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The haemorrhaging
  trauma patient
     Dr Peter Sherren
Objectives
• Causes of coagulopathy in trauma

• Describe damage control resuscitation

• Describe new strategies for managing
  traumatic haemorrhage

• Explain relevance to pre-hospital care
Background
• Uncontrolled haemorrhage is the commonest
  cause of preventable trauma deaths. Holcomb et al
  Ann Surg 2008.



• Damage control resuscitation (DCR) improves
  outcomes and mortality. Cotton BA et al Ann Surg 2011

• DCR should start at the time of injury not in the
  ED
Haemorrhage in trauma
• Surgical - Massive haemorrhage, 1 on the
  floor and 4 more

• Medical - bleeding diathesis,
  anticoagulants, DIC, lethal triad and ATC
•   ~1800 pts HEMS admissions to the RLH
•   ~1 in 4 pts admitted with coagulopathy
•   Independent of fluid administration
•   Significant association with mortality
•   ATC = ACoTS
ATC correlates with ISS
Pathophysiology
• ATC ≠ DIC

• Tissue/endothelial injury and
  hypoperfusion

     • Increased endogenous anticoagulants

     • Fibrinolysis and hyperfibrinolysis
•   APC
•   TFPI
•   AT III


             TERMINATION
Anticoagulation in ATC
Hyperfibrinolysis in ATC
Can we predict ATC?
• Several tools for predicting massive transfusion
  but not validated in ATC or pre-hospital arena
• Trauma Associated Severe Haemorrhage
  (TASH) Score (J Trauma 2006;60:1228-1237) and others
      •   Male
      •   Unstable pelvic fracture
      •   Open or deformed femur fracture
      •   HR >120 bpm
      •   SBP <100 mmHg
      •   FAST positive for intra-abdominal fluid
      •   Hb <11 g/dL
      •   Base deficit > -2
Case Presentation
Case presentation
• 16.05 – High speed MBC

• Ground crew on scene 16.18 hand over to HEMS at
  16:24
   – M ~40 yr old male involved in high speed MBC
   – I Complete traumatic Rt forequarter amputation++
     +blood, ?pelvis, CHI
   – S Agonal breaths, SpO2 not recording, HR 160,
     weak/thready carotid pulse only, GCS 7→3/15, Pupils 4/4
     sluggish.
   – T O2 NRB, 1XIV, 500ml CSL
HEMS management
•   2xIO - IV tissued
•   Sux only RSI - ETCO2 quantatively low but present.
•   Rt thoracostomy
•   Direct compression wound
•   Sam Sling
•   1g TXA
•   250ml HTS, 500ml 0.9%NaCl
•   Persistent volume issues
•   Depart scene 16:47 (scene time 29 mins)
•   Massive transfusion pre-alert, 2xPRBC given on
    helipad arrival
On arrival in the ED
• AB ok
• C
   – Haemodynamically unstable but volume
     responsive with haemostatic resuscitation with
     Level 1
   – pH 6.7, BE -26, Lact 16
   – Bloods on arrival Hb 10.6, HCT 0.28, INR 2.6
     APTTR 2.1
• Taken to theatres for surgical haemostasis
• Debrief points? Good level of care?
Damage Control Resuscitation
• 3 essential components:
  1. Damage control surgery
   2.   Haemostatic resuscitation
   3.   Permissive hypotension



• DCR improves outcomes and mortality.
  No level 1 evidence. Cotton BA et al Ann Surg 2011
1. Damage Control surgery
• Unstable patients with major trauma do not
  survive prolonged definitive surgery
• Normalise physiology at expense of anatomy
     • Stop haemorrhage (Packing, clamping, resection
       +/- IR)
     • Minimise contamination
     • Limb saving procedures
     • Good wash out of cavities
     • Drains and low threshold for Laparostomy
     • Definitive surgery another day
• Optimise lethal triad on the ICU
2. Haemostatic resuscitation
• Aggressive and simultaneous management of
  the lethal triad and ATC in major trauma
     • Minimise Crystalloid transfusion, NO COLLOID.
     • PRBC - HCT~0.5-6 & K+ 10-40mmol/L. Important for oxygen
       carriage and volume.
     • FFP – FII, V, VII-XII, fibrinogen, vWF and ATIII
     • Platelets
     • Cryoprecipitate – fibrinogen, FVIII, FXIII and vWF
     • Ideal PRBC:FFP:platelet ratio not clear but should be <2:1:1
• Use of adjunctive therapies
     • Tranexamic acid Crash 2, NNT 67→ lower with MT&SBP<75
     • Calcium vital for clotting, +ve inotrope & myocardial
       protection
Blood component therapy problems
• When reconstituted poor
  relative of fresh whole blood
• Time to thaw
• Reduced 2,3 DPG levels
  and O2 carrying ability
• Short shelf life
• High volume and antigenic
  load -> ARDS/SIRS/ACS
• ABO issues
• Finite resource
• Citrate load
• Viral/bacterial
  contamination
• Transfusion reactions
PT & APTT?
ROTEM
• Rotational viscoelastive
  test
• NPT
• Whole blood
• Rapid
• Functional/dynamic vs
  quantative lab test
• Clotting factors,
  fibrinogen&platelets
• CA5 ≤35mm predictive of
  ATC and MT, Davenport et al
  Crit Care Med 2011
ROTEM on ED admission (1/4)
   Case - 2u PRBC, 1g TXA, 500ml CSL, 250ml HTS
ROTEM (2/4) leave ED
Case - PRBCx6, FFPx4, 1g TXA, 1000 CSL, 250ml HTS
ROTEM (3/4) theatres
Case - PRBCx12, FFPx8, 1g TXA, 1000 CSL, 250ml HTS
ROTEM 4/4- Good DCR and patient survival
   Case - PRBCx23, FFPx16, 2g TXA, Cyro/Platx3, CaCL 3g,
   1000ml CSL, 250ml HTS -> HAEMOSTASIS
Bad DCR = unfavourable
ROTEM = high mortality rate
3. Permissive hypotension
• Titrated volume resuscitation to maintain organ viability
  and not normality until haemorrhage is controlled
• First clot is often the best = preserve it
• Aggressive early fluid resuscitation in penetrating trauma
  with uncontrolled bleeding may be detrimental, Bickell WH N
  Engl J Med 1994.
• Poor evidence to inform resuscitation strategies in blunt
  trauma with uncontrolled bleeding
• The evidence for maintaining CPP in head injuries is
  much stronger
• ATLS provides a framework for those who are not
  experts in trauma
Permissive hypotension
• The end points for resuscitation will
  depend on age, premorbid autoregulatory
  state and acute pathology

• ‘Rule of thumb’ resuscitation end points:
     • Penetrating trauma - maintain cerebration or central pulse or
       SBP~60mmHg
     • Blunt trauma – maintain radial pulse or SBP >80mmHg
     • Head injury – maintain temporal pulse or SBP >100mmHg
     • SCI – Spinal cord perfusion can be improved with SBP>90mmHg,
       but no functional outcome data as yet
The future for DCR
• PCC (FII, VII, IX and X) in non-warfarin
  pts. Joseph B et al, J Trauma Acute Care Surg 2012 & Schochl H et al, Crit Care
   2011.

• FDP – French military and porcine models
• FCC (fibrinogen and FXIII) over
  cryoprecipitate. Schochl H et al, Crit Care 2010 and 2011
• rFVIIa out of favour
• Fresh warm whole blood, I wish!!
The future for DCR
• Alkalising agents – Tris-hydroxymethyl
  aminomethane (THAM) in MT with severe
  acidaemia
• Novel hybrid resuscitation strategies. Doran CM et al, J
  Trauma Acute Care Surg 2012

• High flow/low pressure resuscitation –
  endothelial resuscitation and microvascular
  washout, Richard Dutton
• Suspended Animation
• Platelet function - validation of platelet mapping
  and aggregometry vs traditional PF-100
• Use of thromboelastometry (TEG/ROTEM)
Early and individualized
goal-directed therapy for
TIC
Schöchl H et al. Scand J Trauma
Resusc Emerg Med 2012
Pre-hospital Management
• C-ABCDE/MARCH – Tourniquets, Haemostatic agents,
  foley catheter
• Meticulous DCR
      • DCS is the key critical intervention so limit scene time
      • Haemostatic resuscitation – Early use of PRBC, TXA and for the
        future PCC/FCC/FDP/alkalising agents
      • Permissive hypotension - good individualised endothelial
        resuscitation
• Lethal triad management
      • Hypothermia- Limit exposure, Enflow fluid warmer, HMEF, insulation
        and active warming pads in cold climates.
      • Acidaemia- A/w further evidence for alkalising agents and high
        flow/low pressure resuscitation.
      • Coagulopathy- Limit crystalloid resuscitation
• Pre alert MTC of need for MT protocol activation
Additional Hospital management
• DCR
     • Damage control surgery
     • Haemostatic resuscitation
        – Initially protocolised <2:1:1 ratios of PRBC:FFP:platelets
          with fibrinogen supplementation.
        – Adjuncts: TXA, Calcium and consider alkalising agents
        – Viscoelastive NPT to guide on going transfusions
     • Permissive hypotension until haemorrhage control

• Lethal triad
     • Hypothermia – ↑ambient temperature, active warming/forced
       air warmers, radiant heaters. Temp no lower than 34̊C.
     • Acidaemia – good resuscitation and control of bleeding is the
       priority. If pH < 7.1 consider THAM/NaHCO3?
Future for GSA-HEMS
• Haemostatic agents – Hemcon and Quikclot →
  Combat gauze, ChitoGauze and Celox
• Foley catheters
• MAT → SOF tactical tourniquet
• TXA – part of Victorian trial or introduce?
• PCC – for warfarin + ATC?
• State wide pre-alert for MTC (Code Crimson) –
  SOP?
     •   sBP<90
     •   Unresponsive to resuscitation
     •   With active bleeding
     •   E-FAST +ve
• Good temp control – EnFlow & improved packaging
Summary
• Early coagulation dysfunction is common in
  trauma patients with haemorrhagic shock

• Tailored management of the ‘lethal triad’ and
  ATC is essential

• DCR is an emerging standard of care, however,
  some of its components are pushing the
  boundaries of what is good EBM
QUESTIONS?

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Managing Traumatic Hemorrhage with Damage Control Resuscitation

  • 1. The haemorrhaging trauma patient Dr Peter Sherren
  • 2. Objectives • Causes of coagulopathy in trauma • Describe damage control resuscitation • Describe new strategies for managing traumatic haemorrhage • Explain relevance to pre-hospital care
  • 3. Background • Uncontrolled haemorrhage is the commonest cause of preventable trauma deaths. Holcomb et al Ann Surg 2008. • Damage control resuscitation (DCR) improves outcomes and mortality. Cotton BA et al Ann Surg 2011 • DCR should start at the time of injury not in the ED
  • 4. Haemorrhage in trauma • Surgical - Massive haemorrhage, 1 on the floor and 4 more • Medical - bleeding diathesis, anticoagulants, DIC, lethal triad and ATC
  • 5.
  • 6. ~1800 pts HEMS admissions to the RLH • ~1 in 4 pts admitted with coagulopathy • Independent of fluid administration • Significant association with mortality • ATC = ACoTS
  • 8. Pathophysiology • ATC ≠ DIC • Tissue/endothelial injury and hypoperfusion • Increased endogenous anticoagulants • Fibrinolysis and hyperfibrinolysis
  • 9.
  • 10. APC • TFPI • AT III TERMINATION
  • 13. Can we predict ATC? • Several tools for predicting massive transfusion but not validated in ATC or pre-hospital arena • Trauma Associated Severe Haemorrhage (TASH) Score (J Trauma 2006;60:1228-1237) and others • Male • Unstable pelvic fracture • Open or deformed femur fracture • HR >120 bpm • SBP <100 mmHg • FAST positive for intra-abdominal fluid • Hb <11 g/dL • Base deficit > -2
  • 15. Case presentation • 16.05 – High speed MBC • Ground crew on scene 16.18 hand over to HEMS at 16:24 – M ~40 yr old male involved in high speed MBC – I Complete traumatic Rt forequarter amputation++ +blood, ?pelvis, CHI – S Agonal breaths, SpO2 not recording, HR 160, weak/thready carotid pulse only, GCS 7→3/15, Pupils 4/4 sluggish. – T O2 NRB, 1XIV, 500ml CSL
  • 16. HEMS management • 2xIO - IV tissued • Sux only RSI - ETCO2 quantatively low but present. • Rt thoracostomy • Direct compression wound • Sam Sling • 1g TXA • 250ml HTS, 500ml 0.9%NaCl • Persistent volume issues • Depart scene 16:47 (scene time 29 mins) • Massive transfusion pre-alert, 2xPRBC given on helipad arrival
  • 17. On arrival in the ED • AB ok • C – Haemodynamically unstable but volume responsive with haemostatic resuscitation with Level 1 – pH 6.7, BE -26, Lact 16 – Bloods on arrival Hb 10.6, HCT 0.28, INR 2.6 APTTR 2.1 • Taken to theatres for surgical haemostasis • Debrief points? Good level of care?
  • 18. Damage Control Resuscitation • 3 essential components: 1. Damage control surgery 2. Haemostatic resuscitation 3. Permissive hypotension • DCR improves outcomes and mortality. No level 1 evidence. Cotton BA et al Ann Surg 2011
  • 19. 1. Damage Control surgery • Unstable patients with major trauma do not survive prolonged definitive surgery • Normalise physiology at expense of anatomy • Stop haemorrhage (Packing, clamping, resection +/- IR) • Minimise contamination • Limb saving procedures • Good wash out of cavities • Drains and low threshold for Laparostomy • Definitive surgery another day • Optimise lethal triad on the ICU
  • 20.
  • 21. 2. Haemostatic resuscitation • Aggressive and simultaneous management of the lethal triad and ATC in major trauma • Minimise Crystalloid transfusion, NO COLLOID. • PRBC - HCT~0.5-6 & K+ 10-40mmol/L. Important for oxygen carriage and volume. • FFP – FII, V, VII-XII, fibrinogen, vWF and ATIII • Platelets • Cryoprecipitate – fibrinogen, FVIII, FXIII and vWF • Ideal PRBC:FFP:platelet ratio not clear but should be <2:1:1 • Use of adjunctive therapies • Tranexamic acid Crash 2, NNT 67→ lower with MT&SBP<75 • Calcium vital for clotting, +ve inotrope & myocardial protection
  • 22. Blood component therapy problems • When reconstituted poor relative of fresh whole blood • Time to thaw • Reduced 2,3 DPG levels and O2 carrying ability • Short shelf life • High volume and antigenic load -> ARDS/SIRS/ACS • ABO issues • Finite resource • Citrate load • Viral/bacterial contamination • Transfusion reactions
  • 24. ROTEM • Rotational viscoelastive test • NPT • Whole blood • Rapid • Functional/dynamic vs quantative lab test • Clotting factors, fibrinogen&platelets • CA5 ≤35mm predictive of ATC and MT, Davenport et al Crit Care Med 2011
  • 25. ROTEM on ED admission (1/4) Case - 2u PRBC, 1g TXA, 500ml CSL, 250ml HTS
  • 26. ROTEM (2/4) leave ED Case - PRBCx6, FFPx4, 1g TXA, 1000 CSL, 250ml HTS
  • 27. ROTEM (3/4) theatres Case - PRBCx12, FFPx8, 1g TXA, 1000 CSL, 250ml HTS
  • 28. ROTEM 4/4- Good DCR and patient survival Case - PRBCx23, FFPx16, 2g TXA, Cyro/Platx3, CaCL 3g, 1000ml CSL, 250ml HTS -> HAEMOSTASIS
  • 29. Bad DCR = unfavourable ROTEM = high mortality rate
  • 30. 3. Permissive hypotension • Titrated volume resuscitation to maintain organ viability and not normality until haemorrhage is controlled • First clot is often the best = preserve it • Aggressive early fluid resuscitation in penetrating trauma with uncontrolled bleeding may be detrimental, Bickell WH N Engl J Med 1994. • Poor evidence to inform resuscitation strategies in blunt trauma with uncontrolled bleeding • The evidence for maintaining CPP in head injuries is much stronger • ATLS provides a framework for those who are not experts in trauma
  • 31. Permissive hypotension • The end points for resuscitation will depend on age, premorbid autoregulatory state and acute pathology • ‘Rule of thumb’ resuscitation end points: • Penetrating trauma - maintain cerebration or central pulse or SBP~60mmHg • Blunt trauma – maintain radial pulse or SBP >80mmHg • Head injury – maintain temporal pulse or SBP >100mmHg • SCI – Spinal cord perfusion can be improved with SBP>90mmHg, but no functional outcome data as yet
  • 32. The future for DCR • PCC (FII, VII, IX and X) in non-warfarin pts. Joseph B et al, J Trauma Acute Care Surg 2012 & Schochl H et al, Crit Care 2011. • FDP – French military and porcine models • FCC (fibrinogen and FXIII) over cryoprecipitate. Schochl H et al, Crit Care 2010 and 2011 • rFVIIa out of favour • Fresh warm whole blood, I wish!!
  • 33. The future for DCR • Alkalising agents – Tris-hydroxymethyl aminomethane (THAM) in MT with severe acidaemia • Novel hybrid resuscitation strategies. Doran CM et al, J Trauma Acute Care Surg 2012 • High flow/low pressure resuscitation – endothelial resuscitation and microvascular washout, Richard Dutton • Suspended Animation • Platelet function - validation of platelet mapping and aggregometry vs traditional PF-100 • Use of thromboelastometry (TEG/ROTEM)
  • 34. Early and individualized goal-directed therapy for TIC Schöchl H et al. Scand J Trauma Resusc Emerg Med 2012
  • 35. Pre-hospital Management • C-ABCDE/MARCH – Tourniquets, Haemostatic agents, foley catheter • Meticulous DCR • DCS is the key critical intervention so limit scene time • Haemostatic resuscitation – Early use of PRBC, TXA and for the future PCC/FCC/FDP/alkalising agents • Permissive hypotension - good individualised endothelial resuscitation • Lethal triad management • Hypothermia- Limit exposure, Enflow fluid warmer, HMEF, insulation and active warming pads in cold climates. • Acidaemia- A/w further evidence for alkalising agents and high flow/low pressure resuscitation. • Coagulopathy- Limit crystalloid resuscitation • Pre alert MTC of need for MT protocol activation
  • 36. Additional Hospital management • DCR • Damage control surgery • Haemostatic resuscitation – Initially protocolised <2:1:1 ratios of PRBC:FFP:platelets with fibrinogen supplementation. – Adjuncts: TXA, Calcium and consider alkalising agents – Viscoelastive NPT to guide on going transfusions • Permissive hypotension until haemorrhage control • Lethal triad • Hypothermia – ↑ambient temperature, active warming/forced air warmers, radiant heaters. Temp no lower than 34̊C. • Acidaemia – good resuscitation and control of bleeding is the priority. If pH < 7.1 consider THAM/NaHCO3?
  • 37. Future for GSA-HEMS • Haemostatic agents – Hemcon and Quikclot → Combat gauze, ChitoGauze and Celox • Foley catheters • MAT → SOF tactical tourniquet • TXA – part of Victorian trial or introduce? • PCC – for warfarin + ATC? • State wide pre-alert for MTC (Code Crimson) – SOP? • sBP<90 • Unresponsive to resuscitation • With active bleeding • E-FAST +ve • Good temp control – EnFlow & improved packaging
  • 38. Summary • Early coagulation dysfunction is common in trauma patients with haemorrhagic shock • Tailored management of the ‘lethal triad’ and ATC is essential • DCR is an emerging standard of care, however, some of its components are pushing the boundaries of what is good EBM

Editor's Notes

  1. DIC (consumptive coagulopathy with thrombosis/bleeding) derranged APTT/PT/TT, thrombocytopnea, hyperfibriolysis (FDPs and fibrinogen levels)
  2. Cell based vs Int/Ex pathways. Platelet plug initiation, propagation, amplication and thrombin burst, termination
  3. Low ionised Ca2+ secondary to citrate washing vital for clotting factors, myocardial protection with K+ load
  4. Ex and InTEM whole blood NPT. ApTEM Aprotinin antifibrinolytic to look at platelet function FibTEM cytocalasin D inhibit platet function HepTEM heparinase used to eliminate effect of Heparin
  5. Freeze dried plasma equally effective in porcine. Produced by lyophilisation of plasma. Low volume, long shelf life and quick reconstitution. FCC FVIIa 1% fatal thrombotic events