How is SIADH managed?
SIADH should resolve if the underlying cause is eliminated—something often easier said than done. Discontinuation of culprit medications, antimicrobial therapy for pulmonary or CNS infections, and treatment of an underlying malignancy will be helpful. Treatment is otherwise dictated by chronicity and severity of symptoms of the hyponatremia. Asymptomatic or minimally symptomatic patients with chronic SIADH should be water restricted initially. The degree of fluid restriction can be estimated by calculating the ratio of the sum of urinary potassium and sodium concentrations to plasma sodium concentration. A ratio less than 1 allows for more liberal water restriction (i.e., 1 L/day); a ratio greater than 1 requires stricter (and often impractical) measures (<500 mL/day). Unsurprisingly, the effectiveness of water restriction is limited by patient compliance. Alternatively, increased protein and salt consumption may be helpful. Oral urea supplementation (30 g/day), by increasing solute intake and hence urine volume, is effective but has been poorly tolerated historically, though newer formulations have proven to be more palatable. When these interventions fail, the vaptans can be used for euvolemic, mild-to-moderate hyponatremia with mild attributable symptoms. The vaptans do not reliably increase the serum sodium in a rapid fashion. Meta-analyses of randomized controlled trials have demonstrated a mean rise in the plasma sodium concentration of approximately 5 mEq/L occurring over several days in the case of tolvaptan. Thus, these medications should not be given for hyponatremia with severe neurologic symptoms, which would otherwise merit more rapid correction. In such cases, hypertonic saline should be administered.