Time for my 2nd donation tweetorial and this one is for @jmugele who let me pick any topic related to the ER.

So let’s learn about the coagulopathy of trauma!

1/n

It is estimated that between 25-35% of injured trauma patients have coagulopathy on arrival to the ER!

This can be 2/2 acidosis, hypothermia, hemodilution or

just the trauma itself

TIC. Trauma induced coagulopathy.

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Patients w/ TIC have
longer stays
more transfusions
more days of mechanical ventilation
multiorgan dysfunction.

Also
3-4x greater mortality
are 8x more likely to die in 1st 24hrs

Most deaths 2/2 hemorrhage in the hospital occur in 1st 6 hrs.

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Other factors contribute to coagulopathy

Acidosis dysfunction of factor complexes involving negatively charged phospholipids and calcium

Hypothermia platelet dysfunction and enzymatic function

this would not be seen on std testing as blood rewarmed 1st

4/n

Resuscitation associated: alterations in hemostatic balance induced by large volumes of IV fluids or unbalanced components.

DIC. Tissue injury Tissue factor exposure, activation of extrinsic pathway. Embolism of thromboplastins from sites of injury risk.

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TIC is independent of, but compounded by those factors.

It involves impairment of hemostasis and activation of fibrinolysis (clot breakdown).

It occurs early and risk with
hypotension
base deficit
injury severity
head injury
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Normally tissue injury clot formation locally thru extrinsic(PT) pathway.

Thrombin (T) can escape injury site but systemic coagulation inhibited by circulating ATIII or by T binding to thrombomodulin(TM) on intact endothelium.

This complex (T-TM) activates protein C.

7/n

Patients w/ TIC have

activated protein C (APC)
inactive PC
soluble TM

Injury severity and shock correlate w/
APC
factors I, II, V, VIII, X

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In addition to dysregulated coagulation, there is

Hyperfibrinolysis
Systemic endothelial dysfxn
inflammation 2/2 APC
Platelet dysfxn

Micro particle release and damage associated molecular patterns may also play a role.

9/n

Prolongation of PT and PTT can be seen. PT prolongation is more common and PTT more specific.

A cutoff of >1.5x reference value is commonly used.

Decreased platelet count contributes to coagulopathy and poor outcomes.

10/n

platelet function plays a role but dedicated testing is not typically available.

Thromboelastography (TEG) and it’s cousin ROTEM, are holistic assessments of clot formation.

Whole blood is used and provides info on clot initiation, strength AND breakdown!
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These are particularly helpful to evaluate platelet function and fibrinolysis.

In TIC, there are 2 problematic fibrinolytic phenotypes.

hyperfibrinolysis is related to TPA release w/o normal compensatory in PAI-1 and is related to the degree of shock

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finrinolytic shutdown correlates with tissue injury and is near complete inhibition of normal clot breakdown

Both of these are associated with mortality compared to patients with normal fibrinolysis (17% in hyper, 3% in normal and 44% in shutdown!)

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Other lab findings include

D-dimer
fibrinogen
factor levels

Several clinical scoring systems exist but aren’t widely used.

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Tx of TIC often includes empiric or TEG based transfusion.

RBCs perfusion and O2 carrying capacity but exacerbate coagulopathy.

For empiric transfusion, most data support 1:1:1 ratio of plasma to RBC to platelets in patients at risk for massive transfusion (MTP).

15/n

If pts not at risk for MTP, transfusions can be based on lab parameters.

Multiple studies have shown improved outcomes using TEG based protocols.

In addition to transfusion, TXA is often used.

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TXA has been shown to all cause and hemorrhage related mortality if given w/in 3 hrs of injury.

One study showed mortality with NNT of 7 in patients requiring MTP.

Other meds used in salvage situations include Novoseven, PCC and DDAVP but data is needed.

17/n

TIC is pretty scary.

Thank goodness for ER doctors like @jmugele that take care of these patients.

18/fin