PORTAL HYPERTENSION

 Normal hepatic venous pressure: 5-6mmHg

 Portal HTN is clinically significant when gradient exceeds 10mmHg and risk
of variceal bleeding increases beyond 12mmHg.
 C/Fs:
 Splenomegaly- cardinal finding
 Collateral vessels on anterior abdominal wall, radiate from umbilicus to form a
‘caput medusa’. Rarely, a large umbilical collateral vessel has a blood flow
sufficient to give a venous hum on auscultation. Most important collateral vessel
formation occurs in esophagus and stomach and this can be a source of severe
bleeding. Rectal varices also cause bleeding.
 Fetal hepaticus d/t portosystemic shunting of blood, which allows mercaptans to
pass directly to lungs.
 Ascites
 Pathophysiology
increased portal vascular resistance leads to increase in portal venous pressure
which further leads to formation of collateral vessels that divert a large fraction
of portal blood bypassing the liver into systemic circulation i.e portosystemic
shunting occurs.
 Investigations:
 Diagnosis is often made clinically.
 Pressure measurements are done by using a balloon catheter using the
transjugular route.
 Thrombocytopenia, leucopenia
 Endoscopy: most useful investigation
 Ultrasonography
 CT scan and MRI
 Management:
1. Primary prevention of variceal bleeding: beta-adrenoreceptor antagonist
therapy with propranolol or nadolol. Carvdilol, a non cardioselective
vasodilating beta-blocker, is also effective. Prophylact banding, particularly
in pateints who are unable to tolerate or adhere to beta-blocker thepary.
2. Management of acute variceal bleeding:
 Complications :
1. Variceal bleeding: esophageal, gastric, other(rare).
2. Congestive gastropathy
3. Ascites
4. Hypersplenism
5. Iron deficiency anemia
6. Renal failure
7. Hepatic encephalopathy