PORTAL HYPERTENSION
Normal pressure in the portal system varies between 5 and 10 mmHg.
Normal hepatic blood flow of 550-900 ml/min (~ 25 % of cardiac output) passes through portal system (2/3) and through hepatic artery (1/3) [1].
Portal hypertension is defined as portal venous pressure greater than 10 mmHg.
Two important factors exist in the pathopysiology of portal hypertension[2]:
1. Vascular resistance and
2. Blood flow.
The relation between these two factors and portal pressure is defined by the following formula:
P=FR
Where P- pressure gradient through the portal venous system,
F- volume of blood flowing through the portal venous system.
R- resistance to the flow.
Changes in either F or R affect the pressure.
In most types of portal hypertension,
both the blood flow and the resistance are altered.
Increased portal resistance
The initial factor is the increase in vascular resistance in portal blood flow from a combination of deposition of collagen in the spaces of Disse and hepatocyte swelling.
Each of them increases the sinusoidal pressure and causes relative resistance to sinusoidal flow.
Portal vascular resistance can be defined by the Poiseuille law,
which states that,
R=8hL/pr4 where:
- h is the viscosity of blood,
related to the hematocrit
- L is the length of blood vessel which are relatively constant
- r is the radius of blood vessel
Changes in portal vascular resistance are determined primarily by the blood vessel radius.
Because portal vascular resistance is indirectly proportional to the four power of the vessel radius,
small decreases in the vessel radius cause large increases in portal vascular resistance and,
therefore,
in portal blood pressure.
Liver disease is responsible for decrease in portal vascular radius due to hepatic architectural disorder and dynamic component (active contraction of myofibroblast ,
activated stellated cells and vascular smooth muscle cells of intrahepatic veins).
Increase in portal blood flow
The second factor that contributes to the pathogenesis of portal hypertension is the increase in blood flow in portal veins due to splanchnic arteriolar vasodilatation caused by an excessive release of endogenous vasodilators.
The increase in portal blood flow aggravates the increase in portal pressure and contributes to existence of portal hypertension despite the formation of an extensive network of portosystemic collaterals that may divert as much as 80% of portal blood flow.
Formation of varices
Varices form when the hepatic venous pressure gradient exceeds 10 mmHg.
The hypertensive portal vein is decompressed by diverting up to 90% of portal flow through portosystemic collaterals and resulting in enlargement of these vessels.
CLASSIFICATION OF CAUSES OF PORTAL HYPERTENSION[1]
Dynamic /hyperkinetic portal hypertension
|
Congenital,
traumatic,
neoplastic arterioportal fistula
|
Increased portal resistance
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prehepatic
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Portal vein thrombosis
|
Portal phlebitis,
oral contraceptives,
coagulopathy,
neoplastic invasion,pancreatitis,
neonatal omphalitis
|
Portal vein compression
|
Tumor,
trauma,
lymphadenopathy,
portal phlebosclerosis,
pancreatic pseudocyst
|
Intrahepatic (obstruction of portal venules)
|
presinusoidal
|
Congenital hepatic fibrosis
Idiopathic noncirrhotic fibrosis
Primary biliary cirrhosis
α1-antytripsin deficiency
wilson disease
sarcoid liver disease
toxic fibrosis
reticuloendotheliosis
myelofibrosis
Felty syndrome
Schistosomiasis
Cystic fibrosis
Chronic malaria
|
sinusoidal
|
Hepatitis
Sickle cell disease
|
postsinusoidal
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Cirrhosis: Laennec cirrhosis,
postnecrotic cirrhosis from hepatitis
Venoocclusive disease of the liver
|
posthepatic
|
Budd-Chiari syndrome
Constrictive pericarditis
CHF (tricuspid incompetence)
|