Module 7: Neurosensory Disorders: Traumatic Spinal Cord Injury
Marnie Quick, RN, MSN, CNRN
Etiology/Pathophysiology of Spinal Cord Injury
1. Normal spinal cord physiology as it relates to spinal cord injury. (Lewis 1446 Fig 565; 56-6;1449 Fig 56-11)
a. Cord begins at foramen magnum; ends L1-L2 vertebra level.
b. Spinal cord is protected by vertebral bones with discs in-between vertebral
bodies for flexibility, internal/external ligaments that hold the vertebra in
place, meninges surround cord (including tough dura that is difficult to
penetrate), and cerebral spinal fluid flows in the subarachnoid space that
allows movement of cord.
c. Autonomic nervous system- Sympathetic chains on both sides of the spinal
column; parasympathetic cranial-sacral branches.
d. Cord is composed of white tracts that send sensory and motor messages to
and from the brain. (Lewis 1446 Fig 56-5)
1)
Pyramidal tract- voluntary movement (crosses in medulla)
2)
Posterior columns (Dorsal)- touch, proprioception, vibration
3)
Lateral spinothalamic tract- pain and temperature (only tract that
crosses within the cord)
e. Gray matter in the center (‘H’ shape) is composed of cell bodies for the reflex
arcs that leave the spinal cord to the rest of the body (sensory-posterior and
motor- anteriorly) through the opening in vertebra (Lewis 1446 Fig 56-5; 566)
f. Dermatomes- Skin innervated by the spinal nerve. It is also helpful in
understanding motor innervations. (Lewis 1593 Fig 61-9)
g. When referring to spinal cord level, it is the reflex arc level not the vertebral
or bone level. Note that the lower (thoracic/ lumbar) reflex arcs are higher
that where the spinal nerves actually leave through the opening in their
respective vertebral (Lewis 1446 Fig 56-5)
h. Upper/lower motor neurons (Lewis 1445)
1)
Upper motor neurons describe the motor neurons located in the
brain and descend down the white tracts into the spinal cord to
just before the anterior horn cell in the reflex arc. Damage or
interruption to upper motor neurons result in spastic paralysis and
hyperreflexia.
2)
Lower motor neurons are the motor neurons located in the anterior
horn cell of the reflex arc of the spinal cord, motor nuclei of the
brainstem and the axons that end in the motor end plate of the
skeletal muscles. Damage or interruption of lower motor neurons
result in flaccid paralysis, muscle atrophy and hyporeflexia
2. Etiology of traumatic spinal cord injury
a. Most SCI caused by MVA (50%). Also caused by falls, violence
(bullets/knives), sport injuries.
b. Cervical and lumbar regions usually areas injured- most flexible area
c. Injury to the cord typically occurs from indirect injury from displaced
vertebral bones compressing the cord. Also interruption of blood supply to
cord and traction resulting from pulling the cord. Less frequently is the cord
torn or cut because of the tough dura surrounding it, but may occur with
gunshot or knife. SCI, especially cervical, frequently occur with head injuries.
d. Hemorrhage, edema, ischemia and vasospasm occur in the cord post injury,
causing secondary damage to the cord. It is progressive and may not know
extent of cord damage till 72 hrs post SCI. (Lewis 1590 Fig 61-4)
e.
3.
4.
5.
6.
7.
Extension of the cord injury from edema can occur over the first few
days. In cervical SCI- watch for phrenic nerve (C3,4,5) involvement!
f. Spinal shock- approx 50% of SCI individuals initially experience spinal shock.
It is the temporary depression of all cord (reflexes, sensory and motor
function) & autonomic nervous system function below level of spinal cord
injury. (See below clinical manifestations/complications)
g. Risk factors- male 16-30 yr age, risk taker. Seeing more females as they
become more active and involved with sports. 78% are male, most common
age is 19.
Prognosis:
a. Five years less than individuals without SCI
b. Death usually related to respiratory
c. 90% discharged to home; 10% nursing home or chronic care facility
Classification of SCI: Mechanism of Spinal Cord Injury (Lewis 1591 Fig 61-5)
a. Flexion (hyperflexion) - normal protective position is flexing the body/head.
b. Flexion-rotation- Generally causes unstable fractures because the ligaments
are stretched or torn. Severe neuro deficits usually result.
c. Hyperextension- caused by the chin hitting a surface area, such as a
dashboard or bathtub.
d. Compression- caused by force from above (hit on top of head) or below
(landing on butt, or feet from a tall building) usually lumbar region.
Classification of SCI: Level of skeletal injury means which vertebral bone is injured.
a. Spinal cord reflex arcs are higher than vertebral level, except for the cervical
vertebra, that comes straight off the cord arc.
Classification of SCI: Level of spinal cord injury (Neurological level). (Lewis Fig 61-6)
a. The lowest cord segment (reflex arc) or dermatome level functioning
normally on both sides cord- as C6; L4; etc. (Lewis 1592 Fig 61-6 and 1593
Fig 61-9)
Classification of SCI: Degree of completeness of cord injury after spinal shock
a. Complete spinal cord injury- totally damaged cord horizontally and post
spinal shock the individual will have:
1)
Motor deficits- hyperreflexia/spastic paralysis below the level of
injury.
2)
Sensory deficits- loss of touch pressure, temperature, pain,
vibration and proprioception from below the level of injury.
3)
Autonomic deficits- vasomotor failure resulting in orthostatic
hypotension, poikilothermic (take on the temperature of the
environment); and parasympathetic spastic bladder
b. Incomplete spinal cord injury- various white tracts damaged at the level of
spinal cord injury. (Lewis 1591 Fig 61-5)
1)
Central Cord Syndrome- injury to the center of the cervical cord by
edema and hemorrhage; usually cord is compressed between
vertebra; weakness in both upper extremities- legs are not
affected as much; varied loss of sensation.
2)
Anterior Cord Syndrome- injury to the anterior part of the cord;
usually caused by injury to anterior spinal artery; loss of motor
(Pyramidal tract) below the level of injury; loss of pain and
temperature below the level of injury; retains the posterior column
function- touch, vibration and proprioception.
3)
Brown-Sequard Syndrome- hemisection of the cord (injury to ½
cord); ipsilateral paralysis (pyramidal tract) on the same side as
spinal cord injury; ipsilateral superficial sensation, proprioception,
and vibration loss; contralateral loss of ability to get information
regarding pain and temperature to the brain from below the level
of cord injury. The lateral spinothalamic white tract is only major
white tract that crosses within the cord segments, rather than in
the medulla.
4)
Posterior Cord Syndrome- Posterior columns affected, therefore,
direct touch, proprioception, and vibration sense are not
functioning.
5)
Cauda equina Syndrome- lowest part of cord- flaccid paralysis of
lower extremity with areflexic bladder
8. Classification of SCI: American Spinal Injury Association Impairment Scale (ASIA)
Used for classifying severity of impairment resulting from spinal cord injury (Lewis
1592 Fig 61-7; 1593 Fig 61-9)
Clinical Manifestations/Complications of Spinal Cord Injury
1. Immediate post injury- Depends on extent and level of injury;
sensory/motor/autonomic deficits; airway/ventilation difficulty; blood volume
changes; cord extension from secondary edema/bleeding
2. The higher the cord injury the more serious the sequelae
3. By body systems
a. Respiratory: decrease chest expansion (intercostals); decrease cough reflex
and vital capacity; diaphragm function controlled by phrenic nerve (C3-5);
may need mechanical ventilation.
b. Cardio: Bradycardia; loss of sympathetic nervous system control over blood
vessels (vasomotor control) decrease venous return, orthostatic hypotension;
decrease CO; decrease blood return to heart
c. GU: upper/lower motor bladder; impotence; sexual dysfunction
d. GI: stress ulcers with bleeding (decreased hemoglobin and hematocrit;
continued hypotension despite treatment; expanding girth); paralytic ileus;
gastric distention; bowel- impaction & incontinence.
e. Skin: pressure ulcers which can lead to infections/sepsis
f. Thermoregulation: poikilothermic (take on temperature of the environment).
Unable to sweat or shiver below level of SCI. Occurs because SNS
interruption prevents peripheral temperature sensations from reaching
hypothalamus. Degree depends on level of cord injury.
g. Metabolic needs: Nasogastric suctioning may lead to metabolic alkalosis.
Nutritional needs to keep body weight and prevent complications- positive
nitrogen and high-protein diet.
h. Peripheral vascular: DVT; pulmonary embolism (a leading cause of death)
i. Neuro: pain at the level of injury; sensory loss; upper/lower motor deficits;
autonomic dysreflexia
j. Musculoskeletal: joint contractures; bone demineralization; osteoporosis;
muscle spasms; muscle atrophy; pathologic fractures; para/tetraplegia
(paralysis) or paresis(weakness).
4. Spinal shock
a. Approx 50% of SCI experience spinal shock and is characterized mainly by
flaccid paralysis and loss of sensation.
b. Spinal shock is the result of inflammatory process in the cord after injury and
causes depression of spinal cord and autonomic nervous system function
below the level of spinal cord injury. It lasts from a few minutes to months
and results in:
1)
Motor loss results in flaccid paralysis below the level of spinal cord
injury.
2)
Sensory loss results in loss of touch, pressure, temperature, pain
and proprioception below the level of spinal cord injury.
3)
Sympathetic nervous system loss results in parasympathetic
domination with vasomotor failure. This causes neurogenic shock,
bradycardia, orthostatic hypotension, and poor temperature
control. There is no vasomotor response to environmental
temperature changes including loss of ability to perspire below
injury and the individual becomes poikilothermic- (individual takes
on the temperature of the environment).
4)
Parasympathetic nervous system loss at the S 3,4,5 reflex arks
results in flaccid bladder.
c. The effect on the sympathetic nervous system is neurogenic (distributive)
shock causing peripheral vasodilation, venous pooling and decreased cardiac
output.
d. After spinal shock is over then the individual may recover or be left with
either complete or incomplete cord injury. Reflexes begin to return such as
spontaneous empting of the bladder and clonus (hyperreflexia). Clonus is the
first sign that spinal shock is over. (See assessment)
5. Upper and lower motor neuron deficits
a. See above ‘Etiology/pathology’ section.
6. Terms used:
a. Prefix: para- two extremities affected; tetra- (or quadra-) all four extremities.
b. Suffix: -paresis meaning weakness; -plegia meaning paralysis.
c. Therefore tetraplegia means all four extremities paralyzed.
7. Functional goals expected of complete lesion by cord segments: (Lewis 1594 Table
61-3)
a. C1-C3 spinal cord injury- usually fatal because loss of the phrenic nerve
inervation (C3,4,5) and breathing stops; can use electric wheel chair with
chin/mouth control; uses portable ventilator; no vasomotor control below
lesion- loss of ability to control temperature and orthostatic hypotensionvagus domination; no bowel or bladder control. Bladder usually spastic UMN
type. 24 hr care.
b. C6 spinal cord injury- has weak grasp, but have use of shoulder/biceps to
transfer & push wheel chair; can use assistive devices; has a decrease
respiratory reserve (intercostals); loss of vasomotor control; no bowel or
bladder (spastic) control. This is the level that is considered the ‘level of
independence’ for a spinal cord injured individual.
c. T1-T6 spinal cord injury- has full use of upper extremity to transfer, drive car
with hand controls and do ADL’s; decreased trunk stability; no bowel or
bladder control- spastic.
d. Prognosis for life- 5 years less than without SCI. Cause of premature death
usually respiratory complication.
e. 90% discharged to home.
Collaborative Care for Spinal Cord Injury
1. Diagnostic tests- X-ray of the spinal column for vertebral fracture; CT/MRI; blood
gases if respirations compromised; comprehensive neuro exam.
2. Initial goals- sustain life and prevent further cord damage.
3. Emergency care- Assessment & Interventions see Lewis 1596 Table 61-4
a. Transport with cervical collar; preserve cord function; O2
b. Assessment of ABC’s- NVS; maintain BP; possible tracheotomy/ventilator
c. IV for life line- to give drugs
d. NG tube to suction- may have paralytic ileus
e. Foley for flaccid bladder from spinal shock
4. Treatment- nonoperative stabilization (Lewis 1601 Fig 61-10; 61-11; 61-12)
a. Stabilization/immobilization- traction (Gardner-Wells tongs)/external traction
(Halo)/casts/splints/collars or brace
b. Special beds- kinetic bed, Rotorest, air; etc- to decrease immobility
complications
5. Treatments- Surgical Therapy:
a. Manipulation to correct dislocation or to unlock vertebrae (facet part of
vertebra gets subluxed)
b. Decompression laminectomy (Refer to Module 8 HNP)
c. Spinal fusion (refer to Module 8)
d. Wiring or rods to hold vertebrae together
6. Treatment- Drug Therapy:
a. IV metylprednisone (Solu-Medrol) within 8 hrs of spinal cord injury to
decrease cord edema/inflammation.
b. Medications to control or to prevent complications from lack of nerve
innervations and immobility; such as
1) Vasopressors to treat bradycardia, hypotension, maintain mean
arterial pressure
2) Histamine H2 blockers to prevent stress ulcers
3) Anticoagulants- immobility
4) Stool softeners decreased bowel function/immobility
5) Antispasmodics for muscle spasms- Dantium
6) BP meds (as Procardia) is symptoms persist with autonomic
dysreflexia
Nursing Assessment Specific to Spinal Cord Injury
1. Subjective and objective data (Lewis 1597 Table 61-6) plus the following:
a. Cognitive-perceptual, coping-stress tolerance
b. By systems- clinical manifestations- see above
c. LOC and pupils- may have indirect SCI from head injury
d. Respiratory status- phrenic nerve (diaphragm) and intercostals (thoracic
and abdominal muscles); lungs sounds
e. Vital signs- bradycardia problem with cervical injury
f. Motor- movement, strength and symmetry. Hand grips; with and without
resistance have individual flex and extend arm at elbow; flex and extend leg
at knee; dosi and planter flex feet. Check for clonus (shows return of reflex
arc- spinal shock over) by flexing the patient’s leg at knee, quickly dorsiflex
the foot with your hand. Clonus causes the foot to have repetitive
movements against your hand. Note spontaneous movement
g. Sensory- With eyes closed and with the sharp and dull ends of a broken
cotton tip applicator (pain) and soft end (touch) have the individual, with
their eyes closed identify. Use the dermatomes as reference to identify
level. C6= thumb; T4= nippleline; T10= naval
h. Proprioception- With eyes closed, move big toe up and down- stop- ask
patient if big toe is up or down
i. Bowel and bladder function
j. Other injuries?
Pertinent Nursing Problems and Interventions for SCI (Nursing Process)
1. Nursing diagnosis (Lewis 1598-1600 Nursing Care Plan 61-1)
a. Impaired gas exchange
b. Decreased cardiac output
2.
3.
c. Impaired skin integrity
d. Constipation
e. Impaired urinary elimination
f. Ineffective physical mobility
g. Risk for autonomic dysreflexia
h. Ineffective coping
i. Interrupted family process
Health promotion
Acute intervention
a. Immobilization- Also add:
1. Body should always be aligned; log rolling
2. Traction- apply principles and provide nursing care of patient with
traction.
3. Braces (cervical and body) and special beds (kinetic bed).
4. Flaccid paralysis- High top tennis shoes or splints to prevent
contractures. Remove frequently to perform ROM (active when
possible)
5. Spastic paralysis- (assess for clonus)
a. Prevent spasms by avoiding: sudden movements or jarring
of the bed; internal stimulus (full bladder/skin infections);
use of footboard; staying in one position too long; fatigue
b. Treat spasms by decreasing causes; using a hard hand roll
or hand splints; hot or cold packs; passive stretching;
antispasmodic medications such as Dantrium
b. Respiratory dysfunction- also add:
1. Phrenic nerve (C3-5) controls the diaphragm bilaterally (if
nonfunctioning individual is ventilator dependent); thoracic nerves
control the intercostals muscles for breathing; abdominal muscles aide
in coughing.
2. Monitor vital capacity, respiratory effort, and arterial blood gases.
Assess for possible respiratory infection or arrest.
3. Assess signs of impending extension of spinal cord injury up the cord to
the phrenic nerve level (C3-5) esp during first 48 hrs
4. Quad cough (assistive cough)- as individual attempts to cough, push
with your hand in and up from the area between the individuals
umbilicus and the xiyphoid process. (similar to Heimlich maneuver.
(Lewis 1809 Fig 68-6)
c. Cardiovascular instability- Also add:
1. Prevent/treat orthostatic hypotension by the use of abdominal binder,
calf compressors, and/or TED hose.
2. Unopposed vagal response; vagal stimulation- cardiac arrest
3. Assess BP, especially when rising.
4. Assist Physical Therapy with tilt table- A table (similar to a stretcher with
a foot board) that allows for PT to raise the head by degrees and
assesses the patients blood pressure. The SCI patient’s blood pressure
gradually gets used to being in an upright position before getting into a
chair.
d. Fluid and nutritional maintenance
1. May have a nonfunctioning GI tract first 48-72 hrs, therefore may need
NG to suction.
2. Monitor fluid/electrolytes
3. As soon as possible high protein/high calorie diet
e. Bladder and bowel management- Also add:
1. Bladder
1) Reflex arc for both bladder function and male errection is Sacral 2,
3, 4.
2) Flaccid bladder (lower motor neuron lesion) has no reflex from
S2,3,4; therefore no automatic empting of bladder. Urine fills the
bladder and dribbles out (incontinence) Use foley, external catheter
or intermittent self catherization.
3) Spastic bladder (upper motor neuron lesion) has reflex ark, but no
connection to or from the brain. Reflex fires at will. Bladder training
for this individual is directed toward ability to empty bladder at a
socially accepted time and place. Use the trigger points (stroking
down inner aspect of thigh, across lower abdomen, pulling pubic
hair) to stimulate parasymathic reflex arc S 2,3,4.
4) Use a bladder scan to see amount of urine in bladder (residual or
otherwise).
5) Some individuals may need suprapubic catheter.
6) Assess effectiveness of medication (such as Urecholine) to stimulate
bladder contraction and effectiveness of urinary antiseptic.
b. Bowel
1) Bowels rely more on bulk than on nerves.
2) Stimulate bowels at the same time each day. Best after a meal
when normal peristalsis occurs.
3) Individual may progress from Dulcolax suppository; to glycerin
suppository; then to gloved finger for digital stimulation
4) Assess bowels sounds prior to giving food for the first time, may
have a paralytic illus.
f.
Temperature control
1. Poikilothermic
2. Monitor environment and body temperature
g. Stress ulcer
1. Physiologic response to severe trauma
2. High-dose corticosteroids
3. 6-14 days post SCI
h. Sensory deprivation
1. Stimulate patient above cord level
2. Prism glasses
3. Keep patient social
i. Reflexes
1. Others, family or individual, may see hyperreflexia as return of
‘normal’ functioning, when in fact it may be clonus post spinal shock.
j. Autonomic Dysreflexia(autonomic hyperrflexia)(Lewis1604 Table 61-7)
1. Occurs in some patients with spinal cord injury above T6 and after
spinal shock is over.
2. Results in loss of normal compensatory mechanisms when
sympathetic nervous system is stimulated.
3. Stimuli include: full bladder (most common), fecal impaction (next
most common), pressure ulcers, labor contractions, etc.
4. When patient recognizes symptoms early may be helpful in bladder
training, because it tells the individual that the bladder needs
emptying. Will feel beginning symptoms before severe hypertension.
5. However, it is considered life threatening- if autonomic dysreflexia
goes unchecked the blood pressure rises and can result in cerebral
hemorrhage- death. (BP may go as high as 300/160)
6. Symptoms:
a. Vasodilatation symptoms above the level of spinal cord
injury- sweating flushed face, nasal congestion,
headache, etc.
b. Vasoconstriction symptoms below the level of spinal
cord injury- cool, pale skin, etc.
7. Treat:
a. Elevate head of bed (causes orthostatic hypotension)
b. Assess for cause and alleviate- if full bladder- cath; skinremove pressure, assess bowels- empty, etc.
c. Remove support hose/abdominal binder
d. Monitor blood pressure
e. Give PRN medication to lower blood pressure- Diazoxide
(Hyperstat); PRN ganglionic blocking agents- nifedipine
(Procardia) or hydralazine (Apresoline).
f. Notify MD, if above not effective
k. Rehabilitation and home care
1. Respiratory- IS; assisted cough; ventilator care
2. Neurogenic bladder- residual urine; infections
3. Neruogenic bowel- hi fiber diet; adequate fluid; digital stimulation
4. Neurogenic skin- prevention of pressure ulcers; thermal injury
5. Sexuality- Also add:
a. Assess readiness/knowledge
b. Male sexual function- reflexogenic (reflex arc- S2,3,4) erections;
psychogenic erections (psychological stimulation- think sexual
thoughts). Ejaculation and fertility may be a problem.
c. Suggestions: empty bladder before sex; withhold fluids and
antispasmotics (although spasms may help some individuals);
certain positions may increase spasms; explore new erogenous
zones; penile implants, medication. (Lewis 1436 Fig 55-11; 55-12;
55-13)
d. Female- hormones more than nerves regarding fertility. May have
C-section, because of chance for autonomic dysreflexia during
labor. Lack sensation and movement can affect sexual
performance.
6. Grief and depression- Also add:
1. Assess thoughts on ‘quality of life’; body image; role changes.
2. Most common SCI is 15-30 years old and generally a risk taker. This
greatly affects their perception of life and rehabilitation progress.
3. Support groups