Brief explanation about portal hypertension causes and management

1. PORTAL HYPERTENSION
• By : - Gowhar Ahmad Dar

2. INTRODUCTION
• The hepatic circulation carries blood from GI tract (i.e.
from the distil esophagus to anorectal junction ) to the
liver
• Porto systemic anastomosis occurs in junctional areas
of venous drainage
• Portal venous blood drain into liver venous sinusoids
and hence in to the heatic veins

3. Definition
• Portal hypertension is defined as the elevation of the
hepatic venous pressure gradient to > 5 mmhg
• Clinically significant portal hypertenstion is present when
gradient exceeds 10 mmhg
• Risk of variceal bleedding increses beyond a gradient of
12 mmhg

4. Anatomy
• Portal vein is formed by the union of the sauperior
mesenteric vein and the splenic vein just posterior of the
head of the pancreas at the level of second lumbar vertebra
• Portal blood flow in man is about 1000 to 1200 ml/min

5. Classification and
Causes
• Preheptic
Portal vein thrombosis
splenic vein thrombosis
Massive spleenomegaly

6. Classification and
Causes
• Hepatic
1. Presinusoidal:
Schistosomiasis
Congenital hepatic fibrosis
2. Sinusoidal:
Cirrhosis of liver
Alcoholic hepatitus
3. Postsinusoidal:
Hepatic sinusoidal obstruction(veno occlusive syndrome )

7. Classification and
Causes
• Posthepatic
Budd Chiari Syndrome
Inferior vena cava obstruction
cardiac causes:
Restrictive cardiomyopathy
Constrictive pericarditis
Severe congestive cardiac failure

8. Etiology
• Most common cause is liver cirrhosis
• It may be :
1. presinusoidal
2. sinusoidal
3. postsinusoidal

9. Etiology cont.

10. Clinical Features
• haematemesis duo to gastro-esophageal varices
• splenomegaly associated with hypersplenism causing
pancytopenia
• caput medusa duo to umbilical vein opening, you may h
audible
venouse hum( Cruveilhier_ Baumgarten murmu
• ascites
• anorectal varices
• increasing cardiac out put causing generalised
vasodilatation.

11. Pathophysiolo
gy
• The fundamental haemodynamic abnormality is an increased resistance
to the blood flow.
• Increased portal vascular resistance leads to gradual reduction in the
flow of portal blood to the liiver and simultaneously to the development
of collateral vessels, allowing portal blood to bypass the liver and enter
the systemic circulation directly.
• Collaterals devlop when the pressure gradient between the portal and
hepatic vein rises above a certain threshold, a process involves
angiogenic factors.
• At the same time portal flow increases in the splanchnic bed due to
splanchnic vasodilatation and increased cardiac output.

12. Pathophysiolo
gy
• Portal vascular resistance is incrteased in chronic liver disease.
Liver cell injury
Stellate cell activation
Stellate cells transform into myofibroblast
De novo expression of specific smooth muscle protein alpha actin
Endothellin, NO Prostaglandins
Contraction of activated cellls
Abnormal blood flow pattern causing increased resistance
fibrogenesis
Increased resistance leads to portal hypertension

13. PATHOPHYSIOLOGY IN CIRRHOSIS
• Portal venous blood is diverted into collateral channels and
some bypass the liver cells and is shunted directly into the
hepatic venous radicles in fibrous septa
• . These portohepatic anastomosis develop from pre-existing
sinusoids enclosed in the septa

14. • The regenerating nodules become divorced from their portal blood supply and are nourished by
the hepatic artery
• The obstruction to portal flow is partially due to nodules which compress hepatic venous radicles

15. Clinical Manifestation
• Upper gastrointestinal hemorrhage
• Ascite
• Enlarged spleen hypersplenia
• Hepatic coma

16. Ascite

17. Laboratory tests
• Blood test
• Hepatic function:
aminotransferase
alkaline phosphatase
• serum bilirubin level
• a-fetoprotein level
• CT CTA
• Magnetic resonance imaging
• ultrasound Doppler ultrasonography

18. A three-dimensional reconstruction of a CT angiogram

19. Liver Biopsy
• A useful technique for establishing the cause of cirrhosis and for
assessing activity of the liver disease.
• Laparoscopic biopsy

20. Pressure test
• portal pressure can be indirectly estimated by
measurement of hepatic venous wedge pressure (HVWP)

21. Child-Pugh criteria for hepatic functional reserve

22. Diagnosis
• History
• Symptom and Physical examination
• Laboratory examination
Hematology exam
CT. CTA
USG
Endoscopic examination

23. • Nonoperative treatments
• operative treatments
Treatment

24. Nonoperative treatments
• Pharmacotherapy
• Endoscopic treatment
• Balloon Tamponade
• Transjugular intrahepatic portosystemic shunt
(TIPS)

25. Pharmacotherapy
• Vasopressin: a bolus dose of 20 units over 20 minutes and a continuous
infusion of 0.2 to 0.4 unit/minute
• Somatostatin is a250-µg intravenous bolus and a continuous infusion of 250
µg/hour for 2 to 4 days
• Octreotide an intravenous bolus of 50 µg andan infusion of 25 to 50 µg/hour
for a similarlength of time
• B-adrenergic blockade

26. Endoscopic treatment
Sclerosis Ligation

27. Balloon
Tamponade
• Complications
Esophageal perforation
ischemic necrosis of the esophagus

28. Transjugular inytrahepatic portosystemic shunt (TIPS)
• Access is gained to a major intrahepatic portal venous
branch through puncture through a hepatic vein. A
parenchymal tract between hepatic and portal veins is
then created with a balloon catheter, and a 10-mm
expandable metal stent is inserted, thereby creating the
shunt

29. Operative Treatment
• operative mortality rates for Child-Pugh classes A, B, and C
• patients are in the range of 0 to 5%, 10% to 15%, and greater
than 25%, respectively.

30. Operative method
• A shunt procedure
• A nonshunt operation
• Hepatic transplantation

31. Non selective shunts
• The end to side portacaval shunt
• The side to side portacaval shunt
• The large diameter interpositon shunt
• The conventional splenorenel shunt

32. Selective shunts
• The disltal splenorenal shunt
• The left gastric vena caval shunt
• A vain graft between the left gastric (coronary)
vain and the inferior vena cava

33. Partial shunts
• A small diameter interposition portacaval
shunt

34. Non shunt operation
• Esophagogastric devascularization
procedures

35. Removal

36. New liver implantation

37. Schematic of completed
liver

38. Piggyback technique

39. Conclusion
• Portal hypertension - widespread disease, in most case caused by
hepatic cirrhosises.
• Treatments and prevention of bleedings from esophageal VRV and
stomach makes up the basis of indications for surgical intervention
when portal hypertension.
• Surgical intervention are limited compensated by stages of portal
hypertension.
• Maloinvazivnye interference covers all the forms category and stages
of portal hypertension and are able to effectively
• to korregirovatj affected the portopechenochnuyu hemodynamics -to
head off and to treat of bleeding from esophageal VRV and stomach-
• affect the functional state of most liver

40. Biblography
• Google
• Wikipedia
• Dr. mohit choudary’s ppt
• Dr. syed al shomimi ppt
• Dr. gunjan malviya
• Shanghai jiaotong university school of medicine ppt
https://slideplayer.com/slide/12935318/