Poisoning — Written Clinical Reasoning

SAQ 1 — Mixed Overdose: Systematic Approach and Integrated Management (20 marks, 30 minutes)

Prompt: Construct a problem list, identify the toxidrome(s), make the decontamination and antidote decisions with justification, and outline an integrated management plan. [1]

Model Answer

Toxidrome identification (2 marks): [1]

The picture is dominated by an anticholinergic toxidrome from the amitriptyline — dilated pupils, dry flushed skin, absent bowel sounds, tachycardia and an agitated-drowsy conscious state. The tricyclic additionally confers sodium-channel blockade, evidenced by the widened QRS (120 ms) and the terminal R wave in aVR, which places him at risk of ventricular dysrhythmia and seizures. The paracetamol and alcohol are, at this stage, asymptomatic but time-critical to manage. [1]

Problem list (4 marks): [1]

1. Tricyclic antidepressant overdose with early cardiotoxicity (QRS 120 ms) — impending ventricular dysrhythmia and seizures.
2. Paracetamol overdose (15 g, level 220 mg/L at four hours) — well above the Rumack-Matthew treatment line, hepatotoxicity risk; requires N-acetylcysteine.
3. Anticholinergic delirium with a falling GCS — airway threat.
4. Alcohol co-ingestion — risk of hypoglycaemia (his glucose is currently normal but must be monitored) and a contributor to CNS depression.
5. Underlying psychiatric crisis — deliberate self-harm; risk assessment once medically stable. [1]

Decontamination decision (3 marks): [1]

Activated charcoal is the decontamination modality of choice for a charcoal-binding ingestion (amitriptyline and paracetamol both bind), taken recently (within 4 to 6 hours). However, his GCS is 12 and falling, and his airway is not protected — this is the single most important contraindication to charcoal. The position paper states that charcoal is contraindicated unless the airway is intact or protected [3]. The decision is: secure the airway by rapid sequence intubation first, then give 50 g activated charcoal via nasogastric tube. Do not give charcoal before intubation. Whole bowel irrigation is not indicated here — the ingestion is recent and the drugs bind charcoal [4].

TCA cardiotoxicity management (3 marks): [1]

The QRS of 120 ms and the terminal R wave in aVR indicate sodium-channel blockade and impending cardiotoxicity. Give intravenous sodium bicarbonate 1 to 2 mmol per kilogram as a bolus, repeated to narrow the QRS, then an infusion to maintain a serum pH of 7.50 to 7.55. Avoid class Ia and Ic antiarrhythmics (they worsen the blockade). If ventricular dysrhythmia develops and is refractory to bicarbonate, give 20 per cent lipid emulsion. [1]

Paracetamol management (3 marks): [1]

The four-hour paracetamol level of 220 mg/L (1400 micromol/L) is well above the Rumack-Matthew treatment line (approximately 150 mg/L or 1000 micromol/L at four hours). Start N-acetylcysteine immediately: 150 mg per kilogram over one hour, then 50 mg per kilogram over four hours, then 100 mg per kilogram over 16 hours. NAC replenishes glutathione and is a sulphate donor for the toxic NAPQI metabolite. Send baseline liver function and coagulation, and repeat after the infusion. The alcohol co-ingestion does not change the NAC indication but does increase the baseline risk of hepatotoxicity. [1]

Resuscitation and airway (2 marks): [1]

ABCDE first. Pre-oxygenase, then rapid sequence intubation given his falling GCS and the need to protect the airway before charcoal. Continuous cardiac monitoring. Two large-bore cannulae. Check a venous gas, electrolytes including magnesium, liver function, coagulation, lipase, and a beta-hCG (if applicable). Send a salicylate level on every overdose. [1]

Psychiatric and disposition (2 marks): [1]

Once medically stable and the NAC course is complete with a reassuring liver profile and coagulation, refer for psychiatric risk assessment. Document the assessment of capacity and the suicide-risk formulation. [1]

Communication and safety: Explain to the family that the immediate priority is to protect the airway and the heart — the QRS widening signals a real risk of a lethal rhythm — and that the paracetamol component is fully treatable with NAC if started now. The psychiatric review follows once he is medically safe. [1]

SAQ 2 — Salicylate Toxicity: Enhanced Elimination and the Dialysis Decision (10 marks, 20 minutes)

Prompt: A 45-year-old woman presents after ingesting 40 tablets of aspirin (300 mg, 12 g) over the preceding 12 hours. She is agitated, tachypnoeic (respiratory rate 32), tinnitus-affected, and has a temperature of 37.8. Blood gas: pH 7.42, PaCO2 18 mmHg, bicarbonate 11 mmol/L, anion gap 22. Salicylate level 5.5 mmol/L (76 mg/dL). She is managed with intravenous sodium bicarbonate for urinary alkalinisation. One hour later she becomes confused and her oxygen saturation falls to 91 per cent with new bibasal crackles. Outline the enhanced-elimination strategy, the dialysis decision, and the airway management. [1]

Model Answer

The acid-base pattern (1 mark): A mixed respiratory alkalosis (PaCO2 18 driving the pH up) and high anion gap metabolic acidosis (bicarbonate 11, anion gap 22) is the classic early pattern of salicylate toxicity — direct medullary stimulation causes the respiratory alkalosis, and uncoupling of oxidative phosphorylation drives the high anion gap metabolic acidosis. [1]

Urinary alkalinisation (3 marks): For moderate salicylate toxicity, the first-line enhanced-elimination strategy is urinary alkalinisation with intravenous sodium bicarbonate to a urine pH of 7.5 to 8.0. Give 1 to 2 mmol per kilogram as a bolus, then an infusion of approximately 100 to 150 mmol sodium bicarbonate in 1 litre of 5 per cent dextrose with 20 to 40 mmol potassium chloride at 1.5 to 2 times maintenance. The target is the urine pH, not the serum pH. Hypokalaemia must be corrected first, because potassium depletion prevents the distal tubule from excreting hydrogen ion and alkalinising the urine. [1]

The dialysis decision (4 marks): Her deterioration — new confusion and hypoxia with pulmonary infiltrates (salicylate-induced non-cardiogenic pulmonary oedema) — meets two EXTRIP indications for haemodialysis: altered mental status, and acute respiratory compromise requiring supplemental oxygen [6]. EXTRIP also recommends dialysis for a salicylate level over 7.2 mmol/L (100 mg/dL) regardless of symptoms, for refractory acidosis (pH under 7.20), and for failure of standard therapy. Intermittent haemodialysis is the preferred modality.

The airway trap (2 marks): Intubating a salicylate-toxic patient removes their compensatory hyperventilation, causing a precipitous rise in PaCO2, a fall in serum pH, and a shift of salicylate into the brain — which can precipitate cardiac arrest. The safe approach is to arrange concurrent haemodialysis and dialyse before, or simultaneously with, intubation. Do not intubate first and dialyse later. [1]

The principle: salicylate toxicity is one of the few poisonings in which the loss of the patient's own compensatory physiology (hyperventilation) under sedation is itself a lethal event. The registrar who recognises this will dialyse before intubating; the one who intubates in isolation may lose the patient on the table. [1]