DAMAGE CONTROL RESUSCITATION

acknowledgementsInspiration for this talk from multiple sources, among them

--Interview of Karim Brohi MD @ http://emcrit.org/podcasts/severe-trauma-karim-brohi/

--Lecture by Karim Brohi MD on hypoT resus@ http://www.trauma.org/index.php/main/article/1424/

--Interview with Richard Dutton MD @ http://emcrit.org/podcasts/trauma-resuscitation-dutton/

-- Conference lecture with Brian Cotton MD, Jay Johanning MD

--Cath Hurn MD “There will be blood” http://podbay.fm/show/648203376/e/1371743460?autostart=1 (also available at Social Media and Critical Care website scmm.org )

Definition“Keeping things from getting too crazy or out of hand.”

“Emergency control of situations that may cause the sinking of a ship”

Damage Control Resuscitation

permissive hypotension limiting crystalloids delivering higher ratios of plasma and

platelets and/or clotting adjuncts as appropriate

What are we after in the trauma bay?

Think before you high-five

Where did we get our resuscitation strategies from?? After World War II, Wiggers developed the classic

‘controlled’ hemorrhagic shock model, which documented that if severe shock was allowed to persist for several hours, an irreversible shock state occurred from which the animals could not be resuscitated.

In the 1960s, Shires and associates used the ‘Wiggers Preparation’ to document that extracellular fluid deficits coexist with hemorrhagic shock and are best replenished with balanced salt solutions. This resulted in the standard 3:1 crystalloid-blood ratio of resuscitation

LR resuscitation resulted in 0-10% mortality vs. 80% mortality with replaced blood only. (Wolfman, 63)

Less is more: Permissive Hypotension

Fink, M. Hayes,M. Soni, N. Classic papers in critical care. Ch. 12: “Fluids”. Springer-Verlag London Limited 2008.

New Paradigm:Permissive Hypotension

“Resuscitation is limited to keep blood pressure at 90 mm Hg, preventing renewed bleeding from recently clotted vessels.” (Holcomb, 2007)

Examples from vascular specialties, the military:

Crawford ES. Ruptured abdominal aortic aneurysm. J Vasc Surg 1991;13:348-50

Holcomb JB. The 2004 Fitts Lecture: current perspective on combat casualty care. J Trauma 2005;59:990-1002

Aggressive volume resuscitation of patients with rAAAs before proximal aortic control predicted an increased perioperative risk of death, which

was independent of systolic blood pressure…volume resuscitation should be delayed until surgical control of bleeding is achieved

Evidentiary Basis: Animal studies

Bickell, 1991: 16 swines treated with fluid or nothing Treatment group achieved higher MAPs. However, after 30-

minutes 5 animals in the treatment group had died whereas all 8 animals in the control group had survived. They had significantly less blood loss as well.

Others Nine trials compared hypotensive versus normotensive

resuscitation (MAP >80) . The relative risk of death with hypotensive resuscitation was 0.37.

“The effect of hypotensive resuscitation was to reduce the risk of death in all the trials. This suggests that using a lower than normal blood pressure as a guide to fluid resuscitation consistently reduces the risk of death regardless of the severity of injury”

Bickell WH, Wall MJ Jr, Pepe PE, et al. Immediate versus delayed fluid resuscitation for hypotensive patients with penetrating torsoinjuries. N Engl J Med. 1994;331:1105–1109.

Meanwhile, in humansBickell et al, 1994. Prospective controlled trial. N= 598 Control= standard practice Experimental= NO IV Fluid. Fluids and blood were then initiated at time of operation for SBP goal 100

OUTCOMESControl group got 1L additional fluid, had a higher MAP at presentationSurvival rate was significantly higher (p=.04) in the delayed-resuscitation group. Control group also had a trend (p=.11) toward more blood loss intraop and trend (p=.08) toward more post-op complications

Bickell WH, Wall MJ Jr, Pepe PE, et al. Immediate versus delayed resuscitation for hypotensive patients with penetrating torso injuries. N Engl J Med 1994;331:1105-9

Others

Dutton RP, et al. 2002 RCT. N= 55 Randomized to SBP goal 70 or 100. No difference in

mortality. (injury severity scores higher in low-BP group…possible benefit?)

Morrison et al, 2011. Number so far= 90 Allocated to MAP goal >50 or >65. The lower MAP goal group shows less blood

products, less IV fluid, less perioperative mortality, trend toward less 30-day mortality.

However the complete f/up article is still not in print.

Dutton RP, MacKenzie CF, Scalea TM. Hypotensive resuscitation during active haemorrhage: impact on in-hospital mortality. J Trauma. 2002;52: 1141-1146.

Morrison CA et al., Hypotensive resuscitation …l. Trauma. 2011 Mar;70(3):652-63.

Theory

“Lower blood pressure enhances regional vasoconstriction and facilitates clot formation and stabilization. Controlled volume administration reduces the development of hypothermia and limits dilution of red cell mass, platelets, and clotting factors. Weighed against this is the potential for worsening hypoperfusion, with a risk for increased acidosis and organ system injury.” Dutton, 2007

Practice Points Delay aggressive fluid resuscitation until operative

control is achievable. SBP >70 and MAP >55 appear safe*.

An SBP of 91-97 has been identified as the pressure at which clots blow in animal models

Still under investigation: Should hypotensive resuscitation extend beyond the trauma bay/ambulance into the OR?

(probably)it depends on the individual patient and the need to balance the potential for worsening hypoperfusion to end-organs. Example elderly, traumatic brain injured patients, patients with cardiac/valvular disease.

* Except in the above populations

Hypotensive Resuscitation (Dr. Jay Johanning)

Goals of Fluid Resuscitation Therapy Improved state of consciousness (if no TBI) Palpable radial pulse corresponds roughly to

systolic blood pressure of 80 mm Hg Avoid over-resuscitation of shock from torso

wounds. Too much fluid volume may make internal

hemorrhage worse by “Popping the Clot.”

• “There are things that you think you will never need to know, things you may need to know only one time in

your life, but you can save a life because you have that knowledge.”

- Eric Thomas

II. Written in Blood

Blood Product Ratios and Limiting the Use of Crystalloids.

Historical Practice• Data from the 1950s and 60s noted altered sodium, water distribution and

retention following trauma with surgical management. Treatment surrounded management of intravenous fluids to balance input and output. (Cotton et al., 2006)

• The 1970s brought forward the thought of a “Golden Hour,” a concept emphasizing rapid diagnosis, surgery and resuscitation. Resulting in prolonged “fix everything now” surgeries. (Dutton, 2005)

• Chief publications in the 1980s stressed the importance of “supranormal resuscitation,” and the infusion of large amounts of fluid regardless of objective measurements.

• The late 1980s marked a major movement toward abbreviated laparotomy, with a definitive surgery only after correction of acidosis, coagulopathy and hypothermia.

• Coinciding with these advances, Intra-abdominal compartment syndrome (ACS) became attributed to major interstitial swelling secondary to “supranormal resuscitation.”

• This led to the present day management of trauma with Damage Control Laparotomy and the minimization of crystalloids with increased use of blood products. (Cotton et al., 2006)

Damage Control Laparotomy• Phase 1 consists of transport to the OR in order to

control hemorrhage and prevent contamination and further injury. The abdomen or site of injury is packed and left open with wound vac in place.

• Phase 2 starts in the OR with extended focus in the ICU where the patient can be physiologically stabilized, resuscitated and warmed in order to correct both acidosis and coagulopathy.

• Phase 3 is a staged definitive surgery to reconstruct the abdomen and close.

Concentration on Phase 2-Resuscitation

• Beginning in the Trauma Bay or OR, Resuscitation can happen concurrently with surgery.

• The Anesthesia and MTP response team is focused on correcting the lethal triad: Acidosis, Hypothermia and Coagulopathy

• This is done by administration of fluids, PRBC, FFP, platelets, Vitamin K, tranexamic acid, buffers, electrolytes and other interventions

Damage Control Anesthesia Recommendations During Surgery

• SBP 90 mm Hg• Urine Output

present• PaCO2 < 50 • pH> 7.25• Lactate Stable• INR < 1.6• Plt > 50,000• Hct > 25%• Deep Anesthesia

Stabilization in ICU– SBP >100– Urine Output >

0.5ml/kg/hr– PaCO2 < 40– pH >7.35– Lactate WNL– INR < 2– Plt > 50,000– Hct >20– Lactate WNLDutton, R.P., (2005). Damage Control Anesthesia, International

Trauma Care, 197-201.

Current trends

• Extensive discussion is present in scholarly research regarding the ratio of PRBCS to FFP in order to ensure the best possible outcome for our patients.

• Furthermore there is increased awareness of the theoretical benefits of limiting use of crystalloids (NS and LR).

(Cotton et al., (2006). The cellular, metabolic, and systemic consequences of aggressive fluid resuscitation strategies. Shock, 26(2), 115-121.)

Literature Review-

Blood Product Ratios

246 Military patients: US Army Combat Support Hospital (retrospective chart review, 2007)

• RESULTS: • For the low ratio group the plasma to RBC median ratio was 1:8

• mortality rate was 65%,• For the medium ratio group, 1:2.5

• mortality rate was 34%• For the high ratio group, 1:1.4

• mortality rate was 19%

(Borgman, M.A., (2007). The ratio of blood products transfused affects mortality in patients receiving massive transfusions at a combat support hospital.

Journal of Trauma, 63(4), 805-813.)

150 Civilian patients: University of Alabama. (2005-2007)

• RESULTS:• HRR= 40% mortality • LRR= 58% mortality

• However, “survival bias was introduced as the patients in the low-ratio group died early which effectively fixed them at a low FFP-PRBC ration for the remained of the resuscitation period (p. 361).”

(Snyder, C.W. et al., (2009). The Relationship of Blood Product Ratio to Mortality:Survival Benefit of Survival Bias?. Journal of Trauma, 66(2), 358-364.)

Clinical review: Fresh frozen plasma in massive bleedings - more questions than answersBartolomeu et al. Critical Care 2010, 14:202 

Hallet, J., Lauzier, F., Mailloux, O., Trottier, V., Archambault, P., Zarychanski, R., & Turgeon, A. (2013) The Use of Higher Platelet: RBC Transfusion Ratio in the Acute Phase of Trauma Resuscitation: A Systematic Review. Critical Care Medicine. 41(12). 2800-2811. DOI: 10.1097/CCM.0b013e31829a6ecb

• Initial studies have reported significant reductions in mortality, but are uncontrolled and methodologically flawed, particularly by survivorship bias. Presently, clinical decisions should be based in assessing the pros and cons of both strategies while considering local resources and individual clinical context.

The Prospective, Observational, Multicenter, Major Trauma Transfusion (PROMMTT) Study: Comparative Effectiveness of a Time-varying Treatment with Competing RisksJohn B. Holcomb, et al. JAMA Surg. Feb 2013; 148(2): 127–136.

• PROMMTT was a prospective, multicenter observational cohort study (10 centers)

Conclusions• In the first 6 hours, patients with ratios < 1:2 were 3–4

times more likely to die than patients with ratios ≥1:1. ‘• After 24 hours, plasma and platelet ratios were

unassociated with mortality, when competing risks from non-hemorrhagic causes prevailed.

Theoretical basis of improved results with High Ratio Infusion

• “FFP is hypothesized to include a mechanism at the cellular level in combination of the replacement of coagulation factors... FFP repairs and normalizes the vascular endothelium by restoring tight junctions, building the glycocalyx, and inhibiting inflammation and edema.”

• (Pati, M.N. et al., 2010). Protective effects of fresh frozen plasma on vascular endothelial permeability, coagulation, and resuscitation after hemorrhagic shock are time dependent and dimnish between days 0 and 5 after thaw. Journal of Trauma. 69, 55-62.)

Literature Review-

Limiting Crystalloids

365 Civilian patients: Multi-Institutional analysis of MTPs (prospective comparative study therapeutic, 2007-2010)

RESULTS

• Patients who received less blood product received more crystalloid over 24-hour period.

• A direct relationship was seen between increased crystalloid use and VAP, bacteremia and sepsis.

• Of the “MTP patients (10 or more units) an increased fourfold morbidity was seen in patients with a 24 hour crystalloid volume in excess of 5 L.”

(Duchesne, J.C. et al., (2013). Diluting the benefits of hemostatic resuscitation: A multi-institutional analysis. Trauma Acute Care Surgery, 75(1), 76-82.)

Theoretical basis of improved results with decreased Crystalloid use.

• “Cellular volume seems to drive many of the basic metabolic changes responsible for protein synthesis, cell turnover, and overall cellular performance. The cellular membranes…do not tolerate significant gradients in hydrostatic pressure.”

(Cotton et al., (2006). The cellular, metabolic, and systemic consequences of aggressive fluid resuscitation strategies. Shock, 26(2), 116)

Complications Associated with Aggressive Crystalloid Resuscitation-Cellular acidification-Inflammation-Altered glucose production

and metabolism-Insulin disturbances-Disruption of cardiac myocyte

action potential-Decreased cardiac output-Cardiac arrhythmias and

ventricular dysfunction-Pulmonary Edema and ARDS-Increase gut permeability/

bacterial translocation

-Ileus-Anastomic dehiscence-Decreased tissue healing-Abdominal Compartment Syndrome-Dilution of coagulation factors-Decreased blood viscosity-Disordered neurotransmitter metabolism-Disturbances in the release of catecholamines, glutamate, and acetylcholine.

(Cotton et al., (2006). The cellular, metabolic, and systemic consequences of aggressive fluid resuscitation strategies. Shock, 26(2), 115-121.)

Current recommendations

• “Effective and aggressive incorporation of high ratio resuscitation is essential to correct the combination of metabolic acidosis, hypothermia, and acute coagulopathy of trauma shock associated with severe tissue injury and tissue hypoperfusion.” (Duchesne et al., 2013)

• Limit excessive crystalloid resuscitation in the acute phase of trauma/hemorrhage

• ATLS Guidelines• Initial infusion of 1-2 L of crystalloid followed by PRBC if there is no

response, when hemorrhagic shock is suspected.

“Greatness, is a lot of small things done well.”

- Eric Thomas

“Just enough education to perform”

REVERSAL OF COAGULOPATHY&THROMBOELASTOGRAPY DIRECTED THERAPY

OBJECTIVES• After this presentation the audience will be

able to:– Discuss pharmacology of novel oral agents

– Describe risk factors for hemorrhage

– Describe agents used to stop hemorrhaging

– Develop an algorithm for life threatening hemorrhages

CLOTTING CASCADEDamaged surface

XII XIIa

XI

XIa

IX

IXa X Xa X

Prothrombin II (Thrombin)

Fibrinogen Fibrin

VIIIa

Va

VIIa VII

Trauma

Fibrin clot

Tissue factor

XIIIa

UFH

LMWH

Xa inhibitors

VKA

DTI

* Investigational

FDA INDICATIONSFDA Supported Indications

Reduce the risk of systemic embolism in patientswith non-valvular AFib

Apixaban

Dabigatran

Rivaroxaban

DVT prophylaxis in knee/hip replacement Rivaroxaban

Treatment of DVT/PE and extended Tx Rivaroxaban

Non-FDA Approved Indications

Treatment of DVT/PE Apixaban

Dabigatran

DVT prophylaxis in knee/hip replacement Apixaban

Dabigatran

Acute Coronary Syndromes* Rivaroxaban

Warfarin, Dabigatran, Rivaroxaban, Apixaban. LexiComp. Hudson, OH. 2013.

Pharmacokinetic ComparisonWarfarin Dabigatran Rivaroxaban Apixaban Edoxaban

Dosing Interval Daily BID Daily BID

Half life (t1/2) hr 40 12-17 4-9 12

Onset Slow Rapid Rapid Rapid

Peak Effect 5-7dys 1-2hrs 2-4hrs 3hrs

Monitoring Yes No No No

DrugInteractions

HighDrugs/food

ModerateP-gp

Moderate3A4, P-gp

Low3A4, P-gp

Reversal Yes No No No

Renal Dose No Yes Yes Yes

Bleeding ++ + + +/-

Hemorrhage RiskFactors

• Demographics– Age (>75y/o)– Low Body Mass

(<50kg)

• Comorbidities– Renal Insufficiency– Liver Disease– Prior hemorrhage– Stroke Hx– Peptic Ulcer

Disease

• Concomitant Meds– Intensity of

anticoagulation

– P2Y12 inhibitor (clopidogrel, prasugrel, ticagrelor)

– Aspirin

– others

Ageno. Chest 2012; 141: e44s-e88s.

BLEEDING AND REVERSAL• Warfarin

– Vitamin K• PO or IV

– Fresh Frozen Plasma– Recombinant Factor VII– Prothrombin Complex Concentrates (PCC)

THEN

Ansell. CHEST. 2008;133;160-198

Now

Holbrook. CHEST. e152-e184

* Low dose reduces INRs 6.0-10 to < 4.0 in 1.4 days after PO or 24 hrs after IV. High dose IV vit K begins reducing INR within 2 hrs with a correction to normal generally by 24 hrs.

INR Bleeding Therapeutic Options> 3.0 – 10 No

bleedingHold warfarin until INR returns to normal range

>10 No bleeding

Hold warfarin and give vitamin K 2.5 - 5mg PO*

Any INR Serious or life-

threatening bleeding

Hold warfarin and administer PCC and supplement with vitamin K 5-10mg IV* infusion and repeat as necessary

Alternatively, FFP or recombinant VIIa may be supplemented with vitamin K 5-10 mg IV infusion may be used instead of PCC

CHEST and ICHGuidelines

Holbrook. CHEST. e152-e184, AHA/ASA ICH Guidelines. Stroke 2010;41:2108-2129.

BLEEDING AND REVERSAL• DTI

– No direct antidote– Prothrombin Complex Concentrates (PCC)– Recombinant Factor VII– Fresh Frozen Plasma– Dabigatran is dialyzable

• Xa Inhibitors( Xarelto)– No direct antidote

• Under development (Andexanet alfa, Portola Pharmaceuticals)– Prothrombin Complex Concentrates (PCC)– Recombinant Factor VII– Fresh Frozen Plasma

AGENTS

Kcentra Package Insert. CSL. April;2013.Feiba. Medical letter. Baxter.

2;2011. Profilnine SD. Factor Levels. Grifols. 03/12. NovoSeven. LexiComp.

Hudson, OH. 2013.

Generic Name Brand Name Approved Uses

PCC - 4 Factor Kcentra (Octaplex, Beriplex)

Reversal of acute major bleeding due to warfarin

Activated PCC - 4 Factor(anti -inhibitor coagulant complex)

Feiba Hemophilia A and B

PCC – 3 Factor Profilnine® SD Hemophilia B with factor IXdeficiency

Recombinant Factor VIIa NovoSeven® RT Patients with factor VII deficiency or with hemophilia

A or B

FACTOR CONTENT

Kcentra

Kcentra Package Insert. CSL. April;2013.Feiba. Medical letter. Baxter.

2;2011. Profilnine SD. Factor Levels. Grifols. 03/12. NovoSeven. LexiComp.

Hudson, OH. 2013.

4 18 11 16 23 19 14

Feiba NF 4 18 12 21 19 15 15

Profilnine SD 3 40Trace

37 23

rFVIIa N/A 100

Imberti et al(Blood Transf Apr.’11,9(2)117- 119).

- Non inverse relationship between plasma factor VII levels and INR.

- Noted that with INR < 4.5, usually sufficient levels of factor VII to allow 3 factor PCC to be effective.

- When higher, levels are usually too low(<10%) and 4 factor PCC is more effective.

- Unlike other clotting factors, only 10- 15% of factor VII is needed for adequate hemostasis.

PRO & CON TABLE

Feiba. LexiComp. Hudson, OH. 2013. Profilnine SD. LexiComp. Hudson, OH.

2013. NovoSeven. LexiComp. Hudson, OH. 2013. Cupp. Pharmacist’s Letter 291012.

Oct. 2013.

Kcentra. LexiComp. Hudson, OH. 2013.

Agent Co s

t

Av a i

l

Vol um e

Infus Time

Admix Time

On se t

Effectiv eness

Infect Risk

Thrombo sis Risk

FFP ¢ + Lg 120 min - - - ++ -

Kcentra $$ - Sm 20 min ++ ++ ++ + +

FEIBA $$$ - Sm 15 min + ++ ++ + ++

Profilnine $ - Sm 15 min + + + + +

NovoSeven $$ - Sm Push + + - - +++

REBOUND DRUG EFFECTSAnticoagulation Reversal Pharmacokinetics

Agent Onset Duration Rebound of AnticoagulantProtamine 5 min Irreversible Likely with SBQ dosing from

postponed drug deliveryVitamin K 4-12hrs Days for

INRDose dependent

Fresh Frozen Plasma (FFP)

1-4hrs 6hrs 4-6hrs

Prothrombin Complex

Concentrate (PCC)

10-15min

12-24hrs ≈12hrs

rFactor VII 10min 4-6hrs 6-12hrs

Full Anticoagulation Reversal for Life Threatening HemorrhageOral Drug Generic Brand Reversal StrategyVit K

AntagonistWarfarin Coumadin PCC - 4 factor + Vitamin K 10mg IV

Factor Xa Inhibitor

Rivaroxaban Apixaban Edoxaban

Xarelto Eliquis PCC - 4 factor

DTI Dabigatran Pradaxa PCC - 4 factor

UFH Heparin N/A

Immediately after IV UFH bolus: 1mg protamine per 100

units heparin

30-60min post UFH: 0.5mg protamine per

100 units heparin

LMWH

Enoxaparin Lovenox≤8hrs since dose:

1mg of protamine per 1 mg of enoxaparin

8-12hrs since dose: 0.5mg of protamine per

1 mg of enoxaparin

Dalteparin Fragmin≤8hrs since dose: 1 mg of protamine

per 100 anti-Xa units

8-12hrs since dose:0.5 mg of protamine per

100 anti-Xa units

Factor Xa Inhibitor

Fondaparinux Arixtra PCC - 4 Factor

DOSING• As literature comes forth, focus on the outcome!

– Laboratory reversal versus hematoma reduction!• The goal is to stop the bleed, not the surrogate marker lab value

that may lag behind.

Pre-Treatment INR Dose of 4F-PCC (Units of Factor IX)

Maximum Dose (Units of Factor IX)

2 to <4 25 units/kg 2500 units

4-6 35 units/kg 3500 units

>6 50 units/kg 5000 units

THROMBOELASTOGARPHY( TEG)

THROMBOELASTOGARPHY( TEG) Developed by H. Hartert in Germany in

1948 as a research tool. First clinical application in liver

transplantation by Kang 25 years later. Historically, widest use in CPB and liver

transplantation. More recently, with advent of damage

control and hemostatic resuscitation, increased use for directed blood therapy.

TEG predicts blood product usage in trauma patients. J Trauma. 1997;42(4):716-22 TEG accurately measures coagulopathy in trauma patients . Anesth Analg.

1998;86(2S):88S

THROMBOELASTOGRAPHY

Functional assay Global

evaluation of(from initiation of protein coagulation through lysis)clot.

Factor Deficiencies Fibrinogen

Function Platelet Function Clot Strength Lysis

COAGULOPATHY OF TRAUMA

Pro-thrombotic State

DVT / PE

(Majority)

Hemorrhagic State

Bleeding

Ongoing hypotension

Coagulopathy of trauma is dynamic.

CONTACT TISSUE

COMMON PATHWAY

THROMBIN / FIBRINOGEN

• Hemostasis profile:R time - Angle MA LY

Fibrin strands clot kinetics strength/elasticity dissolution

LY

TEG COMPONENTS

R (reaction) timeCoagulation factors

K (clotting) time Interaction of factors,

fibrin & platelets

Alpha angleFibrin & platelets

Maximal Amplitude (MA)Platelet function

Lysis 30/60 (LY30/60)Fibrinolysis

GRAPHIC RESULT

PLATELET ABNORMALITY

Probable causes:• Factor deficiency• Low platelet count• Low platelet function

Patient status: bleeding

JW’S TEG PROFILE

FIBRINOGEN DEFICIENCY

Probable cause: fibrinogen deficiencyCommon treatment: Cryoprecipitate, FFP, or prothrombin complex

Patient status: bleeding

TEG DIRECTED THERAPY- PT. 1 Gsw to pelvis and right LE Rectal, Small Bowel, Sacral, & Open

Femur Fx Arrived in Class IV Shock

SAME PATIENT

Intra-op after 11 PRBC, 2 Plt, 4 Cryo, 6 FFP, 3 WB, & 1 Factor VIIa

Post-op after 19 PRBC, 2 Plt, 4 Cryo, 6 FFP, 6 WB, & 1 Factor VIIa

GSW TO LEFT FLANK- PT. 2

Sigmoid Colon, Small Bowel, and Abdominal Wall Injury

2 PRBC given intra-op

GSW TO LEFT FLANK- PT. 2

• Post-op TEG shows early fibrinolysis

• TEG after Amicar infusion

Clinical Randomisation of an Antifibrinolytic in Significant Hemorrhage

Guideline for Blood Product Use

Abnormal TEG

Prolonged R time

Transfuse 4 units FFP

Decrease Maximum Amplitude

Transfuse platelets

Prolonged K time orDecrease a-Angle

Transfuse 4 units FFP then 4 units Cryoprecipitate

Consider rVIIa if abnml after above

Increase LY30

Amicar or Tranexamic Acid

Hemorrhage is the enemy (early) Hypercoagulability is the enemy (late) Diagnosis: time consuming and confusing TEG is extremely useful “Whole blood coagulation measurement” Fast One test Easily repeatable It’s what you want-clot measurement

QUESTIONS???