Clinical Effects

The most common side effects (Table 1.5.6-2.) are hand tremor, polyuria due to loss of urinary concentration ability, and rash. Hand tremor occurs in up to 65 percent of patients at some time,6 and worsening of a baseline tremor is an important signal of developing toxicity. A decrease in urinary-concentrating ability occurs in most patients but is largely asymptomatic. Up to 12 percent of patients will develop nephrogenic diabetes insipidus. 7 In some patients, incomplete distal renal tubular acidosis develops (defect in urine acidification without acidemia). Neurologic side effects include memory loss, decreased mental concentration, and fatigue. Ataxia and dysarthria can develop and will often improve with cessation of therapy. Long-term lithium treatment can lead to electroencephalographic changes, including diffuse slowing, an increase in theta and delta waves, and a decrease in alpha activity.

TABLE 156-2 Side Effects with Chronic Lithium Therapy

Gastrointestinal (GI) side effects are common at initiation of treatment and are generally transient. GI symptoms that develop during the course of treatment may signal toxicity. Cardiovascular changes develop in part because lithium interferes with the sodium-potassium pump, leading to intracellular hypokalemia. This results in electrocardiographic findings of U waves, flattened or inverted T waves, and ST depression. Conduction abnormalities are less common.

Lithium toxicity may result from acute intentional overdose, from chronic overdose, or as a result of a change in lithium excretion (medications, dehydration, or salt depletion). Toxicity developing in patients taking chronic lithium therapy may be due to a change in the daily dose of medication or physiologic changes impairing the elimination of the drug. Renal failure or intravascular volume depletion is a precipitating cause in nearly all cases of chronic toxicity. 7 Other factors known to precipitate lithium toxicity are listed in T§b.!e.,J„56z3.

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