compact presentation on TIC

1. Trauma Induced Coagulopathy
Ruby Kataria
Senior Resident (Mch)
Trauma Surgery & Critical care
AIIMS, Rishikesh

2. Introduction
• Trauma Induced Coagulopathy (TIC) → Mortality rate
of 50%
• ↑sed transfusions/ organ injury sepsis/ ICU stay
• Normal coagulation = hemostatis vs fibrinolysis
• Cause = Acidosis-hypothermia-coagulopathy*
* Traumatic induced coagulopathy in adult trauma patients with bleeding (Protocol)
Copyright © 2013 The Cochrane Collaboration.

3. Definition
Trauma Induced Coagulopathy –
“Biochemical response to injury and shock
leading to hyperfibrinolysis & hypocoagulability
,mediated by dysregulation of protein C system”
Up to Date Apr 11, 2019

5. Normal Hemostasis Pathway

6. Drivers of trauma-induced coagulopathy
Impaired clot formation
1.Activation of protein C
2.Auto heparinization
3.DIC and consumptive coagulopathy
4.Lethal triad
Dysregulation of Fibrinolysis
1.Acute release of t-PA-induced hyperfibrinogenolysis
2.Coagulation activation-induced fibrinogenolysis
Platelet dysfunction

7. Activation of protein C
• Protein C - Systemic anticoagulant & anti inflammatory
• Protein C ---> activated protein C (Thrombin –TM complex )
• Sustained hypoperfusion --> ↑ TM levels---> ↑ TM- thrombin
complex
• Thrombin is diverted from procoagulant to pathologic
anticoagulant via excess activation of protein C
Activated protein C cleaves peptide bonds of F Vα and F VIIIα preventing their assembly into the prothombinase (Vα/Xα) and
tenase (VIIIα/Ixα) complexes.

8. Auto heparinization From Glycocalyx Degradation
• Vascular endothelial cells is covered by –ve charged carbohydrate-
rich layer--endothelial glycocalyx
• Glycocalyx is antiadhesive & anticoagulant
• Endothelial glycocalyx = proteoglycans & glycoprotein
(MC are syndecan-1 and glypican)
• Proteoglycans have glycosaminoglycan comprise of heparan sulfate
(heparin-like)
• Injury  degradation of glycocalyx release of heparan sulfate 
hypocoagulability = endogenous auto-heparinization

9. Lethal Triad

10. Hypothermia
• Affects hemostasis below
33°C
• Inhibits Initiation phase
of clotting
• Enhanced platelet
activation and
aggregation

11. Acidosis
• pH 7.4 7.0 6.8
↓ ↓ ↓
↓ Activity VIIa -90% Xa- 70% PC- 55%
• pH of 7.1 marked ↓↓ in clot strength
 Inhibition of propagation phase
• Acidosis- ↑ fibrinogen degradation
• pH< 7  Impaired platelet aggregation & adhesion

12. Hemodilution
• Overzealous resuscitation  ↑↑coagulopathy and
↓coagulation proteins
• Resuscitation-associated coagulopathy (RAC)/ iatrogenic
coagulopathy
• Storage time on packed RBCs  "storage lesion“
↓
• Decreased Ph
• Chelation of calcium
• Low 2,3 DPG
• Decreased clotting
factor

13. Hyperfibrinolysis
• Fibrinolysis - active degradation of polymerized fibrin through
plasmin.

14. Diagnosis
Standard coagulation tests
• Prothrombin time (PT) >18 seconds
• INR >1.5
• aPTT >60 seconds
Platelet Function
• Platelet function analyzer (PFA-100)
• electrical impedance whole blood aggregometer
Viscoelastic Hemostatic Assays- standard of care

15. Thromboelastography
• Assess viscoelastic properties of clot
• Information regarding clot initiation, clot
strength, and fibrinolysis
• Standard coagulation test vs Thromboelastography

18. ASSAY INTERPRETATION
• R-time, activated clotting time (ACT) – time to start clot initiation &
clotting factors activation
K-time- time from clot initiation to 20 mm clot formation
• Alpha angle- rate of clot formation by measuring the slope b/w
R-time and K-value
K-value & a-angle are inverse proportion
• Maximum amplitude (MA)- Platelet aggregation
• Lysis at 30 minutes (LY30) % of clot fibrinolysis that occurs within
30 minutes after the MA point

20. Prolonged R – FFP
↓amplitude- Platelet
↑ K-value ↓ a-angle –Cryo
Both FFP & RDP
↑LY 30- TXA

22. Rotational Thromboelastometry
(ROTEM)
• Differncence between TEG & ROTEM

23. Types Of TEG

24. Types Of TEG
Functional fibrinogen (FF-TEG)
• To quantify fibrinogen levels
• Use antibody to glycoprotein IIb-IIIa to eliminate
platelets function
Platelet mapping assay (PM-TEG)
• Quantify platelet dysfunction
• Use heparin to eliminate thrombin activation
• Eliminate fibrin contribution to clot strength.

25. Types of ROTEM

26. Management Of TIC
1 Empiric transfusion strategies
• 1:1:1 Vs Whole blood
• 2 studies: Validity of "hemostatic" resuscitation
• PROMMTT (PRospective, Observational, Multicenter, Major Trauma Transfusion)
• PROPPR (Pragmatic, Randomized Optimal Platelet and Plasma Ratios)
2.Thromboelastography-based transfusion
3. Management of fibrinolysis
4. Hemostasis Adjuncts

31. Management of fibrinolysis
• Clinical Randomization of Antifibrinolytic in Significant
Hemorrhage (CRASH-2) trial
• The Military Application of TXA in Trauma Emergency
Resuscitation (MATTERs) study

35. Hemostasis Adjuncts
Fibrinogen / Cryo –
If Fibrinogen levels -1.5-2gm/dl
• Initial dose of 50mg/Kg
• Repeated dose guided by TEG
Prothrombin complex concentrate – factors II,VII, IX,X,
protein C and S & for Urgent warfarin reversal
r VIIa -amplify coagulation through thrombin burst
Presence of TF & functional platelets
absence of hypothermia or acidosis IS MUST

36. Resuscitation Strategies for TIC

38. Heamostatic Resuscitation
• Permissive hypotension

39. In Nutshell

40. THANK YOU