Jose Russe-Russe, MD, James Pellegrini, MD, Kristen Farraj, DO, Melvin Joy, MD, Paul Mustacchia, MD, MBA Nassau University Medical Center, East Meadow, NYIntroduction: Acute liver failure (ALF), characterized by acute liver injury, hepatic encephalopathy, and an increased international normalized ratio, is subcategorized based on the timeline as hyperacute (< 7 days) and acute (7 to 21 days), where cerebral edema is typical, or subacute ( >21 days and < 26 weeks).Case Description/Methods: A 54-year-old female with a history of diabetes complained of fevers, chills, headache, chest pain, abdominal pain, nausea, vomiting, diarrhea, body aches, and back pain for three days. Two days prior, the patient had tested positive for COVID-19. On admission, the patient did not have any respiratory compromise. Initial biochemical tests were unremarkable, except for elevated inflammatory markers and imaging suggestive of atypical pneumonia. After the third day in the hospital, the patient began developing worsening respiratory status and was transferred to critical care; the following day, the patient was intubated for acute respiratory failure. On day eight of admission, the patient began having elevated liver-related proteins and worsening inflammatory markers (Figures 1). Two days later, the patient passed despite aggressive therapeutic measures on day ten after admission.Discussion: In COVID-19, ALF may result from the virus invasion, which directly infects cells via angiotensin-converting enzyme receptor-2 present in the liver cells, including cholangiocytes (60%) and hepatocytes (3%); and are absent in Kupffer cells, where direct viral impact, systemic inflammation, drug-induced damage, congestion abnormalities, and hypoxia-induced damage contribute to liver damage. In a cytokine storm, an acute hyperinflammatory response is responsible for critical illness in many conditions, including viral infections, cancer, sepsis, and multi-organ failure. However, the exact mechanisms of COVID-19 in the induction of ALF have not been identified. Empiric therapy is often started with the diagnostic workup when hyperacute or ALF is suspected, consisting of N-acetylcysteine (NAC). However, management is directed based on the specific clinical requirements of each patient; NAC, anticoagulants, monoclonal antibodies, plasmapheresis, and symptomatic treatment may be used concomitantly to improve outcomes. Cases of hyperacute liver failure itself are a rare disorder. Therefore, when hyperacute or ALF is suspected in COVID-19 disease, early recognition, and prompt action are required to improve patient survival.Figure: Figure 1. A: Inflammatory markers trending from day one of admission to day ten. [Ferritin (blue line), Lactose Dehydrogenase (LDH; red line), C-reactive protein (CRP; yellow line), D-Dimers (DD; green line), Erythrocyte sedimentation rate (ESR; orange dot), Fibrinogen (turquoise line), Interleukin-6 (IL-6; gold diamond)]. B: Liver-related proteins trending from day one of admission to day ten. [Alanine aminotransferase (ALT; blue line), Aspartate aminotransferase (AST; red line), Alkaline phosphatase (ALP; yellow line), Total bilirubin (TB; green line), Total protein (TP; orange line), Albumin (Alb; turquoise line)]. Disclosures:Jose Russe-Russe indicated no relevant financial relationships. James Pellegrini indicated no relevant financial relationships. Kristen Farraj indicated no relevant financial relationships. Melvin Joy indicated no relevant financial relationships. Paul Mustacchia indicated no relevant financial relationships. Jose Russe-Russe, MD, James Pellegrini, MD, Kristen Farraj, DO, Melvin Joy, MD, Paul Mustacchia, MD, MBA. A0512 - Hyperacute Liver Failure Resulting From COVID-19 Infection, ACG 2022 Annual Scientific Meeting Abstracts. Charlotte, NC: American College of Gastroenterology.
