AACN Advanced Critical Care
Volume 32, Number 1, pp. 64-75
© 2021 AACN
Critical Care Considerations for
Damage Control in a Trauma Patient
Shannon Gaasch,
MS, RN, CRNP-BC
ABSTRACT
Traumatic injury remains the leading cause
of death among individuals younger than
age 45 years. Hemorrhage is the primary
preventable cause of death in trauma patients.
Management of hemorrhage focuses on
rapidly controlling bleeding and addressing
the lethal triad of hypothermia, acidosis,
and coagulopathy. The principles of damage
control surgery are rapid control of hemorrhage, temporary control of contamination,
resuscitation in the intensive care unit to
restore normal physiology, and a planned,
delayed definitive operative procedure. Damage control resuscitation focuses on 3 key
components: fluid restriction, permissive
T
raumatic injury is a leading cause of death
worldwide among individuals younger
than 45 years and is the primary source of
productive years of life lost.1 Survivors experience considerable morbidity and long-term disability, which lead to substantial increases in
direct and indirect health care costs.1 Traumatic
brain injury (TBI) is the single greatest cause
of death after trauma, and hemorrhage is the
leading cause of preventable death from trauma,
with a fatality rate of 30% to 40%.1-3
In 1993 Rotondo et al4 first described early
damage control strategies, which focused on the
management of surgical bleeding from wounds
that can be sutured, ligated, or cauterized3-5:
“planned temporary sacrifice of normal anatomy to preserve vital physiology.”3 Shifting
the focus from definitive treatment to rapid
control of bleeding and peritoneal contamination, combined with packing the peritoneal
cavity to temporize the injury and restore
64
hypotension, and fixed-ratio transfusion.
Rapid recognition and control of hemorrhage and implementation of resuscitation
strategies to control damage have significantly improved mortality and morbidity
rates. In addition to describing the basic
principles of damage control surgery and
damage control resuscitation, this article
explains specific management considerations for and potential complications in
patients undergoing damage control interventions in an intensive care unit.
Key words: damage control, permissive
hypotension, resuscitation, trauma-induced
coagulopathy
homeostasis, revolutionized trauma care and led
to a drastic reduction in mortality from hemorrhagic shock.6 This article describes the basis
for damage control surgery (DCS) and damage
control resuscitation (DCR), as well as the
management of patients receiving care in the
intensive care unit (ICU) after resuscitation.
Traumatic Injury and
Physiological Impact
Numerous complex physiological derangements can occur after traumatic injury. Direct
tissue injury generates a local response,
Shannon Gaasch is Senior Nurse Practitioner II, R Adams
Cowley Shock Trauma Center, University of Maryland Medical Center, 22 S Greene St, Baltimore, MD 21201 (Shannon.
gaasch@umm.edu).
The author declares no conflicts of interest.
DOI: https://doi.org/10.4037/aacnacc2021817
VO L U M E 32 • N U MB E R 1 • S PRING 2021
Historically, coagulopathy in traumatic injury
was thought to be related to fluid administration and hypothermia. Current studies, however, suggest that 30% of trauma patients
present with “trauma-induced coagulopathy”
(TIC)1 (Figure 2). This state develops quickly,
usually within 30 minutes of injury and before
significant dilution.14 Injury prompts the activation of the clotting cascade, which responds
lat
ion
oa
gu
De
cre
as
ed
c
sis
do
Coagulopathy
aci
Hypothermia, defined as a core body temperature less than 35 °C, can occur from
physical exposure (both at the scene of injury
and at the hospital), intoxication, circulatory
changes, and administration of cold fluids.10
This condition is exacerbated by the loss of
thermoregulatory control as a result of the
uncoupling of normal metabolic pathways.10
Hypothermia has a profound impact on coagulation, inhibiting platelet aggregation and
reducing coagulation factor activity by approximately 10% for every degree decrease in temperature.10,11 The severity of hypothermia has
been linked with poor prognosis and may be
an independent predictor of mortality in
trauma: mortality rates as high as 70% to
100% have been reported in patients with
severe hypothermia.1,10,12 When a trauma patient
is admitted, providers should take steps to
prevent hypothermia—minimizing exposure,
applying warm sheets and convection blankets, administering warmed fluids, and reducing time spent in the operating room—with
all efforts targeted toward achieving a core
temperature higher than 35 °C.1,3,11,13 Rapid
control of hemorrhage is of paramount importance in correcting hypothermia.
Hypothermia
c
cti
Hypothermia
Coagulopathy
La
propagating a systemic reaction that can be
significantly amplified and harmful.7 Rapid
recognition and control of hemorrhage is critical to preventing systemic effects that may
occur. In a landmark 1982 study, Kashuk et al8
first described the lethal triad of trauma (LTOT)
(Figure 1), which includes hypothermia, coagulopathy, and acidosis.5 Kashuk et al observed
that 89% of trauma-related deaths were attributed to hemorrhage; 51% of those patients
who died had exsanguinated after satisfactory
repair of vascular injury.6,8 If the characteristics
of LTOT are not corrected quickly, it becomes
a vicious, self-perpetuating cycle that can rapidly lead to death.1,10
CONSID E RAT IONS IN DA M AGE CONT ROL
Metabolic acidosis
Decreased myocardial performance
Figure 1: The lethal triad in trauma. Reprinted via
open access from Leibner et al.9
by forming a clot that in turn depletes platelets and coagulation factors, causing a consumptive coagulopathy. This coagulopathy is
worsened by administration of crystalloid
solutions and packed red blood cells (PRBCs)
without the administration of clotting factors.1 Delaying transfusion of clotting products until after large quantities of PRBCs
(> 10 U within 24 hours) and crystalloid have
been given exacerbates coagulopathy by diluting the blood and reducing the concentration
of clotting factors, further driving the cycle of
the LTOT.10 Trauma-induced coagulopathy is
associated with poor outcomes related to the
release of inflammatory mediators from
direct tissue injury and from secondary tissue
hypoperfusion or cellular hypoxia, leading to
systemic anticoagulation via activated protein
C and depletion of clotting factors.1,3,7,10 The
early development of coagulopathy after
trauma is another independent predictor of
mortality.14 Fibrinolysis, a key feature of TIC,
occurs within the first hour after trauma and
is associated with mortality rates as high as
90%.3 It is important to understand and recognize TIC early during the resuscitation phase
in order to improve mortality rates; however,
published clinical scoring systems designed to
detect TIC do not reliably identify patients
who are at risk for this complication.3
Acidosis
The decreased circulatory volume derived
from hemorrhage affects oxygen delivery to
tissues, leading to the development of toxic
metabolites, anaerobic metabolism, and lactic
acidosis.10 Disruptions to pH homeostasis
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Preexisting conditions
Age
Genetics
Comorbidities
Preinjury medication
Trauma
Tissue damage
Hemorrhage
Shock
Hypoperfusion
Sympathoadrenal activation
Inflammation
Systemic
endotheliopathy
Glycocalyx shedding
Endogenous heparinization
Platelet activation and dysfunction
Reduced clotting factor activity
Hyperfibrinolysis
Trauma-associated factors
Resuscitation-associated factors
Coagulation factor loss
Coagulation factor dilution
Coagulation factor consumption
Hypothermia
Acidosis
Traumatic coagulopathy
Figure 2: Trauma-induced coagulopathy. Reprinted via open access from Spahn et al.11
negatively impact enzymatic function throughout the body, and multiple organ dysfunction
develops, evidenced by reduced cardiac contractility and cardiac output, vasodilatation,
hypotension, and bradycardia.1,10 The degree
of acidosis and the level of lactate at admission have been used to predict mortality in
trauma patients.10,13 The goal is to optimize
oxygen delivery through blood transfusion
and augment cardiac output with pharmacologic agents while controlling hemorrhage in
order to deter acidosis.10,11,15
Damage Control Surgery
Rotondo et al4 described DCS in the management of penetrating abdominal injuries
66
and enumerated 3 distinct phases: (1) surgical
control of hemorrhage and contamination
followed by intraperitoneal packing and temporary closure of the abdomen; (2) resuscitation of the patient in the ICU in order to
reverse coagulopathy and achieve normal
physiology; and (3) definitive surgical management once normal physiology has been
restored.4,5,10,15 This strategy significantly reduced
mortality from 89% to 23%, and it can also
be applied in patients with musculoskeletal
trauma, in whom temporary stabilization with
external fixation can reduce hemorrhage and
mortality.10,16 The initial goal is to correct
metabolic derangements and restore normal
physiology, rather than provide definitive
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CONSID E RAT IONS IN DA M AGE CONT ROL
Table 1: Indications for Damage Control Resuscitationa
Anatomic Parameters
Estimated ISS > 36
Penetrating abdominal injuries
Penetrating chest injuries
Open pelvic fracture
Long bone fracture with head injury
Long bone fracture with lung contusion
Truncal hemorrhage and amputation
Physiologic Parameters
Weak or absent radial pulse
Core body temperature < 35 °C
Systolic BP < 100 mm Hg
Heart rate > 100
PaO2/FiO2 < 250
Urinary output < 50 mL/h
Lab Parameters
Lactate > 2.5 mmol/L
Platelet count < 90 000/mL
Fibrinogen > 1 g/dL
PT > 16 s
INR > 1.5
Hg < 11
pH < 7.2
Base deficit < 6
Abbreviations: BP, blood pressure; FiO2, fraction of inspired oxygen; Hg, hemoglobin; INR, international normalized ratio; ISS, injury severity
score; PaO2, partial pressure of oxygen; PT, prothrombin time.
a
Reprinted via open access from Giannoudi and Harwood.10
surgical control, particularly for patients who
display evidence of imminent demise.5
In phase 1, the goal of surgery is to achieve
hemostasis through direct or indirect measures
(eg, packing, aortic balloon occlusion, stabilization of fractures) and to control peritoneal
contamination.11,15,17 Once this goal is achieved,
the surgeon packs the abdomen, applying direct
pressure to tamponade bleeding from solid
organs, then temporarily closes the wound with
simple skin closure or by applying a vacuumsealing device.11,15,17 Ideally, this phase should
be performed within 90 minutes to decrease
significant metabolic derangements. The patient
is then transferred to the ICU, where resuscitation and reversal of metabolic derangements can be continued. The goal is to reverse
coagulopathy and hypothermia, and restore
a normal acid-base status. When the patient
becomes stable they are taken back to the operating room where the surgeon attempts definitive treatment; ideally, this occurs within 24
hours of DCS surgery.17
Damage Control Resuscitation
During the past decade, a new concept of
DCR has emerged as a result of improved
understanding of the negative impact the LTOT
has on morbidity and mortality. Often used in
combination with DCS,5 DCR was designed
to support actively bleeding trauma patients
by restoring homeostasis and preventing or
mitigating tissue hypoxia, oxygen debt, and
coagulopathy.3,18 A systematic approach to
major trauma minimizes blood loss and optimizes patient outcomes, resulting in dramatically reduced mortality from hemorrhage and
a lower incidence of—and less severe—complications such as multiple organ dysfunction
and infection.3 The success of this approach
requires a coordinated effort and multidisciplinary approach.3 Damage control resuscitation should be initiated upon the first contact
with the patient in the prehospital environment and should continue throughout care
until hemorrhage is controlled and physiology corrected.10 Patients who have a major
abdominal or thoracic visceral injury, significant pelvic trauma, amputation, multiple longbone fractures, or head injury have a high risk
for deterioration and should be evaluated as
candidates for DCR3,19 (Table 1). The core
principles of DCR are permissive hypotension, fluid restriction, and fixed-ratio blood
product transfusion5,11 (Figure 3).
Permissive Hypotension
Targeting a normal blood pressure (BP) has
been associated with worse outcomes in patients
with active hemorrhage. The exception is
patients with TBI or spinal cord injury, who
require a higher perfusion pressure to preserve neural tissue.5,10 Resuscitation to a normal BP can displace clots formed during the
body’s attempt to achieve primary hemostasis
and will likely lead to dilutional coagulopathy
as a result of overresuscitation, causing more
bleeding and worsening tissue perfusion.3,5,10
The goal of permissive hypotension is to
achieve the minimal BP necessary to perfuse
organs. Current data suggest a target systolic
BP of 80 to 100 mm Hg.9 For patients with
TBI who are 50 to 69 years old, a desirable
systolic BP target is more than 100 mm Hg;
for such patients who are younger than 49
years, a systolic BP more than 110 mm Hg
should be targeted.9,20 These values equate to
restoration of a palpable radial pulse. Permissive
hypotension has been linked with improved
mortality in trauma patients, likely because
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Rapid diagnosis
Limit
crystalloids
Antifibrinolytics
Damage
control
resuscitation
Rapid anatomic
control
Early 1:1:1
transfusion
strategy
Permissive
hypotension
Figure 3: Principles of damage control resuscitation.
1:1:1 transfusion strategy is 1 packed red blood cells:
1 plasma: 1 platelet. Reprinted via open access from
Leibner et al.9
of fluid restriction and not the specific BP
target.9,21,22 Although this strategy has been
linked to improved survival rates, it should
be used with caution in elderly patients and
patients with chronic hypertension.21 Once
bleeding has been controlled, a normal BP
should be obtained.2
Fluid Restriction
Aggressive fluid resuscitation in an actively
hemorrhaging patient leads to increased bleeding and dilutional coagulopathy. Administration
of large volumes of fluid may temporarily
increase BP, but it counteracts compensatory
vasoconstriction and innate primary hemostasis,
leading to more hemorrhage and rebleeding
from spontaneously clotted vessels.3 Advanced
Trauma Life Support recommendations have
changed from “aggressive resuscitation” to a
more balanced approach, endorsing a maximal
infusion of 1 L isotonic crystalloid solution
and early transfusion of blood products.1,13,23
Further administration of fluids is then guided
by an assessment of the patient’s responsiveness to the administered fluids.23 Ultimately,
large volumes of intravenous fluid negatively
impact organ function.3
Patients with a high crystalloid-to-PRBC
ratio during the first 24 hours have increased
68
mortality and higher rates of acute respiratory
distress syndrome (ARDS), multiple organ
dysfunction, and abdominal compartment
syndrome (ACS) than patients without a high
crystalloid-to-PRBC ratio; the abdominal
viscera can sequester liters of fluid and can
double in size after resuscitation with massive amounts of intravenous fluids.1,5 In a retrospective study, Neal et al24 found that a
crystalloid-to-PRBC ratio more than 1.5:1.0
in patients receiving massive transfusions was
associated with a 70% higher risk of multiple
organ failure and a 2 times higher risk of
ARDS and ACS.9,24 A fluid-restrictive guideline, as suggested in the Advanced Trauma
Life Support manual,23 is recommended. Balanced crystalloid solutions should preferentially be administered, whereas normal saline
solutions should be avoided because of the
high incidence of hyperchloremic acidosis
and renal failure.11
Fixed-Ratio Blood Transfusion
Historically, large-volume infusions of crystalloid solution and PRBCs were administered
before plasma and platelet transfusions would
be considered, contributing to dilutional coagulopathy and other complications in severely
injured patients. Landmark studies from the
US military demonstrated a significant survival
advantage in patients who received infusions
with higher ratios of fresh frozen plasma to
PRBCs.5,25-28 This survival benefit, however,
was not demonstrated in a large, multicenter
civilian study.29 Unlike crystalloid transfusion,
balanced product transfusion resolves acidosis, prevents endothelial damage, treats TIC,
and begins to reverse (rather than contribute
to) DC.1 Early use of platelets in a balanced
transfusion strategy has been associated with
improved survival after trauma.1,18 Fixed-ratio
transfusions—defined as transfusion of PRBCs,
plasma, and platelets at a 1:1:1 ratio—are
effective in approximating the makeup of
whole blood; in addition, administration of
cryoprecipitate should be considered during
administration of large amounts of blood
products.1,5,18 The Eastern Association for the
Surgery of Trauma consensus practice guidelines suggest that early resuscitation with
blood product (ie, plasma and platelets) followed by administration of PRBCs is a safe
guiding principle, though further data are
needed to support this recommendation.25 The
therapeutic targets for DCR are outlined in
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CONSID E RAT IONS IN DA M AGE CONT ROL
Table 2: Therapeutic Goals During Damage Control Resuscitation
Without Neurotrauma
With Neurotrauma
Arterial pressure (mm Hg)
Before hemostasis:
80 < systolic BP < 100
After hemostasis: MAP > 65
Before and after hemostasis:
systolic BP > 100 or MAP > 80
Hemoglobin (g/dL)
7-9
7-9
International normalized ratio
<2
< 1.5
Platelet count/mm
> 50 000
> 100 000
Calcium (mmol/dL)
> 10
Fibrinogen (mg/dL)
150-200
pH
> 7.2
Temperature (°C)
> 36
3
Abbreviations: BP, blood pressure; MAP, mean arterial blood pressure.
Reprinted via open access from Malgras et al.17
Table 2. Point-of-care thromboelastography
may help detect coagulation abnormalities
and allow for a targeted goal-directed transfusion strategy.11
Hypocalcemia is a common complication
associated with blood transfusions; the citrate
added to stored blood in order to prevent coagulation binds to calcium in the serum. Calcium,
in its free ionized state, is present in the extracellular plasma and is essential in the formation and stabilization of fibrin, assists in platelet
function, and is important for cardiac contractility and for maintaining systemic vascular
resistance.11 Platelet and plasma transfusion
products require even higher citrate concentrations, making hypocalcemia more likely to occur
than when PRBCs alone are administered.11,13
Care Considerations in the ICU
After DCS the patient is transferred to the
ICU for continued resuscitation until their transition to the postresuscitation phase of care.
The primary management strategies are to
prevent and mitigate the LTOT by avoiding
hypothermia, correcting acidosis, reversing
coagulopathy, and assessing for ongoing bleeding. An initial evaluation should focus on the
presence and extent of shock, hemodynamics,
end-organ perfusion, intravascular volume
status, neurologic examination, and a general
head-to-toe survey of injuries. After initially
resuscitating the patient, nurses should focus
attention on common ICU considerations such
as ensuring a patent airway, maintaining ventilatory status, providing sufficient nutrition,
managing pain, preventing and treating delirium, promoting early mobility, and avoiding potential complications—all of which
help optimize outcomes for patients who
undergo DCS.
End Points of Resuscitation
One common misconception by clinicians
in the ICU is that vital signs can be relied on
to diagnose hypovolemia, whereas various clinical conditions that cause vital signs to change
may not necessarily represent hypovolemia.30,31
Shock is the consequence of inadequate tissue
perfusion, which results in metabolic acidosis.
The presence and extent of shock are evident
through altered physiologic parameters such
as serum lactate and arterial blood gas (but
not necessarily BP). Patients with severe shock
may also have “normal” vital signs as compensatory mechanisms transiently maintain BP
in the face of profound metabolic acidosis.32
This phenomenon is particularly evident in
young trauma patients.
Several modalities are available to assess
hemodynamics and volume status, including
echocardiography and invasive and noninvasive hemodynamic monitoring; each has advantages and disadvantages.33,34 Static indices give
a representation of the cardiac preload; they
do not, however, accurately predict responsiveness to fluid administration.35 Such indices
include central venous pressure, pulmonary
artery occlusion pressure, and right ventricular
end-diastolic volume.36 Dynamic indices allow
a better understanding of a patient’s volume
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status and help determine whether the patient
should receive fluid or a vasopressor. The passive leg raise maneuver is a dynamic assessment
that has been validated and in use for many
years. If the patient will respond to fluids, a
10% to 12% increase in cardiac output and
stroke volume will occur when the legs are
passively raised.35
Bedside ultrasonography has become an
invaluable tool in determining intravascular
volume.31 The clinician should first determine
fluid volume via point-of-care ultrasound, then
evaluate the patient’s responsiveness to fluids.
Collapse of the inferior vena cava during the
respiratory cycle implies that the patient would
respond to fluids. Because of the impact of
changes in thoracic pressure on the inferior
vena cava, irregular respiratory mechanics limit
the applicability this assessment method.37
Assessing left ventricular size and function can
help determine fluid status: if the patient has
a small, hyperdynamic left ventricle with “kissing ventricles,” hypovolemia is likely to be
present.37 After assessing fluid status and cardiac function, the clinician should determine
responsiveness to fluids.31 Stroke volume variation is typically measured on the basis of the
velocity time integral (VTI) through point-ofcare ultrasound in patients receiving positivepressure ventilation. The VTI measures the
velocity at and distance to which blood ejects
during each myocardial contraction.31,37 Clinicians should obtain multiple measurements of
VTI. A VTI variation greater than 12% indicates that the patient will respond to fluids;
variation more than 14% is highly predictive
of fluid responsiveness, whereas variation
less than 10% is a highly negative predictive
value.31,37 When used together, VTI measurements and the passive leg raise test provide
an ideal assessment of fluid responsiveness.35
A concern with using point-of-care ultrasound to assess intravascular volume is the
variability of clinicians’ skill in performing
the study.31,37
Lactate and base deficit are markers of
anaerobic metabolism, and trends should be
analyzed in order to track recovery from shock
at the cellular level.11,30 The level of lactate,
produced through anaerobic glycolysis, has
prognostic value in patients with hemorrhagic
shock: an elevated level in serum is associated with an increased risk of death and a
likelihood of infectious complications and
multiorgan failure.11 Early clearance of lactic
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acidosis correlates with improved survival.11
Base deficit, measured through arterial blood
gas, is an indirect estimation of global tissue
acidosis due to impaired perfusion; it more
reliably identifies shock 24 hours after presentation, by which time the effects of shock
have been established.11,31,38,39 The time to clear
a base deficit has not been correlated with
prognosis, and lactate may have better clinical applicability after resuscitation with intravenous fluids.30 Many factors can affect base
deficit, including gastrointestinal losses, diabetic ketoacidosis, and renal dysfunction—
again making lactate a more reliable marker.31
Lactate may, however, be less accurate than
base deficit in patients with concurrent liver
failure. Persistent metabolic acidosis indicates
ongoing blood loss or inadequate resuscitation;
sodium bicarbonate should not be administered to treat acidosis related to hypovolemic
shock.23 If a nurse suspects ongoing blood loss,
they should notify the surgeon, who can then
assess the need for reexploration or angioembolization. Urine output can be a surrogate
for adequate renal blood flow, though this
has limitations. Acceptable urine output is
0.5 mL/kg/h in adults.23
Airway and Ventilation
Management
Airway and ventilation complications are
the most common issues identified during
the early management of severely injured
patients.23,30 Signs of sudden or rapidly progressive desaturation—which may or may
not be accompanied by tachycardia, arrhythmia, and agitation—should be evaluated as
an airway emergency.30 Pulse oximetry is
essential to recognizing inadequate peripheral arterial oxygenation and allows immediate assessment of interventions to improve
oxygenation.23 An advanced airway (eg, endotracheal intubation, surgical airway) should
be placed in patients who have altered mental
status (Glasgow Coma Scale score < 8); are
severely agitated or apneic; have multiple
complex facial fractures, inhalation injury,
neck hematoma, or a laryngeal or tracheal
injury; have severe metabolic disturbances; or
are unable to maintain a patent airway.23 One
common sequela of traumatic injury is ARDS,
which is a result of the neurohormonal and
inflammatory responses that occur after
injury. Patients with thoracic trauma are at
particularly high risk for this complication.40
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Lung-protective ventilation strategies can prevent secondary lung injury and ARDS.40
Secondary and Tertiary Survey
The primary survey of the patient is completed upon their arrival in the trauma bay,
addressing life-threatening injuries. A secondary survey begins after airway, breathing, and
circulatory concerns have been addressed and
resuscitation has been initiated.23 When the
patient is transferred to the ICU, a head-totoe assessment is completed to identify other
potential injuries, radiographs and laboratory
tests are ordered to further investigate potential injuries, and fractures are stabilized.23
Despite this thorough assessment and initial
workup, injuries are occasionally missed until
a tertiary survey is performed.30 A full head-totoe examination in the ICU is imperative; the
nurse should assess for tenderness and joint
stability once the patient is clinically stable.
Such extended assessment has reduced the number of missed injuries by 40% to 57%.30,41
Nutrition
Critical illness produces a catabolic state,
making nutrition exceedingly important;
sometimes, however, it is overlooked. Guidelines recommend that full enteral nutrition
(EN) be initiated within 24 to 48 hours of
admission to the ICU to maintain gut integrity, modulate the systemic inflammatory
response, and reduce mortality and infectious
morbidity.36,42,43 Enteral nutrition should, however, be delayed in patients with intestinal
discontinuity or high-output fistulas.44 Barriers to providing sufficient EN exist because
of the multiple interruptions in therapy that
often occur for surgical and procedural interventions; an estimated 60% of interruptions
to enteral feeding in the ICU are due to fasting for procedures.42 A randomized controlled
trial demonstrated that EN can be safely continued in intubated patients until their operation and is not associated with a higher risk
of aspiration.42
Traumatic injury results in dramatic changes
in metabolism and the body’s utilization of
lean tissue to support gluconeogenic substrates
and immune repair functions.43 The hormonal
stress response overrides the normal starvation
pattern that preserves lean muscle, instead
promoting progressive loss of skeletal muscle.43
Survival is strongly correlated with early EN,
and thus it is recommended for patients with
CONSID E RAT IONS IN DA M AGE CONT ROL
TBI.43 This patient population has high energy
and protein requirements as a result of the
significant catabolic state that accompanies
TBI.43 Patients with an open abdomen have
increased fluid, electrolyte, and protein requirements because of large-volume losses—an
estimated 2.0 to 4.6 g of nitrogen are lost per
liter of abdominal fluid output—putting them
at risk of being underfed.36 Enteral nutrition
may still be considered safe in patients who
require vasopressors, although they should be
monitored closely for signs of intolerance to
enteral feeding (eg, abdominal distention,
increasing gastric tube output or gastric residuals, decreased passage of flatus or stool,
worsening metabolic acidosis and base deficit); if such signs are present, the patient
should be evaluated for intestinal ischemia.43
Promotility agents should be initiated for
patients with gastroparesis and high risk for
aspiration. Although these agents improve
gastric emptying and tolerance of EN, studies
have not demonstrated any significant impact
on clinical outcome in patients in the ICU.43
Last, glucose control is important in critically
ill patients, and glucose should be maintained
at 150 to 180 mg/dL.43 Tight glucose control
(defined as 80 to 110 mg/dL) is associated with
higher risk of hypoglycemia and mortality.43
Pain Management
Multimodal analgesia is essential for all
surgical patients. A patient’s pain regimen
should be tailored to their individual injury
and clinical situation; such customization
requires multidisciplinary collaboration.45 The
use of multimodal analgesia reduces opioid
use and opioid-related adverse effects, and
enhances the patient’s postoperative recovery,
function, and satisfaction.45 Multimodal analgesia is achieved by administering nonopioid
medications (eg, nonsteroidal anti-inflammatory
drugs, acetaminophen, gabapentinoids,
N-methyl-D-aspartate receptor antagonists,
_2 agonists, or a combination of them) synergistically with opioid medications.45 Excessive use of opioids has many deleterious
effects such as confusion, sedation, hypotension, constipation, and respiratory depression—to name only a few—and prolonged
use of opioids can lead to physical dependence
and addiction.45 Additional approaches to
pain management, such as patient-controlled
analgesia and neuroaxial or peripheral nerve
blocks, can also be considered.45
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Nonpharmacologic interventions such as
massage, guided imagery, distraction, and
cold compresses decrease pain, anxiety, and
opioid use, and should also be incorporated.45
Delirium and Early Mobility
Delirium is a common problem that affects
up to 90% of hospitalized patients and is
associated with longer hospital length of
stay, more ventilator days, higher cost of
care, and long-term cognitive impairment.46
The incidence of delirium is high among
patients in the ICU: delirium affects up to
80% of mechanically ventilated patients.46
Delirium is defined as an acute change in
mental status from baseline, and patients are
unable to maintain or focus attention for a
sustained period of time.46 Risk factors include
medications, older age, multiple comorbidities, prolonged mechanical ventilation, major
surgery, and septic shock.46 Nurses should use
validated tools to screen for the presence of
delirium; the Confusion Assessment Method
for the Intensive Care Unit and Intensive Care
Delirium Screening Checklist are among the
most widely used tools.46
Prevention of delirium is crucial, and nurses
should emphasize interventions embodied in
the ABCDEF bundle: assess, prevent, and
manage pain; both spontaneous awakening
and spontaneous breathing trials; choice of
analgesia and sedation; assess, prevent, and
manage delirium; early mobility and exercise;
and family engagement and empowerment.47,48
Examples of strategies aimed at preventing
delirium include performing sleep hygiene,
promoting normal circadian rhythms, reducing
noise, frequently reorienting the patient, mobilizing early, minimizing sedation, and avoiding
use of benzodiazepines.46-48 Pharmacologic
treatment with typical and atypical antipsychotic drugs has not decreased the incidence
of delirium and may have associated harmful
effects (QT prolongation, neuroleptic malignant syndrome, and oversedation).46
Early mobility reduces ICU and hospital
lengths of stay, delirium, and mechanical ventilation days and increases functional independence at discharge.49 Unfortunately, early
mobility is not always feasible in trauma
patients because of mobility restrictions and
ongoing resuscitation needs, which may render the patient immobile for prolonged periods.
Myopathy and neuropathy are complications
that can develop in patients in the ICU and
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occur in one-third of critically ill patients as a
result of muscle wasting; these conditions can
leave patients with permanent residual mobility
limitations.50 Bed rest is the most common modifiable risk factor.50 A multidisciplinary approach
to early mobility is imperative to reducing the
incidence of ICU-acquired weakness.
Prophylaxis for Venous
Thromboembolism
Hospital-acquired venous thromboembolism
occurs in more than 50% of patients who sustain multiple traumatic injuries; pulmonary
embolism is the third leading cause of death
among those who survive the first 72 hours
after injury.11 Early mechanical prophylaxis is
encouraged, and European guidelines recommend initiating pharmacologic prophylaxis
for venous thromboembolism within the first
24 hours after bleeding has been controlled,
although commencement may be delayed if
concern exists about a hemorrhagic neurologic injury.11 Low-molecular-weight heparin
(eg, enoxaparin) is recommended as such a
prophylaxis (unless it is contraindicated).51
Complications Related
to DCS and DCR
Transfusion-Related Acute Lung Injury
One of the risks associated with administration of blood products is the development
of transfusion-related acute lung injury, a
syndrome of noncardiogenic pulmonary edema
associated with hypoxia.52 The diagnostic criteria include onset of symptoms within 6 hours
of blood transfusion in the absence of other
clinical conditions that could lead to acute lung
injury.52 Patients may become tachycardic,
febrile, hypotensive, and hypoxemic, and radiographs may show evidence of bilateral chest
infiltrates, without signs of fluid overload.50
In such cases, blood transfusion should be
terminated; low-tidal-volume ventilation
may be initiated, as the pathophysiology for
transfusion-related acute lung injury mimics
that of ARDS.52
ACS and Intra-abdominal Ischemia
Patients who develop ACS can deteriorate
rapidly and develop progressive hypotension
with a transient fluid response.36 If ACS goes
unrecognized and untreated, it can lead to
reduced pulmonary compliance and worsening
respiratory acidosis, ultimately developing into
metabolic acidosis as a result of hypoperfusion.36
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Abdominal distention can worsen and elevated
airway pressure, hypoxia, oliguria, or anuria
can occur in patients with ACS; a bladder pressure more than 20 cm H2O with new organ
dysfunction or failure is diagnostic of the condition.5,44,53 The risk of developing ACS is lower
with DCR than with traditional resuscitation
methods, despite whether temporary or definitive closure has occurred.5 If rapid decompression is required, circulatory collapse can
occur from the sudden reestablishment of
perfusion and the associated acid washout.
High minute ventilation and administration
of sodium bicarbonate and calcium can help
stabilize the patient in this circumstance.36
In severe shock, circulation is preferentially shunted away from the gastrointestinal
tract to the vital organs, especially if a patient
requires a high-dose vasopressor.22 Mesenteric
venous return can be impaired in patients
with intra-abdominal packing or increased
intra-abdominal pressure, and they may
develop congestive intestinal ischemia.36 As
intravascular volume is replete with intravenous fluid, the compromised bowel is reperfused and mucosal damage caused by free
radicals may occur, followed by worsened
bowel edema.36
Failure to Achieve Primary Closure
Inability to close the fascia in a patient
with a midline abdominal wound is the most
feared complication of temporary abdominal
closure and is independently associated with
increased mortality.6,36 Patients in whom surgeons are able to close the abdomen during
the first return to the operating room have a
lower risk for pulmonary, wound, infectious,
and noninfectious complications.5 Volume
overload, prolonged duration of an open
abdomen, and development of enterocutaneous fistulas or intra-abdominal abscesses are
risk factors for the inability to achieve primary
closure.36 Failure to close the fascia results in
a large ventral hernia, and the patient will
require abdominal wall reconstruction. These
patients have a high risk for infection and
enteroatmospheric fistulas.36 Vacuum-mediated
closure methods are preferred for temporary
skin closure following trauma-related DCS
because they allow peritoneal effluent to drain
while providing fascial traction toward the
midline.6 Direct peritoneal resuscitation by
continuously irrigating the peritoneal cavity
and removing inflammatory cytokines has
CONSID E RAT IONS IN DA M AGE CONT ROL
been associated with fewer intra-abdominal
infections, a shorter time to definitive abdominal closure, and lower mortality rates.54
Infection-Related Considerations
Trauma patients are at risk for a number
of infectious complications because of alterations in immune defense, disruption of tissue
integrity, and the effects of indwelling catheters.44 Patient-specific risk factors (eg, age, sex,
and comorbidities) and the mechanism of
trauma (eg, site of injury) contribute to the
risk of posttraumatic nosocomial infections.44
Prophylactic antibiotics should be administered
early to patients with a penetrating abdominal
or brain injury or an open fracture.30 Preoperative administration of antimicrobial prophylaxis is recommended for patients undergoing
colon, neurosurgical, head and neck, cardiothoracic, vascular, facial, and orthopedic procedures.55 Patients with an open abdomen are
at an increased risk of infectious complications:
about one-quarter of such patients develop
wound infections, deep abdominal abscesses,
or intestinal fistulas.36,44 The risk of infectious
complications, including bloodstream infections, increases after 8 days of having an open
abdomen because of an inability to achieve
primary fascial closure.36
Pneumonia is a common complication among
patients in the ICU and occurs secondary to
prolonged intubation and sequelae from the
injury that alter mental status or pulmonary
mechanics.44 Aspiration pneumonia is particularly prevalent; severely ill trauma patients with
brain injury or a depressed level of consciousness are at high risk. Individuals who experience microaspiration typically require a longer
ICU stay and prolonged mechanical ventilation.44
Diligence in providing measures to prevent
ventilator-associated pneumonia, including
elevating the head of the bed more than 30°,
providing oral hygiene with chlorhexidine
mouthwash, and minimizing the use of sedatives and narcotics, can reduce the incidence
of the condition.43 Trauma patients and those
with complicated injury patterns are at risk
for urinary tract infections and bloodstream
infections related to prolonged use of invasive devices during the resuscitative phase.44
When a patient requires a catheter, nurses
should use proper sterile insertion technique,
when feasible; catheters that were placed emergently should be replaced within 24 hours, and
early removal is recommended. Clinician
73
G A ASC H
collaboration with pharmacists and infectious
disease specialists is encouraged in order to
prevent and treat infectious complications
among patients in the ICU.
Conclusion
Significant physiologic and metabolic
derangements occur after a traumatic injury.
Wartime experiences have provided a better
understanding of the pathophysiology of
trauma and coagulopathy and have led to
revolutionary changes in management and
resuscitation strategies. When used synergistically, DCS and DCR considerably improve
morbidity and mortality rates. The central
focus of DCR includes permissive hypotension,
minimizing fluid administration, and balanced
blood product transfusion; hemorrhage must
also be controlled early. These approaches
require multidisciplinary collaboration to recognize signs of a patient’s imminent demise
or TIC so that treatment can be promptly
initiated to halt the LTOT, thereby reducing
hemorrhage and any resulting sequelae.
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CE Evaluation Instructions
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following objectives:
1. Discuss the 3 key components of damage control resuscitation.
2. Describe hemodynamic parameters to assess in patients undergoing damage control resuscitation.
3. Identify the critical care management of patients following damage control surgery including preventing potential complications.
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