Ascites: Causes, Symptoms, Diagnosis, Treatment

Ascites are a condition in which a free fluid accumulates in the abdominal cavity. The most common cause is portal hypertension. The main symptom of ascites is an increase in the abdomen in size.

Diagnosis is established on the basis of physical examination, ultrasonography or CT. Treatment of ascites includes bed rest, a diet with limited sodium content, diuretics and therapeutic paracentesis. Ascetic fluid can become infected (spontaneous bacterial peritonitis), which is often accompanied by pain and fever. Diagnosis of ascites includes investigation and seeding of ascites fluid. Treatment of ascites is based on antibacterial therapy.

What causes ascites?

Typically, ascites serves as a manifestation of (portal) hypertension (> 90%) as a result of chronic liver disease, resulting in cirrhosis. Other causes of ascites are less common and include chronic hepatitis, severe alcoholic hepatitis without cirrhosis and obstruction of the hepatic veins (Badd-Chiari syndrome). Thrombosis of the portal vein usually does not cause ascites unless the hepatocellular structure of the liver is affected.

Extrahepatic causes of ascites include general fluid retention associated with systemic diseases (eg, heart failure, nephrotic syndrome, severe hypoalbuminemia, compressive pericarditis) and diseases of the abdominal cavity (for example, carcinomatosis or bacterial peritonitis, bile flow after surgery or other medical procedures). Rare causes include renal dialysis, pancreatitis, systemic lupus erythematosus and endocrine disorders (eg, myxedema).

Pathophysiology of ascites

The mechanism of development of ascites is complex and has not been fully studied. Known factors include the change in Stirling pressure in the portal vein vessels (low oncotic pressure due to hypoalbuminemia and elevated pressure in the portal vein), active retention of sodium by the kidneys (normal urinary sodium concentration <5 meq / l) and, possibly, increased lymphatic formation in the liver.

Mechanisms that affect the retention of sodium in the kidneys include the activation of the renin-angiotensin-aldosterone system; increased sympathetic tone; Intrarenal shunting of blood past the cortical layer; increased formation of nitric oxide; change in the production and exchange of antidiuretic hormone, kinin, prostaglandin and atrial natriuretic peptide. Expansion of the vessels of the visceral arterial blood flow may be a trigger mechanism, but the significance of these disorders and the relationship between them remain not completely understandable.

Spontaneous bacterial peritonitis (SBP) is associated with infection of ascites without an explicit source. Spontaneous bacterial peritonitis occurs usually with cirrhotic ascites, especially often in patients with alcohol dependence, and often leads to death. It can be the cause of severe complications and death. Most often, spontaneous bacterial peritonitis is caused by gram-negative bacteria Escherichia coli and Klebsiella pneumoniae, as well as Gram-positive Streptococcus pneumoniae; As a rule, only one microorganism is sown from the ascites fluid.

Symptoms of ascites

A small amount of ascites does not cause symptoms. A moderate amount leads to an increase in the volume of the stomach and body weight. A large amount leads to a nonspecific diffuse tension of the abdomen without pain syndrome. If as a result of ascites the diaphragm is depressed, dyspnea may be observed. Symptoms of spontaneous bacterial peritonitis can be supplemented by a feeling of discomfort in the abdomen and fever.

Objective signs of ascites include displacement of blunting with percussion of the stomach and fluctuation. The volume of liquid less than 1500 ml during a physical examination may not be diagnosed. Large ascites causes stress in the abdominal wall and protrusion of the navel. In liver diseases or peritoneal lesions, ascites is usually not associated with peripheral edema or is disproportionate to it; in systemic diseases (for example, heart failure), on the contrary, peripheral edema is more pronounced.

Symptoms of spontaneous bacterial peritonitis may include fever, malaise, encephalopathy, exacerbation of hepatic insufficiency, and unexplained clinical worsening. There are peritoneal signs of ascites (for example, abdominal tenderness in palpation and the Shchetkin-Blumberg symptom), but they can be smoothed due to the presence of ascites fluid.

Diagnosis of ascites

The diagnosis can be made on the basis of a physical examination in the case of a significant amount of fluid, but instrumental studies are more informative. Ultrasonography and CT can detect a much smaller volume of fluid (100-200 ml) compared with a physical examination. Suspicion of spontaneous bacterial peritonitis occurs when a patient with ascites has abdominal pain, fever, or unexplained worsening of the condition.

Diagnostic laparocentesis with dye is indicated in case if ascites is detected recently, its cause is unknown or there is a suspicion of spontaneous bacterial peritonitis. Approximately 50-100 ml of fluid is collected for macroscopic evaluation, protein content studies, cell counting and differentiation, for cytology, bacteriological culture, and, in the presence of clinical indications, for zil-Nielsen acid resistance stain and / or amylase test . In contrast to ascites, ascitic fluid with portal hypertension appears transparent and straw-yellow in inflammation or infection, has a low protein concentration (usually <3 g / dL, and sometimes> 4 g / dL), low PMN (<250 cells / μl), a higher serum albumin concentration gradient than ascitic fluid, which is determined by the difference between albumin concentration in serum and albumin concentration in ascites fluid (more informative). A gradient of more than 1.1 g / dL indicates that the most likely cause of ascites is portal hypertension. Mute ascites fluid and PMN number of more than 500 cells / μl indicate infection, whereas hemorrhagic fluid is usually a sign of a tumor or tuberculosis. Milk (chyle) ascites is rare and usually associated with lymphoma.

Clinical diagnosis of spontaneous bacterial peritonitis can be difficult; its verification requires a thorough examination and mandatory diagnostic laparocentesis, including bacteriological culture of the fluid. Bacteriological culture of blood is also shown. Sowing ascitic fluid on the blood culture before incubation increases sensitivity by almost 70%. Since spontaneous bacterial peritonitis is usually caused by a single microorganism, the detection of a mixed flora in bacteriological culture may suggest perforation of the hollow organ or contamination of the test material.

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Treatment of ascites

Bed rest and a diet with a limited sodium content (20-40 meq / day) are the main and least safe treatment for ascites in portal hypertension. Diuretics should be used if a strict sodium restriction does not lead to sufficient diuresis within a few days. Spironolactone is usually effective (orally on average 50-200 mg twice a day). In case of insufficient efficiency of spironolactone, a loop diuretic can be added (for example, furosemide 20-160 mg orally, usually once a day or on average 20-80 mg twice a day). Since spironolactone can cause potassium retention, and furosemide - its excessive excretion, a combination of these drugs often provides an optimal diuresis with little risk of hyper- or hypokalemia. The restriction of fluid intake is favorable, but only if the Na content in the serum is less than 130 meq / l. Changes in body weight and sodium content in the urine reflect the effectiveness of treatment. Optimal loss is approximately 0.5 kg per day, since the accumulation of ascites can not be more intense. More significant diuresis reduces the volume of intravascular fluid, especially in the absence of peripheral edema; it can cause kidney dysfunction or electrolyte imbalance (eg, hypokalemia), which can accelerate the development of portosystemic encephalopathy. Inadequate sodium restriction in food is usually the cause of permanently persistent ascites.

An alternative is a therapeutic laparocentesis. Removal of 4 liters of ascitic fluid per day is safe provided intravenous infusions of albumin with a low salt content (about 40 g in one procedure) to prevent fluid from escaping from the vascular bed. The therapeutic laparocentesis reduces hospital stay with a relatively small risk of developing electrolyte imbalance or impaired renal function; However, patients need further administration of diuretics, and this does not exclude the recurrence of ascites, and much faster than without laparocentesis.

The technique of autologous infusion of ascitic fluid (for example, the peritoneovenous shunt LeVeen) often leads to complications and, as a rule, is no longer used. Transyugulyarnoe intrahepatic portosystemic shunt ( transjugular intrahepatic portal-systemic Shunting, the TIPS) may reduce portal pressure and effectively resolve ascites resistant to other treatments, but involve significant risk and may lead to complications, including portosystemic encephalopathy and impairment of hepatocellular function.

If there is a suspicion of spontaneous bacterial peritonitis and more than 500 PMN / μl is found in the ascitic fluid, an antibiotic, eg cefotaxime, 2 g IV every 4 to 8 hours (Gram stain and bacteriological culture) should be prescribed for at least 5 days until the ascitic fluid is less than 250 PMN / μl. Antibiotics increase the likelihood of survival. Since spontaneous bacterial peritonitis recurs throughout the year in 70% of patients, antibiotic prophylaxis is indicated; the most widely used quinolones (eg, norfloxacin 400 mg / day orally). The prophylactic use of antibiotics in patients with ascites and bleeding from varicose veins reduces the risk of spontaneous bacterial peritonitis.