OBJECTIVE: To explore three-dimensional reconstruction of hepatic portal vein by laminagraphy of cast specimens to provide anatomic basis for hepatectomy.
Conclusion: The early use of salivia miltiorrhia, low molecular dextrar and dipyridamole can effectively prevent and treat the portal thrombosis after portal-azygous disconnection.
Methods Spiral CT appearances of 18 cases with PSPH were reviewed and compared with those of 30 cases with protal hypertension (PH),especially perigastric collateral channel formation were evaluated.
The common bile duct passes inferiorly, anterior to the epiploic foramen, where it is anterior to the right edge of the portal vein and on the right side of the hepatic artery.
Protein C or protein S deficiency is also sometimes suspected when a venous thromboembolism develops in an unusual site like the portal, mesenteric, or cerebral veins.
Portal hypertension leads to the formation of Portosystemic shunts, which is when blood is diverted away from the portal venous system and backs up into the systemic veins.
This happens because blood flow follows the path of least resistance and shunts away from the portal system and towards the systemic system of circulation.
The features of portal hypertension can be remembered as ABCDE, where A stands for Ascites, B for Bleeding, C for Caput Medusae, D for Diminished liver function, and E for Enlarged spleen.
Higher portal vein pressure means that fluid in blood vessels is more likely to get pushed into tissues and across tissues into large open spaces like the peritoneal cavity.
The fibrotic tissue, pressure buildup, and diversion of blood from the hepatic circulation essentially reduces the number of functional sinusoidal veins, and the number of functional portal triads in general.