ERA UNIVERSITY COLLEGE OF NURSING

LUCKNOW

MSN ASSIGNMENT
ON
“SPINAL CORD INJURY”

SUBMITTED TO-: SUBMITTED BY-:

INTRODUCTION
Spinal cord injury is caused by trauma or damage to the spinal cord. It can result in temporary
permanent alteration in the function of the spinal cord. Younger adult men between 16 & 30
years have the greatest risk for SCI. with improved treatment strategies even the very young
patient with SCI can anticipate a long life. The number of older adults with SCI has
increased. This increase is related to people with SCI living longer and older age at the time
of injury.
The potential for disruption of individual growth and development, altered family dynamics,
economic loss in terms of employment, and the high cost of rehabilitation and long term
health care make SCI a major problem. Although many people with SCI can care for
themselves independently, those with the highest level of injury may require around the clock
care at home or in a long term care facility.

ETIOLOGY
 SCI is usually a result of trauma.
 The most common cause are motor vehicle collisions (38%), violence (14%), sports
injuries (9%), and other miscellaneous causes (95).
 Blunt trauma
 Compression
 Flexion, extension, or rotation injuries to spinal column
 Motor vehicle crash
 Pedestrian accidents
 Falls
 Diving
 Penetrating trauma
 Stretched, torn, crushed or lacerated spinal cord
 Gunshot wounds
 Stab wounds

PATHOPHSIOLOGY
The extent of neorulogic damage caused by SCI result from primary injury (initial physical
disruption of the spinal cord) and secondary injury (from process such as ischemia, hypoxia,
hemorrhge and edema).
I. PRIMARY INJURY- can result from cord compression by bone displacement,
interruption of blood supply to the cord, or traction from pulling on the cord.
 Penetrating trauma, such as gunshot and stab wounds can cause tearing and
transection. The initial mechanical disruption of axons as a result of stretch or
laceration is referred
to as the primary injury
II. SECONDARY INJURY- secondary injury refers to the ongoing progressive damage
that occurs after the primary injury

Causes leads to vascular changes due to haemorrhage, vasospasm, thrombosis of

Leads to free radicals formation, lipid peroxidation, release of glutamate, disruption of the
ionic balance of potassium, sodium and calcium

Leads to neural cell death and reduced spinal cord blood flow

Apoptosis (programmed cell death)

Contribute to post injury demyelination

These process leads to scare tissue formation, irreversible nerve damage and permanent
neurologic deficit

Hypoxia reduces O2 levels below the metabolic needs of the spinal cord

Lactate metabolic accumulate and an increase in vasoactive substances, including

High levels of these vasoactive substances cause vasospasm and hypoxia with subsequent
necrosis

Spinal cord has minimal ability to adapt to vasospasm

Thus compression of the spinal cord occurs

Edema extends above and below the injury, increasing ischemic damage

He injury progress overtime, the extent of the injury and prognosis for recovery are most
accurately determined 72 hours or more after injury

CLASSIFICATION
SCI is classified by the-
1. MECHANISM OF INJURY-the major mechanism of injury are flexion,
hyperextension, flexion-rotation, extension-rotation and compression. The flexion-
rotation injury is the most unstable because ligaments that stabilize the spine are torn.
This injury most often contributes to severe neurologic deficits.
2. LEVEL OF INJURY- skeletal level of injury is the vertebral level with the most
damage to vertebral bones and ligaments. Neurologic level is the lowest segment of
the spinal cord with normal sensory and motor function on both sides of the body.
Cervical and lumber injury are most function on both sides of the body. Cervical and
lumbar injuries are most common because they are associated with the greatest
flexibility and movement.
 If the cervical cord is involved, paralysis of all four extremities occurs,
resulting in tetraplegia.
 If the thoracic, lumbar or sacral spinal cord is damaged, the result is paraplegia
(paralysis and loss of sensation in the legs).
3. DEGREE OF INJURY- the degree of degree of spinal cord involvement may be
complete or incomplete
 Complete cord involvement results in total loss of sensory and motor function
below the level of injury.
 Incomplete cord involvement results in a mixed loss of voluntary motor
activity and sensation and leaves some tracts intact.
 Five major syndromes are associated with incomplete injuries- central cord
syndrome, anterior cord syndrome, brown-sequard syndrome, cauda equine
syndrome, and conus medullaris syndrome.

CLINICAL MANIFESTATION
  Problem walking
 Loss of control of the bladder or bowels
 Inability to move the arms or legs
 Feelings of spreading numbness or tingling in the extremities
 Unconsciousness
 Headache
 Pain, pressure, and stiffness in the back area
 Signs of shock
 Unnatural positioning of the head
 Loss of altered sensation, including the ability to feel heat, cold and touch
 Exaggerated reflex activities or spasms
 Difficulty breathing, coughing or clearing secretions from the lungs
 Weakness, incoordination or paralysis in any part of the body.
 Spinal cord disruption is also marked by decreased ability to sweat or shiver below
the level of injury, which affects the ability to regulate body temperature.
 Spinal cord injury has increased nutritional needs due to increased metabolism and
more protein breakdown. Lean body mass is lost and muscle atrophy leads to weight
loss.

DIAGNOSTIC STUDIES
 History and physical examinations, including complete neurologic examination
 Arterial blood gases
 Electrolytes, serum glucose, coagulation profile, haemoglobin and hemocrit
 Urinalysis
 CT scan, MRI, EMG.
 Anterioroposterior, lateral and oclontoid spinal x-rays
 Serial bedside PFTs.
 Duplex Doppler ultrasound, impedance plethysmography

MANAGEMENT
 MEDICAL MANAGEMENT
 Ensure patent airway and adequate respiration
 Maintain SaO2>90%: administer O2 via nasal cannula, non-rebreather mask,
or endotracheal tube.
 Maintain SBP.90mmHg
 Establish IV access with two large bore catheters to infuse normal saline or
lactated ringer’s solution as appropriate.
 Immobilize and stabilize cervical spine.
 Assess other injuries
 Control external bleeding
 Monitor vital signs, level of consciousness.
  Intubation if indicated by ABGs, PFTs.
 Assessment and management of nutrition
 Insertion of nasogastric tube and attach to suction
 Pain management
 Pressure ulcer prevention
 VTE prophylaxis
 Physical, occupational, speech therapy and physiatrist consults.

 PHARMACOLOGICAL MANAGEMENT
 Low-molecular-weight heparin (enoxaparin) is used to prevent VTE unless
contraindicated.
 Oral anticoagulation alone is not recommended as a prophylactic treatment
strategy.
 Vasopressor agents, such as phenylephrine or norepinephrine, are used in the
acute phase as adjuvants; these maintain the mean arterial pressure (MAP) at
greater than 85 to 90 mmHg to improve perfusion.
 Methylprednisolone, is no longer approved by the FDA; high dose of MP is
associated with harmful side effects including GI bleeding, sepsis, even death.

 SURGICAL MANAGEMENT
 The type of surgery depends on the severity and level of the injury,
mechanism of injury.
 Early spinal cord depression may reduce secondary injury.
 Surgery within the first 24 hours after SCI is safe and associated with
improved neurologic outcome.
 Surgery to stabilize the spine can be performed from the back of the spine
(posterior approach) or from the front of the spinal (anterior approach).
 Fusion involves attaching metal screws, plates or other devices to the bones of
the spine to keep them aligned.

 NURSING MANEGEMENT
 Overall goals are that the patient with SCI will-
1) Maintain an optimum level of neurologic functioning.
2) Have minimal or no complications of immobility.
3) Learn new skilled, gain new knowledge and acquire new behaviours to
be able to care for self or successfully direct others to do so.
4) Return home at an optimal level of functioning.
 NURSING DIAGNOSIS
a. Ineffective breathing pattern related to respiratory muscle fatigue,
neuromuscular paralysis and retained secretions.
b. Imbalanced nutrition: less than body requirement related to paralytic ileus and
metabolic demands of body.
c. Ineffective peripheral tissue perfusion related to hypotension and lack of
mobility.
d. Impaired skin integrity related to immobility and poor tissue perfusion.
e. Impaired urinary elimination related to spinal injury and limited fluid intake.
 f. Constipation related to neurologic bowel, inadequate fluid intake and
immobility.
 EVALUATION
Expected outcomes are that the patient with SCI will-
i. Maintain adequate ventilation and have no signs of respiratory distress.
ii. Maintain adequate circulation & BP.
iii. Maintain intact skin over bony prominence
iv. Maintain adequate nutrition
v. Establish a bowel and bladder management program base on neurologic
function and personal preference
vi. Experience no episodes of autonomic hyperreflexia.