Acquired Brain Injury (Exam 2) Flashcards

1
Q

What is a Traumatic Brain Injury?

A

Bump, blow or jolt to the head that disrupts normal function of the brain

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2
Q

Who is at greatest risk of TBI?

A
  • Older adults (>75)
  • Infants
  • Older adolescents/young adults (15-34)
  • Males 2x as likely>females
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3
Q

In a moderate to severe TBI what is brain damage a result of?

A
  • External forces (primary injury)
  • Rapid acceleration/deceleration forces (primary injuries)
  • Blast waves from an explosion (Blast injury)
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4
Q

What is a closed head injury (CHI)?

A
  • Non penetrating head injuries
  • Accelerating or decelerating blow
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5
Q

What damage can be done as a result of a CHI?

A
  • Minor to severe & irreversible brain damage
  • May see brainstem damage, contusions, diffuse white matter lesions, injury to blood vessels, damage to cranial nerves or CSF rhinorrhea
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6
Q

What is an open head injury and what causes it?

A
  • Meninges have been breached
  • Caused by:
  • Penetrating head injuries
  • May be caused by accelerating or decelerating force
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7
Q

What damage can be done as result of OHI?

A

Amount of functional damage depend on areas affected

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8
Q

What classifies a TBI as a primary injury?

A

Direct trauma to paraenchyma

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9
Q

What are the 2 ways a primary injury (TBI) can occur?

A
  • Brain tissue come in contact with an object (skull, bullet, sharp object) can be OHI or CHI
    OR
  • Rapid Acceleration/ Deceleration of the brain causing cortical disruption (diffusion axonal injury, tissue tearing, intracerebral hemorrhages)
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10
Q

Primary injuries are generally a (BLANK) injury and where do these injuries occur?

A
  • Focal Injury
    Occurring:
  • Anterior temporal poles
  • Frontal poles
  • Lateral & inferior temporal cortices
  • Orbital frontal cortices
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11
Q

What is a coup-contrecoup injury and what TBI classification does it fall under?

A
  • Brain bouncing causes diffusion axonal injury (DAI)
  • Falls under primary injury
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12
Q

What is a diffuse axonal injury (primary injury)?

A

Microscopic injury of the white matter axons related to shear/stretch/ tensile strain
- Axons twist & tear at the gray & white matter junctions

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13
Q

Where do diffuse axonal injury typically occur?

A
  • Parasagittal white matter of cerebral cortex
  • Corpus callosum
  • Brainstem (pontine mesencephalic junction)
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14
Q

T/F: Diffuse Axonal Injury is the predominant MOI in moderate to severe brain injury

A

True

  • Acute medical management is to prevent secondary injury
  • Intensive rehab warranted
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15
Q

Describe the grade of Diffuse Axonal Injury:
Grade 1
Grade 2
Grade 3

A

Grade 1: Microscopic level evidence in cortex
Grade 2: Grade I & corpus callousum
Grade 3: Grade 2 & brainstem lesion

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16
Q

What are the 3 mechanism of primary blast injury?

A
  1. Direct transcranial blast wave propagation
  2. Transfer of kinetic energy from blast wave through the vasculature, triggering pressure oscillations in the blood vessels leading to the brain
  3. Elevations in CSF or venous pressure caused by compression of the thorax & abdomen & by propagation of the shock wave through the blood vessels or CSF
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17
Q

What can cause a secondary blast injury?

A

Shrapnel & other object being hurled at a person

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18
Q

What can cause a tertiary blast injury?

A

Victim flung backwards & strikes an object/ground

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19
Q

What can cause a quaternary blast injury?

A

Can be caused by exposure to resulting fire/fumes/toxins from explosion

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20
Q

What causes a secondary injury and what happens as a result?

A
  • Caused from the reaction to primary trauma
  • Occurs over hours to days
  • Secondary injuries cause metabolic cascade & secondary cell death
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21
Q

What is Metabolic Cascade? And what causes secondary cell death?

A

Metabolic Cascade: Excitotoxicity & free radical formation

Secondary cell death is caused by:
- Elevated ICP
- Herniation (Secondary to edema)
- Vascular changes (Hypoxia/ischemia and/or hemorrhage)
- Neurochemical changes
- Infections

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22
Q

What is ICP?

A
  • Intracranial Pressure
  • Pressure within the skull & on the brain comprised of a fixed volume of neural tissue, blood & CSF
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23
Q

What is the normal value of ICP?

A

5-19 mmHG

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24
Q

What are some causes of increased ICP with TBI?

A
  • Hematoma (epidural, subdural or intracerebral)
  • Swelling (inflammatory response)
  • Increased blood volume due to vascular damage (creates mass effect or midline shift)
  • Blockage of typical drainage of venous outflow
  • Impaired reabsorption of CSF
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25
Q

What can cause a herniation?

A
  • Increased ICP or edema can cause herniation
  • Brain shifts across structures within the skull (Cerebral herniation)
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26
Q

What is the location and effect of subfalcine/Cingulate herniation?

A
  • Location: Frontal/parietal brain extends under falx cerebri
  • Effects: Compress anterior Cerebral A with hemiparesis LE > UE
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27
Q

What is the location & effect of Uncal herniation?

A

Location: CNIII, Cerebral peduncle, Reticular activating system (RAS), PCA

Effects: CNIII paralysis & pupillary dilation, contra-hemiparesis, coma, homonymous & hemianopia

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28
Q

What is the location & effect of central transtentorial herniation?

A

Location: Midbrain & pons, RAS

Effects: Decerebrate rigidity, Coma

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29
Q

What is the location & effect of Tonsillar herniation?

A

Location: Cerebellar tonsils, Indirect activation pathways, RAS, Vasomotor centers

Effects: Neck pain & stiffness, cerebellar sxm, flaccidity, coma, Alt HR, RR, BP

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30
Q

Where do cerebral contusions most frequently occur at?

A
  • The poles
  • Inferior frontal & temporal lobes
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31
Q

What are the 4 main types of hematoma and where do they occur?

A
  • Epidural: between skull & dura
  • Subdural: Under dura
  • Subarachnoid: Between brain & meninges
  • Intracerebral
32
Q

What can hypoxia/hypotension be related to?

A
  • Impaired cardio/respiratory function associated with the injury (Low blood pressure)
  • Not adequate perfusion to the brain
33
Q

What area are most affect by hypoxia/hypotension?

A

Watershed areas

34
Q

What areas of the brain are most affected by anoxia?

A
  • Hippocampus
  • Basal Ganglia
  • Cerebellum
35
Q

Neurochemical changes occur as a result of an inflammatory result what are 3 way this occurs?

A
  1. Increased release of excitatory neurotransmitters, glutatmate (Exacerbates ion channel leakage increasing swelling & ICP)
  2. Membrane depolarization (non selective opening of calcium channels leading to abnormal accumulation of calcium & other ions within the cell causing cell death
  3. Release of free radicals & cytokines
36
Q

What are some brain infections?

A
  • Encephalitis (sub-dural/epidural)
  • Meningitis (membranes surrounding the brain)
  • Abscess (within the brain)
37
Q

What can cause a fever?

A
  • Damage to the brain that regulates temperature
    OR
  • Infection
38
Q

What is brain death?

A
  • Irreversible cessation of all functions of the entire brain, including brainstem
  • Person is in permanent coma, brainstem reflexes have stopped working, breathing has permanently stopped
  • Electrocerebral silence (EEG w/ absence of electrical potential of cerebral organs over 2 microvolts)
39
Q

What are the tests carried out to determine if someone is brain dead?

A

-Pupillary response
- Corneal reflex
- Snout reflex (pressure applied to forehead & nose is pinched to see if any movement)
- Cough reflex (thin plastic tube is placed down windpipe)
- Apnea (disconnected from ventilator)

40
Q

Mild TBI:
LOC?
Alteration of consciousness?
Post Traumatic Amnesia?
GCS?
Neuroimaging ?

A

LOC: 0-30 min
Alteration of consciousness: Brief, <24 hr
Post Traumatic Amnesia: 0-1 day
GCS: 13-15
Neuroimaging: normal

41
Q

Moderate TBI:
LOC?
Alteration of consciousness?
Post Traumatic Amnesia?
GCS?
Neuroimaging ?

A

LOC: >30 min but <24 hr
Alteration of consciousness: >24 hr
Post Traumatic Amnesia: >1 & <7 days
GCS: 9-12
Neuroimaging: Normal or Abnormal

42
Q

Severe TBI:
LOC?
Alteration of consciousness?
Post Traumatic Amnesia?
GCS?
Neuroimaging ?

A

LOC: >24 hr
Alteration of consciousness: >24 hour
Post Traumatic Amnesia: >7 days
GCS: <9
Neuroimaging: Normal or Abnormal

43
Q

What is involved in emergency evaluation of acute medical management of TBI?

A
  • Priority: Airway, Breathing, Circulation (stabilize CV & respiratory systems for brain perfusions)
  • Manage other high priority injuries
  • Glasgow Coma Scale at scene
44
Q

What is the Glasgow Coma Scale?

A

Widely accepted scale to document level of consciousness

45
Q

What 3 areas are patients graded on using the Glasgow Coma Scale?

A

Eye opening: 1-4
Best Motor Response: 1-6
Best verbal response: 1-5

46
Q

Using the GCS what score indicates:
Mild
Moderate
Severe

A

Mild: 13-15
Moderate: 9-12
Severe: 8 or less

47
Q

What are some acute care goals of TBI management?

A
  • Determine severity (neuroimaging)
  • Minimize secondary brain damage
  • Control for:
    Elevated ICP, Edema, Cerebral blood flow & O2, hypotension, bleeding
48
Q

When is ICP monitoring recommended?

A
  • GCS = 8 or less
  • Abnormality on CT
  • SBP <90mmHg
  • Age > 40 y/o
  • Motor posturing
49
Q

How is ICP measured?

A
  • Extra ventricular drain
  • Subdural bolt
  • Fiber optic catheter
50
Q

Name some ways to manage ICP

A
  • sedating meds
  • head position
  • osmotherapy
  • hypothermia
  • barbituates
  • induce pharmacological coma
  • surgical decompression
51
Q

What is normal cerebral perfusion pressure (CPP)?

A

Normal = 60-80 mmHg

52
Q

How do you calculate CPP?

A

MAP-ICP

53
Q

What are the goals of neurosurgery and the common ones?

A

Goals:
- Relieve pressure
- Evacuate blood
- Debridement

Surgeries:
- Craniotomy (burr holes)
- Cranioectomy

54
Q

What is a craniotomy?

A
  • Bone flap is removed
  • (replaced after repair)
55
Q

What is craniectomy?

A

Removal of part of the skull to relieve pressure

56
Q

What is a cranioplasty?

A

Skull back on

57
Q

What is the appropriate first aid when someone has a seizure?

A
  • Ease person to floor
  • Turn person gently to side
  • Clear area
  • Put something soft & flat under the head
  • Remove glasses
  • Loosen ties or anything around the neck
  • Time the seizures
58
Q

When should you call 911 if someone has a seizure?

A
  • Never had one before
  • Difficulty breathing or waking after
  • Last longer than 5 min
  • Has another one soon after 1st
  • They are hurt
  • Other health condition
  • Happens in water
59
Q

What is paroxysmal sympathetic hyperactivity or sympathetic storming and what does this result in?

A
  • Sympathetic nervous system activity can become overactive after TBI

Results in:
- increase HR, RR, BP
- Diaphoresis
- Hyperthermia
- Posturing/hypertonia
- Teeth grinding

60
Q

What is the PT management is a patient has sympathetic storming?

A
  • Monitor patient
  • Call MD & RN
  • Terminate therapy for the day
61
Q

What is the focus on in pharmacology in acute care?

A
  • Focused on minimizing secondary injury
62
Q

with the use of pharmacology how can reducing the rate of secondary injury be achieved?

A

Mannitol: diuretic used to reduce ICP
System management: HR, BP, RR

63
Q

What is the management of Fx?

A
  • Stabilization
  • Immobilization
  • Weight bearing precautions
64
Q

What is the contracture prevention/management?

A
  • Orthosis
  • Serial casting
65
Q

What are some caused of pediatric TBI?

A
  • Falls
  • Shaken baby syndrome
  • Drowning
66
Q

What scale is used for pediatric TBI?

A

Pediatric Glasgow Coma Scale (modified for children under 2)

67
Q

Where is injury most like to occur in a pediatric TBI?

A

Temporal & orbitofrontal lobes

68
Q

Why are infants less likely to have skull fx?

A

B/c pliancy of the skull

69
Q

Describe the Rancho Los Amigos Levels of Cognitive Functioning (LOCF)

A
  • Descriptive scale that classifies levels of cognitive & behavior recovery
  • 8 categories/kevels
  • Helps track change over time
  • Develops & guides interventions
  • Provides method of communication between professional
70
Q

Describe Level 1: No response of LOCF

A
  • Pt not responsive to any stimuli
  • Appears in a deep sleep
  • No sleep wake cycle
  • Reflexive motor movement only
71
Q

Describe Level 2: Generalized response of LOCF

A
  • Inconsistent & non purposeful responses
  • Limited Amt of repsonse
  • Response is not specific to stimuli
72
Q

Describe Level 3: Localized response of LOCF

A
  • Response continues to be inconsistent
  • Response is directly related to the type of stimulus presented
  • May follow one step commands
  • Visual tracking
73
Q

Describe Level 4: Confused and agitated of LOCF

A
  • Heightened state of activity
  • Behavior is not purposeful & bizarre relevant to environment
  • Pt is driven by confusion
  • Attention is brief
  • Memory is impaired
  • Pt may be aggressive
  • Unable to cooperate directly w/ treatment efforts
  • Unable to learn new info
74
Q

Describe Level 5: Confused and inappropriate of LOCF

A
  • Pt is now able to follow simple commands consistently
  • In a more complex environment/task the response are more random
  • W/ structured environment may be able to socialize on an automatic level for short period
  • Extremely distractible
  • Verbalizations (inappropriate, confabulatory)
  • Memory severely impaired
  • Unable to learn new info
  • Poor safety awareness
75
Q

Describe Level 6 of LOCF (Confused - appropriate)

A
  • Goal directed behavior w/ external input
  • Recognizes basic needs & perform automatic task
  • Shows carryover of re-learned tasks
  • Follows simple command consistently
  • able to follow a schedule
  • Memory probs (long term is better than short term)
76
Q

Describe Level 7 of LOCF (Automatic - Appropriate )

A
  • Patient is now oriented in environment
  • Follows daily schedule & routine in a robot-like way
  • Unable to recall all details of daily events
  • New learning possible w/ extra time
  • Ongoing safety concerns & impaired judgment
77
Q

Describe Level 8 of LOCF (Purposeful - appropriate)

A
  • Able to recall & integrate past and recent events
  • Aware of & responsive to environment
  • Independent in the home
  • Developing community reentry skills
  • Shows carryover w/ new skills & no supervision required once skill is learned