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Topic 4

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Topic 4: Toxicology — Common Poisons (Organophosphates, Corrosives, Opioids, Cocaine), Signs and Management

General Principles of Toxicology

A poison is any substance that, when introduced into or applied to the body, produces harmful effects or death. Toxicology encompasses the identification of poisons, understanding their mechanisms of action, recognition of clinical features, and the administration of specific antidotes and supportive care. In forensic medicine, toxicology addresses whether poisoning was accidental, suicidal, or homicidal, and establishes the role of poison in any death through postmortem examination and toxicological analysis.

Routes of Poison Administration

Poisons can enter the body through several routes. The oral route is the most common, with absorption occurring primarily in the gastrointestinal tract. Inhalation (gases and vapours absorbed via alveoli) provides the most rapid systemic absorption. Parenteral administration (injection) is the fastest route for achieving systemic effects. Dermal absorption is particularly significant in infants whose skin is more permeable. Rectal, vaginal, and percutaneous routes are less common but documented.

Organophosphorus Compounds

Mechanism

Organophosphorus compounds (OPCs) such as malathion, parathion, chlorpyrifos, and dichlorvos are irreversible inhibitors of acetylcholinesterase (AChE). This leads to accumulation of acetylcholine at synapses, causing overstimulation of cholinergic receptors throughout the nervous system. This produces the characteristic cholinergic crisis, remembered by the mnemonic SLUDGEM or DUMBELS.

Clinical Features (SLUDGEM/DUMBELS)

  • S: Salivation, Sweating, Salivation
  • L: Lacrimation
  • U: Urination
  • D: Defaecation, Diarrhoea
  • G: GI distress, Giddiness
  • E: Emesis (vomiting)
  • M: Miosis, Muscle fasciculations, bradycardia

Additional features include bronchospasm (causing wheezing), bronchorrhoea (copious secretions in the airway), hypotension, and tachycardia or bradycardia depending on the receptor predominance. Death results from respiratory failure due to paralysis of respiratory muscles, central respiratory depression, and overwhelming secretions.

Treatment

  • Atropine sulfate: A competitive muscarinic antagonist; the dose is titrated to achieve drying of secretions (atropinization). It reverses the muscarinic effects but not the nicotinic effects (fasciculations, paralysis).
  • Pralidoxime (2-PAM): Reactivates acetylcholinesterase if given early (before “ageing” of the enzyme-inhibitor complex occurs). Most effective within 24–48 hours of exposure.
  • Supportive care: Airway management, mechanical ventilation, control of convulsions with benzodiazepines, management of hypotension.

Postmortem Findings

At autopsy, froth in the airways, pulmonary oedema, and haemorrhagic tracheobronchitis may be seen. Blood, stomach contents, fat tissue, and liver should be preserved for toxicological analysis. The diagnosis is confirmed by demonstrating AChE inhibition in blood.

Corrosive Poisons

Types and Features

Corrosives cause tissue destruction by chemical action. They are classified as acids and alkalis.

Concentrated mineral acids (sulphuric acid — H₂SO₄, nitric acid — HNO₃, hydrochloric acid — HCl) produce immediate burning pain in the mouth, throat, and abdomen. Haematemesis (vomiting of blood) is common. Characteristic oral burns appear: sulphuric acid produces white to black burns (carbonization), nitric acid produces yellow to brown burns. Concentrated acids have a sharp, acidic odour.

Carbolic acid (phenol) is a unique corrosive — it has a local anaesthetic effect, so despite causing severe burns, the victim may report less pain than expected. Burns appear white and wrinkled (like leather) with a characteristic medicine-like odour. The urine may turn dark (due to phenols) and the patient may die rapidly from CNS depression.

Alkalis (sodium hydroxide — caustic soda, potassium hydroxide, ammonia) cause liquefactive necrosis through saponification of fats — deeper and more destructive than acid burns. Severe pain, oesophageal strictures (if survived), and gastric burns are characteristic. Vomiting produces watery or blood-tinged material.

General Management of Corrosive Poisoning

Do not induce vomiting — re-exposure of the oesophageal mucosa to the corrosive causes further damage. Do not give gastric lavage — risk of perforation. Management is primarily supportive: airway management, fluid resuscitation, pain control, antibiotics if perforation is suspected, and nutritional support. Emergency endoscopic evaluation (within 12–24 hours) assesses the extent of injury. Stricture formation is a long-term complication of significant corrosive ingestion.

Opioids (Opium, Morphine, Heroin)

Source and Mechanism

Opioids are derived from the opium poppy (Papaver somniferum). Opium contains morphine (approximately 10%), codeine, papaverine, and noscapine. Heroin (diacetylmorphine) is synthesized from morphine and is more lipid-soluble, crossing the blood-brain barrier more rapidly.

Opioids act primarily on mu receptors in the central nervous system, producing analgesia, euphoria, sedation, and respiratory depression.

Clinical Features

The classic triad of opioid poisoning is: miosis (pinpoint pupils), CNS depression progressing to coma, and respiratory depression (rate may drop to 4–6 breaths per minute). Additional features include hypotension, bradycardia, hypothermia, and constipation. The respiratory depression is the cause of death — it leads to hypoxemia, hypercapnia, and ultimately respiratory arrest.

Management

  • Naloxone: A competitive opioid receptor antagonist that rapidly reverses respiratory depression. Short half-life (30–90 minutes), so repeated dosing or infusion may be required. N-allyl nor-morphine (nalorphine) is an alternative.
  • Airway management and mechanical ventilation
  • Supportive care

Postmortem Findings

Cherry-red brain (due to cerebral hypoxia), froth at the nose and mouth, and pulmonary congestion are typical. The stomach may contain a dark brown fluid (opium solution). Detection of opium alkaloids (morphine) in stomach contents, blood, and urine confirms the diagnosis.

Cocaine

Source and Effects

Cocaine is an alkaloid derived from the coca plant (Erythroxylum coca). It exists as cocaine hydrochloride (water-soluble, used intranasally or intravenously) and crack cocaine (alkaloidal, smoked). Cocaine is a powerful stimulant that blocks the reuptake of catecholamines (dopamine, norepinephrine) and serotonin at synapses, leading to sympathetic overactivity.

Clinical Features

Cocaine produces sympathomimetic toxicity: tachycardia, hypertension, hyperthermia, diaphoresis, mydriasis (dilated pupils), agitation, and euphoria. Severe toxicity leads to hyperthermia (due to increased metabolic activity and vasoconstriction), myocardial infarction, cerebral haemorrhage, stroke, seizures, and death. Excited delirium is a recognized syndrome characterized by agitation, hyperthermia, and sudden cardiorespiratory collapse.

Management

There is no specific antidote for cocaine toxicity. Treatment is entirely supportive: benzodiazepines for agitation and seizures, cooling measures for hyperthermia, vasodilators or alpha-blockers for hypertension, beta-blockers are contraindicated (unopposed alpha stimulation worsens coronary vasoconstriction), and aspirin and anticoagulation for suspected myocardial infarction.

Postmortem Findings

Signs of sympathetic overactivity may be present: cerebral and pulmonary oedema, myocardial infarction or haemorrhage, and evidence of seizures (tongue biting, rhabdomyolysis). The diagnosis is confirmed by toxicological analysis of blood, urine, and stomach contents.

General Management of Poisoning Cases

Emergency Management (ABCD Approach)

  • A (Airway): Ensure patency; intubate if needed
  • B (Breathing): Support ventilation; give oxygen
  • C (Circulation): IV access; fluid resuscitation; vasopressors if needed
  • D (Dextrostix): Check blood glucose; correct hypoglycaemia

Decontamination

  • Oral: Gastric lavage (within 1–2 hours of ingestion, contraindicated in corrosives and petroleum products), activated charcoal (most effective within 1 hour; not effective for corrosives, alcohols, or hydrocarbons)
  • Dermal: Remove contaminated clothing; wash skin with soap and water
  • Inhalation: Remove from source; administer 100% oxygen

Enhanced Elimination

  • Forced diuresis (urine alkalinization for acidic poisons like salicylates)
  • Haemodialysis (for alcohols, metformin, lithium, ethylene glycol)
  • Haemoperfusion (for certain drugs)

Evidence Preservation in Poisoning Deaths

For toxicological analysis at autopsy, the following should be preserved: stomach and its contents (100 mL), blood (10 mL from a peripheral vein — avoid contamination), urine (50 mL), CSF (if CNS symptoms), liver and kidney (50 g each), and hair and nails (for chronic heavy metal poisoning). Viscera should be preserved in saturated common salt solution or rectified spirit. Blood for alcohol analysis should be stored in a fluoride/oxalate tube (grey top). All samples must be sealed, labelled, and sent to the forensic science laboratory with a proper forwarding letter.

  • Section 284 IPC: Negligent conduct with poisonous substances — applies to mishandling of poisons in the course of one’s occupation
  • Section 328 IPC: Causing hurt by a substance known to be likely to cause death — applies to poisoning with intent to cause hurt
  • Section 300 IPC: Murder — where death results from intentional poisoning with knowledge that it will cause death