The Seemingly Benign Abdomen with an Underlying Insidious Pathology: A Rare Presentation of Portal Vein Thrombosis

Abstract

The portal vein is formed by the superior mesenteric vein and splenic vein. Thrombosis within this vessel may occur acutely or chronically over time due to hepatic cirrhosis or other pro-thrombotic disorders. While provoking agents and initial symptoms are variable, the common pathology involves general flow obstruction within the portal vasculature with possible new or worsening liver failure, portal hypertension, or intestinal ischemia.Figure 1Figure 2Our patient is a 61-year-old female with a history of ethanol abuse, who presented to the ER with progressive dyspnea and was admitted with community-acquired pneumonia. On admission, the patient denied any pain and had a benign abdominal exam. Due to an INR of 4.1, the GI service was consulted for suspected cirrhosis. An abdominal US was obtained and showed a near complete thrombosis of the portal and superior mesenteric veins. This was confirmed by an abdominal CT, which also revealed numerous ill-defined masses throughout the liver and at the head of the pancreas. An initial liver biopsy showed no evidence of malignancy but revealed acute and chronic inflammation, microabscess formation, and coagulation necrosis. A second liver biopsy corroborated an infectious etiology when 220 mL of perihepatic purulent fluid was collected. As the etiology of the hepatic and pancreatic lesions was investigated, the proposed mechanism of thrombus formation was attributed to the multiple pancreatic lesions compressing and potentiating venous stasis of the nearby vasculature. Treatment was geared toward anticoagulation initially with full dose lovenox and then with heparin. After 2 weeks of treatment, a repeat CT of the abdomen showed no further evidence of thrombus within the portal vein and anticoagulation was discontinued. This case demonstrates a unique pathologic process and etiology of portal vein thrombosis as attributed to venous stasis secondary from abscesses within the liver and pancreatic head. Although the patient presented with a known history of ethanol abuse, she had no abdominal ascites, GI upset, or pain on admission. Coagulopathy was the only aberrant factor that prompted investigation of hepatic pathology. While many factors are known to promote or exacerbate thrombus formation within the portal system, the infectious etiology in this case has been rarely observed within the literature and therefore underscores the variable symptomatology of this condition and the high clinical suspicion necessary for its detection.