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The most common cause of ascites is cirrhosis of the liver. Liver cirrhosis is the cause in approximately 80% of patients with ascites. The increase in pressure due to cirrhosis (portal hypertension) in the veins (vena porta) that bring blood to the liver from the stomach, intestines, pancreas and spleen and the decrease in the serum level of albumin that cannot be adequately produced by the cirrhotic liver reduces the oncotic pressure and causes the water in the vein to escape into the abdominal cavity.
In addition, the increase in pressure in the intra-abdominal lymphatic vessels due to cirrhosis causes the leakage of lymph fluid from the liver surface and lymphatic vessels in the abdominal cavity into the abdominal cavity.
Another cause of acid formation is the accumulation of salt and water in the body that occurs after cirrhosis. The decrease in the effective blood volume circulating in the body and less blood flow to the kidneys due to cirrhosis cause some neurohormonal mechanisms to be activated, resulting in the kidneys to retain water and salt, and to collect fluid (ascites) in the body and the abdominal cavity.
Even without cirrhosis of the liver, ascites may develop as a result of occlusion of the veins (vena porta and hepatic vein) entering and leaving the liver. Occlusion of the vein that comes out of the liver is called Budd-Chiari syndrome.
In chronic kidney diseases, acid may develop due to both protein loss (albumin) from the kidneys and water and salt retention.
Edema in the legs and fluid in the abdominal cavity are also seen in patients with right heart failure and thickening of the heart membrane (constrictive pericarditis).
Ascites may develop in acute and chronic diseases of the pancreas, thyroid hormone deficiency (hypothyroidism), abdominal cavity infections (peritoneal tuberculosis, etc.) and cancers that spread to the abdominal cavity. Acid development is common in advanced stages of stomach, large intestine and ovarian (ovarian) cancers in women, and advanced lymphomas (tumors originating from lymph nodes). Cancer-associated acids are responsible for approximately 10% of all acids.
Classically, there are 2 types of acids; transudate and exudate. This classification is roughly based on the amount of protein and cells contained in the acid. A third, less common type of acid is the ‘chylous’ acid, which is white in color and has a milky appearance due to the high amount of fat in it. The most commonly used method to distinguish between transudate and exudate is to calculate the difference between serum and acid albumin.
This difference is called the serum-acid albumin gradient (SAAG). A SAAG >1.1 is considered a transudate, and less than 1.1 is considered an exudate. For example, if the patient’s serum albumin level is 3.5g/dl, and the acid albumin level is 1.5g/dl, the SAAG is 2g/dl.
In this case, the acid is ‘transudate’ since SAAG is >1,1. While the amount of fat in ascites increases in chylous acids, pancreatic enzymes such as amylase in ascites due to pancreatic diseases are high.
While transudate acid is seen in liver cirrhosis, non-cirrhotic portal hypertension (Budd-Chiari syndrome, etc.), heart failure and kidney failure, exudate acid is seen in cases of infection, intra-abdominal infections (such as tuberculosis), pancreatitis and tumors.
The number of cells in the ascitic fluid >400/mm3 or the number of polymorph nuclear leukocytes >200/mm3 indicates infection in the ascites. In this case, bacteria can grow in the sample taken from the acid.
When the acid accumulated in the abdominal cavity is more than 500 ml, it can be diagnosed by the doctor during the body examination. The presence of ascites that cannot be detected by examination can be detected by ultrasonography.
Even as little as 50 ml of acid can be detected by experienced hands in ultrasonography. When it is understood that a patient has ascites, the underlying cause must be understood. For this purpose, it may be necessary to use other biochemical tests, endoscopic examinations and advanced imaging methods and to take a sample from ascitic fluid.
When the underlying cause is known to be chronic liver, heart and kidney disease in a patient with ascites, it is generally not necessary to take a sample of ascitic fluid, except in some special cases. In some cases, the underlying cause may be difficult to understand. In this case, it is examined by taking a sample from the acid liquid. The process of taking a sample of ascitic fluid with a thin needle is called ‘diagnostic paracentesis’ (the process of taking some fluid from the abdomen for diagnostic purposes).
This procedure is usually painless. It is sufficient to take 20-30cc of acid to analyze the acid liquid. The taken liquid cell count is sent to the laboratory for biochemical and microbiological tests and cytopathological examinations. A larger amount of fluid may be required for pathological examination. In the biochemical examination, cell count, glucose, albumin, sodium, LDH (lactic dehydrogenase) and amylase are measured in ascitic fluid. Cytopathological examination is especially important in the investigation of tumor-associated ascites.
Ascites treatment differs according to the underlying disease. In cases such as liver cirrhosis, heart failure and kidney failure, improvement can be achieved by limiting salt and fluid intake in the diet and using diuretic drugs when necessary. Salt restriction is done by reducing the daily salt intake to 2 g. In a normal daily diet, 4g of salt per day is taken by eating normal bread by making the food completely salt-free.
If the bread is also unsalted, this amount decreases to about 2g. For this reason, both the food and the bread should be salt-free in the diet to be applied in acid treatment. Whether the patient adheres to a salt-free diet can be understood by measuring the amount of sodium excreted in the urine.
In some cases, a little more salt intake may be allowed, but this will be decided by the doctor monitoring the patient. In patients who cannot be adequately treated with salt restriction and bed rest, diuretic drugs are added to the treatment (Diuretics). The two most commonly used drugs for this purpose are ‘sprinolactone’ and ‘furosemide’. These two drugs can be used together when necessary.
The daily dose is 40-160mg in furosemide and 100-400mg in spironlactone. In patients with heart and kidney failure, the use of additional drugs and hemodialysis may be required.
Your doctor, who will evaluate your laboratory results and clinical findings, will decide which type of drug will be used in which dose. Diuretic drugs should be given in the morning to prevent the patient from waking up frequently during the night. The use of drugs in high doses can disrupt the fluid and electrolyte balance in the body, causing sometimes life-threatening changes in sodium, potassium, urea and creatinine levels. Patients with liver cirrhosis may experience impaired brain function (Hepatic encephalopathy).
For this reason, patients under diuretic therapy should be evaluated at regular intervals and such undesirable changes should be monitored. When an infection is detected in the ascitic fluid, the patient is treated with appropriate antibiotics. This condition is not uncommon in patients with ascites accompanying liver cirrhosis and is termed ‘spontaneous bacterial peritonitis’. The presence of infection in ascites reduces the response to diuretic therapy and can lead to renal failure, hepatic encephalopathy and septic shock if left untreated. It usually does not respond well to acid diuretic therapy due to infection and cancer.
The response to diet and diuretic therapy can be understood by measuring body weight. In an effective diuretic treatment, patients with ascites should lose at least 0.5 kg per day. In patients with edema in their legs with ascites, this loss should be 1 kg per day. Before changing treatment in treatment-resistant ascites, the patient’s compliance with treatment (salt-free diet and drug use) and whether there is an infection in ascites should be checked.
If a weight loss of 1 kg or more is not achieved within a week despite effective drug treatment, it is referred to as ‘treatment-resistant acid’. This is seen in approximately 15% of patients with liver cirrhosis and is an important finding that shortens life expectancy. In such cases, the patient is relieved by emptying 5-10L of acid at a time with paracentesis [Therapeutic (therapeutic) paracentesis, large volume paracentesis].
Especially in cancer-related ascites, this method is more effective than diuretic therapy and sometimes it may need to be done once a week. Since large volume paracentesis can cause low blood pressure, extreme fatigue, kidney failure and electrolyte disturbance in patients with cirrhosis, it should be performed in experienced clinics and under the supervision of a doctor.
TIPS (Transjugular intrahepatic portosystemic shunt) and liver transplantation are the other treatment modalities that can be applied in patients with liver cirrhosis who are resistant to treatment. The procedure performed in TIPS is to reach the hepatic vein by entering the veins in the neck and placing a stent passed through the liver between the hepatic vein and the portal vein (see Why does ascites occur?).
In this way, the portal pressure is reduced and the acid regresses rapidly. Stent occlusion and hepatic encephalopathy (impaired brain functions) are the most common side effects. TIPS is applied by experienced radiologists or gastroenterologists in a hospital environment and under sterile conditions.
Liver transplantation is the last option for patients with cirrhosis of the liver with refractory ascites (see Liver transplantation). Heart failure that does not respond to medical treatmente In appropriate cases, heart transplantation may be a solution in patients with associated ascites.
The prognosis in ascites varies according to the underlying cause. The development of ascites in a patient with liver cirrhosis indicates that the disease has progressed and the cirrhosis has become decompensated (see cirrhosis of the liver). 50% of these patients die within 3 years and 75% within 5 years. In the presence of heart disease, development of acid also has a poor prognosis, and the average life expectancy varies between 2-4 years in patients who receive appropriate treatment. Ascites due to cancer and other tumors has a poor prognosis and these patients usually die within months.
