Renal protection during aortic clamping

Specialties CRNA

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Okay, what do you find to be a beneficial mechanism for renal "protection" during infra/supra renal clamping of the aorta. Lasix, mannitol, low dose dopamine, bicarbonate, fenoldopam, IVF etc... Any anecdotal success with a certain technique? Any pearls of wisdom?

What other factors (pre-op renal insufficiency, clamp time, low intravascular volume, etc..) can help one predict post-op renal failure?

thanks in advance, randy srna

Okay, what do you find to be a beneficial mechanism for renal "protection" during infra/supra renal clamping of the aorta. Lasix, mannitol, low dose dopamine, bicarbonate, fenoldopam, IVF etc... Any anecdotal success with a certain technique? Any pearls of wisdom?

What other factors (pre-op renal insufficiency, clamp time, low intravascular volume, etc..) can help one predict post-op renal failure?

thanks in advance, randy srna

I think the simple answer is that none of the above interventions is proven to avoid renal failure. I think that clamp time along with prexisting renal disease are the crutial factors. It is interesting that clamping BELOW the renals also can have deleterious effects on the kidneys.

Not that we've discussed this in school, but I used to recover AAAs while working in the SICU. I asked this very question to our fellow, and she said mannnitol is commonly used since it provides the added benefit of free radical scavenge. Not sure how this works however.

the only thing that has preliminary good signs for renal protection is fenoldapam... everything else is voodoo - but we use it all the same :)

i find the best indicator for good outcome is who the surgeon is ...

On the subject of fenoldopam. I have had two patients desaturate shortly after starting the infusion. Both patients had pre-existing lung disease.

I have not been able to find any literature/studies regarding the effect of fenoldopam on HPV, but believe that this is probably the mechanism for the desaturation.

Anyone have any similar experiences? Or seen any studies showing a correlation between fenoldopam and interference with HPV.

The desaturations have been rather dramatic with no other obvious cause, much more than with nipride.

That doesn't make too much sense from a pharmacological perspective, since it is my understanding that fenaldopam is a pure D1 agonist. Although D1 receptors are found in the renal, splanic, and mesenteric vasculature, I wasn't aware of any in the pulmonary circulation.

I'm not a CRNA or MDA of course, but I asked this question of the Aneshtesiologist in the OR just last week (as he requested Mannitol during the case). I am intersted to know what is it exactly that happens physiologically when the aorta is clamped above vs below? His answer by the way had to do with "radicals" and he couldn't explain it more...

Thanks. I am often in the OR "helping" but not "helping" if you know what I mean.

There are D1 receptors in the lungs, here are just a couple of the articles from medline that discuss them.

I thought the same thing at one time, so my first search was on whether there were D1 receptors in the pulmonary vasculature. Then I went on to try and find something with regard to stimulation and HPV. No studies that I can find, but that certainly does not mean they don't exist.

At any rate, there is a possibility that this is not what I was seeing. But, within minutes of starting the drug the first patient began to desaturate...I think to myself why is this happening? Nothing has changed EXCEPT that I have started fenoldopam. Next thought what about fenoldopam could do this?....well it is a vasodilator so....disruption of HPV. The next time I started it on a patient with pre-existing pulmonary disease I was on the alert...and once again the patient began to desaturate.

After a little internet research it seemed to me that it could very well be a disruption of HPV. But, it is only a hypothesis. Somebody want to test it?

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9028633&dopt=Abstract

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8529048&dopt=Abstract

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12437142&dopt=Abstract

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10515606&dopt=Abstract

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11956574&dopt=Abstract

smiling,

This may be a laughable question, but is fenoldapam a relatively new drug? I am not familiar with it, but it has been awhile since I was involved with the big, ICU-type cases.

The reason I ask is this. At the national meeting in Boston, there was a speaker from the FDA. It really opened my eyes to the drug approval process. He made it a point to encourage clinicians to report adverse effects. Just because a drug has been tested, and released, doesn't mean there is enough data to predict everything that will happen when it comes into routine use.

So, if this drug is still early in its career, you might be observing an effect that has not yet been documented, or added to the literature. I know this is something I had never really thought about before. But it is very consistent with one of my soapbox beliefs, which is that research is not just for academia in the ivory towers. Those of us in the trenches need to be part of the process too.

This speaker presented the FDA website, which seemed very easy to navigate. I did not keep the specific links, but I think that if you are interested in reporting this, if should be pretty easy to find the correct place on their website to contact them. It will say something like "To report adverse effects..."

loisane crna

I've been using it for a couple of years now. We use it in place of Mucomyst before any procedure using contrasts...CT's, Cardiac cath's, etc...

Donn C.

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