Basic information
Common pathogens in clinical gastroenterology of liver cirrhosis Common symptoms of liver include viral hepatitis, alcoholism, nutritional disorders, industrial poisons, drugs, circulatory disorders, metabolic disorders, cholestasis, schistosomiasis, abdominal distension, hepatosplenomegaly, jaundice, liver palm, spider nevus, ascites, etc.
The cause of disease
There are many causes of liver cirrhosis, which can be divided into viral hepatitis cirrhosis, alcoholic cirrhosis, metabolic cirrhosis, cholestatic cirrhosis, hepatic vein reflux obstructive cirrhosis, autoimmune cirrhosis, toxic and drug-induced cirrhosis, malnutrition cirrhosis, cryptogenic cirrhosis and so on.
1. viral hepatitis
At present, viral hepatitis, especially chronic hepatitis B and C, is the main cause of portal cirrhosis in China.
Step 2 drink too much
Long-term heavy drinking is one of the factors leading to cirrhosis.
3. Malnutrition
Most scholars admit that malnutrition can reduce the resistance of liver cells to toxic and infectious factors and become an indirect cause of liver cirrhosis.
4. Industrial poisons or drugs
Long-term or repeated exposure to arsenic-containing pesticides, carbon tetrachloride, yellow phosphorus, chloroform, etc. Or long-term use of certain drugs such as acetaminophen, isoniazid, cincofen, tetracycline, methotrexate, methyldopa, etc., may lead to toxic or drug-induced hepatitis, and then lead to liver cirrhosis. Aflatoxin can also cause toxic damage to liver cells and cause cirrhosis.
5. circulatory disorder
Chronic congestive heart failure and chronic constrictive pericarditis can cause long-term hyperemia and hypoxia of the liver, leading to necrosis and fibrosis of hepatocytes, which is called congestion cirrhosis, also known as cardiogenic cirrhosis.
6. Metabolic disorder
Such as hemochromatosis and Wilson's disease.
7. Cholestasis
When extrahepatic bile duct obstruction or intrahepatic cholestasis occurs, high concentration of bilirubin is harmful to liver cells, and cirrhosis may occur for a long time. Primary biliary cirrhosis is caused by intrahepatic cholestasis, and secondary biliary cirrhosis is caused by extrahepatic bile duct obstruction.
8. Schistosomiasis
In schistosomiasis, eggs stimulate the proliferation of connective tissue in portal area to become schistosomiasis liver fibrosis, which can cause significant portal hypertension, also known as schistosomiasis cirrhosis.
9. The reason is unknown
The cause of partial cirrhosis is unknown, which is called cryptogenic cirrhosis.
clinical picture
1. Compensation period (generally Child-Pugh A level)
There may be clinical manifestations of hepatitis, or the onset may be hidden. There may be mild fatigue, abdominal distension, mild jaundice of liver and spleen, liver palm and spider nevus.
2. decompensated period (generally Child-Pugh B and c)
Liver function damage and portal hypertension syndrome.
(1) The common symptoms are fatigue, emaciation, dull complexion, oliguria and edema of lower limbs.
(2) Gastrointestinal symptoms: anorexia, abdominal distension, gastrointestinal dysfunction and even malabsorption syndrome, hepatogenic diabetes, polyuria, polyphagia and other symptoms may occur.
(3) Bleeding tendency and anemia, gingival bleeding, nosebleed, purpura and anemia.
(4) Endocrine disorder, spider nevus, liver palm, skin pigmentation, menstrual disorder in women, breast development in men, and parotid gland enlargement.
(5) Hypoalbuminemia, edema of lower limbs, oliguria, abdominal ascites and hepatogenic pleural effusion.
(6) Portal hypertension, splenomegaly, hypersplenism, establishment of collateral circulation of portal vein, esophageal-gastric varices and abdominal varicose veins.
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1. Laboratory inspection
(1) The number of hemoglobin (hemoglobin), platelets and white blood cells decreased.
(2) The liver function was slightly abnormal in compensatory period, serum protein decreased, globulin increased and A/G was inverted in decompensated period. Prothrombin activity decreased with the prolongation of prothrombin time. Transaminase and bilirubin increased. Total cholesterol and cholesterol fat decreased, but blood ammonia increased. Amino acid metabolism is disordered, and the ratio of branched chain to aromatic chain is out of balance. Urea nitrogen and creatinine increased. Electrolyte disorder: low sodium and low potassium.
(3) Etiological examination showed that HBV-M, hepatitis C virus -M or hepatitis D virus -M were positive.
(4) Immunological examination ① Immunoglobulin IgA, IgG and IgM can be increased. ② Autoantibodies such as antinuclear antibody, anti-mitochondrial antibody, anti-smooth muscle antibody and anti-hepatic lipoprotein membrane antibody can be positive. ③ Other immunological tests showed that complement decreased, rosette formation rate and lymph node conversion rate decreased, CD8(Ts) cells decreased and function decreased.
(5) The values of PⅢ P, proline hydroxylase (PHO), monoamine oxidase (MAO) and serum laminin (LM) increased in the fibrosis examination.
(6) Examination of Abdominal Effusion For those who have abdominal effusions and the rapid increase of abdominal effusions with unknown primary causes recently, abdominal puncture should be performed, and abdominal effusions should be taken for routine examination, adenosine deaminase (ADA) determination, bacterial culture and cytological examination. In order to improve the positive rate of culture, the sampling operation of ascites culture should be carried out at the bedside, and aerobic and anaerobic bacteria should be cultured in blood culture bottles respectively.
2. Image inspection
(1)X-ray examination of esophageal and gastric barium showed worm-like or earthworm-like varicose veins in esophageal and gastric veins.
(2)B-ultrasound and color Doppler ultrasound showed that the liver capsule was thickened, the liver surface was not smooth, the echo of liver parenchyma was enhanced, the inner diameter of portal vein was widened, the spleen was enlarged, and ascites was found.
(3)CT showed abnormal proportion of hepatic lobes, decreased density, nodular changes, widened hilum, enlarged spleen and ascites.
3. Endoscopic examination
The presence or absence of esophageal and gastric varices can be determined, and the positive rate is higher than that of barium meal X-ray examination. The degree of varicose veins can be known and the risk of bleeding can be evaluated. Esophageal and gastric varices are the most reliable indicators for the diagnosis of portal hypertension. When complicated with upper gastrointestinal bleeding, emergency gastroscopy can identify the location and cause of bleeding and stop bleeding.
4. Liver biopsy
Liver biopsy can confirm the diagnosis.
5. Laparoscopy
The liver, spleen and other abdominal organs and tissues can be directly observed, and biopsy can be taken under direct vision, which is valuable for those who have difficulty in diagnosis.
6. Portal vein pressure measurement
The wedge pressure and free pressure of hepatic vein were measured by jugular vein intubation. The difference between them is the hepatic vein pressure gradient (HVPG) which reflects the portal vein pressure. Normally, portal hypertension is less than 5mmHg and greater than 10mmHg.
diagnose
The diagnosis of decompensated cirrhosis is not difficult, but the early diagnosis of cirrhosis is more difficult.
1. Compensation period
The history and symptoms of chronic hepatitis can be referred to. If there is a typical spider nevus and liver palm, it should be highly suspected. Hard or uneven liver texture and/or large spleen >: 2cm, hard, and there is no other explanation, which is the basis for the diagnosis of early cirrhosis. Liver function can be normal. Protein electrophoresis may be abnormal, and the increase of monoamine oxidase and serum P-ⅲ-P is helpful for diagnosis. If necessary, liver biopsy or laparoscopy will be performed to facilitate diagnosis.
2. Decompensation period
Symptoms, signs and laboratory tests have obvious manifestations, such as ascites and esophageal varices. Obviously, splenomegaly has hypersplenism and abnormal liver function test, so it is not difficult to diagnose. But sometimes it needs to be differentiated from other diseases.
differential diagnosis
1. Hepatosplenomegaly
Such as hepatosplenomegaly caused by hematological diseases and metabolic diseases, liver biopsy can be done when necessary.
2. Abdominal effusion
There are many causes of ascites, such as tuberculous peritonitis, constrictive pericarditis and chronic glomerulonephritis. According to the medical history, clinical manifestations, relevant examinations and abdominal effusion examination, it is not difficult to distinguish it from ascites due to cirrhosis, and laparoscopy can often make a diagnosis when necessary.
3. Complications of liver cirrhosis
Such as upper gastrointestinal bleeding, hepatic encephalopathy and hepatorenal syndrome.
complication
Liver cirrhosis often dies of complications. Upper gastrointestinal bleeding is the most common complication of liver cirrhosis, and hepatic encephalopathy is the most common cause of death. Hepatic encephalopathy, infectious hepatitis, primary liver cancer, hepatorenal syndrome, portal vein thrombosis, respiratory system injury, abdominal effusion.
treat cordially
Cirrhosis is liver dysfunction caused by disorder of tissue structure. There is no radical cure at present. Mainly lies in the early detection and prevention of disease progress.
(a) for the treatment of liver cirrhosis
1. Support therapy
Intravenous infusion of hypertonic glucose solution to supplement calories, as well as vitamin C, insulin, potassium chloride and so on. Can be added to infusion. Pay attention to maintaining water, electrolyte and acid-base balance. Patients with severe illness can be given albumin and fresh plasma.
2. Active hepatitis
It can be given treatments such as protecting liver, reducing enzyme and eliminating jaundice, such as Gantaile and vitamin C, and intravenous infusion if necessary, such as hepatocyte growth-promoting factor, reduced glutathione and glycyrrhizic acid preparation.
3. Oral drugs to reduce portal vein pressure
(1) Propranolol should be administered gradually in small doses.
(2) Nitrates, such as isosorbide dinitrate.
(3) Calcium channel blockers, such as propranolol, can be taken sublingually for emergency administration.
(4) Supplement B vitamins and digestive enzymes such as Weikangfu and Daji.
(5) Hypersplenism can be treated with drugs (such as Leixuesheng, shark liver alcohol, aminopeptide, etc. ) can increase white blood cells and platelets, and splenectomy or splenic artery embolization can be performed if necessary.
(6) Treatment of ascites ① General treatment includes bed rest and restriction of water and sodium intake. (2) diuretic treatment, such as hydrochlorothiazide, should be every other day or every week 1 ~ 2 times. Triamcinolone acetonide, after meals. Spironolactone and furosemide are mainly used. If the diuretic effect is not obvious, the dosage can be gradually increased. Diuretic therapy should reduce the body weight by less than 0.5 kg per day to avoid inducing hepatic encephalopathy and hepatorenal syndrome. If ascites gradually subsides, diuretics can be gradually reduced. ③ Repeated massive ascites and intravenous albumin infusion were used to treat refractory ascites. Peritoneal effusion was discharged every day or three times a week, and albumin was infused intravenously. ④ Increase the plasma colloid osmotic pressure. Intravenous infusion of a small amount of plasma or albumin is performed several times a week. ⑤ Concentrated reinfusion of ascites is used to treat refractory ascites, or patients with hypovolemia, hyponatremia, hypoproteinemia, hepatorenal syndrome, and patients with massive ascites for various reasons who need to relieve symptoms urgently. ⑥ Abdominal jugular vein drainage is an effective method to treat ascites due to liver cirrhosis. However, due to its many complications, such as fever, bacterial infection and pulmonary edema, its application is greatly limited. ⑦ Transjugular intrahepatic portosystemic shunt (TIPS) can effectively reduce portal vein pressure, with little trauma and high safety. It is suitable for esophageal variceal bleeding and intractable ascites, but it is easy to induce hepatic encephalopathy.
(7) The indication for surgical treatment of portal hypertension is esophageal and gastric varices bleeding, and non-surgical treatment is ineffective; Spleen enlargement with hypersplenism; High-risk patients with esophageal variceal bleeding. Including portosystemic shunt, portosystemic shunt and splenectomy.
(8) Liver transplantation is suitable for end-stage liver diseases that are ineffective in conventional medical and surgical treatment. Including irreversible ascites; Portal hypertension with upper gastrointestinal bleeding; Severe liver function damage (grade C in children); Hepatorenal syndrome; Hepatic encephalopathy with progressive aggravation; Liver cancer based on cirrhosis.
(2) Antiviral treatment of hepatitis B cirrhosis.
1. General signs
Including: ①HBeAg positive, HBV-DNA≥ 105 copy /ml (equivalent to 20000 iu/ml); In HBeAg negative patients, HBV-DNA≥ 104 copy /ml (equivalent to 2000 u/ml); ②ALT≥2×ULN； If treated with IFN, ALT should be ≤ 10×ULN, and serum total bilirubin should be ≤ 2× ULN; ; ③ Alt ≥ 2× ULN, but the liver histology showed KnodellHAI≥4, or inflammatory necrosis ≥G2, or fibrosis ≥S2.
For those who continue to be HBV-DNA positive and fail to meet the above treatment standards, antiviral treatment should also be considered: ① For those whose ALT is greater than ULN and their age is less than 40 years old, antiviral treatment should also be considered (Ⅲ); Elderly people with normal ALT (-40 years old) should be closely followed up, and liver biopsy is best; If the liver histology shows KnodellHAI≥4, or inflammatory necrosis ≥G2, or fibrosis ≥S2, antiviral therapy should be actively given (Ⅱ); ③ If there is evidence of disease progression (such as splenomegaly) through dynamic observation, it is suggested to carry out liver histological examination and give antiviral treatment if necessary (Ⅲ).
Therapeutic drugs include interferon (common interferon, long-acting interferon) and nucleoside (acid) analogues (lamivudine, adefovir dipivoxil, telbivudine, entecavir, tenofovir disoproxil fumarate, clavidine, etc. ).
(3) Other treatments
1. Immunomodulatory therapy
Thymosin and α thymosin are commonly used in acute and chronic hepatitis B, which can regulate the body's immunity.
2. Chinese medicine and Chinese medicine preparation treatment
Liver protection therapy can improve clinical symptoms and liver function indexes.
Treatment of complications
1. Spontaneous peritonitis
Choose antibacterial drugs that mainly take Gram-negative bacilli and give consideration to Gram-positive cocci. Such as the third generation cephalosporins and ciprofloxacin. Adjust antibacterial drugs according to drug sensitivity results and patients' response to treatment. The medication time was 1 ~ 2 weeks.
2. Hepatorenal syndrome
The improvement of renal function depends on the improvement of liver function, so the focus of treatment is the treatment of primary liver disease. On this basis, further treatment. ① Quickly control the inducing factors such as upper gastrointestinal bleeding and infection. ② Control the infusion volume and maintain the balance of water, electrolyte and acid-base. ③ Concentrate dextran, albumin, plasma, whole blood and ascites, and use little or no physiological saline. Can be combined with diuretics and low-dose cardiotonic drugs. ④ The application of vasoactive drugs such as dopamine and prostaglandin E2 can improve renal blood flow and increase glomerular filtration rate. ⑤ Dialysis treatment includes hemodialysis and peritoneal dialysis, which is suitable for acute cases, those with the possibility of liver regeneration, or those with the possibility of liver transplantation. Otherwise, it will only prolong the death process of the patient. ⑥ Surgical treatment and liver transplantation, transjugular intrahepatic portosystemic shunt is suitable for patients with refractory ascites due to liver cirrhosis complicated with hepatorenal syndrome. But the effect is not ideal. Dialysis is still needed after operation. Liver transplantation is currently recognized as the best treatment. ⑦ Other treatments: avoid strong diuresis, simply release a large amount of ascites, and use drugs that damage renal function.
3. Hepatic encephalopathy
① Eliminate incentives and low-protein diet. ② Correction of ammonia poisoning: Oral lactulose can acidify the intestine, keep the stool unobstructed, change the pH value of the intestine, reduce the production and absorption of ammonia in the intestine, and reduce the absorption of endotoxemia and other toxic substances. Generally, combined use with sodium glutamate can offset the side effects and enhance the curative effect. Potassium magnesium aspartate: it combines with ammonia to form asparagine, which can remove ammonia. ③ Branched-chain amino acid therapy and antagonism of related toxins. ④ Actively prevent brain edema. ⑤ Artificial liver and liver transplantation are feasible for all kinds of intractable severe hepatic encephalopathy and end-stage liver disease.
4. Esophageal-gastric varices rupture bleeding
If not rescued in time, it may be life-threatening. Hemodynamic monitoring, volume expansion, blood transfusion, portal vein decompression (somatostatin, octreotide, nitroglycerin+pituitrin), hemostasis, acid suppression, three-cavity compression hemostasis, endoscopic treatment, gastric coronary vein embolization, surgery, and transjugular intrahepatic portosystemic stent shunt.
5. Treatment of primary liver cancer
At present, liver cancer can be treated individually by surgery, intervention (vascular embolization +CT-guided local ablation) and local radiotherapy (gamma knife, linear accelerator, three-dimensional conformal radiotherapy). Likatine, sorafenib, gene therapy and biological therapy can also be used.
prognosis
The prognosis of liver cirrhosis is related to etiology, degree of liver function compensation and complications. Liver cirrhosis caused by alcoholic cirrhosis, biliary cirrhosis and liver congestion. If the cause of liver cirrhosis can be eliminated before the decompensation stage, the lesion can tend to be static, which is better than viral hepatitis cirrhosis and cryptogenic cirrhosis. Child-Pugh grading is closely related to prognosis, with grade A being the best and grade C the worst. The causes of death are often hepatic encephalopathy, hepatorenal syndrome, esophageal variceal bleeding and other complications. The development of liver transplantation has obviously improved the prognosis of patients with liver cirrhosis.
prevent
To prevent this disease, we should first pay attention to the prevention and treatment of viral hepatitis. Early detection and isolation of patients and active treatment. Pay attention to diet, reasonable nutrition, moderate drinking, strengthen labor health care and avoid all kinds of chronic chemical poisoning are also active preventive measures. For patients who are suspected of liver cirrhosis for the above reasons, comprehensive physical examination and related laboratory examination should be carried out in time, so as to get reasonable and active treatment in the compensatory period and prevent it from developing into the decompensated period. Regular physical examination, while avoiding all kinds of incentives, to prevent possible complications.