DIABETES INSIPIDUS AS A SYMPTOM OF COVID-19 INFECTION: CASE REPORT

Abstract

SESSION TITLE: Medical Student/Resident Critical Care Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: COVID-19 disease usually presents as a respiratory infection which can progress to pneumonia, acute respiratory distress syndrome (ARDS) and multi organ dysfunction. The more severe cases occur in older adults, with chronic conditions such as cardiovascular and cerebrovascular diseases and diabetes[1,2]. We present a case of COVID-19 infection complicated by central diabetes insipidus (DI). CASE PRESENTATION: A 68 y/o man with history of HTN, HLD, DM- 2, A flutter presented with fever, headache, diarrhea and productive cough for 10 days. In the ED he was hypoxemic with O2 sat of 70% on room air and had diffuse wheezing throughout the lung fields. Covid PCR was positive. He was started on Lopinavir/Ritonavir x 2 days, which was aborted due to transaminitis. He was then started on Hydroxychloroquine and steroids. His hypoxemia worsened and on hospital day #15 he was intubated. On day #23 his mentation changed, he became nonresponsive to noxious stimuli, gag reflex was absent and he was polyuric. Over 24 hours his urine output increased to 7 L, serum Na increased from 136 to 153 mEq/L, urine osm was 152, specific gravity 1.005, urine specific gravity Na 43, MRI of the head showed no acute infarction, intracranial hemorrhage or mass, no abnormal intracranial enhancement. He was diagnosed with Central Diabetes Insipidus (DI) He was given DDAVP which lead to decreased urine output, increased urine Na, increased urine osm and specific gravity. His mentation returned to baseline, with a good gag reflex. He subsequently required tracheotomy, had a prolonged ICU course, and died due to worsening hypoxic respiratory failure. DISCUSSION: Multiple electrolyte derangements were described in the COVID positive patients; hyponatremia was the most frequent sodium abnormality[2]. Our patient demonstrated rapid and adequate response to DDAVP administration. Central DI can be produced by many entities like idiopathic, autoimmune, trauma or malignancy. He did not have a history of head trauma, cancer or brain surgery. The patient was briefly placed on Ketamine for sedation which was described as a cause of the central DI in some cases[3]. However,Ketamine's half life is 160 min. Patient was placed on Ketamine during the subsequent hospital stay without repeated electrolyte derangements. Hypothalamus and hypophysis infarct was less likely given negative imaging results and continuous AC. No other infectious causes were identified at that time. CONCLUSIONS: Critically ill patients with COVID pneumonia may develop central DI. We assume possible mechanism of central DI can be hypoxic encephalopathy which can occur in the setting of severe ARDS, or some more specific mechanism like autoimmune dysregulation leading to autonomic and neuroendocrine derangements. It can also be a sign of poor prognosis. We believe further studies and data analysis regarding this novel and complex viral infection will give more answers. Reference #1: Harapan H, Itoh N, Yufika A, et al. Coronavirus disease 2019 (COVID-19): A literature review. J Infect Public Health. 2020;13(5):667-673. https://doi.org/10.1016/j.jiph.2020.03.019 Reference #2: Zhang X, Cai H, Hu J, et al. Epidemiological, clinical characteristics of cases of SARS-CoV-2 infection with abnormal imaging findings. Int J Infect Dis. 2020;94:81-87. https://doi.org/10.1016/j.ijid.2020.03.040 Reference #3: Gaffar S, Eskander JP, Beakley BD, McClure BP, Amenta P, Pierre N. A case of central diabetes insipidus after ketamine infusion during an external to internal carotid artery bypass. J Clin Anesth. 2017;36:72-75. https://doi.org/10.1016/j.jclinane.2016.09.024 DISCLOSURES: No relevant relationships by Moses Bachan, source=Web Response No relevant relationships by Zinobia Khan, source=Web Response No relevant relationships by Hana Rajevac, source=Web Response