Presentation on theme: "From the ED to the battlefield and back to the ED/bedside"— Presentation transcript:
1From the ED to the battlefield and back to the ED/bedside Resuscitation from Massive Hemorrhage & Development of the MTP: Perspective of an Obstetrical AnesthesiologistAlan I. Frankfurt, MDPartner, ATLAS AnesthesiaIrving, TexasDepartment of AnesthesiologyTH Dallas-Presbyterian Hospital--Alan I. Frankfurt, MD
2Learning Objectives Maryland Shock Trauma Somalia & Iraq/Afghanistan History lessonIncidence of MTDCR & “5 H’s”Coagulopathy and morbidity in hemorrhagic shockLethal triadEvolution of the MTP: responding to an iatrogenic coagulopathyMaryland Shock TraumaSomalia & Iraq/Afghanistan1:1:1 vs. 1:1:2-it’s a math thingPROMMTTPROPPRRThoughts for your day to day practice in the ED.Alan I. Frankfurt, MD
3HISTORY OF WARTIME PREHOSPITAL/ER SHOCK RESUSCITATION WW I/WW IIVietnamKoreaOIF/OEF50 years of Plasma, Albumin and Whole BloodForward to the past( DCR):Early plasma”WB” equivalentFWWB40 years of Crystalloid/Clear Fluids & WB:3rd space resuscitationFractionation of WBAlan I. Frankfurt, MD
4Damage Control Resuscitation “5 H’s” Hemorrhage controlOR timely fashionDefinitive solution to bleeding is in the OR/IRHypotensive resuscitationSystolic BP=80-90 torr“Tolerate” shock vs. Popping clotsHemostatic resuscitationBlood products early and often: PlasmaPrevention of coagulopathyDilutionACoTSMinimize crystalloid administrationHomeostasisHypothermiaAcidosisHypnosis: having our cake and eating it tooDCAVasoconstriction Vasorelaxed
5Alan I. Frankfurt, MDElements of hemostatic resuscitation, and level of evidence in support: R. Dutton; BJA 2012, Vol109 no. suppl 1 i39RecommendationsEvidence Expedited anatomic control in ORStrong; widely accepted Deliberate (permissive) hypotensionSeveral prospective trials; widely acceptedEarly support of coagulation Antifibrinolytic therapyOne large prospective trial, several smaller studies; emerging standard Early use of early plasma and platelets in massively bleeding patients 1:1:1Controversial; variable application in clinical practice (PROMMTT); PROPPR trial Vasodilation with anesthetic agents aka (DCA)Theory only. Minimal clinical data
6Hypotensive Resuscitation A Historical Perspective Alan I. Frankfurt, MD
7Hypotensive Resuscitation: A Balancing Act Alan I. Frankfurt, MDHypotensive Resuscitation: A Balancing ActPermissive ischemiaTolerating short period of hypotensionVs.Popping a clotMinimize the risk of increased bleeding----- Meeting Notes (9/18/14 10:45) -----LCol. USA, MCNorth Africa and ItalyResuscitationLegion of MeritAlan I. Frankfurt, MD
8Keep the SBP 80-90 torr until the bleeding is controlled. Blood Pressure at which Rebleeding Occurs after Resuscitation in Swine with Aortic Injury Jill L. Sondeen, PhD J of Trauma 54: (5) May Supp 2003Reproducible blood pressure at which rebleeding occurred in test animals.Systolic 94 mmHGDiastolic 45 mmHGMAP 64 mmHGSimilar to resuscitation pressures suggested by Drs. Cannon (WW1) and Beecher (WW2), respectively.Stern SA; Ann Emerg Med 1993 Feb; 22: 155Burris D.; J Trauma 1999;46:Stern SA; Prehosp Emerg Care. 2002;6:81-91Standard component of DCRKeep the SBP torr until the bleeding is controlled.Alan I. Frankfurt, MD
973,000 foot view of Hemorrhage Resuscitation: Keeping the Resuscitation Fluids Administered to a Hemorrhaging Patient, Looking Like Blood Coming OutEarly blood product administration (MTP)Early Plasma? Cryoprecipitate & PlateletsMinimize IV crystalloidsAvoid coagulopathyAlan I. Frankfurt, MD
10If not, what should we be following? BasicsAlan I. Frankfurt, MDHow much do young healthy trauma patients bleed before the patient demonstrates changes in routine vital signs (BP, P, RR, LOC).Do routine vital signs reflect EBL & occult shock?If not, what should we be following?What kills you when you “bleed to death”?
11Clinical Signs Associated with Blood Loss: Alan I. Frankfurt, MDACS ATLSClinical Signs Associated with Blood Loss:ClassEBL-estimated blood loss.%EBV Lost Pulse RateBlood Pressure Mental StatusClass I<750cc<15%<100 Normal Slightly anxiousClass IIcc15-30%>100 Normal Mildly anxiousClass IIILife threatening1500(2000)cc30-40%>120Weak or intermittentRadial pulseDecreaseConfusedClass IVLifeThreatening>2000cc40-50%>140Absent radial pulse.Lethargic, Confused, UnconsciousLoss of EffectiveCompensationAlan I. Frankfurt, MD
12ATLS Clinical Signs Associated with Blood Loss Alan I. Frankfurt, MDATLS Clinical Signs Associated with Blood Loss
13Alan I. Frankfurt, MDClassification of Shock Using ED Admission Arterial Base Deficit Values Defined by JW Davis, MD et al.Admission Base Deficit Predicts Transfusion Requirements and Risk of Complications James W. Davis, MD; Jour of Trauma, Vol. 3, No. 5: 769
14Alan I. Frankfurt, MD2013Questioning the validity of the ATLS classification in hypovolemic shock: the role of (venous) BD/Lactate
15Mutschler et al. Critical Care 2013, 17:R42 Alan I. Frankfurt, MDMutschler et al. Critical Care 2013, 17:R42
16Mutschler et al. Critical Care 2013, 17:R42 Alan I. Frankfurt, MDMutschler et al. Critical Care 2013, 17:R42
17Alan I. Frankfurt, MDMutschler et al.Critical Care 2013,17:R42
18Hemorrhagic death is the result of systemic vascular collapse Alan I. Frankfurt, MD
20Pathway to Vascular Collapse and Decompensated Shock Alan I. Frankfurt, MDPathway to Vascular Collapse and Decompensated ShockPathway to vascular collapse:Continuing hemorrhageExhaustion of physiologic compensatory mechanismsLETHAL TRIAD: Acidosis, Hypothermia, Coagulopathyno cellular damageCompensated shock:Skin, skeletal muscle and boneIschemia tolerant tissue:Vasoconstriction:Decompensated shock:cellular damageIschemia intolerant tissue: Brain and heartVasoconstriction
21Lethal Triad of Trauma: Marker of Physiologic Exhaustion Alan I. Frankfurt, MDCoagulopathyINRAcidosisHypothermiaBest single live/die predictor in trauma & hemorrhage patients.
22The Lethal Triad Lethal Triad Massive Hemorrhage Coagulopathy External bleedingConsumption of clotting factorsDilution IV fluids/MTPFibrinolysisDysfunction: H+/TemperatureAcidosis(Lactate)Oxygen debtpH < 7.250% Factor dysfunctionVascular paralysisLethal TriadHypothermiaCold fluidsVasodilationRoom tempOpen abdomenMassiveHemorrhageAlan I. Frankfurt, MD
23The Lethal Triad Drives Resuscitation Efforts CoagulopathyFloorConsumptionDilutionFibrinolysisDysfunctionAcidosisOxygen debtpH <7.250% Factor dysfunctionVascular paralysisLethal TriadHypothermiaCold fluidsVasodilationRoom tempOpen abdomenHemorrhage control (stop the bleeding)Operating roomInterventional radiologyVolume administration (fill the tank)Preload/Cardiac output/MAPCaO2 (oxygen carrying capacity)Hg x SpO2 x KpRBCCoagulation (make clots)MTPFFPCryoprecipitatePlateletsAntifibrinolyticsHomeostasis (keep the patient warm)Normal physiologic environmentHypothermiaAcidosisCalciumDamage Control ResuscitationAlan I. Frankfurt, MD
25Damage Control Resuscitation Resuscitative measures that are taken to prevent physiologic exhaustion (lethal triad) and patient death.Alan I. Frankfurt, MD
26Damage Control Resuscitation “5 H’s” HomeostasisHypothermiaAcidosisIonized calciumLabsINR/TEGABGBase deficitLactateCBC/Chem 7/plateletsFibrinogenHypnosis: having our cake and eating it tooDCAHypotensionVasoconstriction/Hypovole miaVasodilatation/EuvolemiaHemorrhage controlOR timely fashionHypotensive resuscitationSystolic BP=80 torrIschemia vs. Popping a clotHemostatic resuscitationEarly plasma administrationFibrinogen/EGMinimize crystalloid administrationMTP1:1:1:(1) ratioriaSTAPTXArF7RBCHct 35-40%Platelets>100,000
27Massive Transfusion Protocols Alan I. Frankfurt, MD
28MTP initiation: Bleeding and in hypovolemic shock Massive Transfusion Protocol Version 1.0 Composition and ImplementationAlan I. Frankfurt, MDShipment #pRBCsPlasmaPlatelets1521 apheresis34Role of : rF7a vs. TXAMTP initiation: Bleeding and in hypovolemic shockNot sure what is bleeding.How long it will take to stop the bleeding.What it is going to take to stop the bleeding.When you’re bleeding too fast to wait for the labs.
29Is there a role for rF7 in massive hemorrhage? Massive Transfusion Protocol Version 2.0 (Modify based upon severity of blood loss & institutional capabilities)Early plasmaDay 1-3Plasma ratio vs. Plasma deficitLast in, first out:<14 days oldFibrinogenvWBF8F13FibronectinEurope vs. USALyophilizedfibrinogenAnti-fibrinolyticFibrinogen is the first factor to reach critically low levels during massive bleedingIs there a role for rF7 in massive hemorrhage?
30Advanced Trauma Life Support (ATLS) Alan I. Frankfurt, MDAdvanced Trauma Life Support (ATLS)Hemorrhagingpatient2 large bore PIVEvidence of shock:Pulse > 100/minSBP < 100 torr2000 cc crystalloid fluids to normalize BPShock persist1.Continue IV crystalloids and 2.pRBCFrequent labs (guide FFP and platelet administration)Transient responders> 100cc/min blood loss
31Advanced Trauma Life Support (ATLS) Hemorrhage resuscitation circa1980 Crystalloid infusion:Dilution clotting factorsDoes not carry oxygenHypothermiaWorsening of bleedingpRBC administration:Signs of shockPlaying catch up with coagulationFFP/CryoprecipitateDriven by PT/PTT lab test20” lab result turn around20 minutes to dethawContinued crystalloid fluid administration and pRBCPlateletsIatrogenic driven coagulopathy
32Bloody Vicious Cycle of Biblical Proportion Alan I. Frankfurt, MDBloody Vicious Cycle of Biblical ProportionHemorrhageResuscitation with IV fluidsHemodilutionHypothermiaAcidosisCoagulopathy
33Breaking the Bloody Vicious Cycle Damage Control Resuscitation“5 H’s” Hemorrhage controlOR timely fashionDefinitive hemorrhage controlHypotensive resuscitationSystolic BP=80-90 torr“Tolerate” shock vs. Popping clotsHemostatic resuscitationBlood products early and often: PlasmaPrevention of coagulopathyMinimize crystalloid administrationHomeostasisHypothermiaAcidosisYear 2000 (limited trauma centers)DCSDCR:“WB equivalent”Early plasma
34Is There a Role for Whole Blood in Civilian Hemorrhage Resuscitation? Keeping Fluids Going Into our Patients Looking Like Blood Coming Out During a Hemorrhage ResuscitationIs There a Role for Whole Blood in Civilian Hemorrhage Resuscitation?
35Civilian Use of Whole Blood is Limited Alan I. Frankfurt, MDCivilian Use of Whole Blood is LimitedMilitary: (Fresh Warm) Whole BloodWarm: C*Fresh if < 24 hours oldWalking blood bankPre-testedCivilian: Whole BloodCold: 1-4C*Formal testing for transmissible disease.72 hoursLicensed for 21 daysDifficult to obtain from blood centersFractionation of WBEfficient use of blood productFinancial≠
36Is the MTP (1:1:1) the Modern Day Whole Blood Equivalent: Crystalloid fluidPoor volume expanderCarries no oxygen, coagulation factorsWhat if we administer the fractionated parts of WB as a 1:1(:1) ratio?VolumeOxygen deliveryCoagulation factors
37Origin of the (Civilian) MTP 1:1:1 transfusion ratio Alan I. Frankfurt, MDJohn Hess, MD; Richard Dutton, MD: From ISR to Maryland STU 2000Transfusion Vol. 44, Issue 6 pp , June 2004Blood transfusion rates in the care of acute traumaJohn J. Como, Richard Dutton, Thomas M. Scalea, Bennette B. Edelman, John R. HessTransfus Med Rev. 2003; 17:Treating coagulopathy in trauma patientsArmand R., Hess JR
38Origin of the MTP 1:1:1 Ratio Maryland Shock Trauma, Baltimore Md. Alan I. Frankfurt, MDOrigin of the MTP 1:1:1 Ratio Maryland Shock Trauma, Baltimore Md.Early plasma administrationDr. Como et al.(Transfusion 2004);“Blood transfusion rates in the care of acute trauma”8% (479/5645 trauma admissions 2000) received RBC transfusion3% > 10U RBC/24 hours90% ultimately received plasma5645 trauma admissions to Shock Trauma Center in 20005219 units of RBC5226 units of FFPRBC EDFFP ICULack of immediate availability of plasma1:1 ratio
39Birth of the Massive Transfusion Protocol (MTP) Alan I. Frankfurt, MDBirth of the Massive Transfusion Protocol (MTP)Question:“Are we using FFP in the ICU to rescue an iatrogenic (ATLS) induced coagulopathy from the ED/OR resuscitation?”“What if we gave the FFP at the same time as the pRBC in patients with massive hemorrhage?” (personal communication, Richard Dutton, MD)Drs. Dutton, Hess & Holcomb1:1 RBC/FFP in EDBaltimore, Md. 2000Bagdad, Iraq 2005
401 unit pRBC: 1 unit FFP: = 1 unit (apheresis) platelets Is the Massive Transfusion Protocol 1:1:1 ratio the WB equivalent? (Kinda)1 unit pRBC:1 unit FFP: =1 unit (apheresis) platelets1 unit “whole blood”equivalent?
41MTP 1:1:1 “Hemotherapy induced hemodilution” Alan I. Frankfurt, MDMTP 1:1:1 “Hemotherapy induced hemodilution”TempHctPlateletsCoagulationFactor %FibrinogenAmount of anticoagulant and additivesWhole Blood500ccWFWB37* C38-50%150,000to400,000100%1500 mg63ccComponentTherapy680cc1 unit: PRBC, FFP,Platelet-30-0*C29%88,00065%950 mg205cc
42MTP 1:1:1 “Hemotherapy induced hemodilution” Alan I. Frankfurt, MDMTP 1:1:1 “Hemotherapy induced hemodilution”TempHctPlateletsCoagulationFactor %FibrinogenAmount of anticoagulant and additivesWhole Blood500ccWFWB37* C38-50%150,000to400,000100%1500 mg63ccComponentTherapy680cc1U: PRBC, FFP,Platelet-30-0*C29%(10%)26%88,000(30%)55,00065%750 mg205cc
43MTP 1:1:2 “Hemotherapy induced hemodilution” Alan I. Frankfurt, MDMTP 1:1:2 “Hemotherapy induced hemodilution”TempHctPlateletsCoagulationFactor %FibrinogenAmount of anticoagulant and additivesWhole Blood500ccWFWB37* C38-50%150,000to400,000100%1500 mg63ccComponentTherapy680cc2PRBC,1FFP,1Platelet-30-0*C29%88,00065%750 mg205cc40%55,00052%Storage related lossesAny crystalloid administered will further dilute all 3 blood components.36%37,00052%1:1:21:1:126%55,00065%
44PROPPR Trial: JAMA 2015, 313(5): 471-482 Study Question In patients with severe trauma and predicted to require massive transfusion, does the use of a transfusion protocol using a 1:1:1 ratio of plasma to platelets to red blood cells (RBCs) compared to 1:1:2 improve mortality?Alan I. Frankfurt, MD
45PROPPR Trial: Results 24 hour/30 day all cause mortality Alan I. Frankfurt, MDPROPPR Trial: Results24 hour/30 day all cause mortalityNo difference between 1:1:1 vs 1:1:2Reduced mortality in 1:1:1 group from exsanguination in the first 24 hours.The Kaplan-Meier survival curves for a 3 hour endpoint:Statistically significant mortality difference between the two groups.This was not one of the allowed primary outcomes.Our current definitions of massive transfusion are outdated.Critical Administration Threshold (CTA): 3 units/hour
47ROTEM Radically Alters Transfusion in Combat Casualty Resuscitation Andrew P. Cap1, Philip C. Spinella1,3, Nichole K. Ingalls5, Christopher E. White1,2, Alejandra G. Mora1, Heather F. Pidcoke1, Nicolas Prat1, Lorne H. Blackbourne1, Joseph J. DuBose41United States Army Institute of Surgical Research, Fort Sam Houston, TX , 2San Antonio Military Medical Center, Fort Sam Houston, TX 782343 Washington University in St. Louis, St. Louis, MO 63108, 4 Baltimore CSTARS, R. Adams Cowley Shock Trauma Center / University of Maryland School of Medicine, Baltimore, MD 21201, 5 Nellis Air Force Base, NV 89191MTP RATIO DRIVEN RESUSCITATIONROTEM DRIVEN RESUSCITATIONx5*There were 16 and 15 transfused patients respectively in each period that did not receive RBC.
48ROTEM Radically Alters Transfusion in Combat Casualty Resuscitation Andrew P. Cap1, Philip C. Spinella1,3, Nichole K. Ingalls5, Christopher E. White1,2, Alejandra G. Mora1, Heather F. Pidcoke1, Nicolas Prat1, Lorne H. Blackbourne1, Joseph J. DuBose41United States Army Institute of Surgical Research, Fort Sam Houston, TX , 2San Antonio Military Medical Center, Fort Sam Houston, TX 782343 Washington University in St. Louis, St. Louis, MO 63108, 4 Baltimore CSTARS, R. Adams Cowley Shock Trauma Center / University of Maryland School of Medicine, Baltimore, MD 21201, 5 Nellis Air Force Base, NV 89191Conclusions1. DCR utilizing a 1:1:1 ratio driven MTP may underestimate the need for cryoprecipitate and platelets2. ROTEM driven resuscitation more closely approximated a 1:1:1:1 transfusion ratio.*There were 16 and 15 transfused patients respectively in each period that did not receive RBC.
49How Much Difference Does Additional Cryoprecipitate and Platelets Make? 2003 Iraq2012 AfghanistanMortality: >20%No platelets and cryoprecipitate available in theaterMortality: <10%Greater cryoprecipitate and platelets availability.ISS scores higher in casualties in 2012 than those in 2003.Evolving MTP1:1:1:1
50Putting it all together Alan I. Frankfurt, MDPutting it all togetherMassive Transfusion ProtocolTHR Dallas
51MTP & Uncontrolled Hemorrhage Alan I. Frankfurt, MDMTP & Uncontrolled HemorrhagePYXIS/L&D resuscitationBLOOD BANK resuscitationTXA1-2 grams IV slowly1 gram IVPB over 8 hoursriaSTAP2-4 grams IVO negative pRBC(+/- Liquid Plasma)iSTATHgb; ABG/VBG; ionized CaLactateRound 1 MTPO negative pRBCAB negative FFP(+/- cryoprecipitate)(+/- platelets)Round 2 MTPType specific pRBCType specific FFP( +/- platelets)
52Uijttewall WS et al., Am J Physiol Rethinking the Acceptable Hematocrit and Platelet marginalization during massive hemorrhageHigher Hct increased platelet interaction with the endothelium.Platelet concentrations along the endothelium remains almost x7 that of the average blood concentration.Uijttewall WS et al., Am J Physiol1993, 264: H1239-H1244
53Maintain a Hct 35%: Shear stress & platelet margination Alan I. Frankfurt, MDMaintain a Hct 35%: Shear stress & platelet margination35%21%Hardy JF et.Can J Anaesthe 2006, 53: S40-S58
57Plasma deficit vs. Plasma ratio pRBC:FFPVs.Plasma deficit:(Total RBC)-(Total FFP)
58BLOOD PRODUCT USE IN TRAUMA RESUSCITATION: Plasma deficit versus plasma ratio as predictors of mortality in trauma Andreas R. de Biasis, Lynn G. Stansbury, Richard P. Dutton, Debra M. Stein, Thomas Ml Scalea, and John R. HessPlasma deficit(Total RBC)-(Total FFP)<2Mortality was related to plasma deficit, not plasma ratio0-3 hours post injuryEarly plasma availabililtyGold:Red:Gold:Red…..Simultaneous administration of plasma along with pRBCThawed plasma/Liquid (never frozen) plasma in ED/L&DLyophilized plasmaUnavailable in USA? Lyophilized fibrinogen
59Future Developments Lyophilized FFP Alan I. Frankfurt, MDFuture Developments Lyophilized FFPLogistic requirements:StorageNo refrigeration requiredRoom temperatureEasily transportedQuickly reconstitutedRapid volume expansionRapid 1:1 pRBC/FFP ration obtainedContains all clotting factorsShelf life2 yearsClotting factorABO considerationsNo blood typing requiredFrench military medicine1994FDA: compassionate approval for the US militarySpecial forces
60Plasma & the Endothelium (The other 50% of making a strong clot) Alan I. Frankfurt, MD
61Role of the Endothelia Glycocalyx and Resuscitation Fluids Choice Alan I. Frankfurt, MDRole of the Endothelia Glycocalyx and Resuscitation Fluids ChoiceExtremely fragileCompositionGlycoproteinsProteoglycansKey determinants of membrane permeability in various vascular organ systems.mm thickness1000 cc plasma embedded in the EG.
63Plasma: 1000 different proteins Plasma: 1000 different proteins Coagulation factors Immunoglobulin AlbuminCoagulationProcoagulantAnticoagulantsOverall health of the endotheliumResuscitation/Repair of the EGHemorrhagic shock
64Early Plasma vs Crystalloid Effects of Resuscitation Fluids on the Integrity of the Endothelial Glycocalyx:Alan I. Frankfurt, MDIatrogenic Injury
65Review: Transfusion Protocol Version 2.0 We are here
67PlateletsPlatelet Storage: “One size does not fit all” Decisions that shaped the policy on PLT storage temperature
68Platelet Aggregation 2 hours 22*C FIRM, BUT REVERSIBLE ADHESION IRREVERSIBLEScanning electron micrograph of discoid, dormant plateletsActivated, aggregating platelets illustrating fibrin strandsFlowingdisc-shapedplateletRollingball-shapedHemisphere-shapedSpreadingPlatelet Aggregation2 hours22*CAdapted from: Kuwahara M et al. Arterioscler Thromb Vasc Biol 2002; 22: 329–34.
69Platelet Storage: Effects of temperature 5 day life span1-2 hours to “activate”4*C48 hour life spanImmediately “activated”Refrigeration of platelets abandoned in 1970’s.Logistics vs. Patient requirements
70Historical perspective on platelet storage 2 patient populations with different platelet requirementsPatient population:Trauma, OB(PPH, Abruption, Accreta)Requirement:Immediate bleeding problemImmediate clot formation & hemostasis(activated platelets)4*C plateletsImmediately primedSurvival time: hoursPatients receiving chemotherapyprophylaxis against future bleedingLong circulation time(platelet survival)22*C platelets1-2 hours for primingSurvival time: days
71Fibrinogen & Clot strength The 80% Solution Non pregnant state: mg%Pregnant state: (1000) mg%
72Fibrinogen (F1) is the Weak Link in the Clotting System Alan I. Frankfurt, MDHemorrhageRapid depletion of F1 (fibrinogen)Clot formationFibrin precursorPlatelet interactionActivationBindingAggregation
73What is the Optimal Fibrinogen Threshold for Optimal Clot Formation?
74Plasma Fibrinogen levels & Optimal Hemostasis mg/dlLinear increase in clot strength with increasing F1 levels.625 mg/dlClot strength equal to whole bloodPregnancy level > 28 weeks1000 mg/dlClot strength equal to x3 whole bloodClot strength vs. HypercoagulabilityNielsin V, Levy J: Fibrinogen and Bleeding: Old Molecule-New IdeasAnesth Analg 2007; 105: 902-3
75Sources of Fibrinogen: Volume considerations &Preparation time.Allogenic blood productsThawingTyping (ABO if possible)InfectionFresh frozen plasma (FFP)CryoprecipitateFibrinogen concentrateriaSTAP1 grams of riaSTAP/bottle50cc sterile waterUS “off label”Acquired hypofibrinogenemiaEuropeEliminated cryoprecipitateInternational Journal of Obstetric Anesthesia (2010) 19,
79Mode of Action of Lysine Analogue Tranexamic Acid (TXA) Mannucci PM, Levi M. N Engl J Med 2007;356:TXAFigure 1. Mode of Action of Lysine Analogues (Aminocaproic Acid and Tranexamic Acid). Activation of plasminogen by endogenous plasminogen activators results in plasmin, which causes degradation of fibrin. Binding of plasminogen to fibrin makes this process more efficient and occurs through lysine residues in fibrin that bind to lysine-binding sites on plasminogen (Panel A). In the presence of lysine analogues, these lysine-binding sites are occupied, resulting in an inhibition of fibrin binding to plasminogen and impairment of endogenous fibrinolysis (Panel B).
81Resuscitation in a drawer Alan I. Frankfurt, MDResuscitation in a drawerFactor 1 (fibrinogen)riaSTAPTXArF7aCombat gauzeCalciumFactors: 2, 7, 9, 10PCC (prothrombin concentrate complex)Vitamin K dependent factorsFactor 8/vWBEndotheliumLyophilized plasmaPlateletsFactor 5EntegrionLyophilized plateletsLocated in the ED/L&D unit pyxisFuture
82Citrate Intoxication & “ionized "Calcium Alan I. Frankfurt, MDCitrate Intoxication & “ionized "CalciumCitrate intoxication90% citrateFFP & PlateletsCalcium & MagnesiumRate of transfusion, not total blood productsMeasured calcium vs. Ionized calciumTotal calcium is normal even when ionized calcium of critically lowTotal calcium measures both calcium bound to citrate and free, ionized calcium
84Maintain or re-establishing a survivable physiologic state Damage control:Maintain or re-establishing a survivable physiologic stateDamage Control SurgeryHemostasis(definitive)If you need to be in the OR, get there quicklyDamage Control ResuscitationHypotension (permissive)Avoid popping clotsHemostatic resuscitationClotting factors early and often:MTPPlasma deficitPharmacologicHomeostasisKeep the patient warmDamage Control AnesthesiaHypnosisGet them anesthetizedAlan I. Frankfurt, MD
85Damage Control Resuscitation Goals Fibrinogen> mg%FFPCryoprecipitaterisSTAP: fibrinogen concentrateHct35-40%Platelet interactionPlatelet concentration>100,000PlasmaPlasma deficit < 2Early plasma administrationEndothelial glycocalyxCoagulation factorsAnticoagulantspHBase deficit & LactateTemperatureActive warming measuresIonized calcium4 will get you 4Hypotension unresponsive to volume
86Alan I. Frankfurt, M.D. F7040@aol.com Questions??Alan I. Frankfurt, M.D.