Lithium is an effective mood stabilizer with a narrow therapeutic window and is primarily cleared by the kidneys. Conditions such as acute illness, fluid volume depletion, disturbances in sodium levels, and concurrent drug use can elevate the risk of lithium-induced neurotoxicity. A 57-year-old man with bipolar disorder, type 2 diabetes, hypertension, and ischemic heart disease was admitted due to vomiting, reduced oral intake, and diabetic ketoacidosis. He had been taking lithium carbonate 400 mg twice daily for about four months, along with torsemide and spironolactone. During hospitalization, he exhibited mild slurred speech, tremors, and drowsiness. His serum lithium level was 1.43 mmol/L. Although kidney function remained relatively stable, blood urea nitrogen was elevated, and mild hyponatremia was present. Lithium was discontinued, leading to marked improvement in neurological symptoms within approximately 24 hr. The medication was later resumed at a lower dose of 300 mg twice daily. This case underscores that lithium-related neurotoxicity can occur even when serum levels are below the typical toxicity threshold, especially during acute medical conditions and in the presence of factors affecting fluid and sodium balance. Thorough clinical evaluation, medication review, and therapeutic drug monitoring are crucial for patients on lithium therapy.
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Keywords
Adverse Drug Reaction
Bipolar Disorder
Diuretics
Lithium
Neurotoxicity
Therapeutic Drug Monitoring
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