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

2. Change in Platelet Shape
Cascade Model: Tests PT
aPTT
Platelet count
Platelet
Endothelial Cells
Change in Platelet Shape
Area of Injury
Collagen
ADP AA
tPA
Plasminogen
Plasmin
Fibrin Strands
Degradation Products
Fibrinolysis
Red Clot
Thrombin Generation
White Clot
Coagulation Cascade
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
In the cascade model, hemostasis is represented as two somewhat independent coagulation protein activation pathways that converge at the final common pathway, resulting in thrombin generation and fibrin formation.
Two of the routine coagulation tests, PT and aPTT, are based on this cascade model; in these tests, components are separated and tested in isolation. The end point for both tests is initial fibrin generation (5% of the fibrin to be generated), and thus the tests measure only a minor part of the entire hemostatic process — the lag phase until initial thrombin generation. In addition, the tests measure only how coagulation factors interact in solution, rather than on a cellular surface.
Finally, PT and aPTT determine only if the coagulation factors are present at levels adequate for clot formation. Platelet counts provide the number of platelets available, but not the functionality of the platelets. D-DIMER and FDP levels provide a quantitative rather than a functional description of fibrinolysis.

3. [Monroe, DM. et al. Arterioscler Thromb Vasc Biol. 2002;22:1381]
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
Tissue factor
bearing cells
1. Initiation
IIa
2. Amplification
Platelets
3. Propagation
A newer hemostasis paradigm is presented in the cell-based model. The addition of cellular elements is reflected in the cell-based model of hemostasis. This model represents thrombin generation as a process occurring on two types of cell surfaces — tissue factor bearing cells and platelets. It occurs in three overlapping phases:
Initiation
Amplification
Propagation
During the initiation phase, factor VII interacts with the tissue factor expressed on the surface of cells, such as extravascular tissue cells, endothelial cells, or monocytes. This interaction activates the extrinsic pathway, which leads to the generation of a small amount of thrombin which in turn activates platelets and factors V, VIII, and XI of the intrinsic pathway during the amplification phase.
In the propagation phase, the combination of platelet and coagulation factor activation generates a burst of thrombin sufficient to form a stable hemostatic platelet-fibrin clot.
The coagulation cascade still plays a role in hemostasis, but the pathways are dependent on interactions at a cellular surface, rather than in plasma. In the cell-based model, the extrinsic pathway works on the surface of tissue factor bearing cells, and the intrinsic pathway works on the surface of platelets.
The waterfall coagulation cascade model still plays a role in hemostasis, but the pathways are dependent on interactions at a cellular surface, rather than in plasma. In the cell-based model, the extrinsic pathway works on the surface of tissue factor bearing cells, and the intrinsic pathway works on the surface of platelets.
IIa
Activated platelets
[Monroe, DM. et al. Arterioscler Thromb Vasc Biol. 2002;22:1381]

4. Defining the Position Looking at Clot Function
Thrombosis
Bleeding
Rate
Stability
Strength
There are three general characteristics of the clot that determine where along the continuum a patient’s coagulation status exists. These three characteristics are:
The rate of clot formation – If the rate of clot formation is too slow, then the position would shift to the bleeding end of the spectrum. On the other hand if the rate of clot formation is too fast, then it is possible that the position will be shifted toward the thrombotic end of the spectrum.
Clot strength is the second characteristic. Weak clots will be unable to withstand the hemodynamic forces of blood flow and thus result in bleeding. Strong clots are required for normal hemostasis, but clots that are too strong have been associated with a higher risk of a thrombotic event.
The third characteristic that will determine the position along the coagulation continuum is clot stability which is determined by the rate of clot breakdown, commonly known as fibrinolysis.
The thrombelastograph, or TEG, is a whole blood hemostasis monitor that is able to monitor the rate of clot formation, the strength of the clot, and the stability of the clot all with one blood sample. Being a global test of hemostasis, TEG analysis is able to provide the information necessary to determine the position along the coagulation continuum.

5. Global Hemostatic StatusMA
Angle
LY30 R

6. TEG Analysis – Interpretation Examining the parameters
R-time to first fibrin strand
K-rate of clot development (20 mm in height)
Angle-rate of clot development
MA- maximum clot strength
LY/EPL-clot breakdown, clot stability

7. TEG Technology Parameters
Hemostatic
Activity
Component
LY30
30 min a MA MA R
EPL K
Dysfunction
Hypo-
coagulable
Hyper-

8. R Parameter Clot time Dysfunction Hypo- coagulable ­ R (min) ¯ R (min)
IIa generation
Fibrin formation
Coagulation
pathways
Hemostatic
Activity
Hemostatic
Component
Dysfunction
Hypo-
coagulable
­ R (min)
¯ R (min)
Hyper-
coagulable

9. a R K Parameter Clot time Clot rate Dysfunction Hypo- coagulable
IIa generation
Fibrin formation
Coagulation
pathways
Clot rate
Fibrin mesh
Fibrinplatelet
Coag pathways
platelets K a
Hemostatic
Activity
Hemostatic
Component
Dysfunction
Hypo-
coagulable
­ R (min)
¯ R (min)
K (min)
¯ a (deg)
¯ K (min)
­ a (deg)
Hyper-
coagulable

10. Platelet – fibrin interactions
Parameter R
Clot time
IIa generation
Fibrin formation
Coagulation
pathways
Clot rate
Fibrin X-linking
Fibrinplatelet
Coag pathways
platelets K a
Maximum clot strength
Platelet – fibrin interactions
Platelets (~80%)
Fibrin (~20%) MA
Hemostatic
Activity
Hemostatic
Component
Dysfunction
Hypo-
coagulable
­ R (min)
¯ R (min)
K (min)
¯ a (deg)
¯ K (min)
­ a (deg)
¯ MA
­ MA
Hyper-
coagulable

11. 30 min a MA R K ¯ MA ­ MA N/A Parameter Clot time Clot rate
IIa generation
Fibrin formation
Coagulation
pathways
Clot rate
Fibrin X-linking
Fibrinplatelet
Coag pathways
platelets K a
Maximum clot strength
Platelet – fibrin(ogen) interactions
Platelets (~80%)
Fibrin(ogen (~20%) MA
Clot stability
Reduction in clot strength
Fibrinolysis
Hemostatic
Activity
Hemostatic
Component
30 min
LY30
EPL
Dysfunction
Hypo-
coagulable
­ R (min)
¯ R (min)
K (min)
¯ a (deg)
¯ K (min)
­ a (deg)
¯ MA
­ MA
LY30 > 7.5%
EPL > 15%
N/A
Hyper-
coagulable

12. Interpretation: Applying the Parameters TEG Decision Tree
Kaolin sample No

13. Interpretation Practice
Example 1

14. Example 1 At 15 minutes What information is available at this point?
*54.3*

15. Example 1 At 30 minutes
Is this a normal tracing? Yes or No

16. Interpretation Practice
Example 2

17. Example 2 At 15 minutes
Is there a risk for bleeding due to factor dysfunction or heparin?
*1.5*
*10.3*

18. Example 2 At 24 minutes
If this sample was run coming off cardiac bypass pump, what is the bleeding risk after heparin reversal?
*54.8*

19. Example 2 At 45 minutes
If the patient were bleeding, would FFP be the appropriate blood product?

20. Interpretation Practice Not typical (but it happens)
Example 3

21. Example 5 At 24 minutes
Patient is bleeding.
*0.0*
*0.0*

22. Example 5 At 35 minutes Patient is bleeding.
Results suggest Primary Fibrinolyisis.

23. Example 5 At 60 minutes
Consider use of anti-fibrinolytic

24. Interpretation Practice
Example 4

25. Example 6 At 10 minutes
Black = K Green = KH
This patient is in the ICU. Has heparin been reversed? Explain.

26. Example 6 Samples stopped at 35 minutes
Black = K Green = KH
Are any coagulopathies indicated from these results?
What are they?
What are the other possibilities if the patient is bleeding?

27. Interpretation Practice
Example 5

28. Example 7 At 15 minutes
Black = K Green = KH
This patient has been given Protamine. Has heparin been reversed?

29. Example 7 Samples stopped
Black = K Green = KH
What are the other possibilities if the patient is bleeding?
Note the R in both cups.

30. Interpretation Practice Not typical (but it happens)
Example 6

31. Example 8 At 25 minutes What are the other possibilities?
Heparin, No CaCl, or real result.
Call the lab and repeat the test.
*25.3*
2 ― 8

32. Group Exercise #1

33. Exercise 1 At 15 minutes Coagulopathies indicated at this point?
Possibilities if the patient is bleeding?
Hypothermia
Anatomical
VWf
*72.5*

34. Exercise 1 Completed
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?

35. Group Exercise #2

36. Exercise 2 At 6 minutes

37. Exercise 2 At 15 minutes Coagulopathies indicated at this point?
Undetermined coagulopathies at this point?
Possibilities if the patient is bleeding?
*40.7*

38. Exercise 2 Sample Stopped
Possibilities if the patient is bleeding?
Note the MA

39. Group Exercise #3

40. Exercise 3 At 6 minutes

41. Exercise 3 At 20 minutes
*54.2*

42. Exercise 3 Sample Stopped
Coagulopathies indicated at this point?

43. Group Exercise #4

44. Exercise 4 At 8 minutes Coagulopathies indicated at this point?
Undetermined coagulopathies at this point?
*70.7*

45. Exercise 4 At 15 minutes Coagulopathies indicated at this point?
Undetermined coagulopathies at this point?
19.0
*19.0*

46. Exercise 4 Completed Coagulopathies indicated at this point?
Undetermined coagulopathies at this point?
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?

47. Group Exercise #5

48. Exercise 5 At 9 minutes

49. Exercise 5 At 20 minutes
*19.8*

50. Exercise 5 Completed
Coagulopathies indicated at this point?

51. Group Exercise #6

52. Exercise 6 Patient 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?

53. Exercise 6 Completed
What if the patient is oozing? Bleeding?

54. Group Exercise #7

55. Exercise 7 At 12 minutes Coagulopathies indicated at this point?
Undetermined coagulopathies at this point?
*12.2*

56. Exercise 7 At 36 minutes
Note length of R, poor K and Alpha
*24.0*

57. Exercise 7 Completed Requires multiple blood products
FFP, CYRO and Platelets
*24.0*

58. Questions?

59. Back-Up: Additional TEG® Cases Theories and Applications
Intended audience: Perfusionists attending the 2009 Cases in the Sun meeting in Florida.
The purpose of this presentation is educational. The intent is to looks at four customer cases that used the TEG system to gain a better understanding of its use.
Kevin F. Lynch, RN/CCRN, MSN, MBA
Senior Clinical Specialist
Haemonetics

60. Primary Fibrinolysis Case Baseline Heparinase Cup

61. Primary Fibrinolysis Case Products and Drugs
Patient received:
Perioperative
15g Amicar during the case
Post protamine
4 FFP
2 Platelets,
13 mg DDAVP
ICU
1g drip Amicar 24 hrs post
No further blood products

62. Primary Fibrinolysis Case Post Protamine

63. TEG ® Analysis Valve CABG Aortic Tear
Intended audience: Perfusionists attending the 2009 Cases in the Sun meeting in Florida.
The purpose of this presentation is educational. The intent is to looks at four customer cases that used the TEG system to gain a better understanding of its use.

64. Valve CABG Aortic Tear Baseline

65. Valve CABG Aortic Tear Rewarm
Patient came off bypass
Surgeon nicked the aorta

66. Valve CABG Aortic Tear Rewarm
2 FFP given
Patient was reheparinised placed back on bypass

67. Valve CABG Aortic Tear Rewarm
Circ arrested, Came off bypass again
Post protamine
Patient given 2 platelet packs and 1 cryo (10 pack)
Patient was closed with no further bleeding

68. Valve CABG Aortic Tear Post Protamine

69. Valve CABG Aortic Tear Before and After

70. Hemorrhagic TEG Tracing
30 min
This is an example of a hemorrhagic TEG tracing. The R, angle, and MA values are all outside normal ranges. If this patient were bleeding, the likely cause would be a combination of enzymatic pathway and platelet dysfunction.

71. Pradaxa Case Report Kevin F. Lynch, RN/CCRN, MSN, MBA
TEG Clinical Consultant

72. History of Pradaxa (dabigatran)
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

73. 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.)

74. Patient History 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

75. Initial TEG 12 hours after last dose of Pradaxa Creatinine: 6
Initial TEG 12 hours after last dose of Pradaxa Creatinine: 6.3, BUN: 109, INR: 2.18

76. Platelet Mapping ADP

77. Platelet Mapping AA

78. TEG: 24 hours since last dose Creatinine: 6.6, BUN: 109, INR: 2.03

79. TEG: 48 hours since last dose Creatinine: 7.7, BUN: 117, INR: 1.7

80. Transfusions
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

81. TEG after 4 units of FFP INR: 1.73

82. Concerns 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

83. 2 hours after heparin infusion started 500-600 IU/hour, No bolus

84. Heparinase TEG result

85. Following morning, no heparin effect expressed by TEG Creatinine: 7
Following morning, no heparin effect expressed by TEG Creatinine: 7.8, BUN: 117, INR: 1.87

86. Trauma Case Study

87. Blunt injury trauma
42 y/o off-duty firefighter, hanging Christmas lights
Falls onto metal fence from roof (20 feet)
Ruptured spleen and liver laceration, as well as lung contusions and respiratory failure

88. 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.

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

90. 12 hours later, bleeding increasing
12 hours later, bleeding increasing. Heparin effect treated with Protamine, and 2 FFP given for factor deficiency.

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

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

93. This tracing shows extreme response to LMWH
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.

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

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

96. Bleeding stopped over next 3-4 hours.
R decreased from 23.6 with heparinase. Still 15.4, so 3u FFP given. Platelets OK.
Bleeding stopped over next 3-4 hours.

97. Final TEG. All coagulopathies corrected. No more heparinoid effect
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.

98. Haemonetics TEG Case Study: Data Collection Form
Patient 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________________________

99. Cases TEG Analysis
Questions?
Thank You!