Abstract

INTRODUCTION: Esophagogastric varices are a common complication of portal hypertension and can present with life-threatening bleeding. Definitive endoscopic therapy is via band ligation or sclerotherapy. The former is preferred for esophageal varices, but efficacy is lower in gastric varices (GV). Sclerotherapy with cyanoacrylate (CA) has shown better efficacy and is now recommended as first line therapy for bleeding GV. Studies on long-term efficacy and complications remain limited. CASE DESCRIPTION/METHODS: A 62-year-old woman with NASH cirrhosis (MELD 11) presented with hematemesis. She denied any history of SBP, varices, or encephalopathy. She endorsed a previous history of COVID-19 and had reactive IgG but PCR probe for SARS-CoV-2 was negative. She underwent EGD and was found to have oozing GV along the lesser curvature, which were treated with 4cc of CA achieving hemostasis. The following night she had altered mentation and the blood lactate was increased to 7.2 mmol/L. AST and ALT were also increased. She received broad spectrum antibiotics, and a CT angiogram showed evidence of embolization of CA into the left lobe of the liver. On day 3 her level of consciousness declined and she was intubated for airway compromise. An MRCP confirmed the presence of CA within the left hepatic lobe with associated ischemia. The lactate increased to 20 mmol/L and the blood ammonia level to 700 mcg/dL, with MELD 45. Continuous hemodialysis was started for anuric renal failure. She underwent evaluation for liver transplantation, but cerebral edema and multiorgan failure with refractory acidosis occurred and she died on day 7. DISCUSSION: We present a case of GV treated with CA and the subsequent embolization of CA into the left lobe of the liver. This precipitated acute on chronic liver failure with features of fulminant hepatic failure (FHF) complicated by severe hyperammonemia, cerebral edema, multiorgan failure, and death. Although she had a recent diagnosis of COVID-19, the time course, relatively normal initial inflammatory markers, and imaging suggest that CA embolization was likely the injury that led to fulminant hepatic failure. Given the lack of case reports of CA embolization to the liver causing infarction and few cases to the brain or distant vessels, further research on its long-term safety is warranted. Another novel aspect to this case is the development of FHF in a patient with known cirrhosis.

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