bronx43

Word.
10+ Year Member
Apr 22, 2006
1,843
533
281
Status
Attending Physician
I know that the texts say the reason there is no edema in SIADH is that the body can still clear Na. But, can someone explain why there isn't edema simply because plasma becomes hypotonic (due to dilution) to the interstitial fluid, and there is a net movement of fluid into the interstitium? If there isn't edema, where does the increased amount of water go?
 

LukeWhite

USC Pulm/CCM 2014
10+ Year Member
15+ Year Member
Oct 10, 2002
829
8
241
41
New York City
www.facebook.com
Status
Fellow [Any Field]
One way of answering the question is to say that SIADH is definitionally euvolemic. Edema is definitionally hypervolemic. Edema is thus incompatible with SIADH.

But that's just a tricksy way of dodging what seems to be your real question, which is: Why is SIADH necessarily euvolemic? I'm not sure there's a great answer for that, but I'll offer some pathophysiological speculation:

Hyponatremic disorders so severe as to cause third spacing will likely be life-threatening before there's time for any clinically obvious fluid shifts. Another way of saying it: The brain's going to suffer dangerous fluid shifts long before the ankles do. If you're hypervolemic due to SIADH, you died last week.

This isn't true of our other culprits for edema, like hypoalbuminemia, because they're not intrinsically tied to electrically-gated intracellular osmolar regulation like sodium is.
 

obiwan

Junior Member
10+ Year Member
Mar 26, 2006
686
45
261
Texas
Status
Attending Physician
SIADH doesn't have a problem with salt excretion
 

LukeWhite

USC Pulm/CCM 2014
10+ Year Member
15+ Year Member
Oct 10, 2002
829
8
241
41
New York City
www.facebook.com
Status
Fellow [Any Field]
True enough--it's a problem with osmolar balance. Regardless of what the kidneys are doing, though, osmolar balance is always tied to sodium. This is especially true of intracellular/extracellular shifts.
 

Gpan

10+ Year Member
Jul 9, 2007
676
59
271
Status
Attending Physician
DOes anyone know exactly why SIADH pts have EUVOLEMIC ? I tried all the resources and still don't have an answer:(
 

Polish Farmer

Extubated
10+ Year Member
5+ Year Member
Jan 20, 2009
26
2
91
Status
Resident [Any Field]
SIADH doesn't have a problem with salt excretion

Exactly right.
From Burton Rose, who is the God of electrolytes, "The hyponatremia is initially mediated by ADH-induced water retention. The ensuing volume expansion activates secondary natriuretic mechanisms, resulting in sodium and water loss. The net effect is that, with chronic SIADH, sodium loss is as or more prominent than water retention."
 
Mar 15, 2012
1
0
0
Status
Medical Student
Siadh thus will cause hyponatremia alone and no water retension.bcoz the retained water will be drained away by natriuresis.
 

somemaybedoc

ms0
10+ Year Member
7+ Year Member
Jul 4, 2006
961
2
0
Texas
Status
Resident [Any Field]
I think the most direct way to answer your question is that while sodium is what me measure that goes down with SIADH, the free water that is retained is distributed across all compartments, thus excess water is in the interstitial, the vasculature, and intracellular spaces thus reducing solute concentrations in all these spaces. However overall plasma volume is regulated by sodium excretion and thus the patient remains for the most part euvolemic. Imagine for example a patient develops SIADH, his overall volume status is slightly increased by let's say 1 liter, roughly 2/3s of this is intercellular and would have no effect on edema, 1/3 is extracellular and the split the quantity and split of this 1/3 between intra and extra vascular determines the presence of edema. So therefore you would think the SIADH and the resultant free water retention might be able to cause some edema by just increasing extra vascular volume as a whole, but remember that you haven't changed the balance between intra and extra vascular volume, just the total in the intercellular compartment. Therefore the transient intravascular expansion will trigger renal salt excretion and thus volume reduction back to euvolemia albeit with reduced body wide solution concentrations. Hope that was clear enough
 

boaz

shanah alef
10+ Year Member
7+ Year Member
Dec 31, 2007
1,373
25
151
bachelor pad
Status
Medical Student
@somemaybedoc :thanks!, but why does SIADH cause cerebral edema then?
If I recall correctly, in the case of SIADH, cerebral "edema" refers to cellular swelling. The hypotonic ECF causes shift of free water into cells. The pathologic manifestations are due to the fixed volume of the cranial vault resulting in elevated ICP.
 
Oct 29, 2016
1
1
1
Adh causes
@560714"]@somemaybedoc :thanks!, but why does SIADH cause cerebral edema then?
DOes anyone know exactly why SIADH pts have EUVOLEMIC ? I tried all the resources and still don't have an answer:(
ADH will raise only the water level, which will be sensed by heart and produce natriuretic peptide (ANP, BNP) which incresae the GFR and loss Na+&H2O, now previous water gain is corrected by loss. But Sodium get lost. So EVOLEMIC HYPO NATRIMEIA ☺
 
  • Like
Reactions: SA279

Polycherry

2+ Year Member
Nov 21, 2014
45
8
101
Delhi
Status
Medical Student
i understand that in SIADH, there is euvolemia and hyponatremia = hypoosmolarity. So why is there no edema? Why does edema necessarily have to be hypervolemic? In nephrotic syndrome, there's edema due to hypoosmolarity due to albuminuria. Is nephrotic syndrome too a hypervolemic state?