Traumatic Brain Injury PDF

2013 Neurocritical Care Society Practice Update
Traumatic Brain Injury

Joshua M. Levine MD
University of Pennsylvania
Philadelphia, PA
Monisha A. Kumar MD
University of Pennsylvania
Philadelphia, PA
CLINICAL CASE
A 17-year-old man is admitted to the intensive care unit (ICU) from the Emergency Department
(ED) with severe traumatic brain injury from a motor vehicle collision. His initial Glasgow Coma
Scale (GCS) score in the field was 3. His blood pressure was 115/75 mmHg, and his hemoglobin
saturation was 88%. He was bag mask ventilated by EMS, his neck was immobilized with a
cervical collar, and he was transported to the ED. Upon arrival in the ED, blood pressure was
85/60 mmHg, pulse was 120 beats/min, respiratory rate was 8, and hemoglobin saturation was
88%. Rapid sequence intubation was performed. He was mechanically ventilated with 50%
fraction of inspired oxygen to maintain PaO2 > 60 mmHg and a minute ventilation sufficient to
maintain PaCO2 between 35 and 45 mmHg. Two liters of intravenous normal saline were
administered to maintain systolic blood pressure above 90 mmHg. On examination in the ED
his GCS score was 3 and cranial nerve function was intact. He had retroauricuar ecchymosis
and the remainder of his trauma survey was unremarkable. A non-contrast head CT scan
demonstrated small bifrontal contusions and a basilar skull fracture. CT scans of his chest,
abdomen and pelvis were normal. Laboratory evaluation, including a complete blood count,
electrolytes, glucose, coagulation profile, blood alcohol level, and urine toxicology screen was
unremarkable. A ventriculostomy was placed for intracranial pressure (ICP) monitoring and he
was admitted to the ICU. Several hours after admission to the ICU, his intracranial pressure
rose from a baseline of 15 mmHg to 30 mmHg. CSF was drained and a bolus of mannitol was
administered empirically. A STAT repeat head CT scan showed significant expansion of his
contusions. His ICP remained elevated and an intravenous infusion of hypertonic saline was
initiated. Within 30 minutes his ICP declined and remained < 20 mmHg while hypertonic saline
infused. On hospital day #3 weaning of the hypertonic saline infusion was begun and it was
discontinued on hospital day #4. ICP remained stable and a tracheostomy was placed on
hospital day #5. The patient remained comatose and on hospital day #7 an MRI showed
evidence of extensive diffuse axonal injury on diffusion-weighted and gradient echo sequences.
OVERVIEW
Traumatic brain injury (TBI) is a major health problem worldwide. In developed countries it is
the leading cause of death and disability in young adults, and in developing counties its
incidence is steadily increasing. The term, traumatic brain injury encompasses a

heterogeneous group of pathological disorders, each with its own clinical presentation,
pathophysiology, natural history, treatment, and prognosis. TBI may be categorized by
mechanism of injury, clinical severity, radiological appearance, pathology, or distribution (focal
vs. diffuse). A major pathophysiology concept that has become evident in recent years is that
brain damage not only results from the initial physical insult (primary injury), but also continues
to occur in the ensuing hours to days (secondary injury). Mitigation of secondary injury has
become the central goal of pre-hospital and intensive care. In 1995 the Brain Trauma
Foundation published guidelines for the management of severe TBI. These guidelines were
revised in 2000 and again in 2007 [1]. These guidelines serve as the foundation for modern
intensive care management of TBI. Adherence to the guidelines has been associated with
improved outcome, and with reduced mortality and hospital length-of-stay.
EPIDEMIOLOGY
TBI is common and has significant societal impact. In 2009, the Centers for Disease Control
estimated that in the US at least 2.4 million emergency department visits, hospitalizations, or
deaths were related to a TBI. Nearly one third of all injury-related deaths include a diagnosis of
TBI. 5.3 million US residents are living with TBI-related disabilities, including long-term and
psychological impairments. The economic cost of TBI in 2010 was estimated at $76.5 billion
dollars, including both direct and indirect costs, but excluding combat-related TBI treatments
[2].
Risk factors for TBI include lower socioeconomic status, pre-morbid cognitive and psychiatric
disease, and male gender. As with other traumatic injuries, TBI affects more men than women.
Overall, the ratio of men to women affected is between 2:1 and 2.8:1. For severe TBI, the ratio
is closer to 3.5:1.
In the civilian population, the leading causes of TBI are falls (35.2%), motor vehicle crashes
(17.3%), blunt impact (16.5%), and assaults (10%). Falls preferentially account for TBI at
extremes of age, namely <15 years and > 65 years. Motor vehicle collisions (MVC) are the
predominant cause of TBI in teens and young adults. Penetrating TBI is far less common than
blunt (closed head) injury but is associated with worse prognosis. Most civilian penetrating
head injury is the result of high-velocity missiles (bullets). Low-velocity non-missile penetrating
injuries are less common and have better outcomes. While rare in the civilian population, blast
TBI is observed primarily in soldiers exposed to improvised explosive devices.
PATHOPHYSIOLOGY
CEREBRAL HEMODYNAMICS
In a general sense, for patients with TBI, the immediate goal of resuscitation is restoration and
maintenance of adequate tissue metabolism by ensuring sufficient delivery of fuel, typically
oxygen and glucose, to meet cellular metabolic demands. Cerebral blood flow (CBF)
approximates fuel delivery but is difficult to measure. Intracranial pressure (ICP), which is
easier to measure, and cerebral perfusion pressure, which is calculated as mean arterial
pressure (MAP) ICP, are used as surrogates for CBF. If modeled as flow through a rigid tube,
then according to Poiseuilles law, CBF is proportional to CPP and to the radius of the vessel
raised to the 4th power, and is inversely proportional to blood viscosity. Cerebral blood flow is
maintained constant across a wide range of cerebral perfusion pressures through modulation of
vascular diameter (autoregulation). When autoregulation is intact, the primary determinant of
CBF is therefore vessel radius and CPP has little impact. Conversely, when autoregulation is
absent (vessel radius remains constant) changes in CPP significantly impact CBF i.e. blood flow
becomes pressure passive (Figure 1). In patients with TBI, autoregulation may be preserved,
partially intact, or absent, and there is often considerable regional heterogeneity of
autoregulation status within the brain. The use of ICP and CPP as surrogates for CBF therefore
assumes that autoregulation is disturbed.
ICP is defined by the Monro-Kellie hypothesis which states that ICP is the sum of the pressures
exerted by the contents of the intracranial vault, namely, blood, tissue, and CSF. The cranial
compartment can accommodate roughly 150 cc of additional volume before ICP rises. This is
due to compensatory mechanisms. As intracranial volume is added, low-pressure veins
collapse and cerebral blood volume decreases. As further volume is added, there is egress of
CSF from the cranial subarachnoid space into the spinal subarachnoid space. Once these
decreases in cerebral blood and CSF volumes are maximized, the addition of further volume
leads to a sharp rise in ICP. Cerebral compliance is defined as the change in cerebral volume
per unit change in pressure. Cerebral elastance is the inverse of cerebral compliance. Because
of compensatory mechanisms, the cerebral compliance curve is not linear, but rather
logarithmic (Figure 2). TBI patients with intracranial hypertension typically operate on the
steep portion of the compliance curve, where small changes in intracranial volume are
associated with large changes in ICP.
The pathophysiology of a specific TBI is largely dictated by its broad mechanistic category.
Blunt trauma, penetrating trauma, and blast injury each have attendant pathophysiological
consequences that partially overlap. Conversely, an individual patient may have more than one
mechanism of injury. This is especially true in combat-related TBI where blast injury, blunt
injury, and penetrating injury frequently co-exist. Within each mechanistic category, the
pathophysiology may be subdivided into primary (immediate) injury and secondary (delayed)
injury.
PRIMARY CEREBRAL INJURY
Blunt TBI
Primary injury is caused by impact of the head with a blunt object and rapid
acceleration/deceleration. These result in mechanical forces that cause tissue distortion,
compression, shearing, and swelling. Manifestations of these injuries include cerebral
contusions, extra-axial hematomas (epidural, subdural, and subarachnoid hemorrhages), and

diffuse axonal injury.
Contusions are regions of hemorrhagic necrosis due to acceleration/deceleration. They are
commonly observed, particularly in the gyral crests of the orbitofrontal and anterior temporal
regions. Contusions may be ipsilateral to the site of impact (coup) if the head is relatively
immobilized when struck, or contralateral to the site of impact (contra-coup) if the head is not
immobilized. While contusions may appear as multifocal areas of patchy hemorrhage, these
hemorrhages may coalesce into a larger parenchymal hematoma. Roughly one-third of
contusion expand (blossom) in the first 24 hours after injury.
Epidural hematomas (EDH), observed in roughly 5% of patients with TBI, typically occur in the
context of a skull fracture that involves the groove of the middle meningeal artery (MMA).
While laceration of the MMA is most commonly responsible for EDH, epidural bleeding may
also occur from injury to the middle meningeal vein, the diploic veins, or the venous sinuses.
EDH are typically lens shaped (convex) and do not cross skull suture lines.
Subdural hematomas (SDH) are typically caused by rupture of the bridging veins and are often
associated with severe underlying brain injury and high mortality. They usually occur over the
cerebral convexities and are bilateral in roughly 15%, however, they may also occur along the
tentorium or the falx. Subdural hematomas are classically crescent-shaped (concave) and cross
skull suture lines. The mechanism of injury responsible for SDH differs by age group; over 50%
of SDH are caused by MVC in the 18-40 year age group, whereas falls comprise the vast
majority of SDH in those >65 years of age.
Subarachnoid hemorrhage results from tearing of small pial vessels. Blood is typically located
over the cerebral convexities and is often confined to a few sulci or fissures. However,
subarachnoid blood may distribute diffusely over the cortical surface, into the basal cisterns, or
into the ventricles. Isolated intraventricular hemorrhage due to trauma is unusual.
Diffuse axonal injury (DAI) is commonly observed after rapid acceleration and deceleration of
the head, typically in the lateral plane. DAI is both a form of primary and a form of secondary
injury. There may be immediate mechanical damage (primary injury) to structural elements of
axons, such as microtubules, at the time of the trauma. This typically occurs in severe TBI that
involves tearing of tissue. It has become evident, however, that axonal swelling, and ultimately
axotomy, is the consequence of cellular cascades that are initiated by the trauma (secondary
injury). This form of secondary injury may occur in severe, moderate, and even mild TBI
(concussion). In severe cases, DAI is multifocal and bilateral. Regions commonly affected
include the junction between cortex and white matter, white matter structures close to the
midline (corpus callosum, internal capsule), the brainstem, cerebellum, and the corona radiata.
Histopathologically, DAI is characterized by the presence of axonal swellings that are the result
of accumulated material due to interrupted axonal transport. These swellings may have a
periodic arrangement along the length of the axon (axonal varicosities), or there may be a
single point of swelling (axonal bulb or retraction ball) that likely reflects axonal
disconnection. Some have proposed the use of the term, traumatic axonal injury (TAI) or
diffuse traumatic axonal injury (dTAI) to describe theses pathological and pathophysiological
changes [3].
Penetrating TBI
While contusions, epidural hematomas, subdural hematomas, and subarachnoid hemorrhage
are commonly observed in penetrating TBI, the hallmark of penetrating TBI is the cerebral
laceration (figure 3e). In penetrating TBI, the nature of primary injury is largely dictated by the
ballistic properties of the projectile (e.g. bullet) and any secondary projectiles (e.g. bullet
fragments, bone fragments). As a missile penetrates the brain, it tears the parenchyma,
leaving a track with necrosis and hemorrhage (laceration). In the wake of the projectile, tissue
is compressed, collapses and re-expands in a repeating wave-like pattern that further injures
tissue. The degree of tissue injury is dependent on the kinetic energy transferred from the
missile to the tissue. Since kinetic injury = (mass)(velocity)2, higher velocity projectiles cause
more tissue injury than lower velocity projectiles. Projectile paths that cross the hemispheres,
violate the ventricles, or that involve the brainstem have a poor prognosis and are most
frequently fatal.
Blast TBI
Cerebral blast injury occurs when acoustic, electromagnetic, light, and thermal energy (blast
wave) that emanates from an explosion are transferred to the brain directly through the
cranium, and indirectly through oscillating pressures in fluid containing structures, such as
blood vessels. While much remains to be elucidated about the pathophysiology of blast TBI,
some important distinguishing features have been observed. Diffuse axonal injury occurs in a
dose-dependent fashion that likely differs from the DAI observed with closed-head injury.
Malignant cerebral edema may occur rapidly (within an hour) as opposed to the more slowly
developing edema seen in blunt TBI (hours to days). Cerebral vasospasm may occur in up to
50% of moderate to severe blast TBI and may last as long as one month. Lastly, patients with
blast TBI frequently have concomitant blast injury to the eyes and to the auditory and
vestibular systems [4].
SECONDARY CEREBRAL INJURY
Secondary injury involves a host of cellular and molecular cascades that promote cell death,
and that exacerbate cerebral edema and ischemia. While these processes may begin
immediately, they often last for hours to days or longer. Studies of secondary injury are largely
in experimental models and in humans with blunt TBI. Mechanisms of secondary injury include:
neuronal depolarization, disturbance of ionic homeostasis, glutamate excitotoxicity, generation
of nitric oxide and oxygen free radicals, lipid peroxidation, blood-brain barrier disruption,
secondary hemorrhage, ischemia, cerebral edema, intracranial hypertension, mitochondrial
dysfunction, axonal disruption, inflammation, and apoptotic and necrotic cell death. Cerebral
ischemia, intracranial hypertension, systemic hypotension, hypoxia, fever, hypocapnia, and
hypoglycemia have all been shown to independently worsen survival after blunt TBI [5].
Coagulopathy occurs in roughly 1/3 of patients with severe TBI and may exacerbate ischemic
brain injury through microvascular thrombosis and embolism. It is likely that the coagulopathy
of TBI is a distinct entity from the coagulopathy of systemic trauma [6,7].
Clinical Features
The clinical features of TBI are dictated by baseline patient characteristics (e.g. pre-existing
brain injury), type of traumatic injury (e.g. contusion vs. extra-axial hematoma), severity of the
injury, and location of the lesion. The following discussion addresses the clinical features
typically observed in moderate to severe blunt TBI.
Parenchymal contusions are the most commonly observed mass lesion. They may be unilateral
or bilateral, and may be ipsilateral to the site of impact (coup) or contralateral (contra-coup).
Clinical features reflect dysfunction in the affected brain regions, frequently the orbitofrontal
and inferior temporal lobes. Patients may deteriorate within hours of presentation due to
expansion of contusions. On non-contrast computed tomography (CT), contusions appear as
hypodense regions without macroscopic hemorrhage, or as mixed-high density lesions if gross
hemorrhage is present (Figure 3a).
Epidural hematomas may present with focal findings based on the side of injury. They may
expand rapidly and lead to depressed level of consciousness when they exert mass effect
sufficient to cause herniation and brainstem compression. The classic clinical description of
EDH is the lucid interval, in which the patient is initially unconscious, wakes up without
obvious deficit, and subsequently deteriorates. This may be seen in approximately 50% of
patients with surgical EDH. On non-contrast head CT, epidural hematomas appear as lensshaped hyperdense extra-axial collections that do not cross skull suture lines (Figure 3b).
Subdural hematomas, as with epidural hematomas, produce clinical symptoms from local
compression of cortical and subcortical structures, and when large, from herniation and
brainstem compression. Subdural hematomas are most often unilateral but may be bilateral in
15% of cases. Subdural hematomas may enlarge over time and cause clinical deterioration. A
minority of patients may have a lucid interval. On non-contrast head CT, subdural hematomas
appear as hyperdense crescent-shaped extra-axial collections that may cross skull suture lines
(Figure 3c).
Subarachnoid hemorrhage (SAH) may produce clinical symptoms by precipitating acute
hydrocephalus, although this is uncommon. Small volume of SAH is associated with an
increased mortality, and large volumes may increase the odds of death by a factor of 2.
Intraventricular hemorrhages are relatively uncommon, but are associated with significant
morbidity and mortality and may be associated with increased intracranial pressure. CT imaging
demonstrates hyperdense collections in the cerebral sulci, fissues, ventricular system, or basal
cisterns (Figure 3d).
Diffuse axonal injury is rarely fatal but is associated with increased odds of a poor functional
recovery. Classically, patients with DAI have a depressed level of arousal that is out of
proportion to the burden of injury observed on CT scan. Since DAI involves microscopic injury,
it cannot be observed directly on neuroimaging studies; rather, indirect evidence of DAI
(associated, macroscopic injury) is sought. CT imaging may reveal small punctate foci of
hemorrhage but is frequently unremarkable. Magnetic resonance imaging (MRI) is considerably
more sensitive and may display abnormalities on diffusion weighted, gradient-echo, and
diffusion tensor sequences (Figure 3f).
Diffuse cerebral swelling typically occurs hours to days after the insult but may occur within the
first hour, particularly in blast TBI. Signs and symptoms are that of intracranial hypertension
and the herniation syndromes. These include agitation, bradycardia, hypertension, progressive
decrease in level of arousal culminating in coma, abnormalities of the pupillary light reflex, loss
of other brainstem reflexes, abnormal breathing patterns, and abnormal motor posturing. CT
imaging reveals sulcal effacement, loss of differentiation between gray and white matter,
compression of the ventricles, and effacement of the basal cisterns.
Vascular injury from disruption of arterial and venous structures may include arterial dissection,
aneurysms, fistulae, and hemorrhage. The actual incidence of vascular damage is unknown.
Vascular injury is likely under-reported since vascular imaging is usually performed only when
injury is suspected. Blunt injuries to the extracranial carotid and vertebral arteries, although
likely rare (0.1-0.5%), may present with late-onset ischemic strokes. The internal carotid artery
stretches over the lateral masses of the third and fourth cervical vertebrae, perhaps increasing
susceptibility to intimal tearing, dissection, pseudoaneurysm formation, and thrombosis.
Vertebral artery injury may be common in patients with concomitant cervical spine trauma,
although no specic cervical vertebral fracture pattern has a higher association with blunt
vertebral artery injury.
DIAGNOSIS
The diagnosis of TBI is usually made by the history provided by the patient, by bystanders, or by
emergency medical personnel. When history is unavailable, the diagnosis is typically made by
physical examination in conjunction with neuroimaging studies.
On physical examination, superficial evidence of trauma is sought, such as abrasions,
lacerations, and soft tissue swelling of the head. The presence of entrance and exit wounds
should be assessed (penetrating TBI). Sings of a basilar skull fracture may be present, including
retroauricular ecchymosis (Battles sign), periorbital ecchymosis (raccoons eyes),
hemotympanum, and CSF otorrhea or rhinorrhea. A focused neurological assessment is made
to determine the severity of the injury. The Glasgow Coma Scale (GCS) score should be used to
assess, categorize and to communicate severity of injury (table 1). Accordingly, severe TBI is
defined by a GCS of 3-8, moderate TBI by a GCS of 912, and mild TBI by a GCS of 13-15. The
GCS score may be determined quickly, has good inter-rater reliability, has prognostic value, and
is widely used. The GCS has limitations, particularly for use in patients who are intubated or
aphasic. These limitations are addressed in other scales, such as the Full Outline of
UnResponsiveness (FOUR) score, however use of the GCS is presently standard. The
neurological examination should also include assessment of spinal cord and peripheral nerve
function as brain, spinal cord, and nerve injuries may co-exist. A thorough systemic
examination should seek to determine the presence and extent of non-nervous system injuries.
Neuroimaging studies aid in diagnosing the particular types of primary injury present and,
together with the clinical examination, guide decisions about subsequent therapy. The
radiological characteristics of primary injury types are discussed above. While some patients
with mild TBI may not warrant imaging, nearly all patients with moderate or severe TBI do.
Imaging should be performed in all patients with declining level of consciousness, prolonged
loss of consciousness, persistent alteration in consciousness, focal neurological signs, seizures,
penetrating injury, signs of depressed or basilar skull fracture, confusion or agitation. CT is the
imaging modality of choice in the acute setting because it is widely available, may be performed
rapidly, and is highly sensitive for acute blood. MRI is more sensitive for than CT for soft tissue
pathology but is less widely available and may pose logistic challenges.
Neuroimaging studies may also be used to categorize TBI, particularly for research purposes.
Two classification schemes, the Marshall [8] and Rotterdam scores [9], are most commonly
used (table 2). When applied to CT scans in moderate-severe TBI, the Marshall score, an ordinal
numbering scale with 6 categories, aids in predicting risk of intracranial hypertension and
outcome in adults. The Marshall classification is widely used and pragmatic, but has many
recognized and accepted limitations, including difficulties in classifying patients with multiple
injury types and standardization of certain features of the CT scan. The Rotterdam score is a
more standardized CT-based classification system, which uses combinations of findings to
predict outcome.
TREATMENT
Treatment may be divided by phase: pre-hospital, emergency department, and subsequent,
which includes both surgical treatment and intensive care unit (ICU) treatment. The following
recommendations are based on those of the Brain Trauma Foundation for adults with blunt TBI.
Separate guidelines exist for infants, children, and adolescents [10].
I. PRE-HOSPITAL TREATMENT
Minimization of secondary cerebral injury begins in the pre-hospital phase, where the primary
goals of therapy are avoidance and treatment of hypotension and hypoxia, both of which are
associated with worse clinical outcomes. Management strategies that correct these disorders
have been associated with improved outcome. Correction of hypotension is accomplished
through intravenous fluid resuscitation with isotonic crystalloid. Hypertonic saline resuscitation
has not demonstrated benefit and resuscitation with albumin may be associated with harm
[11]. Endotracheal intubation in the field is generally considered for patients with a GCS of < 8,
however, evidence of benefit over bag-mask ventilation is mixed. Endotracheal intubation
should only be performed by paramedical personnel with expertise. Care should be taken to
stabilize the cervical spine and the patient should be rapidly transported to a trauma center.
II. EMERGENCY DEPARTMENT TREATMENT
Initial treatment in the emergency department should proceed according to Advanced Trauma
Life Support (ATLS) guidelines. These include maintenance of adequate oxygenation (PaO 2 > 60
mmHg) and blood pressure (systolic blood pressure > 90 mmHg). Vital signs are monitored and
therapy is adjusted to maintain cardiopulmonary homeostasis. Neurological assessment
includes an initial and then serial determinations of GCS score. Signs of intracranial
hypertension, such as decreased pupillary responsiveness to light, hypertension with
bradycardia, posturing, or respiratory abnormalities, should prompt empiric treatment with
head of bed elevation, hyperventilation, and an osmolar agent (mannitol or hypertonic saline).
The patient is assessed for systemic trauma. Laboratory assessment includes a complete blood
count, electrolytes, glucose, coagulation profile, blood alcohol level, and urine toxicology
screen. Coagulation abnormalities should be rapidly corrected. Imaging, including a noncontrast head CT, is performed to help define the extent of injury and to guide subsequent
management.
III. SURGICAL MANAGEMENT
For mass lesions, indications for surgical evacuation are predicated on clinical and radiological
findings. Table 3 summarizes recommendations for surgical intervention [12-16].
For diffuse TBI, decompressive craniectomy for the treatment of refractory ICP in patients with
diffuse TBI is performed frequently. In the DECRA trial, 155 patients with severe diffuse nonpenetrating traumatic brain injury and refractory intracranial hypertension were assigned to
bifrontal-temporoparietal decompressive craniectomy with durotomy or standard care [17].
Despite a significantly lower mean ICP, functional outcome was worse in the craniectomy
group. A major criticism of the study was a significant difference in patients with unreactive
pupils on admission in the surgical group. A post hoc analysis that adjusted for pupil reactivity
at baseline, found no difference in functional outcome between groups. The authors proposed
that expansion of the swollen brain outside the skull may cause axonal stretch leading to neural
injury or may impair cerebral blood flow or metabolism overcoming any beneficial effect of
lowerering ICP. This is an area of ongoing study [1].) It remains unclear whether unilateral
craniectomy and craniectomy for focal TBI improve outcome.
IV. MEDICAL (INTENSIVE CARE UNIT) MANAGEMENT
Medical management of the patient with severe TBI typically occurs in an intensive care unit
where the focus is on minimization of secondary cerebral injury and on prevention of systemic
complications.
A. Blood pressure and oxygenation

The Brain Trauma Foundation recommends that blood pressure be monitored and that
hypotension (systolic blood pressure < 90 mmHg) be avoided. The threshold value of 90mmHg
to define hypotension was determined by statistical analysis rather than physiological data.
Substantial evidence suggests that considerable secondary brain injury occurs from
hypotension. Both pre-hospital and in-hospital hypotension are associated with worse outcome
after severe TBI. A single episode of hypotension, defined as SBP <90 mmHg, is strongly
associated with worse outcome, independent of age, admission GCS, pupillary function. A
single episode of hypotension is associated with a two-fold increase in mortality compared to
matched controls without hypotension [19, 20].
Guidelines recommend monitoring of oxygenation and avoidance of hypoxia (PaO2 < 60 mmHg
or O2 saturation < 90%). Systemic hypoxemia is an independent predictor of increased
morbidity and mortality. A study of the Traumatic Coma Data Bank, a large prospectively
collected data set, demonstrated a significant and independent association between hypoxemia
and increased morbidity and mortality [19, 20]. Similarly, in patients with peripheral oxygen
saturations of <60% without concomitant hypotension, mortality was 50% compared to 14% in
patients without hypoxia [21]. Manipulative investigation of hypoxia (or hypotension) is
unethical. Therefore, the best available evidence is derived from the large, prospectively
accrued, Trauma Coma Data Bank.
B. Intracranial pressure (ICP)
The Brain Trauma Foundation recommends initiating treatment when ICP exceeds 20 mmHg.
Avoiding and treating intracranial hypertension are central to the management of patients with
TBI. While intracranial hypertension (ICP > 20 mmHg) is associated with increased mortality
and worse outcome, it is not clear that lowering ICP improves outcome. Numerous maneuvers
that successfully reduce ICP, such as craniectomy, hypothermia, and pharmacological coma,
have not been shown to improve outcome. While ICP measurement is relatively easy
compared to measurement of cerebral blood flow and brain biochemistry, it might be
physiologically less meaningful. Nonetheless, control of ICP remains, at present, the
cornerstone of TBI management.
Indications for invasive ICP monitoring are GCS score < 8 and an abnormal head CT that
demonstrates mass effect. An ICP monitor should also be considered for patients with normal
CT scans who have two or more of the following features: age > 40 years; posturing; systolic
blood pressure < 90 mmHg. Typically, ICP is monitored with a ventriculostomy or an
intraparenchymal probe. While invasive ICP monitoring has been standard of care, it has not
been shown to improve outcome. In 2012, a multicenter randomized trial of 324 patients with
TBI conducted in Ecuador and Bolivia found that therapy targeted to maintain ICP < 20 mmHg
with the use of an invasive monitor was not superior to therapy based on clinical examination
[22]. Whether these results are generalizable to TBI populations in developed countries is
unclear.
Initial therapeutic measures in the ICU are largely preventative and include head of bed
elevation, maintenance of the neck in a neutral position, avoidance of neck constriction (e.g.
loosening endotracheal tube ties), prevention of hypercarbia, and adequate treatment of pain,
agitation, fever, and seizures.
When ICP remains > 20 mmHg, a series of tiered therapies are employed.
CSF drainage: CSF drainage through a ventriculostomy should be considered. The optimal
method of drainage (continuous vs. intermittent) has not been established.
Osmotherapy: If CSF diversion is unsuccessful, or if a ventriculostomy is not present, then
osmotic agents, typically mannitol or hypertonic saline, are administered. While both are
effective, there are insufficient data to suggest superiority of one agent over the other. The
optimal concentration and mode of administration (bolus vs. continuous infusion) of hypertonic
saline is unknown. Mannitol (usually 20%) should be administered as a bolus, typically 0.25 1
gm/kg, however, the optimal dose and concentration of mannitol are unknown. When
mannitol is used, great care should be taken to avoid intravascular volume depletion and
hypotension, which are deleterious to the patient with severe TBI. One preventative strategy is
to replace urinary losses on a cc per cc basis for the first few hours after drug administration.
Surgery: Should intracranial hypertension persist despite administration of osmotic agents,
then decompressive craniectomy should be considered. Craniectomy, either unilateral or
bilateral, is the most effective way to lower ICP. As mentioned above, the impact of
decompressive surgery on outcome is unclear.
Metabolic therapy: The goal of metabolic therapy is to suppress cerebral metabolic rate
(CMRO2). A reduction in CMRO2 leads to a reduction in cerebral blood flow (CBF) which lowers
cerebral blood volume and hence ICP. Furthermore, a reduction of CMRO2 in the face of
decreased fuel delivery, might preserve brain tissue. Reduction of CMRO2 may be
accomplished by induction of either a pharmacological coma or hypothermia.
Classically, pharmacologic coma has been achieved with barbiturates, however, it is unclear
whether the risks associated with high-dose barbiturates (e.g. immune suppression,
hypotension, poikilothermia, gastroparesis, decreased mucocilliary clearance) are outweighed
by any cerebral benefit. In clinical practice, multiple sedatives infusions are used, including
opiates, benzodiazepines, and propofol. There is insufficient data to guide choice of sedative
and decisions must be made based on patient characteristics and side-effect profiles. When
pharmacologic coma is employed, the agent should be titrated to an ICP < 20 mmHg, an
isoelectric EEG, or deleterious side effects whichever occurs first.
Hypothermia may also be used to lower CMRO2 and to reduce ICP. Numerous studies have
addressed the role of mild to moderate hypothermia (32-34C) in TBI. Most single-center
studies suggest that induced hypothermia is associated with improved outcome. However, 2
large randomized multicenter studies in adults with severe TBI (National Acute Brain Injury
Study: Hypothermia I and II) failed to show benefit [23, 24], and a randomized study of
hypothermia in children with TBI suggested harm [25]. While mild to moderate hypothermia
has not been shown to improve outcome, the preponderance of literature suggests it is
effective in lowering ICP.
Laparotomy: Perhaps as a last resort, decompressive laparotomy (or thoracotomy) should be
considered to treat refractory intracranial hypertension.
Both intra-abdominal and
intrathoracic hypertension may contribute to raised intracranial pressure, presumably through
transmission of pressure from those cavities to the spinal subarachnoid space (and hence the
cranial subarachnoid space) through the vertebral veins. However, even when intra-abdominal
pressure is normal, opening the abdomen leads to a fall in ICP. In a series of 17 patients, all
with refractory intracranial hypertension and normal intra-abdominal pressure, Joseph et al.
reported a fall in ICP in all patients after laparotomy [26]. Of these, eleven patients maintained
a lower ICP and survived. Further study is needed to define the optimal role of laparotomy and
its impact on functional outcome.
Hyperventilation: Hyperventilation results in blood and CSF alkalosis, which leads to
vasoconstriction, reduced cerebral blood volume and therefore a lower ICP. Sustained and
vigorous hyperventilation may result in cerebral ischemia and is therefore not recommended as
a routine therapy. However, in emergency situations (e.g. acute herniation), hyperventilation
may be used transiently as a bridge to more definitive therapy (e.g. surgery, osmotic agent).
Some suggest that jugular bulb oximetry allows for safer titration of hyperventilation insofar as
it may detect cerebral hypoxia.
C. Cerebral perfusion pressure (CPP)
If cerebral autoregulation is disturbed after TBI, then cerebral perfusion pressure will largely
dictate cerebral blood flow. Therefore, an attempt is made to keep CPP within a range that
prevents cerebral ischemia. It is common practice to maintain CPP > 60 mmHg. The Brain
Trauma Foundation currently recommends maintaining CPP between 50 and 70 mmHg.
Elevating CPP above 70 mmHg with intravenous fluids and vasopressors should be avoided
because of the risk of lung injury. A randomized controlled trial of CPP-targeted therapy versus
ICP-targeted therapy was performed. In the CPP group, CPP was maintained at >70mmHg; in
the ICP group, CPP was maintained at >50mmHg and ICP <20mmHg. There was no difference in
outcome between groups, but the CPP group had a five-fold incidence of acute respiratory
distress syndrome and more frequent use of vasopressor agents [27, 28]. Similarly, data from
an international multicenter trial did not demonstrate benefit of maintaining CPP>60mmHg.
Although lowering CPP below a critical threshold appears deleterious, raising it does not appear
to be advantageous. Optimization of CPP in the normotensive patient should begin with
lowering ICP.
Although CPP is an integral physiological parameter in modern intensive care of the TBI patient,
there is considerable variability in how it is derived. A survey study suggests that placement of
the arterial line transducer (from which MAP is derived for CPP calculations) varies both across
institutions and among the 11 studies cited by the Brain Trauma Foundation for their CPP
recommendations [29]. While some zero the transducer at the level of the heart (phlebostatic
axis), others zero it at the head. If the patient is flat, there is no difference. However, when
head of bed is upright, MAP measured at the right atrium is higher than that measured at the
level of the tragus. Therefore, transducing blood pressure with an arterial line zeroed at the
phlebostatic axis will result in an overestimate of actual CPP. This is particularly problematic in
patients who are nursed with head of bed elevation to >30 degrees for ICP control, as the
discrepancy between CPP measured at the phlebostatic axis versus the tragus could be as high
as 20mm Hg. This lack of uniformity in clinical practice and in the published literature is
problematic and potentially clinically significant.
D. Seizure prophylaxis
BTF guidelines recommend the used of anticonvulsant medication (phenytoin) for one week
following TBI and recommend against longer durations of prophylactic therapy. Many centers
use alternative agents, such as leviteracitam.
Seizures occur in 10% - 30% of patients with TBI. Theoretically, seizures may worsen outcome
by increasing CMRO2 and ICP, thereby increasing the likelihood of cerebral ischemia. In
comatose patients, up to 25% may have non-convulsive seizures. Prophylactic anticonvulsant
medications reduce the incidence of early post-traumatic seizures but do not lessen the odds of
developing post-traumatic epilepsy. The impact of prophylactic anticonvulsant medications on
outcome and their comparative efficacies is unknown.
E. Other general critical care strategies
The Brain Trauma Foundation guidelines address select areas of general critical care of the TBI
patient including, infection prophylaxis, deep vein thrombosis (DVT) prophylaxis, nutrition, and
steroid administration. Recommendations are as follows:
Periprocedural antibiotics for intubation and early tracheostomy are recommended
Graduated compression stockings or intermittent pneumatic compression stockings
should be used until patients are ambulatory. Low molecular weight heparin or low
dose unfractionated heparin should be used but increase the risk for expansion of
intracranial hemorrhage. No recommendations are made regarding the timing,
dose, or duration of pharmacological prophylaxis.
Full caloric needs should be administered by day 7 post-injury
Steroids should not be used to improve outcome or reduce ICP. Steroids are
associated with increased mortality and are contra-indicated.
This was
demonstrated in the CRASH trial, a large (10,008 adults), international, multicenter
placebo-controlled trial of methylprednisolone after head injury. The group that
was treated with steroids had an increased odds of death (relative risk of 1.18),
regardless of injury severity [30].
Fever is strongly, independently, and consistently associated with worse clinical outcomes
across a variety of severe brain injuries. While in experimental models there is a clear causal
relationship, in humans it remains unclear whether fever exacerbates or is merely a marker of
brain injury. Nonetheless it is common practice to treat fever with antipyretic medications, ice
packs, surface cooling devices, or intravascular cooling devices. The impact of fever control on
outcome has yet to be determined.
Similarly, hyperglycemia is associated with worse clinical outcomes after severe TBI. However,
the brain is an obligate glucose consumer and hypoglycemia is also injurious. Avoidance of
both hyper- and hypoglycemia is therefore recommended.
Coagulopathy is frequent in patients with TBI due to the use of anticoagulant and antiplatelet
medications, traumatic brain injury itself, or due to multisystem trauma. Efforts should be
taken to rapidly correct coagulopathy, however the optimal means by which to do so are ill
defined.
F. Multimodality Neuromonitoring
While data are currently insufficient to define the optimal role of advanced neurominitoring
tools, the Brain Trauma Foundation specifically addresses brain oxygenation, and offers a level
III recommendation for use of jugular venous oxygen saturation (SjvO2) and brain tissue oxygen
tension (PbtO2) monitoring. They recommend maintenance of SjvO2 > 50% and PbtO2 > 15
mmHg.
It is increasingly recognized that traditional goals of cerebral resuscitation ICP, CPP, and the
clinical examination are distant surrogates for cerebral perfusion that do not account for
dynamic changes in cerebral autoregulation, tissue metabolic rate, cellular fuel utilization, and
microcirculatory dysfunction, all of which impact tissue metabolic health. Although standard, it
seems intuitively obvious that a uniform approach of maintaining ICP < 20mmHg and CPP
>60mmHg is overly simplistic. This approach, based on statistical averages across large
populations, addresses neither significant baseline differences in patient physiology nor the
complex, dynamic, and variable pathophysiological changes that ensue following severe brain
injury. It is evident that neuronal injury may occur despite apparent physiological homeostasis
(normal SBP, PaO2, ICP, CPP). A more tailored therapeutic strategy that responds to multiple
simultaneously measured and more relevant physiological variables is logically appealing but
has not been subjected to rigorous scientific scrutiny. The emergence of technology that allows
for continuous real-time bedside monitoring of cerebral physiology might facilitate assessment
of therapeutic efficacy and provide more relevant physiological endpoints for resuscitation.
Combining these monitors in a multimodal approach may allow goal-directed cerebral
resuscitation that emphasizes the individual patients unique neurological and systemic
physiology. This approach must ultimately be compared to algorithms that target more
traditional physiological variables.
A variety of monitors are now available that permit bedside assessment of advanced physiology
in real-time or near real-time. CBF may be measured quantitatively in small regions of brain
tissue with thermal diffusion flowmetry probes. Whole brain CBF may be trended in a nonquantitative way with continuous EEG through the use of software that provides a measure of
the ratio of fast waves to slow waves. Cerebral oxygenation may be measures regionally with
the use of a Clark-type electrode (Licox) or non-invasively with near-infrared spectroscopy.
Whole brain oxygenation may be measured with jugular bulb oximetry (SjvO2). Cerebral
biochemistry, including markers of neuronal ischemia and injury (lactate, pyruvate, glycerol,
glutamate, glucose), may be measured regionally with cerebral microdialysis. These monitors
alone or in combination are not expected to help patients; rather, it is hoped that therapeutic
responses to information provided by these tools will improve outcome. Ongoing research
aims to understand better the information provided by these tools and the optimal therapeutic
responses.
PROGNOSIS
Outcomes from TBI span the spectrum from death and vegetative state to full recovery. While
many factors predict poor outcome in large populations (e.g. GCS, age, etc.), these should not
be used for prognostication in individual patients. The IMPACT (International Mission on
Prognosis and Analysis of Clinical Trials) and the CRASH (Corticosteroid Randomization after
Significant Head Injury) scores are externally validated models derived from large datasets that
aid in prediction of 6-month outcome after TBI. However, functional recovery may continue for
at least 18-months following severe injury, and these score are of minimal utility for predicting
ultimate individual patient outcome.
As a general rule, traumatic coma has a better prognosis than coma from hypoxia-ischemia, and
coma from blunt trauma has a better prognosis than coma from penetrating TBI. Much work
remains to be done to better define accurate predictors of outcome. A promising line of
investigation involves the use of advanced MRI imaging (functional and diffusion tensor
sequences) to improve prognostic accuracy.
To date, no medications have proved useful in improving outcome. There have been over 200
failed neuroprotective drug trials. It is unlikely that a single drug will prove efficacious as the
pathways involved in secondary injury are complex and redundant. Perhaps the best hope for
neuroprotection lies in dirty therapies that target multiple pathways, or in combinations of
drugs.
REFERENCES
1. Brain Trauma Foundation, American Association of Neurological Surgeons, Congress of
Neurological Surgeons, et al. Guidelines for the management of severe traumatic brain
injury. Introduction. J Neurotrauma 2007; 24 Suppl 1:S1-S106.
2. www.cdc.gov
3. Johnson VE, Stewart W, Smith DH. Axonal pathology in traumatic brain injury.
Experimental Neurology 2013;246:35-45.
4. Magnuson J, Leonessa F, Ling G. Neuropathology of explosive blast traumatic brain injury.
Current Neurol and Neurosci Rep 2012;12(5):570-579.
5. McHugh GS, Engel DC, Butcher I, et al. Prognostic value of secondary insults in traumatic
brain injury: results from the IMPACT study. J Neurotrauma 2007; 24:287.
6. Stein SC, Smith DH. Coagulopathy in traumatic brain injury. Neurocrit Care. 2004;1(4):47988.
7. Harhangi BS, Kompanje EJ, Leebeek FW, Maas AI. Coagulation disorders after traumatic
brain injury. Acta Neurochir (Wien). 2008 Feb;150(2):165-75; discussion 75.
8. Marshall LF, Marshall SB, Klauber MR, et al. The diagnosis of head injury requires a
classification based on computed axial tomography. J Neurotrauma 1992; 9 Suppl 1:S287.
9. Maas Al, Hukkelhoven CW, Marshall LF, Steyerberg EW. Prediction of outcome in traumatic
brain injury with computed tomographic characteristics: a comparison between the
computed tomographic classification and combinations of computed tomographic
predictors. Neurosurgery 2005; 57:1173.
10. Kochanek PM, Carney N, Adelson PD. Guidelines for the acute medical management of
severe traumatic brain injury in infants, children, and adolescents Second Edition.
Pediatric Critical Care Medicine 2012; 13: S1-S2.
11. SAFE Study Investigators, Australian and New Zealand Intensive Care Society Clinical Trials
Group, Australian Red Cross Blood Service, et al. Saline or albumin for fluid resuscitation in
patients with traumatic brain injury. N Engl J Med 2007; 357:874.
12. Bullock MR, Chesnut R, Ghajar J, et al. Surgical management of acute epidural hematomas.
Neurosurgery 2006; 58:S7.
13. Bullock MR, Chesnut R, Ghajar J, et al. Surgical management of acute subdural hematomas.
14. Bullock MR, Chesnut R, Ghajar J, et al. Surgical management of posterior fossa mass lesions.
15. Bullock MR, Chesnut R, Ghajar J, et al. Surgical management of traumatic parenchymal
lesions. Neurosurgery 2006; 58:S25.
16. Bullock MR, Chesnut R, Ghajar J, et al. Surgical management of depressed cranial fractures.
17. Cooper DJ, Rosenfeld JV, Murray L, et al. Decompressive craniectomy in diffuse traumatic
brain injury. N Engl J Med 2011; 364:1493.
18. Hutchinson PJ, Corteen E, Czosnyka M, et al. Decompressive craniectomy in traumatic brain
injury: the randomized multicenter RESCUEicp study (www.RESCUEicp.com). Acta Neurochir
Suppl 2006; 96:17.
19. Chestnut RM, Marshall LF, Klauber RM, et al. The role of secondary brain injury in
determining outcome from severe head injury. J Trauma 1993;34:216-222.
20. Marmarou A, Anderson RL, Ward JD, et al. Impact of ICP instability and hypotension on
outcome in patients with severe head trauma. J Neurosurg 1991;75:159-166.
21. Stochetti N, Furlan A, Volta F. Hypoxemia and arterial hypotension at the accident scene in
head injury. J Trauma 1996;40:764-767.
22. Chestnut RM, Temkin N, Carney N, et al. A trial of intracranial-pressure monitoring in

traumatic brain injury. New Engl J Med 2012; 367(26): 2471-2481.
23. Clifton GL, Miller ER, Choi SC, et al. Lack of effect of induction of hypothermia after acute
brain injury. N Engl J Med 2001; 344:556.
24. Clifton GL, Valadka A, Zygun D, et al. Very early hypothermia induction in patients with
severe brain injury (the National Acute Brain Injury Study: Hypothermia II): a randomised
trial. Lancet Neurol 2011; 10:131.
25. Hutchison JS, Ward RE, Lacroix J, et al. Hypothermia therapy after traumatic brain injury in
children. N Engl J Med 2008;358(23):2447-56.
26. Joseph DK, Dutton RP, Aarabi B, Scalea TM. Decompressive laparotomy to treat intractable
intracranial hypertension after traumatic brain injury. J Trauma. 2004;57(4):687-93.
27. Robertson CS, Valadka AB, Hannay HJ, et al. Prevention of secondary ischemic insults after
severe head injury. Crit Care Med 1999; 27:2086.
28. Contant CF, Valadka AB, Gopinath SP, et al. Adult respiratory distress syndrome: a
complication of induced hypertension after severe head injury. J Neurosurg 2001; 95:560.
29. Kosty JA, Le Roux PD, Levine J, Park S, Kumar MA, Frangos S, Maloney-Wilensky E, Kofke
WA: A Comparison of Clinical and Research Practices in Measuring Cerebral
PerfusionPressure (CPP): A Literature Review and Practitioner Survey. Anesthesia &
Analgesia In press.
30. Edwards P, Arango M, Balica L, et al. Final results of MRC CRASH, a randomised placebocontrolled trial of intravenous corticosteroid in adults with head injury-outcomes at 6
months. Lancet 2005; 365:1957.
Figure 1. Cerebral autoregulation
Under normal circumstances (a) cerebral blood flow (CBF) is kept constant across a wide range
of cerebral perfusion pressures (CPP) through modulation of vascular diameter. In TBI,
autoregulation may be disturbed (b) and CBF becomes pressure passive as the vessels no
longer change in diameter.
Figure 2. Cerebral compliance curve
The intracranial pressure-volume curve has a flat portion (a) in which compliance ( V/ P) is
high, and a steep portion (b) in which compliance is low. Under normal circumstances, when
compliance is high, a small change in ICV ( V) results in a small change in pressure ( P1).
Patients with intracranial hypertension typically have low compliance, hence small changes in
volume ( V) result in large changes in pressure ( P2). Elastance, P/ V, is the reciprocal of
compliance.
Figure 3. Typical radiological appearance of the various primary injuries in TBI
a) non-contrast axial CT demonstrating right > left frontal lobe contusions with hemorrhage; b)
non-contrast axial CT demonstrating left convexity epidural hematoma; c) non-contrast axial CT
demonstrating left convexity subdural hematoma with mass-effect, effacement of the left
lateral ventricle, and left to right midline shift; d) non-contrast axial CT demonstrating traumatic
subarachnoid hemorrhage; e) non-contrast axial CT demonstrating trans-hemispheric laceration
from bullet with hemorrhage, bullet fragments, and bone fragments in the tract; f) axial
gradient echo MRI sequence demonstrating punctate foci of hemorrhage (black spots)
consistent with diffuse axonal injury.
Table 1. Glasgow Coma Scale

Category
Response
Score
Eye opening
spontaneous
to voice
to pain
none
4
3
2
1
Verbal Response
oriented
confused
inappropriate
incomprehensible
none
5
4
3
2
1
Motor Response
obeys commands
localizes to pain
withdraws from pain
flexion posturing to pain
extensor posturing to pain
none
6
5
4
3
2
1
The Glasgow Coma Scale (GCS) score is widely used for initial and serial neurological
assessment of the TBI patients. Eye opening, verbal responses, and motor responses are each
scored as above. The sum of the scores in each category are added for the total GCS score. The
total GCS score may range from 3 (most severely injured) to 15 (least severely injured).
Patients with endotracheal or tracheostomy tubes are often assigned a verbal score of 1T.
Table 2. Marshall and Rotterdam Scales

a) Marshall CT classification of TBI
Category
Definition
Diffuse injury I
(no visible pathology)
No visible intracranial pathology seen on CT scan
Diffuse injury II
Cisterns are present with midline shift of 0-5 mm; no

high or mixed density lesion > 25 cm3 may include
bone fragments and foreign bodies
Diffuse injury III

(swelling)
Cisterns compressed or absent with midline shift 0-5

mm; no high or mixed density lesion > 25 cm3
Diffuse injury IV
(shift)
Midline shift > 5 mm; no high or mixed density lesion

> 25 cm3
Evacuated mass lesion V
Any lesion surgically evacuated
Non-evacuated mass lesion VI
High or mixed density lesion > 25 cm3; not surgically

evacuated
b) Rotterdam CT classification of TBI

Score
Basal cisterns
Normal
Compressed
Absent
Midline shift
No shift or shift < 5 mm
Shift > 5 mm
Epidural mass lesion
Present
Absent
Intraventricular blood or SAH
Absent
Present
Sum Score
0
1
2
0
1
0
1
0
1
Total + 1
Table 3. Recommendations for Surgical Management of TBI. See references 12-16.

I.
II.
III.
Subdural hematoma
a. Acute SDH with a thickness greater than 10 mm or a midline shift of greater than
5 mm on CT scan should be surgically evacuated, regardless of the patients GCS.
b. All patients with acute SDH (GCS<9) should undergo ICP monitoring.
c. A comatose patient (GCS<9) with a SDH less than 10mm thickness and a midline
shift less than 5mm should undergo surgical evacuation of the lesion if the GCS
decreases by >2 points between time of injury and hospital admission and/or the
patient presents with asymmetric or fixed and dilated pupils and/or the
ICP>20mmHg.
d. In patients with acute SDH and indications for surgery, surgical evacuation
should be performed as soon as possible.
e. If surgical evacuation of an acute SDH in a comatose patient is indicated, it
should be performed using a craniotomy with or without bone flap removal and
duroplasty.
f.
Epidural hematoma
a. An epidural hematoma (EDH) greater than 30 cm3 should be surgically
evacuated regardless of the patients Glasgow Coma Scale (GCS) score.
b. An EDH less than 30 cm3 and with less than a 15-mm thickness and with less
than a 5-mm midline shift (MLS) in patients with a GCS score greater than 8
without focal deficit can be managed non-operatively with serial computed
tomographic (CT) scanning and close neurological observation in a neurosurgical
center.
c. It is strongly recommended that patients with an acute EDH in coma (GCS score
<9) with anisocoria undergo surgical evacuation as soon as possible.
d. There are insufficient data to support one surgical treatment method. However,
craniotomy provides a more complete evacuation of the hematoma.
Parenchymal lesions
a. Patients with parenchymal mass lesions and signs of progressive neurological
deterioration referable to the lesion, medically refractory intracranial
hypertension, or signs of mass effect on computed tomographic (CT) scan should
be treated operatively.
b. Patients with Glasgow Coma Scale (GCS) scores of 6 to 8 with frontal or temporal
contusions greater than 20 cm3 in volume with midline shift of at least 5 mm
and/or cisternal compression on CT scan, and patients with any lesion greater
than 50 cm3 in volume should be treated operatively.
c. Patients with parenchymal mass lesions who do not show evidence for
neurological compromise, have controlled intracranial pressure (ICP), and no
significant signs of mass effect on CT scan may be managed non-operatively with
intensive monitoring and serial imaging.
d. Craniotomy with evacuation of mass lesion is recommended for those patients
with focal lesions and the surgical indications listed above, under Indications.
IV.
V.
e. Bifrontal decompressive craniectomy within 48 hours of injury is a treatment

option for patients with diffuse, medically refractory posttraumatic cerebral
edema and resultant intracranial hypertension.
f. Decompressive procedures, including subtemporal decompression, temporal
lobectomy, and hemispheric decompressive craniectomy, are treatment options
for patients with refractory intracranial hypertension and diffuse parenchymal
injury with clinical and radiographic evidence for impending transtentorial
herniation.
Posterior fossa
a. Patients with mass effect on computed tomographic (CT) scan or with
neurological dysfunction or deterioration referable to the lesion should undergo
operative intervention. Mass effect on CT scan is defined as distortion,
dislocation, or obliteration of the fourth ventricle; compression or loss of
visualization of the basal cisterns, or the presence of obstructive hydrocephalus.
b. Patients with lesions and no significant mass effect on CT scan and without signs
of neurological dysfunction may be managed by close observation and serial
imaging.
c. In patients with indications for surgical intervention, evacuation should be
performed as soon as possible because these patients can deteriorate rapidly,
thus, worsening their prognosis.
d. Methods
e. Suboccipital craniectomy is the predominant method reported for evacuation of
posterior fossa mass lesions, and is therefore recommended.
Depressed skull fractures
a. Patients with open (compound) cranial fractures depressed greater than the
thickness of the cranium should undergo operative intervention to prevent
infection.
b. Patients with open (compound) depressed cranial fractures may be treated nonoperatively if there is no clinical or radiographic evidence of dural penetration,
significant intracranial hematoma, depression greater than 1 cm, frontal sinus
involvement, gross cosmetic deformity, wound infection, pneumocephalus, or
gross wound contamination.
c. Non-operative management of closed (simple) depressed cranial fractures is a
treatment option.
d. Early operation is recommended to reduce the incidence of infection.
e. Elevation and debridement is recommended as the surgical method of choice.
f. Primary bone fragment replacement is a surgical option in the absence of wound
infection at the time of surgery.
g. All management strategies for open (compound) depressed fractures should
include antibiotics.
TRAUMATIC BRAIN INJURY QUESTIONS

1. All of the following are examples of secondary injury except:
a) Free radical formation
b) Inflammation
c) Contusions
d) Hypotension
2. Seizure prophylaxis with an anticonvulsant medication is recommended for how long after a
severe traumatic brain insult?
a) never
b) 3 days
c) 5 days
d) 7 days
e) 2 weeks
f) indefinitely
3. The energy imparted to brain tissue from a projectile is most strongly dependent on the
projectiles:
a) Mass
b) Shape
c) Velocity
d) Material
4. The incidence, nature or time course of which of the following distinguish blast TBI from
blunt TBI:
a) Cerebral vasospasm
b) Malignant cerebral edema
c) Diffuse axonal injury
d) All of the above
e) None of the above
5. The presence of which of the following distinguishes penetrating traumatic brain injury
from blunt traumatic brain injury?
a) Contusions
b) Epidural hematoma
c) Subdural hematoma
d) Brain laceration
e) Subarachnoid hemorrhage
6. The currently accepted threshold for treatment of intracranial hypertension is intracranial

pressure:
a) > 12 mmHg
b) > 15 mmHg
c) > 20 mmHg
d) > 25 mmHg
e) > 30 mmHg
7. Use of vasopressors and intravenous fluids to maintain cerebral perfusion pressure > 70
mmHg is associated with:
a) Better clinical outcomes
b) Increased incidence of lung injury
c) Fewer cerebral infarctions and less ischemia
d) Increased diffuse cerebral edema
8. The relationship between cerebral blood flow and cerebral perfusion pressure becomes
more linear:
a) In all patients with severe TBI
b) When cerebral vascular autoregulation is impaired
c) When cerebral oxygen demand exceeds cerebral metabolic rate
d) When intracranial pressure is low
9. The DECRA study demonstrated that
a) Unilateral craniectomy for focal TBI improved outcome
b) Bifrontal craniectomy for diffuse TBI reduced ICP
c) Bifrontal craniectomy for diffuse TBI improved outcome
d) Unilateral craniectomy for focal TBI reduced ICP
10. Corticosteroids:
a) Are useful as a primary therapy for diffuse traumatic cerebral edema
b) Are useful as an adjunctive therapy for diffuse traumatic cerebral edema
c) Should not be used to treat cerebral edema from TBI
d) Should be used only to treat focal cerebral edema from traumatic injuries
TRAUMATIC BRAIN INJURY ANSWERS

1. The correct answer is C. Primary injury is injury that occurs immediately at the time of the
trauma and is typically caused by mechanical forces. Contusion, or bruising of the brain, is a
form of injury caused by acceleration/deceleration. Secondary (delayed) injury may begin
at the time of the traumatic insult or may begin in the subsequent hours to days. Secondary
injury involves a host of cellular, biochemical, and organ-level pathological cascades,
including free radical formation, inflammation, and hypotension that exacerbate brain
damage. The central goal of TBI management is minimization of secondary injury.
2. The correct answer is D. Anticonvulsants decrease the risk of early post-traumatic seizures
but do not impact the likelihood of developing post-traumatic epilepsy. Brain Trauma
Foundation guidelines therefore recommend prophylactic treatment with an anticonvulsant medication for 7 days post-injury and no longer.
3. The correct answer is C. While a projectiles shape, angle of penetration, and the material
influence the type of injury, kinetic energy is a product of its mass and the square of its
velocity. Therefore velocity is the primary determinant of the energy transferred to brain
tissue.
4. The correct answer is D. Diffuse axonal injury in blast TBI occurs in a dose-dependent
fashion that likely differs from the DAI observed with closed-head injury. Malignant
cerebral edema may occur rapidly (within an hour) as opposed to the more slowly
developing edema seen in blunt TBI (hours to days). Cerebral vasospasm may occur in up to
50% of moderate to severe blast TBI and may last as long as one month. Additionally,
patients with blast TBI frequently have concomitant blast injury to the eyes and to the
auditory and vestibular systems.
5. The correct answer is D. While epidural, subdural, and subarachnoid hemorrhages may
occur in both blunt and penetrating TBI, cerebral lacerations, or tearing of tissue, are the
hallmark of penetrating TBI. Contusions typically result for acceleration/deceleration.
6. The correct answer is C. The Brain Trauma Foundation recommends initiation of therapy
once ICP exceeds 20 mmHg. This is based on observational studies that established a
correlation between ICP > 20 mmHg and poor outcome. There is a lack of convincing
evidence that therapy guided by invasive ICP monitoring is superior to therapy guided by
clinical (and radiological) examinations.
7. The correct answer is B. While initial studies suggested that using volume expansion and
vasopressors to maintain CPP> 70 mmHg improved outcome, subsequent studies suggested
that this approach does not improve outcome and is associated with increased risk of
extracerebral injury, including acute respiratory distress syndrome. Brain Trauma
Foundation guidelines therefore recommend a CPP target of 60 mmHg and avoidance of
CPP < 50 mmHg and CPP > 70 mmHg. Optimization of CPP in a normotensive patient should
start with efforts to lower ICP.
8. The correct answer is B. Normally, cerebral blood flow (CBF) is maintained constant across
a wide range of cerebral perfusion pressures (CPP). This is accomplished by modulation of
vascular diameter. As CPP increases, vascular diameter decreases to maintain constant
cerebral blood flow. This is termed cerebrovascular autoregulation. In patients with TBI,
autoregulation may be abnormal due to vasoplegia and the relationship between CPP and
CBF becomes more linear.
9. The correct answer is B. The DECRA (DEcompressive CRAniectomy) trial randomized
patients with severe diffuse blunt traumatic brain injury and refractory intracranial
hypertension to to bifrontal-temporoparietal decompressive craniectomy with durotomy or
standard care. The surgical group had a significantly lower mean ICP and worse functional
outcomes.
10. The correct answer is C. Multiple studies have examined the effects of corticosteroids on
outcome after TBI. Most recently, the CRASH (Corticosteroid Randomization After
Significant Head injury) study, a large international randomized placebo-controlled study of
early administration of methylprednisolone, found that steroid administration was
associated with increased risk of death. Steroids are therefore contraindicated for the
treatment of cerebral edema due to TBI.

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2013 Neurocritical Care Society Practice Update