Liver cirrhosis is a pathological stage characterized by the progression of various chronic liver diseases, ultimately characterized by chronic liver inflammation, diffuse fibrosis, pseudolobules, regenerative nodules, and intrahepatic and extrahepatic vascular proliferation. While the compensated stage is asymptomatic, the decompensated stage is clinically characterized by portal hypertension and decreased liver function. Patients often die from chronic multi-organ failure, including complications such as esophageal and gastric variceal bleeding, hepatic encephalopathy, infection, hepatorenal syndrome, and portal vein thrombosis.
Clinical classification
1. International guidelines for staging
(1) Compensation period
① Stage 1: Stage 1a and Stage 1b. Stage 1a has no obvious symptoms. Stage 1b has significant portal hypertension but no gastrointestinal varices.
② Stage 2: There are varicose veins in the digestive tract, but no bleeding or ascites.
(2) Decompensation stage
① Stage 3: ascites, no gastrointestinal varicose bleeding, with or without gastrointestinal varicose veins.
② Stage 4: There is varicose bleeding in the gastrointestinal tract, with or without ascites or hepatic encephalopathy.
③ Stage 5: Sepsis, difficult-to-control gastrointestinal varicose bleeding or refractory ascites, acute kidney injury-hepatorenal syndrome and hepatic encephalopathy and other multiple organ dysfunction.
2. Classification by nodule morphology
(1) Micronodular cirrhosis
The nodules are uniform in size, generally 3 to 5 mm in diameter and no larger than 1 cm. Alcoholic cirrhosis caused by long-term excessive drinking is a typical form of micronodular cirrhosis. Micronodular cirrhosis can also be seen in patients with malnutrition and anemia.
(2) Macronodular cirrhosis
The nodules are large and uneven in size, generally ranging from 1 to 3 cm in diameter. Liver cirrhosis caused by chronic viral hepatitis is often macronodular cirrhosis.
(3) Mixed nodular and macronodular cirrhosis
That is, there are two pathological forms of large and small nodules in the liver at the same time, and most cirrhosis is mixed cirrhosis.
Epidemiology
Contagious
Cirrhosis is not contagious, but some causes, such as viral hepatitis, can be contagious. The source of infection is viral hepatitis patients and hepatitis virus carriers, and transmission routes include fecal-oral, blood-borne, and mother-to-child transmission.
Incidence
Cirrhosis is a common chronic disease in clinical practice, but there is no large-sample data statistics on its specific incidence rate.
High-risk population
Patients with various types of hepatitis, liver disease and long-term alcoholics.
Causes
Overview
There are over 10 causes of liver cirrhosis. Hepatitis B virus (HBV) is still the most common cause in my country. In Europe and the United States, alcohol and hepatitis C virus (HCV) are common causes. Fatty liver disease, immune disorders, and drug or chemical toxins are also common causes of liver cirrhosis.
Basic cause
1. Hepatitis virus infection
HBV or HCV infection can cause viral hepatitis. If poorly controlled, it can gradually develop into chronic hepatitis and eventually progress to cirrhosis.
2. Alcoholic liver disease
Liver disease caused by heavy drinking continues to develop until the liver lobule structure is damaged, forming structural fibrosis and pseudolobules, with the morphology of micronodular cirrhosis.
3. Non-alcoholic fatty liver disease
If it is not caused by alcohol and has no other clear cause, the liver cells will undergo fatty degeneration, develop into fatty liver hepatitis, and gradually progress to cirrhosis.
4. Autoimmune liver disease
Including primary biliary cirrhosis (primary biliary cholangitis), autoimmune hepatitis and primary sclerosing cholangitis.
5. Genetic and metabolic diseases
Due to genetic or congenital enzyme defects, certain metabolic products accumulate in the liver, causing hepatocyte necrosis and connective tissue hyperplasia, ultimately leading to cirrhosis. Common diseases include Wilson’s disease, hemochromatosis, and hepatic amyloidosis.
6. Drugs or chemical poisons
Long-term exposure to or use of hepatotoxic drugs or poisons, such as acetaminophen, anti-tuberculosis drugs, and anti-tumor chemotherapy drugs, can cause drug-induced or toxic hepatitis, which can then develop into cirrhosis.
7. Parasitic infection
After infection with schistosoma japonicum, mature eggs are phagocytosed by hepatic macrophages and then develop into fibrocytes, forming fibrous nodules. Clonorchis sinensis parasitizes the intrahepatic and extrahepatic bile ducts, causing biliary obstruction and inflammation, which can gradually progress to cirrhosis.
8. Circulatory disorders
When patients have Budd-Chiari syndrome or right heart failure, circulation disorders occur, liver cells suffer from long-term congestion and hypoxia, leading to liver cell degeneration and fibrosis, and eventually developing into cirrhosis.
9. Unknown cause
The cause of some cirrhosis is unknown, which is called cryptogenic cirrhosis.
Risk factors
1. Obesity.
2. Insulin resistance.
symptom
Overview
Most patients with cirrhosis are asymptomatic or have mild symptoms during the compensated stage, but may experience abdominal discomfort, fatigue, loss of appetite, etc. In the decompensated stage, there are two main manifestations: decreased liver function and portal hypertension (distortion of small blood vessels caused by liver tissue fibrosis and nodule regeneration, which hinders blood flow).
Typical symptoms
1. Compensatory symptoms
There are no symptoms or the symptoms are mild, which may include abdominal discomfort, fatigue, loss of appetite, etc. These symptoms usually occur when tired, nervous or accompanied by other diseases. Rest and digestive aids can relieve the symptoms.
2. Decompensation symptoms
(1) Decreased liver function
①Maldigestion and absorption: loss of appetite, nausea, abdominal distension, worsening after meals, and diarrhea after eating meat.
② Malnutrition: The patient is generally in poor condition, with symptoms of weight loss, fatigue, lack of energy, or even being bedridden. The skin may be dry or swollen.
③ Jaundice: yellowing of the skin and sclera, and dark urine.
④ Bleeding and anemia: There are often mucosal ecchymosis, nasal and gum bleeding or gastrointestinal bleeding.
Endocrine disorders: Patients may experience hepatic facies (i.e., hyperpigmentation of the face and other exposed areas, a dark, sallow complexion, and a dull, dull complexion), spider angiomas, palmar erythema, and ascites. Male patients may also experience decreased libido, testicular atrophy, hair loss, and breast development; female patients may experience menstrual irregularities, amenorrhea, and infertility.
⑥ Irregular low fever: caused by reduced inactivation of pyrogenic factors by the liver or secondary infection.
⑦ Hypoalbuminemia: often accompanied by lower limb edema and ascites.
(2) Portal hypertension
① Hypersplenism and splenomegaly: Portal hypertension causes congestive enlargement of the spleen. Intestinal antigens that should enter the systemic circulation are absorbed by the spleen, stimulating hypersplenism and causing proliferative anemia, infection, and bleeding. Splenomegaly is often prominent in schistosomal cirrhosis.
② Ascites: It is one of the most prominent clinical manifestations of decompensated cirrhosis. Patients often experience abdominal distension and bloating, and may even develop umbilical hernia, dyspnea, and palpitations.
complication
1. Gastrointestinal bleeding
(1) Esophageal varicose bleeding
Portal hypertension is the main cause of esophageal variceal bleeding, with clinical manifestations including sudden massive vomiting of blood or tarry stools, and in severe cases, hemorrhagic shock.
(2) Peptic ulcer
Portal hypertension slows down the venous return of the gastric mucosa, impairs the barrier function, and makes gastric and duodenal ulcers and even bleeding more likely to occur.
(3) Portal hypertensive gastrointestinal disease
Portal hypertensive gastropathy often presents with recurrent or persistent vomiting of small amounts of blood and melena. Portal hypertensive enteropathy often presents with recurrent melena or hematochezia.
2. Cholelithiasis
The prevalence is about 30%, and gallbladder and extrahepatic bile duct stones are more common.
3. Infection
(1) Spontaneous bacterial peritonitis
Acute bacterial peritonitis caused by ascites in patients with cirrhosis.
(2) Biliary tract infection
The obstruction caused by cholelithiasis can cause infection, and patients often have abdominal pain and fever; when there is common bile duct obstruction, obstructive jaundice occurs; when the infection further damages liver function, hepatocellular jaundice may occur.
(3) Lung, intestinal and urinary tract infections
Patients with cirrhosis may develop lung, intestinal and urinary tract infections due to liver microcirculation disorders and decreased immune function.
4. Hepatic encephalopathy
Hepatic encephalopathy is a syndrome of central nervous system dysfunction based on metabolic disorders. About 50% of patients with cirrhosis will develop hepatic encephalopathy.
5. Portal vein thrombosis or cavernous change
(1) Portal vein thrombosis
① Acute portal vein thrombosis: Symptoms include acute abdominal pain, and severe cases can cause intestinal ischemia and intestinal obstruction.
② Chronic portal vein thrombosis: It may be asymptomatic and often ignored, and is often first discovered by imaging examinations.
(2) Cavernous transformation of the portal vein
After portal hypertension causes intravenous obstruction, a network of small and tortuous blood vessels forms around the portal vein.
6. Electrolyte and acid-base imbalance
Patients with cirrhosis often have ascites and need to restrict sodium intake and undergo diuretic treatment, which can lead to electrolyte imbalance.
7. Hepatorenal syndrome
Severe portal hypertension reduces systemic blood flow, preventing the liver from inactivating various vasodilators. This leads to dilation of the systemic vascular bed, decreased renal blood flow, and renal failure. Clinical manifestations include oliguria, anuria, and azotemia.
8. Hepatopulmonary syndrome
Hepatopulmonary syndrome is a condition characterized by dyspnea and signs of hypoxia, such as cyanosis and clubbing of fingers and toes, occurring on the basis of cirrhosis after exclusion of primary cardiopulmonary disease.
9. Primary liver cancer
In my country, about 85% of primary liver cancer occurs on the basis of cirrhosis.
examine
Scheduled inspection
Patients experiencing symptoms such as fatigue, loss of appetite, abdominal distension, diarrhea, and weight loss should seek medical attention promptly. After inquiring about the patient’s medical history and performing a physical examination, the doctor may recommend routine blood and urine tests, abdominal ultrasound, and gastroscopy to confirm the diagnosis and determine the cause.
Physical examination
1. Visual examination
Patients with cirrhosis may have physical signs such as liver disease face, yellowing of skin and mucous membranes, liver palms, spider nevi, varicose veins of the abdominal wall, and abdominal distension.
2. Palpation and percussion
The liver is located in the right lower abdomen. Normally, it is soft and its lower edge cannot be palpated. However, in patients with cirrhosis, the lower edge of the liver can be palpated beneath the ribs. The liver is firm and has blunt edges. Some patients may also have an enlarged spleen.
Laboratory tests
1. Blood routine test
The blood routine of patients with early cirrhosis may be normal; patients in the decompensated stage may experience anemia, and their white blood cell count may increase when they have an infection; when the spleen is hyperactive, both white blood cells and platelets may decrease.
2. Urinalysis
Normally, urine protein is positive in patients with hepatitis B cirrhosis and hepatitis B nephritis. In jaundice caused by cholestasis, urine bilirubin is positive and urobilinogen is negative. In jaundice caused by hepatocellular damage, urobilinogen is increased. Patients with ascites should routinely measure 24-hour urine sodium and potassium.
3. Routine bowel movements
Generally normal, when bleeding occurs due to esophageal varicose veins or portal hypertensive gastropathy, black stools, tarry stools or even dark red bloody stools may appear, and the stool occult blood test may be positive.
4. Liver function test
(1) Serum bilirubin: Conjugated bilirubin and total bilirubin may increase during the decompensated stage. Continuous increase in bilirubin is an important indicator of poor prognosis.
(2) Protein metabolism: The liver is the only place where albumin is synthesized. In the absence of protein loss (such as proteinuria), the amount of serum albumin can often reflect the liver’s reserve function. When liver function is significantly impaired, albumin synthesis decreases.
(3) Prothrombin time: It is an important prognostic indicator reflecting the liver’s reserve function. It is significantly prolonged in late-stage liver cirrhosis and liver cell damage.
(4) Serum enzyme examination: When liver cells are damaged, alanine aminotransferase (ALT) increases; when liver cells are necrotic, aspartate aminotransferase (AST) increases. Extremely low cholinesterase (ChE) indicates a poor prognosis.
(5) Fat metabolism: Blood cholesterol levels are normal or low in patients in the compensated stage, but elevated in patients with primary biliary cirrhosis and non-alcoholic fatty liver disease. Total cholesterol, especially cholesterol esters, are significantly reduced in the decompensated stage.
(6) Blood ammonia: Determination of arterial blood ammonia helps diagnose hepatic encephalopathy.
5. Serum electrolytes
Determine whether the patient has electrolyte imbalance.
6. Alpha-fetoprotein (AFP)
When cirrhosis is active, AFP increases. When primary liver cancer is present, transaminases are normal but AFP remains elevated.
7. Viral hepatitis marker determination
It helps to identify the cause of the disease and determine whether the patient has hepatitis B, hepatitis C or hepatitis D.
8. Serum immunological examination
In primary biliary cirrhosis, serum anti-mitochondrial antibodies are positive. In autoimmune liver disease, anti-smooth muscle antibodies and antinuclear antibodies are positive.
9. Serum ceruloplasmin
It is decreased in Wilson’s disease, accompanied by increased urinary copper.
Imaging examinations
1. Ultrasound examination
It can diagnose portal vein thrombosis and differentiate cirrhotic nodules from liver cancer.
2. CT
Helps differentiate between cirrhosis and primary liver cancer.
3. MRI
It can be used to evaluate liver fibrosis and cirrhosis.
4. Radionuclide imaging
The heart/liver ratio measured by radionuclide 99m Tc-scanning can indirectly reflect the degree of portal hypertension and portosystemic shunt.
5. Upper gastrointestinal tract barium meal radiography
The patient needs to drink a liquid called barium, which can cover the esophagus, stomach and small intestine and show up on X-rays, and can detect varicose veins in the esophagus and gastric fundus.
Pathological examination
Liver biopsy: Under the guidance of ultrasound or laparoscopy, the doctor quickly performs liver puncture and takes liver tissue for pathological examination to confirm early cirrhosis.
Other tests
Gastroscopy: This procedure involves passing a thin tube (endoscope) through the esophagus to examine the stomach lining. Patients must fast overnight before the procedure. This procedure allows direct visualization and identification of varices in the esophagus and stomach, as well as portal hypertensive gastropathy.
diagnosis
Diagnostic principles
Doctors diagnose cirrhosis mainly through a comprehensive assessment of clinical manifestations, physical examination, laboratory tests, imaging tests and liver puncture biopsy to confirm the diagnosis.
Diagnostic basis
1. Diagnostic basis for compensated cirrhosis (one of the following four)
(1) Histology is consistent with the diagnosis of cirrhosis.
(2) If endoscopy shows esophageal and gastric varices or ectopic varices in the digestive tract, portal hypertension not caused by cirrhosis needs to be excluded.
(3) Ultrasound, CT, and other imaging examinations indicate features of cirrhosis or portal hypertension, such as splenomegaly and portal vein ≥1.3 cm.
(4) For patients without histological, endoscopic or imaging examinations, abnormalities in the following examination indicators suggest the presence of cirrhosis (two of the four items must be met):
①PLT is less than 100×10 9 /L and there is no other reason to explain it.
② Serum albumin is less than 35g/L, excluding other causes such as malnutrition or kidney disease.
③INR greater than 1.3 or PT prolonged (thrombolytic or anticoagulant drugs discontinued for more than 7 days).
④AST/PLT ratio index (APRI): The APRI score for adults is greater than 2. The effects of enzyme-lowering drugs and other factors on APRI should be noted.
2. Diagnostic basis for decompensated cirrhosis
(1) Possesses diagnostic evidence for cirrhosis.
(2) Complications related to portal hypertension occur: such as ascites, esophageal and gastric variceal bleeding, sepsis, hepatic encephalopathy, hepatorenal syndrome, etc.
Differential diagnosis
1. Chronic hepatitis
The clinical manifestations of this disease are the same as those of compensated cirrhosis, but the liver is not enlarged and has a smooth surface, which can be distinguished by ultrasound examination.
2. Primary liver cancer
Primary liver cancer may present with liver pain and unexplained fever, hepatomegaly on palpation, ascites with or without blood on biopsy, and persistently elevated serum alpha-fetoprotein with normal transaminases. Liver biopsy can differentiate this disease.
3. Intra-abdominal tumors
It is usually refractory ascites that is bloody. Abdominal puncture, which collects the ascites and tests it, can reveal tumor cells. Ultrasound and CT scans can also reveal the primary tumor lesion.
treat
Treatment principles
Once a diagnosis of cirrhosis is confirmed, comprehensive treatment should be initiated as soon as possible. Prioritize treatment of the underlying cause, including anti-inflammatory and anti-fibrotic measures when necessary, and proactively prevent and treat complications. Follow-up should include dynamic assessment of the patient’s condition. If medical therapy is ineffective, consider gastroscopy and interventional therapy. Liver transplantation may be considered for eligible patients.
Treatment of the cause
1. Liver cirrhosis caused by HBV and HCV
(1) Compensatory stage: Antiviral treatment is performed. Patients with good liver function can also choose interferon under close monitoring, with a course of treatment of 1 year. The purpose is to delay and reduce the occurrence of liver decompensation and primary liver cancer.
(2) Decompensated stage: Long-term or even lifelong oral antiviral treatment with strong antiviral efficacy and low resistance to drug nucleoside analogues, such as entecavir or tenofovir, is required.
2. Alcoholic cirrhosis
Abstinence from alcohol should be enforced. Treatment is often with medications such as glucocorticoids, metadoxine, and S-adenosylmethionine. Metadoxine accelerates the clearance of ethanol from the serum, while S-adenosylmethionine improves symptoms and serum markers.
3. Non-alcoholic fatty liver disease
Weight loss and liver protection treatment should be given.
4. Cirrhosis caused by autoimmune liver disease
Combination therapy with prednisone and azathioprine or budesonide and azathioprine is generally recommended.
5. Wilson’s disease cirrhosis
Commonly used drugs include penicillamine, trientine, etc. Oral zinc preparations such as zinc acetate and zinc gluconate can also be taken.
6. Hemochromatosis and cirrhosis
Dietary iron intake should be restricted, and therapeutic phlebotomy, often with drugs such as deferoxamine and deferasirox, may be used.
7. Cirrhosis caused by drugs and chemicals
Discontinue suspected liver-injury drugs promptly, and avoid re-use of suspected or similar drugs. Severe symptoms should also be treated with N-acetylcysteine or glucocorticoids.
8. Schistosomiasis-induced cirrhosis and Clonorchiasis-induced cirrhosis
Praziquantel is the preferred treatment.
Acute treatment
1. Treatment of massive gastrointestinal bleeding
(1) To correct hypovolemic shock, give the patient rapid fluid and blood transfusion.
(2) Prevent complications related to gastrointestinal bleeding (infection, electrolyte acid-base imbalance, hepatic encephalopathy, etc.), such as using third-generation cephalosporin antibiotics to prevent infection.
(3) Effectively control bleeding, monitor vital signs and urine output, and admit patients to the ICU if conditions permit.
2. Treatment of hepatic encephalopathy
(1) Rapid infusion of mannitol to reduce intracranial pressure.
(2) Patients can be given drugs to lower blood ammonia, such as ornithine aspartate, branched-chain amino acids, etc.
3. Treatment of sepsis and shock
(1) Injection of norepinephrine for anti-shock treatment.
(2) Administer vasoactive drugs to improve visceral organ perfusion and correct tissue ischemia and hypoxia.
(3) Use antibacterial drugs.
(4) Large doses of human albumin can be given.
General treatment
1. Patients in the compensated stage can participate in light work, while patients in the decompensated stage, especially those with complications, should rest in bed.
2. Patients should control their sodium and water intake, limiting sodium to 1.5-2.0g per day and water intake to about 1000ml per day.
For malnourished patients with cirrhosis, ensure adequate energy supply, avoid hypoglycemia, supplement with various vitamins, and administer plasma or albumin transfusions as appropriate. For patients with severe hepatic encephalopathy, abstain from protein for several days. Once the patient regains consciousness, gradually increase protein intake to the target amount based on the patient’s tolerance. Avoid prolonged hunger. It is recommended to eat small, frequent meals, 4 to 6 times daily, primarily consisting of plant protein.
Drug treatment
1. Anti-inflammatory and liver-protecting drugs
Such as glycyrrhizic acid preparations, bicyclol, polyene phosphatidylcholine, etc., which have anti-inflammatory, antioxidant, and liver cell membrane protection effects.
2. Diuretics
Spironolactone, furosemide, mannitol (such as Shuanghe Pharmaceutical’s mannitol injection), etc. can be used to treat ascites, but attention should be paid to monitoring electrolyte changes.
3. Drugs that lower portal pressure
Such as terlipressin, octreotide, etc., can reduce portal vein pressure, prevent and treat gastrointestinal bleeding.
4. Anti-infective drugs
Such as cefoperazone sulbactam, piperacillin-tazobactam, etc., are used to prevent and treat secondary infections.
5. Anti-hepatic encephalopathy drugs
Such as lactulose, rifaximin, etc., can promote ammonia metabolism and clearance, and alleviate the symptoms of hepatic encephalopathy.
Related drugs
Bicyclol, polyene phosphatidylcholine, spironolactone, furosemide, mannitol (such as Shuanghe Pharmaceutical’s mannitol injection), terlipressin, octreotide, cefoperazone-sulbactam, piperacillin-tazobactam, lactulose, rifaximin
Surgical treatment
1. Transjugular intrahepatic portosystemic shunt (TIPS)
(1) Indications: TIPS can slow down the progression of renal impairment from slowly progressive to rapidly progressive, and can also effectively treat splenomegaly with hypersplenism. Patients with massive bleeding and low success rate of endoscopic treatment should undergo TIPS within 72 hours.
(2) Principle of the operation: A special coated metal stent is placed between the intrahepatic portal vein branch and the hepatic vein to establish an intrahepatic portosystemic shunt and reduce portal vein pressure.
(3) Advantages: This procedure has the advantages of being minimally invasive, precise, repeatable, and long-term effective. It can effectively prolong the patient’s survival. Most patients do not need to restrict salt or water or use diuretics for a long time after surgery, and the patient acceptance is higher.
2. Liver transplantation
(1) Indications: Liver transplantation can be performed for patients with terminal cirrhosis, severe complications, and who are unable to be cured by drugs or other treatments.
(2) Principle of the operation: After the patient receives general anesthesia, the doctor makes an incision in the right upper abdomen, removes the diseased liver, and implants the new liver into the abdominal cavity. The doctor sutures the blood vessels and bile ducts, observes whether the blood supply is good, and finally sutures the incision.
(3) Advantages and Disadvantages: The advantage is that it can restore normal liver function. The disadvantages are high surgical costs, the need to wait for organ donation, and the need for long-term use of immune preparations after surgery.
Other treatments
1. Endoscopic treatment
(1) Indications: Simple esophageal varicose bleeding without gastric varices.
(2) Treatment principle: This is a local disconnection surgery. With the assistance of endoscope, the varicose veins are ligated with a rubber band, causing local ischemia and necrosis of the esophageal veins. Granulation tissue then proliferates, forming scars and closing the varicose veins.
2. Airbag compression hemostasis treatment
(1) Indications: Massive gastrointestinal bleeding that is ineffective with drug therapy and does not require endoscopy or TIPS.
(2) Therapeutic principle: A three-chamber, two-balloon tube is inserted through the nasal cavity, and air is injected into the gastric balloon. Pressure is applied outward to compress the gastric fundus. If bleeding fails to stop, air is injected into the esophageal balloon to compress the esophageal varicose veins. To prevent mucosal erosion, the compression should generally not exceed 24 hours. If bleeding persists after a period of deflation, this method can be repeated.
(3) Advantages and disadvantages: Balloon compression is effective in stopping bleeding temporarily, but it causes great pain to the patient and is associated with many complications, so it is not suitable for long-term use.
Treatment cycle
The treatment cycle is affected by factors such as the severity of the disease, treatment plan, treatment timing, age and physical condition, and may vary from person to person.
Treatment costs
The cost of treating cirrhosis of the liver may vary significantly from person to person, and the specific cost is related to the selected hospital, treatment plan, medical insurance policy, etc.
Prognosis
General prognosis
Liver function impairment in patients with cirrhosis cannot be reversed, and treatment can only control the progression of the disease. Patients with hematemesis, jaundice, infection, and ascites generally have a poor prognosis. Liver transplantation can reduce mortality, improve prognosis, and enhance quality of life.
Hazards
1. Cirrhosis may be complicated by hepatic encephalopathy, gastrointestinal bleeding, infection and hepatorenal syndrome. If not treated in time, it may lead to the death of the patient.
2. If cirrhosis of the liver progresses further, it may lead to primary liver cancer.
Self-healing
Cirrhosis generally does not heal on its own, and patients should actively seek treatment to avoid further development of the disease.
Curative
Active treatment of this disease can relieve symptoms and prolong the patient’s survival time.
Cure rate
The cure rate is low.
daily
Overview
Patients with cirrhosis should maintain a positive attitude in their daily lives, actively cooperate with treatment, quit smoking and drinking, and avoid taking medications that damage the liver. Furthermore, patients should have regular checkups so that their doctors can understand the effectiveness of treatment and adjust their treatment plans in a timely manner.
Psychological care
1. Psychological characteristics
Patients with cirrhosis often feel anxious, depressed and fearful due to the severity of their condition and poor prognosis, and worry that their condition will further deteriorate and affect their quality of life or even endanger their lives.
2. Nursing measures
(1) Family members should provide more guidance to patients, help them deal with the disease correctly, and enhance their confidence in overcoming the disease.
(2) Patients should actively participate in cultural and recreational activities and use appropriate methods to vent their negative emotions.
Medication care
Patients should strictly follow their doctor’s instructions when taking medication and avoid blindly or abusing medication to avoid increasing the burden on the liver. During medication, they should also pay attention to whether there are any gastrointestinal reactions such as abdominal pain, diarrhea, nausea, and vomiting.
Life Management
1. Maintain a regular work and rest schedule, get enough sleep, and avoid staying up late and overworking.
2. After the condition stabilizes, you can do moderate walking, Tai Chi and other low-intensity exercises to enhance your physical fitness.
3. Keep the room clean and tidy, well ventilated, and avoid moisture and mildew.
4. Pay attention to personal hygiene, take a bath and change clothes frequently to prevent infection.
Follow-up Instructions
Patients with cirrhosis should undergo medical follow-up every 3 to 6 months if their condition is stable, mainly reviewing liver function and ultrasound, CT and MRI.
diet
Dietary adjustment
Patients with cirrhosis should pay attention to dietary conditioning. A scientific and reasonable diet can ensure the normal functioning of the body’s functions, and play a role in assisting in controlling the disease, maintaining treatment effects, and promoting recovery from the disease.
Dietary recommendations
1. Patients with cirrhosis should supplement high-calorie foods to ensure sufficient glycogen reserves in the liver.
2. Patients can eat more high-protein foods such as soy products, eggs, milk, fish, chicken, lean pork, etc.
3. Patients with ascites should maintain a low-salt or salt-free diet.
4. To promote digestion, food should be cooked by steaming, boiling, stewing and braising as much as possible.
5. Patients with esophageal varices should eat soft food and chew slowly when eating to avoid upper gastrointestinal bleeding.
Dietary taboos
1. When the patient’s blood ammonia level is elevated, protein intake should be restricted or abstained from. After the condition improves, protein intake should be gradually increased, mainly with plant protein.
2. Patients should limit their sodium and water intake and avoid eating high-sodium foods, such as braised meat, pickles, soy sauce, canned food, sodium-containing MSG, etc.
3. Patients with esophageal varices should avoid eating foods with thorns, bones or hard foods to avoid upper gastrointestinal bleeding.
4. Patients with Wilson’s disease cirrhosis should avoid eating foods rich in copper, such as shellfish, nuts, mushrooms and animal offal.
5. Patients should be strictly prohibited from drinking alcohol, especially patients with alcoholic cirrhosis should be forced to abstain from alcohol.
prevention
Preventive measures
1. Actively treat primary liver diseases, such as alcoholic liver disease, viral hepatitis, etc.
2. Do appropriate exercise to enhance your physical fitness.
3. Maintain a healthy weight and prevent obesity.
4. Eat a diversified diet and regularly consume high-quality proteins such as soy products, fish and shrimp.
5. Reduce the intake of smoked and grilled foods, and avoid eating moldy and salty foods.
6. Quit smoking and drinking.
7. Try to reduce the use of unnecessary medications, such as various health products, to reduce the burden on the liver.
Medical Guide
Emergency (120) indications
1. Sudden vomiting of large amounts of blood.
2. Drowsiness, confusion, and hallucinations occur.
3. Other critical situations occur.
All of the above require urgent treatment. Go to the emergency department in time and call the emergency number 120 if necessary.
Outpatient indications
1. Frequent abdominal discomfort, loss of appetite, indigestion, diarrhea, etc.
2. Malnutrition, fatigue, jaundice, anemia, etc.
3. Other severe, persistent or progressive symptoms and signs occur.
All of the above require prompt medical consultation.
Treatment department
1. If the situation is critical and the symptoms are severe, please go to the emergency department immediately.
2. Patients with stable conditions can go to the hepatobiliary surgery or gastroenterology department for treatment.
Medical preparation
1. Make an appointment in advance and bring your ID card, medical insurance card, medical card, etc.
2. A comprehensive physical examination may be performed, and it is recommended that you wear clothing that is easy to put on and take off.
3. A blood test may be performed, and it is best to have the visit in the morning on an empty stomach.
4. If you have had medical treatment recently, please bring relevant medical records, examination reports, laboratory test results, etc.
5. If you have taken some medicine to relieve symptoms recently, you can bring the medicine box with you.
6. Family members can be arranged to accompany the patient to seek medical treatment.
7. Patients can prepare a list of questions they want to ask in advance.
Questions your doctor may ask
1. What is wrong with you? Where do you feel uncomfortable?
2. How long have you been feeling unwell? Are there any regular patterns in your symptoms? Has your discomfort worsened recently?
3. Are there any factors that make your uncomfortable symptoms worse or better?
4. Are you tired in your daily life? When you feel uncomfortable, does it get better after rest?
5. Do you have a history of liver disease? When was it diagnosed? How was it discovered?
6. How is your bowel movement recently? Do you have black stools?
7. What tests have you undergone? What were the results?
8. Have you ever been treated before? How was it treated? What was the effect?
9. Are you taking any medications for a long time?
10. Do you smoke or drink alcohol regularly? Do you drink a lot?
11. Do any of your family members have similar symptoms?
What questions can patients ask?
1. Is my condition serious? Is it definitely cirrhosis?
2. Why did I get cirrhosis?
3. Is this disease contagious?
4. What tests do I need to do?
5. What will happen if I don’t receive treatment?
6. How is it treated? How long does it take? Is it curable?
7. Are there any risks associated with these treatments?
8. What medications do I need to take? Are there any side effects? Do I need to take medication long-term?
9. Will it relapse if cured?
10. What should I pay attention to in my daily life? Should I stop smoking or drinking?
11. Do I need follow-up examinations? How often?