Coagulopathy and Goal Directed Hemostatic … Trauma... · Coagulopathy and Goal Directed...

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Coagulopathy and Goal Directed Hemostatic Resuscitation in Pediatric Trauma Adam M. Vogel, MD Assistant Professor, Division of Pediatric Surgery Washington University in St. Louis School of Medicine December 3, 2013

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  • Coagulopathy and Goal Directed Hemostatic Resuscitation in Pediatric


    Adam M. Vogel, MD Assistant Professor, Division of Pediatric Surgery

    Washington University in St. Louis School of Medicine December 3, 2013

  • Disclosure

    I have no relevant financial or nonfinancial relationships to disclose

  • Outline

    Acute coagulopathy of trauma TEG

    Mechanics Interpretation

    TEG in adults trauma TEG in pediatric trauma SLCH

  • Acute Coagulopathy of Trauma

  • Acute Coagulopathy of Trauma Multifactorial coagulopathy associated with severely

    injured patients

    Distinct from: dilutional coagulopathy transfusion related coagulopathy

    Related to: Tissue factor release Protein C activation Hypoperfusion Hyperfibrinolysis

  • 3287 patients, 391 patients transfused Acute coagulopathy (INR > 1.5) on arrival: 38% Mortality (+) coagulopathy 24% (vs. 4%)

  • Retrospective study 1,088 patients PT, aPTT, thrombin time >1.5 times nL

    On admission, 24.4 % (+) coagulopathic

    Coagulopathy: higher mortality (46% vs. 11%)

  • 211 patients receiving MTP or TEP Prevalence of coagulopathy 70% (INR>1.5)

    Mortality in non-coagulopathic 42% Mortality in coagulopathic 67%

  • N=23,506 2000-2006

  • In Children . . .

  • Retrospective review, children < 18y

    2002-2009; 744 patients Coagulopathy: INR >1.5

  • Retrospective review 102 trauma patients

    requiring a blood transfusion

    Coagulopathic PT > 15.9 s PTT > 42.1 s Fibrinogen < 180 mg/dl Platelets < 185

  • We therefore conclude . . .

    Acute coagulopathy of trauma is real and is BAD

  • Goal Directed Resuscitation Restore normal physiology Reversal of the shock state

    End Organ Perfusion

    Mental status, capillary refill, urine output Vital signs

    HR, BP, MAP, RR, SaO2 Laboratory data

    ABG base deficit, lactate Real-time imaging

    FAST-ECHO, IVC filling

  • Goal Directed Hemostatic Resuscitation

    Conventional coagulation tests (CCT) PT/INR PTT Platelet count Fibrinogen D-dimers

  • Thrombelastography TEG

    Assesses global function of clotting proteins, platelets, and the fibrinolytic system

    Viscioelastic mechanical properties of blood Useful point-of-care assay

    Different devices: TEG vs. ROTEM

    Different names for the parameters

    Multiple flavors of activating agents: Celite Kaolin Tissue factor Rapid: Kaolin + tissue factor

  • How It Works Cup oscillates Pin is attached to a torsion

    wire Clot binds pin to cup Degree of pin movement

    is a function of clot kinetics

    Magnitude of pin motion is a function of the mechanical properties of the clot

    System generates a hemostasis profile

    From initial formation to lysis

    PresenterPresentation NotesThe TEG analyzer has a sample cup that constantly oscillates at a set speed through an arc of 445; each oscillation lasts ten seconds. A whole blood sample of 360 l is placed into the cup, and a stationary pin attached to a torsion wire is immersed in the blood. When fibrin first forms, it begins to bind the cup and pin, causing the pin to oscillate in phase with the cup. The degree of pin movement is a function of the kinetics of clot development.

    The torque of the rotating cup is transmitted to the immersed pin only after fibrin or fibrin-platelet bonding has linked the cup and pin together. The strength of these fibrin-platelet bonds affects the magnitude of the pin motion.

    The magnitude of the output is directly related to the strength of the forming clot. As the clot retracts or lyses, the bonds between the cup and pin are broken, and the transfer of cup motion is diminished. The movement of the pin is converted by a mechanical-electrical transducer into an electrical signal, which can be monitored by a computer.

    The movement of the pin generates a hemostasis profile, which is a measure of the time it takes for the first fibrin strand to form, the kinetics of clot formation, the strength of the clot (in shear elasticity units of dyn/cm2), and the dissolution of clot.

  • R value or ACT: time to initial clot formation K time time for tracing to reach 20mm angle: rate of clot formation Maximum amplitude (MA): clot strength LY30: percent amplitude reduction in 30 minutes

    PresenterPresentation NotesThis is an example of a TEG tracing showing both coagulation and fibrinolysis . . .

    The R value or ACT in rTEG is the time to initiate clot formation, and is thought to reflect clotting factors. Normal range, 0-118 seconds

    The K time is the time for the tracing to reach 20mm. Normal range, 1-2 minutes.

    The alpha angle represents the rate of clot formation. Normal range, 66-82 degrees.

    Both k and alpha are thought to reflect fibrinogen

    The MA or maximum amplitude represents maximal clot strength and is thought to reflect platelet function. Normal range, 54-72 millimeters.

    Finally, the LY30 is the percent degradation of the tracing formthe MA over 30 min and reflects fibrinolysis. Normal range, 0.0-7.5%.

  • Normal TEG Tracing

  • Hemorrhagic TEG Tracing

  • Monitoring Hemostasis

    Need whole blood sample TEG analysis uses whole blood CCT and platelet counts use plasma

    Measure interaction of components TEG analysis reflects interaction CCT and platelet counts isolate components

    Measure dynamic changes from start to finish of process TEG analysis reflects dynamic changes CCT and platelet counts reflect one point in time

    PresenterPresentation NotesMonitoring hemostasis using the cell-based model requires a whole blood test, as in TEG analysis. Whole blood is needed to measure the interactions among platelets, coagulation factors, and other cellular or plasmatic factors. Many laboratory tests including PT, aPTT, TT, D-DIMER, and platelet counts use plasma, and as a result miss the impact of the cellular elements.

    TEG analysis reflects the cell based model and extends beyond it by measuring the net effect of all the blood-borne components of hemostasis. These include coagulation factors, fibrinogen, platelets, fibrinolytic factors, inflammatory cells, blood cells, mediators and most pharmacological agents.

    The hemostatic process is dynamic, and the components interact differently as the process moves from activation to clot formation to clot lysis. Monitoring should reflect the dynamic changes of all components from start to finish, as in TEG analysis. Most tests like PT, aPTT, TT, and platelet count focus on just one component at a specific, isolated point in the process.

  • TEG in Adult Trauma

  • Prospective, observational N=300 ATC: PT > 1.2 Low CA (MA in ROTEM) at 5 min < 35

    Likelihood of PRBC and FFP Likelihood of MTP

  • Prospective, TBI by CT N= 69; TEG and CCT Hypocoagulability

    TEG (R

  • Prospective data collection > 6 units PRBC within 6 hours of admission Pre-rTEG (N=34) and post-rTEG(N=34)

    Trend towards fewer products in the post-rTEG Improved lower FFP:PRBC in the post-rTEG Improved mortality 65% to 29%

    Small N, ISS differences

  • 20 patients rTEG, kTEG, CCT Time to results (MA)

    rTEG: 19.2 3.1 min kTEG: 29.9 4.3 min CCT: 34.1 14.5 min

    rTEG is the fastest

  • rTEG and kTEG

  • Prospective data collection 10/2009 2/2010 272 major trauma activations rTEG: kaolin + tissue factor CCT: PT, aPTT

  • Timing: specimen clocked-in to results Early rTEG values (ACT, K,): 5 min Late rTEG values (, MA): 15 min CCT: 48 min p < 0.001

    Transfusions ACT > 128 s (first to result) predicts PRBC, plasma, platelet,

    and MTP ACT < 105 s identifies patients who did not receive a


  • Prospective, 9/2009-2/2011 N=1974

    Multiple linear regression controlling for age,

    gender, mechanism w-RTS, ISS, and base deficit

  • ACT predicted patients with substantial bleeding and RBC transfusion better than PT/PTT or INR (p = 0.03)

    -angle was superior to fibrinogen for predicting plasma transfusion (p < 0.001)

    mA was superior to platelet count for predicting platelet transfusion (p < 0.001)

    Can TEG replace CCTs?

  • These correlations improved for transfused, shocked or head injured patients

    The charge for r-TEG ($317) was similar to the five CCTs (>$400)

    Admission conventional coagulation tests can be

    replaced with r-TEG

    Can TEG replace CCTs?

  • TXA: antifibrynolytic agent Randomized, prospective, blinded, placebo-

    controlled in 40 countries, 274 hospitals Adult trauma pts with hemorrhage < 8hrs from

    injury w/: SBP < 90, HR > 110 or at risk TXA (N=10060) vs placebo (N=10067) TXA reduced mortality

  • TEG in Pediatric Trauma

  • 5yM s/p peds v. auto CHI, pulmonary contusion Grade IV liver w/ Hepatic artery injury Damage control laparotomy: packing Interventional radiology Serial TEGs, goal directed therapy (w/ factor VII)

  • rTEG in Pediatric Trauma Retrospective

    January 1, 2007 July 31, 2011

    Pediatric code III trauma activations

    Age 14 years Pediatric level I trauma center Admission rTEG

    PresenterPresentation NotesThis was a retrospective review over a two year period of the highest level trauma activations at an ACS verified level 1 pediatric trauma center of patients that received an admission rTEG

  • Methods Demographic, clinical, outcome data

    Transfusions (6 hours) Life saving interventions (6 hours)

    Endotracheal intubation Bedside surgical procedure (ICPm, CT, CVL) Emergent surgical procedure

    Statistical analysis Spearmans correlation Multivariate analysis (age, gender, ISS)

    PresenterPresentation NotesDemographic, clinical, and outcome data were extracted from the patients electronic medical record and trauma registry and data relating to transfusion requirement and life saving interventions were obtained.

    Spearmans correlation was used to relate rTEG parameters to conventional coagulation tests .

    Multivariate analysis controlling apriori for age, gender, and ISS was performed top evaluate rTEG parameters with transfusion requirements and life saving interventions.

  • Demographics Number of patients 86

    Male gender, % 67%

    Median age in years (IQR) 8 (3, 12)

    Blunt mechanism of injury, % 88%

    Median scene GCS (IQR) 9 (3, 15)

    Median EC GCS (IQR) 3 (3, 15)

    Median Injury Severity Score, ISS, (IQR) 21 (9, 33)

    30-day survival, (%) 88%

    PresenterPresentation NotesPatient demographics are as follows:For background, over the 2 year period, there were 2955 pediatric trauma activations, 326 were classified as code 3, and 86 of these patents received an rTEG on admission.

    The majority were male and the predominant mechanism was blunt. The median ISS was 21.

    There was an 88% survival.

    TBI Head AIS >3 was 55%

  • rTEG and CCT ACT k-time -angle MA

    aPTT r=0.68


  • Early Transfusion

    Controlling for age, gender, ISS

    ACT, R, K, , and MA Predict PRBC and FFP transfusion

  • Life Saving Interventions

    Only MA predicted life saving interventions OR 0.84; 95% CI 0.72-0.98; p=0.032

  • Limitations

    Single center


    Sample size

    PresenterPresentation NotesThis study has several limitations most notably its retrospective nature, its single center and small sample size.

  • Conclusions

    rTEG correlates with conventional coagulation tests

    rTEG predicts transfusion requirements

    rTEG predicts life saving interventions


    PresenterPresentation NotesDespite these limitations, we conclude the rapid thromboelastography may be very useful in pediatric trauma.

    rTEG values do correlate with conventional coagulation tests

    It also predicts the need for transfusion and other life saving interventions.

    Rapid thromboelastography may be a valuable tool in pediatric trauma and may serve as a guide for goal directed hemostatic resuscitation.

  • A word (or two) on Massive Transfusion

  • Here at Childrens . . .

  • Goal Directed Hemostatic Resuscitation at SLCH

    TEG provides rapid, valuable, actionable data on hemostasis and coagulopathy

    The goal for goal directed therapy Massive Transfusion Protocol

    Add TEG to admission labs for patients identified at

    risk for bleeding/coagulopathy GCS/TBI Penetrating trauma (t-shirt and boxer shorts) Massive transfusion protocol

  • Thank you

    Coagulopathy and Goal Directed Hemostatic Resuscitation in Pediatric TraumaDisclosureOutlineAcute Coagulopathy of TraumaSlide Number 5Slide Number 6Slide Number 7Acute Coagulopathy of TraumaSlide Number 9Slide Number 10Slide Number 11Slide Number 12Slide Number 13In Children . . .Slide Number 15Slide Number 16We therefore conclude . . .Goal Directed ResuscitationGoal Directed Hemostatic ResuscitationSlide Number 20ThrombelastographyHow It WorksSlide Number 23Normal TEG TracingSlide Number 25Hemorrhagic TEG TracingMonitoring HemostasisTEG in Adult TraumaSlide Number 29Slide Number 30Slide Number 31Slide Number 32rTEG and kTEGSlide Number 34Slide Number 35Slide Number 36Can TEG replace CCTs?Can TEG replace CCTs?Slide Number 39TEG in Pediatric TraumaSlide Number 41Slide Number 42rTEG in Pediatric TraumaMethodsDemographicsrTEG and CCTEarly TransfusionLife Saving InterventionsLimitationsConclusionsSlide Number 51A word (or two) on Massive TransfusionSlide Number 53Slide Number 54Here at Childrens . . .Goal Directed Hemostatic Resuscitation at SLCHThank you