| disease | Liver Cirrhosis |
Liver cirrhosis is a condition caused by various diseases leading to diffuse necrosis of hepatocytes, regeneration, and the induction of fibrous connective tissue proliferation. It involves the destruction of lobular structures, the formation of pseudolobules, and nodular hyperplasia. Clinically, it is characterized by liver function impairment and portal hypertension, with severe complications often occurring in the advanced stage.
bubble_chart Diagnosis
Medical History and Symptoms
The causes of cirrhosis are diverse, with viral hepatitis—especially hepatitis B and C—being the primary causes domestically, followed by alcohol abuse, schistosomiasis, and others. Since cirrhosis develops slowly or remains in a long-term compensated phase, symptoms lack specificity. Only in the decompensated phase do symptoms of liver dysfunction and portal hypertension appear. Therefore, it is essential to inquire in detail about the patient's occupation, lifestyle habits, place of residence, or history of exposure to contaminated water. For suspected hepatitis cases, relevant examinations should be conducted.
Physical Examination Findings
The patient may exhibit a dark complexion, spider angiomas, palmar erythema, and some may present with jaundice, splenomegaly, ascites, or collateral circulation development, such as varicose veins in the abdominal wall, lower esophagus, gastric fundus, or hemorrhoids.
Complications
Common complications include: ① Upper gastrointestinal bleeding, which in cirrhosis is often due to esophageal varices rupture. However, it should be noted that about one-third of cases result from portal hypertensive gastropathy, such as ulcers or acute gastric mucosal lesions. Emergency endoscopy is valuable for both diagnosis and treatment. ② Hepatic encephalopathy. ③ Spontaneous bacterial peritonitis. ④ Hepatorenal syndrome.
Auxiliary ExaminationsIn the compensated phase of cirrhosis, liver function may appear entirely normal, necessitating a combination of medical history for diagnosis. In the decompensated phase, liver function abnormalities emerge, such as elevated serum bilirubin, prolonged prothrombin time, varying degrees of ALT and AST elevation, and an increased AST/ALT ratio, reflecting the severity of hepatocyte injury. GGT elevation is particularly pronounced in alcoholic cirrhosis. Serum albumin decreases while globulin increases, leading to an inverted albumin/globulin ratio. Liver fibrosis serum markers such as PⅢP, type IV collagen, laminin, fibronectin receptor, and hyaluronic acid (HA) are elevated.
Imaging: B-mode ultrasound and abdominal CT reveal changes in liver morphology, disproportionate lobe sizes, widened liver fissures, splenomegaly, portal vein diameter exceeding 1.4 cm, and splenic vein diameter exceeding 1.0 cm.
Esophageal X-ray barium meal and gastroscopy are performed to confirm the presence and severity of esophageal and gastric varices.
bubble_chart Treatment Measures
The treatment of cirrhosis is comprehensive, with attention to avoiding fatigue, catching cold, etc. A high-calorie, high-protein (for those without hepatic encephalopathy), low-salt diet is recommended, supplemented with vitamins B, C, E, and others.
Hepatocyte-protective drugs such as Liver-Tonic 0.2g 3 times a day orally. Proheparin 80–160mg, intramuscular injection once a day. Ursodeoxycholic acid can reduce the cytotoxic effects of hydrophobic bile acids. Additionally, urosodeoxycholic acid, silymarin, and others may also be used. γ or α-interferon can inhibit the proliferation of stellate cells and the expression of extracellular matrix, reducing serum PⅢ levels in liver disease patients. Chinese medicinals such as Salvia and Astragalus Root have anti-fibrotic effects. For patients with ascites, sodium intake should not exceed 1.5g per day, and water intake should not exceed 1500ml; for refractory ascites, limit to 500–700ml/day.
Patients with complications should be admitted to the hospital or sent to the emergency room for treatment.
