6/2/2016
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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OBJECTIVES
DEFINE RESUSCITATION
ENDPOINTS OF RESUSCITATION
ACUTE COAGULOPATHY OF
TRAUMA-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 NONE
MUST USE ALL AVAILABLE DATA
THE WHOLE IS GREATER THAN
THE SUM OF ITS PARTS
DYNAMIC PROCESS THAT
WARRANTS CONSTANT
RE-EVALUATION
OXYGEN DELIVERY
DO2 = 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 POINT
PRESSURE
≠
FLOW
≠
PERFUSION
FINALLY
OXYGEN DELIVERY
≠
OXYGEN
CONSUMPTION
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LACTATE
OXYGEN 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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LACTATE
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
10. AM J PHYSIOL REGUL INTEGR COMP PHYSIOL. 2004;3:502-16.
LACTATE
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
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.
LACTATE
INDIRECT 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 RESUSCITATION
1.
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.
ACoTS
ALL 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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APC
INACTIVATES FACTOR VIII AND V
INCREASES FIBRINOLYSIS
CONSUMES:
PLASMINOGEN ACTIVATOR INHIBITOR
THROMBIN ACTIVATABLE FIBRINOLYSIS
INHIBITOR
5. MINERVA ANESTESIOLOGICA. 77;3:349-59.2011
6. ANESTHESIA AND ANALGESIA.108;6:1760-68.2009
ACoTS
WORSENED 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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ACoTS
SHOULD 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 SHOCK
ACoTS 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 CRITICAL
ILLNESS. CRIT CARE MED 1993;21:218-23.
GIVE MORE VOLUME
WHO 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 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 TRAUMA
PATIENTS: 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
FFP
DECREASED 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 MT
LOTS OF SCORING SYSTEMS
MCLAUGHLIN
TASH
ABC
PWH
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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REFERENCES
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24.
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.
K. BROHI, J. SINGH, M. HERON, AND T. COATS, “ACUTE TRAUMATIC COAGULOPATHY,” THE JOURNAL OF TRAUMA, VOL. 54, NO. 6, PP. 1127–1130, 2003.
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
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.
M. CUSHING AND B. H. SHAZ, “BLOOD TRANSFUSION IN TRAUMA PATIENTS: UNRESOLVED QUESTIONS,” MINERVA ANESTESIOLOGICA, VOL. 77,NO. 3, PP.
349–359, 2011.
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.
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.
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.
BROHI K, SINGH J, HERON M, COATS T. ACUTE TRAUMATIC COAGULOPATHY.J TRAUMA. 2003;54:1127–1130.
ROBERGS ET AL. AM J PHYSIOL REGUL INTEGR COMP PHYSIOL.287;3:R502-16.2004.
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.
J TRAUMA.54:S110-S117.2004
SHIRES ET AL. WORLD J SURG. 25:592-597.2001.
SCALEA ET AL. J TRAUMA.52(6);1141-1146.2002.
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.
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.
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.
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.
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.
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.
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.
BROHI. J TRAUMA. (76):3:561-568.
HOLCOMB. JAMA SURG. 148:127-136.2013.
BARANIUK. INJURY. 45(9):1287-95.
TRENDS IN TRAUMA
RESUSCITATION
LEVI PROCTER, MD, FACS
[email protected]
25