Transcript THE ROLE OF THE PHYSIATRIST IN TRAUMATIC BRAIN INJURY

Traumatic Brain Injury
Dayna Ryan, PT, DPT
Winter 2012
TRAUMATIC BRAIN INJURY
• Lesion: Brain
• ~ 5 million
persons living
with TBI
• ~$60 billion in
the United
States in 2000
TBI INCIDENCE
(March 2010 CDC data)
• ~ 1. 7 million TBI occur in the US annually
• TBI rates among individuals younger than 65 y. o.
– Male : Females = 1.4 : 1
~ 80% of TBI
treated & released
TBI INCIDENCE BY AGE
(March 2010 CDC data)
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Highest incidence among ages
 0-4 (children), 15-19 (teens), 65+ (elderly)
~ 90% ER visits by children aged 0-14 y. o.
Highest rates of TBI-related hospitalizations & deaths
occur in adults aged > 75 y. o.
CAUSE OF TBI
(March 2010 CDC data)
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Falls are #1 cause of TBI among all age groups
Highest rates of fall-related TBI in children 0-4 y.o.
& adults > 75 y.o.
Highest rates of motor vehicle & assault-related TBI
among adults aged 20-24 y.o.
Alcohol involved in >50% of cases
RISK FACTORS
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Young (average age of TBI = 29 y. o.)
Male
Risk taking behaviors (age 15-24 y. o.)
Low income inner city dwellers
Substance abuse (50% hospitalizations by TBI due
to alcohol intoxication)
Availability of firearm
Previous TBI (e.g. sports-related concussions)
Old age (more susceptible to tearing of blood
vessels, declines in cerebrovascular circulation,
slower reaction time, movements & gait)
CLASSIFICATION OF TBI (BY
MECHANISM)
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Open
 meninges have been breached, brain is exposed
Closed
 no skull fracture or laceration of the brain
 coup-contrecoup
Primary injury at impact
2nd injury at the opposite side
Blast
 Blast wave from explosion hits the body
 Air-filled organ or brain surrounded by fluid are
particularly at risks of blast injuries
Coup-Countercoup Injury
CLASSIFICATION OF TBI
- BY TYPES OF INJURIES
• Primary vs. Secondary (Biomolecular
response to injury)
– Primary = direct injury to the brain
– Secondary = damage after the traumatic
event, caused by brain hypotension, hypoxia,
or herniation
• Focal vs. Diffuse or a Combination of the Two
– Focal = localized trauma (gun shot)
– Diffuse = trauma over a large area (swelling)
CLINICAL CLASSIFICATION OF TBI
- BY SEVERITY OF DAMAGE
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Mild (i.e. concussion): ~ 75% of TBI *
Moderate
Severe
Classification Criteria & Prognosis
Types
Mild
(Concussion)
Moderate
Severe
Loss of
Glasgow
Memory
Consciousness Coma
Loss
(LOC)
Scale
< 30 min
> 30 min
< 24 hr
> 24 hr
13-15
8-12
<8
< 24 hr
Prognosis
 Good
 Most recover
completely
> 24 hr
< 7 days
 Good
 Learn to manage
problems resulting
from TBI
> 7 days
 Most impossible to
recover completely
 Physical and/or
cognitive disability
(* Centers for Disease Control and
Prevention (CDC), National Center
for Injury Prevention and Control.
Report to Congress on mild
traumatic brain injury in the United
States: steps to prevent a serious
public health problem. Atlanta (GA):
Centers for Disease Control and
Prevention; 2003. )
SPECIFIC INJURIES
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Concussion (= mild TBI)
Diffuse axonal injury
Contusion
Skull fracture
Intracerebral hematoma
Subdural hematoma
Epidural hematoma
Subarachnoid hemorrhage
Patient: MILD T.B.I.
(Concussion)
COMMON SYMPTOMS
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headache
dizziness
irritability
decreased memory
&concentration
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depression/anxiety
fatigue
sleep disturbance
pain
THESE SYMPTOMS ARE ALSO COMMON
IN THE GENERAL POPULATION AND AMONG
CHRONIC PAIN PATIENTS
CONCUSSION (MILD TBI)
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Most common head injury
Alteration of consciousness & memory
Non-penetrating (non-opened) injury
CT or MRI usually normal
Good prognosis
Cumulative effects of repeated concussion
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can cause chronic dementia
50-100% mortality rate in second impact
syndrome seen in athletes
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a 2nd TBI while the 1st is NOT yet resolved
Post-Concussion Syndrome
Characterized by: dizziness, disorientation,
nausea, headache, fatigue
 Also see decreased control of emotions and
personality changes
 Attention deficit usually present
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**If concussion lasts >2 minutes, patient should
be kept under observation
DIFFUSE AXON INJURY (DAI)
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Severe and fatal head injuries
Widespread axonal damage
As a result of shear and tensile forces within
the brain
Coma and decerebrate posturing
Poor prognosis
CT or MRI usually unremarkable
CONTUSION
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Coup-countercoup injuries
Can involve a small (mild) or large (severe)
area
Most common in the frontal & temporal lobes
Lesion often enlarge during the first week
after injuries
HEMORRHAGE
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Intracerebral hematoma
Subdural hematoma
Subarachnoid hemorrhage
Epidural hematoma
• Intracerebral hematoma
– In brain parenchyma
– hematoma may enlarge during
the first few days after injury
• Subdural hematoma
– Beneath the dura
– Acute or chronic (>2 wk)
– Laceration of bridging
cortical veins during sudden
head deceleration
– A feature of shaken
baby syndrome
• Subarachnoid hemorrhage
– Poor prognosis if bleeding
into ventricular system
– Need to r/o aneurysm
• Epidural hematoma
– In epidural space
– Between dura mater & skull
– Acute bleeding
– Common in temporal bone fracture
Severe TBI
Assess severity of brain injury
 Acute surgical care: expanding mass lesion
from increasing ICP
 Address life-threatening injuries (ABC – airway,
breathing, circulation)
 Prevent complications
 Preventative Rehab interventions
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GENERAL SYMPTOMS & SIGNS
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Altered Level of Consciousness
Cognitive & Behavioral Deficits
Cranial Nerve Damages
Motor Deficits
Sensory Deficits
Altered Level of Consciousness
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Reduction in response to stimuli
Due to diffuse bilateral cerebral hemispheric
damage or a lesion in the brainstem
Arousal is associated with wakefulness and
depends on an intact reticular formation and upper
brainstem
Coma rarely last > 4 wks
Coma is used to determine current status and
prognosis
Altered Level of Consciousness
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Coma: state of unresponsiveness; not opening eyes
Persistent vegetative state or stupor: no evident
cerebral cortical function; eye opening with sleepwake cycles
Obtundity: decreased interest in the environment;
slowed responses to stimulation; sleep more than
normal; drowsiness between sleep states
Lethargy: severe drowsiness; aroused by moderate
stimuli & then drift back to sleep
Confusion: disorientation, bewilderment, and
difficulty following commands
Clouding: inattention & reduced wakefulness
COGNITIVE IMPAIRMENT
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Difficulties in:
 Attention, concentration
 Learning, memory
 Abstract thinking, information processing
 Problem solving
 Initiation, executive functions
 Inaccurate perception (leaning)
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Deficits often remain despite a full return of consciousness
MEMORY DEFICITS IN TBI
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Retrograde amnesia
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Loss of memory of events immediately preceding the injury
Post-traumatic amnesia (PTA) (impaired
anterograde memory) (50 first dates)
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Unable to recall events that occur after the injury
Inability to form new memory
No carryover or tasks requiring memory / learning
Duration of PTA indicates the severity of injury
BEHAVIORAL IMPAIRMENT
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Mood disturbances including depression and
anxiety
Symptoms depending on brain area involved
 Inappropriate, excessive social behaviors
 Inappropriate sexual behaviors
 Irritability; rage; refuse to cooperate
 Euphoria; involuntary laughing or crying
 Apathy; indifference
 Motor, sensory, verbal perserveration
CRANIAL NERVE DAMAGE
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Usually occur following focal damage in the
brainstem or herniation
Disturbances in CN function
 e.g. gaze and tracking deficits, diplopia, ptosis,
facial sensory deficits, absent corneal reflex,
hearing & vestibular dysfunction, cardiac
irregularities, dysphagia, loss of gag reflex
CN dysfunction reflects level of lesion
 Normal pupillary reflex (to light) indicates a
lesion rostral to the midbrain
MOTOR DEFICITS
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Usually flaccid at onset
Increased tone, spasticity and rigidity develop
gradually
Decortical posturing
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Hyperactive UE flexors
Hyperactive LE extensors
Decerebrate posturing
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Hyperactive UE & LE extensors
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A. Decerebrate posturing
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seen in cerebral hemisphere/white matter, internal
capsule and thalamic lesions
B. Decortical posturing
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seen with midbrain lesions/compression; also with
cerebellar and posteria fossa lesions
MOTOR DEFICITS
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Monoplegia, hemiplegia
Abnormal reflexes (e.g. palmar grasp & Babinski
reflex)
Abnormal balance reactions
Cerebellar and BG dysfunction: e.g. ataxia,
dysmetria, tremor, bradykinesia
SENSORY DEFICITS
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Somatosensory dysfunction is determined by the
brain area involved
COMPLICATIONS
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Increased intracranial pressure (ICP)
Heterotoptic ossification:
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osteoclast destroy bone, so increase od Ca in blood, form
boney spurs at joint.
DVT
Spasticity / Contracture
Decubitus ulcer (tuberosity)
Seizure
INCREASED INTRACRANIAL PRESSURE
(ICP)
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Secondary complications develop over hours or days
after the primary injury
Cause: swelling, fluid build-up in the brain &
hematomas
Increased ICP compresses the brain within the rigid
skull
Serious, life-threatening
ICP monitoring:
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Medications
Fluid management
Decompressive craniectomy
Lynda Yang
http://www-personal.umich.edu/~chronis/ICP.html
Cycle of Primary and Secondary Injury
Cerebral Perfusion Pressure =
Mean Arterial Pressure - Intracranial Pressure
HETEROTOPIC OSSIFICATION
• Abnormal bone growth around a joint
• Most commonly in hips, elbows, shoulders
and knees
• Onset 4-12 wk after injury
• Diagnostic test
– X-ray
– Bone scan with increased uptake
– Elevation of alkaline phospatase
• Symptoms and signs
– loss of ROM, tenderness, palpable mass,
redness, swelling, pain with movement
DIAGNOSIS OF TBI
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History
Clinical exam
Imaging
Functional capacity
HISTORY
• Magnitude of injury
• Altered consciousness and memory
– witnessed
– self-report
• Duration of coma correlates with severity of
injury
CLINICAL EXAM
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Evidence of trauma
Glasgow Coma Scale
Ranchos Los Amigos Cognitive Scale
Post-traumatic amnesia
GLASGOW COMA SCALE
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EYE OPENINGSCORE
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spontaneous
to speech
to pain
none
E4
E3
E2
E1
GLASGOW COMA SCALE
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VERBAL RESPONSE
SCORE
appropriate
confused, disoriented
inappropriate words
unintelligible
none
V5
V4
V3
V2
V1
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GLASGOW COMA SCALE
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MOTOR RESPONSE
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Follows commands
Localized (to pain)
Generalized (to pain)
Decorticate posturing (flexion)
Decerebrate posturing (extension)
None
SCORE
M6
M5
M4
M3
M2
M1
GLASGOW COMA SCALE
 Most
accurate early in course
>12 = Mild
 9-12 = Moderate
 <8 for longer than 6 hours = severe
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3 = Dead
RANCHO LOS AMIGOS
COGNITIVE SCALE
I. no response
V.
II. generalized
response
VI. confused, appropriate
III. localized
response
IV. confused, agitated
confused, inappropriate
VII. automatic, appropriate
VIII. purposeful, appropriate
Diagnostic Imaging
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CT
MRI
DTI
SPECT
PET
Computed Tomography
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Anatomic
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1st line of imaging studies
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Bone & brain tissue
Can see damage to gray matter
Rapid (< 1 min for whole brain)
Less costly
Accessible (even with monitor, life-support equipment, or
combative patient)
Best for skull fx, hemorrhage vs. edema, &
intracerebral hemorrhage
Computed Tomography
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Abnormal findings in ~ 18% of patients without
neurologic deficits
Severity of findings correlates with outcome
Not sensitive enough in detecting mild TBI
(concussion)
May underestimate non-hemorrhagic lesion
May not show non-hemorrhagic parenchymal
(neurons and glial cell) injuries
M.R.I.
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Anatomic
Most sensitive 24-48 hours after injury
Higher resolution than CT
Better for hemorrhagic contusions (after first 24
hours)
More sensitive than CT to diffuse axon injury
Scans > 6 months post-injury correlate with outcome
Disadvantage compared to CT
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Duration of scan time, more costly
Not for combative patients
Diffusion Tensor Imaging
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Neuroimaging that builds on MRI technology
Study movement of fluid in the brain
Detect damage in the white matter (axons)
Axons are colored according to orientation
Single Photon Emission Computed
Tomography (S.P.E.C.T.)
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Injection of a small amount of short-lived
radioactive particles into the blood
Image of regional blood flow
More sensitive than MRI
Limited value in acute stage
Abnormal in many patients with normal
neurologic exam, CT, and MRI
Poor image resolution
Not readily available
Positron Emission Tomography
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Study metabolic activity and function
Used in mild TBI
NEUROPSYCHOLOGICAL TESTING
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Standardized measure to assess
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Memory
Concentration
Attention
Motor control
Processing / Decision making
Use testing findings to
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Plan and implement treatment
Monitor progress
Return to work
ACUTE TBI MEDICAL AND
SURGICAL MANAGEMENT
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Surgery (e.g. for hemorrhage; reduce ICP)
Monitor intracranial pressure (ICP)
Cerebral vasoconstrictive agents to decrease
cerebral blood volume
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Mannitol
Barbiturates
Etomidate
Proprofol
SUBACUTE AND CRHONIC TBI
MEDICAL AND SURGICAL
MANAGEMENT
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Spasticity medications
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Seizure control
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Bacolfen
Diazepam
Dantrolene
Depakote
Depression
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Non-tricyclic antidepressants
CONDITONS PREDICTING POOR
PROGNOSIS IN TBI
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Loss of pupillary light reflexes
Oculomotor deficits
Significant damage to brainstem
Midline shift of brain structures
Acute hemispheric swelling with extra-cerebral
hematoma
Multiple small hemorrhages
Skull is fractured
Subarachnoid hemorrhage
Diffuse axon injury
Rigidity persists
Epilepsy develops within first 7 days of injury
Long duration of post-traumatic amnesia
FUNCTIONAL CONSIDERATIONS
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If with NG tube is in place
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Head of bed > 30º to avoid aspiration
If chest tubes are in place
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Drainage tube should be kept below level of chest
at all times
PRECAUTIONS AND
CONTRAINDICATIONS
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In presence of increased intracranial pressure
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Pulmonary PT (percussion and vibration) may be
contraindicated
Hetertopic ossification developed 4-12 weeks
following TBI
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Palpable tenderness and mass by a joint from
abnormal bone growth
Can decrease ROM