Abstract: FR-PO0631
Vasopressin as a Cause of Inducible Central Diabetes Insipidus in the Intensive Care Unit
Session Information
- Fluid, Electrolyte, and Acid-Base Disorders: Clinical - 2
November 07, 2025 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Fluid, Electrolytes, and Acid-Base Disorders
- 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical
Authors
- Gerardot, Shori, Medical University of South Carolina, Charleston, South Carolina, United States
- Budisavljevic, Milos N., Medical University of South Carolina, Charleston, South Carolina, United States
Introduction
Hypotension is a common diagnosis in intensive care unit (ICU) population from a variety of causes. Arginine Vasopressin is a medication growing in popularity as a method of treatment for vasoplegic shock in ICU population. Diabetes Insipidus (DI) has been well described in literature as a cause of polyuria. The gold standard for differentiation of Primary Polydipsia, Central DI and Nephrogenic DI has been the water deprivation test. Newer methods for differentiation have been developed such as Copeptin.
Case Description
A 50 year old male with a medical history of type 2 diabetes Mellitus and hypertension was being treated in the cardiovascular ICU for Ludwigs angina. The patient had undergone multiple mediastinal washouts and debridement for necrotizing mediastinitis. He had prolonged hypotension requiring a month-long course of continuous vasopressin for treatment of hypotension. When Vaso was discontinued he became polyuric, with 1.0 – 1.5 L per hour of urine output (UoP). Urine Osmolarity was measured when Vaso was discontinued and re-initiated, 286 and 648 mmol/L respectively. After restarting Vaso, the his UoP decreased significantly. When Vaso was discontinued again, the patient became polyuric and hypernatremic (150 mmol/L). At this time the patient was treated with two doses of desmopressin which corrected both his polyuria and hypernatremia. After three days without vasopressin and close monitoring his UoP and serum sodium had both normalized. Throughout the hospitalization the patient had normal renal function.
Discussion
Medications have been described in literature as a cause of reversible DI. Since the widespread use of Vaso for hypotension, few case reports of Vaso induced DI have been described. While this patient was being treated for prolonged hypotension with vaso, it appears that his intrinsic production of antidiuretic hormone had decreased. This was evident with the changes of UoP with changes in Vaso dosage. Treatment of this patient’s Central DI was done with weaning of Vaso and monitoring of UoP and serum sodium. Desmopressin was used for stabilizing serum sodium until natural regulation ADH was achieved.