When Should Dialysis be Performed in Lithium Poisoning? A Kinetic Study in 14 Cases of Lithium Poisoning

Abstract

Lithium kinetics were studied in 14 patients with lithium poisoning. Three patients were treated by hemodialysis. Serum lithium peak concentrations ranged between 1.4 and 9.6 mmol/L. The apparent mean serum half-life was 23.16 +/- 9 h, the mean total clearance was 26.5 +/- 13.3 mL/min and the mean renal clearance was 17.2 +/- 5.4 mL/min. The kinetic parameters were dependent on the duration of the study and on the type of the poisoning: acute, acute upon chronic or chronic. During the first 12 h after admission ten patients were in a distribution phase, three were in an elimination phase and one was in an absorption phase. The serum half-life during hemodialysis ranged from 3.6 to 5.7 h and hemodialysis clearance was 63.2 to 114.4 mL/min. The mean volume of distribution calculated in six cases was 0.63 +/- 0.09 L/kg. The evolution of the lithium pools showed a different kinetic pattern between the extra- and the intracellular pool which decreased more slowly. During hemodialysis the decrease of the extracellular pool was about twice that of the cellular pool. Among the factors which may modify lithium toxicity and kinetics, are the type of the poisoning, the presence of an underlying disease and renal impairment. No general and rigid indication for hemodialysis can be set, but the need for hemodialysis should be based on clinical and kinetic data determined during the 12 h following admission.

Extracorporeal Treatment for Lithium Poisoning

“…The central nervous system (CNS) is the organ system predominantly affected, particularly in those patients with chronic lithium poisoning: mild lithium poisoning typically encompasses drowsiness, nausea, vomiting, tremor, hyperreflexia, agitation, muscle weakness, and ataxia (18,21). More prominent symptoms include stupor, rigidity, hypertonia, and hypotension.…”

“…More prominent symptoms include stupor, rigidity, hypertonia, and hypotension. The most severe cases manifest as coma, convulsions, myoclonus, and cardiopulmonary collapse (18,21). Because the distinction between these gradations can often be subtle, they are best thought of as a natural progression of a potentially severe overdose.…”

“…Tissue distribution of lithium follows a multiple compartment model with a delayed diffusion from the extracellular to the intracellular compartment (18). Lithium is rapidly taken up by the kidney, thyroid, and bone (15,18). However, diffusion into the cerebrospinal fluid and the brain is delayed by approximately 24 hours compared with its appearance in plasma (15,19).…”

“…The initial volume of distribution of lithium is 0.5 L/kg; however, it subsequently increases to 0.7-0.9 L/kg with time (8,13). Tissue distribution of lithium follows a multiple compartment model with a delayed diffusion from the extracellular to the intracellular compartment (18). Lithium is rapidly taken up by the kidney, thyroid, and bone (15,18).…”

“…Chronic lithium poisoning occurs in patients on maintenance lithium therapy in the clinical context of a recently increased lithium dose, a decline in kidney function, or a drug-drug interaction that impairs elimination (13,21 (18,21,28), whereas they may be prominent in chronic toxicity, with serum lithium concentrations as low as 1.5 mEq/L, reflecting higher brain lithium concentrations (18,21). The delayed diffusion of lithium to the brain explains the absence or delay of symptoms in patients with acute lithium poisoning, despite highly elevated [Li + ] (18,21,29). For these reasons, these serum lithium concentrations are only a guide to potential risk of toxicity and should always be interpreted in the context of the patient's history, clinical findings, and kidney function.…”