Lithium salts (most commonly, lithium carbonate) are frequently used to treat bipolar disorder. According to experimental animal data and case reports in humans, lithium can interfere with anesthetic agents and neuromuscular blockers. In an animal model, Hill et al. observed that lithium prolonged the latency (time to onset) and the duration of neuromuscular blockade produced by succinylcholine. In the same study, lithium was found to potentiate (increased duration) the effects of pancuronium but not gallamine and d-tubocurarine on the duration of neuromuscular blockade. Lithium had no effect on pseudocholinesterase activity in this study. Several case reports have been published, describing lithium-associated prolongation of NM-blockade produced by both depolarizing and non-depolarizing NM blockers. The physiologic mechanism of these phenomena is thought to be due to lithium-induced inhibition of synthesis and release of acetylcholine at the neuromuscular junction as well as competition with sodium ions during depolarization event. Therefore, it is not unreasonable to reduce the dose of neuromuscular blocker in patients on lithium therapy, in order to avoid prolonged neuromuscular blockade. Finally, there have also been several reports describing prolongation of barbiturate anesthesia and ethanol-induced narcosis by lithium.
H S Havdala, R L Borison, B I Diamond Potential hazards and applications of lithium in anesthesiology. Anesthesiology: 1979, 50(6);534-7
G E Hill, K C Wong, M R Hodges Lithium carbonate and neuromuscular blocking agents. Anesthesiology: 1977, 46(2);122-6