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Spinal Cord Injury
Spinal cord injury (SCI) is an insult to the spinal cord resulting in a change either temporary or
permanent, in its normal motor, sensory or autonomic function. Spinal cord trauma is damage
to the spinal cord. It may result from direct to the spinal cord itself or indirectly from damage to
surrounding bones, tissues or blood vessels.
A spinal cord injury refers to any injury to the spinal cord that is caused by trauma instead of
disease. Depending on where the spinal cord and nerve roots are damaged, the symptoms can
vary widely, from pain to paralysis to incontinence. Cervical and lumber vertebras are the most
common site of spinal injury.
A Spinal Cord Injury (SCI) is termed complete when there is a total loss of motor and sensory
function below the level of the injury. Complete injuries are more common in the thoracic spine
because the spinal canal is quite narrow in that region. An incomplete lesion is one in which
there is some preservation of motor and/or sensory function below the level of the injury.
American Spinal Injury Association (ASIA) has developed the level of spinal cord injury / SCI
impairment scale. They are;
1) A- Complete Injury:
 No motor function or sensation below the level of lesion or injury.
2) B- Incomplete injury:
 Selected sensation is preserved, but there is no evidence of motor function
preservation below the level of injury.
3) C- Incomplete injury:
 Motor function is evident distal to the area of injury; however, key muscles are
assessed at less than antigravity strength.
4) D- Incomplete injury:
 Motor function is evident distal to the area of injury and key muscles are
assessed at better than antigravity strength.
5) E- Normal:
 Motor and sensory function assessed as normal.
Etiology
1) Sudden impingements on the spinal cord as a result of trauma.
2) Fractures of the vertebrae can cut, compress or completely sever the spinal cord;
3) Highest incidence between ages 16-30 years as more than 60% of SCIs occur in this age
group's people.
Pathophysiology
Total or partial spinal cord injury
Resulting spinal shock with sudden loss of reflexes below level of injury
Loss of autonomic nervous system affecting vital organs causing the blood pressure and heart
rate to decrease, decrease cardiac output, venous pooling in the extremities and peripheral
vasodilation. (Neurogenic Shock)
Spasticity paralysis occurs as a results of an upper motor neuron lesion or injury as there is
preserved reflex arc below the level of injury.
Flaccid paralysis and atrophy of the affected muscle occurs as a result of damage in lower
motor neurons between the muscle and the spinal cord
Exaggeration of sympathetic response causing Hypertension accomplished by a pounding
headache, nausea and blurred vision,Vasodilation above the injury level results in skin flushing
and profuse perspiration (diaphoresis),Vasoconstriction in areas below the level of injury cause
cool pale skin and piloerection (goosebumps), which is also known as Autonomic dysreflexia.
Paralysis associated with spinal cord injury can affect a whole extremity, both extremities or
an entire half of the body( e.g. haemiplegia, paraplegia and quadriplegia/ teraplegia).
Clinical Features
The symptoms depend on the location (lumbar, thoracic, cervical) and extent of the damage
and may be temporary or permanent; the sensation and mobility of areas that are supplied by
nerves below the level of the lesion are affected.
A. Subjective:
 Paresthesia or loss of sensation below the level of injury.
 Pain (e.g. cutting, burning, radiating) may occur when there is intact sensation.
B. Objective:
 Inability to move body below level of injury.
 Early signs SCIs injury:
1) Spinal shock: The spinal shock is associated with SCIs reflects;
 A sudden loss of reflexes bellow level of injury; particularly bowel and
bladder, which may lead to paralytic ileus and urinary retention.
 Flaccid paralysis (immobility by weak,soft, flabby muscles) below the
level of injury.
2) Neurogenic shock:
 Neurogenic shock develops due to the loss of autonomic nervous system
below the level of the injury.
 The vital organs are affected causing the blood pressure and heart rate
to decrease.(hypotension and bradycardia).
 Loss of sympathetic innervations includes a decrease in cardiac output,
venous pooling in the extremities and peripheral vasodilation.
 Later symptoms of spinal cord injury:
1) Spasticity paralysis (Reflex hyperexcitibility):
 Spasticity paralysis occur as a results of an upper motor neuron
lesion or injury as there is preserved reflex arc below the level of
injury.
 Muscle below site of injury become spastic and hyperreflexic with the
resolution of spinal shock as muscle remain permanently tense.
 Paralysis associated with upper motor neuron lesions can affect a
whole extremity, both extremities or an entire half of the body( e.g.
haemiplegia, paraplegia and quadriplegia/ teraplegia).
2) Diminished reflex excitability (flaccid paralysis):
 Flaccid paralysis occurs as a result of damage in lower motor
neurons between the muscle and the spinal cord.
 Reflexes are lost and the muscle become flaccid and atrophied from
disuse.
 Flaccid paralysis and atrophy of the affected muscles are the principal
signs of lower motor neuron
3) Total cord damage:
 Both upper and lower motor neurons are destroyed; signs and symptoms
depend on location of injury; loss of motor and sensory function present at time
of damage usually is permanent.
a) Sacral region: Paralysis of lower extremities (Paraplegia) accompanied by
atonic bladder and bowel with impaired of sphincter control.
b) Lumber region: paralysis of lower extremities that may extend to pelvic
region accompanied by spastic bladder and loss of bladder and anal sphincter
control.
c) Thoracic region: Same symptoms as lumber region except paralysis extends
to the trunk below level of the diaphragm.
d) Cervical region: same symptoms as thoracic region except paralysis extends
from neck down and includes paralysis of all extremities (quadriplegia).If
injury is above C4 there is an absence of independent respirations.
4) Partial cord damage:
 Either upper or lower motor neurons, or both, may be destroyed.
 Signs depend not only on location but also on the type of neurons involved.
 Destruction of lower motor neurons results in atrophy and flaccid paralysis of
involved muscles whereas destruction of upper motor neurons causes spasticity.
5) Autonomic dysreflexia (hyperreflexia):
 Autonomic dysflexia is a unique complications of SCI that occurs in patients with
cord injuries at T6 or above.
 The problem is the most common in patients with cervical injuries.
 Autonomic dysreflexia is an exaggerated sympathetic response.
 The clinical manifestations are:
o Hypertension is the classic defining feature accomplished by a pounding
headache, nausea and blurred vision.
o Vasodilation above the injury level results in skin flushing and profuse
perspiration (diaphoresis).
o Vasoconstriction in areas below the level of injury cause cool pale skin
and piloerection (goosebumps).
o The bradycardia produced by excess vagal stimulation can be severe.
o The abnormal stimuli that trigger autonomic dysreflexia arise from
localized areas below the level of injury. Common precipitating factors
for autonomic dysreflexia are distended bladder and distended bowel.
Diagnostic Investigation
1. History taking and neurological assessment by using American Spinal Injury Association
Assessment.
2. Radio Lumber puncture
3. X-ray, MRI and CT scan.
4. Blood test.
Treatment
A. Management of spinal injury:
1. Immobilization especially head and neck; rigid collar, sandbags and straps, spine
board, log-roll to turn, move only adequate personnel and stabilized head and
neck before transferring.
2. Stabilize visual functions.
3. Cut off clothing if rusticated tight
4. Prevent hypotension and manage shock.
5. Corticosteroid to reduce edema on spinal cord
6. Maintain oxygenation through O2 per nasal cannula, if intubation is needed do
not move the neck.
7. NG tube to suction in order to prevent aspiration.
8. Insert indwelling catheter, insert NG.
Nursing Management
A. Assessment:
1. Respiratory status
2. Neurologic status
3. Abdomen for bladder or bowel distension.
4. Health problems that impact on recovery
5. Client's coping skills and support systems.
B. Nursing Diagnosis
1. Ineffective breathing patterns related to weakness or paralysis of abdominal and
intra-costal muscles.
2. Ineffective airway clearance related to paralysis or weakness of abdominal and
intra-costal muscles.
3. Decrease cardiac output related to decreased venous return with pooling of
blood in the periphery.
4. Impaired bed and physical mobility related to motor and sensory impairments.
5. Risk for impaired skin integrity related to sensory losses and physical immobility.
6. Impaired urinary elimination related to neurologic impairment.
7. Risk for constipation related to atonic bowel and immobility.
8. Self-care deficit related to paralysis.
C. Implementation/ Interventions
1. Promoting adequate breathing and airway clearance.
 Maintain frequent observation of respiratory and neurologic functioning.
 Open airway with Jaw thrust or chin lift while maintaining cervical spine
immobilization.
 Suction airway.
 Obtain blood sample for ABG analysis.
 Assist with endo-tracheal intubation.
2. Maintaining fluid balance.
 Cannulate two veins with large bore catheters and initiate.
 Infusion of lactated Ringer's solution or normal saline; monitor rate
carefully.
 Insert urinary catheter.
 Monitor hemo-dynamics.
3. Maintain surgical asepsis with skeletal traction or spinal surgery.
4. Maintain body parts in a functional position; prevent dysfunctional contractures.
5. Institute active and passive range-of-motion exercises as soon as approved; plan
for early ambulation; exercises may be performed in water.
6. Teach use of unaffected extremities to manipulate, move and stabilize affected
parts.
7. Maintaining body temperature.
 Warm or environmental control and monitor room temperature.
 Warm IV fluids and use hypothermia blanket.
8. Attempt to establish a scheduled pattern of bowel function.
 Compare client's bowel habits illness to current pattern; establish a
specific and definite time for bowel movement.
 Provide a diet with bowel-stimulating properties; with emphasis on fruits,
vegetables, cereal grains and legumes because these are rich source of
dietary fiber.
 Encourage sufficient fluid intake: 2000 to 3000 ml per day.
 Schedule evacuation after a meal to utilize the gastrocolic reflex
(peristaltic wave in the colon induced by entrance of food into a fasting
stomach).
 Determine if there is an awareness of the need to defecate e.g. feeling of
fullness or pressure in the rectum, flatus).
 Encourage assumption of a position most near the physiologic position
for defecation.
 Utilize assistive measures to induce defecation by:
o Teach leaning forward to increase intra-abdominal pressure by
compressing the abdomen against the thighs.
o Using enemas only as a last resort.
 Provide for adaptation of equipment as necessary (e.g. elevated toilet
seat, grab bars)
 Teach the family the bowel training programs.
9. Attempt to establish bladder function.
a. Determine the type of bladder problem.
o Neurologic bladder: any disturbance in the bladder functioning
cause by a lesion of the nervous system.
o Spastic bladder: disorder caused by a lesion of spinal cord above
bladder reflex center, in the conus medullaris; there is a loss of
conscious sensation and cerebral motor control; the bladder
empties autonmically when the destrusor muscle is sufficiently
stretched (about 500 ml).
o Flaccid bladder: disorder caused by a lesion of the spinal cord
below the level of injury; the bladder continues to fill, becomes
distended and periodically overflows; the bladder muscle does
not contract forcefully and therefore does not empty except with
a conscious effort.
b. Review the client's bladder habits before illness as well as the current
pattern of elimination; record output, voiding times, and times of
incontinence.
c. Encourage sufficient fluid intake: 3000 to 4000 mal per 24 hours period, a
glass of water with each attempt to void.
d. Restrict fluid after 6 pm to limit amount of urine in bladder during night.
e. Encourage assumption of as normal a position as possible for voiding.
f. Establish a voiding schedule:
o Begin trial voiding at the time the client is most often incontinent.
o Attempt voiding every 2 hours all day and 2 to 3 times during the
night.
o Time intervals between voiding should be shorter in the morning
than later in the day.
o As ability to maintain control improves, lengthen the time
between attempts at voiding.
o Time of intervals is not as important as regularity.
10. Maintaining skin and joint integrity.
 Preventing skin breakdown requires continuing nursing assessment and
intervention.
 Special attention is given is given to avoid pressure.
 Maintain skin integrity by 2 hourly positions changed.
 Keep skin clean and dry and use pressure relieving devices.
 Consider placement on special bed.
11. Determine whether there is an awareness need or act of urination (e.g. fullness
or pressure, flushing, chilling, goose pimples, cold sweats).
12. Discuss need for sexual expression and options available; discussion of penile
implants.
13. Care for the client experiencing autonomic dysreflexia:
 Place in a high-fowler's position.
 Ensure patency of urinary drainage system.
 Assess for fecal impaction.
 Eliminate other potential stimuli such as drafts.
 Notify physician; administer prescribed anti-hypertensives.
14. When permitted, encourage and support use of tilt table to imitate weight
bearing and reduce loss of calciumfrom bones.
D. Evaluation

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Spinal cord injury

  • 1. Spinal Cord Injury Spinal cord injury (SCI) is an insult to the spinal cord resulting in a change either temporary or permanent, in its normal motor, sensory or autonomic function. Spinal cord trauma is damage to the spinal cord. It may result from direct to the spinal cord itself or indirectly from damage to surrounding bones, tissues or blood vessels. A spinal cord injury refers to any injury to the spinal cord that is caused by trauma instead of disease. Depending on where the spinal cord and nerve roots are damaged, the symptoms can vary widely, from pain to paralysis to incontinence. Cervical and lumber vertebras are the most common site of spinal injury. A Spinal Cord Injury (SCI) is termed complete when there is a total loss of motor and sensory function below the level of the injury. Complete injuries are more common in the thoracic spine because the spinal canal is quite narrow in that region. An incomplete lesion is one in which there is some preservation of motor and/or sensory function below the level of the injury. American Spinal Injury Association (ASIA) has developed the level of spinal cord injury / SCI impairment scale. They are; 1) A- Complete Injury:  No motor function or sensation below the level of lesion or injury. 2) B- Incomplete injury:  Selected sensation is preserved, but there is no evidence of motor function preservation below the level of injury. 3) C- Incomplete injury:  Motor function is evident distal to the area of injury; however, key muscles are assessed at less than antigravity strength. 4) D- Incomplete injury:  Motor function is evident distal to the area of injury and key muscles are assessed at better than antigravity strength. 5) E- Normal:  Motor and sensory function assessed as normal.
  • 2. Etiology 1) Sudden impingements on the spinal cord as a result of trauma. 2) Fractures of the vertebrae can cut, compress or completely sever the spinal cord; 3) Highest incidence between ages 16-30 years as more than 60% of SCIs occur in this age group's people. Pathophysiology Total or partial spinal cord injury Resulting spinal shock with sudden loss of reflexes below level of injury Loss of autonomic nervous system affecting vital organs causing the blood pressure and heart rate to decrease, decrease cardiac output, venous pooling in the extremities and peripheral vasodilation. (Neurogenic Shock) Spasticity paralysis occurs as a results of an upper motor neuron lesion or injury as there is preserved reflex arc below the level of injury. Flaccid paralysis and atrophy of the affected muscle occurs as a result of damage in lower motor neurons between the muscle and the spinal cord
  • 3. Exaggeration of sympathetic response causing Hypertension accomplished by a pounding headache, nausea and blurred vision,Vasodilation above the injury level results in skin flushing and profuse perspiration (diaphoresis),Vasoconstriction in areas below the level of injury cause cool pale skin and piloerection (goosebumps), which is also known as Autonomic dysreflexia. Paralysis associated with spinal cord injury can affect a whole extremity, both extremities or an entire half of the body( e.g. haemiplegia, paraplegia and quadriplegia/ teraplegia). Clinical Features The symptoms depend on the location (lumbar, thoracic, cervical) and extent of the damage and may be temporary or permanent; the sensation and mobility of areas that are supplied by nerves below the level of the lesion are affected. A. Subjective:  Paresthesia or loss of sensation below the level of injury.  Pain (e.g. cutting, burning, radiating) may occur when there is intact sensation. B. Objective:  Inability to move body below level of injury.  Early signs SCIs injury: 1) Spinal shock: The spinal shock is associated with SCIs reflects;  A sudden loss of reflexes bellow level of injury; particularly bowel and bladder, which may lead to paralytic ileus and urinary retention.  Flaccid paralysis (immobility by weak,soft, flabby muscles) below the level of injury. 2) Neurogenic shock:  Neurogenic shock develops due to the loss of autonomic nervous system below the level of the injury.  The vital organs are affected causing the blood pressure and heart rate to decrease.(hypotension and bradycardia).  Loss of sympathetic innervations includes a decrease in cardiac output, venous pooling in the extremities and peripheral vasodilation.
  • 4.  Later symptoms of spinal cord injury: 1) Spasticity paralysis (Reflex hyperexcitibility):  Spasticity paralysis occur as a results of an upper motor neuron lesion or injury as there is preserved reflex arc below the level of injury.  Muscle below site of injury become spastic and hyperreflexic with the resolution of spinal shock as muscle remain permanently tense.  Paralysis associated with upper motor neuron lesions can affect a whole extremity, both extremities or an entire half of the body( e.g. haemiplegia, paraplegia and quadriplegia/ teraplegia). 2) Diminished reflex excitability (flaccid paralysis):  Flaccid paralysis occurs as a result of damage in lower motor neurons between the muscle and the spinal cord.  Reflexes are lost and the muscle become flaccid and atrophied from disuse.  Flaccid paralysis and atrophy of the affected muscles are the principal signs of lower motor neuron 3) Total cord damage:  Both upper and lower motor neurons are destroyed; signs and symptoms depend on location of injury; loss of motor and sensory function present at time of damage usually is permanent. a) Sacral region: Paralysis of lower extremities (Paraplegia) accompanied by atonic bladder and bowel with impaired of sphincter control. b) Lumber region: paralysis of lower extremities that may extend to pelvic region accompanied by spastic bladder and loss of bladder and anal sphincter control. c) Thoracic region: Same symptoms as lumber region except paralysis extends to the trunk below level of the diaphragm.
  • 5. d) Cervical region: same symptoms as thoracic region except paralysis extends from neck down and includes paralysis of all extremities (quadriplegia).If injury is above C4 there is an absence of independent respirations. 4) Partial cord damage:  Either upper or lower motor neurons, or both, may be destroyed.  Signs depend not only on location but also on the type of neurons involved.  Destruction of lower motor neurons results in atrophy and flaccid paralysis of involved muscles whereas destruction of upper motor neurons causes spasticity. 5) Autonomic dysreflexia (hyperreflexia):  Autonomic dysflexia is a unique complications of SCI that occurs in patients with cord injuries at T6 or above.  The problem is the most common in patients with cervical injuries.  Autonomic dysreflexia is an exaggerated sympathetic response.  The clinical manifestations are: o Hypertension is the classic defining feature accomplished by a pounding headache, nausea and blurred vision. o Vasodilation above the injury level results in skin flushing and profuse perspiration (diaphoresis). o Vasoconstriction in areas below the level of injury cause cool pale skin and piloerection (goosebumps). o The bradycardia produced by excess vagal stimulation can be severe. o The abnormal stimuli that trigger autonomic dysreflexia arise from localized areas below the level of injury. Common precipitating factors for autonomic dysreflexia are distended bladder and distended bowel. Diagnostic Investigation 1. History taking and neurological assessment by using American Spinal Injury Association Assessment. 2. Radio Lumber puncture 3. X-ray, MRI and CT scan. 4. Blood test.
  • 6. Treatment A. Management of spinal injury: 1. Immobilization especially head and neck; rigid collar, sandbags and straps, spine board, log-roll to turn, move only adequate personnel and stabilized head and neck before transferring. 2. Stabilize visual functions. 3. Cut off clothing if rusticated tight 4. Prevent hypotension and manage shock. 5. Corticosteroid to reduce edema on spinal cord 6. Maintain oxygenation through O2 per nasal cannula, if intubation is needed do not move the neck. 7. NG tube to suction in order to prevent aspiration. 8. Insert indwelling catheter, insert NG. Nursing Management A. Assessment: 1. Respiratory status 2. Neurologic status 3. Abdomen for bladder or bowel distension. 4. Health problems that impact on recovery 5. Client's coping skills and support systems. B. Nursing Diagnosis 1. Ineffective breathing patterns related to weakness or paralysis of abdominal and intra-costal muscles. 2. Ineffective airway clearance related to paralysis or weakness of abdominal and intra-costal muscles. 3. Decrease cardiac output related to decreased venous return with pooling of blood in the periphery. 4. Impaired bed and physical mobility related to motor and sensory impairments. 5. Risk for impaired skin integrity related to sensory losses and physical immobility. 6. Impaired urinary elimination related to neurologic impairment. 7. Risk for constipation related to atonic bowel and immobility. 8. Self-care deficit related to paralysis.
  • 7. C. Implementation/ Interventions 1. Promoting adequate breathing and airway clearance.  Maintain frequent observation of respiratory and neurologic functioning.  Open airway with Jaw thrust or chin lift while maintaining cervical spine immobilization.  Suction airway.  Obtain blood sample for ABG analysis.  Assist with endo-tracheal intubation. 2. Maintaining fluid balance.  Cannulate two veins with large bore catheters and initiate.  Infusion of lactated Ringer's solution or normal saline; monitor rate carefully.  Insert urinary catheter.  Monitor hemo-dynamics. 3. Maintain surgical asepsis with skeletal traction or spinal surgery. 4. Maintain body parts in a functional position; prevent dysfunctional contractures. 5. Institute active and passive range-of-motion exercises as soon as approved; plan for early ambulation; exercises may be performed in water. 6. Teach use of unaffected extremities to manipulate, move and stabilize affected parts. 7. Maintaining body temperature.  Warm or environmental control and monitor room temperature.  Warm IV fluids and use hypothermia blanket. 8. Attempt to establish a scheduled pattern of bowel function.  Compare client's bowel habits illness to current pattern; establish a specific and definite time for bowel movement.  Provide a diet with bowel-stimulating properties; with emphasis on fruits, vegetables, cereal grains and legumes because these are rich source of dietary fiber.  Encourage sufficient fluid intake: 2000 to 3000 ml per day.  Schedule evacuation after a meal to utilize the gastrocolic reflex (peristaltic wave in the colon induced by entrance of food into a fasting stomach).  Determine if there is an awareness of the need to defecate e.g. feeling of fullness or pressure in the rectum, flatus).
  • 8.  Encourage assumption of a position most near the physiologic position for defecation.  Utilize assistive measures to induce defecation by: o Teach leaning forward to increase intra-abdominal pressure by compressing the abdomen against the thighs. o Using enemas only as a last resort.  Provide for adaptation of equipment as necessary (e.g. elevated toilet seat, grab bars)  Teach the family the bowel training programs. 9. Attempt to establish bladder function. a. Determine the type of bladder problem. o Neurologic bladder: any disturbance in the bladder functioning cause by a lesion of the nervous system. o Spastic bladder: disorder caused by a lesion of spinal cord above bladder reflex center, in the conus medullaris; there is a loss of conscious sensation and cerebral motor control; the bladder empties autonmically when the destrusor muscle is sufficiently stretched (about 500 ml). o Flaccid bladder: disorder caused by a lesion of the spinal cord below the level of injury; the bladder continues to fill, becomes distended and periodically overflows; the bladder muscle does not contract forcefully and therefore does not empty except with a conscious effort. b. Review the client's bladder habits before illness as well as the current pattern of elimination; record output, voiding times, and times of incontinence. c. Encourage sufficient fluid intake: 3000 to 4000 mal per 24 hours period, a glass of water with each attempt to void. d. Restrict fluid after 6 pm to limit amount of urine in bladder during night. e. Encourage assumption of as normal a position as possible for voiding. f. Establish a voiding schedule: o Begin trial voiding at the time the client is most often incontinent. o Attempt voiding every 2 hours all day and 2 to 3 times during the night. o Time intervals between voiding should be shorter in the morning than later in the day. o As ability to maintain control improves, lengthen the time between attempts at voiding.
  • 9. o Time of intervals is not as important as regularity. 10. Maintaining skin and joint integrity.  Preventing skin breakdown requires continuing nursing assessment and intervention.  Special attention is given is given to avoid pressure.  Maintain skin integrity by 2 hourly positions changed.  Keep skin clean and dry and use pressure relieving devices.  Consider placement on special bed. 11. Determine whether there is an awareness need or act of urination (e.g. fullness or pressure, flushing, chilling, goose pimples, cold sweats). 12. Discuss need for sexual expression and options available; discussion of penile implants. 13. Care for the client experiencing autonomic dysreflexia:  Place in a high-fowler's position.  Ensure patency of urinary drainage system.  Assess for fecal impaction.  Eliminate other potential stimuli such as drafts.  Notify physician; administer prescribed anti-hypertensives. 14. When permitted, encourage and support use of tilt table to imitate weight bearing and reduce loss of calciumfrom bones. D. Evaluation