Cirrhosis of the liver and its complications
Etiology.
It varies from region to region. Hepatitis virus cirrhosis is the most common in China, followed by schistosomiasis liver fibrosis, and the proportion of patients with alcoholic cirrhosis is gradually increasing. Overseas, alcoholic cirrhosis is the most common. There are many types of cirrhosis, specifically divided into seven categories: alcoholic cirrhosis, post-hepatitis cirrhosis, parasitic cirrhosis, toxic cirrhosis, biliary cirrhosis, circulatory disorder (stasis) cirrhosis and dystrophic cirrhosis.
Diagnosis and differential diagnosis.
I. Laboratory tests
Routine blood count: decreased hematocrit, platelets, and white blood cells.
Liver function test: mild abnormalities in compensated stage, decreased serum protein, increased globulin, and A/G inversion in decompensated stage. Prothrombin time is prolonged and prothrombin activity is decreased. Transaminases and bilirubin are elevated. Total cholesterol and cholesterol lipids are decreased and blood ammonia may be elevated. Amino acid metabolism is disturbed and the branching/aromatic ratio is imbalanced. Urea nitrogen and creatinine are elevated. Electrolyte disorders: low sodium, low potassium.
Pathogenic tests: positive for HBV-M or HCV-M or HDV-M.
Immunological examination.
(1) Immunoglobulins: lgA, lgG, lgM may be elevated.
(2) Autoantibodies: anti-nuclear pit body, anti-mitochondrial antibody, anti-smooth muscle antibody, anti-hepatic lipoprotein membrane antibody may be positive.
(3) Other immunological examinations: decreased complement, decreased roseola node formation rate and lyophilization rate, decreased CD8 (Ts) cells and decreased function.
Fibrosis examination: increased PIIIP value, increased prolyl hydroxylase (PHO), increased monoamine oxidase (MAO), increased serum laminin (LM).
Ascites examination: those with newly developed ascites or those with rapid increase in pre-existing ascites for unknown reasons should undergo laparotomy and draw ascites for routine examination, adenosine deaminase (ADA) determination, bacterial culture and cytological examination. To improve the culture positivity rate, ascites culture should be performed at the bedside, using blood culture bottles for aerobic and anaerobic bacteria, respectively.
II. Imaging examinations
X-ray examination: barium imaging of esophagogastric fundus, which shows worm-like or earthworm-like variceal changes in esophagogastric fundic veins.
B-type and color Doppler ultrasonography: thickened liver peritoneum, unsmooth liver surface, enhanced echogenicity of liver parenchyma, roughness and disproportion, widened portal vein diameter, splenomegaly, ascites.
CT examination: the ratio of liver lobes was out of proportion, density decreased, nodule-like changes, widening of the hepatic hilar, splenomegaly, and ascites.
Endoscopy: It can determine the presence of esophagogastric fundic varices, and the positive rate is higher than that of barium meal X-ray, and it can also understand the degree of varices and assess the risk of bleeding. Esophagogastric fundic varices are the most reliable indicator for the diagnosis of portal hypertension. In case of complicated upper gastrointestinal bleeding, emergency gastroscopy can determine the site and cause of bleeding and provide hemostatic treatment.
Liver biopsy: Liver puncture biopsy can confirm the diagnosis.
V. Laparoscopy: It can directly observe the liver, spleen and other abdominal organs and tissues, and biopsy can be taken under direct vision, which is valuable for those who have difficulty in diagnosis.
Portal vein pressure measurement: The difference between the wedge pressure and free pressure of hepatic vein is the hepatic vein pressure gradient (HVPG), which reflects the portal vein pressure. Normal is mostly less than 5mmHg, and greater than 10mmHg is considered portal hypertension.
Complications.
When cirrhosis develops to an advanced stage, a variety of complications can occur, including ascites, primary peritonitis, portal hypertensive gastropathy, ruptured bleeding from esophagogastric fundic varices, hepatorenal syndrome, electrolyte disorders, and hepatic encephalopathy.
The treatment of cirrhosis mainly includes.
(1) treatment of etiology.
(2) Treatment of cirrhosis.
(3) Treatment of complications.
(4) liver transplantation.
(1) treatment of etiology: such as antiviral therapy for viral hepatitis cirrhosis, hormone therapy for autoimmune cirrhosis in active stage, interventional therapy for cirrhosis due to vascular causes, etc.
(2) Treatment of cirrhosis: support, vitamin supplementation, liver protection, enzyme lowering, anti-yellowing, etc.; if there is bleeding tendency, oral drugs to lower portal pressure can be given; hypersplenism can be treated with leukocyte- and platelet-raising drugs, and splenectomy is feasible if necessary.
(3) Treatment of complications: Patients with complications such as spontaneous peritonitis, hepatorenal syndrome, hepatic encephalopathy, ruptured esophagogastric fundic varices and bleeding should seek timely medical attention and be treated according to the examination results
(4) Liver transplantation: Patients with complications of cirrhosis should be evaluated for liver transplantation. Patients whose conservative medical treatment is ineffective and whose expected survival time is less than 1 year should be considered for liver transplantation.
Preventive care.
The treatment of cirrhosis is a long-term process, and patients should adhere to treatment and regular follow-up. The diet should be reasonably matched, such as a diet based on light foods, Hunsu should also be reasonably matched, avoid spicy, greasy, hormone-containing foods, and in life, quit smoking, quit drinking, and keep enough rest time