Abstract
Introduction: Transient Central Diabetes Insipidus (tCDI) induced by vasopressin withdrawal is a rare condition which is possibly under recognized. It occurs in very sick, often critically ill patients and usually complicates an already complex clinical picture, so early recognition and treatment are critical to reduce morbidity.
Case Description: A 47-y/o male with a PMH of Coffin Lowry syndrome, atrial fibrillation, and GERD presented with abdominal pain and flu like symptoms. His home medications were metoprolol, loratadine and colestipol. Work up revealed bowel perforation for which he was taken to the OR for repair. Intraoperatively he developed septic shock requiring pressor support with norepinephrine and vasopressin. He was weaned off norepinephrine on post-op day (POD)1, and vasopressin on POD 2. Approximately three hours after withdrawal of vasopressin support his urine output increased dramatically up to a peak of 350 cc/hour with a recorded 24hr urine volume of >5L. Concurrently, his serum sodium was found to have increased from 147 mmol/L to 173 mmol/L (n 135-145) over the course of 13 hours. Clinically, he became increasingly lethargic with abnormal eye movements. His sodium did not improve with fluid management with D5W. His other laboratory values included a urine osmolality of 141 mOsm/kg, urine sodium of 60 mmol/L and a peak serum sodium of 177mmol/L. He was administered 1mcg desmopressin and his D5W rate was increased. His urine output dropped gradually to ~150cc/hr, his serum sodium level started to trend down to 168 mmol/L and his urine osmolality increased to 439 mOsm/kg five hours after desmopressin administration, with improvement in mental status. The patient received a total of two doses of desmopressin and continued support with IV fluids. His sodium eventually normalized, and his polyuria did not return.
Discussion: This patient’s clinical picture is consistent with tCDI secondary to discontinuation of vasopressin. Transient Central diabetes insipidus due to vasopressin withdrawal is a phenomenon that is not well understood, but there is a strong male preponderance, and it tends to occur more commonly in patients with underlying neurological conditions, as did our patient. Current proposed mechanisms include decreased production and release of exogenous ADH due to negative feedback, down regulation of the V2 receptors, and hypoperfusion to the posterior pituitary. This condition deserves more investigation to better understand the incidence, risk factors and pathophysiological mechanisms.
Sodium valproate – can it mask neurohypophyseal diabetes insipidus?
