Treatment: SIADH

Fluid intake should be restricted to 500 mL less than urinary output. In pts with severe symptoms or signs, hypertonic (3%) saline can be infused at ≤0.05 mL/kg body weight IV per minute, with hourly sodium levels measured until Na increases by 12 meq/L or to 130 meq/L, whichever occurs first. However, if the hyponatremia has been present for >24-48 h and is corrected too rapidly, saline infusion has the potential to produce central pontine myelinolysis, a serious, potentially fatal neurologic complication caused by osmotic fluid shifts. Vasopressin antagonists (conivaptan, tolvaptan) are now available, but experience with these agents in SIADH treatment is limited. Oral vaptan (tolvaptan), a selective V₂ antagonist increases urinary water excretion by blocking the antidiuretic effect of AVP. It should be initiated in the hospital (typically 15 mg PO qd) to evaluate the clinical response and avoid excessive diuresis. Other options include demeclocycline, 150-300 mg PO tid or qid, or fludrocortisone, 0.05-0.2 mg PO bid. The effect of the demeclocycline manifests in 7-14 days and is due to induction of a reversible form of nephrogenic DI. The effect of fludrocortisone also requires 1-2 weeks and is partly due to increased retention of sodium and possibly inhibition of thirst. It also increases urinary potassium excretion, which may require replacement through dietary adjustments or supplements and may induce hypertension.

For a more detailed discussion, see Robertson GL: Disorders of the Neurohypophysis, Chap. 404, p. 2274, in HPIM-19.