Anesthesia for Patients

w i t h Tra u m a t i c B r a i n
Injuries
Bishwajit Bhattacharya, MD, FACS, Adrian A. Maung, MD, FACS, FCCM*

KEYWORDS
 Traumatic brain injury  Management  Anesthesia  Perioperative

KEY POINTS
 Traumatic brain injury is one of the leading causes of morbidity and mortality worldwide,
especially in younger age groups.
 Long-term outcomes after traumatic brain injury are influenced by the initial medical man-
agement, including in the perioperative arena.
 Traumatic brain injury is commonly divided into primary and secondary brain injury.
Although primary brain injury occurs before medical attention at the time of the initial
trauma, secondary brain injury can be decreased through optimal evidence-based med-
ical management.
 Even brief episodes of hypotension and hypoxemia should be avoided because they have
been associated with worse outcomes. Appropriate airway management is therefore
crucial.
 An algorithmic approach should be used to maintain intracranial pressure less than
20 mm Hg and cerebral perfusion pressure between 50 and 70 mm Hg.

INTRODUCTION

Traumatic brain injury (TBI) is one of the leading causes of morbidity and mortality in
the United States. It is estimated that there are 2.5 million new TBI cases every year
in the United States alone, with an estimated economic burden of $60 billion a
year.1,2 It is also estimated that by the year 2020 TBI may surpass many diseases
as the leading cause of death worldwide because of the increasing use of motor ve-
hicles in developing countries.3

Conflicts of Interest: None.

Disclosures: None.
a
Section of General Surgery, Trauma & Surgical Critical Care, Department of Surgery, 330 Cedar
Street, BB 310, New Haven, CT 06510, USA
* Corresponding author.
E-mail address: [email protected]

Anesthesiology Clin - (2016) -–-

http://dx.doi.org/10.1016/j.anclin.2016.06.009 anesthesiology.theclinics.com
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2 Bhattacharya & Maung

TBI can vary in a spectrum of significance ranging from mild concussions with no
long-term sequelae to severe nonsurvivable injuries. Although the outcome after TBI
depends on the severity of the original injury, the initial and subsequent medical
care can significantly affect the ultimate recovery. Health care practitioners providing
anesthesia to patients with TBI in the operating room can influence the eventual
outcome, which may not be apparent for months or even years after the encounter,
by providing optimal evidence-based medical management that prevents additional
brain injury.

CLASSIFICATION

The severity of TBI can classified by a quick and reproducible neurologic examination:
the Glasgow Coma Scale (GCS). The GCS score is based on 3 components (1) eye
opening, (2) verbal communication, and (3) motor function (Table 1). Patients can
score a minimum of 1 point on each section with a minimal total score of 3 and a
maximal score of 15. Intubated patients are distinguished by adding the suffix T and
can only have a maximum score of 11T because of the inability to verbally communi-
cate. The GCS stratification can be used to triage patients to the appropriate level of
trauma system activation and can also help guide work-up based on the likelihood of
TBI. TBI with a GCS score of 3 to 8 is classified as severe, 9 to 12 as moderate, and 13
to 15 as mild. According to advanced trauma life support guidelines, patients with a
GCS of 8 or less should be intubated for airway protection.4
However, the GCS score has been criticized for interuser variability, which may be
experience dependent.5–7 Confounding factors, such as facial trauma, intoxication,
and intubation, may also diminish the reliability of its tabulation.8 Despite these limita-
tions, GCS score has been shown in multiple studies to be a valid prognosticator of
survival and outcome.9–14

Table 1
GCS score

Eye Opening
Spontaneous 4
In response to speech 3
In response to pain 2
None 1
Verbal Response
Oriented 5
Confused 4
Inappropriate words 3
Incomprehensible sounds 2
None 1
Motor Response
Obeying 6
Localization to pain 5
Withdrawing in response to pain 4
Flexor response (decorticate) 3
Extensor response (decerebrate) 2
None 1
 Anesthesia for TBI 3

TBI is a broad term that represents a variety of 1 or more pathologic injuries identi-
fied on head computed tomography (CT) (Table 2). Some anatomic injuries are not
readily seen on CT scans and require MRI imaging; in particular, diffuse axonal injury,
which has been associated with worse functional prognosis.15,16

PATHOPHYSIOLOGY

The disorder in TBI is commonly considered to be caused by 2 separate but related

events: primary and secondary injury. Although primary brain injury occurs at the
time of the initial trauma as a result of the external forces being transmitted to the intra-
cranial structures, secondary brain injury occurs hours to days after the injury, partly
because of histopathologic and molecular changes initiated by the initial trauma.

Table 2
Various pathologic injuries in TBI

Diagnosis Disorder CT Findings Notes

Epidural hematoma Arterial bleeding Hyperdense mass Patients classically
into the space with biconvex present with a
between the inner layers. Does not lucid interval and
table of the skull cross cranial suture proceed to
and the dura lines deteriorate in
mental status
Subdural hematoma Tearing of the High-density —
bridging veins or crescentic
small arteries collection across
causing bleeding the hemispheric
into the layer convexity
between the inner
dura and the
surface of the
brain
Subarachnoid Disruption of vessels Hyperdense lesions Can also occur
hemorrhage leading to that conform to because of
bleeding in the the sulci and aneurysmal
subarachnoid cisterns rupture
space
Cerebral contusion Punctate areas of May or may not Often associated
hemorrhage and appear on initial with other injuries
necrosis CT scans
Intraparenchymal Areas of hemorrhage Hyperdense lesions in Often associated
hemorrhage in brain the parenchyma with other injuries
parenchyma
Intraventricular Hemorrhage within Hyperdense lesion Most commonly as a
hemorrhage the ventricular within the result of other
system ventricles intracerebral or
subarachnoid
hemorrhage
Diffuse axonal injury Shear injury between Not readily seen on Better seen on MRI
gray and white initial CT scan May be responsible
matter, commonly unless severe for many cognitive
as a result of deficits
sudden
deceleration
4 Bhattacharya & Maung

Episodes of hypotension and hypoxemia have also been linked with secondary brain
injury. Although the exact pathways are not fully known, inflammatory changes, cell
apoptosis, electrolyte disturbances, and tissue ischemia have been implicated along
with increased cerebral edema and intracranial pressure (ICP).
According to the Monroe-Kelli hypothesis, even though the total volume inside the
rigid skull is fixed, the volume of the individual components (blood, cerebrospinal fluid
[CSF], and brain parenchyma) can vary.17 An increase in the volume of one component
thus results in the decrease of one or both of the others. After TBI, the increased vol-
ume caused by extra-axial bleeding and/or parenchymal tissue edema is initially
compensated by a decrease in CSF volume. However, this compensation is limited,
and further increases in the space-occupying lesion result in increased ICP. As ICP in-
creases, the blood inflow into the skull is restricted, leading to tissue ischemia.

Cerebral perfusion pressure (CPP) 5 Mean arterial pressure (MAP) –ICP

The increased ICP is also transmitted to the brain parenchyma and can cause her-
niation across natural orifices, such as the foramen magnum (uncal herniation), or rigid
membranes (eg, falx). This movement can compress vital structures and lead to
further tissue injury and death. For example, uncal herniation leads to brainstem
compression, loss of the brainstem reflexes, and death.

PREVENTION OF SECONDARY INJURY

Primary brain injury can only be mitigated through injury prevention and engineering of
safety equipment. Medical management of TBI therefore focuses on preventing sec-
ondary injury to viable brain tissue by controlling ICP and ensuring adequate perfusion
and oxygen delivery as well as preventing other commonly associated complications.
Both hypotension and hypoxemia have been associated with increased morbidity and
mortality in TBI.18–22

INTRACRANIAL PRESSURE/CEREBRAL PERFUSION PRESSURE MANAGEMENT

The Brain Trauma Foundation published evidence-based Guidelines for the Manage-
ment of Severe Traumatic Brain Injury in 2007.23 The management, whether in the
intensive care unit or in the operating room, includes maintaining appropriate cerebral
blood flow and oxygenation to avoid secondary brain injury. In the past, this therapy
was directed toward the management of ICP but more recently there has been a shift
toward a strategy of also maintaining adequate CPP (Box 1). ICP monitoring is used to
guide both strategies; however, a recent randomized multicenter trial (BEST:TRIP
[Benchmark Evidence From South American Trials: Treatment of Intracranial Pres-
sure]) and a published meta-analysis have raised concerns that intensive ICP moni-
toring does not provide additional benefits.24,25
Common targets of TBI management are maintaining ICP less than 20 mm Hg and
cerebral perfusion pressure between 50 and 70 mm Hg.23 Aggressive therapy to in-
crease CPP to more than 70 mm Hg has been linked to increased incidence of acute
respiratory distress syndrome and other adverse events. Brain tissue oxygen tension
monitoring can also be used as a marker for resuscitation with a treatment threshold of
an oxygen tension level less than 15 mm Hg.23,26
Initial management to decrease ICP includes simple techniques to promote cerebral
venous drainage by head-of-bed elevation to 30 as well as keeping the neck in a
neutral position and ensuring that the cervical collar is not too tight. Reverse Trende-
lenburg position can be used intraoperatively if head-of-bed elevation is not feasible.27
 Anesthesia for TBI 5

Box 1
Management strategies for increased ICP

 Elevate head of bed more than 30 (be aware of any spinal precautions)
 Position head midline
 Ensure that the cervical collar is not too tight and no occlusive dressings are present that may
impair venous drainage
 Implement appropriate sedation and analgesia
 Propofol drip
 Fentanyl drip
 Titrate to Richmond Agitation-Sedation Scale 4 to 5
 Hyperosmolar therapy
 Monitor serum Na and osmolality
 Mannitol: bolus of 0.25 to 1 g/kg (avoid in hypotensive patients)
 3% sodium chloride: bolus of 250 mL over 30 minutes via central access
 23.4% sodium chloride: 30 mL over 15 minutes via central access
 CSF drainage via an external ventricular drain
 Increase MAP with pressors to maintain CPP (50–70 mg Hg)
 Surgical management
 Evacuation of extra-axial blood collections
 Decompressive craniectomy

Sedation is often used to reduce ICP and cerebral metabolic demand as well as to
blunt the effects of tachycardia and hypertension. Propofol is commonly used in the
intensive care setting because of its quick onset and short duration of action, which
facilitates frequent neurologic assessment. However, there is no conclusive evidence
that one agent is more efficacious than another in improving Glasgow Outcome Scale
scores, mortality, ICP, or CPP.28,29 Propofol has also been associated in rare in-
stances with propofol infusion syndrome; risk factors for this syndrome include young
age, TBI, high doses, and prolonged (>48 hours) use.30 Sedatives may also induce hy-
potension and cerebral vasodilation and thus exacerbate cerebral hypoperfusion. Bar-
biturates have been traditionally used as third-line agents for refractory intracranial
hypertension to induce barbiturate coma but there is no clear clinical evidence to sup-
port this practice.31 High-dose barbiturates also cause hypotension in more than 25%
of patients.
Hyperosmolar medications can decrease ICP by creating an osmolar gradient that
draws water across the blood-brain barrier into the intravascular space and thus de-
creases the interstitial volume. Commonly used agents include mannitol and hyper-
tonic saline. Although definitive data are lacking, hypertonic saline has been
observed in small trials to have some advantage compared with mannitol in reducing
ICP and improving outcomes.32 In addition to the osmolar effect, mannitol may also
promote cerebral blood flow by temporarily reducing blood viscosity. It is generally
dosed 0.25 to 1 g/kg every 4 to 6 hours but becomes less effective with repeat dosing.
Serum osmolality should be measured serially during mannitol therapy to maintain it at
less than 320 mOsm/L and caution should be used in hypovolemic patients because
of its diuretic effects. Hypertonic saline is available in a variety of concentrations
(1.5%–23.4%) with concentrations 3% or higher requiring administration via central
venous access. Bolus administration seems to be superior to continuous infusion.32
Although the ideal serum sodium concentration is not well established, clinicians
commonly target levels of 150 to 160 mEq/L. The effects of intravascular
6 Bhattacharya & Maung

administration of hyperosmolar agents changes in the presence of a rupture in the

blood-brain barrier, which is frequently present in patients with TBI.
Mechanical ventilation should be adjusted to prevent hypoxemia and maintain nor-
mocarbia (goal PaCO2 35–40 mm Hg). Both hypocarbia and hypercarbia can have
deleterious effects. Hyperventilation induces cerebral vasoconstriction, resulting in
not only decreased ICP but also decreased cerebral blood flow leading to secondary
ischemia and worse outcomes.33 It can be used briefly as a temporizing measure in
patients with evidence of herniation while other therapies are being implemented.
Although decreasing ICP is first-line therapy, hemodynamic support with pressors is
sometimes used to maintain CPP by increasing the MAP. Norepinephrine is the
preferred agent because of its hemodynamic profile, although it may cause reflex
bradycardia.34 However, artificial increase of CPP to more than 70 mm Hg has been
linked with increased complications and is not recommended.
Hypovolemia should be corrected before the initiation of pressors. Isotonic normal
saline should be used because hypotonic saline can exacerbate cerebral edema and
the use of albumin in patients with TBI may be harmful as well.35 In patients with poly-
trauma, hypovolemia may be caused by acute blood loss. Patients with acute blood
loss anemia should be transfused with blood products to correct hemorrhagic hypo-
volemia and may require procedures to stop the source of ongoing hemorrhage.
Transfusion triggers for critically ill patients are typically hemoglobin level less than
7 g/dL and patients with TBI do not seem to have improved neurologic outcome if
transfused to a higher hemoglobin target.36,37
In addition to the medical therapy described earlier, several surgical options may be
appropriate in the management of TBI. CSF drainage via an external ventricular drain,
which can be placed at the bedside in the intensive care unit, can be used to reduce
ICP; continuous rather than intermittent drainage of CSF may be more effective.38 Sur-
gical drainage of space-occupying extra-axial lesions such as subdural or epidural he-
matomas also decreases ICP. Decompressive craniectomy, an operation in which a
portion of the skull is removed to allow the brain to herniate outward, has been
used for some patients with uncontrolled intracranial hypertension. A randomized trial
(DECRA [Decompressive Craniectomy] trial) published in 2011, which showed
decreased ICP but more unfavorable outcomes in the decompressive craniectomy
group, has stimulated extensive discussion regarding the proper role of this proce-
dure.39 However, the DECRA trial had significant limitations and has left many ques-
tions unanswered; questions that may be answered by another trial of 400 patients
that has recently completed enrollment.40

MONITORING DEVICES

Various technologies are available to assist in ICP/CPP management. ICP can be moni-
tored through 2 categories of devices. One type, which is commonly referred to as bolt,
is only able to measure the pressure, whereas a second type (ventriculostomy, or
external ventricular drain) is able to both measure ICP and also drain CSF as a therapeu-
tic maneuver to decrease the ICP. The Brain Trauma Foundation recommends that all
patients with salvageable severe brain injury (GCS 3–8) with a CT scan abnormality
should have an ICP monitor.23 However, this recommendation is controversial because
studies have questioned whether ICP monitoring improves outcomes.41–44
Continuous or intermittent jugular venous oximetry can be used as a surrogate for
cerebral oxygen use. A catheter is placed retrograde into the jugular vein with the
tip at the jugular bulb (level of the mastoid on a plain film). The blood obtained at
this level is a sample of mixed cerebral blood. Jugular venous oxygen saturation is
 Anesthesia for TBI 7

an indirect measure of the balance between cerebral blood supply and metabolic de-
mand. Normal jugular venous oxygen saturation is 60% to 70%. A decrease in the
saturation suggests an imbalance between oxygen delivery and oxygen demand
(the brain has to extract more oxygen to compensate for the deficiency in the delivery).
This condition may arise from a variety of causes, including hypotension, vasospasm,
increased ICP, decreased CPP, and/or cardiopulmonary insufficiency.45 There are
several limitations with the use of jugular venous oximetry, including sampling errors
from either catheter malposition or possible nondrainage from infarcted territories. A
high incidence of false-positive desaturation episodes has also been observed in
studies.46
Near-infrared spectroscopy (NIRS) is a noninvasive cerebral oxygen monitoring
technique. Near-infrared wavelengths of light are able to penetrate the skull and are
absorbed differently by oxygenated and deoxygenated hemoglobin as well as cyto-
chrome aa3 within brain parenchyma. Their relative concentrations can therefore be
measured by using spectroscopy applied to the forehead. NIRS has been reported
to be more sensitive in detecting episodes of jugular venous desaturation compared
with jugular oximetry.47 However, the accuracy of NIRS can be limited by brain tissue
edema and inaccuracies in distinguishing oxygenation changes in intracranial versus
extracranial tissues. Studies of outcomes of the use of tissue oxygenation versus ICP
monitors have provided mixed results.48–50
Brain tissue oxygenation monitoring is an invasive approach to monitoring the brain
tissue oxygen partial pressure by introducing a catheter into brain parenchyma via a
surgical site or a bolt. Research to validate this technique is ongoing. A more elaborate
way to monitor the metabolic state of the brain is to measure metabolites of the brain
via microdialysis. A catheter is introduced into the parenchyma and perfused with a
physiologic solution. Numerous metabolites such as glucose, lactate, pyruvate, in-
flammatory markers, and neurotransmitters can be measured using this technique.
The ratio of metabolites, in particular the lactate/pyruvate ratio, has been shown to
correlate with severity of injury.45

INTRAOPERATIVE MANAGEMENT

Patients with TBI commonly require operative management of other concomitant

injuries and occasionally of the brain injury. A well-planned and well-executed intra-
operative anesthetic management is crucial to avoid secondary brain injury. An
early secure airway is essential to maintain adequate oxygenation. Patients with
trauma who require emergent intubation for depressed GCS or emergent operative
intervention should undergo rapid sequence intubation. All patients with trauma
should be assumed to have unstable cervical injuries and a full stomach until
proved otherwise. Patients should be intubated by maintaining a manual inline sta-
bilization of the cervical spine. The need for a difficult airway algorithm should be
anticipated, especially in patients with facial or neck trauma. Nasal tubes (endotra-
cheal or gastric) should be avoided in patients with skull base fractures or
coagulopathy.
Induction is usually performed with etomidate to avoid hypotension, although there
are concerns for possibly inducing adrenal insufficiency.51 Other agents, such as pro-
pofol and thiopental, should be used with caution, especially in hypovolemic or hypo-
tensive patients, because of their suppressive effect on the cardiovascular system.
Ketamine has traditionally been avoided in patients with TBI because of its ability to
increase cerebral blood flow and thus increase ICP. However, more recent studies
have challenged this dictum.52 Short-acting paralytic agents are usually chosen for
8 Bhattacharya & Maung

intubation. Hypotonic fluids should be avoided, as discussed earlier, because they can
worsen cerebral edema.
All volatile agents decrease cerebral oxygen metabolic rate but may cause cerebral
vasodilation and increased ICP, although the effect is likely to be low at concentrations
less than 1 minimum alveolar concentration.53 Nitrous oxide should be avoided
because it is a cerebral vasodilator and may increase ICP. Certain anesthetic agents
may be beneficial in TBI. Isoflurane has been shown in animal studies to have a neuro-
protective effect by inhibiting the apoptosis cytokine cascade.54,55 Similarly, other an-
imal studies have shown a theoretic benefit of xenon as a general anesthetic by acting
as an N-methyl-D-aspartate (NMDA) antagonist that prevents ischemic and excitotoxic
injury.56 Other more conventional agents also have purported benefits in the setting of
TBI. Propofol may act as a cerebral protector because of its ability to suppress brain
electrical activity and preserve cerebral pressure autoregulation. In addition, it may
also act as an antioxidant agent that protects against additional neuroinjury.

PERIOPERATIVE CARE

Anesthesia teams caring for patients with TBI should also be aware of the other ther-
apies that may be used in this population.

Seizures
Up to 30% of patients with severe TBI develop early (within 7 days) posttraumatic sei-
zures. Prophylactic antiepileptic drugs have been shown to reduce the incidence of
the early, but not late, seizures. Common regimens include a 7-day to 14-day course
of phenytoin or levetiracetam. Development of seizures can cause an increase in ce-
rebral metabolism, which, coupled with the increase in ICP and decreased cerebral
blood flow, can exacerbate secondary brain injury.23 Treatment of seizures is similar
to the management in patients without TBI.

Endocrine
Both hyperglycemia and hypoglycemia have been associated with worse outcomes
after TBI.57 Hyperglycemia has been shown to contribute to metabolic acidosis and
increased oxidative radicals that ultimately lead to neuron death. However, intense
glucose therapy (goal, 80–120 mg/dL) has become contentious because it has been
linked to increased incidence of hypoglycemic episodes.58 Current recommendation
for critically ill patients in general is to target a glucose level less than 180 mg/dL,
but this may vary depending on the patient population as well as the presence of pre-
existing diabetes.59,60 Both intermittent and continuous insulin infusion can be used,
depending on the glucose levels.
Although glucocorticoids have been used in the past for the treatment of TBI, more
recent studies have shown that steroids in this population are associated with more
harm than benefit. The CRASH (Corticosteroid Randomization After Significant
Head Injury) trial, which randomized 10,008 patients with TBI to 48 hours of steroids
or placebo, revealed an increased risk of death in the steroid group at 2 weeks (Rela-
tive Risk [RR], 1.18) and 6 months (RR, 1.15) independent of injury severity.61,62

Hematological
Patients with trauma are at an increased risk for developing venous thromboembo-
lisms; however, the presence of TBI may represent a relative contraindication to phar-
macologic prophylaxis because of concerns for potentially exacerbating the bleeding.
There is currently wide variability in clinical practice in the timing and use of
 Anesthesia for TBI 9

pharmacologic venous thromboembolism prophylaxis. Patients with TBI may also be

on antiplatelet and/or anticoagulation agents before injury, and TBI may induce coa-
gulopathy that will need to be corrected in the perioperative state. Although anemia
is common in severely injured patients with trauma, including those with TBI, transfu-
sion of red blood cells above a hemoglobin of 7 g/dL has been associated with an
increased incidence of adverse events without any improvement in neurologic
outcomes.37
In the setting of TBI, patients who are on antiplatelet or anticoagulation therapy for
cardiovascular comorbidities may require quick and effective reversal of the agents. In
addition to warfarin, clinicians are now encountering more patients who are anticoa-
gulated with newer-generation factor Xa inhibitors and direct thrombin inhibitors.
Although these drugs are more convenient for patients because they do not require
blood level monitoring, the activity of these drugs cannot be quantified by routine he-
matologic laboratory tests and readily available antidotes are just coming on the mar-
ket. Fresh frozen plasma, which is the mainstay for the reversal of warfarin, is not
beneficial in the reversal of the factor Xa inhibitors. Administration of prothrombin
complex concentrate may have some utility in the reversal of these agents. The direct
thrombin inhibitor is renally excreted and emergent dialysis has been used in in-
stances of life-threatening hemorrhage. A direct inhibitor for dabigatran was approved
by the US Food and Drug Administration in October 2015.

Pharmacy
Agitation and delirium are common after TBI and often require multimodal therapy,
including narcotics, benzodiazepines, antipsychotic agents, clonidine, methadone,
and/or dexmedetomidine. b-Blockers, most commonly propranolol, are used not
only for their sedative effects but also to block excess catecholamines. Their admin-
istration has been linked to improved survival and outcomes.63,64 A course of aman-
tadine, a weak antagonist of the NMDA-type glutamate receptor used in Parkinson
disease and for the treatment of influenza (before the development of widespread
resistance), has also been shown to accelerate functional neurologic recovery.65

Temperature Management
Temperature should be carefully controlled because hyperthermia increases cerebral
metabolism and possibly aggravates secondary brain injury. Management strategies
include antipyretic medications, external surface cooling devices, as well as endovas-
cular temperature management catheters.
Therapeutic hypothermia has shown promise in improving neurologic outcomes in
patients following cardiac arrest. It was therefore hypothesized that therapeutic hypo-
thermia may also benefit the traumatically injured brain by slowing the inflammatory
cascade following injury, thus preventing reperfusion injury and directly decreasing
ICP. Although studies have shown the ability of induced hypothermia (32 C–35 C)
to reduce ICP, it does not seem to have any significant outcome benefit to patients
with TBI and has increased risk of infectious complications.66 The currently available
studies that have shown improved outcomes are of low quality67 and thus induced hy-
pothermia in patients with TBI currently should be reserved for research studies.66,68

MULTIPLE INJURED PATIENTS WITH TRAUMA AND PRIORITIES OF SURGERIES

Patients with severe TBI often have other injuries that may require operative interven-
tion. Life-threatening intra-abdominal or intrathoracic bleeding typically take prece-
dence over neurosurgical interventions, although ideally the 2 teams (eg, trauma
10 Bhattacharya & Maung

and neurosurgery) would perform simultaneous operations. If the patient has intracra-
nial hypertension, limb-threatening injuries should be addressed with abbreviated
damage-control operations rather than definitive repair. Less urgent procedures,
especially if they may potentially result in significant blood loss or hypotension, should
be postponed. The overall goal is to balance the need for the surgical procedure with
the risk of inducing secondary brain injury.

SUMMARY

TBI represents a wide spectrum of disease and disease severity. Because the primary
brain injury occurs before the patient enters the health care system, medical interven-
tions seek principally to prevent secondary injury. Anesthesia teams that provide care
for patients with TBI both in and out of the operating room should be aware of the spe-
cific therapies and needs of this unique and complex patient population.

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