Cirrhosis is a common chronic, progressive, diffuse liver disease. The liver is subjected to long-term or repeated action of one or more pathogenic factors, resulting in necrosis and regeneration of hepatocytes, proliferation of fibrous connective tissue, destruction of normal liver lobule structure, pseudobullet formation, and hardening of texture. This physiopathological change is clinically known as cirrhosis. Cirrhosis occurs in men, mostly in middle-aged adults. It has a chronic clinical course, manifested by varying degrees of liver function impairment and symptoms of portal hypertension. Serious complications often occur in the late stage.
I. Etiology and clinical manifestations of cirrhosis.
The etiology of cirrhosis, alcoholic cirrhosis is common in Europe and America, and post-hepatitis cirrhosis is common in Asian and African countries. Seventy percent of cirrhosis in China has viral hepatitis causes. Most of them are hepatitis B. In recent years, alcoholic liver disease has increased rapidly due to the improvement of living standards. Complication of hepatitis B virus (HBV) or hepatitis C virus (HCV) infection on top of alcoholic liver disease can make the disease more aggravated and more likely to form cirrhosis. Other causes include cholestasis, chronic heart failure, vascular obstruction, poisoning, parasitic infections, metabolic disorders, and severe malnutrition.
The clinical manifestations of cirrhosis are generally divided into two stages: compensated and decompensated stages: because cirrhosis starts slowly, a few can be asymptomatic for ten to several decades. Subsequently, the liver gradually shrinks and the spleen progressively enlarges. Patients in the compensated stage have mild or no symptoms, and splenomegaly may be found inadvertently or during physical examination.
The symptoms of compensated patients are mainly two major syndromes: hepatic decompensation and portal hypertension
1. Symptoms of hepatic decompensation: weakness, emaciation, poor appetite, abdominal distension, nausea, vomiting, diarrhea, jaundice, gum bleeding, nasal bleeding, ankle swelling, grayish face, liver palms, spider nevus. Male patients may have breast development and hypogonadism; female patients may have amenorrhea and menstrual irregularities.
2.Symptoms of portal hypertension: splenomegaly, abdominal wall varices, esophagogastric-fundus varices, rectal varices, portal hypertensive gastropathy. Vomiting blood and blood in stool can occur when varices rupture, especially bleeding from ruptured esophagus-fundus varices is one of the main causes of death in liver cirrhosis.
Prevention and treatment of major complications
1, upper gastrointestinal bleeding: ruptured esophagus-fundus varices bleeding, portal hypertensive gastrointestinal disease and peptic ulcer are the main causes of cirrhosis combined with gastrointestinal bleeding, the most serious is ruptured esophagus-fundus varices bleeding. Clinically, it manifests as vomiting blood, blood in stool and shock. The incidence is about 20-40% in patients with untreated cirrhosis. Of these, 40-80% die during the first bleed. Survivors have a risk of rebleeding of up to about 70%. Another 60% of patients with cirrhosis have gastrointestinal bleeding as a result of portal hypertensive gastric disease. The treatment varies with the cause of bleeding. Therefore, even if the diagnosis is clear that upper gastrointestinal bleeding is due to cirrhosis, gastroscopy is necessary to confirm the specific cause of the bleeding. Once the cause of bleeding is clear, it is important to guide the patient’s life and prevent rebleeding. In case of severe esophageal varices, gastroscopic esophageal vein ligation, sclerosis, and local injection of tissue glue can be performed. In cases with splenomegaly and hypersplenism (anemia, thrombocytopenia, leukopenia), surgical splenectomy and peripancreatic vascular dissection may be performed. For those who do not receive surgery or endoscopic treatment temporarily, medications can be used to reduce portal pressure and prevent bleeding, commonly used are: insulin, hypocretin, cardiac pain, and ambrisentin. In case of acute bleeding, octreotide, growth inhibitor, posterior pituitary hormone, terlipressin, etc. can be given. In case of portal hypertensive gastropathy or peptic ulcer bleeding, acid suppressants and gastric mucosal protective agents are given along with the lowering of portal pressure as symptomatic treatment.
2, hepatic encephalopathy: The cause of its occurrence is the failure of hepatocyte function, unable to remove toxic metabolites or portal hypertension, the toxic substances in the portal vein bypass the liver, through the collateral vessels directly into the body circulation, reaching the brain, causing changes in consciousness-based central nervous metabolic disorders. Triggering factors are mainly upper gastrointestinal bleeding, infection, electrolyte disturbance, high protein diet, constipation, etc. It can be divided into prodromal phase, pre-coma phase, coma phase and coma phase. At the beginning, it may only manifest as depressed mood, sleep disorder, abnormal behavior, dryness and mania, etc. The treatment principle is to eliminate the causative factors, reduce the absorption of toxic substances in the intestine, and correct the amino acid imbalance. Lactulose can be routinely taken orally to prevent it.
3.Primary liver cancer: current research shows that there is a close relationship between cirrhosis and hepatocellular carcinoma, about 60% of patients with hepatocellular carcinoma have cirrhosis at the same time, and all kinds of cirrhosis can be secondary to liver cancer. Among them, the rate of hepatitis B cirrhosis and hepatitis C cirrhosis complicating liver cancer is higher. To the maximum extent, long-term sustained inhibition of viral replication can delay or stop the progression of liver disease, and ultimately achieve the reduction or prevention of cirrhosis, hepatic decompensation, and hepatocellular carcinoma. Therefore, in addition to long-term effective antiviral therapy according to virological testing, patients with cirrhosis should also have regular liver function and tumor markers such as fetoprotein and ultrasound for early detection of liver cancer and timely surgery, interventional or liver transplantation treatment.
4. Other complications: such as ascites, spontaneous peritonitis, hepatic pleural fluid, hepatitis-related nephritis, hepatorenal syndrome, hepatopulmonary syndrome, hepatogenic diabetes, hepatic myelopathy, portal vein thrombosis, cholecystitis, gallstones, etc. all have corresponding manifestations and can be given symptomatic treatment.
III. Prognosis of cirrhosis
The prognosis of cirrhosis is influenced by various factors, such as etiology, pathological type, liver function status and complications. The following points are available for reference.
1. The prognosis is better if the cause is clear and eliminated. For example, alcoholic cirrhosis can survive for a long time after strict abstinence from alcohol, or be maintained in the compensatory stage.
2. Those with enlarged liver have better prognosis than those with shrunken liver. It has been reported that the three-year survival rate of those who can reach the liver is 64%, and those who cannot reach the liver is 45%. This may be related to the fact that those with larger liver size have a higher number of functioning hepatocytes.
Once ascites is formed, it often suggests a poor prognosis. Especially those who need high dose diuretics to control ascites, the prognosis is worse.
4, jaundice appears sharply or severe prognosis is poor, mild jaundice has no major impact on the prognosis.
5.The more severe the degree of esophagogastric varices, the higher the chance of bleeding. The worse the prognosis.
6.The appearance of hepatic encephalopathy suggests a poor prognosis, especially for those who have no obvious causative factors.
Fourth, the patient’s daily health care and holiday considerations.
1. If you have suspicious symptoms of cirrhosis, such as weakness, poor appetite, abdominal distension, jaundice, gum bleeding or find splenomegaly, you should visit the gastroenterology department or liver disease department of a regular hospital and have a comprehensive examination. For example, liver function, blood routine, virological index, immune function measurement, liver fibrosis index, abdominal ultrasound, CT, gastroscopy. Recently, the liver stiffness has been measured by instruments to determine cirrhosis in foreign countries. After the diagnosis of cirrhosis is confirmed, liver function, ultrasound and fetoprotein need to be reviewed regularly. They can be checked every 4-6 months. When antiviral treatment is given, blood count and viral load should also be tested regularly according to the type of virus and medication. Liver biopsy and laparoscopy are the gold standard for the diagnosis of cirrhosis.
2. Patients in the compensated stage should reduce their activities and engage in light physical work. Patients in the decompensated stage should mainly rest in bed. Before hiking and traveling, you should carefully consider your body’s tolerance to avoid aggravation of the disease due to boat travel and even accidents such as bleeding.
3. Diet should be high in calories, high in protein, multivitamins and easy to digest. When there are precursors of hepatic encephalopathy, protein should be restricted. When there is ascites, should be low salt or salt-free diet.
4.Avoid too rough and hard food. Those with severe esophageal-fundus varices should also pay attention not to be too full, lifting heavy objects, constipation, too fast infusion and other factors that can increase abdominal pressure, portal pressure and food reflux.
5.Prohibit alcohol and drugs that damage the liver. Although abstaining from alcohol cannot reverse the formed cirrhosis, it can slow down the disease. The large amount of alcohol consumed during the holidays can even induce upper gastrointestinal hemorrhage and hepatic encephalopathy. Antipyretic analgesics are a common trigger for bleeding. Barbiturates sedative-hypnotics are damaging to the liver and should be avoided as much as possible.
6. Currently, it is believed that antiviral therapy for post-hepatitis cirrhosis can delay and stop the progress of the disease and even reduce the occurrence of hepatocellular carcinoma, but long-term continuous medication is required. Drugs such as cardiotonic to reduce portal pressure to prevent rebleeding should also be applied continuously for a long time, and sudden discontinuation of drugs may cause rebound hemorrhage.