Paeds SAQs · acute-care-resuscitation-and-toxicology
Iron, salicylate and toxic alcohol poisoning — formative SAQs
Two MedVellum formative short-answer questions on the child who has ingested iron, salicylate or a toxic alcohol: reading the shared high-anion-gap metabolic acidosis and the poison-specific signature, giving the correct weight-based antidote (desferrioxamine for iron, urinary alkalinisation for salicylate, fomepizole for the toxic alcohols), decontaminating by poison, and avoiding the three lethal traps. 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 — A toddler with iron tablet ingestion
Question 1 — 10 formative marks; suggested time 15 minutes [1]
A 12 kg two-year-old girl is brought to the emergency department one hour after being found with an open bottle of her mother's ferrous sulphate 325 mg tablets. Eight tablets are missing. She has vomited twice, once with streaks of blood, and is pale and tachycardic. [1]
- Calculate the elemental-iron dose in mg per kg and state the severity category. (2 marks)
- Outline your immediate investigations and the timing of the serum iron level, including any modification for formulation. (3 marks)
- State the decontamination of choice and the antidote, with the dose, route and trigger. (3 marks)
- Six hours later the child looks comfortable and has stopped vomiting, but the venous gas shows a high-anion-gap metabolic acidosis. What is this phase, and why is discharge on clinical grounds dangerous? (2 marks) [1]
Full-credit answer — SAQ 1
Reveal full-credit answer for SAQ 1
1. Elemental-iron dose and severity
Ferrous sulphate 325 mg contains 65 mg elemental iron, so eight tablets equal 520 mg elemental. In a 12 kg child this is about 43 mg per kg of elemental iron. This is a SIGNIFICANT ingestion (over 40 mg per kg): emergency department assessment, serum iron, whole-bowel irrigation and consideration of intravenous desferrioxamine. The dose must be calculated from the elemental iron content, not the salt weight. [1] [2]
2. Investigations and timing
Take bloods BEFORE any antidote: serum iron, venous gas, electrolytes and anion gap, glucose, full blood count, coagulation, LFTs and renal function, plus a paracetamol and salicylate level to exclude co-ingestion. Draw the serum iron at 4 to 6 hours (the peak for immediate-release). For sustained-release or enteric-coated formulations, repeat the level at 8 to 12 hours because the peak is delayed. An abdominal X-ray may show radiopaque tablets and guide decontamination. [1]
3. Decontamination and antidote
The decontamination of choice is whole-bowel irrigation with polyethylene glycol via a nasogastric tube (20 to 40 mL per kg per hour, around 500 mL per hour in a young child) until the rectal effluent is clear and no tablets remain on a repeat X-ray. Activated charcoal is useless because iron is a metal and is not adsorbed. The antidote is intravenous desferrioxamine (deferoxamine) 15 mg per kg per hour, indicated for a serum iron over 500 microgram per dL, a high-anion-gap metabolic acidosis, shock, severe gastrointestinal symptoms or altered consciousness; the urine turns vin-rose as ferrioxamine is excreted. [1]
4. The latent phase
This is stage 2, the deceptive latent phase (6 to 24 hours). The child looks well precisely while absorbed iron is being sequestered by transferrin and is about to spill into tissues and trigger stage 3 systemic toxicity. Clinical appearance is a lie; only the serum iron and the acid-base status tell the truth. Discharge on clinical grounds in this window risks missing the transition to shock, hepatic failure and acidosis, which is why disposition must rest on the serum iron and the metabolic acidosis. [1]
SAQ 2 — An adolescent with a toxic-alcohol ingestion
Question 2 — 10 formative marks; suggested time 15 minutes [9]
A 15-year-old boy is brought from a rural community 14 hours after drinking illicitly distilled alcohol with friends. He is hyperventilating, confused, and reports blurred vision like a snowstorm. The venous gas shows pH 7.18 with a high anion gap and a low bicarbonate. The measured osmolal gap is elevated. The serum methanol level will take many hours to return. [9]
- What is the most likely diagnosis, and which two laboratory findings form the signature? (2 marks)
- State the immediate specific antidote, with the dose, route and timing rationale, and explain why you would not wait for the methanol level. (3 marks)
- List the metabolic cofactor and the role of sodium bicarbonate and haemodialysis. (3 marks)
- Explain why a normal osmolal gap measured later in the course would not exclude the diagnosis. (2 marks) [9]
Full-credit answer — SAQ 2
Reveal full-credit answer for SAQ 2
1. Diagnosis and signature
The most likely diagnosis is methanol poisoning. The signature is the high-anion-gap metabolic acidosis PLUS the elevated osmolal gap (the dual gap), together with the visual symptoms (snowstorm vision, optic disc changes) that are specific to formic acid toxicity. The history of illicit alcohol and the delayed onset (methanol has a latent period of 12 to 24 hours) support the diagnosis. [9] [10]
2. Antidote, dose and timing
Start intravenous fomepizole 15 mg per kg loading over 30 minutes IMMEDIATELY on suspicion, followed by 10 mg per kg every 12 hours for four doses and then 15 mg per kg every 12 hours. I would NOT wait for the methanol level because the entire clinical syndrome is downstream of a single enzyme, alcohol dehydrogenase: blocking it prevents all conversion of methanol to formic acid, and every hour of delay converts more parent alcohol into toxic metabolite. The level confirms the diagnosis and guides duration of therapy; it does not decide whether to treat. [9]
3. Cofactor, bicarbonate and dialysis
Give folinic acid (leucovorin) 1 mg per kg intravenously (up to 50 mg) every 4 to 6 hours, because folate-dependent metabolism speeds formate clearance. Give intravenous sodium bicarbonate to target a serum pH over 7.20 to 7.30; in methanol this also traps formate in its anionic form and speeds renal clearance. Arrange haemodialysis for a methanol level over 50 mg per dL, severe or worsening acidosis, visual symptoms, renal failure or significant electrolyte disturbance; continue fomepizole through and after dialysis because fomepizole is dialysable (give every 4 hours during dialysis). [9] [10]
4. The falling osmolal gap
The osmolal gap is high early because the unmetabolised parent methanol is osmotically active. As alcohol dehydrogenase converts methanol to formic acid, the parent disappears (the osmolal gap falls) and the organic acid accumulates (the anion gap rises). The two gaps are inversely related over time, so a single late measurement can show a normal osmolal gap with a high anion gap. A normal osmolal gap late does NOT exclude methanol poisoning; treat on the clinical picture and the anion gap. [10]
References
- [1]Chang, Timothy P; Rangan, Cyrus Iron poisoning: a literature-based review of epidemiology, diagnosis, and management Pediatric Emergency Care, 2011.PMID 21975503
- [2]Manoguerra, Anthony S; Erdman, Andrew R; Booze, Laura L; Christianson, George; Wax, Paul M; Scharman, Elizabeth J; Woolf, Alan D; Keyes, Daniel C; Olson, Kent R; Chyka, Peter; Caravati, E Martin; Troutman, William G Iron ingestion: an evidence-based consensus guideline for out-of-hospital management Clinical Toxicology, 2005.PMID 16255338
- [6]Snodgrass, Wirt Salicylate toxicity Pediatric Clinics of North America, 1986.PMID 3960612
- [7]Juurlink, David N; Gosselin, Sophie; Kielstein, Jan T; Ghannoum, Marc; Lavergne, Valerie; Nolin, Thomas D; Hoffman, Robert S; EXTRIP Workgroup Extracorporeal treatment for salicylate poisoning: systematic review and recommendations from the EXTRIP workgroup Annals of Emergency Medicine, 2015.PMID 25986310
- [9]Brent, Jeffrey Fomepizole for ethylene glycol and methanol poisoning New England Journal of Medicine, 2009.PMID 19458366
- [10]Kraut, Jeffrey A; Xing, Xuejing Toxic Alcohols New England Journal of Medicine, 2018.PMID 29342392