A RARE AND FATAL CASE OF ACUTE FULMINANT LIVER FAILURE INDUCED BY COVID-19 INFECTION

Abstract

TOPIC: Chest Infections TYPE: Medical Student/Resident Case Reports INTRODUCTION: The SARS-CoV-2 virus, in accordance with the name designated to it by viral taxonomists, primarily causes severe acute respiratory distress syndrome. A challenge of this novel coronavirus has been discovering and preventing its indiscriminate and catastrophic effect on other organs. We present a rare case of the SARS-CoV-2 virus precipitating fulminant hepatic failure in a patient without respiratory symptoms or prior evidence of liver disease. CASE PRESENTATION: A 60 year-old female with history of atrial fibrillation, emphysema, and renal cell carcinoma status post left radical nephrectomy presented with weakness and fatigue. On day 12 of admission, she became hemodynamically unstable due to atrial fibrillation with rapid ventricular response, requiring electrical cardioversion, emergent intubation and transfer to ICU. Repeat SARS-CoV-2 PCR test was positive, although negative on admission. Dexamethasone, vancomycin and piperacillin-tazobactam were initiated, and one dose of Remdesivir was given after an unremarkable liver panel. No further Remdesivir was given, as six hours later, the patient had abrupt worsening of her liver function tests, with eventual peak AST of 2610 IU/L, ALT of 14860 IU/L and INR of 9.12. Fibrinogen was 136 mg/dL, ammonia 290 mcmol/L, lactate 11.51 mmol/L and IL-6 143.9 pg/mL. Viral causes for acute hepatitis were negative and abdominal ultrasound was unremarkable. The patient was treated with N-acetylcysteine, methylprednisolone, lactulose and rifaximin. She was ineligible for transfer to a liver transplant center due to her COVID-19 positive status. Unfortunately, despite conservative management, patient expired after developing severe disseminated intravascular coagulation, renal failure, and refractory septic shock. DISCUSSION: In recent literature, SARS-CoV-2 has primarily been recognized for causing mild liver injury, while fulminant hepatic failure is a rare occurrence (1,2). Remdesivir, which this patient received only one dose of, is known to cause mild transaminitis. It has been shown to cause severe liver injury only when used in combination with amiodarone, due to the latter's role as a moderate inhibitor of CYP3A4 and p-glycoprotein (3). This patient did not have exposure to hepatotoxic agents, prolonged state of shock, evidence of metastatic liver lesions or acute viral hepatitis to explain profound liver failure. Hence, we postulate that the SARS-CoV-2 virus may have directly targeted the hepatobiliary cells. Further studies of the pathophysiology of liver injury from this virus may allow better prevention and treatment. CONCLUSIONS: Understanding SARS-CoV-2's effects on a hepatocellular level may allow for anticipatory monitoring and prevention of liver damage from this virus. For those more severely affected, better treatments would help avoid the difficult course of emergency liver transplantation and resultant need for lifelong immunosuppression. REFERENCE #1: Gupta A, Mahhavan MV, Sehgal K, et al. Extrapulmonary manifestations of COVID19. Nature Medicine 26:1017-1032, July 2020 REFERENCE #2: Melquist S, Estepp K, Aleksandrovich Y, et al. COVID-19 presenting as fulminant hepatic failure. Medicine 99:issue 43, October 23, 2020 doi 10.1097 REFERENCE #3: Remdesivir in LiverTox: Clinical and Research Information on Drug-Induced Liver Injury (Internet). National Institute of Diabetes and Digestive and Kidney Diseases, November 4, 2020; https://www.ncbi.nlm.nih.gov/books/NBK564049/?report=printable DISCLOSURES: No relevant relationships by Chester Choi, source=Web Response No relevant relationships by Madlena Nalbandian, source=Web Response No relevant relationships by Eulia Tlisov, source=Web Response