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.