Phyu M Hlaing1,2, Katherine Z Isoardi2,3, Colin B Page2,3, Peter Pillans2,4. 1. Department of Internal Medicine, Redland Hospital, Brisbane, Queensland, Australia. 2. Faculty of Medicine, University of Queensland, Brisbane, Queensland, Australia. 3. Clinical Toxicology Unit and Emergency Department, Brisbane, Queensland, Australia. 4. Department of Clinical Pharmacology, Princess Alexandra Hospital, Brisbane, Queensland, Australia.
Abstract
BACKGROUND: Lithium-induced neurotoxicity typically occurs with chronic accumulation rather than following acute overdose. There is little emphasis in the literature on the protracted nature of lithium neurotoxicity long after the lithium concentration returns to the therapeutic range. AIMS: To characterise lithium neurotoxicity, with a view of increasing awareness of this important phenomenon. METHODS: This is a retrospective observational study of patients presenting with lithium-induced neurotoxicity over a 5-year period to a clinical toxicology unit. Patients were identified through the unit's database, and clinical notes were analysed. RESULTS: There were 22 patients, with a median age of 65 (range: 36-89) years. Six patients (27%) had previous lithium toxicity, and nine (41%) were regularly prescribed medications that impair lithium excretion. The median lithium concentration on presentation was 2.2 mmol/L, taking a median of 3 days to return to the therapeutic range. Reversible acute kidney injury was observed in 21 patients (95%) on presentation. The median length of stay was 13 (range: 3-95) days due mostly to delayed neurological recovery. Confusion was the predominant symptom, present in 21 (95%) patients, followed by tremors (18(82%)) and ataxia (16(73%)). Multiple investigations were performed to exclude delirium differentials, including 11 computed tomography (CT) and five magnetic resonance imaging (MRI) brain scans, all unremarkable. CONCLUSIONS: Lithium neurotoxicity has a prolonged course. Its severity correlates poorly with lithium concentrations, which normalise quickly. Most poisonings occur in elderly patients with acute kidney injury. Prolonged delirium often prompts multiple unnecessary investigations. Rationalisation of lithium therapy is important in elderly patients.
BACKGROUND:Lithium-induced neurotoxicity typically occurs with chronic accumulation rather than following acute overdose. There is little emphasis in the literature on the protracted nature of lithiumneurotoxicity long after the lithium concentration returns to the therapeutic range. AIMS: To characterise lithiumneurotoxicity, with a view of increasing awareness of this important phenomenon. METHODS: This is a retrospective observational study of patients presenting with lithium-induced neurotoxicity over a 5-year period to a clinical toxicology unit. Patients were identified through the unit's database, and clinical notes were analysed. RESULTS: There were 22 patients, with a median age of 65 (range: 36-89) years. Six patients (27%) had previous lithiumtoxicity, and nine (41%) were regularly prescribed medications that impair lithium excretion. The median lithium concentration on presentation was 2.2 mmol/L, taking a median of 3 days to return to the therapeutic range. Reversible acute kidney injury was observed in 21 patients (95%) on presentation. The median length of stay was 13 (range: 3-95) days due mostly to delayed neurological recovery. Confusion was the predominant symptom, present in 21 (95%) patients, followed by tremors (18(82%)) and ataxia (16(73%)). Multiple investigations were performed to exclude delirium differentials, including 11 computed tomography (CT) and five magnetic resonance imaging (MRI) brain scans, all unremarkable. CONCLUSIONS:Lithiumneurotoxicity has a prolonged course. Its severity correlates poorly with lithium concentrations, which normalise quickly. Most poisonings occur in elderly patients with acute kidney injury. Prolonged delirium often prompts multiple unnecessary investigations. Rationalisation of lithium therapy is important in elderly patients.