TABLE 1563 Factors Precipitating the Development of Lithium Toxicity Excluding Drug Interactions

Patients with acute overdose can tolerate higher levels without toxicity. Acute ingestions classically cause more GI toxicity and less CNS toxicity. After ingestion, there is delay in transport of lithium into the intracellular compartment and across the blood-brain barrier. With time, equilibration occurs and toxicity develops. Neurologic symptoms often develop as GI symptoms are abating. Levels in patients with an acute ingestion do not correlate well with either symptoms or prognosis.

Patients with chronic overdose have lower serum levels, higher cellular levels, and classically display earlier and greater neurologic changes. Levels in such patients correlate better with prognosis and toxicity. Acute-on-chronic ingestions have aspects of both profiles of ingestion. As in most toxicities, the best guideline for therapy is the patient's condition, not the drug level.

Recognizing lithium toxicity is not always easy, particularly in patients with chronic overdose. CNS symptoms are the hallmark of chronic lithium toxicity. Table 156-4.

lists a common grading system for toxicity. Patients commonly present with muscle fasciculations, ataxia, agitation or lethargy, and muscle weakness. At times, it may be difficult to distinguish between lithium toxicity and organic delirium. Although most patients present with slowing of their cognitive function, cases of lithium overdose presenting as mania have been reported. As toxicity worsens, confusion, lethargy, stupor, and, finally, coma develop. Rarely, extrapyramidal signs develop. Proximal muscle weakness, extensor plantar response, and auditory, visual, and tactile hallucinations have been reported. The electroencephalogram shows diffuse slowing and disorganization, with frontal intermittent rhythmic delta activity in severe cases.

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