Liver cirrhosis in the decompensated phase



OVERVIEW

Definition

On the basis of cirrhosis, there are two types of clinical manifestations: portal hypertension complications and hepatic decompensation.

Complications of portal hypertension include hepatic ascites, rupture and bleeding of esophagogastric fundic varices, sepsis, hepatic encephalopathy, hepatorenal syndrome, etc.

Hepatic decompensation manifests as poor digestion and absorption, malnutrition, jaundice, hemorrhage and anemia, endocrine disorders, and so on.

Staging

Cirrhosis is divided into 5 stages according to complications such as ascites, bleeding from esophagogastric fundus varices and hepatic encephalopathy.

Stages 1 and 2 are the compensated stages of cirrhosis.

Stages 3, 4 and 5 are the decompensated stage of cirrhosis.

Morbidity

The incidence of cirrhosis due to different etiologic factors varies greatly in different countries and regions due to differences in geography, environment and living habits.

Alcoholic cirrhosis is the main cause of cirrhosis in western developed countries, accounting for more than 2/3 of all cirrhosis. The increase in the number of alcoholics is the main reason for the increasing incidence of cirrhosis in these countries in recent years.

In Asian and African countries, cirrhosis caused by viral hepatitis is the main cause.

In China, chronic hepatitis B virus (HBV) infection is still the main cause of cirrhosis, accounting for about 50%-60%.

The peak age of onset of cirrhosis in China is 40-50 years old, and the 5-year survival rate of cirrhosis in decompensated stage is only 14%-35%.

Questions you may be concerned about

Is cirrhosis of the liver in the decompensated stage contagious?

There are many causes of cirrhosis decompensated stage, and in the case of cirrhosis decompensated stage caused by viral infection, the virus may be transmitted to others when there is still virus replication in the body.

The causes of decompensated stage of cirrhosis include long-term heavy drinking, drugs, fatty liver, viruses, autoimmune diseases, etc. If it is not caused by viral infection, it is not contagious.

If cirrhosis decompensated stage is caused by hepatitis B or C viruses, and viral DNA or RNA is still detected in the body, it may be transmitted to others through blood transmission, body fluid transmission, and mother-to-child transmission.

It is recommended that patients with decompensated cirrhosis should receive timely treatment for the cause of the disease, such as timely antiviral treatment for hepatitis B and hepatitis C patients, pay attention to the prevention of cirrhosis complications, and visit the gastroenterology clinic regularly to slow down the progression of the disease.

Causes

Causes

Liver cirrhosis decompensated stage is on the basis of liver cirrhosis compensated stage, the common causes of liver cirrhosis are listed below:

Chronic viral hepatitis

In China, the main cause of liver cirrhosis is hepatitis B. The main cause of liver cirrhosis is chronic viral hepatitis.

Hepatitis C virus infection is easily chronicized and can further develop into cirrhosis.

Alcoholic hepatitis

In recent years, there has been a significant increase in cirrhosis caused by long-term heavy drinking.

Chronic drinking is defined as drinking alcohol for a period of time greater than 5 years.

The diagnostic criteria for heavy drinking are different for men and women, with the equivalent amount of ethanol being ≥40 g/d for men and ≥20 g/d for women.

Non-alcoholic steatohepatitis

With the improvement of living standards, the incidence of hyperlipidemia, obesity, diabetes mellitus, and metabolic syndrome has increased significantly.

All of the above factors can lead to hepatic steatosis, which can progress to cirrhosis.

Drugs and poisons

Acute or chronic liver injury caused by drugs and poisons can cause cirrhosis.

Western drugs include anti-tuberculosis drugs, chemotherapeutic drugs, anti-rheumatic drugs, and acetaminophen.

Herbal medicines include Lei Gong Teng, Tu San Qi, He Shou Wu, etc.

Poisons include poisonous mushrooms and carbon tetrachloride.

A variety of so-called “nutritional supplements” have complex ingredients, and the good and bad are mixed, resulting in a significant increase in reports of liver injury in recent years.

Autoimmune liver disease

Generally associated with heredity.

The body’s immune response is abnormal, producing autoantibodies against liver cells.

Mainly includes primary biliary cholangitis, primary sclerosing cholangitis and autoimmune hepatitis.

Inherited Metabolic Disorders

Hemochromatosis (impaired iron metabolism), hepatomegaly (impaired copper metabolism), amyloidosis, glycogen accumulation, galactosemia, hypertyrosinemia, alpha-antitrypsin deficiency, and porphyria can cause cirrhosis.

Cholestasis

Obstruction of the intra- and extrahepatic bile ducts and persistent cholestasis can develop into biliary cirrhosis.

Circulatory disorders

Bugart’s syndrome, right heart failure, constrictive pericarditis, resulting in prolonged siltation of hepatic tissue, can develop into cirrhosis.

Parasitic infection

Schistosoma haematobium, Schistosoma oryzae infection, more common in the south compared to the north.

Cryptogenic cirrhosis

The absence of any of the above factors and the unknown etiology of the disease are called cryptogenic cirrhosis.

Pathogenesis

Cirrhosis in the decompensated stage is mainly characterized by portal hypertension and hepatic decompensation.

Portal hypertension

On the one hand, the formation of cirrhotic pseudolobules compresses the hepatic sinusoids and small hepatic veins, intrahepatic vascular deformation, vascular neovascularization, and hepatic circulatory disorders, leading to the obstruction of portal venous reflux, which is the main reason for the elevation of portal venous pressure.

On the other hand, vasoconstrictor substances such as angiotensin, norepinephrine, and 5-hydroxytryptamine increase, vasoactive substances are imbalanced, intrahepatic veins continue to constrict, and portal venous pressure is further elevated.

Decreased liver function

Chronic inflammation of the liver leads to necrosis of hepatocytes, and the newborn hepatocytes are unable to compensate completely, resulting in hepatic decompensation.

Hypoproteinemia, reduced synthesis of coagulation factors, impaired metabolism of bile pigments, abnormal inactivation of estrogen, and detoxification dysfunction occur, which leads to various clinical manifestations such as poor digestion and absorption, malnutrition, jaundice, hemorrhage and anemia, and endocrine disorders.

Symptoms

Main Symptoms

Compared with the compensated stage of cirrhosis, the symptoms of the decompensated stage are obvious.

Multiple plasma cavity effusion

Including ascites, pleural fluid, pericardial effusion, of which ascites is the most common.

Cirrhotic celiac ascites is rare, with an incidence of 0.5-1%.

Cirrhotic hemorrhagic ascites, appearance can be washed meat-like, can be venous blood-like.

Cirrhotic pleural fluid, more common on the right side. Combined with bacterial infection the prognosis is poor.

Pericardial effusion can also occur in the decompensated stage of cirrhosis.

Digestive tract bleeding

The most common cause of gastrointestinal bleeding in cirrhosis is bleeding from esophagogastric fundus varices, sudden massive vomiting of blood, tarry stools, and in severe cases, shock or even life-threatening.

Portal hypertensive gastropathy is the second cause of gastrointestinal bleeding in cirrhosis.

Other causes are portal hypertensive enteropathy and internal hemorrhoids.

Infection

The development of infection in the abdominal cavity on the basis of cirrhosis, with the exception of intestinal perforation, intestinal abscesses, and other definite sources, is called spontaneous bacterial peritonitis (SBP).

Infections of the urinary tract, biliary tract, respiratory tract, gastrointestinal tract, and skin may also occur, and sepsis may develop.

Hepatic encephalopathy

Hepatic encephalopathy occurs when liver function is significantly impaired during the decompensated phase of cirrhosis, portal shunting is abnormal, and the metabolism of various substances is severely disturbed.

Neuropsychiatric abnormalities of different degrees of severity appear, including anxiety, apathy, amnesia, drowsiness, slurred speech, coma or abnormal behavior.

Hepatic hypoplasia

Poor digestion and absorption, malnutrition manifested as loss of appetite, weakness, emaciation, abdominal distension and so on.

Gum bleeding, nose bleeding, skin petechiae and ecchymosis may also occur.

Women may have menstrual disorders, infertility, or even amenorrhea. Men may have endocrine disorders such as mammary gland development.

Complications

Spontaneous peritonitis (SBP)

Peritoneal fluid is a good culture medium for various bacteria, and intestinal flora shift is easily complicated by peritoneal fluid bacterial infection.

SBP is a common complication of decompensated cirrhosis with an incidence of 40-70%.

Most of the symptoms are atypical and may include fever, abdominal pain, diarrhea, and persistent and unabated ascites.

Hepatorenal syndrome

On the basis of severe liver dysfunction in cirrhosis, functional renal failure occurs without organic damage to the kidney itself.

The main manifestations are oliguria, anuria, and elevated creatinine.

Gallstones

The incidence of gallstones in cirrhotic patients is about 30%.

They are commonly found in gallbladder stones and extrahepatic bile duct stones.

Others

There may also be complications such as portal vein thrombosis, spongiform changes, hypokalemia, hyponatremia, hepatopulmonary syndrome, and hepatocellular carcinoma.

Consultation

Department of Medicine

Gastroenterology

If you have symptoms such as yellowing of the skin and eyes, bloating, abdominal distension, vomiting of blood, black stools, fever, abdominal pain, etc., it is recommended that you consult a gastroenterologist in a timely manner. Some hospitals have liver disease centers and hepatology departments.

Emergency Department

If there is sudden onset of vomiting blood, black stool, or accompanied by dizziness, black haze, drop in blood pressure, oliguria and other signs of shock, it is recommended to go to the Emergency Department immediately.

Preparation

Consultation: Registration, Preparation of documents, Frequently Asked Questions

Tips for seeking medical treatment

Try to keep a record of the symptoms you have experienced, the time of day, and information about your previous medical treatment to make it easier for the doctor to treat you.

Preparation List

Symptom list

Pay particular attention to the time of onset of symptoms, special symptoms, and so on.

Do you have abdominal distension or bloating?

Fever, abdominal pain, diarrhea?

Is there a decrease in urine output, swelling of the legs?

Do you have a good appetite and mental status?

Any recent change in weight?

Any vomiting of blood, blackened stools?

Any drowsiness, coma, or failure to wake up?

Any slurred speech, urination or defecation, or unusual behavior?

Any yellowing of the skin or eyes all over the body?

Do you have bleeding gums, bleeding mucous membranes of the nose, petechiae on the skin?

How long have the above symptoms persisted?

List of medical history

Any history of liver disease such as hepatitis B, hepatitis C, fatty liver? What is the treatment history?

Any long-term heavy drinking or recent alcohol abuse?

Any blood transfusions?

Any drug use?

Have you donated blood at an unregulated blood donation site?

Is there any family history of hepatitis virus infection or hereditary liver disease?

Have you dyed your hair recently?

Have you taken any health supplements or herbal medicines?

Have you been in contact with chemical reagents or harmful substances at work?

Checklist

Test results in the past six months, which can be brought along to the doctor.

Laboratory tests: blood routine, liver and kidney function, electrolytes, coagulation index, viral hepatitis markers, autoantibodies.

Imaging tests: abdominal ultrasound, CT or MRI to assess the presence of cirrhosis, abdominal fluid, abnormal hilar shunt.

Gastroenteroscopy.

Medication list

Medication used in the last 3 months, if available in boxes or packages, carry with you to the doctor’s office

Hepatoprotective medications: liver protection tablets, silymarin.

Antimicrobials: cefuroxime, amoxicillin, vancomycin.

Glucocorticoids: dexamethasone, prednisone acetate.

Diuretics: furosemide, spironolactone.

Diagnosis

Diagnostic basis

The diagnosis of decompensated cirrhosis is based on history, clinical manifestations, physical examination, laboratory tests and imaging.

Medical History.

The following medical history may be present:

History of chronic hepatitis B, chronic hepatitis C, and fatty liver disease.

History of chronic heavy alcohol consumption.

History of blood transfusions, drug abuse.

Frequent hair coloring.

Taking a variety of health supplements and herbs on their own.

Contact with a large number of chemical reagents at work.

Family history of viral hepatitis, hereditary metabolic liver disease, liver cancer.

Clinical manifestations

Symptoms

Weakness, lethargy, poor appetite, and mental instability.

Jaundice, skin petechiae and ecchymosis, bleeding gums, bleeding from nasal mucosa.

Abdominal distension, bloating, decreased urine output, bilateral lower extremity edema.

Fever, abdominal pain, diarrhea.

Vomiting blood, black stools.

Drowsiness, coma, unclear speech, urinating and defecating anywhere, abnormal behavior.

Physical Signs

The following signs may be present:

Visualization: yellowing of the skin and sclera, hepatic palms, spider nevi, distended abdomen.

Palpation: abdominal pressure, rebound pain and muscle tension, bilateral lower extremity depressed edema.

Palpation: cirrhotic ascites >1000 ml, positive mobile turbidities.

Laboratory examination

Blood routine

Find out the presence of pancytopenia, anemia, thrombocytopenia.

White blood cell count and inflammatory indexes to clarify whether there is co-infection.

Biochemistry

Tests for transaminases, biliary enzymes, bilirubin, to assess liver injury.

Albumin, reflecting liver synthesis function.

Creatinine, urea nitrogen, to understand whether the liver and kidney function is normal.

Electrolytes, to clarify the presence of hypokalemia and hypocalcemia.

Coagulation function

Including PT, APTT, PTA, INR, D-dimer, to clarify whether there is coagulation dysfunction, liver failure, thrombosis.

Hepatitis virus markers

Detect hepatophilic virus, non-hepatophilic virus to know whether there is viral infection.

If antibody positive, test for viral DNA/RNA, can distinguish between previous infection and current infection.

Ascites test

Ascites occurs in the decompensated stage of liver cirrhosis, most of them are leakage fluid, and can be exudate or even celiac or bloody when complicated with bacterial infection or tumor.

Diagnostic peritoneal puncture, extracting ascites, sending ascites routine, biochemical, cytological examination, tumor markers, to clarify the diagnosis of ascites in liver cirrhosis and provide the basis for treatment.

Gastroenteroscopy

The appearance of esophagogastric fundus varices suggests the decompensated stage of liver cirrhosis.

It can also detect portal hypertensive gastropathy and portal hypertensive enteropathy.

Assess the risk of gastrointestinal bleeding.

Hepatic venous pressure gradient (HVPG)

HVPG normal value 3-5 mmHg.

HVPG 6-10 mmHg, mild portal hypertension.

HVPG >10 mmHg, significant portal hypertension, may show marked esophagogastric fundal varices.

HVPG >12 mmHg, increased risk of ascites, rupture of esophagogastric varices, and increased morbidity and mortality.

Imaging

Ultrasonography

B-mode color Doppler ultrasonography has diagnostic value in cirrhosis.

CT or magnetic resonance imaging (MRI) examination

Helps in the differential diagnosis of cirrhosis and hepatocellular carcinoma.

Liver transient elasticity scan

Allows assessment of liver fibrosis and grading of the degree of fibrosis.

This test is one of the preferred modalities currently used to monitor the progression of cirrhosis. It is fast, convenient and safe.

The normal reference value is 2.8-7.4 kilopascals (kPa), and a value of more than 17.5 kPa suggests cirrhosis.

Pathological examination

Liver puncture biopsy is very important to confirm the diagnosis of cirrhosis, and is the “gold standard” for clinical diagnosis of cirrhosis.

Differential diagnosis

Diseases causing ascites and abdominal distension

Cardiogenic ascites

Similarity: both can present with ascites.

Differences: Patients with cardiogenic ascites may show signs of heart failure, such as sedentary breathing and coughing up pink foamy sputum.

Carcinogenic ascites

Similarity: Ascites can occur in both advanced liver cancer and decompensated cirrhosis, and the mechanisms are similar.

Difference: Hepatocellular carcinoma may be accompanied by markedly elevated alpha-fetoprotein value, while cirrhosis usually does not. It can be differentiated by imaging and pathologic examination.

Liver nodular lesions

Primary hepatocellular carcinoma

Similarity: symptoms such as pain in the liver area and yellowing of the skin and sclera may occur.

Differences: Liver cancer may be accompanied by malignant disease, manifested by extreme wasting, etc. Differential diagnosis can be made by imaging and pathologic examination.

Malaria

Similarities: both may present with hepatosplenomegaly, and both may be preceded by a history of blood transfusion.

Differences: malaria may be preceded by a history of living in a malaria-endemic area or being bitten by mosquitoes, etc.; typical intermittent chills, profuse sweating, etc. may be present, and the intermittent episodes have a certain regularity; Plasmodium vivax may be detected in the laboratory tests.

Treatment

Treatment purpose: improve liver function, treat complications, delay liver transplantation, improve quality of life and prolong survival time.

Treatment principle: protect and improve liver function, reduce complications of portal hypertension, nutritional support therapy.

General treatment

More bed rest, no heavy physical labor.

Abstain from alcohol.

Avoid unnecessary medication, do not listen to irregular prescriptions and health products of unknown composition.

For patients with esophageal varicose veins, eating should not be too fast, too much, too hard, too spicy, too hot.

High energy, high protein, high fiber, low sodium (<4-6g/d) diet; blood sodium level is less than 125mmol/L, need to limit water.

Pay attention to personal hygiene, avoid catching cold, ventilate frequently to avoid infection.

Treatment of primary disease

Cirrhosis due to HBV and HCV infection may require antiviral therapy.

Consider applying immunosuppressant, interventional or surgical treatment for IgG4-associated cholangitis.

Copper-rich foods such as shells, nuts, mushrooms, and animal offal should be avoided in hepatomegaly cirrhosis. Drug therapy includes penicillamine, tretinoin, and zinc.

Hemochromatosis cirrhosis restricts iron intake, therapeutic venous bloodletting, serum ferritin is maintained at 50-100 μg/L, and iron chelators (e.g., desferrioxamine or deferasirox) are applied.

Anti-inflammatory treatment

Hepatoprotective drugs: glycyrrhizic acid, reduced glutathione, silymarin, polyene phosphatidylcholine, dicyclomine, etc. to protect and improve liver function.

Proprietary Chinese medicines: Anluohua Fibrin Pill, Fuzheng Huayu Capsule, Soft Liver Tablet of Tetrapterygium, which are beneficial to improve liver cirrhosis and liver fibrosis.

Treatment of ascites

Diuretics: spironolactone, furosemide, tolvaptan, etc.

Therapeutic discharge of ascites combined with albumin infusion: 4000-5000ml per discharge of ascites, 20-40g of albumin supplementation.

Transjugular intrahepatic portosystemic shunt (TIPS): diuretics are ineffective and recalcitrant hepatic ascites, early TIPS.

Surgical treatment: consider liver transplantation for recalcitrant ascites.

Treatment of spontaneous peritonitis (SBP)

Choose broad-spectrum antibiotics against G- bacilli taking into account G+ bacilli, quinolones, third-generation cephalosporins or carbapenems, combined with anti-anaerobic antibiotics, such as levofloxacin, cefoperazone, imipenem + metronidazole or tinidazole. The course of treatment is greater than 2 weeks.

Pay attention to keep the bowel clear and adjust the intestinal flora imbalance.

Control the ascites well and reduce the occurrence of infection in the abdominal cavity.

Treatment of esophagogastric fundus varices bleeding

Supplement blood volume and maintain circulatory stability.

Balloon compression hemostasis: can only be used temporarily and acts as a bridge.

Prophylactic application of third-generation cephalosporin antibiotics.

Hemostatic drugs: growth inhibitor, octreotide, terlipressin, posterior pituitary hormone.

Endoscopic treatment: endoscopic sclerotherapy or sleeve treatment.

TIPS: TIPS should be performed within 72 hours when bleeding is heavy and the success rate of endoscopic treatment is low.

Questions you may be concerned about

What to do if cirrhosis decompensated stage turns into liver cancer?

Cirrhosis decompensated stage combined with hepatocellular carcinoma needs to be treated with causative therapy, antifibrotic therapy, and supportive therapy.

Cirrhosis is a risk factor for hepatocellular carcinoma and the two go hand in hand. The main treatment principles of decompensated stage of cirrhosis combined with hepatocellular carcinoma include controlling the causes, removing the triggers, maintaining liver function, and promoting ammonia metabolism and elimination.

1. Recognize and remove the triggers of hepatic encephalopathy attack in time:

(1) Correcting electrolyte and acid-base balance imbalance: mainly preventing internal environment disorders such as hypokalemic alkalosis, attention should be paid to the nutritional support of patients, and excessive diuresis should not be used.

(2) Prevent and control infection.

(3) Improve the intestinal microecology, reduce the generation and absorption of intestinal nitrogenous toxins: ① prevent constipation; ② oral antibiotics, inhibit intestinal urease-producing bacteria, reduce the generation of ammonia; ③ careful use of sedative drugs and drugs that impair liver function.

2. Nutritional supportive therapy: ensure the supply of calories, avoid hypoglycemia, supplement vitamins; transfuse plasma, clear protein, etc. as appropriate; avoid large amounts of protein intake, etc.; also need to use drugs to protect/improve liver function.

3. Promote the metabolism of ammonia in the body: L-ornithine-L-aspartic acid, etc. are commonly used.

4. Treating the cause of liver cirrhosis, the cause of liver cirrhosis is more complicated and needs symptomatic treatment, if it is caused by viral hepatitis, it needs to be treated with antiviral drugs; if it is caused by alcoholic liver disease, it needs to be treated with liver-protecting drugs at the same time in a timely manner, and it needs to be treated with antiviral drugs.

5. According to the condition of liver cancer, surgical resection, liver transplantation, intervention, radiotherapy and targeted therapy should be chosen.

If the cancer is combined with decompensated cirrhosis, it is recommended to go to regular hospitals to evaluate the condition and follow the doctor’s instructions to actively cooperate with the treatment, so as to avoid delaying the condition.

Is shunt operation in decompensated stage of liver cirrhosis effective?

Shunt in the uncompensated stage of liver cirrhosis is very effective. Jugular intrahepatic portal stent shunt is the most effective treatment for severe liver cirrhosis complications, but the treatment effect varies due to individual differences.

If cirrhosis reaches the decompensated stage, liver function will further deteriorate, liver synthesis function will be reduced, coagulation factors will be reduced, bleeding or anemia will occur, and there will also be esophagogastric fundal varices. Cirrhosis shunt will place a stent between the portal vein and hepatic vein to reduce portal hypertension and to achieve the therapeutic effect.

However, due to individual differences, the severity of cirrhosis is different, some patients also have local bleeding during the treatment, local edema, internal circulation disorders and impaired consciousness, etc. After the surgery, drink more water and rest, avoid spicy and stimulating food, exercise according to their own conditions, enhance their immunity, and regular review to avoid recurrence of the disease.

Treatment and maintenance of decompensated stage of liver cirrhosis

Treatment of decompensated stage of liver cirrhosis includes anticause treatment, oral drug treatment and complication treatment, etc. Maintenance usually focuses on daily care.

1. Anti-causal treatment: if it is caused by viral hepatitis, antiviral treatment should be carried out; if it is caused by drug-induced cirrhosis, relevant or suspicious drugs should be discontinued immediately, and oral medication should be taken to improve liver function and anti-hepatic fibrosis, including compound turtle shell soft liver tablets, etc., which can dissipate the blood stasis and detoxify the toxin and may cause nausea, vomiting and other adverse reactions after taking them.

2. Treatment of complications: If patients have serious complications, such as ascites, bleeding, liver injury, hepatorenal syndrome, etc., they need to be actively treated for the complications to prevent endangering their lives.

3. Maintenance: Cirrhosis decompensated period maintenance is mainly based on daily care, diet should limit the intake of vegetable protein and salt, should also avoid eating high fat, greasy and spicy stimulating food, pay attention to dietary rules and hygiene, avoid overeating, you can eat more vitamin-rich foods, such as fresh vegetables, fruits and so on.

Cirrhosis patients should actively consult the doctor and standardize the treatment under the doctor’s guidance. The use of the above drugs should follow the doctor’s instructions.

Prognosis

Cure

The prognosis is poor and often requires regular outpatient visits or hospitalization for comprehensive treatment.

Surgical treatment of cirrhosis, using a relatively intact liver for transplantation, can reverse cirrhosis from the root and is currently the only way to cure cirrhosis.

The development of liver transplantation has significantly changed the prognosis of cirrhosis, with a 1-year survival rate of about 90% and a 5-year survival rate of about 80% after transplantation, and the quality of life has been greatly improved.

The 1-year morbidity and mortality rates for cirrhotic decompensated stages 3, 4, and 5 are approximately 10%, 21%, and 87%.

Hazards

Hepatic encephalopathy can occur in the decompensated stage of cirrhosis and is the most common cause of death in cirrhosis.

Rupture of esophagogastric fundic varices can lead to hemorrhage manifested by vomiting of blood and dark stools, and massive bleeding can lead to shock and even death.

Cirrhosis is easily complicated by various infections due to hypersplenism and reduced immune function of the body.

About 10% to 25% of cirrhosis can eventually transform into liver cancer.

Liver cirrhosis decompensation stage can lead to hepatorenal syndrome, which is mainly manifested as oliguria, renal hypoplasia, hyponatremia and so on.

Daily

Daily Management

Dietary management

Diet should be light, soft, easy to digest, non-stimulating, small amount of meals, chewing and swallowing slowly.

Cooking should be processed finely and avoid hard and rough foods, such as fried foods and hard fruits; if there is upper gastrointestinal bleeding, the above foods are strictly prohibited.

Staple food should be chosen softer, rice and noodles should be softer than normal, buns, steamed buns, wontons, dumplings can be (pay attention to the filling of wontons or dumplings to choose less fiber).

Recommended high-quality protein diet, such as soybeans and their products such as tofu, tofu brain, soy milk, milk and dairy products, a variety of lean meats.

Eat more vegetables and fruits with lower fiber content to supplement vitamins and minerals, such as winter squash, pumpkin, cauliflower, apples, oranges, etc. Chopping, juicing and pureeing are preferred for cooking.

Avoid high protein diet if hepatic encephalopathy occurs.

Life management

Quit smoking and drinking, avoid using unnecessary drugs and health supplements to avoid aggravating liver damage.

Avoid heavy physical labor and take adequate rest.

Do not catch cold and avoid infection.

Psychological support

Maintain emotional stability and reduce anxiety.

Disease monitoring

Treat for the cause, protect liver function, and reduce the recurrence of cirrhosis portal hypertension complications.

Regular gastroenterology outpatient review, hospitalization and medication adjustment are required.

Follow-up review

Review blood routine, biochemistry, electrolytes, coagulation function, recommended every three months.

Surveillance for primary liver cancer: refinement of alpha-fetoprotein (AFP), abdominal ultrasound in three to six months.

Screening for esophagogastric fundal varices: review gastroscopy annually to prevent rupture and rebleeding of esophagogastric fundal varices.

Prevention

Cirrhosis decompensated stage is mainly prevented by etiology, early detection and treatment and adjustment of life and diet habits.

Active treatment of viral hepatitis, alcoholic liver disease, fatty liver and chronic heart failure and other diseases.

Newborns and high-risk groups should be injected with hepatitis B vaccine for prevention.

Abstain from alcohol and do not use drugs for liver damage.

Adhere to antiviral treatment for hepatitis B to avoid progression to the decompensated stage of cirrhosis.

Cure hepatitis C to avoid chronic progression to cirrhosis.