Traumatic Coagulopathy

[Karim Brohi]

Claudia

Thanks for the plug! (and sorry for the delay)

In a nutshell, the paper ascribes the acute coagulopathy we previously
identified (present on admission in 25% of cases and with a 5-fold
associated increase in mortality) as being due to the shocked state and
tissue hypoperfusion, and not related to consumption, acidosis or dilution.


Next it characterizes the coagulopathy as a systemic anticoagulation and
hyperfibrinolysis, and presents evidence that this is due to systemic
activation of protein C in the hypoperfused state.  

Our feeling is that a) this is real, b) shock is the primary determinant of
coagulopathy prior to transfusion, c) we probably need to rethink how we
treat traumatic coagulopathy and d) this has revealed promising targets for
novel therapies.

It's an exciting time for coagulation, transfusion and trauma.  We'll see
how things pan out over the next few years.

Thanks again Claudia

Karim

-----Original Message-----
From: trauma-list-bounces at trauma.org [mailto:trauma-list-bounces at trauma.org]
On Behalf Of claudia
Sent: 25 May 2007 16:56
To: Trauma &amp, Critical Care mailing list
Subject: Traumatic Coagulopathy

Dear listmembers,

I came out from lurking mode to send this  to those who haven´t seen it yet.
I think the study would be greatly complemented by an analysis of thrombin
generation in parallel.
But, overall, it is quite original due to the early timing of the testing.

Congratulations from Brazil, Dr Brohi.

Claudia Teles
Hemostasis Lab Coordinator - Lamina Unit at Pro Cardiaco Hospital Rio de
Janeiro Diagnosticos da America, Brazil