Inspiration for this talk from multiple sources,
among them





--Interview of Karim Brohi MD @
http://emcrit.org/podcasts/severetrauma-karim-brohi/
--Lecture by Karim Brohi MD on hypoT
resus@
http://www.trauma.org/index.php/mai
n/article/1424/
--Interview with Richard Dutton MD @
http://emcrit.org/podcasts/traumaresuscitation-dutton/
-- Conference lecture with Brian Cotton
MD, Jay Johanning MD
--Cath Hurn MD “There will be blood”
http://podbay.fm/show/648203376/e/1
371743460?autostart=1 (also available at
Social Media and Critical Care website
scmm.org )
“Keeping things from getting too crazy or out of hand.”
“Emergency control of situations that may cause the sinking
of a ship”



permissive hypotension
limiting crystalloids
delivering higher ratios of plasma and platelets
and/or clotting adjuncts as appropriate

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)
Fink, M. Hayes,M. Soni, N. Classic papers in critical care. Ch. 12: “Fluids”. Springer-Verlag London Limited 2008.


“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:
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
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
Bickell, 1991: 16 swines treated with fluid or nothing
 Treatment group achieved higher MAPs. However, after 30minutes 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. 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.
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 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
OUTCOMES
Control group got 1L additional fluid, had a higher MAP at
presentation
Survival rate was significantly higher (p=.04) in the delayedresuscitation 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
Dutton RP, et al. 2002
 RCT. N= 55
 Randomized to SBP goal 70 or 100. No difference
in mortality. (injury severity scores higher in lowBP 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.
Morrison CA et al., Hypotensive resuscitation …l. Trauma. 2011 Mar;70(3):652-63.
Dutton RP, MacKenzie CF, Scalea TM. Hypotensive resuscitation during active
haemorrhage: impact on in-hospital mortality. J Trauma. 2002;52: 1141-1146.

“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


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 endorgans. Example elderly, traumatic brain injured patients,
patients with cardiac/valvular disease.

* Except in the above populations
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
Stabilization in ICU
• SBP 90 mm Hg
• Urine Output
present
• PaCO2 < 50
• pH> 7.25
• Lactate Stable
• INR < 1.6
• Plt > 50,000
• Hct > 25%
• Deep Anesthesia
– SBP >100
– Urine Output >
0.5ml/kg/hr
– PaCO2 < 40
– pH >7.35
– Lactate WNL
– INR < 2
– Plt > 50,000
– Hct >20
– Lactate WNL
Dutton, R.P., (2005). Damage Control Anesthesia, International Trauma Care,
197-201.
• 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.)
Current trends
Literature ReviewBlood 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.)
• 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.
Clinical review: Fresh frozen plasma in
massive bleedings - more questions than
answers
Bartolomeu 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
The Prospective, Observational, Multicenter, Major
Trauma Transfusion (PROMMTT) Study: Comparative
Effectiveness of a Time-varying Treatment with
Competing Risks
John 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 ReviewLimiting 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.)
• “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.
Current recommendations
“Greatness, is a lot of small things done well.”
- Eric Thomas
“Just enough education to
perform”
•
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
Damaged surface
XII
Trauma
XIIa
XI
XIa
IX
VIIa
IXa
Tissue
factor
VIIIa
X
Xa
UFH
LMWH
Xa inhibitors
VKA
DTI
VII
X
Va
Prothrombin
II (Thrombin)
Fibrinogen
Fibrin
XIIIa
Fibrin clot
FDA Supported Indications
Reduce the risk of systemic embolism in patients
with non-valvular AFib
Apixaban
Dabigatran
DVT prophylaxis in knee/hip replacement
Rivaroxaban
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*
* Investigational
Rivaroxaban
Pharmacokinetic Comparison
Warfarin
Dabigatran
Rivaroxaban
Apixaban
Dosing Interval
Daily
BID
Daily
BID
Half life (t1/2) hr
40
12-17
4-9
12
Slow
Rapid
Rapid
Rapid
Peak Effect
5-7dys
1-2hrs
2-4hrs
3hrs
Monitoring
Yes
No
No
No
Drug
Interactions
High
Moderate
3A4, P-gp
Low
Drugs/food
Moderate
P-gp
3A4, P-gp
Reversal
Yes
No
No
No
Renal Dose
No
Yes
Yes
Yes
Bleeding
++
+
+
+/-
Onset
Edoxaban
Warfarin, Dabigatran, Rivaroxaban,
Apixaban. LexiComp. Hudson, OH. 2013.
Hemorrhage Risk Factors
•
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.
• Warfarin
– Vitamin K
• PO or IV
– Fresh Frozen Plasma
– Recombinant Factor VII
– Prothrombin Complex Concentrates (PCC)
Ansell. CHEST. 2008;133;160-198
Now
INR
> 3.0 – 10
>10
Any INR
Bleeding
Therapeutic Options
No
Hold warfarin until INR returns to normal range
bleeding
No
Hold warfarin and give vitamin K 2.5 - 5mg PO*
bleeding
Serious or
Hold warfarin and administer PCC and
lifesupplement with vitamin K 5-10mg IV* infusion
threatening
and repeat as necessary
bleeding
Alternatively, FFP or recombinant VIIa may be
supplemented with vitamin K 5-10 mg IV
infusion may be used instead of PCC
* 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.
Holbrook. CHEST. e152-e184
CHEST and ICH
Guidelines
Holbrook. CHEST. e152-e184, AHA/ASA ICH Guidelines. Stroke 2010;41:2108-2129.
• 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
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)
PCC – 3 Factor
Feiba
Hemophilia A and B
Profilnine® SD
Hemophilia B with factor IX
deficiency
Recombinant Factor VIIa
NovoSeven® RT
Patients with factor VII
deficiency or with hemophilia
A or B
Kcentra Package Insert. CSL. April;2013.
Feiba. Medical letter. Baxter. 2;2011.
Profilnine SD. Factor Levels. Grifols. 03/12.
NovoSeven. LexiComp. Hudson, OH. 2013.
Kcentra
4
18
11
Feiba NF
4
18
12
Profilnine SD
3
40
Trace
rFVIIa
N/A
21
16
23
19
19
15
15
37
23
14
100
Kcentra Package Insert. CSL. April;2013.
Feiba. Medical letter. Baxter. 2;2011.
Profilnine SD. Factor Levels. Grifols. 03/12.
NovoSeven. LexiComp. Hudson, OH. 2013.

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.
-
-
Infus
Time
Admix
Time
O
n
s
e
t
Effectiv
eness
Infect
Risk
Thrombo
sis
Risk
+
V
o
l
u
m
e
Lg
120 min
-
-
-
++
-
$$
-
Sm
20 min
++
++
++
+
+
FEIBA
$$$
-
Sm
15 min
+
++
++
+
++
Profilnine
$
-
Sm
15 min
+
+
+
+
+
NovoSeven
$$
-
Sm
Push
+
+
-
-
+++
Agent
C
o
s
t
A
v
a
i
l
FFP
¢
Kcentra
Kcentra. LexiComp. Hudson, OH. 2013.
Feiba. LexiComp. Hudson, OH. 2013.
Profilnine SD. LexiComp. Hudson, OH. 2013.
NovoSeven. LexiComp. Hudson, OH. 2013.
Cupp. Pharmacist’s Letter 291012. Oct. 2013.
Anticoagulation Reversal Pharmacokinetics
Agent
Onset
Duration
Rebound of Anticoagulant
Protamine
5 min Irreversible Likely with SBQ dosing from
postponed drug delivery
Vitamin K
4-12hrs
Days for
Dose dependent
INR
1-4hrs
6hrs
4-6hrs
Fresh Frozen
Plasma (FFP)
1012-24hrs
≈12hrs
Prothrombin
15min
Complex
Concentrate (PCC)
rFactor VII
10min
4-6hrs
6-12hrs
Full Anticoagulation Reversal for Life Threatening Hemorrhage
Oral Drug
Vit K
Antagonist
Generic
Brand
Reversal Strategy
Warfarin
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
Enoxaparin
Lovenox
Dalteparin
Fragmin
LMWH
Factor Xa
Fondaparinux
Inhibitor
Arixtra
Immediately after IV
30-60min post UFH:
UFH bolus: 1mg
0.5mg protamine per
protamine per 100
100 units heparin
units heparin
≤8hrs since dose:
8-12hrs since dose:
1mg of protamine per 0.5mg of protamine per
1 mg of enoxaparin
1 mg of enoxaparin
≤8hrs since dose:
8-12hrs since dose:
1 mg of protamine
0.5 mg of protamine per
100 anti-Xa units
per 100 anti-Xa units
PCC - 4 Factor
• 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
 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

 Functional
assay
 Global evaluation
of(from initiation
of protein
coagulation
through lysis)clot.
 Factor
Deficiencies
 Fibrinogen Function
 Platelet Function
 Clot Strength
 Lysis
Pro-thrombotic
State
Hemorrhagic
State
DVT / PE
Bleeding
(Majority)
Ongoing
hypotension
Coagulopathy of trauma is dynamic.
CONTACT
TISSUE
COMMON
PATHWAY
THROMBIN / FIBRINOGEN
LY
• Hemostasis profile:
R time
Fibrin strands
 Angle
MA
LY
clot kinetics strength/elasticity dissolution
 R (reaction) time

Coagulation factors
 K (clotting) time

Interaction of factors,
fibrin & platelets
 Alpha

angle
Fibrin & platelets
 Maximal

Platelet function
 Lysis

Amplitude (MA)
30/60 (LY30/60)
Fibrinolysis
Patient status: bleeding
Probable causes:
• Factor deficiency
• Low platelet count
• Low platelet function
Patient status: bleeding
Probable cause: fibrinogen deficiency
Common treatment: Cryoprecipitate, FFP, or prothrombin complex
 Gsw
to pelvis and right LE
 Rectal, Small Bowel, Sacral, & Open
Femur Fx
 Arrived in Class IV
Shock

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
 Sigmoid
Colon, Small
Bowel, and Abdominal
Wall Injury
 2 PRBC given intra-op
• 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
Prolonged K time or
Decrease a-Angle
Transfuse 4 units FFP
Transfuse 4 units FFP
then 4 units Cryoprecipitate
Consider rVIIa if abnml after above
Decrease Maximum Amplitude
Increase LY30
Transfuse platelets
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