1. Portal Hypertension
Dr. HAMID HINDI

2. What is portal hypertension ?
Preamble
What is portal hypertension ?
How does it present ?
How do we manage it ?

3. Superior mesenteric vein
Splenic vein
Superior mesenteric vein
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.

4. Portal vein is not a true vein
Because it does not conduct blood directly into the heart. It drains blood from the GIT and spleen into the liver

5. 20 %
Portal vein supplies 80% of the blood to the liver. The remaining 20% is supplied by the Hepatic artery
80 %

6. Portal venous pressure > 10 mm Hg
Increased resistance to
portal flow
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.

7. Posthepatic
Hepatic
Prehepatic

8. Prehapatic (portal vein obstruction)
Thrombosis of portal vein
Congenital atresia / stenosis
Extrinsic compression

9. Hepatic
Cirrhosis
Schistosomiasis

10. Posthepatic
Budd-Chiari syndrome
Cardiac disease

12. Portal hypertension has no symptoms

13. Ascites

14. Variceal Bleeding Caput Medusae Haemorrhoids
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.
Haemorrhoids

15. Investigations in Ascites
CT with IV contrast
Aspiration of fluid
Portal pressure measurement
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.

16. Ascites Shrunken Liver Portal vein thrombosis Splenomegaly
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
Splenomegaly

17. Investigations in Ascites
CT with IV contrast
Aspiration of fluid
Portal pressure measurement
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.

18. Investigations in Ascites
CT with IV contrast
Aspiration of fluid
Portal pressure measurement
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.

19. Portal Pressure Measurement
Wedged hepatic venous pressure
Splenic pulp pressure
Catheterization of umbilical vein

20. Treatment Medical Treatment Peritoneo-venous shunting TIPS
Liver transplantation

21. Medical Treatment
Salt restriction
Diuretics
Paracenteses

22. Peritoneo-venous shunt
(LeVeen shunt, Denver shunt)

25. TIPS
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.

26. TIPS

27. … in summary Pressure > 10 mm Hg Secondary to resistance to flow
Presents as ascites / variceal bleeding

28. … in summary Ascites can be treated with Medical treatment PJ shunt
TIPS
Liver transplantation