PE14.1-3 | Childhood Poisoning — Practice Quiz

Correct. For kerosene ingestion, supportive care is the mainstay. Emesis and lavage are contraindicated because of the high aspiration risk — the volatile hydrocarbon causes severe aspiration pneumonitis far more dangerous than the swallowed dose. Activated charcoal does not adsorb hydrocarbons effectively.

In kerosene and other hydrocarbon ingestions, emesis and gastric lavage are CONTRAINDICATED due to aspiration pneumonitis risk. Activated charcoal is also ineffective. Supportive care, O2, and close respiratory monitoring are the standard of care.

Both emesis induction and gastric lavage are contraindicated in kerosene/hydrocarbon ingestion because they dramatically increase aspiration risk, causing aspiration pneumonitis — a complication far more dangerous than GI absorption. Activated charcoal is ineffective for hydrocarbons. Supportive care, oxygen monitoring, and observation are the correct approach.

Correct. Radiological changes in kerosene aspiration pneumonitis characteristically lag 4–6 hours (sometimes longer) behind clinical symptoms. A normal early CXR does not exclude aspiration; the child must be observed with serial clinical monitoring and repeat imaging if required.

Chest X-ray changes in hydrocarbon/kerosene aspiration pneumonitis may lag 4–6 hours behind symptom onset. Never discharge a symptomatic child on the basis of a normal early CXR; clinical reassessment and serial monitoring are mandatory.

A normal chest X-ray in the first few hours does NOT exclude aspiration pneumonitis from kerosene. Radiological changes typically lag 4–6 hours or more after aspiration. Clinical signs — tachypnoea, cough, fever — take precedence.

Correct. Atropine is the first-line antidote for organophosphorus (OP) poisoning. It blocks muscarinic acetylcholine receptors, countering the SLUDGE syndrome (Salivation, Lacrimation, Urination, Defaecation, GI upset, Emesis). The endpoint of atropinisation is drying of secretions (not tachycardia). Pralidoxime should follow but only after adequate atropinisation.

In organophosphorus poisoning, the sequence is: ATROPINE first (0.05 mg/kg IV; endpoint = secretion dryness) then PRALIDOXIME within 24–48 hours. The SLUDGE syndrome reflects muscarinic excess; atropine reverses it. Pralidoxime reactivates cholinesterase but is ineffective after ageing.

Atropine is always the FIRST antidote in OP poisoning — it is life-saving by counteracting the life-threatening muscarinic excess (bronchospasm, hypersecretion). Pralidoxime is important but is the SECOND agent. Diazepam addresses seizures but not the primary poisoning mechanism.

Correct. The clinical endpoint of atropinisation in OP poisoning is the DRYING of bronchial secretions and salivation. Heart rate and pupil size are unreliable endpoints. Tachycardia may reflect hypoxia or volume depletion, and pupils may not fully dilate despite adequate atropinisation. Secretion dryness indicates sufficient muscarinic blockade to protect the airway.

The endpoint of atropine therapy in OP poisoning is DRYING OF SECRETIONS (bronchorrhoea, salivation). Do not target heart rate or pupil size. Adequate atropinisation protects the airway from flooding with secretions, which is the most common cause of death in OP poisoning.

The correct endpoint for atropine therapy in OP poisoning is SECRETION DRYNESS — dry mouth, dry tracheal secretions. Targeting a heart rate or pupil size is incorrect and can lead to over- or under-atropinisation. Blood pressure normalisation is not an endpoint of atropine therapy.

Correct. Pralidoxime (PAM) reactivates inhibited acetylcholinesterase — but only before the enzyme–OP complex undergoes 'ageing' (irreversible phosphorylation). Ageing occurs within 24–48 hours depending on the OP compound. At 36 hours, ageing is likely well advanced, rendering PAM clinically ineffective or potentially harmful. Atropine (for muscarinic symptoms) remains the principal treatment.

Pralidoxime (PAM) must be given within 24–48 hours of OP exposure, before the cholinesterase–OP complex undergoes irreversible ageing. After this window, PAM is ineffective. Atropine for muscarinic blockade remains effective at any time post-exposure.

PAM is ineffective after the cholinesterase-ageing window of 24–48 hours. Beyond this point, the OP-enzyme complex is irreversible. PAM and atropine are used together — they are NOT contraindicated with each other. Atropine is always the first-line agent regardless of timing.

Correct. The ingested dose is 15 tablets × 500 mg = 7,500 mg in a 15 kg child = 500 mg/kg — far exceeding the toxic threshold of 150 mg/kg. The Rumack-Matthew nomogram requires a serum paracetamol level obtained AT LEAST 4 hours after ingestion (earlier levels are unreliable for predicting toxicity). This level then guides NAC initiation.

Paracetamol toxic dose in children = >150 mg/kg. Rumack-Matthew nomogram requires a serum level at ≥4 hours post-ingestion. N-acetylcysteine (NAC) is the antidote. Asymptomatic presentation at 2 hours is typical — toxicity (hepatic injury) manifests 24–72 hours later. Never wait for symptoms to appear before acting.

The toxic threshold for paracetamol in children is 150 mg/kg. The ingested dose (7,500 mg ÷ 15 kg = 500 mg/kg) far exceeds this. The standard protocol is to obtain a serum paracetamol level at 4 hours post-ingestion and plot on the Rumack-Matthew nomogram. Levels before 4 hours are not interpretable on the nomogram.

Correct. Paracetamol overdose depletes hepatic glutathione; the toxic metabolite NAPQI then accumulates and covalently binds to hepatocytes, causing liver necrosis. NAC replenishes glutathione stores (acting as a precursor) and directly conjugates with NAPQI, detoxifying it. This is why NAC is most effective when given early (within 8–10 hours of ingestion).

NAC prevents paracetamol hepatotoxicity by replenishing hepatic glutathione and directly conjugating NAPQI. It is most effective within 8–10 hours of ingestion and remains indicated (though less effective) up to 24 hours. Weight-based IV protocol: 150 mg/kg loading dose over 1 hour, then maintenance infusions.

NAC works by replenishing depleted glutathione stores. Glutathione normally conjugates NAPQI (the hepatotoxic metabolite of paracetamol). When glutathione is exhausted, NAPQI binds hepatocytes causing necrosis. NAC provides the cysteine backbone for glutathione synthesis and can also directly bind NAPQI.

Correct. A paracetamol level above the Rumack-Matthew treatment line at ≥4 hours post-ingestion is the indication for NAC therapy. Immediate initiation reduces hepatotoxicity risk significantly. Delaying for repeat levels or waiting for symptoms allows NAPQI to accumulate and glutathione to deplete.

The Rumack-Matthew nomogram: if the 4-hour (or later) serum paracetamol level plots ABOVE the treatment line, start NAC IMMEDIATELY. The nomogram is only valid for ≥4 hours post-ingestion. Early NAC (within 8 hours) is highly effective at preventing hepatic failure.

A level ABOVE the Rumack-Matthew treatment line at ≥4 hours post-ingestion is a clear indication for immediate NAC therapy. Waiting for symptoms, delaying for repeat levels, or discharging is dangerous. Hepatic injury from paracetamol develops 24–72 hours later — by then the treatment window is narrowing.

Correct. This child has aspiration pneumonitis from kerosene — the most feared complication. With SpO2 86%, immediate oxygen supplementation is the priority. If there is progressive respiratory failure, intubation and mechanical ventilation may be required. Gastric lavage and activated charcoal are both contraindicated. Bronchoscopy is not standard management for liquid hydrocarbon aspiration.

Aspiration pneumonitis is the life-threatening complication of kerosene ingestion. Management = supportive oxygen therapy, respiratory monitoring, and escalation to ventilation if needed. ALL decontamination procedures (lavage, emesis, activated charcoal) are contraindicated. Antibiotics are given only if secondary bacterial pneumonia develops.

This child has established aspiration pneumonitis (hypoxia, respiratory distress). The priority is AIRWAY and OXYGENATION — supplemental O2 first, consider escalation to ventilatory support. Gastric lavage, emesis, and activated charcoal are all contraindicated in kerosene ingestion. Bronchoscopy is not indicated.

Correct. Seizures in OP poisoning are driven by nicotinic receptor and central acetylcholine excess. Benzodiazepines (diazepam or lorazepam) are the first-line agents for OP-induced seizures due to their GABAergic mechanism which counteracts the hyperexcitability. Phenobarbitone is a second-line option if benzodiazepines fail. Atropine does not control nicotinic/CNS seizures.

Seizures in OP poisoning are treated with benzodiazepines (diazepam or lorazepam) first-line. Atropine controls the muscarinic (SLUDGE) features but not seizures. Phenobarbitone is second-line. Aggressive seizure control is essential to prevent secondary brain injury.

Benzodiazepines are the first-line treatment for seizures in OP poisoning. Atropine controls muscarinic symptoms but NOT nicotinic or CNS-driven seizures. Phenobarbitone is second-line. Magnesium sulphate has no role in OP-induced seizures.