CNS TRAUMA

EPIDEMIOLOGY
Traumatic brain injury (TBI) is a critical public health and socioeconomic
problem throughout the world
Leading cause of mortality and disability among young individuals in high
income countries
The incidence is rising sharply, mainly because of increasing use of motor
vehicles in low- and middle income countries
In high-income countries, falls are a main cause of TBI, particularly in elderly
people
CLASSIFICATION OF TBI
SCORING SYSTEMS are applied to classify the severity of the injury
Clinical severity of intracranial injuries is commonly assessed according to
the degree of depression of the level of consciousness, assessed by the
Glasgow Coma Scale (GCS)
GCS score is the sum score of three components (eye, motor, and verbal
scales)
GCS CLASSIFICATION
Severe TBI is defined by a GCS score of 3 to 8
Moderate TBI by a GCS score 9 to 13
Mild TBI by a GCS score 14 to 15
Limitation of classifying clinical severity with the GCS is that assessment
may be confounded by prior alcohol or substance use, prehospital sedation
and paralysis
PRIMARY BRAIN INJURY
occurs at the moment of impact and consists of multiple mechanisms,
including blast force, high-velocity penetrating injury, direct force, and
rapid accelerating/ decelerating-type injuries
Two pathologic processes are uniquely characteristic of TBI: diffuse axonal
injury (DAI) and contusion/hematoma formation
SECONDARY BRAIN INJURY
characterized by a cascade of molecular derangements related to the primary injury and the
body’s response to injury in the initial minutes to days
This process is primarily mediated by cellular response mechanisms, which should be
differentiated from secondary brain injury events that may be preventable (e.g., hypoxia and
hypotension)
This complex cascade of events involves neurotransmitter-mediated cell injury,
inflammatory responses, microvascular occlusion and injury, electrolyte imbalances,
mitochondrial dysfunction, and cellular apoptosis
Manifested clinically by the development of intracranial hypertension and cerebral ischemia
IMAGING MODALITIES
Skull radiographs are not indicated in acute closed head injury
Beginning in 2002,1 and reiterated in 2009,2 the Centers for Disease Control
and Prevention (CDC) and American College of Emergency Physicians
(ACEP) practice guidelines have stated that “skull film radiographs are not
recommended in the evaluation of mild TBI
Although the presence of a skull fracture increases the likelihood of an
intracranial lesion, its sensitivity is not sufficient to be a useful screening test
COMPUTED TOMOGRAPHY
Noncontrast head CT plays a critical role in immediate decisions, including the need for
hospitalization, intensive care unit admission, detection of intracranial hematoma and early
surgical management, such as evacuation of mass lesions, decompressive hemicraniectomy,
an external ventricular drainage catheter, or intracranial pressure monitor placement
initial imaging modality of choice in acute TBI for many reasons, including its high
sensitivity for acute intracranial hemorrhage, particularly intracranial hematomas large
enough to warrant immediate neurosurgical intervention, and for its superb delineation of
bony detail allowing highly sensitive and specific evaluation for skull, facial, and cervical
spine fractures within a single brief imaging session
INDICATIONS FOR CT SCAN

Generally, the CDC/ACEP guidelines recommend that head CT be

performed for:
Most patients with GCS score less than 15 or any LOC or PTA
INDICATIONS FOR CT SCAN
GCS SCORE

GCS plays an important role in

categorizing injury severity, allowing for
standardize determination of clinical
neurological status, and detecting
episodes of neurological deterioration
FOCAL BRAIN INJURIES
Result in contusions and traumatic intracranial hematomas
Contusions: focal regions of subpial hemorrhage and swelling and are present in 22% to 31% of patients
on initial CT scan
Most common in regions that contact bony surfaces in the cranial vault during trauma: frontal and
temporal poles, orbitofrontal gyri, perisylvian cortices, and inferolateral temporal lobe surfaces
Fracture contusions result from direct contact injuries and occur immediately adjacent to a skull fracture
Coup contusions refer to those that occur at the site of impact in the absence of a fracture, whereas
contrecoup contusions are those that are diametrically opposite to the point of impact
Contusions can cause significant mass effect owing to surrounding edema or hemorrhagic progression to
an intracerebral hematoma
TRAUMATIC INTRACRANIAL
HEMATOMA
Represent mass lesions that are potential therapeutic targets of surgical
intervention
The three major types of traumatic intracranial hematomas:
1. Epidural
2. Subdural
3. Intracerebral
TRAUMATIC INTRACRANIAL
HEMATOMA
EPIDURAL HEMATOMA
Occur in 10.6% of TBI patients admitted to the hospital
Account for 5% to 15% of fatal head injuries
In adults, EDH is far less common than subdural or intracerebral hemorrhages.
In pediatric patients, however, EDH is 1.96 times more common after TBI.
This is likely because of abundant diploic and dural vascularization normally
present in infants and young children, notwithstanding the tight adherence of
dura to the inner table of the skull
EPIDURAL HEMATOMA
Result from vascular injuries to dural vessels or the skull and are often
associated with overlying skull fractures
Classic EDH occurs beneath a temporoparietal skull fracture as a result of
damage to the middle meningeal artery
Separation of dura and bone is thought to occur at the time of injury rather
than in a delayed fashion owing to “stripping” of the dura from the inner
table because of clot enlargement
EPIDURAL HEMATOMA
The classic clinical course of a patient with EDH was first described by
Jacobson in 1886: initial loss of consciousness after trauma, transient complete
recovery (“lucid interval”), then rapid progression of neurological deterioration
This classic presentation occurs in only 14% to 21% of patients with an EDH
Neurological deterioration from an expanding EDH typically results in
obtundation, contralateral hemiparesis, ipsilateral oculomotor nerve paresis,
decerebrate rigidity, arterial hypertension, cardiac arrhythmias, respiratory
disturbances, and, finally, apnea and death
EPIDURAL HEMATOMA
Pure EDHs have an excellent prognosis after surgical evacuation, whereas
those with associated intradural lesions experience good outcome in only
44% of cases
Morbidity and mortality from a pure EDH are primarily caused by delay in
diagnosis and appropriate treatment
EPIDURAL
HEMATOMA
located in the potential space between the outer layer of the dura
mater and the inner table o the skull
Most epidural hematomas result from arterial bleeding from a
branch of the middle meningeal artery
CT shows a well-defined biconvex hyperdense collection
skull fracture is identified in approximately 90% of cases in adults
EDH is less common in children because the skull is more compliant
and the middle meningeal artery is not yet or only shallowly
indented into the inner table
 EPIDURAL HEMATOMA
Mortality from acute EDH ranges from 9% to 33%, but
when the lesion is evacuated before alteration of
consciousness, the mortality rate may approach zero
surgical management guidelines recommend evacuation of
the acute EDH when the volume exceeds 30 mL regardless
of the patient’s GCS score
Patients can be managed conservatively, with proper
monitoring, if the EDH volume is less than 30 mL and is
less than 15 mm thick with less than a 5-mm midline shift
and the patient has a GCS score greater than 8 without
focal neurological deficit.
SUBDURAL HEMATOMA
located between the dura and arachnoid layer and may result from arterial
or venous hemorrhage
caused by tearing of bridging veins that span the subdural space to drain
cortical blood directly into dural sinuses
Pathologically, an acute SDH is composed of clot and blood (within 48
hours), a subacute SDH represents a mixture of clotted blood and fluid (2-
14 days), and a chronic SDH is one that is in fluid phase (>14 days
SUBDURAL HEMATOMA
SUBDURAL HEMATOMA
Acute SDHs account for 50% to 60% of all SDHs
They are most common after sudden head movements that occur with
assaults or falls
Acute SDH may occur spontaneously (or after minor trauma) in patients
receiving chronic anticoagulation therapy
Despite the often relatively minor underlying brain damage, prognosis is
generally poor in these patients unless the hematoma is rapidly evacuated
SUBDURAL HEMATOMA
Cerebral ischemia plays a critical role in the pathology of SDH
likely related to compressive effects of the hematoma and elevated ICP with
resultant compromised CPP
 develops within the potential subdural space

SUBDURAL
between the arachnoid mater and the inner
layer of the dura
Subdural hematomas most commonly result

HEMATOMA
from tearing of cortical bridging veins
most commonly appears as a crescent
shaped extra-axial collection overlying a
cerebral convexity
SUBDURAL HEMATOMA
associated with high rates of mortality, ranging from 40% to 90%
A low admission Glasgow Coma Scale (GCS) score, advanced age, and
postoperative intracranial hypertension have been identified as significant
prognostic indicators for poor outcome in patients with acute SDH
SUBDURAL HEMATOMA
Acute SDH with thickness greater than 10 mm or causing greater than 5
mm of midline shift should be evacuated regardless of the patient’s GCS
score
For those with SDH thickness less than 10 mm or midline shift less than 5
mm, the hematoma should be evacuated if the GCS score declines 2 or
more points from injury to admission, if pupillary function is abnormal, or
if ICP is greater than 20 mm Hg
INTRACEREBRAL
HEMATOMA
account for 20% to 30% of all traumatic intracranial hematomas
They are associated with extensive lobar contusions, from which they are often
difficult to distinguish
ICHs differ from cerebral contusions in that a large proportion of these lesions are
composed of blood, but they often result from growth and/or coalescence of
smaller cerebral contusions
is a parenchymal lesion composed of at least two thirds blood; otherwise, the
lesion is described as disrupted tissue with areas of microscopic hemorrhage
INTRACEREBRAL
HEMATOMA
most traumatic ICHs occur in the orbitofrontal and temporal lobes
ICHs are most common in focal head injuries, such as missile injuries,
perforating wounds, and depressed skull fractures
Patients on chronic anticoagulation therapy are at increased risk of
developing ICH, even after mild head injury
INTRACEREBRAL
HEMATOMA

appears as a focal area of patchy hemorrhage and edema

within a superficial portion of the brain that lies
immediately adjacent to the skull
INTRACEREBRAL
HEMATOMA
On CT they tend to occur in highly characteristic locations, often in
portions of the brain that lie immediately adjacent rough inner surfaces of
the skull
Most common locations are the anterior temporal lobes along the greater
sphenoid wings (50%), followed by the frontal lobes (30%), particularly the
orbitofrontal brain above the cribriform plate and orbital roofs
INTRACEREBRAL
HEMATOMA
The presence of extravasated blood in the brain parenchyma is considered neurotoxic
Mass effect from the hematoma along with perilesional edema also contributes to secondary brain
injury
Patients with parenchymal mass lesions and associated signs of progressive neurological
deterioration, or
medically refractory intracranial hypertension, or signs of mass effect on CT scan should be treated
with surgery
Patients with any parenchymal lesion greater than 50 cm3, or frontal or temporal contusions greater
than 20 cm3 with midline shift greater than 5 mm or cisternal compression and GCS scores of 6 to 8,
should also undergo operative management
INTRACEREBRAL
HEMATOMA
DIFFUSE BRAIN INJURIES
Concussion

Diffuse Axonal Injuries

CONCUSSION
the mildest form of diffuse injury and is thought to be caused by rotational
acceleration of the head in the absence of significant mechanical contact
patients with concussion experience a transient loss of consciousness followed by
a rapid return to a normal state of alertness
repeat concussions often result in some degree of permanent neurological
impairment
pathophysiology of concussion may be related to disturbances of consciousness
from lesions of the brainstem and diencephalon
DIFFUSE AXONAL INJURY
results from severe angular and rotational acceleration and deceleration that
delivers shear and tensile forces to axons
DAI may result in severe neurological impairment despite lack of gross
parenchymal contusions, lacerations, or hematomas
shearing injury, diffuse damage to the white matter of the immediate impact
type or diffuse white matter shearing injury
DIFFUSE AXONAL INJURY
histologic findings of DAI have been well described and include disruption and
swelling of axons, “retraction balls” (swollen proximal ends of severed axons), and
punctate hemorrhages in the pons, midbrain, and corpus callosum
DAI is often associated with punctate hemorrhages, termed Strich hemorrhages, that
represent bleeding from small cerebral vessels
Strich hemorrhages are typically found in areas that experience maximal acceleration
forces during trauma: corpus callosum, peri-third ventricular structures (hypothalamus,
columns of the fornix, anterior commissure), internal capsule, basal ganglia,
dorsolateral brainstem, and superior cerebellar peduncles
 CRITICAL CARE
MANAGEMENT OF TBI
Damage to the brain that occurs following traumatic injury is usually
divided into two general types, primary and secondary
The primary injury occurs prior to the patient’s arrival at the hospital and,
other than trauma preventive programs, cannot be modified by the
physicians treating the individual patient
the primary injury often initiates a cascade of secondary injury processes
that evolve over the first few postinjury hours to days
 CRITICAL CARE
MANAGEMENT OF TBI
These secondary pathologic processes may be of intracranial or systemic origin
Intracranial secondary insults include intracranial hypertension or elevated ICP, cerebral
edema (fluid-mediated swelling), and cerebral ischemia
Systemic events include systemic arterial hypotension hypoxemia, and hyperthermia
In severe forms of TBI, the secondary responses include changes in cerebral blood flow
(CBF), local and systemic inflammation, alterations in oxygen delivery and metabolism, and
both ischemic and apoptotic death of neural cells
injured brain is exquisitely sensitive to ischemia, and secondary ischemic insults can
additionally damage the brain
PRIMARY BRAIN INJURY
Occurs at the moment of impact and consists of multiple mechanisms,
including blast force, high-velocity penetrating injury, direct force, and
rapid accelerating/ decelerating-type injuries
Two pathologic processes are uniquely characteristic of TBI: diffuse axonal
injury (DAI) and contusion/ hematoma formation
SECONDARY BRAIN INJURY
Trauma initiates secondary brain injury mechanisms that are characterized by a cascade of
molecular derangements related to the primary injury and the body’s response to injury in the
initial minutes to days
This process is primarily mediated by cellular response mechanisms, which should be
differentiated from secondary brain injury events that may be preventable
This complex cascade of events involves neurotransmitter-mediated cell injury, inflammatory
responses, microvascular occlusion and injury, electrolyte imbalances, mitochondrial dysfunction,
and cellular apoptosis
These processes are manifested clinically by the development of intracranial hypertension and
cerebral ischemia
SECONDARY BRAIN INJURY

duration of hypotensive, febrile, and hypoxic insults was significantly

associated with mortality
the major reason that the traumatized brain is so sensitive to secondary
insults is that the regulatory processes that normally preserve CBF during
reductions in blood pressure, arterial partial pressure of oxygen (PO2), and
hemoglobin concentration are dysfunctional after trauma
The goal for these physiologic parameters must be to optimize cerebral
perfusion in the traumatized brain
INTRACRANIAL HYPERTENSION

the water content of the brain is increased while the cerebral blood volume
is decreased, suggesting that edema is the major component of brain
swelling after trauma
clinical manifestation of brain swelling is intracranial hypertension, which
develops in 50% of patients in a coma caused by severe head injury
CRITICAL CARE OF TBI
To assess the neurological status of the patient, evaluation of mental status
and cranial nerve, pupillary, and motor functions should be included in the
periodic neurological examination whenever possible
INTRACRANIAL
HYPERTENSION
ICP cannot be reliably estimated from any clinical feature after severe head injury
Clinical symptoms of raised ICP, such as headache, nausea, and vomiting, are impossible to
elicit in comatose patients
Papilledema is uncommon after head injury, even in patients with intracranial hypertension
CT scan signs of brain swelling, such as midline shift and compressed basal cisterns, are
predictive of raised ICP, but intracranial hypertension can occur without these findings
ICP monitoring has been the cornerstone of management of severe neurological injury of
different etiologies and most notably in the TBI patient population
INTRACRANIAL
HYPERTENSION
Normally, resting ICP in adults is less than 10 mm Hg
A sustained ICP greater than 20 mm Hg is clearly abnormal
An ICP between 20 and 40 mm Hg is considered moderate intracranial hypertension
An ICP greater than 40 mm Hg represents severe, usually life-threatening,
intracranial hypertension
The current TBI guidelines (Table 349-4) recommend treating ICP above 20 mm Hg
GUIDELINES FOR
MANAGEMENT
Blood pressure and oxygen
• Monitor blood pressure and avoid hypotension (systolic blood pressure <90 mm
Hg)
• Monitor oxygenation and avoid hypoxia (arterial PO2 <60 mm Hg or O2
saturation <90%)
Hyperosmolar therapy
• Mannitol is effective for control of ICP after severe head injury at doses of0.25-1
g/kg
GUIDELINES FOR
MANAGEMENT
Infection prophylaxis
• Give periprocedural antibiotics for intubation to reduce the incidence of
pneumonia (does not alter mortality or length of hospital stay)
• Perform early tracheostomy to reduce days of mechanical ventilation (does not
alter mortality rate or incidence of pneumonia)
Deep vein thrombosis prophylaxis
• Apply graduated compression stockings or intermittent pneumatic compression
stockings to reduce risk of thrombophlebitis
GUIDELINES FOR
MANAGEMENT
Anesthetics, analgesics, and sedatives
• Do not use prophylactic barbiturate coma to control ICP or improve outcome
• High-dose barbiturate administration may control elevated ICP refractory to maximum
standard medical and surgical treatment
Antiseizure prophylaxis
• Prophylactic phenytoin or valproate does not prevent late posttraumatic seizures.
• Prophylactic anticonvulsants decrease the incidence of early posttraumatic seizures (do
not improve outcome)
GUIDELINES FOR
MANAGEMENT
Hyperventilation
• Do not use prophylactic hyperventilation (arterial PCO2 of ≤25 mm Hg)
to control ICP
• May use hyperventilation as a temporizing measure for the reduction of
elevated ICP
• Avoid hyperventilation during the first 24 hr after injury when cerebral
blood flow is often critically reduced
GUIDELINES FOR
MANAGEMENT
Steroids
• Steroids do not improve outcome or reduce ICP.
• In patients with moderate to severe TBI, high-dose methylprednisolone
is associated with increased mortality
SPINAL CORD
INJURIES
CAUSES OF SPINAL CORD
INJURY
Motor vehicle accidents (50%)
Falls and work related injuries (30%)
Violent crime (11%)
Sports-related injuries (9%)
56% of all SCIs occur in the cervical spine
EPIDEMIOLOGY
SCI most commonly affects young otherwise healthy and productive
individuals
The male-to-female ratio is about 4 : 1
PHASES OF INJURY
Primary injury
1. damage that occurs at the time of the initial trauma and that causes immediate severing of axons and
death of spinal cord cells
2. involve shearing, laceration, and acute stretching which disrupt axons, blood vessels, and cell membranes
Secondary injury
3. refers to delayed, progressive damage that continues after cessation of primary injury and that can last for
weeks or even years
4. highly interrelated cellular processes lead to cell and axonal loss in a delayed fashion, these events
represent potential therapeutic targets
5. secondary SCI processes include apoptosis, ischemia, ion-mediated cell damage and excitotoxicity,
neuroinflammation, mitochondrial dysfunction, and oxidative cell damage
SPINAL CORD ISCHEMIA
Oxygen supply insufficient to meet metabolic demands can result from
causes such as vascular disruption, hypotension from hemorrhagic or
neurogenic shock, and respiratory insufficiency, all of which are
unfortunately common following SCI
Systemic hypoxia is seen particularly frequently in patients with SCI
because of respiratory muscle compromise and fatigue
SECONDARY INSULTS
Distinct from secondary injury
Occur at the level of the patient and lead to deficient provision of nutrients to
injured CNS tissue
Hypotension and hypoxia, two secondary insults commonly seen after SCI, are
believed to exacerbate secondary injury processes and worsen neurological
injury
top priority in managing acute SCI is assessment and stabilization of vital signs
NEUROGENIC SHOCK
Neurogenic shock refers to hypotension and bradycardia due to interruption of the
descending sympathetic tracts after severe CNS damage (brain or cervical or high
thoracic [T6 or above]
Neurogenic shock is typified by preserved urine output and warm extremities
recommended to maintain systolic blood pressure above 90 mm Hg
SCI guidelines currently recommend efforts to optimize spinal cord perfusion by
maintaining mean arterial pressures higher than 85 mm Hg for the first 7 days
after injury
SPINAL SHOCK
characterized by the loss of reflexes, bladder function, and muscle tone below the level of
injury
Spinal shock usually lasts for days or weeks after SCI, the average duration being 4 to 12
weeks
The identification of clinical signs that define the duration of spinal shock is controversial
Different writers have defined the termination of spinal shock as the appearance of the
bulbocavernosus reflex, the recovery of deep tendon reflexes, or the return of reflex
detrusor functions
ASIA SCALE
NEURO IMAGING OF SCI
Plain Radiographs

rapidly obtained, relatively inexpensive, and widely available

they involve low radiation exposure and pose limited risks to the patient

Plain radiographs of the spine are useful for the visualization of bony structures and are most
commonly used to evaluate the alignment of bony anatomy, grafts, and instrumentation

Used to look for abnormal motion of vertebrae during flexion and extension; and to assess
stability in traumatic injuries or spondylolisthesis during weight-bearing

The principal disadvantage of radiographs is that they poorly define soft tissues, such as the
disk, ligaments, nerves, and paraspinal tissues
COMPUTED
TOMOGRAPHY
CT quickly provides accurate images of the spine
Delineation of bony anatomy is excellent, allowing for
detailed evaluation of fractures
Differences in tissue attenuation enable the identification of
disk herniation and canal stenosis. Intraspinal and paraspinal
pathologic conditions and bone marrow changes, however, are
poorly visualized
CT is much more sensitive than plain radiographs for
diagnosing fractures (sensitivity 98% versus 52%,
respectively)
COMPUTED
TOMOGRAPHY
CT is the modality of choice because of its rapid
image acquisition and negative predictive value—
especially in patients with severe head trauma and
those who are hemodynamically unstable so would
not tolerate the time needed for MRI
All symptomatic, major trauma, or obtunded
patients with potential SCI should receive a high-
quality computed tomography (CT) scan, because
CT has a sensitivity approaching 100% for
detecting fractures, canal patency, and alignment
MAGNETIC
RESONANCE IMAGING

In trauma cases, MRI is often necessary to classify

a spinal cord injury, evaluate the extent of
ligamentous injuries, determine the chronicity of a
fracture, and identify the presence of a disk
herniation or hemorrhage
Highly detailed visualization of spine anatomy can
be obtained in a noninvasive fashion and does not
require the use of ionizing radiation
MAGNETIC RESONANCE
IMAGING
For patients with neurological deficits or CT abnormalities, magnetic
resonance imaging (MRI) can further define the level and nature of SCI
MRI can identify the pattern and anatomic level of cord injury for
prognostication, and also can identify soft tissue injury, ligamentous
disruption, or intervertebral disk herniation that must be included in patient
management
METHYLPREDISOLONE
NASCIS III compared the 24-hour MPSS infusion used in NASCIS II with a 48-hour MPSS
infusion and with tirilazad mesylate, a 21-aminosteroid with antioxidant but not glucocorticoid
effects
Overall this trial demonstrated no sustained benefit to MPSS administration. A post hoc
analysis noted that patients receiving MPSS 3 to 8 hours after injury demonstrated improved
neurological function at 6 weeks and 6 months but not at 1 year, when administered MPSS for
48 hours rather than 24 hours
This finding led to the recommendation that if MPSS were given within 3 hours of injury, the
24-hour infusion would suffice, but if treatment was initiated between 3 and 8 hours after
injury, a 48-hour MPSS regimen was better than the 24-hour regimen
In the context of inconsistent benefits, the role of corticosteroids in SCI
continues to be controversial and should be considered on an individual
patient basis
It remains an option for patients presenting within 8 hours of
nonpenetrating, incomplete SCI in the young, nondiabetic, and
immunocompetent population