Ascites

Introduction to ascites Under normal conditions, there is a small amount of liquid (usually less than 200ml) in the abdominal cavity of the human body, which acts as a lubrication for intestinal peristalsis. Any pathological condition leads to an increase in the amount of fluid in the peritoneal cavity. When it exceeds 200 ml, it is called ascites. basic knowledge The proportion of illness: 0.005% Susceptible people: no special people. Mode of infection: non-infectious Complications: anemia, polyneuritis

Cause of ascites

Plasma colloid osmotic pressure decreased (25%):

Plasma colloid osmotic pressure is mainly maintained by albumin. Plasma albumin is less than 25g/L or accompanied by portal hypertension. Liquid easily leaks into the interstitial space and abdominal cavity from capillaries. If water leaks into the abdominal cavity, ascites is formed. Found in severe liver dysfunction, advanced cirrhosis (reduced protein synthesis), nutritional deficiencies (insufficient protein intake), nephrotic syndrome and protein-losing gastrointestinal disorders.

Sodium, water retention (30%):

Common in heart, renal insufficiency and advanced cirrhosis with secondary aldosteronism, liver cirrhosis and right heart failure, the activity of natriuretic factors is reduced, so that the renal proximal tubules increase sodium reabsorption, in recent years, it is considered The sodium reabsorption mechanism of tubules is more important than the action of aldosterone on distal convoluted tubules; cardiac insufficiency and advanced cirrhosis cause a large amount of ascites to reduce effective blood volume, stimulate volume receptors and glomerular devices; enhance sympathetic activity and activate renin - angiotensin-aldosterone system; increased release of vasopressin, decreased renal blood flow, decreased glomerular filtration rate, increased renal tubular resorption, promoted sodium, water retention, so that ascites continued to retreat, so the kidney Sodium, water retention is a persistent factor in ascites.

Endocrine disorders (15%):

When liver cirrhosis or hepatic insufficiency, liver degradation is reduced. On the one hand, the inactivation function of antidiuretic hormone and aldosterone reduces sodium and water retention; on the other hand, the concentration of some vasodilators in the blood circulation increases, and these substances cause Peripheral and visceral arteriolar resistance decreased, cardiac output increased, visceral was in a high-powered circulation state, due to splanchnic vascular bed dilatation, visceral congestion, resulting in insufficient circulating blood volume and hypotension, the body compensated release of angiotensin II and norepinephrine to maintain blood pressure, so that due to the reflective excitatory sympathetic nervous system release some vasoconstrictor substances, so that renal blood flow decreased, glomerular filtration rate decreased, coupled with the release of antidiuretic hormone, causing renal tubules Sodium, water back absorption increases, causing sodium, water retention and formation of ascites.

(1) Causes of the disease

Ascites is a manifestation of various diseases. According to its traits and characteristics, it is usually divided into three categories: leakage, exudation and blood. Common causes of leakage of ascites are: hepatogenic, cardiogenic, venous obstructive, renal source. Sex, nutritional deficiencies, chyle, etc.; common causes of exudative ascites are: spontaneous bacterial peritonitis, secondary peritonitis (including cancerous ascites), tuberculous peritonitis, pancreatic, biliary, chyle fungal Peritonitis, etc.; common causes of bloody ascites are: acute portal vein thrombosis, hepatocellular carcinoma nodules rupture, acute sub-macro hepatic necrosis, hepatic traumatic rupture, hepatic aneurysm rupture, ectopic pregnancy, etc.

(two) pathogenesis

The formation of ascites is the result of the loss of homeostasis in the production and absorption of fluid in the peritoneal cavity. The formation mechanism of ascites in each disease is caused by several factors combined or alone.

Local factors:

(1) Increased hydrostatic pressure: As the cirrhosis and external pressure of the portal vein or its own thrombosis, the pressure in the portal vein and its capillaries increases, which in turn causes ascites.

(2) Increased lymphatic flow, obstruction of reflux: due to portal vein and sinus pressure increased significantly in cirrhosis, subcapsular lymphatic vessels such as dead branches, absorption area shrinks, lymph growth increases, exceeding the ability of lymphatic circulation reabsorption, Causes lymphatic deposition, leakage from the lymphatic vessels through the peritoneal visceral or liver surface into the abdominal cavity, aggravating the accumulation of ascites, obstruction of the thoracic duct or chyle in the retroperitoneal tumor, mediastinal tumor, filariasis, etc., and rupture of the rupture The chyle leaks into the abdominal cavity to form chylorrhea ascites.

(3) increased peritoneal vascular permeability: peritoneal inflammation, cancer infiltration or perforation of organs, causing bile, pancreatic juice, gastric juice, blood stimulation, can promote the peritoneal vascular permeability increased ascites.

(4) abdominal visceral rupture: substantial or hollow organ rupture and perforation can cause pancreatic ascites, biliary ascites, bloody ascites and blood abdomen.

Ascites prevention

There is no effective preventive measure for this disease. Early detection and early diagnosis are the key to the prevention and treatment of this disease.

Ascites complications Complications anemia polyneuritis

Generally can be expressed as: poor nutritional status, weight loss, fatigue, cachexia, physical weakness, bedridden or dry skin, gray complexion dark and dark. There are often complications such as glossitis, polyneuritis and edema, such as cirrhosis and ascites, and may also cause anemia, nutrient deficiencies, intestinal absorption, spleen hyperactivity and gastrointestinal blood loss.

Ascites symptoms Common symptoms Diffuse drum sounds Lymph node enlargement Hepatosplenomegaly Peritonitis Abdominal tenderness Ascites Liver failure Esophageal peristalsis is weakened

Physical examination of ascites often has signs of primary disease in addition to mobile voiced sounds. Ascites caused by heart disease can be seen with cyanosis, peripheral edema, jugular vein engorgement, enlarged heart, tremor in the anterior region, and liver and spleen. Swollen, arrhythmia, heart valve murmur and other signs, liver disease often have dull or dull yellow, skin sclera yellow stain, face, neck or chest can have spider mites or liver palm, abdominal wall varicose veins, hepatosplenomegaly Major signs, ascites caused by kidney disease can be pale, surrounded by edema and other signs, flushing, fever, abdominal tenderness, abdominal wall with flexibility can consider tuberculous peritonitis, patients with weight loss, cachexia, swollen lymph nodes or abdominal mass Mostly malignant tumors.

Ascites examination

Laboratory tests are often an important means of finding the cause, liver function is impaired, hypoproteinemia may suggest cirrhosis, massive proteinuria, elevated blood urea nitrogen and creatinine suggest impaired renal function, immunological examination of liver and kidney The diagnosis of the disease is also important.

The nature of ascites and the cause of the identification of ascites can be determined by examination of the peritoneal puncture.

1. General inspection

(1) Appearance: Most of the leakage liquid is light yellow, thin and transparent, and the exudate can be different color or turbid. The ascites of different causes can have different appearances, such as purulent infection with yellow purulent or pus and blood; The ascites of the bacillus infection is green; the yellow sputum is yellow; the bloody ascites is found in acute tuberculous peritonitis, malignant tumor; the chyle ascites is milky white and self-coagulated, because it is a non-inflammatory product, it is still a leakage.

(2) Relative density: The relative density of the leakage liquid is more than 1.018; the relative density of the exudate is more than 1.018.

(3) Clot formation: The exudate contains fibrinogen and tissue, and the cell destroys the released thromboplastin, so it is easy to coagulate into a lump or floc.

2. Biochemical examination

(1) Qualitative test of mucin test: the leakage is negative; the exudate is positive, the quantitative, the leakage is less than 0.25g / L; the exudate is greater than 0.25g / L.

(2) Increased amylase in pancreatic ascites.

(3) bacteriological and histocytological examination: smear staining after ascites can be found in bacteria, acid-fast staining can be found in tuberculosis, if necessary, bacterial culture or animal inoculation, tumor cells can be examined in ascites, The diagnosis of abdominal tumors is very necessary, and its sensitivity and specificity can reach 90%.

3. Ultrasound and CT examination

Not only can show a small amount of ascites, but also the size of the liver, the smoothness of the liver capsule, the intrahepatic space-occupying lesions, the size of the heart, the structure, the inflow and outflow tract of the heart, the blood flow, and the size of the kidney. , form, structure, etc.

4. ECG examination

Changes in heart rhythm can be found, and blood supply to the heart.

Ascites diagnosis

Diagnostic criteria

The diagnosis of ascites is generally easier. The intra-abdominal effusion exceeds 500ml. The abdominal movement can be detected by percussion. When there is a lot of ascites, there can be fluid tremor. Less than 500ml of ascites can be detected by ultrasound and abdominal puncture. There is a dark area at the junction, the sensitivity of CT is not as good as ultrasound, causing leakage of ascites, and the common causes or diseases of exudative ascites (including chylorrhea ascites, bloody ascites) can be summarized as follows for reference or reference.

Leaky ascites

(1) Hepatic origin: common in severe viral hepatitis, toxic hepatitis, various types of cirrhosis, primary liver cancer and the like.

(2) Malnutrition: It is rare to see that long-term malnutrition patients often have lower plasma albumin, which can cause edema and leakage of ascites.

(3) Kidney-derived: seen in acute, chronic nephritis, renal failure, systemic lupus erythematosus and other connective tissue diseases.

(4) Cardiac: seen in chronic right heart dysfunction or constrictive pericarditis.

(5) Gastrointestinal origin: diseases mainly caused by various gastrointestinal diseases, such as intestinal tuberculosis, gastrointestinal Crohn's disease, malignant lymphoma, small intestinal lymphatic dilatation, congenital Intestinal lymphatic dysplasia, celiac disease in children and adults.

(6) venous obstruction: common in hepatic vein obstruction syndrome (Budd-Chiari Syndrome), inferior vena cava obstruction or compression, portal venous inflammation, portal vein obstruction, thrombosis or compression.

(7) mucus edema: seen in hypothyroidism, hypopituitarism caused by mucinous edema.

2. Exudative ascites

(1) peritoneal inflammation: common in tuberculous peritonitis, spontaneous bacterial peritonitis, acute infectious peritonitis caused by perforation of peritoneal organs, cancerous peritonitis (including peritoneal metastasis of abdominal or pelvic malignant tumors), fungal peritonitis, eosinophilic Cell invasive peritonitis and the like.

(2) Pancreatic origin: more common in acute necrotizing pancreatitis, pancreatic pseudocyst, chronic pancreatitis, pancreatic cancer, pancreatic duct dysplasia.

(3) biliary: more common in gallbladder perforation, bile duct rupture, gallbladder, bile duct surgery or bile duct puncture injury.

(4) chyle: the cause of chylorrhea ascites is more complicated, can be found in intra-abdominal or peritoneal infections (tuberculosis, filariasis), malignant tumors (such as lymphoma, gastric cancer, liver cancer), congenital intra-abdominal or intestinal lymphatics Dysplasia, lymphatic vessel dilatation or local compression, abdominal trauma or intra-abdominal iatrogenic injury and a small number of cirrhosis, portal vein thrombosis and nephrotic syndrome.

3. Bloody ascites

Although there are many causes of bloody ascites, there must be factors such as rupture of blood vessels or capillaries or increased osmotic pressure or coagulopathy, and blood can penetrate or leak into the abdominal cavity.

(1) Liver disease: severe hepatitis, fulminant hepatic failure, post-necrosis cirrhosis, advanced liver cancer (mainly coagulation mechanism, blood oozing from the surface of the liver capsule), hepatocellular carcinoma nodules ruptured, spontaneous during pregnancy Hepatic rupture, rupture of hepatic aneurysm, rupture of giant hepatic hemangioma and rupture of hepatic trauma.

(2) peritoneal disease: tuberculous peritonitis, peritoneal metastasis of malignant tumors in the abdominal or pelvic cavity, primary peritoneal mesothelioma, peritoneal or omental blood supply disorders.

(3) Other lesions in the abdominal cavity: such as abdominal aortic rupture, acute hemorrhagic necrotizing pancreatitis, traumatic or traumatic spleen rupture, other organ damage in the abdominal cavity, mesenteric artery or vein embolism or thrombosis, portal hypertension Empty, ileal varices, intra-abdominal lymphoma, primary spleen lymphoma, gastric cancer and colon cancer serous involvement, chronic nephritis, uremia.

(4) pelvic lesions: ectopic pregnancy, corpus luteum rupture, endometriosis, ovarian cancer or ovarian mucinous cystic carcinoma.

Differential diagnosis

1. huge ovarian cyst

Female patients should be differentiated from giant ovarian cysts. When the ovarian cysts are in the supine position, the abdomen bulges forward more obviously, slightly shifting upwards, and there are more drum sounds on both sides of the abdomen; the voiced sound of ovarian cysts is not mobile, the ruler pressure test: For ovarian cysts, the pulsation of the abdominal aorta can be transmitted to the hard scale through the cyst, showing rhythmic beats. If it is ascites, the hard foot is not beaten, and both vaginal and ultrasonography are helpful for identification.

2. Identification of leakage and exudate

3. Identification of benign and malignant ascites

There are many indicators for benign and malignant ascites, mainly ascites cytology, biochemistry, immunology and imaging, but all are non-specific indicators. In order to reduce and avoid misjudgment, comprehensive analysis and joint detection should be combined with clinical data. It is not appropriate to rely too much on an indicator. Gerbes believes that the diagnosis of good, malignant ascites is: the first step is to use higher sensitivity cholesterol as a screening to exclude benign ascites, cholesterol is significantly increased in malignant ascites, especially greater than 2.85 mol / L, the identification value is greater; the second step combined with high specific carcinoembryonic antigen (CEA), lactate deoxygenase (LDH), ascites ferritin (FA) content and cytology as a basis for diagnosis, ascites CEA> 15mg /L, ascites CEA/serum CEA>1; ascites LDH>1270U/L or ascites LDH/serum LDH>1.0, ascites FA>100g/L, ascites FA/serum FA>1, malignant ascites is likely, if ascites The diagnosis can be confirmed by finding the tumor cells; followed by imaging diagnosis to determine the location and extent of the lesion.

4. Tumor marker detection

In recent years, the detection of a variety of malignant tumor markers in blood and ascites has been widely carried out, which is of great significance for the identification of benign and malignant ascites. The commonly used markers are as follows.

(1) Carcinoembryonic antigen (CEA)-related cancer: colon cancer, gastric cancer, primary liver cancer, cervical cancer, ovarian cancer, breast cancer, pancreatic cancer, lung cancer, cholangiocarcinoma, liver metastatic adenocarcinoma, CEA is the first A characteristic marker of gastrointestinal adenocarcinoma.

(2) Alpha-fetoprotein (AFP)-related cancer: AFP is significantly increased in 70% to 80% of primary liver cancer, metastatic liver cancer, gastric cancer, gonad embryo, and primary liver cancer.

(3) Prostate cancer-associated antigen: PSA, FreePSA.

(4) Breast cancer-specific antigen: CA15-3 or BR.

(5) Ovarian cancer-specific antigen: CA12-5 or OV.

(6) Digestive tract tumors with multiple specific related antigens: CA19-9, CA24-2, CA50.

Combined detection of multiple tumor markers can increase the diagnostic positive rate.

5. Other ascites tumor markers studied in recent years

(1) Endotheliolysin (ET): ET is produced in vascular endothelial cells and has a strong and sustained vasoconstriction. In recent years, it has been found to have many extravascular functions: it is a cell mitogenic agent involved in cell growth and metabolism. It has certain influence on cell DNA synthesis, original gene expression and cell proliferation. ET-1 has been introduced into the field of oncology research abroad, and radioimmunoassay has confirmed that ET exists in tumor cells such as lung cancer, kidney cancer, breast cancer and pancreatic cancer. -1, it is generally believed that endothelin levels are significantly elevated in tuberculous and malignant ascites.

(2) Cadherin (Cad): Four types of Cad's allotype factors - E, N, P and L, have been found, while mutant E-cad is mainly expressed in diffuse gastric cancer, and Lymphatic metastasis of cancer cells, liver and peritoneal metastasis, hematogenous dissemination and prognosis of tumors were significantly correlated. It was found that the expression of mutant E-Cad in ascites-precipitated cells was detected by routine immunostaining, and the specificity of benign and malignant ascites was identified. Sex and sensitivity can reach 97% and 72%, respectively.

(3) Telomerase: Telomerase activation is a significant biological feature of malignant tumors. It is the fundamental difference between tumor cells and normal cells. The positive rate of telomerase in cancerous ascites is also significantly higher. A variety of benign ascites, the study found that the sensitivity and specificity of telomerase for the identification of benign and malignant ascites were 76% and 95.7%, respectively, but false positives can also occur.

(4) Vascular endothelial growth factor (VEGF): A large number of studies have shown that many tumor tissues have high expression of VEGF, such as breast cancer, brain tumor, kidney cancer, ovarian cancer, etc. The formation, development and metastasis are closely related. The increase of VEGF in serum can be detected in more than 60% of patients with tumor metastasis. The content of CEGF in 46% to 96% of malignant ascites specimens exceeds 675pg/ml.

(5) -chorionic gonadotropin (HCG): Chorionic gonadotropin is a glycoprotein hormone secreted by placental trophoblast cells, with two subunits and , which are determined by beta subunits. The specificity of hormones, so most of the detection of subunits, many malignant tumors can increase the HCG value, which identifies the sensitivity of benign and malignant ascites, specificity and accuracy can reach 61%, 94% and 83%.

(6) Polyamine detection: combined detection of spermatophore (SPD), cadaverine (CA) and total polyamine (TPA) in polyamines can better identify benign and malignant ascites, polyamines and Cell growth and proliferation are related to the regulation of intracellular DNA, RNA and protein biosynthesis. The content of polyamines in tumor tissues and body fluids is significantly increased in normal humans.

(7) IL-6, IL-2 (SIL-2R), TNF- combined detection: these three tumor markers can be increased in a variety of malignant ascites, domestic studies have shown that the combined detection of the three on the liver Sclerotherapy ascites with spontaneous peritonitis also has diagnostic value, so it can be used to identify cancerous ascites.

In summary, although some indicators can better identify benign and malignant ascites, so far, no detection method can achieve 100% accuracy, and some detection methods are difficult to promote clinical application, it should be emphasized Combined detection of multiple tumor markers can improve the accuracy of identification of ascites. Clinically, the diagnosis of malignant ascites should be combined with other methods such as imaging examination and pathological examination.

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