HEPATITIS C CIRRHOSIS, HEPATITIS B SUPERIMPOSED INFECTION, AND THE EMERGENCE OF AN ACUTE PORTAL VEIN THROMBOSIS

Document Type

Conference Proceeding

Publication Date

6-23-2023

Publication Title

J Gen Intern Med

Abstract

CASE: A 65-year-old man presented with generalized fatigue for one month. His history was notable for liver cirrhosis secondary to hepatitis C, treated and in sustained virologic response. Patient was alert and oriented and exam was notable for scleral icterus, abdominal distension, and bilateral leg swelling. Workup showed new liver profile abnormalities with AST 467, ALT 470, and total bilirubin 10.9; his MELD-Na score was 26. Hepatitis C RNA was undetectable. Hepatitis B surface antigen and core antibody were positive, surface antibody was negative, and DNA level was 1,481,240. Ultrasonography with doppler and CT liver demonstrated patent vasculature. Patient was diagnosed with decompensated liver disease in the setting of active hepatitis B infection and was treated with Entecavir. Patient initially responded to treatment and had improvement in his symptoms and laboratory abnormalities, however, five days after presentation he became confused with hepatic encephalopathy. Infectious workup was unremarkable and he did not improve after empiric antibiotics, lactulose, and rifaximin. His liver profile worsened with AST 1147, ALT 407, total bilirubin 42.3; MELD-Na score increased to 39. He was escalated to the ICU where a repeat ultrasonography with doppler demonstrated an interval absence of color flow visualization in the main, right, and left portal veins indicative of acute portal vein thrombosis (PVT). Management with intravenous heparin resulted in improvement in laboratory markers. IMPACT/DISCUSSION: PVT involves occlusion of the portal vein by a thrombus and occurs in the setting of prothrombotic states or decompensated liver disease. Acute PVT presents with abdominal pain, fever, or gastrointestinal bleeding but is often asymptomatic. Chronic PVT results in portal hypertension which causes ascites and varices. Diagnosis is made with abdominal ultrasonography with doppler imaging, CT, or MRI. Management for patients with acute PVT involves anticoagulation to promote recanalization, although the indication for anticoagulation in chronic PVT remains unclear. This case offers a unique presentation of acute PVT that developed within several days of a hospitalization for decompensated liver disease, as proven by the interval absence of portal venous flow on repeat imaging. Despite the workup on initial presentation being negative for PVT, reconsideration of differentials after the change in our patient's clinical status led to the diagnosis. Active hepatitis B infection was likely the initial trigger for the patient's cirrhosis decompensation and presentation; the subsequent coagulopathy and alteration in the portal blood flow triggered the development of an acute PVT. CONCLUSION: Patients with cirrhosis are at risk for both prothrombotic and antithrombotic complications. Superimposed infections with hepatitis viruses and abnormal flow through the hepatic portal system increase the risk for PVT. This case demonstrates the importance of reevaluating cases to reduce anchoring bias.

Volume

38

Issue

Suppl 3

First Page

S474

Find It @ Sladen

Share

COinS