From the Guidelines
Portal hypertension in patients with cirrhosis and normal liver function is a significant concern, as it can lead to complications such as variceal bleeding and ascites, and management should focus on preventing these complications. The condition, sometimes called compensated cirrhosis, occurs due to structural changes in the liver that create increased resistance to blood flow through the portal vein system, despite the liver cells still functioning adequately 1.
Key Considerations
- Patients should undergo endoscopic screening for esophageal varices; if large varices are found, non-selective beta-blockers like propranolol (starting at 20mg twice daily, titrated to heart rate) or carvedilol (starting at 6.25mg daily, maximum 12.5mg daily) are recommended 1.
- For patients with varices who have already bled, a combination of beta-blockers and endoscopic band ligation is needed 1.
- Salt restriction (less than 2g sodium daily) and diuretics like spironolactone (starting at 100mg daily) may be necessary if ascites develops 1.
- Patients should avoid alcohol completely, limit NSAID use, and receive vaccinations against hepatitis A, B, and pneumococcal infections 1.
- Regular monitoring with ultrasound every 6 months for hepatocellular carcinoma screening is essential, even with normal liver function, as the underlying cirrhosis still poses significant risks despite preserved synthetic function 1.
Prevention of Complications
- Clinically significant portal hypertension occurs when the HVPG is 10 mmHg, at which point complications such as esophageal varices and ascites may develop 1.
- 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.
- Non-invasive methods for the diagnosis of cirrhosis and portal hypertension, including ultrasonography (US) and transient elastography, can be used to assess liver fibrosis and cirrhosis 1.
From the Research
Portal Hypertension and Cirrhosis
- Portal hypertension (PH) is a common complication of cirrhosis and a major driver of hepatic decompensation, leading to ascites, variceal bleeding, and hepatic encephalopathy 2, 3.
- The goal of PH treatment in patients with compensated cirrhosis is to reduce the risk of hepatic decompensation, while in decompensated patients, the aim is to prevent further decompensation and improve survival 2.
Pathophysiology of Portal Hypertension
- Portal hypertension is initiated by increased intrahepatic vascular resistance and a hyperdynamic circulatory state, characterized by high cardiac output, increased total blood volume, and splanchnic vasodilatation 4.
- The hyperdynamic circulatory state results in increased mesenteric blood flow, which contributes to the development of portal hypertension 4.
Treatment of Portal Hypertension
- Non-selective beta-blockers (NSBBs) are the primary treatment for portal hypertension, aiming to reduce cardiac output and splanchnic vasodilatation 2, 3, 4, 5, 6.
- Carvedilol, a non-selective beta-blocker, has shown superior efficacy in lowering PH in patients with cirrhosis and may be the NSBB of choice for the treatment of clinically significant portal hypertension 2.
- Other treatments, such as statins, angiotensin converting enzyme inhibitors, and angiotensin II type receptor 1 blockers, have been investigated, but their use is limited by off-target effects and the need for further randomized clinical trials 4.
Clinical Significance
- Portal hypertension is responsible for the most severe and often lethal complications of cirrhosis, including bleeding oesophageal varices, ascites, renal dysfunction, and hepatic encephalopathy 3.
- Reducing portal pressure is associated with a lower long-term risk of developing complications and an improved long-term survival 3.
- The use of NSBBs, such as carvedilol, has been shown to improve patient survival and reduce the risk of variceal bleeding in patients with cirrhosis and portal hypertension 2, 3, 4.