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Thromboelastography  in Trauma Thromboelastography  in Trauma

Thromboelastography in Trauma - PowerPoint Presentation

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Thromboelastography in Trauma - PPT Presentation

June 5 2015 What is TEG TEG is a functional assay which measures the bloods ability to form a clot Measures clot formation via the tensile strength of fibrinpolymerplatelet complex First developed in Germany in 1948 ID: 933075

trauma teg blood patients teg trauma patients blood time coagulopathy mortality platelet induced coagulation product clot parameters transfusion 001

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Slide1

Thromboelastography in Trauma

June 5, 2015

Slide2

What is TEG?

TEG is a functional assay which measures the blood’s ability to form a clotMeasures clot formation via the tensile strength of fibrin-polymer-platelet complexFirst developed in Germany in 1948

Slide3

How does it work?

The patient’s whole blood sample is placed in a small cup at 37° CA metal pin goes into the center of the cup

The machine slowly spins the cup

As the clot forms, it connects the inside of the cup with the metal pin, and the energy used to move the cup is transferred to the pin

A wire connected to the pin measures the strength of the clot and creates a computerized tracing

J Periop US App Tech. 2012;1(1).

 

Slide4

http://emmedonline.com/emergency_medicine/thromboelastogram

Slide5

Parameters

R (reaction time): Time from activation of the clotting cascade to the formation of fibrinDepends on coagulation factors

Treat short R with

coumadin

Treat prolonged R with coagulation factor replacement/ FFP

Slide6

Parameters

k: Time from formation of fibrin to a defined amplitudeRepresents speed of clot formation

Slide7

Parameters

α (angle): Measures the speed of fibrin build-up and cross-linking

Depends on fibrinogen

Treat a low angle with fibrinogen

replacement/ cryoprecipitate

Slide8

Parameters

MA (maximum amplitude): Represents strength of the fibrin clot correlated to platelet function (80% platelets/20% fibrinogen)Depends on platelets

Treat a low MA with

platelets

Treat an increased MA with ASA/Plavix

Slide9

Parameters

LY30: Percentage decrease in amplitude 30 minutes after the MA is measuredMeasures degree of

fibrinolysis

May consider treatment with

antifibrinolytics

or anticoagulants (primary vs. secondary)

Slide10

Examples

Int

J

Periop

US

Appl

Tech. 2012;1(1).

Slide11

J Periop US App Tech. 2012;1(1).

 

Slide12

Types of TEG

Standard TEGCoagulation initiated with kaolinRapid TEG

Coagulation initiated with tissue factor; ACT (activated clotting time) instead of

r-value

Heparinase

cup

TEG is run twice, once with

heparinase and once without; compare two curves and if no change then no effect from heparinPlatelet mappingBaseline TEG compared to two additional patient samples with maximal stimulation of platelets with AA and ADP; computer calculates difference in MA as % inhibition

Slide13

Trauma induced coagulopathy

1981 to ̴2007: “Bloody vicious cycle" Acidosis from tissue injury and shock, hypothermia from fluid infusions and exposure, and

hemodilution

from blood and fluid

administrations (“lethal triad”)

Leads to secondary development of trauma induced coagulopathy

https://www.aacc.org/publications/cln/articles/2014/july/coagulation 

Slide14

Trauma induced coagulopathy

2007: Distinct primary

disorder, cell-based model

Initiation (tissue factor on cells), amplification (platelet activation), propagation (thrombin generation)

H

ypoperfusion

leads to excess activation of protein C, which inhibits thrombin generation, impairs clot formation, and degrades any clots that have

formed

Inten Care Med. 2011;37.

 

Slide15

Trauma induced coagulopathy

Occurs in 30% of trauma patientsMost common preventable cause of postinjury mortality

Associated with:

8x increased 24 hour mortality

4x increased total mortality

longer ICU and total hospital stay

increased

risk for renal insufficiency and multiple organ failurelonger need for ventilatory support

tendency

towards increased lung injury

Classical coagulation tests (PT/PTT) are only weakly predictive of bleeding in trauma patients, do not predict extent of bleeding, and results are not available rapidly enough

Inten Care Med. 2011;37.

 

Slide16

Trauma induced coagulopathy

J Trauma. 2003;54(6).

 

Slide17

Guidelines

We recommend that routine practice to detect post-traumatic coagulopathy include the measurement of international normalised ratio (INR), activated partial thromboplastin

time (APTT), fibrinogen and platelets. INR and APTT alone should not be used to guide

haemostatic

therapy (Grade 1C). We suggest that

thrombelastometry

also be performed to assist in characterising

the coagulopathy and in guiding haemostatic therapy (Grade 2C).

Crit Care. 2010;14:R52.

Slide18

TEG in trauma induced coagulopathy

Turn around timeDiagnosis of TICPrediction of blood product use Prediction of mortality

Critical

Care. 2014;18.

Slide19

Turn around time

Slide20

Turn around time

J Trauma. 2009 Apr;66(4

).

Slide21

Turn around time

Prospective study of 272 trauma patientsEarly r-TEG (activated clotting time, k-time) available within 5 minutesLate r-TEG (

α

angle, MA) within 15 minutes

Standard clotting tests (PT/INR/PTT/platelet count) within 48 minutes (p=<0.001)

J Trauma. 2011;71(2).

Slide22

Diagnosis of trauma induced coagulopathy

Slide23

Diagnosis of trauma induced coagulopathy

Observational study of 69 blunt trauma patients

7

hypocoagulable

by TEG (mean ISS 28.6)

1

hypocoagulable by PT/PTT

6/7 hypocoagulable patients received blood45 hypercoagulable by TEG (mean ISS 13.1)17 normal by TEG (mean ISS 3.7)

Only ISS and TEG were predictive of blood product use in the first 24 hours (p=<0.05)

J Trauma. 1997;42(4).

 

Slide24

Diagnosis of trauma induced coagulopathy

20 traumatic brain injury patients versus 10 healthy controlsTBI patients have a lower platelet count (180,000 per microliter vs 256,000 per microliter in healthy controls, p<0.005) and reduced platelet response to AA on platelet mapping (mean 22% vs 73% in healthy controls, p<0.001)

J Neurotrauma. 2007;24(11).

 

Slide25

Diagnosis of trauma induced coagulopathy

Review from 1970 to 2013 to determine diagnostic accuracy of TEG or ROTEM for diagnosing TIC3 studies using ROTEM and 0 studies using TEG

300, 90, and 40 patients

Clot amplitude was the only potential indicator

5 min: 70-96% sensitivity and 86-58% specificity

10 min: 100% sensitivity and 70% specificity

15 min: 88% sensitivity and 100% specificity

TIC was defined as INR of 1.2 or greater or 1.5 or greater

Cochrane Library. 2015;2.

 

Slide26

Prediction of blood product usage

Slide27

Prediction of blood product usage

Observational study of 69 blunt trauma patientsTEG, PT, PTT, revised trauma score, ISS6 patients received transfusion in first 24 hours

Only ISS and TEG were predictive of blood product use in the first 24 hours (p=<0.05)

J Trauma. 1997;42(4).

 

Slide28

Prediction of blood product usage

Retrospective study of 44 penetrating trauma patientsINR, PT, and PTT were increased in 39%, 31%, and 37% but did not correlate with use of blood products (p>0.05)

MA correlated with blood product use as well as platelet count (p,0.01)

Patients with reduced MA (23) used more blood products and had lower platelet counts and hematocrit.

J Trauma. 2008;64(2).

 

Slide29

Prediction of blood product usage

Prospective study of 272 trauma patientsRapid TEG available in trauma bayACT predicted RBC (p < 0.001), plasma (p < 0.001) and platelet (p <0.001) transfusions within 2 hours of arrival

ACT > 128 sec predicted massive transfusion > 10 units in first 6 hours (p = 0.01)

ACT < 105 sec predictions patients who did not receive any transfusions in first 24 hours (p = 0.04)

J Trauma. 2011;71(2).

Slide30

Mortality

Slide31

Mortality

23 trauma patients5 patients with hyperfibrinolysis H

igher injury severity score (75 vs 20, p<0.05)

Higher INR (8.2 vs 1.3, p<0.05)

Lower fibrinogen (0.0 vs 2.2 g/L, p<0.05)

Higher mortality rate (100% vs 11%, p<0.05)

Br J Anaesth. 2008;100(6).

 

Slide32

Mortality

Prospective study of 795 major trauma patientsElevated Ly30 was an independent predictor of mortalityCombined with GCS ≤ 8, SBP ≤ 90mmHg,

Hgb

< 11g/

dL

, and BE < -6mEq/L to create 5-variable 24 hour mortality predictive model (AUROC 0.88, HL goodness-of-fit 0.90)

All parameters available within 30 minutes.J Trauma

. 2014 May;207(5).

 

Slide33

Mortality

Retrospective review 131 trauma patients with pelvic fractureTEG R > 6 was independently associated with death independent of injury severity (OR 16, P=0.0001); death rate 52%No significant association between traditional coagulation tests (PT/INR/PTT) and death rate

Orthopedic Surgery 2015;7(1).

 

Slide34

Additional points

Slide35

Additional points

What about hypercoagulable TEG results? What does this mean in the trauma setting?

Slide36

Hypercoagulable TEG in cardiac surgery patients

124 patients scheduled for CABGDivded

into two groups: TEG-

hypercoagulable

and TEG-

normocoagulable

3 months post-op, all had CT to evaluate graft patency

359 grafts, 186 TEG-HC and 173 TEG-NCNo difference in bypass graft occlusion (p=0.9)Rate of major adverse cardiovascular and cerebral events significantly higher in TEG-HC (30% vs 9%, p=0.004)

Scandinavian Cardiovascular Journal 2013;47(2).

 

Slide37

TEG-based blood administration algorithms

Studies in other populations (cardiac surgery) have found some benefit to TEG-based blood administration algorithms, does this apply to trauma patients?

Slide38

TEG-guided transfusions in pediatric surgery patients

78 pediatric cardiac surgery patientsConventional transfusion vs algorithm/TEG guided transfusion for 12 hours post-op

TEG-guided transfusion significantly reduced post-op bleeding (9 vs 16 mL/kg, p<0.001), PRBC transfusion requirement (11 vs 23 mL/kg, p=0.005), and ICU stay (60 vs 71 h, p=0.014)

Platelet and plasma transfusions were similar, but occurred earlier in TEG-guided group

Brit J Anesth. 2015;114(1).

 

Slide39

Special populations

Slide40

Special populations

Effect of differing baseline TEG results in special populations, and potential impact during trauma:NeonatesAlcohol intoxication

Use of newer anticoagulants

Uremia

Slide41

Neonates

Limited data in neonates, particularly no data on premature neonatesSmall number of healthy infants showed age dependent accelerated initiation and propagation of coagulation despite prolonged standard coagulation tests; clot firmness and fibrinolysis similar to adults

J Maternal-Fetal and Neonatal Med 2012;25(s4).

 

Slide42

Effect of alcohol

35-50% of trauma patients are acutely intoxicated Alcohol has little effect on standard coagulation tests, transfusion requirements, or outcome, but does affect TEG results:

Prolonged R time (5.91 vs 4.43 min, p=0.013)

Decreased angle (66.5 vs 70.2 degrees, p=0.001)

Trend toward decreased MA (63.44 vs 64.93 mm, p=0.063)

J Trauma Acute Care Surg 2014;77(6).

 

Slide43

Newer anticoagulants

It is unclear how newer anticoagulants may or may not affect TEG parameters

Slide44

Uremia

Baseline TEG r-time, k-time, α angle, and MA are hypercoagulable in uremic patients compared to controls (p<0.05), and fibrinolysis was decreased in uremic patients

J Clin Anesth. 1997;9(6).

 

Slide45

Summary

Many small, single center, observational studies of TEG in traumaTEG results are available more rapidly than standard coagulation testsSome evidence to suggest TEG may allow for early diagnosis of trauma induced coagulopathy and may predict blood product usage and mortality, but associations with specific parameters are variable

Randomized trials are lacking

It’s unclear how baseline differences in TEG in various populations might impact TEG results during trauma