Monday, January 9, 2017

The SAAG solution (Serum-Ascites Albumin Gradient simplified)

Yo people!

A good friend of mine asked me to review the concept of SAAG. So let's dive into a "Puddle" of ascitic fluid. :P

As you guys all know, SAAG stands for Serum-Ascites Albumin Gradient and it helps to differentiate the causes of ascites. What it means is pretty self explanatory, it is the difference (gradient) between the levels of albumin (a plasma protein) in two compartments i.e. Serum and Peritoneal fluid.

SAAG = Serum Albumin - Albumin of Ascitic fluid.

The normal value of serum albumin is 4g/dL and the normal level of protein in ascitic fluid is 3g/dL and majority of that is albumin. To make our lives easy, let's take these values as values of albumin.

SAAG = 4-3 = ~1 to 1.1g/dL.

Now, we have an idea of what normal is.

Different pathologies can alter SAAG level, which can result in increase to > 1.1g/dL indicating a "High SAAG" or decrease to < 1.1g/dl indicating a "Low SAAG".

Since the calculation of SAAG has only 2 variables, there are 2 ways of either increasing or decreasing it.

Let's deal with low SAAG first because it is fairly straight forward. A low SAAG can be obtained by either "Decreasing" the serum albumin eg. Nephrotic Syndrome, where your protein is in the toilet bowl or "Increasing" the albumin in ascitic fluid eg. Tuberculosis, inflammatory conditions, malignancy etc. So the "exudative" ascites usually has a low SAAG.

Exudative ascitic fluid is checked for different things like culture, neutrophils, hemorrhage etc which aid in narrowing the exudative causes.

Now, the fun part, "High" SAAG. High SAAG can be achieved by either increasing the serum albumin level or decreasing the albumin in peritoneal fluid. Before we start read this, it is important to know the concept proposed by IkaN's Darling, Mr. Starling. According to Starling the net flow of fluid is influenced by 2 important forces i.e. Yin and Yang... Not really... :P
The 2 important forces are, the hydrostatic force (drives out the fluid - like diarrhea drives out the poop from your bowel) and oncotic force (holds in the fluid - like decreased peristalsis holds in the feces) which act in the opposite direction. Under normal circumstances, these two are in a state of balance, be it in kidneys, capillaries etc and are responsible for filtration, edema etc.

Let us consider the example of cirrhosis (Because for all practical purposes, the major cause of ascites is cirrhosis) and try to understand this. In Cirrhosis, there is fibrosis, especially, around the sinusoids which are like the conduits connecting the portal circulation with the systemic circulation.
When there is fibrosis, these channels become narrow and unyielding, making the flow of intravascular fluid very sluggish and difficult (Like squeezing amazon river through a garden hose :P). This causes increased amount of fluid in the portal circulation causing an increase in the hydrostatic (hydro=water, static=stationary) pressure which causes "Portal hypertension" (portal HTN).

The increased hydrostatic pressure (portal HTN) drives the intravascular fluid into extravascular space of Disse and into hepatic interstitium. From there the fluid seeps into the peritoneal cavity causing small "puddles" of fluid. When the accumulation exceeds the lymphatic drainage of the peritoneal cavity (into thoracic duct) it results in "Ascites".

This fluid has less amount of proteins because the proteins like albumin don't escape as easily as the liquid component (mostly water) through the fenestrae. So the shift of low protein fluid from intravascular compartment increases the albumin level in serum (relatively concentrated, since the production is not affected) and decreases the albumin content of ascitic fluid (again, relatively diluted.)

So the SAAG becomes "High". The conditions which increase SAAG would be conditions which cause portal hypertension like Cirrhosis, Budd Chiari, IVC obstruction and good old cardiac failure.

SAAG can be further used with another factor i.e. Total ascitic protein, to further differentiate the causes of ascites. Liver is the war factory of proteins and after they are spilled into the sinusoids for further transport. When the sinusoids are patent, they allow the passage of proteins into the ascites, but when they are damaged in cirrhosis this movement into ascites is hampered, thereby decreasing the total ascitic protein. The magic number for this is 2.5g/dL. A level of  < 2.5 g/dL indicates liver sinusoidal pathology like cirrhosis, late budd chiari etc and level of > 2.5g/dL indicates a non hepatic pathology like CHF.
Total Protein
< 2.5 g/dL
> 2.5 g/dL
< 1.1 g/dL
Nephrotic Syndrome
TB, Cancer
> 1.1 g/dL
So thats the whole shebang about SAAG. If you guys want, I can teach you how to cook SAAG aloo too. :P

Until then, Peace.

- DJ AweSpear


  1. Nice! You made it crystal clear
    Thank you

    1. You are welcome A medico.....
      Hope that helps.....
      Stay tuned for some more concepts, mnemonics.....
      Until then, peace .....

  2. Excellent explanation, thank you!

  3. Excellent explanation, thank you!

  4. SAAG aloo hahahaha... Why is the total protein decreased in nephrotic syndrome though?

  5. I love you for this


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