S5696 Double Trouble in a Stable Cirrhotic: Simultaneous Superior and Inferior Mesenteric Vein Thrombosis, Recent Variceal Banding, and the Endless Anticoagulation Dilemma

Introduction: Cirrhosis induces complex alterations in hemostasis, shifting the balance between bleeding and thrombosis. These changes involve reduced hepatic synthesis of procoagulant and anticoagulant factors, thrombocytopenia due to hypersplenism, and compensatory elevations in factor VIII and von Willebrand factor. Endothelial dysfunction, and impaired fibrinolysis contribute to a fragile yet prothrombotic state. This “rebalanced” hemostatic system may predispose even patients with compensated cirrhosis to thrombotic complications. While portal vein thrombosis is a known complication, concurrent thrombosis of both the superior and inferior mesenteric veins is infrequently observed. We present a case of compensated cirrhosis complicated by superior mesenteric vein (SMV) and inferior mesenteric vein (IMV) thrombosis, despite normal platelet count and mildly elevated international normalized ratio (INR), illustrating the paradoxical hypercoagulable state in cirrhosis. Case Description/Methods: A 65-year-old woman with alcoholic liver cirrhosis (Child-Pugh A, Model for End-Stage Liver Disease-Na 10) presented with 2 weeks of progressive lower abdominal pain radiating to the back. The pain was cramping, sharp, and rated 8/10. Patient was unable to identify any specific triggers or alleviating factors and denied GI bleeding or bowel habit changes. A week prior, she had undergone band ligation for large esophageal varices. Labs showed INR 1.3, platelets 111,000, normal AST/ALT. Computed tomography (CT) revealed hypodense SMV and IMV with inflammatory changes. MRI confirmed nonocclusive thrombi in both veins. There was no hepatocellular carcinoma or infection. Hypercoagulability workup was unremarkable. She was started on full-dose enoxaparin, later transitioned to apixaban, with symptom improvement. Discussion: Simultaneous thrombosis of the SMV and IMV is a rare complication of cirrhosis, particularly in compensated cirrhosis without portal vein involvement. Even in patients with compensated cirrhosis, the risk of thrombotic events is high due to the complex hemostatic balance. In this case, a comprehensive hematologic workup ruled out inherited or acquired hypercoagulable states, suggesting that local factors such as altered venous flow and endothelial dysfunction likely contributed to thrombosis. Anticoagulation posed bleeding risks, particularly in the setting of recent variceal banding but the need to prevent complications outweighed the risk. This case underscores the importance of individualized risk-benefit analysis when managing thrombosis in cirrhotic patients, despite being clinically stable and compensated.