Neurocrit Care
DOI 10.1007/s12028-017-0461-0
Emergency Neurological Life Support: Severe Traumatic Brain
Injury
Rachel Garvin1 • Halinder S. Mangat2
 Neurocritical Care Society 2017
Abstract Severe traumatic brain injury (TBI) causes sub-
stantial morbidity and mortality, and is a leading cause of
death in both the developed and developing world. The
need for a systematic evidence-based approach to the care
of severe TBI patients within the emergency setting has led
to its inclusion as an Emergency Neurological Life Support
topic. This protocol was designed to enumerate the practice
steps that should be considered within the first critical
hours of neurological injury from severe TBI.
Keywords Severe traumatic brain injury
Neurotrauma

Neurocritical care
Emergency
Introduction
The Centers for Disease Control (CDC) estimates that
approximately 2.5 million people sustain a traumatic brain
injury (TBI) each year in the United States. Of these
individuals, 283,000 are hospitalized and 52,000 die, con-
tributing to a third of all injury-related deaths. 5.3 million
individuals are living with TBI-related disability [1–3].
Worldwide, TBI is the leading cause of death and disability
for children (>1 year old) and young adults. Motor vehicle
accidents, falls, and blunt injuries account for the largest
portion of TBI in civilian populations in the U.S [4]. In
2010 the economic cost of TBI was estimated to be $76.5
& Rachel Garvin
doctorgarvin@gmail.com; garvinr@uthscsa.edu
Halinder S. Mangat
hsm9001@med.cornell.edu
1
UT Health San Antonio, San Antonio, TX, USA
2
Weill Cornell Medical College, New York, NY, USA
billion, 90% of which was spent on hospital care of patients
with TBI [5].
In patients who survive their initial traumatic event, a
cascade of secondary injury occurs and can be a major
determinant of clinical outcome. Secondary injury occurs
on both a microscopic cellular level (e.g., as a result of
hypoxemia) and a macroscopic level (e.g., mass effect from
a subdural hematoma). The goals of severe TBI manage-
ment are treatment of surgical injuries, prevention and
early detection of secondary injury, and then institution of
therapeutic means to mitigate and reverse further injury
caused by hypoxia, ischemia (due to hypotension or
hypocarbia), developing hematomas, seizures and
intracranial hypertension.
The ENLS suggested algorithm for the initial manage-
ment of traumatic brain injury is shown in Fig. 1.
Suggested items to complete within the first hour of eval-
uating a patient with traumatic brain injury are shown in
Table 1.
Traumatic Brain Injury: Diagnosis
and Classification
TBI is defined as an alteration in brain function or other
evidence of brain pathology caused by an external force
[6]. The diagnosis of TBI then is based on identifying a
mechanism consistent with TBI and/or physical signs of
trauma in a patient with neurological signs or symptoms.
TBI patients are evaluated using the Glasgow Coma Scale
(GCS), [7] and severe TBI is diagnosed in a patient with
GCS score <9. The physical findings (e.g., scalp lacera-
tion, depressed skull fracture) and the mechanism of injury
(e.g., fall from a height, high speed motor vehicle accident)
are key to anticipating the extent of injury for each patient.
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Fig. 1 Traumatic Brain Injury Algorithm
Table 1 Traumatic Brain Injury checklist for the first hour
Checklist
h Secure airway
h Keep SBP >90 mmHg and O2 saturation >90%
h C-spine precautions
h Head CT
h Treat herniation
h Neurologic examination
A neurological evaluation is an integral component of
initial evaluation of a patient who has suffered trauma or is
unable to coherently express oneself. Since acute car-
diorespiratory insufficiency may also affect neurological
status, a GCS score must be recorded following full
resuscitation, but prior to administration of any sedative or
paralytic agents. The best score possible should be given.
For example, if the patient follows commands with the
right upper extremity but only withdraws with the left
upper extremity, a score of 6 for motor should be given.
The GCS score should be recorded frequently during
transport and resuscitation, as well as in the emergency
department and intensive care unit, to identify worsening or
improvement over time. When the mechanism of injury is
not clear or history is lacking, non-traumatic causes of
decreased level of consciousness (LOC) must be consid-
ered, especially if appropriate neuro-imaging does not
match the clinical exam.
Information gathered at the scene and from witnesses
and companions by pre-hospital personnel may be helpful
in confirming and determining the mechanism of TBI.
Patients involved in single motor vehicle accidents and
those without significant signs of external trauma may raise
suspicion for other non-traumatic causes of decreased
LOC. For example, a patient may have sustained a TBI
after a stroke, seizure, or intracranial hemorrhage. Causes
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of altered LOC that are reversible in the field may include
airway obstruction, hypoxia due to pneumothorax or aspi-
ration, hypoglycemia, and drug or alcohol intoxication.
Pre-hospital Care
The pre-hospital management of TBI patients by trained
paramedical personnel is critical to outcome. Fifty percent
of deaths from TBI occur within the first few hours of
injury [4]. Basic life support maneuvers are directed at
establishing and maintaining a patent airway, achieving
adequate ventilation and oxygenation, ensuring adequate
circulation, and stabilization of the cervical spine (C-spine)
[8]. If any of these are compromised, secondary injury
proceeds at an accelerated pace, and the risk of mortality
increases.
Balancing the priorities of expeditious transport to a
trauma center and the provision of best resuscitative mea-
sures in the field remains a priority. National paramedic
standards call for expedited transport with treatment en
route. The largest pre-hospital study to compare the
effectiveness of advanced life support (ALS) to basic life
support (BLS) is the Ontario Pre-hospital Advanced Life
Support (OPALS) study. This study compared a large
population of patients before and after the implementation
of ACLS in pre-hospital care. No improvement was
detected in the outcomes of trauma patients subsequent to
the addition of ACLS transport [9].
The limited studies available suggest that the perfor-
mance of advanced invasive procedures in the field or
during transport, in particular, endotracheal intubation,
may worsen outcomes in some patients. Most studies that
examine pre-hospital intubation are retrospective and suf-
fer from selection bias (i.e., the patients that are intubated
are likely sicker, making intubation seem deleterious). A
recent meta-analysis published in 2015 examined mortality
in adult severe TBI patients who were intubated in the
field, and demonstrated that endotracheal intubation by
inexperienced providers was associated with increased
rates of mortality up to two-fold compared to providers
with significant intubation experience [10]. It is clear
however, should pre-hospital intubation be attempted, it be
performed by experienced practitioners in a way that does
not substantially increase field time.
The use by pre-hospital personnel of paralytic medica-
tions in the field to facilitate endotracheal intubation in
patients with head injuries has received considerable
attention. There are numerous case series of successful
advanced airway management by paramedics and nurses in
tightly regulated and highly specialized systems. However,
the best data comes from a large, controlled trial on field
rapid sequence intubation (RSI) that was performed
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including a variety of ground based paramedic units. When
compared to historical controls, patients who received RSI
for intubation in the field had a higher rate of mortality and
a decreased likelihood of a favorable neurological outcome
than historical controls. The study involved mostly rapid
transport times in urban areas, and the paramedics included
received a limited amount of training in RSI [11]. Analysis
of field records from this study revealed that RSI doubled
scene time from 13 to 26 min. Oximetry and capnography
records revealed that prolonged episodes of hypoxemia,
hypercapnia and hypocapnea, often lasting several minutes,
were associated with field RSI. These observations may
explain the poor outcomes in the RSI cohort and the con-
ditions present in this study may not adequately represent
the expertise or capability of many pre-hospital systems.
With continued concerns about the safety of prehospital
intubation in trauma, there has been a renewed focus on
supraglottic devices, which are easier and faster to place.
These have been adopted in many EMS systems as either a
primary or rescue airway device when conventional
endotracheal intubation has failed or in lieu of endotracheal
intubation as they can be placed rapidly. A recent sys-
tematic review of the prehospital literature concluded there
are no statistically significant differences in patient ori-
ented outcomes between patients managed with alternative
airway devices and with field attempts at conventional
endotracheal intubation [12]. However, clear clinical trial
data is lacking.
Hypotension in the field disproportionately worsens
outcome in trauma patients with TBI, hence aggressive
fluid administration is indicated in TBI patients with shock
[13]. Systolic blood pressure should be maintained at a
minimum of 100 mmHg. For patients ages 15–49 years or
>70 years, SBP > 110 mmHg is the goal [14]. However,
a recent study has also highlighted that mortality
improvement may not be related to a single threshold point
and was inversely related to systolic blood pressure across
a large range (40–119 mmHg) [15].
Normal saline is the preferred solution for initial
resuscitation. Hypertonic saline (HTS) has been studied
extensively as a resuscitation fluid in patients with TBI.
HTS is theoretically ideal in TBI patients with multiple
injuries, as it is both an effective volume expander and
capable of decreasing brain edema. However, it has not
been shown to decrease mortality or improve neurological
outcome in a randomized, controlled trial in patients with
severe TBI and hypotension when HTS was used during
prehospital care [16].
ENLS Recommendations for Pre-hospital Care
Airway
Basic and advanced airway management by experienced
personnel is indicated to maintain oxygen saturation
greater than 90%.
In the patient who is breathing spontaneously, the air-
way should be monitored while maintaining spinal
stabilization. Supplemental oxygen should be delivered if
required by face-mask. If easily tolerated (considering
C-spine precautions), insertion of an oral airway device is
helpful to prevent the tongue from occluding the airway.
The use of paralytics to assist endotracheal intubation in
the pre-hospital setting is only recommended for personnel
specially trained in rapid sequence intubation. In situations
where transport times will be short, endotracheal intubation
may not be preferred. If more airway support is needed,
supraglottic airway devices, such as an LMA (laryngeal
mask airway), can be used until a definitive airway can be
established.
Breathing
Normal breathing should be maintained with goal pCO2 of
35–40 mmHg. End-tidal CO2 (ETCO2) can be used for
monitoring in the pre-hospital environment. If there are
clinical signs of herniation (e.g. unilateral or bilaterally
dilated pupil), then hyperventilation (ETCO2 28–35 mm
Hg) can be used as a temporary measure (until signs of
herniation resolve or until further assessment by emer-
gency room personnel). If ETCO2 is not available and
patient is receiving assisted ventilation (i.e. with bag valve,
endotracheal tube or supraglottic airway), goal respiratory
rate should be 10–14 breaths/min. Oxygenation via pulse
oximetry, should be monitored continuously with a goal
SaO2 of >90%. Supplemental oxygen should be used as
needed to maintain this parameter.
Circulation
Adequate blood pressure (BP) needs to be maintained in
order to keep an appropriate cerebral perfusion pressure
(CPP), as hypotension contributes to secondary brain
injury. For adults, maintain systolic BP > 100 mmHg. For
children, systolic BP should be maintained >5th percentile
for age (70 mmHg + age X 2). Hypotensive patients
should be treated with rapid infusion of isotonic fluids
(20–40 ml/kg of normal saline). Hypotonic fluids, such as
D5W or ‘ NS should be avoided, as they may exacerbate
brain edema.
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Additional Parameters
In-line spinal stabilization should be maintained until the
spine is cleared of injury. Blood glucose should be checked
and hypoglycemia (blood glucose <60 mg/dl) should be
treated with dextrose (25 gm dextrose, either Dextrose 10
or 50% IV push in adults and 0.5 gm/kg of dextrose 10% in
children). Assess and re-assess GCS frequently during the
resuscitation process for improvement or worsening. Pupils
should be monitored frequently throughout the resuscita-
tion. Pupil asymmetry is defined as >1 mm difference in
diameter. An unreactive pupil is defined as <1 mm
response to bright light. Eye, scalp and facial trauma may
mimic or mask the signs of herniation and should be
considered in each case.
Initial Emergency Department/Hospital
Management
Upon arrival to the emergency department (ED), the major
priorities from the field are maintained: maintenance of
airway, breathing and circulation are performed first, fol-
lowed by assessment of neurologic status and avoiding
hypothermia (ABCDE trauma evaluation). Secondary sur-
vey and further imaging must wait until the patient is
stabilized. A GCS score should be evaluated and docu-
mented. Blood glucose should be assessed and c-spine
stabilization should be maintained.
Airway
Although a GCS score B8 during the initial evaluation is
an indication for endotracheal intubation, severe extra-
cranial injuries, agitation, intoxication or a risk for
declining mental status are also indications. Rapid
sequence intubation (RSI) should be used to optimize first
pass attempt. RSI drugs should be chosen carefully as
certain drugs, such as propofol, can profoundly drop blood
pressure. Induction agents such as etomidate or ketamine
may be more appropriate choices. Patients must be pre-
oxygenated initially with 100% oxygen and then titrated to
maintain SaO2 > 90%. In addition to pulse oximetry and
electrocardiography (ECG) monitoring, capnography is
extremely helpful to guide cerebral resuscitation. However,
it must be understood that capnography often underesti-
mates actual paCO2. An increase in ventilatory dead space
results in lower capnography readings. This physiology is
often present in critically ill patients and those with low
cardiac output.
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Circulation
In patients with multiple injuries, hemostasis should be
made an initial priority. Two large bore intravenous can-
nulae should be inserted. An intraosseous (IO) cannula can
be used if there is difficulty with intravenous access. In the
adult, systolic BP should be kept >100 mmHg and in the
child, the goal systolic BP should be >5th percentile for
age (70 mmHg + age in years X2). For infants 12 months
and younger, a goal systolic BP of >60 mmHg is rec-
ommended. Avoidance of hypotension is particularly
important in the first 6 h post-injury [11]. Even mild
decreases in blood pressure in children (SBP < 75% per-
centile for age) have been associated with risk of poor
outcome [17]. A FAST exam can be performed to evaluate
for possible internal hemorrhage. Evaluation for coagu-
lopathy should be part of standard laboratory tests, and
anticoagulant reversal should be administered if required.
The initial resuscitation may be followed by more defini-
tive therapy in the operating room or procedural suite for
exsanguinating injuries.
Immediate surgical intervention for life-threatening
systemic hemorrhage may mean that neuroimaging is not
performed initially. Emergency neurosurgical procedures,
such as ventriculostomy, may, in some cases, be performed
concurrently with other life-saving measures.
Imaging
Head computed tomography (CT) remains the emergency
neuroimaging modality of choice. Despite advances in
magnetic resonance imaging (MRI) technology, CT
acquisition is much faster, is reliable in identifying surgical
lesions, and is more practical for the critically injured
patient. The primary purpose of the initial head CT is to
identify any hemorrhagic lesions that require surgery. As a
general guide, an extra-axial hematoma (extra- or subdural)
>1 cm in thickness, an intra-parenchymal hematoma
>20 cc in volume, and a >5 mm midline shift associated
with a hematoma are to be considered for surgical inter-
vention. In addition, any extra-axial hematoma in a
comatose patient with or without evidence of cerebral
herniation should be considered for surgically removal
[18–20].
Acute blood is hyperdense, but, in some patients, it may
be iso- or hypodense if the patient is coagulopathic, ane-
mic, or the CT is obtained very soon following injury.
Acute contusions can be hyperdense with admixed hypo-
density, or have a ‘‘salt and pepper’’ appearance.
Intracranial air suggests an open skull fracture, craniofacial
trauma, or injury to an air sinus. Surgical decision-making
is often guided by the amount of mass effect. Therefore, it
should be determined whether the perimesencephalic
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cisterns are open, compromised, or closed, and the degree
of midline shift at the level of the third ventricle should be
quantified. These findings are useful but not always diag-
nostic of abnormal intracranial pathophysiology [21].
Therefore, they should be interpreted with clinical findings
in mind.
The cranial vault and facial bones should be assessed for
fractures, displacement of bone fragments, or penetrating
objects. Because C-spine injuries occur in up to 10% of
head-injured patients, radiologic imaging of TBI should
include cervical-spine (C-spine) CT. The C-spine should
remain immobilized until it can be cleared from either a
radiographic or clinical standpoint by an appropriate
provider.
In some patients, the cerebral vasculature, including the
intracranial or extracranial vessels, must be imaged to
assess for injury based on mechanism or site of injury [22].
This imaging may be accomplished through CT angiogra-
phy, MR angiography or venography, or conventional
angiography in select patients. These studies should be
considered when there is:
Penetrating head injury
Fracture over a venous sinus
A neurologic deficit that is not explained by head CT scan
Select C-spine injuries (e.g., severe flexion or extension
injury or a fracture through the transverse foramen)
Petrous bone fracture
Lefort II or III facial fractures
A suspected cause for the injury (e.g., aneurysm rupture)
In addition, patients who are victims of near hanging,
have seat belt abrasions over the neck, or have soft tissue
swelling of the anterior neck should undergo vascular
imaging to exclude blunt injury to the carotid or vertebral
arteries.
Summary of Recommendations
Advanced airway management should be performed to
ensure airway protection, adequate ventilation and oxy-
genation (SaO2 > 90%) and normotension (SBP > 100
mmHg).
Oxygenation, blood pressure, cardiac rhythm and pCO2
should be continuously monitored and maintained.
Parenteral access (IV or IO) should be acquired.
Spinal precautions should be maintained at all times.
GCS and pupillary light reaction should be evaluated and
documented frequently.
Patient should be evaluated for hypoglycemia and if blood
glucose <60 mg/dl give adults D50W 50 ml IV and give
children 5 ml/kg of D10 IV.
Address immediate, life-threatening, extracranial injuries.
Evaluate and reverse coagulopathy.
Obtain and review appropriate imaging to include non-
contrast head CT, C-spine CT, in addition to imaging
related to extracranial injuries.
Obtain neurosurgical consultation for identified brain
injuries and for all trauma patients with impaired
consciousness.
Transfer
Patients with severe TBI should be transferred to a trauma
center with neurosurgical capabilities, including availabil-
ity of pediatric neurosurgical expertise for pediatric
patients. When communicating to an accepting or referring
physician about this patient, consider including the key
elements listed in Table 2.
Fundamentals of Intracranial Pressure (ICP)
and Cerebral Perfusion Pressure (CPP) Physiology
An understanding of two fundamental aspects of brain
physiology—the Monro–Kellie doctrine and cerebral auto-
regulation (CAR)—provides a framework on which to base
ICP management [23]. These are discussed in detail in the
ENLS ICP module which describes the dynamic effect of
shifting volumes of the intracranial contents (brain, blood
and CSF) on cerebral compliance and ICP.
It follows that if there is an expanding mass lesion (e.g.,
a post-traumatic hematoma), ICP will remain normal,
provided there are reductions in volume of the other
compartments. In this compensated state, the volume
increase associated with a mass lesion or edema is offset by
shifting CSF into the spinal subarachnoid space and shift-
ing venous blood out of the intracranial space. However, as
the volume of the mass lesion increases, ICP begins to
Table 2 Traumatic Brain Injury communication regarding assess-
ment and referral
Communication
h Patient age and mechanism of injury
h Pre-injury health, including home medications
h Head CT findings
h Post resuscitation GCS with detailed neurologic exam
h Completed interventions
h Focal motor findings
h Coagulation status and other pertinent laboratory findings
h Other injuries
h State of C-spine: cleared, not cleared, injury
h Current vital signs
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increase, and—once compensation is exhausted—a rapid
increase in ICP occurs. When ICP is elevated or a pressure
gradient arises, brain tissue begins to shift from areas of
high pressure to areas of low pressure.
Adequate CPP is the mainstay in maintaining cerebral
blood flow and is the difference between mean arterial BP
(MAP) and ICP (CPP = MAP - ICP). Therefore, changes
in MAP and ICP influence CPP. Though there are regional
differences in CBF, normal CBF is generally considered to
be approximately 50 mL/100 g/min. When CBF is
<30 mL/100 g/min, cerebral ischemia results, and when
CBF is <10–18 ml/100 g/min, cell death occurs. Cell
death also depends on the duration and extent of low blood
flow [24, 25].
Cerebrovascular autoregulation (CAR) refers to the
ability of the brain to maintain a constant CBF despite
variations in systemic perfusing pressures. There are sev-
eral forms of CAR: metabolic, pressure and biochemical.
Metabolic CAR maintains CBF related to cerebral meta-
bolism and is also known as the flow-metabolism coupling.
In pressure CAR, vasoconstriction or dilation of the cere-
bral arteriolar bed helps maintain constant CBF across a
broad range of perfusion pressures, believed to be
MAP 50–150 mmHg in the normal individual. However,
when CAR is absent, as may occur after severe TBI, CBF
response to MAP can become passive and can simply
parallel changes in MAP, which results in severe increases
in ICP and exacerbates ischemia. Eventually, inadequate
tissue oxygen and glucose delivery may result and when
ICP equals CPP, CBF can no longer be maintained, and
cerebral circulatory arrest occurs. Biochemical CAR refers
to CBF responses to tissue pH and CO2 and also occurs
rapidly as in hyperventilation.
In resuscitation and management, the fundamental goal
is to ensure normal ICP and adequate CPP. The Monro–
Kellie doctrine and CAR provide the framework on which
to base management. For example, if a large mass lesion is
present, surgery is required to manage ICP. Alternately,
when diffuse injury and cerebral edema are present,
osmotherapy is indicated, since much of the edema is
cytotoxic in origin [26].
Recommendations for Management of Initial
Cerebral Herniation
During the initial resuscitation of trauma, placement of an
ICP monitoring device is often impractical, but must be
carried out as soon as possible in a safe manner. Empiric
therapy for presumed raised ICP also carries risks. Pro-
phylactic hyperventilation is associated with increased
cerebral ischemia, while hypothermia has not been shown
to provide outcome benefit. Treatment of presumed
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intracranial hypertension should be reserved for patients
with evidence of intracranial hypertension which includes
dilated, non-reactive or asymmetric pupils, extensor pos-
turing or absent motor response, progressive decline in
neurologic condition (decrease in GCS score >2 points),
and Cushing’s response (increased BP, decreased pulse,
and irregular respirations). In these circumstances, empir-
ical treatment of presumptive cerebral herniation may be
necessary prior to monitor placement. Immediate measures
may include hyperosmotic therapy or hyperventilation.
Hyperosmotic Therapy
Mannitol is a sugar alcohol that acts an osmotic diuretic. A
dose of 20% mannitol 0.5–1 gm/kg may be given intra-
venously as a rapid bolus in patients with concerns for
cerebral herniation. For patients who are hypotensive,
hypertonic saline rather than mannitol can be used as it has
volume expansion properties. This may be administered
intravenously as 30 ml of 23.4% saline administered over
5–10 min or 3% NaCl (2–4 ml/kg) intravenously over
10 min; 5–10 ml/kg intravenously in children). Central
venous access is preferred for hypertonic saline due to the
high osmolarity of the solution.
Transient Hyperventilation
Target a paCO2 of 28–35 mmHg or ETCO2 of 25–30 (20
breaths/min in an adult) for a short period of time while
awaiting definitive intervention to treat cerebral herniation.
Prolonged and prophylactic hyperventilation should be
avoided.
Recommendations for CPP Maintenance
The cerebral perfusion pressure (CPP) goal is approxi-
mately 60–70 mmHg. A CPP of 45–60 mmHg may be
targeted in children, with infants in the lower end of this
range and older children and teenagers in the upper end.
If the patient has been appropriately resuscitated,
administration of a vasopressor may be indicated to
maintain cerebral perfusion. Vasopressors should not be
used to augment CPP >70 mmHg. For anemic or actively
bleeding patients, a red blood cell (RBC) transfusion can
be considered.
Physiological Targets for Goal Directed TBI Care
To facilitate management of intracranial pathology, the
following physiological parameters should be targeted as
part of goal-directed TBI care, during both resuscitation
and subsequent ICU care. However, it is important to
recognize that each patient has individual physiologic
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needs and therapeutic targets should take these circum-
stances into consideration, particularly when clinical or
monitoring evidence of secondary injury is evident.
Pulse oximetry C90%
PaCO2 35–40 mmHg
SBP C 100 mmHg
ICP < 22 mmHg
CPP 60–70 mmHg (45–60 mmHg in children)
PbtO2 C 15 mmHg
Temperature (core) 36.0–38.3 C
Glucose 140–180 mg/dL
Platelets C 100 9 103/mm3
Hgb C 7 gm/dl
In summary, during the initial phases of severe TBI
management, MAP is the most important physiological
parameter to follow as it directly influences CPP
(CPP = MAP - ICP). Other parameters should be
appropriately adjusted to optimize CPP and brain oxy-
genation. Once resuscitated, care can be guided by
placement of intracranial monitors, including ICP and brain
tissue oxygen tension (PbtO2). In adult patients, a MAP of
C80 mmHg is a reasonable goal if ICP is assumed to be
>20 mmHg. However, the optimal blood pressure levels
for brain resuscitation remain the subject of debate, and
higher targeted MAP may increase the risk of pulmonary
dysfunction.
Coagulopathy and Reversal
The occurrence of coagulopathy in TBI patients, including
those with isolated TBI, is high. Incidence approaches
40–50% in severe TBI. Coagulopathy associated with
trauma has several possible mechanisms, but in TBI and
isolated TBI, the principal process involves tissue factor
(TF) release. Several factors, such as increased age,
hypotension at the scene of injury, a low GCS (B8), injury
severity score (ISS) C16, severity of TBI reflected by the
head abbreviated injury score (AIS), intraparenchymal
lesions, penetrating injury, and base deficit are associated
with TBI coagulopathy [27–29]. In industrialized countries,
approximately 1% of the population receives anticoagula-
tion with warfarin and increasing numbers of patients are
taking novel oral anticoagulants (NOACs). Therefore,
many TBI patients may have a pharmacological cause of
coagulopathy. Many more adults take antiplatelet agents,
such as aspirin or clopidogrel. Alcohol abuse and nutri-
tional status can also affect coagulation parameters
Coagulopathy may compound secondary brain injury by
allowing expansion of intracranial injury. The presence of
coagulopathy is an independent factor associated with the
evolution of intracranial hematomas and with poor out-
come. In addition, the presence of a coagulopathy can
affect the appearance of an acute intracranial hemorrhage
on head CT (i.e., it may appear hypo- or isodense rather
than hyperdense, or a fluid level will be present). Identifi-
cation of a pre-existing or rapidly acquired coagulopathy is
important in the first critical hour and during the remainder
of the hospital stay [30].
Laboratory measures of prothrombin time (PT)/
INR/partial thromboplastin time (PTT), platelet counts and
fibrinogen levels should be routine in neurotrauma. If
available, thromboelastography (TEG) can also be used as
a dynamic assessment of coagulopathy. At present, some of
the NOACs do not have antidotes. Nonetheless, some
trauma centers have advocated use of prothromin complex
concnetrates (PCCs) for patients known to be taking
NOACs. Regardless, it is important to know whether a
patient has taken such agents, as this may alter surgical
options or lead to more diligent hemostasis. The Pharma-
cotherapy module outlines an appropriate approach to
coagulopathy and anti-platelet medication reversal.
Recommendations
Seizure Prophylaxis
Seizures that occur after head injury may be classified as
early (within 7 days of TBI) or late (occurring >7 days
after head injury). Early post-traumatic seizures (PTS)
should be prevented. Particularly during the acute phase, a
seizure can cloud the neurologic evaluation, aggravate
intracranial pathology, and in some patients, be the pre-
cipitating event that leads to herniation. Patients may have
convulsive and/or non-convulsive seizures.
Prolonged seizures (>30 min) can cause secondary
cerebral injury. Convulsive PTS occur in approximately
5% of patients admitted to hospital with closed head
injuries and in 15% of those with severe TBI. The inci-
dence of PTS may be even higher in children, particularly
in infants who are victims of abusive TBI [31]. In comatose
TBI patients at high risk for seizures who undergo con-
tinuous electroencephalography (cEEG), non-convulsive
seizures are identified in up to 30%. There are several risk
factors for PTS in adult TBI patients including a GCS
<10, cortical contusion, subdural hematoma, epidural
hematoma, intracerebral hematoma, depressed skull frac-
ture, penetrating head wound, and seizure within 24 h of
injury. Phenytoin has proven efficacy in preventing early
PTS in TBI patients [32]. Phenytoin (or fosphenytoin) is
therefore recommended as seizure prophylaxis in severe
TBI patients when the benefits outweigh the drug risk. The
seizure prophylaxis is stopped after 7 days if no seizure
occurs. Late prophylactic therapy (i.e., after 7 days) in
patients without evidence of a previous seizure is not
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effective and may cause harm to the patient. Therefore,
prophylactic use of anti-epileptic medications (AED) is not
recommended to prevent late PTS [33]. Levetiracetam is
another AED that is commonly used and is supported by a
growing volume of data especially in regards to safety and
adverse effect profile in comparison to phenytoin. How-
ever, there are currently no high quality studies to support
its use in the severe TBI patient in comparison to
phenytoin.
Recommendations:
• Use of prophylactic antiepileptic drugs (AEDs) may be
used to decrease incidence of early post-traumatic
seizures in patients with severe TBI if benefit of the
drug outweighs the risk.
• Consider continuous EEG monitoring to rule out non-
convulsive seizures
Administer 20 mg/kg loading dose of phenytoin (50 mg/
min) or fosphenytoin (150 mg/min) intravenously followed
by a daily maintenance dose. Levetiracetam may be an
acceptable alternative prophylactic agent. Patients who
have continuous seizures classified as status epilepticus
need immediate treatment to stop their seizures. For full
treatment regimen, see the NCS Status Epilepticus proto-
col. Antiepileptic medications should be stopped after
seven days if there is no clinical or EEG seizure activity.
ICP Monitoring
Both primary and secondary injuries contribute to poor
outcome, morbidity and mortality in TBI patients.
Intracranial hypertension develops in about 50% of severe
TBI patients [34]. An ICP > 22 mmHg, particularly if
sustained is associated with significantly increased mor-
tality [14]. Similar data supports treatment in pediatric
patients with intracranial hypertension after severe TBI
[35].
It is difficult to diagnose elevated ICP by clinical means
alone. The physical exam early in the course of TBI may
reveal signs of brain herniation or intracranial hyperten-
sion. While brain CT findings indicate mass effect and risk
for increased ICP, a reliable relationship does not exist
between the admission CT and subsequent development of
intracranial hypertension during a patient’s ICU course
[21]. Therefore, an ICP monitor is essential for timely
diagnosis and ICP management.
There are several published TBI guidelines that describe
monitoring in adults after TBI, including the European
Neurointensive Care and Emergency Medicine consensus
on neurological monitoring [36], European Brain Injury
Consortium [37], Multimodality Monitoring Consensus
Statement [38], and the Brain Trauma Foundation (BTF)
Guidelines [14]. The 2016 BTF Guidelines are currently
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the most widely accepted international guidelines for TBI
management [14].
At present, there are no reliable non-invasive ICP
monitors. ICP is best monitored invasively, with a ven-
tricular catheter or an intraparenchymal monitor [39, 40].
These devices are typically placed by neurosurgeons, yet,
in some institutions, appropriately trained neurointensivists
may also insert ICP monitors [41].
Hemorrhage is the most common procedural complica-
tion, identified rarely with parenchymal monitors and in up
to 5% of ventriculostomies. The majority of hemorrhages
identified on post-placement imaging are not of clinical
significance. An INR B 1.6 is considered acceptable to
place a ventricular catheter after TBI [42]. A platelet count
of >100,000 is preferred to safely place an ICP monitor;
however, minimal literature on the topic is available.
A ventriculostomy or external ventricular drain (EVD)
to monitor ICP also allows therapeutic drainage of CSF.
Control of elevated ICP is observed in approximately 50%
of patients where an EVD is inserted after other initial
measures fail [43]. However, a ventricular catheter with an
external transducer only allows intermittent ICP measure-
ments when the drain is closed. Simultaneous ICP
monitoring and CSF drainage is feasible with commer-
cially available catheters that have a pressure transducer
within their lumen. Ventricular catheters can be difficult to
insert after TBI due to small ventricular size or shift of
brain structures due to focal lesions. In addition, catheter
blockage and displacement can occur, causing ICP to be
poorly estimated [44].
Intraparenchymal devices require less precision in
placement than EVDs and are inserted into the brain par-
enchyma through a small burr hole at the bedside. These
monitors are secured in the skull by a specially designed,
transcranial access device known as a bolt. Many bolts also
permit insertion of other monitors (e.g., brain oxygen,
temperature, microdialysis, CBF probes). Parenchymal ICP
monitors are typically placed into what appears to be
normal white matter on the admission CT, in the non-
dominant frontal lobe in diffuse injuries or on the side of
maximal pathology in cases of focal abnormality. Different
values may be obtained depending on device location and
its proximity to a focal abnormality. Therefore, ICP values
must be interpreted in context with the clinical examination
and imaging studies.
There are several different intraparenchymal monitor
technologies, including fiber-optic, strain gauge, and
pneumatic technologies. Zero-drift occurs with fiberoptic
ICP probes and must be kept in mind when a discrepancy is
suspected. The risk associated with intraparenchymal ICP
monitors is generally considered significantly less than that
for external ventricular catheters. Hemorrhage seen on
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imaging is reported in less than 1% of devices, and
infections are reported even less frequently.
Continuous ICP recording is feasible and preferable
over intermittent readings. Technical complications (e.g.,
catheter breakage, dislodgement) may occur in approxi-
mately 4% of cases. The complications often occur during
transport, nursing maneuvers, or patient movement (See
ENLS protocols Elevated ICP and Herniation, and Coma
for further discussion on ICP management).
Recommendations
General indications for ICP monitoring may include:
GCS 3–8 and abnormal CT scan (applies to adults and
children)
GCS 3–8 with normal CT and two or more of the
following:
• Age >40 years
• Motor posturing
• Systolic Blood Pressure (SBP) <90 mmHg
GCS 9–12 and CT scan:
• Mass lesion (extra-axial >1 cm thick temporal contu-
sion, intracranial hemorrhage, or ICH >3 cm)
• Effaced cisterns
• Brain Shift >5 mm
Following craniotomy
Neurological examination cannot be followed (i.e.,
requires another surgical procedure, sedation)
Sedation and Analgesia
Patients with severe TBI are often intubated for airway
protection. Analgesia and sedation are often needed to
ensure pain is relieved and that patients are not agitated. In
choosing sedative medications, short acting agents with
minimal hemodynamic effects are optimal. No single
medication has been shown to be superior in patients with
severe TBI and nearly all medications decrease blood
pressure. Propofol and benzodiazepines though preserve
the flow-metabolism coupling and are ideal agents. A
combination of a sedative and an analgesic agent can
reduce the dose of each agent. A detailed discussion of
sedation may be found other ENLS modules (See ENLS
protocol Airway, Ventilation and Sedation).
Consultation
A neurosurgical consultation is appropriate for a patient
with TBI if:
• GCS B 13
• The patient has seizures
• There are lateralizing findings on neurological exami-
nation (e.g., unequal pupils, focal weakness)
• Head CT scan is abnormal
• Head CT is not consistent with the clinical signs
• Signs of CSF leak (otorrhea or rhinorrhea of clear fluid)
• Signs of skull fracture
• Penetrating head injury
• Cerebrovascular injury
• Suspected C-spine injury
Surgery
The decision to perform a hematoma evacuation or a
decompressive craniotomy following TBI depends on a
number of factors, and should be made with the guidance
of neurosurgical consultation. In general, extra-axial (ex-
tra-dural or subdural) hemorrhage or mass >1 cm in
thickness, midline shift >5 mm, ICH >20 cc, penetrating
injury, depressed skull fracture, or refractory intracranial
hypertension (ICH) are all indications for surgery
[18–20, 45].
In general, acute extra-axial (i.e., extra-dural and sub-
dural, hematomas C1 cm thick or associated with C5 mm
of midline shift or coma) hematomas should be considered
for emergent surgery [33–37]. Similarly, intracerebral
hematomas >20 cc in volume particularly with mass
effect, should be considered for surgical evaluation, though
the decision to operate will often depend on hematoma
location. In the posterior fossa, minimal enlargement of a
small lesion has the potential to result in brainstem com-
pression. Midline cerebellar lesions may result in
obstructive hydrocephalus.
Depressed skull fractures that are displaced greater than
the thickness of the skull table, and particularly those that
are open or compound, typically require surgical repair
[46]. Any depressed fracture immediately over a major
venous sinus requires surgical consideration. Fractures of
air sinuses, penetrating trauma, or craniofacial injuries all
require special consideration.
Decompressive craniectomy (DC) can be used to treat
refractory intracranial hypertension. There is strong evi-
dence that DC in select patients effectively controls ICP
and reduces mortality though the effect on improving
patient functional outcome is not dramatic [47–51]. Ipsi-
lateral DC may be considered when there are focal
contusions or hematomas that risk herniation and com-
promise of cerebral perfusion pressure.
123

Pediatric Considerations
Pediatric TBI accounts for 3000 deaths and almost 474,000
ED visits in the US each year [52]. TBI is the leading cause
of injury-related pediatric deaths. The goals of initial
management include rapid identification of intracranial
injuries requiring surgical intervention and prevention of
secondary brain insults that worsen outcome. For the most
part, the approach and emergent care of a child with TBI is
similar to adult management as outlined in the previous
sections.
Causes of TBI in children vary by age with falls being
the most common cause in young children. Motor vehicle
and bicycle accidents and sports-related injuries are the
most common cause of TBI in older children [52]. Abusive
head trauma is the leading cause of death from traumatic
brain injury in infants (B1 year old) and the leading cause
of death from physical abuse in the United States. Gener-
ally, pediatric patients with TBI have a known and often
witnessed history of trauma described by the accompany-
ing caregiver. However, infants and children with trauma
or unwitnessed trauma presenting with altered mental sta-
tus and an unreliable history, make the diagnosis of TBI
challenging. trauma is an important concern in infants and
children with unexplained injuries, or physical findings of
TBI not consistent with the mechanism of injury and this
cause of TBI carries a worse prognosis for recovery.
Due to variations in verbal and motor skills, a pediatric
GCS score was developed to assess disability and should be
used in the setting of TBI. The standard GCS has been
validated for use in children 3 years of age and older and
the pediatric GCS should be used for infants through
2 years of age [53–57]. Additionally, evaluation of the
anterior fontanelle is important in infants with TBI as
increased fullness with decline in neurologic condition may
raise suspicion of intracranial hypertension. Predictors of
poor outcome in children with severe TBI include
hypotension, hypothermia, and trauma [17].
In children with severe TBI or those with less severe
brain injury but inability to maintain the airway, airway
management should be performed to ensure airway pro-
tection, oxygen saturation >90%, and control of
ventilation. (see ENLS AVS module for discussion of
appropriate sizing of pediatric airways) If unable to suc-
cessfully perform endotracheal intubation, adequate bag-
mask ventilation or maintenance of the airway by the most
appropriate means available should be assured [8].
Spinal cord injury is less frequent in children compared
to adults, but spinal precautions should be maintained at all
times. Importantly, young children are at risk of spinal cord
injury without radiographic abnormality (SCIWORA).
Prompt recognition, use of MRI and electrophysiological
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verification, and timely bracing of SCIWORA patients
remain the chief measures to improve outcome [58].
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