SCI Flashcards
(128 cards)
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
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
3
Q
why are incidences of SCI decreasing in regards to MVA
A
seat belt laws, air bags
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
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
6
Q
what does C5 SCI commonly result in
A
quadriplegia/tetraplegia (all 4 extremities involved)
7
Q
what does T12 SCI commonly result in
A
paraplegia
8
Q
what are other common locations for SCI
A
C7 and L2
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
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
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
12
Q
what type of injury is distraction common in
A
cervical whiplash injury
13
Q
occurs due to impingement by fx bone, soft tissue or both; causes primary damage to SCI
A
contusion
14
Q
types of primary damage to SC
A
- contusion
- microscopic hemorrhage/tissue laceration/tissue necrosis
- demyelination
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
16
Q
process of demyelination begins in peripheral spinal N roots and spreads over _____ segments
A
1-3
17
Q
once swelling and traumatic response subsides, necrotic SC tissue is replaced by
A
scar tissue
cysts
cavities
18
Q
does primary or secondary damage cause more damage
A
secondary
19
Q
examples of secondary damage to SC
A
ischemia
inflammation
ion deranagement
apoptosis
scarring
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
21
Q
how quickly does blood flow diminish to gray matter first
A
only 2-3 hours
22
Q
CNS is very intolerant to ischemia, irreversible damage to neurons can occurs in _____ following trauma
A
15-30 seconds
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
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
25
temporary dysfunction of the SC due to effects of trauma
spinal shock
26
what does spinal shock result in
- 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
27
how long can spinal shock last
2 days - 2 weeks
28
what signals the end of spinal shock
return of distal reflexes
29
what typically replaces flaccidity
spasticity and hyperreflexia
30
is a component of spinal shock syndrome and describes the hemodynamic changes resulting from a sudden loss of autonomic (sympathetic) tone due to SPI
neurogenic shock
31
refers to the loss of all sensation below level of injury that occurs immediately after injury and is not circulatory in nature
spinal shock
32
interruption of sympathetic NS below the level of injury, loss of vascular tone in LE
neurogenic shock
33
neurogenic shock results in cardiac dysregulation if injury occurs above
T6
34
what is the classic sx triad presentation for neurogenic shock
hypotension
bradycardia
hypothermia
35
what is NOT considered neurologic return following spinal shock
return of reflexive function below the level of lesion
36
where does spasticity/hypertonicity occur in regards to lesion and where does flaccidity occur
- spasticity/hypertonicity below lesion
- flaccidity above lesion
37
partial or complete paralysis and/or sensory loss of all 4 extremities and trunk including respiratory muscles
tetraplegia/quadriplegia
38
what levels does tetraplegia/quadriplegia occur with
C1-C8
39
partial or complete paralysis and/or sensory loss of all or part of the trunk and both LE's
paraplegia
40
paraplegia results from injuries to what
thoracic and lumbar cord or sacral roots
41
ASIA
American Spinal Cord Injury Association
42
standardized classification system for determining neurogenic level of impairment for SCI
ASIA
43
what determines the level of lesion with SCI
- most distal segment with intact motor (3/5) and sensory
44
what signifies complete SCI on ASIA
NOOOON
45
NO sensory or motor function below the level of injury in the lowest sacral segment (S4&5)
complete lesion
46
cause of complete lesion
Caused by complete transection, severe compression or vascular impairment to the cord
47
how to determine if someone has complete injury
Determined by insertion of dinge into rectum
Absent sensation
Inability to contract external anal sphincter around the finger
48
Preservation of some motor or sensory function below the level of injury and in sacral segments
Some viable neural tissue still exists
incomplete lesion
49
causes of incomplete lesion
Often results from contusions to the cord, from displaced bone or swelling within the spinal canal
50
refers to dermatomes and myotomes that are caudal to the neurological level that remain partially innervated
zone of partial preservation (ZPP)
51
what can only be used to describe complete injuries
zone of partial preservation (ZPP)
52
what are the different types of incomplete SCI syndromes
brown-sequard
anterior cord
central cord
posterior cord
cauda equina
53
traumatic hemisection as result of GSW, stabbing or MVA
brown-sequard syndrome
54
presentation of brown sequard syndrome
- 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
what does anterior cord syndrome typically occurs with
Often occurs with flexion injuries to C/s that result in compression of anterior spinal artery and hypotension
56
presentation of anterior cord syndrome
- 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
what does central cord syndrome commonly occur with
Most commonly occurs with hyperextension injuries or congenital narrowing of the spinal canal
- Causes compression of the central cord
58
presentation of central cord syndrome
- 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
extremely rare injury to the dorsal columns
posterior cord syndrome
60
presentation of posterior cord syndrome
- 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
location of conus medullaris and what is it comprised of
L1-2
sacral spinal N roots S1-5
62
causes of conus medullaris syndrome
Compression due to midline HNP, tumor, trauma
63
presentation of conus medullaris syndrome
- 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
describe what levels present as UMN/LMN in conus medullaris syndrome
LMN at level of lesion
UMN below level of lesion
65
what means horses tail
cauda equina
66
where does cauda equina syndrome occur (level)
L2 or below
67
what causes cauda equina syndrome
Compression of spinal nerves by HNP
68
presentation of cauda equina syndrome
- 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
patient may need to be intubated during acute management if the injury is thought to be above _____, if _____ or _____
C5
hypoxix
respiratory distress
70
_____ in the first 48 hours improves prognosis
steroids - because it decreases inflammation
71
what occurs to breathing if injury is above C4
quad breathing - flail chest breathing
72
why does flail chest/quad breathing occur and what will patient require
- 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
complications of respiratory management in SCI
pneumonia
atelectasis
PE
74
what will complete injuries above T6 experience
neurogenic shock
75
loss of supraspinal control of the sympathetic nervous system
symphatectomy
76
sympathetic NS has _______ outflow; parasympathetic NS has _______ outflow
- thoracolumbar (T1-L2)
- craniosacral (CN 3, 7, 9, 10 ans S2-4)
77
how to treat hypotension in SCI
vasopressors
- epinephrine, norepinephrine, and dopamine cause vasoconstriction to bring BP up to maintain MAP at 85-90 mmH
78
initially may mobilize via skeletal ____ until pt is stable for surgery
traction
79
inserted laterally on the skull with traction rope applied rostrally; usually about 12 weeks until healing occurs
tongs
80
stryjer frame allows positional changes with spinal stabilization; limited to prone and supine and cannot accommodate obese or large patients
turning frames/bed
81
provides continuous oscillation and side-to-side rotation to improve pulmonary and kidney drainage and prevents pressure sores
roto-test kinetic table
82
prevents further neurologic compromise by decompressing neural tissue via bone grafting/wiring; allows for early mobilization
surgical stabilization
83
how long must patient where spinal orthosis following spinal stabilization
3 months
84
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
halo frame for C/s injuries
85
what devices are just post-op for thoracic and lumbar SC injuries
body cast/jacket orthosis (TLSO)
86
list complications following SCI
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
what structure is unable to control blood flow or level of sweating that impairs temperature control
hypothalamus
88
describe the impaired temperature control following SCI
- 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
impaired temperature control is common in what types of lesions
c/s lesions or injuries above T6
90
diaphoresis (increased sweating) typically occurs where
above level of injury
91
what nerve innervates the diaphragm
phrenic nerve
92
muscle involvement to cough
- 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
what is the most common cause of death in tetraplegia SCI in early stages
pneumonia and PE
94
what does paralysis of mm of inspiration lead to
decreased chest wall expansion and lower inspiratory volume
95
poor innervation of abs often results in what
intrathoracic pressure which effects total lung capacity (TLC) and expiratory reserve volume (ERV)
96
what can altered breathing patterns lead to
permanent postural changes
97
what typically develops once spinal shock has subsided bc SCI is a UMN lesion
spasticity, hypertonicity
98
how long does spasticity typically gradually increase until leveling off
6 months
99
what are some examples of things that can increase spasticity in SCI patients
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
what is the most frequent medical condition following SCI
UTI
101
what spinal cord levels primarily control the bladder
S2, 3, 4
102
occurs when lesions are in the cord above the conus medularis
reflex bladder (spastic)
103
occurs when lesion is in the conus medularis or cauda equina
arereflexic bladder (flaccid)
104
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
reflexive bladder
105
how to manage reflexive bladder
intermittent catherization to empty at regular/predictable times
106
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
2000
107
flaccid due to LMN lesion; no reflex action of detrusor mm
areflexive bladder
108
how to empty areflexive bladder
increasing intraabdominal pressure via valsalva maneuver or by manually compressing lower abdomen (crede maneuver)
109
how to manage bowel dysfunction following TBI
- 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
erectile capacity in M is greater in _____ vs _____ and in _____ vs _____
UMN vs LMN
incomplete vs. Complete
111
occur in response to external stimulation - mediated through reflex arc at S2-4 - most common in UMN lesion
reflexogenic erection
112
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
psychogenic erection
113
caused by impaired sensation resulting in unrelieved pressure or shearing forces
pressure injuries
114
contributing factors to pressure injuries
- 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
what can cause a major delay in rehab and can eventually lead to death in SCI
pressure injuries
116
pathologic autonomic reflex typically occurring with lesions above T6
autonomic dyreflexia
117
autonomic dysreflexia is the acute onset of excessive autonomic activity due to some noxious stimulation that leads to
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
what is the most common cause of autonomic dysreflexia; list other causes
bladder distention from urinary retention
pressure sores, urinary or kidney stones, UTI, excessive environmental temperature changes, following passive stretching of the hip
119
is autonomic dysreflexia a medical emergency
yes
120
how to treat autonomic dysreflexia when it occurs
- 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
decrease in BP that occurs when assuming an erect position or vertical positional changes above 60 deg
orthostatic hypotension
122
what causes orthostatic hypotension and what is it often associated/caused by
loss of sympathetic vasoconstriction control due to lack of LE muscle tone
- prolonged bed rest/immobilization
123
sx of orthostatic hypotension
lightheaded, dizzy, syncope
124
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
heterotropic ossification
125
when are contractures irreversible
once capsular tissues are involved
126
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
nerve root pain
127
peculiar, often painful sensations below level of lesion that do not follow dermatomal distribution; burning, numbness, tingling, pins and needles, phantom type pain
spinal cord dysesthesias
128
most common location for MSK pain
shoulders (or above level of injury)
