Ascites

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In medicine (gastroenterology), ascites (also known as 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.

Contents 1 Signs and symptoms 2 Classification 3 Diagnosis 4 Causes 5 Pathophysiology 6 Treatment 6.1 High SAAG 6.2 Low SAAG 7 Cultural significance 8 References

[edit] 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.

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.

[edit] Classification

Ascites exists in three grades:^[1]

• Grade 1: mild, only visible on ultrasound
• Grade 2: detectable with flank bulging and shifting dullness on physical examination
• Grade 3: directly visible, confirmed with fluid thrill (or fluid wave)

[edit] Diagnosis

In addition to the routine complete blood count (CBC), basic metabolic profile, liver enzymes, and coagulation, a diagnostic paracentesis should be performed to sample about 50 to 100 mL of fluid. 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.^[2]

The serum-ascites albumin gradient (SAAG) is probably a better discriminant than older measures (transudate versus exudate) for the causes of ascites.^[3] 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.

[edit] Causes

Causes of high SAAG ("transudate") are:^[2]

• 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

[edit] 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.^[2]

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.

[edit] 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. If both ascites and peripheral edema is present, the goal of loss is no more than 1.0 kg/day and no more than 0.5 kg/day for those with ascites alone. In those with severe ascites, hospitalization is generally necessary.^{[citation needed]}

[edit] High SAAG

In cirrhotic/transudative ascites, salt restriction is generally the baseline step in therapy, which allows diuresis (production of urine) since the patient now has more fluid than salt concentration. 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. Generally, the starting dose is oral spironolactone 100 mg/day (max 400 mg/day). A loop diuretic may also be added to the regimen to further enhance diuresis and generally, furosemide is added at a dose of 40 mg/day (max 160 mg/day), or alternatively (bumetanide or torasemide). Serum potassium level and renal function should be monitored closely while on these medications.^[4]

In those with severe ascites, therapeutic paracentesis may be needed in addition to medical treatments listed above. As this may deplete serum albumin levels in the blood, albumin is generally administered intravenously in proportion to the amount of ascites removed.

Ascites that is refractory to medical therapy is considered to be a classic indication for liver transplantation.

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.

[edit] 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.

[edit] Cultural significance

It has been suggested that ascites was seen as a punishment especially for oath-breakers among the Proto-Indo-Europeans.^[5] This proposal builds on the Hittite military oath as well as various Vedic hymns (RV 7.89, AVS 4.16.7). A similar curse dates to the Kassite dynasty (12th century BC), threatening oath-breakers: "May Marduk, king of heaven and earth, fill his body with dropsy, which has a grip that can never be loosened".^{[citation needed]} Comparable is also Numeri 5:11ff, where a confirmed adulteress is punished with swelling of the abdomen.

[edit] References

1. ^ Moore KP, Wong F, Gines P, Bernardi M, Ochs A, Salerno F, Angeli P, Porayko M, Moreau R, Garcia-Tsao G, Jimenez W, Planas R, Arroyo V. The management of ascites in cirrhosis: report on the consensus conference of the International Ascites Club. Hepatology 2003;38:258-66. PMID 12830009.
2. ^ ^{a b c} Warrell DA, Cox TN, Firth JD, Benz ED. Oxford textbook of medicine. Oxford: Oxford University Press, 2003. ISBN 0-19-262922-0.
3. ^ Runyon BA, Montano AA, Akriviadis EA, Antillon MR, Irving MA, McHutchison JG. The serum-ascites albumin gradient is superior to the exudate-transudate concept in the differential diagnosis of ascites. Ann Intern Med 1992;117:215-20. PMID 1616215.
4. ^ Gines P, Cardenas A, Arroyo V, Rodes J. Management of cirrhosis and ascites. N Engl J Med 2004;350:1646-54. PMID 15084697.
5. ^ Oettinger, Norbert. Die Militärischen Eide der Hethiter. Wiesbaden, 1976. ISBN 3-447-01711-2.