Poisoning Viva

Long Case Viva Defence

Candidate's opening statement (model answer)

"Mr David Chen is a 28-year-old software engineer who presents with a deliberate mixed overdose of amitriptyline and paracetamol with alcohol, an uncertain 4 to 6 hours ago. He is drowsy with a GCS of 12, tachycardic at 124, hypotensive at 96 over 58, with dry flushed skin, dilated pupils and absent bowel sounds — an anticholinergic picture consistent with the tricyclic. His ECG shows a QRS of 120 milliseconds with a terminal R wave in aVR, signalling early sodium-channel blockade. His four-hour paracetamol level is 220 milligrams per litre, well above the Rumack-Matthew treatment line." [1]

"His main problems are:

1. Tricyclic antidepressant overdose with early cardiotoxicity — the widened QRS is the prognostic marker and mandates intravenous sodium bicarbonate.
2. Paracetamol overdose at a hepatotoxic dose and level — N-acetylcysteine is indicated.
3. A falling GCS with an unprotected airway — intubation is required before any decontamination.
4. Alcohol co-ingestion with a risk of hypoglycaemia.
5. An underlying psychiatric crisis." [1]

"My immediate priorities are to secure the airway, give sodium bicarbonate for the QRS widening, start N-acetylcysteine for the paracetamol, and give activated charcoal once intubated." [1]

Examiner probing questions and model answers

Q1: "Walk me through your decision to give charcoal — or not." [1]

"Charcoal binds both amitriptyline and paracetamol, and the ingestion was within the last four to six hours, so it is the correct decontamination modality. But his GCS is 12 and falling, and his airway is not protected. The single most dangerous contraindication to charcoal is an unprotected airway — aspiration of charcoal causes a catastrophic chemical pneumonitis. My plan is to perform rapid sequence intubation first, then give 50 grams of activated charcoal via nasogastric tube. I would never give charcoal before the airway is secured. If his GCS were 15 and his airway intact, I would give charcoal without intubation." [1]

Q2: "His QRS is 120 ms. How does that change your management, and what is your threshold?" [1]

"A QRS over 100 milliseconds after a tricyclic overdose warrants intravenous sodium bicarbonate. Over 160 milliseconds carries a 50 per cent seizure risk. I would give 1 to 2 millimoles per kilogram of sodium bicarbonate as an intravenous bolus, repeated to narrow the QRS, then an infusion to maintain a serum pH of 7.50 to 7.55. Sodium bicarbonate works by two mechanisms — the sodium load overcomes the channel blockade, and the alkalinisation shifts the drug off the sodium channel into its neutral form. I would avoid class Ia and Ic antiarrhythmics entirely, because they worsen the blockade. If he develops refractory ventricular dysrhythmia, the next step is 20 per cent lipid emulsion." [1]

Q3: "When will you start the N-acetylcysteine, and what regimen?" [1]

"I start it now — his four-hour paracetamol level is 220 milligrams per litre, well above the treatment line. The regimen is 150 milligrams per kilogram over one hour, then 50 milligrams per kilogram over four hours, then 100 milligrams per kilogram over 16 hours. N-acetylcysteine replenishes glutathione and is a sulphate donor for the toxic NAPQI metabolite. I send baseline liver function and coagulation, and repeat them after the infusion and at 24 hours. The alcohol co-ingestion does not change the NAC indication. If his level had been below the line, I would not give NAC." [1]

Q4: "He becomes more drowsy. Would you give flumazenil to reverse the sedation?" [1]

"No. Flumazenil is contraindicated in a mixed overdose with a pro-convulsant such as a tricyclic — it precipitates seizures that are refractory to standard treatment. I would reserve flumazenil for isolated, iatrogenic benzodiazepine over-sedation in a benzodiazepine-naive patient. For his sedation, the correct response is to protect the airway by intubation, not to reverse the sedation pharmacologically." [1]

Q5: "His paracetamol ingestion was staggered over several hours. Can you still use the nomogram?" [1]

"No. The Rumack-Matthew nomogram applies only to a single acute ingestion with a known time. For a staggered ingestion or an unknown time, the nomogram cannot be plotted, and the standard practice is to treat with N-acetylcysteine on clinical grounds. I would give NAC and monitor the liver function and coagulation, continuing beyond the standard course if there is any hepatotoxicity." [1]

Short Case Discussion

Scenario: "This patient is unconscious. Examine him and tell me the toxidrome."

Provided data: The patient is unconscious, with a respiratory rate of 6, a heart rate of 48, pinpoint pupils, and a normal temperature. Bedside glucose is 5.5 mmol/L. [1]

Candidate presentation (model): [1]

"I have examined an unconscious patient. He has a respiratory rate of 6, pinpoint pupils, a heart rate of 48, and a normal temperature and glucose. This is the classic opioid toxidrome — the triad of pinpoint pupils, respiratory depression and coma. My immediate action is to give naloxone, starting at 0.04 milligrams intravenously and titrating to his respiratory effort, while preparing to secure his airway if he does not respond. I would not give a large bolus, because if he is a chronic opioid user, a full reversal will precipitate acute withdrawal." [1]

Examiner: "What is the maximum naloxone dose, and what does a non-responder mean?" [1]

"I would titrate, doubling the dose every two minutes, up to a total of 10 milligrams. A patient who does not respond to 10 milligrams is not primarily opioid-toxic, and I would broaden the differential to include a sedative-hypnotic, alcohol, a structural brainstem lesion, or a severe metabolic encephalopathy such as a profound hypoglycaemia that I may have missed, or a hepatic or uraemic encephalopathy. If the opioid is long-acting — methadone, a fentanyl patch, sustained-release morphine — I would start a naloxone infusion after the initial reversal, because the opioid will outlast the antidote." [1]

Examiner: "Name three toxidromes that cause a depressed conscious state, and the antidote for each." [1]

"First, the opioid toxidrome — naloxone, a competitive mu-receptor antagonist, titrated to respiratory effort. Second, the benzodiazepine toxidrome — flumazenil, used only in a benzodiazepine-naive patient with an isolated overdose, because in a chronic user or a mixed overdose with a pro-convulsant it precipitates seizures. Third, there is no specific antidote for the alcohol or barbiturate toxidrome; the management is supportive — airway, ventilation and time. A fourth, if useful, is the cholinergic toxidrome from organophosphates, which in its later phase causes a depressed conscious state, and is treated with atropine for the muscarinic effects and pralidoxime to reactivate acetylcholinesterase and reverse the nicotinic muscle weakness." [1]

Examiner: "What is the most common error candidates make when managing an opioid overdose?" [1]

"Giving naloxone to fully reverse the patient rather than titrating to respiratory effort. A full reversal in a chronic opioid user precipitates acute withdrawal — agitation, vomiting, aspiration, and severe pain — and it does not improve outcome. I titrate to restore an adequate respiratory rate, accepting that the patient may remain drowsy. The end-point is breathing, not wakefulness." [1]

Examiner: "Name three causes of a high anion gap metabolic acidosis in the poisoned patient that have a specific antidote." [1]

"First, methanol — fomepizole to inhibit alcohol dehydrogenase, folate as a cofactor, and haemodialysis; the clue is visual symptoms with a high anion gap and osmolar gap. Second, ethylene glycol — the same fomepizole-based approach, with thiamine and pyridoxine as cofactors and haemodialysis; the clue is renal failure and calcium oxalate crystals. Third, salicylate toxicity — urinary alkalinisation and haemodialysis for severe toxicity; the clue is the mixed respiratory alkalosis and high anion gap metabolic acidosis with tinnitus. The osmolar gap is the key discriminator between these and a lactic acidosis, which does not raise the osmolar gap." [1]