Transient Central Diabetes Insipidus Occurring After Vasopressin Infusion

The common causes of central diabetes insipidus (CDI) include trauma to the pituitary, hypoperfusion, and malignancy. However, CDI can also be transient. An emerging cause of transient diabetes insipidus is through the use and withdrawal of vasopressin. Here, we present a case of transient CDI that developed during an intensive care unit admission.

A Caucasian woman presented to the emergency room after a fall. On presentation, the patient was found to be in shock and was admitted to the surgical intensive care unit. Treatment with norepinephrine, vasopressin, and intravenous antibiotics was started. On day 5 of hospitalization, the patient's blood pressure improved, and treatment with vasopressin was discontinued. On day 6 of hospitalization, the patient's urine output increased and serum sodium level was elevated. Despite increasing free water, serum sodium level continued to rise. Endocrinology division was consulted, and urine osmolality was consistent with diabetes insipidus (DI). Urine osmolality at 30 and 60 minutes after desmopressin (1-desamino-8-d-arginine vasopressin [DDAVP]) was consistent with CDI. Magnetic resonance imaging scan of the brain showed no intracranial pathology. Over the next day with scheduled DDAVP, serum sodium level decreased below the goal level. Thus, DDAVP was held. Prior to discharge, the patient did not require additional DDAVP. She was discharged without DDAVP.

Our patient's workup was initially consistent with CDI. However, the DI resolved spontaneously, supporting transient CDI secondary to vasopressin infusion. Different theories have emerged about why this occurs with vasopressin. However, further investigation is needed.

Although rare, it is important to monitor for DI after vasopressin infusion and have a suspicion that DI may be transient in the absence of a clear cause.