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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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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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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