TEG article Flashcards
What is a major cause of preventable death in trauma patients?
uncontrolled coagulopathic hemorrhage
What are the 3 phases of hemorrhagic shock due to coagulopathy?
- Compensated shock
- uncompensated but reversible
- irreversible hemorrhagic shock
- once this phase is entered, fluid replacement or inotropic agents will not improve BP, tissue oxygenation or perfusion
- goal of resuscitative care is to delay or prevent transition to irreversible hemorrhagic shock
What are factors that contribute to coagulopathy in trauma patients?
- blood loss
- hemodilution by physiologi vascular refill
- consumption of platelets
- hypothermic plt dysfunction
- reduction enzyme activity
- acidosis-induced reduction in coag factor activity
- unopposed fibrinolysis
What is a teg?
- real-time viscoelastic assay
- measures strength of fibrin-plt bonds in whole blood
- result of this process is functional hemostatic plug
- 0.36mL of whole blood placed in cup and heated to 37 degrees
- cup rotated back and forth at constant set speed, through and arc
- sluggish flow mimics venous circulation and activates coag process
- pin attached to torsion wire inserted into cup
- speed and strength of clot formation converted to mechanical-electrical transducer and electrical signal is analyzed by computer
- converted to numeric values
What is the R value?
Normal?
Intervention if low or high?
start of clot or fibrin formation
- Normal 7.5-15 minutes
- If prolonged (>15 min)- deficiency in coag factors, effect of endogenous heparin release during trauma, and/or hemodilution
- TXMT- FFP
-
If shortened (less than 3 mintes)
- state of hypercoagulability
- treatment with anticoag of choice may be beneficial
- state of hypercoagulability
What is the K value?
Normal?
Interventions?
fibrin kinetics or speed of clot formation
- Normal= 3-6 minutes
- low vlaue= fibrinogen administration needed
- High value= hypercoagulability
What is the maximum amplitude?
Normal?
Treatment?
Width of tracing representing clot strength
- Normal 50-60mm
- Low value= hypofibrinogenemia, decreased PLT function or quality
- TXMT- PLT transfusion
- High value (>75)= prothrombotic state, need anticoagulant)
What values to you expect to see on TEG when hemodiluation is present?
Treatment?
- R value= high
- K and alpha= normal
- MA= normal
- Treatment= no treatment necessary
What do you expect to see on TEG when you have factor deficiency? Treatment?
- R value= high
- K and alpha= low or normal
- MA= low or normal
- Treatment= FFP
What do you expect to see on TEG with fibrinogen deficiency?
- R time= normal
- K and alpha= low
- MA= low or normal
- Treatment= cryoprecipitate
What do you expect to see on TEG when PLT low or dysfunctional?
Treatment?
- R time= normal
- K and alpha= normal
- MA= low
- Treatment= platelets
What do you expect to see on TEG with primary fibrinolysis?
- R value= normal
- K and alpha= normal
- MA= low
- Treatment= antifibrinolytics, TXA, Aproptinin
What do you expect to see on TEG in DIC stage 1 and 2?
DIC stage 1= hypercoagulability with fibrinolysis
- R time= low
- K and alpha= high
- MA= high
- treatment= Treat DIC
DIC Stage 2= hypocoaguability after consumption
- R time= high
- k and alpha= low
- MA= low
- treatment- treat DIC
Why isnt’ PT/INR sufficent?
Only covers factor VII and III (extrinsic pathway) only accounts for 3% of clot strength
doesn’t account for platelets role in clot strength
What does a aPTT assay assess?
- Intrinsic pathway
- factors XII, XI, IX, VII
- 3 natural anticoagulant proteins C, S, Z
- 10% of overall clot strength
At what point inthe coag cascade do all routine coag tests stop analysis?
When the formation of fibirn polymers occus
Does not capture full effects of thrombin (II)
What is thrombin
- involved in final common pathway
- huge role in platelet activation
- most potent platelet activator in body
- serves as catalyst for hemostatic process
- very small amounts of thrombin are required to cleave fibrinogen and activate platelets
- however, need large amount thrombin to produce network of platelet-fibrin polymers.
What are some negative consequences of using stored blood to resuscitate pt?
- decreased 2,3 dpg
- lower pH
- increased levels potassium
this can exacerbate considitons of trauma patient
Benefits of using TEG?
- One study in cardac surgery showed 75% reduction in umber of patients receiving FFP and 50% reduction in platelet transfusion
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What are current studies suggesting for trauma resus?
- RBC, FFP and PLT resus 1:1:1 improve survival rates rather than use of crystalloid and/or colloid
- Whole blood is considered superior replacement for massively transfused trauma patient (out of studies looking at Operations in the Middle East)
- However, increased FFP associated with acute lung injury.
