SEIZURES AS THE INITIAL PRESENTATION OF COVID-19: A NOVEL CASE OF SYNDROME OF INAPPROPRIATE ANTIDIURETIC HORMONE

ABSTRACT

SESSION TITLE Medical Student/Resident Critical Care Posters SESSION TYPE Med Student/Res Case Rep Postr PRESENTED ON October 18-21, 2020 INTRODUCTION: The rapid and unprecedented spread of severe acute respiratory syndrome coronavirus disease 2019 (COVID-19) has significantly limited our understanding of this disease. As the pandemic continues to evolve, cardio-pulmonary symptoms predominate, however new atypical manifestation of COVID are increasingly recognized. CASE PRESENTATION A previously healthy 70-year-old man presents with a witnessed episode of new-onset seizures. Per family accounts, the episode lasted three minutes with tonic-clonic movements of all extremities, followed by a period of confusion. He had endorsed worsening fatigue and headaches with a declining appetite over the preceding two weeks. There was no history of cough, respiratory symptoms, sick contacts or prior similar episodes. Travel history was significant for a trip to California two weeks prior. He denied any medication, health supplement or illicit substance use. Past medical, surgical and family histories were unremarkable. On examination, the patient was obtunded and afebrile (37.3°C). He appeared visibly dyspneic, with an SpO2 of 85% on room air and RR of 34 /minute, but remained hemodynamically stable. Lung auscultation revealed scattered bilateral crackles while the neurological exam was non-focal. Clinically the patient appeared euvolemic. Computed tomography of the brain was unrevealing with no additional explanation for his prolonged altered mentation. Chest-radiography revealed bilateral air-space opacities. Labs indicated mild leukocytopenia (3.2 x109/L) with lymphopenia (0.6 x109/L) and a profound hyponatremia of 104 mEq/L. Renal and liver parameters were normal. Workup of his hyponatremia revealed a serum and urine osmolality of 230 mOsm/kg and 693 mOsm/Kg respectively with a urine sodium of 58 mmol/L. TSH and Cortisol levels were normal. Inflammatory markers were significantly elevated as summarized in Table 1. Influenza PCR, respiratory viral PCR panel, legionella urine antigen and blood cultures were all negative;however, the COVID-19 PCR assay was subsequently found to be positive. Based on the patient’s clinical and biochemical data, he was diagnosed with severe symptomatic hyponatremia secondary to SIADH in the setting of COVID-19 pneumonia. DISCUSSION: SIADH in the setting of pneumonia has been extensively studied and reported. A number of potential mechanisms have been postulated including extensive cytokine release, hypoxemia, nausea and stress. Additionally, inflammation (IL-6 in particular) itself has been reported to directly impair osmoregulation leading to hyponatremia. We hypothesize that milder forms of hypercytokinemia and hyper-inflammation could result in a number of less dramatic atypical presentations including SIADH. CONCLUSIONS: A high index of suspicion and awareness of this association is essential to mitigate SIADH related complications as cases of COVID-19 continue to rise. Reference #1 Edmonds, Z. V. (2012). Hyponatremia in pneumonia. Journal of Hospital Medicine, 7(S4). doi 10.1002/jhm.1933 Reference #2 Swart RM, Swart RM, Hoorn EJ, Betjes MG, Zietse R. Hyponatremia and Inflammation The Emerging Role of Interleukin-6 in Osmoregulation. NEP. 2011;118(2)p45–51. DISCLOSURES No relevant relationships by Yasmin Herrera, source=Web Response No relevant relationships by Kam Sing Ho, source=Web Response no disclosure on file for Bharat Narasimhan;No relevant relationships by Archana Pattupara, source=Web Response No relevant relationships by Joseph Poon, source=Web Response no disclosure on file for James Salonia;