Ascites
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Overview
| Ascites Classification and external resources | |
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| ICD-10 | R18. |
| ICD-9 | 789.5 |
| DiseasesDB | 943 |
| eMedicine | ped/2927 med/173 |
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In medicine (gastroenterology), ascites (also known as peritoneal cavity fluid, peritoneal fluid excess, hydroperitoneum or more archaically as abdominal dropsy) is an accumulation of fluid in the peritoneal cavity. Although most commonly due to cirrhosis and severe liver disease, its presence can portend other significant medical problems. Diagnosis of the cause is usually with blood tests, an ultrasound scan of the abdomen and direct removal of the fluid by needle or paracentesis (which may also be therapeutic). Treatment may be with medication (diuretics), paracentesis or other treatments directed at the cause.
Signs and symptoms
Mild ascites is hard to notice, but severe ascites leads to abdominal distension. Patients with ascites generally will complain of progressive abdominal heaviness and pressure as well as shortness of breath due to mechanical impingement on the diaphragm.
Ascites is detected on physical examination of the abdomen by visible bulging of the flanks in the reclining patient ("flank bulging"), "shifting dullness" (difference in percussion note in the flanks that shifts when the patient is turned on the side) or in massive ascites with a "fluid thrill" or "fluid wave" (tapping or pushing on one side will generate a wave-like effect through the fluid that can be felt in the opposite side of the abdomen).
Other signs of ascites may be present due to its underlying etiology. For instance, in portal hypertension (perhaps due to cirrhosis or fibrosis of the liver) 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 exercise intolerance.
Classification
Ascites exists in three grades:[1]
- Grade 1: mild, only visible on ultrasound
- Grade 2: detectable with flank bulging and shifting dullness
- Grade 3: directly visible, confirmed with fluid thrill
Diagnosis
Routine complete blood count (CBC), basic metabolic profile, liver enzymes, and coagulation should be performed. Most experts recommend a diagnostic paracentesis be performed if the ascites is new or if the patient with ascites is being admitted to the hospital. The fluid is then reviewed for its gross appearance, protein level, albumin, and cell counts (red and white). Additional tests will be performed if indicated such as Gram stain and cytology.[1]
The Serum-ascites albumin gradient (SAAG) is probably a better discriminant than older measures (transudate versus exudate) for the causes of ascites.[1] A high gradient (> 1.1 g/dL) indicates the ascites is due to portal hypertension. A low gradient (< 1.1 g/dL) indicates ascites of non-portal hypertensive etiology.
Ultrasound investigation is often performed prior to attempts to remove fluid from the abdomen. This may reveal the size and shape of the abdominal organs, and Doppler studies may show the direction of flow in the portal vein, as well as detecting Budd-Chiari syndrome and portal vein thrombosis. Additionally, the sonographer can make an estimation of the amount of ascitic fluid, and difficult-to-drain ascites may be drained under ultrasound guidance. Abdominal CT scan is a more accurate alternate to reveal abdominal organ structure and morphology.
Fetal Ascites
Differential diagnosis of fetal ascites.
- Urinary ascites
- Bowel rupture (i.e. meconium peritonitis)
- Ruptured ovarian cyst
- Hydrops
- Pseudoascites
- Infection
Causes
Causes of high SAAG ("transudate") are:[1]
- Cirrhosis - 81% (alcoholic in 65%, viral in 10%, cryptogenic in 6%)
- Heart failure - 3%
- Budd-Chiari syndrome or veno-occlusive disease
- Constrictive pericarditis
Causes of low SAAG ("exudate") are:
- Cancer (primary peritoneal carcinomatosis and metastasis) - 10%
- Tuberculosis - 2%
- Pancreatitis - 1%
- Serositis
- Nephrotic syndrome
Pathophysiology
Ascitic fluid can accumulate as a transudate or an exudate. Amounts of up to 25 liters are fully possible.
Roughly, transudates are a result of increased pressure in the portal vein (>8 mmHg), e.g. due to cirrhosis, while exudates are actively secreted fluid due to inflammation or malignancy. As a result, exudates are high in protein, high in lactate dehydrogenase, have a low pH (<7.30), a low glucose level, and more white blood cells. Transudates have low protein (<30g/L), low LDH, high pH, normal glucose, and fewer than 1 white cell per 1000 mm³. Clinically, the most useful measure is the difference between ascitic and serum albumin concentrations. A difference of less than 1 g/dl (10 g/L) implies an exudate.[1]
Portal hypertension plays an important role in the production of ascites by raising capillary hydrostatic pressure within the splanchnic bed.
Regardless of the cause, sequestration of fluid within the abdomen leads to additional fluid retention by the kidneys due to stimulatory effect on blood pressure hormones, notably aldosterone. The sympathetic nervous system is also activated, and renin production is increased due to decreased perfusion of the kidney. Extreme disruption of the renal blood flow can lead to the feared hepatorenal syndrome. Other complications of ascites include spontaneous bacterial peritonitis (SBP), due to decreased antibacterial factors in the ascitic fluid such as complement.
Diagnosis
Images shown below are courtesy of Professor Peter Anderson DVM PhD and published with permission. © PEIR, University of Alabama at Birmingham, Department of Pathology
Ascites in a patient with cirrhotic liver disease. Dilated abdominal veins are visible |
 Ascites, the same patient, lateral view. |
 A 2 month old child with ascites. Ascites is a common form of tuberculosis in higher incidence areas. |
 Ascites: Postmortem findings |
Treatment
Ascites is generally treated simultaneously while an underlying etiology is sought in order to prevent complications, to relieve symptoms and to prevent further progression. In patients with mild ascites, therapy is usually as an outpatient. The goal is weight loss of no more than 1.0 kg/day for patients with both ascites and peripheral edema and no more than 0.5 kg/day for patients with ascites alone.[1] In those with severe ascites causing a tense abdomen, hospitalization is generally necessary for paracentesis.[1][1]
High SAAG
Salt restriction
Salt restriction is the initial treatment, which allows diuresis (production of urine) since the patient now has more fluid than salt concentration. Salt restriction is effective in about 15% of patients.[1]
Diuretics
Since salt restriction is the basic concept in treatment, and aldosterone is one of the hormones that acts to increase salt retention, a medication that counteracts aldosterone should be sought. Spironolactone (or other distal-tubule diuretics such as triamterene or amiloride) is the drug of choice since they block the aldosterone receptor in the collecting tubule. This choice has been confirmed in a randomized controlled trial.[1] Diuretics for ascites should be dosed once per day.[1] Generally, the starting dose is oral spironolactone 100 mg/day (max 400 mg/day). 40% of patients will respond to spironolactone.[1] For nonresponders, a loop diuretic may also be added and generally, furosemide is added at a dose of 40 mg/day (max 160 mg/day), or alternatively (bumetanide or torasemide). The ratio of 100:40 reduces risks of potassium imbalance.[1] Serum potassium level and renal function should be monitored closely while on these medications.[1] Monitoring diuresis: Diuresis can be monitored by weighing the patient daily. The goal is weight loss of no more than 1.0 kg/day for patients with both ascites and peripheral edema and no more than 0.5 kg/day for patients with ascites alone.[1] If daily weights cannot be obtained, diuretics can also be guided by the urinary sodium concentration. Dosage is increased until a negative sodium balance occurs.[1] A random urine sodium-to-potassium ratio of > 1 is 90% sensitivity in predicting negative balance (> 78-mmol/day sodium excretion).[1] Diuretic resistance: Diuretic resistance can be predicted by giving 80 mg intravenous furosemide after 3 days without diuretics and on a 80 mEq sodium/day diet. The urinary sodium excretion over 8 hours < 50 mEq/8 hours predicts resistance.[1]
Water restriction
Water restriction is needed if hyponatremia < 130 mmol per liter develops.[1]
Paracentesis
In those with severe (tense) ascites, therapeutic paracentesis may be needed in addition to medical treatments listed above.[1][1] As this may deplete serum albumin levels in the blood, albumin is generally administered intravenously in proportion to the amount of ascites removed.
Liver transplantation
Ascites that is refractory to medical therapy is considered an indication for liver transplantation. In the United States, the MELD score (online calculator)[1] is used to prioritize patients for transplantation.
Shunting
In a minority of the patient with advanced cirrhosis that have recurrent ascites, shunts may be used. Typical shunts used are portacaval shunt, peritoneovenous shunt, and the transjugular intrahepatic portosystemic shunt (TIPS). However, none of these shunts has been shown to extend life expectancy, and are considered to be bridges to liver transplantation. A meta-analysis of randomized controlled trials by the international Cochrane Collaboration concluded that "TIPS was more effective at removing ascites as compared with paracentesis...however, TIPS patients develop hepatic encephalopathy significantly more often" [1]
Low SAAG
Exudative ascites generally does not respond to manipulation of the salt balance or diuretic therapy. Repeated paracentesis and treatment of the underlying cause is the mainstay of treatment.
Complications
Spontaneous bacterial peritonitis
References
ar:استسقاء (مرض)
de:Aszitesfr:Ascite
it:Ascite
nl:Ascites (medisch)
ja:腹水sv:Ascites
uk:Асцит
Acknowledgement and Attribution Regarding Sources of Content
Some of the initial content on this page may be incorporated in part from copyleft sources in the public domain including wikis such as Wikipedia and AskDrWiki. Drug information for patients came from the The National Library of Medicine. Infectious disease information may have come from the Centers for Disease Control (CDC). Differential Diagnoses are drawn from clinicians as well as an amalgamation of 3 sources: 1.The Disease Database; 2. Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:3; 3. Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:7 .
