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TRENDS IN TRAUMA RESUSCITATION

LEVI PROCTER, MD, FACS

TRAUMA, ACUTE CARE SURGERY AND SURGICAL CRITICAL CARE

DISCLOSURES

“NO RELEVANT FINANCIAL

RELATIONSHIP(S) EXIST.”

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OBJECTIVESDEFINE RESUSCITATION

ENDPOINTS OF RESUSCITATION

ACUTE COAGULOPATHY OFTRAUMA-SHOCK

THROMBOELASTOGRAPHY

MASSIVE TRANSFUSION

TRANEXAMIC ACID

SHOCK

INADEQUATE CELLULAR PERFUSION

TO MAINTAIN CELL LIFE

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RESUSCITATION

TO RESTORE CONSCIOUSNESS, VIGOR OR LIFE

END POINTS OF RESUSCITATION

BLOOD PRESSURE

MENTAL STATUS

PULSE

LACTATE

BASE DEFICIT

CVP

UOP

CARDIAC INDEX

SCVO2/SVO2

PULMONARY ARTERY OCCLUSION PRESSURE

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THERE ARE NONEMUST USE ALL AVAILABLE DATA

THE WHOLE IS GREATER THAN THE SUM OF ITS PARTS

DYNAMIC PROCESS THAT WARRANTS CONSTANT

RE-EVALUATION

OXYGEN DELIVERYDO2 = CO X CACO2

= [(HR X SV)] X [(HG X 1.34 X SAO2) + (PAO2 X 0.003)]

NOTICE THERE IS NO PRESSURE VARIABLE

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KEY POINTPRESSURE ≠ FLOW ≠ PERFUSION

FINALLY

OXYGEN DELIVERY ≠

OXYGEN CONSUMPTION

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LACTATEOXYGEN DEBT…

MADE IN ANAEROBIC CONDITIONS…

RIGHT?

LACTATE

LACTIC ACIDOSIS MAKES US SICK…

RIGHT?

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LACTATE

10. AM J PHYSIOL REGUL INTEGR COMP PHYSIOL. 2004;3:502-16.

LACTATE

10. AM J PHYSIOL REGUL INTEGR COMP PHYSIOL. 2004;3:502-16.

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BUFFER FOR INTRACELLULAR ACIDITY

USED FOR FUEL

WHEN CELL CAN’T MAKE ENOUGH LACTATE:

– PH DROPS MORE

– CELL DIES

– LACTATE SPILLS OUT (SOME IS TRANSPORTED OUT PRIOR VIA H+/LACTATE TRANSPORTER)

– HYDROGEN ION DERIVED FROM HYDROLYSIS OF ATP

LACTATE

10. AM J PHYSIOL REGUL INTEGR COMP PHYSIOL. 2004;3:502-16.

LACTATE DERIVED FROM CONVERSION OF PYRUVATE VIA LDH

– OCCURS WHEN INSUFFICIENT O2

PRESENT (SHOCK) TO ALLOW MITOCHONDRIA TO OXIDIZE GLUCOSE TO ATP

– ALSO OCCURS IN PRESENCE OF ADEQUATE OXYGEN

LACTATE

10. AM J PHYSIOL REGUL INTEGR COMP PHYSIOL. 2004;3:502-16.

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LACTATE OR LACTIC ACID

PKA OF LACTIC ACID IS 3.85

LACTATE TO LACTIC ACID IS IN A RATIO OF 3548:1 AT PH 7.4

ACID LOAD COMES FROM HYDROLYSIS OF ATP->ADP->AMP

10. AM J PHYSIOL REGUL INTEGR COMP PHYSIOL. 2004;3:502-16.

LACTATEINDIRECT MARKER OF SHOCK

MORE INDICATIVE OF ADRENERGIC DRIVE!

AKA…SOMETHING BAD IS PROBABLY GOING ON….

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HEMORRHAGIC SHOCK RESUSCITATION

CRYSTALLOIDS ARE OUT

COLLOIDS ARE OUT

PERMISSIVE HYPOTENSION IS IN

BLOOD AND PLASMA ARE IN

COAGULOPATHY GUIDED RESUSCITATION

HEMORRHAGIC SHOCK RESUSCITATION

STOP THE BLEEDING

GIVE THEM WHAT THEY NEED….

AND NOT A DROP MORE

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ACUTE COAGULOPATHY OF TRAUMA-SHOCK (ACoTS)

SYNDROME OF COAGULOPATHY THAT FAVORS BLEEDING

PRESENT IN 25-30% OF TRAUMATICALLY INJURED ON PRESENTATION 1-2

8X AND 4X-INCREASED RISK OF MORTALITY AT

24 HOURS AND 30 DAYS.

MORE TRANSFUSION, LONGER ICU AND HOSPITAL LOS, MORE MOF3-4

REVERSAL REQUIRES FACTOR DRIVEN RESUSCITATION1. J TRAUMA. (55).1.39–44, 2003.2. J TRAUMA. (54).6.1127-1130.2003.3. CURRENT OP CRITICAL CARE. (13)6.680-5.2007.4. INTENSIVE CARE MEDICINE. (37)4.572-82. 2011.

ACoTSALL MECHANISMS NOT KNOWN YET

DEPENDS ON:DEGREE OF TISSUE INJURY

DEGREE OF HYPOPERFUSION

2 COMPONENTS ARE:ACTIVATION OF PROTEIN C (APC) –

BLOOD LOSS CAUSING HYPOPERFUSION

HYPERFIBRINOLYSIS –TISSUE DAMAGE CAUSES RELEASE OF TPA

(TISSUE PLASMINOGEN ACTIVATOR)

3. CURRENT OP CRITICAL CARE. (13)6.680-5.2007.

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APCINACTIVATES FACTOR VIII AND V

INCREASES FIBRINOLYSIS

CONSUMES:PLASMINOGEN ACTIVATOR INHIBITOR

THROMBIN ACTIVATABLE FIBRINOLYSIS INHIBITOR

5. MINERVA ANESTESIOLOGICA. 77;3:349-59.20116. ANESTHESIA AND ANALGESIA.108;6:1760-68.2009

ACoTSWORSENED BY BUT NOT CAUSED BY5:

DILUTION – CRYSTALLOID AND COLLOID

HYPOTHERMIA

ACIDEMIA

5. ANESTHESIA AND ANALGESIA, VOL. 108, NO. 6, PP. 1760–1768, 2009.

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ACoTSSHOULD BE CONSIDERED IN ALL4:

SEVERELY INJURED PATIENTS

HIGH ENERGY TRAUMA

CLINICALLY ILL

EVIDENCE OF SHOCK

4. INTENSIVE CARE MEDICINE, VOL. 37, NO. 4, PP. 572–582, 2011..

ACoTS

J TRAUMA. 2008;64:1211–1217

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ACoTS AND SHOCKACoTS IS DOSE DEPENDENT

ACoTS SEVERITY BASED ON:

SEVERITY OF HYPOPERFUSION

BD > 6 MMOL/L7

PT/PTT > 1.5 X NL8

7. ANN SURG. 2007;245:812-818.8. J TRAUMA. 54;6.1127-30.2003.

PERMISSIVE HYPOTENSION

CLOT LYSIS WHEN SBP > 80 MMHG

12. J TRAUMA.54:S110-S117.2004

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PERMISSIVE HYPOTENSION

SBP 80-90 MMHG

AND/OR

MAP 50 MMHG

12. J TRAUMA.54:S110-S117.2004

WHAT ABOUT TBI?HYPOTENSION INCREASES TBI

MORTALITY

SBP TARGETED FLUID RESUSCITATION

WILL NOT

IMPROVE SBP DURING ACTIVE HEMORRHAGE

13. SHIRES ET AL. WORLD J SURG. 25:592-597.2001.14. SCALEA ET AL. J TRAUMA.52(6);1141-1146.2002.

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NEED LOTS OF HEMORRAHGE

ONLY WHEN ~50%

BLOOD VOLUME LOST

=

FALL IN SBP

15. WO CJ, SHOEMAKER WC, APPEL PL, BISHOP MH, KRAM HB, HARDIN E. UNRELIABILITY OF BLOOD PRESSURE AND HEART RATE TO EVALUATE CARDIAC OUTPUT IN EMERGENCY RESUSCITATION AND CRITICALILLNESS. CRIT CARE MED 1993;21:218-23.

GIVE MORE VOLUMEWHO CARES?

WORSE COAGULOPATHY

WORSE SIRS

MORE ARDS

MORE ACS

MORE PULM EDEMA

MORE DEATH

16. COTTON BA, GUY JS, MORRIS JA JR ET AL: THE CELLULAR, METABOLIC, AND SYSTEMIC CONSEQUENCES OF AGGRESSIVE FLUID RESUSCITATION STRATEGIES. SHOCK 2006;26(2):115–121.

17. D AUGHERTY EL, LIANG H, TAICHMAN D ET AL: ABDOMINAL COMPARTMENT SYNDROME IS COMMON IN MEDICAL INTENSIVE CARE UNIT PATIENTS RECEIVING LARGE-VOLUME RESUSCITATION. J INTENSIVE CARE MED 2007;22(5):294–299.

18. O’MARA MS, SLATER H, GOLDFARB IW ET AL: A PROSPECTIVE, RANDOMIZED EVALUATION OF INTRA-ABDOMINAL PRESSURES WITH CRYSTALLOID AND COLLOID RESUSCITATION IN BURN PATIENTS. J TRAUMA 2005;58(5):1011–1018.

19. G IANNOUDIS PV, FOGERTY S: INITIAL CARE OF THE SEVERELY INJURED PATIENT: PREDICTING MORBIDITY FROM SUB-CLINICAL FINDINGS ANDCLINICAL PROTEOMICS. INJURY 2007;38(3):261–262.

20. KLEIN MB, HAYDEN D, ELSON C ET AL: THE ASSOCIATION BETWEEN FLUID ADMINISTRATION AND OUTCOME FOLLOWING MAJOR BURN: A MULTICENTER STUDY. ANN SURG 2007;245(4):622–628.

21. KASOTAKIS G, SIDERIS A, YANG Y ET AL: AGGRESSIVE EARLY CRYSTALLOIDRESUSCITATION ADVERSELY AFFECTS OUTCOMES IN ADULT BLUNT TRAUMAPATIENTS: AN ANALYSIS OF THE GLUE GRANT DATABASE. J TRAUMA ACUTE CARE SURG 2013;74(5):1215–1221;DISCUSSION 1221–1222.

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THROMOBOELASTOGRAPHY

MECHANICAL GRAPHICAL DISPLAY OF CLOT FORMATION AND STABILITY

TAKES 30-45 MINUTES

REAL TIME DISPLAY OF CLOT

REQUIRES EQUIPMENT AND TRAINING FOR GRAPH INTERPRETATION

TEG

INCREASED R TIME � FFPDECREASED ANGLE � CRYOPRECIPTATE

DECREASED MA � PLATELETS (CONSIDER DDAVP)FIBRINOLYSIS � TRANEXAMIC

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WHAT ABOUT INR?IF INR > 1.5 IT IS VALUABLE

WILL MISS FIBRINOLYSIS

ONLY ASSESSES FIRST 60 SECONDS OF CLOTTING IN PLASMA

BLOOD IS WARMED TO RUN THE TEST

NOT A TRUE REFLECTION OF HEMOSTATIC ENVIRONMENT

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TRANEXAMIC ACID

ANTIFIBRINOLYTIC

INHIBITS PLASMINOGEN ACTIVATION

DECREASES PLASMIN ACTIVITY

REDUCES CLOT LYSIS

TRANEXAMIC ACID

CRASH-2 TRIAL

LOWERED MORTALITY

GIVE WITHIN 3 HOURS OF INJURY

RECOMMENDED FOR ANY PATIENT YOU FEEL IS AT RISK FOR BLEEDING

IF YOU HAVE ACCESS TO TEG – USE IT TO GUIDE YOUR ADMINISTRATION

22. CRASH2 INVESTIGATORS. The Lancet, Vol. 377, No. 9771, p1096–1101

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HYPERFIBRINOLYSIS

INCREASED RISK OF DEATH

TREATMENT INCLUDES TRANEXAMIC ACID

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WHAT DO WE DO?STOP BLEEDING

USE HIGH RATIO TRANSFUSION(1:1:1)

ALLOW PERMISSIVE HYPOTENSION*

* OUTSIDE OF HEAD INJURY

WHAT DO WE DO?AVOID/CORRECT:

HYPOTHERMIA

ACIDEMIA

DILUTION

HYPOCALCEMIA

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MASSIVE TRANSFUSION

ARBITRARY DEFINITION

2-3% OF CIVILIAN TRAUMA10

MIMICS WHOLE BLOOD TRANSFUSION

1:1:1

PLASMA:PLATELETS:PRBCS

NO BEST RATIO OUTSIDE OF 1:1:1

11. INJURY. 38;3:298-304.2007.

HEMOSTATIC RESUSCITATION

USE OF AGGRESSIVE RATIOS OF BLOOD AND PRODUCTS TO ATTEMPT

TO REVERSE ACoTS

UNABLE TO COMPLETELY REVERSE WITHOUT ARREST OF HEMORRHAGE

22. BROHI. J TRAUMA. (76):3:561-568.23. HOLCOMB. JAMA SURG. 148:127-136.2013.24. BARANIUK. INJURY. 45(9):1287-95.

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PREDICTING MTLOTS OF SCORING SYSTEMS

MCLAUGHLINTASHABCPWH

NOT ALL PATIENTS HAVE THE DATA TO USE THESE

CURRENTLY LACK A GOLD STANDARD PREDICTOR

STABLE PATIENTS

DON’T NEED:

BLOOD

CRYSTALLOID

COLLOID

IT’S OK TO NOT INTERVENE

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SUMMARY

STOP BLEEDING

ALLOW HYPOTENSION

MINIMIZE CRYSTALLOID AND COLLOID

ACoTS INCREASES MORTALITY

RELATED TO DEGREE OF HYPOPERFUSION AND INJURY

SUMMARY

EARLY USE OF COMPONENT BLOOD PRODUCT RESUSCITATION

TRANEXAMIC ACID GOOD AND GIVE EARLY

TEG CAN GUIDE BLOOD RESUSCITATION

LACTATE A MARKER OF SEVERITY OF ILLNESS

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REFERENCES1. J. B. A. MACLEOD, M. LYNN, M. G. MCKENNEY, S. M. COHN, AND M. MURTHA, “EARLY COAGULOPATHY PREDICTS MORTALITY IN TRAUMA,” THE JOURNAL

OF TRAUMA, VOL. 55, NO. 1, PP. 39–44, 2003.

2. K. BROHI, J. SINGH, M. HERON, AND T. COATS, “ACUTE TRAUMATIC COAGULOPATHY,” THE JOURNAL OF TRAUMA, VOL. 54, NO. 6, PP. 1127–1130, 2003.

3. K. BROHI, M. J. COHEN, AND R. A. DAVENPORT, “ACUTE COAGULOPATHYOF TRAUMA: MECHANISM, IDENTIFICATION AND EFFECT,” CURRENTOPINION IN CRITICAL CARE, VOL. 13, NO. 6, PP. 680–685, 2007

4. AH. LIER, B.W. B¨OTTIGER, J.HINKELBEIN, H. KREP, AND M. BERNHARD, “COAGULATION MANAGEMENT IN MULTIPLE TRAUMA: A SYSTEMATICREVIEW,” INTENSIVE CARE MEDICINE, VOL. 37, NO. 4, PP. 572–582, 2011.

5. M. CUSHING AND B. H. SHAZ, “BLOOD TRANSFUSION IN TRAUMA PATIENTS: UNRESOLVED QUESTIONS,” MINERVA ANESTESIOLOGICA, VOL. 77,NO. 3, PP. 349–359, 2011.

6. B. H. SHAZ, C. J. DENTE, R. S. HARRIS, J. B. MACLEOD, AND C. D. HILLYER, “TRANSFUSION MANAGEMENT OF TRAUMA PATIENTS,” ANESTHESIA AND ANALGESIA, VOL. 108, NO. 6, PP. 1760–1768, 2009.

7. BROHI K, COHEN MJ, GANTER MT, MATTHAY MA, MACKERSIE RC, PITTET JF. ACUTE TRAUMATIC COAGULOPATHY: INITIATED BY HYPOPERFUSION: MODULATEDTHROUGH THE PROTEIN C PATHWAY? ANN SURG. 2007;245:812–818.

8. BROHI K, COHEN MJ, GANTER MT, MATTHAY MA, MACKERSIE RC, PITTET JF. ACUTE TRAUMATIC COAGULOPATHY: INITIATED BY HYPOPERFUSION, MODULATED THROUGH THE PROTEIN C PATHWAY? ANN SURG. 2007;245:818–818.

9. BROHI K, SINGH J, HERON M, COATS T. ACUTE TRAUMATIC COAGULOPATHY.J TRAUMA. 2003;54:1127–1130.

10. ROBERGS ET AL. AM J PHYSIOL REGUL INTEGR COMP PHYSIOL.287;3:R502-16.2004.

11. M. MAEGELE, R. LEFERING, N. YUCEL ET AL., “EARLY COAGULOPATHY IN MULTIPLE INJURY: AN ANALYSIS FROM THE GERMAN TRAUMA REGISTRYON 8724 PATIENTS,” INJURY, VOL. 38, NO. 3, PP. 298–304, 2007.

12. J TRAUMA.54:S110-S117.2004

13. SHIRES ET AL. WORLD J SURG. 25:592-597.2001.

14. SCALEA ET AL. J TRAUMA.52(6);1141-1146.2002.

15. WO CJ, SHOEMAKER WC, APPEL PL, BISHOP MH, KRAM HB, HARDIN E. UNRELIABILITY OF BLOOD PRESSURE AND HEART RATE TO EVALUATE CARDIAC OUTPUT IN EMERGENCY RESUSCITATION AND CRITICAL ILLNESS. CRIT CARE MED 1993;21:218-23.

16. COTTON BA, GUY JS, MORRIS JA JR ET AL: THE CELLULAR, METABOLIC, AND SYSTEMIC CONSEQUENCES OF AGGRESSIVE FLUID RESUSCITATION STRATEGIES. SHOCK 2006;26(2):115–121.

17. D AUGHERTY EL, LIANG H, TAICHMAN D ET AL: ABDOMINAL COMPARTMENT SYNDROME IS COMMON IN MEDICAL INTENSIVE CARE UNIT PATIENTS RECEIVING LARVOLUME RESUSCITATION. J INTENSIVE CARE MED 2007;22(5):294–299.

18. O’MARA MS, SLATER H, GOLDFARB IW ET AL: A PROSPECTIVE, RANDOMIZED EVALUATION OF INTRA-ABDOMINAL PRESSURES WITH CRYSTALLOID AND COLLOID RESUSCITATION IN BURN PATIENTS. J TRAUMA 2005;58(5):1011–1018.

19. G IANNOUDIS PV, FOGERTY S: INITIAL CARE OF THE SEVERELY INJURED PATIENT: PREDICTING MORBIDITY FROM SUB-CLINICAL FINDINGS AND CLINICAL PROTEOMICS. INJURY 2007;38(3):261–262.

20. KLEIN MB, HAYDEN D, ELSON C ET AL: THE ASSOCIATION BETWEEN FLUID ADMINISTRATION AND OUTCOME FOLLOWING MAJOR BURN: A MULTICENTER STUDY. ANN SURG 2007;245(4):622–628.

21. KASOTAKIS G, SIDERIS A, YANG Y ET AL: AGGRESSIVE EARLY CRYSTALLOIDRESUSCITATION ADVERSELY AFFECTS OUTCOMES IN ADULT BLUNT TRAUMAPATIENTS: AN ANALYSIS OF THE GLUE GRANT DATABASE. J TRAUMA ACUTE CARE SURG 2013;74(5):1215–1221;DISCUSSION 1221–1222.

22. BROHI. J TRAUMA. (76):3:561-568.

23. HOLCOMB. JAMA SURG. 148:127-136.2013.

24. BARANIUK. INJURY. 45(9):1287-95.

TRENDS IN TRAUMA RESUSCITATION

LEVI PROCTER, MD, FACS

LEVI.PROCTER@UKY.EDU