Sounds rather counter intuitive doesn't it?
But is it?
Reuters Health Information
Antiplatelet Therapy May Protect in Severe Blunt Trauma
Dec 31, 2012
http://www.medscape.com/viewarticle/776900?src=wnl_edit_medn_surg&spon=14
This arrived in my mailbox and found its way to my "to do list" rather quickly.
For those who have been around a while, or know me personally, I have a rather good understanding of shock. But I must say that this one even caught me by surprise.
So, since I know that coagulation and inflammatory cascades are linked, I figured I would explore this idea a little more.
For those of you just joining us, a bit of background:
Clotting, anticlotting, inflammation, antiinflammatory, kininogen, and it's mediators are all linked by common molecules.
That means, anytime you have one, you have them all.
Clinically managing shock patients of any kind requires trying to manage both inflammation and O2 delivery. (it is so important I don't even think of them as seperate issues anymore)
The trouble is mediating immunity is very difficult, largely lacks supporting evidence, and is extremely expensive. Basically a winning trifecta of "why the hell would we do that?"
Now this article talks about modulating proclotting and so by default, proinflammatory mediators. It perhaps overgenerously alludes that ARDS is the major problem in blunt trauma. But ARDS is caused by inflammation. Several molecular level treatments (aka drugs) directly affecting inflammation have not yiedled promising evidence. Or really significant evidence at all. But there have been some.
Now I wrote this up here in an EMS forum, really to organize my thinking on it, but there is a very major EMS implication.
We all know that resuscitation of blunt trauma arrest is basically futile. The focus on treating shock in EMS is entirely on restoring O2 delivery. The inflammatory aspects of shock are not even mentioned, much less taught.
But this article calls into question whether or not EMS should be involved in the inflammatory response and treatments and how.
It might mean that blunt arrest survival increases or morbidity from blunt trauma not at the arrest level decreases.
Before you become a nay sayer though, some of us older people remeber protocols for steroid injection in spinal injury. That was postulated to reduce swelling from inflammation that impinges on the cord. It also was supposed to reduce direct inflammatory damage to injured cells so they may survive and return to normal function. All in all, it went away because it didn't work fast enough to reduce spinal damage. But nobody ever considered it may be doing something else.
That is one of the biggest problems with "EBM" experiments that focus on what to do with no concern for why.
Focusing on single organ or system specific treatments instead of total organismal homeostasis is the plague of modern medicine.
In multiple pathologies, acute reversal is often just as detrimental as the pathology itself. EMS has always looked at the pinnacle of hemorrhage control as stopping bleeding. Maybe it is time to consider not acutely revering that either.
Afterall, control of hemorrhage is not the same as stopping it.
Perhaps you have a thought on this or an experience to share?
But is it?
Reuters Health Information
Antiplatelet Therapy May Protect in Severe Blunt Trauma
Dec 31, 2012
http://www.medscape.com/viewarticle/776900?src=wnl_edit_medn_surg&spon=14
This arrived in my mailbox and found its way to my "to do list" rather quickly.
For those who have been around a while, or know me personally, I have a rather good understanding of shock. But I must say that this one even caught me by surprise.
So, since I know that coagulation and inflammatory cascades are linked, I figured I would explore this idea a little more.
For those of you just joining us, a bit of background:
Clotting, anticlotting, inflammation, antiinflammatory, kininogen, and it's mediators are all linked by common molecules.
That means, anytime you have one, you have them all.
Clinically managing shock patients of any kind requires trying to manage both inflammation and O2 delivery. (it is so important I don't even think of them as seperate issues anymore)
The trouble is mediating immunity is very difficult, largely lacks supporting evidence, and is extremely expensive. Basically a winning trifecta of "why the hell would we do that?"
Now this article talks about modulating proclotting and so by default, proinflammatory mediators. It perhaps overgenerously alludes that ARDS is the major problem in blunt trauma. But ARDS is caused by inflammation. Several molecular level treatments (aka drugs) directly affecting inflammation have not yiedled promising evidence. Or really significant evidence at all. But there have been some.
Now I wrote this up here in an EMS forum, really to organize my thinking on it, but there is a very major EMS implication.
We all know that resuscitation of blunt trauma arrest is basically futile. The focus on treating shock in EMS is entirely on restoring O2 delivery. The inflammatory aspects of shock are not even mentioned, much less taught.
But this article calls into question whether or not EMS should be involved in the inflammatory response and treatments and how.
It might mean that blunt arrest survival increases or morbidity from blunt trauma not at the arrest level decreases.
Before you become a nay sayer though, some of us older people remeber protocols for steroid injection in spinal injury. That was postulated to reduce swelling from inflammation that impinges on the cord. It also was supposed to reduce direct inflammatory damage to injured cells so they may survive and return to normal function. All in all, it went away because it didn't work fast enough to reduce spinal damage. But nobody ever considered it may be doing something else.
That is one of the biggest problems with "EBM" experiments that focus on what to do with no concern for why.
Focusing on single organ or system specific treatments instead of total organismal homeostasis is the plague of modern medicine.
In multiple pathologies, acute reversal is often just as detrimental as the pathology itself. EMS has always looked at the pinnacle of hemorrhage control as stopping bleeding. Maybe it is time to consider not acutely revering that either.
Afterall, control of hemorrhage is not the same as stopping it.
Perhaps you have a thought on this or an experience to share?
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