Spinal Cord Injury Flashcards
(35 cards)
What is the most common cause of traumatic SCI?
MVA (40.4%)
How are they classified?
Traumatic or non-traumatic
Mechanisms of injury
Flexion (most common in lumbar injury)
Flexion-rotation (most common in cervical injury)
Axial compression
Hyperextension
Penetrating injuries
Spinal shock
A transient period of areflexia immediately following SCI
Approximately 24 hours
Hypotension, loss of control of sweating
Goosebumps
Will eventually lead to hyper reflexia (UMN S&S)
Tetraolegia
All four extremities
Lesions of Cx SC
56%
Paraplegia
Tx Lx L2 (caudal equina)
46%
How is SCI standardized
international standards for neurological classification of SCI *ISNCSCI
Neurological level of injury
Most caudal level of SCI level with INTACT motor and sensory fxn
Motor and sensory level
Most caudal level Intact
Complete and incomplete SCI
Complete is every paralysis below neurological level
Incomplete are those with some persevered function (zones of partial preservation)
ASIA impairment scale
A- complete
B- incomplete: has sensory
C- incomplete: has sensory and motor but muscle grade is less than 3
D- incomplete: has sensory and motor but muscle grade is more than 3
E- normal
Clinical syndromes
Incomplete
- brown-sequard
- anterior cord
- central cord
- posterior cord
Other
- conus medullaris
-caudal equine
Brown- Sequard syndrome
Damage to one half of the spinal cord (usually penetrating injury)
Ipsilateral loss of:
- all sensory modalities at the level of lesion
- motor function (descending: lateral corticospinal tract)
- proprioception, discriminative touch, and vibratory sense (ascending- dorsal column)
Contrateral loss:
- pain and temperature (spinalthalamic tract)
Anterior cord syndrome
Commonly due to flexion injuries
Loss of motor fxn, pain and temp below level of lesion
Central cord syndrome
Hyperextension in Cx- compressive forces cause edema
Loss of motor > sensory
motor loss UL>LL
Posterior cord syndrome
Loss of proprioceptions, pressure, and vibratory sense
NO motor loss
Caudal Equina
Damages to the nerve roots below L1
Flaccid paralysis
LMN injury, areflexive bowel/ bladder, and sacral anesthesia
Autonomic Dysreflexia
Sympathetic over activity in the body
Typically in lesions above T6
EMERGENCY SITUATION
Pathophysiology of autonomic dysreflexia
Noxious stimulus, increased sympathetic outflow, wide spread vascoconriction (Increase HR an BP), basorecetirs stimulate increase in fatal output causing decreased HR, but insufficient to counteract Increased BP
Most common triggers of AD
Bladder and bowel distenson/irritation
Lots more
AD S&S
Hypertension
Initial tachycardia but then bradycardia
Severe headache
Profuse sweating
Increased spasticity/ hypertonia
THERES MORE
AD interventions
Sit patient up to decrease BP
Notify nearby nurse or doc
Check catheter for kink, block or fullness
Loosen tight clothing
Look for other potential noxious stimulus below NLI
Document
Functional outcomes: NLI C1-4
Most severe
Paralysis of arms, hands, trunk and legs
Require assistance with breathing and secretion clearance
Dependent in all ADLs
Dependent in transfers
Power wheelchair
Functional outcomes: NLI C5
Can breathe but labored because lack of abdominal tone so no diaphragm counterpressure
Dependent in transfers
Manual wheelchair with propulsion aids for short distances
Can drive a van using adaptive hand controls
Power wheelchair with adapted joystick for communities