What is Cirrhosis?

Cirrhosis is a clinically common chronic progressive liver disease. It is a diffuse liver damage caused by long-term or repeated effects of one or more causes. In China, most of them are post-hepatitis cirrhosis, and a few are alcoholic cirrhosis and schistosomiasis cirrhosis. Histopathologically, there are extensive hepatic necrosis, nodular regeneration of residual hepatocytes, connective tissue hyperplasia and fibrous septum formation, leading to the destruction of hepatic lobular structure and the formation of pseudolobules. The liver gradually deforms and hardens to develop cirrhosis. In the early stage, there are no obvious symptoms due to strong liver compensatory function. In the later stage, liver function damage and portal hypertension are the main manifestations, and there are multiple system involvements. In the later stage, upper gastrointestinal bleeding, hepatic encephalopathy, secondary infection, and spleen are often present. Complications such as hyperfunction, ascites, canceration.

Basic Information

English name

liver cirrhosis

Visiting department

Gastroenterology

Common locations

liver

Common causes

Viral hepatitis, alcoholism, nutritional disorders, industrial poisons, drugs, circulation disorders, metabolic disorders, cholestasis, schistosomiasis, etc.

Common symptoms

Fatigue, abdominal distension, hepatosplenomegaly, jaundice, palm of the liver, spider mole, ascites, etc.

Causes of cirrhosis

There are many causes of cirrhosis, which can be divided into viral hepatitis, cirrhosis, alcoholic cirrhosis, metabolic cirrhosis, cholestasis cirrhosis, hepatic venous obstruction, liver cirrhosis, autoimmune cirrhosis, toxicants and drug Cirrhosis, dystrophic cirrhosis, cryptogenic cirrhosis, etc.

Viral hepatitis

At present in China, viral hepatitis, especially chronic hepatitis B and C, is the main cause of portal cirrhosis.

2. Alcoholism

Long-term heavy drinking is one of the factors that cause cirrhosis.

3. Nutrition disorders

Most scholars acknowledge that malnutrition can reduce the resistance of liver cells to toxic and infectious agents 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 diacetophene, isoniazid, simoxifen, tetracycline, methotrexate, methyl poly Bar, can produce toxic or drug-induced hepatitis, which can lead to cirrhosis. Aflatoxin can also cause toxic damage to liver cells and cause cirrhosis.

5. Circulatory disorders

Chronic congestive heart failure and chronic constrictive pericarditis can cause long-term congestion and hypoxia in the liver, causing necrosis and fibrosis of liver cells. It is called congestive cirrhosis, also known as cardiogenic cirrhosis.

6. Metabolic disorders

Such as hemochromatosis and hepatolenticular degeneration (also known as Wilson disease).

7. Cholestasis

High concentrations of bilirubin during extrahepatic bile duct obstruction or intrahepatic cholestasis can damage liver cells. Liver cirrhosis can occur over time. People with intrahepatic cholestasis are called primary biliary cirrhosis. The cause said secondary biliary cirrhosis.

8. Schistosomiasis

In schistosomiasis, schistosomiasis liver fibrosis can be caused by schistosomiasis due to worm eggs stimulating connective tissue proliferation in the manifold area, which can cause significant portal hypertension.

9. Unexplained

Part of the cause of cirrhosis is unknown, known as cryptogenic cirrhosis.

Clinical manifestations of cirrhosis

1. Compensation period (generally Child-Pugh A)

May have clinical manifestations of hepatitis, can also hide the onset. May have mild fatigue, abdominal distension, mild liver and spleen, mild jaundice, palm of the liver, spider mole.

2. Decompensation period (generally Child-Pugh B, C)

Have liver function damage and portal hypertension syndrome.

(1) Systemic symptoms: fatigue, weight loss, dull complexion, oliguria, and lower limb edema.

(2) Gastrointestinal symptoms: loss of appetite, bloating, gastrointestinal dysfunction, and even malabsorption syndrome, liver-induced diabetes, and symptoms such as polyuria and polyphagia can occur.

(3) bleeding tendency and anemia, gum bleeding, epistaxis, purpura, anemia.

(4) Endocrine disorders: spider mole, liver palm, skin pigmentation, menstrual disorders in women, male breast development, and parotid enlargement.

(5) Hypoproteinemia: edema of both lower limbs, oliguria, peritoneal effusion, and hepatic pleural effusion.

(6) Portal hypertension: splenomegaly, hypersplenism, portal collateral circulation establishment, esophageal-gastric varices, abdominal wall varices.

Cirrhosis

Laboratory inspection

(1) Hemoglobin (hemoglobin), platelets, and white blood cell counts are reduced.

(2) Liver function test : slight abnormalities in the compensatory period, decreased serum protein, increased globulin, and A / G inversion during the decompensated period. Prothrombin time prolongs and prothrombin activity decreases. Transaminase and bilirubin increased. Total cholesterol and cholesterol lipids decrease, and blood ammonia can increase. Disorders of amino acid metabolism, imbalance of branch / aromatic ratio. Urea nitrogen and creatinine increased. Electrolyte disorders: low sodium, low potassium.

(3) Etiology test is positive for HBV-M or HCV-M or HDV-M.

(4) Immunological examination IgA, IgG, IgM can be increased. Autoantibodies Antinuclear antibodies, antimitochondrial antibodies, antismooth muscle antibodies, and antihepatic lipoprotein membrane antibodies can be positive. Other immunological examinations: Decrease in complement, decrease in rosette formation rate and leaching rate, decrease in CD8 (Ts) cells, and decrease function.

(5) Fibrosis examination PP value increased, prolyl hydroxylase (PHO) increased, monoamine oxidase (MAO) increased, and serum lamin (LM) increased.

(6) Examination of peritoneal effusion: Those who have recently had peritoneal effusion and whose original peritoneal effusion has rapidly increased are unknown. Abdominal puncture should be performed. Abdominal effusion should be drawn for routine inspection, adenosine deaminase (ADA) measurement, bacterial culture and Cytological examination. In order to increase the positive rate of culture, the sampling operation of peritoneal effusion culture should be performed by the bedside, using blood culture bottles for aerobic and anaerobic bacteria cultures.

2. Imaging examination

(1) X-ray examination of esophagus-gastric barium contrast showed that esophageal-gastric vein showed worm-like or earthworm-like varices.

(2) Type B and color Doppler ultrasound examination: thickened liver capsule, liver surface is not smooth, liver parenchyma is enhanced, rough and uneven, portal vein diameter is widened, splenomegaly, and peritoneal effusion.

(3) CT examination showed that the proportion of liver leaves was abnormal, the density was reduced, and nodules were changed. The hepatic hilarity was widened, splenomegaly, and peritoneal effusion.

3. Endoscopy

The presence or absence of esophageal-gastric varicose veins can be determined, and the positive rate is higher than that of barium meal X-ray examination. The extent of varicose veins can be understood and the risk of bleeding can be evaluated. Esophageal-gastric varices are the most reliable indicator for the diagnosis of portal hypertension. In cases of upper gastrointestinal bleeding, emergency gastroscopy can identify the bleeding site and cause, and perform hemostatic treatment.

4. Liver biopsy

A liver biopsy can confirm the diagnosis.

5. Laparoscopy

Can directly observe the abdominal organs and tissues such as liver and spleen, and can take biopsy under direct vision, which is valuable for those who have difficulty in diagnosis.

6. Portal vein pressure measurement

Hepatic vein wedge pressure and free pressure were measured via jugular vein intubation. The difference between the two was the hepatic vein pressure gradient (HVPG), which reflected portal pressure. Normally less than 5mmHg, more than 10mmHg is portal hypertension.

Cirrhosis diagnosis

Diagnosis of decompensated cirrhosis is not difficult, and early diagnosis of cirrhosis is difficult.

Compensation period

The history and symptoms of chronic hepatitis are available for reference. If there is a typical spider mole, the liver palm should be highly suspect. The liver texture is hard or uneven and / or the splenomegaly is larger than 2 cm. The liver is hard without any explanation, which is the basis for diagnosis of early liver cirrhosis. Liver function can be normal. Protein electrophoresis may be abnormal, and elevated monoamino oxidase and serum P-III-P may help diagnosis. Liver biopsy or laparoscopy is necessary to confirm the diagnosis.

Decompensation period

Symptoms, signs, and laboratory tests have more prominent manifestations, such as peritoneal effusion and esophageal varices. Obvious splenomegaly, hypersplenism and abnormal liver function tests are not difficult to diagnose. But sometimes it needs to be distinguished from other diseases.

Differential diagnosis of cirrhosis

Hepatosplenomegaly

If hepatosplenomegaly is caused by blood disease or metabolic disease, liver biopsy can be performed if necessary.

Peritoneal effusion

There are many causes of peritoneal effusion, such as tuberculous peritonitis, constrictive pericarditis, and chronic glomerulonephritis. According to the medical history and clinical manifestations, relevant examinations and examination of the peritoneal effusion, it is not difficult to distinguish the peritoneal effusion from cirrhosis, and a laparoscopy can often confirm the diagnosis if necessary.

3. Complications of Cirrhosis

Differential diagnosis of upper gastrointestinal bleeding, hepatic encephalopathy, hepatorenal syndrome, etc.

Cirrhosis complications

Cirrhosis often dies due to complications. Upper gastrointestinal bleeding is the most common complication of cirrhosis, and hepatic encephalopathy is the most common cause of death. Hepatic encephalopathy, infectious hepatitis, primary liver cancer, hepatorenal syndrome, portal vein thrombosis, respiratory damage, and peritoneal effusion.

Cirrhosis Treatment

Cirrhosis is liver dysfunction caused by structural disorders. There is currently no cure. Mainly lies in early detection and prevention of disease progression.

(A) treatment for cirrhosis

Supportive treatment

Hypertonic glucose solution is input intravenously to supplement calories. Vitamin C, insulin, potassium chloride, etc. can be added to the infusion. Pay attention to maintaining water, electrolyte and acid-base balance. In severe cases, albumin and fresh plasma can be imported.

2. Hepatitis active period

Can be given liver protection, enzyme reduction, Huanghuang and other treatments: such as liver Taile, vitamin C. If necessary, intravenous infusion therapy, such as hepatocyte growth promoting hormone, reduced glutathione, glycyrrhizic acid preparations, etc.

3. Oral drugs that lower portal pressure

(1) Propranolol should start from a small amount and increase the dose.

(2) Nitrate esters, such as Xiaoxintong.

(3) Calcium channel blockers, such as heartache, can be administered sublingually in acute cases.

(4) Supplement B vitamins and digestive enzymes, such as Wellcome, Daji.

(5) Treatment of hypersplenism Drugs that can increase leukocytes and platelets (such as reserine, shark liver alcohol, aminopeptin, etc.) can be used, if necessary, splenectomy or splenic artery embolization can be used.

(6) Treatment of peritoneal effusion General treatment Including bed rest, limiting water and sodium intake. Diuretic therapy, such as dihydrodiuretic, is taken every other day or 1 to 2 times a week. Ampicillin, take after meals. The main use of spironolactone and furosemide. If the diuretic effect is not obvious, you can gradually increase the amount. It is advisable to dilute weight not exceeding 0.5 kg per day for diuretic treatment, so as not to induce hepatic encephalopathy and hepatorenal syndrome. Those with ascites gradually subsiding, can gradually reduce the amount of diuretics. Repeatedly put a large amount of peritoneal effusion plus intravenous infusion of albumin for the treatment of refractory peritoneal effusion. Drain the peritoneal effusion daily or 3 times a week while injecting albumin intravenously. Increase plasma colloid osmotic pressure . Intravenous infusion of plasma or albumin in small amounts or multiple times a week. Concentrated peritoneal effusion is used to treat refractory peritoneal effusion, or patients with hypovolemia, hyponatremia, hypoproteinemia, and hepatorenal syndrome, and a large number of peritoneal effusions caused by various reasons Patients in need of fluid relief. Abdominal cavity-jugular vein drainage, or PVS, is an effective method to treat liver cirrhosis and peritoneal effusion. But because of its many complications, such as fever, bacterial infection, pulmonary edema, etc., its application is greatly limited. Transjugular intrajugular intrahepatic portosystemic shunt (TIPS) can effectively reduce portal vein pressure with less trauma and high safety. For esophageal varices bleeding and refractory peritoneal effusion, but easy to induce hepatic encephalopathy.

(7) Surgical treatment of portal hypertension: The indication is esophageal-gastric fundus varices bleeding and non-surgical treatment; giant spleen with hypersplenism; high-risk patients with esophageal varices bleeding. Including portal-caval vein shunt, portal-odd vein shunt and splenectomy.

(8) Liver transplantation is suitable for end-stage liver disease in which conventional medical and surgical treatment is ineffective. Includes irreversible peritoneal effusion; portal hypertension and upper gastrointestinal bleeding; severe liver damage (Child grade C); hepatorenal syndrome; progressively worsening hepatic encephalopathy; cirrhosis basis Complicated by liver cancer.

(B) Antiviral treatment of hepatitis B cirrhosis

General indication

Including: HBeAg positive, HBV-DNA 105 copies / ml (equivalent to 20000IU / ml); HBeAg negative, HBV-DNA 104 copies / ml (equivalent to 2000U / ml); ALT 2 × ULN; if used IFN treatment, ALT should be 10 × ULN, serum total bilirubin should be 2 × ULN; ALT 2 × ULN, but liver histology showed KnodellHAI ₄ , or inflammatory necrosis G ₂ , or fibrosis S2.

Antiviral therapy should also be considered for those who are persistently HBV-DNA positive and fail to meet the above treatment standards, but in one of the following cases: Antiviral therapy should also be considered for those with ALT greater than ULN and age 40 ); Those with persistently normal ALT but older ( 40 years old) should be closely followed up, and liver biopsy is best; if liver histology shows KnodellHAI ₄ , or inflammatory necrosis G ₂ , or fibrosis S2, antiviral therapy should be given actively (II); If dynamic observation shows evidence of disease progression (such as enlarged spleen), liver histological examination is recommended, and antiviral therapy should be given if necessary (III).

Therapeutic drugs include interferon (common interferon, long-acting interferon) and nucleoside (acid) analogs (lamivudine, adefovir dipivoxil, telbivudine, entecavir, tenofovir disoproxil, kraft Scheduled, etc.).

(Three) other treatments

Immunomodulatory therapy

Thymosin and alpha thymosin are commonly used in acute and chronic hepatitis B and can regulate body immunity.

2. Traditional Chinese medicine and traditional Chinese medicine treatment

Hepatoprotective treatment has certain effects on improving clinical symptoms and liver function indicators.

(D) Treatment of complications

Spontaneous peritonitis

Choose antibacterial drugs that mainly target Gram-negative bacilli and take into account Gram-positive cocci. Such as three generations of cephalosporins, ciprofloxacin and so on. Adjust antimicrobials based on drug sensitivity results and patient response to treatment. Medication time is 1-2 weeks.

2. Hepatorenal syndrome

The improvement of renal function depends on the improvement of liver function, so the treatment focuses on the primary liver disease. On this basis further treatment. Quickly control the inducing factors such as major gastrointestinal bleeding and infection. Control the amount of infusion to maintain water, electrolyte and acid and alkali balance. Dextrose, albumin, plasma, whole blood, and its own peritoneal effusion are used for volume expansion treatment. Can be used in combination with diuretics and low-dose cardiotonics. The application of vasoactive drugs such as dopamine and prostaglandin E ₂ can improve renal blood flow and increase glomerular filtration rate. Dialysis treatment includes hemodialysis and peritoneal dialysis, which is suitable for acute cases, those with liver regeneration potential, or those with liver transplantation potential. Otherwise, it just prolongs the patient's death process. Surgical treatment and liver transplantation, transjugular intrahepatic portosystemic shunt is suitable for patients with liver cirrhosis accompanied by refractory ascites complicated by hepatorenal syndrome. But the effect is not yet satisfactory. Postoperative dialysis is still needed. Liver transplantation is currently recognized as the best treatment. Other treatments: Avoid strong diuresis, simply put a large amount of ascites, and use drugs that damage kidney function.

3. Hepatic encephalopathy

Eliminate incentives and low protein diet. Correct ammonia poisoning: oral lactulose, lactulose can acidify the intestine, keep the stool open, change the pH of the intestine, reduce intestinal ammonia production and absorption of ammonia, and reduce endotoxemia and absorption of other toxic substances . Generally combined with sodium glutamate can offset side effects and enhance efficacy. Potassium and magnesium aspartate: Combined with ammonia to form asparagine and have ammonia removal effect. Branch-chain amino acid treatment and antagonistic related toxins. Actively prevent brain edema. All kinds of stubborn and severe hepatic encephalopathy and end-stage liver disease can be treated with artificial liver and liver transplantation.

4. Esophageal-gastric fundus varices bleeding

If not rescued in time, it can be life threatening. Establish hemodynamic monitoring, volume expansion, blood transfusion, reduction of portal pressure (somatostatin, octreotide, nitroglycerin + pituitary hormone), hemostasis, acid suppression, hemostasis with triple-lumen compression, endoscopic treatment, gastric coronary vein embolism , Surgery, transjugular intrahepatic portal stent shunt.

5. Treatment of primary liver cancer

Surgery, interventional (vascular embolization + CT guided local ablation), local radiotherapy (-knife, linear accelerator, three-dimensional conformal radiotherapy) and other treatment methods can be applied to individualize liver cancer. Can also be used licatin, sorafenib, gene therapy, biological therapy and so on.

Prognosis of cirrhosis

The prognosis of cirrhosis is related to the etiology, degree of liver function compensation and complications. Cirrhosis caused by alcoholic cirrhosis, biliary cirrhosis, hepatic congestion, etc. If the cause can be eliminated before the cirrhosis has progressed to the decompensated stage, the lesions may tend to stand still. Source cirrhosis is good. Child-Pugh classification is closely related to prognosis, with A being the best and C being the worst. The cause of death is often complications such as hepatic encephalopathy, hepatorenal syndrome, esophageal = gastric fundus rupture and bleeding. The development of liver transplantation has significantly improved the prognosis of patients with liver cirrhosis.

Cirrhosis prevention

Prevention of this disease must first attach importance to the prevention and treatment of viral hepatitis. Early detection and isolation of patients give active treatment. Paying attention to diet, proper nutrition, moderate drinking, strengthening labor health, and avoiding various chronic chemical poisoning are also positive measures for prevention. Those who have the above-mentioned diseases and suspect cirrhosis should promptly conduct a comprehensive physical examination and relevant laboratory inspections in an effort to obtain reasonable and active treatment during the compensation period to prevent the development of the decompensation period. Regular physical examination while avoiding various inducements, prevention and treatment of possible complications.