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Semester 5 PMNM Exam 8 > Spinal Cord Injury (Tighe - PA) > Flashcards

Spinal Cord Injury (Tighe - PA) Flashcards

1
Q

4 mechanisms of SC trauma

A

transection
compression
contusion
vascular injury

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2
Q

what happens in transection

A

glia are disrupted and SC tissue is torn

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3
Q

causes of transection 4

A

penetrating trauma
blunt trauma
bony fragments
disc herniation

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4
Q

cauases of compression injury to SC

A

violent shaking or direct blow

temporary loss of function

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5
Q

describe contusion injury to SC

A
  • glial tissue and SC surface are intact

- may have loss of grey and white matter which creates a cavity with white matter rim at periphery

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6
Q

when do you suspect vascular injury to the SC?

A

suspect vascular injury if discrepancy between clinical neurological deficit and level of spinal injury

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7
Q

examples of vascular injury

A
  • lower cervical dislocation compresses vertebral arteries

- thrombosis, decreased BF through anterior spinal artery

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8
Q

anterior spinal artery originates where

A

originates at C1 from both vertebral arteries and appears as C1 or C2 loclization

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9
Q

primary injury

A

damage that occurs immediately at time of injury due to forces such as compression, contusion, shear injury, penetrating, GSW
- spared tissues and axons may remain and are important in recovery

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10
Q

secondary injury

A

begins within minutes of injury and evolves over hours, includes: ischemia, hypoxia, inflammation, edema, electrolyte distrubances

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11
Q

describe blood flow changes from secondary inuury

A

occur within 2 hours following injury. Decreased SC BF, rapid swelling at level of injury, pressure on SC increases, ischemia, necrosis

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12
Q

edema occurs when

A

within hours after injury (secondary injury), occurs first at injury site and spreads to adjacent and distal segments

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13
Q

immediate treatment of SCI includes what

A

manual immobilzation of C spine with hands, followed by using a C collar. next do CAB’s and full spinal immobiliztion

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14
Q

what happens if the c collar is too short or too tall?

A

too short = cervical flexion

too tall = cervical extension

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15
Q

consults with what 5 areas

A

neurosurgeon, orthopedist, trauma specialist, general surgeon, others as needed

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16
Q

describe the cord in a complete cord injury

A

the cord is transected in a complete cord injury

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17
Q

complete cord injury: sensory and motor fxn

A

complete loss of sensory and motor function occurs below the level of the lesion in a complete cord injury

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18
Q

complete cord injury what ASIA grade

A

A

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19
Q

acute stages of complete cord injury (symptoms)

A

absent reflexes, no response to plantar stimulation, flaccid muscle tone, priapism, urinary retention and bladder distension

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20
Q

ASIA grade for incomplete cord injury

A

grades B-D

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21
Q

motor and sensory fxn in incomplete cord injury

A

partial loss of sensory and motor function below the level of the lesion in an incomplete cord injury

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22
Q

incomplete cord injury caused by

A

contusion, edema, bony fragments

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23
Q

causes of complete cord injury

A

transection of cord, severe compression, or extensive vascular dysfunction

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24
Q

which is more preserved in an incomplete cord injury, sensation or motor fxn

A

sensation preserved more than motor fxn becuase sensory tracts are more peripheral and less vulnerable

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25
Q

incomplete cord injury - motor and sensation

A

various degrees of muscle motor fxn and sensation in dermatomes

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26
Q

the more incomplete the injury, the more what recovery?

A

the more incomplete the injury, the more favorable the potential for recovery, especially on initial eval and 72 hrs to 1 week after injury

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27
Q

ASIA impairment scale

A

A = complete
B - D = incomplete
E = normal

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28
Q

how are deficits determined in SCI?

A

deficits determined by neurological levels/lesions

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29
Q

tetraplegia aka and what levels

A

aka quadriplegia

levels C1-C8

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30
Q

paraplegia levels?

A

thoracic, lumbar, or sacral segments

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31
Q

define central cord syndrome

A

damage to the central part of the SC. the peripheral fibers are not affected

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32
Q

central cord syndrome caused by

A

cervical hyperextension with pre-existing cervical spondylosis

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33
Q

central cord syndrome: more severe motor impariment where

A

more severe motor impairment in UE than LE!

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34
Q

bladder and sensory issues with central cord syndrome

A

bladder dysfunction and variable sensory loss below the injury level

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35
Q

pain and temp - central cord

A

loss of pain and temp sensation at the site of injury and surrounding dermatomes due to crossing of spinothalamic fibers - “suspended sensory loss”

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36
Q

central cord pain and temp above and below

A

intact pain and temp at dermatomes above and below the injury

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37
Q

central cord vibration and proprioception

A

vibration and proprioception often spared in central cord syndrome

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38
Q

cause of anterior cord syndrome

A

loss of blood supply from anterior spinal artery, which supplies 2/3 of SC

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39
Q

anterior cord syndrome - tactile, position and vibratory sense

A

are normal.

40
Q

what is lost in anterior cord syndrome

A

urinary incontinence

41
Q

anterior cord syndrome is caused by what 4 things

A

flexion injuries, IVD herniation, SC infarction, radiation myelopathy

42
Q

how common is posterior cord syndrome

A

rare

43
Q

how is the CST impacted in posterior cord syndrome

A

acute: weakness, flaccidity, hyporeflexia
chronic: hypertonia, hyperreflexia

44
Q

characteristics of posterior cord syndrome

A

loss of proprioception causing wide-based gait ataxia, loss of vibratory sense, bladder dysfunction, paresthesias

45
Q

causes of posterior cord syndrome

A

MS, friedreich ataxia, tumors, cervical spondylotic myelopathy, tabes dorsalis

46
Q

characteristics of brown-sequard

A

unilateral involvement

weakness, loss of vibration/proprioception on the same side of the lesion and loss of pain/temp on opposite side

47
Q

causes of brown-sequard

A

knife, GSW, demyelination, disc herniation, infarction, infection, tumor

48
Q

conus medullaris syndrome is what type of injury

A

sacral cord injury

49
Q

conus medullaris syndrome is associated with what lesion

A

L2 - often affects conus medullaris

50
Q

characteristics of conus medullaris syndrome

A

early, prominent sphincter dysfxn, flaccid paralysis of rectum/bladder, impotence, saddle anesthesia, leg muscle weakness

51
Q

causes of conus medullaris syndrome

A

disc herniation, spinal fracture, tumors

52
Q

Cauda equina syndrome is due to injury of what

A

injury of lumbosacral nerve roots

53
Q

what happens in cauda equina

A

loss of fxn of 2+ of the 18 nerve roots in the cauda equine - usually central lumbar disc herniation

54
Q

characteristics of cauda equine syndrome

A

LBP w/ radiating pain, PF weakness, bladder and rectal sphincter paralysis (S3-5), sensory loss in dermatomes, saddle anesthesia

55
Q

T/F cauda equine is a medical emergency

A

true. refer to neurosurgery

56
Q

what is syringomyelia

A

a clinical syndrome that affects 2% of paraplegics

57
Q

most common site for syringomyelia

A

thoracic area

58
Q

causes of syringomyelia

A

cystic cavitation and gliosis of SC (cyst develops and grows down the SC)

59
Q

when does syringomyelia usually occur

A

within 4-9 years post trauma but can develop up to 30 years after initial lesion

60
Q

S/S of syringomyelia

A

initial sharp pain, LMN dysfxn, sensory loss, Horner’s syndrome
- changes difficult to assess - below site of injury

61
Q

3 sx of Horner’s

A

ipsilateral ptosis, miosis, anhydrosis

62
Q

syringomyelia may have what additional s/s

A

spasms, reflex changes, phantom sensations, sexual dyscn, spasticity, weakness, HA, loss of b/b, sensation loss in hands

63
Q

neurapraxia

A
  • transient neuro deficits
  • transient tetraplegia from axial loading (diving into pool)
  • athletic injuries
  • sudden decrease in AP diameter of SC = compression
  • seen w/ hypertext and hyperflex
64
Q

What is spinal shock

A

transient (!!!!) physiological deficit of cord fxn below the level of injury
- complete loss of all neuro fxn but will resolve

65
Q

s/s of spinal shock

A
  • initial: tachycardia, htn due to release of catecholamines
  • then bradycardia and hypotension
  • paralysis, b/b dysfxn, priapism
66
Q

what is neurogenic shock

A
  • severe autonomic dysfxn
  • interruption of SNS
  • usually does not occur with injury below T6!!
67
Q

neurogenic shock does not usually occur with an injury below which level

A

T6

68
Q

KEY s/s of neurogenic shock (3)

A
  • HYPOTENSION
  • BRADYCARDIA
  • PERIPHERAL VASODILATION
69
Q

other s/s of neurogenic shock

A

hypothermia, priapism, decreased shivering/sweating below injury, loss of body temp control below injury, b/b incontinence

70
Q

what do you consider with a spinal injury below T6?

A

consider hemorrhagic until proven otherwise.

71
Q

goals of sCI

A
  • mean arterial BP at least 90
  • fluids bu tdon’t overhydrate
  • pressors to maintain BP
  • maintain BS to SC
72
Q

what occurs with BP in injuries above T6

A

baseline BP is reduced as well as HR (50-60bpm)

don’t push too hard with exercise

73
Q

orthostiatic hypotension

eval

A

eval BP and PULSE in supine, sitting and standing

74
Q

orthostatic hypotension dx if

A

decreased SBP > 20 and/or

decreased DBP > 10

75
Q

autonomic dysreflexia occurs in SC injuries above what level

A

T6

76
Q

what is autonomic dysreflexia

A

an uninhibited sympathetic response to stimuli. leads to diffuse VC and HTN. compensate via PSNS above the lesion w/ bradycardia and VD but not enough to compensate

77
Q

when does autonomic dysreflexia usually occur

A

in first month/first year after injury

20-70% of SCI w/ lesions above T6 will have it

78
Q

autonomic dysreflexia - medical emergency?

A

YES!

79
Q

stimuli of autonomic dysreflexia

A

bladder distension, bowel impaction, pressure sores, bone frx, sexual activity, labor, menstrual cramps

80
Q

S/S of autonomic dysreflexia

A 
headache - pounding!
HTN 20-40 above normal for pt
brady or tachy
diaphoresis above injury
flushing
blurred vision 
anxiety
nausea
81
Q

complications of autonomic dysreflexia

A

HTN, HTN crisis, bradycardia, cardiac arrest, IC hemorrhage, seizures

82
Q

management of autonomic dysreflexia

A

check BP, sit pt up, remove tight clothing, search for cause - often from crimped catheter. could also be UTI or fecal impaction

83
Q

management of autonomic dysreflexia

A

meds to lower BP

84
Q

keys of autonomic dysreflexia

A

recognition and avoidance of causative stimuli

85
Q

CAD

A

mortality great in SCI w/ lesions above T5. may have atypical s.s of cardiac ischemia such as autonomic dysreflexia and changes in spasticity

86
Q

CAD

A

Cardiac arrhythmias
Acute cervical SCI - due to
Excess vagal tone
Hypoxia, hypotension, fluid and electrolyte imbalances
Less frequently seen in chronic SCI
Complete cervical SCI – ongoing risk for cardiac arrest

87
Q

Ventilatory fxn

A

respiratory muscles not working in cervical and high thoracic SCI

88
Q

issues with ventilation

A

dyspnea, decreased ex tolerance, impaired cough, lung secretions, increased risk of pneumonia

89
Q

DVT

A

common early complication from lack of mvmt. prevent via exercise, turning in bed, drugs, ted hose, etc

90
Q

what to do if suspect DVT

A

stop mobilization, report findings, Doppler ultrasound, D dimer blood test

91
Q

why do SCI pt’s have difficulty with temp regulation

A

due to disruption of autonomic pathways

92
Q

who are most vulnerable for lack of temp regulation

A

SCI T6 and above

93
Q

impaired cooling mechanism (temp regulation) -

A

loss of SNS: insensate skin and reduced sweating
autonomic dysfxn below lesion, loss of muscle pump
increased metabolic heat

94
Q

T/F those with SCI have difficulty cooling themselves

A

true (or heating)

95
Q

definition of hypothermia (body temp must be)

A

core body temp below 95 F (35 C)

96
Q

2 types of bladder dysfxn

A

spastic and flaccid. goal is bladder volume less than 500 ml to avoid distention

Semester 5 PMNM Exam 8 (2 decks)

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