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Serum-ascites albumin gradient

Pathophysiology sample values
BMP/ELECTROLYTES:
Na+ = 140 Cl = 100 BUN = 20 /
Glu = 150
K+ = 4 CO2 = 22 PCr = 1.0 \
ARTERIAL BLOOD GAS:
HCO3 = 24 paCO2 = 40 paO2 = 95 pH = 7.40
ALVEOLAR GAS:
pACO2 = 36 pAO2 = 105 A-a g = 10
OTHER:
Ca = 9.5 Mg2+ = 2.0 PO4 = 1
CK = 55 BE = −0.36 AG = 16
SERUM OSMOLARITY/RENAL:
PMO = 300 PCO = 295 POG = 5 BUN:Cr = 20
URINALYSIS:
UNa+ = 80 UCl = 100 UAG = 5 FENa = 0.95
UK+ = 25 USG = 1.01 UCr = 60 UO = 800
PROTEIN/GI/LIVER FUNCTION TESTS:
LDH = 100 TP = 7.6 AST = 25 TBIL = 0.7
ALP = 71 Alb = 4.0 ALT = 40 BC = 0.5
AST/ALT = 0.6 BU = 0.2
AF alb = 3.0 SAAG = 1.0 SOG = 60
CSF:
CSF alb = 30 CSF glu = 60 CSF/S alb = 7.5 CSF/S glu = 0.4

The serum-ascites albumin gradient or gap (SAAG) is a calculation used in medicine to help determine the cause of ascites.[1] The SAAG may be a better discriminant than the older method of classifying ascites fluid as a transudate versus exudate.[2]

The formula is as follows:

SAAG = (serum albumin) − (albumin level of ascitic fluid).

Ideally, the two values should be measured at the same time.

This phenomenon is the result of Starling's forces between the fluid of the circulatory system and ascitic fluid. Under normal circumstances the SAAG is < 1.1 because serum oncotic pressure (pulling fluid back into circulation) is exactly counterbalanced by the serum hydrostatic pressure (which pushes fluid out of the circulatory system). This balance is disturbed in certain diseases (such as the Budd–Chiari syndrome, heart failure, or liver cirrhosis) that increase the hydrostatic pressure in the circulatory system. The increase in hydrostatic pressure causes more fluid to leave the circulation into the peritoneal space (ascites). The SAAG subsequently increases because there is more free fluid leaving the circulation, concentrating the serum albumin. The albumin does not move across membrane spaces easily because it is a large molecule.

Contents

DifferentialEdit

High gradientEdit

A high gradient (> 1.1 g/dL, >11g/L) indicates the ascites is due to portal hypertension, either liver related or non-liver related, with approximately 97% accuracy.[2] This is due to increased hydrostatic pressure within the blood vessels of the hepatic portal system, which in turn forces water into the peritoneal cavity but leaves proteins such as albumin within the vasculature.

Important causes of high SAAG ascites (> 1.1 g/dL, >11 g/L) include: cirrhosis of the liver, heart failure, Budd-Chiari syndrome, portal vein thrombosis, and idiopathic portal fibrosis.[3]

Low gradientEdit

A low gradient (< 1.1 g/dL, <11 g/L) indicates causes of ascites not associated with increased portal pressure: tuberculosis, pancreatitis, infections, serositis, various types of peritoneal cancers (peritoneal carcinomatosis) and pulmonary infarcts.

SAAG vs Total ascities protein
SAAG
<1.1 >1.1
Total Protein <2.5 Tuberculous Peritonitis, Nephrotic syndrome Cirrhosis, Budd-Chiari (late)
>2.5 Cancer, Tuberculosis, Chylous ascites, Pancreatitis Right HF, Budd-Chiari (early), veno-occlusive disease

ReferencesEdit

  1. ^ Wong CL, Holroyd-Leduc J, Thorpe KE, Straus SE (March 2008). "Does this patient have bacterial peritonitis or portal hypertension? How do I perform a paracentesis and analyze the results?". JAMA. 299 (10): 1166–78. doi:10.1001/jama.299.10.1166. PMID 18334692. 
  2. ^ a b 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". Annals of Internal Medicine. 117 (3): 215–20. doi:10.7326/0003-4819-117-3-215. PMID 1616215. 
  3. ^ Ginès, Pere; Cárdenas, Andrés; Arroyo, Vicente; Rodés, Juan (15 April 2004). "Management of Cirrhosis and Ascites". New England Journal of Medicine. 350 (16): 1646–1654. doi:10.1056/NEJMra035021. PMID 15084697.