Portal hypertension occurs when hepatic venous pressure gradient exceeds 10 mm Hg and risk of variceal bleeding increases above 12 mm Hg. It can be caused by prehepatic issues like portal vein thrombosis, intrahepatic issues like cirrhosis, or post-hepatic issues like Budd-Chiari syndrome. Clinical signs include splenomegaly, ascites, collateral veins, and risk of gastrointestinal bleeding from esophageal varices. Management involves beta-blocker therapy to reduce pressure, antibiotics and endoscopic therapy for acute bleeding, and TIPSS or shunting for refractory cases. Complications include variceal bleeding, ascites, and hypersplenism.

1. PORTAL HYPERTENSION

2. PORTAL HYPERTENSION
The normal hepatic venous pressure gradient
(difference between the wedged hepatic venous
pressure and free hepatic venous pressure, see below)
is 5–6 mm Hg. Clinically significant portal hypertension
is present when the gradient exceeds 10 mm Hg and
risk of variceal bleeding increases beyond a gradient of
12 mm Hg.
Portal vein: superior mesenteric vein+ Splenic vein.
It carries nutrition to the liver.

3. Causes
1) Prehepatic pre-sinusoidal:
i) Portal vein thrombosis due to sepsis or secondary to cirrhosis
ii) Abdominal trauma including surgery.
2) Intrahepatic pre-sinusoidal:
i) Schistosomiasis*
ii) Congenital hepatic fibrosis
iii) Drugs
iv) Sarcoidosis
3) Sinusoidal:
i) Cirrhosis
ii) Polycystic liver disease
iii) Nodular regenerative hyperplasia
iv)Metastatic malignant disease
4) Intrahepatic post-sinusoidal:
i) Veno-occlusive disease.
5) Extrahepatic post-sinusoidal:
i) Budd-Chiari syndrome

5. Clinical presentation
• Splenomegaly
• Ascites
• Collateral veins: Caput medusa
• Hypersplenisim
• Hematemesis & Melaena( Due to ruptured esophageal varices).
• Bed side clinical sign in cirrhotic patient:
i) Splenomegaly
ii) ascites
iii) Collateral veins( Caput medusa)

6. Site of collateral Vessel formation
• distal oesophagus
• stomach and rectum.
• in the anterior abdominal wall
• In the renal, lumbar,ovarian and testicular
vasculature

7. Investigations
• Endoscopy: to determine whether gastro-
oesophageal varices are present.
• Ultrasonography: often shows features of portal
hypertension, such as splenomegaly and collateral
vessels, and can sometimes indicate the cause,
such as liver disease or portal vein thrombosis.
• CT and MRI
• Portal venous pressure measurement.
• To see features of hypersplenisim: TC &
DC of WBC, platelet, Hb%

8. Portal Pressure measurement
• Pressure measurements are made by using
a balloon catheter inserted using the
transjugular route (via the inferior vena cava
into a hepatic vein and then hepatic venule)
to measure the wedged hepatic venous
pressure (WHVP). This is an indirect
measurement of portal vein pressure.
• Another is direct method.

9. Management:
• Primary prevention of variceal bleeding:
i) β-adrenoceptor antagonist (β-blocker) therapy with propranolol (80–
160 mg/day) is effective in reducing portal venous pressure.
*Administration of these drugs at doses that reduce the heart rate by 25%
has been shown to be effective in the primary prevention of variceal
bleeding.
ii) In patients that are unable to tolerate
β-blocker therapy. Carvedilol, a non-cardioselective
vasodilating β-blocker, is also effective.

10. Management…………
• Management of acute variceal bleeding:
i) I/V fluid: Normal saline/ Colloids
ii) Terlipressin: The dose is 2 mg IV 4 times daily until bleeding
stops, and then 1 mg 4 times daily for up to 72 hours.
iii) Antibiotics: I/V Cephalosporin or Oral Ciprofloxacin.
iv) Endoscopic therapy: band ligation or sclerotherapy.
v) Balloon temponade.
vi) TIPSS(Transjugular intrahepatic portosystemic stent
shunting)
• Treatment of comlications.

12. Complications
• Variceal bleeding: Esophageal, gastric
• Congestive gastropathy.
• Hypersplenisim
• Ascites
• Iron deficiency anemia
• Renal failure
• Hepatic Encephalopathy.

13. Hypersplenisim
• It is characterized by clinical triad of---
i) Splenomegaly.
ii) Anemia, leucopenia, thrombocytopenia,
alone or in combination.
iii) After splenectomy, there will be correction
of the blood cytopanias.