What Is the Relationship Between Cirrhosis and Hepatitis C?

According to the cause, it can be divided into hepatitis B cirrhosis and hepatitis C cirrhosis.

Xing Huichun	(Chief physician)	Liver Disease Center of Beijing Ditan Hospital
Ou Ni	(Deputy Chief Physician)	Liver Disease Center of Beijing Ditan Hospital
Cheng Danying	(Attending physician)	Liver Disease Center of Beijing Ditan Hospital

Viral hepatitis cirrhosis is currently believed to develop from chronic viral hepatitis B, C, and D. 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.

Western Medicine Name: Hepatitis cirrhosis
English name: viral hepatitis cirrhosis
Affiliated Department: Internal Medicine-Gastroenterology

Disease site: liver
The main symptoms: Mild fatigue, bloating, wasting, etc.
Main cause: Hepatitis B, Hepatitis C, etc.

Hepatitis Cirrhosis Disease Classification

According to the cause, it can be divided into hepatitis B cirrhosis and hepatitis C cirrhosis.

According to the classification of pathological morphology, it can be divided into small nodular cirrhosis, large nodular cirrhosis, mixed nodules of large and small nodules, and incompletely separated cirrhosis.

Causes of hepatitis cirrhosis

In China, viral hepatitis B and viral hepatitis C are the main causes of cirrhosis, and most of them develop portal cirrhosis. The HBsAg positive rate in patients with liver cirrhosis was as high as 76.7%.

Pathogenesis and pathophysiology of hepatitis cirrhosis

The main pathogenesis of cirrhosis is progressive fibrosis. Collagen (types I and III) of normal liver tissue is mainly distributed in the portal area and around the central vein. During cirrhosis, type I and type III collagens increased significantly and settled around the lobules. With the continuous deposition of collagen in the sinusoidal space, the window holes of the endothelial cells are significantly reduced, which gradually evolves the hepatic sinus into capillaries, resulting in obstacles to the material exchange between blood and liver cells. A large amount of collagen in cirrhosis comes from fat-storing cells (Ito cells) located in the sinus space (Disse cavity). The cells proliferate actively and can be transformed into fibroblast-like cells. Although the fibrous tissue that is initially proliferated forms small strands, but it has not yet been connected to each other to form a space to modify the hepatic lobular structure, it is called liver fibrosis. If it continues to progress, the fibrous spaces in the central lobular area and the portal area will be connected to each other, and the liver lobular structure and blood circulation will be reconstructed to form cirrhosis. ^[1]

Clinical manifestations of hepatitis cirrhosis

1. Compensation period (generally Child-Pugh Grade A): may have clinical manifestations of hepatitis, and may also hide the onset. May have mild fatigue, abdominal distension, mild swelling of the liver and spleen, mild jaundice, palm of the liver, spider mole. Imaging, biochemical, or blood tests have evidence of hepatocyte synthesis dysfunction or portal hypertension (such as hypersplenism and esophageal gastric varices), or histologically consistent with a diagnosis of liver cirrhosis, but no esophageal gastric varices rupture, bleeding, Serious complications such as ascites or hepatic encephalopathy.

2. Decompensation period (generally Child-Pugh B, C): liver function impairment and portal hypertension syndrome.

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

2) Gastrointestinal symptoms: anorexia, bloating, gastrointestinal dysfunction, and even malabsorption syndrome, liver-induced diabetes, and symptoms such as polyuria and polyphagia.

3) Bleeding tendency and anemia: bleeding gums, epistaxis, purpura, anemia.

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

5) Hypoproteinemia: edema in both lower limbs, oliguria, ascites, and liver-derived pleural effusion.

6) Portal hypertension: ascites, pleural effusion, splenomegaly, hypersplenism, establishment of collateral circulation of portal vein, esophageal gastric fundus varicose veins, and abdominal wall varicose veins.

3. Complications

1) Infection: Primary peritonitis is most common. The incidence is about 3 to 10%. There is tenderness in the abdomen, rebound pain, ascites is exudate, and peripheral blood is increased.

2) Upper gastrointestinal bleeding: esophageal gastric fundus varices rupture and bleeding and liver-derived gastrointestinal mucosal ulcer bleeding.

3) Hepatic encephalopathy: On the basis of cirrhosis, patients with excessive protein intake, gastrointestinal bleeding, infection, and electrolyte disorders can induce hepatic encephalopathy.

4) Hepatorenal syndrome: manifested as oliguria, anuria, azotemia, low sodium, high potassium, liver coma, and hypotension shock. ^[2]

Diagnosis and identification of hepatitis cirrhosis

Hepatitis cirrhosis auxiliary examination

I. Laboratory inspection

1. Blood routine: Hemoglobin, platelets, and white blood cells are reduced.

2. Liver function test: mild 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. Etiological examination: HBV-M or HCV-M or HDV-M is positive.

4. Immunological examination:

(1) Immunoglobulins: lgA, lgG, and lgM can be increased.

(2) Autoantibodies: antinuclear pits, antimitochondrial antibodies, antismooth muscle antibodies, and antihepatic lipoprotein membrane antibodies can be positive.

(3) Other immunological examinations: decreased complement, decreased rosette formation and leaching rate, decreased CD8 (Ts) cells, and decreased function.

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

6. Ascites examination: those who have recently had ascites and those whose original ascites have increased rapidly for unknown reasons should undergo abdominal puncture. Ascites should be drawn for routine examination, adenosine deaminase (ADA) measurement, bacterial culture and cytology examination. In order to increase the positive rate of culture, ascites culture should be performed by the bedside, using blood culture bottles for aerobic and anaerobic bacteria cultures.

Imaging examination

1. X-ray examination: esophagus gastric fundus barium contrast, visible esophageal gastric fundus veins worm-like or earthworm-like varicose veins changes.

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

3. CT examination: abnormal proportion of liver leaves, decreased density, nodular changes, widened hilar, splenomegaly, and ascites.

Third, endoscopic examination: can determine the presence of esophageal gastric varicose veins, the positive rate is higher than barium meal X-ray examination, can still understand the degree of varicose veins, and evaluate the risk of bleeding. Varicose veins of the esophagus and gastric fundus are the most reliable indicators 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.

Fourth, liver biopsy: liver biopsy can confirm the diagnosis.

Fifth, 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. Measurement of portal vein pressure: Wedge pressure and free pressure of the hepatic vein were measured via jugular vein cannula. The difference between the two was the hepatic vein pressure gradient (HVPG), which reflected the portal vein pressure. Normally less than 5mmHg, more than 10mmHg is portal hypertension.

Differential diagnosis of hepatitis and cirrhosis

1. Alcoholic liver cirrhosis: has a long history of a large amount of alcohol addiction, a history of alcoholic hepatitis, and the etiology indicators are negative. Pathological changes: extensive steatosis and hepatic cells may contain alcoholic Mallory's hyaline degeneration.

2. Schistosomiasis cirrhosis: He has been to the epidemic area and had a history of schistosomiasis infection, and the hepatitis virology index is negative. Pathological changes: The liver tissue showed specific schistosomiasis arterial fibrosis, eosinophil-based cell infiltration occurred in the manifold area, and egg nodules and calcified egg eggs were also seen.

3. Congestive liver cirrhosis: There is a long history of heart failure, especially heart failure caused by tricuspid insufficiency and constrictive pericarditis is more prone to congestive cirrhosis.

4. Other cirrhosis: obstructive biliary cirrhosis, primary biliary cirrhosis, malnutrition cirrhosis, genetic diseases and chemical drug cirrhosis.

5. Identification with diseases that cause ascites or abdominal distension: such as tuberculous peritonitis and constrictive pericarditis.

Tuberculous peritonitis has a history of tuberculosis, abdominal pain, bloating, ascites or (and) abdominal masses. Ascites examination is exudate, mainly lymphocytes. Barium meal examination found intestinal adhesions and a strong positive tuberculin test was helpful in diagnosis. Constrictive pericarditis, renal failure, dyspnea, and dyspnea associated with fatigue, abdominal distension. On examination, the jugular veins were swollen, liver was large, ascites, heart dullness was not large, heart sounds were reduced, and pericardial throbbing sounds could be heard. X-rays, echocardiography, and right heart catheterization can help diagnose.

6. Identification with complications of liver cirrhosis: Upper gastrointestinal bleeding: It should be distinguished from peptic ulcer and gastric cancer. Gastroscopy can be performed to confirm the diagnosis. Hepatic encephalopathy: It should be distinguished from hypoglycemic coma, uremia, diabetic ketoacidosis, etc. A detailed inquiry about the history of liver disease, examination of liver and spleen size, liver function, blood ammonia, EEG and other examinations are helpful for diagnosis. Hepatorenal syndrome: It should be distinguished from chronic glomerulonephritis and acute tubular necrosis. Has a history of cirrhosis, spontaneous oliguria or anuria, azotemia, dilute hyponatremia, and hyponatremia, but no significant pathological changes in the kidney can help diagnose liver and kidney syndrome.

Hepatitis Cirrhosis Treatment

Hepatitis cirrhosis (a) treatment for cirrhosis

1. Supportive therapy: Intravenous hypertonic glucose solution is added 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. Patients with hepatitis activity can be given treatments such as liver protection, enzyme reduction, and yellowing. Such as glucurolactone tablets, vitamin C. If necessary, intravenous infusion therapy, such as hepatocyte growth promoting hormone 80-120mg / day, reduced glutathione 1.2g / day, glycyrrhizic acid preparations, etc.

3. Oral medications to reduce portal pressure: 1, propranolol: 10-20mg commonly used in China, 3 times a day or 40mg each time, 2 times a day. It should be started in small amounts and given incrementally. 2. Nitrate esters: such as Xiaoxintong 5 10mg each time, 2 3 times a day, extreme amount 20mg each time. 3. Calcium channel blockers: such as heartache 10 to 20 mg each time, 3 times a day, can be administered sublingually in acute cases.

4. Supplement B vitamins and digestive enzymes. Such as Wellcome 2 tablets, once a day. Dage 2 capsules, wait 3 times a day.

5, the treatment of hypersplenism: can take leukocyte and platelet drugs, such as Lixuesheng 20mg, 3 times a day. Squalol 50mg 3 times a day. 1 g of aminopeptide 3 times a day. If necessary, splenectomy or splenic artery embolization can be performed.

6.Treatment of ascites

(1) General treatment: including bed rest, limiting water and sodium intake. Sodium intake is 250 to 500 mg per day. If the sodium in the urine is 10-50 mmol / 24h, it means that the sodium retention is not very serious. The daily intake of sodium is 500-1000 mg, that is, sodium chloride 1200-2400 mg, which is equivalent to a low-salt diet. Once obvious diuresis or ascites subsides, sodium intake can increase by 1000 to 2000 mg per day. Generally the daily water intake should be limited to 1500 ml. If serum sodium is less than 130 mmol / L, the daily water intake should be controlled below 1000 ml. Serum sodium is less than 125 mmol / L, and the daily water intake should be reduced to 500 ml to 700 ml.

(2) Diuretic therapy: such as dihydrodiuretic urine, 25 to 100 mg each time, taken once or twice a week. Ampicillin, 50-100 mg daily, taken after meals. The main use of spironolactone and furosemide. The ratio of spironolactone and furosemide was 100mg: 40mg. Start with spironolactone 100mg / day and furosemide 40mg / day. 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.

(3) Repeatedly adding ascites and intravenous infusion of albumin: used to treat refractory ascites. Put ascites 3 times a day or 4 times a week, 4000 ~ 6000 ml each time, while injecting 40g of albumin.

(4) Increase plasma colloid osmotic pressure: Plasma or albumin is infused intravenously in small amounts or multiple times a week.

(5) Ascites enrichment and infusion: for the treatment of refractory ascites, or patients with hypovolemia, hyponatremia, hypoproteinemia, and hepatorenal syndrome, and a large number of ascites due to various reasons urgently need to be relieved Symptoms. Contraindications include: infectious ascites, cancerous ascites, and endogenous endotoxin-induced ascites; severe hepatic impairment (serum bilirubin greater than 85 umol / L), severe coagulopathy or hepatic encephalopathy (stages 3 to 4) Patients; patients with recent esophageal varices rupture and bleeding; patients with severe cardiopulmonary insufficiency. Generally put 5000 ~ 10000 ml of water each time. Concentrate and add 5-10 mg of heparin per 1000 ml of ascites. It was processed into 500 ml by concentration, and then intravenously infused.

(6) Abdominal cavity-jugular vein drainage: PVS, which is an effective method for the treatment of cirrhosis and ascites. But because of its many complications, such as fever, bacterial infection, pulmonary edema, etc., its application is greatly limited. At present, it is mainly applicable to the following patients: patients with refractory ascites who cannot perform liver transplantation; patients with refractory ascites who have many abdominal surgical scars who cannot undergo ascites and ascites; patients with refractory ascites who are repeatedly treated with ascites without condition.

(7) Transjugular intrahepatic portosystemic shunt (TIPS): It can effectively reduce portal vein pressure with less trauma and high safety. It is suitable for esophageal varices bleeding and refractory ascites, but it is easy to induce hepatic encephalopathy.

7. Surgical treatment of portal hypertension: The indication is rupture and bleeding of esophageal and gastric varices, which is not effective after 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. Postoperative complications include hepatic encephalopathy and postoperative bleeding.

8. Liver transplantation: It is suitable for end-stage liver disease in which conventional medical and surgical treatment is ineffective. Including: difficult to reverse ascites; portal hypertension and upper gastrointestinal bleeding; severe liver damage (Child grade C); hepatorenal syndrome; progressive hepatic encephalopathy; cirrhosis Complicated by liver cancer.

Hepatitis cirrhosis (II) Antiviral treatment of hepatitis B cirrhosis

1. Compensatory hepatitis B cirrhosis

HBeAg-positive patients were treated with HBV DNA 104 copies / ml, and HBeAg-negative patients were HBV DNA 103 copies / ml, with normal or elevated ALT. The goal of treatment is to delay and reduce the occurrence of liver decompensation and HCC. Due to the need for longer-term treatment, it is best to use nucleoside (acid) analogs with a low incidence of resistance. Optional: Lamivudine 100 mg orally once daily; adefovir dipivoxil 10 mg orally once daily; entecavir 0.5 mg (1 mg for lamivudine resistant patients) once daily Oral; telbivudine 600 mg orally once daily. Interferon should be very careful because of its potential to cause complications such as decompensation of liver function. If it is deemed necessary, it should be started from a small dose and gradually increased to a predetermined therapeutic dose according to the patient's tolerance.

2. Decompensated hepatitis B cirrhosis

For patients with decompensated liver cirrhosis, as long as HBV DNA can be detected, regardless of whether ALT or AST is elevated, it is recommended that antiviral treatment with nucleoside (acid) analogs be initiated in a timely manner based on their informed consent to improve liver function And delay or reduce the need for liver transplantation. Due to the need for long-term treatment, it is best to use nucleoside (acid) analogs with a low incidence of drug resistance. The drug cannot be stopped at will. Once drug resistance mutations occur, other approved nucleosides that can treat drug resistance mutations should be added in time. (Acid) analogs. Interferon treatment can lead to liver failure, so it is contraindicated in patients with decompensated cirrhosis.

Hepatitis cirrhosis (3) Antiviral treatment of hepatitis C cirrhosis

The American Liver Association recommends the following treatment options:

(1) Patients with liver function compensated liver cirrhosis (Child-Pugh A), although the tolerance and effect of the treatment are reduced, but in order to stabilize the disease, delay or prevent complications such as liver failure and HCC, It is recommended to give antiviral treatment under close observation. The protocol is as follows: 1) pegylated interferon combined with ribavirin treatment plan, to detect HCV RNA by 12 weeks, if the decline of HCV RNA is less than 2 logarithmic levels, consider discontinuation; Negative conversion, or below the minimum detection limit of the quantitative method, continue treatment to 48 weeks; if HCV RNA does not turn negative, but decreases 2 logarithmic levels, continue treatment to 24 weeks; such as HCV RNA turns negative Treatment can be continued to 48 weeks; if the disease does not turn negative at 24 weeks, stop the drug observation. 2) Common interferon combined with ribavirin treatment plan: recommended treatment for 48 weeks.

(2) In patients with decompensated liver cirrhosis, it is difficult to tolerate the adverse reactions of interferon treatment, and those who have the conditions should perform liver transplantation.

Hepatitis cirrhosis (d) treatment for complications

1. Spontaneous peritonitis: Use antibacterial drugs mainly for Gram-negative bacilli and both 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 kidney 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 infusion volume and maintain the balance of water, electrolyte and acid and alkali. Expansion therapy: dextran, albumin, plasma, whole blood, and its own ascites are concentrated and transfused, with little or no saline. Can be used in combination with diuretics and low-dose cardiotonics. Application of vasoactive drugs: such as dopamine and prostaglandin E2 can improve renal blood flow and increase glomerular filtration rate. The effect of terlipressin plus albumin infusion on type 1 HRS has been confirmed. The use of terlipressin is 0.5 1mg / time, once every 4 6h, and it can be doubled every 2 days when it is ineffective. The maximum amount is 12mg / d; albumin 1 1g / (kg · d) per day, followed by 20 40g / d (if hemoglobin> 45g / L or pulmonary edema should be stopped). Dialysis treatment: including hemodialysis and peritoneal dialysis. Applicable to acute cases, those with liver regeneration potential, or those with liver transplantation. 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. It has been reported that TIPS can promote the recovery of renal function and the resolution of refractory ascites in patients with HRS, and can improve the survival rate of patients with type 1 HRS. For patients with type 1 HRS that have a poor response to medication, try it if there are no contraindications.

3. Hepatic encephalopathy: 1. Eliminate incentives and low protein diet. 2. Correction of ammonia poisoning: oral lactulose, lactulose can acidify the intestine, maintain smooth stools, change the pH of the intestine, reduce intestinal ammonia production and ammonia absorption, and reduce endotoxemia and other toxic substances absorb. The starting dose is 30-50 ml, 3 times a day, taken at meals. After adjusting the dosage, it is better to discharge the paste twice a day. Available lactulose + saline high enema. Can also be used acidic enema, such as 500 ml of normal saline plus an appropriate amount of 0.25% to 1% acetic acid or vinegar. Sodium (potassium) glutamate 4 at a time, added intravenously to glucose solution, 1-2 times / day, suitable for exogenous HE, metabolic acidosis. 10 to 20 g of arginine is added to the glucose solution intravenously once per day, which is suitable for metabolic alkalosis or when sodium glutamate is not effective. 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. 3. Branch-chain amino acid treatment and antagonistic related toxins. 4. Actively prevent brain edema. 5. All kinds of stubborn and severe hepatic encephalopathy and end-stage liver disease can be treated with artificial liver and liver transplantation.

4. Esophageal and gastric varices rupture and 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, intervention (vascular embolization + CT guided local ablation), local radiotherapy (r-knife, linear accelerator, three-dimensional conformal radiotherapy) and other treatment methods can be applied to individualize liver cancer. Licatine, sorafenib, gene therapy, and biotherapy can prevent recurrence. ^[3]

Prognosis of hepatitis cirrhosis

The prognosis is related to the degree of liver function compensation and complications. 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.

Hepatitis Cirrhosis Prevention

The most common cause in China is viral hepatitis B, followed by hepatitis C, so 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.

Hepatitis cirrhosis diet attention

The dietary principles of patients with cirrhosis are high in calories, high in protein, high in carbohydrates, high in vitamins, high in fat and easy to digest. When liver function is significantly reduced and there are signs of liver coma, protein intake should be properly controlled. Do regular, quantitative, and small meals. Promote a low-salt diet or avoid salt. The daily intake of salt should not exceed 1 to 1.5 grams, and the amount of drinking water should be within 2000 milliliters. In severe ascites, the intake of salt should be controlled within 500 milligrams and the water intake should be within 1000 milliliters. Spicy spicy products and hard cold foods should be avoided. Overheated foods should not be eaten to prevent blood from coming out.

Hepatitis Cirrhosis Care

The liver is very closely related to mental sentiment. Poor mood, depression, and anger can all affect liver function and accelerate the development of lesions. Establishing a strong will, a cheerful mood, a rejuvenating spirit, and eliminating the burden of thought will help improve the condition. Compensation for cirrhosis is impaired, and patients with ascites or infection should stay in bed. In the period of full compensation and stable disease, you can do some light work or proper activities, and carry out useful physical exercises. The amount of activity is not to feel fatigue.