Paeds SAQs · clinical-pharmacology-and-therapeutics
Poisoning antidotes and toxicology pharmacology — formative SAQs
Two MedVellum formative short-answer questions on poisoning antidotes and toxicology pharmacology in children: defending the N-acetylcysteine regimen and timing in paracetamol poisoning, and choosing and dosing the correct antidote across opioid, iron, lead, and snake-envenomation scenarios by mechanism and weight. The marks and timing support transparent self-assessment. They are not an official board format or pass standard.
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Target exams
SAQ 1 — N-acetylcysteine for paracetamol poisoning
Question 1 — 10 formative marks; suggested time 15 minutes [1]
A previously well three-year-old, 14-kilogram girl is brought in six hours after her mother found her with an open bottle of adult paracetamol tablets. The exact number ingested and the precise time are uncertain. She is clinically well. The team asks whether a paracetamol level should guide treatment and whether N-acetylcysteine is indicated. [1] [2]
- Explain the pharmacological mechanism by which an overdose of paracetamol causes hepatotoxicity, and how N-acetylcysteine prevents it. (3 marks)
- State the full intravenous N-acetylcysteine dosing regimen by weight for this child, and the circumstances under which you would start it regardless of a level. (4 marks)
- Describe the commonest adverse reaction to N-acetylcysteine and how you would manage it without abandoning the antidote. (3 marks)
Full-credit answer — SAQ 1
Reveal full-credit answer for SAQ 1
1. Mechanism of hepatotoxicity and how NAC prevents it
At therapeutic doses paracetamol is cleared by glucuronidation and sulfation, with only a small fraction metabolised by cytochrome P450 2E1 into the reactive intermediate NAPQI, which is immediately detoxified by glutathione. After an overdose the conjugation pathways saturate, more paracetamol is shunted into the P450 pathway, NAPQI accumulates, glutathione is depleted, and free NAPQI binds hepatocyte proteins and causes centrilobular necrosis. N-acetylcysteine works by replenishing glutathione and supplying sulfhydryl groups that directly detoxify NAPQI — but only while the hepatocyte is still salvageable, which is why timing governs its use. [1] [2]
2. The IV regimen and when to start regardless of level
For a 14-kilogram child the intravenous N-acetylcysteine regimen is 150 mg per kilogram over one hour (about 2.1 g), then 50 mg per kilogram over four hours (about 0.7 g), then 100 mg per kilogram over sixteen hours (about 1.4 g) — a 21-hour total course. I would start it regardless of the level whenever the ingestion is staggered or timed-unknown (as here, where the time and number are uncertain), for sustained-release preparations, or when there is any evidence of hepatotoxicity, because the Rumack-Matthew nomogram cannot be applied in those situations and the default is to treat. A level at four hours or later plotted against a known time selects treatment when on or above the line. [1]
3. The commonest adverse reaction and its management
The commonest adverse reaction is an anaphylactoid reaction — rash, flushing, urticaria, and occasionally bronchospasm — which is rate-related rather than a true IgE allergy. I would manage it by pausing or slowing the infusion and treating the symptoms with an antihistamine, and then resuming the N-acetylcysteine at a slower rate, because the reaction is rarely a reason to abandon a life-saving course. In a small child I would also adjust the diluent volume to avoid fluid overload from the large weight-based dose. [1] [2]
SAQ 2 — Choosing and dosing the antidote across scenarios
Question 2 — 10 formative marks; suggested time 15 minutes [3]
You are the registrar covering the emergency department. Four children arrive over the shift: an adolescent unconscious from an opioid overdose with pin-point pupils and a respiratory rate of six; a toddler who has taken adult iron tablets with vomiting and a metabolic acidosis; a school-age child with a blood lead level of 70 microgram per decilitre and abdominal pain; and a country child bitten by a brown snake with evolving coagulopathy. [3] [8]
- For the opioid-overdose adolescent, give the antidote, the weight-based dose, the route, and the principle of titration. Explain why you would observe for renarcotisation. (3 marks)
- For the iron-toxic toddler and the lead-exposed child, name each antidote, its mechanism class, and the key dosing or threshold point, including the caveat from the TLC trial. (4 marks)
- For the snake-envenomated child, defend why antivenom is given early and intravenously, and how you would prepare for its adverse effects. (3 marks)
Full-credit answer — SAQ 2
Reveal full-credit answer for SAQ 2
1. Opioid overdose — naloxone
The antidote is naloxone, a competitive mu-opioid receptor antagonist (receptor antagonist class). I would give 10 microgram per kilogram intravenously, repeated every two to three minutes until the respiratory effort recovers, titrated to respiratory rate and arousability, not to full consciousness, because a large bolus precipitates acute withdrawal, severe pain, and agitation. If intravenous access is delayed, intramuscular or intranasal naloxone is rapidly absorbed. I would observe for renarcotisation because naloxone has a half-life of only about 30 to 80 minutes — shorter than most opioids — so the child can re-sedate as the naloxone wears off, and a naloxone infusion may be needed for a long-acting opioid. [3] [4]
2. Iron and lead — the chelators
For the iron-toxic toddler the antidote is deferoxamine, a binding-agent chelator that wraps free ferric iron to form the water-soluble ferrioxamine excreted in the urine (vin-rose). I would give 15 mg per kilogram per hour intravenously, continued until the child is stable and the acidosis resolves, titrated to avoid hypotension. For the lead-exposed child with a level of 70 microgram per decilitre and symptoms, I would use intravenous calcium-disodium EDTA for severe poisoning, with oral succimer reserved for moderate poisoning. The crucial caveat is the TLC trial (Rogan, NEJM 2001): succimer lowered blood lead levels but did not improve neuropsychological outcome at low-to-moderate exposure, so chelation is reserved for higher levels or symptomatic disease, and environmental abatement is emphasised alongside pharmacological chelation. [8] [10] [11]
3. Snake envenomation — early intravenous antivenom
Antivenom is antibody therapy that binds and neutralises circulating venom so it can no longer reach its target tissue. I would give it early and intravenously for systemic envenomation because it does not reverse tissue injury already inflicted — coagulopathy, neurotoxicity, and myotoxicity are best prevented by neutralising the venom before damage is established. The dose is species-specific, guided by venom detection or regional expert advice. Because antivenom can cause an anaphylactoid reaction and serum sickness, I would give it where resuscitation facilities are available, with adrenaline drawn up, and observe the child afterwards for recurrence and for delayed serum sickness. Pre-medication is controversial and not routine. [6]
References
- [1]Dart, Richard C; Mullins, Michael E; Matoushek, Tomas; et al Management of Acetaminophen Poisoning in the US and Canada: A Consensus Statement JAMA Network Open, 2023.PMID 37552484
- [2]Chiew, Angela L; Gluud, Christian; Brok, Joergen; Buckley, Nicholas A Interventions for paracetamol (acetaminophen) overdose Cochrane Database of Systematic Reviews, 2018.PMID 29473717
- [3]Boyer, Edward W Management of opioid analgesic overdose New England Journal of Medicine, 2012.PMID 22784117
- [4]Malmros Olsson, Elisabet; Lonnqvist, Per-Arne; Stiller, Cari O; et al Rapid systemic uptake of naloxone after intranasal administration in children Paediatric Anaesthesia, 2021.PMID 33687794
- [6]Isbister, Geoffrey K; Jenkins, Sarah; Downes, Margaret A; et al Randomised controlled trial and prospective cohort investigating antivenom for red-bellied black snake envenomation Clinical Toxicology, 2024.PMID 38913734
- [8]Fine, Jerri S Iron poisoning Current Problems in Pediatrics, 2000.PMID 10742921
- [10]Bradberry, Sally; Vale, Allister Dimercaptosuccinic acid (succimer; DMSA) in inorganic lead poisoning Clinical Toxicology, 2009.PMID 19663612
- [11]Rogan, Walter J; Dietrich, Kim N; Ware, John H; et al Effect of chelation therapy with succimer on neuropsychological development in children exposed to lead New England Journal of Medicine, 2001.PMID 11346806