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Portal Hypertension

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Portal hypertension is defined as an increase in portal venous pressure above 5 millimeters of mercury.

When it exceeds 10 to 12 mmHg, the condition becomes clinically significant and starts to disrupt normal circulation.

The most common cause is cirrhosis, where fibrotic scarring within the liver obstructs blood flow.

Other causes can be classified as prehepatic, such as portal vein thrombosis, intrahepatic, like schistosomiasis, and posthepatic, like right heart failure.

As liver resistance increases, blood from the gastrointestinal tract is rerouted through collateral vessels that bypass the liver. These collateral pathways—such as those in the esophagus—help reduce portal pressure but also allow blood to bypass hepatic metabolism.

This reduced processing causes toxins, like ammonia, to accumulate in the blood and reach the brain, leading to hepatic encephalopathy.

Meanwhile, the rising pressure causes venous congestion in nearby organs. Varices can form in vulnerable areas such as the esophagus and stomach. These varices may rupture, leading to severe bleeding.

Overview

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Portal hypertension is an increase in blood pressure within the portal venous system. Normally, this pressure is less than 5 mmHg. It is considered clinically significant when it rises above 10 mmHg. At this threshold, complications from altered blood flow and venous congestion emerge.

Etiology

Portal hypertension arises from conditions that impede blood flow through the liver. The most common cause is cirrhosis, in which chronic liver injury leads to fibrotic scarring. This fibrosis narrows or obstructs the intrahepatic vasculature, increasing resistance to portal blood flow.

Other contributing causes include:

Hepatic vein thrombosis (Budd-Chiari syndrome): Obstructing outflow from the liver increases upstream pressure.
Right-sided heart failure: Elevated central venous pressure is transmitted backward into the hepatic circulation.
Schistosomiasis: This parasitic infection affects the hepatic portal system and often leads to periportal fibrosis.

Pathophysiology

When resistance within the liver increases, blood returning from the gastrointestinal tract cannot pass through the portal system efficiently. To compensate, the body redirects this blood through collateral vessels that bypass the liver. These newly formed pathways—known as portosystemic collaterals—relieve some of the pressure but also produce significant consequences.

As a result:

Hepatic encephalopathy may develop when unfiltered toxins—such as ammonia—enter systemic circulation and reach the brain.
Varices, or dilated veins, form in vulnerable areas such as the esophagus and stomach. These fragile veins are prone to rupture, posing a risk of life-threatening gastrointestinal bleeding.
Pulmonary complications may arise due to altered circulation, including:
- Hepatopulmonary syndrome is characterized by intrapulmonary vascular dilation and impaired oxygenation.
- Portopulmonary hypertension is characterized by elevated pulmonary arterial pressure resulting from changes in vascular tone.

These physiological changes illustrate how portal hypertension extends beyond the liver, affecting multiple organ systems and leading to serious complications in chronic liver disease.

Transcript

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