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Clin Med Fall 2015 > Traumatic Brain Injury (TBI) Test 2 > Flashcards

Traumatic Brain Injury (TBI) Test 2 Flashcards

1
Q

Traumatic brain injuries can occur

A

prior to birth, during birth or anytime after

-also called transient brain ischemia

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2
Q

Incidence of TBI ( in US)

A
  • Every 5 min an individual dies from a head injury and another is permanently disabled
  • 2 million head injuries/year
    • 500,000 require hospitalization
    • 90,000 left with life long permanent disabilty
  • 3:1 male to female ( risktakers)
  • majority ages 15-24 y/o
  • in peds bimodal peaks:
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3
Q

Healthy people 2020 goal

A

decrease TBI due to accidents and violence
-car seats/seat belts
-legislation
The greatest cure is prevention

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4
Q

Prevalence of TBI

A
  • 5 million Americans are living with TBI related disablities
  • Mechanisms of injury
    • MVA-50%
    • Falls
    • Violence (firearms ~10% -leading cause of TBI related death , has been increasing)
  • Overall mortality due to TBI has decreased 20% since 1980 ( due to decline in MVA)
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5
Q

Risk Factors for TBI >65 y/o

A
  • female
  • poor vision
  • history of previous falls (increased risk in elderly due to falls)
  • dementia
  • polypharmacy (overlapping meds for the same thing ie Tylenol & Motrin, increase # of meds taken-> increase risk of falls)
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6
Q

Closed Head injury( CHI)

A
  • non penetrating head injury
  • accelerating or decelerating blow
  • minor-severe and irreversible brain damage
  • may see brainstem damage,contusions,diffuse white matter lesions, injury to blood vessels,damage to cranial nerves or CSF rhinorrhea
    ie. concussion, blow to the head
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7
Q

Edema due to a closed head injury

A
  • increased protein and NT in brain tissue (toxic) leads to 2ndary damage
  • increased intracranial pressure (max threshold~ impair/stop circulation)
  • mass effect; swelling -> shift in midline
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8
Q

Open Head Injury (OHI)

A

-meninges have been breached
-penetrating head injuries
-may be caused by accelerating or decelerating forces
-amount of damage due to areas affected
-increased likelihood of CNS infection
ie gunshot wound ( may leave lines of force in brain tissue on image), knife, golf club

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9
Q

Fractures associated with head injury

A

-skull fx - can just be depressed

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10
Q

Primary injury

A

occurs at time of impact

ie shear or tension on brain tissue, laceration, depression etc

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11
Q

Secondary injury

A

occurs after the impact secondary to the bodys response to injury
-due to cascade of cellular events (dumping of NT into interstitial space, dead neurons-> increased proteins-> increased fluid vol & swelling-> further damage

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12
Q

Primary damage

A

Local Brian Damage or Diffuse Brain injury

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13
Q

Local Brain damage

A

localized to area of brain under site if impact on skull

  • primary damage
  • likely MOI: direct contact
  • coup-contrecoup
  • polar brain damage( brain moves forward inside skull, suddenly stops due to impact with skull- ant& post type of coup contrecoup)
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14
Q

Coup contrecoup

A

Intial injury and force causes brain to shift in opposite direction or any direction and leads to damage in both areas
-Ant/Post region: polar brain damage

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15
Q

Diffuse brain damage

A 
diffuse axonal injury
-primary damage
-likely MOI: non-contact
-acceleration or deceleration or rotational forces (shear is placed on brain w/great force-> axonal injury)
ie MVA or amusmant ride
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16
Q

Secondary Injury

A
  • Hypoxic-ischemic injury(may be due to insult to specific vascular territory due to brain shift or diffuse injury caused by arterial hypoxemia
  • intracranial hematoma
  • mass effect (shift in brain caused by edema)
  • increased intracranial pressure (ICP) (rises above 40mgHg it can stop circulation to other areas of brain- heart can’t fight against it-> further damage)
  • hydrocephalus
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17
Q

Causes of secondary injury

A
  • neurochemical and cellular changes
  • hypotnesion->
  • hypoxia
  • increased ICP which leads to decreased CPP(cerebral perfusion pressure)
  • electrolyte imbalances
  • ischemia
18
Q

Dx of head injury

A

-xray and CT

19
Q

Intracranial hemorrhage

A
  • bleed in brain parenchyma

- due to accelerating/decelerating forces

20
Q

Pathogenesis of head injuries

A
  • Vasoparalysis: arrest in circulation w/ instaneous rise in ICP( > 40 mmHg)
  • shearing forces :due to blow to cranium causing rotation of the brain within the skull
  • contusions:lead to hemorrhage and an increase in ICP
  • lacerations cause direct damage to neural tissue (ie gunshot/knife)
21
Q

Shear injury

A
  • commonly seen in acute injuries due to the differences between white and gray matter
  • when you stop quickly these layers will separate
  • typically separate at corticomedullary junctions and they typically have blood in them
  • Poor prognosis
22
Q

Immediate complications of head injuries

A

Edema

  • Vasogenic edema: occurs in regions bordering those damage during ischemia. Increased permeability-> increased vol of extracellular fluid; most common edema
  • Cerebrospinal fluid: in steady state with extracellular fluid
  • Cytotoxic edmea: follows cerebral ischemia or hypoxia; caused by swelling of endothelial cells, neurons, and glia
23
Q

Diffuse Cerebral Edema leads to

A

other immediate problems:
-Herniation
-infection
(shear injury, swelling throughout brain)

24
Q

Dx imaging of head injury

A
  • X-rays ( gives idea of stability/ instability of structures- need for immobilization/fx)
  • CT scan( integrity of brain tissue)
  • MRI ( useful but not done in emergency room)
  • Cerebral bloodflow mapping( Pet or SPECT- look at brain function)
  • EEG ( mild-severe head injury - brain dead or vegetative state
25
Q

Glasgow Coma Scale (GCS)

A
  • nuerosurgical defintion of coma is ; no eye opening, no recognizable speech, no following of motor commands.
  • commonly used to assess level of consciousness of pts in the early stages or minimal response phase after suspected brain injury
  • gives info on motor/ sensory / cognitive function
26
Q

Eye opening on Glasgow Coma Scale (GCS)

A 
graded on 4 pt scale
1-none
2-to pain
3-to speech
4- spontaneous
27
Q

Motor response on Glasgow Coma Scale (GCS)

A 
movements graded on a 6 pt scale
1-none
2-extension
3-abnormal flexion
4-withdrawl
5-localizes pain
6- obeys commands
28
Q

Verbal response on Glasgow Coma Scale (GCS)

A 
talking graded on 5 pt scale
1-none
2-incomprehemsible sounds
3- inappropriate words
4-confused conversation
5-oreinted
29
Q

Glasgow Coma Scale (GCS)

A
  • scored on a scale of 3-15pts
  • equal to the total of the three categories of response; eye opening, motor (movement), and verbal response
  • max score is 15 and min score is 3
    • scores from 13-15 represent mild injury
    • scores from 9-12 represent moderate brain injury
    • scores of 8 or less represent severe brain injury
  • can tract over time to see improvements or deterioration
30
Q

Degrees of head injury

A
  • minor head injury (better prognosis, multiple casues)
  • moderate head injury
  • severe head injury ( may be brain dead or in consistent veg. state)
31
Q

Minor head injury

A

-uncomplicated course
-observation of patent at home by family
-minor signs and symptoms may progress to more serious pathology
-common complaints: “see stars”, stunned, nervous, poor memory of events just prior to or just following event
(microscopic damage- not visible on CT, likely doesn’t get imaging, ie fall or concussion in sports, may lose consciousness but not likely)

32
Q

Concussion

A

-violent jarring or shaking that results in a disturbance
of brain function
-momentary interruption of brain function w/ or w/out loss of consciousness
-considered a mild form of diffuse axonal injury
-microscopic changes in neurons and glia within hours of injury
(obsevre; behavior/cognitive/nausea/vomiting/ consciousness )
-dx based on subjective pr report( not objective tests)

33
Q

Return to play guidlines

A
  • depends on sport/league
  • Cantu
  • NATA ( national AT association)
  • how to manage results post
  • return to sports based on some objective test taken before and after concussion-impact test, reaction time
34
Q

Post Concussive Syndrome

A

-Persistence of mild symptoms such as headache, irritability, insomnia, poor concentration and memory (sensitivity to light/noise, drowsy/diff to stay awake,)-not prescribed to take pain meds for headches bc cant monitor symptoms and meds may impact blood flow
-can be persistent for weeks-months
-organic basis for post concussive syndrome is suspected
-some controversy due to psychological/subjective complaints
-may limit ability to complete ADLs or employment ( esp. if repeated concussion)
-may need cognitive retraining or pyschological support (esp. if repeated concussion)
( 2 concussions in 1 game -> accelerated injury/rate of damage -> serous problems)

35
Q

Moderate Head injury

A
  • acute epidural hemorrhage
  • acute subdural hemorrhage
  • chronic subdural hemorrhage
  • cerebral hemorrhage
  • subarchnoid hemorrhage
36
Q

Acute Epidual Hemorrhage

A
  • moderate head injury
  • no initial coma but deterioration in neuro status if left unresolved
  • resolved w/surgical intervention
37
Q

Acute Subdural Hemorrhage

A
  • results quickly in coma
  • arterial bleed
  • bleed arrested by increased ICP (pressure increases to a point that it stops bleeding from getting worse)
  • requires surgical intervention (craniotomy; may go into brain tissue-evacuate blood accumulation-risky surgery may create damage)
38
Q

Chronic Subdural Hematoma

A

-slow venous leak
-neuro deterioration over period of weeks
-CT scan-encapsulated mass often mistaken as tumor
-surgical intervention(evacuate bleed/seal vessel)
ie elderly person falls and mental status deteriorates

39
Q

Cerebral Hemorhage

A
  • disruption of intrinsic cerebral circulation (due to acceleration or deceleration or blow to brain)
  • managed similar to hypertensive stroke
  • surgery may be necessary
40
Q

Subarchnoid hemorrhage

A

-managed similar to epidural hemorrhage

41
Q

Severe Head injuries

A

-present with immediate LOC(loss of conciousness)
-complete paralysis of cerebral function (coma)
may see immediate cerebral lacerations, SAH (subarchnoid hemorrhage), subdural hemorrhage, coup-countrecoup sites, damage along the lines of the force of injury
-multiple system involvement
-permanent deficits will persist
ie MVA, ejected from vechile

42
Q

Severe Head injury-incompatible with life

A

-deep coma
-initially may be flaccid, become spastic or rigid with posturing (decerebrate or decorebate)
-unresponsive to pain and all stimuli( 3 on coma scale)
-ventilator required to maintain breathing
-deregulation of body temperature and BP
-poor EEG
(may result in death, brain dead(lack of electrical activity), or persistent vegetative state)
-autonomic / brainstem affected

Clin Med Fall 2015 (10 decks)

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