Spinal Cord Injury Pathology and Acute Management Flashcards
Neuroanatomy: sensory nerve root
impulses about bodily sensations from sensory nerve fibers converge to form nerve roots at the back of the spinal cord
- impulses are conveyed to the brain via nerve fiver tracts
Neuroanatomy: sensory root ganglion
a cluster of nerve cell bodies, connects to sensory spinal root
Neuroanatomy: motor nerve root
bundles of fibers that leave the front of the spinal cord, the fibers conduct impulses from the central nervous system
- control voluntary movement and involuntary processes (like digestion)
Neuroanatomy: meninges
protective connective tissue around the spinal cord
Neuroanatomy: central canal
space where CSF fills to provide nourishment to nerve cells
Causes of a spinal cord injury:
39.2% MVA
14.6% acts of violence
28.3% falls
9.7% other/unknown
8.2% sports
Who is more commonly affected by SCI?
men (80.9%) > women (19.1%)
Common SCI injury sites:
C4, C5, C6
Prevention of SCI
- distraction while driving with phones
- child safety seats
- fall prevention in elderly
- wear your seatbelt
- helmets with bikes/scooter
- watch where you dive when swimming
- don’t dive head first at the beach
Classification of SCI
cervical = tetraplegia
thoracic = paraplegia
lumbar = paraplegia
What did most people expire from in the early 1900s?
respiratory or circulatory problems
What year was the radical shift in medical care?
1970s
What did the radical shift in medical care create?
reductions in complete injuries
- improvements in precautions in the emergency room
- intermittent bladder cauterization for renal failure
What did they use to stabilization unstable spinal cord before the use of vertebral internal stabilization?
stryker frames (bed that patient is tied to that turns used for SCIs and burns)
THINK JOHNNY IN THE OUTSIDERS- HE WAS FLIPPED FACING THE FLOOR
Medical improvements in SCI
- surgical interventions in the 1970s (vertebral stabilization)
- spasticity medications (baclofen, intrathecal baclofen, botox)
- urological management
- lighter wheelchairs
- lightweight orthotics
Types of SCI: traumatic
- rarely complete disruption of the spinal cord
- burst fracture or vertebral body
- usually a younger age
Types of SCI: non-traumatic
- lower incidence of complete SCI
- shorter length of stay
- lower secondary complications
- usually 55+ years
- transverse myelitis
- epidural hematoma
Etiology: direct trauma
- fractured vertebrae
- edema and bone fragments
- vertebral dislocation
Non-traumatic SCI:
Transverse myelitis
- inflammation of the spinal cord
- lesions on the C spine from antibodies when a person becomes sick (virus/bacteria)
- antibodies build up and attack spine
Initial presentation of transverse myelitis
- sharp pain at level of inflammation
- sensory alterations (paresthesia)
- bowel and bladder dysfunction (voiding problems)
- arm and leg weakness
- headache
- nausea/vomiting
Viral etiology of transverse myelitis
- herpes
- enterovirus
- epstein barr
- west nile
- hep B
- measles
- mumps
Bacterial etiology of transverse myelitis
- syphilis
- tuberculosis
- middle ear infection
- GI infections
- tetanus
Inflammatory disorder etiology of transverse myelitis
- sjogren’s
- lupus
- mixed connective tissue disease
- scleroderma
Vascular disorders that cause SCI
- ischemia (anterior or posterior spinal arteries)
- vasculitis of spinal arteries
- vascular malformations (arterial or venous)
Spinal cord compression can be caused by:
- epidural hematoma
- metastasis
- spinal stenosis
Etiology of spinal stenosis
- OA
- DDD/DJD
- facet joint enlargement
- narrow spinal canal
- scoliosis
- spondylolisthesis
- RA
Syringomyelia
fluid within the spinal cord from a cyst grows or distention of the central canal
Phases of a traumatic SCI
acute, cell death, chronic
Traumatic SCI: acute phase
- spinal shock 30-60 mins
- flaccid paralysis
- no DTRs for 24 hrs
Traumatic SCI: cell death phase
- glutamate 6x higher for 15 mins to weeks
- apoptosis
Traumatic SCI: chronic phase
- apoptosis continues days to years
- demyelination
- changes in neural circuitry
- chronic pain
- spasticity
SCI pathology: inflammation acute
0-48 hrs
- 3 levels above and below site
- compression of neural tissue
- hemorrhage
- spinal shock
SCI pathology: subacute
2-14 days
- hemorrhage
- edema
- glial scar tissue
- ischemia
- excitotoxicity
- cytokine number increases
- oxidative stsess
Chronic phase: SCI
- white matter disruption (demyelination axons)
- gray matter disruption
- glial cell cyst formation
- axonal sprouting (regeneration and sprouting after SCI)
What happens to the injured area several weeks after injury?
- damaged tissue is cleared my microglia and macrophages
- a cavity is formed and is filled with fluid
- a glial scar is formed with astrocytes
What does the glial scar do at the injury site?
the scar secretes molecules that inhibit regrowth of severed axons
What is the fluid filled cavity called?
syrinx
- it forms a barrier to the reconnection of the two sides of the damaged spinal cord
What do oligodendrocytes do in an injury?
IN NORMAL BODY - produce neurotrophic factors to support the maintenance of nerve cells
IN SCI - oligodendrocytes are lost due to the toxic environment resulting in loss of myelin and neuronal regeneration
Differential diagnosis of SCI
- spinal epidural hematomas and abscesses may cause acute cord compression
- spinal cord compression from metastatic disease
- aortic artery dissection
- epidural and subdural infections
- syphilis
- transverse myelitis
- acute intervertebral disc herniation
Central cord syndrome
UE deficits are greater than the LE deficits
- LE corticospinal tracts are located lateral in the cord
- the most common incomplete cord syndrome
- frequently in elderly with underlying spondylosis or younger people with severe extension injury (forced extension!!)
- average prognosis
WILL HAVE:
- complete loss of motor function in UE
- incomplete loss of motor function in torso
- UE > LE
- distal muscles > proximal muscles
Anterior cord syndrome
- caused by an extreme flexion injury (flexion tear drop fracture), burst fracture, or herniated disc
- presents with immediate paralysis bc the corticospinal tracts are located on the anterior aspect of spinal cord
- poor prognosis
WILL HAVE:
- loss of motor function below lesion (ipsilateral)
- loss of pain and temp below lesion (contralateral)
- preserved position, touch, and vibration
Posterior cord syndrome
- uncommon
- disruption of dorsal columns
- due to extension injury
- good prognosis
WILL HAVE:
- loss of positioning sense
Brown sequard syndrome
- rotational injury (fracture, dislocation, penetrating trauma)
- hemisection of spinal cord
- extradural compression
- hyperreflexia in weak leg
WILL HAVE:
- ipsilateral motor weakness and decreased joint position/vibration
- contralateral sensory deficit (pain/temp)
What are the 2 things we do for immediate management of SCI?
stabilization and pharmacology/modalities
Immediate management of SCI: stabilization
short term –> traction to stabilize
C SPINE
- surgical = fusion with philadelphia collar
- traction = halo for bone healing 6-12 weeks
T/L SPINE
- internal fixation
- TSLO (thoracic lumbar sacral orthosis)
Immediate management of SCI: pharmacology
NO MEDS
- hypothermia to reduce edema/inflammation (ice packs)
What does hypothermia do for SCI?
- reduces inflammation/edema
- protects against ischemia
- MAY increase complications (pneumonia)
*** not a certain benefit in neurologic recovery/outcomes
Motor recovery prognosis for incomplete lesions
- C spine 2x greater recovery if incomplete
- preservation of sensation at the motor level improves the probability of motor return
- recovery at 72 hours post injury is predictive
Motor recovery prognosis for incomplete lesions: walking function
- increased motor scores between one month and one year
- first six months has the GREATEST recovery
- one month post injury ambulate with orthosis
What ASIA scores are needed to begin ambulation training?
- 10/50 motor score
- at least 2/5 in hip flexors and knee extensors
5 areas of critical concern for the SCI team:
- cardiovascular/hypotension
- autonomic changes
- bowel/bladder dysfunction
- respiratory
- skin integrity
What complications result from autonomic dysfunction?
hypotension and cardiovascular complications
Autonomic dysreflexia
above T6 level is LIFE THREATENING
- loss of supraspinal regulation of autonomic function
- irritation below the point of SCI sends nerve signals up the spine
- nerve signals are blocked at the SCI causing blood vessels to tighten and raise in BP
- brain sends signals to lower BP but but the signals are blocked so other symptoms result (sweating/headache)
Common causes of autonomic dysreflexia
- bladder distention
- UTI
- constipation
- hemorrhoids
- pressure ulcers
- bone fractures
S/S of autonomic dysreflexia
- headache
- high BP
- bradycardia
- sweating
- cardiac arrhythmias
- flushing of the skin
