Non-pitting vs. pitting edema

[MudPhud20XX]

1. Kaplan physio says if the edema responds to diuretics it's pitting and if not, it's non-pitting.
Does anyone know how they end up using the term "pitting?" Is it just a description for the respond to diuretics?

2. Would it be safe to consider:
pitting = cardiogenic
non-pitting = non-cardiogenic

3. Transduate for pitting edema, exduate for non-pitting edema, correct?

So an example of pitting edema is CHF. So let's say that you have a Lt. CHF which leads to increased hydrostative pressure in pulmonary circuit leading to pulmonary edema (pure water gets into lung interstitial tissue due to the increased hydrostatic pressure). So that's why you get transduate in case of CHF, correct?

I guess in nephrotic syndrome where you also end up with pitting edema, the rationale that you get transduate is the same since increased oncotic pressure will lead water to get into interstitial space. Can anyone confirm that I got this right?

Then, how do you explain exudate for non-pitting? Increased permeability via inflammtory respond right? So how do you get exudate in lymphedema (distrubance of the lymphatic system), which is non-pitting edema? Is it also associated with increased permeability? How come if there is no inflammation going on?

Many thanks in advance.

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[govnah]

"pitting" refers to whether the edema pits on exam, i.e. when you physically press on a CHF patient's ankles whether the dimple remains after you remove your hand or not. I wouldn't think of it in terms of equating pitting to cardiogenic. I would more think of it as a marker of severity, i.e pitting edema is worse than non-pitting edema. Both should be transudate.

 

[ArmyTiger]

1. Kaplan physio says if the edema responds to diuretics it's pitting and if not, it's non-pitting.
Does anyone know how they end up using the term "pitting?" Is it just a description for the respond to diuretics?

2. Would it be safe to consider:
pitting = cardiogenic
non-pitting = non-cardiogenic

3. Transduate for pitting edema, exduate for non-pitting edema, correct?
So an example of pitting edema is CHF. So let's say that you have a Lt. CHF which leads to increased hydrostative pressure in pulmonary circuit leading to pulmonary edema right? So that's why you get transduate in case of CHF or I guess in nephrotic syndrome where you also end up with pitting edema, the rationale that you get transduate is the same since increased oncotic pressure will lead water to get into interstitial space. Can anyone confirm that I got this right?

Then, how do you explain exudate for non-pitting? Increased permeability via inflammtory respond right? So how do you get exudate in lymphedema (distrubance of the lymphatic system), which is non-pitting edema?

Many thanks in advance.

1. Pitting vs. non-pitting is a clinical feature that tells you whether an edema is a transudate or an exudate/lymphatic blockage. Pitting edema stays pitted after you press and release with a finger; non-pitting usually won't give to pressure.

2. Not quite. See above.

3. Correct on this point. Right heart failure (by any means, although left heart failure is certainly a fairly likely cause) or nephrotic syndrome will cause pitting edema. So would liver cirrhosis (decreased oncotic pressure + increased hydrostatic pressure).

 

[MudPhud20XX]

"pitting" refers to whether the edema pits on exam, i.e. when you physically press on a CHF patient's ankles whether the dimple remains after you remove your hand or not. I wouldn't think of it in terms of equating pitting to cardiogenic. I would more think of it as a marker of severity, i.e pitting edema is worse than non-pitting edema. Both should be transudate.

Thanks for the reply. I just checked Goljan path and it says "Lymphedema: 1. protein-rich fluid (exduate) 2. nonpitting edema." I think non-pitting should give you exudate, right?