Cirrhosis of the liver is caused by persistent or repeated damage to liver cells by disease-causing factors, leading to degeneration, necrosis, regeneration, destruction of the normal structure of liver lobules, formation of regenerative nodules, fibrosis, and scarring. The main clinical manifestations are symptoms of liver function impairment and portal hypertension. It is classified into three types: portal cirrhosis, post-necrotic cirrhosis, and biliary cirrhosis. Cirrhosis is less common in children. Diseases that can cause cirrhosis in children include viral hepatitis, neonatal hepatitis, malnutrition, hepatolenticular degeneration (Wilson's disease), clonorchiasis, galactosemia, hepatic glycogen storage disease, α1-antitrypsin deficiency, and congenital biliary atresia. Some cases have unknown causes.

bubble_chart Auxiliary Examination

1. B-mode ultrasonography: May suggest a diagnosis.
2. Barium meal fluoroscopy of the esophagus: If positive X-ray signs of esophageal and gastric varices are found, it has definitive diagnostic significance, but a negative result does not rule out cirrhosis.
3. Liver biopsy: Has confirmatory significance. However, it is only used in cases where there is high suspicion and the diagnosis remains unclear after various examinations.
4. Serum total protein may be normal or decreased, albumin is decreased, and globulin is elevated. Prothrombin time may be prolonged. In cases of portal hypertension, the white blood cell count and platelets are reduced.

bubble_chart Diagnosis

1. Medical history: The onset is insidious, with a history of neonatal hepatitis, pestilential hepatitis, or hepatolenticular degeneration.
2. Symptoms: Weakness, loss of appetite, abdominal distension and fullness, irregular diarrhea, emaciation, etc.
3. Signs: Spider angioma, liver palms, splenomegaly, abdominal wall varices, ascites, etc. The liver may be slightly enlarged in the early stage and shrink in the advanced stage.

bubble_chart Treatment Measures

1. General treatment: Rest. Provide an appropriate protein diet, sufficient calories, a high-vitamin, low-fat diet.
2. Liver-protecting treatment: Supplement deficient vitamins. The efficacy of liver-protecting drugs remains to be determined. Intravenous infusion of glucose solution or multiple amino acid solutions when food intake is insufficient or impossible.
3. Disease cause treatment: Such as correcting malnutrition, eradicating schistosomiasis, or treating extrahepatic biliary obstruction.
4. Treatment of complications:
   1. Ascites treatment: The basic approach includes bed rest, enhanced nutrition, and restriction of water and sodium intake. Diuretics may be used, such as hydrochlorothiazide, 2 mg/kg per day, plus spironolactone, 2–3 mg/kg per day, each divided into two oral doses. Potassium salts should be appropriately supplemented. Ascites drainage should be minimized.
   2. Treatment of upper gastrointestinal bleeding:
      1. Intravenous injection of posterior pituitary hormone, 0.3 IU/kg each time, dissolved in 25 ml of normal saline, slowly injected intravenously over 10 minutes. Effective when blood pressure rises and bleeding stops, but side effects such as abdominal pain, urge to defecate, and pale complexion may occur. This medication can be repeated.
      2. The three-lumen tube hemostasis method is the most commonly used hemostatic technique. It directly compresses the ruptured esophageal and gastric varices to stop bleeding. However, this is an emergency measure and does not achieve long-lasting hemostasis. If norepinephrine is added to frozen saline and injected into the stomach via a gastric tube, combined with the three-lumen tube compression method, the hemostatic effect can be enhanced.
      3. Maintain airway patency to prevent suffocation. Administer oxygen or blood transfusion if necessary.
      4. Surgical treatment may be required if necessary.