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529 Neuro 2 > L11 SCI Pathology > Flashcards

L11 SCI Pathology Flashcards

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1
Q

Causes of SCI

A

MVA
falls
violent act
sports
unknown
as age increases, falls out weight sports, violence, and MVA as cause of SCI

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2
Q

Age of most SCI pts

A

16-30 y/o
mean 40 y/o

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3
Q

gender of SCI pts

A

80% male, 20% female

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4
Q

most common SCI injury levels

A

C5
C4
C6

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5
Q

prevention of SCI

A

driving: seatbelt, no distracted driving, car seats
fall prevention in elderly
recreation: helmets, no diving head first

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6
Q

tetraplegia caused by injury to what levels?

A

C6 and above

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7
Q

paraplegia caused by injury to what levels

A

T6 and below

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8
Q

why did SCI pts not survive in the past?

A

spinal precautions in ER not developed
renal failure due to lack of bladder catheter
respiratory and circulatory problems
1970s added movement precautions, bladder catheter, and reduction of complete SCI

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9
Q

stryker frame

A

pt sandwiched between two large frames and rotated every couple hours to relieve pressure
necessary in the past before the ability to surgically provide internal fixation

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10
Q

medical interventions that revolutionized SCI pt care and survival

A

vertebral stabilization
spasticity medication
urological management w catheter to prevent renal failure
power wheelchairs
lighter manual wheelchairs
lightweight orthotics

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11
Q

types of SCI (general)

A

traumatic: often incomplete, due to vertebral burst fracture, common in younger pts
non traumatic: older pts, not often complete with few secondary complications

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12
Q

how do Fxs cause SCI?

A

fracture causes:
bone fragments: impinging spinal cord and causing compression or severing SC
edema: compressing SC
dislocation: compressing SC

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13
Q

transverse myelitis definition

A

non traumatic SCI, umbrella term for lesions near SC

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14
Q

epidural hematoma

A

common cause of non traumatic SCI
swelling over dural layer compresses SC
treated with surgery and medication

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15
Q

transverse myelitis presentation

A

sharp pain at level
paresthesia
B& B dysfunction
arm/leg weakness
headache
n/v

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16
Q

transverse myelitis etiology

A

virus; herpes, entero, epstein barr, west nile, hep B, measles, mumps
bacterial: syphilis, TB, middle ear infection, GI infection, tetanus
inflammatory: sjorgrens, lupus, CT dxs, scleroderma

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17
Q

vascular causes of non traumatic SCI

A

ischemia of anterior/posterior aa.
vasculitis of spinal aa.
arterial venous malformation

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18
Q

types of non traumatic SCI

A

transverse myelitis
epidural hematoma
metastasis
spinal stenosis
vascular cause
syringomyelia
surgical error

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19
Q

stenosis etiology

A

OA
DDD
facet joint enlarged
narrowing spinal canal
scoliosis
spondylolisthesis
RA

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20
Q

syringomyelia

A

very rare
central canal where CSF flows in the center of the SC
the fluid becomes distended and compresses SC
often in C spine

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21
Q

acute traumatic SCI presentation

A

affected 3 levels above and below injury
spinal shock 30-60 min
flaccid paralysis
no DTRs
edema causing compression of neural tissue
hemorrhage
glutamate starts to increase up to 6x higher and cause cell death almost immediately

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22
Q

subacute/chronic traumatic SCI presentation

A

hemorrhage, edema, glial scar tissue, and ischemia
glutamate levels increase causing apoptosis in SC
continued cell death complicates recovery
demyelination occurs with cell death causing SC changes in circuitry leading to spasticity and chronic pain
oxidative stress and cytokines

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23
Q

changes to the SC in chronic SCI

A

white matter disruption due to demyelination
gray matter disruption
glial cell cyst formation
axonal sprouting

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24
Q

syrinx

A

fluid filled cavity resulting from area of damaged tissue
once damaged tissue is cleared away by immune system, a glial scar forms made of astrocytes
this cavity blocks the reconnection of the two sides of the SC from regenerating together

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25
why does demyelination occur after SCI
oligodendrocytes are lost in area of injury due to toxic environment (glutamate excitotoxicity) causes loss of myelin and regeneration
26
differential of SCI
epidural hematoma metastatic disease AAA epidural infection syphilis transverse myelitis acuet IV disc herniation
27
central cord syndrome
incomplete cord syndrome UE>LE deficit due to LE corticospinal tracts being located laterally in the SC (somatotopic organization)
28
etiology of central cord syndrome
elderly: spondylosis younger: severe extension injury
29
s/s of central cord syndrome
complete loss of UE motor function incomplete loss of thoracic motor function variable degrees of sensory loss
30
anterior spinal cord injury etiology
flexion injury in C spine burst fracture flexion tear drop fracture herniated disc
31
anterior spinal cord injury presentation
immediate paralysis due to corticospinal tract involvement in anterior spinal cord pain and temperature sensation are impaired vibration and proprioception are intact motor deficits at and below the injury
32
posterior cord syndrome etiology
extension injury
33
posterior cord syndrome presentation
loss of proprioception/vibration due to disruption of dorsal column (sensory)
34
brown sequard syndrome etiology
rotational injury causing fracture/dislocation penetrating trauma like a stab wound
35
brown sequard syndrome presentation
spinal cord hemisection IL motor weakness on side of lesion due to corticospinal tract CL sensory deficit; - dorsal column loss on side of lesion - spinothalamic tract loss on opposite side of lesion below level and at IL side level of lesion
36
immediate medical management of SCI
stabilize: traction, surgical, halo traction, TLSO no meds currently hypothermia: reduce edema/inflammation/ischemia but can lead to pneumonia
37
prognosis for motor recovery: incomplete lesions
c spine: 2x greater chance of recovery for incomplete than complete greater prognosis of motor return if sensation at motor level is preserved recovery at 72 hours post injury is predictive of future motor function
38
prognosis for walking function in SCI
incomplete paraplegia: - increased motor scores between one month and one year - greatest recovery in the first 6 months - at least 10-50 ASIA and 2/5 in hip flexors allowing to ambulate in orthosis and community ambulation
39
five areas of critical concern for SCI management
1. CV: hypotension 2. autonomic dysfunction 3. B&B dysfunction 4. respiratory 5. skin integrity
40
autonomic dysreflexia occurs in pts with injury above what level?
T6 these patients lose supraspinal regulation of autonomic function
41
cause of autonomic dysreflexia
sensory information from irritation gets sent up the SC but can't reach the brain this causes BP vessels to contract which is detected by baroreceptors sending info to brain however brain can't regulate BP with descending control due to SCI
42
s/s of autonomic dysreflexia
sweating severe headache high BP bradycardia arrhythmia skin flush
43
common irritations that can cause autonomic dysreflexia
bladder distension UTI constipation hemorrhoids pressure ulcers restrictive clothing fracture
44
how to address autonomic dysreflexia
sit pt upright address irritant: remove tight clothing check B&B, catheter monitor BP every 2-5 min if systolic BP reaches 150+ needs immediate meds management monitor for at least 2 hours
45
pressure ulcer: steps to address once identified
1. measure 2. stage 3. pressure relief 4. contact med team stage 1 may be appropriate to just provide pressure relief and monitoring
46
Pts with an injury T12 and below will have a spastic or flaccid bladder?
flaccid loss of reflexive/voluntary control and sensation requires catheter
47
Pts with an injury above T12 will have a spastic or flaccid bladder?
spastic increased tone and pressure in bladder
48
level of breathing support needed by spinal cord level
C1-3: vent dependent C4: nighttime ventilation, daytime off C5-T6: need diaphragm strengthening and assisted cough T6-T12: intercostal and diaphragm support
49
heterotrophic ossification
secondary complication of SCI ectopic bone formation caudal to injury caused by inflammatory process with soft tissue trauma
50
s/s of heterotrophic ossification
knee, shoulder, elbow ROM limitation w hard end feel joint warmth/swelling palpation: extra bone growth 53% of SCI pts
51
interventions for heterotopic ossification
early ROM, PROM or AROM NSAIDs to reduce inflammation and prevent Ca deposits Ca prevention: etidronate
52
DVT in SCI pts incidence
17-60% most in 2 weeks after initial injury
53
s/s of DVT in SCI pts
distal LE swelling increased temperature Homan's sign can lead to thrombus breaking free into PE
54
positive sign
a sign where a symptom is present, indicating disease/syndrome/etc
55
negative sign
sign where something is lacking indicating disease/symptoms/etc
56
presentation of spasticity in SCI
not present initially at injury develops in 60-80% of pts aberrant processing of sensory information results in exaggerated central response changes in interneurons in the SC result in reduced presynaptic inhibition mechanical properties of muscle change lack of movement results in less input from muscle spindle to AHC
57
expected functional outcomes: C1-3
vent dependent total assist in: B&B bed mobility transfers pressure relief eating dressing grooming
58
expected functional outcomes: C4
use of: upper traps, diaphragm dependent for: ADLs, mobility nocturnal ventilator operate electric wheelchair w head/chin
59
expected functional outcomes: C5
use of: deltoid, biceps needs assistance w: ADLs, bed mobility, transfers independent w device for feeding electric wheelchair w hand control
60
expected functional outcomes: C6
use of: pec major, lats, SA, wrist extensors can be independent with some ADLs, bed mobility, transfers tenodesis grasp manual WC drive w wheel modifications live independent w support
61
expected functional outcomes: C7-T1
use of: triceps, wrist flexors, finger extensors independent in ADLs, bed mobility, transfer, some grasp, manual WC drive w modifications live independently w equipment
62
precautions when working with SCI pts
stress at fracture site skin integrity BP fall risk overstretching overuse/stress

529 Neuro 2 (16 decks)

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