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IM 7 Test 3 > TBI and Spinal Cord Injuries > Flashcards

TBI and Spinal Cord Injuries Flashcards

1
Q

Monro-Kellie theory

A

when the volume of one component of ICP goes up, the others must go down

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2
Q

what is the easiest component of ICP to displace

A

CSF

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3
Q

second easiest thing to displace in ICP

A

blood volume

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4
Q

MAP formula

A

(SBP+2(DBP))/3

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5
Q

CPP

A

MAP-ICP

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6
Q

approximate cerebral blood flow

A

50 mL/min/100g

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7
Q

most common cause of cerebral edema

A

vasogenic

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8
Q

where does vasogenic cerebral edema mostly occur

A

mainly in white matter

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9
Q

s/s of vasogenic cerebral edema

A

range from HA to coma

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10
Q

what is cytotoxic edema

A

disruption of the integrity of the cell membranes

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11
Q

what does cytotoxic edema lead to

A

inappropriate ADH secreiton

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12
Q

what causes interstitial edema

A

usually a result of hydrocephaly

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13
Q

where do VS changes in cushing’s triad come from

A

changes in pressure at the thalamus, hypothalamus, ons and medulle

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14
Q

how to treat increased ICP X3

A

head midline and elevated 30 degrees

cluster care

low stimulation

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15
Q

care of ICP monitors X6

A

minimize infection risk

label tubing

keep dressing clean/dry

keep off floor

do not give meds

don’t allow d/c

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16
Q

drugs used in IICP X2

A

corticosteroids - dexamethasone

hypertonic saline

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17
Q

what is a head injury

A

any trauma to scalp, skull, brain

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18
Q

what is head trauma

A

includes an alteration in consciousness - no matter how brief

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19
Q

highest risk of head injury

A

males 15-24, then little kids, then old people

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20
Q

when is death likely in a head injury

A

immediately after the injury

within 2 hours after injury

3 weeks after injury

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21
Q

why does death occur immediately after a head injury

A

catastrophic injury

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22
Q

why does death occur 2 hours after head injury

A

bleeding out

swelling out of control

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23
Q

why doesdeath occur 3 weeks after a head injury

A

3 weeks after injury

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24
Q

what is the primary head injury

A

the actual damage

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25
Q

what is the secondary head injury

A

what occurs in the coming days

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26
Q

key characteristic in scalp lacs

A

bleed profusely but heal quickly

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27
Q

how do you know if a skull fracture is open

A

feel for mushy spots

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28
Q

s/s of basilar skull fractures

A

ear/nose bleeding

leaking straw colored CSF

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29
Q

CI in basilar fractures

A

no NG tube

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30
Q

CI in any injury with a CSF leak

A

do not do anything that would introduce bacteria

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31
Q

concussion s/s X2

A

brief disruption in the level of consciousness

retrograde amnesia

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32
Q

what happens with repeat concussions

A

may make future concussions worse

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33
Q

what is a diffuse axonal injury

A

widespread sheared axonal damage that occurs primarily in the white matter after any brain injury

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34
Q

axonal injury presentation

A

will arrive unconscious with a blank initial CT

repeat CT shows small bleeds in parenchyma

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35
Q

diffuse axonal injury interventions

A

head elevated

comfort

midline

clustur care

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36
Q

CI in diffuse axonal injury

A

no surgery

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37
Q

prognosis for diffuse axonal injury

A

if they don’t improve within 24 hours they probably wont

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38
Q

x3 focal injuries

A

brain lacerations

contusions

coup-contrecoup

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39
Q

DAI s/s X4

A

decreased LOC

IICP

decerebration or decortication

global cerebral edema

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40
Q

what is an epidural hematoma

A

bleeding between dura and inner surface of the skull

bleeding from middle meningeal artery

hemorrhage in epidural space

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41
Q

s/s of epidural hematoma X4

A

initial period of unconsciousness

brief lucid interval

decrease in LOC

HA, N/V

42
Q

epidural hematoma nickanme

A

walking dead - go straight to OR

43
Q

acute subdrual hematoma s/s

A

similar s/s to brain tissue compression in IICP

44
Q

when do acute SDH’s occur

A

within 24-48 hours

45
Q

what is a subacute SDH

A

the SDH may appear to enlarge overtime after the initial bleeding

46
Q

when do subacute SDH’s occur

A

within 2-14 days

47
Q

what kind of bleed is a acute SDH

A

arterial bleed

48
Q

what kind of bleed is a subacute SDH

A

venous bleed

49
Q

chronic SDH s/s X4

A

increased ICP

N/V

vomiting w/o nausea

decreased LOC

50
Q

peak incidence in chronic SDH

A

sixth and seventh decades of life

51
Q

who is most likely to have a chronic SDH

A

alcoholics d/t chronic falling

52
Q

are chronic SDH’s emergent

A

no - probably will not require OR

53
Q

what is a intracerebral hematoma

A

occurs from bleeding within the parenchyma usually between the frontal and temporal lobes

54
Q

what determines outcome in an intracerebral hematoma

A

size and location

55
Q

tx of intracerebral hematoma

A

cannot be removed - must wait to heal

tx s/s

56
Q

common causes of SAH X3

A

SA aneurysm, head trauma, HTN

57
Q

s/s of SAH X3

A

sudden severe HA often confused with migraine

photophobia

nuchal rigidity

58
Q

what happens 3-14 days after a SAH

A

clot lyses and gets reabsorbed

59
Q

how do you prevent vasospasm in SAH

A

use Nimodipine (Ca Channel blocker)

60
Q

where do CN I and II occur

A

above the medulla and are hard to assess in an unconscious patient

61
Q

how long does cell death continue after spinal cord injuries

A

weeks or months

62
Q

why does permanent injury occur in spinal cord injuries around 24 hours

A

edema

63
Q

what is spinal shock

A

temporary neurologic syndrome

concussion of the spinal cord that resolves as soft tissue swelling goes away

64
Q

how long does spinal shock last

A

hours to weeks

65
Q

spinal shock s/s

A

flaccid areflexia

warm and dry

66
Q

neurogenic shock

A

loss of vasomotor tone - true shock

67
Q

how does neurogenic shock resolve

A

usually on its own

68
Q

when should you assume it’s neurogenic shock

A

if they don’t respond to fluid - then give pressors

69
Q

causes of neurogenic shock X4

A

GB syndrome

spinal anesthesia

ANS toxins

Down’s Kids

70
Q

s/s of neurogenic shock

A

loss of sympathetic tone to heart and vascular system

deadly triad

71
Q

deadly triad in neurogenic shock

A

hypotension

bradycardia

peripheral vasal dilation

72
Q

what causes hyperflexion

A

sudden forward motion

73
Q

what does starring the windshield mean

A

hitting the windshield with forehead

74
Q

most mobile section of spine

A

C5-6

75
Q

hyperextension

A

head accelerates and rapidly decelerates

vertebrae might fracture/subluxate

76
Q

axial loading

A

vertical force results in vertebral shatter - diving accident

77
Q

safest thing to do in combative axial loading pts

A

medicate and intubate

78
Q

rotational injury

A

displacement of the spinal column

79
Q

skeletal level of injury

A

at the vertebral level

most damage to vertebral bones and ligaments

80
Q

neurological level of injury

A

lowest segment of spinal cord with normal sensory and motor function on both sides of the body

81
Q

what occurs if the thoracic or lumbar cord is damaged

A

paraplegia

82
Q

when are arms rarely damaged in spinal cord injuries

A

high C damage

83
Q

what happens in high atlas fractures

A

death likely - internal decapitation

84
Q

complete cord involvement

A

results in total loss of sensory and motor function below level of lesion

85
Q

incomplete/partial cord involvement

A

mixed loss of voluntary motor activity and sensation and leaves some tracts intact

86
Q

central cord syndrome

A

damage to the scentral spinal cord

87
Q

where do central cord syndrome injuries commonly occur

A

commonly in the cervical region in older adults

88
Q

s/s of central cord syndrom

A

motor weakness and sensory loss in all limbs but worse in arms than in legs

89
Q

anterior cord syndrome

A

caused by damage to anterior spinal artery leading to compromised blood flow

90
Q

what causes anterior cord syndrome

A

injuries causing acute compression of anterior portion of spinal cord

91
Q

brown sequard syndrome

A

result of damage to one half of the spinal cord

92
Q

brown sequard syndrome s/s X3

A

loss of motor function and position and vibration sense on same side of injury

paralysis on same side as injury

opposite side has loss of pain and temp sensation below level of lesion

93
Q

respiratory complications with a C3 and above injury

A

near total ventilatory muscle paralysis

artificial airways provide direct access for pathogens

94
Q

respiratory complications for a C3-C5 injury

A

loss of phrenic nerve function

95
Q

respiratory complication for C6-T8

A

loss of phrenic nerve and intercostals

96
Q

respiratory complications for T7-T12 injury

A

loss of abdominal muslces

97
Q

cardiovascular implications and tx for a T6 and up injury

A

sympathetic nervous system is reduced

heart rate is slowed

IV fluids

SCD’s, lovenox, TCDB

98
Q

urinary system implicatoins during spinal cord injuries

A

urinary retention and hyperirritability common

99
Q

GI system implicatoins T5+

A

primary issue is hypomotility

100
Q

GI issues T12 down

A

decreased sphincter tone

101
Q

autonomic dysreflexia X4

A

HTN

blurred vision

throbbing headache

marked diaphoresis above lesion level

102
Q

autonomic dysreflexia NI

A

elevate HOB at 45 degrees+

assess cause (bladder fullness)

notify physician

immediate catheterization

IM 7 Test 3 (5 decks)

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