Interpreting the Coagulopathy of Trauma-Shock

Interpreting the Coagulopathy of Trauma-Shock

FacultyFaculty

2

Bryan A. Cotton, MD, MPH

The University of Texas Health Science Center

Houston, Texas

Richard P. Dutton, MD, MBA

University of Maryland School of Medicine

R Adams Cowley Shock Trauma Center

Baltimore, Maryland

Martin A. Schreiber, MD, FACS

Oregon Health & Science University

Portland, Oregon

Mortality After TraumaMortality After Trauma

Stewart RM, et al. J Trauma . 2003;54:66-71.3

Retrospective review of trauma death at level I trauma center (Stewart et al, 2003)

● Leading causes of death CNS, 51% Shock, 21% CNS + Shock, 16%

Time to DeathTime to Death

• Within 12 h of arrival to ED

50% of trauma patients are dead

• Within 48 h of arrival to ED ≈70% of trauma patients are dead

• Early interventions can impact a patient’s life

Stewart RM, et al. J Trauma. 2003;54:66-71. 4

Coagulopathy and MortalityCoagulopathy and Mortality

• Retrospective review

• N=1867, 24.4% of patients significantly coagulopathic

• Coagulopathy defined as:

1.5 x normal• Mortality

Overall, 19.5% Noncoagulopathic, 10.9% Coagulopathic, 46%

Brohi K, et al. J Trauma. 2003;54:1127–1130. 5

Adapted from Brohi K, et al. J Trauma. 2003;54:1127–1130.

Coagulopathy and Mortality

6

100

80

60

40

20

0

Mortality

0-14 15-29 30-44 45-59 59-64

Injury Severity Score

Per

cen

t M

ort

alit

y

Normal

Coagulopathy

Acute Coagulopathy of TraumaAcute Coagulopathy of Trauma

7

2.1

Acute Coagulopathy of TraumaAcute Coagulopathy of Trauma

8

Adapted with permission from Brohi K, et al. Ann Surg. 2007;245:812-818.

101112131415161718

2.2-4.1 4.2-7.6

Base Deficit (mEq/L)

Pro

thro

mb

in T

ime

(s)

7.7

Shock as a Mechanism of CoagulopathyShock as a Mechanism of Coagulopathy

9Adapted from Hoffman M. Blood Rev. 2003;17:S1-S5.

7.72.1

Base Deficit and Protein CBase Deficit and Protein C

10

Adapted with permission from Brohi K, et al. Ann Surg. 2007;245:812-818.

20

40

60

80

2.2-4.1 4.2-7.6

Base Deficit (mEq/L)

Th

rom

bo

mo

du

lin(n

g/m

L)

Base Deficit and Protein CBase Deficit and Protein C

11Brohi K, et al. Ann Surg. 2007;245:812-818.

● Activated protein C is potent anticoagulant Activates fibrinolysis

• In shock state, protein C activation→coagulopathy

• Decrease in protein C concentration associated with marked increase in mortality

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Protein C Pathway

● Thrombomodulin increased

● Binds protein C

● Produces activated protein C

● Inhibits factors V, VIII

● Accelerates fibrinolysis

Rate of Heat TransferRate of Heat Transfer

Gentilello LM. In: Maull KI, et al, eds. Advances in Trauma and Critical Care. Vol 9. St Louis, MO: Mosby; 1994:39-79.

Q=mc(T2 - T1)

Rewarming TechniqueHeat Transfer (kcal/hr)

Airway rewarming 8-12

Overhead radiant warmer 17

Heating blankets 20

Convective warmers 15-26

Body cavity lavage 36

Continuous arteriovenous rewarming 92-139

Cardiopulmonary bypass 710

13

Effect of Hypothermia and DilutionEffect of Hypothermia and Dilution

Gubler KD, et al. J Trauma. 1994;36:847-851.14

Dilution

No Dilution

PT

(se

c)

Temperature (°C)

13

15

17

19

21

23

25

27

28 30 32 34 36 38

Martini WZ, et al. J Trauma. 2005;58:1002-1010.

Changes of Plasma Fibrinogen Concentration and Platelet Count

15

• Porcine trauma model

• HCI-induced hypothermia and acidosis pH, 7.1 Temperature, 32°C

• Results: Increased hypothermia and acidosis significantly decreased fibrinogen concentration and PLT counts

Thrombin GenerationThrombin Generation

Posted with permission from Martini WZ, et al. J Trauma. 2005;58:1002–1010.

Control

Hypothermic

Acidotic

Combined

*P.05, different from normal value at the same quench time point.

16

0

1500

3000

4500

6000

7500

9000

0 1 2 3 4 5 6 7Quench Time (min)

[TAT

] (µg

/L)

*

*

* **

*

*

**

*

*

*

Acute Coagulopathy of Trauma (ACOT)Acute Coagulopathy of Trauma (ACOT)

Hess JR, et al. J Trauma. 2008;65:748-754. 17

Trauma Hemorrhage

ShockResuscitation

Coagulopathy ACoTS

FactorConsumption

FibrinolysisAcidemia

HypothermiaHypothermia

Dilution

Inflammation

Other Diseases

Medications

Genetics

ConclusionsConclusions

• Coagulopathy following trauma is complex

• Severely injured are coagulopathic immediately following injury

• Most of what we do makes it worse

• Early treatment should focus on stopping bleeding and correcting coagulopathy

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Bryan A. Cotton, MD, MPH

Associate Professor of Surgery

The University of Texas

Health Science Center and

Center for Translational Injury Research

Houston, Texas

Has the way in which you manage the coagulopathy of trauma changed considerably over the course of your career as a surgeon?

20

Historically

• Treatment delayed

• Resuscitation emphasized

Currently

• Arrest bleeding

• Correct coagulopathy early

• Downplay resuscitation

• Adequate organ perfusion

• Limit fluids

21

22

Richard P. Dutton, MD, MBA

Professor of Anesthesiology

University of Maryland School of Medicine

Attending Anesthesiologist

R Adams Cowley Shock Trauma Center

Baltimore, Maryland

In the upcoming year, what types of research can we expect to see disseminated in the medical literature concerning resuscitation methods and strategies for managing the coagulopathy of trauma, and what will be the focus of those papers?

23

• Papers on role of recombinant factor VIIa in trauma

Results from prospective, randomized trial expected ≈600 patients enrolled

Third or fourth largest trauma study ever conducted

• Papers on plasma:red cell ratio

Match therapy to patient

Base ratio on needs of particular patient

Prospective and randomized trials24

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