Resuscitation from Massive Hemorrhage & Development of the MTP: Perspective of an Obstetrical Anesthesiologist Alan I. Frankfurt, MD Partner, ATLAS Anesthesia

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Resuscitation from Massive Hemorrhage & Development of the MTP:Perspective of an Obstetrical Anesthesiologist

Alan I. Frankfurt, MDPartner, ATLAS Anesthesia

Irving, Texas

Department of AnesthesiologyTH Dallas-Presbyterian Hospital

From the ED to the battlefield and back to the ED/bedside

Alan I. Frankfurt, MD

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Learning Objectives

History lesson Incidence of MT DCR & “5 H’s” Coagulopathy and morbidity in hemorrhagic shock Lethal triad Evolution of the MTP: responding to an iatrogenic coagulopathy Maryland Shock Trauma Somalia & Iraq/Afghanistan 1:1:1 vs. 1:1:2-it’s a math thing PROMMTT PROPPRR Thoughts for your day to day practice in the ED.

HISTORY OF WARTIME PREHOSPITAL/ER SHOCK RESUSCITATION

WW I/WW II VietnamKorea OIF/OEF

50 years of Plasma, Albumin and Whole Blood

40 years of Crystalloid/Clear Fluids & WB:1. 3rd space resuscitation2. Fractionation of WB

Forward to the past( DCR):1. Early plasma2. ”WB”

equivalent3. FWWB

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Damage Control Resuscitation“5 H’s”

• Hemorrhage control▫ OR timely fashion

Definitive solution to bleeding is in the OR/IR• Hypotensive resuscitation

▫ Systolic BP=80-90 torr “Tolerate” shock vs. Popping clots

• Hemostatic resuscitation▫ Blood products early and often: Plasma

Prevention of coagulopathy Dilution ACoTS

▫ Minimize crystalloid administration• Homeostasis

▫ Hypothermia▫ Acidosis

• Hypnosis: having our cake and eating it too▫ DCA

Vasoconstriction Vasorelaxed

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Elements of hemostatic resuscitation, and level of evidence in support:

R. Dutton; BJA 2012, Vol109 no. suppl 1 i39

Recommendations Evidence

Expedited anatomic control in OR

Strong; widely accepted

Deliberate (permissive) hypotension

Several prospective trials; widely accepted

Early support of coagulation

Antifibrinolytic therapy One large prospective trial, several smaller studies; emerging standard

Early use of early plasma and platelets in massively bleeding patients 1:1:1

Controversial; variable application in clinical practice (PROMMTT); PROPPR trial

Vasodilation with anesthetic agents aka (DCA)

Theory only. Minimal clinical data



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Hypotensive ResuscitationA Historical Perspective


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Hypotensive Resuscitation:A Balancing Act

Permissive ischemiaTolerating short

period of hypotension

Vs.

Popping a clotMinimize the risk of increased bleeding

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Blood Pressure at which Rebleeding Occurs after Resuscitation in Swine

with Aortic InjuryJill L. Sondeen, PhD

J of Trauma 54: (5) May Supp 2003

• Reproducible blood pressure at which rebleeding occurred in test animals. ▫Systolic 94 mmHG▫Diastolic 45 mmHG▫MAP 64 mmHG

Similar to resuscitation pressures suggested by Drs. Cannon (WW1) and Beecher (WW2), respectively. Stern SA; Ann Emerg Med 1993 Feb; 22: 155 Burris D.; J Trauma 1999;46:216-223 Stern SA; Prehosp Emerg Care. 2002;6:81-91

• Standard component of DCRAlan I. Frankfurt, MD

Keep the SBP 80-90 torr until the bleeding is controlled.

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73,000 foot view of Hemorrhage Resuscitation:Keeping the Resuscitation Fluids Administered to a Hemorrhaging Patient,

Looking Like Blood Coming Out

Early blood product administration (MTP) Early Plasma

? Cryoprecipitate & Platelets

Minimize IV crystalloids Avoid coagulopathy


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Basics

How 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”?


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Class

EBL-estimated blood loss.

%EBV Lost Pulse Rate

Blood Pressure

Mental Status

Class I <750cc <15% <100 Normal Slightly

anxious

Class II 750-1500cc 15-30% >100 Normal Mildly

anxious

Class IIILife threatening

1500(2000)cc30-40%

>120Weak or intermittentRadial pulse

Decrease Confused

Class IVLifeThreatening

>2000cc 40-50% >140Absent radial pulse.

DecreaseLethargic, Confused, Unconscious

ACS ATLSClinical Signs Associated with Blood

Loss:


Loss of Effective

Compensation


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Classification 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

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Questioning the validity of the

ATLS classification in

hypovolemic shock:

the role of (venous) BD/Lactate


2013


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Mutschler et al. Critical Care 2013, 17:R42


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Hemorrhagic death is the result of systemic vascular collapse

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40%

MAP

EBV~5000cc/70 kg personVenoconstrictionArterial constriction

Vascular capacitance= X3 EBV

Increasing blood loss• Endothelial ischemia &

Acidosis pH<7.2• Loss of vascular reactivity

•Catecholamines

• Systemic vasodilatation• Vascular collapse

10% 20% 30% 50-60%

Systemic vascular collapse

Baseline

vascular

tone

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Pathway to Vascular Collapse and Decompensated Shock


Pathway to vascular collapse:

Continuing hemorrhage

Exhaustion of physiologic

compensatory mechanisms

LETHAL TRIAD: Acidosis,

Hypothermia, Coagulopathy

Compensated shock:

no cellular damage

Vasoconstriction:Ischemia tolerant

tissue:Skin, skeletal muscle

and bone

Decompensated shock:

cellular damage

VasoconstrictionIschemia intolerant tissue: Brain and

heart


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Lethal Triad of Trauma: Marker of Physiologic Exhaustion

CoagulopathyINR

AcidosisHypothermia

Best single live/die predictor in trauma & hemorrhage patients.

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The Lethal Triad


Coagulopathy•External bleeding•Consumption of clotting factors

•Dilution IV fluids/MTP

•Fibrinolysis•Dysfunction: H+/Temperature

Acidosis(Lactate)•Oxygen debt•pH < 7.2•50% Factor dysfunction

•Vascular paralysis

Lethal Triad

Hypothermia•Cold fluids•Vasodilation•Room temp•Open abdomen

MassiveHemorrhag

e

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The Lethal Triad Drives Resuscitation Efforts

• Hemorrhage control (stop the bleeding)▫ Operating room▫ Interventional radiology

• Volume administration (fill the tank)▫ Preload/Cardiac output/MAP

• CaO2 (oxygen carrying capacity)▫ Hg x SpO2 x K

pRBC

• Coagulation (make clots)▫ MTP

FFP Cryoprecipitate Platelets Antifibrinolytics

• Homeostasis (keep the patient warm)▫ Normal physiologic environment

Hypothermia Acidosis Calcium


Coagulopathy•Floor•Consumption•Dilution•Fibrinolysis•Dysfunction

Acidosis•Oxygen debt•pH <7.2•50% Factor dysfunction

•Vascular paralysis

Lethal Triad

Hypothermia•Cold fluids•Vasodilation•Room temp•Open abdomen

Damage Control Resuscitation


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Damage Control

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•Resuscitative measures that are taken to prevent physiologic exhaustion (lethal triad) and patient death.


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Damage Control Resuscitation“5 H’s”


• Hypotensive resuscitation▫ Systolic BP=80 torr

Ischemia vs. Popping a clot• Hemostatic resuscitation

▫ Early plasma administration Fibrinogen/EG

▫ Minimize crystalloid administration

▫ MTP 1:1:1:(1) ratio

riaSTAP TXA rF7

▫ RBC Hct 35-40%

▫ Platelets >100,000

• Homeostasis ▫ Hypothermia▫ Acidosis ▫ Ionized calcium▫ Labs

INR/TEG ABG

Base deficit Lactate CBC/Chem 7/platelets Fibrinogen

• Hypnosis: having our cake and eating it too▫ DCA

Hypotension Vasoconstriction/

Hypovolemia Hypotension

Vasodilatation/Euvolemia


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Massive Transfusion Protocols

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Shipment # pRBCs Plasma Platelets

1 5 5

2 5 5 1 apheresis

3 5 5

4 5 5 1 apheresis

Role of : rF7a vs. TXA

Alan I. Frankfurt, MDMassive Transfusion Protocol Version 1.0

Composition and Implementation

MTP initiation: Bleeding and in hypovolemic shock

• Not 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.

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Massive Transfusion Protocol Version 2.0

(Modify based upon severity of blood loss & institutional capabilities)

Last in, first out:<14 days old

Early plasma

Day 1-3

Plasma ratio vs. Plasma deficit

FibrinogenvWBF8F13Fibronectin

Europe vs. USA

Lyophilizedfibrinogen

Fibrinogen is the first factor to reach critically low levels

during massive bleeding

Is there a role for rF7 in massive

hemorrhage?

Anti-fibrinolytic


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Advanced Trauma Life Support (ATLS)

Hemorrhaging patient

2 large bore PIV

Evidence of shock:Pulse > 100/min

SBP < 100 torr

2000 cc crystalloid fluids to

normalize BP

Shock persist

1.Continue IV crystalloids and 2.pRBC

Frequent labs (guide FFP and

platelet administration)Transient

responders

> 100cc/min blood loss

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Advanced Trauma Life Support (ATLS)Hemorrhage resuscitation circa1980

• Crystalloid infusion: ▫ Dilution clotting factors▫ Does not carry oxygen▫ Hypothermia▫ Worsening of bleeding

• pRBC administration: ▫ Signs of shock

• Playing catch up with coagulation▫ FFP/Cryoprecipitate

Driven by PT/PTT lab test 20” lab result turn around 20 minutes to dethaw

▫ Continued crystalloid fluid administration and pRBC

▫ Platelets

Iatrogenic driven

coagulopathy

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Bloody Vicious Cycle of Biblical Proportion

Hemorrhage

Resuscitation with IV

fluids

HemodilutionHypothermia

Acidosis

Coagulopathy


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Breaking the Bloody Vicious CycleDamage Control Resuscitation“5 H’s”


Definitive hemorrhage control• Hypotensive resuscitation

▫ Systolic BP=80-90 torr “Tolerate” shock vs. Popping clots

• Hemostatic resuscitation▫ Blood products early and often: Plasma

Prevention of coagulopathy▫ Minimize crystalloid administration

• Homeostasis ▫ Hypothermia▫ Acidosis

Year 2000 (limited trauma centers)

DCSDCR:

“WB equivalent” Early plasma

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Is There a Role for Whole Blood in Civilian Hemorrhage Resuscitation?

Keeping Fluids Going Into our Patients Looking Like Blood Coming Out During

a Hemorrhage Resuscitation


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Civilian Use of Whole Blood is Limited

• Military: (Fresh Warm) Whole Blood▫ Warm: 20-24 C*▫ Fresh if < 24 hours old▫ Walking blood bank

Pre-tested

• Civilian: Whole Blood▫ Cold: 1-4C*▫ Formal testing for

transmissible disease. 72 hours

▫ Licensed for 21 days▫ Difficult to obtain from

blood centers Fractionation of WB

▫Efficient use of blood product

▫Financial

≠

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Is the MTP (1:1:1) the Modern Day Whole Blood Equivalent:

• Crystalloid fluid▫ Poor volume expander▫ Carries no oxygen,

coagulation factors

• What if we administer the fractionated parts of WB as a 1:1(:1) ratio?▫ Volume▫ Oxygen delivery▫ Coagulation factors

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Origin of the (Civilian) MTP 1:1:1 transfusion ratio

• John Hess, MD; Richard Dutton, MD: From ISR to Maryland STU 2000

• Transfusion Vol. 44, Issue 6 pp. 809-813, June 2004• Blood transfusion rates in the care of acute trauma

• John J. Como, Richard Dutton, Thomas M. Scalea, Bennette B. Edelman, John R. Hess

• Transfus Med Rev. 2003; 17: 223-31• Treating coagulopathy in trauma patients

• Armand R., Hess JR

• Alan I. Frankfurt, MD


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Origin of the MTP 1:1:1 RatioMaryland Shock Trauma, Baltimore

Md. • Early plasma administration

▫ Dr. Como et al.(Transfusion 2004); “Blood transfusion rates in the care of acute trauma”

8% (479/5645 trauma admissions 2000) received RBC transfusion

3% > 10U RBC/24 hours▫ 90% ultimately received plasma

5645 trauma admissions to Shock Trauma Center in 2000 5219 units of RBC 5226 units of FFP

RBC ED FFP ICU

Lack of immediate availability of plasma

1:1 ratio


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Birth 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 & Holcomb 1:1 RBC/FFP in ED

Baltimore, Md. 2000 Bagdad, Iraq 2005

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Is the Massive Transfusion Protocol

1:1:1 ratio the WB equivalent?(Kinda)

1 unit pRBC:

1 unit FFP: =1 unit (apheresis) platelets

1 unit “whole blood”

equivalent?

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MTP 1:1:1“Hemotherapy induced hemodilution”

Temp Hct Platelets CoagulationFactor %

Fibrinogen

Amount of anticoagulant and additives

Whole Blood

500cc

WFWB

37* C 38-50%

150,000to 400,000

100% 1500 mg 63cc

Component Therapy

680cc

1 unit: PRBC, FFP,Platelet

-30-0*C

29% 88,000 65% 950 mg 205cc


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Fibrinogen


Whole Blood

500cc

WFWB

37* C 38-50%

150,000to 400,000

100% 1500 mg 63cc

Component Therapy

680cc

1U: PRBC, FFP,Platelet

-30-0*C

29%(10%)26%

88,000(30%)55,000

65% 750 mg 205cc


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Fibrinogen


Whole Blood

500cc

WFWB

37* C 38-50%

150,000to 400,000

100% 1500 mg 63cc

Component Therapy

680cc

2PRBC,1FFP,1Platelet

-30-0*C

29% 88,000 65% 750 mg 205cc


52%

55,00040% Storage related losses

36%

37,000 52%

Any crystalloid administered will further dilute all 3 blood components.

26%

55,000 65%

1:1:1

1:1:2


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PROPPR 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?


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PROPPR Trial: Results• 24 hour/30 day all cause mortality

▫No difference between 1:1:1 vs 1:1:2 • Reduced 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


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Cryoprecipitate

1:1:1:1(?)

ROTEM Radically Alters Transfusion in Combat Casualty Resuscitation

D

E DI C AT I ON

D

UT Y S E R V I C

E

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. DuBose4

1United States Army Institute of Surgical Research, Fort Sam Houston, TX 78234-6315, 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 89191

0

10

20

30

40

50

pRBC FFP Cryo PLT

Per

cen

t of s

ub

ject

s

PRE POST

*There were 16 and 15 transfused patients respectively in each period that did not receive RBC.

x5

MTP RATIO DRIVEN RESUSCITATIONROTEM DRIVEN RESUSCITATION

Conclusions

1. DCR utilizing a 1:1:1 ratio driven MTP may underestimate the need for cryoprecipitate and platelets

2. ROTEM driven resuscitation more closely approximated a 1:1:1:1 transfusion ratio.

ROTEM Radically Alters Transfusion in Combat Casualty Resuscitation

D

E DI C AT I ON

D

UT Y S E R V I C

E

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. DuBose4

1United States Army Institute of Surgical Research, Fort Sam Houston, TX 78234-6315, 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 89191

*There were 16 and 15 transfused patients respectively in each period that did not receive RBC.

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How Much Difference Does Additional Cryoprecipitate and Platelets Make?

2003 Iraq 2012 Afghanistan

• Mortality: >20%▫ No platelets and

cryoprecipitate available in theater

• Mortality: <10%▫ Greater cryoprecipitate

and platelets availability. ISS scores higher in

casualties in 2012 than those in 2003.Evolving MTP

1:1:1:1


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Putting it all together

Massive Transfusion ProtocolTHR Dallas

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MTP & Uncontrolled Hemorrhage

PYXIS/L&D resuscitation BLOOD BANK resuscitation

• TXA▫ 1-2 grams IV slowly▫ 1 gram IVPB over 8

hours• riaSTAP

▫ 2-4 grams IV• O negative pRBC• (+/- Liquid Plasma)• iSTAT

▫ Hgb; ABG/VBG; ionized Ca

▫ Lactate

• Round 1 MTP▫ O negative pRBC▫ AB negative FFP▫ (+/- cryoprecipitate)▫ (+/- platelets)

• Round 2 MTP▫ Type specific pRBC▫ Type specific FFP▫ (+/- cryoprecipitate)▫ ( +/- platelets)

Rethinking the Acceptable Hematocrit and Platelet

marginalization during massive hemorrhage

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• Higher 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

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Maintain a Hct 35%: Shear stress & platelet margination


35%

21%

Hardy JF et. Can J Anaesthe 2006, 53: S40-S58

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HCT & Platelet count:Synergistic Effect on Clotting

Hct level Platelet count Percentage platelet interaction with subendothelium

Hct =40% 200,000 19.3 +/- 7.8

100,000 7.5 +/- 2.8

50,000 2.5 +/- 0.8

Hct=20% 200,000 3.3 +/- 4.0

100,000 2.8 +/- 0.7

50,000 0.6 +/- 0.2

Transfusion 1994, Vol. 34, No.6


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Plasma


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Plasma

Frozen: “FFP” < 8 hrs;“FP” < 24 hrs

Thawed FFP/FP <24 hrs

Thawed plasma 24 hrs-5 days

Never Frozen: “Liquid Plasma”

Thawed shelf life: 5 days

Shelf life: 26 days

RBCPlatelet

s

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Plasma deficit vs. Plasma ratio

Plasma ratio:pRBC:FFP

Vs.Plasma deficit:

(Total RBC)-(Total FFP)

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BLOOD PRODUCT USE IN TRAUMA RESUSCITATION: Plasma deficit versus plasma

ratio as predictors of mortality in traumaAndreas R. de Biasis, Lynn G. Stansbury, Richard P. Dutton, Debra M.

Stein, Thomas Ml Scalea, and John R. Hess

• Plasma deficit▫ (Total RBC)-(Total FFP)<2

Mortality was related to plasma deficit, not plasma ratio 0-3 hours post injury Early plasma availabililty

• Gold:Red:Gold:Red…..• Simultaneous administration of plasma along with pRBC

• Thawed plasma/Liquid (never frozen) plasma in ED/L&D• Lyophilized plasma

• Unavailable in USA• ? Lyophilized fibrinogen


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Future DevelopmentsLyophilized FFP

• Logistic requirements: ▫ Storage

No refrigeration required Room temperature Easily transported

▫ Quickly reconstituted• Rapid volume expansion

▫ Rapid 1:1 pRBC/FFP ration obtained• Contains all clotting factors• Shelf life

▫ 2 years Clotting factor

• ABO considerations▫ No blood typing required

• French military medicine▫ 1994

• FDA: compassionate approval for the US military▫ Special forces

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Plasma & the Endothelium (The other 50% of making a strong clot)



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Role of the Endothelia Glycocalyx and Resuscitation Fluids Choice

• Extremely fragile• Composition

▫ Glycoproteins▫ Proteoglycans

• Key determinants of membrane permeability in various vascular organ systems.

• 0.2-1.0 mm thickness• 1000 cc plasma embedded

in the EG.


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Plasma: 1000 different proteins Coagulation factorsImmunoglobulin

Albumin

Coagulation Procoagulant Anticoagulants

Overall health of the endothelium Resuscitation/Repair of the EG

Hemorrhagic shock


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Early Plasma vs Crystalloid Effects of Resuscitation Fluids on the Integrity of

the Endothelial Glycocalyx:

Iatrogenic Injury

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Review: Transfusion Protocol Version 2.0

We are here


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Platelets

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PlateletsPlatelet Storage: “One size does not fit all”Decisions that shaped the policy on PLT storage temperature

Adapted from: Kuwahara M et al. Arterioscler Thromb Vasc Biol 2002; 22: 329–34.

Platelet Aggregation

FIRM, BUT REVERSIBLEADHESION

IRREVERSIBLEADHESION

Scanning electron micrograph of discoid, dormant platelets

Activated, aggregating platelets illustrating fibrin strands

Flowingdisc-shaped

platelet

Rollingball-shaped

platelet

Hemisphere-shapedplatelet

Spreadingplatelet

22*C

2 hour

s

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Platelet Storage:Effects of temperature

•22*C▫5 day life span▫1-2 hours to “activate”

•4*C▫48 hour life span▫Immediately “activated”

Refrigeration of platelets abandoned in 1970’s.

•Logistics vs. Patient requirements

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2 patient populations with different

platelet requirements

Patient population: Trauma, OB(PPH,

Abruption, Accreta)

Requirement:Immediate bleeding problem

Immediate clot formation & hemostasis(activated platelets)

4*C platelets

Immediately primed

Survival time: hours

Patient population:Patients receiving

chemotherapy

Requirement: prophylaxis against

future bleeding

Long circulation time

(platelet survival)

22*C platelets

1-2 hours for priming

Survival time: days

Historical perspective on platelet storage

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Fibrinogen & Clot strength

The 80% Solution

Non pregnant state: 200-400 mg%Pregnant state: 400-700(1000) mg%


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Fibrinogen (F1) is the Weak Link in the Clotting System

•Hemorrhage▫Rapid depletion of F1 (fibrinogen)

•Clot formation▫Fibrin precursor

•Platelet interaction▫Activation▫Binding▫Aggregation

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What is the Optimal Fibrinogen Threshold for Optimal Clot

Formation?

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Plasma Fibrinogen levels & Optimal Hemostasis

• 150-300 mg/dl▫ Linear increase in clot

strength with increasing F1 levels.

• 625 mg/dl▫ Clot strength equal to

whole blood Pregnancy level > 28

weeks• 1000 mg/dl

▫ Clot strength equal to x3 whole blood

Clot strength vs. Hypercoagulability

Nielsin V, Levy J: Fibrinogen and Bleeding: Old Molecule-New Ideas

Anesth Analg 2007; 105: 902-3

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Sources of Fibrinogen:

• Fresh frozen plasma (FFP)

• Cryoprecipitate

• Fibrinogen concentrate▫ riaSTAP

1 grams of riaSTAP/bottle 50cc sterile water

▫ US “off label” Acquired hypofibrinogenemia

▫ Europe Eliminated cryoprecipitate

Volume considerations &

Preparation time. Allogenic blood

productsThawing

Typing (ABO if possible)Infection

International Journal of Obstetric Anesthesia (2010) 19, 218-234

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Fibrinogen ConcentrateRiaSTAP

• Human donor▫Pooled plasma

product Lyophilized

• Viral inactivation• Predictable mg

content/vial▫1000 mg/vial

• No thawing required▫Pyxis storage

• ? Thrombogenic potential

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Tranexamic Acid (TXA)Lysine analogue antifibrinolytics

Resuscitation in a drawer (pyxis)

Mode of Action of Lysine Analogue Tranexamic Acid (TXA)

Mannucci PM, Levi M. N Engl J Med 2007;356:2301-2311

TXA


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CRASH-2 Study


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Resuscitation in a drawer• Factor 1 (fibrinogen)

▫ riaSTAP• TXA• rF7a• Combat gauze• Calcium• Factors: 2, 7, 9, 10

▫ PCC (prothrombin concentrate complex) Vitamin K dependent factors

▫ Factor 8/vWB Endothelium

▫ Lyophilized plasma▫ Platelets

Factor 5 Entegrion

Lyophilized platelets

Located in the ED/L&D unit pyxis

Future


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Citrate Intoxication & “ionized "Calcium

•Citrate intoxication▫90% citrate

FFP & Platelets▫Calcium & Magnesium

•Rate of transfusion, not total blood products•Measured calcium vs. Ionized calcium

▫Total calcium is normal even when ionized calcium of critically low Total calcium measures both calcium bound to

citrate and free, ionized calcium


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Summary


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Damage control:Maintain or re-establishing a survivable physiologic state

Damage Control Surgery

Hemostasis(definitive)

If you need to be in the OR, get there quickly


Hypotension (permissive)

Avoid popping clots

Hemostatic resuscitation

Clotting factors early and often:

MTPPlasma deficitPharmacologic

Homeostasis

Keep the patient warm

Damage Control Anesthesia

Hypnosis

Get them anesthetized

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Damage Control Resuscitation Goals

• Fibrinogen▫ >250-400 mg%

FFP Cryoprecipitate risSTAP: fibrinogen concentrate

• Hct▫ 35-40%

Platelet interaction• Platelet concentration

▫ >100,000• Plasma

▫ Plasma deficit < 2 Early plasma administration

▫ Endothelial glycocalyx▫ Coagulation factors▫ Anticoagulants

• pH▫ Base deficit & Lactate

• Temperature▫ Active warming measures

• Ionized calcium▫ 4 will get you 4

Hypotension unresponsive to volume

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Questions??

Alan I. Frankfurt, [email protected]

Documents

Resuscitation from Massive Hemorrhage & Development of the MTP: Perspective of an Obstetrical Anesthesiologist Alan I. Frankfurt, MD Partner, ATLAS Anesthesia