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Portal hypertension
- 1. Portal Hypertension Dr.Shahzad Ahmad Daula MID,DMLT,DDC TheUniversity of Lahore
- 2. Portal Hypertension An elevation of pressure >6mmHg in the portal venous system. Portal vein Normally <13mm in diameter.
- 3. Superior mesenteric veinSuperior mesenteric vein Splenic veinSplenic vein
- 4. Portal vein is not a true vein
- 5. 20 % 80 %
- 6. Portal venous pressure > 10 mm Hg Increased resistance to portal flow
- 8. Prehapatic (portal vein obstruction) ⢠Thrombosis of portal vein ⢠Congenital atresia / stenosis ⢠Extrinsic compression
- 10. Posthepatic ⢠Budd-Chiari syndrome ⢠Cardiac disease
- 12. Portal hypertension has no symptoms
- 13. AscitesAscites
- 15. Investigations in Ascites â˘CT with IV contrast â˘Aspiration of fluid â˘Portal pressure measurement
- 16. AscitesAscites ShrunkenShrunken LiverLiver Portal veinPortal vein thrombosisthrombosis SplenomegalySplenomegaly
- 17. Ascites â˘CT with IV contrast â˘Aspiration of fluid â˘Portal pressure measurement
- 18. Portal Pressure Measurement ⢠Wedged hepatic venous pressure ⢠Splenic pulp pressure ⢠Catheterization of umbilical vein
- 19. Treatment ⢠Medical Treatment ⢠Peritoneo-venous shunting ⢠TIPS ⢠Liver transplantation
- 20. Medical Treatment ⢠Salt restriction ⢠Diuretics ⢠Paracenteses
- 21. Peritoneo-venous shunt (LeVeen shunt, Denver shunt)
- 24. TIPS
- 25. TIPS
- 26. ⌠in summary ⢠Pressure > 06 mm Hg ⢠Secondary to ďŠresistance to flow ⢠Presents as ascites / variceal bleeding
- 27. ⌠in summary ⢠Ascites can be treated with ⢠Medical treatment ⢠PJ shunt ⢠TIPS ⢠Liver transplantation
Hinweis der Redaktion
- The portal vein is formed by the confluence of the Superior mesenteric vein and splenic vein. It collects blood from the GI tract and drains it into the liver.
- Because it does not conduct blood directly into the heart. It drains blood from the GIT and spleen into the liver
- Portal vein supplies 80% of the blood to the liver. The remaining 20% is supplied by the Hepatic artery
- Portal pressure normally ranges from 7-10 mm Hg. In portal hypertension, portal pressure exceeds 10 mm Hg, averaging 20 mm Hg and sometimes rising as high as50-60 mm Hg. In all but few cases, the basic lesion is increased resistance to portal flow.
- The obstacle to flow through the liver promotes expansion of collateral channels between the portal and systemic venous system. As the pathologic process develops, portal pressure increases until a level of 30 mm Hg is reached. At this point increasing hepatic resistance diverts a greater fraction of portal flow through collaterals. These collaterals give rise to esophageal and gastric varices. Othe rspontaneous spontaneous collaterals are through te recanalized umbilical vein to the abdominal wall, from the superior haemorrhoidal veininto the middle and inferior hemorrhoidal veins, and through numerous small veins (of Retzius) connecting the retroperitoneal viscera with posterior abdominal wall. Of the many large collaterals, sponatneous bleeding is relatively uncommon except from those at the gastroesophageal junction.
- Imaging by CT will confirm acsites and demonstarte the irregular, shrunken nature of cirrhotic liver and associated splenomegaly. Intravenous cntrast enhancement will allow oesophageal varices to be demonstrated and patency of portal vein, as portal vein thrombosis is a common predisposing factor to the development of ascites in CLD. Aspiration of ascitic fluid allows the measurement of protein to determine whether the fluid is an exudate or transudate, and an amylase content will exclude a pancreatic ascites. Cytology will exclude malignancy, and both microscopy and culture will exclude primary peritonitis and tuberculous peritonitis.
- 79-year-old woman with cirrhosis, portal hypertension, hypertensive gastropathy, esophageal varices, and hepatopulmonary syndrome. Axial contrast-enhanced CT scan shows nodular liver, portal vein thrombosis (white arrow), ascitis, and left gastric varices (black arrows
- Imaging by CT will confirm acsites and demonstarte the irregular, shrunken nature of cirrhotic liver and associated splenomegaly. Intravenous cntrast enhancement will allow oesophageal varices to be demonstrated and patency of portal vein, as portal vein thrombosis is a common predisposing factor to the development of ascites in CLD. Aspiration of ascitic fluid allows the measurement of protein to determine whether the fluid is an exudate or transudate, and an amylase content will exclude a pancreatic ascites. Cytology will exclude malignancy, and both microscopy and culture will exclude primary peritonitis and tuberculous peritonitis.
- TIPS is a minimally invasive means of creating a portosystemic shunt by creating a direct communication between the portal and the hepatic venous systems within the liver. A catheter is introduced through the internal jugular veinand under radiological control, is positioned in the hepatic vein. From here, the portal vein is accessed through the liver, the tract is dilated and and the channel is kept open by placing an expandable metallic stent. This technique is of great value in controlling portal hypertension and variceal bleeding. The shunts remain open in ost patients for up to a year, at which point intimal overgrowth leads to thrombosis and occlusion.