Euroasian journal of hepato-gastroenterology

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VOLUME 2 , ISSUE 1 ( January-June, 2012 ) > List of Articles


Subacute Hepatic Failure: Its Possible Pathogenesis

Santosh Man Shrestha, Shobhana Shrestha

Citation Information : Man Shrestha S, Shrestha S. Subacute Hepatic Failure: Its Possible Pathogenesis. Euroasian J Hepatogastroenterol 2012; 2 (1):41-46.

DOI: 10.5005/jp-journals-10018-1030

License: CC BY-NC 4.0

Published Online: 01-08-2018

Copyright Statement:  Copyright © 2012; The Author(s).


Background: Subacute hepatic failure (SAHF) is a complication of acute hepatitis (AH) characterized by progressive jaundice and development of ascites within 24 weeks of the onset of icterus. Its pathogenesis is unknown and its treatment is unsatisfactory. This study highlights on the possible pathogenesis of the disease. Materials and methods: Thirty-two with SAHF among 798 patients of AH who had tests for markers of acute hepatitis A, B, C and E had blood and ascitic fluid study and ultrasonogram (US) of liver. US and risk factors for infection were compared with consecutive uncomplicated AH. Blood culture was done in consecutive 307 AH patients at the time of the first visit. Patients with SAHF and control were followed for at least 6 months. Results: SAHF developed in 4% of the patients with AH. Bacteremia was detected in 50% and ascitic fluid showed features of hepatic venous outflow obstruction (HVOO) and bacterial peritonitis. Thrombus was detected in IVC in all. Seventy-five percent of the patients who received antibiotic recovered. Recurrence of the symptoms in five and development of cirrhosis in seven patients were noted at follow-up but none among patients with uncomplicated acute hepatitis (AH). Bacteremia was also detected in 25% of consecutive AH patients presenting with fever, with high incidence in those with complications. Conclusion: Bacteremia was common among patients with AH. Clinical features of SAHF could be explained by occurrence superadded bacterial infection that caused thrombophlebitis of hepatic portion of the IVC resulting in HVOO.

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