DISCUSSION
Cavernous transformation of the portal vein (CTPV) is a very rare condition usually characterized by tiny tortuous blood vessels formed around a thrombosed portal vein 3. This condition is mostly accompanied by portal hypertension and the formation of porto-systemic collaterals and varices 8. CTPV have been mostly recorded in individuals with long-term thrombosis of the portal vein without evidence of liver cirrhosis or hepatoma1–3.
In CTPV, two types of collateral circulations are observed namely portoportal and portosystemic. In the event of the occurrence of portal vein thrombosis, re – canalization usually takes place in patients without cirrhosis or any liver disease which causes an increased resistance to blood flow 6. This leads to increase in hepatic arterial blood flow at the acute phase and mesenteric collaterals compensates for the obstruction. Subsequently, there is dilatation of collateral vascular channels within the hepatoduodenal and hepatocolic ligaments, around common bile duct, hepatic ducts and gall bladder draining in to the intrahepatic portal veins to bypass the obstruction 9; and this was evident in our case where gallbladder wall thickening with evidence of pericholecystic varices under Color Doppler interrogation were observed. This “venous rescue” process continues and subsequently organizes into a cavernous transformation in about 3 – 5 weeks. This compensatory process however has deleterious effect on intestinal circulation as it is known to be associated with bowel ischemia 6. When the portal cavernoma persists for a long time, the collaterals encase and compress the biliary tree which causes damage to the intra and/or extra hepatobiliary ducts and this may lead to loss of functional liver tissue.
Clinically, most patients affected with CTPV present with symptoms such as hematemesis and melena secondary to possible bleeding esophageal varices 6,8. These symptoms may however be non-specific for CTPV since patients with gastrointestinal disease conditions may also present with hematemesis and melena; and this was observed in our case where the patient’s initial diagnosis was directed towards bleeding peptic ulcer and likely Mallory-Weiss tear. Other signs associated with portal hypertension such as anemia, splenomegaly, ascites and abnormally low platelets count (thrombocytopenia) have also been reported in patients with CTPV 8. All these aforementioned clinical symptoms of CTPV were evident in the patient in our case study.
Administering of medication and surgery are known interventions for the management of CTPV; with the success of treatment depending on the etiology of the disease 4. The surgical procedure which involves the creation of shunts decreases the portal pressure, enables hepatopetal blood from portal vein to the liver and also alleviate the abnormal hemodynamic status in the portal system10. This have been known to be associated with favorable outcomes.
In our case study, the etiology of the CTPV could not be determined since the patient had no history of liver cirrhosis, hepatoma or pancreatitis. A chronic portal vein thrombosis from a likely systemic vascular disorder could be the cause of the CTPV.