Ascites

Encyclopedia : A : AS : ASC : Ascites

In medicine (gastroenterology), ascites 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. Typically described in terms of transudate (low protein concentration) and exudate (high protein), the serum-ascites albumin gradient (SAAG) is probably a better discriminantRunyon 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.

Contents

1 Causes
2 Signs and symptoms
3 Diagnosis
4 Classification
5 Pathophysiology
6 Treatment
7 Cultural significance
8 References
9 See also

Causes

Causes of high SAAG are:

Cirrhosis - 81%
* alcoholic - 65%
* viral - 10%
* cryptogenic - 6%
Heart failure - 3%
Budd-Chiari syndrome or veno-occlusive disease
Constrictive pericarditis

Causes of low SAAG are:

Cancer (primary peritoneal carcinomatosis and metastasis) - 10%
Tuberculosis - 2%
Pancreatitis - 1%
Serositis
Nephrotic syndrome

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. In those with portal hypertension, such as due to cirrhosis, patients may also complain of lower extremity swelling, progressive problems with clotting after major trauma/surgery, hematemesis, or mental status changes. In some cases, patients will also complain of gynecomastia (due to hyperestrogenism), spider angiomata, palmar erythema, or caput medusa. Jaundice and skin itching may or may not be present depending on the level of liver congestion and bilirubin build-up.

Those with ascites due to cancer (peritoneal carcinomatosis or peritoneal cavity seeding from metastases from elsewhere) 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.

Ascites can also be due to tuberculosis, in which case patients may complain of night sweats, dry cough, and chronic fatigue.

Rarely, ascites may be a component of Meigs' syndrome --- a combination of ascites, hydrothrorax (unilateral pleural effusion), and benign tumors of the ovary.

Diagnosis

In addition to the routine complete blood count (CBC), basic metabolic profile, liver enzymes, and coagulation factors, 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, serum-ascites albumin gradient (SAG, SAAG), and cell counts (red and white). Additional tests will be performed if indicated such as gram stain and cytology.

The serum-ascites albumin gradient is important because it is paramount to determine if the ascites is due to portal hypertension or otherwise, since the diagnostic pathways are different for each cause. A high gradient (> 1.1 g/dL) indicates the ascites is due to uncomplicated cirrhotic ascites and is likely due to portal hypertension. A low gradient (< 1.1 g/dL) indicates ascites of non-portal hypertension etiology.

If the cause is not apparent, serology for viruses known to cause hepatitis may contribute to the analysis. Iron studies (serum iron, ferritin, TIBC) may reveal rare causes such as hemochromatosis. Serum copper and ceruloplasmin may reveal Wilson's disease. a1-antitrypsin may reveal a1-antitrypsin deficiency disease. All of these causes may contribute to formation of cirrhosis.

Ultrasound investigation with doppler studies can be an important help, and may identify vessel architecture and reveal such problems as Budd-Chiari syndrome, portal vein thrombosis and cirrhosis. Additionally, the sonographer can make an estimation of the amount of ascitic fluid.

Abdominal CT scan is an alternate to reveal abdominal organ structure and morphology.

Classification

Ascites exists in three grades:

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)

Pathophysiology

Ascitic fluid can accumulate as a transudate or an exudate. Amounts of up to 25 litres 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.

Portal hypertension lays 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.

Treatment

Ascites is generally treated simultaneously while an underlying etiology is sought (see above, diagnosis) in order to prevent complications (i.e., spontaneous bacterial peritonitis) and to prevent further progression. In patients with mild ascites, therapy can be done in the outpatient but should be gradual. 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.

Salt restriction is generally the baseline step in therapy, which allows diuresis 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 spironolactone PO 100 mg/day (max 400 mg/day). A loop diuretic (furosemide, bumetanide, torasemide) may also be added to the regimen to further enhance diuresis and generally, furosemide (Lasix) is added at a dose of 40 mg/day (max 160 mg/day). Serum potassium level and renal function should be monitored closely while on these medications.

In those with severe ascites, therapeutic paracentesis may be needed in addition to medical treatments listed above.

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.

Cultural significance

It has been suggested that ascites was seen as a punishment especially for oath-breakers among the Proto-Indo-Europeans (Oettinger, StBoT 22:71). 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". Comparable is also Numeri 5:11ff.

References

Oxford textbook of medicine
Gines P, Cardenas A, Arroyo V, Rodes J. Management of cirrhosis and ascites. N Engl J Med 2004;350:1646-54. PMID 15084697.