albumin and hypotension

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I have always thought that with hypotensive liver patients who also have low albumin levels, the correct treatment is to give albumin. This seems to make sense since they need the protein to maintain the osmotic gradient so that they can keep fluid in their intravascular space. However, now I'm told that repleting albumin will not help with correcting their hypotension, or at least not for long. What am I missing?!

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You're not missing anything...you've waded into controversy. In your post you identify several problems: hypotension, liver disease and hypoalbuminemia, all of which can have causes and consequences that are mutually exclusive.

While it is universally accepted that hypotension and hypoalbuminemia increase mortality in ICU patients, just how albumin figures into their treatment is another conversation altogether.

I personally like albumin because in stays intravascularly longer than crystalloid and there is some evidence that I like that indicates better renal perfusion with it. Also, I get a faster response in hemodynamic indices with 250 of 5% albumin, because I can get it in faster than 750 of crystalloid...but that's me. This all assumes, of course, that the hypotension is because of an issue that responds to volume. Pressors and inopressors play a big role here too, but you probably know that.

As far as correcting hypoalbuminemia with it, that is not a consideration when giving it for hypotension, because, in the end, it just extravasates anyway.

Just by way of perspective, 250 of albumin stays intravascular for very roughly 4 hours, assuming a physiologically normal vascular system which none of these patients have. After one hour, 250 mls of a liter of crystalloid stays intravascular, again, assuming the above.

Good question. The above is not nearly a complete answer, but it might get you started.

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Thanks for your reply.

Okay, so albumin IV is not the correct treatment for hypoalbuminemia, correct? This is also what I've read, but it didn't quite make sense to me. So, the albumin soon just extravasates out of the blood vessels, along with the fluid? I thought large proteins like that would stay in the blood.

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Specializes in Critical care.

I agree that this is some pretty unsettled territory, even for those staunch supporters of evidence based medicine.

I remember reading research spurred by the big Cochrane Review done in the late 90's, (so, early 2000's?) that showed no statistical difference in outcomes between 5% Albumin and good ole NS for resuscitation fluids in several thousand ICU pts. We need some solid Level II RCT's to guide our future practice.

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Thanks for your reply.

Okay, so albumin IV is not the correct treatment for hypoalbuminemia, correct? This is also what I've read, but it didn't quite make sense to me. So, the albumin soon just extravasates out of the blood vessels, along with the fluid? I thought large proteins like that would stay in the blood.

It's associated with different problems that have different management objectives. Treating hypotension and treating hypoalbuminemia are two different things.

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Thanks for your reply.

Okay, so albumin IV is not the correct treatment for hypoalbuminemia, correct? This is also what I've read, but it didn't quite make sense to me. So, the albumin soon just extravasates out of the blood vessels, along with the fluid? I thought large proteins like that would stay in the blood.

As mentioned by offlabel, treating hypotension along with hypoalbuminemia is different than just treating hypoalbuminemia. But in any case, try to familiarize yourself with the concept of 'all cause mortality' because it applies to this situation as well as many others in medicine and critical care especially.

The fact of the matter is that by most accounts, the common understanding of what albumin does in the bloodstream is correct - it is more inclined to stay in the bloodstream than crystalloids, etc. And despite this, experiments to this point have not generally found a benefit to all cause mortality (i.e. mortality from any cause) from albumin administration to hypotensive critical care patients. Now, why exactly that might be is still very much up for debate. There's speculation about albumin's drug binding tendencies, speculation about albumin's effects on the lungs and kidneys, and speculation about the possibility that the studies so far on the matter have been flawed among other possible explanations. Here's one overview:

Debate: Albumin administration should be avoided in the critically ill

You'll find similar controversies in some instances of blood transfusions or administration of bicarb, just for a couple particularly common examples.

Just for fun, here's one of my favorite gomerblog articles, which touches on the subject:

With First Date Going Badly, ICU Fellow Tries Albumin | GomerBlog

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Thanks for all the responses so far.

One thing I don't understand is how the albumin gets out of the vasculature. Probably I'm forgetting something from physiology class. I understand how the water that's infused with the albumin goes out of the vasculature into the interstitial space, but aren't the proteins too big to go out?

Also I'd like to get some opinions on how the following patients should be treated...

1) Normotensive liver-cirrhosis patient with an albumin of 1.0 and a significant amount of peripheral edema.

2) Hypotensive liver-cirrhosis patient with an albumin of 1.0. His BP is 70 systolic.

3) Hypotensive liver-cirrhosis patient with an albumin of 1.0, BP 70 systolic, who is undergoing CRRT.

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The altered distribution in critical illness is related to an increase in capillary leakage.26 It involves dysfunction of the endothelial barrier, resulting in capillary leakage and loss of protein, inflammatory cells and large volumes of fluid into the interstitial space. The precise mediators of this capillary leakage are still being discovered and currently include: • endotoxin from Gram‐negative bacteria;3 71

• cytokines—TNF‐α and IL‐6;12 15

• arachidonic acid metabolites—leukotrienes and prosta glandins;10 31

• complement components C3a and C5a;31

• other vasoactive peptides—bradykinin, histamine;71

• chemokines—macrophage inflammatory protein 1α.95

The normal transcapillary escape rate for albumin increases by up to 300%

The above is a very brief and incomplete treatment of what causes the normal capillary permeability to albumin to increase. If you're getting the idea that your questions exceed the scope of any medical forum, let alone this one, you're correct.

As above, treating hypotension is a matter of priorities and what the specific patient is presenting with. No one can give a coherent plan of treatment of your 3 patients bases on 3 sentences besides saying "restore oxygen delivery to demand requirements".

Since you've chosen albumin as a starting point for your questions I'll offer this paper:

http://bja.oxfordjournals.org/content/85/4/599.full

Start with it and it will bring up different questions in your mind that you'll want to chase down. These are really good questions that you're going to learn a lot from.

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Thanks. The fact that albumin does not stay in the vasculature makes it much easier to understand some of the other processes involved.

I'm half way through the article now. Very interesting so far.

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Specializes in Dialysis.

Liver failure patients have low BPs because they have low systemic vascular resistance due to the hepatic congestion. Albumin would increase the preload but that isn't the problem.

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