Traumatic Brain Injury

Definition:

Traumatic brain injury (TBI) is physical injury to brain tissue that temporarily or permanently impairs
brain function.

Pathology:

• Injuries are commonly categorized as open or closed.

• Open injuries involve penetration of the scalp and skull (and usually
the meninges and underlying brain tissue).
 They typically involve bullets or sharp objects.
• A skull fracture with overlying laceration due to severe blunt force is
also considered an open injury.

• Closed injuries typically occur when the head is struck, strikes an object,
or is shaken violently, causing rapid brain acceleration and deceleration.
• Acceleration or deceleration can injure tissue at the point of impact
(coup), at its opposite pole (contrecoup), or diffusely.
• The frontal and temporal lobes are particularly vulnerable.
• Axons, blood vessels, or both can be sheared or torn.

Common Types of Traumatic Brain Injury

• Concussion:
– Concussion is defined as a transient and reversible posttraumatic
alteration in mental status (eg, loss of consciousness or memory,
confusion) lasting from seconds to minutes and not more than 6 h.
– No gross structural brain lesions and serious neurologic residua.
– Temporary disability can occur due to symptoms, such as nausea,
headache, dizziness, memory disturbance, and difficulty
concentrating (postconcussion syndrome) that usually resolve
within weeks.

• Brain Contusions:
– Contusions (bruises of the brain) can occur with open or closed
injuries.
– Contusions can impair a wide range of brain functions, depending
on contusion size and location.
– Larger contusions may cause brain edema and increased
intracranial pressure (ICP).
– Contusions may enlarge in the hours and days following the initial injury and cause
neurologic deterioration

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 • Diffuse axonal injury:
– Diffuse axonal injury (DAI) occurs when there is generalized
disruption of axonal fibers and myelin sheaths.
– No gross structural lesions but small petechial hemorrhages
are present.
– DAI is sometimes defined clinically as a loss of consciousness
lasting > 6 h in the absence of a specific focal lesion.
– Edema from the injury often increases ICP, leading to various manifestations.

• Hematomas:
– Hematomas can occur with open or closed injuries.
– They may be epidural, subdural, or intracerebral.
– Subarachnoid hemorrhage is common

• Subdural hematomas are collections of blood between the dura mater

and the pia-arachnoid mater.
o It arises from laceration of veins.
o They occur from falls and motor vehicle crashes.
o Compression of the brain by the hematoma and swelling of the
brain can increase ICP.
o High ICP increases mortality and morbidity.
o A chronic subdural hematoma cause symptoms gradually over
several weeks after trauma.
 These hematomas occur often in alcoholics and elderly
patients (especially in those taking antiplatelet or anticoagulant drugs, or in
those with brain atrophy).
 Elderly patients may consider the headinjury relatively trivial or may have even
forgotten it.
 Edema and increased ICP are unusual.

• Epidural hematomas are collections of blood between the skull and

dura mater and are less common.
o Epidural hematomas that are large or rapidly expanding are
usually caused by arterial bleeding, from the middle
meningeal artery caused by a temporal bone fracture.
o Without intervention, hematomas may rapidly deteriorate
and cause death.
o Small, venous epidural hematomas are rarely lethal.

• Intracerebral hematomas are collections of blood within the brain itself.

o They result from coalescence of contusions.
o Increased ICP, herniation, and brain stem failure can subsequently
develop, particularly with lesions in the temporal lobes.

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Skull fractures:

• Skull fractures may be linear, depressed, or comminuted.

• The presence of a fracture suggests that significant force was
involved in the injury.
• Patients with any fracture associated with neurologic impairment are
at increased risk of intracranial hematomas.
• Fractures that involve special risks include:
– Depressed fractures can tear the dura and damages the
underlying brain, or both.
– Temporal bone fractures that cross the area of the middle
meningeal artery can caused an epidural hematoma.
– Fractures that cross one of the major dural sinuses cause
significant hemorrhage and venous epidural or venous subdural
hematoma.
– Injured venous sinuses can later thrombose and cause cerebral
infarction.
– Fractures that involve the carotid canal can result in carotid
artery dissection.
– Fractures of the occipital bone and base of the skull (basilar bones).
– These bones are thick and strong, so fractures in these areas indicate a high-intensity
impact and so increases the risk of brain injury.
– Basilar skull fractures that extend into the petrous part of the temporal bone often
damage middle and inner ear structures and can impair facial, acoustic, and vestibular
nerve function.
– A linear skull fracture in infants can trapped the meninges with subsequent
development of a leptomeningeal cyst and expansion of the original fracture (growing
fracture)

Pathophysiology :

• Brain function may be immediately impaired by direct damage (eg, crush, laceration) of brain
tissue or occurs shortly thereafter from the cascade of events triggered by the initial injury.
• TBI of any sort can cause cerebral edema and decrease brain blood flow.
• Any swelling from edema or an intracranial hematoma has nowhere to expand and thus
increases ICP.
• The brain becomes ischemic.
• Systemic complications from trauma (eg, hypotension, hypoxia) can also contribute to cerebral
ischemia (secondary brain insults).
• Excessive ICP initially causes global cerebral dysfunction.
• If excessive ICP is unrelieved, it can push brain tissue across the tentorium or through the
foramen magnum, causing herniation and increased morbidity and mortality

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 • The Glasgow Coma Scale.
– It is a scoring system used during the initial examination to estimate severity of TBI.
– It is based on eye opening, verbal response, and the best motor response.
– The lowest total score (3) indicates likely fatal damage, especially if both pupils fail to
respond to light and oculovestibular responses are absent.
– Higher initial scores tend to predict better recovery.
– The severity of headinjury is initially defined by the GCS score:
 14 or 15 is mild TBI
 9 to 13 is moderate TBI
 3 to 8 is severe TBI.

– The Glasgow Coma Scale:

Area Assessed Response Points

Eye opening Open spontaneously 4

Open to verbal command 3

Open in response to pain applied to the limbs or sternum 2

None 1

Verbal Oriented 5

Disoriented, but able to answer questions 4

Inappropriate answers to questions; words discernible 3

Incomprehensible speech 2

None 1

Motor Obeys commands 6

Responds to pain with purposeful movement 5

Withdraws from pain stimuli 4

Responds to pain with abnormal flexion (decorticate posture) 3

Responds to pain with abnormal (rigid) extension (decerebrate 2

posture)
None 1

Combined scores < 8 are typically regarded as coma.

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Symptoms of specific types of TBI:

• Symptoms of various types of TBI may overlap considerably.

• Epidural hematoma symptoms usually develop within minutes to several hours after the injury
(the period without symptoms is the so-called lucid interval) and consist of increasing headache,
decreased level of consciousness, and focal neurologic deficits (eg, hemiparesis).
• Pupillary dilation with loss of light reactivity usually indicates herniation.
• Some patients lose consciousness, then have a transient lucid interval, and then gradual
neurologic deterioration.
• Most patients with subdural hematomas have immediate loss of consciousness.
• Intracerebral hematoma and subdural hematoma can cause focal neurologic deficits such as
hemiparesis, progressive decrease in consciousness, or both.
• Progressive decrease in consciousness may result from anything that increases ICP (eg,
hematoma, edema, hyperemia).
• Increased ICP sometimes causes vomiting.
• Classically, it manifests as a combination of hypertension, bradycardia, and respiratory
depression (Cushing triad).
• Severe diffuse brain injury or markedly increased ICP may cause decorticate or decerebrate
posturing.
o Both are poor prognostic signs.

• Transtentorial herniation may result in coma, unilaterally or bilaterally dilated and unreactive
pupils, hemiplegia (usually on the side opposite a unilaterally dilated pupil), and Cushing triad
(hypertension, bradycardia and poor respiration).

• Basilar skull fracture may result in

o leakage of CSF from the nose (CSF rhinorrhea) or ear (CSF otorrhea).
o blood behind the tympanic membrane (hemotympanum) or in the external ear canal if
the tympanic membrane has ruptured.
o ecchymosis behind the ear (Battle sign) or in the periorbital area (raccoon eyes).
• Loss of smell and hearing is usually immediate, usually aware after regain consciousness.
• Facial nerve function may be impaired immediately or after a delay.
• Other fractures of the cranial vault are sometimes palpable, particularly through a scalp
laceration, as a depression or step-off deformity.
• Chronic subdural hematoma may manifest with increasing daily headache, fluctuating
drowsiness or confusion, and mild-to-moderate hemiparesis or other focal neurologic deficits.

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Long-term symptoms:

• Retrograde and anterograde amnesia may persist.

• Postconcussion syndrome, commonly after a moderate or severe concussion, includes
headache, dizziness, fatigue, difficulty concentrating, variable amnesia, depression, apathy, and
anxiety.
• Smell and taste, sometimes hearing, or rarely vision is altered or lost.
• Symptoms usually resolve spontaneously over weeks to months.
• Common problems such as amnesia, behavioral changes (eg, agitation, lack of motivation),
emotional laibility, sleep disturbances, and decreased intellectual function can persist.
• Late seizures (> 7 days after the injury) develop in some patients, often weeks, months, or even
years later.
• Spastic motor impairment, gait and balance disturbances, ataxia, and sensory losses may occur.
• A persistent vegetative state can result from a TBI that destroys forebrain cognitive functions
but spares the brain stem.
• The capacity for self-awareness and other mental activity is absent.
• Few patients recover normal neurologic function when a persistent vegetative state lasts for 3
mo after injury, and almost none recover after 6 mo.
• Neurologic function may continue to improve for a few years after TBI, most rapidly during the
initial 6 mo.

Diagnosis:

1. Initial rapid trauma assessment

2. Glasgow coma scale and neurologic examination.
3. CT

• Initial measures:
– Perform a rapid, focused neurologic evaluation.
– Assess adequacy of the airway and breathing.
– Perform pupillary light response.
– Assessed before paralytics and sedatives are given.
– Reassessed at frequent intervals (eg, every 15 to 30 min initially, then every 1 h after
stabilization)
• Complete neurologic examination is done as soon as the patient is sufficiently stable.
• CT scan of the head is indicated for the following:
– Patients with impaired level of consciousness.
– GCS score < 15.
– focal neurologic findings.
– persistent vomiting.
– Seizures.
– a history of loss of consciousness.
– clinically suspected fractures.
• CT can detect hematomas, contusions and skull fractures.
• MRI may be useful later in the clinical course to detect more subtle contusions, DAI, and brain
stem injury.

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Prognosis:

• The vast majority of patients with mild TBI retain good neurologic function.
• With moderate or severe TBI, the prognosis is not good.
• The assessment of TBI outcomes is usually based on the GCS score as follows:
o 14 or 15 - Good recovery (return to previous level of function).
o 9 – 13 - Moderate disability (capable of self-care).
o 3 – 8 - Severe disability (incapable of self-care).
o < 8 - Vegetative (no cognitive function).
• Occurrence and duration of coma after a TBI are strong predictors of disability.
• Of patients whose coma exceeds 24 h, 50% have severe persistent neurologic sequelae, and 2 to
6% remain in a persistent vegetative state at 6 mo.
• Cognitive deficits, with impaired concentration, attention, and memory, and various personality
changes are a more common cause of disability.
• Posttraumatic anosmia and acute traumatic blindness seldom resolve after 3 to 4 mo.
• Hemiparesis and aphasia usually resolve at least partially, except in the elderly.

Treatment:

1. For mild injuries, discharge and home observation

2. For moderate and severe injuries, optimization of ventilation, oxygenation, and brain perfusion;
treatment of complications (eg, increased ICP, seizures, hematomas); and rehabilitation.

At The Scene:
• A clear airway is secured and external bleeding is controlled before the patient is moved.
• Avoid displacement of the spine or other bones to protect the spinal cord and blood vessels.
• Proper immobilization should be maintained with a cervical collar and long spine board.
• After the initial rapid neurologic assessment, pain should be relieved with a short-acting
opioid (eg, fentanyl ).

In the hospital:
• After quick initial evaluation, neurologic findings (GCS and pupillary reaction), BP, pulse, and
temperature should be recorded frequently for several hours because any deterioration
demands prompt attention.
• The cornerstone of management for all patients is -
 maintenance of adequate ventilation, oxygenation, and brain perfusion to avoid
secondary brain insult.
 aggressive early management of hypoxia, hypercapnia, hypotension, and increased
ICP helps avoid secondary complications.
 Bleeding from injuries (external and internal) is rapidly controlled.
 intravascular volume is promptly replaced with crystalloid (eg, 0.9% saline) or
sometimes blood transfusion to maintain cerebral perfusion.
 Hypotonic fluids (especially 5% D/W) are contraindicated because they contain
excess free water, which can increase brain edema and ICP.

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 • Other complications to check for and to prevent include hyperthermia, hyponatremia,
hyperglycemia, and fluid imbalance.

1. Mild injury:
• Injury is mild (GCS score 14-15) in 80% of patients.
• If there is brief or no loss of consciousness, vital signs are stable, a normal head CT scan,
and normal mental and neurologic function, they may be discharged home provided
family members or friends can observe them closely for an additional 24 h.
• The patients are brought back to the hospital if any of the following develop:
– Decreased level of consciousness
– Focal neurologic deficits.
– Worsening headache.
– Vomiting
– Deterioration of mental function (eg, seems confused, cannot recognize people,
behaves abnormally)
– Seizures.

2. Moderate and severe injury:

• Injury is moderate in 10% of patients.
• Because deterioration is possible, these patients should be admitted and observed even
if head CT is normal.
• Because airway protective reflexes are usually impaired and ICP may be increased,
patients are intubated endotracheally.
• Close monitoring using the GCS and pupillary response should continue.
• CT is repeated, particularly if there is an unexplained ICP rise

3. Increased intracranial pressure :

• Treatment principles for patients with increased ICP include
– Rapid sequence orotracheal intubation.
– Mechanical ventilation.
– Monitoring of ICP and Cerebral Perfusion Pressure (CPP)
– Ongoing sedation as needed
– Maintaining euvolemia and serum osmolality of 295 to
320 mOsm/kg
– For intractable increased ICP, possibly CSF drainage,
temporary hyperventilation, decompressive craniotomy,
or pentobarbital coma.
• Patients who require airway support or mechanical ventilation need rapid sequence
intubation (RSI) orally rather than awake nasotracheal intubation, which can cause
coughing and gagging and thereby raise the ICP.
– RSI requires an induction agent (eg. IV etomidate 0.3mg/kg for adult) and a
muscle relaxant (eg. IV succinylcholine 1.5mg/kg).
• Pulse oximetry and ABGs (if possible, end-tidal CO2) should be used to assess adequacy
of oxygenation and ventilation.
– The goal is a normal Paco2 level (38 to 42 mm Hg).

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 • Cerebral venous drainage can be enhanced (thus lowering ICP) by elevating the head of
the bed to 30° and by keeping the patient's head in a midline position.
– The goal is to maintain ICP at < 20 mm Hg.
• Preventing agitation, excessive muscular activity (eg, due to delirium), and pain can also
help prevent increases in ICP.
– For sedation, inj propofol is often used in adults because it has quick onset and
very brief duration of action; dose is 0.3 mg/kg/h continuous IV infusion,
titrated gradually upward as needed (up to 3 mg/kg/h).
– Opioids are often needed for adequate pain control.
• Patients should be kept euvolemic and iso-osmolar or slightly hyperosmolar (target
serum osmolality 295 to 320 mOsm/kg).
• To control ICP, hypertonic saline solution (usually 2% to 3%) is more effective as
osmotic agent compared to mannitol. It is given as a bolus of 2 to 3 mL/kg IV as needed
or as a continuous infusion of 1 mL/kg/h.
• Serum Na level is monitored and kept ≤ 155 mEq/L.

• When increased ICP is refractory to other interventions,

decompressive craniotomy is considered. A bone flap is removed
(to be replaced later), and duraplasty is done to allow outward
brain swelling.

• Next option for intractable increased ICP is pentobarbital coma.

• Coma is induced by giving pentobarbital 10 mg/kg IV over 30 min,
5 mg/kg/h for 3 h, then 1 mg/kg/h maintenance infusion. This will
suppress bursts of EEG activity.

4. Seizures:
• Seizures can worsen brain damage and increase ICP and therefore should be treated
promptly.
• In patients with significant structural injury (eg, larger contusions or hematomas, brain
laceration, depressed skull fracture) or a GCS score < 10, a prophylactic anticonvulsant
should be considered.
• Inj phenytoin is commonly used. A loading dose of 20 mg/kg IV is given followed by
maintenance dose of 2 to 2.7 mg/kg tid for adult.

5. Skull fractures:
• Aligned closed fractures require no specific treatment.
• Depressed fractures sometimes require surgery to elevate fragments, manage lacerated
cortical vessels, repair dura mater, and debride injured brain.
• Open fractures may require surgical debridement unless there is no CSF leak and the
fracture is not depressed by greater than the thickness of the skull.

6. Surgery:
• Intracranial hematomas may require urgent surgical evacuation to prevent or treat brain
shift, compression, and herniation.
• Small intracerebral and subdural hematomas rarely require surgery.
• Factors that suggest a need for surgery include -
 a midline brain shift of > 5 mm.

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  compression of the basal cisterns.
 worsening neurologic examination findings.
• Chronic subdural hematomas may require surgical drainage but much less urgently than
acute subdural hematomas.
• Large or arterial epidural hematomas are treated surgically.
 Small epidural hematomas that are thought to be venous in origin can be
followed with serial CT.

7. Rehabilitation:
• When neurologic deficits persist, rehabilitation is needed.
• Rehabilitation is best provided through a team approach that combines physical,
occupational, and speech therapy, skill-building activities, and counseling to meet the
patient's social and emotional needs.
• Brain injury support groups may provide assistance to the families of brain-injured
patients.

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