Pathogenesis
Portal pressure can be defined by the equation P (portal pressure) = Q (blood
flow in the portal venous system) x R (hepatic resistance). Any condition
causing increased portal venous flow, or increased hepatic resistance, can develop
into portal hypertension. In practice, most conditions associated with portal
hypertension are due to a combination of these 2 factors.
In the West, cirrhosis of any etiology is the most common cause of portal hypertension.
In the cirrhotic liver, architectural disorganization with nodular regeneration
and fibrosis results in a large increase in resistance due to vascular destruction
and distortion. The normally smooth, regular vascular channels become tortuous
and irregular, which also increases resistance. Further splanchnic arterial
inflow and thus flow in the portal vein also increase. Although it appears that
increased resistance is the prime factor in cirrhosis, increased flow also contributes
to portal hypertension.
Rare conditions causing purely an increased flow into the portal venous system
are almost always associated with only mild portal pressure elevation. However,
secondary structural changes in the liver microcirculation lead to increased
resistance (eg, a splanchnic arteriovenous [A-V] shunt may develop after abdominal
trauma). Although significant portal hypertension with this condition has been
documented, when the liver is carefully examined in detail, subtle but significant
microcirculatory changes are present (eg, collagen deposition in the space of
Disse). Conditions associated purely with increased portal venous flow (eg,
massive splenomegaly and splanchnic A-V malformations and shunts) are associated
with significant portal hypertension only in the presence of secondary intrahepatic
microcirculatory changes.
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