Damage Control Resuscitation: Directly Addressing the Early
Coagulopathy of Trauma
John B. Holcomb, MD, FACS, Don Jenkins, MD, FACS, Peter Rhee, MD, FACS, Jay Johannigman, MD, FS, FACS,
Peter Mahoney, FRCA, RAMC, Sumeru Mehta, MD, E. Darrin Cox, MD, FACS, Michael J. Gehrke, MD,
Greg J. Beilman, MD, FACS, Martin Schreiber, MD, FACS, Stephen F. Flaherty, MD, FACS,
Kurt W. Grathwohl, MD, Phillip C. Spinella, MD, Jeremy G. Perkins, MD, Alec C. Beekley, MD, FACS,
Neil R. McMullin, MD, Myung S. Park, MD, FACS, Ernest A. Gonzalez, MD, FACS, Charles E. Wade, PhD,
Michael A. Dubick, PhD, C. William Schwab, MD, FACS, Fred A. Moore, MD, FACS, Howard R. Champion, FRCS,
David B. Hoyt, MD, FACS, and John R. Hess, MD, MPH, FACP
J Trauma. 2007;62:307–310.
verely injured casualties expedites the process.1Historically,
these conditions have converged during times of conflict,
improving the care of combat casualties and subsequently
that of civilian trauma patients.1,2
In the most severely injured casualties, we know that
when the lethal triad of hypothermia, acidosis, and coagu-
lopathy are present, death is imminent.3Current teaching is to
avoid reaching these conditions by using “damage control
surgery.”4–6However, conventional resuscitation practice for
damage control focuses on rapid reversal of acidosis and
prevention of hypothermia, and surgical techniques focus on
controlling hemorrhage and contamination. Direct treatment
of coagulopathy has been relatively neglected, viewed as a
byproduct of resuscitation, hemodilution, and hypothermia,
and delayed by blood banking logistics. Damage control
resuscitation addresses the entire lethal triad immediately
upon admission to a combat hospital.7,8
By demonstrating that in the severely injured the coagu-
lopathy of trauma is present at admission, recent studies have
apid progress in trauma care occurs when the results of
translational research are promptly integrated into clin-
ical practice. Experience with a high volume of se-
brought back to light the importance of treating this disorder
at an earlier stage.9–12Reports of lactated Ringer’s solution
and normal saline increasing reperfusion injury and leukocyte
adhesion lead one to conclude that the standard crystalloid-
based resuscitation guidelines in prehospital trauma life sup-
port (PHTLS) and advanced trauma life support (ATLS) may
worsen the presenting acidosis and coagulopathy in severely
injured trauma patients, and possibly increase ARDS, SIRS,
and MOF.13–17The safety of withholding PRBCs in hemo-
dynamically stable patients has been demonstrated,18and the
risks associated with blood transfusion are well described.19,20
Further, massive transfusion in military and civilian casual-
ties has been associated with an increased risk of death.21–23
Taken together, these observations suggest that the most
severely injured may need a resuscitative approach tailored
specifically to their needs. However, even in the largest
civilian academic trauma centers, patients with injuries at the
outer limits of survivability, such as those massively trans-
fused with more than 10 units of RBCs in the first 24 hours,
are uncommon and constitute only 1% to 2% of the patient
population, making it difficult to develop and test new resus-
citation concepts.21Because 7% of combat casualties require
massive transfusion, we have had just such an opportunity to
observe the effects of new resuscitation strategies in the
combat hospitals of Iraq and Afghanistan.
The military munitions used in Southwest Asia can in-
flict severe multisystem injuries on both combatants and
civilians. These patients frequently present to American mil-
itary medical personnel shortly after being wounded. Unlike
civilian systems, where treatment of coagulopathy is often lim-
ited by standard blood bank logistics, in Iraq we frequently have
immediate access to PRBCs and thawed AB or A plasma, and
rapid access to apheresis platelets, prepooled cryoprecipitate,
fresh whole blood, and rFVIIa, as indicated.24–29Thus, the
opportunity to formally evaluate the immediate and direct
treatment of the coagulopathy of trauma is available.
Submitted for publication September 22, 2006.
Accepted for publication December 20, 2006.
Copyright © 2007 by Lippincott Williams & Wilkins, Inc.
From the USAISR (J.B.H.), Fort Sam Houston, TX; CENTCOM
Trauma (D.J.), Camp Victory, Iraq; Navy Trauma Training Center (P.R.), Los
Angeles, CA; 332nd Expeditionary Medical Group (J.J.), Balad Air Base, Iraq;
ADMEM RCDM (P.M.), Birmingham, United Kingdom; Emergency Depart-
ment (S.M.), 10th Combat Support Hospital, Baghdad, Iraq; Department of
Surgery (E.D.C.), 10th Combat Support Hospital, Baghdad, Iraq; Chief of
Anesthesia (M.J.G.), 10th Combat Support Hospital, Baghdad, Iraq.
Address for reprints: COL John B. Holcomb, MD, FACS, Trauma
Consultant for the Surgeon General, Commander, US Army Institute of
Surgical Research, 3400 Rawley E. Chambers Avenue, Fort Sam Houston,
TX 78234-6315; email: email@example.com.
The Journal of TRAUMA?Injury, Infection, and Critical Care
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The trauma patients who are most severely injured (ap-
proximately 10%) also represent the majority of in-hospital
trauma deaths. Considerable attention has been directed to-
ward the technical details of damage control surgery and
reversing the acidosis and hypothermia present at admission.
Less attention has been directed toward reversing the coagu-
lopathy related to blood loss that is present at the same time.
Clinical experience in Operation Iraqi Freedom and Opera-
tion Enduring Freedom suggests that coagulopathy may be
present at the time of admission before significant resuscita-
tive fluid has been given, as a consequence of acidosis-
induced coagulation factor dysfunction, coagulation factor
consumption, and hypothermia-induced failure of platelet ac-
tivation. Failure to recognize and immediately address the
coagulopathy found in severely injured patients can be linked
to several factors. Most studies of trauma-induced coagulopa-
thy have measured the laboratory changes that happen in the
OR or ICU after dilution with crystalloid and PRBCs, and
have concluded that the coagulopathy could be fully ex-
plained by the resuscitation and/or hypothermia.30
The goal of shock resuscitation efforts in the past has
been largely to support blood pressure and urine output and to
reverse the metabolic derangements associated with the isch-
emia associated with acute blood loss.31,32Although these
goals are obviously important, the studies supporting this
concept were based on controlled animal hemorrhage studies,
and the results were not evaluated in randomized human
trials.33–35Additionally, the potential benefits of mitigating
ischemia-induced reperfusion injury after standard crystalloid
resuscitation were not fully recognized.14,36Furthermore, re-
cent resuscitation studies have overlooked the importance of
an integrated and coherent prehospital, ED, OR, and ICU
shock resuscitation plan that incorporates intravascular treat-
ment of coagulopathy.32,37Finally, the current generation of
clinicians has been taught to not use plasma as a resuscitation
fluid.38We agree that current standard resuscitation methods
are appropriate policy for the approximately 90% of trauma
patients who are not in shock and are hypercoagulable after
injury.39–42However, for the approximately 10% of casual-
ties who constitute the most seriously injured, are in shock
and coagulopathic, and represent the potentially preventable
hemorrhagic deaths, liquid plasma may be the optimal resus-
citation fluid currently available.43–50
Based on (1) previous civilian clinical studies, (2) the
recommendations of an international consensus conference
on early massive transfusion for trauma,51and (3) consider-
able experience in the current war, we think patients at high
risk for coagulopathy can be readily identified at admission
and prompt simultaneous treatment of hypothermia, acidosis,
and coagulopathy initiated. Hypothermia, an independent fac-
tor for increased mortality in trauma patients, was an earlier
focus for active prevention and treatment,52–54but application
of training and equipment recommendations of the Commit-
tee on Tactical Combat Casualty Care and the Joint Theater
Trauma System has made it an uncommon finding.55Acido-
sis significantly impairs the thrombin generation rates, criti-
cal to optimal coagulation function56and is thus aggressively
managed by use of THAM and volume loading with blood
components once hemostasis is obtained, with restoration of
a normal blood lactate, base deficit, or pH as the ultimate
goal. Damage control resuscitation as a structured interven-
tion begins immediately after rapid initial assessment in the
ED and progresses through the OR into the ICU. All efforts
are directed toward this goal by repeated point of care testing
and the use of multiple blood products and drugs readily
available in theater, albeit in new ratios and amounts. Com-
pared with civilian practice, damage control resuscitation
efforts are largely completed in the OR, with little resuscita-
tion required in the ICU. Achieving this goal quickly in the
OR may allow a shift from limited damage control surgery to
earlier definitive surgical interventions, including sophisti-
cated limb salvage techniques, and improved outcomes.
In the severely injured casualty, damage control resusci-
tation consists of two parts and is initiated within minutes of
arrival in the ED. First, resuscitation is limited to keep blood
pressure at approximately 90 mm Hg, preventing renewed
bleeding from recently clotted vessels.15,17,39,57–62Second,
intravascular volume restoration is accomplished by using
thawed plasma as a primary resuscitation fluid in at least a 1:1
or 1:2 ratio with PRBCs.8,10,48–50Our initial clinical experi-
ence shows these ratios decrease mortality in similarly in-
jured casualties (Borgman MA, et al. unpublished data).
Recombinant FVIIa is occasionally used along with the early
units of red cells and as required throughout the resuscitation.
For casualties who will require continued resuscitation, the
blood bank is notified to activate the massive transfusion
protocol and deliver to the operating room 6 units of plasma,
6 units of PRBCs, 6 packs of platelets, and 10 units of
cryoprecipitate stored in individual coolers.50The most se-
verely injured of this group also receive fresh warm whole
blood as a resuscitative fluid.47,63Additional coolers, con-
taining the same mix of blood products, are provided as
needed until the massive transfusion order is cancelled. Crys-
talloid use is minimized and serves mainly as a drug carrier
and to keep lines open between the units of blood products.
In combat casualties requiring major resuscitation
(10–40 units of blood products), we have found as little as
5 L to 8 L of crystalloid are utilized during the first 24 hours,
representing a decrease of at least 50% when compared with
current standard resuscitation practices. Using the damage
control resuscitation approach, the lack of intraoperative co-
agulopathic bleeding has been remarkable, allowing surgeons
to focus on surgical bleeding. Patients treated in this fashion
almost always arrive in the ICU warm, euvolemic, and non-
acidotic, with a normal INR and minimal edema. In the
majority of patients the abnormalities of the lethal triad are
absent. These patients appear to be easily ventilated and more
quickly extubated than patients with similar blood loss treated
with the standard crystalloid resuscitation volumes and blood
component ratios. These admittedly anecdotal yet compelling
The Journal of TRAUMA?Injury, Infection, and Critical Care
observations cause us to question further the use of excessive
crystalloid resuscitation and to begin to formulate hypotheses
that can be tested to demonstrate beneficial effects of pre-
emptive control of coagulopathy.14
For the first time in US warfare, data for all admitted
trauma casualties in the current conflict in Southwest Asia are
entered into a joint theater trauma registry (JTTR).64A de-
ployed combat research team is being sent into theater for the
first time since Vietnam, operating under the same standards
of IRB approval as practiced in the United States. Data
collected by this team, along with outcome data from the
JTTR, will allow an analysis of the effects of resuscitation
with thawed plasma, fresh whole blood, administration of
rFVIIa, and limited crystalloid. Additionally, focused effort
will be required to describe the mechanisms causing the early
coagulopathy of trauma present at admission. The clinical
effects and consequences of damage control resuscitation will
be measurable in patient outcomes. We will know if we are
saving more severely injured soldiers, if reducing coagulopa-
thy and edema leads to better outcomes, and, ultimately,
whether we are creating more blood exposure or less. We will
soon have sufficient data to assess the full benefits of damage
control resuscitation in the population of critically injured for
whom it matters most. As in the past, perceptive observation,
thoughtful discussion, and insightful analysis concerning
medical care during war from experienced military medics,
surgeons, and scientists, in concert with our civilian col-
leagues, will generate recommendations for new and im-
proved medical practice, with continuous modification as
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The Journal of TRAUMA?Injury, Infection, and Critical Care