REVIEW

CURRENT
OPINION Bleeding and damage control surgery
Roseny R. Rodrigues a, Maria José C. Carmona b,
and Jose Otavio C.A. Junior c

Purpose of review
Bleeding is still a major cause of death in trauma patients. Damage control surgery is a strategy that aims
to control bleeding and avoid secondary contamination of the cavity. This article checks the principles and
indications of damage control surgery, bleeding management, and the role of the anesthesiologist in
trauma context. The efficient treatment of severe trauma and exsanguinated patients includes a surgical
approach to the patient performed as quickly as possible. Volemic resuscitation, hemostatic transfusion,
prevention and/or treatment of coagulopathy, hypothermia, and acidosis are strategies that reduce
bleeding, as well as permissive hypotension.
Recent findings
Specialized literature shows us that the adoption of all of these principles along with reduced surgical time
has led to a broader concept called damage control resuscitation.
Summary
Damage control resuscitation is a treatment strategy in which the recovery of physiological variables is
initially prioritized over anatomical variables and can be required in severe trauma patients.
Keywords
bleeding, damage control resuscitation, damage control surgery

INTRODUCTION conditions have improved, usually 36–48 h after

Trauma is the leading cause of death in individuals
up to 40 years of age. Hemorrhagic shock is respon-
sible for 30–40% of deaths from trauma, and it is
believed to be the most common cause of poten-
the initial trauma. Definitive surgical reprogram-
ming is performed under conditions optimized for
the patient. At this stage, a search is also conducted
for unobserved injuries that were not detected or
&

tially preventable deaths. The cause of death of
approximately 50% of patients, who die within
the first 24 h after trauma, is bleeding [1]. The rapid
control of bleeding remains one of the most import-
ant measures in the management of hemorrhagic
shock. Damage control surgery (DCS) is a strategy
that aims to control bleeding and avoid secondary
contamination of the cavity. According to the liter-
ature, an estimated 10% of severe multiple trauma
patients can benefit from DCS [2–4].
Damage control surgery is divided into three
temporal phases: phase I – involves reduced surgical
time and is aimed at the rapid control of hemor-
rhaging and cavity contamination control; phase II
or resuscitative – the main objective of this phase, is
the re-establishment of physiological functions,
including temperature control, prevention and
treatment of hypothermia, and acidosis beyond
the hemostatic therapy; This phase can take
between 24 and 48 h after trauma. Phase III or
definitive surgery occurs after the physiological
repaired during the first surgical approach [4,5,6 ]
(Table 1).
The efficient treatment of severe trauma and
exsanguinated patients includes a surgical approach
to the patient performed as quickly as possible.
Volemic resuscitation, hemostatic transfusion, pre-
vention and/or treatment of coagulopathy, hypo-
thermia, and acidosis are strategies that reduce
bleeding, as well permissive hypotension. The adop-
tion of all of these principles, along with reduced
a
Anesthesia and Intensive Care Department, Hospital das Clı́nicas,
b
Central Institute, Hospital das Clı́nicas – São Paulo University and
c
Hospital das Clı́nicas, São Paulo, Brazil
Correspondence to: Roseny R. Rodrigues, MD, PhD, Anesthesia and
Intensive Care Department, Hospital das Clı́nicas – São Paulo University,
Avenida Dr Enéas de Carvalho Aguiar, 255, São Paulo-SP, 05403-000,
Brazil. Tel: +55 11 2661 6335;
e-mail: ny_rodrigues@yahoo.com.br
Curr Opin Anesthesiol 2016, 29:229–233
DOI:10.1097/ACO.0000000000000288

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Copyright © 2016 Wolters Kluwer Health, Inc. All rights reserved.

Trauma and transfusion
KEY POINTS
 DCR can be required in severe trauma victims.
 Hypothermia, coagulopathy, and acidosis should be
aggressively treated.
 Strategies such as permissive hypotension can be used
to decrease the loss of blood.
 Hemostatic therapy may also contribute to a better
outcome for these patients.
surgical time, has led to a broader concept called
damage control resuscitation (DCR), described by
Rotondo and collaborators in 1993.
DCR is a treatment strategy in which the recov-
ery of physiological variables is initially prioritized
over anatomical variables. The objective of this
article is to review the principles and indications
of DCR, bleeding management, and the role of the
anesthesiologist in this context.
DAMAGE CONTROL RESUSCITATION
Rapid identification of severely traumatized patients
with metabolic and hemodynamic disturbances is
the cornerstone of indication for damage control.
The most acceptable indications for damage control
are the association of a patient’s severe clinical
condition with the presence of several specific types
of trauma mechanisms. The most relevant clinical
conditions, include the presence of hypothermia
(T < 358C) or coagulopathy (evidenced by microvas-
cular bleeding), the need for multiple transfusions
(defined as the need for transfusion of more than
10 U of packed red blood cells), and the presence of
metabolic acidosis (pH < 7.3), especially if there is
associated hyperlactatemia. The trauma mechan-
isms most closely associated with the need for dam-
age control include those involving high kinetic
energy; among the most common trauma mechan-
isms include large abdominal traumas with vascular
lesions and/or the presence of visceral lesions, and
multiple penetrating traumas to the torso with
exsanguination [4,7,8] (Table 2).
Table 1. Damage control surgery
Indications Phases
Rapid control of bleeding Reduced surgical time
Control and prevention of cavity Resuscitation phase
contamination
—————————————— Definitive surgical correction
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Table 2. Damage control surgery indications
Related to the patient Related to the trauma
Acidosis (pH < 7.3) High kinetic energy trauma
Hypothermia Abdominal trauma with vascular injury
Coagulopathy Abdominal trauma with visceral injury
Hemodynamic instability Penetrating trauma(s) in the torso
Part of the anesthesiologist’s role is to identify
risk factors inherent to each patient, as well as to
institute early actions to address, in a timely man-
ner, the conditions that may worsen the hemody-
namic and clinical status of the patient. Strategies
for the prevention and treatment of hypothermia,
metabolic acidosis, and coagulopathy are discussed
below, along with other measures to reduce bleed-
ing (Table 3).
Hypothermia
Although hypothermia reduces metabolic demands
and oxygen consumption, it is known to affect the
coagulation cascade by reducing the activity of
enzymes that are involved in platelet function
and to promote endothelial and fibrinolytic system
changes; a decrease of 18C in body temperature
reduces the activity of coagulation proteases
between 4 and 10%, which can result in bleeding
[5,9]. In addition, a 15% decrease in the thrombox-
ane B2 production rate occurs, which also leads to a
reduction in platelet aggregation [9].
Coagulation cascade enzymatic reactions are
strongly inhibited by decreasing temperature; a
temperature of 348C is the critical point [5]. Tem-
peratures lower than 358C lead to a reduction in the
metabolic rate of coagulation factors [5,9]. It is
recommended that the temperature of all critical
patients should be monitored using an esophageal
and/or rectal thermometer for maintenance of body
temperature at values close to normothermia
(36–378C). The effects of hypothermia on coagul-
opathy may be reduced by early infusion of heated
Table 3. Damage control resuscitation
Damage control surgery
Prevention and treatment of hypothermia
Prevention and correction of acidosis
Prevention and treatment of coagulopathy
Hemostatic transfusion
Permissive hypotension
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 Bleeding and damage control surgery dos Reis Rodrigues et al.
fluids, the use of warming devices, such as heated
blankets and mattresses, and operating room
temperature control.
Acidosis
Metabolic acidosis resulting from anaerobic
metabolism secondary to tissue hypoperfusion is
one of the major triggers of trauma coagulopathy,
and may therefore worsen existing bleeding. Lactic
acidosis leads to decreases in coagulation factors,
optimal enzyme activity, and platelet activity.
Factor VII function is reduced by approximately
90% when the blood pH is reduced from 7.4 to 7.0.
Acidosis should be corrected at the expense of
volemic replacement, guided by goals and effec-
tive transfusion therapy to avoid cell dysoxia
resulting from anemia and hypoflow situations
[10–12].
The perioperative replacement of goal-directed
fluid, involving the administration of fluids and
inotropics to optimize hemodynamic goals, is a
technique that has been known for some time
and has been proven beneficial in reducing compli-
cations and the length of the hospital stay, especi-
ally after elective surgery [13]. The excessive use of
fluids in an attempt to correct metabolic acidosis
can lead to dilutional coagulopathy and worsening
of bleeding.
Coagulopathy
Coagulopathy is recognized as an integral com-
ponent of the ‘lethal trauma triad’. Its appearance
is directly associated with systemic inflammation
and is in most cases caused by multiple factors.
Coagulopathy may be the result of a vicious cycle
of dilution, consumption of coagulation factors,
hypothermia, acidosis [14], the presence of previous
diseases, and previous use of medications, especially
antiplatelets and anticoagulants.
The concept of trauma-induced coagulopathy
has introduced a new paradigm in the last decade,
and it has become accepted that coagulopathy is a
primary trauma event. This concept of primary and
early coagulopathy is supported by trials, which
have reported a change in traditional coagulation
tests at hospital admission in approximately
10–34% of trauma patients. Coagulopathy has also
been shown to be a mortality predictor [12]. In 2003,
a retrospective study of 1088 trauma patients who
had undergone coagulation analysis prior to the
administration of large amounts of fluids found that
approximately 25% of trauma patients arrived at the
emergency department with clinically significant
coagulopathy. The study showed that four times
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more deaths occurred in the group of patients with
coagulopathy on admission than in the other
groups [13].
The hypothesis postulates that a state of shock
and tissue hypoperfusion leads to an increase in
thrombomodulin expression in the endothelium,
which in turn forms a complex with thrombin,
causing protein C activation and subsequent hyper-
fibrinolysis [12–14].
Recognition of the pathophysiology of trauma
coagulopathy has opened discussions and possibil-
ities of new approaches to bleeding, such as the use
of antifibrinolytics. Antifibrinolytics are used as
fibrinolysis inhibitors. They interfere with plasmin
formation, blocking the binding site of enzymes or
plasminogen, and prevent plasmin conversion and
the consequent disruption of clot formation and
fibrin degradation products. In severe multiple
trauma patients (Injury Severity Score > 15), the
Clinical Randomization of an Antifibrinolytic in
Significant Hemorrhage-2 and Millitary Application
of Tranexamic Acid in Trauma Emergency studies
validated the use of tranexamic acid in patients with
active bleeding in the early hours of trauma and
noted a reduction in mortality related to bleeding
[15,16].
Permissive hypotension
Permissive hypotension is a strategy that has been
increasingly used to reduce bleeding in patients
with traumatic hemorrhage, especially in vascular
and penetrating trauma. Systemic blood pressure
reduction is the pathophysiological rationale for
bleeding reduction. A study of an experimental
uncontrolled shock model in rats used different
levels of mean arterial pressure to achieve volemic
resuscitation (40, 50, 60, 70, 80, and 100 mmHg).
Animals undergoing resuscitation with blood press-
ures of approximately 80–100 mmHg exhibited
more bleeding, mortality, and organ dysfunction
than those subjected to permissive hypotension
(50 and 60 mmHg). Animals resuscitated with an
average pressure of 40 mmHg showed less bleeding
but at the expense of increased organ dysfunction
and mortality. The tolerance time for permissive
hypotension in this study was 90 min, after which
increased mortality occurred [17].
Caution must be exercised in the selection of
patients, as the presence of associated head trauma
is a contraindication for the application of this
bleeding reduction strategy. In these patients, lower
pressure levels can cause a reduction in cerebral
perfusion pressure, and hence, contribute to the
introduction or deterioration of secondary brain
injury.
www.co-anesthesiology.com 231
Trauma and transfusion
There is universal agreement in the medical
literature that patients who are actively bleeding
should have their losses initially restored with fluids
to replace the extracellular space [18]. This approach
should, however, be conducted according to
criteria. Because of the increase in the blood pres-
sure, the hemorrhage can be worsened by the rup-
ture of newly formed clots. Transfusion of blood
components should be considered in cases of sig-
nificant losses, especially when the goal is to achieve
an optimized oxygen supply to the tissue and also,
to correct the incipient coagulopathy.
Prospective and randomized clinical trials that
definitively evaluate the possible benefits of per-
missive hypotension are lacking. Most studies are
experimental and are subject to limitations associ-
ated with this type of research.
Transfusion
Patients with blunt or penetrating trauma and mas-
sive hemorrhage require quick and complex resus-
citation to prevent and correct dilutional and
consumption coagulopathy [19]. There are no stud-
ies in the medical literature offering guidance as to
precisely how much and when to start transfusing
patients suffering from acute bleeding.
Based on studies, particularly retrospective stud-
ies, various scoring systems have been proposed for
predicting the effect of transfusion in this category
of patients [20]. In clinical practice, the different
degrees of hemorrhagic shock are still the most often
used guides. Attention, however, should be given to
the indiscriminate use of other hemocomponents.
A retrospective analysis of studies with civilian
trauma patients reported that a high ratio of fresh
frozen plasma : red blood cells (FFP : RBC) (>1 : 1)
significantly reduces intraoperative coagulopathy
and mortality at 24 h and 30 days [21]. However,
the optimum FFP : RBC ratio is still under discus-
sion [22,23]. There is no doubt that coagulopathy
should be corrected early, as it is directly associ-
ated with increased mortality in trauma patients.
More recently, Davenport and collaborators [22]
found no improvement in coagulation status
when patients were transfused with a ratio of
1 : 1 compared with ratios of 1 : 2 or 3 : 4. Simmons
and collaborators [24] reported in their study,
based on data collected in the Iraq war, that a
change in clinical practice, following transfusion
guidelines with a higher FFP : RBC ratio resulted in
significantly higher plasma transfusion but with
no improvement in patient survival. In contrast
to a fixed FFP : RBC : platelet ratio, some European
studies advocate directing coagulation therapy to
adapt the treatment individually to the patient’s
232 www.co-anesthesiology.com
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actual needs. For this purpose, the use of viscoe-
lastic tests such as the rotational thromboelastom-
etry and thromboelastography systems are needed
to guide coagulation transfusion therapy [25,26].
Massive transfusions are used to treat uncon-
trolled hemorrhages. Early and definitive control of
hemorrhages is extremely important for satisfactory
patient outcomes. According to the literature, mas-
sive blood transfusions are indicated in less than
10% of patients, even in major trauma centers [27].
Studies in the medical literature that compare
the effect of different hemoglobin triggers on the
decision to transfuse patients with acute traumatic
brain injury are lacking. It is assumed that liberal
transfusion strategies (hemoglobin of approxi-
mately 9–10 g/dl) should be used to prevent secon-
dary injury and additional ischemic cerebral insults
because the traumatized brain cannot compensate
for the decrease in oxygen supply associated with
anemia [28,29 ].
&
CONCLUSION
Severe multiple trauma patients with active bleed-
ing may be candidates for DCR. Early identification
of these patients is critical to reduce the surgical
time; adopt measures to prevent and treat coagul-
opathy, hypothermia, and metabolic acidosis; and
produce a consequent reduction in bleeding. The
use of strategies such as permissive hypotension and
adequate hemostatic therapy may also contribute to
a better outcome for these patients.
Acknowledgements
All trauma patients that teach us every day; General
Trauma Team from Hospital das Clı´nicas – São Paulo
University.
Financial support and sponsorship
None.
Conflicts of interest
Eventual lectures do CSL Behring; TEM Innovations is
sponsor of trials.
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