1. Basic Clinician Training Module 3
Basic bleeding profiles

2. Introduction to bleeding
Causes of bleeding
Mechanical – vascular injury
Pathophysiological – imbalance between the anticoagulant/antithrombotic and prothrombotic forces of the hemostatic system
Monitoring hemostasis – finding where the imbalance resides

3. Monitoring bleeding with the TEG
TEG analysis – monitoring hemostatic components and their interactions.
Mechanical – Normal TEG parameters
Pathophysiological
R: enzymatic pathway abnormality
Angle (a): fibrinogen deficiency
MA: platelet abnormality
LY30: fibrinolysis (See Module 6)

4. Decision Tree Hemorrhage Fibrinolysis Hypercoagulable C.I. > 3.0
EPL > 15% No or
Yes
LY30 > 7.5%
Hemorrhage No
C.I. > 3.0
Yes
C.I.
< 1.0
> 3.0 No
R > 10min
R < 3min
Yes
Primary fibrinolysis
Secondary fibrinolysis No
Yes
Low clotting
factors
Platelet
hypercoagulability
Fibrinolysis No
MA < 55mm
Yes
MA > 73mm No
Yes
Low platelet
function
Enzymatic
hypercoagulability
Enzymatic & platelet
hypercoagulability
a < 45º i
Yes
Hypercoagulable
Low fibrinogen
level

5. Mechanical bleeding
Characterized by bleeding patient with a normal TEG tracing.
Probable cause: Surgical injury to blood vessel with insufficient repair of the blood vessel.
Other possible explanations
Clot development not confined to injury site – suggests vWF deficiency
Presence of platelet inhibitors

6. Patient status: bleeding
Probable cause (3):
Vessel injury
vWF deficiency
Presence of platelet inhibitor

7. Patient status: bleeding
Probable cause  Common treatment:
Vessel injury  Suture
vWF deficiency  DDAVP
Presence of platelet inhibitor  Run Platelet Mapping

8. Enzymatic pathway abnormalities
Characterized by a bleeding patient and a TEG tracing with an abnormally long R value.
Factor deficiency may also cause abnormalities in other TEG parameters (angle, MA)
Probable causes:
Coagulation factor(s) deficiency
Coagulation factor dysfunction
Presence of anticoagulant (i.e. residual heparin)
Effect:
Slow rate of thrombin generation leading to slow clot development
Insufficient thrombin generation leading to insufficient clot development

9. Causes of enzymatic pathway abnormalities
Coagulation factor deficiency
Hemodilution
Liver disease or liver congestion
Trauma with significant blood loss and/or blood salvage
Congenital – i.e. hemophilia
Factor consumption > synthesis
Cardiopulmonary bypass, ECMO
Disseminated intravascular coagulation (DIC)
Coagulation factor dysfunction
Vitamin K deficiency
Warfarin treatment
Presence of anticoagulant
Residual heparin

10. Enzymatic pathway abnormality: Coagulation factor deficiency
Patient status: bleeding
Patient condition: bleeding
Probable cause: factor deficiency
Probable cause: Factor deficiency

11. Enzymatic pathway abnormality: Coagulation factor deficiency
Patient status: bleeding
Probable cause(s):
Factor deficiency
Platelet deficiency/dysfunction

12. Enzymatic pathway abnormality: Coagulation factor deficiency
Patient status: bleeding
Probable cause(s)  Common treatment(s)
Factor deficiency  FFP
Platelet deficiency/dysfunction  platelets

13. Enzymatic pathway abnormality: Residual heparin
Characterized by a bleeding patient and a TEG tracing with an abnormally long R value (non-heparinase sample)
Probable causes:
Residual heparin after protamine administration due to insufficient protamine dose.
Heparin rebound – reappearance of heparin in circulation after initial reversal with protamine
Release of endogenous sources of heparin (i.e. reperfusion of transplanted liver)
Effect: inhibition of thrombin action resulting in reduced fibrin formation and clot development.

14. Enzymatic pathway abnormality: Residual heparin
Post Protamine
Patient status: Bleeding
Probable cause(s):
Residual heparin
Factor deficiency
First TEST for residual heparin

15. Testing for residual heparin with the TEG analyzer
Run blood sample on two channels simultaneously
K = kaolin activated (clear cup)
KH = kaolin with heparinase (blue cup)
Results:
If R for K  KH, long R is not due to heparin
If R for K is long and for KH is normal, heparin is present in blood sample

16. Testing for residual heparin with the TEG analyzer
R for K > KH suggests presence of heparin

17. Fibrinogen deficiency
Characterized by a bleeding patient and a TEG tracing with only an abnormally low angle (a).
Probable cause: low fibrinogen levels
Effect: slow rate of clot development
Note: The angle parameter is influenced by the enzymatic and platelet pathways, thus correcting a deficiency or defect in these pathways will typically correct the angle.

18. Causes of fibrinogen deficiency
Liver disease or congestion
Disseminated intravascular coagulation (DIC) – hypocoagulable stage
OB-GYN complications – placental abruption
Hemodilution
Excessive consumption

19. Fibrinogen deficiency
Patient status: bleeding
Probable cause: fibrinogen deficiency

20. Fibrinogen deficiency
Patient status: Bleeding
Probable cause: Fibrinogen deficiency
Common treatment: Cryoprecipitate or FFP

21. Platelet abnormality
Characterized by a bleeding patient and a TEG tracing with an abnormally low MA value
A low MA value may also be associated with an elongated R and/or a low angle values
Probable causes:
Low platelet number
Low platelet function
Note: The TEG cannot distinguish between a low platelet count and low platelet function
Effect: formation of a clot with low clot strength that is insufficient to stop vascular bleeding.

22. Platelet abnormality: A note on low platelet counts
In certain disease states platelet counts may be reduced, but the remaining platelets may be hyperfunctional and hypersensitive, resulting in normal or high clot strength (normal to high MA).
Example: cancer patients

23. Platelet abnormality Low platelet counts - causes
Bone marrow disorders (i.e. leukemia)
Chemotherapy
Congenital disorder
Lupus
Trauma with significant blood loss and/or blood salvage
Hemodilution
Cardiac valve dysfunction – regurgitation
Consumption and/or sequestration
Platelet antibodies - HITT

24. Platelet abnormality Platelet dysfunction - Mechanisms
Activation – inhibition or dysfunction of platelet receptors
Adhesion – inhibition or dysfunction of GPIb receptor preventing adhesion of platelet to endothelium
Aggregation – inhibition or dysfunction of GPIIb/IIIa receptors preventing the development of a platelet plug
Secretion – inhibition or dysfunction of secretory pathways resulting in reduced platelet activation
Procoagulant activity – reduction of thrombin generation on platelet surface

25. Platelet abnormality Low platelet function - causes
Cardiopulmonary bypass
Antiplatelet therapies
Platelet antibodies
Congenital disorders
Liver disease
Uremia
Consumption

26. Patient status: bleeding
Platelet abnormality
Patient status: bleeding
Probable cause(s):
Low platelet count +/or
Low platelet function

27. Patient status: bleeding
Platelet abnormality
Patient status: bleeding
Probable cause(s)  Common treatments:
Low platelet count  platelet transfusion
Low platelet function  platelet transfusion

28. Patient status: bleeding
Platelet abnormality
Patient status: bleeding
Probable cause(s):
Low platelet count +/or
Low platelet function

29. Patient status: bleeding
Platelet abnormality
Patient status: bleeding
Probable cause(s)  Common treatment
Low platelet count  platelet transfusion
Low platelet function  platelet transfusion

30. Patient status: bleeding
Platelet abnormality
Patient status: bleeding
Probable cause(s):
Factor deficiency +/or
Low platelet count +/or
Low platelet function

31. Patient status: bleeding
Platelet abnormality
Patient status: bleeding
Probable cause(s)  Common treatment(s):
Factor deficiency  FFP +/or
Low platelet count  platelet transfusion
Low platelet function  platelet transfusion

32. Platelet abnormalities Special considerations
The inhibition of platelets by platelet inhibitors may not be revealed by the TEG using a kaolin activated sample. This is due to thrombin generation in the blood sample which results in maximum activation of platelets which overrides other activation pathways.
An important factor to consider in induced platelet dysfunction (i.e., treatment with antiplatelet drugs) is the monitoring of platelet inhibition.
PlateletMapping™ assays measure the degree of inhibition at the ADP receptor and arachadonic acid pathways as well as provide a reference point against which to interpret the inhibition (See Module 6)

33. Interpretation Exercises
Hemorrhage

34. Exercise 1 Answer Next Black tracing: Kaolin
Green tracing: Kaolin with heparinase
Using the TEG Decision Tree, what is your interpretation of this TEG tracing?
[Select all that apply]
Factor deficiency
Platelet deficiency or dysfunction
Low fibrinogen level
Fibrinolysis
Normal
Has heparin been reversed in this patient? Yes or No.
Answer
Next

35. Patient status: bleeding
Exercise 2
Post-protamine
Patient status: bleeding
Using the TEG Decision Tree, what is your interpretation of this TEG tracing?
[Select all that apply]
Factor deficiency
Platelet deficiency or dysfunction
Low fibrinogen level
Fibrinolysis
Normal
What treatment(s) would you consider for this patient?
Answer
Next

36. Patient status: Bleeding
Exercise 3
Patient status: Bleeding
Using the TEG Decision Tree and the available information from the TEG tracing:
Is it likely the patient will require more protamine as a treatment for bleeding? Yes or No.
Is it likely the patient will require FFP as a treatment for bleeding? Yes or No.
Next
Answer

37. Patient status: Bleeding
Exercise 4
Patient status: Bleeding
Using the TEG Decision Tree what is a likely cause(s) of bleeding in this patient?
[Select all that apply]
Factor deficiency
Platelet deficiency or dysfunction
Low fibrinogen level
Fibrinolysis
Surgical bleeding
What treatment(s) would you consider for this patient?
Answer
Next

38. Exercise 5
Using the TEG Decision Tree what is your interpretation of this TEG tracing?
[Select all that apply]
Factor deficiency
Platelet deficiency or dysfunction
Low fibrinogen level
Fibrinolysis
Normal
If this patient was bleeding, what treatment(s) would you consider?
Answer
Next

39. Patient status: bleeding
Exercise 6
Post-protamine
Patient status: bleeding
Using the TEG Decision Tree what is your interpretation of this TEG tracing?
[Select all that apply]
Factor deficiency
Anticoagulant effect
Platelet deficiency or dysfunction
Low fibrinogen level
Surgical bleeding
What treatment(s) would you consider for this patient?
Answer
Next

40. Patient status: bleeding
Exercise 7
Black tracing: Kaolin
Green tracing: Kaolin with heparinase
Patient status: bleeding
Using the TEG Decision Tree what is your interpretation of this TEG tracing?
[Select all that apply]
Factor deficiency
Anticoagulant effect
Platelet deficiency or dysfunction
Low fibrinogen level
Surgical bleeding
How would you treat this patient?
Answer
Next

41. Exercise 8
Post-protamine
- The above patient is bleeding after administration of protamine. What are the possible
causes of bleeding (select all that apply)?
- For each selection, identify one treatment consideration.
Surgical bleeding
Factor deficiency
Residual platelet inhibitor effect
Diminished platelet adhesion
Anticoagulant effect
Answer
Next

42. Exercise 9
The above is the baseline TEG (post-induction) of a female patient (70 yr, 54kg) requiring
CABG with CPB. The patient has not been taking aspirin for 7 days (81 mg/d).
Based on this TEG and the patient history, is this patient at risk for bleeding post-CPB? Yes or No.
If so, what will be the most likely cause(s) of bleeding?
Surgical bleeding
Factor deficiency
Platelet deficiency/dysfunction
Fibrinolysis
Anticoagulant effect
Answer
Next

43. Exercise 10
Green: Post-protamine
Black: ICU
The above patient has started bleeding approximately 1 hr post-op. What is the most likely
cause(s) of bleeding?
Surgical bleeding
Factor deficiency
Platelet deficiency/dysfunction
Fibrinolysis
Anticoagulant effect
How would you treat this patient?
Answer
END

44. Exercise 1 Back Black tracing: Kaolin
Green tracing: Kaolin with heparinase
Using the TEG Decision Tree what is your interpretation of this TEG tracing?
Factor deficiency
Platelet deficiency or dysfunction
Low fibrinogen level
Fibrinolysis
Normal – all parameters are within normal range
Has heparin been reversed in this patient? Yes or No. Since the R values for both
the kaolin and kaolin with heparinase samples are the same suggests that the
heparin has been reversed.
Back

45. Patient status: bleeding
Exercise 2
Post-protamine
Patient status: bleeding
Using the TEG Decision Tree what is your interpretation of this TEG tracing?
[Select all that apply]
Factor deficiency
Platelet deficiency or dysfunction
Low fibrinogen level
Fibrinolysis
Normal
What treatment(s) would you consider for this patient? After completion of protamine
administration, consider treating with platelets first. Repeat TEG. If R value is still
elongated and the patient is bleeding, consider treating with FFP.
Back

46. Patient status: Bleeding
Exercise 3
Patient status: Bleeding
Using the TEG Decision Tree and the available information from the TEG tracing:
Is it likely the patient will require more protamine as a treatment for bleeding? Yes or No.
This is a tracing from a kaolin activated sample. The presence of heparin in a kaolin sample
would result in an elongated R value. An R within normal range suggests heparin is not present,
thus additional protamine is not required.
Is it likely the patient will require FFP as a treatment for bleeding? Yes or No.
An R value within normal range suggests that factor deficiency is not the cause
of bleeding in this patient.
Back

47. Patient status: Bleeding
Exercise 4
Patient status: Bleeding
Using the TEG Decision Tree what is a likely cause(s) of bleeding in this patient?
[Select all that apply]
Factor deficiency
Platelet deficiency or dysfunction
Low fibrinogen level
Fibrinolysis
Surgical bleeding
A slightly elongated R may suggest factor deficiency, however surgical bleeding cannot
be ruled out.
What treatment(s) would you consider for this patient? The R value is less than the
trigger point for FFP transfusion. If patient is oozing, wait an hour and repeat the
TEG. If R is still elongated and the patient is still oozy, consider treating with FFP.
Back

48. Exercise 5
Using the TEG Decision Tree what is your interpretation of this TEG tracing?
[Select all that apply]
Factor deficiency
Platelet deficiency or dysfunction
Low fibrinogen level
Fibrinolysis
Normal
If this patient was bleeding, what treatment(s) would you consider?
Cryoprecipitate or FFP
Back

49. Patient status: bleeding
Exercise 6
Post-protamine
Patient status: bleeding
Using the TEG Decision Tree what is your interpretation of this TEG tracing?
[Select all that apply]
Factor deficiency
Anticoagulant effect
Platelet deficiency or dysfunction
Low fibrinogen level
Surgical bleeding
What treatment(s) would you consider for this patient? Platelet transfusion
Back

50. Patient status: bleeding
Exercise 7
Black tracing: Kaolin
Green tracing: Kaolin with heparinase
Patient status: bleeding
Using the TEG Decision Tree what is your interpretation of this TEG tracing?
[Select all that apply]
Factor deficiency (cannot rule out)
Anticoagulant effect (incomplete reversal of heparin)
Platelet deficiency or dysfunction (cannot rule out)
Low fibrinogen level
Surgical bleeding
How would you treat this patient? A common treatment protocol would likely
include administration of additional protamine to reverse the heparin effect.
If the patient continues to bleed, repeat the TEG to determine the probable
cause. Most likely platelet deficiency/dysfunction.
Back

51. Exercise 8
Post-protamine
- The above patient is bleeding after administration of protamine. What are the possible
causes of bleeding (select all that apply)?
- For each selection, identify one treatment consideration.
Surgical bleeding: check for bleeding site and repair
Factor deficiency
Residual platelet inhibitor effect: platelet transfusion
Diminished platelet adhesion: DDAVP
Anticoagulant effect: Since this is a KH sample, there is a possibility of
residual heparin. Compare R values for the K and KH samples. If they are
similar, the cause of bleeding is not residual heparin.
Back

52. Exercise 9
The above is the baseline TEG (post-induction) of a female patient (70 yr, 54kg) requiring
CABG with CPB. The patient has not been taking aspirin for 7 days (81 mg/d).
Based on this TEG and the patient history, is this patient at risk for bleeding post-CPB? Yes or No.
If so, what will be the most likely cause(s) of bleeding?
Surgical bleeding
Factor deficiency (cannot be ruled out)
Platelet deficiency/dysfunction (Most likely cause of post-CPB bleeding since the patient is
starting out with a low platelet count/function. Consider using aprotinin as antifibrinolytic agent.
Rewarming TEG should demonstrate effect of CPB on platelets and factors).
Fibrinolysis
Anticoagulant effect
Back

53. Exercise 10
Green: Post-protamine
Black: ICU
The above patient has started bleeding approximately 1 hr post-op. What is the most likely
cause(s) of bleeding?
Surgical bleeding
Factor deficiency
Platelet deficiency/dysfunction
Fibrinolysis
Anticoagulant effect (since kaolin sample, a heparin effect is not considered)
How would you treat this patient? Return to OR for re-exploration.
Back

54. End of Module 3