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Adipsic Diabetes Insipidus ‑ the Challenging Combination of Polyuria and Adipsia : a Case Report and Review of Literature

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Adipsic Diabetes Insipidus ‑ the Challenging Combination of Polyuria and Adipsia : a Case Report and Review of Literature This document is downloaded from DR‑NTU (https://dr.ntu.edu.sg) Nanyang Technological University, Singapore. Adipsic Diabetes Insipidus ‑ the challenging combination of polyuria and adipsia : a case report and review of literature Dalan, Rinkoo; Chin, Hanxin; Hoe, Jeremy; Chen, Abel; Tan, Huiling; Boehm, Bernhard Otto; Chua, Karen SuiGeok 2019 Dalan, R., Chin, H., Hoe, J., Chen, A., Tan, H., Boehm, B. O., & Chua, K. S. (2019). Adipsic Diabetes Insipidus ‑ the challenging combination of polyuria and adipsia : a case report and review of literature. Frontiers in Endocrinology, 10, 630‑. doi:10.3389/fendo.2019.00630 https://hdl.handle.net/10356/142472 https://doi.org/10.3389/fendo.2019.00630 © 2019 Dalan, Chin, Hoe, Chen, Tan, Boehm and Chua. This is an open‑access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. Downloaded on 03 Oct 2021 23:00:13 SGT CASE REPORT published: 18 September 2019 doi: 10.3389/fendo.2019.00630 Adipsic Diabetes Insipidus—The Challenging Combination of Polyuria and Adipsia: A Case Report and Review of Literature Rinkoo Dalan 1,2,3*, Hanxin Chin 1, Jeremy Hoe 1, Abel Chen 1, Huiling Tan 4, Bernhard Otto Boehm 1,2 and Karen SuiGeok Chua 5 1 Department of Endocrinology, Tan Tock Seng Hospital, Singapore, Singapore, 2 Metabolic Medicine, Lee Kong Chian School of Medicine, Nanyang Technological University Singapore, Singapore, Singapore, 3 Department of Medicine, Yong Loo School of Medicine, National University of Singapore, Singapore, Singapore, 4 Department of Anaesthesiology, Intensive Care and Pain Medicine, Tan Tock Seng Hospital, Singapore, Singapore, 5 Department of Rehabilitation Medicine, Tan Tock Seng Hospital, Singapore, Singapore Adipsic Diabetes Insipidus is a rare hypothalamic disorder characterized by a loss of thirst in response to hypernatraemia accompanied by diabetes insipidus. These occur secondary to a congregation of defects in the homeostatic mechanisms of water balance. A 27-year old Chinese female presented with Adipsic Diabetes Insipidus after cerebral arteriovenous malformation (AVM) surgery. Initial diagnosis and management Edited by: was extremely challenging. Long term management required a careful interplay between Vincent Geenen, low dose vasopressin analog treatment and fluids. Detailed charts of medication and University of Liège, Belgium sodium balance are described in the case presentation. We performed a literature search Reviewed by: Daniel Georges Bichet, of similarly reported cases and describe the possible pathogenesis, etiology, clinical Université de Montréal, Canada presentation, acute and chronic management, and prognosis. Joseph George Verbalis, Georgetown University, United States Keywords: adipsia, diabetes insipidus, water balance, thirst and drinking, hypothalamus and neuroendocrinology *Correspondence: Rinkoo Dalan [email protected] BACKGROUND AND INTRODUCTION Specialty section: Hypothalamic Adipsic Diabetes Insipidus (ADI), a rare syndrome with heterogenous clinical This article was submitted to presentation, is characterized by a congregation of defects in the homeostatic mechanisms for water Neuroendocrine Science, balance. These include osmoregulation of thirst mechanism, arginine vasopressin secretion, and a section of the journal renal ability to concentrate urine. Less than one hundred severe cases have been reported worldwide Frontiers in Endocrinology over the last four decades (1). Received: 26 June 2019 The management of such patients is extremely challenging as these patients tend to suffer from Accepted: 30 August 2019 wide swings in plasma sodium even when the DI is well-controlled(2). Published: 18 September 2019 We report a case of severe ADI which occurred postoperatively after cerebral arteriovenous Citation: malformation (AVM) surgery. We describe the possible pathogenesis in this case and review the Dalan R, Chin H, Hoe J, Chen A, literature for all similarly reported cases and describe the potential mechanisms involved, clinical Tan H, Boehm BO and Chua KS presentation, acute as well as chronic management, and prognosis. (2019) Adipsic Diabetes Insipidus—The Challenging Combination of Polyuria and Adipsia: CASE PRESENTATION A Case Report and Review of Literature. Front. Endocrinol. 10:630. A 27-year-old lady presented with left frontal intracerebral hemorrhage with intraventricular doi: 10.3389/fendo.2019.00630 extension secondary to a basal ganglia large complex (AVM) with complex arterial feeders from left Frontiers in Endocrinology | www.frontiersin.org 1 September 2019 | Volume 10 | Article 630 Dalan et al. Adipsic Diabetes Insipidus middle cerebral arteries (MCA), and anterior cerebral arteries Figure 1). The serum cortisol, growth hormone, insulin like (ACA) with Spetzler Martin Grading Scale of 3 (3). growth factor-1, thyroid function, and prolactin levels were all After initial recovery from decompressive craniotomy and within the normal range. clot evacuation surgery, she underwent an elective AVM excision After a ventriculoperitoneal shunt insertion (done to maintain surgery ∼2 weeks later. During the AVM surgery, the surgeons intracranial pressure) 6 weeks after the AVM excision, she reported brisk bleeding from the feeder vessels (the MCA, was transferred to rehabilitation wards and the intravenous ACA, and the choroidal vessels) with severe intracerebral desmopressin regime converted to a subcutaneous (SC) regime hemorrhage and intra-ventricular hemorrhage requiring massive (see Figure 1). When nasogastric tube feeding was discontinued, blood transfusion of up to 32 units intraoperatively. She was we tried to regulate fluids by thirst. Blood investigations placed on barbiturate-induced coma and induced hypotension to showed rising sodium levels up to 165 mmol/L and she minimize cerebral oedema (4). felt no thirst during this period of hypernatraemia despite She started to have polyuria with large volumes of urine a serum osmolality of 350 mosm/kg. She remained adipsic intra-operatively soon after the episode of profuse intraoperative despite recovery of aphasia. A thirst scale was not used as bleeding. Although pre-operatively her sodium concentrations upon questioning, she verbalized that she felt no thirst at all, were normal, sodium concentrations were higher immediately and a thirst scale could not be applied. Hence, fluids had to (within the 1st hour) postoperatively within the range of 151– be regulated to maintain sodium balance. Her urine output 160 mmol/L in tandem with a low urine osmolality <130 was fixed and her sodium balance well-regulated on a SC mosm/L. Transient DI was considered and she was started on regime of desmopressin 0.5 mcg in the morning and 0.375 intravenous desmopressin (IV desmopressin) 1 mcg which was mcg at night, with regulated fluids of 1.5–2L per day. She given daily along with 3.5–4 L half strength saline infusion for 3 did not have any evidence of thermoregulatory disturbances. consecutive days. Polyetheretherketone (PEEK) cranioplasty was performed ∼4 However, she since developed pulmonary oedema (likely months after initial surgery. a consequence of massive blood transfusion intraoperatively, After 5 months of intensive multidisciplinary rehabilitation, intravenous hypotonic fluids, and concurrent IV desmopressin) she still had a non-functional dominant right hand and on postoperative day 4, IV desmopressin was discontinued, significant residual cognitive deficits, and safe dosing and self- and fresh frozen plasma and diuretics (intravenous furosemide administration of subcutaneous desmopressin was not possible 40 mg) were administered to reduce the extra-vascular oedema. in the long term. In the subsequent hour, she started to develop polyuria again A trial of nasal desmopressin and oral desmopressin showed with a urine output of 800 mL in a single hour and her sodium significant variable absorption leading to greater fluctuations concentrations up trended to 172 mmol/L. In view of the in the sodium concentrations. Hereafter, we decided to use concomitant postoperative cerebral oedema, it was decided to the sublingual desmopressin available as desmopressin Melt. lower the sodium concentrations in a targeted manner such that After several trials of different dosing regimens we were rate of decrease in sodium remained within 5–10 mmol/L/day, able to fix the urine output to approximately 2 L/day using with a target level of 155 mmol/L. A low dose of IV desmopressin desmopressin Melt oral lyophilizate 120 mcg (2 tablets) in the 0.25 mcg was administered, and titration regime suggested with morning and 60 mcg (1 tablet) in the evening. However, at a view to maintain an hourly urine output of lower than 100 this dose she was having hyponatremia at certain times of mL/h. She required IV 0.75 mcg desmopressin on postoperative the day. We performed further dose titration by cutting the day 5, and then IV 0.25 mcg twice daily on day 6 when she desmopressin tablets using tweezers/forceps to lift the tablets reached a target level of 155 mmol/L. This sodium concentration from the blister pack and cut the tablets into exact quarter could be maintained with the desmopressin dosing for pieces (each 15 mcg) with the help of a pill
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