hepatic ascites



OVERVIEW

Definition

Various liver diseases cause body fluids to enter the peritoneal cavity faster than the peritoneal membrane can absorb them, and free fluid accumulates in the peritoneal cavity, forming ascites.

Normally, only a small amount of plasma is present in the abdominal cavity for lubrication, not exceeding 200 ml.

In pathological conditions, there is an increase in the accumulation of fluid in the peritoneal cavity.

Classification

According to the nature of ascites, it is divided into leakage, exudative and mixed.

According to the etiology of ascites, it is divided into benign and malignant ascites.

Morbidity

Hepatic ascites, which accounts for approximately 75% of patients with ascites [1].

Questions you may be concerned about

What is the difference between a large stomach and a pot belly with hepatic ascites

The difference between hepatic ascites with a big belly and a big belly is that the morphology is different, the skin of the abdominal wall is different in different manifestations, and the causes and physical examination results are different.

1. Different morphology:

Hepatic ascites abdominal shape can change with the position changes, such as lying position when the ascites sink to the sides, can be manifested as the abdominal wall shape wide flat shape, called frog-like abdomen; sitting position or side lying position when the ascites move down, can be manifested as the lower part of the abdomen bulge; there are also umbilical protrusion of the performance.

The common large belly is diffusely distended, spherical or oval, with more subcutaneous fat in the abdominal wall and a concave umbilicus. Abdominal morphology has little to do with body position.

2. The skin of the abdominal wall behaves differently:

Hepatic ascites can be due to high intra-abdominal pressure, abdominal wall varicose veins, visible obvious dark blue blood vessels tortuous shape, from the umbilicus to the four sides of the extension of the sea serpent’s head; or visible subcutaneous hemorrhagic foci of small blood vessels, touching the fading, loosening is revealed, known as the spider nevus.

Ordinary belly abdominal wall skin smooth, no spider nevus, varicose veins and so on.

3. Different causes:

Hepatic ascites belly is due to liver lesions caused by abdominal fluid accumulation, most commonly seen in cirrhosis, but also seen in primary liver cancer metastatic peritoneal cancer and other cases.

Other cases of big belly can be seen in obesity, late pregnancy and nephrotic syndrome, heart failure and other conditions.

4. Physical examination results are different:

Hepatic ascites with a big belly feels hard on palpation, and there can be positive mobile turbid sound on percussion Other causes can be percussion drum sound or turbid sound.

Hepatic ascites macrosomia requires prompt medical attention and treatment as prescribed.

Can hepatic ascites be passed on to those who care for him?

Hepatic ascites is not contagious to those who care for it.

The mechanism that produces ascites is a decrease in albumin synthesis due to liver disease, which causes a decrease in the colloid osmotic pressure in the blood, and leakage of fluid from the blood vessels into the abdominal cavity and the interstitial spaces of the tissues, resulting in the formation of ascites. In addition, liver disease can also lead to obstruction of portal vein blood flow, portal vein pressure increases, causing fluid extravasation, but these extravasated fluids do not contain pathogens and are not infectious.

In addition, if the patient has cirrhosis due to hepatitis B, people who have not been vaccinated against hepatitis B or whose antibodies to the hepatitis B virus have disappeared from their bodies may become infected with the hepatitis B virus if they are in close contact with the patient or if they come into contact with the patient’s bodily fluids, but there is no relationship with hepatic ascites.

If the patient has hepatic ascites, it is recommended to consult a doctor in time to clarify the cause of the disease and targeted treatment under the guidance of the doctor, do not take medication on your own to avoid delaying the condition.

What is the difference between renal ascites and hepatic ascites?

The difference between renal ascites and hepatic ascites is mainly due to different causes, different manifestations and different treatment methods.

1. Different causes: renal ascites is mainly caused by glomerulonephritis, hypertensive nephropathy, diabetic nephropathy and other causes of renal insufficiency, renal failure, resulting in sodium and water retention; hepatic ascites is mainly due to the decline in liver function and cirrhosis caused by the formation of hepatic ascites.

2. Different performance: renal ascites can be accompanied by elevated blood pressure, abdominal pain and distension, nausea, vomiting, and symptoms of lumbago and leg weakness; hepatic ascites can be manifested as swelling of both lower limbs, jaundice, pain in the liver area and other symptoms.

3. Different treatments: renal ascites caused by nephritis can be treated by hormone shock, and albumin can be inputted for treatment if a serious drop in protein content is detected; hepatic ascites can be treated by intravenous input of albumin, and diuretics such as furosemide and spironolactone can also be used for treatment.

Patients with ascites need to go to the hospital in time to get a clear diagnosis and treatment plan, use drugs under the guidance of the doctor and avoid self-medication.

Causes

Causes

Hepatic ascites is common in viral hepatitis, cirrhosis and primary liver cancer. Cirrhosis is the most common cause of liver ascites. The various causes of liver ascites are as follows:

Chronic viral hepatitis

In China, hepatitis B is the main cause of cirrhosis.

Hepatitis C can also develop into cirrhosis if it continues to develop.

Cirrhosis of the liver

Cirrhosis is the most prominent cause of ascites.

Hepatic ascites is a common complication of cirrhosis, which occurs when patients with cirrhosis enter the decompensated phase.

Alcoholic Liver Disease

In recent years, the incidence of alcoholic liver disease has increased in China.

Due to long-term heavy drinking, intake of ethanol ≥40g/d for men and ≥20g/d for women for >5 years may cause alcoholic liver disease.

It includes alcoholic hepatitis, alcoholic fatty liver, alcoholic liver fibrosis, cirrhosis and liver cancer.

Autoimmune liver disease

Abnormal autoimmune response in which the body produces autoantibodies against liver cells.

Includes autoimmune hepatitis, primary biliary cirrhosis, and primary sclerosing cholangitis.

Drug induced liver disease

The incidence is increasing year by year with the increase in the number of new types of drugs.

Liver injury can be induced by chemicals, herbs, health products and hair dyes.

It may manifest as acute or chronic liver injury and progress to cirrhosis.

Circulatory disorders

Buga syndrome, cardiac insufficiency, constrictive pericarditis, leading to prolonged liver stasis and eventual development of liver fibrosis and cirrhosis.

Parasitic infection

Schistosoma haematobium, Schistosoma oryzae infection, parasitized in the liver, can gradually progress to cirrhosis.

Liver tumor

Malignant tumors in the liver, such as primary liver cancer and metastatic liver tumors, may present symptoms such as liver ascites, jaundice and anemia in the advanced stage.

Pathogenesis

The formation of ascites is the result of the loss of dynamic balance between the production and absorption of fluid in the abdominal cavity. Each disease leading to ascites can be caused by one mechanism alone or by the combined effect of multiple mechanisms.

Elevated hydrostatic pressure

Hydrostatic pressure is the pressure exerted on the walls of blood vessels by the fluid within them. When the pressure within the blood vessels becomes high, fluid tends to move from the blood vessels into the abdominal cavity, forming ascites.

Decreased plasma colloid osmotic pressure (hypoproteinemia)

The proteins in plasma have the function of “water locking” (that is, they play a role in maintaining the “colloid osmotic pressure”). When the protein concentration in plasma decreases, the plasma’s ability to “lock water” decreases, and water can easily escape from the blood vessels. When the protein concentration in plasma decreases, the ability of plasma to “lock up water” decreases, and water can easily “escape” from the blood vessels into the peritoneal cavity, forming ascites.

Peritoneal capillary permeability increases

The peritoneum has a strong ability to exchange substances, because there are many windows for substance exchange – capillaries – distributed on the peritoneum. However, this window can pass only a very small amount of “cargo”. In a disease state, these windows may open up, allowing fluids and certain substances to leak into the peritoneal cavity through them.

Lymphatic reflux or lymph node compression

The lymphatic system consists of lymphatic vessels and lymph nodes that are responsible for recycling excess fluid from the tissues. When the flow of lymphatic fluid is impeded, the fluid that cannot be recycled can build up in the abdominal cavity and form ascites.

Mixed

Many diseases are caused by a combination of the above mechanisms.

Questions you may be concerned about

Is it possible to wake up from a shallow coma caused by liver ascites?

Shallow coma due to hepatic ascites can usually be awakened.

Hepatic ascites is usually caused by cirrhosis or liver cancer, although the condition is quite complicated, but the condition of shallow coma caused by timely treatment can be improved, and the patient can gradually wake up.

Hepatic coma usually refers to hepatic encephalopathy, which can cause shallow coma when complex metabolic disorders occur. If the attack is acute, protein intake should be restricted as soon as possible. Lactulose enemas are administered, and ammonia elimination is promoted by the use of ornithine aspartate. For patients with primary diseases, such as cirrhosis and hepatocellular carcinoma, the primary disease should be treated as soon as possible.

When hepatic ascites causes shallow coma, hospitalization should be chosen, and targeted treatment and medication under the guidance of the doctor to avoid accidents.

Is it true that there are 3 signs of hepatic ascites?

There is no accurate reference value for the authenticity of the three signs of hepatic ascites. The appearance of hepatic ascites is generally characterized by abdominal distension and pain, abdominal distension, venous swelling of the lower extremities, and respiratory distress.

1. Abdominal distension and pain: when suffering from liver diseases, such as cirrhosis, liver cancer and other diseases, if there is a feeling of abdominal distension and pain, it is necessary to promptly check whether there is a sign of hepatic ascites or peritonitis.

2. Abdominal distension: If the patient has a history of liver disease and feels abdominal distension, obvious varicose veins in the abdomen, weight gain and other manifestations, it is necessary to check whether there is hepatic ascites in time.

3. Swelling of the lower limbs: after the emergence of hepatic ascites, especially a large amount of ascites will compress the lower limb veins, causing laparoscopic lower limb venous return obstruction, which can lead to swelling of the lower limbs.

4. Difficulty in breathing: when suffering from hepatic ascites, patients can have difficulty in breathing, chest tightness, panic and other symptoms when lying down.

If the above symptoms occur, it is recommended to go to the hospital in time to check the specific cause and treatment, so as not to delay the condition.

Can liver ascites cause swelling of the scrotum and penis?

Liver ascites can cause swelling of scrotum and penis.

Cirrhosis of liver failure will have ascites, scrotum and penis swelling is mainly due to hypoproteinemia, due to liver failure protein synthesis obstacle, blood colloid osmotic pressure drop caused by local tissue edema, mainly in the lower limbs, the involvement of the penis and scrotum is more serious, pay attention to supplemental nutrition, high-quality protein, low-salt and low-fat diet, supplemental human albumin if necessary.

In addition, if the presence of penile foreskin and scrotum inflammation can also cause edema, touching the allergens will also be edema, should be anti-inflammatory, anti-allergy, keep clean and hygienic.

If there is a case of hepatic ascites, timely medical treatment, by the doctor to identify the cause of the disease to clarify the diagnosis, individualized treatment, do not unauthorized use of medication, so as not to cause adverse consequences.

Symptoms

Main Symptoms

Ascites more than 1500ml before the obvious symptoms.

Abdominal distension

When standing and lying down, the appearance of the abdomen is different, shaped like a frog’s abdomen, or even with umbilical hernia.

Abdominal distension

Patients with ascites often have abdominal distension.

Gasping and Panic

A large amount of ascites forces the diaphragm upward, restricts movement, and affects respiration and circulation, which can lead to stridor, panic, and dyspnea.

Complications

Spontaneous peritonitis

Ascites is a good culture medium for bacteria, cirrhotic patients with ascites are prone to bacterial infection.

It may manifest as fever, abdominal pain, abdominal distension, persistent ascites, hepatic encephalopathy.

Hepatorenal syndrome

There is no substantial lesion of kidney, and functional renal failure occurs on the basis of liver dysfunction.

A large amount of ascites causes a significant increase in intra-abdominal pressure and a decrease in renal blood flow, resulting in hepatorenal syndrome. It manifests as small amount, anuria and azotemia.

Consultation

Department of Medicine

Gastroenterology

If you have a history of abdominal distension or bloating, especially if you have a history of liver disease or a history of drinking large amounts of alcohol over a long period of time, it is recommended that you consult a doctor promptly.

Hepatology

Patients with ascites caused by viral hepatitis, etc. may also consult the Department of Hepatology or the Department of Infectious Diseases.

Preparation

Consultation: Registration, Preparation of Documents, Frequently Asked Questions

Tips for medical treatment

Try to keep a record of symptoms, duration, and information about previous consultations and treatments, so that you can give your doctor more information.

Preparation Checklist

Symptom list

Pay particular attention to the time of onset of symptoms, special manifestations, etc.

Any bloating, abdominal pain, diarrhea, fever?

Is there any change in weight, urine output?

Any yellowing of the skin and sclera, red rash?

Any bleeding gums, nosebleeds, petechiae?

How long have the above symptoms lasted?

List of medical history

Any history of hepatitis B, hepatitis C, fatty liver? Has it been treated?

Do you drink alcohol? What strength of alcohol? Amount of alcohol consumed per day? Number of years?

Any history of blood transfusions, trauma, surgery?

Any family history of viral hepatitis, hereditary liver disease?

Any recent frequent hair coloring? Changed hair dyes?

Any prolonged exposure to chemicals, poisons at work?

Checklist

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

Laboratory tests: blood test, biochemistry, coagulation function, viral hepatitis markers.

Abdominal ultrasound, echocardiogram.

Medication list

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

Hepatoprotective drugs: e.g. compound glycyrrhizin, silymarin, etc.

Diuretics: e.g. aldosterone, furosemide, etc.

Antivirals: e.g. entecavir, interferon, etc.

Diagnosis

Diagnosis is based on

medical history

The following medical history may be present:

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

History of prolonged heavy alcohol consumption.

History of blood transfusions, trauma, and surgery.

Frequent hair coloring and recent change of hair dye.

Long-term exposure to chemicals and poisons at work.

Family history of viral hepatitis, hereditary liver disease.

Clinical manifestations

Symptoms

Bloating, abdominal rumbling, wheezing, panic.

Abdominal pain, diarrhea, fever.

Physical signs

Visual examination: abdominal distension, even with froggy belly and umbilical hernia.

Percussion: mobile turbidity (+) if the amount of ascites is greater than 1000 ml.

Laboratory tests

Blood routine

Detect red blood cells, hemoglobin, white blood cells, platelets, to find out whether there is a total blood cell reduction, anemia, and whether there is any co-infection.

Biochemistry

Detect liver enzymes, bilirubin level, creatinine, potassium and other indicators to understand the liver and kidney function and electrolytes are normal.

Coagulation function

To find out whether there is coagulation dysfunction, liver failure, thrombosis.

Hepatitis Virus Markers

Test for Hepatitis B two half pairs, Hepatitis C antibody, Hepatitis A antibody, Hepatitis E antibody to know whether there is hepatitis virus infection.

If the above antibodies are positive, check for hepatitis virus DNA/RNA to clarify whether it is a previous or current infection.

Ascites test

Ascites in cirrhosis is mostly leakage fluid, and can be exudate fluid when combined with infection or tumor.

The appearance, color, specific gravity, bacterial culture and histological culture of ascites can be used to know whether there is bacterial infection, whether there are cancer cells and the nature and type of ascites.

Routine tests for ascites include cell count, classification, quantification of albumin, total protein, and amylase.

Ascites cell count and classification are the primary indicators of ascites examination, and the total number of cells in ascites of cirrhosis without complications is <500 x 10 6 cells/L.

Ascites culture/smear, sugar, LDH, triglycerides, gram stain, decidual cells, bilirubin, etc. may also be examined.

Positive ascites ADA suggests the possibility of tuberculous peritonitis.

Pathologic detection of cancer cells in ascites helps in the diagnosis of neoplasia.

Cirrhotic ascites is considered if serum-ascites albumin gradient (SAAG) ≥11g/L and ascites protein <25g/L. If SAAG ≥11g/L and ascites protein ≥25g/L , consider cardiogenic portal hypertensive ascites.SAAG <llg/L, ascites caused by neoplastic and tuberculosis etc. should be considered.

Gastroscopy

Find out whether there is a serious complication of cirrhosis portal hypertension: esophagogastric fundus varices.

Liver histopathology

Liver histopathology is essential for the diagnosis of unexplained abnormal liver function.

Assess the degree of hepatocellular damage, degree of hepatic fibrosis.

Differential diagnosis

Hepatogenic ascites should be differentiated from cardiogenic, nephrogenic, and tuberculous ascites:

Cardiogenic ascites

Similarity: SAAG ≥ 11 g/L.

Points of difference:

Hepatogenic: total protein <25g/L; history of liver disease such as chronic viral hepatitis and alcoholic liver disease.

Cardiac origin: total protein >25g/L; history of heart disease such as heart failure, pericarditis, cardiomyopathy; echocardiography is helpful in determining cardiac function.

Nephrogenic ascites

Similarities: ascites, bilateral lower extremity edema, hypoproteinemia.

Points of difference:

Hepatogenic: SAAG ≥11 g/L, total protein <25 g/L; history of chronic liver disease.

Nephrogenic: history of renal disease such as nephritic syndrome and nephrotic syndrome; massive proteinuria with urinary protein ≥3.5 g/d; hyperlipidemia.

Tuberculous ascites

Similarities: may have symptoms such as ascites, abdominal distension, and fever.

Points of difference:

Hepatogenic: history of chronic liver disease; ascites is leaky, SAAG ≥11 g/L, total protein <25 g/L.

Tuberculous: history of old tuberculosis; ascites may be yellow-green in appearance, exudate, SAAG <11g/L, total protein >25g/L; adenosine deaminase (ADA) is markedly elevated.

Treatment

Therapeutic objectives: control ascites, improve symptoms, improve quality of life, prolong survival time.

Treatment principle: mainly for removing the cause of liver injury and drug symptomatic treatment. Now focus on the symptomatic treatment of ascites.

General treatment

Take sufficient rest and avoid exertion.

Eating too hard, too spicy, too hot food should be avoided.

High energy, high protein, high fiber, low salt (<4-6g/d) diet.

Avoid non-steroidal anti-inflammatory drugs such as ibuprofen and loxoprofen.

Avoid aminoglycoside antibiotics, e.g. streptomycin, gentamicin.

Diuretics

Aldosterone antagonists

Commonly used drugs: spironolactone.

Application: For those with initial moderate ascites, monotherapy is recommended. For recurrence of 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, amphotericin.

Therapeutic ascites release combined with albumin infusion

4000-5000 ml of ascites release and 20-40 g of albumin supplementation each time can effectively control persistent ascites and improve the patient’s prognosis.

It is not recommended to place drainage tubes in the abdominal cavity to release ascites to avoid infection.

Interventional therapy

Poor effect of diuretics and persistent ascites, early transjugular intrahepatic portosystemic shunt (TIPS).

Indications: recalcitrant ascites, frequent ascites release, transitional treatment for liver transplantation.

Contraindications: hepatic encephalopathy, cardiopulmonary disease, hepatic failure (bilirubin 5.8mg/dL or more), sepsis, advanced age over 70 years old Child-Pugh score of 12 or more.

Advantages: decreases portal pressure, increases renal perfusion, significantly reduces or eliminates peritoneal fluid.

Surgical treatment

Consider liver transplantation in patients with persistent ascites in cirrhosis.

Ascites Concentration Reinfusion

Cell-free ascites concentrate transfusion, a palliative approach to the treatment of recalcitrant ascites. Most patients will have fever.

Traditional Chinese Medicine (TCM)

Chinese medicine has unique theory and experience in the treatment of chronic liver disease, which can improve liver function in some patients, or even delay the progress of chronic liver disease. It is recommended to go to a regular medical institution and use the medication under the guidance of a Chinese medicine practitioner.

Proprietary Chinese medicines, such as Anluohua Fibrin Pill, Fuzheng Huayu Capsule, Soft Liver Tablet of turtle shell, are beneficial to improve cirrhosis and liver fibrosis.

Complications treatment

Spontaneous peritonitis (SBP)

About 1/3 of patients have typical manifestations, fever, abdominal pain, diarrhea, abdominal pressure and rebound pain.

Most patients present atypically, with recalcitrant ascites, shock, and hepatic encephalopathy suggestive of SBP.

Broad-spectrum, anti-Gram-negative & anaerobic, combination anti-infective regimen, tertiary cephalosporin antibiotics + anti-anaerobic antibiotics, e.g., cefepime + metronidazole, or, carbapenems + anti-anaerobic antibiotics, e.g., meropenem + ornidazole.

Rifaximin is not absorbed orally and acts locally in the gut to prevent recurrent SBP.

Hepatorenal syndrome (HRS)

Poor prognosis, divided into rapidly progressive type 1 and slowly progressive type 2.

HRS should be considered when patients with cirrhotic ascites have rapidly diminishing renal function, spontaneous peritonitis, massive diuresis, massive discharge of ascites, upper gastrointestinal bleeding, severe vomiting, diarrhea, and electrolyte disorders.

Once diagnosed, treat as early as possible to prevent further deterioration of renal function.

Terlipressin combined with albumin therapy. Discontinue non-selective beta-blockers, e.g. propranolol, carvedilol. Vasodilators are not recommended.

Type 1 HRS that does not respond well to medications can be treated with renal replacement therapy, artificial liver support system.

TIPS can be done for type 2 HRS that does not respond well to medications and has a large amount of ascites.

Liver transplantation should be prioritized for either type 1 or type 2 HRS.

Prognosis

Cure

The prognosis for hepatic ascites depends on the etiology.

Ascites appears more rapidly, often with an obvious trigger, and has a better prognosis.

Patients with cirrhosis have a poorer prognosis. The appearance of ascites in patients with cirrhosis represents entry into the decompensated phase, with a 1-year mortality rate of up to 20%.

With the recurrence of ascites, bleeding from esophagogastric fundus varices, hepatic encephalopathy, sepsis and other complications in the decompensated stage of cirrhosis, the patient’s death rate increases significantly, and the prognosis is very poor.

Harmfulness

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

Liver cirrhosis in the decompensated stage will also increase the risk of hepatocellular carcinoma and liver failure.

In the advanced stage of the disease, the risk of death increases due to systemic multi-organ dysfunction.

Daily

Daily Management

Dietary management

Eat easy-to-digest food, low-salt, high-calorie, high-protein and high-vitamin diet.

Avoid high protein diet when hepatic encephalopathy occurs.

Avoid raw, cold, hot, spicy and stimulating diet.

Life management

Quit smoking and drinking, avoid taking hepatotoxic drugs.

Avoid strenuous work, take sufficient rest and ensure enough sleep.

Keep warm and avoid infection.

Appropriate sports during the period of remission to enhance immunity.

Psychological support

Maintain a positive mindset, avoid anxiety, depression and other negative emotions.

Disease monitoring

Emphasize the treatment of primary disease, improve liver function, delay or reverse liver fibrosis and cirrhosis.

Cirrhosis patients need regular outpatient review or hospitalization to adjust the medication regimen.

Follow-up review

Long-term outpatient review allows the doctor to evaluate the condition and adjust the medication regimen.

Every 3 months for routine blood test, liver and kidney function, electrolytes, coagulation function.

Review of alpha-fetoprotein and abdominal ultrasound every 3-6 months to screen for primary liver cancer.

Review gastroscopy every 12 months to find out whether there is esophagogastric fundal varices and clarify its severity.

Prevention

Do not share razors and other invasive household items.

Stop smoking and drinking.

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

Pay attention to reasonable nutrition.

Avoid the application of drugs that can damage the liver.

Actively treat viral hepatitis, autoimmune liver disease and other primary diseases, delay the progress of liver disease, or even reverse liver fibrosis and cirrhosis, and prevent the emergence of hepatic ascites.