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Causes[edit]
Causes of high SAAG ("transudate") are:[3]
Heart failure - 3%
Hepatic venous occlusion: Budd-Chiari syndrome or veno-occlusive
disease
Constrictive pericarditis
Pancreatitis - 1%
Serositis
Nephrotic syndrome[4]
Hereditary angioedema[5]
Meigs syndrome
Vasculitis
Hypothyroidism
Renal dialysis
Peritoneum mesothelioma
Abdominal tuberculosis
Diagnosis[edit]
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 microbiological
culture, Gram stain and cytopathology.[3]
The serum-ascites albumin gradient (SAAG) is probably a better discriminant
than older measures (transudate versus exudate) for the causes of ascites.[6] 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(thrombosis of the hepatic vein)
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. An abdominal CT scan is a more accurate
alternate to reveal abdominal organ structure and morphology.[citation needed]
Classification[edit]
Ascites exists in three grades:[7]
Pathophysiology[edit]
Ascitic fluid can accumulate as a transudate or an exudate. Amounts of up to
35 liters are possible.
Roughly, transudates are a result of increased pressure in the hepatic portal
vein (>8 mmHg, usually around 20 mmHg[8]), 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 morewhite blood cells. Transudates
have low protein (<30 g/L), low LDH, high pH, normal glucose, and fewer than
1 white cell per 1000 mm. 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.[3]
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, notablyaldosterone. 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 hepatorenal syndrome. Other complications of ascites include spontaneous
bacterial peritonitis (SBP), due to decreased antibacterial factors in the ascitic
fluid such as complement.
Treatment[edit]
Diet[edit]
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.[12] Water restriction is needed
if serum sodium levels drop below 130 mmol L1.[13]
Diuretics[edit]
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 distaltubule diuretics such as triamterene oramiloride) 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.[14] Diuretics for ascites should
be dosed once per day.[15] Generally, the starting dose is oral spironolactone
100 mg/day (max 400 mg/day). 40% of patients will respond to
spironolactone.[12] 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
Paracentesis[edit]
Main article: Paracentesis
In those with severe (tense) ascites, therapeutic paracentesis may be needed
in addition to medical treatments listed above.[10][11] As this may deplete serum
albumin levels in the blood, albumin is generally administered intravenously in
proportion to the amount of ascites removed.
Surgery[edit]
Ascites that is refractory to medical therapy is considered an indication
for liver transplantation. In the United States, the MELD score (online
calculator)[20] is used to prioritize patients for transplantation.
In a minority of people with advanced cirrhosis that have recurrent ascites,
shunts may be used. Typical shunts used are portacaval
Low SAAG[edit]
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[edit]
Hepatorenal syndrome[edit]
Main article: Hepatorenal syndrome
Thrombosis[edit]
Complications involve portal vein thrombosis and splenic vein thrombosis:
clotting of blood affects the hepatic portal vein or varices associated with
splenic vein. This can lead to portal hypertension and reduction in blood flow.
When a liver cirrhosis patient is suffering from thrombosis, it is not possible to
perform a liver transplant, unless the thrombosis is very minor. In case of
minor thrombosis, there are some chances of survival using cadaveric liver
transplant.
References[edit]
1.
2.
3.
^ Jump up to:a b c Warrell DA, Cox TN, Firth JD, Benz ED. Oxford
textbook of medicine. Oxford: Oxford University Press, 2003. ISBN 0-19262922-0.
4.
Jump up^ Kumar & Clark's Clinical Medicine e.8 Chapter 7: Liver,
biliary tract and pancreatic disease Pg. 335
5.
6.
Jump up^ Runyon BA, Montano AA, Akriviadis EA, Antillon MR, Irving
MA, McHutchison JG (August 1992). "The serum-ascites albumin gradient is
superior to the exudate-transudate concept in the differential diagnosis of
ascites". Ann. Intern. Med. 117 (3): 21520.doi:10.7326/0003-4819-117-3215. PMID 1616215.
7.
Jump up^ Moore, K. P.; 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 (2003). "The Management of Ascites in Cirrhosis:
Report on the Consensus Conference of the International Ascites
Club". Hepatology. 2003 (38): 258
66.doi:10.1053/jhep.2003.50315. PMID 12830009.
8.
9.
10.
11.
13.
14.
Jump up^ Fogel MR, Sawhney VK, Neal EA, Miller RG, Knauer CM,
Gregory PB (1981). "Diuresis in the ascitic patient: a randomized controlled
trial of three regimens". J. Clin. Gastroenterol. 3 Suppl 1: 73
80. doi:10.1097/00004836-198100031-00016. PMID 7035545.
15.
16.
Jump up^ Runyon BA, Heck M (1996). "Utility of 24-hour urine sodium
collection and urine Na/K ratios in the management of patients with cirrhosis
and ascites". Hepatology. 24: 571A.
17.
18.
Jump up^ Hunt SA, Abraham WT, Chin MH, et al. (2005). "ACC/AHA
2005 Guideline Update for the Diagnosis and Management of Chronic Heart
Failure in the Adult: a report of the American College of Cardiology/American
Heart Association Task Force on Practice Guidelines". Circulation. 112 (12):
154235.doi:10.1161/CIRCULATIONAHA.105.167586. PMID 16160202.
19.
Jump up^ Adams KF, Lindenfeld J, Arnold JM, Baker DW, Barnard
DH, Baughman KL, Boehmer JP, Deedwania P, Dunbar SB, Elkayam U,
Gheorghiade M, Howlett JG, Konstam MA, Kronenberg MW, Massie BM,
Mehra MR, Miller AB, Moser DK, Patterson JH, Rodeheffer RJ, SacknerBernstein J, Silver MA, Starling RC, Stevenson LW, Wagoner LE (2006).
"Heart Failure Society of America (HFSA) 2006 Comprehensive Heart Failure
Practice Guideline.". J Cardiac Failure. 12 (1): e1
e122. doi:10.1016/j.cardfail.2005.11.005.PMID 16500560.
20.
21.
Jump up^ Saab S, Nieto JM, Lewis SK, Runyon BA (2006). "TIPS
versus paracentesis for cirrhotic patients with refractory ascites". Cochrane
database of systematic reviews (Online) (4):
CD004889. doi:10.1002/14651858.CD004889.pub2. PMID 17054221.
22.