S2907 Portal Vein Thrombosis in the COVID-19 Era: A Rare Presentation

Abstract

Introduction: An increased incidence of venous thromboembolism (VTE) has been reported with SARS-COV2 (severe acute respiratory syndrome coronavirus 2) infections. VTE in unusual sites like the portal vein is limited to case reports. This report adds to the growing body of literature about thrombotic complications with SARS-COV2 infections. Case Description/Methods: A female aged 39 with a medical history of diabetes, hypertension and cholecystectomy presented with three days of right upper quadrant (RUQ) pain. She denied substance use, cirrhosis, autoimmune disease or previous VTE. On presentation, vitals were stable. She had RUQ tenderness. Blood work revealed elevated alkaline phosphatase and transaminases. White cell count, bilirubin and coagulation were normal. Imaging revealed occlusive thrombus of the right portal vein proximal to the bifurcation with peripheral extension (images 1 and 2). Extensive hypercoagulable and infectious workup was negative. She was immediately started on enoxaparin. A chest x ray was suggestive of SARS-COV2 infection and confirmatory testing was positive. Her symptoms improved and lab abnormalities resolved. She was discharged home with oral anticoagulants and instructions to self-isolate. Discussion: Most reported cases of Portal vein thrombosis (PVT) with SARS-COV2 are incidental. Our patient presented with RUQ abdominal pain, highlighting an unusual presentation. PVT is rare and occurs with cirrhosis, connective tissue disease, malignancies, pancreatitis and thrombophilia. These were absent in our patient and other causes of hypercoagulability such as antiphospholipid syndrome, proteins C, S and antithrombin deficiencies, Factor V mutations were ruled out. SARS-COV2 infected patients experience a hypercoagulable state with the incidence of thrombotic complications as high as 31%. Some have suggested that systemic inflammation leads to endothelial dysfunction, causing Von-Willebrand Factor and toll-like receptor activation, leading to platelet aggregation and coagulation cascade initiation. Others have speculated that inflammatory cytokines bind to endothelial surface angiotensin converting enzyme receptor leading to lymphocytic endotheliitis and prothrombotic gene overexpression. Anticoagulation should be used in PVT to reduce complications of intestinal infarction and portal hypertension. Recanalization occurs in 60% of cases with anticoagulation in the first week. We used therapeutic enoxaparin and switched to an oral anticoagulant for a 6-month course.Figure 1.: Image 1 a and b: CT scan showing right portal vein thrombosis, just at its bifurcation (blue arrows) c: chest x ray showing bilateral patchy opacities.