure to air. Active principle: Bhilawanol (15%) and semicarpol (0.1%). FD: 5-10 g. Signs and symptoms after ingestion: Vomiting ularrhoea, dyspnoea, hypotension, tachycardia, delirium, coma and death. Management: Gastric lavage and demulcents. Atopsy features: Blisters mouth and throat. Stomach is congested. LAArtificial bruises--(1) juice of marking nut applied on the skin to bruise-like produce false bruise. The lesions are actually raised, blackisth, isters, the scratching of which can Cause According similar lesions on the tips of fingers.

the marginto some uthors the blisters are on of bruise. The

acrid serum produces uptions of the hbouring skin it come may mes into ntact. Later on ulcers be produce produced. Artificial (false) bruise must with which

ns

357

be differentiated from true bruise. (2) Accidental poisoning is common. (3) Criminal abortion. (4) Malingering-a dilute solution of the fluid is instilled in the eyes to produce conjunctivitis. (5) Vitriolage-juice may be thrown on the face. (6) Dhobi mark dermatitis is seen in Indian washermen who use marking nut in their work and the chemical urushiol is responsible.

and

pain from mouth to death. causes a vesicating agent and thus Croton oil is suppuration redness, vesication and burning on skin. when applied Managenment: astric lavage, demulcents and Signs

Organic Irritant Po

Capsicum(CHILLIES, RED PEPPER) It

organic irritant (vegetable) poison. Active principle: capsaicin and capsicin. FD: It is not fatal. Hunan's hands: Severe burning lesions of fingers in people handling dried red chilli powder with bare hands (i.e. without using gloves) for prolonged period. Features are severe burning pain, hyperalgesia, erythema and dermatitis. It was common in Hunan province of China. Mechanism of skin/mucosal irritation: Capsaicin releases substance P from afferent sensory neurons, which causes pain. (1) Criminal purpose: The chilli powder can MLI: be thrown by the robbers into the eyes to commit robbery. (2) The chilli powder can be used by ladies in the west to drive away potential rapists. (3) Hyderabadi goli: It is a method of introducing lathi plastered with chilli powder into the anus for causing torture. It also has been used by police to extort confession. (4) Accidental poisoning: The seeds of capsicum are confused with the seeds of Datura. So acute Datura poisoning can occur. (5) Burning of red chilli (or its powder) by supersti tious people to scare away ghosts and spirits and also to decrease the effect of negative energy. is an

Calotropis (MADAR, AKDO) tis

MILKWEED,

poison. It is a an organic irritant (vegetable) the roadside. Tivo Weed very commonly seen at Culotropis gigantean and Important species are cut, a leaves and stem are Calotropis procera. When milky latex comes out. calactin Calotropin, calatoxin, Active principle: Uncertain. FP: 6-12 h. application on and uscharin. FD: (1) Local symptoms: eruptions; SIgns and vesication and bullous

skin-redness,

SECTION

II

Forensic Toxicology

(2) instillation in eyes-conjunetivitis, keratitis, corneal oedema and dimness of vision; (3) ingestion: acrid bitter taste, burning pain in mouth, throat and stomach. Vomiting, diarrhoca, pupils dilated, convulsions, coma and death. Management: Gastric lavage, demulcents and symptomatic. MLI: The juice can be used in many ways. (1) Artificial bruise (or false bruisc)--redness and vesication. (2) Abortifacient-used in abortion stick. (3) Infanticide. (4) The root is highly poisonous to some poisonous snakes (including cobra). The snakes even cannot stand its smell. So the snake charmers use it to control the newly caught snakes. (5) Cattle poisoning (juice smeared on a cloth and pushed into rectum). Cattle do not eat because of their unpleasant smell and taste. (6) In folk

SNAKEBITTE

Classification of Snakes A.

Step 1: Look at belly scales. (A) If bellv se are small (or moderat large), that is, es do cover entire breadth of belly, the snake is not non poisonous' and (B) if belly scales are large, that is cover entire breadth of belly, the snake maybe nonpoisonous or poisonous. 2) Step 2: Look at the scales at the top of the head. (A) If scales are small, the snake is 'poisonou (e.g. viper) and (B) if scales are large, the snake may be nonpoisonous or poisonous. 3) Step 3: Look at the side of face. (A) If there is a pit between eye and nostril, the snake is 'poisonous (pit viper); (B) if third labial touches the eye and nasal shield, it is 'poisonous' (cobra and coral snakes) and (C) if there is a large shield on top of head, but no pit and third labial does not touches eye and nostrils, then proceed to fourth step. 4) Step 4: Look for central row of scales on back if enlarged, and at under surface of mouth, only four infralabials present, the fourth one being largest (do not count central scale, which is mental), it is 'poisonous' (krait) which has bands or half rings across back. 1)

medicine.

CANTHARIDES (SPANISH FLY)

(Lytta vesicatoria OR Cantharis

vesicatoria)

It

is an emerald green beetle. Size: 2 cm X 0.5 cm. Active principle: Cantharidin. Amount of cantharidin in a beetle varies from 0.2-0.7 mg. It is a milky fluid synthesised predominantly by male beetle and exuded from their joints as a milky fluid when disturbed.

FD: 10-80 mg. FP: 24-36 h.

Acute

poisoning: Local application on skin Burning pain, redness and blister. On ingestion: (1) GIT-blistering of lips and tongue, burning sensation in mouth and epigastrium, thirst, dysphagia, dysarthria, nausea, vomiting, abdominal colic, tenesmus and bloody diarrhoea; (2) strangury increased desire to pass urine but scanty urine and haematuria and (3) priapism, abortion, convulsions, coma and death. Priapism is the persistent painful erection of penis lasting longer than 4 h. Management: Gastric lavage, demulcents (dilute milk) and vasopressors for peripheral vascular col-

Japse

popularity as an aphMLI:(1) Cantharidesitgained priapism. (2) Causes rodisiac but actually causes woman. abortion n pregnant grcen particles' found features: "shiny is conAutopny mucosa. GIT mucosa gastric the sticking to

ested,

Venomous snakes and nonvenomous c. D/W-8]. Steps to differentiate venomous 1akes ake from nonvenomous snakes:

B.

On the basis of toxicity of venom: 1) Neurotoxic: A. Colubridae: Boomslang, rat snake, tree snake and mountain racer. B. Elapidae: (1) Cobra, for example, comntu cobra (Naja naja) and king cobra (Ope* phagus/Naja hannah); (2) krait (Bungurs caeruleus), for example, common krait banded krait and (3) coral snake (Calliepi 2) Vasculotoxic

(Viperidae):

Russell's

(Daboia russelii), saw-scaled viper natus), pit viper and rattle snakes. 3) Myotoxic (sea snakes).

The Big Four

(Echis

sna

whie

These are four very important species of a. lnaltt are responsible for virtually all snakebites in 1) Common cobra (Naja naja)(naag) ch Size (1.5-2 m). Hood with spectacle hood. of marking present at underside

CHAPTER 16 Third labial touches cye as well as

Eye

nasal shield

Hood

Eye

without

(spectacle mark

maTA Nasal shield

Common (ndian)

Ein.

16.1

King

cobra

cobra

king cobra Common cobra and

as well as head, third labial touches eye king (in both common cobra and Oviparous. cobra). Pupil is round. sidc of nasal shield

differentiated

from Common cobra has to be (Ophiophagus hannah; naagraj): king cobra a cobra and it is the sole king cobra is not true It is the member of the genus Ophiophagus. world's longest venomous snake. It eats other snakes, so the name Ophiophagus (Greek, ophis = serpent, phagos = eater of). When confronted, it can raise up to one-third of its body straight off the ground and still move forward to attack. King cobra is the only one snake of the world which builds the nest. It is bigger (size =2.5-4.5 m) than comnmon cobra. The hood is without spectacle marking. It can inject 40 times the fatal dose in a single bite (Fig. 16.1). 2)

Common krait (Bungarus caeruleus):

It

Organic Irritant Poisons

59

is responsible for maximum snakebite cases

and deaths. is considered as world's most dangerous snake because of its aggressive and easily excitable temperament. Triangular head. Brownish with white markings. Scales are small on head, but scales are broad with serrated edges (so called saw scaled) on the body. When it moves, a peculiar rustling sound is created due to saw-like scales on the body. Most species are viviparous but Indian species are oviparous.

It

Approximate Yield of Venom per Bite (Table 16.4)

TABLE 16.4 Approximate Yield

of Venom per Bite and Lethal Dose Usual Lethal

Snake

Dose

Krait

obra Russell viper

6 mg

8-20 mg

12 mg

170-300

15 mg

130-250 mg

mng

40-60 mg

Pit viper Saw-scaled

Approximate Yield of Venom per Bite

viper

8 mg

20-30 mg

Components of Snake Venom (Table 16.5)

Size: 1.5 m.

Usually steel black in colour. The back of whole body bear single/double narrow bands, and belly creamy white. Head is oval with one enlarged Central row of hexagonal scales on the back. Undersurface of the mouth has only four infralabials-the fourth one is largest. Third labial Scale does not touch nose and eye. very active Itis at night. ) Russell's 1S

viper (Daboia russelii): body (1-1.5 m; stouter than other akes), triangular head with narrow neck. cales at head are small, Three longitudi bigger nostrils. gular chain-like pattern or rows on the back. Very large Sa-scaled hissing sound. viper (Echis Smallest carinatus) (growing to just a foot) among above tour. Life span 2-5 years.

TABLE 16.5 Venom

Components of Snake

Venom of Colubridae It is predominantly neurotoxic, primarily toxic for respiratory and cardiac

centres

He

Venom of Viperidae It is predominantly

haemotoxic and haemolytic. It produces cytolysis of cells of vascular endothelium, ysis of BCs and other tissues and coagulation

disorders NeurotOxins and cardiotoxins

.Phospholipaseand

phospho-tidase Cholinesterase and ribonuclease

Proteinase

Hemolysin, leucolysin and cytolysin

Haemorrhagin Lecithinase and

phospholipase-4

Proteolysin and fibrinolysin Colubridao and Viperidae Venom common to both thromboplastin) Hyaluronidase, protease and

360

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Forensic Toxicology

Dry Bite When poisonous snake bites without injecting venom, the bite is known as dry bite. About 20% of viper bites and even a higher percentage of bites inflicted by some other snake families (up to 75% of sea snakes) are dry.

Clinical Features in a Case of Snakebiteor Oophitoxaemia [SN-2]

Management in a Case of Snakebite [SN-3, 4 and 5] It includes first aid measure as well as hospital man-

agement.

Postmortem Findings in a Case of Snakebite (1) Fang marks-mostly two bite marks (1 cm deep

in elapid bite and 2 cm deep in viper bite). They may not be visible, so a magnifying lens may be used. (2) In elapid bite-local changes are minimal. Brain congested. (3) In viper bite-oozing of blood from bite marks. Swelling and cellulitis. Lungs are haemorrhagic. Extravasation of blood in serous membranes (pleura and pericardium). Haemorrhage may be found in other organs. Regional lymph nodes are swollen and haemorrhagic. (4) In sea snakebite-rhabdomyolysis. Kidneys are congested. (5) In snakebite, the venom can be found in urine, saliva or milk as venom is excreted into these fluids. MLI of 1)

Snakebite Ingestion of venom is not poisonous: If a person

ingests snake venom accidently, it will not cause any harm to that person. Reason is that the proteins of venom are digested in GIT and so intact protein molecules of venom are not available to be absorbed from mucosa. A rescuer who sucks venom from wound will not be poisoned if he swallows. However if he has abrasions in mouth, then the venom may be absorbed. Even the animals killed due to snakebite may be eaten without ill effects. 2) Cattle poison: A cobra is shut up in an earthen vessel containing a banana and the mouth of the vessel is closed. Then vessel is heated which irritates the snake and snakebites banana many times and in this way the snake injects most of its venom

into the banana pulp. Then pulp is taken taken smeared on a rag. 'The gis thrust into outand the rectum of animal by a bamboo. 3) Manner of death is usually accidental. Queen Cleopatra committed suicide by snakebite. 4) It was a method of ecution in past. The convic were thrown into a deep pit containing venom snakes.

ARTHROPODS

Scorpions Neurotoxin of scorpions is highly lethal than neuro. toxin of snake. Management of scorpion bite [SN-7].

Centipedes 'Forcipules (poison caws) are the modified first pair of legs around the head. They are used to capture pray and inject venom. Local symptoms are pain, erythema, oedema, lymphadenitis and local skin necrosis. These features resolve within 2 days except tissue necrosis which may take a week to heal. Systemic features are fever, palpitations and anxiety. Clean the wound, give local anaesthetics (lignocaine) for pain and give TT injection.

Honeybees Female worker bees are the only one that can sting When a honeybee stings a person, it leaves benlnd not only the stinger, but also part of its abdomen and digestive tract, plus muscles and nerves. This massive abdominal rupture kills the honeydee Within minutes. Signs and symptoms are nt local pain with erythema and swelling (1 cm areah urticaria, dyspnoea (due to laryngeal oedema hypotension and abdominal pain. As the hone bee leaves its stinger behind, the venom sac ot stinging apparatus left at the skin continues top Sate and it delivers its whole content Withn min must of the sting. Due to this reason, the stinger De removed immediately without wasting tine teroids, colcd sponging. Treatment: antihistaminics, stet

i

adrenalin and beta2-agonist.

Wasps Wasps

their

Wasps can sting several times, they do1not leave after sting at the skin of man and they do not de stinging like honeybees.

CHAPTER 16

IMPORTANTQUESTIONS FOR EXAMINATION

SHORT

NOTES (SN)

Sui in a case of snakebite or ophitox.Clinica features

1.

acmia 3.

Management in 2010)

aid 4. First

case of snakebite |CCU 2004,

of snakebite snakebite case of

measures to be taken in

management Anti-snake venom thherapy Scorpion bite

a

case

Hospital

in a

DIFFERENCE

BETWEEN (D/W)

5.

6. 7.

8.

9.

d

a

10. 11.

12.

[DU Poisonous snake and nonpoisonous snakes 2001, 2006, 2009] [CCU 2014] Cobra and viper

marks [DU 2010] Colubrine and viperine bite [DU 2004] Elapid bite and viperine bite Cobra and viper bite

ANSWERS SN-1: Sui

4

Sui (or sutari) is a sharp tapering needle made up of Abrus precatorius used for killing cattle and can be even used for homicidal purpose. The preparation of sui: The ratti seeds are first soaked in water, decorticated, then mixed with opum, onion, Datura and water to make a paste and then this paste is shaped like small sharp Tapering needle about 2.5 cm long. These needles are then dried in the sun. Uses ofsuis Killing cattle (cattle poison): Two suis are fixea Dy their bases to the hole of a bamboo pole (or a Small piece of wood or at the end of a lathi) and that that end of the bamboo is forcefully hit/ stabbed on the skin of the cattle so that both are implanted into the skin. Both suis are Placed nearby each other on one end ol lathi becau the wound used by two suis resemble the wound aused by two fangs of snake. In this way, it creates confusion.At and around the of inoculation, there will be inflamnman, oedema or even necrosis with oozing of

s

Organic Irritant

Poisons

361

haemorrhagic fluid from the puncture. First the animal will not take food and by third day will be unable to stand or move and it dies within 3-5 days. 'These signs and with snake (viper) bite. symptoms resemble 2) Killing human (i.c. homicidal purpose): The sui can be kept between any two fingers of hand with the pointed ends towards ventral aspect of hand and then other person is slapped so that sui is inserted into the skin of the cheek. Clinical features of injection of sui: The symptoms (local and systemic) resemble viperine snakebite. The wounds caused by two suis resem ble the wounds caused by the fangs in snakebite.

A. Local features: Painful swelling and oedema,

ecchymoses, inflammation, oozing of haemorrhagic fuid and necrosis around the site of puncture. The wound consists of two needle prick marks, the fragments of the needle along with sui may be found in the wound. B. Systemic features: Weakness, faintness, vertigo, anorexia, titanic convulsions, decreased temper ature, drowsiness, coma and death in 3-5 days. Advantage of using sui to the killer: Since the symptoms resemble viper snakebite, the killer is

not under suspicion. Management of the case with injected sui into the skin: A. Surgical: The sui should be dissected out. B. For systemic effects: 1) Sodium bicarbonate (NaHCo,) 10 g orally urine. It per day to maintain alkalinity of prevents agglutination of RBCs. 2) Diazepam to control convulsions.

of SN-2: Clinical features in a case

snakebite Common Features Seen in all Snakebite (hypotension, a

Psychological trauma: Fright pallor, sweattransient increasecd respiratory rate, vonmiting)> Fight> skin and ing cold clammy absorption of venom> PsyIncreased systemic death. delayed chological shock and It is a hypersensitivity reaction: even after Type lI may present discharge patient the manifestation, informed during be should h, so he 24

regarding this.

362

SECTIONII ForensicToxicology

Signs and Symptoms in a Case of Neurotoxic Snakebite (e.g. Cobra Bite) DLocal symptoms: Local symptoms in case of neurotoxic snakebite o

ecchymosis, necrosiS and gangrene (of s. subcutaneous tissues and muscles), hl: suppuration, sloughing and regional lym adenopathy. 'Persistent bleeding from bitee is a constant feature in site viper bite. Swelling (initially around bite site) quickly spread. reads over the entire limb

are minimal and include-(1) bite (fang) mark with minimal swelling and (2) bloodstained fluid oozing out. Systemic symptoms: Nausea and vomiting, headache, vertigo,sleepiness, convulsions, ptosis, blurring of vision and diplopia. Muscular weakness and paralysis: Paralysis initially involves lower limbs, trunk, head and neck

Oedema of limb Increased intracomnpartmental pressure Tense swelling

then

Paralysis of palate and vocal cord leads to inability to speak (i.e. dysphonia)

Muscle compartment syndrome (Severe pain which increases on stretching intracompartmental muscles) Blisters containing clear or blood stained fluid start appearing in and around the bite site within 12h and spread around to involve entire limb. They heal in around 4 weeks if the patient

then

Paralysis of muscles of jaws, tongue and pharynx leads to inability to swallow (i.e. dysphagia)

then

Paralysis of respiratory muscle leads to respiratory

Hypoxia and acidosis

then Coma

Death

Signs and Symptoms in a Case of Neurotoxic Snakebite (e.g. Krait Bite) Most patients are bitten while asleep on the floor and thus any part of the body (head, neck, shoulder, hands, chest, abdomen and legs) may be bitten. The bite mark is invisible or scarcely visible. The local swelling is either negligible or even absent. Mild tenderness, itching, nunmbness, paraesthesia, abdominal pain, drowsiness, fasciculations and paralysis.

Signs and Symptoms in a Case of Vasculotoxic Snakebite (e.g. Viper) o

Local features: The local symptoms are more pronounced in viperine bite as compared to other snakebite. Pain, tenderness, reddening, persistent bleed ing, swelling, oedema, discolouration and

Man

mea

survives.

failure

then

SI

o

Systemic features are haematologic and haemor rhagic abnormalities: Haematologic manifestation: decreased plate lets, increased bleeding time and increased clotting time. Urine contains blood, sugr and protein. Intravascular hemolysis> Hac maturia and haemoglobinuria > Acute renal failure. Haemorhagic manifestations: (bleeding from nose), haemop Epistaxis tysis (blood in sputum), subconjunctiva haemorrhage and gingival bleeding. Bleeding in gastrointestinal tract (eg. rect haenar bleeding), genitourinary tract (e:g. turia) and peritoneum udla Intracranial haemorrhage: (1)Severe nei noid haemorrhage (SAH) > ICH)

-

ache. (2) Intracerebral haemorrhage unconscou

Convulsions, hemiplegia,

ness. (3) Bleecding in anterior pituitary Hlc "CVS: Hypotension, tachycardia >

weuk rhagic shock. dizzines Headache, features: General blurriu ness, pupils dilated and fixed and vision. shock ofdeath is haemorrhagic

Cause

SN

The=

abso Vent

Tabl

Reco

) Re Snc

ina

Reco

Re

CHAPTER 16

Case of Symptoms in a Case and Signsand kebite (e.g. Sea Snake) signs lotoxic Local

The bite

swelling.

local no Headache, Systemic:

thirst sweating, vomiting, weakness and nderness of muscles. stiftness, muscles persists or several months. Weakness of MyoglobiGeneralised rhabdomyolys myoglobinuria) and hypernaemia (and Acuterenal failure. kalaemia Polymyositis, frismus, ptosis and later progres,

paralysis.

sive flaccid

reddish brown. occurs from cardiac arrest (due to

.Urine is dark . Death

hyperkalaema) or

respiratory paralysis.

SN-3: Management in a snakebite

case of

Management of a case of snakebite includes first aid measures (SN-4] and hospital management [SN-5]. aematolosr

Poisons

363

snakes may not always inject a lethal dose. We must tell this fact to the person who has been bitten. Telling him this is very helpful as it reassures him and allays anxiety and freight. Fear increases the sympathetic drive and thus increases heart rate, which consequently hastens the circulation of venom.

usually ainless with minimal or

is

Organic Irritant

2) Arrange for rapid transport of patient to the nearest hospital where anti-snake venom is available. 3) Remove jewellery/watch/ring/bracelets or cloth-

ing

4) Immobilisation of the bitten limb by using a splint or a sling. Movement inçreases the spread of venom in circulation. 5)

Pressure immobilisation technique (lympho-oc

clusive bandages): is used in neurotoxic (elapid) bite where local It tissue damage is less. It should not be used for vasculotoxic (viper) bites because of the danger of increasing the local effects of the necrotic

venom. limb is wrapped immediately with a bandage, for example, crepe/elastic (4.5 m long and 10 cm wide). The bandage is bound firmly around the entire bitten limb, starting distally around the fingers or toes and moving proximally, to include a igid splint. Wrap pressure should be 40-70 mmHg for upper extremity and 55-70 mmHg for lower extremity. The limb is is then immobilised by a splint. The bandage bound as tightly as for a sprained ankle, but not (radial, pos so tightly that the peripheral pulse occluded or that terior tibial dorsalis pedis) is slipped between its a finger cannot easily be

Entire

r

SN-4: First in a

aid measures to be taken

case of snakebite

of first aid measures is to retard systemic absorption of venom and preserve life and preent complications before receiving medical care The aim

(Table 16.6).

Recommended )

Measures

Reassurance: 'All snakes are

not poisonous; most are nonvenomous and all poisonous

S1akebites

layers.

TABLE

16.6 FirstAid Measures in a Case of Snakebite

Recommended

1. Reassurance

for rapid ge transport of patient

3. Rernove

accessories

4 Immobilisation of limb , Pressure bitten

2

Not Recommended

thne

immobilisation

1echnique Occlusive (lympho

bandages)

1. Wash (saline cleaning) 2. Sterile dressing 3. Local incision

4. Mechanical suction/

mouth suction

5. Topical instillation or

application of chemicals, herbs or ice packs 6. Tourniquets 7. Electric current 8. Do not give food or drink

offending

should be used only when: (1) known to be snake is reliably identitied and in rescuer is skilled (2) neurotoxic; primarily (3) victim can be pressure wrap application and carried to medical care. tight tourniquet It

(1) Release of compression bandage

Caution:

aay

result in the systemic or development of severe compression bandramatic ldeally, envenoming. (2) released until the patient are be lages should not resuscitation facilitiesbeen hospital, treatment has IS in antivenom

available and started.

SECTION I

364 Do It RIGHT

Approach. It

Forensic TOxicologyY is

For airway and breathing: If airway is patent (i.e. silent breathinoiD Place the patient in recovery position. If airway is compromised (1Le. a noisy breathin. thing c.g. gurgling and whistling): do a head tilt and chin lift manoeuvre to open the airway. If the patient is not breathing: start bao and mask ventilation and itiate CPR (Cardiopul. monary resuscitation). If patient is not able to maintain respiration endotracheal intubation and mechanical venti. lation. For circulation: decure a wide-bore peripheral Iw line as soon as possible. Rapid and low.-volume pulses indicate hypotension which needs immedi.

now recommended to

RIGHT approach, adopt what has been called 'do it Getting to Hospithat is Reassurance, Immobilisation, thhe doctor of any signs tal without delay and Telling and symptons that develop. Not Recommended Measures 1) Wash (saline cleaning): Do not wash the wound with soap or any other solution. 2) Sterile dressing: Not to apply. 3) Local incision: Do not give. 4) Mechanical suction/mouth suction: Do not do. 5) Topical instillation or application of chemicals, herbs or ice packs: Do not apply. 6) Tourniquets: The techniques to limit venom spread (e.g. lympho-occlusive bandages or tourniquets) are not recommended because there is a high risk of 'arterial compression' and 'subsequent gangrene' with a tight tourniquet. It may also lead to greater local tissue damage, loss of function of the limb or even amputation. In case the patient presents with a tourniquet applied elsewhere, then look for distal pulses. If distal pulses are present, avoid removing the tourniquet until ASV has been administered. If distal pulses are absent, remove tourniquet immediately but with gradual release of pressure. Sudden release of pressure may cause two things: (a) It releases large amount of venom in bloodstream in a very short time which may suddenly deteriorate the condition of the patient. (6) It releases deoxygenated blood and many harmful metabolites into the circulation which leads to severe metabolic acidosis, vasodilatation and profound hypotension which can cause sudden

cardiac arrest. 7) Electric current. 8) Do not give food or drink (especially avoid alcohol), but small sips of water are acceptable if there is a great delay in the victim being transported to hospital.

SN-5: Hospital management in a of snakebite 1.

ate I/V fluids. 2.

epistaxis.

examination: Bleeding or not. Loin pain and tenderness suggests acute renal ischaemia (in Russell's viper bites). 3. Rapid history 4. Laboratory Investigations Blood: test (20WBCT). 20 min whole blood clotting (com ABG (arterial blood gas) analysis, CBC timeh plete blood count), PT (prothrombin PTT (partial thromboplastin time) and N (international normalised ratio). Aminotransferases, creatine kinase and alu

Gingival

local dans* lase are elevated if there is severe damage: or particularly generalised muscle ised nitrogen ra

Creatinine,

urea or blood urea

in the renal failure. seen may De hyperkalaemia Early Potassium:

tollowing extensive rhabdomyolysis snakebites. acidosis (es metabolic Low Bicarbonate:

case

Rapid clinical assessment and resuscitation: Assess the level of consciousness. ABC (i.e. airway breathing and circulation).

Rapid general physical examination: Local examination: Examine the bitten part. Look for tense oedema and extent of swelling Elicit tenderness to palpation. CVS: Arterial pulses, BP/HR, lymphadenopathy and lymphangitis, compartmental syndrome, petechiae, purpura and ecchymoses and

in

renal failure). Urine may contain RBC casts, globin or protein.

5.

Iemoglobin/nyo-

Anti-snake venom (PAV) therapy [SN-6J|

CHAPTER 16 (i.e. ten part): Apply dry Treatmeni of wound Aseptic debridement of essing. Apply splint. 6.

Do not touch intact blisters but we with aseptic echnique. debride ruptured listers

necrotic tissue.

can 7,

Other

measures:

immunisation.

Mannitol I/V. cholinergics. When neurotoxic features:

signs: When neuroparalysis

neostigmine (0.25-0.5 mg I/V half hourly). Give atropine neostig0.6 mg I/V before every injection of effects. mine to block its muscarinic side Fasciotomy in case of muscular compartment syndrome: In case intracompartmental pres1 sure is high (>40 mmHg) even after h of I/V mannitol, fasciotomy is done to do decompress the compartment just to preserve nerve function.

Anti-snake venom therapy

Anti-snake venom therapy: Polyspecific (polyvalent) serum is prepared by using the venoms of tour snakes (common cobra, common krait, Russell's viper, and saw-scaled viper). Most commercial antivenoms are of ori81n.

equine are prepared from horses. Two are there: MOnospecific (monovalent) serum: Prepared USing the venom of a single snake. It is not available in India.

m india, antivenins types of serum

4)

Polyspecific

(polyvalent)

Dy

serum:

Prepared

using the venoms of >one snake. It is pre pared at Haffkine Institute in Mumbai, lndia ánd Central Research

Institute (CRI) in Kasauli, ndia. It is in the form of a lyophilised powaer of horse serum oduced by the immunisation of horses with the venom common of four snakes cobra, mon krait, Russell's viper, and saw-scaled

by drying

vacuum.

Indications

it

viper), The serum is lyophilised from the frozen state under high

AVHaemostatic

hemical abnormalities, spontaneous bleeding from gums,

is

present. So

adrenaline should be ready (i.e. loaded) before administering ASV. Hypersensitivity testing: Not recommended nowadays, as it does not reliably predict which patient will have an allergic reaction to equine antivenom. Adrenaline injection should be immediately available to treat anaphylaxis. Antivenins: Initial dose 8-10 vials I/V stat. For neuroparalysis, if there is no response or worsening over the 2 h after an infusion, a second and final dose of 8-10 vials should be given. Effectiveness: Antivenom has proved effective up to 2 days (after hydrophid bites) and weeks (after Viperidae bites). It is almost never too late to give antivenom while signs of systemic envenoming persist, but ideally it should be given as soon as it is indicated.

SN-7: Scorpion bite venomous scorpion species belong to a large family Buthidae, for example, Leiurus quinque: triatus and Mesobuthus tamulus. MOA: Neurotoxins in the venom of scorpion affect voltage gated Na-channels and K-channels.

All

Clinical features:

Severe pain at the site of sting. Systemic manifestations:'Autonomic storm. 1) Profuse sweating (= skin diarrhoea). 2) Thick ropey salivation due to stimulation of bronchial mucous glands, which is dithcult to expectorate. It persists for of adults. It 3) Priapism in all children and 20%

Local:

24h.

4) 5) 6)

for xample, and nose, etc.

365

2) Hypotension and shock. 3) Ncurotoxicity and general rhabdomyolysis. 4) Tender local lymphadenopathy is suggestive of systemic spread of venom. 5) Severe local swelling.

Risk of hypersensitivity reactions

Tetanus Prophylactic antibiotics. PCM). Analgesics («.g.

SN-6:

Organic Irritant Poisons

7)

persists for 5-15 h. Dilatation of pupils (mydriasis). severe vasoconstriction Cold extremities due to catecholamine. due to liberated circulatory and is due to Hypotension is short lastirng vonniting, sweating hypovolaemia as a result of Hypertension and pulmonary salivation. receptors. and stimulation ofalpha Oedema due to Acute pancreatitis.

SECTION

II

Forensic Toxicology

D/w-9: Cobra and viper (Table 16

Management:

is the specific Scorpion antivenom (SAV) as carly treatment. It must be administered l/V route withas possible (within 4 h) by rcaction to out skin testing. Hypersensitivity SAV is not secn. Why? Becausc high circulating catecholamine induced by SAV prevents a reaction to SAV and acts as a prophylaxis agent anaphylaxis. 2) Prazosin (a,-blocker as well as phosphodiesterase inhibitor): It is widely used for Mesobuthus tamulhus sting. Prazosin with SAV enhances recovery time. Patients given SAV with Prazosin required significantly fewer doses of Prazosin than the Prazosin singly. Dose: 250-300 g every 3 h interval. 3) Other drugs: (1) vasodilators, for example, Hydralazine, Nifedipine and isosorbide dinitrate; (2) ACE inhibitors, for example, Capto pril improve the diuretic induced pulmonary oedema and cardiogenic shock due to scorpion sting and (3) dobutamine improves pulmonary oedema. 1)

D/W-8: Poisonous (venomous) and

nonpoisonous (nonvenomous) snakes

TABLE 16.8 Dfference Between Cobra and Viper Sr. No.

Characters

Cobra

Viper

1.

Body

Long, cylindrical

Short, stout

2

Head

Small (and same width as neck)

Larger fand broader

then

neck and body), triangular

3.

Scales on head

Large

Small

Upper jaw

Two fangs+ other teeth

Two fangs only

5.

Fangs

Short, fixed and grooved

Long, mobile and

6.

Tail

Round

Tapered

Pupil

Round

Vertical

8

Venom

Neurotoxic

Haemotoxic

9.

Parity

Oviparous

Viviparous

canalised

DW-10: Cobra bite marks and viper bite marks (Table 16.9)

(Table 16.7)

TABLE

TABLE 16.9 Difference Between Cobra Bite Marks and Viper Bite Marks

Difference Between Nonpoisonous Snakes and Poisonous Snakes

Sr. No.

1

16.7

Nonpoisonous

CharactersSnakes Belly scale

2.

Scales at

head

Small, do not cover entire breadth of belly Usually large

4 6.

Two fang marks

associated with following features

Swelling

Minimal or absent

Two fang marks

associated with following features Extensive aind to may spread

Usually small (e.g. viper) except elapid and

3.

Haemorrhage

Minimal or absent

Persistent

4

Tenderness

Less

More

Short and solid

Hollow

Compressed

Nocturnal/Diurnal Nocturnal Two fang marks + Two fang marks marks of other marks of

small teeth

Bite Marks

2.

Blunt (not markedly

Bite marks

Fang marks

Viper Marks

Bite

Large, cover entire breadth of belly

Tail

5.Habits

Characterss

Snakes

Fangs

compressed)

1.

Cobra

Poisonous

krait

TF3

Sr.

No.

other teeth

entire limb

and pain

D/W-11: Colubrine bite and

viperine bite

viperm

and Same as differences between elapid bite an. bite (Table 16.10) because snakes of Colubri ta ily are neurotoxic as the snakes of Elapidae

|

CHAPTER 16 Organic Irritant Poisons

Elapid bite and viperine bite (Talble 16.10) oM-12: TABLE 116.10 Str. No.

Difference Between Elapid Bite and Viperine Bite Elapid Bite

(Cobra Bite)

Features

Neurotoxic

Venom

symptoms Onset of signs and 2.

Local reaction

(haemorrhage,

Late (i.e. within 10-20 min) Minimal

Viperine Bite

(Viper Bite)

Vasculotoxic Early (i.e. within seconds to 10 min)

Extensive

swelling and pain)

Gangrene

Wet type

Dry type

Paralysis

Present

Absent

Lost (due to paralysis of tongue and throat muscles)

Not so

Hypersalivation with trickling of saliva from the mouth

Absent

Pupils

Normal

Dilated, nonreactive to light

Respiration

Slow, weak, laboured

Quick and laboured

Normal

Hypotension

Coagulability

Not affected

Greatly affected

12.

Haemorrhagic manifestations

Absent

Prominent feature

13.

Cause of death

Respiratory failure

Speech and deglutition Saliva

9 0.

Blood

367

pressure

Haemorrhagic shock

17 Poisons Acting on Nervous System Chapter 17A CNS Depressants CLASSIFICATION OF CNS DEPRESSANTS 1.

Inebriants: Alcohols: Ethanol and methanol. b. Sedative hypnotics: Barbiturates, benzodiazepines, paraldehyde, chloral hydrate and potassium bromide. c. General Anaesthetics: chloroform and ether. Somniterous poisons: Opium and its derivatives, for example, heroin, codeine, thebaine and papaverine. a.

2.

INTRODUCTION TO ALCOHOLS Alcohol is classified as inebriant' or cerebral neurotoxic poison' or 'sedative hypnotic.

Alcohol

(i.e. ethyl alcohol) is a socially acceptable drug. Among socially acceptable drug it is the third most common drug of abuse after caffeine and nicotine. Concentrations ofalcohol in various alcoholic beverages: Rum (45%-90%); vodka (40%-50%); whisky, gin, brandy, arrack and tequila 45%); liquors (35%-40%); fortified wine, for example, sherry and port (15%-20%); champagne (10%-15%) and beer (4%-8%) and port (3%-7%). Surgical spirit: Ethanol (90%-95%) + methanol (5%-10%) along with traces of castor oil and methyl salicylate. Types of alcohol: (1) Absolute alcohol (dehydrated alcohol) (alcohol dehydratum) 99,95% ethyl alco hol by volume (i.e. etlhyl alcohol containing40% is the optimum for rapid sherry and port) (eg brandy, arrack

absorption.

Absorption

80%, rapi absorption occurs Maximunm (up to jejunum). 20% small intestine (duodenum and in

occurs in stomach. Absorbed GIT via portal vein to liver. phase, blood alcohol concenSo during absorptive elsetration (BAC) in portal vein exceeds that of (slower absorption) alcohol is carried from

where in body. Factors which affect the rate of hol (Table 17A.1).

absorption of alco-

reached, distribution of alcohol is urine (1.3) > spinal fluid (1.10-1.27), serum/ plasma (1.12-1.20), whole blood (1.00) and brain

When equilibrium

is

and liver (0.85).

After absorption, alcohol gets fairly and evenly distributed throughout the body tissues except in the bones and fats. Actually body tissues take alcohol in

proportion to their water content. Bones and

TABLE 17A.1

Factors Which Affect the Rate of Absorption of Alcohol Factors Which

Increase

the Rate of Absorption_ 1 Empty stomach: Absence of proteins, carbohydrates and fats 2. Rapid gastric emptying:

Factors Which Decrease the Rate of Absorption 1.

Carbonated

beverages, champagne because the bubbles greatly increase the Surface for example,

area carrying

alcohol 3. Dilution

to 20%. about s the optimum for20% rapid absorption Strength of

4. Absence of congeners 5. Gastrectomised patients: Increased of absorption

8. Prostigmine

1.

Carbonation

rate

2.

Fatty nmeal: Beverages with higher Concentrations of alcohol (>40%), for example, Vodka, rum, whisky gin, brandy, arrack and

tequila- Pylorospasm, gastric iritation, decreases gastric motility and forms a barrier of mucous (to decrease absorption) Chronic gastritis and GIT diseases

3. Adrenaline and

atropine

4. Co-ingestion of drugs, for example, aspirin and

butyl scopolamine drink

taken to ingest 5. Time Individual variations 6.

Poisons Acting on Nervous

System

369

fatty tissues contain less water, amount of water. With intake so they retain less of known amount of alcohol, BAC will be higher in obese man in comparison to a lean person of same After death, alcohol in stomach weight. may diffuse into the blood and tissues. This results in higher blood level than existed during life, if the blood sample is taken from the part into which postmortem diffusion has taken place. Alcohol interferes absorption of vitamins [A, B, B, (nicotinic acid or niacin), B, (pyridoxine) and folacin or folic acid) in small intestine and decreases their storage in liver.

Metabolism 90% ingested alcohol is metabolised (oxidised) in liver, rest 10%% is excreted (5% in urine and 5% in breath). The most important pathways of metabolism are: A. First pathway (= alcohol dehydrogenase pathway) (main pathway, 90%): It occurs in 'cytosol' of hepatocytes. Alcohol, in the presence of alcohol dehydrogenase, is converted into acetaldehyde. Acetaldehyde, in the presence of aldehyde dehydrogenase, is converted into acetate and acetyl CoA. B. Second pathway [= MEOS (microsomal ethanol-oxidising system) or CYP2E1] (>10%): It occurs in 'microsomes' of sarcoendoplasmic retic oxidaulum. It is responsible for 210% of ethanol It is an tion at high blood alcohol concentration. inducible pathway. catalase pathway): It C. Third pathway (peroxidase hepatocytes. Least com Occurs in peroxisomes' of

mon.

Pharmacokinetics

rela-

saturated at Aldehyde dehydrogenase: It is concentration. As the sysethanol blood low tronm tively elimination changes tem is saturated, ethanol kinetics. first-order to zero-order elimiunation is Normal rate of chronic alcomination: mg9%/h). A 12-27 (range mg9%/h) than mg%/h 18 (>40 faster eliminate far sutters severe holic can until he least at addiction. ne average person stages of his centres are later the ver damage in actions: Higher thalamus, armacological midbrain and followed by first, medulla. alfected finally the and spinal cord

370

SECTION IIForensic Toxicology

Fatal Dose Ingestion: Adults-5-8 g/kg absolute ethanol (or 6-10 mL/kg); children--3 g/kg absolute ethanol (or 4 mL/kg). Larger doses especially taken quickly may not kil, because of violent emesis due to gastric irritation. Blood concentration > 500 mg% is fatal.

ACUTE ETHANOL P0ISONING

Acute Ethanol Poisoning [L0-1] Differential Diagnosis of Acute Alcohol Poisoning (1) Head-head injury, CVA, intracranial tumours,

epilepsy and parkinsonism; (2) psychological dis-

orders, for example, general paralysis of insane and

hypomania; (3) metabolic disorders, for example, coma (diabetic, hypoglycaemic and uremic); (4) disseminated sclerosis; (5) drugs, for example, insulin, atropine, barbiturates, morphine, hallucinogens and antihistaminics; (6) high fever and (7) CO poisoning.

CHRONIC ALCOHOL POISONING

Clinical Syndromes Associated With Chronic Alcohol Poisoning Alcohol abstinence syndrome: Seen 6-8 h after cessation of alcohol intake and is characterised by tremors (in hands, legs and trunk), agitation, sweating, headache, nausea and insomnia. 2) Alcoholic withdrawal seizures (rum fits): It may be seen after 24 h after cessation of alcohol intake. GTCS. 3) Alcoholic hallucinosis: Seen 48 h after cessation of alcohol intake. Auditory or visual hallucinations. 1)

4) Alcoholic ketoacidosis: It develops

24-72

cessation of alcohol intake. Increased h after metabolic acidosis and hypokalaemia. anion gap 5) Alcoholic paranoia: Delusions of persecuti reference/infidelity and violent quarrels, 6) Alcoholic polyneuritis (or peripheral uropathy): Pain and tenderness in extremities, loss af deep reflexes, unsteady gait, weakness, wrist an foot drop. 7) Cardiac problems: (1) Beriberi heart occurs d to deficiency of thiamine; (2) alcoholic cardiomy. opathy and (3) dysrhythmias. 8) GIT problems: Gastric ulcerations, Mallory Weiss syndrome, liver cirrhosis and malnutrition. 9) Delirium tremens [SN-6]. 10)

Neuropsychiatric symptoms (Table 17A.2).

Treatment of Alcohol Dependence (1) Aversion therapy-a type of behaviour therapy. It involves (a) using an emetic, for example apomorphine mixed with alcohol and (b) subthreshold electric shock. (2) Psychotherapy and group therapy. (3) Deterrent agents (alcohol sensitising agents), for example disulfiram, metronidazole, cephalosporins, chlorpropamide and so on. (4) Anti-cra ing agents, for example naltrexone, fluoxetine and

acamprosate.

Vire

1or

ion

sble 1994

dryb

rk

Erik

POS Ale

di bl an the Alc

S hoE OCC

less

Alcohol and Sudden Death During struggle, catecholamines are released which on combination with alcohol produces arrhythmia Cardiac arrest > Death. Conduction system lesions predispose to arrhythmia that may be further agra vated by alcohol and catecholamine.

Alo

Colt

mp

will alco

s

Whe

TABLE 17A.2 Neuropsychiatric Symptoms Associated With Chronic Alcoholism

Wemicke's Encephalopathy

An acute reaction due to thiamine (vitamin B1) deficiency, which

characteristically develops aftera period of persisting vomiting Triad

Global confusion (disturbance of higher mental functions + recent memory) 2) Ophthalmoplegia (nystagmus and sixth cranial nerve palsy) 1)

3)

Ataxia (cerebellar)

Korsakoff's Psychosis A delayed or long-term complication

which often follows Wernicke's

encephalopathy Consists of amnestic syndrome 1) Amnesla (both retrograde and anterograde) 2) Confabulatlon (a false memory that the patient believes to be true)

Marchiafava-Bignami Disease

Widespread demyelination of corpus callosum and optic tract Disorientation, epilepsy, ataxia anu SO on

but WEDN

ETHY

yCon

brou

ser &octd

e

CHAPTER 17

BORATORY ANALYSIS OF ALCOHOL and urine are good for alcohol anal-

s humour alffected by putrefaction for a longer not theyare s glucose. Laboraand also they do not conlain dependence are: (1) GGT narkers of alcohol (2) MCV (mcan corpuscular (7ghtyt transferase); and cath analysers. EstimnaBAC (3) olume) and analysis is legally admisVitreo

based on breath of BAC 185, Motor Vehicle Act, 1988 (Amnended ble as per S. nmL of breath is received in to a 1994). About 60-100 and analysed by breath analyser. dry balloon tio

Erik

Widmark's formula (1932) [SN-7]

POSTMORTEM ALCOHOL ANALYSIS

.Alcohol diffuses after death: After death, alcohol difuses through stomach wall to surrounding blood, cavities (pleural, pericardial and peritoneal) and tissues. So blood should not be collected from the areas in vicinity of stomach. Alcohol and head injury: If death is due to head injury, EDH or SDH should be preserved for analysis, as it will contain the same concentration of alco-

blood at the time when incidence occurred. Also the effect of putrefactive changes is less in EDH/SDH due to good protection by skull. Alcohol and putrefaction: Alcohols can be produced due to action of enzymes, bacteria (e.g. Escherichia coli), yeast and fungi on carbohydrates and proteins in putrefied bodies. Longer the time since death, more will be the production of alcohols. Concentration of alcohols in advanced putrefaction could be as high as 0.29%, so when PM levels of alcohols are EuphoExcitement. ria Higher centres of brain are inhibited, for example decreased cognitive function, decreased inhibitions, decreased attention span (i.e. concentration), decreased sensory perceptions and decreased capacity of critical judgement.

Signs and 1)

It

Euphoria, increased self-confidence, increased sociability and increased talkativeness. Inci dence of motor vehicle accidents increases. Loss of self-control, excitement, memory and reasoning impaired and pupils are dilated. Nystagmus occurs due to effect of alcohol on vestibulocochlear system. Two types are AGN and PAN (Table 17A.6). Due to loss of critical judgement, the person may disclose his secretes. Visual acuity is decreased.

TABLE

Nutshell

17A.5 Action of Alcohol in

Blood Alcohol

Concentration

0-50 50-100 100-150

150-200

200-300 300-500

500

(mg

Behaviour Sobriety Euphoria

Excitement

Confusion Stupor Coma

Death

0

Poisons Acting on Nervous System

3755

2) Stage of incoordination (at BAC of 150-300 mg%): Higher centres as described above are inhibited further.

It

includes two more conditions: confusion and stupor. Stage of confusion: (1) Incoordination ofthought; (2) speech slurred, incoherent and difficulty in pronouncing consonants; (3) staggering gait and ataxia and (4) disorientation and vertigo. Skilled movements impaired and increased reaction time. Stage of stupor: Painful stimuli not felt, drows iness, loss of muscle coordination (inability to stand or walk), pupil dilated and vision blurred. 3) Stage of narcosis/coma (at BAC of > 300 mg%): Eyes: McEwan's sign may be seen. The pupils are constricted but on painful stimulus (e.g. pinching or slapping or pulling beard or hair), the contracted pupils dilate which then again return slowly to the contracted stage. The pupils may take up to 20 min to reach their previous contracted state. The patient does not regain consciousness to any degree during this sign. This sign is not found in coma due to other conditions, for example concussion, apoplexy and so on, so it is helpful in differentiating alco holic coma from other comatose conditions. Incontinence of urine and faeces. Temperature is subnormal.

Respiratory Strenuous respiration and cold depression clammy cyanotic skin. Unconsciousness (or coma) and pupils are dilated. Death occurs at BAC > 500 mg% due to respiratory failure. Investigation. (1) Blood alcohol level and (2) CT a scan of head-head injury should be excluded as differential diagnosis of acute alcohol poisoning. Management. Treatment is mainly supportive as the patient will improve slowly. Death is rare in pure eth prolonged anol ingestion and there is recovery after (hangover). sleep with some residual after-effects 1) ABC: Airway, breathing and circulation. bicarbonate. It is of 2) Gastric lavage with sodium in early stage. great value if the patient is brought the is brought late or It is not done if the patient patient is unconscious. 3) Thiamine 100 mg I/V. + 15 unit insulin. 4) I/V fluids: 10% glucose peritoneal dialysis. 5) Haemodialysis and

Progressive medullary paralysis

TABLE 17A.6

Nystagmus Positional Alcohol Nystagmus (PAN)

(AGN Alcohol Gaze Nystagmus

vertical (sitting or standing) position It is of two types: 1) Horizontal gaze nystagmus (HGN, seen at blood alcohol concentration 80 mg% is consistently associated with HGN. It is onset at an angle s40 degree from the midline is a sensitive indicator of blood alcohol concentration of >100 mg% Presence of HGN should not be taken as proof of alcohol intoxication as HGN may be noted in pathological conditions, ingestion of sedatives and tranquillisers

PM findings. (1) Alcoholic smell on opening the body cavities and stomach. (2) Organs (liver, lungs

and brain) and GIT are congested. Pulmonary and cerebral oedema. (3) Blood is dark and tluid.

Classify poisons. Discuss the clinical manifestations, investigation, management and postmortem findings in a case of 'acute methanol poisoning Classification of Poisons [LO-1, Chapter 15]1 Acute Methanol Poisoning LO-2:

Clinical features Methyl alcohol produces symptoms of drunkenness in the same way as ethyl alcohol but inebriation (drunkenness) is not prominent and the effects on CNS are more intense and persistent (prolonged). FD: 60-200 mL. Blood level of 200 mg% are fatal. GIT: Nausea/vomiting, abdominal pain (severe cramps) and pancreatitis. CNS: Headache, neck stiffness, drunkenness as prominent as in ethanol), vertigo, confusion, delirium and coma. Eyes: Effects in the eyes are mainly due to formic acid. [Mnemonic. Very Red Scratch Causes Pain], that is: 1) Visual disturbance (photophobia and blurred vision). 2) Retinal oedema.

It is seen in horizontal (supine) position when head to either right side or left side is turned It is caused by alcohol acting on 'vestibular system' .It is best seen if eyes are closed, that is it is seen as movement of cornea through eyelids Types: PAN 1:The nystagmus is in the direction towards whichthe head is turned, that is nystagmus occurs to the when head is turned to right SIde and vice versa.right side It occurs within 30 min and lasts for 3-4 h. Mostly seen at 280 mag PAN II:The nystagmus is in the opposite direction to seen in PAN I, that is nystagmus occurs to the right that side when head is turned to left side and vice versa. It appears about 4-5 h after ingestion and lasts for 4-5 h

3) Scotoma (central and peripheral) and nystagmus, 4) Complete blindness (due to inhibition of cytochrome oxidase by formic acid in optic nerve

Optic neuritis and atrophy). 5) Pupils dilated and fixed in later stage. Acute tubular necrosis: Urine is strongly acidic and may contain acetone and a trace of albumen. High anion gap metabolic acidosis.

Others:

Muscular weakness, dyspnoea, hypoten sion and tachycardia.

Investigation. Blood for methanol

level and meta

bolic acidosis.

Management of methanol (methyl alcohol) pois0 ing [SN-8]

Mention different alkaloids of opium. Discuss signs, symptoms management and postmortem findings of 'acute opium/morphine poisoning LO-3:

4E

17A.7) Alkaloids of Opium (TablePoisonin9

Acute Opium/Morphine

very Clinical features stage s This excitement): 1) First stage (stage of dose 15 tu short but it may be absent if a large flushing ess, chil Buphoria, excitement, talkativeness seizures neonatal and hallucinations face, dren. Restlessness.

Na essar

Sion

ter

CHAPTER 17

Alkaloids of Opium TABLE 17A.7 Deivatives lsoquinoline Derivatives (9%-14%) 1) Narcotine (noscapine) (6%) Morphine

henanthn

1) Codeine (2%-4%) 2) Thebaine(0.5%) 3)

2)

3)

Papaverine (1%) Narceine (0.2%)

(stage ot sfupor): Initially drowsjheadache, itchin sensation nausea ness, giddi uncontrollable desire to and vomiting. Later on by external stimsleep, patient cannot be aroused uli, cyanoSIs and pupils are contracted. 3) Third stage (Stage of narcosis): Coma with all reflexes lost. Pinpoint pupik Initially the pupils are contracted (pinpoint pupils) and they do not react to light. This is the most important characteristics. The pupils dilate at the end. Classical triad of opioid toxicity: Miosis, CNS depression and respiratory depression. Face is pale and covered with perspiration, so the skin is cold and clammy. BP and RR are decreased. )

Second stage

Noncardiogenic pulmonary oedema.

Death

is

Management 1)

due to asphyxia.

ABCDE of resuscitation: Patent

ventilation.

Grastric lavage

airway and assisted

with KMnO,. Gastric lavage should

done even if opiates are taken parenterally. It is aue to the reason that opiates De

undergo enterohe-

circulation and so they are resecreted into the Stomach. For the same region, leave MgSO, in the onach (as a purgative and to minimise reabsorpLon of opiates). Also give MDAC. 3) patic

Multidose

4) Evacuationactivated charcoal

(MDAC). of intestines to prevent reabsorp tionn of opiates: Sodium lphate 30 g orally and enema.

5) Antidotes:

nal naloxone, naltrexone (50 mg/day nalmefene and 'sostigmine for reversng respiratory depression. Naloxor Dose is 1-2 mg 1/V. Since duration of One is only essary 2-3 h, the repeat dose may be necfor patients intoxicated by eg,codeine).f longer acting drugs ion. Alternatively, it can be given as an infuThepatient after should be onitored for at least 4h the last naloxone dose. orally),

Poisons Acting on Nervous

System

377

Treat convulsions (by benzodiazepines) hypotension (by 1/V fAluids). and Postmortem findings 1) General: Evidences of drug abuse may be present, for example, injection/prick marks, abscesses, old scars and so on. Signs of asphyxia, for example, cyanosed face and nails. PM staining is cyanotic. Froths at mouth and nostrils. 2) Internal: (1) Stomach contains opium; (2) smell of opium present; (3) brain meninges are congested; (4) blood is dark and fluid; (5) all viscera are congested; (6) lungs are congested and oedematous and (7) bladder is full of urine.

LO-4:

What are somniferous poisons? Describe clinical features, management, postmortem findings and medicolegal significance in a case of facute morphine poisoning' DU 2008, 2010] Somniferous Poisons 1)

Opium is obtained from poppy plant (Papaver

somniferum). 2) Opiates: These are the natural derivatives or drugs obtained from opium. Example: morphine, codeine, thebaine, papaverine, narcotine and heroine. 3) Opioids: These are the synthetic analogues which have similar action to opiates but are not derived from natural opium. Examples: methadone, pethidine and tramadol.

Acute Morphine Poisoning [La-3].

poisons. Discuss the clinical manifestations, investigation, managenment and postmortem findings in a case of 'acute barbiturate poisoning. How will you preserve viscera in such a case? LO-5: Classify

Classification of Poisons [La-1, Chapter Acute Barbiturate Poisoning

15]

Clinical features 1) CNS depression: contusion, delirium, Synptoms: Drowsiness, loss of inhibitions, excitement, euphoria,

SECTION

378

II

Forensic Toxicology

hallucinations, paresthesia, ataxia, slurred stuspeech, ystagmus, visual disturbance, por and coma. response Signs: Babinski's sign positive, loss of contracted, to painful stimuli, pupils slightly but may be dilated during terminal stage. Reflexes are lost.

Respiratory depression due to depression of respiratory centres in medulla leads to bronchopneumonia and respiratory acidosis. In terminal stages, Cheyne-Stokes respiration> Death. 3) Cardiovascular depression: Cardiac output is decreased, hypotensive shock, cyanosis and pulse 2)

and rapid. 4) GIT: Bowel sounds absent due to decreased peristalsis. It occurs in deeply comatose patient and is a bad prognostic sign: With improvement in condition, the peristalsis returns to normal but again due to drug absorption, the condition deteriorates. So there are 'fluctuating levels of consciousness. 5) Kidneys: Urine is scanty and suppressed and contains albumin and sugar. 6) Barbiturate blisters: Found in only 6%-10% is weak

cases.

subepidermal blisters which develop within 48-72 h of the onset of unconsciousness. A b. blister contains clear serous fluid. On rupture, leaves a red, raw surface which later dries to a it brown parchment-like area. C. Most common sites are where friction or pressure has been exerted between two skin surfaces, for example axillae, interdigital clefts, buttocks, back of thigh and knee joints and calves and forearms. d. These may be mistaken for burns by hot water bottle. e. Blisters are also seen in BB-PCM (Barbiturates, Benzodiazepines, Phencyclidine, CO and Meprobamate). 7) Body temperature is decreased but may be increased in bronchopneumonia. 8) Death: In early stages, the COD is respiratory failure and ventricular fibrillation. In later stages, COD may be bronchopneumonia, pulmonary oedema, acute renal failure or cerebral oedema. Investigation 1) Dille-Koppanyi test: Specimen (gastric lavage sample) + two drops of 1% cobalt acetate in methanol, a. These are tense

then add one drop of2%isopropylamine A lavender methanol. blue colour developed e in i is slo presence of barbiturates. 2) Calorimetric method. 3) GC-HPLC. Management. It is supportive. 1) Gastric lavage with warm water mixed KMNO, and activated charcoal. Gastric with lavao should be done even if barbiturates are takenvage par. enterally. It is due to the reason that barbiturates undergo enterohepatic circulation and so they are resecreted into the stomach. Por the same region. leave MgSO, in the stomach (as a purgative andto minimise reabsorption of barbiturates). Also give MDAC. 2) MDAC.

3) Scandinavian method: It uses (1) antishock measures; (2) patent/clean airway (by removing mucous from throat); (3) respiratory (ventilation) support and (4) fluid replacement therapy

used but not vasopressors. 4) Evacuation of intestines to prevent reabsorption of barbiturates: sodium sulphate 30 g orally and enema. 5) Specific antidote: None. CNS stimulants (analeptics) are not used. 6) Urine alkalinisation: We know that ionised drug molecules cannot freely pass through biological membrane. Barbiturates are acidic drugs and So they become ionised more in alkaline urine. excrete if we want barbiturate (an acidic drug) to so through urine, we have to alkalinise the urine so and that the drug molecules become ionised and so they are not reabsorbed in renal tubules they are eliminated through urine 7) Haemodynamic support for hypotensiOn. exchange 8) Haemodialysis, haemoperfusion and transfusion. counteraet 9)ntravenous lipid emulsion (1LE): Tolocal anae the action of lipophilic poisons (e.g. injection thetics, barbiturates and so on), /V drug lipophilic hne lipid emulsion are given. The are sequesterecd from the plasna. tris-hydroxynmethyi 10) THAM (trometamol, NaHCO, n nomethane): It is an alternative to and treatment of acidosis. conma, DVT prolonged T) Management of orthostatic pneumonia. 12) Antibiotics to treat bronchopneumon

Fasim

d

bl an

6)He

7K

8)

In

Br

10) Bl

Prese 1)

Bes

p 2)

The

nte the SN=

De

Ito

sho ture

Pne Se nene

A

HAPTER 17

indingsS Postmortem venous system illed with dark Cyanosis hole

)

deoxygenated blood).

blisters. Barbiturate 2) mouth. Froths at nose and 3) cnsely congested, or even may turn Lungs are 4) mpletely black due to dark deoxygenated oedema hlood). In late deaths, lungs may show bronclhopneumonia. and Ctomach: Haemorrhagic, congestion and erosion ofmucosa, white particles of ingested drugs. Funor haemorrlhagic. dus may be thickened, granular Subendocardial haemorrhage. 6) Heart: are degenerated. 7 Kidneys: Convoluted tubules S) In delayed deaths, necrosis of globus pallidus and

Poisons Actin

Nervous System

379

5) Hyperactivity of CNS, convulsions, psychomotor agitation and anxiety, restlessness and

insomnia. 6) Tendency to commit suicide, homicide, violent assault or to damage to the property. Management: (1)Benzodiazepines, for example diazepam and chlordiazepoxide and (2) thiamine. Death occurs in 5%-15% cases and the cause of death may be cardiac arhythmias, hypokalaemia, infections and respiratory failure. MLI: (1) It is a medical emergency and should be attended by doctors immediately. (2) If such a person commits a crime, he is not held responsible for his criminal acts because he is considered to be mentally unsound [S.84, IPC].

corpus callosum.

oedematous in late death. 10) Blood will remain fluid and dark. Preservation of viscera in such a case 1) Best preservative is rectified spirit but can also be preserved in saturated solution of common salt. 2) The samples to be preserved are stomach, small intestine (30 cm), liver with gall bladder (because the drug is excreted in bile) and brain. 9) Brain

SN-6: Delirium tremens

Delirium tremens: It

is an acute episode of delirum seen 3-5 days after sudden withdrawal of alcohol in about 5% patients. It is the most severe alcohol withdrawal syndrome. It occurs in (1) sudden withdrawal of alcohol; (2) shock after receiving injuries, for example fracture of bone and (3) acute infections, for example pneumonia and influenza. een within 3-5 days of complete or significant absti nence from heavy drinking in about 5% patients. Symptoms: It is a form of acute insanity. ) Clouding of consciousness with disorientation O time, place and person. Poor attention span and distractibility and loss of memory. 4 Hallucinations (visual> auditory > tactile) and illusion are very frightening. Autonomic disturbances: Uncontrollable fear, ncreased heart rate/respiratory rate, fever, Sweating and dilated pupil. Tremors of face, tongue and hands.

SN-7: Widmark's formula

Erik

Widmark's formula (1932): It

is a formula calculate the to amount of consumed alcohol (i.e. total amount of alcohol in body) if his blood alcohol level is known and vice versa.

Formula is: A = PCR,where A total body alcohol (in g) P= total bodyweight (in kg) C blood alcohol concentration (BAC) (in mg/kg or) = Note: 100 g of blood 94.7 mL of blood or 100 mL of blood = 105.6 g of blood. Widmark's distribution factor which is a R constant (0.68 for males, 0.55 for females, var ies between 0.5 and 0.9).

Widmark's

formula becomes: A = PCR X expressed in (g/100 mL) or (g%).

The

10 when BAC is

factor: It is calculated as Concentrationof alcoholin body After R Concentrationof alcoholin blood absorption, alcohol gets fairly and evenly distributed throughout the body tissues except in the alcohol bones and fats. Actually body tissues take Bones and n proportion to their water content. retain less tatty tissues contain less water, so they known amount of amount of water. With intake of in com-

Distribution

obese man alcohol, BAC will be higher in same weight. parison to a lean person of different in males

is Why distribution distribution factor tac Why soluble; is water and females? Alcohol

the water

380

Toxicology SECTIONII Forensic

will therefore detercontent of any tissue/organ dissolve in it. It means mine how much alcohol can content can have that tissues with higher water morec dissolved. Men have alcohol of amount more have less musmuscles and less fats but women reason, man have cles and more fats. Due to tlhis body tissues but higher concentration of alcohol in to lower blood alcohol concentration as compared alcohol females who have lower concentration of in body tissues but higher blood alcohol concentration. So distribution factor is higher in men as Compared to woman. Sex diffterence in Widmark's factor is due to different fat: water ratio, male having 54% and female 44% water partition by weight. This formula is controversial and several variations have been suggested. is useful only after the completion of alco It hol absorption and when equilibrium has been reached between blood and body tissues.

B.

ness, rash, increased aminotransterases and

SN-8: Management of methanol

(methyl alcohol) poisoning

1) Gastric lavage with 5% bicarbonate solution. Leave 500 mL of it in stomach. 2) Antidote A. Ethanol: Ethanol competes with methanol for alcohol dehydrogenase. The affinity of 'alcohol

dehydrogenase' is 15 times more for ethanol as compared to methanol. So, if we give ethanol, it engages 'alcohol dehydrogenase' and blocks the formation of formaldehyde and formic acid which are actually the main culprit of methanol toxicity. Dose: 10% ethanol in a dose of 10 mL/kg I/V. Maintain a serum concentration of 100 mg%. Complications are hypotension, respiratory depression, flushing, hypoglycaemia, hyponatraemia, gastritis, pancreatitis and inebriation. So due to these side effects, the patient is admitted to ICU to give ethanol. Orally ethanol is also effective and may be considered when ICU monitoring is unavailable especially in rural areas. Oral dose:

mL/kg of 95% ethanol is given in 200 of fruit juice over 30 min. For maintenanc 0.2 mL/kg/h as 50% ethanol in fruit Fomepizole (4-methyl pyrazole): It juice. is a com ompetitive antagonist of alcohol dehydrogenas nase and so inhibits this enzyme. Due to ome advantages over ethanol, the fomepizole is preferred nowadays. a. Dose: 15 mg/kgI/V as an initial loading dose (diluted in 100 mL of NS or D5W) followed by 10 mg/kg every 12h for 4 doses. b. After 48 h, fomepizole induces its own metabolism, so its dose must be increased after 48 h to 15 mg/kg every 12 h. c. Side-effects: Local reaction at the site of infusion (if the concentration is >25 mg/mL in urine), nausea, anxiety, headache, dizzi1

3) 4) 5) 6)

eosinophilia. d. Advantage over ethanol: (1) Fomepizole does not cause inebriation whereas ethanol causes. (2) Fomepizole acts quickly whereas ethanol takes time and so acts late. (3) Fomepizole has fewer side effects as compared to ethanol. (4) To administer fomepizole, there is no need to be admitted in ICU whereas ethanol administration needs the patient to be admitted in ICU to monitor serum concentration. (5) In case of fomepizole, serum concentration does not need to be monitored as with ethanol. iS e. Disadvantage over ethanol: Fomepizole very costly and not easily available whereas ethanol is cheap and easily available. Folinic acid (also known as leucovorin). Haemodialysis nmust begin when blood levels arc 20 mg% or arterial pH is Limbs (Thorax). Death occurs due to respiratory paralysis. Treatment: (1) Atropine (0.6-1.2 mg) followed by acetylcholinesterase inhibitors, for example physostigmine (1-2 mg) and neostigmine (0.5-1 mg) subcutaneously; (2) aminopyridine and (3) supportive-artificial respiration and stimulants.

Autopsy features: Asphyxial. MLI: (1) Arrow poison; (2) poisoning

mainly accidental but homicidal is also possible only if curare is administered parenterally and (3) use with general anaesthesia-rare nowadays. is

Poison Hemlock (Conium maculatum) Also known as 'spotted hemlock (due to the presence of purple spots on the stem) or 'poison of exe Cution (because Socrates, the Greek philosopher, was executed in 399 BC by this) or 'deadly hemlock, All parts of the plant are highly toxic and emit a strong mousy odour, Active principle: coniine content is highest in leaves during flowering time and in roots during summer. MOA: act on motor end

plates and causes paralysis of motor nerve terminals in the muscles, Fatal dose: 60 mg of coniine, Death

5. Strychnine poisoning and tetanus

L

ANSWERS

SN-1: Strychnine poisoning Fatal Dose One crushed or powdered seed. Strychnine: 15-50 FP:1-2 h.

mg

Mechanism of Action [SN-2] Signs and Symptoms [SN-3] Treatment [SN-4] Autopsy Findings Autopsy findings are not characteristic but the 'signs of asphyxia' are present mortis starts early and persists for longer Rigor duration.

Stomach is congested, may contain fragments of seeds vio Muscles may show microscopic tears (due to

lent convulsions) leading to the extravasation o the blood. All organs and spinal cord are congested. Postmortem caloricity (due to violent convulsions may be seen. cord and brain have to be preserved sm Spial strychnine is spinal poison.

Medicolegal Importance

Poisoning may be accidental (especially in cu its vey dren), suicidal or homicidal (rare due to strong bitter taste). stray ao 2) Has been used as cattle poison (e.g. to kill Malaysia. rodenticide (rats) and arrow poison in 1)

CHAPTER 17

Poisons Acting on Nervous System

athletics.

nine binds at another separate site on the same glycine receptor and lowers the affinity of glycine for the receptor. Simply the glycine is unable to bind its receptor. So inhibitory effects of glycine are lost. When there is no inhibitory effect, the AHMC do not stop their activity and cause release excitation with greatly increased reflex excitability. Since hyperpolarisation developed at the postsynaptic membrane inhibits the activity of AHMC « spinal cord and thus inhibits the neuronal firing, it is called inhibitory postsynaptic potentials (IPPs). In a sense, strychnine depresses IPPs in spinal cord and so prevents the effect of glycine resulting in release excitation. So a slight stimulus (e.g. noise, light and breeze) causes a violent reflex action producing general contraction of all muscles simultaneously, producing convulsive seizures.

has been used by poison can be detected in Aph putrefaction,.so 3)Resist after death. It may be found in time long 4) years. to 4 it was cadaver up Since it is bitter in taste, Homicidal idal use: by mixing it in bitter alcoholic the victim ac. Also

5)ven to

subject

is

already under the influe

inks. If the unable ble to etect it in further drinks. drink,he is ychnine in therapeuof use of Banned: Today the 6) preparations has been banmned. It is used as an drugs. tic adulterant in street

Diferential Diagnosis 1)

D/VW Tetanus: See the

tetanus. 2)

3)

4)

strychnine poisoning and

fts are

difterentiated by history. In epilepsy, clonic with loss of consciousness and the

Teflexes

are

Epilepsy: It is

normal. Meningitis: Fever and neck rigidity are present. Hysteria: At times two are difficult to distinguish so it is better to treat for poisoning.

SN-2:

Mechanism of action of

strychnine

poisoning spinal poison (stimulant) and acts horn motor nerve cells' (AHMC) of

Strychnine is a on 'anterior spinal cord.

SN-3: Signs and symptoms in

strychnine poisoning

If

intact uncrushed seeds are ingested, there will be

no effect and all seeds are passed intact in stool. If crushed' seeds are ingested, there will be signs and symptoms within 1 h. taste, dysphagia, increased perception, musBitter cular twitching, rigidity of muscles, convulsions,

Normal physiology

of AHMC: The AHMC of excitatory in nature to excitation of muscles. Glycine is an inhibitory neurotransmitter Wich binds at glycine receptor (a ligand-gated chloride channel), highly enriched in the postnaptic membrane of AHMC. Glycine binds with chloride channel Chloride channel opens Influx of Cl ions Hyperpolarisation of PSLsynaptic membrane Inhibition of AHMC O Spinal cord. In this way the glycine controls by the Ding it is obvious excitatory functions of AHMC. So inhibitory that if glycine itself is inhibited, its effect on AHMC is lost and so cause release excitation. Whatdoess primarily strychnine do (Fig. 17C.3): Strychnine affects'AHMC as a glycine of inal cord by acting gonist. strychnin Actually both glyeine and bind Same glycine at two eparate binding sites on the an example ceptor in an allosteric manner. tis of allosteric inhibition where strych

391

Posterior horn

spinal cord (Fig. 17C.2) are and naturally they lead

-

AHMC

in spinal cord are excitatory in nature

nerve cells in 17C.2 Anterior horn motor spinal cord Fig.

392

SECTION

II

Forensic Toxicology Anormal physiological mechanism in the body

Effects of strychnine Strychnine

(Glycine

-Glycine

receptor

Ligand gated CI ion

Glycine is replaced by

channel

strychnine

Ligand gated

CIion

channel

Inhibition of AHMC

No inhibition of AHMC

Suppression of excitation

Release excitation

Muscular activities are controlled and within normal limit

Violent muscular contractions (convulsions)

Fig. 17C.3 Mechanism of action of strychnine

froths at mouth and prominent eyeballs with

dilated pupils.

Convulsions:

1) The violent convulsive seizures affect all muscles of the body at a time.

2) The seizures initially are 'clonic (i.e. intermittent) in nature, but very soon become 'tonic' (i.e. sustained). 3) Convulsions last for 1-2 min and reoccur after an interval of 5-15 min. 4) The duration of the convulsive seizure becomes longer and intervals between seizures become

with the occiput of head and the heels touching the ground (Fig. 17C.4). b. Emprosthotonos: Forward bending of the body due to violent spasmodic contraction of abdominal muscles. C. Pleurosthotonos: Lateral bending of body 8) Renal failure: Convulsions leads to rhabdomyolysis (i.e. skeletal muscle damage), so myoglobin is released into blood which blocks renal tubules

> Renal failure. Period between convulsions: Between two epr sodes of convulsions, the muscles are completely' relaxed but the patient looks exhausted, takes breath, cyanosis decreases and there is cold persp ration. The dilated pupil during convulsive phase may contract.

shorter. 5) During convulsions, the patient has anxious look, cyanotic (because he is not able to breath), eyes are prominent and staring, pupils are dilated and mouth is covered with froths. 6) Risus sardonicus is a peculiar characteristics of strychnine poisoning in which the corners of the mouth are drawn back due to sustained contraction of jaws and facial muscles, so there is widening of the mouth. 7) Any one out of the following three types of positions may be found during convulsions: position) a. Opisthotonos: Body assumes a bow-like Fig. 17C.4 Opisthotonos (bow-like position (arched and concave) on the back, strychnine poisoning

CHAPTER 17

Poisons Acting on Nervous Syster

393

convulsions: After 5-15 min (or Resumption of impulse) Ise) anotlher convulsion occurs. lightest increases, lactic on vulsions, the temperature renal failure may occur. may develop and sis Durin convulsions and between sciousness: Consci convulsions, he person remains isodes of two conscious. Paticnt remains conscious till

Muscle relaxants (e.g. curare, mephenesin, pancuronium bromide and succinylcholine). General anaesthesia may be given if all measures fail to control convulsions. other lational anaesthetics (e.g. ether) have Inhato be given in the period between convulsions because in convulsive phase he does not take

five conusualy ocurs after four to Dea last convulsion, the patient canrulsions. In the spasm ofrespiratory breathe because of the not diaphragm and oracic muscles). muscles (the causes hypoxia of respiratory muscles So spasm

2) After control of convulsions: Gastric lavage: Gastric lavage has to be done only after the control of convulsions by medications. So avoid gastric lavage directly as done in other ingested poisons because it can start a new convulsion. It is done with activated char-

fully theend. ath: Death

which causes

SN-4:

medullaryY paralysis.

coal and KMnO,.

Fluid and electrolyte balance. Treat lactic acidosis. Forced acidic diuresis enhances the excretion of strychnine in urine. Urine alkalinisation can

Treatment of strychnine

poisoning 1)

Control of convulsions:

patient in dark, noise-free room because any sensory stimulus can start convulsion. Diazepam 0.1-0.5 mg/kg slow I/V followed by Keep

phenobarbital 1/V;

short acting barbiturates

(pentobarbital sodium) are also useful.

1ABLE

be used as a prophylaxis against renal failure.

D/W-5: Strychnine poisoning and tetanus (Table 17C.2)

Tetanus [D/W-5 17C.2 Difference Between Strychnine Poisoning and

St. No. Features

.

brcath.

Strychnine Poisoning

Onset

Sudden and rapid

History of

Poisoning

Convulsions

Generalised

State in between convulsions Nature of paroxysm

Complete relaxation

Lower jaw

timee All parts of body involved at same during fixed Chest (respiratory muscles) convulsions

Initially clonic (i.e. intermittent) but

later tonic (i.e. sustained) lower jaw Convulsions do not start from

Fever

Absent

Fatal Period

1-2.h

Lab analysis

in suspected food Poison may be detected

Tetanus

Gradual and delayed Injury

Localised Affects jaw and then face not fixed Chest (respiratory muscles) during convulsions

Never complete relaxation Tonic lower jaW Convulsions usually start from

Present >24 h demonstrated Clostridjum tetani can be microscOpY in culture and

aHCCF L)2NP

18 Cardiac PoisonS Cardiac poisons are [Mnemonic DNA of Cute Queen 1) Digitalis (Digitalis purpurea) 2) Nicotine (Nicotina tabacum [tobacco]) 3) Aconite (Aconitum Imitha bish/mitha zahar, monk's hood]) 4) Oleander: White oleander (Nerium odorum [kaner]), Yellow oleander: Cerebra thevetia and Cerbera odallam 5) Cleistanthus collinus 6) Quinine (Cincona)

Digitalis purpurea Entire

plant is toxic. Only leaves are used for medicinal purpose. Active principles: (1) Cardiac stimulants, for example, Digitoxin, Digitalin; (2) cardiac depressant, for example, Digitonin. Digoxin is the only glycoside that is currently in use. It is present only in the leaves of Digitalis lanata (not D. purpurea). MOA: It acts directly on heart muscles and prolong diastolic period. Signs and symptoms: GIT is affected first and then CVS. (1) GIT-NV, anorexia, abdominal watery pain, diarrhoea. (2) CVS-dysrhythmias, extrasystoles and

fibrillation. (3) Visual--chromatopsia (aberrations in colour vision), photopsia (flashes of light), xanthopsia (yellow halos), photophobia and pupil dilated. Fatal dose: Digitalis (2-3 g); Digitoxin (4 mg); Digoxin (5 mg); Digitalin (15-20 mg). FP 40%):

1.

3. Treatment

Moderate (COHb

2) ABC. 3) Cytochrome C.

ring min to D 40 takes O, 100% 4) Oxygen therapy: halfits valut to blood the in level COHb of the

5

C Pos

b

10-

Cln ina Pois

ass Table Acxute

atald 30m

Ainic

Resy

CHAPTER 19 Asphyxiants

mospheric pressure is choice in ssevere CO exposure treatment ot hoice

Hyperbaric O, at 2-3 the

selected

cascs.

Cyt. oxidase ag (Fes [ferric))

Cyanide Cyt. oxidase ag-cyanide Complex

in onvulsants, antibiot Antconv asphyxia. 5) death: Nonmechanical of de

401

Oxy-Hb (Fe* [ferrous])) Amyl nitritel

sodium nitrite Met-Hb (Fe* [ferric)

of

Cause

features: (pink) colour of skin (especially Cherry red 1) extremitics and the regions of postmortem in hvpostasis), mucous membrane and nail beds, blisters at wrists, interdigital surfaces of 2)Skin calves and buttocks. fingers, knees, Postmortem

3) 4) 5)

6)

Blood is fluid.

Congested and pulmonary oedema. myocardial Heart: Pericardial haemorrhage, infarction and focal areas of necrosis. Brain: Necrosis and cavitation in basal ganglia

Cyt. oxidase ag gets free

Rhodanase

Excreted in

Lungs:

Acc.

Classify poisons. Discuss the clinical manifestations, investigation, management and postmortemfindings ina case of acute

cyanide

poisoning.

Classification of Table 13.1). dose: HCN

300 mg).

Clinical

Poisons (Refer Chapter 13,

Poisoning (50-60 mg) and NaCN/KCN (200-

features:

Gll: Burningtaste, throat constriction ess, salivation, frothing epigastric

and numb-

at the mouth, nausea and

pain. Dizziness, headache,

S:Usion,

seizures, coma

3)Respiratory

anxiety, sweating, con and death.

system: Tachypno and dyspnoea (due stimulation of respiratory centre and carotid chemorecept caused by local poxia). later stage,1 respiratory depression. Ditter almond-like odour' be in breatn detected.

In

early stage:

In

Pulmonary

Thiosulphate (Sulphur Hhodanase onor)

°****

ROHN.

Cyanide Hydroxy-

cobalamine

(Vitamin Bi2)

Cyanocobalamine (Vitamin B12)

Fig. 19.1 Mechanism of action of antidotes used in cyanide poisoning

L0-2:

Fatal

No..oS 3

Date.il:22

globus pallidus and putamen) in delayed death. Punctiform and ring-shaped haemorrhages in white matter. Cerebral

Acute Cyanide

-Thiocyanate urine BEDKAR ME, EDICA LIBRARY

(especially in

oedema.

Cyan-Met-Hb

i

intoxication.oedema: It is found in oral cyanide

4) Cardiovascular system: Initially hypertension with reflex bradycardia, but later on, hypotension with reflex tachycardia. 5) Eyes:(1) on fundoscopic examination, retinal veins and arteries are both equally red, because the 0, remains in the veins (as it is not utilised by tissues) and (2) eyes are prominent. Cornea is bright, glassy and glistening. Pupils are dilated and nonreactive to light. 6) Anion gap metabolic (lactic) acidosis. 7) Death is due to respiratory failure. Investigation: The decision for the treatment needs level to be based on clinical findings. A blood cyanide level of >0.2 ug/mL is considered toxic, whereas level should >1 ug/mL is fatal. ABG for blood lactate be done. immediately Management: Start the treatment Three things because the fatal period is very short. antidote (Fig. 19.1) are very important: 100% oxygen, and gastric lavage. adnministration

Stabilisation: ABC, 1009% 0, do ABG to check I/Vaccess, carcdiac monitoring, Vasopressors tor acidosis. Tor metabolic (lactic) steps hypotension. given in three are They cytochrome 2) Antidotes: aim is to make 1)

(Table 19.2). The main

oxidase free. How?

402

SECTION IForensic Toxicology

TABLE 19.2 The Steps ofThree Antidotes in Cyanide Poisoning

Postmortem examination:

External examination: )

Third Step

First Step Amyl Nitrite ampoule of is broken between two pads of gauze and placed over the airway. It is inhaled for 30 s of each minute. Use a fresh ampoule every 3 min. It should be done until second step begins

A 0.2 mL

Second Step Sodium Nitrite

(3% Solution) Dose: 10 ml slow IW

Sodium Thiosulphate

(25% Solution) Dose: 50 mL slow IW infusion

infusion Over 5-10 min

MOA of amyl nitrite or sodium nitrite: It con verts Hb (Fe2*) into methaemoglobin (Fe*"). Level of methaemoglobin has to be kept Al (OH), + PH,. Phosphine is

toxic to insects and rodents. b) After ingestion (i.e. in stomach): On coming in contact with HCl, ALP liberates phosphine (PH). ALP +3HCl> AIcl,+ PH,

Acute Aluminium Phosphide Poisoning [LO-2

as

ZINCPHOSPHIDE(Zn,P

Zinc

phosphide poisoning [LQ-3]:

Mechanism

ot

managencent

action, clinical features, investigation, to alunil and postmortem findings are similar is responsio ium phosphide. The phosphine' gas for toxicity. FD =5gand FP = 24 h.

CHAPTER 20

IMPORTANT QUESTIONS FOR EXAMINATION

L0N

QUESTIO

(LO)

ONG

insecticides insecticides. Discuss the mode of action, Classify I. ana and symptoms, vestigations, managesigns postniortem findings in a case of 'acute nd

organophosphates poisoning. Discuss the clinica manifestaClassily poisons

2.

postmortem in a case of findings and medicolegal importance [DU poisoning aluminium phosphide tions,

investigation, management and

acute

2009). 3.

poisons. Discuss the clinical manifestations, investigation, management and postmortem findings in a case of 'acute zinc phosphide' Classify

poisoning.

SHORT

NOTES (SN)

4.

Carbamate poisoning

5.

Plant penicillin

6.

Paraquat poisoning

ANSWERS LO-1: Classify

insecticides. Discuss the mode of action, signs and sympP foms, investigation, management andpostmortem findings in a case of acute organophosphate poisoning.

Agricultural Poisons

3) Organochlorines

(chlorinated

hydrocarbons): DDT, aldrin, endrin, endosulfan, GBH, lindane (gamma hexachlorocyclohexane), gammexane. Vegetable 4) origin: Nicotine, pyrethrins and rotenone.

Organophosphate Poisoning

Clinical features: A. Muscarinic or parasympathetic symptoms Mnemonic Semal-Dust]: Sweating, Emesis (vomiting), Miosis (Constriction of pupil or pinpoint pupil), Abdominal cramps, Lacrimation, Diarrhea/defecation, Urination, Salivation, Tracheobronchial secretion. MyoB. Nicotinic symptoms [Mnemonic HMT watches]: u

ypertention,

Muscular weakness with twitch-

ing. fasciculations and cramps, Tachycardia.

C. CNS symptoms [Mnemonic MAD-RAT]: Muscular weakness, Anxiety, Depression of respiration and CVS, Restlessness, Ataxia, Tremors. oFatal period: 24 h. Cause of death is respiratory

failure. o Diagnosis: Cholinesterase level in RBC and plasma is decreased. Normaly, symptoms may not appear until RBC level of cholinesterase falls by 25% or less. aManagement: 1) ABC: Airway should be cleared because there are lots of bronchial secretions which occlude the airway. 2) Antidotes: Atropine is used to counteract mus carinic effects, whereas oximes are used to counteract nicotinic and central effects (Fig. 20.1).

Classification

of Insecticides )Organophosphates:

Nerve ending

Akyl phosphates: HETP phosphate)

(hexaethyl tetraTEPP (tetraethyl pyrophosphate A(octamethyl Pyrophosphoramide), malathion and others, Demeto for example, Dimefox, Isopestox, Sulfotep, Aryl Trichlorion. sphates: Parathion (nitrostigmine -parathion, chlorthion. aoxone, diazinon and Damates: aminocarb,

Carbaryl, Approbarb.

carbofuran,

05

aldicarb,

Postsynaptic membrane

Choline AcetylcholinestaraseACO

Acetate

rocoptors

M Oceplors

Atroplne

Muscarinia effects

Nicotinlc/Pralidaximne

effects

(2-PAM)

oximes action of atropine and of Mechanism Fig. 20.1

406

SECTIONI Forensic ToxicologY

Atropine: (Primarily acts on muscarinic receptors). is a competitive antagonist, highly It cffective in controlling muscarinic symptoms, but higher doses are required to antagonising central effects. does not reverse 'peripheral muscular It paralysis' (which is a nicotinic action), and for this purpose, the oximes are required which act on nicotinic receptors. Ty ofatropine is I min. Dose: repeated every 2-5 mg 5-10 min till signs of atropinisation appear (the signs of atropinisation are clear lungs, reversal of muscarinic toxic syndrome, HR 280/min, systemic BP 280 mmHg, dry axillae, and wider than pinpoint pupil). Do not consider dilatation of pupils as the end point for the use of atropine. Atropine is administered in lower maintenance doses and at less frequent intervals so as to maintain atropinisation for 1-2 days. Oximes (cholinesterase reactivators): (Primarily acts on nicotinic receptors) Oximes include pralidoxime (2-PAM), obidoxime and diacetyl monoximne (DAM). Oximes are ineffective in carbamate poi-

Pro-2-PAM:

A.

B.

soning.

Pralidoxime (2-PAM): Oximes primarily act to counter the nicotinic effects of OPs (where the atropine is ineffective), though they can reverse some of the CNS effects also. Oximes are always given with atropine (both acting synergisticallyT, but the use of oximes in OP poisoning is secondary to that of atropine, that is atropine is the mainstay treatment of OP poisoning Mechanism of action: 2-PAM by binding with OP liberates acetylcholinesterase so that additional Ach can

be

Since 2-PAM (i.e. pra-

lidoxime) is a quaternary nitrogen compound, it is not expected to cross BBB. So to improve central effects of 2-PAM, a prodrug was developed called Pro-2-PAM, which allow pas. sage through blood brain barrier (BBB). After crossing BBB, spontaneous in vivo oxidation converts Pro2-PAM to 2-PAM (pralidoxime) in brain. So desired central effects are achieved.

Obidoxime

chloride

is

more (10-20

times) effective than pralidoxime. Protopam (pralidoxime chloride). Effective against nerve gases: NAAK (nerve agent antidote kit), Hagedorn oximes (H-oximes) and methoxime. C. Diazepam: For convulsions and muscle fasciculations. Dose: 5 mg I/V every 10 min (maximum dose 15 mg). D. Isoproterenol and lidocaine for ventricular tachycardia.

Postmortem

findings: Findings of asphyxia, for example, congestion offace and cyanosis of lips, nails and mucous membrane present. froth in nose and mouth may be Blood-tinged

present. Blood-stained froth is present in respiratory tract. Smell of kerosene may be present on opening the oesophagus and stomach due to dilutton mucosa of the poison. Gastric and intestinal congested with submucosalpetechial haemor rhages. are All organs are congested. Brain and lungs Congested and oedematous with petechia haemorrhages. Toxicological analysis: OPs resist postmorten autolysis and can be recovered trom putretied bod ies for a long time.

metabolisedr

Dosel1-2gI/Vn 100 mL of slowly over 15-30 min. Dose

given can be h weakness if muscle in and repeated fasciculations are not relieved. Thereafter, the dose may be repeated every 3-8 h as long as signs of poisoning persist. 1

NS

D

Enumerate poisons. Discuss the clinical manifestations, investigato management, postmortem findings case and medicolegal importance in a of 'aluminium phosphide poisoning LO-2:

2

orea

blar

Hep Rend

ONS

Tesl

Neta

me

CHAPTER 20

Poisons: of Po gssification ijon of 13.1)

Table

uminiun

(Refer Chapter 13,

features:

halation of phosphine

through lungs and kidneys. 1) Reduction of absorption of PH,: Gastric lavage with Na,CO, or KMnO,. Activated charcoal can given orally to adsorb PE, from GIT. Liquid paraffin can be given to accelerate excretion of ALP and PH, from gut. 2) Reduction of absorbed PH,: The liberated PH, cannot be detoxified as there is no specific antidote. Organ toxicity can be prevented by using membrane stabilisers, for example, MgSO, which corrects hypomagnesaemia, a precipitating factor for arrhythmias. 3) Enhancement of excretion of PH,:PH, is excreted through lungs. To enhance its excretion through kidneys, adequate hydration and renal perfusion must be maintained with I/V fluids. Dialysis may be done in presence of acute renal failure. 4) Treatment of shock: Fluids, low-dose dopamine infusion and hydrocortisone. 5) Treatment of arrhythmias: Conventional antiarrhythmic drugs are not effective. Magnesium sulphate (MgsO,) due to its membrane stabilis ing action is effective, especially during first 24 h. It also corrects hypomagnesaemia, the precipitating factor for arrhythmias. Dose: 3 g bolus

gas (1PH,)

Dueto inhalation: Aucous membrane irritaheadache, Mild respiratory distress, tion, acute

tightness in chest. paraesthesia, .More muscular wealknumbness, tremor, diplopia, incoordination, paralysis and jaundice. ness, toxicity: ARDS (acute respira, Very severe syndrome), cardiac arrhythtory distress CHE pulmonary oedema, convulsions diarrhoca, dizziness and severe toxicity: Ataxia,

mias,

and coma. of ALP: Due to ingestion GIT: Nausea, vomiting and

retrosternal pain.

CVS:

and tachycardia/bradycardia are due to (1) cardiogenic causes, for example, arrhythmias and myocardial dam age; (2) peripheral circulatory failure and (3) fluid loss due to vomiting. 2) Acute cardiotoxicity is due to binding of eytochrome oxidase in mitochondria by PH, leading to anoxic myocardial damage. Cardiac arrhythmias are due to direct toxic effects or hypomagnesaemia brougnt oy focal myocardial damage by the action of PH, Cardiogenic shock is the most common 1)

Shock (hypotension)

followed by 6 g as infusion over 24 h for 5-7 days. 6) Treatment of metabolic acidosis: Soda bicarbonate I/V for 3-4 days. If the patient becomes haemodynamically stable but metabolic acidosis persists, peritoneal or haemodialysis may be useful. 7) Other supportive measures: Oxygen artiñcial

cause of death.

Respiratory system: Garlic fishy odour from Dreath cough, dyspnoea, cyanosis, rhonchi, bilateral basal crepts and respiratory failure. Hepatobiliary: Jaundice, hepatitis, soft tender hepatomegaly. Renal failure. CNS: Headache,

and

dizzines altered mental state,

estlessness, convulsions, acute hypoxic encep alopathy and coma. Metabolic

Iavestigationacidosis. 1) The

gnosis of ALP ingestio can be confirmedby detecting phosphine in exhaled air or instomach irate. Using:silver nitrate impreg nated 2) ECG: strips could get good results. ST elevation tion in V1-V5, T inversion in all leads.

4073

3) Chest X-ray suggestive of pulmonary oedema. Management: There is no specific antidote, so treatment is mainly conservative. Main object of treatment is to sustain life till PH, is excreted

Phosphide (ALP) Poisoning

Clinical

Agricultural Poisons

D

respiration. PMappearance: Blood-stained froths at the mouth and nostrils. Garlic fishy odour on opening stom myocarditis ach. Heart shows the features of toxic

oedematous (pulwith fibrillar necrosis. Lungs are congested. monary oedema). Internal organs are poisoning1s Medicolegal importance: Suicidal Uttar Pradesh more common in India (Haryana, Accidental in farmers. especially Rajasthan), and especially in children. poisoning is also frequent ALP poisoning has rare. lomicidal poisoning is most common cause of the been reported to be India. suicidal death in North

SECTION

LO-3:

II

Forensic Toxicology

Classify poisons. Discuss

the clinical manifestations, investigations, management and postmortem findings in a case of acute zinc phosphide poisoning. Classification of Poisons (Refer Chapter 13, Table 13.1). Zinc Phosphide Poisoning: Similar to Aluminium Phosphide Poisoning [LO-2].

SN-4: Carbamate poisoning Carbamate: They are the compounds derived from carbamic acid and are the popular insecticides after OP compounds. Examples highly toxic (e.g. aminocarb, carbaryl, carbofuran and propoxur) and less toxic (e.g. aldicarb and pirimicarb). MOA: Carbamates, such as OPs, are acetylcholinesterase (AchE) inhibitors, but they carbamylate the serine moiety at the active site instead of phosphorylation. Since this is a reversible type of binding the symptoms are less severe and of shorter duration. Carbamate (unlike OPs) does not penetrate CNS so CNS toxicity is less. Clinical features: They are same as that of OPs but of less severity and short duration. Management: (1) Atropine is the drug of choice. (2) Oximes are contraindicated. Oxime therapy is usually not needed due to rapid regeneration of ChE. However, oximes may be given in patients exposed to aliphatic oxime carbamates (aldicarb and methomyl). Autopsy findings: Similar to OP poisoning.

SN-5: Plant penicillin Endrin is known as plant penicillin. It is a commonly used popular agricultural pesticide. Since it is effective against a wide variety of pests of plants, for example, cotton, tobacco, sugarcane and paddy, it is also known as plant penicillin. Endrin is classified as polychlorinated hydrocarbon (DDT is another example). It is most toxic among

polychlorinated hydrocarbons and is 10 times more toxic than DDT. In market: Endrin is sold under the trade names Endrex, Endox-DB and so on. These products of contain 25%-50% of endrin mixed with petroleum hydrocarbons, for example, aromax which smells like kerosene. These products are used as spray on plants. g and FP: 1-2 h. FD:5 Its absorption through skin or mucosa increasesif it is mixed with oil. is neurotoxic primarily acting on CNS It causing respiratory paralysis. Acute poisoning: Nausea, vomiting, abdominal pain, restlessness, mental confusion, delirium, tremors, tonic-clonic convulsions, profuse frothing at mouth and nose, dilated pupils, coma and death due to respiratory failure. Treatment: (1) General-maintain airway, breathing and circulation; (2) gastric lavage-with 2% KMn0; (3) No known antidote, so treatment is entirely supportive and symptomatic; (4) atropine and (5) to control convulsions, for example, thiopentone sodium- and Ca-gluconate. appearance: (1) Pupils are dilated: (2) bloodstained frothy fluid is at mouth and nose with kerosene smell'; (3) stomach is congested with kerosene smell; (4) lungs are congested and oedematous and (5) all organs are congested. MLI: (1) Mostly used for suicidal purpose because it is cheap and easily available. Accidental deaths are common during spraying. Homicide is rare but it has been reported to have been used by miung it with alcohol (especially 'toddy) which masks its smell. (2) Endrin resists putrefaction for a long time, so it can be detected in viscera for long after death. (3) It has been banned in India.

PM

SN-6: Paraquat poisoning herbicide sprayed on unwanted plants betore planting crops. FD:3-5 g. FP: 1-7 days. is Mechanism of action: Highest concentration found in lungs, so maximum damage ccursand lungs. Paraquat enters pneunmocytes (type NADPH-dependen tYpe ) where it undergoes react with reduction Free radicals death. Superoxide and hydroxyl radicals > cell It is a

CHAPTER 20

Vmptoms:(1) GIT-nausea, vomiting, and haematemesis, dysphagia, oral ulcerSi diarrhoea, oesophagea perforation and pancreatitis, pain. Pharyngeal pseudomemebrane abdomin. is also found; (2) in diphtheria) (sinmidlarto to that

Agricultural Poisons

409

causes lung damage and it causes death within 2 weeks.

Management: (1) Remove all clothes and wash the

(hepatorenal)

body with soap and water; (2) gastric lavage with Fuller's earth (1 L of 15%-30% aqueous suspension) or 'bentonite (7%). Some is left in stomach to adsorb paraquat. It is followed by 200 mL of 20% mannitol. Lavage can be done with activated charcoal; (3) haemodialysis and haemoperfusion; (4) antioxidants and glucocorticoids and (5) fluid and electrolyte balance. Autopsy: (1) GIT-ulceration around mouth and lips. A pharyngeal pseudomembrane (similar to that of diphtheria) found. Stomach shows patchy haemorrhage and erosions; (2) liver-pallor, mottled, fatty changes and centrilobular necrosis; (3) kidneys-cortical pallor and ATN and (4) lungs PPLD: stiff and rigid lungs.

(5)

MLI: Accidental and suicidal.

entrilobular necrosis; (3 kidneys-acute necrosis; (4) lungs-most typical and

bular

paraquat poisoning are found proliferative lung and that is progressive in lungs damage (PPLD). It includes proliferative pulmohaemorrhages, fibrinous nary fibrosis, pulmonary pulmonary pleurisy and stittened lungs and diffuse Oedema (absent in diquat poisoning), cough, haecharacteristic sign or

moptysis

and dyspnoea. After 5 days,

pulmonary

fibrosis.

Causes of death: (1) Oesophageal perforation or corrosive effects of GIT; (2) multiorgan

failure--immediate cause and PPLD-the progressive pulmonary fibrosis

21 Drug Abuse INTRODUCTION (self-administration) of any drug Drug abuse: Use the approved medin a manner that deviates from ical or social pattern within a given

culture. dependence Drug dependence: The term 'drug was suggested by WHO committee in 1964 to replace 'addiction' and 'habituation. So the term drug dependence includes two terms-drug addiction' and drug habituation-which have to be differentiated from each other (Table 21.1). commonly abused drugs: Legal (caf Most

feine> nicotine> alcohol). Illegal/Tllicit (Cannabis > cocaine).

BASICS ABOUT DRUGS OF ABUSSE

Classification of Drugs of Abuse A. B.

Narcotic (hard drugs): Opium straw, coca leaf, Cannabis (hemp) and all manufactured drugs. Non-narcotic (soft drugs): Hypnotics/Downers (e.g. barbiturates); antidepressants (e.g. TCAs and MAO inhibitors); hallucinogens (e.g. Cannabs

TABLE 21.1

[bhang, ganja and charas|, cocaine, mescaline. lysergic acid diethylamide [LSD], phencycli. dine [PCP] and methaqualone); sedatives (hypnotic + tranquillisers), for example, BZDs and alcohols and deliriants.

Routes of Administration of Drugs of Abuse (1) Oral. (2) Inhalation: nicotine inhalation from tobacco and charas. (3) Chasing heroin is put inside a rolled cigarette foil or Rs 5/10 note and then put fire from a matchstick under it. Deep white smoke is drawn inside mouth through a tube made of currency note. Here addict chases the columns of smoke. (4) Snorting (sniffing): cocaine. (5) Injection: three methods-(a) skin popping (injection via s/c route); (b) mainlining (injection via I/V route), used for the most potent opioid analgesics and (c) I/M route. (1) Accidental overdosage usually occurs with I/V route. (2) Toxicity due to contaminants: the substances, tor example, quinine, are commonly used to cut the drugs in order to reduce the cost. These are used by

Drug Addiction

Drug Habituation

Definition

Physical and psychological (or emotional) dependency resulting from repeated consumption of a drug is known as drug addiction

Psychological (or emotional) dependency resulting from repeated consumption of a drug is known as drug habituation

Dependence

Physical> psychological

Psychological

3.

Example

Alcohol, opiates Cannabis, cocaine, amphetamines and barbiturates

Caffeine, nicotine and tea

4.

There is

Compulsive use of drugs (i.e, craving)

2

Tendency to increase dosePresent 6. 8.

410

compulsion Only a desire to take drug (i.e. no

Absent

Harm to

Individual and society

Individual

Relapse

Occurs Characteristic

Nil

Withdrawal symptoms

IErdos

de to

Hazards of Drugs of Abuse

Difference Between Drug Addiction and Drug Habituation [D/W-9]

Sr. No. Features

)AIL

Mild or nil

TAE

CHAPTER 21

preparing the drug for injection. Pulm whilc devel vclop due to these contamianulomas may gram hepatitiss B, HIV, bacterial absco nary Infections: (3) cndocardi rditis and moniliasis. (4) nantsbophlebitis, ( thnonmbo Anaphylactic reaction (6) Risks of body (5) Cngrene y stifing:for illegal drug smuggling by

pckingandb

smugeler, der, these

tvwo

DRUGS OF ABUSE o

sarevery common-body

stuffers SN-1] and body

Causes of

SN-2].

and concentration.

Death in Drug Abuse (Drug

Complications) nfections (endocarditis, hepatitis and tetanus) (pulmonary and cerebral). and septicaemia. (2) Abscess complications. (4) Suicidal tendency from (3) AIDS

n

of certain drugs, the effect of for example, amphetamine. (5) Under drugs,person may die due to electrocution, head injury due to fall and drowning. (6) Choking due to accidental1 aspiration of food, vomitus or artificial dentures. overdose

of drugs during withdrawal

Autopsy

Findings in a Case of Drug Abuse

Table 21.2)

ABLE 21.2 Autopsy Findings in a Case of Drug

Abuse

Internal

Extermal

Fingertips may be stained with different types drugs used

of

Mainliners: IW addicts with typical linear needle

priCK

cScarmarks usually over veins of cubital fossa, dms,dorsum of hands, lower extremities, neck and of

penis 5) Skinpoppers:

s/c heroin addicts with typical depressed, scars and ulcers 6) Turkey skin: Punctate areas of tattooing are seen along the needlet tracks due to sition of carbonaceous material along the needle track Various recent zones inflammationand old injectior sites may show and perivenous fibrosis utiple recent and old healed abscesses Perforation ofnasal septum by snorting and snuffing Ot cocaine Crcular, atrophic

of

and heroin

or cellulose

Gastrointestinal tract: Pills/capsules. Starch/talk mucosa may be seen adherent to the gastric often shows foreign scars various of 2) Microscopic examination talk or dirt particles material, for example, fibres of cloth, near veins in muscle and at injection sites 3) Abscess formation due to repeated injections hepatis): (enlarged LNs in porta 4) Hepatic lymphadenopathy non-specitic Microscopy shows A very common finding. hyperplasia Lungs Froths in respiratory tract, oedema, pulmonary 5) Respiratory system: non-specific oedematous, contents. Right Congested and of gastric bronchopneumonia and aspiration presence of present due to may be hypertrophy ventricular pulmonary embo extensive microcrystalline increased in spleen and LNs surrounding concentration muscles and veins opposite 6) 1gM and IgG tissues, of skin, s/c control from reservationrecent injections along with for chemical analysis area of saline 1)

Ferson on emaciated, with lots of scars and tattooss 2) Foths at nose and mouth

dorsal vein

MDA (methylene-dioxy-amphetamine),

MDMA (methylene-dioxy-meth-amphetamine) (ccstasy) and MDEA (methylene-dioxy-eth-amphetamine) (eve). Tricyclic antidepressants (TCAs): Amitryptyline, imipramine, trimipramine, doxepin and clomipramine. Hallucinogens (psychedelics):LSD. is the most powerful hallucinogen known to It man. FD: 200 ug/kg or 14 mg. Signs and symptoms: Increased RR (tachypnoea), increased HR (tachycardia), increased BP (hypertension), increased temperature (hyperpyrexia), pupils dilated with photophobia and tremors. most important features: Four 1) Bad trips [SN-5]: It is defined as 'panic attacks' or 'extreme anxiety experienced by a person on consuming LSD. 2) Flashback phenomenon SN-6]: Abrupt abstinence following continues use of LSD does not produce withdrawal symptoms but

(1able 21.3).

Symptoms of Drugs of Abuse

impairment of memory

411

Amphetamines and its derivatives: Natural: Methamphetamine, fenfluramine, phentermine, mephentermine and methylphenidate. Synthetic amphetamines (designer's drugs)

SN-4:

Signs and appetite and weight, unstcady gait, tremors, loss of ftiness of eyes, slurring of speech roddening and and Withdrawal syTmptoms

Drug Abuse

he preserved in SIde should be

normal

SECTION

TABLE 21.3

II

ForensicToxicology

Difference Between Body Packers and Body Stufer

Sr. No. Features

3

Body Stuffer

Body Packer

Definition

The person who swallows drugs for the purpose of smuggling across cOuntries

User or seller who swallows the drug or inserts the drug in ear/nose/vagina when police comes to arrest

Smuggling

Smuggles the drug

Packing

Carefully packed in condoms, balloons and so on

Does not smuggle the drug Not packed due to nonavailability of time

Drug

Usually very high quality

Usually poor quality and adulterated

Poisoning

Rare

Very common

Radiography

Usually helpful in detection

Not always helpful

Treatment when arrested

Observation

According to the drug ingested

the effects of LSD may be re-experienced without further exposure to the drug. 3) Withdrawal symptoms: LSD does not show withdrawal symptoms. 4) Tolerance to LSD: It develops in 2-3 days with daily intake. Loss of tolerance occurs in 4-6 days if LSD is not taken. Treatment: Chlorpromazine. The death is attributed to the bizarre ML: behaviour induced by the drug that can result in accidental and suicidal deaths. Suicidal and homicidal tendency occurs. The person explores his own feelings. Phencyclidine (Cadillac,Angel Dust): Pleasurable effects, for example, euphoria, feeling of dissoci ation, numbness, perpetual distortion and visual hallucinations. Common mode of intake involves sprinkling of drug on parsley or marijuana leaves and smoking the same. Addiction leads to violent tendency, psychosis and suicidal as well as homicidal behaviour.

ILLICIT USE OF DRUGS IN SPORTS

(DOPING) Many sports men use performance enhancing substances in an effort to gain edge over others. Dope=a drug given to a race horse to influence its speed/performance. In the world of sports, 'doping' means the deliber ate use of a substance or method banned by Medical Commission of International Olympic Committee (1OC). Due to health (death and ill effects) and ethical reasons, 1OC in 1967 agreed to ban or

restrict certain substances and methods that could be used to enhance performance. Examples: Anabolic steroids, nonsteroidal anabolic agents (eg. 52-agonist), stimulants or psychomotor drugs, for example, amphetamines.

IMPORTANT QUESTIONS FOR EXAMINATION SHORT NOTES (SN) 1.

2.

3. 4. 5. 6. 7. 8.

Body packers Withdrawal syndrome/symptom Glue sniffing Designer's drugs Bad trip Flashback phenomenon Ecstasy Date rape drugs or drug-facilitated sexual assault

DIFFERENCE BETWEEN (D/W) Drug addiction and drug habituation 10. Body packers and body stuffers 9.

L

ANSWERSS

SN-1: Body packers

Body

snmuggle illicit ingesting them or ears, vagina or

packers: The person who

drugs across countries by either inserting them in body cavities (e.g. rectum). high-quality For smuggling of financially lucrative morphime)» drugs (Cannabis, cocaine, heroin and

CHAPTER 21

commonly wrapped in aluminium Commonly wr. reare drugs capsules les, condom or balthe cellophane paper, fois make small packets. Smugglers then swal recovered| later from vomitus loon to Jowpacketswhich are after reaching their estination. faeces fter or person allows drugs for the purpose of The as body cker' or 'mule' or smuggling is known courier packers usually attempt to transport the Thebody ional borders so body packers are drugs acrosS airports. detected and arrested usually at the motility during transportation, the reduce gut Tosmuggler may take the drugs which reduce GIT antidiarrhoeals, antiemetics motility, for example, and

antipropulsives (e.g. diphenoxylate and loper.

reaching destination, the smuggler takes laxatives, detecates and then retrieves the packets from faeces to deliver them to the drug amide). After

dealer.

Detection

occur, for example: (1) Acidental poisoning occurs due to bursting/ leaking of ingested packets in the GIT and (2) acute intestinal obstruction. B. Abdominal X-ray and CT scan detects the nature of packets and their contents. Unusual number of homogeneous rounded or oblong densities with a complete gas halo. C. Physical examination of rectum/vagina. Management ofpoisoning: 1)Give nothing to eat/drink till packets are within A.

When complications

GIT

Kemoval of packets by whole bowel irrigation. 3) Antidotes specific to the drug causing poison-

ing

4) Symptomatic.

Autopsy findings: (1) Ruptured as well as intact ckets of drugs in stomach and intestines. (2) dstric and intestinal mucosa is congested. (5) All organs are congested. (4) Lungs and brain are oedematous.

SN-2:

Withdrawal syndrome

symptoms Withdrawal

a

sýndromes are the symptoms seen in addict due t aepends upon to sudden stoppage of ugs. dose and type of drug, duration of addiction an uddenness of withdrawal. The a drug

Drug Abuse

413

newborn born to an addicted mother also shows withdrawal symptoms within 2 days after birth in the form of hyperactivity, twitching and convulsions.

Substances showing: 1) Marked

withdrawal symptoms: Opioids, alcohol, scdatives and hypnotics and anxiolytics. 2) Weak withdrawal symptoms: Amphetamine, Cannabis, cocaine and nicotine. 3) No withdrawal symptoms occur with phencyclidine and hallucinogens (e.g. LSD).

Iypical withdrawal symptoms of opiates: They begin within 6-8 h of stoppage of drugs and are maximal in 72 h. Three stages are seen: 1) First (early, up to 12 h) stage: Intense fear, tachycardia, lacrimation, rhinorrhoea, sweating, craving, cold sensation, muscle aches, irritability/restlessness and yawning 2) Second (intermediate, 12-24 h) stage: Increased bronchial secretions predispose to chest infections, dilated pupils, piloerection and tremors. 3) Third (late, 24 h-10 days) stage: Sleep lasting 8-16 h. Upon awakening, all previous symptoms become intense. Painful abdominal cramps, leg pains, fever, hypertension, sweating vomiting, diarrhoea and increased heart rate. The symptoms pass off in 7-10 days. The newborn of addicted mother may develop withdrawal symptoms within 1 h of birth and require treatment. The symptoms are hyperactivity, convulsions and twitching.

Management of withdrawal symptoms: Benzodiazepines.

SN-3: Glue sniffing It means volatile substance abuse. inhalation of Volatile substance abuse: It is the which pro(inhalants/solvents)

volatile substances duces a feeling of euphoria. initially most common sub Glue sniffing: Sincetoluene-based adhesive/glue, so stance inhaled was broad term, also known the term'glue sniffing, as a as volatile substance abuse. hydrocarbons): Commonly abused inhalants: (mainly products Houselhold fuels), a) glues, paints and (in benzene permanent Acetone, xylene (in toluene, CCl4, kerosene, gasoline or petrol,

markers),

414

SECTION I

Forensic Toxicology

trichloroethylene, nitrites and so on. Toluene (in paint thinner, inks, varnishes, adhesives, glues and fuels) is the most commonly misused volatile solvent. b) Anaesthetic gases: Chloroform, ether, halothane and nitrous oxide.

It

is seen mainly in adolescents, especially of lower

socioeconomic classes because these substances are cheap and easily available. Methods of glue sniffing: 1) Bagging: Abuser empties the solvent into a plastic bag and then put their face inside and breathing deeply. 2) Dusting: Spraying an inhalant directly in mouth or nose 3) Gladding: The volatile substance is sprayed in the room and then inhaled deeply. 4) Huffing: The cloth is saturated with the volatile substance and is then kept over mouth. 5) Sniffing (snorting): The volatile substance is inhaled directly from the neck of a bottle containing the volatile substance. Signs and symptoms: Acute poisoning: It produces effects like alcoholic intoxication. Euphoria, excitement, a sensation of floating, dizziness, ataxia, slurred speech, powerful dreams and irrational behaviour. Chronic poisoning (occurs in painters, shoemakers, AC mechanics, drycleaning workers, anaesthesiologist, etc.). 1) Solvent syndrome: Headache, insomnia, Also restlessness/irritability. depression and seen in painters (known as painter's syndrome) due to chronic exposure to paint thinner. 2) Degreaser's flush: It is seen in industrial workers coming in contact with trichloroethylene for a long time. When they drink beer after work, red blotches develop on face known as degreaser's flush. 3) Solvent psychosis: Dementia. Cause of death: In acute poisoning: (1) Sudden cardiac arrest due to ventricular fibrillation is the most common cause of death; (2) hypoxia, anoxia and accidental asphyxia and (3) aspiration and accidents. In chronic poisoning: Liver and renal failure Autopsy findings: Surrounding skin around nose and mouth may be reddened or excoriated from the irritant action of solvent.

SN-4: Designer's drugs

Designer's drugs:

By altering chemical structure a new drug IS produced which is

of a known drug, called 'designer's drug. These drugs usually are highly potent and oflong duration as compared to their parent drugs. Illegal or banned drug. They include: A. Synthetic amphetamines: They act as stimulants, for example: 1) MDA = Love drug. 2) MDMA = Ecstasy (developed in 1914): Usually taken orally but may be injected/inhaled. Its effect last for 3-6 h. It may cause sudden death through cardiac arrhythmia. It can induce hyperthermia and hallucinations. 3) MDEA= Eve.

Methaqualone group: They act as depressants. C. Opioid group: They are narcotics, for example, fentanyl, pethidine and so on. D. Phencyclidine group: They cause hallucinoB.

gens.

Designer's

drugs are used in rave parties.

SN-5: Bad trip Bad trip: It is defined as panic attacks' or 'extreme anxiety experienced by a person on consuming LSD. LSD is classified as 'hallucinogen (or psyche

delic). a Actually the same LSD user may have either bad trip' or 'good trip. The term good trip

pleasurable used when the user experiences effects. tor and symptoms: (1) Hallucinations,hears Signs (i.e. example visual (of colours) and auditory and space voices); (2) disturbance in sense of time, simultaneous distances (3) dream-like state and (4) happiness experience of depression and elation, and sadness. up ceases after sometime, may persist tor or It events all the of flashback a give it may h 24 but dreamy state even for up to 2 years. treatment is essenta Treatment: (1) Prolonged Supportive-reassurance to treat flashbacks. (2) dark anu Take the patient in exam psychotherapy). (or Anxiolytic drugs, for avoid loud noise. (3) ple, diazepam. 1s

CHAPTER 21

Flashback phenomenon or

SN-6 flashbacks'

phenomenon: Abrupt abstinence folcontinuous use of LSD does not produce lowing but the effects of LSD may be awal symptoms wthdh ienced without further exposure to the drug. ccur wecks to months after the last experi-

Fashback

It

may

ence.

persist for 12-18 h even half-life of the drug is only 3 h.

action of LSD may

The though the

induced by alcohol 11take, n1arijuana intoxicastress. severe plysical illness, fatigue or

is

tion,

Sometimes it can be self-induced by will for positrips). tive re-experiences (free of most psychotomimetIt may occur with abuse psilocybin and ics, for exammple, LSD, mescaline,

trptamines.

MLI: It may lead to eccentric behaviour, for example, homicide

SN-7:

or suicide.

Ecstasy

Ecstasy is the name given to MDMA (i.e.

ylenedioxymethamphetamine), also molly.

t

is a

known as

synthetic psychoactive drug which was

developed by Merck 1912.

Usually

3,4-meth-

Pharmaceutical Company in

taken orally but may be injected/inhaled.

Its effect lasts

for 3-6 h. Cinical features: (1) euphoria; (2) a sense of intinacy (emotional closeness) with others, that 1s, cmpathy, compassion and forgiveness; (3) hyperactivity, increased alertness, wakefulness and awareness and (4) bruxism (teeth grinding) and Trismus (spasm of muscles

of mastication).

unical use: Posttraumatic

stress disorder (PTSD) a/w terminal cancer. Lause of death: (1) riorsagittalsinus, DIC Thrombosis of supe: (2) hypert failure. erthermia and (3) renal and anxiety

Test: Simon's

test.

MLI: (1) Sexstasy-combinatio

of 'ecstasy' with to increase sexual pleasure; (2) candyflapping-cor combination of 'ecstas with LSD' and (3) stacking"'alcohol'.The -combination of 'ecstasy danger nger of overdose increases because denafil'

Drug Abuse

415

ecstasy (stimulant) and alcohol (depressant) mask each other's effect.

SN-8: Date rape drug or 'drug-

facilitated sexual assaul

Date rape drug (or predator drug): A drug used to induce unconsciousness in woman, thus incapacitating her, for the purpose of sexual assault is known as date rape drug. Such rape is known as date rape' or 'drug-facilitated sexual assault. Such rape is called 'date rape' or 'drug-facilitated sexual assault' because the girl was called for dating and the drug was secretly mixed in her food or drink to make her unconscious for the purpose of rape. drugs used in DFSA currently include: (1) The Alcohol--most common drug used for DFSA; (2)) GHB (gamma hydroxy butyrate) is especially sometimes called date rape drug: (3) Ecstasy = MDMA and (4) others, for example, sedative-hypnotics (e.g. zolpidem), lunitrazepam (Rohypnol), ketamine, chloral hydrate and benzodiazepines (phencyclidine). The commission of date rape is usually preplanned and so drugs are purchased, kept safely and administered without the knowledge of victim. of these drugs favouring the Characteristics accused: 1) It should be rapidly acting (i.e. impairs judgment immediately) and short acting (i.e. it is quickly metabolised and excreted) so blood level becomes undetectable after 24 h. 2) It should cause anterograde amnesia, that is it should become very dificult for the girl to remember or recall the sexual events accurately. to the In many cases, even victim may not report authorities for many days after sexual assault. and taste 3) It should be colourless, odourless less, Drug is usually

added to a food or drink adding such subvictim's knowledge. The act of spiking. stances to drinks is known as'drink on body on examinaIn case of death: No injuries tion of victim. specimen tor Urine is a better investigation: in hair Lab can be detected care chemical analysis. Drugs DFSA seeks medical of victim Unless a also.

without

16

SECTION

II

Forensic Toxicology

within 72h of the assault, there are less chances that the tests would successfully detect the presence of these drugs, since most of them metabolise and get eliminated from the body within that period. (1) DFSA can take place not only between ML: two strangers but also within a happily married couple (Case box 22.1). (2) During examination of date rape victim, she should be asked about the effects of drugs felt by her after its administration.

By knowing the effects

screening can be done.

of drug, a specific

drug

DW-9: Drug addiction and drug habituation (Table 21.1) D/W-10: Body packer and body stuffer (Table 21.3)

1E3

22

Miscellaneous Poisons VEGETABLE

FOOD POISONS

It is a cLathyrus sativus (kesari dal, grass pea): drought-resistant pulse, that is, it can grow in conin poor soil. dition of extreme drought, tamine and reliable yield. It When all other crops fail, it produces js resistant to pests. It causes neurolathyrism |SN-1.

Argemone mexicana (Mexican poppy, prickly poppy, pila dhatura, satyanashi): Argemone seeds are similar to mustard seeds. Argemone seeds have spiny edges and burst with a report when.pressed on a slide. Mustard seeds have no spiny edges and collapse quietly when pressed. Argemone seeds contain several poisonous alkaloids like berberine, protopine, sanguinarine and dihydrosanguinarine. It causes epidemic dropsy [SN-2]. Poisonous mushroom: The genus Amanita (species muscaria, phylloides

and pantherina) is responpoisoning. most poimushroom in the world. Toxic principles

for most cases of mushroom Amanita nuscaria (death cap) is the Sstble

Sonous

amatoxins.

PHARMACEUTICAL TOXICOLOGY

Paracetamol Poisoning Paracetamol = para-acetylaminophenol. The term paracetamol' is used in India and the term 'acetaminophen' in United States and Canada. Metabolism: It is metabolised in liver by four pathways: sulphation (60%), glucoronidation (35%), gation with cysteine (3%) and Cyt-P450-mediated N-hydroxylation. Signs and symptoms: seI (30 min to 24 h): nausea, vomiting, dlaphoresis, pallor, drowsiness ase II (24-48 h): symptomless Phase days): symptoms of severe hepatic necrosis, -5 for exampl asterixis (i.e. coarse flapping

tremors of hands), right upper quadrant tenderness, coagulation defect, haemorrhages, foetor hepaticus, hypoglycaemia and hepatic encephalopathy Fatal dose: 40-50 tablets (i.e. 20-25 g); more dangerous in alcoholics. Children 6 months. If a diet containing>30% of kesari dal is taken for >6 months, spastic paralysis results. Kesari dal is a staple food for low income groups in some States, for example, Uttar Pradesh, Madhya Pradesh, Odisha and Bihar. It is similar to the arhar dal, so is frequently adulterated. Toxie principle responsible for neurolathyrism is a neurotoxin beta-oxalyldiamino-propionic acid (ODAP) also known as beta-oxalyl-amino-alanne (BOAA). affects mainly men (especially young men ot It 10-20 years). Initially: weakness of legs; walking with short steps and jerky movements. Patient wvalks on toes because heals don't touch the ground completely while walking. Patient may also have ditficulty in sitting down and getting up. Later: cross-legged gait (scissor gait), patien egs LIses a stick to walk; Ted muscle tone in muscle weakness; inversion of feet and knee jerks Ted. A unique feature is atrophy of gluteal muscle (buttocks). Still later: complete spastic paraplasia that ie to crawling as knee joints can't support the weight of the body.

CHAPTER 22

Prevention:

method method: Steepingme

BOAA is

eping

water soluble and

about 70% of BOAA

is

boiling for1 h, can be removed also by soaking removed. They

for 2 h. the soaking in lime water overarboiling: simple. boiling. followed by water pulse in hot

night

SN-2: Epidemic

dropsy

due to consumption of edible oil adulterated with the poisonous 'argemone oil. mustard oil, so it is used Argemone oil resembles adulterant of mustard oil. as an

Epidemic dropsy: is

Miscellaneous Poisons

419

Argemone oil is rich in two poisonous alkaloids:

guinarine (more toxic) and dihydrosanguinarine.sanMechanism of action of sanguinarine: It affects blood vessels > widespread capillary dilatation and increased capillary permeability and leakage of protein-rich plasma into extravascular compartment marked pitting oedema of legs. It also inhibits Nat-K*-ATPase activity of heart degenerative changes in cardiac muscles. Symptoms: marked oedema of legs associated with diarrhoea; dyspnoea, CCE, glaucoma, and bluish mottling on skin which blenches on pressure. Case: outbreak in New Delhi (Aug.-Oct., 1998); 2552 cases were reported and 65 deaths occurred.

-

SECTIONI Practicals IIA.

Specimens, 423

Examination IlB. Injury Report, 446

IC.

Age Estimation

Report, 455

IID. Grand Viva in Forensic Medicine, 465 IIIE. Grand Viva in Forensic Toxicology, 483

421

IIIA Specimens (For Spotting and Grand Viva) 3.

WEAPONS

Type of weapon: Heavy hard weapon with sharp edge and blunt edge. 2) Injuries caused: Abrasion, bruise, laceration, fracture. 1)

mechanical devices which, when hostile manner, will produce lesions or

weapons are the The Dplied in a

Chopper (Gandasa) (Fig. IIIA.3)

HOunds.

ypes of Weapons A.

heavy and B.

These may be light, moderately

Blunt weapons:

heavy.

weapons: (1) Sharp cutting (sharp edged)-these also may be light, moderately heavy and heavy. They may have single cutting edge or Sharp

both edges spear, needle

sharp cutting. (2) Sharp pointed and so on.

C.

Mixed.

1.

Knife (Fig. IIIA.1) 1)

Type of weapon:

ting weapon. 2)

Incised wound, lacerated cut-throat wounds, stab wound, abrasions and contusions. WOund,

Blunt Dack

4. Axe (Kulhari) (Fig. IIIA.4) 1) Type of weapon: Heavy, hard, sharp edged weapon. 2) Injuries caused: Laceration, fracture, abrasion,

bruise.

Light, single-edged sharp cut-

Injuries caused:

Siarpend

Fig. IWA.3 Chopper

Blade

Handle

Fig. IlIA.4 Axe 5.

Arrow (Fig. IIIA.5) 1) Type of weapon: Heavy, hard, pointed weapon. 2) Injuries caused: Stab, laceration, abrasion, bruise.

pOint

Sharp edge

Fig. IMA.1

Ricasso Crossquar

guard or hi

or

Knife and its parts

2. Hammer

(Fig. IlIA.2) ) Type of weapo Heavy, hard blunt. njuries caused: Abrasion, contusion, laceration, fracture.

Fig.IMA.2

Hammer

Fig. IMA.5 Arrow 6. Sword (Fig.

IlA.6)

hard, sharp edged Type of weapon: Heavy, weapon. Laceration, fracture. Also abra2) Injuries caused: sion and bruise. 1)

Fig. lWA.6 Sword

423

424 7.

SECTION II

Practicals 12.

Chisel (Fig. IlIA.7) 1) Type of weapon: Heavy, hard, sharp cdged weapon. 2) Injurics caused: Laceration, fracture, abrasion, bruise.

Ice pick (Fig. IIIA.12)

Type of weapon: Light weapon. 2) Injuries caused: Stab by the sharp pointed end, abrasion, bruise. 1)

Fig. IMA.12 lce pick Fig. IlIA.7 Chisel 8. Sickle (Fig. 1IIA.8)

13. Basuli (Fig. IIA.13) 1) Type of weapon: Heavy,

hard weapon.

2) Injuries caused: Laceration, abrasion, bruise,

Type of weapon: Sharp curved light weapon. 2) Injuries caused: Laceration, abrasion, bruise. 1)

fracture.

Fig. I1A.13 Basuli Fig. IIA.8 Sickle 9. Saw (Aari) (Fig. IlIA.9)

Type of weapon: Light, sharp cutting weapon with serrated edge. 2) Injuries caused: Laceration, abrasion, bruise. 1)

SLIDES

Haemochromogen Crystals (Fig. IIA.14) 1)

What is haemochromogen (Takayama) test? Ans. It is a confirmatory test to differentiate blood stains from other similar looking stains. Pink, feathery, rhomboidal crystals of haemochromogen or reduced alkaline haematin arranged in clusters are seen.

Fig. lIA.9 Saw 10. Rope (Fig. IIIA.10)

Type of weapon: Soft blunt weapon. 2) Injuries caused: Abrasion (patterned), bruise. 1)

Fig.

lMA. 14

Haemochromogen crystals

Haemin Crystals (Fig. llIA.15) 1)

Fig. IlIA.10 Ropes 11.

Trishul (Fig. IIA.11) 1) Type of weapon: Heavy hard sharp pointed weapon. 2) Injuries caused: Stabs, abrasion, bruise,

Fig. IlIA.11 Trishul

What is haemin (Teichmann) test? Ans. It is a confirmatory test to differentiate blood stains from other similar looking stains. Faint ye lowish red (or dark brownish/brownish black rhombic crystals of haematin chloride arranged single or in clusters are seen.

Fig. IWA.15 Haemin crystals

CHAPTER

tals (Fig. lIA.16) Picrate Picrate spemine mine test?

Barberio's Whatis screening test of semen which detects a spermine present in the prostatic Ans. If is presence ofs the Yellowish needle-shaped spermine secretions.

crystals are picrate

IMA

Specimens

425

TABLE IA. 1 Difference Between

AnimalHair and Human Hair Features 1.

Animal Hair

General

Thick and coarse Thin and fine Each scale is Each scale is

2. Cuticular scale

seen.

imbricate(i.e. it does not

Florence test? What is ) screening test of semen which detects Ans It is a in seminal vesipresence of 'choline present

completely Surround the

brown needle-shaped/rhombic choline seen. iodide crystals are

shaft)

e. Dark

Human Hair

3. Medulla

coronal (i.e. it completely Surrounds the shaft)

Broader, usually Narrow, Continuous

noncontinuous

or fragmented or entirely

absent Very narrow

4. Cortex

Broader (4-10 times broader than medulla)

Fig. MIA.16

Hair (Fig.

Spermine picrate crystals

5. Medullary Index (M)

Diameter of medulla Diameter of shaft

IIA.17)

medullary index? Ans. It is the ratio of the diameter of medulla to the diarneter of shaft (not the cortex). 2) What is the difference between animal hair and 1)

Always >0.5

Always 149 mm, and in females is Acute hyperflexion > Head strikes the front object, then Reactionary hyperexten sion. b) Hit from behind: Hyperextension -> Hyperflexion. c) Violent hyperflexion and hyperextension movement Atlanto-occipital dislocation (30% cases) or C5-C6 dislocation. Spinal

injury t

CHAPTER IIB

What

the major

site of hypertensiv haemor-

Mrhage?

ommon site of hypertensive haemorputamen, 55%). basalganglia (especially rhage thalamus (15%), white matter (10%), Others are (10%). (10%) and cerebellum

ns.Most

Sr.

No.

2.

2

PART

1.

iferentiate between and

ante-mortem abrasion

3.

postmortem abrasion. Refer Table IlIB.3.

Postmortem Hypostasis/ Bruise (Contusion)

Lividity

Cause: Distension of vessels with blood Site: Most dependent parts

Anywhere

Margins: Clearly defined

Not clearly defined

Colour: Uniform bluish

Different colours depending upon the age of bruise

purple

Ans.

TABLE I1B.3 Difference Between Ante-mortem Abrasion and Postmortem

5.

Abrasion: Not present

6.

It is

absent areas of contact flattening

Abrasion St

No.

Postmortem Abrasions

Ante-mortem Abrasions Site:

Anywhere on the

body

may be of any

colour

5.

Exudation: More, slightly raised

scab

Cause may be according to the typee of abrasions.

and congestion

4

Ans. Margins

Less, scab often lies slightly below the level of skin

contact

No change

MLI: It suggests the position

t suggests the nature

of

weapon used and also the nature of injury

inner canthus of eyes, axilla, underfold of female breasts, vagina, rectum, nape of neck. 46. What is assault?

Cause may be

handling during transport to mortuary

1) Manual

seen

ante-mortem bruise

and

of ante-mortem bruise are less sharp Or indistinct indicating vital reaction, but margins postmortem bruise are quite sharply deined. What are the causes of black eye Ans.(1) Blunt impact on forehead; (2) direct trauma the eye and (3) acture of anterior cranial fossa. 44. How will you rom differentiate a bruise contusion) om postmortem Ans. hypostasis/lividity. Postmortem Sion 0stasis is due to the distenVessels with blood at the most dependent parts of death body due to the effect of ravity after (Table IlIB.4). at is concealed incture wounds? cealed uncture wounds caused on conparts of body, for cample, strils, ears,

.

Lighter over the area of

Yellowish parchment like

reaction Not seen

Difference between postmortem bruise?

May be present

changes after death

2) Ant bite Microscopic: Vital

Rupture of vessels

Effect of pressure: Colour blanches but reappears on its release

time since death

Do not show colour

according to the time since injuryY

4

in

of the body at death and

prominences

Show colour changesS during life It

8.

Usually on the bony

451

TABLE IIB.4 Difference Between Postmortem Hypostasis and Contusion

pons

S

Injury Examination Report

47. 48.

49.

50.

Ans. In simple words, assault is defined as an attempt, offer or threat to appy criminal force to the body of another in a hostile manner. S.351, IPC defines assault as whoever makes any gesture or any preparation, intending or knowing it to be likely that such gesture or preparation will cause any person present to apprehend that he who makes that gesture or preparation is about to use criminal force to that person, is said to commit an assault. What is battery? Ans. Execution of assault is known as battery. What is hurt? causes Ans. S.319, IPC defines hurt as 'whoever person, is any bodily pain, disease or infirmity to said to cause hurt What is sinple hurt? serious nor extensive Ans. Sinmple hurt is neither category of grievous and does not fall under the heals rapidly withand hurt. It is simple in nature deformity (e-g. scar) out leaving any peranent such term in law. no or distiguration. Tlhere is What is concussion? cerebral dystunction (i.e. Ans. lt is a temporarystatus) immediately after alteration in mental confusion (disorientation), head injury. Features:

52

SECTION I

Practicals

amnesia, loss of consciousness may be there, headache, nausea, irritability, clumsiness, sweating, hypotention and visual disturbance. 51. What is bevelled cut? Ans. When any hcavy sharp-cdged weapon is struck obliquely on the body part, it will cause bevelling of one edge and undermining of other edge. In this wound, one edge (or flap) is visible. MLI: (1) The undermining edge indicates the direction from which the slashing stroke was made. (2) It also gives clue about the relative position of the victim and assailant. (3) These cuts are usually homicidal and are usually caused by heavy sharp-cutting weapons. 52. What is dowry death? Ans. According to S.304B (clause 1) of IPC, where the death of a woman is caused by any burns or bodily injury or occurs otherwise than under normal circumstances within 7 years of her marriage and it is shown that soon before her death she was subjected to cruelty or harassment by her husband (or any relative of her husband) for any demand for dowry, such death shall be called 'dowry death. 53. What is the punishment for causing dowry death? Ans. According to S.304B (clause 2) of IPC imprisonment for 7 years, which may extend to imprisonment for life.

VIVA

VIVA OF FIREARM

PART1 Classify firearmns. Ans. Table IIIB.5.

1.

TABLE IJB.5 Classification of Firearms

Smooth Bore Forearms

(Shotguns)

On the basis of length of barrel:

(1) long barrelled (e.g. Musket) and (2) short barrelled .On basis of number of barrel: (1) single barrelled and (2) double barrelled

On basis of loading: (1) muzzle loader and (2) breach loader

On basis of interior of barrel:

(1) cylinder bore and (2) choke bore Miscellaneous: (1) pump action and (2) slug shotguns

Rifled Firearms

(Rifles)

Shoulder

arms (Long barrel) Rifles (1) Single shot (2) Multiple shot Hand arm8 (Short barrel) (1) Plstol (2) Revolver

What is caliber of a weapon? Ans. It is the distance between two opposite lands in a rifled fircar 3. What is choking? Ans. Terminal/Distal a few cm (7-10 cm) of bore near muzzle end is slightly constricted in some the shotguns. This constriction of bore is known of as choking. 4. What are the various degrees of choking? 2.

Ans. Table IIIB.6.

TABLE IB.6 Degrees of Choking Degree 1.

Full

of

Choking

(minimum dispersion)

2. Three

quarter (4)

Constriction Inch

mm

0.04 0.03

0.75

3. Half (%)

0.02

0.50

4. One-fourth (4)

0.01

0.25

5. Open/lmproved/Cylinder (maximum dispersion)

0

0

What are the functions of choking? Ans. (1) It decreases or limits the spread of shot. (2) It increases the explosive force, velocity shot of and the range. 6. What are the differences between entry wound and exit wound? Ans. Refer Table IIIB.7. 7. What is rifling? Ans. The inner aspect (i.e. internal surface) of the wall of the barrel is cut longitudinally into a series of parallel spiral grooves from the breech end to the muzzle end. The elevated areas are called lands and the depressed areas are called grooves. 8. What are the functions of rifling? Ans. (1) It gives spin (rotator nmotion) bullet in to its long axis. (2) It prevents from wobbling în ar. (3) It increases the power of penetration. (4) ensures longer range. 9. What is abrasion collar? Ans. It is the abrasion of the skin caused by the bullet around entry vound. 10. What is tattooing? Ans. Numerous reddish-brown punctuate abra* Sions surrounding the wound of entrance in case of firearm injury. It is due to embedding of burnt, semiburnt and unburnt powder particles in the 5.

Superficial layers of the skin.

CHAPTER MB E IIB. TABL

Betweeen 7 Difference Wound

Woun and Exit und Entry Entry reaures

Exit

Wound

Smaller than the

Larger

17.

diameter of bullet Eages Abrasid

and grease

Inverted

Everted

Present

Absent

May be present

Absent

May be present

Absent

collar Blackening and

18.

19.

tattooing Burning with

singeing

20.

of hair

6

May be present

Cherry red (bright

Absent

near discharge

in

pink) colour of

tissues due to carboxyhaemoglobin Lead (metal) ring

Seen on X-ray

Absent

Positive for lead and carbon monoxide

Negative

around the wound

8

Chemical

tests

21.

PART2 11.

12.

What is primer? Ans. Primer is a 'small metallic cup, which tains priming mixture (or detonator).

con-

22.

What is 'priming

mixture? mixture or detonator is a chemi cal substance present in the primer in cartridge. t consists of three compounds, that is barium itrate, lead (styphate and peroxide) and tetraEne. Blow of firing pin on primer cup crushes tne Pining mixture (detonator) against anvil centre

Ans. Priming

and burns

it.

wnat are the components of black powder: Three components: PCS, 8. that is Potassium nitrate

.

(75%), Charcoal (15%), Sulphur (10%). What re the component of smokeless powder? Single base: nitrocellulose (gun cotlon) Ouble base: Nitrocellulose + Nitroglycerine.

ple

base:

Nitrocellulose

Ine + Nitroguanidine.

5. What

+

Nitroglycer

is paradox gun

Ans. Son

1otguns in which small part of ils bore paradox its muzzle end is rifled are knoWn as

argun.

453

16. What is

Wound

No

njury Examination Rep eport

23.

improvised firearm? Ans. Unlicensed country made firearms, for example desi katta. It is the smooth bored firearms used by criminals in India. What is dumdum bullet? Ans. It is .303 centrefire rifle cartridge loaded with a soft point bullet. What is Yawning bullet? Ans. A bullet travelling in irregular fashion instead of travelling nose-on. What is tumbling bullet? Ans. A bullet that tumbles, that is rotates end-onend during its motion. What is Souvenir bullet? Ans. Sometimes a bullet enters the body but does not cause fatality, and it is retained in the body for a long time. The person survives and usually does not show ill effects of the retained bullet. This type of bullet, which is present in the body for a long time is called Souvenir bullet. What is ricochet bullet? Ans. The bullet ricochets off or reflected from a surface, for example internal surface of skull bone. Ricocheting of a bullet may occur with an old unused firearm and a low velocity bullet. Jacketed bullets have a greater ricochet potential than unjacketed bullets. What is incendiary (explosive) bullet? Ans. It catches fire on hitting the target due to the is presence of phosphorus. If an incendiary bullet present in the body, the use of USG or microwave diagnostic techniques must be avoided as they can cause the bullet to cdetonate and explode. What is frangible bullet?

inmpact and Ans. The bullet which fragments on completely disintegrates. bore of a weapon? 24. What do you nmean by the term be 12 bore, 18 bore, Ans. The bore of aweapon may term'bore"'by the tollowin etc. We understancd the Pound (454 gm) example: 12 Bore gun means equal size (volunie and of lead- 12 Lead balls of into barrel, so Lead ball which tits weight) barrel. I ball = Diameter of Diameter of a single lead Which a pistol. a revolver and satety his tor 25. If a criminal have to kill a person choose he will One remains purpose? the cartridlge revolver, Ans. ln the case of chamber atter tiring The revolving with him in the the revolver 1

away perpetrator takes

4

SECTION I1

Practicals

along with cartridge, so at the crime scene, there is no cvidence left. In the case of pistol, the cartridge is ejected out of pistol and when the perpetrator leaves the place of crime scene along with his pistol, he leaves the cartridge at crime scene. This cartridge if found at the crime scene, it will help to identify the weapon and consequentiy may help to identify the criminal.

26. What is Kennedy phenomenon?

Ans. Surgical intervention of firearm wound during treatment makes the wound difficult to interpret during autopsy whether it is entry wound or exit wound. (It happened in John F. Kennedy's case, the 35th President of the United States.)

IIIC Age Estimation Report age report of a boy been brought to you

hypothetical write a Case years) wholhas (alleged age 16 entioning two police,

(Pill the following proforma and take the help of fol-

lowing X-rays provided to you.)

tification marks.

by

Report no.

...

...

.Ime

Dr.... *********e*nsenen************************ examinatlon..... ... Varitai Status... Sex

onducted

***********************************.

....

by

.....Fldce or

*******************************************

Date... ********************* age ********************* PrObable Name. .....Occupation... ...R/O.. ********************************************************** ********************* S/o, D/o, W/o..... FIR/DD

No..

Brought by constable....sr************************** Alleged history

.. mm

***********s

Photo

*aase***************

******************"

********************************"""********' IP****** *****'"********************

**************************************************************************************************"*************************************************

*********************************************************************** *************************************************************

************************************************************************************************ ******

******************************************************************** ****************************** ********************* *********************************** ******

************************************************************************************** Consent..... *******************************************************************************************************"****** *********************************************************************** ******************************************************** ***************************

**************************** ********|

**********************

Signature (Thumb impression)

Signature of witness General physical examination

and Nourishment..*****"******"********************************* **************************** .Built Weight... Pubic Hair.******************************* Scalp hair. ...Beard ...Moustache... Axillary hair..... ****************************** ********* ******************* ..Body. *************** ********* ***************************************** Chest.. *********************************.********** Date of menarche (in females).. *** ************** J********************************************** Breast development (in *************************************************************** .Voice... ************************************************* Genitals. **************** Height.

*******************.V

****

*************

Marks of identification 1.

2.

********************************************************************************°******"****************"******** *****

'************

*

*

*****************************************************************************************

*****'****************************************

*

Dental Examination: Dental charting

Radiological Examination:

NO,O1X- ray Plates examined.. X-ray plate number

Bearing No. Part of the body x-rayed

.

***

ddle

"*

*****°**********

Findings

of the opinion that rom the general physical, dental and radiological examination, am person examined by .yedls, me is between dna I

the age or tne

Dere

Officer

Signature of Medical number, Date & Seal) (with Name, Registration

455

56

SECTION I

Practicals

Example: Write a hypothctical age report of a boy (alleged age 16 years) who has been brought to you by police, mentioning two identilication marks.

34

2

(Note: Take the help of following four X-rays pro0vided to you.)

NO

CHAPTER IIC AA/AAAA.... AA/AAAA......

Report no.

DD.MM.YYYY.

lE...****************

Date Name..

s/o, Bfo,

AYL.......

**

wfo:.ABC.

FIR/BENo. ht by

by

Dr.

.....

Chand... ime.1.30A.M..Place of examination. ..Alleged (Probable) age.. 12 Years... Sex S.

0....... O00.

XX/XXXX.....

constable..

Conducted

Dated.....

EP.

NO....

...

TU

.

0CCupatlon

.

DD.MM.YYYY..

...Police station...

AA/BBB,...P/S...

Alleged history

all

Age Estimation Report

457

***********************

ABC.....

Male...

**********

********

****

..ATL...... ABCD... ***********

ABC...***********************************

edly on DD.MM.YYYY at around 9 PM, the person was caught in a theft in a house in ABC in XYz. been brought here for the purpose of age estimation.

He hos

Consent

, XYz, s/o ABC, R/0 JKL, give my full, free and

voluntary consent for a complete medical examination and other relevant investigations for the purpose of making an age report. The nature and consequences of such examination have been told to me by the doctor in my own language.

Signature of witness

Signature (Thumb impression))

examination Built and Nourishment..Average..*************************************" .150 cm... Weight. 40 Kg.. Scalp hair..Present... Beard...some hair present..Moustache..some hair present ...Axillary hair.. some hair present. Present extending to medial surface of thigh.. Pubic Hair. Chest.. ******************. Body... ***********e****.LC No hair..**** * Respiratory rate...14/min...Pulse rate..78/min..BP..132/82 mmHg... Abdomen...NAD Others...Ni.. Genital.Adult in shape & size, Testicular volume is 30 Voice.. .Normal. General physical Height

*******************

e**o*nssonns*****nne**ono

c.

Marks of identification

********************

L. A mole, 3 mm x2 mm, black,

raised, non-hairy, present at right side of forehead, 2 cm above the middle of right eyebrow 1/3 and 2.5 cm away from midline. An old healed scar, 2 cm x 0.3 cm, yellowish, glistening, non-contracted, non-raised, present at right side of forehead, 2 cm above the middle 1/3" of right eyebrow and 2.5 cm away from midline. Dental Examination: Dental hygiene: Good Dental charting: X means tooth not erupted. X 17 16 15 14 13 12 11 21 22 23 24 25 26 27 X x 47 46 45 44 43 42 41 31 32 33 34 35 36 37 X The age is < 18 years but > 12 years. Radiological Examination: No. ot X- ray Plates examined. ************************ .Bearing No *********************** X-ray plate Findings body Part of the

.

..

number

X-rayed

Upper end of humerus not united (i.e. < 17 years) < years) 2 Lower end of humerus not united (i.e. 16 Elbow joint 24 h, it is known as near-drowning. If he dies after 24 h due to some complications, then it is known as secondary drowning. 29. What is cutis anserina (or goose skin)? Ans. Cutis anserine: In a case of drowning, the skin may show a granular and puckered appearance like an orange peel. may be an ante-mortem (contraction of It erector pilorum) or postmortem phenomenon. In case of postmortem phenomenon, it can occur when dead body is immersed in water soon after death while the muscles are still irritable, that is before molecular death. can be due to the rigor mortis of erector It pilorum muscle of skin. 30. What are diatoms? Ans. Diatoms are microscopic unicellular algae found in water.

2.

3.

4.

5.

6.

Define impotency in males. Ans. Inability of male to achieve and/or maintain penile erection for satisfactory sexual intercourse. Define sterility in relation to males. Ans. Failure to impregnate; or inability of a male to beget children. Define sterility in relation to females. Ans. Failure to conceive or inability of female to conceive children. What is impotence quoad hoc? Ans. A man is impotent with a particular woman (e.g. wife) but not with others. Which one is the ground for divorce impotency or sterility? Ans. Impotency. What is the most common cause of impotence in males? Ans. Psychogenic.

Virginity, Pregnancy, Delivery and

Legitimacy Who is a virgin? Ans. A virgin is a female who has never experi enced sexual intercourse. 2. Who is a true virgin? Ans. A woman who has not experienced sexual intercourse and her hymen is intact. 1.

Part 2 31. Tell the anatomy and ossification of hyoid bone.

Ans. Hyoid bone consists of body (the central part), greater cornua (one on each side), lesser cornua (one on each side) at the junction of body and greater cornua. Ossification: Hyoid bone ossifies from six ossification centres (Table IIID.11). 32. What is emphysema aquosum? Ans. In ante-mortem drowning, water enters the voluminous, lungs and on autopsy the lungs are filling the bulky, water logged and over inflated, bulges chest cavity and overlapping the heart and Surface removed. out of chest when sternum is and indentation appearance may show pale grey of ribs

3. Define virginity.

4. 5.

6.

Ans. The state of being virgin is known as virginity. What is defloration? Ans. Loss of virginity is known as defloration. When a woman is said to be deflorate? sexual interAns. A woman who has experienced course and her hymen is torn or ruptured. Who is a false virgin? experienced sexual interAns. A woman who has is intact. course and in spite of that her hymen

IIID

ABLE ID.12

Signs of

Amenorrhea

sickness

Morning Quickening

3. Hyperpigmentation

4. Disturbances: Sympatihetic and urinary 7

Fatigue and (2) vagina Changesin (1) breast

Mnemoic A

7.

Manager Quits

HDFC

Can a false virgin take

Probable Signs Abdominal enlargement (Intermittent uterine contractions) 3. Changes in (1) cervix and (2) uterus 4. Oseander sign 5. Tests: Biological tests and immunological tests 6. Uterine soufflé 7. Ballottement Mnemonic: A Black Cat on TUB

1.

2. Foetal parts

herself in the court to be

true virgin. What are the features of hymen in true virgin and false virgin? Ans. In true virgin, hymen is intact, rigid, inelasti, thin membrane. It admits only the tip of little finger through the orifice painfully. In false virgin, hymen is intact, loose, elastic, thick/fleshy. It easily admits two fingers through the orifice. 9. What are the various types of hymen? Ans. [Mnemonic AS,-I Can Ignite Fire] (1) Annular, (2) Semilunar (or Crescentric), (3) Septate, (4) Subseptate, (5) Infantile, (6) Cribriform, 8.

(7) Imperforate and (8) Fimbriated. What are the signs of pregnancy? Ans. Table IIID.12. 11. What is quickening? Ans. It means the first perception of foetal movements by the mother. It occurs at 16th-20th weeks of pregnancy. It is a presumptive sign of pregnancy. 12. What is Braxton Hick's sign? Ans. Intermittent 10.

uterine contractions felt after They last about 1 min period of 2-3 min. It is a

16th week of pregnancy. followed by a relaxation

probable sign

Foetal movements

1.

Sinity?

of pregnancy. Hagar sign? Ans. It is a probable sign of pregnancy. It 1s a Dimanual examination in which one hand is placed on abdomen and two fingers of other hand in vagina. It is most valuable sign in early pregnancy, seen at 6th week.

13. What is

Positive Signs

2. Braxton Hick's sign

advantage of her false vir-

Ans. Yes, she can claim

477

Pregnancy

Presumptive Signs

2.

Grand Viva in Forensic Medicine

3. Foetal heart sounds 4. Foetal cells in mother's blood 5. Placental soufflé and umbilical soufflé 6. USG 7. X-ray

Mnemonic:

F-Please Use X-ray

What is superfecundation? Ans. It is fertilisation of two or more than two ova in the same menstrual cycle by two or more than two separate acts of intercourse. Two living foetuses are born. 15. What is superfetation? Ans. It is the fertilisation of ovum in an already pregnant woman. Only one living foetus is born. Other one is not foetus but foetus papyraceou 16. What is lochia? Ans. It is the discharge for 2-3 weeks after delivery. It has a peculiar sour, disagreeable odour (Table IIID.13). What are different types of lochia? Ans. The appearance of lochia after delivery var ies with the passage of time. 18. What is the medicolegal importance of lochia? Ans. It indicates that the woman has delivered a child. It also indicates the time since delivery. 19. Who is a suppositious child' Ans. When a woman claims a child as her own but actually it is not her child. This child is known as suppositious child. 14.

TABLE ID. 13 After Delivery Time ldays) For first 4 days For next 4 days i.e. 5-8 days)

After 9 days

Appearance of Lochia Type of lochia Lochia rubra (bright red

containing blood clots)

in colour) Lochia serosa (pale

Lachia alba turbid)

(yellowish green or

478

SECTION 1

Practicals

20. Who is a

posthumous child? Ans. One who is born after the death of his father, begotten during the lifetime of his father, the mother being conceived by said father.

5. What are the methods to induce criminal abortion? Ans.

General violence: Kicks, blows, jumping, kneeling, violent exercise, cupping, very hot and cold bath alternatively, massaging abdominal wall. 2) Local violence (instruments): Abortion stick, slipperyelm (Ulmusrubra), pastes, for example, Utus pastes and Fetex paste, air insufflations, syringing, rupture of amniotic membrane. 3) Abortifacient drugs: a) Ecbolics: The drugs which increase uterine contraction and cause abortion, for example, ergot, cotton root bark, posterior pituitary extract. b) Emmenagogues: The drugs which increase menstrual flow, for example, pros taglandins, borax, and so on. c) Irritants of genitourinary tract: Turpentine oil, cantharides, KMnO d) Organic irritants: Unripe fruit of papaya and pineapple, seeds of carrot and so on. 1)

Abortion 1.

What are the indications ofMTP? Ans. [Mnemonic English is Tough-Hindi

Simple

1) Eugenic:

is

When there is substantial risk to the

newborn.

2) Therapeutic: When there is risk to the life of

pregnant woman.

3) Humanitarian: When pregnancy is caused by

rape.

4) Social: Failure of any contraceptive device or method used by any married woman or her

husband. 2. Who can perform MTP legally? Ans. It depends upon the duration of pregnancy. Up to 12 weeks of pregnancy: Only one doc tor only if he has assisted an RMP in 25 cases of MTP, of which 5 have been performed by him independently in a hospital/institution approved by the government. After 12th week up to 20th week of preg nancy: Two doctors. Doctor should have PG degree/diploma in 0&G or he has completed 6 months of house residency in O&G or has experience at any hospital for 2l year in the practice of O&G. 20 weeks of pregnancy: It should not be After terminated except only in emergency when there is risk to the life of pregnant woman. In the case of emergency, only one doctor can ter minate pregnancy but it should be in good faith. Here PG degree/diploma in 08G not required. 3. Who can give consent for MTP? Ans. A woman of age>18 years can give consent for medical termination of her pregnancy. If she is