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Lithium toxicity with AKI — FFICM MCQ

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HardObstetric and ToxicologyLithium toxicity with AKIFFICM

A 58-year-old woman taking lithium presents with confusion, coarse tremor, ataxia and vomiting after dehydration from gastroenteritis. Creatinine is 310 micromol/L and lithium concentration is 4.1 mmol/L. ECG shows T-wave flattening. She remains symptomatic after initial intravenous fluids. What is the most appropriate management?

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Correct answer: ADiscuss urgent haemodialysis with renal and toxicology services

The correct answer is A, discuss urgent haemodialysis with renal and toxicology services. This woman has severe lithium toxicity (level 4.1 mmol/L, well above the 2.5 mmol/L threshold generally used to trigger extracorporeal removal), acute kidney injury (creatinine 310 micromol/L reducing lithium clearance), and significant neurotoxicity (confusion, coarse tremor, ataxia) with cardiac changes on ECG, and she has failed to improve with intravenous fluids. Haemodialysis criteria include a lithium level above 4.0 mmol/L in a patient with renal impairment, or severe neurological or cardiovascular toxicity irrespective of level, both of which apply here. Dialysis rapidly removes lithium (endogenous clearance is only about 15 to 20 mL/min, but high-efficiency haemodialysis increases this markedly) and corrects the renal impairment perpetuating toxicity, so urgent multidisciplinary discussion with renal and toxicology teams is mandatory. Why the other options are wrong: E. Activated charcoal as definitive treatment: lithium is a small, fully ionised inorganic cation that is not adsorbed by activated charcoal, so it has no role in decontamination or definitive treatment. C. Sodium bicarbonate infusion: bicarbonate alkalinises urine to enhance elimination of weak acids like salicylates, not lithium, which is renally handled independently of urinary pH and is unaffected by bicarbonate. D. Flumazenil: this is a benzodiazepine receptor antagonist used for benzodiazepine-induced sedation or coma, entirely irrelevant to lithium's neurotoxic mechanism. B. Restart lithium at a lower dose: reintroducing any lithium during active severe toxicity with AKI would worsen accumulation and neurotoxicity; lithium must be withheld until levels normalise and renal function recovers. Key point: severe symptomatic lithium toxicity with renal impairment and a level above 4.0 mmol/L (or life-threatening neuro/cardiac features at any level) mandates urgent haemodialysis discussion, since charcoal, bicarbonate and antidotal drugs have no role in lithium elimination.

Reference: The Pharmaceutical Journal, Lithium monitoring and toxicity management, https://pharmaceutical-journal.com/article/ld/lithium-monitoring-and-toxicity-management