What are the complications of cirrhosis?

Cirrhosis is the advanced stage of progressive liver fibrosis, characterized by distortion of liver architecture and formation of regenerative nodules. Cirrhosis is caused by long-term or repeated effects of one or more etiologies on the liver. Patients with cirrhosis are prone to multiple complications and their life expectancy is significantly shortened.

Today we will learn about the complications of cirrhosis.

(1) Portal hypertension

In cirrhosis, due to the formation of fibrous tissue, the liver lobule structure is destroyed, and the portal vein blood flow is blocked, causing a large amount of blood flow from the stomach, intestines, spleen, etc. to stagnate in the portal vein, increasing the portal vein pressure. When it reaches a certain level, portal hypertension is formed. Many complications of cirrhosis are caused by portal hypertension (increased pressure in the portal vein system). Portal hypertension can lead to the formation of venous collateral circulation (varicose veins) and circulatory, vascular, functional and biochemical abnormalities, which in turn lead to the occurrence of ascites and other complications.

(2) Esophageal varices.

When portal vein pressure increases to a certain level, a large amount of portal vein blood will be shunted to the esophageal and gastric fundus venous plexus, causing esophageal and gastric fundus varices. When the tension of varicose veins reaches a certain level, the mucosa will become thinner. Coupled with the effects of other factors, such as hard food and constipation, bleeding is very likely to occur. Patients with varicose bleeding often present with vomiting blood and/or black stools. Conventional treatment measures are endoscopic treatment. The mortality rate of varicose bleeding is very high. In the past, the mortality rate of a single varicose bleeding was 30%, and only 1/3 of patients could survive for 1 year.

3) Portal hypertensive gastropathy.

Although portal hypertensive gastropathy (congestive gastropathy) is very common in patients with portal hypertension, it rarely causes significant bleeding in these patients. If portal hypertensive gastropathy is the only cause of bleeding, it is diffuse mucosal effusions in the absence of other lesions such as varicose veins that cause gastrointestinal bleeding and anemia. The gastric mucosa is very fragile, and bleeding may be due to rupture of dilated blood vessels. The severity of gastropathy is related to the level of portal pressure, the level of hepatic vascular resistance, and the degree of reduced hepatic blood flow.

(4) Ascites and edema

Ascites is the accumulation of fluid in the peritoneal cavity and is the most common complication of cirrhosis. Portal hypertension is the first step leading to fluid retention and ascites in patients with cirrhosis. Patients without portal hypertension will not develop ascites and edema.

Plasma albumin is mainly synthesized in the liver. Due to severe damage to liver function, patients with cirrhosis suffer from protein synthesis disorders and hypoproteinemia. When the protein level decreases to a certain level, pleural effusion, ascites and lower limb edema will occur.

(5) Hepatic encephalopathy

Hepatic encephalopathy refers to a series of potentially reversible neuropsychiatric abnormalities in patients with liver dysfunction. Disrupted circadian sleep patterns (insomnia and hypersomnia) are common early features, usually before obvious neurological signs appear. Ammonia produced by the metabolism of protein foods is one of the causes of hepatic encephalopathy. Due to the impaired metabolic clearance of ammonia after cirrhosis, ammonia produced by protein metabolism in the body, or ammonia produced in the body due to the intake of a large amount of protein foods at one time, increases the ammonia concentration in the blood and induces hepatic encephalopathy.

(6) Spontaneous bacterial peritonitis.

Abbreviated as SBP. This refers to the infection of the patient's existing ascites in the absence of evidence of secondary pathogens in the abdominal cavity (such as visceral perforation). SBP is almost always seen in patients with end-stage liver disease. The clinical manifestations of SBP include fever, abdominal pain, abdominal tenderness and mental changes. Due to impaired liver detoxification function and decreased immune function, bacteria and toxins that enter the body through the intestinal wall cannot be effectively cleared, forming bacteremia. After entering the abdominal cavity, spontaneous bacterial peritonitis is formed. In severe cases, symptoms such as refractory ascites and abdominal pain may occur.

(7) Primary liver cancer.

Patients with cirrhosis have a significantly increased risk of developing hepatocellular carcinoma. For most types of chronic hepatitis, the risk of liver cancer increases only after cirrhosis develops. The exception is patients with chronic hepatitis B virus infection, who can develop HCC even without cirrhosis. In cirrhosis, due to severe damage to liver cells, a large number of liver cells proliferate to compensate for liver function, and the new liver cells may become cancerous due to abnormal proliferation. Due to the strong reserve of liver function, HCC patients are often asymptomatic in the early stages of the disease, so diagnosis is often delayed.

(8) Hepatorenal syndrome.

Hepatorenal syndrome is the development of renal failure in patients with advanced liver disease caused by cirrhosis, severe alcoholic hepatitis, acute liver failure, or (rarely) metastatic disease. Hepatorenal syndrome is not a new disease, but is often the end stage of progressive liver damage leading to a continuous decrease in renal perfusion.

(9) Hepatic hydrothorax - Hepatic hydrothorax refers to the presence of pleural effusion in patients with cirrhosis who have no evidence of underlying cardiopulmonary disease. It is caused by ascites entering the pleural cavity through a defect in the diaphragm and is often located on the right side.