spinal cord injury

Spinal Cord Injury

Definition

Spinal cord injury is damage to the spinal cord that causes loss of sensation and motor control.

Description

Approximately 10,000 new spinal cord injuries (SCIs) occur each year in the United States. About 250,000 people are currently affected. Spinal cord injuries can happen to anyone at any time of life. The typical patient, however, is a man between the ages of 19 and 26, injured in a motor vehicle accident (about 50% of all SCIs), a fall (20%), an act of violence (15%), or a sporting accident (14%). Alcohol or other drug abuse plays an important role in a large percentage of all spinal cord injuries. Six percent of people who receive injuries to the lower spine die within a year, and 40% of people who receive the more frequent higher injuries die within a year.Short-term costs for hospitalization, equipment, and home modifications are approximately $140,000 for an SCI patient capable of independent living. Lifetime costs may exceed one million dollars. Costs may be three to four times higher for the SCI patient who needs long-term institutional care. Overall costs to the American economy in direct payments and lost productivity are more than $10 billion per year.

Causes and symptoms

Causes

The spinal cord is about as big around as the index finger. It descends from the brain down the back through hollow channels of the backbone. The spinal cord is made of nerve cells (neurons). The nerve cells carry sensory data from the areas outside the spinal cord (periphery) to the brain, and they carry motor commands from brain to periphery. Peripheral neurons are bundled together to make up the 31 pairs of peripheral nerve roots. The peripheral nerve roots enter and exit the spinal cord by passing through the spaces between the stacked vertebrae. Each pair of nerves is named for the vertebra from which it exits. These are known as:

C1-8. These nerves enter from the eight cervical or neck vertebrae.
T1-12. These nerves enter from the thoracic or chest vertebrae.
L1-5. These nerves enter from the lumbar vertebrae of the lower back.
S1-5. These nerves enter through the sacral or pelvic vertebrae.
Coccygeal. These nerves enter through the coccyx or tailbone.

Peripheral nerves carry motor commands to the muscles and internal organs, and they carry sensations from these areas and from the body's surface. (Sensory data from the head, including sight, sound, smell, and taste, do not pass through the spinal cord and are not affected by most SCIs.) Damage to the spinal cord interrupts these signals. The interruption damages motor functions that allow the muscles to move, sensory functions such as feeling heat and cold, and autonomic functions such as urination, sexual function, sweating, and blood pressure.Spinal cord injuries most often occur where the spine is most flexible, in the regions of C5-C7 of the neck, and T10-L2 at the base of the rib cage. Several physically distinct types of damage are recognized. Sudden and violent jolts to nearby tissues can jar the cord. This jarring causes a temporary spinal concussion. Concussion symptoms usually disappear completely within several hours. A spinal contusion or bruise is bleeding within the spinal column. The pressure from the excess fluid may kill spinal cord neurons. Spinal compression is caused by some object, such as a tumor, pressing on the cord. Lacerations or tears cause direct damage to cord neurons. Lacerations can be caused by bone fragments or missiles such as bullets. Spinal transection describes the complete severing of the cord. Most spinal cord injuries involve two or more of these types of damage.

Symptoms

PARALYSIS AND LOSS OF SENSATION. The extent to which movement and sensation are damaged depends on the level of the spinal cord injury. Nerves leaving the spinal cord at different levels control sensation and movement in different parts of the body. The distribution is roughly as follows:

C1-C4: head and neck.
C3-C5: diaphragm (chest and breathing).
C5-T1: shoulders, arms and hands.
T2-T12: chest and abdomen (excluding internal organs).
L1-L4: abdomen (excluding internal organs), buttocks, genitals, and upper legs.
L4-S1: legs.
S2-S4: genitals and muscles of the perineum.

Damage below T1, which lies at the base of the rib cage, causes paralysis and loss of sensation in the legs and trunk below the injury. Injury at this level usually does no damage to the arms and hands. Paralysis of the legs is called paraplegia. Damage above T1 involves the arms as well as the legs. Paralysis of all four limbs is called quadriplegia or tetraplegia. Cervical or neck injuries not only cause quadriplegia but also may cause difficulty in breathing. Damage in the lower part of the neck may leave enough diaphragm control to allow unassisted breathing. Patients with damage at C3 or above, just below the base of the skull, require mechanical assistance to breathe.Symptoms also depend on the extent of spinal cord injury. A completely severed cord causes paralysis and loss of sensation below the wound. If the cord is only partially severed, some function will remain below the injury. Damage limited to the front portion of the cord causes paralysis and loss of sensations of pain and temperature. Other sensation may be preserved. Damage to the center of the cord may spare the legs but paralyze the arms. Damage to the right or left half causes loss of position sense, paralysis on the side of the injury, and loss of pain and temperature sensation on the opposite side.DEEP VENOUS THROMBOSIS. Blood does not flow normally to a paralyzed limb that is inactive for long periods. The blood pools in the deep veins and forms clots, a condition known as deep vein thrombosis. A clot or thrombus can break free and lodge in smaller arteries in the brain, causing a stroke, or in the lungs, causing pulmonary embolism.PRESSURE ULCERS. Inability to move also leads to pressure ulcers or bed sores. Pressure ulcers form where skin remains in contact with a bed or chair for a long time. The most common sites of pressure ulcers are the buttocks, hips, and heels.SPASTICITY AND CONTRACTURE. A paralyzed limb is incapable of active movement, but the muscle still has tone, a constant low level of contraction. Normal muscle tone requires communication between the muscle and the brain. Spinal cord injury prevents the brain from telling the muscle to relax. The result is prolonged muscle contraction or spasticity. Because the muscles that extend and those that bend a joint are not usually equal in strength, the involved joint is bent, often severely. This constant pressure causes deformity. As the muscle remains in the shortened position over several weeks or months, the tendons remodel and cause permanent muscle shortening or contracture. When muscles have permanently shortened, the inner surfaces of joints, such as armpits or palms, cannot be cleaned and the skin breaks down in that area.HETEROTOPIC OSSIFICATION. Heterotopic ossification is an abnormal deposit of bone in muscles and tendons that may occur after injury. It is most common in the hips and knees. Initially heterotopic ossification causes localized swelling, warmth, redness, and stiffness of the muscle. It usually begins one to four months after the injury and is rare after one year.AUTONOMIC DYSREFLEXIA. Body organs that regulate themselves, such as the heart, gastrointestinal tract, and glands, are controlled by groups of nerves called autonomic nerves. Autonomic nerves emerge from three different places: above the spinal column, in the lower back from vertebrae T1-L4, and from the lowest regions of the sacrum at the base of the spine. In general, these three groups of autonomic nerves operate in balance. Spinal cord injury can disrupt this balance, a condition called autonomic dysreflexia or autonomic hyperreflexia. Patients with injuries at T6 or above are at greatest risk.In autonomic dysreflexia, irritation of the skin, bowel, or bladder causes a highly exaggerated

The extent of sensory and motor loss resulting from a spinal cord injury depends on the level of the injury because nerves at different levels control sensation and movement in different parts of the body. The distribution is as follows: C1-C4: head and neck; C3-C5: diaphragm; C5-T1: shoulders, arms, and hands; T2-T12: chest and abdomen (excluding internal organs); L1-L4: abdomen (excluding internal organs), buttocks, genitals, upper legs; L4-S3: legs; S2-S4: genitals, muscles of the perineum. (Illustration by Electronic Illustrators Group.)response from autonomic nerves. This response is caused by the uncontrolled release of norepinephrine, a hormone similar to adrenaline. Uncontrolled release of norepinephrine causes a rapid rise in blood pressure and a slowing of the heart rate. These symptoms are accompanied by throbbing headache, nausea, anxiety, sweating, and goose bumps below the level of the injury. The elevated blood pressure can rapidly cause loss of consciousness, seizures, cerebral hemorrhage, and death. Autonomic dysreflexia is most often caused by an over-full bladder or bladder infection, impaction or hard impassable fecal mass in the bowel, or skin irritation from tight clothing, sunburn, or other irritant. Inability to sense these irritants before the autonomic reaction begins is a major cause of dysreflexia.LOSS OF BLADDER AND BOWEL CONTROL. Bladder and bowel control require both motor nerves and the autonomic nervous system. Both of these systems may be damaged by SCI. When the autonomic nervous system triggers an urge to urinate or defecate, continence is maintained by contracting the anal or urethral sphincters. A sphincter is a ring of muscle that contracts to close off a passage or opening in the body. When the neural connections to these muscles are severed, conscious control is lost. In addition, loss of feeling may prevent sensations of fullness from reaching the brain. To compensate, the patient may help empty the bowel or bladder by using physical maneuvers that stimulate autonomic contractions before they would otherwise begin. However, the patient may not be able to relax the sphincters. If the sphincters cannot be relaxed, the patient will retain urine or feces.Retention of urine may cause muscular changes in the bladder and urethral sphincter that make the problem worse. Urinary tract infection is common. Retention of feces can cause impaction. Symptoms of impaction include loss of appetite and nausea. Untreated impaction may cause perforation of the large intestine and rapid overwhelming infection.SEXUAL DYSFUNCTION. Men who have sustained SCI may be unable to achieve an erection or ejaculate. Sperm formation may be abnormal too, reducing fertility. Fertility and the ability to achieve orgasm are less impaired for women. Women may still be able to become pregnant and deliver vaginally with proper medical care.

Diagnosis

The location and extent of spinal cord injury is determined with computed tomography scans (CT scans), magnetic resonance imaging (MRI) scans, and x rays. X rays may be enhanced with an injected contrast dye.

Treatment

A person who may have a spinal cord injury should not be moved. Treatment of SCI begins with immobilization. This strategy prevents partial injuries of the cord from severing it completely. Use of splints to completely immobilize suspected SCI at the scene of the injury has helped reduce the severity of spinal cord injuries in the last two decades. Intravenous methylprednisone, a steroidal anti-inflammatory drug, is given during the first 24 hours to reduce inflammation and tissue destruction.Rehabilitation after spinal cord injury seeks to prevent complications, promote recovery, and make the most of remaining function. Rehabilitation is a complex and long-term process. It requires a team of professionals, including a neurologist, physiatrist or rehabilitation specialist, physical therapist, and occupational therapist. Other specialists who may be needed include a respiratory therapist, vocational rehabilitation counselor, social worker, speech-language pathologist, nutritionist, special education teacher, recreation therapist, and clinical psychologist. Support groups provide a critical source of information, advice, and support for SCI patients.

Paralysis and loss of sensation

Some limited mobility and sensation may be recovered, but the extent and speed of this recovery cannot be predicted. Experimental electrical stimulation has been shown to allow some control of muscle contraction in paraplegia. This experimental technique offers the possibility of unaided walking. Further development of current control systems will be needed before useful movement is possible outside the laboratory.The physical therapist focuses on mobility, to maintain range of motion of affected limbs and reduce contracture and deformity. Physical therapy helps compensate for lost skills by using those muscles that are still functional. It also helps to increase any residual strength and control in affected muscles. A physical therapist suggests adaptive equipment such as braces, canes, or wheelchairs.An occupational therapist works to restore ability to perform the activities of daily living, such as eating and grooming, with tools and new techniques. The occupational therapist also designs modifications of the home and workplace to match the individual impairment.A pulmonologist or respiratory therapist promotes airway hygiene through instruction in assisted coughing techniques and postural drainage. The respiratory professional also prescribes and provides instruction in the use of ventilators, facial or nasal masks, and tracheostomy equipment where necessary.

Pressure ulcers

Pressure ulcers are prevented by turning in bed at least every two hours. The patient should be turned more frequently when redness begins to develop in sensitive areas. Special mattresses and chair cushions can distribute weight more evenly to reduce pressure. Electrical stimulation is sometimes used to promote muscle movement to prevent pressure ulcers.

Spasticity and contracture

Range of motion (ROM) exercises help to prevent contracture. Chemicals can be used to prevent contractures from becoming fixed when ROM exercise is inadequate. Phenol or alcohol can be injected onto the nerve or botulinum toxin directly into the muscle. Botulinum toxin is associated with fewer complications, but it is more expensive than phenol and alcohol. Contractures can be released by cutting the shortened tendon or transferring it surgically to a different site on the bone where its pull will not cause as much deformity. Such tendon transfers may also be used to increase strength in partially functional extremities.

Heterotopic ossification

Etidronate disodium (Didronel), a drug that regulates the body's use of calcium, is used to prevent heterotopic ossification. Treatment begins three weeks after the injury and continues for 12 weeks. Surgical removal of ossified tissue is possible.

Autonomic dysreflexia

Autonomic dysreflexia is prevented by bowel and bladder care and attention to potential irritants. It is treated by prompt removal of the irritant. Drugs to lower blood pressure are used when necessary. People with SCI should educate friends and family members about the symptoms and treatment of dysreflexia, because immediate attention is necessary.

Loss of bladder and bowel control

Normal bowel function is promoted through adequate fluid intake and a diet rich in fiber. Evacuation is stimulated by deliberately increasing the abdominal pressure, either voluntarily or by using an abdominal binder.Bladder care involves continual or intermittent catheterization. The full bladder may be detected by feeling its bulge against the abdominal wall. Urinary tract infection is a significant complication of catheterization and requires frequent monitoring.

Sexual dysfunction

Counseling can help in adjusting to changes in sexual function after spinal cord injury. Erection may be enhanced through the same means used to treat erectile dysfunction in the general population.

Prognosis

The prognosis of SCI depends on the location and extent of injury. Injuries of the neck above C4 with significant involvement of the diaphragm hold the gravest prognosis. Respiratory infection is one of the leading causes of death in long-term SCI. Overall, 85% of SCI patients who survive the first 24 hours are alive 10 years after their injuries. Recovery of function is impossible to predict. Partial recovery is more likely after an incomplete wound than after the spinal cord has been completely severed.

Prevention

Risk of spinal cord injury can be reduced through prevention of the accidents that lead to it. Chances of injury from automobile accidents, the major cause of SCIs, can be significantly reduced by driving at safe speeds, avoiding alcohol while driving, and using seat belts.

Resources

Organizations

National Spinal Cord Injury Association. 8300 Colesville Road, Silver Spring, Maryland 20910. (301) 588-6959. http://www.erols.com/nscia.

Key terms

Autonomic nervous system — The part of the nervous system that controls involuntary functions such as sweating and blood pressure.Botulinum toxin — Any of a group of potent bacterial toxins or poisons produced by different strains of the bacterium Clostridium botulinum.Computed tomography (CT) — An imaging technique in which cross-sectional x rays of the body are compiled to create a three-dimensional image of the body's internal structures.Magnetic resonance imaging (MRI) — An imaging technique that uses a large circular magnet and radio waves to generate signals from atoms in the body. These signals are used to construct images of internal structures.Motor — Of or pertaining to motion, the body apparatus involved in movement, or the brain functions that direct purposeful activity.Motor nerve — Motor or efferent nerve cells carry impulses from the brain to muscle or organ tissue.Peripheral nervous system — The part of the nervous system that is outside the brain and spinal cord. Sensory, motor, and autonomic nerves are included.Postural drainage — The use of positioning to drain secretions from the bronchial tubes and lungs into the trachea or windpipe.Range of motion (ROM) — The range of motion of a joint from full extension to full flexion (bending) measured in degrees like a circle.Sensory nerves — Sensory or afferent nerves carry impulses of sensation from the periphery or outward parts of the body to the brain. Sensations include feelings, impressions, and awareness of the state of the body.Voluntary — An action or thought undertaken or controlled by a person's free will or choice.

spinal cord injury

Spinal cord compression, spinal cord trauma Neurology Traumatic damage to the spinal cord resulting in a significant or complete loss of voluntary control of extremities or autonomic nervous system at and below the level of injury Epidemiology 10,000 to 15,000 new cases/yr; 200,000 currently with chronic SCI–US; MVAs cause 45%, falls 22%, acts of violence 16%, sports–eg, diving into shallow water 13%, etc–industrial accidents, gunshot wounds, assault; ♂:♀ ratio 4:1; mean age = 31; 59% occur at age 16-30 Clinical SC compression due to fluid or blood in sub- and epidural spaces, paralysis, loss of bladder, bowel control Complications-2nd yr UTI 59%, spasticity 38%, chills and fever 19%, pressure sore 16%, autonomic hyperreflexia, contractures Complications-≥ 30 yrs Pressure sores 17%, muscle and joint pain 16%, GI or cardiovascular problems, UTIs or other infections Management Depending on the severity; surgical if acute or unstable; physical therapy for chronic SCI. See SCIWORA.

Spinal Cord Injury

DRG Category:	53
Mean LOS:	3.5 days
Description:	MEDICAL: Spinal Disorders and Injuries Without CC or Major CC

Spinal cord injury (SCI), trauma to the spinal cord, affects approximately 12,000 Americans every year. Half of the injuries produce paraplegia and half quadriplegia. A physiological cascade of events occurs at the time of an SCI and leads to neuronal damage and neurological deficit.

The initial injury causes a release of glutamate, which causes cellular damage and petechial hemorrhages at the injury site. Calcium influx into the neuron is caused by thrombus formation. This alteration in calcium triggers the arachidonic acid cascade to be initiated, leading to free radical formation, lactic acidosis, and lipid peroxidation. This final series of events hastens ischemia of the white matter and microvasculature destruction, with resultant neuronal damage and permanent neurological deficit. This series of physiological and chemical events associated with acute SCI lead to the permanent neurological deficit. With aggressive medical interventions and nursing management, approximately 90% of patients with acute SCI survive.

SCI can be classified by a variety of methods: complete and incomplete cord injury, mechanism of injury, and the level of injury. In a complete SCI, the patient loses all function below the neurological injury level (the lowest neurological segment with intact motor and sensory function). In an incomplete SCI, some motor or sensory function below the neurological injury level remains intact (Table 1).

Types of Incomplete Spinal Cord Injury

Table 1. Types of Incomplete Spinal Cord Injury
INJURY	MECHANISM	DESCRIPTION	FUNCTIONS PRESERVED	FUNCTIONS IMPAIRED
Brown-Séquard syndrome	Penetrating trauma	One side of the cord is affected	Opposite-side pain and temperature sensation	Opposite-side movement, proprioception, light touch
			Same-side movement, proprioception, light touch	Same-side pain and temperature sensation
Posterior cord syndrome	Extension	Loss of posterior column sensory function; motor paralysis	Pain sensation Temperature sensation	Vibratory sensation Proprioception
Anterior cord syndrome	Flexion	Hypalgesia; hypesthesia, motor paralysis, posterior column sensory function preserved	Light touch, proprioception, vibratory sensation	Pain sensation, motor function, temperature sensation
Central cord syndrome	Flexion or extension	Injury to central gray matter	Motor functions of lower extremities	Motor functions of upper extremities

Causes

Leading causes of SCI include motor vehicle crashes (MVCs), falls, acts of violence, and sporting injuries. SCIs caused by violence have increased dramatically in the last decade. The mechanism of injury influences the type of SCI and the degree of neurological deficit.

Genetic considerations

No clear genetic contributions to susceptibility have been defined.

Gender, ethnic/racial, and life span considerations

Acute SCIs occur in both children and adults, although the majority occur between the ages of 16 and 18. The vast majority, approximately 80%, involve men. The financial impact of acute SCIs is tremendous, but it is related to the age of most patients and the degree of disability. Older adults have greater functional and mental status decline after a SCI as compared to their younger counterparts. There are no known racial or ethnic considerations.

Global health considerations

Experts estimate that each year, there are approximately 225,000 cases globally of traumatic SCI from injuries and violence. Transportation injuries from motor vehicle crashes are decreasing in developed regions but increasing in developing regions due to the growing number of vehicles on the road, poor infrastructure, and difficulty enforcing laws. As populations age, traumatic SCI from falls among older adults is increasing in developed and developing regions; falls from heights of less than 5 meters are the leading cause of injury overall, and in developing countries, falls are common from trees, roofs, and balconies, and at construction sites. Traumatic SCI occurs in young people in developing regions from carrying heavy loads on their heads.

Assessment

History

Determine the mechanism of injury in addition to taking a detailed report from prehospital professionals about the patient with an acute SCI. Question the prehospital care provider, significant others, or witnesses about the situation surrounding the injury. If the patient was in an MVC, determine the speed and type of the vehicle, whether the patient was restrained, the patient’s position in the vehicle, and if the patient was thrown from the vehicle on impact. If the patient fell, the distance of the fall is important to know during the initial assessment and evaluation phase. A key component of the history in the patient with a suspected acute SCI is information about the patient’s motor and sensory function at the scene of the injury.

Physical examination

Common symptoms include pain, changes in strength and motion of the extremities, changes in sensation, and changes in bowel and bladder function. Changes may be an autonomic response (urinary retention, constipation, paralytic ileus, hypotension, hypothermia, and bradycardia), a motor response (hemiplegia or hemiparesis, paraplagia or paraparesis, tetraplegia or tetraparesis), or sensory changes at a particular cord level. Assess the patient as soon as possible after the primary injury and again each hour during the acute period. Neurological assessments usually include the Glasgow Coma Scale and pupil reflexes.

The initial assessment is conducted at the injury site. This primary survey generally takes about 30 seconds and focuses on assessing airway, breathing, and circulation (ABCs) and implementing life-saving intervention. Stabilizing the cervical spine prevents an incomplete SCI from progressing to a complete one. The secondary survey is a complete head-to-toe assessment. Sometime during the first 48 hours, a tertiary survey is performed to discover any subtle injuries that may have been missed during the initial assessment.

Assess the patient’s injury level. Test the patient’s ability to distinguish a pinprick from dull pain at each level of the dermatomes. Rectal examination helps determine if the sphincter tone is normal and if the SCI is complete or incomplete. Normal sphincter tone and anal winking indicate an incomplete SCI. Evaluate the patient’s motor strength to help determine the injury level. Test the patient’s motor movement.

Examine the patient for signs of neurogenic shock, which usually occurs within 30 to 60 minutes after the SCI when sympathetic nerves have lost their normal connections to the central nervous system (CNS). Signs to look for include decreased heart rate and pronounced hypotension (systolic pressure below 90 mm Hg).

Psychosocial

Acute SCI is catastrophic and alters not only the lives of patients but also the lives of their families, friends, and the community they live in. Physiological alterations are significant in patients with acute SCIs, as are the psychosocial adjustments. Ongoing assessment of the patient’s and family’s coping skills is critical in planning meaningful support and interventions to assist the patient in reaching her or his functional potential.

Diagnostic highlights

Test	Normal Result	Abnormality With Condition	Explanation
Spine x-rays	Normal body structures	May show spine fractures or injury such as dislocation or subluxation	Determines the integrity of bony structures of spine
Computed tomography scan	Normal body structures	Determines degree and extent of injury; may show spine fractures or injury such as dislocation or subluxation	Determines the integrity of bony structures of spine
Magnetic resonance imaging	Normal body structures	Determines degree and extent of injury; may show spine fractures or injury such as dislocation or subluxation	Determines the integrity of bony structures of spine

Other Tests: Electromyography, somatosensory-evoked potentials, motor-evoked potentials, complete blood count, urinalysis, arterial blood gases

Primary nursing diagnosis

Diagnosis

Ineffective airway clearance related to hypoventilation or airway obstruction

Outcomes

Respiratory status: Gas exchange and ventilation; Safety status: Physical injury

Interventions

Airway insertion; Airway management; Airway suctioning; Oral health promotion; Respiratory monitoring; Ventilation assistance

Planning and implementation

Collaborative

Maintenance of ABCs is the highest priority in patients with SCI. The patient with a cervical or high thoracic injury is at risk for developing pulmonary insufficiency, problems with airway clearance, and ineffective breathing patterns. The patient may require endotracheal intubation or tracheostomy with mechanical ventilation. Assess tidal volume and vital capacity every 2 hours in the patient who is not endotracheally intubated. Hydration may be provided by intravenous (IV) crystalloid fluids or by dextran, a plasma expander that may be used to increase capillary blood flow.

The benefits of early spinal stabilization are decreased morbidity and decreased length of hospital stay, but the neurological benefits are controversial. Although this is a temporary intervention, external stabilization may be accomplished by Gardner-Wells tongs, which can be applied until surgical stabilization can be performed. A halo apparatus can be applied either as a primary intervention or to protect a surgical repair. This device immobilizes the cervical spine but allows the patient increased mobility. Patients with stable thoracolumbar spine fractures require only support with a rigid external brace for several months. Timing for surgical (internal) stabilization of cervical spine injuries is controversial. Some suggest that early surgical stabilization enhances neurological recovery and decreases morbidity, but others believe that early stabilization may increase biochemical alterations and vascular instability.

Patients with unstable thoracolumbar spine fractures are managed with metal rods and surgical decompression. Neurological outcome may be improved by postponing surgery until spinal cord edema is decreased.

Postoperative patients may require a rigid cervical collar or rigid external brace to protect the surgical repair. Patients with acute SCI from penetrating trauma may require surgical intervention for débridement and closure of the dura if cerebrospinal fluid leakage persists. If x-ray films demonstrate that a bullet or other foreign body is within the spinal cord, surgical removal may be recommended to decrease the likelihood of chronic radicular pain.

Pharmacologic highlights

Medication or Drug Class	Dosage	Description	Rationale
Methylprednisolone	30 mg/kg IV as a loading dose, followed by a 48-hr IV infusion of 5.4 mg/kg per hr	Corticosteroid; dexamethasone may also be used	Reduces inflammation and improves motor and sensory function
Inotropic agents	Varies by drug	Dopamine, dobutamine	Improve systemic vascular resistance and blood pressure
Atropine	1 mg IV as needed	Anticholinergic	Manages symptomatic bradycardia

Other Drugs: Prophylactic anticoagulants may prevent the formation of deep vein thrombosis when the patient is no longer at risk for hemorrhage. Histamine-receptor antagonists decrease gastric acid secretion by inhibiting the receptor sites in the parietal cells and reducing the risk of stress ulcers. Antacids may be administered to neutralize gastric acid.

Independent

The most critical nursing intervention for the patient with an acute SCI is to maintain airway, breathing, and circulation. Maintain cervical alignment and immobilization. An abdominal binder may be beneficial in patients with SCIs to provide additional support of the abdominal musculature, a major contributor to respiratory excursion. A potentially life-threatening complication associated with acute SCI is autonomic dysreflexia. This dysfunction may occur after the acute phase and is characterized by a hypersympathetic response to some noxious stimuli; this response is commonly found in patients with SCIs above the T8 level (Box 1). Deep vein thrombosis may also occur. Apply sequential compression devices or foot pumps as prescribed.

Autonomic Dysreflexia

Table .
Precipitating Factors Bladder distension or urinary tract infection Bowel distention Pressure ulcers Thrombophlebitis Gastric ulcers, gastritis Pulmonary emboli Menstruation Constrictive clothing Pain Sexual activity; ejaculation Manipulation of bowel or bladder Spasticity Exposure to hot or cold stimuli	Clinical Manifestations Paroxysmal hypertension Pounding headache Blurred vision Bradycardia Diaphoresis above the level of injury Piloerection Nasal congestion Nausea Pupillary dilation

Check bony prominences and areas under the brace or jacket for skin breakdown. Aggressive physical and occupational therapy early in the acute phase may be beneficial to the patient’s overall rehabilitation. Joint range-of-motion exercises prevent contractures and severe muscle wasting. Some patients may require splints for the upper and lower extremities to prevent flexion contractures and footdrop.

Prevent urinary tract infections by instituting an intermittent catheterization protocol early. Protocols vary, but most begin with catheterizing every 4 hours. Monitor the residual urine volume; when it is less than 400 mL, catheterization can be done every 6 hours. Record the amount of urine voided and the postvoid residuals. As the amount of residual volume decreases, increase the time intervals between catheterizations. Before catheterization, assist the patient in emptying the bladder by Crede’s method or by gently tapping or percussing the bladder. Establish bowel continence early in the acute phase.

When the patient is eating by mouth or is being tube fed, administer stool softeners as ordered. If the patient has not had a bowel movement, administer bisacodyl (Dulcolax) suppository. If the patient is NPO (nothing by mouth), administer bisacodyl every other night. Digital stimulation is used in conjunction with the bowel program. Adequate fluid volume status is important for a successful bowel and bladder program.

Provide diversionary activities to help pass the time. Arrange for the patient or family to consult with a clinical nurse specialist, chaplain, or social worker to assist in coping with anxiety and stress if it is deemed necessary. If the patient has little hope for recovery, consider speaking with the family about donating the patient’s organs if appropriate.

If the patient is scheduled for discharge, teach the patient and family about the recommended activity level and rehabilitative exercises. Explain how to recognize the signs and symptoms of infection or a deteriorating level of consciousness. Instruct the patient and family in the name, dosage, action, and potential adverse effects of all prescribed medications. Show them the proper care for wounds and lacerations. Make sure the patient and family are aware of the schedule for follow-up medical care.

Evidence-Based Practice and Health Policy

Krassioukov, A., Eng, J.J., Claxton, G., Sakakibara, B.M., & Shum, S. (2010). Neurogenic bowel management after spinal cord injury: A systematic review of the evidence. Spinal Cord, 48(10), 718–733.

Investigators conducted a systematic review of 52 studies reporting strategies for neurogenic bowel management in patients with an SCI and evaluated them according to the following levels of evidence: level 1 includes randomized controlled trials (RCTs) with good to excellent methodological quality; level 2 includes RCTs with fair to good methodological quality and nonrandomized cohort studies; level 3 includes case-control studies; and level 4 includes pretest and posttest or case series.
There is level 4 evidence that support the use of multifaceted bowel management programs to reduce gastrointestinal transit time and the duration of time required for bowel management. There is also level 4 evidence that support the use of digital rectal stimulation to increase motility as well as the use of abdominal massage to shorten colonic transit time, reduce abdominal distension, and increase the frequency of bowel movements per week.
Additionally, there is level 1 evidence that supports the use of polyethylene glycol-based suppositories to decrease total bowel care time, and there is level 2 evidence that supports the use of cisapride, prucalopride, and intravenous metoclopramide to decrease constipation, improve stool consistency, and correct impairment in gastric emptying. However, level 4 evidence from one case series revealed that the use of a high-fiber diet increased rather than decreased the colonic transit time among SCI patients in that study.
Lastly, there is level 4 evidence that supports the placement of a colostomy to simplify bowel care routines, reduce the number of hours spent on bowel care, reduce the number of gastrointestinal-related hospitalizations, and improve patients’ health-related and psychosocial quality of life.

Documentation guidelines

Physical findings: Vital signs, hemodynamic parameters, urinary output, tidal volumes, vital capacity, level of consciousness
Presence of complications: Pulmonary infections, urinary tract infection, deep vein thrombosis, alterations in skin integrity, autonomic dysreflexia
Presence of bowel and bladder continence

Discharge and home healthcare guidelines

Encourage the patient to participate in therapies. Instruct the patient to communicate any abnormalities that are recognized. Explain the use of compression stockings as prescribed, with correct application. Teach the patient to maintain the bowel and bladder program. Verify that the patient and family understand the causes and symptoms of autonomic dysreflexia. Be sure the patient understands any medication prescribed. Verify that the patient and family have demonstrated safe use of all assistive devices: wheelchair, transfers, adaptive feeding equipment, and toileting practices. Review with the patient and family all follow-up appointments that are arranged. Verify that all at-home arrangements have been completed.