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2) Patho 2 > 13) TBI > Flashcards

13) TBI Flashcards

1
Q

TBI

A

Caused by a bump, blow, or jolt to the head or penetrating head injury that disrupts normal fxn of the brain

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2
Q

Who is more at risk for TBI?

A

Males

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3
Q

Risk factors for hospitalization/death post-TBI

A
  • Male
  • Age
  • Previous TBI
  • Drugs & alcohol use
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4
Q

Primary Injury

A

Occurs at the moment of impact

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5
Q

Focal Injury

A

Occurs at moment of impact

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6
Q

Diffuse Injury

A

Widespread brain tissue damage

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7
Q

2° Injury

A

Triggered by primary injury, causing even more brain damage

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8
Q

What does 2° injury cause?

A
  • Inflammation
  • Cell receptor-mediated dysfxn
  • Free-radical & oxidative damage
  • Ca2+/Ion-mediated Damage
  • Cerebral Edema
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9
Q

Contusion

A

Bruising

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10
Q

Coup Injury

A

At site of impact

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11
Q

Contre Coup Injury

A

Injury to the opposite side

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12
Q

Diffuse Axonal Injury

A

Shearing, tensile stress, & widespread injury

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13
Q

Open Head Injury

A

Skull Fx

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14
Q

Epidural Bleeding

A

Bleeding btwn the skull & dura; Caused by a blow to the head

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15
Q

What can epidural bleeding cause?

A

High ICP & brain shift

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16
Q

Why do epidural bleeds progress so quickly?

A

Bc the bleeding is usually arterial

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17
Q

What is the 1st sx of epidural bleed?

A

Fixed/dilated pupil on ipsilateral side bc of CN3 compression

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18
Q

What region of the brain is the most common place for epidural bleeds to occur & why?

A

Temporal region bc the temporal bones are the most commonly fx’ed

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19
Q

Tx for Epidural Bleed

A

Evacuation via burr hole or craniotomy

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20
Q

What gives a more favorable prognosis for epidural bleed?

A

If pt was conscious immediately after injury

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21
Q

Subdural Bleeding

A

Venous bleeding btwn the dura & brain

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22
Q

What determines the severity of a subdural bleed?

A

Speed of Onset

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23
Q

True or False: Sx’s of subdural bleed can appear immediately or be delayed.

A

True

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24
Q

Who are subdural bleeds most common in?

A

Very young & elderly

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25
Q

Tx for Subdural Bleed

A

Craniotomy w/dural incision

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26
Q

Subarachnoid Bleeding

A

Bleeding into the subarachnoid space bc of a ruptured blood vessel or severe blow to the head

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27
Q

Sx’s of Subarachnoid Bleed

A
  • Severe HA
  • Vomiting
  • Confusion
  • Altered Consciousness
  • Sometimes seizures
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28
Q

What are the most common complications of subarachnoid hemorrhage?

A

Hydrocephalus, Seizure, & Re

29
Q

Intraparenchymal Hemorrhage

A

Bleeding into the brain tissue

30
Q

What is the most common cause of intraparencyhmal hemorrhage?

A

Non-traumatic mechanisms

31
Q

What can intraparenchymal hemorrhages cause?

A

HIgh ICP & fatal herniations

32
Q

Intraventricular Hemorrhage

A

Bleeding into the ventricles

33
Q

What is intraventricular hemorrhage associated w/?

A

SAH & IPH

34
Q

Subfalcine Herniation

A

Compression of pericallosal arteries, which causes HA & contralateral leg weakness

35
Q

Transtentorial Hernia

A

Compression of PCA & CN3 causing:

  • CN3 paresis
  • Ipsilateral dilated pupil
  • Abn EOM’s
  • Contralateral hemiparesis
36
Q

Tonsilar Hernia

A

Compresses pons & medulla & causes obtundation

37
Q

What are the 2° mechinisms of injury associated w/TBI?

A
  • Acidosis
  • Cerebral edema
  • Hypoxia
  • Hypotension
  • Hypercapnia
  • Incr ICP
  • Ischemia
38
Q

Level 1 LOC

A

Coma; No eye opening, no sleep/wake cycle, & no response to stimuli

39
Q

Level 2 LOC

A

Vegetative State; Have sleep/wake cycle, but no purposeful responses

  • Means brainstem fxn is intact but cortical fxn is severly impaired
  • Pt has general response to noxious stimuli
  • Complex reflexes may be present
40
Q

Level 3 LOC

A

Minimally conscious state; Inconsistent purposeful responses (Level 3)

41
Q

Minimally conscious state (Level 3 LOC)

A

Inconsistent, but clearly discernible behavioral evidence of consciousness

  • Pt will have localized response to stimuli
  • Pt can inconsistantly follow 1 or 2-step motor commands
42
Q

When is pt said to have “emerged” from a minimally conscious state?

A
  • When they can use 2 different objects on 2 consecutive days
  • Ability to answer 6/6 visual or auditory situational questions
43
Q

Favorable Prognostic Indicators

A
  • Initial GCS >5
  • Pupillary response
  • Younger age
  • Limited trauma
  • Short duration of PTA
  • Low injury severity
  • Higher intelligence
  • Higher education level
44
Q

Unfavorable Prognostic Indicators

A
  • Midline shift
  • Repeat injury
  • Anoxia
  • Mass lesion
  • High ICP
  • Hypotension
  • Premorbid distability
  • Poor work hx
  • Hx of violence, drug, or alcohol use
45
Q

What outcome measures are used to asses TBI outcomes?

A
  • Brain Injury Awareness Questionnaire
  • Coma/Near Coma Scale
  • Community Integration Questionnaire
  • Disability Rating Scale
  • JFK Coma Recovery Scale
  • Fxnl Independence Measure
  • GCS
46
Q

Acute care TBI management

A
  • Early mobes in ICU
  • PROM/Contracture management
  • Positioning for skin integrity
  • Behavior management
  • Ongoing monitoring for 2° complications
47
Q

2° complications of TBI

A
  • Agitation
  • Physiological shifts
48
Q

What causes TBI-related agitation?

A

Damage to the frontal & temporal lobes

49
Q

What kinds of meds are given to TBI pt’s?

A
  • Anti-epileptics
  • Dopamine agonists
  • Anti-depressants
  • Anti-psychotics
  • Beta-blockers
50
Q

Spasticity

A

Motor disorder characterized by a velocity-dependent incr in tonic stretch reflexes w/exaggerated DTR bc of UMN involvement, loss of descending inhibitory control from the reticulospinal tract, & overactive vestibulospinal tracts

51
Q

Management for spasticity

A
  • WB
  • Stretching
  • Serial casting
  • Splinting
  • Botox
  • Oral meds
  • Baclofen
52
Q

Sx’s of Seizures

A
  • Uncontrolled movements
  • Unresponsiveness/Staring
  • Chewing movements
  • Hallucinations
  • Sudden fatigue or dizziness
  • Language changes
  • High fever
  • Loss of sleep/extreme fatigue
53
Q

Side effects of anti-epileptic drugs

A
  • Sleepiness
  • Balance deficits
  • Lightheadedness
  • Dizziiness
  • Trembling
  • Double vision
  • Confusion
54
Q

What causes post-traumatic hydrocephalus?

A
  • Overproduction of CSF
  • CSF blockage
  • Insufficient CSF absorption
55
Q

True or False: Pt’s w/hydrocephalus can have either normal or high ICP.

A

True

56
Q

Is a non-communicating hyrocephalus classified as communicating or non-communicating?

A

Non-communicating

57
Q

Actue Post-Traumatic Hydrocephalus

A

Coma & focal neurological deficits

58
Q

How will a pt w/chronic Post-Traumatic Hydrocephalus present?

A

Gradual decline in fxnl status or failure to improve

59
Q

Who usually picks up on chronic post-traumatic hydrocephalus?

A

PT’s

60
Q

What are the 3 cardinal signs of post-traumatic hydrocephalus?

A

1) Progressive gait disorder
2) Impaired cognition
3) Urinary incontinence

61
Q

Sx’s of non-communicating hydrocephalus

A

Papilledema & cognitive changes

62
Q

Management of hydrocephalus

A

Shunt placement & rehab

63
Q

Concussion

A

Traumatically induced physiological disruption of brain fxn manifested by LOC, loss of memory for events right before/after the accident, altered mental state, or focal neurological deficits

64
Q

How does concussion present?

A

Constellation of varied physical, cognitive, emotional, & sleep-related sx’s

65
Q

Tx for Concussion

A
  • Rest
  • Rehab
    • Cervical strengthening
    • HA management
    • Balance
    • Vestibular Therapy
    • Vision therapy
  • Psychotherapy
  • Sx-based meds
66
Q

Why has there been an incr incidence of concussion?

A

Bc of incr youth sports participation

67
Q

Consequences of concussion

A
  • Predispostion for more concussions
  • Cognitive slowing
  • Early-onset alzheimers
  • 2nd Impact Syndrpme
  • Chronic Traumatic Encephalopathy
68
Q

How long does it take for most concussions to resolve?

A

1wk

69
Q

Do pt’s w/post-concussion syndrome return to baseline fxn?

A

No

2) Patho 2 (20 decks)

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