Poisoning — Clinical Case

DCE Long Case

Patient brief (provided to trainee)

Patient: Mr David Chen, 28 years old, software engineer. [1]

Presenting complaint: Found drowsy at home by his partner after a suspected deliberate overdose. Empty blister packs of amitriptyline 50 mg (perhaps 40 tablets, a total of 2 g) and paracetamol 500 mg (perhaps 30 tablets, a total of 15 g) were found beside him, together with an empty bottle of wine. The time of ingestion is uncertain but the partner estimates 4 to 6 hours ago. [1]

Past history: Major depressive disorder (diagnosed 2 years ago, treated with amitriptyline by his general practitioner), a previous overdose 6 months ago (paracetamol, no hepatotoxicity), no other medical history of note. He is not on any other regular medication. He drinks 30 to 40 standard drinks per week. [1]

Examination findings (trainee elicits):

• GCS 12 (E3 V3 M6), drowsy but rousable to voice, mumbling incoherently
• Airway patent, respiratory rate 14, oxygen saturation 96 per cent on room air
• Heart rate 124, blood pressure 96/58, temperature 37.2 degrees Celsius
• Skin dry and flushed, pupils dilated at 6 mm and poorly reactive, mucous membranes dry, bowel sounds absent, bladder not palpable
• No focal neurological deficit, no muscle fasciculations [1]

Investigations:

• Bedside glucose 4.8 mmol/L
• ECG: sinus tachycardia, QRS 120 ms, prominent terminal R wave in aVR, QTc 480 ms
• Venous gas: pH 7.32, bicarbonate 18 mmol/L, anion gap 14, lactate 1.8
• Sodium 140, potassium 4.0, chloride 104, urea 5.0, creatinine 80, albumin 40
• Liver function normal at baseline; coagulation normal
• Four-hour paracetamol level 220 mg/L (1400 micromol/L); salicylate level not detected
• Blood alcohol concentration 0.12 per cent [1]

Candidate's structured presentation (model)

Opening statement (SASPOP): [1]

"Mr 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 has a background of major depressive disorder and a previous overdose. 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 and impending cardiotoxicity. His four-hour paracetamol level is 220 milligrams per litre, well above the treatment line." [1]

"His main problems are:

1. Tricyclic antidepressant overdose with early cardiotoxicity (QRS 120 ms) — the prognostic marker that mandates intravenous sodium bicarbonate, with a risk of ventricular dysrhythmia and seizures.
2. Paracetamol overdose at a hepatotoxic dose and level — N-acetylcysteine is indicated immediately.
3. A falling GCS with an unprotected airway — rapid sequence intubation is required before any decontamination.
4. Alcohol co-ingestion with a risk of hypoglycaemia (currently normal but to be monitored) and a contribution to his CNS depression.
5. An underlying psychiatric crisis with a previous overdose — a high suicide-risk patient requiring risk assessment once medically stable." [1]

"My immediate priorities are to secure the airway by rapid sequence intubation, give intravenous sodium bicarbonate for the QRS widening, start N-acetylcysteine for the paracetamol, and give activated charcoal once the airway is protected." [1]

Management plan: [1]

1. Airway and resuscitation: 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.
2. TCA cardiotoxicity: intravenous sodium bicarbonate 1 to 2 millimoles per kilogram 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; have 20 per cent lipid emulsion ready for refractory dysrhythmia.
3. Decontamination: once intubated, give 50 grams of activated charcoal via nasogastric tube — both amitriptyline and paracetamol bind charcoal, and the ingestion was within the window. Charcoal was contraindicated before intubation because of the unprotected airway.
4. Paracetamol management: start N-acetylcysteine now — 150 milligrams per kilogram over one hour, then 50 over four hours, then 100 over 16 hours. Send baseline liver function and coagulation; repeat after the infusion and at 24 hours.
5. Monitoring and investigations: continuous ECG, serial GCS, hourly glucose, repeat venous gas and electrolytes, magnesium (replace if low), lipase, beta-hCG if applicable. ICU referral for the cardiotoxicity and intubation.
6. Psychiatric: once medically cleared and the NAC course is complete with a reassuring profile, refer for psychiatric risk assessment. [1]

Communication and shared decision-making: explain to the family that the immediate priorities are 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. Document the capacity assessment and the suicide-risk formulation once he is alert. [1]

Examiner discussion questions

Q: "Would you give charcoal before intubation?" [1]

"No. His GCS is 12 and falling, and his airway is not protected. The single most dangerous contraindication to activated charcoal is an unprotected airway — aspiration of charcoal causes a catastrophic chemical pneumonitis. The position paper is explicit: charcoal is contraindicated unless the airway is intact or protected. My plan is to intubate first, then give 50 grams of charcoal via nasogastric tube. If his GCS were 15 and his airway intact, I would give charcoal without intubation." [1]

Q: "The QRS widens to 160 ms while you are waiting for the bicarbonate. What does this mean, and what do you do?" [1]

"A QRS over 160 milliseconds after a tricyclic overdose carries approximately a 50 per cent risk of a seizure, and the risk of ventricular dysrhythmia rises steeply. I would give intravenous sodium bicarbonate 1 to 2 millimoles per kilogram as a bolus immediately, repeated to narrow the QRS, and start an infusion to maintain a serum pH of 7.50 to 7.55. I would not use amiodarone, lignocaine, or any class Ia or Ic antiarrhythmic, because they worsen the sodium-channel blockade. If ventricular dysrhythmia develops and is refractory to bicarbonate, the next step is 20 per cent lipid emulsion — 1.5 millilitres per kilogram bolus then 0.25 millilitres per kilogram per minute." [1]

Q: "How confident are you in the time of ingestion, and does it affect your paracetamol management?" [1]

"I am not confident — the partner's estimate of 4 to 6 hours is uncertain. The four-hour paracetamol level is 220 milligrams per litre, which is well above the Rumack-Matthew treatment line at four hours, so N-acetylcysteine is clearly indicated regardless of the uncertainty. The bigger concern is whether the ingestion was staggered. If it was staggered over several hours, the nomogram cannot be applied, and the standard practice is to treat with NAC on clinical grounds. Either way, he gets NAC." [1]

Q: "Why is his anion gap only 14 when you would expect a lactic acidosis from a seizure or hypoperfusion?" [1]

"At this stage he has not yet seized and his blood pressure is holding. The mild acidaemia (pH 7.32, bicarbonate 18) is most likely a mild lactic acidosis from hypoperfusion and agitation, and it is not yet dominant. The anion gap may rise if he seizes or deteriorates. The key point is that the anion gap is not the driver of his presentation — the cardiotoxicity and the airway are." [1]

Q: "When would you involve the toxicologist or the poison information centre?" [1]

"Now. For any complex mixed overdose with cardiotoxicity, I would call the poison information centre (13 11 26 in Australia) early and involve the medical toxicologist. I would also refer to ICU for admission given the intubation, the cardiotoxicity, and the need for continuous monitoring. The toxicologist can advise on the lipid emulsion threshold, the duration of the bicarbonate infusion, and the timing of NAC discontinuation in the setting of any hepatotoxicity." [1]

Q: "What is the single most dangerous error a registrar could make in this patient?" [1]

"Giving charcoal before securing the airway. The aspiration of charcoal into an unprotected bronchial tree causes a chemical pneumonitis that is frequently fatal, and it is entirely avoidable. The second most dangerous error is treating the TCA ventricular dysrhythmia with a class Ia or Ic antiarrhythmic instead of sodium bicarbonate. The third is failing to start N-acetylcysteine because the time of ingestion is uncertain — uncertainty is a reason to treat, not to withhold." [1]

DCE Short Case — Toxidrome at the Bedside

Instruction

"This patient was brought in unconscious. Examine him and tell me the toxidrome and your immediate action. You have 4 minutes to examine and 6 minutes for discussion." [1]

Provided data: The patient is unconscious (GCS 8). Respiratory rate 6, heart rate 48, blood pressure 100/60, temperature 35.8 degrees Celsius. Pupils pinpoint (1 mm). Skin normal, no fasciculations, no diaphoresis. Bedside glucose 5.5 mmol/L. [1]

Presentation template

"I have examined an unconscious patient. He has a respiratory rate of 6, a heart rate of 48, a slightly low temperature of 35.8, and pinpoint pupils. His glucose is normal. The skin is normal, there are no fasciculations and no secretions. 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 respiratory effort, while preparing to secure his airway. I would check a bed-side glucose, which I have done, and I would send a paracetamol and salicylate level on every overdose." [1]

Discussion

Examiner: "What is your naloxone end-point, and why not give a large bolus?" [1]

"My end-point is an adequate respiratory rate — I titrate to restore breathing, not to full wakefulness. A large bolus that fully reverses a chronic opioid user precipitates acute withdrawal — agitation, vomiting, aspiration, and pain. I start at 0.04 milligrams intravenously, doubling every two minutes, up to a maximum of 10 milligrams. A non-responder at 10 milligrams is not opioid-toxic, and I would then broaden the differential to a sedative-hypnotic, alcohol, a structural brainstem lesion, or a metabolic encephalopathy." [1]

Examiner: "The patient responds to naloxone, but 30 minutes later he is again bradypnoeic. What has happened, and what do you do?" [1]

"This indicates a long-acting opioid — methadone, a fentanyl patch, or sustained-release morphine — whose half-life exceeds that of naloxone. The opioid outlasts the antidote. I would start a naloxone infusion: two-thirds of the bolus dose that initially reversed him, given per hour as an infusion, titrated to respiratory effort. I would observe him in a monitored setting for at least 6 to 12 hours after the infusion is ceased." [1]

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

"First, the opioid toxidrome — naloxone, titrated to respiratory effort. Second, the benzodiazepine toxidrome — flumazenil, reserved for isolated, iatrogenic, benzodiazepine-naive overdose because it precipitates seizures in chronic users and in mixed overdoses with pro-convulsants. Third, the organophosphate cholinergic toxidrome, which in its later phase causes coma — atropine for the muscarinic effects and pralidoxime to reactivate acetylcholinesterase and reverse the nicotinic muscle weakness. There is no specific antidote for the alcohol or barbiturate toxidrome; the management is supportive." [1]

Examiner: "What is the most dangerous toxidrome to miss in a hot, agitated patient?" [1]

"A sympathomimetic or anticholinergic toxidrome with severe hyperthermia — temperatures over 40 degrees precipitate rhabdomyolysis, disseminated intravascular coagulation, multi-organ failure and death within hours. The immediate management is active cooling and benzodiazepines (first-line, for both the agitation and the heat generation), plus alpha-blockade for hypertension in a sympathomimetic overdose. I would never give a beta-blocker alone for a sympathomimetic overdose, because unopposed alpha stimulation worsens the vasospasm and the hypertension. The discriminator between the sympathomimetic and anticholinergic toxidromes is the skin — diaphoretic in the former, dry and flushed in the latter." [1]