Damage Control
Resuscitation
Gregory W. Jones M.D.
CDR MC USN
Naval Hospital Camp Pendleton
“Damage Control Resuscitation
represents the most important advance
in trauma care for hospitalized civilian
and military casualties from this war.”
Cordts, Brosch and Holcomb, J Trauma, 2008
Acknowledgment
Thanks to
COL Jay Johannigman, MC, USAF, for his
significant contributions to this
presentation.
Case Data
25 year old SGT involved in IED blast
Tourniquet applied at scene one hour ago
Systolic BP 90
Mental Status: Awake, confused
Blood oozing from superficial wounds
Temp 96 F
Patient Assessment
Sick or Not Sick
What are reliable criteria for initial
assessment?
Which criteria can predict outcomes and
direct therapy?
New Diagnostic criteria
Avoids the “but he looked good”
phenomenon
Within the first five minutes in the ED
– Identify patients in trouble
– Identify patients with increased mortality
– Identify patients with increased probability of massive transfusion
The Lethal Triad
Acidosis
Hypothermia
Death
Coagulopathy
Brohi, K, et al. J Trauma, 2003.
Damage Control Resuscitation
Acidosis- Base Deficit > - 6
Coagulopathy – INR > 1.5
Hypotension – Systolic B/P < 90
Hemoglobin - < 11
Temperature - < 96. 5
Pattern recognition
Weak or absent radial pulse
Abnormal mental status
Severe Traumatic Injury
Challenges
Requires robust Medical setting
Need system approach to deliver
casualties to most capable facilities
Isolated and far forward facilities can still
benefit from these principles
Acidosis
Base deficit (BD) ≥ 6 identifies patients that
–
–
–
require early transfusion,
increased ICU days and
risk for ARDS and MOF
BD of ≥ 6 is strongly associated with the need for
MT and mortality in both civilian and military
trauma.
Patients have an elevated BD before their blood
pressure drops to classic “hypotension” levels.
Acidosis contributes more to coagulopathy more
than hypothermia (not reversible)
Coagulopathy on Presentation
An initial INR ≥ 1.5 reliably predicts those
military casualties who will require MT.
Pts who have a significant injury present with a
coagulopathy.
Severity of injury and mortality is linearly
associated with the degree of the initial
coagulopathy.
Coagulopathy and
Trauma
Derangements in
coagulation occur rapidly
after trauma
By the time of arrival at
the ED, 28% (2,994 of
10,790) of trauma
patients had a detectable
coagulopathy that was
associated with poor
outcome
(Brohi et al., 2003)
Brohi Graph Here
Hypotension
A systolic blood pressure of 90 mm Hg or less is
indicative casualties that have lost over 40% of
their blood volume
– (~2000 ml in an adult)
– They have impending cardiovascular collapse
and have significantly increased mortality.
Hemoglobin
Otherwise young healthy soldiers with a Hgb of
< 11 have only one reason for their anemia,
namely acute blood loss.
Temperature
A temperature < 96°F or 35°C is
associated with an increase in mortality.
Trauma patients that are hypothermic
are not perfusing their tissue
The coagulation cascade is an enzymatic
pathway that degrades with temperature
and ceases at 92 F
Diagnosis done
Diagnosis Done
– How to resuscitate these
casualties?
Damage Control Resuscitation
1. Hypotensive resuscitation
2. Hemostatic resuscitation
Hypotensive Resuscitation
Time Honored technique developed by Military
physicians during WWI and WWII
Maximizing the resuscitation benefit to the
mitochondria while minimizing rebleeding by
avoiding “popping the clot”
Supported by a significant body of scientific data.
This approach preserves the resuscitation fluid
within the vascular system
Logistically sound by preventing needless waste
of blood and fluids.
Hemostatic Resuscitation
Damage control philosophy can be extended to
hemostatic resuscitation
restoring normal coagulation
minimizing crystalloid
Traditional resuscitation strategies dilute the already deficient
coagulation factors and increase multiple organ failure
The aggressive hemostatic resuscitation should
be combined with equally aggressive control of
bleeding
Standard Resuscitation Paradigm
Crystalloid 3:1 Ratio
Transient or no response
Blood
6-10 u PRBC
FFP
Oh- By the way:
show me the data
Crystalloid
Hemostatic Resuscitation
1. Early Dx in ED
2. 1:1 ratio (PRBC to FFP)
3. ED use of rFVIIa
4. Call for FWB from the ED
5. Frequent cryo and platelets
6. Repeated doses of rFVIIa in OR and ICU
as required
7. Minimal crystalloid
Thawed Plasma
Thawed plasma should be used as a primary
resuscitative fluid.
This product should be present upon arrival of the
casualty in the ED
This approach not only addresses the metabolic
abnormality of shock, but initiates reversal of the
coagulopathy present in the .
Plasma Composition
Electrolytes (mmol/L) average unit of FFP ~
300cc
Na
165 (48mmol/unit)
K
3.3 (1.0mmol/unit)
Glucose
20
Calcium
1.8
Citrate
20
Lactate
3
pH
7.2-7.4 (LR 6.5, NS 5.0)
Phosphate
3.63
1:1 Ratio of PRBC to Plasma
Increased FFP transfusions within
first 24 hrs of admission were
independently associated with
increased survival.
Median ratio of FFP: RBC was
1:1.7 in survivors compared to 1:3
in non-survivors (p<0.001).
Mortality PRBC:FFP
Cause of Death
100
Hemorrhage
90
80
70
Sepsis
60
50
40
Airway/Resp
30
20
CNS
10
0
low
medium
Plasma ratio
high
Fresh Whole Blood
Fresh whole blood (FWB) must be called for
early after ED arrival, takes 60 minutes
– Injury Pattern recognition
FWB is the optimal resuscitation fluid for
severely injured casualties.
FWB is the best fluid for hypotensive
resuscitation for hemorrhagic shock.
Component Therapy vs Fresh Whole
Blood
Plt
5.5x1010
50 mL
PRBC
Hct 55%
335 mL
FFP
80%
275 mL
So Component Therapy Gives You
1U PRBC + 1U PLT + 1U FFP + 10 pk Cryo =
660 COLD mL
•Hct 29%
•Plt 87K
•Coag activity 65%
•750 mg fibrinogen
•Armand & Hess, Transfusion Med. Rev., 2003
500 mL Warm
Hct: 38-50%
Plt: 150-400K
Coags: 100%
1500 mg
Fibrinogen
Scoring System
n=57
90
SBP <
110
Hct < 32
pH <
7.25
% Probability of Massive Transfusion
HR >
105
80
n=115
70
60
n=153
50
40
n=203
30
n=180
20
10
0
0
1
2
Score
3
4
rFVIIa
In military casualties requiring massive transfusion, early
administration of rFVIIa decreased pRBC use by 23%
rFVIIa increases the SBP at which arterial rebleeding
occurs
– suggesting the formation of a tighter, stronger fibrin plug
in the presence of high concentrations of rFVIIa
Seven prospective, randomized surgical trials have
documented the safety of this drug.
The clinical goal is a subnormal PT or INR, ensuring that if
bleeding is still occurring then surgical intervention is
required.
The Effect of Recombinant Activated Factor VII
on Mortality in Combat-Related Casualties With
Severe Trauma and Massive Transfusion
Philip C. Spinella, MD, Jeremy G. Perkins, MD, Daniel F. McLaughlin, MD, Sarah E. Niles, MD,
MPH,Kurt W. Grathwohl, MD, Alec C. Beekley, MD, Jose Salinas, PhD, Sumeru Mehta, MD, Charles E.
Wade, PhD,and John B. Holcomb, MD
J of Trauma- Feb 2008
When comparing rFVIIa (+) to rFVIIa (-) patients
– 24 hour mortality was 7/49 (14%) and 26/75 (35%),
(p=0.01)
– 30 day mortality was 15/49 (31%) and 38/75 (51%),
(p=.03).
SBP was higher in the rFVIIa (+) group
The use of rFVIIa was associated with improved early and
late survival after severe trauma and massive transfusion.
rFVIIa was not associated with increased risk of thrombotic
events.
Retrospective Study of Combat Casualties
Who did and did not Receive rFVIIa
Jan 2004 - Oct 2006
n = 615
329 US casualties did
not receive rFVIIa
ISS = 21 ± 14
Complications = 17%
– Thrombotic = 11%
ICU days = 6 ± 24
Hospital days = 27 ± 40
PRBCs = 8 ± 7
Mortality = 19%
* P < 0.05
286 US Casualties did
receive rFVIIa
ISS = 24 ± 13*
Complications = 23%*
– Thrombotic = 14%
ICU days = 10 ± 15*
Hospital days = 37 ± 35*
PRBCs = 18 ± 22*
Mortality = 21%
Summary
Recognize Shock
– Five Critical Criterion
– Identify the critical 10 %
Resuscitate Immediately
– Devote attention to Hemostatic
resuscitation
Provide volume that also restores the
hemostatic cascade
Minimize crystalloid
Stop the bleeding
Stay out of trouble
Thawed or liquid plasma
– Whole Blood