25 Closed Head Injury

Trauma
PART 4 Trauma
25
Closed Head Injury
JAMES W. BALES, ROBERT H. BONOW,
RICHARD G. ELLENBOGEN
CLINICAL PEARLS
• As with all trauma patients, traumatic brain injury (TBI) patients • Hyperventilation is an effective means of reducing intracranial
must be promptly resuscitated and surveyed. A focus on hypertension in acutely worsening patients but prophylactic,
oxygenation, ventilation, blood pressure, and determination of long-term use is associated with poor outcomes and should be
the Glasgow Coma Scale should be the immediate priority avoided.
followed by a neurologic exam, which is the basis of all TBI • Antiepileptic medications show reduction in early onset
treatment. seizures (<7 days after injury) but no reduction in late-onset
• Even single episodes of hypoxia or hypotension are associated seizures (>7 days after injury). Dilantin or Keppra is
with increased morbidity and mortality after a severe head recommended for the first 7 days after TBI to help reduce the
injury and should be avoided. risk of early onset seizures.
• Glucocorticoids are associated with worse outcomes, and • Intracranial pressure monitors can assist greatly in the
routine use of steroids is not recommended in treatment of identification and treatment of elevated intracranial pressure in
traumatic brain injury. patients with TBI. In the absence of intracranial pressure
• Mannitol and hypertonic saline have both been shown to be monitoring, a meticulous treatment algorithm by skilled
effective in reducing intracranial hypertension and improving clinicians using clinical and appropriate radiologic exams can
cerebral perfusion pressure. provide equivalent outcomes.
• Maintaining cerebral perfusion pressure (CPP) greater than • Concussion often occurs without loss of consciousness and can
60 mm Hg may help avoid cerebral ischemia after severe head lead to complete clinical recovery but can also have long-term
injury. Attempts to maintain CPP at greater than 70 mm Hg is consequences when complicated by multiple events without
associated with respiratory complications and does not chance for recovery.
improve outcomes.
E
ach year, traumatic brain injury (TBI) contributes to a but also on society as a whole, and that it is a pressing public
large number of deaths and permanent disability. In health and medical problem.
2010 the Centers for Disease Control and Prevention The neurosurgical practitioner in combination with the
(CDC) estimated that TBI accounted for approximately 2.5 trauma team in the emergency department is often asked to
million emergency department (ED) visits, hospitalizations, evaluate and manage patients with a TBI or closed head injury.
and deaths in the United States, either as an isolated injury or These patients can present with or without skull fractures,
in combination with other injuries. Amazingly, these numbers intracranial hemorrhages, or associated systemic injuries. From
underestimate the actual occurrence of TBI, as those who did a neurosurgical perspective, immediate consideration must be
not receive medical care or had outpatient or office-based visits given to any intracranial mass lesion; in TBI this constitutes
are not counted.1 intracranial hemorrhage.
It is estimated that by the year 2020 TBI will surpass many Subdural hematomas, epidural hematomas, intraparenchy-
diseases as the major cause of death and disability.2 In 2013 mal hemorrhages, intracerebral contusions, and traumatic sub-
the direct costs of TBI was estimated to be $13.1 billion. An arachnoid hemorrhages can all be seen after a TBI and may
additional $51.2 billion ($64.7 billion in 2013) was lost present an immediate surgical consideration. Intracranial hem-
through missed work and lost productivity.3 It is clear that TBI orrhages of the aforementioned variety affect 25% to 45% of
not only has a devastating impact on individuals and families, severe TBI (Glasgow Coma Scale [GCS] < 8) cases and 3% to
366
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CHAPTER 25 Closed Head Injury 367
12% of nonsevere cases.4 It is important for both surgical plan- The first evidence-based guidelines for the management of
ning and in subsequent treatment of TBI patients to under- TBI patients were published in 1995,6 with the most recently
stand the forces involved in injury. The classic coup-contrecoup updated version published in 2016.7,8 Also in 2000, the
injury seen in patients who have suffered a significant trau- Cochrane Library published a series of reviews that provided
matic impact to the head is further complicated by rotational evidence-based standards and guidelines for the management
forces, which together can lead to intracranial shearing of of TBI patients.9–11 The fourth edition of evidence-based
vascular structures and subsequent bleeds. With the increasing guidelines for the management of severe traumatic brain injury
use of anticoagulation in the aging population, these types of was published in 2016, and these are the most up-to-date
injuries will likely be encountered throughout a neurosurgeon’s recommendations on the management and treatment of TBI.
career. Evidence-based guidelines for the management of penetrating
Fortunately with historical improvements in the resuscita- head injury have also been published,12 as well as guidelines
tion of general trauma patients, improvements in field care, for prehospital and pediatric TBI management.13–15 The Brain
and the presence of dedicated neurologic intensive care units Trauma Foundation (BTF) maintains and updates most of
(NICUs), there has been a steady decline in the mortality rate these guidelines every few years, and they can be reviewed in
from severe TBI.5 Current treatment strategies discussed in this full at the BTF website (www.braintrauma.org).
chapter serve as a guideline to limit the types of secondary Current treatment strategies based on the guidelines for
brain injury (Fig. 25.1) that evolve within TBI patients follow- TBI are focused on the monitoring and control of elevated
ing their initial resuscitation. intracranial pressure (ICP). In the United States and most
CONTRE-
IMPACT COUP COUP
ROTATIONAL
IMPACT
PRIMARY INJURY SECONDARY INJURY

(at time of injury) (hours, to days, to weeks)
• Due to force associated with mechanism • Cellular mechanism and microenvironment

- fall changes of further dysfunction
- motor vehicle accident
- assault • Astrocyte foot swelling
- breakdown of the blood-brain barrier
• Coup – Contrecoup
- contusions • Gliosis
• Shearing of blood vessels • Glutamatergic release

- epidural, subdural hematomas - activation of NMDA and AMPA receptors
• cellular depolarization
• Rotational forces causing axonal shearing • excitotoxicity
- diffuse axonal injury • mitochondrial dysfunction
• caspace cascade
• Figure 25.1 Schematic of primary and secondary injuries that occur due to head trauma.
368 PART 4 Trauma
high-income countries, this includes the use of an intracranial separate category of injury known as blast injury, which is
monitoring device. A 2016 study published in the New England unique in injury pattern and considerations. Although the
Journal of Medicine by Chesnut and coworkers, demonstrated average neurosurgical practitioner may not need to manage the
that in the absence of the availability of ICP monitoring, the acute consequences of a blast-induced head injury, the long-
use of a strict treatment algorithm, which includes a clinical term consideration of this type of head injury will likely be
and radiologic exam designed to treat the correlates of elevated important as more servicemen and women experience a blast
ICP, can be equally beneficial to patient outcomes.16 injury.
Traditionally, research in recovery of function after TBI has
focused on preventing or manipulating early events in order Blast-Induced Head Injury
to prevent chronic dysfunction. Drugs inhibiting apoptosis,
blocking glutamate-induced excitotoxicity, or attenuating oxi- Blast-induced head injury has become the most common type
dative stress were designed to reduce cell loss with the premise of military head injury, affecting close to 500,000 service
that neuronal sparing would enhance recovery.17,18 Unfortu- members. This type of injury occurs when a high-velocity,
nately, the neuroprotective effects observed in the TBI labora- high-energy blast wave encounters the human head and reflects
tories have not translated successfully to the clinic.19,20 and diffracts with its energy interacting with the structures
within.21 Experimental models have demonstrated that the
Classification primary cause of damage to biologic structures is this sudden
increase in pressure followed by a rapid decrease.22 Blast injury
Although experimentally the classification of head injury can is a spectrum disorder ranging from mild to severe, with the
be difficult given how variable injury patterns can be in the latter being frequently associated with polytrauma. Since 2001
patient population, from a clinical perspective the most practi- approximately 1.5 million service members were deployed to
cal way to approach a head injury is based on mechanism, Afghanistan and Iraq, where nearly 15% to 30% suffered a
severity, and imaging characteristics (Fig. 25.2). form of TBI. Approximately 80% of those TBIs were caused
by an explosive blast. Of those cases, 5% were severe with the
Mechanism rest on the spectrum of mild to moderate brain injury.23
A blast injury leads to a number of neurobehavioral symp-
Head injuries can be classically classified as closed or penetrat- toms including transient confusion, coma, headaches, impaired
ing. A closed head injury is typically used to describe falls, memory and learning, forgetfulness, poor concentration, mood
automobile accidents, and assaults, whereas a penetrating imbalances, and increased anxiety and depression.24 Many of
injury describes gunshot wounds or stab injuries. The use of these symptoms are mild in nature, can adversely affect the
improvised explosive devices in military warfare has created a overall quality of life, and keep the soldiers from returning
Traumatic brain injury classifications
By mechanism By morphology
Penetrating
Closed head injury Skull fractures Focal Diffuse
head injury
High
Low
velocity
Gunshot Stab velocity Blast Vault Epidural Subdural Intracerebral Diffuse
(motor Basilar fracture Concussion
wounds wounds (fall/ injury fracture hematoma hematoma hemorrhage injury
vehicle
assault)
accident)
With or With or
Linear Depressed without without
or versus CSP CN
stellate not leak VII palsy
• Figure 25.2 Simplified classification scheme for evaluation of head-injured patients.
to duty.25 Repeated exposures to blast injuries increases the commands. Among patients who could neither obey nor speak,
probability of developing more severe acute and long-term 16% opened their eyes and were therefore judged not to be in
symptoms.26 Another major challenge facing the medical pro- coma. Patients who open their eyes spontaneously, obey com-
fessional evaluating a patient with a potential blast injury is mands, and are oriented score a total of 15 points, whereas
the similarity that the symptoms share with posttraumatic flaccid patients who do not open their eyes or talk score the
stress disorder (PTSD). Both share similar neurobehavioral minimum of 3 points. No single score within the range of 3
impairments including memory difficulties, anxiety, and to 15 forms the cutoff point for coma. However, 90% of all
depression. Currently there is a lack of definitive objective patients with a score of 8 or less, and none of those with a
measurements to evaluate blast TBI (eg, imaging, molecu- score of 9 or more, are found to be in a coma according to the
lar biomarkers), but ongoing research in magnetic resonance preceding definition. Therefore for all practical purposes,
imaging (MRI) technology and biomarkers may change this in someone with a GCS score of 8 or less has become the gener-
the future.27 ally accepted definition of a comatose patient.
The distinction between patients with severe head injury
Severity and those with mild to moderate injury is relatively clear.
However, distinguishing between mild and moderate head
In 1974 Teasdale and Jennet28 designed the Glasgow Coma injury is more of a problem.30 Somewhat arbitrarily, head-
Scale (Table 25.1) in an attempt to minimize interobserver injured patients with a GCS score of 9 to 13 have been catego-
variability in the description of head injury severity. Jennett rized as “moderate,” and those with a GCS score of 14 or 15
and Teasdale defined coma as the inability to obey commands, have been designated “mild.” Authors have variably classified
to utter words, and to open the eyes.29 A patient needs to meet the GCS 13 patients with the mild or moderate TBI groups,
all three aspects of this definition to be classified as comatose. but studies suggest that patients with a GCS of 13 at admission
In a series of 2000 patients with severe head injury, these fit better into the moderate rather than mild TBI group. Eighty
authors observed 4% who did not speak but could obey com- percent of head injuries are categorized as mild, 10% as moder-
mands and another 4% who uttered words but did not obey ate, and 10% as severe. Williams and colleagues reported that
the neurobehavioral deficits in patients with mild head injury
(GCS 14 or 15) and an intracranial lesion on initial computed
tomography (CT) scan were similar to those in patients with
TABLE moderate head injury (GCS 9 to 13), but patients with mild
25.1 Glasgow Coma Scale (GCS) Components head injury uncomplicated by an intracranial lesion on CT
Points scan did significantly better.31 Although it is important to
Component Assigned recognize that initial GCS does correlate with patient out-
comes, most recent literature does not discretely distinguish
Eye opening (E) between mild and moderate head. In truth, closed head injury
Spontaneous 4
To voice 3
that is not severe is best considered as a “spectrum of TBI,”
To pain 2 which includes the traditional characterization of “mild” and
Does not open 1 “moderate.” For the purpose of this chapter we will discuss
Motor response (M)
severe head injury as a separate clinical entity but other closed
Follows commands 6 head injury as a spectrum of disorders.
Localizes to painful 5
stimulus
Withdrawal from 4 Morphology
painful stimulus
Abnormal flexion 3
Easily attainable CT scans in most developed countries have
(decorticate) allowed for clear and accurate descriptions of the morphology
Extension 2 of injury related to trauma. For neurosurgical practitioners this
(decerebrate) has largely eliminated the need for exploratory burr holes or
None 1 craniotomy and allows for treatment management decisions
Verbal response (V) that can be guided by frequent CT follow-up to evaluate the
Oriented 5 evolution of head injury. Imaging is particularly helpful in
Confused 4 guiding management of skull fractures and intracranial lesions.
Inappropriate words 3
Incomprehensible 2 Skull fractures may involve the cranial vault or skull base,
sounds be linear or stellate, and be depressed or nondepressed. Pneu-
None 1 mocephalus seen on CT scanning can be another indication
of probable skull fracture. A skull fracture by itself does not
GCS sum score: (E +
M +V); best possible necessarily warrant hospital observation, but it does increase
score = 15; worst the risk of underlying intracranial hematomas and should be
possible score = 3 properly evaluated with appropriate imaging and clinical
consideration.
370 PART 4 Trauma
The identification of basal skull fractures are particularly the nasofrontal outflow tract, and cosmetic deformity caused
important, as persistent cerebrospinal fluid (CSF) leakage as a by the fracture.32,33 Antibiotic prophylaxis in these patients
consequence of a basal skull fracture can occur. The majority does not reduce the rate of meningitis.
of these leaks heal on their own, but some may require tem-
porary CSF drainage via a lumbar drain or operative repair if Intracranial Lesions
refractory. Leakage of CSF from the nose (rhinorrhea) or ear Focal lesions include epidural hematomas, subdural hemato-
(otorrhea), blood behind the ear (hemotympanum), bruising mas, and contusions/intracerebral hematomas. Diffuse brain
behind the ear (the Battle sign), and bruising around the eyes injury, also referred to as diffuse axonal injury (DAI), may have
(raccoon eyes) are all clinical indications of a possible basal a relatively benign-appearing CT scan (Fig. 25.3A); however,
skull fracture and should increase suspicion. small punctate hemorrhages may be noted, particularly at
Linear, nondepressed skull fractures rarely require any oper- midline structures. Patients with diffuse axonal injury typically
ative intervention; however, a depressed skull fracture can be have a poor neurologic examination with altered sensorium or
associated with a dural injury and may require operative fixa- even deep coma out of proportion to the findings on their
tion. Generally a depressed fracture more than the thickness imaging workup.
of the skull requires elevation. Open or compound skull frac- MRI analysis can assist in the understanding of DAI as it
tures with direct communication between the scalp laceration relates to an individual patient, as injuries to white matter
and cerebral surface require early surgical repair and appropri- tracts are more apparent on magnetic resonance studies.34
ate antibiotic coverage. Although attempts have been made to classify the extent of
Fractures can also involve the anterior or posterior tables of DAI based on imaging characteristics, to date the most relevant
the frontal sinus. These fractures can lead to inadequate drain- imaging finding to prognosis is the amount of injury
age and recurrent sinusitis if the communication between the apparent.35
sinus and nasal cavity (nasofrontal outflow tract) is obstructed.
Furthermore, if the posterior table is violated with obstruction Epidural Hematoma
of the nasofrontal outflow tract, there is an increased risk of Most commonly located in the temporal or temporoparietal
intracranial infections. Treatment of such fractures should be regions, this type of bleeding is located between the inner table
based on the fine cut CT bone window findings, patency of of the skull and the dura (Fig. 25.3B). Classically these are
A B
C D
• Figure 25.3 Common lesions seen on CT scans in traumatic brain injury: diffuse axonal injury, epidural
hematoma, subdural hematoma, and intraparenchymal hemorrhages/contusions.
associated with injury to the middle meningeal artery as a or signs of significant mass effect on CT should be treated
consequence of a calvarial fracture. Epidural hematomas may operatively. Also in patients with GCS scores of 6 to 8 with
be associated with bleeding from the bone (up to one-third of frontal or temporal contusion greater than 20  cm3 with midline
cases), tearing of venus structures, or arterial bleeding. Non- shift greater than 5 mm or cisternal compression on CT scan
surgical epidural hematomas are reported in 2.7% to 4% of and patients with any lesion greater than 50 cm3 in volume
TBI patients.14,36–39 In patients presenting with coma, up to should be surgically treated.14
9% may harbor an epidural hematoma. Epidural hematomas
tend to affect patients between 20 and 30 years old and are Diagnostic Procedures and Monitoring: General
most commonly seen in traffic accidents (53%), falls (30%),
Guidelines and Considerations
and assaults (8%).14 The mortality rate in all age groups and
GCS scores undergoing surgery for epidural hematoma is Computed Tomography
approximately 10%.14 More specifically, in patients not in a CT scanning is the procedure of choice in the evaluation of
coma the mortality rate approximates 0%, for obtunded the head-injured patient and has probably significantly
patients it is 9%, and for patients presenting in a coma it improved outcome after head injury.43 It is strongly recom-
approaches 20%. Patients with epidural hematomas tend to mended that an emergency CT scan be obtained as soon as
have better neurologic outcomes than those with other types possible (preferably within half an hour) after admission with
of intracranial pathology. a severe head injury. Centers dealing with a large number of
such patients must make arrangements to have CT technicians
Subdural Hematoma in the hospital on a 24-hour basis or within easy accessibility
In patients with a severe TBI, 12% to 29% present with a in an emergency. CT scans should also be repeated whenever
subdural hematoma (SDH; Fig. 25.3C). The BTF review of there is a change in the patient’s clinical status or an unex-
surgical subdural hematomas showed that in 2870 patients, plained rise in intracranial pressure.
21% presented with SDH. They occur most frequently from
a tearing of bridging veins between the cerebral cortex and the Imaging in Concussion/Mild Traumatic Brain Injury
draining sinuses. The mechanism of SDH is age dependent In 1999, a task force on mild traumatic brain injury was
with younger patients (18–40 years) presenting with SDH devised under the support of the European Federation of Neu-
after a motor vehicle accident (MVA) 56% of the time, whereas rological Societies. The efforts of the task force produced the
in older patients (over 65 years) a SDH is frequently associated recommendations for the initial management of mild trau-
with falls (56%).40 The injury in patients with SDH is usually matic brain injury.44
much more severe, and the prognosis is much worse compared Routine ordering of skull films has in most instances become
to epidural hematomas. Brain damage seen in SDH results obsolete with the availability of CT scanners. Studies compar-
from direct pressure, cerebral swelling, increased intracranial ing skull radiography with CT have shown a low sensitivity
pressure, and diffuse axonal injury. MVA is described as the and specificity of the presence of a skull fracture on skull
mechanism of injury in 53% to 75% of patients who are radiographs for intracranial hemorrhage.45 A meta-analysis
comatose with SDH. The mortality rate in a general series may confirmed that skull radiography is of little value in the clinical
be around 60% but can be lowered by rapid surgical interven- assessment of mild TBI.46
tion and aggressive medical management.41 Multiple studies CT is considered the gold standard for the detection of
show that the morbidity and mortality rates increase if the intracranial abnormalities in the acute setting after mild TBI.
surgery is performed after 3 to 4 hours, and the timing of acute It is recommended for those with loss of consciousness or
SDH surgical intervention should be done within 2 to 4 hours posttraumatic amnesia and is considered mandatory in all
of TBI if possible.14 patients with GCS scores of 13 or 14, or in the presence of
risk factors.
Contusions/Intracerebral Hemorrhage
Cerebral contusions are fairly common, found in 8% of all TBI Imaging in Moderate-Severe Traumatic Brain Injury
cases14,42 and 13% to 35% of severe injuries.14 Contusions of In a prospective study of CT scan abnormalities in 207 patients
the brain are often concomitant with SDH. Most contusions with severe TBI, the initial CT scan was found to be normal
occur in the frontal and temporal lobes, although they can in 30% of cases. The remaining 70% of patients had CT scan
occur at almost any site, including the cerebellum and brain- abnormalities: low-density lesions in 10%, high-density non-
stem. The distinction between contusions and traumatic intra- surgical lesions in 19%, and high-density lesions requiring
cerebral hematomas (Fig. 25.3D) remains somewhat ill defined. surgery in 41%.47
Management of the intracerebral hematoma is dependent Edema is seen on CT as a zone of low density associated
on the neurologic status of the patient. Rapid surgical evacu- with mass effect on the adjacent ventricles reflected as compres-
ation decompression is recommended if there is a significant sion, distortion, and displacement of the ventricular system.
mass effect (generally, a 5-mm or greater actual midline shift). The edema may be focal, multifocal, or diffuse. With diffuse
The current BTF guidelines state that patients with parenchy- cerebral edema it may be hard to appreciate the lower density
mal mass lesions and signs of progressive neurologic deteriora- because no area of normal brain density is available for com-
tion related to the lesion, refractory intracranial hypertension, parison. In such cases there is usually bilateral ventricular
372 PART 4 Trauma
compression, which may be so gross that the ventricular system are clearly seen by 7 days. Contrast enhancement improves the
is not seen, especially in children. diagnostic yield by nearly 15%, and MRI is even more
Cerebral contusions are seen as nonhomogeneous areas of sensitive.
high density, often interspersed with areas of low density (“salt A noncontrast CT scan of the brain is a quick and accurate
and pepper” appearance). The CT appearance results from diagnostic tool for initial and serial assessment in TBI patients.
multiple small areas of hemorrhage within the brain substance, Studies have demonstrated that CT findings can also be used as
associated with areas of edema (see Fig. 25.3D). The margin a prognostic tool in TBI.41,48–50 Each of the following parame-
is usually poorly defined. A mass effect is often seen, although ters appears to be important in outcomes and prognostication:
this appearance may be minimal. Depending on the extent of status of basal cisterns, midline shift, traumatic subarachnoid
hemorrhage, the degree of edema, and the time course, a con- or intraventricular hemorrhage, and presence of different types
tusion may appear predominantly dense or lucent. of mass lesions.51
Although it is not always possible to differentiate between Cervical spine injuries are also commonly seen in TBI
subdural and epidural hematomas on CT, the latter are typi- patients, and cervical spine films (cross-table lateral and antero-
cally biconvex or lenticular in shape, because the close attach- posterior) or a thin-cut cervical spine CT scan are the first to
ment of the dura to the inner table of the skull prevents the be taken in the severely traumatized patient prior to neck
hematoma from spreading (see Fig. 25.3B). Approximately mobilization. Cervical spine CT is indicated for the uncon-
20% of patients with an extracerebral hematoma have blood scious patient with suspicious or inadequate cervical radio-
in both the epidural and subdural spaces at operation or graphs and with all cervical fractures or suspected fractures on
autopsy. Because there is little chance of epidural blood mixing initial plain films. Several studies have demonstrated the value
with CSF, these lesions appear as uniformly dense collections of the full CT scan, with sagittal and coronal reconstructions,
and are rarely isodense. However, they may develop in a for the exclusion of significant spinal injury.52 Widening, slip-
delayed fashion, especially after evacuation of a contralateral page, or rotational abnormalities of the cervical vertebrae
“balancing” lesion. For that reason we recommend obtaining suggest soft tissue injury. An absence of such signs appears to
an intraoperative CT scan after evacuation of a contralateral exclude significant instability.
lesion, if available at your institution.
The typical subdural hematoma is more diffuse than an Ventriculography
epidural hematoma and has a concave inner margin that As a historical note, ventriculography was once used prior to
follows the surface of the brain (see Fig. 25.3C). Most acute the era of CT scanning to help identify mass lesions causing
subdural hematomas are hyperdense, most subacute lesions are ventricle compression and shift. In current practice, there is
isodense or of mixed density, and most chronic hematomas are essentially no indication for ventriculography.
hypodense as compared with brain tissue. Effacement of the
cerebral sulci over the convexity and distortion of the ipsilateral Angiography
lateral ventricle may suggest the presence of an isodense Prior to the advent of CT scanning, angiography was used to
hematoma. diagnose mass lesions and shift of the brain by examining the
Traumatic intracerebral hematomas are usually located in pattern of the blood vessels and looking for shift or displace-
the frontal and anterior temporal lobes, although they can ment. In patients with neck injuries or skull base fractures near
occur in virtually any area. Most hematomas develop immedi- the carotid canal, angiography may be performed for diagnosis
ately after the injury, but delayed lesions are often noted, and possible treatment of carotid or vertebral injuries, such as
usually within the first week. They are high-density lesions and dissection. Angiography may still be useful in the diagnosis
are usually surrounded by zones of low density caused by of patients with Horner syndrome, dysphagia, hemiparesis,
edema. Traumatic hematomas are more often multiple than obtundation, and monoparesis when CT scanning does not
hematomas from other causes. elicit an abnormality. With the advent of computed tomog-
Traumatic intraventricular hemorrhage was previously raphy angiography (CTA) and magnetic resonance imaging
believed to have a uniformly poor prognosis, but this is no (MRA), true invasive cerebral angiography is not used as
longer considered true. It is frequently associated with paren- much, with the newer tests being less invasive and having
chymal hemorrhage. The blood becomes isodense relatively less risk.
rapidly and often disappears completely within a couple of
weeks. If indicated, a ventriculostomy may be placed in the Computed Tomography Angiography
less bloody ventricle, and CSF drainage can be used to monitor Patients who have skull base fractures through the petrous
and reduce intracranial pressure and drain away the blood. bone, cervical trauma, or cervical fractures through the trans-
Acute obstructive hydrocephalus may develop secondary to verse foramen are at risk for carotid and vertebral artery dis-
a posterior fossa hematoma that obstructs the ventricular path- section. CTA offers a rapid means of cervical and intracranial
ways. However, delayed hydrocephalus is far more common, vascular injury assessment while the patient is the emergency
occurring in about 6% of patients with severe head injury. department.53–56 Contraindications to CTA use include aller-
Acute ischemic infarction appears as a low-density area gies to iodine-based contrast dye as well as underlying renal
compared with the adjacent brain. The infarction may be disease. Most centers have protocols in place to guide specific
detectable on CT scan within 24 hours of onset, and over 60% criteria in regard to dealing with such patients.
Magnetic Resonance Imaging AUTOREGULATION CURVE

A wide range of CT findings in patients with closed head 100
90
injury can represent a specific GCS score. Furthermore, repeat
80
CBF (mL/100g/min)
CT scans offer a cumulative risk or iatrogenic pathology
70
because of the radiation used to obtain the images.57 The use
60
of MRI in TBI patients can help in diagnosis, especially in Normal
50
those with nonspecific CT findings. Particularly helpful
40
imaging sequences include diffusion-weighted imaging (DWI), 30 Impaired
susceptibility-weighted imaging (SWI), diffusion tensor 20 or absent
imaging (DTI), MRI spectroscopy, and functional MRI with 10
established protocols.58–60 0
DTI, in particular, has garnered a lot of interest from the 0 20 40 60 80 100 120 140 160 180 200
TBI community in an effort to better understand the prognosis MAP
and symptomology of patients who have experienced a mild
• Figure 25.4 Autoregulation curve and demonstration of impaired
TBI. In a structurally intact axon, water molecules have a autoregulation.
higher degree of diffusion in the axial direction compared to
radial direction as they are bounded by the membrane. Struc-
tural damage to the axon by trauma will result in a reduction given) detected more lesions than CT or MRI and significantly
of this axial diffusion. DTI utilizes this disruption to demon- reduced CBF.64
strate the compromise of structural integrity. Current and Although SPECT imaging gives a cost-effective means of
ongoing research has shown the sensitivity of DTI in detecting assessing the CBF post TBI, one question that it does not
white matter damage and demonstrated a positive correlation answer is what a patient’s individual physiologic response is to
of DTI findings with cognitive deficits, even in mild TBI.60 alterations in CBF. Autoregulation, the process by which the
Given the rising popularity of DTI in the research and clinical brain controls CBF, is known to be disrupted in TBI.65 Indeed
communities, it is an imaging modality to be familiar with for nearly any insult to the central nervous system has the potential
potential uses in prognostication of TBI. to alter the autoregulation curve as depicted in Fig. 25.4.
Although this is a simplistic view of autoregulation, it under-
Clinical Electrophysiology scores how a loss in autoregulation can significantly change the
Electroencephalography (EEG) measures difference in electri- way the brain responds to systemic factors. In patients with
cal potential between two points where electrodes are placed. disrupted cerebral autoregulation, blood pressure parameters
Conventional EEG in the clinical setting uses data collected and indeed ICP control become more complex as the natural
from 21 scalp electrodes arranged according to the international protective system employed by a patient’s CNS is nonfunc-
10-20 system and was the first tool that allowed characteriza- tional. Methods of measuring autoregulation can thus lead to
tion of cerebral physiology in post-TBI patients.61,62 The utili- meaningful changes in the management of TBI patients.
zation of conventional EEG often depends on the severity of Transcranial Doppler techniques to assess dynamic and static
brain injury seen in the neurocritical care assessment. Charac- cerebral autoregulation are powerful tools to assess the level of
teristic findings of conventional EEG include generalized or autoregulatory dysfunction.66 Further research is necessary to
focal slowing and attenuated alpha response (7.5–12.5 Hz explain the clinical implications; the patient with an intact
frequency band). The information provided during these autoregulatory system may be partially protected from hyper-
recordings allows detection of abnormal brain patterns and has emia and systemic hypertension, allowing for more liberal
been used in prognostication in severe TBI.63 treatment paradigms. Furthermore, in patients with dysfunc-
tional autoregulation, care must be taken to manage systemic
Cerebral Blood Flow blood pressure and thereby avoid hypo- or hyperperfusion.67
Single-photon emission computed tomography (SPECT)
detects cerebral blood flow (CBF) by using a gamma ray– Intracranial Pressure
emitting isotope such as 99mTc. Agents such as TC-99m
hexamethylpropleneamine oxime (99mTc-HMPAO), 99mTc- Since the early 1970s, there has been an increasing interest in
ethylcysteinate (99mTc-ECD), and iomazenil are commonly ICP monitoring and control, which has been associated with
used for injection in SPECT imaging. These radioactive tracers progressive evolution of related technology. However, the
are injected in the subjects for uptake by brain tissue, and intraventricular catheter (or ventriculostomy) remains the
the uptake of this agent is proportional to the CBF. Photons most widely used device for measuring ICP, helping to control
are emitted by a process named gamma emission during the it, and maintaining cerebral perfusion pressure.68,69
decay of the ray-emitting isotope, and these photons are Cerebral perfusion pressure (CPP) is the mean arterial
detected by gamma cameras. The level of CBF can be mea- blood pressure minus ICP. Because cerebral ischemia may be
sured because the level of gamma emission is proportional to the single most important secondary effect influencing outcome
CBF. In a study of 19 patients with severe head injury, SPECT following severe TBI, it is useful to follow CPP rather than
between 3 to 36 months after injury (no mean interval was ICP alone.70 The guidelines have recommended maintaining
374 PART 4 Trauma
CPP at a minimum of 60 mm Hg to possibly help in the (level I evidence) found no differences in functional outcomes
avoidance of both global and regional ischemia. It has been or neuropsychiatric scores between two protocol-based treat-
demonstrated that pushing the CPP significantly higher than ment strategies, one of which was driven by ICP measurements
60 mm Hg may also have a deleterious effect, particularly with and the other by imaging and clinical examinations.16 That
respiratory complications, and should be avoided.71 there was no difference in outcome between these groups sug-
Head injury is the most common indication for ICP moni- gests that treatment of ICP in response to imaging and clinical
toring. As a general rule, patients who can follow simple com- correlates of intracranial hypertension may be equivalent in
mands need not be monitored and may satisfactorily be experienced clinicians to treatment based on actual ICP values.
followed clinically. In patients who are unable to follow simple However, the protocol nature of the study and its specific
commands and have an abnormal CT scan, the incidence of setting in Latin American countries with skilled ICU staff
intracranial hypertension is high (53%–63%), and monitoring require that the results be generalized with caution when
is warranted.72 Severe TBI patients with normal CT scans exported to other institutions.
generally have a lower incidence of elevated ICP (approxi- Via the LICOX CMP System it is possible to monitor
mately 13%) unless they have two or more of the following cerebral oxygenation. The purpose of this triple-lumen bolt
adverse features at admission: systolic blood pressure less than system is to provide additional data including brain tissue
90 mm Hg, unilateral or bilateral motor posturing, or age over oxygenation (PBTO2) and temperature as well as ICP in
40 years. In the presence of these adverse features, the inci- patients in whom cerebral hypoxia and ischemia are a concern.
dence of intracranial hypertension (even in patients with Mean normal brain tissue oxygen pressure is greater than
normal CT scans) is as high as in those with abnormal CT 30 mm Hg (range 25–50 mm Hg) with ischemia reported at
scans on admission.72 Compression or absence of basal cisterns ranges less than 8 to 12 mm Hg and cell death at less than
has also been associated with elevated ICP.73 5 mm Hg.75
Normal ICP in a relaxed or paralyzed patient who is neither
hypotensive nor hypercarbic is 10 mm Hg (136 mm H2O) or General Management and Initial Evaluation
less (1 mm Hg = 13.6 mm H2O = 1.36 cm H2O). Pressures
in the range of 10 to 20 mm Hg (136–272 mm H2O) may of Traumatic Brain Injury
occur with moderate disturbances of intracranial volumes; General Examination
pressures greater than these herald an intracranial hematoma,
diffuse brain swelling, or both. As with all patients, the approach to individuals with suspected
Most dangerous traumatic intracranial mass lesions shift the traumatic brain injury begins with history taking and physical
midline 5 mm or greater. This is invariably associated with an examination if he or she is stable. Of particular importance to
elevated ICP. Significant temporal lobe lesions may cause only the neurosurgeon are a history of bleeding diathesis and the
a minimal shift of the midline, but the ICP may be elevated use of any medications that increase the risk of bleeding.
and the third ventricle, if seen, will often be shifted more than During the process of cardiopulmonary stabilization, the
the lateral ventricles. If there is little or no midline shift, the clinician conducts a rapid general examination looking for
ICP is elevated, and the patient is not hypercarbic, then either other injuries. In one series of severe TBI patients, more than
there are bilateral mass lesions or there is significant diffuse 50% had additional major systemic injuries requiring care by
brain swelling. other specialists.76
When intracranial pressure demonstrates an upward trend,
certain basic items should be checked. The neck should be in Neurologic Examination
a neutral position to facilitate venous drainage. In most cases,
having the head end of the bed elevated approximately 30 As soon as the patient’s cardiopulmonary status has been sta-
degrees is useful.74 The calibration of the system must be bilized, a rapid and directed neurologic examination is per-
checked, and one should confirm that the transducer is level formed. The neurologic exam is the basis of all TBI management.
with the foramen of Monro. If the patient is fighting the ven- Various factors may confound an accurate evaluation of the
tilator, he or she should be sedated or chemically paralyzed. If patient’s neurologic state (eg, hypotension, hypoxia, intoxica-
these measures are not adequate, various methods exist to tion, sedation or paralytic agents) and should be considered
reduce the ICP, including ventricular drainage, mannitol, and during the initial examination.
hyperventilation. The GCS status of a patient can be determined quickly and
In some patients, these measures are inadequate to control with good intraobserver accuracy but should not be the limit
ICP. These individuals are often considered for decompressive of the examination. A patient’s age, vital signs, pupillary
craniectomy, a surgical procedure in which a large unilateral response, and eye movements are all important in determining
or bifrontal bone flap is removed to provide additional space severity and therapeutic decision making in a head injury.77
for the brain to swell. These procedures effectively reduce ICP, The GCS score provides a simple grading of the arousal and
but evidence from two randomized controlled trials suggests functional capacity of the cerebral cortex, and the pupillary
that they offer limited benefits. Trials also demonstrate that responses and eye movements serve as measures of brainstem
although ICP monitoring is the standard of care, it does not function. Advanced age, hypotension, and hypoxia all adversely
clearly improve outcomes. A large randomized controlled trial affect outcome.
Pupils tone and pupillary constriction. Continued herniation leads to

Careful observation of pupil size and response to light is increasing dilatation of the pupil and paralysis of its light
important during the initial examination Table 25.2. Com- response. With full mydriasis (8- to 9-mm pupil), ptosis and
pression of the oculomotor nerve, which can indicate temporal paresis of the medial rectus and other ocular muscles inner-
lobe/uncal herniation, impairs the parasympathetic axons and vated by the oculomotor nerve appear. A bright light in a
results in mild pupillary dilatation and a sluggish pupillary darkened room is always necessary to determine pupillary light
light response. Bilateral miotic pupils (1–3 mm) can also occur responses. Computerized pupillometry underwent clinical
in the early stages of herniation as a result of compromise of testing in the past with reportedly unclear results initially.78
the pupillomotor sympathetic pathways originating in the With technologic advances the automated pupillometer has
hypothalamus, permitting a predominance of parasympathetic become an important tool in the critical care of severe TBI
TABLE
25.2 Components of the Exam Important for Evaluation of the Head-Injured Patient
Evaluation of the Head Injury Patient

Primary Survey Often done as part of initial Airway: intubate early if GCS < 8
emergency department Blood pressure: avoid hypotension (SBP < 90)
management, but should be Circulation: avoid hypoxia (P02 <90%)
verified prior to focused exam
Neurologic Examination
GCS: 3–8, severe brain injury, 9–13 See GCS scale, eye opening, motor response, verbal response
patients possibly at higher risk for
decompensation, 14–15 at low
risk for worsening
Pupillary examination Findings
Darkened room with bright light Unilateral dilation with sluggish or fixed response → cranial
nerve III compression secondary to tentorial herniation
With advances in automated Bilateral dilation with sluggish or fixed response → anoxic injury
pupillometry it is reasonable to or bilateral cranial nerve III compression due to transtentorial
employ a pupillometer if you are herniation
familiar with its use Unilateral dilation with reactivity to light in opposite eye (Marcus
Gunn pupil) → optic nerve injury.
Bilaterally miotic → opiates, metabolic encephalopathy, pontine
lesion
Unilaterally miotic with intact light response → injury to the
sympathetic pathway (ie, carotid sheath injury)
Oculocephalic (doll’s eye): verify there Turning the head from side to side
is no cervical injury prior to doing Intact brainstem: eyes will move away from the direction head
this maneuver is turned
Evaluation in comatose patient, Brainstem not intact, eyes remain fixed midorbit during
unnecessary in patient who can movement
move eyes voluntarily
Oculovestibular (caloric): can be Can be done with either cold or warm water. Cold water is
performed in patient with cervical usually more easily acquired.
injury which limits oculocephalic
testing
Ensure the tympanic membrane is Slow injection of cold water into ear canal → eyes turn toward
intact and the ear canal is clear of ipsilateral ear with a nystagmus toward contralateral ear;
debris that might limit utility absence of both phases indicates the brainstem is not intact.
Gross Examination
Motor score Normal power—5
Important, as it can indicate Slight weakness (can resist examiner but not easily)—4 Severe
concomitant spinal injury or weakness (cannot resist but able to work against gravity)—3
localize intracranial injury
Important to consider if there is injury Severe weakness (cannot work against gravity)—2
to the limb in question Trace movement—1
Sensory examination Crude touch and light touch evaluation
GCS, Glasgow Coma Scale; SBP, systolic blood pressure.
376 PART 4 Trauma
patients. Direct comparison of automated pupillometry to causes fast-phase nystagmus in the direction opposite to the
standard clinical practice demonstrated that the use of auto- tonic eye deviation. The mnemonic “COWS” (cold opposite,
mated pupillometer in critical care populations was associated warm same) refers to this phenomenon. However, in comatose
with improved reliability in the assessment of a patient’s pupil- patients, functional suppression of the reticular activating
lary response. Current automated pupillometers allow for both system is reflected by the absence of nystagmus in response to
the measurement of pupillary size and their reactivity, even in caloric stimulation so that only the tonic eye deviation is seen
small pupils (< 2 mm). The use of automated pupillary systems (cold same). Thus irrigation with cold water in a comatose
should be considered in any critical care setting to improve patient causes ipsilateral deviation of the eyes toward the stim-
intraobserver reliability.79 ulated side.
Recognition of additional pupillary disorders that can occur While oculocephalic and caloric testing is being performed,
in an unconscious patient is useful in the examination of the infranuclear, internuclear, and supranuclear ocular motility
patient with head trauma. Disruption of the afferent arc of disorders are recognizable. A destructive lesion of a frontal or
the pupillary light reflex within the optic nerve is detected by pontine gaze center results in tonic overaction of the opposite
the swinging flashlight test. As the flashlight is swung from the frontal-pontine axis for horizontal eye movement. This overac-
normal eye to the injured eye, injury to the optic nerve is tion results in ipsilateral deviation of the eyes with frontal lobe
indicated by a paradoxic response of the pupil: dilatation rather lesions, and contralateral gaze deviation with pontine lesions.
than constriction. This paradoxic pupillary dilatation is termed Third and sixth cranial nerve palsies are generally not dif-
an afferent pupillary defect or Marcus Gunn pupil, and in the ficult to recognize in patients with head injury. Fourth cranial
absence of opacification of the ocular media it is evidence of nerve palsies cannot ordinarily be identified in coma because
optic nerve injury. of the select action of the superior oblique muscle. In alert and
Bilaterally small pupils suggest opiate use, metabolic recovering patients, however, superior oblique paresis causes
encephalopathies, or a destructive lesion of the pons. A unilat- troublesome double vision, especially with downward and
eral Horner pupil is seen occasionally with brainstem lesions, inward gaze. Head tilt opposite the side of the paretic muscle
but in the trauma patient attention should be given to the lessens the diplopia, whereas ipsilateral tilt of the head increases
possibility of a disrupted efferent sympathetic pathway at the it. Internuclear ophthalmoplegia is suggested by select adduc-
apex of the lung, base of the neck, or ipsilateral carotid sheath. tion paresis without additional involvement of the pupil, lid,
Midposition pupils with variable light responses can be or vertical muscles innervated by the third nerve. This ophthal-
observed in all stages of coma. Traumatic oculomotor nerve moplegia results from disruption of the ipsilateral medial lon-
injury is the diagnosis in patients with a history of a dilated gitudinal fasciculus that connects the oculomotor subnucleus
pupil from the onset of injury, an improving level of conscious- for medial rectus neurons to the contralateral horizontal gaze
ness, and appropriate ocular muscle weakness. A mydriatic center. Either bilateral or unilateral internuclear ophthalmo-
pupil (6 mm or more) occurs occasionally with direct trauma plegia may be seen, depending on the extent of the brainstem
to the globe of the eye. This traumatic mydriasis is usually trauma.
unilateral and is not accompanied by ocular muscle paresis.
Finally, bilaterally dilated and fixed pupils in patients with Motor Function
head injury may be the result of inadequate cerebral vascular The basic examination is completed by a gross test of motor
perfusion caused by hypotension secondary to blood loss or strength, although severely head-injured patients are not suf-
elevation of intracranial pressure to a degree that impairs cere- ficiently responsive for such a determination to be reliably
bral blood flow. Return of the pupillary response may occur made. Each extremity is examined and graded on the interna-
promptly after the restoration of blood flow, if the period of tionally used scale (Table 25.3). Furthermore, stimuli to assess
inadequate perfusion has not been too long. patients should be standardized. In assessing for localization,
the elbow should be bent at 90 degrees with the forearms
Eye Movements resting on the patient’s chest. If the patient is able to bring the
The evaluation of eye movements allows the physician an hand at or above the chin, localization should be noted. To
objective examination of midbrain function. Unfortunately, in assess withdraw, deep nailbed pressure is applied to the second
many instances patients who have suffered a head injury are digit to test for any movement away from the noxious stimu-
unable to provide voluntary eye movements due to altered lus. Assessing the lower extremities for withdraw is difficult to
sensorium. In states of depressed consciousness the oculoce- differentiate from reflexive triple flexion and thus has dimin-
phalic or oculovestibular responses are used to determine the ished validity.
presence or absence of an eye movement disorder. Prior to
performing oculocephalic testing, the presence of a cervical
Special Consideration: Diffuse Axonal Injury
fracture must be excluded.
The oculovestibular response can be tested with ice water Diffuse Injuries/Concussion
and only a small expenditure of time. Obstructions within the Diffuse brain injuries form a continuum of progressively severe
external auditory canal due to blood or cerumen must be brain damage caused by increasing amounts of acceleration-
removed, and ocular movement may be limited in patients deceleration injury to the brain. In its purest form, diffuse
with orbital edema. In alert patients, cold caloric stimulation brain injury is the most common type of head injury. Diffuse
TABLE concussion have no sequelae other than amnesia for the events
25.3 Motor Strength Scale relating to the injury, some patients may have more long-
lasting and sometimes significant neurologic deficits.
Grade Ability to Move
Efforts have been made to move beyond the simple GCS
5 The muscle can move the join it crosses through a classification when applied to mild TBI or concussion. In the
full range of motion; against gravity, and against past concussion was defined as a loss of consciousness with
full resistance applied by the examiner
transient altered sensorium due to an injury to the head. Gen-
4 The muscles can move the joint it crosses through erally it was felt to be a benign entity with good recovery.
a full range of motion against moderate However, our understanding of concussion has greatly increased
resistance
and we now acknowledge the potential risk and danger of what
3 The muscle can move the joint it crosses through a is essentially a mild traumatic brain injury. About 3% of
full range of motion against gravity but without patients with “mild or concussive” head injuries can deteriorate
any resistance
unexpectedly and become neurologically devastated if the
2 The muscle can move the joint it crosses through a decline in mental status is not noticed early.80 Postconcussive
full range of motion only if the part is properly symptoms have been shown to include memory deficits, sleep
positioned so that the force of gravity is
eliminated
difficulties, and ongoing cognitive dysfunction.81,82
The Brain Trauma Foundation has begun to redefine con-
1 Muscle contraction is seen or identified with cussion for the modern era in an attempt to provide guidelines
palpation, but it is insufficient to produce joint
motion even with elimination of gravityl
at future updates.83 Its recommendation is to define concussion
as (1) a change in brain function, (2) which follows a force to
0 No muscle contraction is seen or identified with the head, (3) may be accompanied by temporary loss of con-
palpation; paralysis
sciousness (LOC), (4) is identified in awake individuals, and
(5) includes measures of neurologic and cognitive dysfunction.
The recognition of a concussed individual has become an
axonal injury is the term used to describe a prolonged post- integral part of neurologic care in sports medicine. To this end,
traumatic state in which there is loss of consciousness from the the International Consensus Meeting of Concussion in Sport
time of injury that continues beyond 6 hours. Severe diffuse developed the Sports Concussion Assessment Tool (SCAT) in
axonal injury usually occurs in vehicular accidents, comprising 2005 and the SCAT 5 (Fig. 25.5) was developed at the 5th
about 36% of all patients with diffuse axonal injury. These International Consensus Meeting of Concussion in Sport in
patients are rendered deeply comatose and remain so for pro- Berlin in 2016.84,85 The Adult SCAT 5 provides a standardized
longed periods of time. They often demonstrate evidence of tool for evaluating injured athletes for concussion and can be
decortication or decerebration (motor posturing) and often used by health care professionals in athletes age 13 years and
remain severely disabled, if they survive. older.86 The Child SCAT 5 is also designed for medical profes-
sionals to be used in children with suspected concussion, ages
Evaluation and Management of Concussion/ 5 to 12.87 The SCAT tool includes a Glasgow Coma Score,
Mild Head Injury Maddocks Score, symptom evaluation, cognitive assessment,
neurologic and neck exam, balance exam, coordination, and
Concussion, like many other forms of TBI, can present as a delayed recall test. The SCAT can be administered by a licensed
spectrum of conditions. Concussion is a TBI in which con- health care professional on the sidelines to help guide field
sciousness is preserved in about 90% of patients, but there is management or in the outpatient clinic to provide follow-up
a diagnosable degree of temporary neurologic dysfunction. and help decide return to play or school status for concussed
These injuries are exceedingly common and, because of their patients.
mild degree, are often not brought to medical attention. The
mildest presentation of concussion results in headache, tran- Concussion in Sports Injuries
sient confusion, or disorientation without amnesia. This syn-
drome is usually completely reversible and is associated with Sports-related injuries are among the most common cause of
no major sequelae. More severe concussive injury can involve concussion in children, adolescents, and young adults. There
confusion with both retrograde and posttraumatic amnesia has been increasing concern over the potential long-term out-
often presenting with a GCS of 14. comes of sports-related concussions. The rates of concussion
Classically a cerebral concussion is that posttraumatic state and recurrent concussions per 10,000 exposures were mea-
that results in loss of consciousness. This condition is always sured by the National Collegiate Athletic Association Injury
accompanied by some degree of retrograde and posttraumatic Surveillance Program from 2009 to 2010 and 2013 to 2014.
amnesia, and the length of posttraumatic amnesia is a good This public health initiative identified a relatively high inci-
measure of the severity of the injury. The loss of consciousness dence of concussion in American football, wrestling, ice
is transient and reversible. The patient returns to full con- hockey, rugby, lacrosse, field hockey, and soccer.88 This high-
sciousness by 6 hours, although it is usually much sooner. Even lights the necessity for medical practitioners to be familiar with
though the great majority of patients with classic cerebral sports concussion tools such as the SCAT 5, which has greatly
378 PART 4 Trauma
• Figure 25.5 Components of the Sports Concussion Assessment Tool (SCAT).
facilitated the culture change that has included the monitoring concentrated in the depths of the cerebral sulci and pathologic
and reporting of concussive injuries. tau inclusions within neurons. Based on the severity of patho-
What remains unclear is the long-term consequence of a logic tau deposition, CTE can be placed into one of four stages
concussive injury. Although the majority of patients who sus- from stage I (isolated focal perivascular tau lesions) to stage IV
tained a sports-related concussion recover within weeks of (cerebral atrophy and neuronal loss associated with widespread
injury, a minority of patients, as many as 30% in some studies, tau pathology).95
can develop persistent “postconcussive symptoms.” The symp- It is unclear what the pathologic mechanism of tau deposi-
toms of postconcussive syndrome include at least three of the tion and CTE is or how it relates to repeat head injuries, but
following: headache, dizziness, fatigue, irritability, impaired it has become an important clinical entity to recognize. Current
memory and concentration, insomnia, and lowered tolerance hypotheses point to possible genetic factors, such as differences
for noise and light.89 The causes of these persistent symptoms in APOE isoforms, that predispose some individuals to devel-
are not known; however, general treatment strategies are aimed oping neurotoxic effects and mitochondrial dysfunction in the
at addressing the symptomology and not the underlying cause. setting of a head injury.96 To date CTE has been documented
Although a single sports-related concussion is unlikely to in amateur and professional athletes, military personnel, and
result in long-term adverse outcomes, the effect of multiple individuals who have been exposed to repetitive brain injury
concussions appears to carry more potential risk.90 In former usually in the form of multiple concussions.97,98 All reported
professional American football players who reported a history pathologically confirmed cases of CTE have had a history of
of multiple concussions, there was an increased risk of depres- multiple brain injuries, and it is a recognized consequence of
sion and memory problems. A number of studies have exam- multiple concussive and subconcussive injuries.99,100
ined both collegiate football players and soccer players with Case reports of CTE (formerly termed dementia pugilistica)
multiple concussions who demonstrated impairment on neu- indicated a number of symptoms in common among the pre-
ropsychologic testing months to years later.91–93 In addition to senting patients, typically boxers, including impairments in
deficits in cognitive domains, repetitive head injuries can also cognition, behavior, and mood. More recently a study examin-
lead to recognized neurodegenerative disease. Chronic trau- ing the clinical profile of 36 neuropathologically confirmed
matic encephalopathy (CTE) is a neurodegenerative disease cases of CTE attempted to give a more complete clinical
characterized by the accumulation of hyperphosphorylated tau profile.101 In this study over 80% of patients presented with
in the brain.94 Mckee and colleagues (2013) introduced the memory impairment that was progressive in nature. In addi-
pathologic criteria for a neuropathologic diagnosis of CTE. tion, over 70% of patients with CTE demonstrated attention
Hallmark features of CTE include focal perivascular tau lesions and concentration difficulties and executive dysfunction at
presentation. Other symptoms were more variable in nature usually confused or somnolent and may have focal neurologic
but included language difficulties, mood alterations including deficits such as a hemiparesis. In patients with mild to moder-
depression and impulsivity, and even motor difficulties in some ate head injury, extracranial injuries play a significant role in
patients. Although this study is an important step in our the overall outcome. Approximately 10% of these patients will
understanding the clinical picture of CTE, there remains many deteriorate and lapse into coma. They should be managed as
questions over who is at risk for developing CTE and how patients with severe head injuries, the only caveat being that
generalizable the findings in these 36 patients are to all repeti- they are not routinely intubated.
tive head-injury patients. In a review of 341 patients with a GCS score of 9 to 12,
As the incidence of repetitive brain injury increases, with 40% of cases had an abnormal initial CT scan and 8% required
both sports-related concussions and blast-induced head injury, surgery.102 It is recommended that patients who present with
the recognition of these long-term consequences is important a GCS score of 9 to 12 are admitted for observation even if
for both the clinical care of patients and appropriate counsel- the CT scan is normal. If a patient improves neurologically
ing. This has led to current concussion management emphasiz- and there is no injury on follow-up scans, he or she can typi-
ing the need for complete player recovery prior to a return to cally be discharged within 1 to 2 days post injury. If the patient
activity. It often falls upon the medical professional to make should deteriorate, then he or she should be managed as a
the final determination as to whether or not a player has fully severe TBI case.
recovered from the injury. It is in this context that again the
detailed concussion examination with the SCAT 5 is impera- Severe Traumatic Brain Injury
tive to determining if a player is safe to return to play or school.
Severe TBI patients are those who are unable to follow simple
Moderate Traumatic Brain Injury commands even after initial resuscitation and stabilization. It
is these patients who are at greatest risk of suffering significant
The evaluation and initial considerations for the management morbidity and death. Prompt diagnosis and treatment are of
of patients with head injury is outlined in the flowchart in Fig. the utmost importance.41,47
25.6. Consideration is given for the initial presenting severity
and points of potential changes in patient care. Management of Traumatic Brain Injury (Severe)
Patients with GCS scores of 9 to 12 constitute approxi-
mately 10% of head injury patients seen in the emergency TBI is a highly variable and extremely complex phenomenon.
room. They are still able to follow simple commands but are Following the acute primary injury, which often consists of a
GCS 15 GCS 15 GCS 15 GCS 9–13 GCS <9

No LOC LOC <30 mins With risk factors Moderate head Severe head injury
No PTA PTA <60 mins injury
No risk factors No risk factors GCS 13–14
CT recommended CT indicated
Ok for discharge home
Full neuro evaluation Full neuro evaluation
Consider Cardiopulmonary
CT scan abnormal stabilization
Cardiopulmonary
Skull fracture Status Airway control
Pneumocephalus CT indicated Coordinated trauma
No EDH evaluation
SDH Primary and secondary
Re-evaluate GCS IVH injuries
Contusion CT indicated when
SAH patient is stable
Initial GCS 13–15 Initial GCS 9–12 Initial GCS <9 Cerebral edema
Management at
IPH
Current GCS 15 Current GCS < Current GCS < neurotrauma center
15 15 required
Yes
Continue Indication for surgery No Hospital admission
Ok for discharge home severe Observe at least 24 hrs
pathway Yes Repeat CT scan 4–6 hrs
after initial scan
Likely to need
evaluation at Evaluation at
trauma center neurotrauma center
• Figure 25.6 Flowchart for evaluation of head injury following a traumatic event. *Risk factors include
age > 40, headache, vomiting, high-risk mechanism (eg, motor vehicle collision), and anticoagulant use.
CT, head compute tomography image; EDH, epidural hematoma; GCS, Glasgow Coma Scale; IPH,
intraparenchymal hemorrhage; IVH, intraventricular hemorrhage; LOC, loss of consciousness; PTA, post-
traumatic amnesia; SAH, subarachnoid hemorrhage; SDH, subdural hematoma.
380 PART 4 Trauma
focal contusion and more diffuse structural damage, there are Although the exact level of hypotension and hypoxia that
a series of subsequent secondary responses, which include, but is detrimental is unknown, current practice dictates avoiding
are not limited to, excitotoxicity, ischemia, oxidative stress, and a systolic blood pressure less than 90 mm Hg and a PaO2 less
ongoing structural and chemical alterations.103–105 Tradition- than 60 mm Hg. Currently there are insufficient data to
ally, research in recovery of function after TBI has focused on support level I or II recommendations. Prior recommendations
preventing or manipulating early events in order to prevent of the BTF suggested evidence for monitoring blood pressure
chronic dysfunction, which has shown limited improvement and avoiding hypotension defined as SBP less than 90  mm  Hg.12
in TBI outcomes.17–20 As such, the current primary aim of TBI The current recommendation is level III and states that main-
management is to prevent secondary damage. Based on the taining SBP at > 100 mm Hg for patients 50 to 69 years old
available data, the Brain Trauma Foundation and American or at >110 mm Hg for patients 15 to 49 or over 70 years of
Association of Neurological Surgeons established treatment age may decrease mortality and improve outcomes.8 Prior
protocols for the management of TBI in 1995.6–8 Recommen- guidelines demonstrated that level III evidence exists for oxy-
dations of care were formulated relying on scientific evidence genation monitoring and avoidance of hypoxia, and it is rea-
rather than expert opinion. The recommendations were classi- sonable to do so in all trauma patients (PaO2 <60 mm Hg or
fied as level I, II, or III, reflecting the degree of clinical cer- O2 saturation <90%).13
tainty. Table 25.4 presents an outline of these recommendations.
The Brain Trauma Foundation updated these guidelines in Hyperosmolar Therapy
2007 and 2016.8,12
Classically the hyperosmolar therapy for elevated intracranial
pressure consisted of mannitol. Literature has supported the
Medical Therapy use of hypertonic saline as a trauma resuscitation fluid, as well
as a therapy for treating elevated ICP.
Blood Pressure and Oxygenation
The indications for mannitol are as a one-time dose to lower
Airway ICP while obtaining further diagnostic studies or while waiting
Patients with a severe TBI should be evaluated for intubation for definitive treatment. Mannitol has been used on an inter-
as early as possible. Transient respiratory rest is frequently seen mittent basis on a more prolonged timeline for the treatment
in the setting of a severe TBI, and prolonged apnea may often of elevated ICP. There are few human trials that validate the
be the cause of “immediate” death at the scene of an accident. currently used regimens of mannitol in most centers.16
Initiation of artificial respiration can improve outcomes.80 Mannitol’s physiologic effect relies on its ability to expand
Apnea, atelectasis, aspiration, and adult respiratory distress plasma, reduce hematocrit, and increase deformability of
syndrome are frequently associated with severe head injury, erythrocytes, reducing blood viscosity and increasing cerebral
and the immediate management of these patients is the estab- oxygenation delivery. Mannitol’s effect takes place in 15 to 30
lishment of a reliable airway. One hundred percent oxygen is minutes while plasma gradients are established. Mannitol
then used for ventilation until blood gases can be checked and should be used with caution in patients with renal issues or on
appropriate adjustments of the Fio2 made. nephrotoxic drugs, as serum osmolality rises and patients are
at risk for acute tubular necrosis. Serum osmolality should not
Cardiopulmonary generally be allowed to go much above 320 mOsm/L, if pos-
sible, to avoid systemic acidosis and renal failure. There is
In a study of 100 consecutive patients with severe brain injury clinical and laboratory evidence to suggest that long-term,
evaluated on arrival in the emergency room, 30% were hypox- repeated use of mannitol can worsen brain edema and hence
emic (Po2 <65  mm  Hg), 13% were hypotensive (systolic blood reverse the initial beneficial effect.44 Mannitol has been shown
pressure [SBP] <95 mm Hg), and 12% were anemic (hemato- to have an effect on ICP lasting from 90 minutes to 6 hours
crit <30%).76 Approximately 35% of patients who arrive in the or more.
setting of trauma are hypotensive. It has been shown consis- Studies on small volume resuscitations have shown the
tently that the presence of hypotension (systolic blood pressure therapeutic effectiveness of hypertonic saline (HS) administra-
<90 mm Hg) in severe TBI patients increases the mortality tion. Hypertonic saline solutions were administered in poly-
rate from 27% to 50%.105 Hypotension at admission (systolic trauma patients with hemorrhagic shock, and the subset of
blood pressure <90 mm Hg) is one of three factors in severe patients in the group with TBI showed an increase in survival
head injury with a normal CT scan (the other two being age and stabilization of hemodynamic properties.13 As a result of
over 40 years and motor posturing) that, when noted at admis- this finding, other studies have been conducted showing its
sion, are associated with subsequent ICP elevation.72 If the utility in the treatment of elevated ICP in trauma, subarach-
patient is hypotensive, it is vital to restore normal blood pres- noid hemorrhage, stroke, and other pathologic insults.
sure as soon as possible. Hypotension is typically a marker of The effect of HS on ICP is theorized to come from mobi-
severe blood loss, which may be overt, occult, or possibly both. lization of water across the blood-brain barrier, decreasing
Associated spinal cord injury (with quadriplegia or paraplegia), cerebral water content. HS also increases plasma volume and
cardiac contusion or tamponade, and tension pneumothorax cerebral blood flow. HS must be used with caution in patients
are also possible causes that should be considered. with underlying cardiac or pulmonary issues as they are at risk
TABLE Level I (Standards), Level II (Guidelines), and Level III (Options) Recommendations in the Care of the Head-
25.4 Injured Patient
Application/
Indication Level I Level II Level III
Trauma systems Insufficient data All regions in the United States should As delineated in the ACS Committee on Trauma
and the have an organized trauma care Resources for Optimal Care of the Injured
neurosurgeon system. Patient, 1993: neurosurgeons should have an
organized and responsive system of care.
Neurosurgeons should initiate neurotrauma
care planning (prehospital management and
triage), maintain call schedules, review trauma
care records for quality improvement, and
participate in trauma education.
Brain-specific Insufficient data Insufficient data The first priority is complete and physiological
treatments resuscitation. No specific treatments should be
during initial directed at intracranial hypertension in the
resuscitation absence of signs of transtentorial herniation or
progressive neurological deterioration not
attributable to extracranial explanation. If signs
of expanding mass lesion or neurological
deterioration mannitol use can be considered.
Literature indicates that hypertonic saline may
be the resuscitation fluid of choice in trauma
patients with head injury.
Resuscitation Insufficient data Blood pressure should be monitored Oxygenation should be monitored and hypoxia
of blood and hypotension (SBP <90 mm Hg) (PaO2 <60 mm Hg or O2 <90%) avoided.
pressure and avoided.
oxygenation
Hyperosmolar Insufficient data Insufficient data Although hyperosmolar therapy may lower
agents intracranial pressure, there is insufficient
evidence to support a specific
recommendation or specific hyperosmolar
agent. Further studies on hypertonic saline and
mannitol are needed to determine ideal
treatment of elevated ICP.
From 3rd: Mannitol is effective for control of raised
intracranial pressure at doses of 0.25 g/kg to
1 g/kg body weight. Arterial hypotension
should be avoided.
Hypothermia Insufficient data Early (within 2.5 hrs), short term Pooled data indicated that prophylactic
(48 hrs post injury), prophylactic hypothermia is not significantly associated with
hypothermia is not recommended decreased mortality rate in comparison with
to improve outcomes in patients normothermic control subjects. Preliminary
with diffuse injury. findings point to a greater decrease in mortality
risk with maintenance of target temperatures
for more than 48 hours.
Infection Insufficient data Routine ventricular catheter exchange or
prophylaxis prophylactic antibiotic use for ventricular
catheter placement is not recommended to
reduce infection. Antimicrobial-impregnated
catheters may be considered to prevent
catheter-related infections during external
ventricular drainage. Early extubation in
qualified patients can be done without
increased risk in pneumonia.
Continued
382 PART 4 Trauma
25.4 Injured Patient—cont’d
Application/
DVT prophylaxis Insufficient data Graduated compression stockings or intermittent
pneumatic compression stockings (IPC) are
recommended, unless contraindicated
secondary to lower extremity injury; they
should be continued until ambulation. Low-
molecular-weight heparin or low-dose
unfractionated heparin should be used in
combination with mechanical prophylaxis; there
is an increased risk for expansion of intracranial
hemorrhage if present. Insufficient data are
available to recommend preferred agent, dose,
or timing of pharmacological initiation of DVT
prophylaxis.
Indications for Insufficient data Management of severe TBI patients Insufficient data
ICP using information from ICP
monitoring monitoring is recommended to
reduce in-hospital and 2-week
post-injury mortality.
CSF drainage Insufficient data Insufficient data An EVD system zeroed at the midbrain with
continuous drainage of CSF may be
considered to lower ICP burden more
effectively then intermittent use.
Use of CSF drainage to lower ICP in patients
with an initial GCS < 6 during the first 12 hours
after injury may be considered.
ICP treatment Insufficient data ICP treatment should be initiated at A combination of ICP values and clinical and
threshold an upper threshold of 22 mm Hg. brain CT findings should be used in the
decision making for duration and type of
ICP-lowering therapy.
CPP Insufficient data The recommended target CPP value Avoiding aggressive attempts to maintain CPP
for survival and favorable outcomes greater 70 mm Hg with fluids and pressors
is between 60 and 70 mm Hg. may be considered because of the risk of adult
Whether 60 or 70 mm Hg is the respiratory failure.
minimum optimal CPP threshold is
unclear and may depend upon the
autoregulatory status of the patient.
Brain oxygen Insufficient data Insufficient data Jugular venous saturation <50% may be a
monitoring threshold to avoid in order to reduce mortality
and and improve outcomes.
thresholds
Anesthetics, Insufficient data Prophylactic administration of None
analgesics, barbiturates to induce EEG
and sedatives suppression is not recommended.
High-dose barbiturate
administration is recommended to
control elevated ICP refractory to
maximum standard medical and
surgical treatment. Hemodynamic
stability is essential before and
during barbiturate therapy. Propofol
is recommended for the control of
ICP but not for improvement in
mortality risk or 6-month outcome.
High-dose propofol can produce
significant morbidity (propofol
infusion syndrome).
25.4 Injured Patient—cont’d
Application/
Nutrition Insufficient data Feeding patients to attain basal Insufficient data
caloric replacement at least by the
fifth day and at most by the
seventh day post injury is
recommended to decrease
mortality.
Transgastric jejunal feeding is not
recommended to reduce the
incidence of ventilator-associated
pneumonia.
Antiseizure Insufficient data Prophylactic use of phenytoin or Insufficient data
prophylaxis valproate is not recommended for
preventing late PTSs.
Anticonvulsants are indicated to
decreased the incidence of early
PTS (<7 days from injury). Early
PTS is not associated with worse
outcomes.
There is insufficient evidence to
recommend levetiracetam
compared with phenytoin regarding
efficacy in prevention early
posttraumatic seizures and toxicity.
Hyperventilation Insufficient data Prophylactic hyperventilation (PaCO2 < Insufficient data
25 mm Hg) is not recommended. Of note: changes from 3rd edition include the
removal of recommending hyperventilation as a
temporizing measure.
Glucocorticoids The use of None None
glucocorticoids is
not recommended
for improving
outcome or
reducing ICP in
patients with
severe head injury.
In patients with
moderate to severe
TBI, high-dose
methylprednisolone
is associated with
increased mortality
risk and is
contraindicated.
Updated by the Brain Trauma Foundation, 2016.
for pulmonary edema. It must also be used with caution in between 0.25 mg/kg and 1 g/kg of body weight.13 Level II
patients with hyponatremia because rapid correction may lead evidence exists to avoid hypotension (SBP <90 mm Hg).13 In
to central pontine myelinolysis. the most recent updated recommendations the BTF recog-
The theoretic advantage of using HS therapy over mannitol nized that there is currently insufficient evidence to support a
lies in the fact the HS pulls water intravascularly, increasing specific recommendation on the use of a hyperosmolar agent.
blood pressure and maintaining cerebral perfusion. Mannitol Studies of HS show its utility in a continuous infusion form
has the unfortunate result of diuresis and potential decrease in or as bolus treatment form equivalent to or superior to man-
blood pressure, decreasing cerebral perfusion pressure. nitol for refractory elevated ICP.106–109 Although the current
Prior Brain Trauma Foundation guidelines show level II recommendations for HS remain the same, multiple meta-
evidence for mannitol’s effective control of raised ICP at doses analyses have demonstrated at least equivalent ICP control and
384 PART 4 Trauma
clinical outcomes with the use of HS in comparison to man- Deep Venous Thrombosis Prophylaxis
nitol.110 Given that there remains some instances where man-
nitol cannot be given (ie, hypotensive patients), HS appears to Trauma patients are at high risk for deep vein thrombosis
be a safe and effective treatment for elevated ICP and should (DVT) and subsequent pulmonary embolism (PE), which are
be considered when mannitol cannot be given or as potential collectively referred to venous thromboembolism (VTE).112,113
first-line or adjuvant therapy. VTE is associated with increased mortality and morbidity and
increased hospitalization duration and costs.114,115 The risk of
Furosemide developing DVT in the absence of prophylaxis was found to
be 20% after severe TBI in a study by Kaufman and associ-
Furosemide (Lasix) has been used alone and in conjunction ates.116 The treatment of DVT and PE in the TBI patient is
with mannitol in the treatment of raised ICP. It has been complicated by the uncertainty of the safety of anticoagula-
shown that diuresis can be enhanced by the combined use of tion, specifically in postcraniotomy patients or those with
these agents with more pronounced and consistent brain intracerebral hemorrhage from their trauma.
shrinkage. A dose of 0.3 to 0.5 mg/kg of furosemide given Prophylaxis options can be considered in two categories:
intravenously is reasonable. Due to the risk of hypotension mechanical versus pharmacologic. These can be thought of in
with the use of diuretics, it is not currently recommended to a graduated fashion ranging from graduated compression
use furosemide in the brain trauma setting. stockings, intermittent pneumatic compression stockings, and
finally anticoagulant medications (low-dose heparin and low-
Prophylactic Hypothermia molecular-weight heparin).
In studies comparing pharmacologic with mechanical treat-
In theory decreasing brain metabolic demand during the initial ment for the prevention of DVT, pharmacologic treatment is
injury period could reduce ICP and hyperemia, and thus affect more efficacious in preventing DVT, but there is a trend toward
functional outcomes. This provides the basis for therapeutic increased risk of intracranial bleeding.8 In patients who did not
hypothermia in TBI. Although initial studies seemed to suggest start enoxaparin until a full 24 hours had elapsed after injury
some utility of hypothermia in TBI, subsequent analysis and in one study, the progression rate of intracranial bleed was only
further examination has met with inconsistent results. 1.8%, which was comparable to anticoagulant-naive historical
Interpretation of trials involving hypothermia is difficult controls.117,118 Current BTF guidelines show level III evidence
secondary to confounding factors affecting outcome. It appears for graduated compression stockings or intermittent pneu-
that patients who are treated with hypothermia have a trend matic compression stockings and low-molecular-weight
to more favorable outcome, as evidenced by Glasgow Outcome heparin or low-dose unfractionated heparin to be used in con-
Scale scores of 4 to 5. Currently there are no level I or level II junction, but they recognize the risk of intracranial hemor-
recommendations for this treatment. A Cochrane Database rhage expansion.8 Given literature on the safety and efficacy of
review in 2014 found no evidence that hypothermia is benefi- VTE prophylaxis after TBI, it can be argued that low-
cial in the treatment of head injury.111 Hypothermia may be molecular-weight heparin or low-dose unfractionated heparin
effective in reducing death and unfavorable outcomes for trau- should be used in combination with mechanical prophylaxis
matic head-injured patients, but significant benefit was only while understanding there is an increased risk for expansion of
found in low-quality trials.13 High-quality trials found no intracranial hemorrhage. Most studies would seem to suggest
decrease in the likelihood of death with hypothermia, but this that beginning pharmacologic prophylaxis at 48 to 72 hours
finding was not statistically significant.13 Early, short-term pro- post stabilization of any intracranial hemorrhage appropriately
phylactic hypothermia is not recommended in patients with balances the risk and benefit of VTE prophylaxis.119
diffuse injury.8
Intracranial Pressure Monitoring
Infection Prophylaxis
Monitoring ICP can be used to check patients for worsening
In polytrauma patients, the risk of infection can be increased intracranial injury, to help predict outcome, to calculate CPP,
significantly secondary to intubation, invasive lines, and place- and, if ventriculostomy is used, for therapeutic CSF drainage.
ment of intracranial monitors. Infections can be broken down When comparing patients with ICP monitoring to prior
into infection/colonization of ICP monitors and infection/ reports of patients without monitoring, monitored patients
colonization of peripheral lines/pneumonia. Most trials of have improved outcome.8,12
prophylactic antibiotics have shown selection of more viru- Monitoring options include intraparenchymal monitors
lent gram-negative organisms. Current BTF guidelines, at (Camino monitor), ventriculostomy catheter, and brain oxygen
level IIa, recommend early tracheostomy to reduce mechani- tension monitors (Licox). Ventriculostomy remains the gold
cal ventilation days but recognize it does not alter mortality standard, as it can monitor ICP as well as drain fluid as a
rate or nosocomial pneumonia rate. Level III evidence sup- therapeutic treatment to lower elevated ICP.115 The Licox
ports the use of antimicrobial-impregnated catheters to prevent monitor has the ability to measure ICP as well as brain oxy-
catheter-related infections during external ventricular drain genation. The utility of these measurements has been suggested
(EVD) use.8 to decrease morbidity and mortality rates, as discussed earlier.
Currently BTF guidelines show level IIb evidence for lowering measures, as values above that level are associated with
placing an ICP monitor in severe TBI, as it may reduce in- increased mortality.8
hospital and 2-week postinjury mortality.8 Prior level III evi- The management paradigm of elevated CPP (>70 mm Hg)
dence for ICP monitoring in patients with severe TBI with a for treatment of TBI became popular in the late 1980s. It has
normal CT and two or more of the following: (1) age over 40 since been found that the optimal CPP ranges between 60 and
years, (2) unilateral or bilateral motor posturing, or (3) systolic 70 mm Hg.8 Current level III evidence recommends avoiding
blood pressure less than 90 mm Hg did not meet the standards driving CPP more than 70 mm Hg because systemic compli-
for current recommendation.13,72 cations are increased when the CPP is elevated above this level.
Current level IIb evidence suggests a CPP less than 60 mm Hg
Intracranial Pressure Monitor Technology should be avoided; the optimal range is somewhere between
60 and 70 mm Hg.8 Ancillary monitoring of blood flow, oxy-
The ideal monitor should have several useful qualities includ- genation, or metabolism helps to facilitate on a patient-by-
ing ease of insertion, safety of insertion, accuracy, reliability, patient basis the optimal CPP.
cost effectiveness, and the need for minimal troubleshooting.
The Association for the Advancement of Medical Instrumen- Brain Oxygenation Monitoring and Threshold
tation (AAMI) was developed in association with a neuro- for Treatment
surgery committee. This association led to the development
of the American National Standard for Intracranial Pressure The monitoring of cerebral oxygenation has taken form in two
Monitoring Devices. The job of this standard is to provide different ways: (1) brain oxygenation monitoring probes and
labeling, safety, and performance requirements for intracranial (2) jugular venous oxygen monitoring. Abnormal venous
monitors. According to the AAMI standard, ICP monitors jugular oxygen levels have been correlated with poor outcomes.
should have (1) pressure ranges of 0 to 100 mm Hg, (2) accu- High and low values have been associated with poor outcomes,
racy ±2 mm Hg in the range of 0 to 20 mm Hg, and (3) which are believed to be related to brain metabolism. Venous
maximum error of 10% in the range of 20 to 100 mm Hg.13 jugular oxygenation is more helpful when arteriojugular differ-
The current ICP monitors work via external strain, cathe- ence in oxygenation is measured, most likely giving a more
ter tip strain, or catheter tip fiberoptics. Catheter tip fiber- accurate picture of cerebral metabolism.
optics are calibrated prior to intracranial insertion and Multiple studies have shown that a diminished oxygenation
are at risk for measurement drift and possible inaccurate of brain tissue (as measured by the partial pressure of oxygen
readings. in brain tissue, PBTO2) is correlated with poorer outcomes and
Current available ICP monitors were ranked based on accu- death.121–123 Treatments to keep PBTO2 greater than 25 mm Hg
racy, reliability, and cost. The order of ranking is as follows: (1) along with CPP and ICP management have shown decreased
intraventricular devices (fluid-coupled catheter), (2) intraven- mortality rates when compared to outcomes of treating CPP
tricular devices (microstrain gauge or fiberoptic), (3) parenchy- and ICP alone.121–123 However, due to contradictory evidence
mal pressure transducers, (4) subdural devices, (5) subarachnoid and the relative lack of quality studies, current recommenda-
fluid couple devices, and (6) epidural devices.13 tions do not include the use of cerebral oxygen monitoring.8
The ventricular catheter connected to an external strain Even though treatments to maintain cerebral oxygenation
gauge remains a cost-effective and reliable method of ICP seem promising, there is only level III evidence for jugular
monitoring.13 However, solid-state monitors such as the venous monitoring.8 The treatment threshold for jugular
Camino or Codman systems are generally reliable, although venous saturation is less than 50%.8
they cannot be recalibrated once they have been inserted.
In addition to cost effectiveness, level III evidence in the Anesthesia, Analgesics, and Sedatives
current BTF guidelines support the use of CSF drainage to
lower ICP in patients with an initial GCS <6 during the first Pain medications and sedatives have often been used to calm
12 hours. An EVD system zeroed at the midbrain with con- patients and prevent a dangerous rise in ICP that may be
tinuous drainage of CSF appears to be more effective than associated with severe agitation. Barbiturates have been used
intermittent use.8 since the 1930s with the knowledge of their ability to lower
ICP.124 Barbiturates are also known to decrease cerebral metab-
Treatment Thresholds and Optimal Cerebral olism having a cerebral protective effect.125,126 The use of bar-
Perfusion Pressure biturates couples blood flow to cerebral metabolism, decreasing
The threshold to treat elevated ICP should be based on the blood flow where metabolism is low and shunting blood flow
patient’s CT scan, clinical picture, and ICP number. Multiple to areas where metabolism is high.
small studies show the optimal treatment window to be Prophylactic administration has not proved to be effective
between 15 and 25 mm Hg. It is important to emphasize that in preventing elevated ICP. The Cochrane group reviewed two
patients with temporal hematomas or posterior fossa hemor- randomized controlled trials of barbiturate use showing no
rhages may have deceptively low ICP despite being under evidence of improved outcomes in severe TBI. They also found
neurologic duress. Current level II evidence recommends treat- that there was a 25% chance of hypotension when receiving
ing patients with ICP greater than 22 mm Hg with ICP barbiturates, offsetting any effect of ICP lowering. To monitor
386 PART 4 Trauma
for appropriate sedation, patients are placed on EEG monitor- administered anticonvulsants, a double-blind study of 404
ing. Dosing to burst suppression reduces cerebral metabolism patients with severe head injury, who were randomized to
to maximal reduction. receive phenytoin or placebo beginning within 24 hours of
Propofol has been studied because of its quick onset of injury and continuing for 1 year, found that phenytoin reduced
action, and its short duration of action allows quick neurologic the incidence of seizures in the first week after injury but not
assessment. Studies have shown that propofol does have a thereafter.131 This study appears to justify stopping prophylac-
minimal effect at lowering ICP, and one study reported high- tic anticonvulsants after the first week in most cases. In patients
dose propofol showing a favorable neurologic outcome when who have had a seizure, anticonvulsants are continued for at
compared to a low-dose propofol.127 Propofol must be used least a year.
with caution, especially in high doses, as some patients develop With the use of Keppra (levetiracetam) as an antiepileptic,
propofol infusion syndrome, which may lead to death. with its relatively low side effect profile, studies have been done
BTF guidelines currently have level II evidence that pro- to evaluate its efficacy compared to the gold standard Dilantin
phylactic administration of barbiturates to burst suppression (phenytoin). It does appear to be as effective as Dilantin at
is not recommended. High-dose barbiturate treatment is preventing early seizures with a lower side effect profile.132,133
recommended for refractory ICP control; however, hemody- It should also be noted the Keppra had a tendency to show
namic stability must be maintained and improved outcomes more seizure activity on EEG analysis in one study.132
have never been proved.8,13 Propofol is recommended for Current BTF recommendations show level II evidence that
the control of ICP, but not for improvement of 6-month Dilantin and valproate are not indicated to prevent late onset
outcomes.8,13 seizure activity.8 Level II evidence shows that antiepileptic
medication is indicated to prevent early onset seizure (within
Nutrition 7 days); however, early onset posttraumatic seizure has not
been proved to be associated with worse outcomes.8
It is known that patients with TBI have metabolism dysfunc-
tion. These patients require a higher nitrogen intake, as their Hyperventilation
nitrogen balance becomes negative. Studies show that TBI
patients’ caloric intake had a mean increase of 140%. Studies Hyperventilation has been used in the treatment of severe TBI
have shown a decreased mortality rate when full caloric replace- since the late 1990s. A pathophysiologic understanding of TBI
ment is achieved by 7 days. Typically to reach this goal caloric and the mechanism of ICP lowering of hyperventilation have
replacement begins around 72 hours after injury. put it under scrutiny. Hyperventilation decreases ICP by
There are three ways to initiate early feeding: gastric, jejunal, decreasing CO2 leading to cerebral vasoconstriction. This in
and parenteral. It is important to maintain normoglycemia in turn leads to decreased cerebral blood flow (CBF). Aggressive
head injury patients, as hyperglycemia has been associated with sustained hyperventilation may lead to cerebral ischemia and
worse outcomes. stroke, especially in the severe TBI patient who may already
Current level II evidence recommends that patients should have alterations in CBF and autoregulation.
be fed to attain basal caloric replacement by the fifth day and Current BTF recommendations show level II evidence
at most seven days after injury.8 Transgastric jejunal feeding is against the routine use of prophylactic hyperventilation to
recommended to reduce the incidence of ventilator-associated PaCO2 less than 25 mm Hg.8 Hyperventilation should be
pneumonia.8 avoided in the first 24 hours after TBI when CBF may be
critically reduced. Prior recommendations for the use of hyper-
Antiseizure Prophylaxis ventilation as a temporizing measure in critically ill patients
The role of prophylactic anticonvulsants in patients with severe were not supported by further evidence in the most recent
head injury has been more clearly defined with the advent of update.8,13
the published guidelines. Posttraumatic seizures are classified
as “early,” occurring within 7 days of injury, or “late,” occurring Steroids
more than 7 days after the injury.128,129 It is desirable to prevent
early and late seizure activity, although these medications have Although steroids are clearly useful in reducing the edema
been associated with adverse and neurobehavioral ill effects. associated with brain tumors, their value in head injury is not
The classic study by Jennett130 found posttraumatic epilepsy to clear. In fact, most studies to date have not demonstrated any
occur in about 5% of all patients admitted to the hospital with beneficial effect associated with steroids in terms of either ICP
closed head injuries and in 15% of those with severe head control or improved outcome from severe head injury. Further-
injuries. Three main factors were found to be linked to a high more, there is some evidence that steroids may have a deleteri-
incidence of late epilepsy: early seizures occurring within the ous effect on metabolism in these patients.
first week, an intracranial hematoma, or a depressed skull Level I evidence currently recommends against the routine
fracture. Posttraumatic seizures are also associated with GCS use of steroids for improving outcome or reducing ICP.8,13
scores lower than 10, a penetrating head wound, or a seizure It has been shown in patients with moderate to severe
within the first 24 hours. Although certain earlier studies TBI on high-dose methylprednisolone that mortality rate is
were unable to show significant benefit of prophylactically increased.8,13
Surgical Therapy explained and reversed or any deterioration in neurologic

Indications for Surgery status warrants prompt repetition of the CT scan followed by
appropriate corrective measures.
An important reason for operating on a mass lesion is a Because there is great concern about increased ICP as a
midline shift of 5 mm or more. Such a shift may be dem- result of a mass lesion, the anesthetic agents that are used in
onstrated by CT scan or occasionally by angiography. Most head-injured patients preferably should not increase the ICP.
epidural, subdural, or intracerebral hematomas associated with Nitrous oxide has only a slight vasodilatory effect and generally
a midline shift of 5 mm or more are surgically evacuated. In a does not cause a significant ICP increase. It is therefore con-
patient who has a small hematoma causing less than a 5-mm sidered a good agent for use in the head-injured patient. A
shift and who is alert and neurologically intact, a conserva- commonly used combination is nitrous oxide with oxygen,
tive approach is justified. However, the patient may deterio- intravenous muscle relaxant, and propofol. Mannitol prior to
rate, and very close observation is vital. Should there be any and during induction can blunt the vasodilatory effect and
change in mental status, a repeat CT scan should be obtained limit intracranial hypertension to some degree while the
immediately. cranium is being opened. If, during surgery, malignant brain
It is reasonable is to operate on comatose patients with an swelling occurs that is refractory to mannitol, pentobarbital in
intracranial mass lesion and 5 mm or more of midline shift large doses (5–10 mg/kg) should be used. This agent can cause
unless they are brain-dead. This is based on evidence that some hypotension, especially in hypovolemic patients, and should
patients with bilaterally nonreactive pupils, impaired oculoce- therefore be used with caution.
phalic responses, and decerebrate posturing can nevertheless
make a good recovery. In one series, 3 of 19 such patients who
were treated maximally ended up in the “good” or “moderately Special Consideration: Surgery for Diffuse
disabled” category, despite the foreboding constellation of Brain Injury or Intracranial Pressure Control
signs.134
The management of brain contusions is somewhat less clear Outcomes in severe brain injury can often be devastating,138
cut. Galbraith and Teasdale,135 in their series of 26 patients and surgical intervention for ICP control or in injuries where
with acute traumatic intracranial hematomas who were no mass lesions are identified remains a difficult topic. The
managed without surgery, found that all patients with ICP Decompressive Craniectomy (DECRA) trial enrolled patients
greater than 30 mm Hg eventually deteriorated and required without mass lesions whose ICP could not be controlled by
surgery. In contrast, only one patient with ICP less than standard measures for 15 minutes and randomized them to
20 mm Hg deteriorated. Patients in the 20 to 30 mm Hg bifrontal craniectomy or continued medical care.139 The sur-
range were about evenly divided between the surgical and gical arm suffered significantly worse functional outcomes,
nonsurgical groups. although this group also had a greater proportion of patients
Patients with brain contusions who could follow com- with bilaterally fixed and dilated pupils. A similar study
mands at admission did not require ICP monitoring and, as examined the efficacy of bifrontal craniectomy or unilateral
a rule, did well with simple observation. However, those who hemicraniectomy in patients with ICP that could not be con-
could not follow commands (in the absence of a focal lesion trolled for between 1 and 12 hours. This study showed a
in the speech area) often had intracranial hypertension and significant mortality benefit, but survivors were more likely
needed to have their ICP monitored. The majority of these to be disabled. There was no difference in the rate of good
patients who had a midline shift of 5 mm or more required neurologic outcomes.140 Analyses of smaller, nonrandomized
surgery.136 studies have demonstrated both benefit and no benefit with
It has been demonstrated conclusively that patients with a the use of decompressive operations, and patients should
large (over 30 mL) temporal lobe hematoma have a much be carefully evaluated prior to the use of decompressive
greater risk of developing tentorial herniation than those with craniectomy.141,142
a frontal or parieto-occipital lesion.137 The bias should there-
fore tilt toward early surgery in such cases. Subdural Hematomas
Once a decision has been made as to whether or not the
patient is a surgical candidate, he or she is promptly moved to Acute subdural hematomas may result from bleeding from
the operating room or to the neurosurgical intensive care unit lacerated brain, ruptured cortical vessels, or an avulsed bridg-
(NICU), respectively. If the patient is harboring a mass lesion, ing vein. The most common sites for brain injury are the
mannitol (1–2 g/kg) should be administered en route to the inferior frontal lobes and the anterior temporal lobes. In the
operating room. As in all the maneuvers undertaken thus far, surgical management of subdural hematomas, a large fronto-
time is of the essence. The sooner the mass lesion is evacuated, temporoparietal question mark–shaped incision is recom-
the better the possibility of a good recovery.41 If, on the other mended. This allows the surgeon to deal with bleeding near
hand, no surgical lesion is found, the patient is carefully moni- the midline as well as to débride effectively parts of the frontal,
tored in the NICU, both clinically and with various physio- temporal, and parietal lobes as needed. If the patient is deterio-
logic parameters, notably ICP recordings and serial CT scans. rating rapidly, a quick temporal decompression can be per-
Any rise in ICP above 22 mm Hg that cannot be readily formed via a small craniectomy before opening up the rest of
388 PART 4 Trauma
the flap. This maneuver could reduce the probability of tento- the use of the operating room for the closure of such wounds
rial herniation. A generous subtemporal craniectomy may be is recommended.
useful in postoperative ICP control. In general patients who
received a craniotomy for SDH evacuation demonstrated Venous Sinus Injuries
better outcomes than those who received a craniectomy.143 This Injuries of the major venous sinuses are among the most dif-
is likely due to differences in the underlying injury in patients ficult problems a neurosurgeon has to face. As a general rule,
who had received a craniectomy, but it highlights that even in ligation of the anterior third of the superior sagittal sinus is
surgery for trauma consideration should be given to how tolerated well; ligation of the posterior third is most likely to
extensive a surgical intervention is necessary. produce massive venous infarction of the brain. Ligation of the
middle third of the superior sagittal sinus has somewhat unpre-
Epidural Hematomas dictable effects. A dominant transverse sinus usually cannot be
safely ligated. Although the use of shunts in the repair of these
Epidural hematomas are most often located in the temporal major sinuses has been often described, simple pressure with
region and often result from tearing of the middle meningeal the use of hemostatic agents is much more practical in the
vessels due to a temporal bone fracture. Venous epidural hema- majority of cases.
tomas may occur as a result of a skull fracture or an associated
venous sinus injury. These tend to be smaller and usually have Posterior Fossa Hematomas
a more benign course. Such hematomas often present several
hours or days after the initial injury and can be managed non- Posterior fossa hematomas, fortunately, are less common than
surgically. However, usually an epidural hematoma represents supratentorial hematomas. In general, an aggressive surgical
a surgical emergency and should be evacuated as rapidly as approach is recommended for most of these lesions because
possible. Every effort should be made to relieve the pressure as the patient can deteriorate rapidly. Because it generally takes
soon as possible. A more localized craniotomy flap is warranted longer to expose the posterior fossa and because the brainstem
for epidural hematomas. structures are likely to suffer irreversible damage from a shorter
period of compression, the surgeon does not have much leeway
Contusions/Intracerebral Hematomas in terms of time.
Contusions are most often located in the anterior and inferior

frontal lobes as well as the anterior temporal lobes. Commonly, Prognosis
the CT appearance of a contusion evolves over several days so
that what are initially small “salt and pepper” lesions coalesce The Glasgow Outcome Scale (GOS) has been widely accepted
to form hematomas. This phenomenon is also termed delayed as a standard means of describing outcome in head injury
traumatic intracerebral hematoma. Patients who are awake and patients.139 The traditional GOS has five categories, which
alert but demonstrate cerebral contusions can be managed were extended to eight for the Glasgow Outcome Scale–
without surgery in the majority of cases.136 However, patients Extended (GOSE) (Table 25.5).145 These categories are some-
who are comatose and have a significant midline shift usually times lumped together as either favorable outcomes (G, MD)
need surgery. Between these two extremes, there are patients or unfavorable outcomes (SD, V, or D). Posttraumatic amnesia
who demonstrate alterations in levels of consciousness or focal is a fairly good prognostic indicator of outcome. First described
neurologic deficits; for these patients, the decision to under- by Russel in 1932, posttraumatic amnesia is defined as the
take surgical débridement is not always easy. As a general duration of time from the point of injury until the patient has
rule, débridement of the left frontal and temporal lobes is continuous memory of ongoing events. In most cases, the
undertaken more reluctantly because the speech area is on retrospective measurement of posttraumatic amnesia is unreli-
this side. able. Therefore Harvey Levin developed the Galveston Orien-
tation and Amnesia Test (GOAT) to provide an objective
Depressed Skull Fractures reliable measurement of posttraumatic amnesia. The duration
of posttraumatic amnesia has proved to be highly correlated
A skull fracture is considered significantly depressed if the with ultimate functional outcomes.146
outer table of the skull lies below the level of the inner table Several statistical studies have reported the use of various
of the surrounding bone. Sometimes the depression may not prognostic indicators for predicting outcome in severe head
be evident on plain radiographs, but it is usually seen clearly injury. Because of unexpected medical and surgical complica-
on the CT scan. Most closed depressed fractures occur in tions and the inherent unpredictability of disease, there is no
young children and may be of the ping-pong ball variety. absolutely unfailing prediction system. Based on experience
Surgery may be undertaken in such cases for cosmetic reasons with a large group of patients, an algorithm has been developed
or because of brain compression. In compound depressed frac- for approximate expected outcomes associated with certain
tures, the wounds are often dirty and contaminated. Hair, skin, prognostic features.147 An attempt to predict mortality with
or other foreign debris may be insinuated between the depressed 100% certainty appeared to work in one center.148 However,
bone fragments. Therefore except in the simplest of injuries, when this system was applied to other patient populations,
TABLE Persistent cognitive deficits can be categorized into one

25.5 Glasgow Outcome Scale Extended of three general domains: attention and processing speed,
memory, and executive function.151–154 Of these, memory dif-
Glasgow
ficulties are the most commonly reported and most difficult
Outcome Score—
for patients and caregivers.153 In addition to cognitive difficul-
Score Extended (GOSE) Description
ties, TBI survivors often experience behavioral difficulties char-
1 Dead (D) acterized by enhanced emotional lability and alterations in
2 Vegetative State Patient exhibits no obvious affect.155 Importantly, a prior TBI has been shown to be a risk
(VS) cortical function factor for developing psychiatric and psychotic disorders,156
3 Lower severe Able to follow commands,
Alzheimer disease, Parkinson disease, depression, and bipolar
disability (SD−) needs help with all disorders.157 Due to its often diffuse nature and the variety of
activities, unable to live cognitive disturbances experienced post TBI, it has been dif-
alone ficult to localize a single disruption in neural function that
4 Upper severe Able to follow commands, could explain such an array of events. Indeed, persistent defi-
disability (SD+) needs help with most cits experienced by TBI patients are probably due to a wide
activities; unable to live spectrum of different neural system dysfunctions. This can
alone make treatment of long-term deficits difficult.
5 Lower moderate Able to live independently, What is clear in both “mild” and more severe forms of TBI
disability (MD−) requires some assistance, is that there remains a significant opportunity to advance the
unable to return to work research in understanding the pathophysiology of TBI, as well
or school
as its long-term neuropsychologic effects, and to translate those
6 Upper moderate Able to live independently, advances into meaningful improvements in clinical care and
disability (MD+) requires little assistance, neurologic outcome.
unable to return to work
or school
7 Lower good Able to return to work or
Acknowledgments
recovery (GR−) school with mild difficulty
Special thanks to Clifford M. Houseman, Shawn A. Belverud,
8 Upper good Able to return to normal and Raj K. Narayan who coauthored the prior chapter on this
recovery (GR+) activities topic.
Selected Key References

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Trauma

PRIMARY INJURY SECONDARY INJURY

• Due to force associated with mechanism • Cellular mechanism and microenvironment

• Shearing of blood vessels • Glutamatergic release

Traumatic brain injury classifications

• Figure 25.2 Simplified classification scheme for evaluation of head-injured patients.

Magnetic Resonance Imaging AUTOREGULATION CURVE

Pupils tone and pupillary constriction. Continued herniation leads to

Evaluation of the Head Injury Patient

GCS, Glasgow Coma Scale; SBP, systolic blood pressure.

• Figure 25.5 Components of the Sports Concussion Assessment Tool (SCAT).

GCS 15 GCS 15 GCS 15 GCS 9–13 GCS <9

Updated by the Brain Trauma Foundation, 2016.

Surgical Therapy explained and reversed or any deterioration in neurologic

Contusions are most often located in the anterior and inferior

TABLE Persistent cognitive deficits can be categorized into one

Selected Key References

References Neurotrauma: Molecular, Neuropsychological, and Rehabilitation

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