Preservation of Viscera in Cases of Poisoning Death

When to Preserve Viscera

1. Death is suspected to be due to poisoning (by police or doctor)
2. Deceased was intoxicated or used drugs
3. Cause of death not found after autopsy
4. Unusual smell, color, or unidentifiable material detected in stomach contents
5. Anaphylactic deaths
6. Deaths due to burns
7. Advanced decomposition
8. Accidental death involving driver of a vehicle or machine operator

Routine Viscera Preserved in ALL Suspected Poisoning Cases

Containers

• Glass bottles: 1-litre capacity, clean, wide-mouthed, white, fitted with glass stoppers
• No rubber inserts under caps - rubber extracts certain poisons (chloroform, phenols)
• Clean with sulphuric acid-chromate solution, rinse with distilled water, dry
• Polyethylene bags can be used but volatile poisons may diffuse through plastic
• Nylon bags must be used for lungs/tissues for volatile substance analysis (nylon is not permeable)
• Blood: collected in screw-capped bottle of ~30 mL

Preservatives

1. Saturated Sodium Chloride (Common Salt) Solution

• Used in all cases EXCEPT poisoning by:
  • Corrosive acids (other than phenol/carbolic acid)
  • Alkalis
  • Corrosive sublimate
  • Aconite

2. Rectified Spirit (Ethanol)

• Used when salt solution is contraindicated
• NOT used in suspected poisoning by:
  • Alcohol, kerosene
  • Chloroform, ether
  • Chloral hydrate
  • Formic acid, formaldehyde, acetic acid
  • Phenol / phosphorus
  • Paraldehyde (Reason: organic acids and paraldehyde are soluble in alcohol; phosphorescence of phosphorus is diminished by alcohol)

3. Blood Preservatives

Note: Heparin and EDTA must NOT be used as anticoagulants as they interfere with detection of methanol.

4. Urine Preservatives

• Saturated common salt solution, OR
• Rectified spirit, OR
• Fine grains of thymol, OR
• 1 gm sodium benzoate, OR
• 5 mL concentrated hydrochloric acid (for 200-500 mL urine)

5. Histopathology

• 10% formalin for tissues meant for histopathological examination

6. Fluoride Addition Required For:

• Urine, CSF, vitreous humor when alcohol estimation is needed
• Samples for cocaine, cyanide, and CO analysis

Additional/Special Viscera (Poison-Specific)

Control specimens from the opposite side of the body must be taken when skin is sampled.

Packing and Dispatch Procedure

1. Separate bottles - Contents of GI tract must NOT contaminate solid viscera
2. Standard arrangement:
   • Bottle 1: Stomach + upper small intestine + contents
   • Bottle 2: Liver, kidney (and spleen pieces)
   • Bottle 3: Urine
   • Separate vials: Blood
   • Additional: Brain in one bottle; vomit/stomach washout in another
3. Fill only two-thirds of bottle capacity - leaves room for decomposition gases
4. Stoppers well-fitted, covered with cloth, tied with tape/string, ends sealed
5. Labeling - Each bottle must include:
   • Name of victim, age, sex
   • Autopsy number
   • Police station and crime number
   • Organs contained
   • Date and place of autopsy
   • Preservative used
   • Signature of doctor
   • Infectious content warning if applicable
6. Preservative control sample: 25 mL rectified spirit OR 25 g sodium chloride sent separately to FSL to exclude contaminants
7. Sealed bottles placed in a locked box, sealed with personal/departmental seal
8. Documents sent to FSL: Inquest report + Postmortem report + Magistrate's authorization
9. Analysis only done with authorization from Magistrate OR police officer not below rank of Deputy Superintendent
10. Viscera box handed to police constable with receipt; personally delivered to FSL

Key Principle

The liver concentrates many poisons to identifiable levels even when blood and urine concentrations have declined. The kidney's excretory function ensures high poison levels in urine. Muscle drug levels more accurately reflect blood levels than liver or kidney. Post-mortem diffusion from GI contents can cause false rises in tissue levels - hence strict separation of viscera is mandatory.

• The Essentials of Forensic Medicine and Toxicology, 36th ed., 2026, pp. 130-132
• Parikh's Textbook of Medical Jurisprudence, Forensic Medicine and Toxicology, pp. 139-140

War Gases (Chemical Warfare Agents)

Definition

Historical Background

Classification of War Gases

1. Lung Irritants (Asphyxiants / Choking Gases)

• Chlorine, Phosgene, Chloropicrin, Diphosgene

2. Lacrimators (Tear Gases)

• Chloroacetophenone (CAP/CN), Bromo-benzyl cyanide (BBC), Ethyl-iodo-acetate (KSK)

3. Vesicants (Blister Gases)

• Mustard gas, Lewisite

4. Sternutators (Nasal Irritants / Vomiting Gases)

• Diphenyl-chlorarsine (DA), Diphenyl-amine-chlorarsine (DM), Diphenyl-cyan-arsine (DC)

5. Paralysants (Blood/Nerve Poisons)

• Carbon monoxide, Hydrocyanic acid (HCN), Hydrogen sulphide (H₂S)

6. Nerve Gases

• Toxic chemicals with acetylcholine-like action

7. Incapacitating Agents

• BZ (3-quinuclidinyl benzilate) - hallucinogen causing disorientation, delirium, amnesia

Detailed Account of Major War Gases

A. NERVE AGENTS

• Volatile liquids at room temperature; heavier than air - stay close to ground, travel downwind and downhill
• Must be aerosolized or evaporated for use as inhalational weapons

• Nerve agents are potent inhibitors of acetylcholinesterase (AChE)
• Normally, AChE breaks down acetylcholine (ACh) at nerve synapses
• When AChE is inhibited, ACh accumulates continuously at cholinergic synapses
• This causes continuous stimulation of muscles and glands, leading to:

• Salivation, Lacrimation, Urination, Defecation, GI cramps, Emesis

1. Atropine - blocks muscarinic receptors, counters ACh accumulation
2. Pralidoxime (2-PAM) - reactivates acetylcholinesterase (must be given early before "aging" of the enzyme)
3. Diazepam - for seizures
4. Pyridostigmine (pretreatment) - carbamylates AChE, preventing nerve agent binding

B. VESICANTS (Blister Agents)

Mustard Gas (Sulfur Mustard, Yellow Cross, HS)

• Chemical: Bis(2-chloroethyl) sulfide
• Odour: Garlic/mustard-like smell
• Delayed action - symptoms appear hours after exposure (insidious)
• Easily penetrates leather and fabric
• Effects: Severe chemical burns to skin, eyes (blindness), respiratory tract; painful fluid-filled blisters; long-term respiratory problems
• Used in WWI (1917), WWII, Iran-Iraq war

Lewisite (Dichloro-2-chlorovinylarsine)

• Organic arsenical compound
• Immediate pain on contact (unlike mustard gas)
• Similar blister/vesicant effects; also systemic arsenic toxicity
• Antidote: British Anti-Lewisite (BAL / Dimercaprol) - chelates arsenic

• Immediate decontamination (remove clothing, copious water irrigation)
• Wound care to prevent infection
• Eye irrigation
• BAL for Lewisite poisoning

C. CHOKING AGENTS (Lung Irritants)

• Chlorine: Bleaching powder smell; kept liquid under pressure
• Phosgene: Musty / freshly mown hay odour; colorless gas; heavier than air
• Chloropicrin: Yellowish oily liquid; fly-paper like odour
• Diphosgene: Oily liquid; phosgene-like smell

• Chlorine when inhaled reacts with water in lungs → hydrochloric acid → corrosive lung damage, suffocation
• Phosgene: Reacts with proteins and lipids in alveolar membranes → non-cardiogenic pulmonary edema
• 80% of WWI chemical warfare deaths were caused by phosgene

• Coughing, choking, chest tightness
• Pulmonary edema (may be delayed 24 hours with phosgene)
• Frothy sputum, respiratory failure
• Chlorine: Lacrimation, conjunctivitis, stinging of eyes/throat

• Immediate removal from exposure
• Supplemental oxygen
• Respiratory support / mechanical ventilation
• Bronchodilators
• No specific antidote for phosgene

D. LACRIMATORS (Tear Gases)

• CN - Chloroacetophenone (Mace)
• CS - Chlorobenzylidenemalononitrile (most common riot control agent)
• CR - Dibenzoxazepine

• Intense lacrimation (tearing)
• Eye pain, blepharospasm
• Nasal and respiratory tract irritation
• Skin burning sensation

E. STERNUTATORS (Vomiting / Nasal Irritants)

• DA - Diphenyl-chlorarsine
• DM - Diphenyl-amine-chlorarsine (Adamsite)
• DC - Diphenyl-cyan-arsine

• Violent sneezing, coughing, nausea, vomiting
• Headache, malaise
• Forces victims to remove gas masks, making them vulnerable to other agents

F. BLOOD / PARALYSANT AGENTS

• Inhibits cytochrome c oxidase (Complex IV of electron transport chain)
• Causes histotoxic anoxia - cells cannot use oxygen despite adequate blood oxygen
• Classic: Bitter almond smell, cherry red color of blood

• Amyl nitrite (inhaled) + Sodium nitrite IV → form methemoglobin (binds CN)
• Sodium thiosulfate IV → converts CN to thiocyanate (non-toxic)
• Hydroxocobalamin (alternative - binds CN directly)

Lethal vs. Incapacitating Classification

• Lethal agents: designed to kill (nerve agents, mustard gas, cyanide)
• Incapacitating agents: < 1/100 of lethal dose causes incapacitation (nausea, visual disturbance, disorientation)
• The distinction is statistical and based on LD50

Protection

General Management of Chemical Agent Exposure

1. Remove victim from contaminated area
2. First responders use PPE (Level A/B suits for liquid nerve agents)
3. Decontamination BEFORE patient enters ED (strip clothing, water irrigation)
4. Triage at scene and again before hospital entry
5. Specific antidotes based on agent class (atropine + pralidoxime for nerve agents; BAL for Lewisite; O₂ for choking agents; nitrites + thiosulfate for cyanide)

International Legal Framework

1. Geneva Protocol (1925): Prohibited chemical and biological weapons in warfare; lacked enforcement
2. Chemical Weapons Convention (CWC, 1993; in force 1997): Prohibits development, production, stockpiling, and use; mandates destruction of existing stockpiles; enforced by the OPCW (Organisation for the Prohibition of Chemical Weapons)

Forensic Significance

• The Essentials of Forensic Medicine and Toxicology, 36th ed. 2026, p. 539-541
• P.C. Dikshit's Textbook of Forensic Medicine and Toxicology, pp. 562-564
• Rosen's Emergency Medicine, 9th ed., Chapter 55

Run Amok

Definition

Classification

• Culture-bound syndrome (DSM-5 / ICD)
• Also classified under dissociative disorders
• Distinguished from Intermittent Explosive Disorder by: a single episode and prominent dissociative features

Geographical Distribution

Epidemiology

• Sex: Essentially unknown in women (only one atypical case in literature, with no deaths)
• Age: 20-45 years
• Typical profile: Males of Malay extraction, Muslim religion, low education, rural origin
• Pattern: Endemic in Malayo-Indonesia with some epidemic increases
• Rates of relapse are unknown, but considered very likely in popular view

Stages / Phenomenology

Stage 1 - Precipitating Event

• Exposure to a stressful stimulus or subacute conflict
• Elicits feelings of anger, loss, shame, and lowered self-esteem
• Stressor usually appears minor in proportion to the resulting behavior (argument with a coworker, verbal insult)
• Occasionally a severe stressor (death of a loved one)

Stage 2 - Brooding (Prodromal Period)

• Period of social withdrawal and brooding over the precipitating conflict
• Often involves aimless wandering
• Sometimes accompanied by visual perceptual alterations

Stage 3 - Frenzied Violent Outburst (Acute Phase)

• Sudden transition to frenzied, extremely violent homicidality
• May be with or without brief prodrome of preparation (locating a preferred weapon, or grabbing whatever is available)
• Indiscriminate victim selection - victims may or may not symbolically represent the original actors in the conflict
• Subject also attacks animals or objects in his path; may wound himself
• Perseveres despite external attempts to bring him under control
• Verbalizations may be frenzied and guttural, or express internal conflict

Stage 4 - Cessation

• Cessation usually results from being overpowered or killed
• Occasionally spontaneous; typically abrupt
• Leads to a change in consciousness - usually stupor or sleep

Stage 5 - Post-episode

• Partial or total amnesia for the acute episode
• Reports of "unconsciousness" or "darkened vision" (mata gelap in Malay)
• Perceptual disturbances or affective decompensation for days or weeks after
• Psychosis or depression sometimes ensues

Precipitants

• Arguments with coworkers
• Non-specific family tensions
• Feelings of social humiliation
• Bouts of possessive jealousy
• Gambling debts
• Job loss

Suicidal intent: Unclear. Anecdotes and cultural views suggest it, but interviews with surviving subjects have refuted the association.

Etiology / Associated Conditions

• Schizophrenia (most common underlying diagnosis in hospitalized cases)
• Dissociative disorder
• Brief psychotic episodes

• Cannabis (Hashish) - Acute psychotic reaction in chronic abusers; person develops homicidal frenzy - "Run Amok" - can commit a killing spree of anyone they encounter; can also meet with accidents or be killed
• Cannabis (Parikh): Following continued use, or rarely after first-time consumption, the person may run amok. Associated with hashish psychosis (sensuous hallucinations, delusions of grandeur/persecution, homicidal crimes of sexual jealousy)
• Rarely described with other psychostimulants

Differential Diagnosis

Medicolegal / Forensic Significance

1. Insanity Defense: In 20th-century Malaysia, afflicted individuals have been exempted from legal or moral responsibility for acts committed during amok, using an insanity defense characterizing the attack as "unconscious" and beyond the subject's control.
2. Outcome of legal proceedings:
   • Hospitalization (sometimes permanent)
   • In the past: banishment or execution
   • Some trials resulted in criminal verdicts and prolonged imprisonment
3. Drug-related criminality: Cannabis-induced amok has direct medicolegal implications - identifying the drug-induced state may influence criminal responsibility assessments.
4. Post-episode amnesia is a key feature that supports the insanity/automatism defense - the subject claims to have been "unconscious" during the act.

Treatment

• Antipsychotic medications (once hospitalized - underlying schizophrenia often diagnosed)
• Psychiatric hospitalization (sometimes permanent in Malaysia)
• Addressing underlying precipitant / social stressors
• Treatment of any drug dependency if amok was drug-induced

Key Points for Exams

• Kaplan & Sadock's Synopsis of Psychiatry, pp. 3223-3225
• The Essentials of Forensic Medicine and Toxicology, 36th ed. 2026
• Parikh's Textbook of Medical Jurisprudence, Forensic Medicine and Toxicology