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General Medicine · Toxicology: chronic lithium toxicity
Sample itemA 55-year-old woman with bipolar disorder on lithium has recently been started on an NSAID for knee pain and a thiazide for hypertension. She now has coarse tremor, vomiting, slurred speech, ataxia, confusion and a generalised seizure. Serum lithium is 3.2 mmol/L and creatinine is raised. What is the most appropriate definitive treatment?
Original practice item, not a recalled exam question. Nothing here is recorded.
The answer and the reasoning
A. Haemodialysis
Lithium is renally cleared, and NSAIDs and thiazides reduce clearance by increasing proximal tubular reabsorption, causing chronic toxicity with neurological features. Lithium is small, water-soluble, not protein-bound and has a small volume of distribution, so haemodialysis removes it efficiently and is indicated for severe neurotoxicity (seizures, reduced consciousness), very high levels or renal impairment. Rebound levels can occur from intracellular redistribution, so levels are rechecked.
Option by option
A. Haemodialysis (correct)
Correct. Dialysis rapidly removes lithium, and severe neurological toxicity with renal impairment is a clear indication.
B. Intravenous sodium bicarbonate for urinary alkalinisation
Bicarbonate alkalinisation enhances salicylate excretion but has no role in lithium elimination.
C. Activated charcoal
Activated charcoal does not adsorb lithium and the toxicity here is chronic, not a recent ingestion.
D. Forced diuresis with furosemide
Loop diuretics cause sodium and volume depletion, which increases proximal lithium reabsorption and worsens toxicity.
Source note: Original NextPrep sample item — pending expert review. This item is original practice material awaiting independent expert review, so confirm important facts in a standard textbook.
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