Spinal cord injury

41 Spinal cord injury




Overview/pathophysiology


Spinal cord injuries (SCIs) are caused by vertebral fractures or dislocations that sever, lacerate, stretch, or compress the spinal cord and interrupt neuronal function and transmission of nerve impulses. Concussive trauma can cause damage from bruising, swelling, and inflammation. When blood supply to the spinal cord is interrupted, the spinal cord swells in response, and this, along with hemorrhage, can cause additional compression, ischemia, and compromised function. Neurologic deficits resulting from compression may be reversible if the resulting edema and ischemia do not lead to spinal cord degeneration and necrosis. Common causes of injury include motor vehicle accidents, diving or other sporting accidents, falls, and gunshot wounds. SCIs are classified in a number of different ways according to type (open, closed), cause (concussion, contusion, laceration, transection), site (level of spinal cord involved), mechanism of injury (compression, hyperflexion, hyperextension, rotational, penetrating), stability and degree of spinal cord function loss (complete, incomplete), or syndromes (central cord, Brown-Séquard [lateral], anterior cord, conus medullaris, cauda equina, and posterior cord). A spinal cord concussion involves a transient loss of cord function caused by a traumatic event, resulting in immediate flaccid paralysis that resolves completely in a matter of minutes or hours.




Prognosis:


Any evidence of voluntary motor function, sensory function, or sacral sensation below the level of injury (lowest level in which motor function and sensation remain intact) indicates an incomplete SCI, with potential for partial or complete recovery. After an acute injury, the spinal cord usually goes into a condition called spinal shock, in which there can be total loss of spinal cord function below the level of injury. During spinal shock there is no reflex activity. Resolution of spinal shock with return of reflexes usually occurs within 1-2 wk, but may take 6 mo or more. If there is no evidence of returning motor function after local reflexes have returned, the spinal cord is considered irreversibly damaged. Generally, SCI does not cause immediate death unless it is at C1 through C3, which results in respiratory muscle paralysis. Individuals who survive these injuries require a ventilator for the rest of their lives. If the injury occurs at C4, respiratory difficulties may result in death, although some individuals who have survived the initial injury have been successfully weaned from the ventilator. Injuries below C4 also can be life threatening because of ascending cord edema, which can cause respiratory muscle paralysis. Immediately after injury, common complications that require treatment include hypotension (systolic blood pressure [SBP] less than 80 mm Hg), bradycardia, paralytic ileus, urinary retention, pneumonia, and stress ulcers. Other long-term, life-threatening complications of SCI include autonomic dysreflexia (AD), pneumonia, decubitus ulcers, sepsis, urinary calculi, and urinary tract infection (UTI).



Health care setting


Acute care, subacute care, rehabilitation center



Assessment



• There are a variety of neurologic assessment and functional outcome scales, including the American Spinal Injury Association (ASIA) Impairment scale in which the impairment is described by whether it is complete, incomplete, or normal, with further differentiations for incomplete injuries.



Acute indicators:


Loss of sensation, weakness, or paralysis below level of injury, localized pain or tenderness over site of injury, headache, hypothermia or hyperthermia, and alterations in bowel and bladder function.



Cervical injury:


Possible alterations in level of consciousness (LOC); weakness or paralysis in all four extremities (tetraparesis or tetraplegia, previously termed quadriparesis or quadriplegia); and paralysis of respiratory muscles or signs of respiratory problems, such as flaring nostrils and use of accessory muscles for respirations. Any cervical injury can result in low body temperature (to 96° F [35.5° C]), slowed pulse rate (less than 60 bpm) caused by vagal stimulation of the heart, hypotension (SBP less than 80 mm Hg) caused by vasodilation, and decreased peristalsis.



Thoracic and lumbar injuries:


Paraparesis/paraplegia or altered sensation in the legs; hand and arm involvement in upper thoracic injuries.



Acute spinal shock:


Can last from 2 days to 4-6 mo but usually resolves in 1-2 wk. Spinal shock results from loss of sympathetic nerve outflow and reflex function in all segments below level of injury. Indicators depend on injury severity and include total loss of spinal cord function, loss of skin sensation, flaccid paralysis or absence of reflexes below level of injury, paralytic ileus and constipation secondary to atonic bowel, bladder distention secondary to atonic bladder, bradycardia, low/falling blood pressure (BP) secondary to loss of vasomotor tone and decreased venous return, and anhidrosis (absence of sweating and loss of temperature regulation) below level of injury. Autonomic instability is more dramatic in higher (e.g., cervical) lesions. Resolution of spinal shock is indicated by return of both the bulbocavernosus reflex (slight muscle contraction when glans penis is squeezed or urinary catheter is pulled, causing scrotal retraction) and the anal reflex (anal puckering on digital examination or gentle scratching around the anus). Remaining reflexes may take weeks to return.



Chronic indicators:


As spinal shock resolves, muscle tone, reflexes, and some function may return, depending on severity and level of injury. Return of reflexes usually results in muscle spasticity. Chronic autonomic dysfunction may be manifested as fever; mild hypotension; anhidrosis; and alterations in bowel, bladder, and sexual function. Chronic neural pain may occur after SCI and tends to occur as either diffuse pain below level of injury or pain adjacent to level of injury. Injuries at or below L1 may result in permanent flaccid paralysis. Orthostatic hypotension is more typical of lesions above T7.



Upper motor neuron (UMN) involvement:


UMNs are nerve cell bodies that originate in high levels of the central nervous system (CNS) and transmit impulses from the brain down the spinal cord. Injury interrupts this impulse transmission, causing muscle or organ dysfunction below level of injury. However, because the injury does not interrupt reflex arcs coming from those muscles or organs to the spinal cord, hypertonic reflexes, clonus paralysis, and spastic paralysis are seen. The patient will have a positive Babinski’s reflex.



Lower motor neuron (LMN) involvement:


LMNs are anterior horn cell bodies that originate in the spinal cord. LMNs transmit nerve impulses to muscles and organs and are involved in reflex arcs that control involuntary responses. Damage to LMNs will abolish voluntary and reflex responses of muscles and organs, resulting in flaccid paralysis, hypotonia, atrophy, and muscle fibrillations and fasciculations. The patient will have an absent Babinski’s reflex. The spinal cord ends at the T12-L1 level. Below that level, a bundle of nerve roots from the spinal cord, called the cauda equina, fills the spinal canal. Injuries at or below L1 that damage nerve fiber after it leaves the spinal cord result in flaccid paralysis because of interrupted reflex arc activity.



Bowel and bladder dysfunction:


Usually conscious sensation of the need to void or defecate is lost. UMN bowel and bladder involvement results in reflex incontinence. Flaccid LMN bladder involvement causes urinary retention with overflow incontinence. Flaccid LMN bowel involvement causes fecal retention/impaction.



Sexual dysfunction:


Degree of dysfunction varies according to degree of completeness and whether injury is UMN or LMN. Males with complete UMN injuries have a loss of psychogenic erection but may have reflex erections. Ejaculation rates with complete UMN injuries are as low as 4%. Females have a loss of psychogenic lubrication but may have reflex lubrication. With complete LMN injuries, about 25% of males will have psychogenic erections but none will have reflex erections. About 50% of both sexes (by questionnaire) say they can experience orgasm regardless of injury level (possibly through other erogenous zones). Incomplete injuries will result in better sexual functioning that may include both erections and ejaculations.



Autonomic dysreflexia:


Also known as autonomic hyperreflexia, AD is the exaggerated and unopposed sympathetic response to noxious stimuli below the SCI lesion and can be life threatening as reflex activity returns. AD is seen most commonly in patients with injuries at or above T6, but it has been reported with injuries as low as T8. Signs and symptoms include gross hypertension (BP more than 20 mm Hg above baseline, but BP can be as high as 240-300/150 mm Hg), pounding headache, blurred vision, bradycardia, nausea, and nasal congestion. Above level of injury, flushing and sweating may occur. Below level of injury, piloerection (goose bumps) and skin pallor, which signal vasoconstriction, may be present. Seizures, subarachnoid hemorrhage, stroke, or retinal hemorrhage also may occur.



Physical assessment




Acute (spinal shock):


Absence of deep tendon reflexes (DTRs) below level of injury, absence of cremasteric reflex (scratching or light stroking of inner thigh for male patients causes testicle on that side to elevate) for T12 and L1 injuries, absence of penile or anal sphincter reflex.



Chronic:


Generally, increased DTRs occur if the spinal cord lesion is of the UMN type.



Diagnostic tests


Complete spine immobilization with a rigid cervical collar and backboard or other firm surface is essential until diagnostic tests rule out injury.




X-ray examination of spine:


To delineate fracture, deformity, displacement of vertebrae, and soft tissue masses such as hematomas.



Magnetic resonance imaging (MRI) scan:


To reveal changes in spinal cord and surrounding soft tissue. MRI scan evaluation is preferred and considered the “gold” standard for evaluation of degree of injury in patients who can tolerate it.



Computed tomography (CT) scan:


To reveal changes in the spinal cord, vertebrae, and soft tissue surrounding the spine.



Arterial blood gas (ABG)/pulmonary function tests:


To assess effectiveness of respirations and detect need for O2 or mechanical ventilation.



Myelography:


To show blockage or disruption of the spinal canal and used if other diagnostic examinations are inconclusive. Radiopaque dye is injected into the subarachnoid space of the spine, using a lumbar or cervical puncture.



Cystometry/urodynamic evaluation/external sphincter electromyogram:


To assess bladder capacity and function after resolution of spinal shock for the best type of bladder training program.



Pulmonary fluoroscopy:


To evaluate degree of diaphragm movement and effectiveness in individuals with high cervical injuries.



Evoked potential studies (e.g., somatosensory):


To help locate level of spinal cord lesion by evaluating integrity of anatomic pathways and connections of the nervous system. Stimulation of a peripheral nerve triggers a discrete electrical response along a neurologic pathway to the brain. Response or lack of response to stimulation is measured in this test.



Deep vein thrombosis (DVT) studies (e.g., venogram, duplex doppler ultrasound, impedance plethysmography):


To monitor for development of DVT.





Nursing diagnosis:


Risk for autonomic dysreflexia

related to exaggerated unopposed autonomic response to noxious stimuli for individuals with SCI at or above T6


Desired Outcomes: On an ongoing basis, patient is free of AD symptoms as evidenced by BP within patient’s baseline range, HR 60-100 bpm, and absence of headache and other clinical indicators of AD. Following instruction, patient and significant other verbalize factors that cause AD, treatment and prevention, and when immediate emergency treatment is indicated.

































































































ASSESSMENT/INTERVENTIONS RATIONALES
Assess for indicators of AD, including hypertension (BP more than 20 mm Hg above baseline, but may go as high as 240-300/150 mm Hg), pounding headache, bradycardia, blurred vision, nausea, nasal congestion, flushing and sweating above the level of injury, and piloerection (goose bumps) or pallor below level of injury. AD is a medical emergency that can occur after spinal shock resolution in patients with injuries at or above T6, but cases have been reported in patients with injuries as low as T8.
If AD is suspected, raise head of bed (HOB) immediately to 90 degrees or assist patient into a sitting position. These actions lower patient’s BP and decrease venous return. Seizures, subarachnoid hemorrhage, myocardial infarction (MI), stroke, or retinal hemorrhage can occur if severe hypertensive episode continues.
Call for someone to notify health care provider; stay with patient, and systematically search to identify and relieve the noxious stimulus. Speed is essential. The noxious stimulus (e.g., distended bladder) must be found and alleviated as quickly as possible in order to remove the stimulus triggering AD.
Assess BP q3-5min during hypertensive episode. This assesses trend of the BP.
Remain calm and supportive of patient and significant other. They will be very anxious.
Assess the following sites for causes, and implement measures for removing the noxious stimulus.  
Bladder: Distention, UTI, calculus and other obstructions, bladder spasms, catheterization, or bladder irrigations performed too quickly or with too cold a liquid. Problems with the bladder are the most likely cause of AD.
Do not use Credé’s method for a distended bladder. The increased bladder pressure could further stimulate the reflex and worsen the condition.
Catheterize patient (ideally using anesthetic jelly) if there is a possibility or question of bladder distention. Consult health care provider stat. Bladder distention is a potential cause of AD and requires immediate intervention. Anesthetic jelly prevents skin stimulation, which could trigger AD.
If a catheter is already in place, check tubing for kinks and lower drainage bag. For obstruction, such as sediment in tubing, slowly irrigate catheter as indicated, using 30 mL or less of normal saline. If catheter patency is uncertain, recatheterize patient using anesthetic jelly. These interventions enable checking for catheter tube patency. Obstruction is a potential cause of AD.
If the bladder is not distended, check for cloudy urine, hematuria, and positive laboratory or x-ray examination results. These are signs of UTI and/or urinary calculi—two potential causes of AD.
Obtain urine specimen. Culture and sensitivity studies will show if UTI, a potential cause of AD, is present.
Instill tetracaine or lidocaine into the bladder if prescribed. These agents will reduce bladder excitability.
Institute preventive measures as prescribed to prevent UTI and urinary calculi. Future episodes may be caused by these factors.
Bowel: Constipation, impaction, insertion of suppository or enema, or rectal examination. Problems with the bowel are the second most likely cause of AD. A good bowel regimen is a key factor in preventing the noxious stimuli that constipation may cause.
Do not attempt rectal examination without first anesthetizing the rectal sphincter and anal canal with anesthetic jelly. Anesthetic jelly prevents skin stimulation, which could trigger AD.
Use large amounts of anesthetic jelly in anus and rectum before disimpacting bowel to remove potential stimulus. Bowel impaction is a potential cause of AD.
Wait 5 minutes and check BP before disimpacting. A lowered BP is a sign that anesthetic jelly has become effective.
Skin: Pressure, infection, injury, heat, pain, or cold. These are possible causes of AD. A good skin integrity program is another key factor in preventing these noxious stimuli.
Loosen clothing and remove antiembolism hose, leg bandages, abdominal binder, or constrictive sheets as appropriate. For male patients, check for pressure source on penis, scrotum, or testicles and remove pressure if present. Pressure on the skin is a potential cause of AD. Removal of hose, bandages, etc., also enables assessment of the skin for redness and other signs of pressure.
Check skin surface below level of injury. Monitor for presence of a pressure area or sore, infection, laceration, rash, sunburn, ingrown toenail, or infected area, or check skin for contact with a hard object. If indicated, apply a topical anesthetic. Skin infection, pain, and injury are potential causes of AD.
Observe for and remove source of heat or cold (e.g., ice pack, heating pad). Topical heat or cold are two potential causes of AD.
Turn patient on side and ensure that bed linen is free of wrinkles. Consider adhering to a more frequent turning schedule. These measures relieve other possible sources of pressure.
Additional causes: Surgical manipulation, incisional pain, sexual activity, menstrual cramps, labor, vaginal infection, or intraabdominal problems such as appendicitis.  
Administer antihypertensive agents such as nifedipine (oral, sublingual), nitroglycerin (sublingual, spray, or topical ointment), hydralazine, diazoxide, terazosin, or phenoxybenzamine as prescribed. These medications lower patient’s BP.
Check for use of sildenafil, an erectile dysfunction medication, before giving nitroglycerin. Sildenafil is contraindicated for people who are taking nitrates (e.g., nitroglycerin) because of the additive hypotensive effect.
Administer mecamylamine, prazosin, or clonidine if prescribed for recurrent AD. These medications reduce severity of recurrent episodes.
On resolution of the crisis, answer patient’s and significant other’s questions about AD. Discuss signs and symptoms, treatment, methods of prevention, and need for regular assessment of causative agents. Prevention is the best way to deal with AD. A bowel regimen and skin integrity program are key factors in preventing the noxious stimuli that constipation and pressure areas may cause.
Encourage patient to wear a medical alert bracelet or tag. These items inform health care providers of patient’s condition in case the patient is unable to do so during AD.
Encourage keeping an AD kit on hand that includes a glove, lubricant jelly, straight catheter, electronic BP machine, and alert card. This kit will help relieve and monitor this medical emergency when it occurs.




Nursing diagnosis:


Ineffective airway clearance

related to neuromuscular paralysis/weakness or restriction of chest expansion occurring with halo vest obstruction


Desired Outcome: Following intervention, patient has a clear airway as evidenced by respiratory rate (RR) of 12-20 breaths/min with normal depth and pattern (eupnea) and absence of adventitious breath sounds.






























ASSESSMENT/INTERVENTIONS RATIONALES

Monitor ventilation capability by checking vital capacity, tidal volume, and pulmonary function tests. Monitor serial ABG values and/or pulse oximetry readings.

Provide oxygen as indicated.
If vital capacity is less than 1 L or if patient exhibits signs of hypoxia (Pao2 less than 80 mm Hg, O2 saturation 92% or less, tachycardia, increased restlessness, mental status changes or dullness, cyanosis), health care provider should be notified immediately.

Oxygen will help keep saturation greater than 92%.
Assess for increasing difficulty with secretions, coughing, respiratory difficulties, bradycardia, fluctuating BP, and increased motor and sensory losses at a higher level than baseline findings. These signs may signal ascending cord edema secondary to effects of contusion or bleeding. If present, patient may require increased respiratory support.
Assess for loss of previous ability to bend arms at the elbows (C5-6) or shrug shoulders (C3-4). If these findings are noted, notify health care provider immediately. Changes from baseline or previous assessment may signal problems such as contusion, compression, bleeding, or damage to blood supply, and they necessitate prompt intervention.
Keep patient’s head in neutral position, and suction as necessary. Be aware that suctioning may cause severe bradycardia in the patient with autonomic dysfunction. If indicated, prepare patient for a tracheostomy, endotracheal intubation, and/or mechanical ventilation to support respiratory function. If appropriate, arrange for transfer to intensive care unit for continuous monitoring. These actions maintain a patent airway and support respiratory function. Patients with injuries above C5 are intubated and put on a ventilator. Nasal intubation or tracheostomy may be used to prevent neck extension (and thus further damage) during intubation. An implanted phrenic nerve stimulator (e.g., diaphragm pacer) eventually may be inserted to enable selected patients on ventilators to be off the ventilator for short periods.

If patient is wearing halo vest traction, assess respiratory status at least q4h or more frequently as indicated.

Assess ability to swallow for patient in halo traction.
This action ascertains whether the vest is restricting chest expansion.

Inability to swallow may indicate improper position of neck and chin or changes in cranial nerve function caused by cranial pin compression or irritation.
Teach use of incentive spirometry. Spirometry promotes adequate ventilation and assesses quality of patient’s inspiratory abilities.
Assess for shortness of breath, hemoptysis, tachycardia, sudden shoulder pain, and diminished breath sounds. These are indicators of venous thromboembolus (VTE)/pulmonary embolus (PE), which can occur because of impaired ventilation, altered vascular tone, and decreased mobility. Pain may or may not be present with VTE/PE, depending on level of SCI. Sudden shoulder pain may be referred pain from VTE/PE.

Encourage coughing exercises.
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Jul 18, 2016 | Posted by in NURSING | Comments Off on Spinal cord injury

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