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Abstract: SA-PO712

Differentiating Vasopressin Withdrawal Syndrome from Gestational and Central Diabetes Insipidus: A Learning Case Study

Session Information

Category: Fluid, Electrolytes, and Acid-Base Disorders

  • 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical

Authors

  • Hansrivijit, Panupong, Massachusetts General Hospital, Boston, Massachusetts, United States
  • Liu, Annie, Massachusetts General Hospital, Boston, Massachusetts, United States
  • Cheung, Pui Susan Wen, Massachusetts General Hospital, Boston, Massachusetts, United States
Introduction

Differentiating vasopressin withdrawal syndrome (VWS) from gestational diabetes insipidus (GDI) and central diabetes insipidus (CDI) in a pregnant woman is challenging. Prolonged administration of exogenous vasopressin can lead to negative feedback on endogenous anti-diuretic hormone (ADH) production from the posterior pituitary gland. CDI can occur following a shock leading to pituitary infarction and usually co-exists with anterior pituitary axis deficits given their enriched blood supply. Finally, GDI is mediated by placenta-derived vasopressinase which degrades endogenous ADH and exogenous vasopressin. GDI typically presents in the 2nd and 3rd trimester and can persist up to 4-6 weeks postpartum. A baseline urine analysis and serum copeptin level is a useful tool in the diagnosis of polyuria in pregnancy.

Case Description

A 32-year-old, 24+2-week pregnant female was admitted to the Intensive Care Unit for peripartum cardiomyopathy requiring Impella device placement. She was started on phenylephrine and vasopressin for hypotension on hospital day (HOD) 1. On HOD13, vasopressin was stopped, and she became polyuric with nine liters of urine output leading to some issues with the Impella device. Urine osmolality was 100 mosm/kg. Vasopressin was then restarted with resolution of polyuria. Nephrology was then consulted. Fortunately, urine analysis was collected on the day of admission and showed urine specific gravity of >1.030. While on vasopressin, the serum sodium was 129 mmol/L, urine osmolality was 678 mosm/kg, copeptin level was <2.8 pmol/L. Anterior pituitary axis work-up was unremarkable. She delivered on HOD21 while on vasopressin. Vasopressin was successfully discontinued on HOD22 with a bridge using desmopressin. Eventually, desmopressin was completely stopped on HOD37 (16 days after delivery).

Discussion

This patient’s presentation favors VWS over GDI. First, the urine specific gravity on admission suggested presence of ADH effect which argues against GDI. Second, low copeptin level was auggestive of VWS. The copeptin level is expected to be within reference range in GDI or elevated in the setting of cardiogenic shock. Finally, absence of anterior pituitary axis dysfunction would make CDI very less likely. In conclusion, urine chemistry and copeptin level are essential in the diagnosis of polyuria in pregnancy.