IM22.1-13 | Poisoning — Graded Quiz

Correct. This is severe OP poisoning. After airway/O2, both antidotes are given concurrently. Atropine: start at 1.8-3 mg IV (NOT 0.6 mg — that is under-dosing) and double the dose every 5-10 minutes until secretions dry. The target is DRY SECRETIONS (clear chest), not tachycardia or mydriasis. Pralidoxime reactivates AChE before ageing occurs (within the first 24-48 hours for most OPs) and is most effective when given early. Naloxone does not treat cholinergic toxidrome. Benzodiazepines may be used for seizures but are not first-line.

Severe OP poisoning requires aggressive atropinisation — starting at 1.8-3 mg IV and titrating to dry secretions, NOT the 0.6 mg dose that is routinely under-used. Pralidoxime should be started simultaneously. Delay in atropine from waiting for SpO2 improvement is dangerous — atropine dries the bronchorrhoea that is causing the hypoxia.

Correct. Paracetamol is metabolised via CYP2E1 to NAPQI; in overdose, glutathione stores are depleted and NAPQI covalently binds hepatocyte proteins — causing centrilobular necrosis. This process is time-dependent and clinically silent for 24 hours. NAC provides cysteine substrate to replenish glutathione, detoxifying NAPQI BEFORE necrosis is established. The Rumack-Matthew nomogram predicts which patients will develop hepatotoxicity — patients above the treatment line must receive NAC whether or not they have symptoms. Waiting for transaminase rise means waiting until the preventable window has closed.

NAC works by replenishing glutathione to neutralise NAPQI before it causes hepatocyte necrosis. The damage is biochemically progressing while the patient is symptom-free. The nomogram identifies those at risk — treatment before injury is the entire logic of NAC therapy. Starting NAC after transaminase rise means the preventable window has passed.

Correct. When fomepizole is unavailable, ethanol is the alternative ADH inhibitor — ethanol has higher affinity for ADH than methanol, competitively preventing methanol's conversion to formaldehyde and formate. Oral/NG ethanol is used to achieve a serum level of 100-150 mg/dL. However, with pH 7.08, severe acidosis, anuria, and likely high methanol/formate levels, haemodialysis is also mandatory — it removes both methanol and formate, corrects acidosis, and treats acute kidney injury. Folic acid accelerates formate breakdown but is an adjunct, not primary therapy. NAC is not indicated for methanol.

When fomepizole is unavailable, ethanol (nasogastric or IV) is the alternative ADH inhibitor, titrated to a serum level of 100-150 mg/dL. In severe poisoning with pH <7.25, anuria, or visual symptoms, haemodialysis is mandatory to remove methanol and formate. Bicarbonate alone does not remove the toxin.

Correct. Aluminium phosphide management requires knowing what NOT to do. Activated charcoal does not adsorb phosphine gas. NG tube insertion triggers vomiting, and phosphine gas in vomitus can be inhaled by healthcare workers in the room — a real occupational hazard. Gastric lavage is dangerous (volatilises more gas) and ineffective once phosphine has been absorbed. Atropine is not the antidote — there is no antidote. Supportive care with vasopressors (noradrenaline/adrenaline for cardiovascular collapse), magnesium sulphate (as an adjuvant for its antioxidant effect, not as a cathartic), and intensive monitoring is the only option.

In AlP poisoning: no NG tube (phosphine in vomitus is a healthcare worker hazard), no activated charcoal (ineffective), no gastric lavage (dangerous). There is no antidote. Management is supportive — vasopressors for cardiovascular collapse, arrhythmia management. The family should be counselled honestly about the grave prognosis.

Correct. Intermediate syndrome (IMS) is a well-recognised delayed complication of OP poisoning occurring 24 hours to 18 days after the acute cholinergic crisis (typically days 1-4 of apparent recovery). It is characterised by: proximal limb weakness, neck flexion weakness (cranial nerve involvement), and potentially respiratory failure requiring re-intubation. It is NOT a recurrence of the cholinergic toxidrome. The mechanism is incompletely understood but relates to prolonged AChE inhibition at the neuromuscular junction. OPIDP occurs weeks to months later (delayed neuropathy). GBS can mimic IMS but context here is clear.

Intermediate syndrome is the specific OP complication presenting 1-18 days after the acute crisis — proximal weakness, neck flexion weakness, and respiratory compromise. It is not a recurrence of cholinergic features. OPIDP is a separate, later complication (weeks-months) causing sensorimotor peripheral neuropathy. ICU patients may develop GBS but the OP poisoning context makes IMS the primary diagnosis.

Correct. Nerium oleander contains oleandrin and neriine — cardiac glycosides that inhibit the Na+/K+-ATPase pump. This leads to intracellular sodium accumulation → Na+/Ca2+ exchanger reversal → intracellular calcium overload → increased automaticity and impaired conduction. The result is virtually identical to digoxin toxicity: bradycardia, AV block, ventricular arrhythmias, and hyperkalaemia. In India, Cerbera manghas (sea mango), Thevetia peruviana (yellow oleander), and Nerium oleander are the major cardiac glycoside plant poisons. Management: digoxin-specific antibody fragments (Fab) can cross-react with plant cardiac glycosides in severe cases; otherwise supportive.

Oleandrin is a cardiac glycoside that inhibits Na+/K+-ATPase — the same mechanism as digoxin. The consequence is intracellular calcium overload causing bradyarrhythmias, AV block, and ventricular arrhythmias. This is NOT beta-blockade or anticholinergic toxicity. Digoxin-specific Fab fragments have been used in severe cases.

Correct. The medico-legal report for poisoning is a factual clinical document. It must include: MLC registration number, date/time of examination, history as given (noting who gave it), clinical findings (level of consciousness, vital signs, specific examination findings), investigations ordered and results, treatment given. Crucially, the physician must NOT opine on suicidal vs homicidal intent — that determination is for the magistrate/court. Unknown quantities should be recorded as 'not known' rather than estimated. Psychiatric diagnosis, while important for management, is a separate clinical document.

The MLR is a factual record, not an opinion document. Record clinical findings, investigations, and treatment. Do NOT opine on suicidal vs homicidal intent — that is for the court. Do NOT estimate unknown quantities. A psychiatric diagnosis is a clinical concern, not an MLR requirement.

Correct. Ethylene glycol is metabolised to glycolic acid and then to oxalic acid (oxalate) via ADH. Oxalate precipitates with calcium in renal tubules as calcium oxalate crystals → acute tubular necrosis and AKI. Optic nerve toxicity and basal ganglia damage are features of methanol (formate), NOT ethylene glycol. Treatment: (1) Fomepizole blocks ADH — stops further oxalate generation; (2) Thiamine and pyridoxine as adjuvants to divert glyoxylate away from oxalate; (3) Haemodialysis is mandatory in AKI, metabolic acidosis pH <7.25, or high ethylene glycol levels. IV calcium may be needed for symptomatic hypocalcaemia but does not treat the primary toxicity.

Ethylene glycol's toxic metabolite is oxalate (not formate — that is methanol). Oxalate crystallises in renal tubules causing AKI. The hallmarks: calcium oxalate crystals in urine, oliguric AKI, high osmolar gap then high anion gap as metabolism proceeds. Fomepizole blocks further oxalate production; haemodialysis treats AKI and removes the toxin.

Correct. Remote telephone advice for corrosive ingestion: NEVER induce vomiting (re-exposes burned mucosa, risk of airway obstruction), NEVER give milk or attempt neutralisation, NEVER pass anything into the throat. Wipe around the mouth. If the child is fully alert and there is no stridor, small sips of water to dilute may be acceptable per some guidelines. The priority is immediate transfer to the nearest emergency facility with resuscitation capability for airway assessment and endoscopy planning. Contacting the National Poison Centre (1800-116-117) for additional guidance is appropriate.

Corrosive poisoning: the only emergency first-aid instruction is DO NOT INDUCE VOMITING. Everything else — milk, charcoal, finger in throat — is either useless or harmful. Wipe the mouth, do not give anything unless the child is fully conscious and you are advised by a poison centre, and seek emergency care immediately.

Correct. Every deliberate self-harm (DSH) case — irrespective of current suicidal ideation — requires mandatory psychiatric consultation before discharge. The treating physician must not assess suicidal risk independently. The psychiatric team will assess: intent, access to means, protective factors, mental illness, and social context; formulate a safety plan; and determine the appropriate level of care (inpatient psychiatric admission vs outpatient follow-up). Denial of current suicidal ideation in the immediate aftermath is unreliable and does not reduce the risk. The absence of suicidal ideation on the day of discharge does not eliminate risk.

All deliberate self-harm admissions require psychiatric consultation before discharge — this is mandatory, not optional. The denial of current ideation in the immediate post-medical period is unreliable. The psychiatrist assesses risk, mental illness, safety plan, and disposition. Discharging a DSH patient without psychiatric clearance is a clinical and medico-legal risk.

Correct. Family counselling in aluminium phosphide poisoning is one of the most difficult conversations in emergency medicine. The key principles are: honesty (the prognosis is genuinely grave — case fatality can exceed 60-90% in severe poisoning), empathy (acknowledge distress), transparency about the limits of medicine (no antidote), and explaining active supportive measures the team is taking. Withholding prognostic information denies families the ability to prepare. Quoting statistics without emotional support is harmful. Restricting information to one family member by gender is inconsistent with patient-centred care. Police involvement is appropriate for MLC registration, not family counselling.

Family counselling in grave poisoning requires honest prognostic disclosure combined with empathy and support. Withholding the prognosis denies informed decision-making. Quoting statistics without support is cold and unhelpful. The goal is honest, kind communication that explains what is being done and allows the family to prepare.