Basic Clinician TrainingModule 3

Basic bleeding profiles

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

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)

EPL > 15%or

LY30 > 7.5%YesNo

R > 10min Yes

MA < 55mm

No

YesNo

Yes

YesNo

Primary fibrinolysis

C.I.

< 1.0 > 3.0

i

Yes

Yes

No

No

Decision Tree

Fibrinolysis

Hypercoagulable

C.I. > 3.0

Low plateletfunction

Low clottingfactors

Low fibrinogenlevel

< 45º

R < 3min

Platelethypercoagulability

MA > 73mm

Enzymatichypercoagulability

Enzymatic & platelethypercoagulability

Secondary fibrinolysis

Hemorrhage

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

Patient status: bleeding

Probable cause (3):• Vessel injury• vWF deficiency• Presence of platelet inhibitor

Patient status: bleeding

Probable cause Common treatment:• Vessel injury Suture• vWF deficiency DDAVP• Presence of platelet inhibitor Run Platelet Mapping

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

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

Enzymatic pathway abnormality:Coagulation factor deficiency

Patient condition: bleedingProbable cause: factor deficiency

Probable cause: Factor deficiency

Patient status: bleeding

Patient status: bleeding

Probable cause(s): • Factor deficiency• Platelet deficiency/dysfunction

Enzymatic pathway abnormality:Coagulation factor deficiency

Patient status: bleeding

Probable cause(s) Common treatment(s)• Factor deficiency FFP• Platelet deficiency/dysfunction platelets

Enzymatic pathway abnormality:Coagulation factor deficiency

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.

Enzymatic pathway abnormality:Residual heparin

Patient status: Bleeding

Probable cause(s):• Residual heparin• Factor deficiency

First TEST for residual heparin

Post Protamine

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

R for K > KH suggests presence of heparin

Testing for residual heparin with the TEG analyzer

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.

Causes of fibrinogen deficiency

• Liver disease or congestion• Disseminated intravascular coagulation

(DIC) – hypocoagulable stage• OB-GYN complications – placental

abruption• Hemodilution• Excessive consumption

Patient status: bleeding

Probable cause: fibrinogen deficiency

Fibrinogen deficiency

Fibrinogen deficiency

Patient status: Bleeding

Probable cause: Fibrinogen deficiencyCommon treatment: Cryoprecipitate or FFP

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.

• 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

Platelet abnormality:A note on low platelet counts

• 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

Platelet abnormalityLow platelet counts - causes

Platelet abnormalityPlatelet 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

Platelet abnormalityLow platelet function - causes• Cardiopulmonary bypass• Antiplatelet therapies• Platelet antibodies• Congenital disorders• Liver disease• Uremia• Consumption

Patient status: bleeding

Probable cause(s):• Low platelet count +/or• Low platelet function

Platelet abnormality

Patient status: bleeding

Probable cause(s) Common treatments:• Low platelet count platelet transfusion• Low platelet function platelet transfusion

Platelet abnormality

Patient status: bleeding

Probable cause(s):• Low platelet count +/or• Low platelet function

Platelet abnormality

Patient status: bleeding

Probable cause(s) Common treatment• Low platelet count platelet transfusion• Low platelet function platelet transfusion

Platelet abnormality

Patient status: bleeding

Probable cause(s):• Factor deficiency +/or• Low platelet count +/or• Low platelet function

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

Platelet abnormality

• 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)

Platelet abnormalitiesSpecial considerations

Interpretation Exercises

Hemorrhage

Exercise 1

Black tracing: KaolinGreen tracing: Kaolin with heparinase

Using the TEG Decision Tree, what is your interpretation of this TEG tracing?[Select all that apply]a. Factor deficiencyb. Platelet deficiency or dysfunctionc. Low fibrinogen leveld. Fibrinolysise. Normal

Has heparin been reversed in this patient? Yes or No.

Answer

Next

Exercise 2

Post-protamine

Using the TEG Decision Tree, what is your interpretation of this TEG tracing?[Select all that apply]a. Factor deficiencyb. Platelet deficiency or dysfunctionc. Low fibrinogen leveld. Fibrinolysise. Normal

What treatment(s) would you consider for this patient?

Patient status: bleeding

Answer

Next

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.

Answer Next

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]a. Factor deficiencyb. Platelet deficiency or dysfunctionc. Low fibrinogen leveld. Fibrinolysise. Surgical bleeding

What treatment(s) would you consider for this patient?

Answer

Next

Exercise 5

Using the TEG Decision Tree what is your interpretation of this TEG tracing?[Select all that apply]a. Factor deficiencyb. Platelet deficiency or dysfunctionc. Low fibrinogen leveld. Fibrinolysise. Normal

If this patient was bleeding, what treatment(s) would you consider?Next

Answer

Exercise 6

Using the TEG Decision Tree what is your interpretation of this TEG tracing?[Select all that apply]a. Factor deficiencyb. Anticoagulant effectc. Platelet deficiency or dysfunctiond. Low fibrinogen levele. Surgical bleeding

What treatment(s) would you consider for this patient? Next

Post-protamine

Patient status: bleeding

Answer

Exercise 7

Black tracing: KaolinGreen tracing: Kaolin with heparinase

Patient status: bleeding

Using the TEG Decision Tree what is your interpretation of this TEG tracing?[Select all that apply]a. Factor deficiencyb. Anticoagulant effectc. Platelet deficiency or dysfunctiond. Low fibrinogen levele. Surgical bleeding

How would you treat this patient? Answer

Next

Exercise 8

Post-protamine

- The above patient is bleeding after administration of protamine. What are the possiblecauses of bleeding (select all that apply)? - For each selection, identify one treatment consideration.a. Surgical bleedingb. Factor deficiencyc. Residual platelet inhibitor effectd. Diminished platelet adhesione. Anticoagulant effect Answer

Next

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?a. Surgical bleedingb. Factor deficiencyc. Platelet deficiency/dysfunctiond. Fibrinolysise. Anticoagulant effect

Answer

Next

Exercise 10

Green: Post-protamineBlack: ICU

The above patient has started bleeding approximately 1 hr post-op. What is the most likely cause(s) of bleeding? a. Surgical bleedingb. Factor deficiencyc. Platelet deficiency/dysfunctiond. Fibrinolysise. Anticoagulant effect

How would you treat this patient?Answer

END

Exercise 1

Black tracing: KaolinGreen tracing: Kaolin with heparinase

Using the TEG Decision Tree what is your interpretation of this TEG tracing?a. Factor deficiencyb. Platelet deficiency or dysfunctionc. Low fibrinogen leveld. Fibrinolysise. Normal – all parameters are within normal range

Has heparin been reversed in this patient? Yes or No. Since the R values for boththe kaolin and kaolin with heparinase samples are the same suggests that theheparin has been reversed.

Back

Exercise 2

Using the TEG Decision Tree what is your interpretation of this TEG tracing?[Select all that apply]a. Factor deficiencyb. Platelet deficiency or dysfunctionc. Low fibrinogen leveld. Fibrinolysise. Normal

What treatment(s) would you consider for this patient? After completion of protamineadministration, consider treating with platelets first. Repeat TEG. If R value is still elongated and the patient is bleeding, consider treating with FFP.

Patient status: bleeding

Post-protamine

Back

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 samplewould 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 causeof bleeding in this patient. Back

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]a. Factor deficiencyb. Platelet deficiency or dysfunctionc. Low fibrinogen leveld. Fibrinolysise. Surgical bleedingA 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 thetrigger point for FFP transfusion. If patient is oozing, wait an hour and repeat theTEG. If R is still elongated and the patient is still oozy, consider treating with FFP.

Back

Exercise 5

Using the TEG Decision Tree what is your interpretation of this TEG tracing?[Select all that apply]a. Factor deficiencyb. Platelet deficiency or dysfunctionc. Low fibrinogen leveld. Fibrinolysise. Normal

If this patient was bleeding, what treatment(s) would you consider?Cryoprecipitate or FFP

Back

Exercise 6

Using the TEG Decision Tree what is your interpretation of this TEG tracing?[Select all that apply]a. Factor deficiencyb. Anticoagulant effectc. Platelet deficiency or dysfunctiond. Low fibrinogen levele. Surgical bleeding

What treatment(s) would you consider for this patient? Platelet transfusion

Post-protamine

Patient status: bleeding

Back

Exercise 7

Black tracing: KaolinGreen tracing: Kaolin with heparinase

Patient status: bleeding

Using the TEG Decision Tree what is your interpretation of this TEG tracing?[Select all that apply]a. Factor deficiency (cannot rule out)b. Anticoagulant effect (incomplete reversal of heparin)c. Platelet deficiency or dysfunction (cannot rule out)d. Low fibrinogen levele. Surgical bleeding

How would you treat this patient? A common treatment protocol would likelyinclude administration of additional protamine to reverse the heparin effect.If the patient continues to bleed, repeat the TEG to determine the probablecause. Most likely platelet deficiency/dysfunction.

Back

Exercise 8

Post-protamine

- The above patient is bleeding after administration of protamine. What are the possiblecauses of bleeding (select all that apply)? - For each selection, identify one treatment consideration.a. Surgical bleeding: check for bleeding site and repairb. Factor deficiencyc. Residual platelet inhibitor effect: platelet transfusiond. Diminished platelet adhesion: DDAVPe. 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 aresimilar, the cause of bleeding is not residual heparin.

Back

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?a. Surgical bleedingb. Factor deficiency (cannot be ruled out)c. 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).a. Fibrinolysisb. Anticoagulant effect Back

Exercise 10

Green: Post-protamineBlack: ICU

The above patient has started bleeding approximately 1 hr post-op. What is the most likely cause(s) of bleeding? a. Surgical bleedingb. Factor deficiency c. Platelet deficiency/dysfunctiond. Fibrinolysise. Anticoagulant effect (since kaolin sample, a heparin effect is not considered)

How would you treat this patient? Return to OR for re-exploration.

Back

End of Module 3