Abstract: PO1440
Development of Hyponatremia and Overcorrection in a Patient with COVID-19 and Vasopressin Exposure
Session Information
- Fluid, Electrolyte, and Acid-Base Disorders: Clinical - 1
October 22, 2020 | Location: On-Demand
Abstract Time: 10:00 AM - 12:00 PM
Category: Trainee Case Report
- 902 Fluid, Electrolyte, and Acid-Base Disorders: Clinical
Authors
- Eswarappa, Meghana, Icahn School of Medicine at Mount Sinai, New York, New York, United States
- Patel, Niralee, Icahn School of Medicine at Mount Sinai, New York, New York, United States
- Farouk, Samira S., Icahn School of Medicine at Mount Sinai, New York, New York, United States
Introduction
Hyponatremia in the setting of elevated antidiuretic hormone (ADH) is a common phenomenon. However, exogenous ADH from vasopressin administration for hemodynamic support does not cause clinically relevant hyponatremia, despite its widespread use. Further, discontinuing vasopressin may lead to rapid rises in sodium that may be missed. Here, we present a case of a critically ill patient who developed hyponatremia in the setting of vasopressin use, with subsequent rapid overcorrection that required re-lowering of serum sodium after discontinuing vasopressin.
Case Description
A 40-year-old male with no known history was admitted to the ICU for respiratory failure due to COVID-19 pneumonia. Initial labs showed normal renal function and electrolytes. He received azithromycin, hydroxychloroquine, and glucocorticoids and required extracorporeal membrane oxygenation. During the first 45 days of hospitalization, he had persistent hypernatremia(sodium as high as 154 mEq/L) despite free water flushes(FWF) and intermittent IV 5% dextrose in water(D5W). On day 45, vasopressin and norepinephrine were initiated for hypotension. Over the next 72 hours, serum sodium decreased from 148 to 128 mEq/L (Figure 1). Urine osmolality(UOsm) and sodium were 684 mOsm/Kg and 145 mEq/L, respectively. During this 72-hour period, the patient received about 1L/day FWF. On day 55, vasopressin was discontinued for 11 hours, during which time the sodium rose from 126 to 138 mEq/L and UOsm decreased from 705 to 82 mOsm/kg. He received D5W to re-lower the sodium. Vasopressin was also restarted, and the sodium stabilized near 132mEq/L.
Discussion
Although pneumonia may have contributed to high ADH release in this patient, the timing of vasopressin administration prior to the development of hyponatremia and the acute rise in sodium after vasopressin discontinuation suggests an important role for exogenous ADH. Clinicians should pay close attention to fluctuations in sodium levels in patients receiving IV vasopressin, particularly when therapy is discontinued, given the risk of rapid overcorrection and development of osmotic demyelination syndrome.