cirrhosis with ascites



Overview

Definition

Cirrhotic ascites is one of the most prominent clinical manifestations in the decompensated stage of cirrhosis. It is the increase of abdominal leakage fluid under the combined effect of hepatic decompensation and portal hypertension, and is aggravated by water and sodium retention, increased vascular permeability and other factors.

Its formation is closely related to the decrease of liver function synthesis, metabolism and detoxification ability caused by hepatocyte degeneration and necrosis, fibrosis, hypoalbuminemia, and impaired metabolism of vasoactive substances.

Classification

Classification according to the amount of ascites

Grade 1 (small amount) ascites

It can only be detected by ultrasonography, and the ultrasonography suggests that the depth of ascites is <3cm.

There is often no abdominal distension.

Mobile turbidities are negative.

Grade 2 (moderate amount) ascites

There is often moderate abdominal distention and symmetrical abdominal elevation.

Mobile turbidities are negative/positive.

Ultrasound suggests ascites flooding the bowel but not crossing the mid-abdomen at a depth of 3-10 cm.

Grade 3 (massive) ascites

Abdominal distension is evident, and there may be abdominal bulging or even umbilical hernia formation.

Mobile turbid sounds are positive.

Ultrasound suggests that ascites occupies the whole abdominal cavity with a depth of >10cm.

Morbidity

Ascites occurs in 5% to 10% of compensated cirrhosis every year and is an important sign of the progression of the natural course of cirrhosis.

The 1-year morbidity and mortality rate of those who develop cirrhotic ascites is about 15%, and the 5-year morbidity and mortality rate is about 44% to 85%.

Refractory ascites accounts for about 5% to 10%, with a poorer prognosis and a 6-month survival rate of about 50%.

Cirrhotic ascites with renal failure, oliguria or azotemia, 3-month morbidity and mortality rate of 50-70%.

Causes

Causes

Hepatitis virus infection

Common hepatitis B virus infection leads to viral hepatitis, due to the rapid progression of the disease or untimely treatment, the development of decompensated stage of viral hepatitis after cirrhosis, cirrhosis ascites.

Cholestasis

Stone, inflammation, drugs and other causes of cholestasis disease, long-term chronic effects of the development of cholestatic cirrhosis, into the decompensated stage of cirrhosis ascites can occur.

Circulatory disorders

Heart disease (e.g. chronic cardiac insufficiency), liver outflow tract obstruction, etc., make the liver cells long-term blood supply circulatory disorders, stagnation, prompting liver cell degeneration and necrosis, followed by the formation of hepatic fibrosis, development of cirrhosis, ascites.

Parasite infection

Adult worms and eggs of Schistosoma haematobium form fibrous nodules in liver cells, blocking the normal circulation of portal vein, long-term chronic obstruction and inflammatory reaction, which may progress to cirrhosis and ascites.

Long-term heavy drinking

Long-term chronic alcohol damage to liver cells, can lead to alcoholic cirrhosis, ascites in the decompensated stage.

Drug damage

Many drugs (such as antitumor drugs, cardiovascular disease drugs, certain proprietary Chinese medicines) can cause damage to liver cells, and long-term chronic damage can lead to drug cirrhosis, and in severe cases, it will progress to decompensated cirrhosis and ascites.

Genetic metabolism

Some hereditary diseases can cause connective tissue proliferation in liver, degeneration and necrosis of hepatocytes, such as copper metabolism disorder in hepatomegaly, excessive iron deposition in hemochromatosis, α1-antitrypsin deficiency leading to a large amount of α1-antitrypsin accumulation, etc., all of which will cause chronic damage to liver cells, leading to cirrhosis and ascites.

Pathogenesis

Portal hypertension

The main cause and initiating factor for the formation of ascites is portal hypertension.

Portal hypertension is the result of the development of cirrhosis to a certain stage.

Increased intra-abdominal pressure allows tissue fluid to leak into the abdominal cavity with reduced reabsorption.

Hypoalbuminemia

Leakage of intracapillary fluid into the peritoneal cavity or tissue interstitium is associated with decreased plasma colloid osmolality when serum protein is less than 30 g/L.

Increased activity of the renin-angiotensin-aldosterone system

This is the main cause of ascites formation and less likely to subside.

It may be characterized by decreased renal blood flow and decreased glomerular filtration rate.

Decreased sodium excretion and urinary output, and water and sodium retention may also occur.

Increased secretion or activity of other vasoactive substances

Such substances include atrial peptides, prostaglandins, and vasoactive peptides.

Resulting in sodium retention effects.

Obstruction of hepatic lymphatic return

Increased production of hepatic lymphatic fluid (increased intrahepatic sinusoidal pressure), which in turn leaks from the surface of the hepatic envelope into the abdominal cavity.

Coeliac ascites: associated with obstruction and rupture of the celiac duct.

Risk factors

All of the following factors are closely associated with an increased risk of developing cirrhotic ascites and are considered high risk factors:

Viral infections: e.g. hepatitis B virus infection.

Bacterial infections: e.g. Escherichia coli.

Alcoholism.

Cholestasis.

Immune disorders: e.g. autoimmune liver disease.

Inherited metabolic diseases: e.g. hepatomegaly.

Drugs: e.g. antitumor drugs, cardiovascular disease drugs, certain traditional Chinese medicines.

Parasites: e.g. schistosomiasis.

Symptoms

Early cirrhosis of the liver with small amount of ascites, often no obvious symptoms and signs, only in the physical examination of the abdomen ultrasound can be found.

In the late stage, with the progress of the disease, the amount of ascites gradually increases, and different degrees of symptoms and signs may appear.

Typical symptoms

Abdominal distension: the most typical symptom of cirrhosis ascites is abdominal distension.

Other symptoms

Umbilical hernia

Large amount of fluid in the abdominal cavity, which may lead to umbilical hernia in severe cases.

Dyspnea and palpitations

When the amount of fluid in the abdominal cavity is too large, the diaphragm moves upward and movement is restricted, compressing the lungs and heart, and dyspnea and palpitations occur.

Abdominal pain

Abdominal pressure and pain may be present when there is a large amount of ascites, and pressure or rebound pain, fever and diarrhea may be present when there is complication of peritonitis.

Systemic symptoms

In severe cases, there may be aggravation of existing symptoms, with weakness, loss of appetite, double lower limb edema, oliguria, hepatic encephalopathy, coagulation dysfunction, jaundice, shock and other manifestations.

Complications

In the process of cirrhosis ascites, complications are more closely related to life and health, which also increase the difficulty of treatment and the important link of prognosis.

Bleeding in digestive tract

The most life-threatening complication.

Pseudolobule formation leading to portal hypertension.

Reduced synthesis of hepatic coagulation factors leads to decreased coagulation function and predisposes to gastrointestinal bleeding.

Hypersplenism leads to thrombocytopenia and decreased coagulation function, predisposing to gastrointestinal bleeding.

Increased pressure in the abdominal cavity and increased pressure in the portal venous system predispose to acute esophagogastric fundic varices rupture and bleeding.

Spontaneous bacterial peritonitis

Not secondary to infection of abdominal organs.

Those with slow onset tend to have low-grade fever, abdominal distension, or persistent unabated peritoneal fluid.

Those with rapid progression have abdominal pain and rapid growth of peritoneal fluid.

In severe cases, hepatic encephalopathy and toxic shock are induced.

Pathogenic bacteria are mostly gram-negative bacilli.

Hepatorenal syndrome

Usually there is no substantial lesion in the kidney.

Manifested as oliguria, anuria, azotemia.

Caused by severe portal hypertension, inability of many vasodilating substances to be inactivated by the liver, and inadequate renal perfusion due to increased intra-abdominal pressure caused by large amounts of fluid in the abdominal cavity.

80% of those with the acute progressive form of hepatorenal syndrome die within approximately 2 weeks.

The slow-onset type often presents with refractory peritoneal effusion, progresses to hepatic failure, and then turns into the acute-onset type and dies under the influence of a causative agent.

Hepatopulmonary syndrome

Primary cardiopulmonary disease should first be excluded.

Hepatopulmonary syndrome occurs on the basis of cirrhosis.

It is characterized by dyspnea and signs of hypoxia (e.g., cyanosis, pestle fingers (toes)).

Severe hypoxemia (PaO2 less than 70 mmHg).

Those who develop hepatopulmonary syndrome have a poor prognosis.

Hepatic encephalopathy

Hepatic encephalopathy usually has a basis of severe liver disease and obvious triggers.

Liver function indexes are obviously abnormal and blood ammonia is increased.

Psychiatric symptoms are prominent.

Hyponatremia

Hyponatremia is associated with prolonged inadequate sodium intake, massive diuresis, massive ascites release, and secondary aldosteronism.

Hyponatremia usually has a poor prognosis.

Consultation

Department of Medicine

Gastroenterology

Patients with cirrhosis are advised to consult the doctor promptly when they notice symptoms such as abdominal distension, bloating, bilateral lower extremity edema, or when their existing symptoms worsen.

Emergency Department

Cirrhosis patients are advised to consult the doctor promptly when they have symptoms such as obvious abdominal distension, dyspnea and palpitation.

Preparation for medical treatment

Consultation: Registration, Preparation of documents, Frequently asked questions

Tips for Consultation

Avoid eating before the visit so that you can have an examination on an empty stomach.

Bring along previous examination reports or medical records.

Keep a record of your daily intake of food, water and urine.

Preparation Checklist

Symptom Checklist

Particular attention needs to be paid to the time of onset of symptoms, special manifestations, etc.

How long has the bloating lasted?

Is there dyspnea or panic?

Is there any yellowing of the skin?

Is there vomiting of blood, black stools?

How is the diet and bowel movements?

Medical History Checklist

Does anyone in the family have hepatitis, cirrhosis, or liver cancer?

Is there a history of heavy alcohol consumption?

Is there any history of drug abuse, drug addiction?

Has there been any treatment for hepatoprotection or ascites release?

Checklist

Test results in the past six months, which can be brought to the doctor’s office

Blood test: liver function, kidney function, blood routine, coagulation function, viral hepatitis index.

Imaging tests: chest X-ray, abdominal ultrasound or CT or MRI.

Medication list

Test results in the last six months, which can be carried to the doctor

Hepatoprotective drugs: compound glycyrrhizin, silymarin, etc.

Diuretics: spironolactone, furosemide, etc.

Antiviral drugs: entecavir, tenofovir, interferon, etc.

Diagnosis

Diagnosis is based on

Medical history

History of heavy drinking, history of taking special drugs, etc.

History of hepatitis, cirrhosis, etc.

Clinical manifestations

Symptoms

Recent onset of fatigue, loss of appetite or aggravation of existing symptoms.

Recent abdominal distension, bilateral lower extremity edema, decreased urine output.

Physical signs

Abdominal examination: abdominal distension in the form of frog-like abdomen, no mass, visible abdominal wall varicose veins.

Positive mobile turbidity suggests that the volume of abdominal fluid is >1000 ml, and negative cannot be excluded.

Skin and mucous membrane examination: yellow staining of skin and mucous membrane, spider nevus are seen.

Laboratory examination

Blood routine: to know whether there is anemia, infection, whether there is hypersplenism.

Liver function: to know the degree of elevation of liver enzymes, whether there is a decrease in albumin.

Electrolytes: to know whether there are electrolyte disorders, acid-base imbalance.

Coagulation function: to know whether there is prolongation of coagulation time.

Ascites biochemistry, microbial culture, cytologic analysis: to determine whether the ascites is leaking and whether there is infection.

Imaging examination

Abdominal ultrasound

It is a relatively simple and inexpensive non-invasive auxiliary diagnostic method.

It can observe the amount of ascites, the location of ascites, whether the liver and spleen have normal morphology, and locate for abdominal puncture.

Chest X-ray

It can observe whether the diaphragm is elevated, whether the heart boundary is normal, and whether there is pleural effusion.

CT or MRI examination

It can determine the amount of ascites, liver and spleen size more accurately.

It can be used in differential diagnosis with abdominal masses.

It can be used for differential diagnosis when progression to hepatocellular carcinoma is suspected.

Differential diagnosis

Tuberculous peritonitis

Similarities: both have an accumulation of fluid in the abdominal cavity.

Differences: Tuberculous peritonitis is characterized by low-grade fever, night sweats, and a history of tuberculosis or family history. Tuberculosis tests and cultures can be used to differentiate.

Intra-abdominal tumor

Similarity: both have abdominal distension and may have abdominal effusion.

Differences: abdominal tumors can be palpable as a mass in the abdomen, and there may be different degrees of fixed abdominal pain, accompanied by symptoms such as emaciation and anemia. Abdominal CT or MRI, tumor markers can be used for differential diagnosis.

Nephrotic syndrome

Similarity: both have the manifestation of abdominal fluid.

Differences: Nephrotic syndrome may have symptoms such as large amount of proteinuria, edema, abdominal distension and fatigue. Urine routine, urine protein quantification, blood lipids, blood biochemical examination to identify, if necessary, feasible renal puncture biopsy to clarify.

Constrictive pericarditis

Similarity: patients have a large amount of abdominal fluid, dyspnea.

Differences: constrictive pericarditis mainly manifests as dyspnea after exertion, abdominal effusion occurs later, and there are also symptoms such as lower limb edema and cough. Chest X-ray, cardiac ultrasound, cardiac CT and MRI can be differentiated.

Giant ovarian cyst

Similarities: The patient has a bulging abdomen and fluid in the abdominal cavity.

Differences: Giant ovarian cysts mostly occur in women of reproductive age, with unilateral abdominal pain, lower abdominal pressure, pain during sexual intercourse and lumbosacral pain. Perform pelvic ultrasound or CT and MRI, tumor markers, blood HCG and other tests can be differentiated.

Treatment

Treatment principle: According to the age, symptoms, complications and the etiology, degree of progress and prognosis of cirrhotic ascites of individuals, reasonable salt restriction (4-6g/d), application of diuretics, discharge of ascites and surgical treatment are used.

Aim of treatment: to improve clinical symptoms, enhance quality of life and prolong survival time.

General treatment

Limit sodium intake

Sodium chloride intake should be 4～6g/d.

Limit protein intake

High-quality protein is the mainstay, with a daily intake of 1～1.2g/kg.

In obvious hepatic encephalopathy, protein intake should be limited to 0.5g/kg per day.

Avoid medication

Avoid drugs that increase the burden on the liver and impair liver function, such as nonsteroidal anti-inflammatory drugs, angiotensin-converting enzyme inhibitors, angiotensin II receptor antagonists, α1-adrenergic blockers and dipyridamole, aminoglycoside antibiotics, and contrast agents.

Medication

Diuretics

To avoid inducing hepatic encephalopathy, hepatorenal syndrome, etc., the rate of diuresis should not be too fast. Theoretically, long-term use is required.

Aldosterone antagonist

Commonly used drugs: spironolactone.

Application: For those with initial moderate ascites, monotherapy is recommended. For recurrent severe ascites, combination with furosemide is recommended.

Adverse effects: hyperkalemia, menstrual disorders in women, gynecomastia and distension.

Diuretics with tabs

Commonly used drugs: furosemide.

Application: often combined with spironolactone for better efficacy.

Adverse effects: postural hypotension, cardiac arrhythmia, low potassium and sodium.

Highly selective vasopressin 2 receptor antagonist

Commonly used drugs: tolvaptan.

Contraindications: hypovolemic hyponatremia.

Adverse effects: renal failure, thirst, hypernatremia.

Others

e.g. hydrochlorothiazide, amiloride hydrochloride, aminopterin.

Vasoconstrictor-activated drugs

Commonly used drugs: Terlipressin.

Contraindications: pregnant women and uncontrolled hypertension, ischemic cardiovascular disease, etc.

Advantages: Combined with human albumin can prevent circulatory disorders and hepatorenal syndrome.

Adverse effects: abdominal cramps, increased stool frequency, headache, increased arterial pressure, etc.

Human albumin and fresh plasma

Indications: when diuretics are ineffective, after large amounts of ascites are released, hypoalbuminemia.

Advantages: It has the effect of reducing the incidence of renal failure, the rate of death during hospitalization, fresh plasma helps to improve the coagulation function.

Antibiotics

Indications: spontaneous bacterial peritonitis and other infections.

Commonly used drugs: cephalosporins, nitroimidazoles.

Application: empirical medication along with early ascites culture to look for sensitive bacteria.

Crystalline solution

Such as sodium chloride solution

Indications: severe hyponatremia (blood sodium <110mmol/L) or the presence of hyponatremic encephalopathy.

Surgical treatment

Usually use peritoneal puncture to drain ascites, transjugular intrahepatic portosystemic shunt (TIPS), ultrafiltration of ascites to concentrate and refill, and renal replacement therapy.

Liver transplantation

For liver failure (Child-Pugh class C), severe cirrhosis combined with recalcitrant ascites.

Prognosis

Cure

If ascites can be detected in time and treated correctly, and if cirrhosis is not serious, ascites can subside quickly and the prognosis is good.

If cirrhosis has progressed to liver failure with jaundice, coagulation disorders, gastrointestinal bleeding or hepatic encephalopathy, the prognosis is worse.

Hazards

Poorly controlled disease may affect normal life and work due to severe abdominal distension, dyspnea, and fatigue.

Uncompensated cirrhosis also increases the risk of liver cancer and liver failure.

The advanced stage of the disease increases the risk of death due to systemic multi-organ dysfunction and severe infections.

Daily

Daily Management

Dietary management

Focus on food types that are easy to digest, produce less gas, and are less irritating.

Moderate intake of high quality protein amount, reduce the intake of high fat food.

Balance nutrition and eat fresh vegetables and fruits.

Eat a light diet that is not too spicy.

Eat a low-salt diet, do not add extra salt when cooking and avoid processed foods.

Strict prohibition of alcohol.

Hygiene Management

The living room should be ventilated.

Practice good personal hygiene.

Avoid cold and unclean food.

Exercise management

Do not engage in heavy physical activities and intense physical exercise.

Rest in bed more often.

Psychological support

Maintain emotional stability and reduce psychological pressure.

Receive health education to understand the knowledge of cirrhosis with peritoneal effusion, correct the wrong perception of the disease and enhance the confidence in treatment.

If you are emotionally unstable, lost, etc., talk to your friends and relatives in time, or seek help from medical personnel, and if necessary, have psychological counseling to avoid affecting the treatment.

Follow-up and review

During treatment and after discharge from the hospital, regular follow-ups will be conducted to observe the treatment effect and monitor the changes of the condition, so that life-threatening situations can be detected in time.

If the condition is stable, biochemistry, blood routine, coagulation function, alpha-fetoprotein and abdominal ultrasound should be rechecked every 3 months.

For those with esophagogastric fundal varices, gastroscopy should be repeated every 12 months.

Prevention

Do not share razors and other invasive household items.

Abstain from smoking and alcohol.

Newborns and high-risk groups should be vaccinated against hepatitis B. Patients with hepatitis B should be given aggressive antiviral drug treatment.

Pay attention to reasonable nutrition.

Avoid the application of drugs that are harmful to the liver.

Strengthen labor health care and avoid all kinds of chronic chemical poisoning in industrial and agricultural production.

Regular physical examination.