Introduction: While portal vein thrombosis (PVT) is a relatively rare disease in the general population, the prevalence of PVT in cirrhosis increases in parallel with the severity of cirrhosis. The pathogenesis of PVT in cirrhosis is thought to be multifactorial resulting mainly from alterations in the different components of Virchow’s triad.
Case Description/Methods: Here we report a case of a 36-year-old woman with history of alcoholic cirrhosis who presented 2 weeks status post c-section complaining of acute onset abdominal pain, bloating, and nausea with two episodes of hematemesis. Her initial vital signs were unremarkable and hemoglobin was 7.4 gm/dL. Her model for end-stage liver disease (MELD) score was 16. She underwent upper endoscopy (EGD) with successful banding of 3 columns of large varices which showed stigmata of recent bleeding. Patient also underwent diagnostic and therapeutic paracentesis which did not show signs of spontaneous bacterial peritonitis (SBP). However, she did have history of wound dehiscence of her cesarean incision with persistent leakage of serous fluid despite prior negative pressure wound therapy. Therefore, CT abdomen/pelvis was obtained which demonstrated nonocclusive thrombus in the main portal vein extending into both the right and left branches. Due to finding of PVT, MRI was also obtained which showed no evidence of malignancy. As her hemoglobin remained stable ( >7 gm/dL) during hospitalization, she was started on therapeutic low molecular weight heparin (LMWH). Unfortunately, patient was re-admitted five days later for hematemesis and drop in her hemoglobin to 5.6 gm/dL. She received blood products, and repeat EGD showed cratered and superficial esophageal ulcers at the site of prior variceal treatment. Ultimately LMWH was held and resumed after hemoglobin stabilized.
Discussion: This case demonstrates the conundrum of if/when to treat PVT in patients with cirrhosis. Current guidelines recommend anticoagulation as the mainstay of PVT treatment. However, this is can be complicated by other sequelae of decompensated cirrhosis such as variceal bleeding. Consequences of non-treatment include further increase in resistance to portal blood thus worsening portal hypertension. In this case, patient’s post-partum status also favors anticoagulation as other society guidelines have recommended anticoagulation with LMWH for postpartum patients with vascular disease of the liver. Therefore, individualized treatment algorithms should be developed and used to guide management.
