Abstract

A 58-year old male presented with hematemesis and melena. He was recently diagnosed with HCC and had two prior episodes of GVB. Prior investigations had revealed a large right liver mass, PVT, splenomegaly, dilated splenic vein with gastric varices. On examination, he was hypotensive and had tender hepatomegaly. Investigations: Hb: 7 gm/dl, platelets: 88,000/cmm, alkaline phosphatase: 139 U/l, AST: 90 U/l, ALT: 132 U/l and INR: 1.3. An upper endoscopy revealed a large cluster of gastric fundic varices and no esophageal varices. He was not a candidate for TIPS as CT scan redemonstrated PVT. This was suspected to represent invasion of HCC into the intra-hepatic vasculature. He was deemed to be at a high risk for re-bleeding and was not a candidate for splenectomy. He underwent SAE; two 8 mm Nestor coils were deployed within the distal splenic artery and six 10mm coils were deployed in the mid-distal aspect of the splenic artery. He tolerated the procedure well and there was no rebleeding. A CT scan obtained 2 weeks later showed an approximately 80% splenic infarction with reduction in gastric varices. Discussion: HCC is the fifth most common cancer and tends to invade the intrahepatic vasculature especially the portal vein. Portal vein tumor thrombosis (PVTT) can be detected in 30–62% of reported patients and portends a poor prognosis. The incidence of variceal bleeding as the presenting feature in HCC ranges from 1–15%. GVB is a common complication of portal hypertension and is associated with high morbidity and mortality rates. Endoscopic sclerotherapy is difficult to perform for GVB and has had varying success rates. Although splenectomy is an option, it is has a high risk of severe hemorrhage and high operative mortality. SAE is an alternative treatment for this group of patients. SAE leads to cessation of GVB by decreasing splenic inflow. Metallic coils and Gelfoam are the most commonly employed agents. Close monitoring is suggested in patients with a volume of splenic necrosis > 50%. The post-embolization syndrome (pain, fever, vomiting) is the most frequent side effect and typically resolves rapidly. Other complications reported include transient ascites, splenic abscess, pneumonia, pleural effusion and sepsis. In conclusion, SAE offers an attractive alternative for treatment of GVB associated with HCC and PVTT in patients with high surgical risk.

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