Craniocerebral Trauma

• Traumatic brain injury (TBI) is

– A silent epidemic in developed nations and
– One of the leading causes of death and disability,
accounting for almost one-third of all trauma-related
deaths.
 EPIDEMIOLOGY

• TBI is most prevalent in the young.

• The elderly have the worst outcome.
– Although only 10 % of TBI occurs in the old, they
account for 50% of TBI-related death.
• Although 50% of all TBI cases are due to road
traffic, falls are the most common cause in the
elderly.
 CLASSIFICATION

• TBI is classified by mechanism, severity, and

morphology
• A. Mechanism
– Blunt injury is the most common mechanism and
includes low- and high-velocity impacts
– Gunshot wounds are the most prevalent penetrating
injuries,
• 35% of deaths from TBI under the age of 45 years in the USA
• Most lethal type of brain injury, 90% resulting in death
• Further damage is done by shock waves
– Blast is a rare mechanism of injury in civilian life, but it
is common in combat.
• Blast injuries occur as
– A direct result of supersonic waves of intense air (primary
blast injury),
– From objects put in motion by the blast hitting people
(secondary blast injury)
– By a person being forcefully put in motion by the blast (tertiary
blast injury)
• B. Injury Severity
– There are different methods for stratifying TBI by
severity,
– Most commonly used is the Glasgow Coma Scale (GCS),

– Mild TBI is eight times more common

– Mild traumatic brain injury and concussion are often
used interchangeably,
• Mild TBI
– Despite its high incidence, no objective test for
diagnosing mild TBI exists currently.
– Only 1 out of 10 head CT scans has a positive finding in
mild TBI patients
– Therefore, special factors need to be considered when
determining the need for a CT scan
• A concussion is defined as injury to the brain
caused by a hard blow or violent shaking,
producing a sudden and temporary impairment of
brain function, such as a brief loss of
consciousness or disturbance of vision and
equilibrium.
– Headache,
– Nausea,
– Dizziness,
– Irritability, and
– Impaired ability to concentrate
• Loss of consciousness is believed to result from
rotational forces exerted on the upper midbrain
and Thalamus, impairing the function of the
reticular neurons
• Persistence of these symptoms for weeks is called
post-concussion syndrome and can last from 1
month to a year.
• C. Morphology
• TBI can be subdivided as injuries to the skull
itself and intracranial injuries, which can be
focal or diffuse
 Skull fractures

• Presence of skull fractures consistently has been

associated with a higher incidence of
– Intracranial lesions
– Neurological deficits
– Poorer outcome

• Hence, CT scanning should be performed in all

patients with a known or suspected cranial
fracture
• Fractures can be located in the calvarium or in the
skull base. Skull base fractures are
– Associated with cranial nerve (CN) palsy
– Depending on their location, CN VII (temporal bone) and CN VI
(clivus) are at risk
– Prone to cause cerebrospinal fluid leaks
 Intracranial Injuries

• Contusions
– The brain moves within the skull enough to collide with it
– Bruising of the brain parenchyma (hemorrhage and
edema)
– Most common locations are the frontal and temporal
poles

• In contrast to concussion, contusions are visible

on a head CT scan.
• Countercoup is seen diagonally across the site
of the direct impact (coup injury) when the
accelerated brain strikes the skull on the opposite
site
 Epidural hematoma (EDH)

– Bleeding between the dura and the skull.

– Peak incidence is in the second decade, and the mean
age of TBI victims with EDH is between 20 and 30 years
– Traffic-related accidents, falls, and assaults account for
53% of EDH in adults
– Falls account for half of the EDH in children

• EDHs are associated with a skull fracture and

bleeding from a lacerated artery or indirect bone
bleeding.
• Arterial bleeding was identified as the source of
the EDH in 36% of adults in a systematic review.
• Rupture of the middle meningeal vein, the diploic
veins, or the venous sinuses also can cause EDH.
• The most common location of EDH is temporal.
• Because the temporal bone is thinner than the
rest of the skull, it breaks more easily, often
resulting in a laceration of the middle meningeal
artery
 Subdural hematoma (SDH)

• Develops between the brain parenchyma and the

dura
• It occurs when the brain moves within the skull
enough to tear a surface vein, also called a
bridging vein, that runs from the brain surface to
the dural venous sinus.
• Most common locations are the frontal and
parietal convexities
• On a CT scan, an acute SDH typically
• Bright (hyperdense) extra-axial crescent shaped,
homogeneous collection of fluid that conforms to
the cerebral surface.
• Unlike an EDH, its spread is not limited by suture
lines; it can spread over the whole convexity, but
it almost never crosses the midline.
• An SDH can be acute or chronic. Herein, “acute
SDH” is defined as an SDH diagnosed within 14
days of TBI.
• Chronic SDH may be of mixed density or isodense
to gray matter. In these cases, it can be identified
by its mass effects including sulcal effacement,
inward buckling of the gray–white interface, and
presence of midline shift.
• Between 37% and 80% of patients with acute
SDH present with an initial GCS score of 8 or less,
and dilated pupils are seen preoperatively in 50%
of these patients.
 Traumatic subarachnoid hemorrhage
(tSAH)
• Seen with mild and severe TBI alike, refers to
microhemorrhages into the subarachnoid space
from crushed or ruptured smaller vessels.
• CT scans show hyperdense linear areas in
superficial brain sulci
• In contrast to aneurysmal SAH, the blood is
superficial in the cortex and not present in the
basal cisterns
• Most of the time, traumatic SAH indicates a more
severe underlying brain injury and is seen in
conjunction with diffuse axonal injury, subdural
hematoma, or epidural hematoma.
• It has been shown that the presence of traumatic
SAH is an independent factor for poor outcome.
• The incidence of post-traumatic vasospasm in
patients with a mean GCS score of 7 (range, 3 to
15) is similar to that following aneurysmal SAH
 Diffuse axonal injury

• Very common severe head injury associated with

significant morbidity
• Characterized clinically by rapid progression to
coma in the absence of specific focal lesions
• DAI is a result of shearing, stretching, and/or
angular forces pulling on axons and small vessels
• Impaired axonal transport leads to focal axonal
swelling and may result in axonal disconnection
• Most common locations are the
– Corticomedullary (gray matter–white matter) junction
(particularly in the frontal and temporal areas),
– Internal capsule,
– Deep gray matter,
– Upper brainstem, and
– Corpus callosum.
• Patients who survive the most severe form rapidly
lapse into coma and remain unconscious,
vegetative, or severely disabled.
• MRI is more sensitive than CT in detecting DAI.
• Gradient echo MRI is most sensitive to areas of
hemorrhage, and fluid attenuated inversion
recovery images are best for visualizing
nonhemorrhagic lesions.
• Diffusion tensor imaging (DTI) is a new imaging
technology more sensitive to DAI than is
conventional MRI.
 PATHOPHYSIOLGY

• Much of the research concerning TBI is directed at

affecting the mechanisms of secondary brain
injury
• These mechanisms include
– Excitatory amino-acid toxicity,
– Hypoxia,
– Impaired cerebrovascular autoregulation,
– Hyperthermia,
– Blood–brain barrier breakdown, and
– Hypercalcemia.
• Hypoxia and hypoperfusion are recognized as
leading contributors to secondary brain injury
• Cerebrovascular dysregulation
– Often seen after TBI
– Decreased CBF (<20 mL/100 g/min) in the initial 24
hours is associated with poor outcome
• Diffuse cerebral swelling
• A significant contributor to elevated ICP
• Result from blood–brain barrier disruption
(vasogenic edema), osmolar changes, and edema
at the cellular level (cytotoxic or cellular edema).
• Hypoxia, hypoperfusion, inflammation, and
oxidative stress also can contribute to cerebral
swelling.
• After a TBI, excitotoxicity occurs upon the release
of excessive amounts of excitatory amino acids
such as glutamate, resulting in neuronal injury.
 TREATMENT

• Evaluation
• Early intervention is essential in successful TBI
care
• Once in the emergency room, further measures
can be taken if necessary to achieve adequate
cardiopulmonary function
• Next, a neurological examination is performed to
triage patients accordingly.
• The GCS score is widely used to convey the
severity of TBI.
• Trauma patients with altered mental status,
pupillary asymmetry, and flexion or extension
posturing are at high risk for a SDH or an EDH
compressing the brain and brainstem and must
be evaluated with a CT scan of the head.
• This rule have 100% sensitivity for neurosurgical
lesions and 83% to 98% sensitivity for
nonoperative lesions.
• Neurocritical care and any therapeutic
intervention, operative or nonoperative, have one
goal:
– The prevention of secondary injury, which, unlike the
irreversible primary injury, can be limited.
• Anticoagulation in patients with traumatic brain
injury is a common complicating factor.
• The use of aspirin, Plavix, Coumadin, and a new
group of Factor Xa inhibitors is seen quite often in
the elderly population presenting with TBI
 Management of Diffuse Injuries

• Patients with complicated mild TBI (positive CT

findings) and moderate TBI are admitted to the
ICU and followed with serial neurological
examinations.
• Although intracranial complications are
uncommon after a mild TBI, in 6% to 12% of
patients, CT shows abnormalities in the form of a
contusion, SAH, SDH, or EDH.
• Concussion is defined as a complex
pathophysiology process affecting the brain,
induced by biomechanical forces.
• Concussions typically result in a rapid onset of
short-lived impairment and they resolve
spontaneously, which may or may not involve the
loss of consciousness.
• Clinical experts suggest a benefit from the use of
mild analgesics for headache; avoidance of
narcotics; and the use of meclizine, or
promethazine, and vestibular exercise for
dizziness.
• Patients with a GCS score ≤8 qualify for ICP
monitoring.
• This can be achieved via an external ventricular
drain (EVD), which allows both ICP measurement
and CSF drainage
• An escalating protocol should be followed to
control ICP , using sedation, hyperosmolar
therapy in the form of mannitol and hypertonic
saline, and hyperventilation.
• Currently, patients with increased ICP initially
receive a continuous 3% saline infusion and 250-
mL boluses if needed.
• Mannitol is reserved for an emergency situation
such as an acutely dilated pupil and imminent
brain herniation.
• Serum sodium can be elevated safely to 155
mEq/L and a serum osmolality of 320 mOsm/kg.
Beyond those levels, renal failure can develop.
• If hypertonic saline administration is stopped
suddenly, rebound intracranial hypertension is a
risk but can be avoided by tapering the
hypertonic saline solution over 48 hours.
• ICP that remains elevated despite maximal
medical efforts is an indication for decompressive
craniectomy or bilateral frontal craniectomy
 Management of Focal Injuries

• Patients with focal TBI and axial or extra-axial

bleeding with mass effect are treated surgically.
• The development of mass effect may result in
secondary brain injury, posing the risk of further
neurological deterioration, herniation, and death.
• A patient with an EDH can go from normal
neurological status to coma within minutes.
• Most often, the patient becomes agitated and
restless and may have an episode of emesis
because of the increased ICP.
• The following guidelines list the criteria for
surgical evacuation of an acute epidural
hematoma:
– An EDH >30 cm3 should be evacuated regardless of the
GCS score.
– An EDH <30 cm3 in volume and <15 mm thick, with a
<5-mm midline shift in patients with a GCS score ≤8
without focal deficit can be managed nonoperatively
with serial CT scanning and close neurological
observation in a facility with neurosurgical coverage.
• Regarding timing, emergent surgical evacuation
is strongly recommended for comatose (GCS
score of ≤8) patients with an acute EDH.
• Emergent craniotomy for evacuation also is
indicated if an EDH thicker than 1 cm develops or
leads to neurological symptoms.
• The following guidelines list the criteria for
surgical management of SDH:
– An acute SDH thicker than 10 mm or causing a midline
shift >5 mm on CT scans should be surgically
evacuated, regardless of the patient’s GCS score.
– A comatose patient (GCS score ≤8) with an SDH <10
mm thick and midline shift <5 mm should undergo
surgical evacuation of the lesion if the GCS score
decreases by 2 or more points between the time of
injury and hospital admission, the pupils are asymmetric
or fixed and dilated, or ICP exceeds 20 mm Hg.
– ICP monitoring should be performed in all comatose
(GCS score ≤ 8) patients with an acute SDH.
• Isolated linear fractures are usually of little
clinical significance unless they are near or
traverse a suture or they involve a venous sinus
groove or vascular channel.
• Patients with simple (“closed”) depressed cranial
fractures may be treated nonoperatively if there
is no :
– clinical or radiographic evidence of dural penetration
(pneumocephalus),
– significant intracranial hematoma,
– depression >1 cm,
– frontal sinus involvement,
– cosmetic deformity, or
– gross wound contamination.
Thank you