Spinal Cord Injury - Pathology Flashcards
1
Q
Main causes of SCI
A
39% - MVA
28% - falls
14% - acts of violence
around 17K new injuries happen each year
2
Q
Demographics
A
3k of 17k for disease and congential anomalies
53% are 16-30 y.o
mean age: 40 y.o
sex: men>women
common sites:
- c5 = 14.9%
- c4 - 13.6%
- c6 = 10.8%
3
Q
classification of SCI
A
c4 - tetraplegia
c6 - tetralplegia
t6 - paraplegia
L1 - paraplegia
4
Q
history of SCI
A
- SCI pt usually die from respiratory or circulatory problems
- 70s had radical shift in medical care
5
Q
medical improvements in SCI
A
vertebral stabilizationin the 70s
spasticity meds
urological management
wheelchairs
lightweight orthotics
6
Q
trauma of SCI
A
rarely complete
- usually burst fx of the vertebral body
- happens in younger age
7
Q
non-traumatic of SCI
A
happens in avg, older (55 y.o)
lower incidence of complete SCI
shorter LOS
lower 2dary complications
8
Q
etiology of direct trauma
A
can be fx vertebrae
- can have edema and bone fragments
- fx and vertebral dislocation
9
Q
non-traumatic SCI
A
tranverse myelitis
epidural hematoma
10
Q
tranverse myelitis
A
is the inflammation of the spinal cord
a non-traumatic SCI
11
Q
tranverse myelitis initial presentation
A
- sharp pain at level of inflammation
- paresthesia
- bowel and bladder dysfunction
- voiding problems
- arm and leg weakness
- headache
- N/V
12
Q
virus etiology
A
- herpes
- enterovirus
- epstein barr
- west nile
- Hep b
- measle, mumps
13
Q
bacterial etiology
A
- syphilis
- TB
- middle ear infection
- GI infections
- tetanus
14
Q
inflammatory disorder
A
- sjogren’s
- lupus
- mixed connective tissue disease
- scleroderma
15
Q
vascular disorders
A
ischemia
- anterior or posterior spinal artery
vasculitis of the spinal arteries
vascular malformation
- arterial venous malformation (AVM)
16
Q
spinal cord compression
A
epidural hematoma
- medication
metastasis
- vertebral body and meninges
spinal stenosis
- spinal cord narrowing
17
Q
etiology of spinal stenosis
A
- OA
- DD
- facet joint enlargement
- narrow spinal canal
- scoliosis
- spondylolisthesis
- RA
18
Q
syringomyelia
A
fluid in the spinal cord from cyst growths or distention of the central canal
19
Q
causes of hemorragic SCI
A
from a bleeding disorder or surgical mishaps
20
Q
acute phase of SCI
A
spinal shock for 30-60 min with flaccid paralysis
no DTRs in 24 hours
21
Q
cell death phase of SCI
A
15 min to weeks where glutamate is 6x higher
apoptosis happens
22
Q
chronic phase of SCI
A
days to years: apoptosis still happens
demyelination causing changes in neural circuits
chronic pain and spasticity
23
Q
pathology during acute inflammation
A
0-48 hours
3 levels above and below the site
compression of neural tissue
hemorrhage
SPINAL SHOCK
24
Q
pathology during subacute phase
A
2-14 days
hemorrhage
edema
glial scar tissue
ischemia
25
pathology during **subacute cellular excitotoxicity**
excess glutamate
immune: cytokines
oxidative stress
26
pathology during chronic phase
disruptions of the white matter (demyelination of axons)
gray matter disruptions
glial cell cyst dysfunction
axonal sproating (regen and sprouting after SCI)
27
scar tissue secretion
after weeks from initial injury, area of injury is cleared by microglial causing a fluid-filled cavity that is surrounded by a glial scar made by astrocytes (called syrinx)
the scar secretes molecules that inhibit regrowth of damaged axons
this forms a barrier to the reconnection of two sides of the damanged spinal cords
28
neural connections after syrinx (fluid-filled cavity)
intact motor control and somatosensory
connections and neural cell bodies above and below are not affected
29
function of oligodendrocytes
production of neurotrophic factors which support nerve cell maintenance or survival
30
oligodendrocytes and SCI
they are lost because of the toxic environment
leads to loss of myelin and neuronal regeneration
31
differential diagnosis and SCI
- spinal epidural hematomas
- abscesses can cause acute cord compression
- compression from metastatic disease
- aortic artery dissection
- epidural and subdural infections
- syphilis
- tranverse myelitis
- acute IV hernitation
32
central cord syndrome
most common incomplete cord syndrome
- frequently found in elderly with hidden spondylosis
- found in younger people with severe extension injury
- **prognosis is average**
33
central cord patterns
| S/S
UE > LE
distal > proximal
loss of motor function mid sternum and UE
incomplete motor function of mid-lower trunk
variable sensory loss
34
anterior cord syndrome
flexion injuries like a burst fracture, flexion tear drop fx or herniated disk
immediate paralysis from corticospinal tract affected
35
anterior cord syndrome pattern
loss of motor power, pain, temp
preserved of position, vibration and touch
36
C5-6 tear drop fx
vertebral displacement into the anterior sc cuz of posterior ligament instability
anterior spinal stabilization
37
Burst fx treatment
spinal stabilization
38
posterior cord syndrome
uncommon syndrome because of extension injury
good prognosis
39
posterior cord syndrome pattern
loss of position sense since dorsal columns are affected
40
brown-sequard syndrome
result from rotation injury like fx-dislocation or penetrating truma
41
brown-sequard syndrome pattern
ipsilateral motor weakness and contralateral sensory deficit because SC hemisection
hyperreflexia in the weak leg
42
short term SCI management
traction to stabilize
43
immediate C-spine stabilization
surgical: fusion with philly collar
halo traction: bone healing is 6-12 weeks and let rehab process begin
44
immediate t and l-spine stabilization
internal fixation
thoracic lumbar sacral orthosis
45
immediate SCI pharmacology
none at this time
**hypothermia** to reduce edema and inflammation to protect against ischemia
- has certain benefits in neuro recovery or outcomes
- pneumonia is a possible complication
46
prognosis for motor recovery for incomplete lesions
c-spine: 2x greater in incomplete
preservation of sensation @ motor level helps with probability
recovery @ 72 hours is predicitive
47
prognosis for walking function for incomplete paraplegia
increased motor scores between 1month-1 year
first 6 months is best recovery
one moth post injury: motor scores 10/50 (asia) and 2/5 hip flex and knee ext
walk with orthosis and community ambulation
48
stabilization of anterior and posterior SCI pathology
internal fixation of the bodies
49
stabilization of c-spine fx/dislocation
halo brace
philly collar
thoracolumbarsacral orthosis
50
Five areas of critical concerns for SCI treatment
1. CV hypotension
2. Autonomic changes
3. bladder and bowel dysfunction
4. respiratory
5. skin integrity
requires close attention or can be life threatening if unmanaged
51
autonomic dysfunction
can cause hypotension and other CV complications
52
autonomic dysreflexia
LIFE THREATENING EVENT
above T6 level: loss of supraspinal regulation of autonomic function
53
pathology of autonomic dysreflexia
1. irritation below area of damage and sends nerve signals to the spine
2. nerve signals are blocked by the SCI causes blood vessels to get tight and raise BP
3. brain sends signals to lower BP but is also blocked by SCI causing sx like sweating and severe sweating
54
autonomic dysreflexia hypertension pathology
once hypertension is identified, baroreceptors in the vessels communicate to CN IX, X
CN X will decrease HR
55
common causes of autonomic dysreflexia
bladder distenion (check foley for kinks or overfilled)
UTI
constipation
hemorrhoids
pressure ulcers
restrictive clothing
bone fx
56
signs of autonomic dysreflexia
hypertension
bradycardia
sweating
cardiac arrhythmias
flushing of the skin
57
pt care if theres an episode of autonomic dystreflexia
1. sit pt up (stay seated or upright until BP normalizes)
2. loosen or remove tight clothing
3. monitor BP every 2-5 min
4. check bowel and bladder
5. insert indwelling cath if not in place
6. systolic BP > 150 or systolic BP 40 over base line --> pharmacology management
7. monitor sys and BP for at least 2 hours after episode
58
normal systolic BP of SCI above t6
90-110 mmHg
59
pressure ulcers
big reason of morbidity after SCI
proper skin care and education is important
prevention for individual or caregiver
60
main areas where pressure ulcers form
bony areas
heel
sacrum
trochanter
ischium (base of the buttocks)
61
steps to take with pressure ulcers
1. measure or circle with pen
2. stage if possible
3. remove pressure
4. contact nurse or primary
62
flaccid bladder
t12 and below
loss of reflexive and voluntary control
intermittent catherization (or foley)
63
spastic bladder
above t12
increased tone
increase in bladder pressure
hydronephrosis
64
respiratory management
c1-c3 = ventilator dependent
c4 = variable: nighttime ventilation, daytime off vent
c5-t6 = diaphragmatic strengthening and assisted cough
t6-t12 = intercostal and diaphragm
65
secondary conditions: heterotrophic ossification
ectopic bone formation occurs caudal to the injury
inflammation with trauma to the soft tissue
53% incidence that happens in the first 4 months
hip is a common site + knee, shoulder and elbow
first sign = ROM limitations (hard end feel) + warm joints and/or swelling
66
intervention for heterotopic ossification
early ROM exercises - PROM or AROM
medical management - prevent calcium going into the bone
NSAIDs
calcium prevention: etidronate
66
secondary conditions: DVT
highest after the first 2 weeks of injury
incidence can be 17-60%
thrombus breaks free which turns to a pulmonary embolus
67
s/s of DVT
swelling in distal LEs
increased temp
homan's sign
68
upper motor syndrome - positive signs
positive:
spasticity
babinski sign
mass reflex
clonus
hyperreflexia
spasm
negative:
weakness
69
spasticity of MS
distinct in stroke and MS
not evident right after injury
**60-80%** of SCI eventually get it
aberrant processing in incoming sensory info
- exaggerated central response
- changes in SC interneuron connections with reduced presynaptic inhibition
changes in medical properties of muscle
70
precautions when performing interventions with people with SCI
orthopedic/stress at fx site
skin integrity
blood pressure
fall risk
overstretching
overuse/stress
