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Portal hypertension
Portal hypertension is hypertension (high blood
pressure) in the portal vein and its branches. It is usually the
result of cirrhosis of the liver. Normally the portal venous pressure
is up to 10mmHg. Portal hypertension denotes a rise of the portal vein
pressure above 10mmHg.
Causes
1. Prehepatic obstruction
- Splenic vein thrombosis
- Portal vein thrombosis
2. Intrahepatic obstruction
- Presinusoidal (fibrosis or infiltration outside the sinusoids)
as in bilharziasis and metastasis.
- Sinusoidal as in cirrhosis
- Postsinusoidal as in veno-occlusive disease
3. Post hepatic obstruction of the portal vein flow
Pathophysiology
Portal hypertension leads to the opening of venous collateral
circulation in many areas of the body (e.g. esophagus). These veins
become dilated and are prone to bleeding.
Clinical picture
The major clinical manifestations of portal hypertension include
hemorrhage from gastroesophageal varices, splenomegaly with
hypersplenism, ascites, and acute and chronic hepatic encephalopathy.
These are related, at least in part, to the development of
portal-systemic collateral channels.
Consequences of portal hypertension
-
Ascites (free fluid in the peritoneal cavity)
-
Esophageal varices (dilated veins in the wall of
the esophagus that are prone to bleed)
-
Hemorrhoids
-
Increased risk of spontaneous bacterial
peritonitis
-
Increased risk of hepatorenal syndrome
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Diagnosis
- Ultrasound and CT scan reveals distention of portal vein and its
collaterals.
- Endoscopy enables easy diagnosis and grading of varices.
- Celiac and superior mesenteric arteriography are used to
determine the site of block and the extent of collaterals which is
essential before procedures such as surgery, TIPS or hepatic
transplantation.
Treatment
Surgical decompression procedures have been used
for many years to lower portal pressure in patients with bleeding
esophageal varices (see below). However, portal-systemic shunt surgery
does not result in improved survival rates in patients with cirrhosis.
Decompression can now be accomplished without surgery through the
percutaneous placement of a portal-systemic shunt, termed a
transjugular intrahepatic portosystemic shunt (TIPS).
B-Adrenergic blockade with propranolol or nadolol
reduces portal pressure through vasodilatory effects on both the
splanchnic arterial bed and the portal venous system in combination
with reduced cardiac output.
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