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Mon Jun 4 22:05:33 BST 2007

I think you're absolutely right.  Teleologically it's easy to see that
during low flow states, organ beds should become relatively hypocoagulable
to avoid intravascular thrombosis.  This would confer a significant
evolutionary survival analysis.  However, global hypoperfusion due to a
systemic insult like severe shock would then lead to a systemic
hypocoagulable, hyperfibrinolytic state, which is bad if you're actually
bleeding!!!

Conventional mechanisms of therapy, augmenting the extrinsic pathway and
thrombin generation (FFP, Factor VII etc) might temporarily overwhelm the
anticoagulant response but would simultaneously, in the presence of shock
and endothelial thrombomodulin presentation, lead to increased activation
of  protein C, reduced fibrinogen utilization and increased fibrinolysis.
This anticoagulant/hyperfibrinolytic state probably persists longer than the
FFP or F7a, and thus patients would be at risk of re-bleeding episodes -
which is certainly something that has been seen both in the laboratory and
clinically.

Probably dilution, hypothermia etc are factors after massive transfusion.
But while patients are systemically hypoperfused, this underlying process
will continue to predominate.  Therapies that particularly target these
derangements may be more effective.  Of course limiting the time in shock is
the best we can do at present.

Paper attached.

Karim

On 04/06/07, Kashuk, Jeffry <Jeffry.Kashuk at dhha.org> wrote:
>
> Agree that acidosis,hypothermia and coagulopathy (consumptive and/or
> dilutional) are the end result of shock/tissue hypoperfusion.... this has
> been known/realized for some time. A fascinating question is: what is the
> reason for this early anticoagulation and hyperfibrinolysis? Could it be a
> mechanism of "protection" from end organ thrombosis?(counter-intuitive if
> there is a 5-fold increase in mortality).
> How do you think we ought to be "re-thinking" our treatment of traumatic
> coagulopathy? Are you suggesting that conventional Rx regimens may really
> not be effective? Do different patients manifest different pathways of
> coagulation disorders?
> JK
> Jeffry L. Kashuk, M.D, FACS
> Surgery, Trauma, Surgical Critical Care
> Denver Health Medical Center
> 777 Bannock St, MC 0206
> Denver, CO 80204
> Ph 303-436-6558
> Fax 303-436-6572
>
>
> -----Original Message-----
> From: Karim Brohi [mailto:karim at trauma.org]
> Sent: Sunday,June 03,2007 5:08 AM
> To: 'Trauma &amp; Critical Care mailing list'
> Subject: RE: Traumatic Coagulopathy
>
> 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
>
>
>
>
>
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