Hepatic encephalopathy in the setting of advanced chronic liver disease, occurs following a precipitating factor and generally responds to correction of the precipitating factor and anticoma measures. We report the case of a lady with Child A cirrhosis who presented with frequent episodes of hepatic encephalopathy without any precipitating factors. She was found to be having a large portosystemic shunt. The shunt was obliterated by coil embolotherapy following which there was no further episodes of encephalopathy. ( J CLIN EXP HEPATOL 2014;4:60-62) A 36-year-old female was diagnosed to have liver cirrhosis since 2 years. She had multiple episodes of hepatic encephalopathy requiring frequent hospitalizations, which responded to lactulose and other anti-encephalopathy measures and supportive care. She never had any episode of hematemesis or melena.General examination was unremarkable except for generalized hyperpigmentation. She did not have mucosal hyperpigmentation. Abdominal examination revealed mild splenomegaly. She had no stigmata of liver disease, KF ring, xanthalesma or other findings. On evaluation she was found to have Child class A liver functional status. Serum hepatitis B surface antigen and antibody against hepatitis C virus was negative. Antibody against core antigen (total) was positive; however HBV DNA was undetectable on PCR quantification. Antinuclear antibody, antimitochondrial antibody, anti-smooth muscle antibody, antiphospholipid antibody (IgG & IgM) were negative. Her serum ferrtin, and ceruloplasmin were within normal limits. She was non-diabetic and her lipid profile was within normal limits. Upper GI endoscopy did not reveal any varices and colonoscopy was also normal except for small hemorrhoids. Fasting arterial ammonia was 140 mmol/L. Her renal function tests and electrolytes were normal.Multiphasic computerised tomography abdomen showed mild splenomegaly, but no focal lesion in liver. Portal vein and splenic vein were dilated. Portal vein was 1.8 cm at porta hepatis. Left branch of portal vein appeared occluded. Right branch was dilated and tortuous and seen to drain into inferior vena cava via hepatic vein (Figure 1). Middle and left hepatic veins were normal.She was taken up for angioembolisation of the fistula. The right portal vein was percutaneously entered using Chiba needle and 6F sheath was introduced. Preliminary angiogram showed large venous sac communicating right anterior division of portal vein with right hepatic vein. Right posterior division was also seen to be communicating with the venous sac. Amplatz closure device was deployed to prevent distal migration of the coils (Figure 2) and after which multiple (12) 8 mm  8 and 6  6 mm (0.035) steel coils were deployed (Figure 3). Post-procedure, angiogram showed good result (Figure 4). Post-procedure period was uneventful and she had fall in arterial and serum ammonia levels. She had no further episodes of encephalopathy and was asymptomatic till 6 months of follow-up. DISCUSSIONOur patient had multiple episodes of he...
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