Diffuse fibrosis occurs in the liver, the tissues are severely damaged to form pseudolobules, and the liver gradually becomes deformed and hardened.
Weakness and loss of appetite may appear in the early stage, and ascites and hepatic encephalopathy may appear with the progress of the disease.
Causes include chronic hepatitis virus infection, alcoholism, toxins and drugs, lipid metabolism disorders, autoimmunity, etc.
Treatment includes symptomatic therapy, hepatoprotective therapy, complication therapy, symptomatic supportive therapy, artificial liver and liver transplantation.
Definition
Cirrhosis is a common chronic progressive liver disease, which is the end stage of diffuse liver disease formed by one or more etiologic factors over a long period of time or repeatedly.
Cirrhosis is characterized by extensive hepatocellular necrosis, nodular regeneration of residual hepatocytes, connective tissue proliferation and fibrous septum formation, resulting in the loss of normal structure and the formation of pseudolobules; the liver gradually becomes deformed and hardened.
Types
Small nodular cirrhosis
The size of nodules is more uniform, the diameter is between 3 and 5 millimeters, usually not more than 1 centimeter, the fibrous septum is finer, and the pseudolobules are more consistent.
It is mostly seen in chronic viral hepatitis.
Large nodular cirrhosis
The nodules are large and of different sizes, with a diameter of more than 5 millimeters and a maximum of several centimeters.
Mostly due to extensive hepatocellular necrosis, which was previously called post-necrotic cirrhosis.
Mixed cirrhosis
It is a mixture of cirrhosis with both large and small nodules.
Incompletely segregated cirrhosis
It is also called regenerative nodular opacity cirrhosis.
Most normal liver lobules are surrounded by fibrous septa to form pseudolobules.
Mainly seen in schistosomiasis cirrhosis.
Pathogenesis
In China, cirrhosis is a relatively common disease of the hepatobiliary system. Cirrhosis accounts for 1% of all hospitalized patients in the same period.
Cirrhosis is most commonly seen in males between the ages of 20 and 50.
The main populations of cirrhosis in China are patients with chronic hepatitis B and metabolic fatty liver disease, as well as people with chronic alcoholism.
The annual incidence rate of cirrhosis in China is about 17.1/100,000 people.
Clinical Classification
The most commonly used clinical classification is Child-Pugh classification. The evaluation criteria include 5 indicators such as hepatic encephalopathy, ascites, total bilirubin, albumin and prothrombin time (see table below).
Child-Pugh Grading Criteria Table
Evaluation indicators 1 point 2 points 3 points
Hepatic encephalopathy (stage) None1～23～4
Hepatic encephalopathy (stage)
None
1～2
3～4
Ascites None Mild Moderate to severe
Ascites
None
Mild
Moderate, severe
Total bilirubin (μmol/L) <3434～51>51
Total bilirubin (μmol/L)
<34
34～51
>51
Albumin (g/L) >3528～35<28
Albumin (g/L)
>35
28～35
<28
Prolongation of prothrombin time (sec) <44～5>6
Prolongation of prothrombin time (sec)
<4
4～5
>6
Child-Pugh grade A: total score ≤6;
Child-pugh grade B: total score 7 to 9;
Child-pugh grade C: total score ≥10.
The higher the score, the worse the liver reserve function.
Causes
Causes
Common causes of cirrhosis include viral hepatitis, long-term alcohol consumption, abnormal fat metabolism liver disease, poisons or drugs causing liver injury, parasitic infections such as schistosomiasis, metabolic liver disease and autoimmune liver disease.
Rare factors include obstruction of hepatic venous return (e.g., chronic right heart failure, Buga syndrome, hepatic sinusoidal obstruction syndrome).
Very rarely the cause is unknown and is called idiopathic.
Chronic viral hepatitis
Viral hepatitis B, C, and D can cause cirrhosis if uncontrolled and prolonged to chronic.
Chronic hepatitis B is one of the major causes of cirrhosis in China.
Alcoholic Liver Disease
Long-term alcohol abuse, alcohol will cause liver cell damage, the liver in the continuous damage repair process, cirrhosis will occur.
Alcoholic liver disease is one of the common causes in Europe and the United States, and there is an increasing trend in China in recent years.
Fat Metabolism Abnormal Liver Disease
With the change of life style, the number of obese people in China, especially the number of abdominal obesity has increased dramatically compared with before, which leads to the increase of the number of people suffering from steatohepatopathy and the number of people suffering from cirrhosis related to it has also increased.
Poison or drug
Prolonged or repeated exposure to hepatotoxic poisons such as arsenic-containing insecticides and carbon tetrachloride, or long-term consumption of hepatotoxic drugs such as isoniazid, cycloheximide and methotrexate can also lead to cirrhosis.
Obstruction of hepatic venous return
Chronic right heart failure, hepatic sinusoidal obstruction syndrome and Buga syndrome (hepatic venous obstruction syndrome) can cause long-term stagnation and hypoxia in the liver, resulting in hepatocellular necrosis and fibrosis, and in severe cases, cirrhosis.
Metabolic diseases
Metabolic diseases such as hemochromatosis and hepatomegaly (Wilson’s disease) can also cause cirrhosis.
Autoimmune diseases
Primary biliary cirrhosis, primary sclerosing cholangitis and other diseases can cause cirrhosis.
Parasitic infections
When suffering from schistosomiasis, due to the eggs of the worms in the confluent area stimulate the connective tissue proliferation to become schistosomiasis hepatic fibrosis, which can cause significant portal hypertension, also known as schistosomiasis cirrhosis.
Idiopathic
Rarely, the cause is unknown, called cryptogenic cirrhosis or idiopathic cirrhosis.
Pathogenesis
Hepatocytes are attacked by pathogenic factors for a long time, and necrosis occurs. Fibrotic proliferation and extracellular matrix deposition occur in the process of hepatocyte repair, resulting in cirrhosis.
Microscopic manifestations include massive necrosis of hepatocytes, nodular regeneration of residual hepatocytes, hyperplasia of connective tissue with formation of fibrous septa, disruption of the normal hepatic lobular structure, and formation of pseudolobules.
Symptoms
Cirrhosis in different stages will show different symptoms. Generally speaking, the symptoms of early and middle stage (compensated stage) cirrhosis are more insidious and not easy to be felt subjectively, while the symptoms of terminal stage (decompensated stage) are more obvious.
Compensated stage
A small proportion of early compensated cirrhosis may be asymptomatic.
Most symptoms are mild and less specific. They include mild fatigue, abdominal distension, mild loss of appetite, weight loss, mild enlargement of the liver and spleen, mild jaundice, etc. Some of them may appear as hepatic palms (reddening of the skin of the palm of the hand near the carpal joints, which fades away when pressure is put on it) and spider nevus (vascular nevus formed by the dilatation of small arteries in the skin, which is similar to that of a spider).
Loss of compensation stage
Systemic symptoms
Weakness.
Wasting away.
Digestive tract symptoms
Loss of appetite.
Bloating.
Some may experience polyuria and polyphagia due to hepatogenic diabetes.
Urinary symptoms
If combined with hepatorenal syndrome, oliguria and anuria will occur.
Skin symptoms
Yellowing of the skin all over the body (jaundice) and darkening of the facial skin.
Liver palms.
Spider nevi.
Bleeding symptoms
Bleeding from the gums.
Nosebleeds.
Skin petechiae, ecchymosis.
Endocrine Disorder Symptoms
Women experience menstrual disorders, infertility, and even amenorrhea.
Males may develop mammary gland development, etc.
Hypoproteinemia
Double lower extremity edema.
Ascites, pleural effusion.
Symptoms of portal hypertension
Varicose veins of the chest and abdominal wall.
Esophagogastric fundal varices.
Bleeding rectal-anal varices.
Complications
Splenomegaly and hypersplenism: anemia symptoms such as pallor, dizziness, and fatigue, as well as decreased resistance manifestations such as susceptibility to infection, may be present.
Spontaneous peritonitis: there may be different degrees of fever, abdominal distension, and poor mental status.
Hepatic encephalopathy: there may be manifestations such as personality, behavior, intelligence change and consciousness disorder.
Esophagogastric fundal varices rupture bleeding: mainly manifested by sudden vomiting of blood, which is bright red or dark red, and shock may occur when the bleeding is large.
Hepatorenal syndrome: there may be oliguria, anuria, jaundice and ascites with varying degrees of yellowing of skin and mucous membranes and increasing abdominal circumference.
Hepatopulmonary syndrome: dyspnea, cyanosis of skin and mucous membranes may occur.
Consultation
Department of Medicine
Gastroenterology
When symptoms such as loss of appetite, fatigue, emaciation, abdominal distension, dark color and jaundice appear, it is recommended to consult a doctor promptly.
Emergency Department
For symptoms such as severe vomiting, vomiting blood, change in consciousness, coma, etc., immediate medical attention is recommended.
Preparation for medical treatment
Preparing for medical treatment: registration, preparation of documents, common problems
Tips for seeking medical treatment
Before seeking medical attention, try to keep a record of the symptoms you have experienced, their duration, etc. for the doctor’s reference.
Preparation Checklist
Symptom list
Pay particular attention to the time of onset of symptoms, special manifestations, etc.
Where is the discomfort? How long has the discomfort lasted?
Any change in stool color?
How has your appetite been recently?
Any recent change in weight?
Have you had any tests and what were the results?
Have you taken any medications recently?
Medical History List
Any previous diseases of the hepatobiliary system?
Has anyone in the family experienced similar symptoms?
What is your occupation?
Do you drink alcohol? How long have you been drinking alcohol? What is the daily amount of alcohol consumed?
Any recent blood transfusions or use of blood products?
Checklist
Test results for the last six months, which can be brought to the doctor’s office
Routine blood test, routine urine test, routine stool test
Liver function, blood lipid, liver fibrosis index test
Virology test
Coagulation function test
Autoantibody test
Abdominal ultrasound, abdominal CT, abdominal MRI
Liver puncture biopsy report
Medication List
Medication used in the last 3 months, if available, you can bring the box or package to the doctor
The diagnosis of cirrhosis of the liver needs to be based on the history, clinical manifestations, physical examination, laboratory tests and imaging tests.
Medical history
History of viral hepatitis and fatty liver.
Long-term alcohol consumption.
Family history of cirrhosis.
Clinical manifestations
There are systemic symptoms such as fatigue and emaciation, digestive symptoms such as abdominal distension and loss of appetite.
There are jaundice, liver palms, spider nevus, liver disease face and portal hypertension.
Some patients have characteristic manifestations of cirrhosis such as hepatosplenomegaly and tenderness to percussion in the liver area.
Laboratory examination
Etiologic tests
Etiologic examination helps to diagnose the cause of cirrhosis and can provide treatment plan for the follow-up.
Hepatitis B five indexes test, Hepatitis B virus (HBV-DNA) test.
Hepatitis C virus (HCV-RNA) test and genotyping.
Serum copper, copper blue protein test, serum iron test.
Autoantibody test.
Routine blood tests
Cirrhosis, if combined with hypersplenism, may have decreased white blood cell count and platelet count.
Urine routine
Abnormal urinary bilirubin and urobilinogen indexes are of significance in determining the jaundice caused by liver cirrhosis.
Stool routine
Fecal occult blood test is significant in determining the gastrointestinal bleeding caused by liver cirrhosis.
Liver function testLiver function tests such as serum bilirubin, serum albumin, serum enzymes and blood ammonia can help diagnose liver cirrhosis by finding out whether the liver is in normal working condition.Liver Fibrosis Indicator TestElevated values of Pre-III collagen peptide (PIIIP), prolyl hydroxylase (PHO), monoamine oxidase (MAO), serum laminin (LM), as well as hyaluronic acid and laminin, etc., indicate the presence of hepatic fibrosis, which is helpful for the diagnosis of liver cirrhosis.APRI scoreRecent studies have used the APRI score for the diagnosis of cirrhosis.
重播Definition: APRI is the aspartate aminotransferase (AST) and platelet (PLT) ratio index.
Calculation method: APRI = [(AST test value/upper limit of normal value) × 100] /PLT (109/L).
Evaluation criteria: When APRI is greater than 2, it suggests the presence of cirrhosis.
Imaging
Ultrasonography
B-mode and color Doppler ultrasonography have diagnostic value for cirrhosis.
CT or magnetic resonance imaging
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), with a value of more than 17.5 kPa suggesting cirrhosis.
Pathological examination
Liver puncture biopsy is important for early diagnosis of cirrhosis and is the “gold standard” for clinical diagnosis of cirrhosis.
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Differential Diagnosis
Differentials from diseases causing hepatosplenomegaly
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 a mosquito; it may also present with typical intermittent chills, profuse sweating, etc., and the intermittent episodes have a certain regularity; laboratory tests may reveal Plasmodium vivax.
Malignant histiocytosis
Similarities: both may present with hepatosplenomegaly, jaundice and abnormal liver function.
Differences: Bone marrow smear or other histopathologic findings of malignant histiocytosis include abnormal histiocytes and multinucleated giant histiocytes.
Hepatocellular carcinoma
Similarity: Early stage of liver cancer is relatively insidious, with no specific symptoms. With the progression of the disease, symptoms such as pain in liver area, hepatosplenomegaly, yellowing of skin and sclera may appear.
Differences: Liver cancer may be accompanied by malignant disease, manifested by extreme emaciation. Differential diagnosis can be made by imaging and pathological examination.
Differences with diseases causing ascites
Cardiogenic ascites
Similarity: both can present with ascites.
Differences: Patients with cardiogenic ascites may show signs of heart failure, i.e. sedentary breathing, 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 elevated alpha-fetoprotein value, whereas cirrhosis usually does not. It can be differentiated by imaging and pathologic examination.
Treatment
Aims and principles of treatment
Aims of treatment: Early detection and prevention of disease progression. Cirrhosis is an irreversible dysfunction of liver function due to the disturbance of tissue structure. At present, it is not only impossible to cure by itself, but also cannot be completely cured even by treatment.
Treatment principle
Comprehensive treatment, personalized treatment for the patient’s condition.
In the early stage of cirrhosis, the main treatment is to treat the cause of cirrhosis (to treat the primary disease that causes cirrhosis); in the late stage, the main treatment is to treat the complications.
Supportive treatment
People with cirrhosis should take rest and try to stay in bed as much as possible.
Nutritional screening and assessment are required before and during the nutritional support therapy. The principles of nutritional and dietary therapy are as follows.
Energy
Cirrhosis energy is supplied at 35-40 kcal per kilogram of body weight per day.
For obesity, energy should be reduced by 500 to 800 kcal throughout the day to ensure 5% to 10% weight loss without compromising protein reserves, provided that protein intake is adequate (>1.5 g per kg of body weight per day).
Protein
For compensated cirrhosis without nutritional risk or malnutrition, the normal dietary protein supply should be 1.2 g per kg body weight per day; for decompensation it should be 1.5 g per kg body weight per day.
If adequate nitrogen intake cannot be obtained orally, consider taking branched-chain amino acid supplements under medical supervision.
Protein diet should be controlled in decompensated cirrhosis.
Fat
The supply should be 25% of total energy.
If steatorrhea is present, it should be a low-fat diet. Patients may also apply a medium-chain triglyceride diet under medical supervision.
Carbohydrates
300 to 450 grams of carbohydrates should be consumed daily to ensure glycogen reserves.
Other Nutrients
Supplementation with multivitamins and trace element preparations is recommended under medical supervision; no special treatment is required for clinically insignificant deficiencies.
Dietary considerations
Eat small and frequent meals, those who can eat by mouth can have 4～6 meals per day (including additional meals before bedtime).
Use less or no spicy and stimulating food, and focus on a light diet (less salt, less sugar, less oil).
Those who have developed esophageal varices need to avoid hard, coarse and dry foods, such as coarse grains, cookies, ham, nuts, vegetables and fruits with high fiber; vegetables and fruits can be chopped and juiced for drinking, and nuts and nuts can be crushed and added to cooked dishes for consumption.
Hypertonic glucose solution can also be fed intravenously to replenish calories, and vitamin C, insulin, and potassium chloride can be added to the infusion.
Ascites should be limited to sodium intake (no more than 2 grams of ingested sodium per day), and attention should be paid to protein supplementation.
Hepatoprotective treatment
The principle of treatment is to protect the liver, reduce enzymes, reduce yellowing, resist liver fibrosis, and promote liver cell regeneration.
Western medicine
Adenosylmethionine, ursodeoxycholic acid, diammonium glycyrrhizinate can be chosen.
If necessary, intravenous infusion treatment, such as hepatocyte growth-promoting hormone, reduced glutathione, glycyrrhizic acid preparations.
Chinese medicine
Fuzheng Huayu capsule, Heluo Huayu pill, Compound turtle shell soft liver tablets, Silymarin-like drugs can be chosen.
Etiologic Treatment
Chronic viral hepatitis
Chronic hepatitis B
Nucleoside analogs: Recommended choices include entecavir, tenofovir or propranolol tenofovir, but also tebivudine, adefovir, lamivudine, etc.
Interferon: Polyethylene glycol interferon can be chosen with caution in compensated cirrhosis, and regular interferon therapy is also available. Interferon is prohibited in decompensated cirrhosis.
Hepatitis C
Currently, direct antiviral drugs (DDAs) are mostly used in clinical treatment.
Commonly used drugs include prozac (a combination of sofosbuvir and viplatasvir, also known as gizandia), asurevir, simeprevir, dalatasvir, lediprevir, and sofosbuvir.
Antiviral drugs should be selected based on viral genotyping. With a course of treatment of 8 to 12 weeks, more than 95% of hepatitis C can be completely cured.
Alcoholic cirrhosis
Abstain from alcohol and do not consume any food containing alcohol.
Hepatomegaly
Copper repellent treatment, commonly used copper repellent drugs include penicillamine, sodium dimercaptopropanesulfonate, and sodium edetate calcium.
Reduce the consumption of oysters, animal liver, walnuts, and soybeans, which are rich in copper.
Secondary biliary cirrhosis
Follow the doctor’s instructions for relevant treatments, such as endoscopic retrograde cholangiopancreatography and papillotomy plus lithotripsy.
Treatment is aimed at relieving biliary obstruction, and surgery may also be performed if necessary.
Autoimmune liver disease
Immunomodulatory therapy.
Complications
Treatment of hypersplenism
Leukocyte and platelet boosting drugs (e.g., lisdexamfetamine, shark liver alcohol, aminopterin, etc.) may be given.
If necessary, splenectomy or splenic artery embolization is feasible.
Treatment of persistent ascites
Diuretic drugs
Use diuretics, such as hydrochlorothiazide, aminopterin, etc., as prescribed by the doctor.
If diuresis is not effective, it may be gradually increased. Diuretic therapy is appropriate to lose no more than 0.5 kg of body weight per day to avoid inducing hepatic encephalopathy and hepatorenal syndrome.
Diuretics may be tapered down gradually if ascites subsides.
Human blood albumin
Albumin can also be infused intravenously to increase colloid osmotic pressure and reduce ascites production.
Refractory peritoneal effusions can be treated with repeated draining of the peritoneal fluid, plus intravenous albumin infusion.
Concentration of peritoneal fluid infusion
For the treatment of refractory peritoneal effusion, or with hypovolemic state, hyponatremia, hypoproteinemia and hepatorenal syndrome, as well as large amounts of peritoneal effusion due to various causes in urgent need of symptomatic relief.
TIPS is a treatment to effectively reduce portal vein pressure and control bleeding from ruptured varices in the fundic vein of the lower esophagus. It is a procedure that creates a hepatic vein-portal vein channel within the liver through an interventional approach, so that high-pressure portal vein blood flows through the channel into the low-pressure inferior vena cava.
Lowering the pressure in the portal vein
The drugs Procainide, Isosorbide Mononitrate, Cardivanol, etc. can be chosen under the guidance of specialized doctors.
Bleeding from rupture of esophageal- fundic varices
If not rescued in time, it can be life-threatening.
It needs to receive volume expansion, blood transfusion, lowering portal pressure, hemostasis, acid suppression, triple lumen tube compression for hemostasis, endoscopic sclerotherapy or sleeve treatment, gastric coronary vein embolization, surgery, and transjugular intrahepatic portal vein stent shunt.
Spontaneous peritonitis
The doctor may use antimicrobial drugs such as third generation cephalosporins and ciprofloxacin.
Antimicrobial drugs will also be adjusted during the course of treatment, based on drug sensitivity results and response to treatment, for 1 to 2 weeks.
Hepatorenal syndrome
Treatment focuses on the treatment of the liver primary and further therapy.
Volume-expanding therapy may be administered, and drugs such as albumin, plasma, whole blood, and concentrated reflux of one’s own peritoneal fluid may be used.
It may also receive concurrent treatment with diuretics, and vasoactive drugs such as dopamine, prostaglandins, and terlipressin.
Sometimes they may also receive dialysis treatment, which includes hemodialysis and peritoneal dialysis.
Hepatic encephalopathy
The first step is to control the protein diet.
Oral lactulose is given as prescribed. Lactulose acidifies the intestines, keeps the stools moving, changes the intestinal acidity (pH) so that the intestines produce less ammonia and absorb less ammonia, and reduces endotoxemia and the absorption of other toxic substances.
It may also be treated with medications such as branched-chain amino acids and mentholated ornithine.
Artificial Liver and Liver Transplantation
Artificial liver or liver transplantation may be considered for the treatment of end-stage liver failure.
Artificial liver therapy
These include plasma exchange, bilirubin adsorption, and molecular adsorbent recirculation system (MARS).
Liver transplantation
For end-stage liver disease where conventional medical treatment is ineffective.
Prognosis
Cure
Medication can slow down, or keep cirrhosis from further deterioration, but there is no way to reverse cirrhosis. Current antifibrotic drugs cannot completely reverse liver fibrosis and cirrhosis, so medical treatment cannot cure cirrhosis.
Surgical treatment of cirrhosis, which involves the transplantation of a relatively intact liver, can reverse cirrhosis from the root and is the only way to cure cirrhosis at present.
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, greatly improving the quality of life.
Survival
Survival in cirrhosis is related to the etiology of the disease, the degree of liver function compensation and complications. According to the Child-Pugh classification of cirrhosis, the estimated survival rates at 1 and 2 years are as follows.
Child-Pugh grade A 100%, 85%.
Child-Pugh B 80%, 60%.
Child-Pugh Class C 45%, 35%.
Hazards
Hepatic encephalopathy can occur in advanced cirrhosis and is the most common cause of death in cirrhosis.
Rupture of esophagogastric fundic varices can lead to hemorrhage, which manifests as vomiting blood and black 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.
About 10% of cirrhosis can be complicated by portal vein thrombosis, which is mainly related to the slow blood flow in portal vein, portal vein hardening and other factors.
End-stage cirrhosis can lead to hepatorenal syndrome, which is the most common and serious complication of cirrhosis, mainly manifested by oliguria, renal hypoplasia, hyponatremia and so on.
Daily life
Cirrhosis should pay attention to many aspects in daily life, such as diet regulation, life regulation and psychological regulation.
Daily management
Dietary management
Diet should be light, soft, easy to digest, non-stimulating, small and frequent meals, chewing and swallowing slowly.
Cooking should be fine, avoid hard and rough food, such as fried food, hard fruit food; if there is upper gastrointestinal bleeding, the above food is 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 replenish vitamins and minerals, such as winter squash, pumpkin, cauliflower, apples, oranges, etc. Chopping, juicing and pureeing are preferred for cooking.