What are the complications of liver cirrhosis?

What are the complications of liver cirrhosis? Cirrhosis of the liver is formed by long-term or repeated effects of one or more causes on the liver. Patients with liver cirrhosis are prone to a variety of complications, and their life expectancy is significantly shortened. Today we will learn about the complications of liver cirrhosis.

Liver cirrhosis is the advanced stage of progressive liver fibrosis, which is characterized by distortion of the liver structure and the formation of regenerative nodules. Cirrhosis of the liver is formed by long-term or repeated effects of one or more causes on the liver. Patients with liver cirrhosis are prone to a variety of complications, and their life expectancy is significantly shortened.

Today we will learn about the complications of liver cirrhosis.

(1) Portal hypertension

In liver cirrhosis, due to the formation of fibrous tissue, the structure of the liver lobules is destroyed, and the blood flow of the portal vein is blocked, causing a large amount of blood flow from the stomach, intestines, spleen, etc. to stagnate in the portal vein, increasing the pressure of the portal vein. After reaching a certain level, portal hypertension is formed. . Many complications of liver cirrhosis are caused by portal hypertension (increased pressure in the portal venous system). Portal hypertension can lead to the formation of venous collateral circulation (varices) and abnormalities in circulation, blood vessels, function and biochemistry, which in turn leads to ascites and other complications.

(2) Varicose veins of the fundus of esophagus and stomach.

When the portal pressure increases to a certain level, a large amount of portal vein blood is shunted to the fundus esophagus and gastric venous plexus, causing esophageal and gastric varices, and when the tension of the varicose vein reaches a certain level, the mucosa will become thinner, and other factors, such as Hard food, constipation, etc., are extremely prone to bleeding. Patients with bleeding from varicose veins often present with hematemesis and/or melena. The conventional treatment is endoscopic treatment. The mortality rate of varicose vein bleeding is very high. In the past, the mortality rate of a single varicose vein bleeding was 30%, and only one-third of patients could live for one year.

3) Portal hypertensive gastropathy.

Portal hypertensive gastropathy (congestive gastric disease) is very common in patients with portal hypertension, but it rarely causes significant bleeding in these patients. If portal hypertensive gastropathy is the only cause of bleeding, the cause of gastrointestinal bleeding and anemia is diffuse mucosal oozing and no other lesions, such as varicose veins. The gastric mucosa is very fragile, and the bleeding may be due to the rupture of dilated blood vessels. The severity of gastric disease is related to the level of portal pressure, the level of hepatic vascular resistance, and the degree of reduction in hepatic blood flow.

(4) Ascites and edema

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

Plasma albumin is mainly synthesized in the liver. In patients with liver cirrhosis, the liver function is severely damaged, resulting in protein synthesis disorders and hypoalbuminemia. When the protein is reduced to a certain level, pleural and ascites and lower limb edema will appear.

(5) Hepatic encephalopathy

Hepatic encephalopathy refers to a series of potentially reversible neuropsychiatric abnormalities in patients with liver insufficiency. Disturbances in circadian sleep patterns (insomnia and drowsiness) are common early features and usually precede obvious neurological signs. Ammonia produced by eating protein food metabolism is one of the causes of hepatic encephalopathy. After liver cirrhosis, the metabolism of ammonia is obstructed, the ammonia produced by protein metabolism in the body, or the ammonia produced in the body by ingesting a large amount of protein food at one time, increases the concentration of ammonia in the blood and induces hepatic encephalopathy.

(6) Spontaneous bacterial peritonitis.

Referred to as SBP. This refers to the infection of the patient’s own ascites when there is no evidence of a secondary source of disease (eg, visceral perforation) in the abdominal cavity. 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 liver detoxification dysfunction and immune function decline, bacteria and toxins that enter the body through the intestinal wall cannot be effectively removed, resulting in bacteremia. After re-entering into the abdominal cavity, spontaneous bacterial peritonitis develops, which may be refractory in severe cases. Symptoms such as ascites and abdominal pain.

(7) Primary liver cancer.

Patients with liver cirrhosis have a significantly higher risk of hepatocellular carcinoma. Most types of chronic hepatitis only increase the risk of liver cancer after cirrhosis. An exception is chronic hepatitis B virus infection. Such patients can develop HCC even without cirrhosis. In liver cirrhosis, due to severe damage of liver cells, a large number of hepatocytes 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, which often delays diagnosis.

(8) Hepatorenal syndrome.

Hepatorenal syndrome refers to renal failure in patients with advanced liver disease caused by liver cirrhosis, severe alcoholic hepatitis, acute liver failure or metastases (rarely). Hepatorenal syndrome is not a new disease, but is often the end stage of continuous reduction in renal perfusion due to increasingly severe liver damage.

(9) Hepatic pleural effusion

Hepatic pleural effusion refers to pleural effusion in patients with liver cirrhosis without evidence of underlying cardiopulmonary disease. It is caused by ascites passing through the defect of the diaphragm and entering the pleural cavity, often located on the right side.

(source:internet, reference only)

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