From the Guidelines
Portal hypertension is a condition characterized by increased pressure in the portal venous system, primarily resulting from obstruction to blood flow, and its pathophysiology involves increased resistance to portal blood flow, splanchnic vasodilation, and hyperdynamic circulation, leading to complications like ascites, hepatorenal syndrome, and hepatic encephalopathy. The pathophysiology of portal hypertension begins with increased resistance to portal blood flow, which can occur at prehepatic, intrahepatic, or posthepatic levels 1. In cirrhosis, the most common cause, structural changes in the liver including fibrosis and nodule formation distort the hepatic vasculature, while dynamic components involve contraction of hepatic stellate cells and myofibroblasts due to decreased nitric oxide production and increased vasoconstrictors. As portal pressure rises above 10 mmHg, collateral vessels develop to bypass the obstruction, leading to varices in the esophagus, stomach, and rectum. Simultaneously, splanchnic vasodilation occurs due to increased production of vasodilators like nitric oxide, which worsens portal hypertension by increasing portal blood flow. This vasodilation, combined with systemic vasoconstriction and sodium retention, leads to increased cardiac output and hyperdynamic circulation. These hemodynamic changes contribute to complications like ascites, hepatorenal syndrome, and hepatic encephalopathy.
Key Factors in Portal Hypertension
- Increased resistance to portal blood flow
- Splanchnic vasodilation
- Hyperdynamic circulation
- Collateral vessel formation
- Varices in the esophagus, stomach, and rectum
Treatment of Portal Hypertension
Treatment focuses on reducing portal pressure through beta-blockers like propranolol or nadolol, which decrease cardiac output and cause splanchnic vasoconstriction, or through procedures like transjugular intrahepatic portosystemic shunt (TIPS) to create alternative flow pathways 1. The management of portal hypertension-related complications, such as variceal bleeding, ascites, and hepatic encephalopathy, should follow AASLD and Baveno/EASL guidelines, which recommend the use of non-selective beta blockers (NSBBs) to prevent portal hypertension-related decompensation, and the combination of vasoactive drugs and endoscopic band ligation (EBL) as the first therapeutic option for acute variceal bleeding 1.
Recent Guidelines and Recommendations
Recent studies have shown that noninvasive liver disease assessments, such as ultrasonography and transient elastography, can be used to diagnose cirrhosis and portal hypertension, and that a reduction of HVPG by >20% of baseline values or 12 mmHg is correlated with considerable reduction of risk of variceal bleeding during treatment with nonselective beta blockers 1. The most recent and highest quality study recommends the use of noninvasive methods for the diagnosis of cirrhosis and portal hypertension, and the management of portal hypertension-related complications according to AASLD and Baveno/EASL guidelines.
From the Research
Pathophysiology of Portal Hypertension
- Portal hypertension is characterized by an increase in the pressure gradient between the portal vein and the inferior vena cava 2
- The main driver of cirrhosis decompensation is portal hypertension, leading to complications such as varices, ascites, and hepatic encephalopathy 3
- Increased resistance within the portal venous system, followed by increased portal venous inflow, contributes to the development of portal hypertension 2
Diagnosis of Portal Hypertension
- The gold standard for measuring portal pressure in cirrhosis and determining its severity is hepatic vein catheterization with determination of the hepatic venous pressure gradient 2
- Non-invasive tests, such as liver stiffness measurement in combination with platelet count, can accurately identify clinically significant portal hypertension 4
- Varices on endoscopy or portosystemic collaterals on imaging can indicate portal hypertension 2
Management of Portal Hypertension
- Non-selective beta blockers, such as propranolol and nadolol, are commonly used to reduce portal pressure and prevent variceal bleeding 5
- Carvedilol is a more potent agent than propranolol in reducing portal pressure and is better tolerated 5
- Combining beta blockers with nitrates, such as isosorbide-5-mononitrate, may be more effective in reducing portal pressure than using beta blockers alone 6
- Hemodynamic monitoring can help select non-responders who may benefit from additional therapies, such as band ligation 5