Hyponatremia lithium toxicity

Fluid and sodium balance are important to the safe use of lithium. Both dehydration and a negative sodium balance (for example a low salt intake, diuretic-induced sodium loss) will reduce renal lithium clearance and predispose to toxicity (331). Hyponatremia (for example, secondary to polydipsia or SIADH) may also increase the risk of lithium toxicity (332). 

Lithium augmentation of antidepressants is a well-established treatment for resistant depression and is usually well tolerated with all classes of antidepressants, although there have been a few reports of the serotonin syndrome with SSRIs (474). It is possible that shared adverse effects could be magnified by combining lithium with various antidepressants (for example tremor, weight gain, gastrointestinal upset). Hyponatremia secondary to the SIADH has been linked to SSRIs and tricyclic antidepressants, especially in elderly patients, and could predispose to lithium toxicity. 

Carbamazepine and lithium can elevate each other s serum levels (the mechanism is unknown). Toxicity is possible while blood levels are within the normal range, and is partially associated with pre-existing brain abnormalities. The diuretic effect of lithium outweighs the antidiuretic effect of carbamazepine. Carbamazepine does not protect against lithium-induced diabetes insipidus. Lithium can enhance carbamazepine-induced hyponatremia. 

ADH antagonists oppose the actions of ADH and other naturally occurring peptides that act on the same Vj receptor. Such peptides are produced by certain tumors (eg, small cell carcinoma of the lung) and can cause significant water retention and dangerous hyponatremia. This syndrome of inappropriate ADH secretion (SIADH) can be treated with demeclocycline. Lithium also works but has greater toxicity. 

Watch patients taking lithium for signs of toxicity when hyponatremia is present. This toxicity can occur even if the lithium dosage has been consistent because hyponatremia causes an increase in lithium retenhon. 

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