Case Report Transient Central Diabetes Insipidus after Discontinuation of Vasopressin Nathaniel Carman , 1 Carl Kay , 1 Abigail Petersen, 2 Maria Kravchenko, 1 and Joshua Tate 1 1 Department of Medicine, Brooke Army Medical Center, Fort Sam Houston, TX, USA 2 Uniformed Services University of the Health Sciences, Bethesda, MD, USA Correspondence should be addressed to Nathaniel Carman; nathaniel.a.carman.mil@mail.mil Received 19 August 2019; Accepted 14 November 2019; Published 11 December 2019 Academic Editor: Eli Hershkovitz Copyright © 2019 Nathaniel Carman et al. is is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Central diabetes insipidus (CDI) is an uncommon condition resulting from lack of vasopressin secretion from the posterior pituitary gland typically caused by some form of destruction of the gland. Here we present a case of transient CDI aſter discontinuation of vasopressin used for septic shock without evidence of overt pituitary damage. Serum sodium concentration peaked at 160 mmol/L in the setting of polyuria within days of vasopressin discontinuation without identified alternative etiologies. Sodium levels and urine output normalized with administration of desmopressin with continued stability aſter desmopressin was discontinued. is is one of few reported cases of diabetes insipidus occurring aſter discontinuation of vasopressin and the rapid and profound response to desmopressin in this case proves a central etiology. is case allows for speculation into predisposing risk factors for this phenomenon including preexisting neurological disease. 1. Introduction Central diabetes insipidus (CDI) is characterized by deficient secretion of vasopressin, a hormone produced in the hypo- thalamus and secreted from the posterior pituitary gland. e lack of vasopressin leads to hallmark findings of polyuria, polydipsia and hypernatremia. e most common and well described causes of CDI are secondary to injury and destruc- tion of the hypothalamus or posterior pituitary including trauma, neurosurgery, tumors, ischemia and autoimmunity [1]. What is less well described is CDI following cessation of therapeutic exogenous vasopressin, a common treatment for patients with vasodilatory shock and refractory hypotension. Few cases of CDI related to withdrawal of vasopressin have been reported with the actual incidence of vasopressin asso- ciated CDI remaining largely unknown [2–6]. While sparse in the literature, there have been reports of this phenomenon allowing for speculation of potential predisposing risk factors as well as underlying mechanisms. We report a case of tran- sient CDI following discontinuation of vasopressin for treat- ment of urinary tract infection-induced septic shock. 2. Case Presentation An 88-year-old male with a history of normal pressure hydro- cephalus and ventriculoperitoneal (VP) shunt presented to the emergency department for altered mental status, fever, and hypotension. Evaluation was notable for hyponatremia [serum sodium 129 mmol/L (reference range 133– 145 mmol/L)] and Pseudomonas aeruginosa positive urine culture. Septic shock was treated via volume resuscitation, vasopressors, and broad-spectrum antibiotics. Vasopressors, norepinephrine and vasopressin (0.04 units/min), were weaned off approximately 24 hours aſter intensive care unit admission (Figure 1). From hospital days 3–5, the patient experienced an acute rise in serum sodium concentration (130 mmol/L–159 mmol/L) associated with a diuresis of 18 liters over 72 hours (average output of 250 mL/hr). e patient received no diuretics and serum glucose was without hyper- glycemic excursions while on a subcutaneous insulin regimen. Serum osmolality was 344 (285–310) mOsm/kg and urine osmolality was 203 (300–1300) mOsm/kg with rise to 545 mOsm/kg aſter administration of desmopressin 2 mcg Hindawi Case Reports in Endocrinology Volume 2019, Article ID 4189525, 4 pages https://doi.org/10.1155/2019/4189525