Paeds Vivas · acute-care-resuscitation-and-toxicology
Iron, salicylate and toxic alcohol poisoning — branching viva
A branching viva following one adolescent who presents with a high-anion-gap metabolic acidosis after a deliberate overdose, through the recognition of the poison-specific signature, the choice of decontamination, the weight-based antidote (desferrioxamine, urinary alkalinisation or fomepizole), the avoidance of the three lethal traps, and the escalation to dialysis and retrieval.
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Target exams
Branching cross-examination
This is a MedVellum formative viva. It is not an official RACP, MRCPCH, ABP, ACGME or RCPSC station, mark scheme, duration or pass standard. Release each update only after the candidate states the failing system, the immediate action and the reassessment endpoint. [1] [9]
Candidate brief
You are the senior paediatric clinician in a rural district emergency department. Speak as you would during resuscitation. Recognise the shared high-anion-gap acidosis and read the poison-specific signature; give the weight-based antidote on its trigger; decontaminate by poison; avoid the three lethal traps; and escalate to dialysis and retrieval before local support is exceeded. This is one continuous case. Each escalation branch leads to the next update. [9]
Question 1 — The doorway and the shared metabolic picture
Stimulus update. A 14-year-old is brought by ambulance after a deliberate overdose. He took a handful of his mother's iron tablets, several aspirin tablets, and a mouthful of windscreen washer fluid about four hours ago. He is drowsy, tachypnoeic with deep sighing respirations, and has vomited once with streaks of blood. The venous gas shows pH 7.22 with a high anion gap and a low bicarbonate. Question: What do you say and do now? [1] [9]
Consultant-level model answer. "I am immediately concerned. This child has a high-anion-gap metabolic acidosis from a mixed overdose of three poisons that share the same metabolic lesion. I call the senior paediatric, resuscitation and poisons-centre teams now, name a leader, allocate roles, and bring weight-appropriate equipment and monitoring. I run ABCDE treating threats as they are found: high-flow oxygen, IV or IO access, isotonic crystalloid with dextrose in aliquots, bedside glucose, and bloods BEFORE antidote (iron, salicylate, paracetamol, osmolality, electrolytes, anion gap, gas, coagulation, LFTs and renal function). I will read the poison-specific signature out of the shared acidosis and give each antidote on its trigger." [1] [9]
Probing follow-up. "Why draw bloods before the antidote?" A strong answer is: "Desferrioxamine and fomepizole alter the assays, and the iron, salicylate and osmolal-gap results drive the antidote and dialysis decisions, so they must be drawn before the antidote is given." [1]
Common weak answer. "I will take a full history, examine the child, and order a chest X-ray." This delays resuscitation for diagnostic completeness in a child with a dangerous metabolic acidosis, and it inverts the order. [1] [9]
Escalation branch. If the candidate recognises the shared lesion and starts resuscitation, release the poison-specific data in Question 2. If they anchor on one poison, ask which antidotes each of the three poisons needs. [9]
Question 2 — Reading the poison-specific signature
Stimulus update. The serum salicylate is 580 mg per L, the capillary glucose is 3.0 mmol per L, the serum iron is pending, the measured osmolal gap is 28 mOsm per kg, and the serum ethanol is zero. Tinnitus is present on questioning. The methanol and ethylene glycol levels will take hours. Question: What is the signature of each poison, and what do you do about each, right now? [6] [9]
Consultant-level model answer. "The salicylate is confirmed by the mixed respiratory alkalosis with tinnitus: I start urinary alkalinisation with intravenous sodium bicarbonate to a urine pH of 7.5 to 8.0, I correct the potassium to over 4 mmol per L so alkalinisation works, and I give dextrose for cerebral hypoglycaemia despite the near-normal plasma glucose. The iron is still pending; with haematemesis and acidosis I will start intravenous desferrioxamine 15 mg per kg per hour once the level returns or if acidosis or shock worsens, and I begin whole-bowel irrigation because charcoal is useless for iron. The toxic alcohol is signalled by the elevated osmolal gap with the high anion gap; I start intravenous fomepizole 15 mg per kg loading NOW, on suspicion, without waiting for the methanol or ethylene glycol level." [6] [7] [9]
Probing follow-up. "Why fomepizole and not ethanol?" A strong answer is: "Fomepizole is preferred over ethanol in children because it has no CNS depressant effect, no hypoglycaemia, and no intensive monitoring burden; ethanol causes CNS depression and hypoglycaemia in children and is second line only where fomepizole is unavailable." [9]
Common weak answer. "I will wait for the methanol level before deciding on fomepizole." This is the classic lethal trap: every hour of delay converts more parent alcohol into toxic metabolite. Start fomepizole on suspicion. [9]
Escalation branch. If the candidate starts all three antidotes on their triggers, release the deterioration in Question 3. If they wait for levels, ask what happens to the retina and the kidney while they wait. [9] [10]
Question 3 — The lethal traps
Stimulus update. The child becomes more tachypnoeic and drowsier, with a rising PaCO2 and a falling pH. The team suggests intubation to protect the airway. Question: What is the danger of intubation here, and how do you do it safely if it is unavoidable? [6]
Consultant-level model answer. "Intubation is the deadliest intervention in salicylate toxicity. This child is keeping himself alive by hyperventilating: the low PaCO2 is the only thing holding his pH near normal and his salicylate out of the brain. Sedation, paralysis and a normally-set ventilator let PaCO2 rise, pH fall, salicylate shift into the central nervous system, and he can crash within minutes. If intubation is unavoidable, I give a bicarbonate bolus and optimise the pH first, pre-oxygenase, use rapid sequence, and set the ventilator to a respiratory rate of 20 to 30 with the minute ventilation matched to his pre-intubation hypocapnia. I also have haemodialysis ready, because the acidosis will worsen." [6] [7]
Probing follow-up. "What about the iron latent phase in this same child?" A strong answer is: "The same child may also look better in a few hours as iron is sequestered by transferrin, and that improvement is deceptive; I will not be reassured by clinical appearance and will keep the desferrioxamine running until the iron is falling and the acidosis has resolved." [1]
Common weak answer. "I will intubate at a standard rate and recheck the gas in an hour." This removes the compensatory hyperventilation and the child arrests. [6]
Escalation branch. If the candidate navigates the intubation and the latent-phase traps, move to Question 4 on dialysis and retrieval. [7]
Question 4 — Dialysis, retrieval and disposition
Stimulus update. The salicylate is now 720 mg per L, the methanol level returns at 60 mg per dL, and the child has acute kidney injury. The rural hospital has no paediatric dialysis circuit and no intensive care. Question: What are your dialysis indications, your cofactor plan, and your retrieval plan? [7] [9]
Consultant-level model answer. "The dialysis indications are met for both salicylate (level over 700 mg per L, plus CNS signs and renal failure) and the toxic alcohol (methanol over 50 mg per dL with severe acidosis and renal failure). I continue fomepizole through and after dialysis, giving it every 4 hours during the run because it is dialysable, and I continue folinic acid 1 mg per kg every 4 to 6 hours. I continue salicylate alkalinisation and recheck the level every 2 to 4 hours for at least 12 to 24 hours after dialysis for rebound. I called retrieval in parallel with resuscitation, before local support was exceeded; I agree the paediatric dialysis destination, the treatment to continue en route, the escort and equipment, the expected deterioration, and the contingency if transfer is delayed." [7] [9] [10]
Probing follow-up. "What is the one principle you most want the team to carry forward?" A strong answer is: "Recognise the shared high-anion-gap acidosis, read the poison-specific signature, give each weight-based antidote on its trigger, decontaminate by poison, and never fall for the three lethal traps of latent-phase reassurance, salicylate intubation without hypocapnia, or waiting for toxic-alcohol levels before fomepizole." [1] [9]
Common weak answer. "I will wait for the retrieval team to arrive before arranging dialysis." Dialysis and retrieval must be arranged in parallel; the child needs ongoing resuscitation, antidote and a contingency for deterioration during the wait. [7] [9]
[1] [6] [7] [9] [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
- [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