Description

Cavernous transformation of the portal vein (CTPV) is primarily caused by portal vein thrombosis (PVT). It is characterized by the formation of a network of tortuous, dilated, and malformed venous channels around the obstructed portal vein-a morphology that macroscopically resembles a sponge, hence the name. While a minority of patients with well-developed collateral circulation may remain asymptomatic, most develop complications of portal hypertension, such as esophagogastric variceal bleeding, ascites, and hypersplenism. Variceal bleeding, in particular, is associated with acute onset and high mortality. The management of variceal bleeding in CTPV generally follows guidelines for cirrhotic portal hypertension, including pharmacological therapy, endoscopic treatment, transjugular intrahepatic portosystemic shunt (TIPS), and surgical intervention. However, the distinct hemodynamics resulting from portal vein occlusion pose specific therapeutic challenges:

1. Limited Efficacy of Conventional Pharmacological and Endoscopic Therapies: The chronic organic obstruction in CTPV renders pharmacological agents that reduce portal pressure-such as non-selective beta-blockers-largely ineffective, as they cannot adequately decrease pressure distal to the occlusion. Furthermore, the extensive and complex collateral circulation that develops (e.g., gastroesophageal varices, retroperitoneal venous networks) is often multifocal and highly interconnected. This makes it difficult for endoscopic band ligation or sclerotherapy to comprehensively address all potential bleeding sources. As a result, CTPV patients experience significantly higher rebleeding rates after endoscopic therapy compared to those with conventional portal hypertension.
2. Challenges of Splenectomy with Periesophagogastric Devascularization: Although this classic surgical procedure is used for variceal bleeding in standard portal hypertension, its application in CTPV is complicated by several factors. The spleen is often markedly enlarged and adherent to adjacent structures due to chronic congestion, and the splenic hilar vessels are tortuous and friable, increasing the risk of intraoperative hemorrhage. Moreover, the abundant collateral circulation requires the ligation of a much larger number of vessels than in typical cases. Incomplete devascularization can lead to rebleeding, while the extensive nature of the surgery-coupled with chronic malnutrition and reduced hepatic reserve-elevates the risks of infection, liver failure, and thrombosis, contributing to high perioperative mortality.
3. Limitations of TIPS: While TIPS has shown efficacy in selected CTPV patients with portal hypertension, its success depends on sufficient portal venous inflow to maintain stent patency. In cases with extensive thrombosis involving the splenic or superior mesenteric veins, inadequate inflow increases the risk of early stent thrombosis and shunt dysfunction. Additionally, TIPS carries a well-established risk of hepatic encephalopathy, necessitating careful patient selection, particularly in those with advanced liver dysfunction (Child-Pugh class C) or high baseline encephalopathy risk.

Evidence suggests that combined variceal embolization and partial splenic artery embolization achieves hemostatic outcomes comparable to modified TIPS in cirrhotic portal hypertension, with similar rebleeding rates. This dual interventional approach may also confer benefits in terms of liver function improvement and could be particularly advantageous for patients at high risk of hepatic encephalopathy or with significant liver impairment. Therefore, the investigators hypothesize that for CTPV patients with extensive portosystemic thrombosis and insufficient portal inflow who are unsuitable for shunt procedures, this combined embolization therapy may reduce portal pressure and mitigate the risk of esophagogastric variceal bleeding.