TEG ® Interpretation Review TRACING BOOTCAMP Kevin F. Lynch, RN/CCRN, MSN, MBA Senior Clinical Specialist Haemonetics

TEG® Interpretation ReviewTRACING BOOTCAMP

Kevin F. Lynch, RN/CCRN, MSN, MBASenior Clinical Specialist

Haemonetics

Copyright © 2009 Haemonetics Corp.

Cascade Model: Tests

Represents hemostasis Two independent activation

pathways Pathways converge at the

final common pathway

PT, aPTT: based on cascade model

Measure coagulation factor interaction in solution

Determine if adequate levels of coagulation factors are present for clot formation

Pr ombin (II) Thr

Ca2+

XI XIa

X

VIIa/TF VII

IX

XII XIIa

XIIIaXIII

+

V V PTaPTT

Platelet count

Platelet

Endothelial CellsChange in Platelet ShapeArea of Injury

Collagen

ADP AA

tPA

Plasminogen PlasminFibrin Strands

Degradation Products

Fib

rino

lysisR

ed C

lot

Th

rom

bin

Gen

eration

Wh

ite Clo

t

Co

agu

lation

Cascad

e


Cell-Based Model

• Reflects in vivo

Occurring on cell surfaces Tissue factor bearing cells Platelets

Overlapping phases: Initiation (TF bearing cells) Amplification (platelets) Propagation (platelets)

• The coagulation cascades are still important, but are cell-based

extrinsic pathway: surface of tissue factor bearing cells

intrinsic pathway: surface of platelets

• Routine coagulation tests do not represent the cell-based model of hemostasis

[Monroe, DM. et al. Arterioscler Thromb Vasc Biol. 2002;22:1381]

Tissue factorbearing cells

1. Initiation

Platelets

Activated platelets

2. Amplification

3. Propagation

IIa

IIa


BleedingThrombosis

Strength StabilityRate

Defining the PositionLooking at Clot Function


Global Hemostatic Status

Initiation

Platelet plug formsFibrin strands form

Clot grows

Maximum clot forms

Clot degradation takes over

Clot dissolvedDamage repaired

R

MA

LY30Angle


TEG Analysis – InterpretationExamining the parameters

1. R-time to first fibrin strand

2.K-rate of clot development (20 mm in height)

3.Angle-rate of clot development

4.MA- maximum clot strength

5.LY/EPL-clot breakdown, clot stability


R

Parameter

HemostaticActivity

HemostaticComponent

Dysfunction

Hypo-coagulable

Hyper-coagulable

K

MAMA

30 min LY30

EPL

a

TEG TechnologyParameters


R

Clot time

IIa generationFibrin formation

Coagulationpathways

Parameter

HemostaticActivity

HemostaticComponent

Hypo-coagulable

Hyper-coagulable

R (min)

¯R (min)

Dysfunction


R

Clot time


Coagulationpathways

Parameter

HemostaticActivity

HemostaticComponent

Hypo-coagulable

Hyper-coagulable

R (min)

¯R (min)

K (min)¯ a (deg)

¯K (min) a (deg)

Clot rate

Fibrin meshFibrinplatelet

Coag pathwaysplatelets

K

a

Dysfunction


R

Clot time


Coagulationpathways

Parameter

HemostaticActivity

HemostaticComponent

Hypo-coagulable

Hyper-coagulable

R (min)

¯R (min)

K (min)¯ a (deg)

¯K (min) a (deg)

¯MA

MA

Clot rate

Fibrin X-linkingFibrinplatelet


K

a

Maximum clot strength

Platelet – fibrin interactions

Platelets (~80%)Fibrin (~20%)

MA

Dysfunction


R

Clot time


Coagulationpathways

Parameter

HemostaticActivity

HemostaticComponent

Hypo-coagulable

Hyper-coagulable

R (min)

¯R (min)

K (min)¯ a (deg)

¯K (min) a (deg)

¯MA

MA

Clot stability

Reduction in clot strength

Fibrinolysis

Clot rate

Fibrin X-linkingFibrinplatelet


K

a

Maximum clot strength

Platelet – fibrin(ogen) interactions

Platelets (~80%)Fibrin(ogen (~20%)

MA

30 min LY30

EPL

LY30 > 7.5%EPL > 15%

N/A

Dysfunction


Interpretation: Applying the ParametersTEG Decision Tree

Kaolin sample

No

Interpretation Practice

Example 1


Example 1At 15 minutes

*54.3*

What information is available at this point?



Is this a normal tracing? Yes or No


Example 2



*10.3*

Is there a risk for bleeding due to factor dysfunction or heparin?

*1.5*



*54.8*

If this sample was run coming off cardiac bypass pump, what is the bleeding risk after heparin reversal?



If the patient were bleeding, would FFP be the appropriate blood product?

Interpretation Practice Not typical (but it happens)

Example 3



Patient is bleeding.

*0.0* *0.0*



Patient is bleeding.

Results suggest Primary Fibrinolyisis.



Consider use of anti-fibrinolytic


Example 4



This patient is in the ICU. Has heparin been reversed? Explain.

Black = K Green = KH


Example 6Samples stopped at 35 minutes

Are any coagulopathies indicated from these results?

What are they?

What are the other possibilities if the patient is bleeding?



Example 5



This patient has been given Protamine. Has heparin been reversed?



Example 7Samples stopped

What are the other possibilities if the patient is bleeding?

Note the R in both cups.


Interpretation PracticeNot typical (but it happens)

Example 6



What are the other possibilities?

Heparin, No CaCl, or real result.

Call the lab and repeat the test.

*25.3*2 ― 8

Group Exercise #1


Exercise 1At 15 minutes

*72.5*

Coagulopathies indicated at this point?

Possibilities if the patient is bleeding?

Hypothermia

Anatomical

VWf


Exercise 1Completed

What actions might a clinician take if this is presurgical? Post surgical?

What is the significance if this patient is on an antiplatelet drug such as Plavix® and is going into surgery? What should be done?

Group Exercise #2





*40.7*


Undetermined coagulopathies at this point?



Exercise 2Sample Stopped


Note the MA

Group Exercise #3





*54.2*


Exercise 3Sample Stopped


Group Exercise #4





*70.7*





19.0 *19.0*


Exercise 4Completed



This is 2 days post-op. If the post-op tracing had indicated the patient was on the edge of the hypercoagulable side, what is the concern?

Group Exercise #5





*19.8*


Exercise 5Completed


Group Exercise #6


Exercise 6Patient after surgery

After surgery, heparin was reversed, and heparin rebound was not present (checked with K vs. KH sample). This is the K sample.

Patient was bleeding and give 6 units of platelets. Why?


Exercise 6Completed

What if the patient is oozing? Bleeding?

Group Exercise #7





*12.2*



Note length of R, poor K and Alpha

*24.0*


Exercise 7Completed

Requires multiple blood products

FFP, CYRO and Platelets

*24.0*


Questions?

Back-Up:Additional TEG® Cases Theories and Applications

Kevin F. Lynch, RN/CCRN, MSN, MBASenior Clinical Specialist

Haemonetics


Primary Fibrinolysis CaseBaseline Heparinase Cup


Primary Fibrinolysis CaseProducts and Drugs

Patient received:Perioperative 15g Amicar during the case

Post protamine4 FFP2 Platelets, 13 mg DDAVP

ICU 1g drip Amicar 24 hrs post No further blood products


Primary Fibrinolysis Case Post Protamine

TEG ® Analysis Valve CABG Aortic Tear


Valve CABG Aortic Tear Baseline


Valve CABG Aortic Tear Rewarm

Patient came off bypass Surgeon nicked the aorta



2 FFP given Patient was reheparinised placed back on bypass



Circ arrested, Came off bypass again

Post protaminePatient given 2 platelet packs and 1 cryo (10 pack)Patient was closed with no further bleeding


Valve CABG Aortic TearPost Protamine


Valve CABG Aortic Tear Before and After

Before

After


Hemorrhagic TEG Tracing

30 min

HAEMONETICS CORPORATION COMPANY CONFIDENTIAL

Pradaxa Case Report

Kevin F. Lynch, RN/CCRN, MSN, MBA

TEG Clinical Consultant

Copyright © 2009 Haemonetics Corp.HAEMONETICS CORPORATION COMPANY CONFIDENTIAL72

Oral direct thrombin inhibitor Indications for use:

Indicated to reduce the risk of stroke or systemic embolism in patients with non-valvular atrial fibrillation

Prescribed in 75mg or 150 mg tablets based on CrCl Trial comparing Pradaxa to Warfarin

Most common reason for discontinuation of Pradaxa Increased bleeding & GI events

Number of patients suffering myocardial infarction greater when taking 150 mg of Pradaxa versus Warfarin

Some P-gp inducers (rifampin) can reduce dabigatran exposure & effectivness

History of Pradaxa (dabigatran)


Rifampin

Rifampin increases the activity of enzymes in the liver that break down various medicines. As a result, it can increase the removal of these medicines from the body, making them less effective.

Anticoagulants such as warfarin and acenocoumarol. (People taking anticoagulants should have their blood clotting time (INR) monitored closely after starting and stopping treatment with rifampin.)


68 year old male History of Coronary Artery Disease 4-vessel bypass in March, 2010 Atrial Fibrillation Symptoms of TIA, stroke in the months following his bypass Placed on Pradaxa

Fall, 2010

Admitted to hospital for Renal & Disc/Spinal Biopsies May, 2011 Diagnosed with renal insufficiency Traditional coagulation tests abnormal

Patient History


Initial TEG 12 hours after last dose of PradaxaCreatinine: 6.3, BUN: 109, INR: 2.18


Platelet Mapping ADP


Platelet Mapping AA


TEG: 24 hours since last doseCreatinine: 6.6, BUN: 109, INR: 2.03


TEG: 48 hours since last doseCreatinine: 7.7, BUN: 117, INR: 1.7


In an attempt to correct his INR & allow physicians to proceed with the procedure: Attending MD ordered 4 units of FFP for transfusion Documentation has shown FFP to be unsuccessful in reversing

Pradaxa

Transfusions


TEG after 4 units of FFPINR: 1.73


FFP transfusions ineffective TEG expressed more dilutional/deficient effect than a procoagulant

effect (R 20.8 mins)

Began to have concerns about further ischemic events As Pradaxa wearing off, TEG platelet function & clot strength

increasing (MA & G)

Decision made to begin heparin infusion Try and reduce risk for thrombosis temporarily Easy to reverse, if needed

Concerns


2 hours after heparin infusion started500-600 IU/hour, No bolus


Heparinase TEG result


Following morning, no heparin effect expressed by TEG

Creatinine: 7.8, BUN: 117, INR: 1.87


Trauma Case Study


42 y/o off-duty firefighter, hanging Christmas lightsFalls onto metal fence from roof (20 feet)Ruptured spleen and liver laceration, as well as lung contusions and respiratory failure

Blunt injury trauma


Baseline shows 100% ADP and AA inhibition, and significant heparinoid effect. Protamine 50 mg given and during surgery received 8 PRBC & 7 FFP. Abdomen open

but packed, with bleeding slowly increasing over next 24 hours.


Bleeding increasing from abd. drain. Heparin effect seen. Protamine 50mg given and also 3u FFP. No Platelets given.


12 hours later, bleeding increasing. Heparin effect treated with Protamine, and 2 FFP given for factor deficiency.


Protamine 25mg and 3u FFP. Bleeding tapers off and hemodynamics stabilize over next few days.


This tracing shows the effects of LMWH started.after bleeding was controlled.


This tracing shows extreme response to LMWH. Bleeding from wound vac started to increase, so LMWH stopped. TEG returned to normal over next 24 hours.


Bleeding continues 3 hours later. Protamine 25mg given and 4 u FFP given.


Protamine 50mg given (R 25.5 min .) and 1 SDP.(Platelets)


R decreased from 23.6 with heparinase. Still 15.4, so 3u FFP given. Platelets OK.

Bleeding stopped over next 3-4 hours.


Final TEG. All coagulopathies corrected. No more heparinoid effect. Thromboprophylaxis not restarted due to patient’s sensitivity to it, and normal TEG

results. MSOF did not resolve, and patient died the following week.


Haemonetics TEG Case Study: Data Collection FormPatient Age: ____ Fill in all data that is applicable and available.

M or F

Admitting diagnosis:__________________________

Relevant History:__________________________________________________________________________________________

_______________________________________________________________________________________________________

Other procedures affecting hemostasis (IABP, VAD, stents, valves, sepsis, etc.):_______________________________________

_______________________________________________________________________________________________________

Meds affecting hemostasis (include supplements) and dosage:_____________________________________________________

_______________________________________________________________________________________________________

Relevant labs: PT/INR____________ PTT_________ Plt Cnt_______ H/h_____________ TT_________ BT______ Fib____

D-dimer_________ FDP/FSP_______ ATIII level______ Prot C________ Prot S_________ FactorVLeiden_____ Lupus Anti_____

vWF______ Russell Viper Venom Time________ Other____________________________________________________

Procedure or Surgery:___________________________________________________ if CV, give CPB time____________

If valve replacement, is it mechanical or tissue, which location?_________________________________________________

Baseline TEG/PM, yes or no?_______ Interpretation_____________________________________________________________

Decisions based upon baseline data (delay, meds, etc.)___________________________________________________________

Intra-op TEG (on-pump, p-prot, etc)?________ Interpretation______________________________________________________

Decisions made (ready products, administer products, what and how much, meds given)______________________________

_______________________________________________________________________________________________________

Post-op TEG (PM if needed)?___________ Interpretation________________________________________________________

Decisions made (products, meds, anticoag/antiplt meds for thromboprophylaxis)_____________________________________

_______________________________________________________________________________________________________

Outcome (bleeding, thrombosis, H/H if no drains, day of discharge)_________________________________________________

______________________________________________________________________________________________________

Savings to hospital (bed days, products saved, other benefits), if not already using TEG protocols________________________

_______________________________________________________________________________________________________


Cases TEG Analysis

Questions?

Thank You!

Documents

TEG ® Interpretation Review TRACING BOOTCAMP Kevin F. Lynch, RN/CCRN, MSN, MBA Senior Clinical Specialist Haemonetics