PowerPoint Presentation (PDF) - Perfusion.com

Emergency Department Use of
Thromboelastography in Trauma: “Goal
Directed” Blood Component Therapy
and Beyond
Mark Walsh MD FACEP
Indiana School of Medicine
Notre Dame Campus, South Bend, Indiana

Notre Dame Study of
Thromboelastographic Decisions Group
Mark Walsh MD,
Scott Thomas MD
Frank Castellino PhD
Deborah Donahue BS
Rudy Navari MD PhD
Ed Evans BA CCP
Andrew Medvecz BS

Objectives
• 1. Acute Traumatic Coagulopathy
• 2. TEG-PM in the Emergency Department (ED)
for “goal directed” BCT. “Art=Science”
• 3. Other indications for ED use of the TEG
• 4. Central importance of the perfusionist for
the implementation of TEG guided goal
directed BCT in the ED.

The generation or exposure of
TF at the wound site, and its
interaction with factor VII, is the
PRIMARY physiologic event
in initiating clotting. The
components of the intrinsic
pathway (ie, factors VIII, IX, XI)
are responsible for
AMPLIFICATION of this
process only after a small initial
amount of thrombin has been
generated through the extrinsic
pathway.

Tissue factor (TF)
is exposed and
binds to FVIIa or
FVII which is
subsequently
converted to
FVIIa
FXa binds to FVa
on the cell surface
The complex between
TF and FVIIa activates
FIX and FX
Trauma,
induces the initiation
of coagulation
Hemostasis: Initiation Phase TF-VIIa=R

The FXa/FVa complex converts
small amounts of prothrombin
into thrombin
FXIa converts FIX to FIXa
The small amount of
thrombin generated
activates FVIII, FV, FXI
and platelets locally.
Activated
platelets
bind FVa,
FVIIIa
and FIXa
Hemostasis: Amplification phase small Th =K

The FVIIIa/FIXa
Complex activates
FX on the surfaces of
activated platelets
The “thrombin
burst” leads to the
formation of a
stable fibrin clot.
FXa in association with FVa converts large amounts of
prothrombin into thrombin creating a “thrombin burst”.
Hemostasis : Propagation Phase TH Burst=alpha

Thrombin binds
Thrombomodulin
The complex
Thrombin-
Thrombomodulin
activates Protein C
APC decreases
FVIIIa and FVa
and induces
D-dimers production
Activated protein C pathway

700 Patients Reviewed 2009
Injury Severity Score and TEG

ISS minor 10-20;20-35;>30

J Trauma. 2007;62:307–310.

“Damage Control Resuscitation”
• Rapid recognition of “trauma-induced
coagulopathy” (massive transfusion prediction)
• Permissive hypotension/minimizing use of
crystalloids
• Early transfusion of RBC:FFP:PLTs in a 1:1:1 ratio
• Appropriate use of rFVIIa and fibrinogen containing
products such as cryoprecipitate
• When available, POC coagulation assays such as
rapid thromboelastography (rTEG) to guide
administration of blood products.

Strategies for Blood Component
Resuscitation in the ED
• Massive Transfusion Protocol (MTP)
definition >10uPRBC/24hr (now 6 hours
Kashuk and Moore)
• 1PRBC:1FFP:1PLTS “DCR”
–1:1:1 we use 6:6:6 plus immediate
calcium
–Never seen a normal calcium in MTP
case
–Multiple Trauma can be a “Living Hell”

The generation or exposure of
TF at the wound site, and its
interaction with factor VII, is the
PRIMARY physiologic event
in initiating clotting. The
components of the intrinsic
pathway (ie, factors VIII, IX, XI)
are responsible for
AMPLIFICATION of this
process only after a small initial
amount of thrombin has been
generated through the extrinsic
pathway.

Massive Transfusion in “Chest”
2009;136:1654-1667
Siler and Napolitano
• p1658 “ Randomized controlled trials of how
to best to administer coagulation factors (FFP,
platelets and cryoprecipitates) in the presence
of ongoing severe traumatic hemorrhage are
difficult to execute and have not been
published”……..”most MTP grossly
underestimate the treatment that is needed
to correct the coagulopathy”

Solution to Blind Adherence to 1:1:1
– “triggers” for MTP ?
–Dr. Thurer: “operative bleeding” =
“trigger”
–Pre hospital and ED bleeding
“triggers
–“triggers and TEGs”

Triggers for MTP

TASH
• Trauma Associated Severe Hemorrhage
• A simple scoring system to predict the need
for massive blood transfusion in severe
trauma patients
• An analysis from the German Trauma
Registry 1993-2006
• 29,353 patients 125 hospitals
• 6044 patients complete data 13.9% MTP
• 4427 patient data set

ABC
• Penetrating mechanism (0 = no, 1 = yes)
• ED SBP of 90 mm Hg or less (0 = no, 1 = yes)
• ED HR of 120 bpm or greater (0 = no, 1 = yes)
• Positive FAST (0 = no, 1 = yes)
2009; 66: 346-352

20 year old motorcycle crash
• Transferred from another facility.
• Spleen and kidney are ruptured with much
intraperitoneal blood.
• Bowel and mesenteric lacerations as well.
• Received 4 liters LR and 2uPRBC prior to
arrival.
• Hypotenisve, tachycardic, no base deficit.

ABC criteria for MTP
• Hypotensive……………………………………………1
• Tachycardic…………………………………………….1
• Blood in CT scan of abdomen………………….1
• Not penetrating………………………………………0
• 3 out of 4 therefore MTP is triggered.

ABC + TASH Criteria are “fluid” in ED
• Male………………………………………………………….1
• Hypotensive120……………………………………….2
• Free Fluid US or CT……………………………………3
• 1+3+2+4=10 initial likelihood of MTP …….20%.
• One hour later BD= -6 for 3 extra points
• One hour later Hb= 8 for 7 extra points
• 10+10=20. >65% chance needing MTP
• Perfusionist runs ISTAT “GC8” with TEG-PM

TEG normal in ED

ADP in ED

AA in ED no NSAID History

ADP post platelet transfusion in OR

AA post platelet transfusion in ER/OR: Total 8 uPRBC,
2uFFP, 2SD plts TEG-PM driven not by blind 1:1:1

TEG post op day 1: DVT prophylaxis

TEG “Goal-Directed” BCT
TEG
abnormality
Prolonged
R
Prolonged k and/or Low MA
reduced alpha angle
Elevated LY30%
BCT FFP
CRYOPPT plts
DDAVP
Address hypothermia,
acidosis, hemorrhage,
dilution, low Calcium.
Consider rFVIIa,
thrombocytopathy
and antifibrinolytics.

36 year old in hemorrhagic shock
• Peutz Jeghers duodenal tumor biopsy site
• Immediate MTP activation
• Requires 6 PRBC/6FFP/”6u”plts units in ED
• IR coiling duodenal vessels after failed clipping
• On Day 2 after 10 units PRBC, 6 units FFP and
2 SD apheresis platelets resumes bleeding and
thrombocytopenic. IF OR = Whipple
• TEG normal but platelet mapping is not

Peutz Jeghers Syndrome Whipple?

35 year old female in shock in ED
rTEG in ED

TEG in ED

ICU AM day 2 plts 54K 2SD plts

ADP ICU in AM DAY 2

AA in ICU AM day 2

TEG in ICU PM day 2 re-bleeding at plts
count 104K low BP Hb 8.6

ADP ICU PM day 2 after 2 more SD plts
given at 54K now 104K

AA in ICU PM day 2 after 2 more SD
plts given at 54K now 104K

TEG ICU AM day 3 after 4 SD platelets since
54k. No bleeding after clip and 2 nd coiling
6uPRBC no more FFP plts=134K

ADP in ICU AM day 3 no bleeding.

AA ICU AM day 3 no bleeding

TEG on floor day 4 stable

ADP on Floor day 4

AA on floor day 4
Final Tally 16uPRBC, 6uFFP, 5SD plts no
cryoppt

Platelet function testing has not been
well studied in trauma
• Brohi on platelet dysfunction in ATC Current
Opinion in Anaesthesiology 2009;22:261–266
“only one study has evaluated platelet
function and activation in injured patients.”
• Elderly patients and patients on platelet
inhibitors not uncommon

Peutz Jeghers Whipple?

Ejection fraction 11 %

Peutz Jegher’s Mom and child

Indications for the Use of TEG in the
ED
Suggested Indications for TEG analysis in Trauma Population
1. Massive transfusion
2. Traumatic and non traumatic brain injury with bleeding
3. Unexplained continued surgical bleeding
4. Suspected platelet dysfunction
5. Recombinant Factor VIIa use
6. Potential organ donor with coagulopathy
7. Early cessation of resuscitation in severe trauma with
poor prognosis due to comorbidity
8. Identification of hypercoagulable patient

TEG is not business
It’s Personal

The Future of Emergency Department
TEG?

Action of rFVIIa

Potential Role of FVIIa in
Acute Traumatic Coagulopathy
Direct thrombin generation even in the
absence of FVIII and FIX
Increase Xa
Direct activate IX on activated platelet
FVIIa
Inhibit
Fibrinolysis