Forensic Toxicology — Classification of Poisons, Common Poisonings, Medicolegal Autopsy & Management

Forensic Toxicology — Classification of Poisons, Common Poisonings, Medicolegal Autopsy & Management

Introduction to Forensic Toxicology

Toxicology is the study of poisons — their source, properties, mode of action, symptoms, fatal dose and period, treatment, and medicolegal aspects. Forensic (medicolegal) toxicology applies this knowledge to questions of law: was a death due to poisoning, was it suicidal, homicidal, or accidental, and what evidence will stand in court. A poison is any substance which, when administered into or applied to the body in a small quantity, produces ill health or death by its chemical action. For FMGE, the high-yield areas are the classification of poisons, the features of poisons common in India (organophosphates, aluminium phosphide, corrosives, arsenic, opioids, and datura), the correct preservation of viscera, and the principles of management.

Relevant Law

A doctor’s handling of a suspected poisoning case is governed by statute. The Poisons Act, 1919 regulates the import, possession, and sale of poisons, and the Drugs and Cosmetics Act, 1940 controls the manufacture and sale of drugs. Under the Indian Penal Code, Section 328 IPC punishes causing hurt by means of poison or any stupefying, intoxicating, or unwholesome substance with intent to commit an offence, and Section 284 IPC punishes negligent conduct with respect to a poisonous substance. Deaths from poisoning with criminal intent are dealt with under the general homicide provisions (Sections 299 and 300 IPC). A case of suspected homicidal or suicidal poisoning is a medicolegal case, and the treating doctor must inform the police.

Classification of Poisons

Poisons are classified by their predominant mode of action.

Corrosives

Substances that produce local destruction (chemical burns) of tissue on contact:

• Strong acids: sulphuric acid (oil of vitriol), nitric acid (aqua fortis), hydrochloric acid. Acids produce coagulative necrosis with a dry, leathery eschar.
• Strong alkalis: sodium and potassium hydroxide. Alkalis produce liquefactive (colliquative) necrosis with a soft, soapy, translucent slough — deeper penetration than acids.
• Organic/weaker corrosives: oxalic acid, carbolic acid (phenol).

Irritants

Produce inflammation and irritation of the tissues:

• Inorganic — non-metallic: phosphorus, chlorine, bromine, iodine.
• Inorganic — metallic: arsenic, mercury, lead, copper, antimony, thallium.
• Inorganic — mechanical: powdered glass, diamond dust.
• Organic — vegetable: castor (ricin), croton, Abrus precatorius (jequirity/rosary pea), calotropis.
• Organic — animal: snake venom, cantharides (Spanish fly), insect and scorpion stings.

Neurotics (acting chiefly on the nervous system)

• Cerebral: somniferous (opium and its alkaloid morphine); inebriants (ethyl alcohol, ether, chloroform); deliriants (datura, cannabis, cocaine, belladonna/atropine).
• Spinal: excitant — strychnine (from nux vomica); depressant — gelsemium.
• Peripheral: curare, conium (hemlock).

Cardiac Poisons

Aconite (the most rapidly fatal vegetable poison), digitalis, oleander (yellow and white), nicotine, and tobacco.

Asphyxiants (irrespirable gases)

Carbon monoxide, carbon dioxide, hydrogen sulphide, and war/irritant gases.

Miscellaneous (agricultural and household)

Organophosphates and carbamates, organochlorines, aluminium phosphide, and kerosene/hydrocarbons.

Factors Modifying the Action of a Poison

The clinical and fatal effect of a poison depends on the dose, the physical form (gas > liquid > powder > solid; a poison must dissolve to act), the concentration, and the route of administration (inhalation and intravenous routes act fastest, followed by intramuscular, subcutaneous, oral, and dermal). Patient factors also matter: age (children and the elderly are more susceptible), state of health, sleep (slows absorption), idiosyncrasy and hypersensitivity, tolerance (as seen with chronic opioid use), and cumulative effect (slowly excreted poisons such as arsenic and lead).

Ideal Homicidal vs. Suicidal Poison

An ideal homicidal poison is cheap, easily available, colourless, odourless, and tasteless (so it can be mixed with food), produces symptoms resembling a natural disease, and leaves no characteristic post-mortem appearance — classic examples are arsenic, aconite, and thallium. An ideal suicidal poison is one that is easily available, cheap, capable of causing painless death with certainty, and acts reliably — examples in India include organophosphates, aluminium phosphide, opium, and barbiturates.

Common Poisonings in India (High-Yield)

Organophosphorus Compounds

Insecticides such as malathion and parathion. They irreversibly inhibit acetylcholinesterase, causing accumulation of acetylcholine. Features are muscarinic (the SLUDGE complex — salivation, lacrimation, urination, defaecation, gastrointestinal cramps, emesis; plus bradycardia, bronchorrhoea, and miosis), nicotinic (muscle fasciculations, weakness, paralysis), and CNS (confusion, convulsions, coma). The breath may smell of garlic. Management: atropine (to reverse muscarinic effects, titrated to drying of secretions) plus pralidoxime / 2-PAM (a cholinesterase reactivator, most useful early before “ageing” of the enzyme).

Aluminium Phosphide (Celphos, “rice tablet”)

A very common fatal poisoning in agricultural India. On contact with moisture and gastric acid it liberates phosphine gas, which blocks cellular respiration. It causes profound, refractory circulatory shock and metabolic acidosis; the breath and gastric contents smell of garlic/decaying fish. There is no specific antidote — management is supportive, with airway protection, correction of acidosis and shock, and gastric lavage (some use potassium permanganate or coconut oil to retard phosphine release).

Arsenic

The classic homicidal poison. Acute poisoning produces severe vomiting and “rice-water stools” with a garlic odour, mimicking cholera or gastroenteritis. Chronic poisoning produces “raindrop” skin pigmentation, hyperkeratosis, Mee’s lines (transverse white bands on the nails), and peripheral neuropathy. Arsenic is deposited in hair and nails and can be detected long after death (the Reinsch and Marsh tests are classic detection methods). Antidote: BAL (dimercaprol), or oral DMSA/DMPS.

Corrosive Poisoning

Acids and alkalis produce chemical burns of the lips, mouth, oesophagus, and stomach with intense pain, dysphagia, and risk of perforation; late complications include oesophageal and pyloric stricture. Gastric lavage and emetics are contraindicated (risk of re-exposing tissues and perforation); management is dilution, airway protection, and supportive care.

Opioids (Opium / Morphine / Heroin)

The classic triad is pinpoint (miotic) pupils, respiratory depression, and coma. Antidote: naloxone, a competitive opioid antagonist.

Datura (Dhatura)

Known as the “poison of highway robbers” for its use in stupefying victims. Its alkaloids (atropine, hyoscine) are anticholinergic, producing the classic picture: “blind as a bat (mydriasis, blurred vision), dry as a bone (dry mouth and skin), red as a beet (flushing), hot as a hare (hyperthermia), and mad as a hatter (delirium, hallucinations).” Management is supportive; physostigmine may be used in severe anticholinergic toxicity.

Carbon Monoxide

A colourless, odourless gas with about 240 times the affinity of oxygen for haemoglobin, forming carboxyhaemoglobin and causing tissue hypoxia. The characteristic post-mortem finding is cherry-red discoloration of the skin, lividity, and blood. Treatment is 100% oxygen (hyperbaric oxygen in severe cases).

Snake Bite

Neurotoxic venom (cobra, krait) causes ptosis, bulbar palsy, and respiratory paralysis; vasculotoxic/haemotoxic venom (vipers) causes local swelling, bleeding, and coagulopathy. Treatment is polyvalent anti-snake venom (ASV) with supportive care.

Medicolegal Autopsy and Preservation of Viscera

In a suspected poisoning death, the autopsy surgeon must preserve viscera for chemical analysis at the Forensic Science Laboratory. The routine samples are: the stomach and its contents, the upper part of the small intestine with contents, about 500 g of liver, half of each kidney, and samples of blood and urine. In suspected metallic poisoning, also preserve hair, nails, skin, and bone.

The standard preservative is saturated saline (common salt) solution. Two important exceptions: for suspected alcohol or carbon monoxide poisoning, the preservative is sodium fluoride with potassium oxalate (fluoride prevents fermentation/neoformation or destruction of alcohol). Formalin must never be used as a preservative for toxicological samples, as it interferes with chemical analysis (and itself destroys or alters many poisons). Each container is sealed, labelled, and dispatched with a sample of the preservative as a control, maintaining an unbroken chain of custody.

Principles of Management of Poisoning

Management follows a logical sequence: (1) stabilise the airway, breathing, and circulation; (2) remove unabsorbed poison — gastric lavage (contraindicated in corrosive and convulsant poisoning and in unprotected airway) and activated charcoal, the “universal antidote,” which adsorbs most organic poisons but is ineffective for metals, corrosives, alcohols, and hydrocarbons; (3) administer antidotes where available — physical, chemical, or physiological/pharmacological (for example atropine and pralidoxime for organophosphates, naloxone for opioids, BAL for arsenic); (4) enhance elimination by forced alkaline diuresis, haemodialysis, or haemoperfusion in selected poisonings; and (5) provide supportive and symptomatic care throughout.