Traumatic Spinal Cord Injury
Marnie Quick, RN, MSN, CNRN
A. Pathophysiology/etiology
Normal spinal cord as it relates to SCI
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Spinal cord begins at
the foramen magnum
in the cranium
Cord ends at the L1L2 vertebra level
Spinal nerves
continue to the last
sacral vertebra
Normal protection of spinal cord from
injury:
Bones- vertebral column
Protection of spinal cord from injury
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Disc between
vertebra
Internal and external
ligaments
Protection of Spinal Cord from Injury
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Meninges
CSF in subarachnoid
space allow for
movement within spinal
canal
Normal spinal cord as relates SCI:
Autonomic Nervous System & Cord
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ANS can be affected
by SCI
Sympathetic chains
on both sides of the
spinal column
Parasympathic
nervous system is the
cranial-sacral branch
Normal spinal cord: White tracks send
messages to and from the brain
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Pyramidal- Voluntary
movements
Posterior column
(Dorsal)- touch,
proprioception, and
vibration sense
Lateral spinothalamic
tract- pain and
temperature sensation
(only tract that crosses
within the cord)
Normal spinal cord: Reflex ark in center
of the spinal cord
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Where sensory and
motor nerves arise
from cord
Sensory fibers enter
posterior
Motor fibers leave
from anterior
Once outside cord
join form spinal nerve
Normal spinal cord: Dermatones: skin
innervated by sensory nerves
Normal spinal cord:
Spinal cord level
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When referring to spinal
cord level, it the reflex
arc level not the vertebral
or bone level.
Note that the thoracic,
lumbar & sacral reflex
arcs are higher than were
the spinal nerves actually
leave through the
opening of there
respective vertebral bone
Upper and Lower Motor Neurons
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Upper motor deficits
results in spastic
paralysis
Lower motor deficits
are flaccid paralysis
and muscle atrophy
Etiology of traumatic spinal cord injury
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MVA- most common cause
Other: falls, violence, sport injuries
Typically occurs from indirect injury from
displaced vertebral bones compressing cord
Frequently occurs with head injuries
Less frequent cord torn/cut, as from direct
trauma from knives or bullets
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Hemorrhage/edema occurs secondary in cord post
injury, causing more damage to cord
Extension of cord injury from cord edema can
occur over 1st few days- watch the phrenic nerve!
Initially SCI experience spinal shock- depression
of all cord & ANS function below injury. Lasts
from few min to wks
Risk factors- male, 16-30 yr, risk taker
90% discharged home; 10% chronic care facility
Events leading to spinal cord
ischemia and hypoxia of 2nd injury
Classification of SCI:
1. Mechanism of Spinal Cord Injury
Mechanism of Injury SCI:
Flexion (hyperflexion)
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Most common
because of natural
protection position.
Generally cause neck
to be unstable
because stretching of
ligaments
Flexion with rotation
can also occur
Mechanism of SCI:
Hyperextention
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Caused by chin
hitting a surface area,
such as dashboard or
bathtub
Usually causes
central cord
syndrome symptoms
Mechanism of SCI:
Compression
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Caused by force from
above, as hit on head
Or from below as
landing on butt
Usually affects the
lumbar region
Classification of SCI:
2. Level of skeletal injury
Classification of spinal cord injury3. Level of Injury to the spinal cord
Neurologic level of Injury
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Neurologic level or
the lowest cord
segment (reflex) or
dermatone level
functioning
Such as C6; L4 SCI
Prefix: Para-, quadSuffix:-paresis,-plegia
Classification of SCI: Level of SCI
Neurologic level
Classification 4. Degree of completeness inj:
Complete (transection) spinal cord inj
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After spinal shock:
Motor deficits- spastic
paralysis below level of
injury
Sensory- loss of all
sensation perception
Autonomic deficitsvasomotor failure
(orthostatic hypotension,
poikilothermic) and
spastic bladder
Classification of SCI:
Incomplete spinal cord injury- what white
tracks are working after spinal shock is over?
Classification of SCI: Degree of completeness
Incomplete spinal cord injury
Incomplete spinal cord injury:
Central cord Syndrome
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Injury to the center of
the cord by edema
and hemorrhage
Weakness in both
upper extremitieslegs are spared
Varied loss of
sensation
Incomplete spinal cord injury:
Anterior Cord Syndrome
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Injury to anterior cord
Loss of voluntary
motor (Pyramidal
track) below
Loss of pain and
temperature
perception
Retains posterior
column function
Incomplete spinal cord injury:
Brown-Sequard Syndrome
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Hemisection of cord
Ipsilateral paralysis
Ipsilateral superficial
sensation, vibration
and proprioception
loss
Contralateral loss of
pain and temperature
perception
Classification of SCI:
5. American Spinal Injury Association
Impairment Scale
Clinical Manifestations & Complications
Spinal Cord Injury
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Depends on extent and
level of injury
Higher cord injury more
serious sequelae
Resp: decrease chest
expansion (intercostals);
decrease cough reflex &
Vital capacity; diaphragm
function controlled by
phrenic nerve (C3-5);
may need mechanical
ventilation
Clinical Manifestations & Complications
Spinal Cord Injury continued
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Cardio: dysrhythmias; bradycardia; loss SNS
control bl vessels spinal shock; loss of
sympathetic nervous system control over blood
vessels (vasomotor control)- dec venous return,
orthostatic hypotension; dec CO; poikilothermic
(takes on temp of room)
GU: upper/lower motor bladder; impotence;
sexual dysfunction
GI: stress ulcers; paralytic ileus; bowelimpaction & incontinence
Clinical Manifestations & Complications
Spinal Cord Injury continued
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Skin: pressure ulcers can lead to infection/sepsis
Thermoregulation: poikilothermic (take on temp
of environment) Unable to sweat or shiver below
level of SCI. Occurs due to SNS interruption;
Degree depends level inj
Metabolic needs: Nasogastric suctioning may
lead to metabolic alkalosis (Paralytic ileus).
Nutritional needs to deep body wt and prevent
complications- need positive nitrogen, highprotein diet
Peripheral vascular: DVT; pulmonary embolism
Clinical Manifestations & Complications
Spinal Cord Injury continued
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Neuro: pain at the level of injury; sensory
loss; upper/lower motor deficits; autonomic
dysreflexia; spinal shock
Musculoskeletal: joint contractures; bone
demineralization; osteoporosis; muscle
spasms; muscle atrophy; pathologic
fractures; para/tetra/Quad; plegia/paresis
Spinal shock: result of inflammatory process in cord
after injury, causing depression of cord & ANS
function below level of injury. Approx 50% develop
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Motor loss- flaccid paralysis below level injury
Sensory loss- loss touch, pressure, temperature
pain and proprioception perception below injury
Sympathetic NS loss results in parasympathic
dominance with vasomotor failure
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Neurogenic shock, bradycardia, orthostatic
hypotension and poor temperature control
(poikilothermic- takes on temp of environment)
Parasympathetic NS loss of the S 2,3,4 reflex arks
results in flaccid bladder
Distributive shock symptoms
Spinal shock lasts from few minutes to wks
How do you know spinal shock is over?
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Clonus is one of the
first signs
Hyperreflexia of foot
Test by flexing leg at
knee & quickly
dorsiflex the foot
Rhythmic oscillations
of foot against hand
Common manifestations&complications:
Functional Goals for Spinal Cord Injury
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C1-3 usually fatal- loss phrenic inervation;
ventilator dependent; no B/B control; spastic
paralysis; electric w/c with chin/mouth control
C6- weak grasp; has shoulder/biceps to transfer &
push w/c; can use assistive devices; dec resp
reserve; loss vasomotor; no bowel /bladder
control.
T1-6- full use of upper extremity; transfer; drive
car with hand controls and do ADL’s; dec trunk
stability; no bowel/bladder control
C6 SCI using a transfer board
Collaborative Care for SCI:
Diagnostic tests
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Comprehensive neuro
exam
X-ray of spinal
column
CT/MRI
Blood gases
Collaborative Care:
Emergency care at scene, ER & ICU
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Initial goals- sustain life
and prevent further cord
damage
Transport with cervical
collar
Assess ABC’s; O2;
tracheotomy/vent
IV for life line- to give
meds
NG to suction
Foley- flaccid bladder
Collaborative Care: Stabilization &
immobilization with traction
Collaborative Care:
Gardner-Wells tongs
Collaborative Care:
External traction
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Halo device
For patients who have
few motor deficits
Experience less
immobility
complications
Collaborative Care:
Casts; splints; collars; braces
Collaborative Care:
Special Beds for SCI
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To decrease
immobility
complications
Rotorest bed provides
for lateral rotation
23 hrs a day
Collaborative Care: Surgery for SCI
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Manipulation to
correct dislocation or
to unlock vertebrae
Decompression
laminectomy
Spinal fusion
Wiring or rods to
hold vertebrae
together
Collaborative Care:
Drug Therapy
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IV metylprednisone (Solu-Medrol) within 8 hrs to
decrease cord edema/inflammation
Medications to control or to prevent
complications SCI and immobility:
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Vasopressors treat bradycardia or hypotension
Histamine H2 blockers to prevent stress ulcers
Anticoagulants- immobility
Stool softeners
Antispastomotics
BP meds (Procardia) if sym persists with autonomic
dysreflexia
Nursing Assessment Specific to SCI
Lewis 1553 Table 61-6
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Subjective data:
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Important health info- health history; cause of SCI
Function health patterns-activity; perceptual;coping
Objective data:
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By systems
LOC/pupils- R/O head injury
VS- bradycardia
Motor & Sensory
Clonus & spontaneous movement
Nursing assessment:
Motor assessment
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Movement, strength
and symmetry
Hand grips
Flex and extend arm
at elbow- with and
without resistance
Nursing assessment:
Motor assessment lower extremity
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Flex and extend leg at
knee with and without
resistance
Planter and dorsi
flexion of foot
Nursing assessment:
Motor assessment- Clonus
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Clonus- hyperreflexia
Flex knee and quickly
dorsiflex the foot with
your hand
If has return of reflex
function the foot will
have repetitive
movements against you
hand
Spinal shock is over
Nursing assessment:
Sensory assessment
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With the sharp and
dull ends of a Q-tip or
paperclip have the
individual, with their
eyes closed identify
Use the dermatome as
reference to identify
level
C6 thumb; T4 nipple;
T10 naval
Pertinent Nsg problems/intervention SCI
Lewis p.1554-5 NCP: 61-1
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Impaired gas exchange
Decrease CO
Impaired skin integrity
Constipation
Impaired urinary elimination
Risk for autonomic dysreflexia
Ineffective coping
Interrupted family process
Pertinent nursing problems/interventions
Acute intervention: Immobilization
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Log roll as a single unit; provide assistance as
needed to keep alignment; teach patient
Care traction, special beds, collars, splints,
braces, assistive devices for ADL’s
Flaccid paralysis- use high top tennis shoes or
splints to prevent contractures. Remove at least
every 2 hrs for ROM (active ROM best)
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Spastic paralysis- assess for clonus
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Prevent spasms by avoiding; sudden movements or
jarring of the bed; internal stimulus (full bladder/skin
breakdown; use of footboard; staying in one position
too long; fatigue
Treat spasms by decreasing causes; hot or cold
packs; passive stretching; antispasmotic medications
Assess skin break down & thrombophlebitis;
remove TED hose at least every shift
Pertinent nursing problems/interventions
Respiratory
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Phrenic nerve; thoracic
and intercstal nerves;
abdominal muscles
Monitor vital capacity,
respiratory effort, ABG’s,
O2 saturation, need for
ventilator assistance
Assess for signs of
impending extension of
SCI up cord to phrenic
nerve level (C3-5)
Quad cough (assistive
cough) as needed
Pertinent nursing problems/interventions
Acute intervention: Cardio/nutrition
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Cardiovascular instablity
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Prevent/treat orthostatic hypotension
Abdominal binder, calf compressors, TED hose when
individual gets up
Assess BP, especially when rising
Assist Physical Therapy with tilt table as individual
gradually gets use to being in an upright position
Fluid and nutritional maintenance
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NG to suction in acute; monitor F&E
High protein/high calorie diet
Pertinent nursing problems/interventions
Acute intervention: Bladder
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Bladder reflex ark- sacral 2,3,4
Flaccid bladder (lower motor neuron lesion) has
no reflex from S2,3,4. Have automatic empting of
bladder. Urine fills the bladder and dribbles out.
Need foley or freq intermittent self catherization
Spastic bladder (upper motor neuron lesion) has
reflex ark, but no connection to or from brain.
Reflex fires at will. Bladder training- trigger
points to stimulate empting; self catherization
Upper/lower motor bladder-Website
http://www.rnceus.com/course_frame.asp?exam_id=56&directory=uro
4. Autonomic Dysreflexia
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SCI above T6
Results in loss of normal
compensatory
mechanisms when
sympathetic nervous
system is stimulated
Life threatening- if goes
unchecked BP can result
in cerebral hemorrhage
Autonomic Dysreflexia- assess
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Vasodilatation
symptoms above SCI
Vasoconstriction
symptoms below SCI
The cause of SNS
stimulation
Autonomic Dysreflexia- treatment
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Elevate head of bed- causes orthostatic
hypotension
Identify cause/alleviate- if full bladder- cath; if
skin- remove pressure, if full bowel- empty, etc
Remove support hose/abdominal binder
Monitor blood pressure- can get > 300 S
Give PRN medication to lower BP
If above not effective– call physician
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Use bladder scan to see amount of urine in
bladder
Goal- residual <100ml/20% bladder capacity
Some individuals may need suprapubic catheter
Assess effectiveness of medication
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Urecholine to stimulate the parasympathic S 2,3,4
reflex to fire and cause bladder contraction
Urinary antiseptic
Pertinent nursing problems/interventions
other
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Bowels
Temperature control
Stress ulcer
Sensory deprivation
Reflexes- may see hyperreflexia as return of
motor function
Rehabilitation and home care: Resp; neurogenic
bladder/bowel; skin care; sexuality;
grief/depression
Bowel
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Bowel rely more on bulk than on nerves
Stimulate bowels at the same time each day. Best
after a meal when normal peristalsis occurs
Individual may progress from ducolax
suppository to glycerin then to gloved finger for
digital stimulation
Assess bowel sounds prior to giving food for the
first time– paralytic illus!
Sexual dysfunction
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Assess readiness/knowledge/your ability
Male sexual function- reflexogenic (S2,3,4)
erections; psychogenic erections (psychological
stimulation) Ejaculation/fertility may be affected
Female- hormones more than nerves regarding
fertility. C-section because of chance for
autonomic dysreflexia during labor. Lack of
sensation/movement affects sexual performance
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Suggestions: empty bladder before sex; withhold
fluids and antispasmodics; certain positions may
increase spasms; explore new erogenous zones;
penile implants
Low self-esteem
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Assess thoughts on ‘quality of life’; body image;
role changes
Physical and psychological support
Most common SCI is 15-30 yeas old and
generally a risk taker– this greatly affects their
perception of life and rehabilitation progress
Home care
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Assess psychological, physical resources, need
for rehabilitation (in-house or outpatient); need
for community resources
Home evaluation