A51-48 Severe Hyponatremia Corrected by Potassium Replacement Alone: Early Desmopressin to Prevent Overcorrection

Abstract Introduction Osmotic demyelination syndrome (ODS) is a rare but potentially devastating complication of overly rapid correction of serum sodium in hyponatremia. Patients at highest risk for ODS include those with serum sodium (SNa) 105 mmol/L, hypokalemia, malnutrition, or liver disease. We present a case of severe hyponatremia with concurrent hypokalemia and metabolic alkalosis secondary to vomiting, poor solute intake, and increased water consumption. Sodium levels and metabolic alkalosis improved with potassium chloride replacement. Desmopressin was administered to prevent overcorrection and reduce the risk of ODS. Case Presentation A 63-year-old woman with diabetes, hypertension, and hypothyroidism presented with one week of confusion, nausea, and vomiting. Her family reported chronically poor solute intake, recent vomiting, and increased water intake. Labs showed severe hyponatremia (102 mmol/L), hypokalemia (1.9 mmol/L), hypochloremia (60 mmol/L), hypomagnesemia (1.7 mg/dL), and metabolic alkalosis (pH 7.61, pCO2 26 mmHg, HCO3⁻ 26 mmol/L). Serum osmolality was 226 mOsm/kg, urine sodium 12 mmol/L, urine potassium 20 mmol/L, and urine osmolality 249 mOsm/kg. In the ICU, she received intravenous potassium chloride through a central line (up to 220 mEq/day). Desmopressin 2 mcg every 8 hours was administered to prevent water diuresis and overcorrection. Serum sodium rose gradually to 110, 116, and 123 mmol/L over the first three days. Desmopressin was stopped on day 3, and intravenous fluids were given for volume repletion. She was discharged with serum sodium 132 mmol/L. Discussion Potassium is as osmotically active as sodium. Replenishing potassium in hypokalemia raises serum sodium through several mechanisms: (1) shifting potassium into cells in exchange for sodium, and (2) extracellular chloride follows potassium into cells, increasing intracellular osmolality and drawing water in, further concentrating serum sodium. These effects should be considered when anticipating the sodium correction rate, especially in severe hyponatremia with hypokalemia. These patients are at high risk for water diuresis, rapid overcorrection, and ODS. To prevent overcorrection and ODS, desmopressin can be given early for 24-48 hours or until serum sodium reaches at least 125 mEq/L (termed ‘DDAVP block’). Desmopressin, a selective agonist of the V2 receptor, prevents aquaresis and allows for more predictable sodium correction during potassium replacement. Frequent sodium assessments (every 2-4 hours) and urine output monitoring are essential to guide safe correction. Conclusion This case demonstrates that severe hyponatremia with hypokalemia can resolve with potassium supplementation and emphasizes the utility of desmopressin use to prevent overcorrection and ODS in high risk groups. This abstract is funded by: None