Abstract

INTRODUCTION: PVT is a rare entity in the absences of liver cirrhosis, malignancy, prothrombotic disorder or an intra-abdominal inflammatory state. In some cases, no clear etiology can be found and it can be triggered by a combination of factors. We report a case of non-cirrhotic woman with a symptomatic and progressive PVT in the setting of low antithrombin activity and liver lesions. CASE DESCRIPTION/METHODS: 48 year old female without past medical or family medical history, was brought to the ED with diffuse abdominal pain. For the past ten weeks, she has experienced post-pandrial abdominal pain associated with nauseas and two episodes of non-bloody vomiting. She denied diarrhea, recent abdominal infections, drug use or OCP use. Patient has not undergone abdominal surgery. Her physical exam was unremarkable except for mild diffuse abdominal pain, no Murphy's sign, no guarding or rebound signs. CBC, BMP, lipase and liver function panel was unremarkable. Recent mammography, EGD and colonoscopy displayed no signs of malignancy or portal hypertension. MRA showed no stenosis or obstruction of arteries. CAT-scan of abdomen and pelvis with IV contrast showed extensive thrombosis of main portal vein, right portal vein, left portal vein and the portosplenic confluence. Also showed collateral vessels extending from the portosplenic confluence into the bilateral retroperitoneum, bilateral renal hilum and extending across the ovarian veins into the pelvis. There were multiple indeterminate hypodense liver lesions. Additional laboratory tests were ordered and samples collected before starting anticoagulation. Laboratory tests showed decrease antithrombin activity, which is a risk factor for PVT. She was admitted on low-molecular weight heparin (LMWH) until stabilization, and then discharged on oral anticoagulation. In this case, outpatient follow up evaluation by hemato-oncology was scheduled to rule out other coagulation disorders and malignancy. DISCUSSION: PVT in a healthy and young patient is not common. The prevalence of PVT is low in patients with cirrhosis; it is even lower in patients non-cirrhotic and without malignancy. It has been estimated that in non-cirrhotic PVT, hypercoagulable states account for 40%-60% of cases. The American Association for the Study of Liver Diseases (AASLD) guidelines recommend treatment with anticoagulation to prevent thrombi extension and to restore blood flow in occluded vessels. The outcome for non-cirrhotic, non-malignant PVT is good if the diagnosis and treatment occurs early.

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