IM22.1-13 | Poisoning — Practice Quiz

Correct. Regardless of the suspected toxin, the initial approach to any poisoned patient follows ABC stabilisation: Airway (GCS 9 means reduced airway protection — prepare for intubation), Breathing (high-flow O2 for bronchospasm and secretions), Circulation (IV access). Decontamination — removing contaminated clothing — is done simultaneously. Atropine is the antidote for OP poisoning but cannot be the first step before the airway is secured.

In any poisoning, ABC stabilisation precedes antidote administration. With GCS 9, the airway must be secured first. Atropine is the correct antidote for OP poisoning but should follow resuscitation steps. Activated charcoal is contraindicated when GCS is reduced (aspiration risk). AChE levels confirm diagnosis but do not delay treatment.

Correct. The cholinergic toxidrome results from excess acetylcholine at muscarinic and nicotinic receptors. Muscarinic features: SLUDGE/DUMBELS (Salivation, Lacrimation, Urination, Defecation, GI cramps, Emesis; Diarrhoea, Urination, Miosis, Bradycardia, Bronchospasm, Emesis, Lacrimation, Salivation). Nicotinic features: fasciculations, weakness. Classic causes: organophosphate and carbamate insecticides, nerve agents.

This picture — miosis, bradycardia, bronchospasm, sweating, fasciculations — is the cholinergic toxidrome (excess acetylcholine). Anticholinergic is the mirror image: mydriasis, tachycardia, dry skin, delirium. Opioid causes miosis but with respiratory depression and no fasciculations. Sympathomimetic causes mydriasis and tachycardia.

Correct. The silent period of paracetamol toxicity is its most dangerous feature. A normal AST at 6 hours means nothing — hepatic necrosis peaks at 72-96 hours. The Rumack-Matthew nomogram uses serum paracetamol level plotted against time since ingestion to identify patients at risk. If above the treatment line (usually >150 mcg/mL at 4 hours), NAC should be started regardless of symptoms. NAC is most effective within 8-10 hours; waiting for transaminase elevation means waiting until the window for effective treatment has passed.

Paracetamol overdose has a treacherous silent phase — the patient is well while hepatic necrosis is developing. The Rumack-Matthew nomogram guides NAC decision based on serum level vs time since ingestion. NAC must be started before transaminases rise; waiting for symptoms means the treatment window has been missed.

Correct. Aluminium phosphide (Celphos) is one of the most lethal agricultural poisons encountered in India, with case fatality rates of 30-100% in severe poisoning. Phosphine gas (released on contact with moisture) inhibits cytochrome c oxidase (Complex IV of the mitochondrial ETC), causing profound cellular energy failure and cardiovascular collapse. There is NO specific antidote. Management is entirely supportive: aggressive vasopressor support for refractory hypotension, arrhythmia management, and supportive care for multi-organ failure. Activated charcoal is relatively ineffective against phosphine and risks aspiration in a haemodynamically unstable patient.

Aluminium phosphide poisoning has NO antidote. Desferrioxamine chelates iron, not phosphine. Fomepizole blocks alcohol dehydrogenase. The only management is supportive: haemodynamic resuscitation, vasopressors, and treatment of arrhythmias. The family must be counselled honestly about the grave prognosis.

Correct. The triad of miosis, respiratory depression (rate 6/min), and reduced consciousness is the classic opioid toxidrome. Naloxone (0.4-2 mg IV, repeated every 2-3 minutes as needed) is the specific opioid antagonist and the correct first antidote. Atropine is for the cholinergic toxidrome, which also causes miosis but with bradycardia, bronchospasm, and secretions rather than pure respiratory depression. Flumazenil reverses benzodiazepines but can precipitate seizures in mixed overdose or BZD-dependent patients and should not be given empirically.

Miosis + respiratory depression + reduced GCS without bronchospasm, bradycardia, or fasciculations = opioid toxidrome. Naloxone is the specific antidote. Atropine targets the cholinergic toxidrome. Flumazenil can precipitate seizures if given empirically. NAC is for paracetamol toxicity.

Correct. Methanol is metabolised by alcohol dehydrogenase (ADH) to formaldehyde and then to formic acid (formate), which inhibits cytochrome c oxidase → optic nerve and basal ganglia toxicity. The treatment strategy is logical: (1) Block ADH with fomepizole (preferred, 15 mg/kg IV loading dose) or ethanol (if fomepizole unavailable) to stop further formate generation; (2) Folate to accelerate formate breakdown; (3) Haemodialysis to remove methanol and formate AND correct severe acidosis — indicated when pH <7.25, methanol level >50 mg/dL, or visual symptoms. Bicarbonate alone does not remove the toxin.

Methanol's toxicity comes from its metabolite formate, not methanol itself. Blocking ADH with fomepizole (or ethanol if fomepizole is unavailable) stops further formate production — this is the most critical intervention. Haemodialysis removes both methanol and formate. Bicarbonate treats acidosis symptomatically but does not remove the toxin.

Correct. Datura stramonium contains tropane alkaloids (scopolamine, hyoscyamine, atropine-like compounds) that BLOCK muscarinic acetylcholine receptors. The result is the anticholinergic toxidrome: dry flushed skin (anhidrosis), hyperthermia, tachycardia, mydriasis (dilated pupils), urinary retention, agitation, and delirium — remembered as 'Mad as a hatter, blind as a bat, red as a beet, hot as a hare, dry as a bone.' There is no specific antidote; physostigmine (a reversible AChE inhibitor) may be used in severe cases under specialist guidance.

Datura alkaloids BLOCK (not stimulate) muscarinic receptors — this produces the anticholinergic toxidrome: hot, dry, flushed, tachycardia, mydriasis, delirium, retention. AChE inhibition would produce the cholinergic toxidrome (opposite picture: miosis, bradycardia, secretions). Serotonin syndrome causes clonus and hyperreflexia, not urinary retention.

Correct. Inducing vomiting in corrosive poisoning is absolutely contraindicated and potentially fatal. Vomiting re-exposes the already-burned oesophagus and larynx to the corrosive, deepening the injury and risking complete airway obstruction from laryngeal oedema. Similarly, nasogastric tube insertion and activated charcoal are contraindicated. The appropriate actions are: IV fluid resuscitation, analgesia (opioids are appropriate), airway monitoring, and early endoscopic assessment to grade the burns (Zargar classification).

The most dangerous error in corrosive poisoning is inducing vomiting — this re-exposes the burned oesophagus to the corrosive and can cause complete airway obstruction. All standard GI decontamination manoeuvres (emesis, NG tube, activated charcoal) are absolutely contraindicated. Airway management, fluid resuscitation, and analgesia are the correct immediate steps.

Correct. The atropine titration endpoint in OP poisoning is DRY SECRETIONS: cessation of bronchorrhoea (the most dangerous feature — it causes drowning in secretions), clearing of wheeze, and drying of oral and airway secretions. This is NOT heart rate, NOT pupil size, NOT GCS. Tachycardia and dry skin are side effects of adequate atropinisation but are not the target endpoint. Under-dosing atropine (giving 0.6 mg and waiting) is the most common fatal error.

The atropine endpoint in OP poisoning is DRY SECRETIONS — the chest must be clear of wheeze and bronchorrhoea. Tachycardia is a side effect of adequate dosing, not the target. Pupils and GCS do not reliably guide atropine dosing. Pralidoxime (not atropine) addresses fasciculations by reactivating AChE.

Correct. Every poisoning case is a medico-legal case (MLC) in India. The doctor MUST inform the police when: the patient is brought in unconscious and cannot give history, when homicidal poisoning is suspected, or when the circumstances suggest an unnatural cause. This is a legal obligation under Section 176 of the BNSS 2023 (formerly CrPC 39) — failure to report is a criminal offence. The patient's consent is not required for mandatory police reporting; patient consent is needed only for MLC registration of a conscious patient who is the victim.

Police notification in poisoning is a legal obligation — not optional and not contingent on patient consent. The mandatory triggers are: unconscious patient, suspected homicide, unnatural cause. All poisoning cases are MLCs. The treating doctor who fails to report when required is liable under the criminal procedure code.