TEG article Flashcards

1
Q

What is a major cause of preventable death in trauma patients?

A

uncontrolled coagulopathic hemorrhage

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2
Q

What are the 3 phases of hemorrhagic shock due to coagulopathy?

A
  1. Compensated shock
  2. uncompensated but reversible
  3. irreversible hemorrhagic shock
    1. 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
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3
Q

What are factors that contribute to coagulopathy in trauma patients?

A
  • 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
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4
Q

What is a teg?

A
  • 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
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5
Q

What is the R value?

Normal?

Intervention if low or high?

A

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
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6
Q

What is the K value?

Normal?

Interventions?

A

fibrin kinetics or speed of clot formation

  • Normal= 3-6 minutes
  • low vlaue= fibrinogen administration needed
  • High value= hypercoagulability
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7
Q

What is the maximum amplitude?

Normal?

Treatment?

A

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)
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8
Q

What values to you expect to see on TEG when hemodiluation is present?

Treatment?

A
  • R value= high
  • K and alpha= normal
  • MA= normal
  • Treatment= no treatment necessary
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9
Q

What do you expect to see on TEG when you have factor deficiency? Treatment?

A
  • R value= high
  • K and alpha= low or normal
  • MA= low or normal
  • Treatment= FFP
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10
Q

What do you expect to see on TEG with fibrinogen deficiency?

A
  • R time= normal
  • K and alpha= low
  • MA= low or normal
  • Treatment= cryoprecipitate
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11
Q

What do you expect to see on TEG when PLT low or dysfunctional?

Treatment?

A
  • R time= normal
  • K and alpha= normal
  • MA= low
  • Treatment= platelets
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12
Q

What do you expect to see on TEG with primary fibrinolysis?

A
  • R value= normal
  • K and alpha= normal
  • MA= low
  • Treatment= antifibrinolytics, TXA, Aproptinin
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13
Q

What do you expect to see on TEG in DIC stage 1 and 2?

A

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
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14
Q

Why isnt’ PT/INR sufficent?

A

Only covers factor VII and III (extrinsic pathway) only accounts for 3% of clot strength

doesn’t account for platelets role in clot strength

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15
Q

What does a aPTT assay assess?

A
  • Intrinsic pathway
  • factors XII, XI, IX, VII
    • 3 natural anticoagulant proteins C, S, Z
  • 10% of overall clot strength
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16
Q

At what point inthe coag cascade do all routine coag tests stop analysis?

A

When the formation of fibirn polymers occus

Does not capture full effects of thrombin (II)

17
Q

What is thrombin

A
  • 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.
18
Q

What are some negative consequences of using stored blood to resuscitate pt?

A
  • decreased 2,3 dpg
  • lower pH
  • increased levels potassium

this can exacerbate considitons of trauma patient

19
Q

Benefits of using TEG?

A
  • One study in cardac surgery showed 75% reduction in umber of patients receiving FFP and 50% reduction in platelet transfusion
    *
20
Q

What are current studies suggesting for trauma resus?

A
  • 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.