Ascites is a buildup of abnormal fluid in the abdomen. Technically, it's more than 25 mL of fluid in the peritoneal cavity. Symptoms may include increased abdominal size, weight gain, abdominal discomfort, and shortness of breath. Complications may include spontaneous bacterial peritonitis.
In developed countries, the most common cause is cirrhosis of the liver. Other causes include cancer, heart failure, tuberculosis, pancreatitis, and blockage of hepatic veins. In cirrhosis, the underlying mechanism involves high blood pressure in the portal system and vascular dysfunction. Diagnosis is usually based on joint examination with ultrasound or CT scan. Liquid testing can help in determining the underlying cause.
Treatment often involves a low-salt diet, drugs such as diuretics, and fluid drainage. Transjugular intrahepatic portosystemic shunt (TIPS) can be placed but associated with complications. Effects to treat underlying causes, such as with liver transplantation can be considered. Of those with cirrhosis, more than half developed ascites within ten years after diagnosis. Once ascites has grown in this group, the average life expectancy is less than three years. The term is derived from the Greek askÃÆ'tes which means "baglike".
Video Ascites
Signs and symptoms
Thin ascites are difficult to notice, but severe ascites cause abdominal distension. Patients with ascites will generally complain of progressive weight and pressure of the abdomen and shortness of breath due to mechanical impingement on the diaphragm.
Ascites are detected on physical examination of the abdomen by visible prominence of the pelvis in lying patients ("bulging flank"), "dull shift" (differences in percussion records in the pelvis that shift when the patient is turned on the side) or in massive ascites with "fluid sensation" or "liquid waves" (tapping or pushing on one side will produce wave-like effects through fluid that can be felt on the opposite side of the stomach).
Other signs of ascites may be present due to underlying causes. For example, in portal hypertension (possibly due to cirrhosis or liver fibrosis) patients may also complain of leg swelling, bruising, gynecomastia, hematemesis, or mental changes due to encephalopathy. Those with ascites due to cancer (peritoneal carcinomatosis) may complain of chronic fatigue or weight loss. Those with ascites due to heart failure may also complain of shortness of breath as well as wheezing and intolerance.
Maps Ascites
Cause
The cause of high serum-asites (SAAG or transudate) glucose levels is:
- Cirrhosis - 81% (alcoholic 65%, viral in 10%, cryptogenic in 6%)
- Heart failure - 3%
- Hepatic vein occlusion: Budd-Chiari syndrome or veno-specific illness
- Constructive pericarditis
- Kwashiorkor (malnutrition of childhood protein)
The cause of low SAAG ("exudate") is:
- Cancer (primary peritoneal metastasis and carcinomatosis) - 10%
- Infection: Tuberculosis - 2% or spontaneous bacterial peritonitis
- Pancreatitis - 1%
- Serositis
- Nephrotic Syndrome
- Hereditary angioedema
Penyebab langka lainnya:
- Meigs syndrome
- Vasculitis
- Hypothyroidism
- Dialisis ginjal
- Peritoneum Mesothelioma
- Tuberculosis cancellation
- Mastositosis
- Level 1: light, seen only on ultrasound and CT
- Class 2: can be detected with bumps on the sides and shifts shift
- Level 3: instantly visible, confirmed by fluid wave/vibration test
Diagnosis
Complete blood count routine (CBC), basic metabolic profile, liver enzymes, and coagulation should be performed. Most experts recommend diagnostic paracentesis is done if new ascites or if patients with ascites are being hospitalized. The fluid is then reviewed for dirty appearance, protein level, albumin, and cell count (red and white). Additional tests will be performed if indicated such as microbiological culture, Gram staining and cytopathology.
The serum-ascites albumin gradient (SAAG) may be a better discriminant than the older size (transudate versus exudate) for the cause of ascites. A high gradient (& gt; 1.1 g/dL) indicates ascites are due to portal hypertension. A low gradient (& lt; 1.1 g/dL) shows ascites of non-portal hypertension as the cause.
Ultrasound investigation is often performed before attempting to remove fluid from the stomach. This may reveal the size and shape of the abdominal organs, and the Doppler study may show the direction of flow in the portal vein, as well as detect Budd-Chiari syndrome (venous hepatic thrombosis) and portal vein thrombosis. In addition, the sonographer can make an estimate of the amount of ascitic fluid, and hard-to-drain ascites can be dried under ultrasound guidance. Stomach CT scan is a more accurate alternative to reveal abdominal organ structures and morphology.
Classification
Ascites exist in three classes:
Pathophysiology
Acetic liquids can accumulate as transudates or exudates. Amount up to 35 liters possible.
Roughly speaking, transudates are the result of increased pressure in the hepatic portal vein (& gt; 8 mmHg, usually about 20 mmHg), for example. because of cirrhosis, while the exudate actively secretes fluid due to inflammation or malignancy. As a result, the exudate is high in protein and dehydrogenase lactate and has a low pH (& lt; 7.30), low glucose levels, and more white blood cells. Transudates have low protein (& lt; 30 g/L), low LDH, high pH, ​​normal glucose, and less than 1 white blood cell per 1000 mm. Clinically, the most useful measure is the difference between serum albumin and ascitic concentration. A difference of less than 1 g/dl (10 g/L) implies exudates.
Portal hypertension plays an important role in ascites production by increasing the capillary hydrostatic pressure in splanchnic beds.
Regardless of the cause, fluid sequestration in the stomach causes additional fluid retention by the kidneys because of the stimulating effects of blood pressure hormones, especially aldosterone. The sympathetic nervous system is also activated, and renin production is increased due to decreased renal perfusion. Extreme disturbance of renal blood flow can cause hepatorenal syndrome. Other complications of ascites include spontaneous bacterial peritonitis (SBP), due to declining antibacterial factors in ascitic fluids such as complement.
Treatment
Ascites are generally treated while underlying causes are sought, to prevent complications, reduce symptoms, and prevent further progression. In patients with mild ascites, therapy is usually performed outpatient. The goal is a weight loss of no more than 1.0 kg/day for patients with ascites and peripheral edema and no more than 0.5 kg/day for patients with ascites alone. In those with severe ascites that cause a tense stomach, hospitalization is generally required for paracentesis.
Treatments in high SAAG ("transudate") are:
Diet
Salt restriction is the initial treatment, which allows diuresis (urine production) because patients now have more fluids than salt concentrations. Effective salt restriction in about 15% of patients. Water restriction is required if serum sodium levels fall below 130 mm L -1 .
Diuretic
Because salt restriction is a basic concept in medicine, and aldosterone is one of the hormones that act to increase salt retention, drugs that fight aldosterone should be sought. Spironolactone (or other distal-tubular diuretics such as triamterene or amiloride) is the drug of choice because they block aldosterone receptors in the collecting tubules. This choice has been confirmed in a randomized controlled trial. Diuretics for ascites should be administered once per day. Generally, the initial dose is oral spironolactone 100 mg/day (maximum 400 mg/day). 40% of patients will respond to spironolactone. For nonresponders, loop diuretics may also be added and generally, furosemide is added at a dose of 40 mg/day (maximum 160 mg/day), or alternatively (bumetanide or torasemide). The ratio of 100: 40 reduces the risk of potassium imbalance. Serum potassium levels and renal function should be closely monitored when using these drugs.
Diuresis monitoring : Diuresis can be monitored by weighing patients daily. The goal is a weight loss of no more than 1.0 kg/day for patients with ascites and peripheral edema and no more than 0.5 kg/day for patients with ascites alone. If daily weight can not be obtained, diuretics can also be guided by urinary sodium concentrations. The dose is increased until a negative sodium balance occurs. Sodium-to-potassium ratio of random urine & gt; 1 is 90% sensitivity in predicting negative balance (& gt; 78-mmol/day of sodium excretion).
Diuretic resistance : Diuretic durability can be predicted by intravenous furosemide of 80 mg after 3 days without diuretics and on 80 mEq sodium/day diet. Urinary excretion of sodium over 8 hours & lt; 50 mEq/8 hours predict resistance.
If the patient shows poor resistance or response to diuretic therapy, ultrafiltration or aquapheresis may be necessary to achieve adequate fluid retention and congestion control. The use of mechanical methods such as fluid removal may yield significant clinical benefits in patients with diuretic resistance and may restore response to conventional diuretic doses.
Paracentesis
In those with severe (tense) ascites, paracentesis therapy may be required in addition to the medical care listed above. Because this can deplete the serum level of albumin in the blood, albumin is generally given intravenously according to the amount of ascites released.
Surgery
Refractory ascites to medical therapy are considered an indication for liver transplantation. In the United States, MELD scores (online calculators) are used to prioritize patients for transplantation.
In a small proportion of people with advanced cirrhosis who have recurrent ascites, shunt may be used. Typical shunts used are portacaval shunts, peritoneovenous shunts, and transjugular intrahepatic portosystemic shunts (TIPS). However, none of these shunts has been shown to prolong life expectancy, and is considered a bridge for liver transplantation. A meta-analysis of randomized controlled trials by the international Cochrane Collaboration concluded that "TIPS are more effective at removing ascites compared to paracentesis... however, TIPS patients develop hepatic encephalopathy significantly more frequently".
Low SAAG
Exudative ascites generally do not respond to salt balance manipulation or diuretic therapy. Recurrent parasentesis and treatment of underlying causes are the mainstay of treatment.
Complications
Spontaneous bacterial peritonitis
Hepatorenal Syndrome
Thrombosis
Complications involve blockage of the portal vein and spleen venous thrombosis: blood clots affect the hepatic portal vein or varicose veins associated with the vein of the lithium. It can cause portal hypertension and decreased blood flow. When a patient with liver cirrhosis suffers from thrombosis, it is not possible to have a liver transplant, unless the thrombosis is very small. In the case of small thrombosis, there are several survival possibilities using cadaveric liver transplantation.
Society and culture
It has been argued that ascites are seen as a punishment especially for an oath-breaker among Proto-Indo-European peoples. This proposal was built on the Hittite military oath as well as various Vedic hymns (RV 7.89, AVS 4.16.7). The curse date is similar to the Kassite dynasty (12th century BC). Comparable is also Numbers 5: 11ff, in which a confirmed adulterer is punished with abdominal swelling.
References
External links
Source of the article : Wikipedia
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