Traumatic Brain Injury
Traumatic Brain Injury
Injury
Ma. Corazon D. Acosta, MD.,
FPARM
University of La Salette
College of Medicine and Allied
Medical Programs
1
Traumatic Brain Injury
Epidemiology
Bimodal age distribution
Peak age at 15 – 24 and 65 – 75 years
old
M > F (2:1)
2
Causes of TBI
General
Population
Other 7%
Sports/Recreation
10%
Vehicle
Firearms
Crashes
12%
50%
Falls
21%
TBI Gender
6
Closed Head Injury
7
Penetrating Head Injury
8
Most common risk
factor is
ALCOHOL
INTAKE
9
Primary Injury in TBI
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Cerebral Contusions and
Lacerations
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Cerebral Contusions and
Lacerations
Contusi
on
12
Diffuse Axonal Injury
Occurs as a result of mechanical
deceleration, causing disruption
following shearing and tearing of
axons
13
Diffuse Axonal Injury
Areas involved
Corpus callosum
Dorsolateral
quadrant of the
midbrain
Midbrain at the
level of the
superior cerebellar
peduncle
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Diffuse Axonal Injury
16
Diffuse Axonal Injury
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Secondary Brain Injury
1. Intracranial Hematoma
2. Cerebral swelling
3. Herniation
4. Cerebral ischemia
5. Infection
18
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Secondary Brain Injury
Intrscranial hematoma
May be extradural (epidural) or
intradural (subdural) hematoma
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Epidural Hematoma
Acute in presentation
Associated with skull fractures
Bleeding from meningeal vessels
and dural sinuses
Lucid interval
May lead to herniation, coma or
death
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Epidural Hematoma
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Epidural Hematoma
23
Subdural Hematoma
Bleeding from bridging veins
Due to acceleration-deceleration
Dissection into subdural space
Acute (0 – 7 days)
Subacute (7 – 22 days)
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Subdural Hematoma
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Subdural Hematoma
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Cerebral Edema
Due to either vasodilatation or an
increase in intra or extracellular
fluid
May lead to increased intracranial
pressure (ICP)
Increased ICP
Headache
Vomiting
Papilledema
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Papilledema
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Herniation
1. Central herniation
> Protrusion of the midbrain and pons
through the tentorial notch
2. Tonsillar herniation
> Protrusion of the medulla and
cerebellar tonsils through the foramen
magnum
3. Uncal herniation
> Protrusion of the uncus and
hippocampal gyrus of the brain
through the tentorial notch
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Cerebral ischemia
Caused by hypoxia or impaired cerebral
perfusion
Infection
May occur in the presence of dural
tears
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Clinical Assessment
Lacerations and bruising
Basal skull fracture
Level of consciousness
Pupil response
Limb weakness
Eye movements
Vital signs
Cranial nerve lesions
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Basal skull fracture
Look for:
1. CSF rhinorrhea
2. Bilateral periorbital hematoma
3. subconjunctival hemorrhage
4. CSF otorrhea
5. Battle’s sign
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Level of Consciousness
Glasgow Coma Scale
Eye opening
Best verbal response
Score : 3 - 15
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Glasgow Coma Scale
Best Eye Response. (4)
1 - No eye opening.
2 - Eye opening to pain.
3 - Eye opening to verbal command.
4 - Eyes open spontaneously.
34
Glasgow Coma Scale
Best Verbal Response (5)
1 - No verbal response
2 - Incomprehensible sounds.
3 - Inappropriate words.
4 - Confused
5 - Orientated
35
Glasgow Coma Scale
Best Motor Response. (6)
1 - No motor response.
2 - Extension to pain.
3 - Flexion to pain.
4 - Withdrawal from pain.
5 - Localising pain.
6 - Obeys Commands.
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Modified Glasgow Coma
Scale
Nonverbal Child's Best Verbal
Response Score
smiles, oriented to sound, follows objects,
interacts oriented and converses (5)
consolable when crying and interacts
inappropriately disoriented and converses
(4)
inconsistently consolable and moans;
makes vocal sounds inappropriate words
(3)
inconsolable, irritable and restless; cries
incomprehensible sounds (2)
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Glasgow Coma Scale
GCS 13 – 15 mild TBI
GCS 9 – 12 moderate TBI
GCS ≤ 8 severe TBI
comatose
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Pupil Response
39
Eye Movements
test)
Spontaneous eye movements
40
Vital Signs
Look for Cushing’s triad
Hypertension
Bradycardia
Abnormal respiration
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Measures of Injury
Severity
Depth and duration of coma
GCS of 8 or less
Coma ≥ 6 hours (severe injury)
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Outcome after TBI
Deficits
Physical or neurobehavioral
Vary from one person to another
Behavioral problems
Minor irritability or passivity to
disinhibited, bizarre or aggressive
behavior
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Cognitive Impairment
Common after moderate to severe
TBI
Attention and arousal
Memory
Sensory/perceptual dysfunction
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Outcomes Measurement
Glasgow Outcome Scale
Disability Rating Scale
Rancho Los Amigos Level of
cognitive functioning
Functional Independence Measure
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Glasgow Outcome Scale
absence seizures
patients given prophylactic
50
Medical Complications
After TBI
Hydrocephalus
May be communicating (within the ventricular
system) or non-communicating (obstruction in
the subarachnoid space)
Symptoms include
Nausea
Vomiting
Headache
Papiledema
Obtundation
Dementia
Ataxia
Urinary incontinence
Treatment – shunting procedure or lumbar
puncture
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Medical Complications
After TBI
Deep Venous Thrombosis
Patients should be given prophylaxis
as early as possible
Prophylaxis include:
Elastic compression
Intermittent pneumatic compression
Vena cava filters
Anticoagulants
52
Medical Complications
After TBI
Heterotopic Ossification
Ectopic bone formation
Common in the hips, knees, elbows,
shoulders, hands and spine
Risk factors include coma lasting > 2
weeks, limb spasticity and decreased
mobility
Spasticity
Velocity dependent increase in tone
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Medical Complications
After TBI
GI and GU complications
Include stress ulcers, dysphagia,
bowel incontinence and elevated liver
functions tests
GU complications include urethral
strictures, UTI and urinary
incontinence
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THERAPEUTIC INTERVENTIONS FOR
THE COGNITIVE AND BEHAVIORAL
SEQUELAE IN TBI
neuropsychological
processes, predominantly
attention, memory, and
executive skills
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Therapeutic
Interventions
Compensatory training focuses
on adapting to the presence of
a cognitive deficit.
Compensatory devices, such
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Therapeutic
Interventions
Behavior modification
used to address the
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RECOMMENDATIONS REGARDING
REHABILITATION OF PATIENTS WITH
TBI
Rehabilitation services should be matched
development program
supported living programs and
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