traumatic brain injury.pdf

8/9/2019 Traumatic Brain Injury.pdf

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© 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 hemoglobinsaturation 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


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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 continuesto 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 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)


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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 Poiseuille’s 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 ofvascular 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


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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 = ½ (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 beginimmediately, 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


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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 lens-

shaped 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 acutehydrocephalus, 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).


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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 considerablymore 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 specific 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, includingretroauricular ecchymosis (Battle’s sign), periorbital ecchymosis (raccoon’s 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 9 –12, 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


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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 primarygoals 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


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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 TraumaLife Support (ATLS) guidelines. These include maintenance of adequate oxygenation (PaO2 > 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 non-

contrast 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 non-

penetrating traumatic brain injury and refractory intracranial hypertension were assigned tobifrontal-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.


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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 fromhypotension. Both pre-hospital and in-hospital hypotension are associated with worse outcome

after severe TBI. A single episode of hypotension, defined as SBP 40 years; posturing; systolicblood 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.


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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 sedativeand 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 (32-34°C) in TBI. Most single-center

studies suggest that induced hypothermia is associated with improved outcome. However, 2


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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 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


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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 thephlebostatic 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-injurySteroids 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].


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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, andmicrocirculatory 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 assessmentof 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 patient’s unique neurological and systemic

physiology. This approach must ultimately be compared to algorithms that target more

traditional physiological variables.


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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 non-

quantitative 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 workremains 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

http://www.cdc.gov/http://www.cdc.gov/


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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):479-

88.

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.Neurosurgery 2006; 58:S47.

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.


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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 randomisedtrial. 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 placebo-

controlled trial of intravenous corticosteroid in adults with head injury-outcomes at 6

months. Lancet 2005; 365:1957.


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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.


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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.


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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

incomprehensiblenone

5

4

3

21

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”.


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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

0

1

2

Midline shift

No shift or shift < 5 mm

Shift > 5 mm

0

1

Epidural mass lesionPresent

Absent

0

1

Intraventricular blood or SAH

Absent

Present

0

1

Sum Score Total + 1


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Table 3. Recommendations for Surgical Management of TBI. See references 12-16.

I. 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 patient’s GCS.

b.

All patients with acute SDH (GCS20mmHg.

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.

II. Epidural hematoma

a. An epidural hematoma (EDH) greater than 30 cm3 should be surgically

evacuated regardless of the patient’s 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


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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 parenchymalinjury with clinical and radiographic evidence for impending transtentorial

herniation.

IV.

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.

V. 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 non-

operatively 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 woundinfection at the time of surgery.

g.

All management strategies for open (compound) depressed fractures should

include antibiotics.


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TRAUMATIC BRAIN INJURY QUESTIONS

1.

All of the following are examples of secondary injury except:

a) Free radical formation

b) Inflammation

c)

Contusionsd) 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

projectile’s:

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 vasospasmb) 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 hematomad) Brain laceration

e)

Subarachnoid hemorrhage


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6.

The currently accepted threshold for treatment of intracranial hypertension is intracranial

pressure:

a)

> 12 mmHg

b) > 15 mmHg

c) > 20 mmHg

d)

> 25 mmHge) > 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


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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. Secondaryinjury 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 anti-

convulsant medication for 7 days post-injury and no longer.

3. The correct answer is C. While a projectile’s 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


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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 constantcerebral 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.

traumatic brain injury.pdf

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