Protracted Acute Hypervolemic Hypernatremia Unmasked After Vasopressin Therapy: Case Report, Literature Review, and Proposed Algorithmic Approach

Abstract

Acute hypervolemic hypernatremia (HHN) is the most common form of hypernatremia in critical care settings. Previous reports implicated acute kidney injury and vasopressin withdrawal-induced central diabetes insipidus. We present the case of a 52-year-old woman who developed HHN after treatment of septic shock due to complicated bowel perforation. After discontinuation of a 30-hour infusion of vasopressin analog, the patient manifested hypernatremia (150 to 156 mEq/L, equivalent to mmol/L) with hyponatriuria (49 mEq/L), hypoosmotic urine (163 mOsm/L), and polyuria (6.9 L/day) in a setting of cumulative positive fluid balance of 20.1 L. A trial of desmopressin yielded incomplete urinary concentration suggestive of renal resistance to desmopressin likely due to fluid overload. Despite positive water balance, her urine sodium was low at 36 to 49 mEq/L compared to serum sodium of 152 to 156 mEq/L. The hypernatremia with polyuria persisted for 16 days and resolved after treatment of the positive cumulative water balance (with controlled diuresis prioritizing natriuresis). HHN may result in insufficient urine sodium clearance. We propose modifying the diagnostic/treatment algorithm by including HHN in a critical care setting, and recommending judicious administration of a loop diuretic to prioritize natriuria in hypernatremia with extreme cumulative fluid overload.