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PT 680 Clinical Medicine > SCI > Flashcards

SCI Flashcards

1
Q

common traumatic causes to SCI and what percent are traumatic

A

70%
high risk activities, MVA, GSW, stabbings, falls, acts of violence, recreational/sports, medical negligence

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2
Q

what percent of SCI are caused by non-traumatic injury and what are examples

A

30%
usually results from disease/pathology
AVM, thrombus/embolus/hemorrhage, subluxation (RA or Down’s syndrome), infections (syphyillis, transverse myelitis), neoplasms, syringomyelia, spinal stenosis

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3
Q

why are incidences of SCI decreasing in regards to MVA

A

seat belt laws, air bags

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4
Q

violence incidence rates of SCI have been increasing, when are they found to be the highest (around what time)

A

in summer
on saturdays and sundays

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5
Q

what is the MOI for traumatic SCI

A

excessive motion/force in any of the planes of spinal motion
- results in fx or dislocation
- intensity and direction of force determine extent of injury
- combinations of force create the most damage

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6
Q

what does C5 SCI commonly result in

A

quadriplegia/tetraplegia (all 4 extremities involved)

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7
Q

what does T12 SCI commonly result in

A

paraplegia

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8
Q

what are other common locations for SCI

A

C7 and L2

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9
Q

what is the MOI of a hangman’s fx and what vertebrae does it involve

A

fx seen with excessive flexion injury
C2 fracture

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10
Q

describe effects of shearing forces on SC

A
  • occurs with horizontal force to the spine
  • disrupts ligamentous stability
  • associated with fx dislocations in thoracolumbar region
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11
Q

describe the effects of distraction forces on SC

A
  • traction force
  • least common MOI
  • occurs with significant momentum of head that creates tensile force on the spine
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12
Q

what type of injury is distraction common in

A

cervical whiplash injury

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13
Q

occurs due to impingement by fx bone, soft tissue or both; causes primary damage to SCI

A

contusion

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14
Q

types of primary damage to SC

A
  • contusion
  • microscopic hemorrhage/tissue laceration/tissue necrosis
  • demyelination
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15
Q

microscopic hemorrhage, tissue laceration, tissue necrosis begin within ___ in _____ matter after initial injury and then spread to ___ matter

A

hours
gray
axonal white

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16
Q

process of demyelination begins in peripheral spinal N roots and spreads over _____ segments

A

1-3

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17
Q

once swelling and traumatic response subsides, necrotic SC tissue is replaced by

A

scar tissue
cysts
cavities

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18
Q

does primary or secondary damage cause more damage

A

secondary

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19
Q

examples of secondary damage to SC

A

ischemia
inflammation
ion deranagement
apoptosis
scarring

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20
Q

describe how ischemia effects the SC

A
  • mechanical trauma to anterior spinal arteries/arterioles and vasospasm disrupts blood flow to gray matter area and tracts
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21
Q

how quickly does blood flow diminish to gray matter first

A

only 2-3 hours

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22
Q

CNS is very intolerant to ischemia, irreversible damage to neurons can occurs in _____ following trauma

A

15-30 seconds

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23
Q

how does inflammation affect SC damage

A
  • cells damaged in initial trauma release proinflammatory substances that attracts neutrophiles to area
  • results in expansion of area of tissue damage 24-48 hours
  • other immune system cells remain in area for up to 8 weeks post-injury to complete process of phagocytosis and oxydation
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24
Q

how does ion derangement effect the SC

A
  • abnormal levels K+ and Na+ accumulate in intra and extracellular spaces that results in loss of neuronal excitability
  • accumulation of Ca+ ions disrupt cellular function, results in demyelination and destruction of cell membrane and leads to cell death (apoptosis)
  • initial apoptosis occurs at level of injury for 4-24 hours but prolonged for up to 3 weeks in segments rostral and caudal to site of injury
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25
Q

temporary dysfunction of the SC due to effects of trauma

A

spinal shock

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26
Q

what does spinal shock result in

A
  • loss of motor reflex activity below site of injury
  • loss of sensation, voluntary motor and autonomic function below level
  • bladder function with urinary retention
  • bowel function with ileus
  • loss of perspiration below level of injury
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27
Q

how long can spinal shock last

A

2 days - 2 weeks

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28
Q

what signals the end of spinal shock

A

return of distal reflexes

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29
Q

what typically replaces flaccidity

A

spasticity and hyperreflexia

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30
Q

is a component of spinal shock syndrome and describes the hemodynamic changes resulting from a sudden loss of autonomic (sympathetic) tone due to SPI

A

neurogenic shock

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31
Q

refers to the loss of all sensation below level of injury that occurs immediately after injury and is not circulatory in nature

A

spinal shock

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32
Q

interruption of sympathetic NS below the level of injury, loss of vascular tone in LE

A

neurogenic shock

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33
Q

neurogenic shock results in cardiac dysregulation if injury occurs above

A

T6

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34
Q

what is the classic sx triad presentation for neurogenic shock

A

hypotension
bradycardia
hypothermia

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35
Q

what is NOT considered neurologic return following spinal shock

A

return of reflexive function below the level of lesion

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36
Q

where does spasticity/hypertonicity occur in regards to lesion and where does flaccidity occur

A
  • spasticity/hypertonicity below lesion
  • flaccidity above lesion
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37
Q

partial or complete paralysis and/or sensory loss of all 4 extremities and trunk including respiratory muscles

A

tetraplegia/quadriplegia

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38
Q

what levels does tetraplegia/quadriplegia occur with

A

C1-C8

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39
Q

partial or complete paralysis and/or sensory loss of all or part of the trunk and both LE’s

A

paraplegia

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40
Q

paraplegia results from injuries to what

A

thoracic and lumbar cord or sacral roots

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41
Q

ASIA

A

American Spinal Cord Injury Association

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42
Q

standardized classification system for determining neurogenic level of impairment for SCI

A

ASIA

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43
Q

what determines the level of lesion with SCI

A
  • most distal segment with intact motor (3/5) and sensory
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44
Q

what signifies complete SCI on ASIA

A

NOOOON

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45
Q

NO sensory or motor function below the level of injury in the lowest sacral segment (S4&5)

A

complete lesion

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46
Q

cause of complete lesion

A

Caused by complete transection, severe compression or vascular impairment to the cord

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47
Q

how to determine if someone has complete injury

A

Determined by insertion of dinge into rectum
Absent sensation
Inability to contract external anal sphincter around the finger

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48
Q

Preservation of some motor or sensory function below the level of injury and in sacral segments
Some viable neural tissue still exists

A

incomplete lesion

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49
Q

causes of incomplete lesion

A

Often results from contusions to the cord, from displaced bone or swelling within the spinal canal

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50
Q

refers to dermatomes and myotomes that are caudal to the neurological level that remain partially innervated

A

zone of partial preservation (ZPP)

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51
Q

what can only be used to describe complete injuries

A

zone of partial preservation (ZPP)

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52
Q

what are the different types of incomplete SCI syndromes

A

brown-sequard
anterior cord
central cord
posterior cord
cauda equina

53
Q

traumatic hemisection as result of GSW, stabbing or MVA

A

brown-sequard syndrome

54
Q

presentation of brown sequard syndrome

A
  • ipsilateral motor and proprioceptive loss (spasticity likely below level of lesion, clonus and babinski reflexes will be positive)
  • contralateral sensory loss to pin prick (pain), light touch and temperature
55
Q

what does anterior cord syndrome typically occurs with

A

Often occurs with flexion injuries to C/s that result in compression of anterior spinal artery and hypotension

56
Q

presentation of anterior cord syndrome

A
  • B/L loss of motor function, pain, light touch and temperature below level of lesion
  • Proprioceptive, kinesthesia and vibration spared (because DCML located dorsally)
57
Q

what does central cord syndrome commonly occur with

A

Most commonly occurs with hyperextension injuries or congenital narrowing of the spinal canal
- Causes compression of the central cord

58
Q

presentation of central cord syndrome

A
  • UE loss > LE because lumbar and sacral tracts are more peripherally located in cord
  • Sensory impairment > motor impairment (Sensory tracts run more medially)
  • Normal bowel, bladder and sexual function
59
Q

extremely rare injury to the dorsal columns

A

posterior cord syndrome

60
Q

presentation of posterior cord syndrome

A
  • Loss of proprioception, kinesthesia, vibration and combined cortical functions below level of lesion
  • Difficulty in coordinating movement of limbs
  • Voluntary motor, pain, light touch and temperature are intact (ALS)
  • Wide based gait pattern may be evident
61
Q

location of conus medullaris and what is it comprised of

A

L1-2
sacral spinal N roots S1-5

62
Q

causes of conus medullaris syndrome

A

Compression due to midline HNP, tumor, trauma

63
Q

presentation of conus medullaris syndrome

A
  • Mixed UMN and LMN signs
  • Symmetric saddle anesthesia
  • Bowel and bladder dysfunction occurs early in presentation (because controlled by sacral levels)
  • Pain occurs later and more mild than in cauda equina
64
Q

describe what levels present as UMN/LMN in conus medullaris syndrome

A

LMN at level of lesion
UMN below level of lesion

65
Q

what means horses tail

A

cauda equina

66
Q

where does cauda equina syndrome occur (level)

A

L2 or below

67
Q

what causes cauda equina syndrome

A

Compression of spinal nerves by HNP

68
Q

presentation of cauda equina syndrome

A
  • LMN injury with absent DTRs
  • Early back and radicular pain
  • Asymmetrical weakness
  • Sensory loss (asymmetrically) to all modalities and numbness
  • Bowel and bladder dysfunction occurring late in course
  • Saddle anesthesia
69
Q

patient may need to be intubated during acute management if the injury is thought to be above _____, if _____ or _____

A

C5
hypoxix
respiratory distress

70
Q

_____ in the first 48 hours improves prognosis

A

steroids - because it decreases inflammation

71
Q

what occurs to breathing if injury is above C4

A

quad breathing - flail chest breathing

72
Q

why does flail chest/quad breathing occur and what will patient require

A
  • loss of phrenic nerve innervation to the diaphragm; leads to respiratory paralysis
  • pt will require ventilator support or phrenic N stimulator if C4 and 5 are intact
73
Q

complications of respiratory management in SCI

A

pneumonia
atelectasis
PE

74
Q

what will complete injuries above T6 experience

A

neurogenic shock

75
Q

loss of supraspinal control of the sympathetic nervous system

A

symphatectomy

76
Q

sympathetic NS has _______ outflow; parasympathetic NS has _______ outflow

A
  • thoracolumbar (T1-L2)
  • craniosacral (CN 3, 7, 9, 10 ans S2-4)
77
Q

how to treat hypotension in SCI

A

vasopressors
- epinephrine, norepinephrine, and dopamine cause vasoconstriction to bring BP up to maintain MAP at 85-90 mmH

78
Q

initially may mobilize via skeletal ____ until pt is stable for surgery

A

traction

79
Q

inserted laterally on the skull with traction rope applied rostrally; usually about 12 weeks until healing occurs

A

tongs

80
Q

stryjer frame allows positional changes with spinal stabilization; limited to prone and supine and cannot accommodate obese or large patients

A

turning frames/bed

81
Q

provides continuous oscillation and side-to-side rotation to improve pulmonary and kidney drainage and prevents pressure sores

A

roto-test kinetic table

82
Q

prevents further neurologic compromise by decompressing neural tissue via bone grafting/wiring; allows for early mobilization

A

surgical stabilization

83
Q

how long must patient where spinal orthosis following spinal stabilization

A

3 months

84
Q

ring with 4 steel screws attaching directly to the skull; attached to a body jacket by 4 steel posts; considered a major improvement in medical management of SCI because they permit early OOB and early rehab

A

halo frame for C/s injuries

85
Q

what devices are just post-op for thoracic and lumbar SC injuries

A

body cast/jacket orthosis (TLSO)

86
Q

list complications following SCI

A

impaired temperature control
spasticity
bowel/bladder dysfunction
autonomic dysreflexia
heterotrophic ossification
joint contractures
osteoporosis
respiratory impairment
sexual dysfunctio
pressure sores
postural hypotension
DVT
pain
renal calculi

87
Q

what structure is unable to control blood flow or level of sweating that impairs temperature control

A

hypothalamus

88
Q

describe the impaired temperature control following SCI

A
  • lost ability to shiver
  • vasodilation does not occur with increased heat
  • vasoconstriction does not occur when cold
  • body temperature significantly influenced by external temperature
  • avoid extremities in external temperature
89
Q

impaired temperature control is common in what types of lesions

A

c/s lesions or injuries above T6

90
Q

diaphoresis (increased sweating) typically occurs where

A

above level of injury

91
Q

what nerve innervates the diaphragm

A

phrenic nerve

92
Q

muscle involvement to cough

A
  • expiration is passive, forced expiration and cough involves T1-12 (intercostals and abdominals)
  • accessory: STM, traps, pec minor, serratus at multiple levels
  • postural drainage, chest PT, breathing exercises, assisted cough techniques
93
Q

what is the most common cause of death in tetraplegia SCI in early stages

A

pneumonia and PE

94
Q

what does paralysis of mm of inspiration lead to

A

decreased chest wall expansion and lower inspiratory volume

95
Q

poor innervation of abs often results in what

A

intrathoracic pressure which effects total lung capacity (TLC) and expiratory reserve volume (ERV)

96
Q

what can altered breathing patterns lead to

A

permanent postural changes

97
Q

what typically develops once spinal shock has subsided bc SCI is a UMN lesion

A

spasticity, hypertonicity

98
Q

how long does spasticity typically gradually increase until leveling off

A

6 months

99
Q

what are some examples of things that can increase spasticity in SCI patients

A

positional changes
cutaneous stimulation
response to change in temperature
tight clothing
presence of kidney stones
fecal impactions
catheter blockage
UTI
decubitis ulcers
emotional stress

100
Q

what is the most frequent medical condition following SCI

A

UTI

101
Q

what spinal cord levels primarily control the bladder

A

S2, 3, 4

102
Q

occurs when lesions are in the cord above the conus medularis

A

reflex bladder (spastic)

103
Q

occurs when lesion is in the conus medularis or cauda equina

A

arereflexic bladder (flaccid)

104
Q

spasticity in bladder due to UMN lesion; empties reflexively in response to a certain level of filling pressure; may be triggered by manual stimulation (stroking, kneading, tapping suprapubic or upper thigh/groin area

A

reflexive bladder

105
Q

how to manage reflexive bladder

A

intermittent catherization to empty at regular/predictable times

106
Q

for reflexive bladder, fluid intake is restricted to _______ ml/d and monitored hourly with intake stopped late in the day to reduce need to cath during the night

A

2000

107
Q

flaccid due to LMN lesion; no reflex action of detrusor mm

A

areflexive bladder

108
Q

how to empty areflexive bladder

A

increasing intraabdominal pressure via valsalva maneuver or by manually compressing lower abdomen (crede maneuver)

109
Q

how to manage bowel dysfunction following TBI

A
  • combo of laxatives and digital stimulation to trigger defecation reflex
  • regulate diet and establish regular pattern of evacuation
  • prone to develop ileus or GI bleed
110
Q

erectile capacity in M is greater in _____ vs _____ and in _____ vs _____

A

UMN vs LMN
incomplete vs. Complete

111
Q

occur in response to external stimulation - mediated through reflex arc at S2-4 - most common in UMN lesion

A

reflexogenic erection

112
Q

occurs in response to cognitive stimulation like erotic fantasy, mediated cortically, most common in LMN lesion but at much lower percentage and only in incomplete lesions

A

psychogenic erection

113
Q

caused by impaired sensation resulting in unrelieved pressure or shearing forces

A

pressure injuries

114
Q

contributing factors to pressure injuries

A
  • loss of vasomotor control
  • spasticity
  • maceration due to excessive exposure to moisture
  • trauma from adhesive or tape
  • nutritional deficiencies
  • poor general skin condition prior to SCI
  • secondary infections
115
Q

what can cause a major delay in rehab and can eventually lead to death in SCI

A

pressure injuries

116
Q

pathologic autonomic reflex typically occurring with lesions above T6

A

autonomic dyreflexia

117
Q

autonomic dysreflexia is the acute onset of excessive autonomic activity due to some noxious stimulation that leads to

A

rapid elevation of BP greater than 20% systolic, with change in HR plus at least one of following: severe pounding HA, profuse sweating, increased spasticity and restlessness, vasoconstriction below level of lesion, vasodilation above, constricted pupils, goosebumps, nasal congestion, blurred vision

118
Q

what is the most common cause of autonomic dysreflexia; list other causes

A

bladder distention from urinary retention
pressure sores, urinary or kidney stones, UTI, excessive environmental temperature changes, following passive stretching of the hip

119
Q

is autonomic dysreflexia a medical emergency

A

yes

120
Q

how to treat autonomic dysreflexia when it occurs

A
  • place pt in upright sitting to lower BP
  • assess drainage system of bladder, check catheter for kinks in tubing or full bag, check for irritating clothing
121
Q

decrease in BP that occurs when assuming an erect position or vertical positional changes above 60 deg

A

orthostatic hypotension

122
Q

what causes orthostatic hypotension and what is it often associated/caused by

A

loss of sympathetic vasoconstriction control due to lack of LE muscle tone
- prolonged bed rest/immobilization

123
Q

sx of orthostatic hypotension

A

lightheaded, dizzy, syncope

124
Q

occurs when abnormal osteogenesis forms in soft tissue below level of lesion; thought to be associated with tissue hypoxia; always extracapsular and extra-articular; develops in tendons, connective tissue layers between mm, aponeurotic tissue, peripheral aspects of mm

A

heterotropic ossification

125
Q

when are contractures irreversible

A

once capsular tissues are involved

126
Q

pain that occurs at or near site of injury around cord due to cute compression or tearing; sharp, shooting, burning, stabbing following a dermatome pattern; most common in cauda equina injuries

A

nerve root pain

127
Q

peculiar, often painful sensations below level of lesion that do not follow dermatomal distribution; burning, numbness, tingling, pins and needles, phantom type pain

A

spinal cord dysesthesias

128
Q

most common location for MSK pain

A

shoulders (or above level of injury)

PT 680 Clinical Medicine (18 decks)

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