Intractable hyponatremia complicated by a reset osmostat: a case report

Abstract

Background: Hyponatremia associated with a low serum osmolality is a common and confounding electrolyte disorder. Correcting hyponatremia is also complicated, especially in the setting of chronic hyponatremia. Here, we provide a rational approach to accurately detecting and safely treating acute on chronic euvolemic hyponatremia in the setting of acute polydipsia with a chronic reset osmostat. Case presentation: A 71-year-old hispanic gentleman with chronic hyponatremia presented with hiccups, polydipsia, and a serum sodium concentration of 120 mEq/L associated with diffuse weakness, inattentiveness, and suicidal ideation. Symptomatic euvolemic hyponatremia warranted hypertonic saline treatment in the acute phase and water restriction in the chronic phase. Both interventions resulted in improvement in symptoms and/or the serum sodium concentration, but to a serum sodium level that persistently remained below the normal range. Remarkably, the urine osmolality appropriately fell when the serum sodium concentration fell below 126 mEq/L. Also remarkable was the appropriate increase in urine osmolality when the serum sodium concentration exceeded 126 mEq/L. The preservation of both concentration and dilution, albeit at a lower-than-normal serum osmolality, shows that the osmostat regulating antidiuretic hormone release had been “reset.” Both physiologic and pharmacologic resetting of the osmostat are discussed. Conclusions: Preservation of urinary concentrating and diluting ability at a lower-than-normal serum sodium concentration, especially in the setting of chronic hyponatremia, is diagnostic of a reset osmostat. The presence of a reset osmostat often confounds the treatment of concomitant acute hyponatremia. Early recognition of a reset osmostat avoids the need to normalize serum sodium concentration, expedites hospital discharge, and limits potential harm from overcorrecting acute hyponatremia.