Cirrhosis is an advanced stage of progressive liver fibrosis characterized by structural distortion of the liver and regenerative nodule formation. Cirrhosis is formed by the long-term or repeated action of one or more causes on the liver. Patients with cirrhosis are prone to a variety of complications and have a significantly shorter life expectancy.
Today we will understand what are the complications of cirrhosis.
(1) Portal hypertension
When cirrhosis of the liver, due to the formation of fibrous tissue, the destruction of the structure of the liver lobules, and the obstruction of portal vein blood flow, resulting in a large amount of blood flow from the stomach, intestine, spleen and other places stagnating in the portal vein, so that the portal vein pressure increases, and after reaching a certain extent, a portal hypertension is formed. Many complications of cirrhosis are caused by portal hypertension (increased pressure on the portal vein system). Portal hypertension can lead to collateral circulation (varicose veins) and abnormalities of circulation, vessels, function, and biochemistry, leading to ascites and other complications.
(2) Varicose veins of the esophagus and gastric base.
When the portal vein pressure increases to a certain extent, a large amount of portal vein blood is shunted to the esophageal gastric floor venous plexus, so that the esophagus gastric varices, varicose vein tone reaches a certain level, the mucous membrane will become thin, coupled with the role of other factors, such as hard food, constipation, etc., it is very easy to bleed. Patients with varicose vein bleeding often present with hematemesis and/or melena. Conventional treatment is endoscopic. The mortality rate from varicose vein bleeding is high. In the past, the mortality rate of a single variceal bleeding was 30%, and only 1 in 3 patients were able to live for 1 year.
3) Portal hypertensive gastropathy.
Portal hypertensive gastropathy (congestive gastropathy), although very common in patients with portal hypertension, rarely causes significant bleeding in these patients. If portal hypertensive gastropathy is the only cause of bleeding, gastrointestinal bleeding and anemia are caused by diffuse mucosal bleeding without other lesions such as varicose veins. The gastric mucosa is fragile, and bleeding may be due to the rupture of dilated blood vessels. The severity of stomach disease is related to the level of portal pressure, the level of hepatic vascular resistance, and the degree of decreased hepatic blood flow.
(4) Ascites and puffiness
Ascites, where fluid accumulates in the abdominal cavity, is the most common complication of cirrhosis. Portal hypertension is the first step leading to fluid retention and even ascites in patients with cirrhosis. Patients without portal hypertension do not develop ascites and edema.
Plasma albumin is mainly synthesized in the liver, cirrhosis patients due to severe damage to liver function, resulting in protein synthesis disorders, hypoproteinemia, when the protein is reduced to a certain extent, there will be chest ascites and lower limb edema.
(5) Hepatic encephalopathy
Hepatic encephalopathy is a series of potentially reversible neuropsychiatric abnormalities in patients with hepatic insufficiency. Disorders of circadian sleep patterns (insomnia and drowsiness) are common early features and usually precede the appearance of obvious neurologic signs. Eating ammonia produced by protein food metabolism is one of the causes of hepatic encephalopathy. Hepatic encephalopathy is induced due to the occurrence of disorders in the 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 food in the body at one time, which increases the concentration of ammonia in the blood.
(6) Spontaneous bacterial peritonitis.
Abbreviated as SBP. This refers to infection with the patient's own pre-existing ascites in the absence of evidence of a secondary source (eg, visceral perforation) in the abdominal cavity. SBP is almost always seen in patients with end-stage liver disease. Clinical manifestations of SBP include fever, abdominal pain, abdominal tenderness, and altered consciousness. Due to liver detoxification dysfunction, the body's immune function is reduced, bacteria and toxins entering the body through the intestinal wall cannot be effectively removed, and bacteremia is formed, and after re-entering the abdominal cavity, spontaneous bacterial peritonitis is formed, and symptoms such as refractory ascites and abdominal pain can occur in severe cases.
(7) Primary liver cancer.
Patients with cirrhosis have a significantly higher risk of developing hepatocellular carcinoma. Most types of chronic hepatitis increase the risk of liver cancer only after the development of cirrhosis. Exceptions are those with chronic hepatitis B virus infection, which can develop HCC even without cirrhosis. In cirrhosis, due to severe damage to liver cells, a large number of hepatocyte hyperplasias occur to compensate for liver function, and newborn liver cells may become cancerous due to abnormal proliferation. Patients with HCC are often asymptomatic early in the course of the disease due to strong liver function reserves, often delaying diagnosis.
(8) Hepatorenal syndrome.
Hepatorenal syndrome is renal failure in patients with advanced liver disease caused by cirrhosis, severe alcoholic hepatitis, acute liver failure, or metastases (rarely). Hepatorenal syndrome is not an emerging disease, but is often the end-stage of increasing liver damage leading to a continuous decrease in renal perfusion.
(9) Hepatic pleural fluid - Hepatic pleural fluid refers to the pleural effusion in patients with cirrhosis without evidence of basal cardiopulmonary disease, which is caused by ascites passing through the defect of the diaphragm into the pleural cavity, often located on the right side.