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Ascitesjpeg
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Severe ascites in a boy with schistosomiasis, leading to portal hypertension Source: CDC
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In
Medicine (
Gastroenterology ), 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. Ascitic fluid can generally be categorized as having a high or low
Serum-ascities Albumin Gradient (SAAG) (see below). Categorization by SAAG has been shown to be superior than categorizing by the previous transudates/exudates method. PMID 1616215
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:
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.
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
Virus es 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.
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)''
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 Cell s. Transudates have low protein (<30g/L), low LDH, high pH, normal glucose, and fewer than 1 white cell per 1000 mm
3. 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.
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.
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.
It has been suggested that ascites was seen as a punishment especially for , 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.
- 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.
