SCI affects young adults most often. Population-based data show the highest incidence, nearly 51.6% of injuries, occurs in the 16- to 30-year age group.³ However, the most recent trends suggest that SCI is occurring with increasing frequency in older persons. The result is that the fastest growing population of new SCI patients is older than 60 years of age. Since 1990, the incidence of SCI in persons older than 60 has increased to 12% from 4.5% in the 1970s.³ The average age at SCI has increased from 28.7 to 38.9 as of 2007. Additionally, while SCI is an injury that occurs primarily in males (81.6% since 1973), some centers are reporting increasing numbers of females suffering SCI.

Life Expectance

Life expectancies for persons with SCI that were so low many years ago continue to steadily increase. Mortality rates, however, while improving, continue to be highest during the first year after injury. Complete injuries still have lower ultimate survival rates than incomplete injuries. The degree of neurologic impairment, as measured by the Frankel Grade or the American Spinal Injury Association (ASIA) Impairment Scale, and level of injury were significantly correlated with mortality risk. For example, the average life expectancy of a 20-year-old who suffers complete paraplegia is 66 years. This compares with 61 years for a C5 to C8 SCI, 57 years for a C1 to C4 SCI, and 43 years for a ventilator-dependent patient. This compares with the normal life expectancy in the general population of 77 years and in a patient with incomplete SCI of 72 years.⁵ The factors that can increase life expectancy are favorable circumstances for good health, community integration, and higher income.⁶

Mortality

Many years ago, the leading cause of death among persons with SCI was renal failure. Pulmonary embolus (PE) usually in the first few weeks after injury, and most often associated with a deep vein thrombosis (DVT), was another frequent cause of death. Advances in urologic management, DVT and PE prevention, and early mobilization have reduced the number of early deaths. Today, renal failure rarely occurs in the acute SCI setting. Because more SCI patients live not only through their first year after injury but also survive to old age, cardiovascular disease has become a more frequent cause of death (Fig. 84–1). Nash and colleagues⁷ demonstrated that SCI is an independent risk factor for developing multiple risks for cardiovascular disease such as increased cholesterol. Respiratory illness, particularly pneumonia, is now the leading cause of death among older SCI patients with cervical injuries.⁸ The cause of death in persons with paraplegia is more varied. In addition to heart disease, cancer, suicide, and septicemia are the leading causes.

FIGURE 84–1 Cause of death after spinal cord injury.

Etiology

The causes of spinal cord injury are typically divided into traumatic and nontraumatic. The top five causes of traumatic SCI in males are auto accidents, falls, gunshot wounds, diving, and motorcycle accidents.³ The top three remain the same in women, but the final two are medical causes and diving³ (Fig. 84–2).

FIGURE 84–2 Etiology of spinal cord injury by gender of patients.

(Adapted with permission from Jackson AB, Dijkers M, DeVivo MJ, Poczatek RB: A demographic profile of new traumatic spinal cord injuries: Change and stability over 30 years. Arch Phys Med Rehab 85:1740-1748, 2004.)

The major trend is that violent injuries have decreased from 20% in the 1990s to 9.8% in 2000s.³ Geographic variations occur depending on the state or city. In the older SCI patients, in addition to falls, nontraumatic causes of SCI such as cancer, vascular injuries, and infection make up a larger proportion of injuries.

Etiology is also reported in terms of major groups. Figure 84–3 illustrates the frequency that each of these groups causes SCI.

FIGURE 84–3 Etiology of spinal cord injury.

Classification of Spinal Cord Injury

The spinal cord has three basic physiologic functions. The ascending tracts in the cord receive sensory information from the somatic and visceral receptors through dorsal root ganglia and transmit this information to higher centers. The descending tracts receive signals from higher centers and ultimately transmit these signals to target sites via the ventral roots. The other basic function of the spinal cord is to modulate these signals via a variety of local mechanisms.

Assessment, treatment, and classification of spinal cord injury flow directly from the anatomy, physiology, and topography of the spinal cord. Classification or grouping of patients allows the rehabilitation physician to predict the outcome and ultimate function in a majority of patients on the basis of others with similar injuries. This allows the rehabilitation team to design a rehabilitation program appropriate for individual SCI patients to give them the best opportunity to maximize their potential functional outcome.

The most accurate way to assess a patient who has suffered an SCI is to perform a standardized physical examination as outlined by the American Spinal Injury Association. The neurologic examination includes two key components—the motor and sensory examination with required and optional elements. The result allows the clinician to compile a score and determination of the completeness of injury. The neurologic level is also determined by rules set forth in the ASIA examination. From these data a functional classification is assigned to each patient. This information can then be used to design each patient’s rehabilitation program and predict his or her functional outcome on the basis of previous patients with similar injury classifications.

Two assessment tools are used in the evaluation of patients after SCI.⁹ One is the neurologic classification of SCI using the ASIA impairment scale. The other is the functional score, or Functional Independence Measure (FIM) score.

The ASIA impairment scale measures the degree of completeness of injury using categories from A to E (Table 84–1). Complete paralysis is defined as the absence of sensory and motor function in the lowest sacral segments and incomplete paralysis as preservation of sensation below the level of the injury including the lowest sacral segments. Sacral sparing is defined as voluntary anal contraction or presence of dull touch and pinprick sensation in the rectal and perianal area.

TABLE 84–1 American Spinal Injury Association (ASIA) Impairment Scale

Scale Grade	Description
A	Complete—No motor or sensory function is preserved in the sacral segments S4-5.
B	Incomplete—Sensory but not motor function is preserved below the neurologic level and includes the sacral segments S4-5.
C	Incomplete—Motor function is preserved below the neurologic level, and more than half of key muscles below the neurologic level have a muscle grade less than 3.
D	Incomplete—Motor function is preserved below the neurologic level, and at least half the key muscles below the neurologic level have a muscle grade of 3 or more.
E	Normal—Motor and sensory function is normal.

In addition to the ASIA impairment scale is a scoring system that measures the strength of each muscle on a 6-point scale (0 to 5) and sensation for pinprick and dull touch on a 3-point scale (0 to 2). The motor level of SCI is defined as the lowest normal motor segment that has a grade 3 or more, providing the muscles above that level are graded as a 5. The motor level best reflects the severity of impairment and disability during rehabilitation.

FIM score is a widely accepted functional assessment tool and is currently used as an indicator of function in patients with SCI. FIM is an 18-item scale. There are two categories of items, motor and cognitive. Individual items in each category score from 1 to 7, from “total assistance” to “complete independence.” There are 13 items of motor scoring important in determination of self-care, sphincter control, and mobility (Box 84–1). Scores falling below 6 indicate that the patient requires another person for assistance. Many rehabilitation units now use FIM scores to measure patient outcomes. Quality assurance units use these data from groups of patients to draw inferences on the effectiveness of the rehabilitation unit.

Clinical Syndromes

In addition to classifying patients on the basis of their individual motor and sensory injury levels, the following specific clinical syndromes have been identified in the literature: central cord, anterior cord, posterior cord, Brown-Séquard, conus medullaris, and cauda equina syndromes.^10,¹¹

Central Cord Syndrome

The most common type of incomplete SCI in the elderly, central cord syndrome also carries with it a relatively favorable prognosis for recovery. The mechanism of injury is usually hyperextension of an already stenotic cervical canal producing central hematomyelia.¹² Because the lumbar and sacral motor tracts are located in the periphery of the white matter, the syndrome is characterized by motor weakness of the upper extremities greater than the lower extremities and sacral sparing. Recovery occurs more favorably in younger patients. Between 87% and 97% of patients younger than 50 will eventually ambulate, versus 31% to 41% of those older than 50. Hand intrinsic function is last to recover, usually incompletely in all ages.

Anterior Cord Syndrome

This is an injury to the anterior two thirds of the spinal cord including both gray and white matter. The posterior columns are preserved. The mechanism of injury is either due to thoracic fractures with retropulsion of disc or bone fragments or lesions of the anterior spinal artery. The resulting SCI is most commonly complete paralysis with spasticity. In the lower extremities deep pressure and proprioception are preserved. However, the prognosis for motor recovery is relatively poor.¹³

Posterior Cord Syndrome

The least common incomplete SCI is characterized by absence of position sense. There is usually preservation of pain, temperature, and touch. Motor function is impaired in varied amounts.

Brown-Séquard Syndrome

This injury occurs with a literal or functional hemisection of the spinal cord. The most common cause is a bullet or knife wound. The classic presentation is ipsilateral loss of motor function, ipsilateral loss of dorsal column sensation, and contralateral loss of pain and temperature below the level of the lesion. Overall, these patients have the greatest potential for functional outcome and ambulation (75% to 90%).¹⁴ Bowel and bladder continence is regained in 82% and 89%, respectively.

Conus Medullaris, Epiconus, and Cauda Equina Syndromes

Patients with these lesions present with similar motor and sensory deficits but are also different in a few distinct ways. Patients present with patchy lower extremity weakness, saddle anesthesia, and incontinence of stool. Urinary retention is more common than incontinence. Lesions of the cauda equina are clearly lower motor neuron with decreased lower extremity motor tone, absent lower extremity and bulbocavernosus reflexes, flaccid bladder, and asymmetric weakness. High conus (epiconus) lesions may have upper motor neuron (UMN) findings mixed with the lower motor neuron findings.

Cauda equina lesions carry a much more favorable prognosis for functional motor and sensory recovery, especially when surgical/medical treatment occurs promptly. Bowel, bladder, and sexual function return less frequently, often leading to adjustment and psychologic difficulties. The long-term difficulties in patients with cauda injuries are compounded by a high incidence of severe neuropathic lower extremity pain not usually seen in conus injuries. Thus patients recovering from cauda equina injuries may have long-term physical and emotional disabilities despite their seemingly “normal” outward appearance even after successful physical rehabilitation.

Therapy Approaches

As stated earlier, rehabilitation of the SCI patient begins from the moment of injury. Quick response, transfer to a level I trauma center, and prompt medical and surgical treatment results in a minimizing of medical complications and preservation of neurologic function. In the acute hospital setting, important recommendations given on consultation with the SCI specialist include treatment of neurogenic bowel and bladder, prophylaxis of DVT and PE, prophylaxis of gastric ulcer, preventing atelectasis and pneumonia via proper pulmonary management, and preventing skin ulcers with proper positioning in bed and turning every 2 hours. Physical and occupational therapies are initiated in the acute hospital unit once the spine is stabilized. Range of motion (ROM) is performed to the shoulders, hips, elbows, and heel cords. ROM should be performed twice daily to prevent joint contractures and can be taught to family members. Splints are made for the upper extremities for the same reason. The patient begins to build tolerance to sitting and is taught weight shifting to prevent pressure ulcers. The goal is to achieve medical stability so that the injured patient can be admitted as quickly as possible to a multidisciplinary inpatient rehabilitation hospital that specializes in SCI treatment.

Once the acute treatment is completed and the patient is deemed “medically stable,” the rehabilitation course is assisted with the quickest possible transfer to the rehabilitation unit. In cases of high tetraplegia, medical stability may be achieved while the patient is still on a ventilator. The result of a shorter length of stay in the acute hospital and quicker move to rehabilitation is to lower the cost to the “health care system” and improve the ability of patients to quickly see functional recovery.

Moving patients quickly through rehabilitation has some negative consequences, too. Sometimes patients do not have a chance to psychologically adjust to their injury fully. Additionally, shorter lengths of stay have also moved to the rehabilitation hospital.

Unfortunately, these shorter lengths of stay that are often forced on patients and rehabilitation providers by insurance company mandates continue a trend that patients will need to complete their physical, functional, and psychologic rehabilitation as outpatients. Therefore it is imperative then that the rehabilitation be focused and aggressive to accomplish as much as possible in a shorter amount of time. The challenge is to provide SCI patients with the highest quality rehabilitative care despite these imposed constraints so that they leave the hospital with the highest possible outcome.

On the rehabilitation unit, the SCI patient begins a new journey. The basic skills of mobility, self-care, and bladder/bowel functions are relearned regardless of the severity of the injury—sometimes quickly but other times painfully slowly. Patients try to achieve independence in each area, although sometimes only modified or partial independence is possible. The level of neurologic injury best predicts the level of independence and mobility each patient can achieve,¹⁵ even though individual differences occur. SCI patients use a significant time in rehabilitation to review a variety of handbooks and computer programs to become educated on their injury. Most patients also receive counseling for emotional and psychologic adjustment, discover initial vocational options for their future, and participate in recreational and leisure activities that ease their reintegration into society. A subset of SCI patients who suffered concurrent head trauma receives cognitive testing and retraining. Another subset of SCI patients who remain on ventilators receives breathing and communication training. Finally, each patient is discharged to the most independent living situation possible. Usually they can only go home after multiple modifications are built and after a myriad of adaptive equipment is prescribed.

Because the tasks of rehabilitation can be so daunting and involve so much of the “whole person” with all organ systems including the psychosocial system affected, only a dedicated multidisciplinary team can accomplish a successful comprehensive rehabilitation. Each member of the multiple rehabilitation disciplines functions together as a team to optimize each patient’s outcome.¹⁶ Historically the leader of the team has been the rehabilitation physician, or physiatrist, who would create the rehabilitation goals, lead weekly team meetings, and decide when the program is complete. More recently, most rehabilitation programs have shifted to a more patient-centered approach with the interdisciplinary team working toward goals set forth together.¹⁷ All disciplines focus their treatments on the patient, so teamwork and treatment overlap are encouraged. With this approach the patient, and often his or her family, is intimately involved in deciding the direction of the rehabilitation and the date of discharge. The individual disciplines are listed in Table 84–2.¹⁸

TABLE 84–2 Interdisciplinary Team

Discipline	Role
Psychiatrist	Medical care, coordination of rehabilitation, team leader
Rehabilitation nurse	Daily care, medication, education, reinforce skills, transfers
Physical therapist	Gross motor skills, transfers, mobility (wheelchair, standing, ambulation)
Occupational therapist	Fine motor skills, activities of daily living (e.g., feeding, dressing, bathing)
Recreational therapist	Leisure activities, community reintegration, assistive technology use
Social worker	Obtain community resources; assist with disposition planning; communicate with insurance companies
Speech therapist	Assess cognitive status; provide communication, swallowing, and cognitive training
Respiratory therapist	Manage patients on respirator; provide respiratory treatments
Prosthetist/orthotist	Design and fabricate upper/lower extremity braces and prosthesis; fit spine braces
Vocational counselor	Test skills and interest; recommend training and assist with placement
Vendor	Wheelchair procurement and fitting, adaptive equipment

Recent advances in rehabilitation techniques have led to both increased functional outcomes and decreased lengths of stay. One of the most influential advances has been in surgical stabilization. Historically, large bulky cervical braces including halos dominated rehabilitation units. Now, better internal fixation has allowed patients to come onto the rehabilitation units almost immediately after surgery and usually with only a hard collar.¹⁹ The less intrusive bracing allows patients to progress more quickly in their mobility training.

Newer medications have also allowed SCI patients to progress more quickly. Patients who were having difficulty with postural hypotension can get upright sooner and for longer time periods. Other medications have decreased the incidence of DVT, pulmonary embolism, and spasticity. Those SCI patients slowed by neuropathic pain now benefit from new pain medications and procedures. Aggressive percussive lung treatments have decreased the incidence of pneumonia and “down time” on the unit.

The functional rehabilitation program begins with a comprehensive assessment of medical impairments, functional deficits, and environmental setup. Then, on the basis of the findings, appropriate goals can be set and a treatment approach to reach those goals can be initiated and completed. Persons with complete SCI share the common situation that in most cases their impairment remains static or permanent.

Therapists may choose from a number of treatment approaches to achieve the goal of functional independence or achieving maximum function. More than one different type of approach may also be used if felt appropriate by the therapist. Additionally, although therapy sessions and tasks are divided by discipline (e.g., transfer training by physical therapy, activities of daily living [ADL] to occupational therapy), all therapists must use expertise from other specialists on the team to maximize functional restoration and treatment. Within that framework, treatment can be either restorative or compensatory. The goal of restorative treatment is simply to reverse the disability, even if the impairment cannot be reversed. The individual is encouraged to perform the ADL task the same way as before the injury. Compensatory treatment aims to reverse the disability and even the handicap by finding other means of traversing the divide created by the impairment without directly restoring the function. Either way, the functional task gets done independently or at least with the least dependence possible leading to the point of discharge.

The choice of which method to use depends on the underlying condition of the patient. Most persons with complete SCI may gain one or two levels of neurologic function but are unlikely to gain any more neurologic return in their immediate future. Therefore therapists most often use compensatory strategies to create independent function. However, persons with incomplete SCI may see tremendous neurologic recovery over time and are more appropriate for restorative therapy immediately. Therefore therapists must carefully observe their patient and try to project the amount and speed of the recovery. If recovery is occurring quickly, restorative treatment strategies are more appropriate. One example would be employing standing balance strategies at the kitchen even when the patient cannot yet ambulate but should in the near future. Areas of focus on the inpatient rehabilitation stay are as follows:

Neurogenic bladder management

Neurogenic bowel management

Assistive devices

Home and environment modifications

Many advances in therapy techniques have improved treatment offered to SCI patients in rehabilitation. Functional electrical stimulation (FES) has been applied to patients both in the acute rehabilitation setting and later in the outpatient setting to upper and lower extremities.²⁰ Assisted or weighted standing and walking, even with patients with complete injuries, is now being tried in a few centers with promising early results.²¹ Technology and equipment innovation has influenced greatly the quality of care SCI patients receive. Power wheelchairs now have standing options, more rugged wheels, and automatic pressure relief. Manual chairs are now fitted with more advanced cushions, sport options, and “power-assist” wheels. Most cars and vans are outfitted with hand controls. Finally, computerized environmental control units and voice-activated systems have improved independence and freedom for patients with high-level tetraplegia.

Because shorter lengths of stay have moved patients home sooner, the majority of rehabilitation gains often occur in the outpatient setting. Patients with “chronic SCI,” some years after their injury, are even seeing benefits from renewed or prolonged rehabilitation. Jacobs and colleagues ²² showed improvements in cardiovascular status after circuit strength training in SCI patients. Competitive sports for patients with disabilities offer not only physical but also psychologic benefits. Technology has also fueled growth in the rehabilitative treatment of SCI patients long after injury. Tendon transfers had been coupled with the “freehand” implant to improve hand function in many tetraplegic patients.²³ Bladder implants or injections of botulinum toxin may reduce incontinence,²⁴ intrathecal baclofen pumps reduce malignant spasticity,²⁵ and FES implants have allowed for limited amounts of standing and ambulation.²⁶ All of these devices can increase functional independence in the appropriate SCI candidate but also require postplacement rehabilitation training.²⁷

Medical Management

Rehabilitation should begin as soon as possible after SCI. The most important medical aspects in the acute period of rehabilitation include neurogenic bowel and bladder care, pulmonary management, thromboembolic and gastric ulcer prevention, and proper positioning in bed. If early medical complications can be prevented, the rehabilitation course is assisted and the cost of care is significantly reduced.

Neurogenic Bowel Dysfunction

Neurogenic bowel dysfunction is common after SCI and has the potential to influence the social, emotional, and physical well-being of patients. Establishment of an effective bowel program during rehabilitation can minimize the development of disability related to neurogenic bowel. The goal is to control severe constipation, promote regularity, and prevent involuntary bowel movements. Two types of neurogenic bowel dysfunction after SCI exist: reflexic and areflexic.²⁸

Reflexic or UMN bowel dysfunction is seen in patients with SCI above the conus medullaris. Voluntary control of bowel is lost in these patients, but conus-mediated reflex activity and intestinal peristalsis are intact. The external anal sphincter becomes spastic because of the spasticity of the pelvic floor preventing stool evacuation. Stool accumulates in the colon unless reflex defecation is triggered. Bowel care in these patients includes (1) nutritional changes with increased fiber and fluid intake, (2) oral medication (lubricants and cathartics), (3) rectal chemical stimulation (suppositories or enema), and (4) mechanical digital stimulation.²⁹

Areflexic or lower motor neuron (LMN) bowel dysfunction is a result of lesions at or below the conus medullaris. Voluntary control of bowel is lost, as well as sacral reflex activity. The external anal sphincter becomes atonic and flaccid, which increases the risk of fecal incontinence. Management of LMN bowel dysfunction includes (1) diet with fiber and some fluid restriction, (2) oral medication (bulk-forming agent), and (3) mechanical digital removal of stool.²⁹

Neurogenic Bladder Dysfunction

Urosepsis was the leading cause of death before introduction of intermittent catheterization (IC).³⁰ Urologic problems are the most common complications of SCI. The rate of urinary tract infections (UTIs) is 50% to 80% in the first year postinjury. The goal of bladder management during rehabilitation is to establish an effective and safe method of emptying the bladder and avoiding incontinence. Two types of neurogenic bladder dysfunction exist: reflexic and areflexic.

Reflexic or UMN bladder is secondary to lesions above conus medullaris. It is characterized by (1) incontinence secondary to conus-mediated reflex contractions of the bladder detrusor muscle, (2) spastic external urethral sphincter, and (3) detrusor/sphincter dyssynergia.

Areflexic or LMN bladder occurs in lesions below the conus medullaris. This condition is characterized by (1) denervated external urethral sphincter and (2) flaccid detrusor muscle leading to overflow or stress incontinence.

Management of neurogenic bladder after SCI is similar for both types. The routine recommendations are based on clinical practice guidelines prepared by the Consortium for Spinal Cord Medicine ³¹:

• Management of fluid intake to maintain daily urine output between 1.5 and 2 L

• Intermittent catheterization using clean or sterile technique

• Indwelling catheter for patients with poor hand control and lack of attendant care

• Suprapubic catheter for, most commonly, patients with urethral lesions

• External (condom) catheter for male patients with UMN bladder with reflex voiding

• Surgery. The two circumstances when surgery is indicated in management of neurogenic bladder after SCI are (1) to correct the failure to store or (2) to correct the failure to empty urine. The most commonly performed corrective procedures are augmentation of small capacity bladder with intestine and sphincterotomy. The most frequent method of bladder management at discharge from SCI rehabilitation centers is intermittent catheterization (59%); however, a relatively high number of patients were discharged with indwelling catheters (13%).⁴

Spasticity

Spasticity is seen frequently in patients after SCI. In 37% of patients the spasticity is significant and requires chronic therapy. Spasticity may interfere with function, daily activities, and sleep. The severity of spasticity during rehabilitation in SCI patients varies. It has been reported that patients with cervical and upper thoracic injuries have a higher incidence of spasticity than patients with lower spine injuries.³² The underlying processes involved in pathogenesis of hyperactive reflexes are multifactorial and involve both inhibitory and excitatory neurotransmitters. The role of neurotransmitters in spasticity is not fully understood; therefore the therapy is generally symptomatic. Immediately after SCI there is a short period (2 to 3 weeks) of areflexia that is followed by a gradual occurrence of increased muscle tone below the level of injury. In mild to moderately severe cases, ROM and static stretching can be used to treat spasticity during rehabilitation. Medication is usually indicated for severe and chronic spasticity. The different drugs that can be used for spasticity are in order (1) baclofen, (2) benzodiazepines, (3) tizanidine, and (4) dantrolene. Baclofen is a GABA agonist, a major inhibitory neurotransmitter in the central nervous system (CNS). The starting dose is 5 mg three times per day and increased slowly to avoid side effects. The standard maximum dose is 80 mg/day divided either into TID or QID dosing (although some practitioners will go higher). For refractory and severe spasticity, baclofen can be given by intrathecal pump, which will reduce the therapeutic dose 100 times and will also markedly decrease sedative side effects of the drug on the CNS.

Benzodiazepines assist the effect of endogenous GABA, and they are a second-choice medication in treatment of spasticity because their sedative CNS side effects exceed that of baclofen. Tizanidine is an alpha-adrenergic receptor agonist with effects similar to noradrenaline. Noradrenaline belongs to the group of inhibitory neurotransmitters that prevent release of excitatory amino acids from nerve terminals. Tizanidine blocks hyperactive spinal reflexes and, similar to other antispastic medication, has a sedative effect on the CNS. Dantrolene has no effects on the CNS, acting directly on skeletal muscle cells, where it inhibits contraction of myofibrils. The inhibitory effect of dantrolene is due to blockade of endoplasmatic release of calcium. Neurolytic nerve blocks and surgery (dorsal rhizotomy) are additional therapeutic modalities in treatment of spasticity. Although these therapies have not been used frequently in recent years, they are indicated for severe spasticity unresponsive to medication.

Cardiovascular Complications

The primary mechanisms underlying cardiovascular abnormalities are related to the disruption of sympathetic control located in the cervical cord. The most frequent symptoms are orthostatic hypotension (68%) and bradycardia (71%).³³ Autonomic dysreflexia develops in patients with SCI above the T6 spinal segment.

Orthostatic hypotension after SCI is caused by passive vasodilatation below the level of injury, while bradycardia is due to uninhibited parasympathetic tone. Frequent associated clinical findings are weakness, dizziness, blurred vision, and fainting during positional changes. The majority of patients gradually develops adaptation to hypotension and may tolerate orthostasis for an extended period of time. During the period of rehabilitation, different measures such as elastic stockings, abdominal binders, and slow mobilization from the bed can be effective. Also, in early periods after SCI, medication may be indicated. Two oral agents with different mechanisms of action can be used: midodrine and fludrocortisone. Midodrine is an alpha-1 adrenergic agonist (ProAmatine); it is the first-choice drug. Fludrocortisone (Florinef), a mineralocorticosteroid, enhances renal resorption of sodium and may be used as an alternative.

Autonomic dysreflexia (AD) is a serious complication after SCI ³⁴. It is characterized by a sudden onset of pounding headache, increase of blood pressure, and bradycardia. AD occurs in patients with SCI above the T6 spine segment. These patients have interrupted central inhibitory control of the thoracic sympathetic system. Therefore, various peripheral noxious stimuli below the injury (i.e. bladder distension, pressure ulcers, ingrown toenails, UTI, constipation, etc.) may lead to overstimulation of the sympathetic system. AD may have different causes, however it is most commonly related to bladder or bowel distension³⁴. Treatment of AD includes immediate repositioning of patient in a sitting position and loosening of clothing or constrictive devices to allow a pooling of blood into the lower extremities. The placement of an indwelling catheter should be performed early because the most common cause of autonomic dysreflexia is bladder distension. If after the catheterization systolic blood pressure remains elevated over 150 mm Hg, an antihypertensive agent with rapid onset and short duration (i.e., nitrates or nifedipine) is recommended³⁴. If bowel distension or impaction is suspected, antihypertensive medication needs to be administered prior to rectal examination for stool.

The incidence of thromboembolism is high in the acute stage of SCI. The routine screening for deep vein thrombosis (DVT) showed positive results in 47% to 100% of patients.³⁵ Studies based on clinical parameters estimated a lower incidence of DVT in acute SCI. The incidence of clinically diagnosed DVT was 11.4% in 1996, which was significantly reduced to 5.2% in 1998. The decline in the incidence of DVT is most likely the result of introduction of low molecular weight heparin (LMWH).³⁶ Prevention of thromboembolism starts after injury and continues throughout rehabilitation. Current methods for prevention of thromboembolism used in the SCI patients are mechanical (compression hose, boots, pneumatic devices), pharmacologic (unfractionated heparin, LMWH, warfarin), and inferior vena cava filter. A consortium organized by Paralyzed Veterans of America in 1997³⁵ recommended mechanical prevention for the first 2 weeks following injury. In patients with motor complete SCI, pharmacologic prevention with unfractionated heparin or LMWH is recommended for a minimum of 8 weeks or until discharge from the rehabilitation center. Patients with motor complete injuries and risk factors such as obesity, heart failure, cancer, lower extremity fractures, previous DVT, or age older than 70 may need their prevention extended after discharge. The most recent recommendation for the prevention of thromboembolism in the rehabilitation phase of patients with SCI is based on the sixth ACCP consensus in 2001.³⁷ LMWH or full-dose oral anticoagulation with warfarin was the initial recommended method with IVCF recommended in patients who failed or have contraindications to anticoagulation. Treatment of thromboembolism in patients with SCI does not differ from treatment currently used in non-SCI patients.

Respiratory Complications

Respiratory complications are the most common early and late causes of death after SCI. Figure 84–4 shows the most common respiratory complications in patients with different levels of SCI.³⁸ Pneumonia is the most common complication in high-level injuries, whereas atelectasis is seen in all groups of patients in similar frequency regardless of level of injury. Smith and coworkers found in more than 18,000 veterans with SCI a steady rate of visits for acute respiratory infection, without a declining trend in frequency.³⁹

FIGURE 84–4 Respiratory complications after spinal cord injury.

(Adapted with permission from Jackson AB, Grooms TE: Incidence of respiratory complications following spinal cord injury. Arch Phys Med Rehab 75:270-275, 1994.)

There are several factors important in genesis of ventilatory abnormalities after SCI ⁴⁰ such as (1) restrictive ventilatory dysfunction as a result of muscle paralysis, (2) inability to cough, which is due primarily to paralysis of abdominal and intercostal muscles, and (3) hypersecretion of mucus. Overproduction of mucus (about 1 L/day) is due to absent sympathetic outflow and unopposed parasympathetic tone that also leads to bronchoconstriction.

The neurologic level of injury mainly determines the management of respiratory complications after SCI. Patients with cervical injuries from C1 to C3 frequently need mechanical ventilation. Patients with C4 to C7 and upper thoracic injuries often require the following treatments during rehabilitation: (1) bronchodilators (beta-adrenergic agonists and/or anticholinergics), (2) mucolytic agents, and (3) chest physiotherapy.

Later in the phase of rehabilitation and with the return of peripheral sympathetic tone, there is a decrease of mucus production. At this stage respiratory treatments are focused on assisted cough and prevention of respiratory complications. All patients with cervical and high thoracic injuries need yearly vaccination for influenza and every 5 years for pneumonia.

Pressure Ulcers

SCI causes profound changes in the structure and physiology of the skin, which leaves patients susceptible to the development of pressure ulcers. The incidence of pressure sores after SCI is high, with approximately 50% of chronic patients with SCI developing a pressure ulcer in their lifetime. Pressure ulcers are seen on the sacrum in 26%, ischium in 23%, heel in 12%, and trochanter in 10% of chronic SCI patients.⁴¹ Several factors are responsible for the development of pressure ulcers after SCI, but most important is prolonged pressure over a bone prominence. The cornerstones in the prevention of pressure ulcers are regular daily inspection of skin and the performance of pressure relief techniques.

The management of pressure ulcers requires a multidisciplinary team approach. It is also important to provide sufficient nutritional support, treatment of comorbid conditions, and special support surfaces (cushions and mattresses). Two types of mattresses, static (foam, gel, air, or water) and dynamic (air pump with alternating pressure), are used to reduce pressure on the ulcer. Medical treatment may include enzymatic débridement and moist wound dressing changes with various products (transparent membranes, hydrogels, foams, alginates, etc.). Surgical repair is recommended when the ulcers are too large and only if nutritional and medical conditions of the patient are satisfactory.

Heterotopic Ossification

Heterotopic ossification (HO) is another early complication after SCI. Often occurring in the first month of rehabilitation, HO is often a cause of “fever of unknown origin.” The incidence of HO after SCI is about 50%.^42,⁴³ The etiology of HO is unknown. The pathology of HO is characterized by bone growth in extra-articular tissue of paralyzed extremities. Clinically, in the acute stage of HO the most common findings are swelling, fever, and reduction in ROM of affected joint(s). The level of creatine phosphokinase (CPK) in serum in the early stage may indicate the severity of muscle involvement. In the chronic stage, HO may limit the functional status of the patient. Diagnosis of HO in the early stages is based on a positive three-phase bone scintigraphy with 99m Tc diphosphonate. Prevention of HO with indomethacin in patients with SCI is effective if started early (3 to 4 weeks) after injury.⁴⁴ Etidronate is often prescribed to treat HO in the acute stage along with aggressive joint motion by a physical therapist. Only when the heterotopic bone is mature up to 1 year after the onset can surgical resection be considered.

Osteoporosis and Fractures

In patients with SCI there is a significant bone loss in paralyzed limbs in the early period after injury. The most severely involved skeletal regions are the distal femur and proximal tibia. Bone densitometric studies showed that patients with complete paralysis might have bone loss of 30% in the first 3 months.⁴⁵ In later periods bone loss will continue at a slower rate, reaching a new steady state after 2 years. At the final stages bone mineral loss can be about 30% in the femoral shaft and 50% in the proximal tibia.⁴⁶ Patients who actually suffer fractures were found to have even higher bone loss; about 40% in femoral shaft and 70% in proximal tibia. Presently there is no cure for osteoporosis after SCI. Many different preventive programs for bone loss have been evaluated. So far, all preventive measures have shown some positive effect on bone mass, but the effects are transient and the bone loss resumes as soon as the intervention stops. The incidence of lower extremity fractures after SCI is about 1% to 2% per year. Lower limb fractures are most often treated using a nonsurgical approach with the goal of maintaining functional independence. Use of splints and early mobilization are generally allowed initially in a supervised setting.

Pain

Pain prevalence is stable over time ranging from 81% at 1 year after injury to 83% at 25 years.⁴⁷ Approximately 90% of patients with SCI have a delayed onset of pain, and many of them are not finding an adequate pain relief from commonly used medication.⁴⁸ Nepomuceno and colleagues⁴⁹ described the negative impact of pain on the life of patients with SCI. Thirty-seven percent of patients with cervical injuries and 23% of patients with lower level of SCI reported that if they had the chance, they would trade pain for loss of bladder, bowel, or sexual function. Most patients describe pain as stable or controlled, while the others report that pain increased their disability. Of the different classifications of pain after SCI, the most commonly described are central neuropathic and musculoskeletal pain.^50,⁵¹ Clinical differentiation between central neuropathic and musculoskeletal pain is shown in Table 84–3.

TABLE 84–3 Characteristics of Pain after Spinal Cord Injury

Several mechanisms have been proposed in the pathogenesis of central pain, but the causes still remain uncertain. In contrast, musculoskeletal pain is most commonly due to spine injury or overuse of joint, tendon, or ligament structures. Treatment measures depend on which type of pain is being treated. There is no known cure for central pain. The most effective strategy in the management of central pain involves an interdisciplinary approach. However, only partial pain relief can be expected. The treatment strategies follow:

1 Nonpharmacologic (transcutaneous electrical nerve stimulation, aerobic and anaerobic exercise, recreational activity, massage, acupuncture, heat or cold)

2 Pharmacologic

Guidelines from the World Health Organization for the treatment of malignant pain can be applied in these patients: (1) Nonopioid analgesics (nonsteroidal anti-inflammatory drug [NSAIDs], acetaminophen) ± adjuvant (tricyclic antidepressants, selective serotonin reuptake inhibitor, anticonvulsants); (2) opioid for moderate pain (oxycodone, codeine, hydrocodone) ± nonopioid ± adjuvant; and (3) opioid for severe pain (hydromorphone, morphine, fentanyl) ± nonopioid ± adjuvant.

3 Psychosocial/Biofeedback

4 Surgical (nerve blocks, dorsal root entry zone, dorsal column stimulator)

Musculoskeletal pain can be treated with mild analgesic, NSAIDs, passive ROM, and trigger point injections.

Outcomes of Rehabilitation

Length of Stay

In general, patients with tetraplegia need a longer period for rehabilitation than patients with paraplegia. Similarly, patients with complete paralysis require a longer stay at rehabilitation centers than with incomplete paralysis. Recent statistical analysis showed that time needed for acute care has not changed during the past 20 years; however, significant changes were found in the length of stay (LOS) at the rehabilitation centers (Fig. 84–5). Figure 84–5 illustrates results from a database derived from the National database.⁵ A dramatic reduction of LOS was documented at rehabilitation centers across the country from 1977 to 2000. The average length of stay was 106 days in 1977, 90 days in 1987, 51 days in 1997, and 39 in 2004. The changes in the LOS of patients after SCI can mainly be attributed to measures that managed care instituted in the early 1990s.

FIGURE 84–5 Length of stay of patients after spinal cord injury in rehabilitation centers.

(Adapted with permission from Fiedler IG, Laud PW, Maiman DJ, Apple DF: Economics of managed care in spinal cord injury. Arch Phys Med Rehab 80:1441-1449, 1999.)

Discharge Disposition

The changes in the length of stay of patients at rehabilitation centers had some effect on the discharge disposition of these patients. The results from the national database ⁴ obtained in 1997 showed that the majority of patients were still discharged home (91.2%); however, the percent of patients discharged to skilled nursing homes also increased (5.3%) as compared with 2.8% in 1990.

Gain of Motor Function

The outcomes of motor function are determined by the previously discussed ASIA standard evaluation by using the ASIA system and data obtained from the national database.⁵² The outcomes of motor function were related to rehabilitation and neurologic recovery and shown in Figure 84–6. As illustrated in Figure 84–6, about 10% to 15% of patients diagnosed as complete (ASIA “A”) will convert in 1 year to incomplete ASIA “B,” “C,” or “D.” Usually neurologic return of motor function starts in the first month after injury but may continue up to 24 months. Despite recent advances in pharmacologic treatment of spinal cord injury, prognosis for recovery of patients with initial ASIA “A” remains poor. The prognosis for motor function recovery of patients with ASIA “B” designation is intermediate. One third of these patients remain unchanged, one third converts to ASIA “C,” and one third to ASIA “D” or “E.” In the group of patients with ASIA “C” designation, 70% will convert to ASIA “D.” Patients with initial ASIA “D” designation showed functional improvement to “E” in 4%, whereas 96% of these patients remained in the “D” category. Even after 5 years from traumatic SCI, results are not very different. Kirshblum and colleagues⁵³ found that only 4.5% of patients with motor complete paralysis regained some motor or sensory recovery.

FIGURE 84–6 The changes in motor function after spinal cord injury. The American Spinal Injury Association (ASIA) scale is used to grade motor function. For ASIA scoring see text.

(Adapted with permission from Marino RJ, Ditunno J, Donovan WH, Maynard F: Neurological recovery after spinal cord injury. Arch Phys Med Rehab 80:1031-1396, 1999.)

Functional Independence (Charting ADL Improvement Objectively)

Currently the most widely used validated ADL evaluation scale is the functional independence measure (FIM).⁵⁴ The FIM instrument evaluates nine areas of self-care and can be applied multiple times throughout the course of treatment not only to provide a baseline of function but also to chart improvement in these key areas. The areas that the FIM reports on are self-feeding; grooming; bathing; dressing upper and lower body; toileting; and transfer to the toilet, tub, or shower. The FIM has demonstrated a high degree of inter-relater reliability.⁵⁵After the SCI patient leaves the hospital, the FIM can be continued in a self-reporting form (FIM-SR). Masedo and colleagues found the FIM-SR motor scales and total FIM-SR score to be reliable and valid measures of perceived functional independence in individuals with SCI.⁵⁶

Figure 84–7 shows the results from the national database on FIM scores.⁵⁷ The data were obtained on admission and discharge from rehabilitation and at the follow-up after 1 year. There is a marked difference in FIM motor scores from admission to discharge from rehabilitation in all neurologic groups of patients. The greatest improvements are seen in patients with lower cervical and thoracolumbar injuries. There was little change in FIM scores in all categories of patients beyond discharge from rehabilitation. Figure 84–7 illustrates mean FIM motor scores for each neurologic group of patients and indicates that a score of 78 (13 motor items with scores of 6), correlating with functional independence, is reached only in patients with thoracolumbar injuries.

FIGURE 84–7 Functional independence measure (FIM) of spinal cord injury patients at admission and discharge from rehabilitation center and 1 year thereafter (YR-1). For FIM scoring see text.

(Adapted with permission from Hall KM, Cohen ME, Wright J, et al: Characteristics of the functional independence measure in traumatic spinal cord injury. Arch Phys Med Rehab 80:1471-1476, 1999.)

Despite the advantages that using a validated comprehensive ADL measure creates, there are significant limitations. Specifically, the FIM is not specific to SCI but is a general measure of any rehabilitation diagnosis. Thus some aspects critical to SCI function such as mastery of the environment and respiratory function are not charted.

Therefore the Spinal Cord Independence Measure (SCIM III, revised three times) created a new, more comprehensive measure applicable to persons with paraplegia and tetraplegia, complete and incomplete.⁵⁸ Itzkovich and colleagues⁵⁹ found total agreement between raters was above 80% in most SCIM III tasks. They also found the SCIM III was more responsive to changes than FIM in the subscales of respiration and sphincter management and mobility indoors and outdoors. The measure is now undergoing final studies to see if it is more sensitive or specific for SCI-injured persons than other measures while maintaining the practicality of the FIM.

Employment

More than half (57.4%) of those persons with SCI admitted to a model system reported being employed at the time of their injury. The postinjury employment picture is better among persons with paraplegia than among their tetraplegic counterparts. By postinjury year 10, 32.4% of persons with paraplegia are employed, whereas 24.2% of those with tetraplegia are employed during the same year. National data from Model System Spinal Cord Centers revealed that the rate of employment of SCI patients is approximately 27% after rehabilitation.⁶⁰ Similar results were found for both genders, 24.1% in female patients and 27.7% in male patients. Important factors in obtaining employment after SCI were age, severity of injury, and educational level before injury.

Community Integration

Community integration of patients with SCI starts during inpatient rehabilitation and continues after discharge from rehabilitation center. The involvement of human services plays a major role in assisting patients in the community. Figure 84–8 depicts the three aspects of community integration after SCI: functional independence, social integration, and occupation. Data obtained from the national database⁶¹ indicate high levels of social integration in all neurologic groups of patients after SCI. The lowest median score of community integration was found in occupation, as discussed in the paragraph earlier. Community and athletic groups increase the levels of community integration. Activities that injured persons used to participate in can be modified for the wheelchair athlete or participant, increasing the quality of life for those injured. The sports include sailing programs, diving programs, wheelchair basketball teams, skiing, rugby, marathon racing, and Paralympic competitions.

FIGURE 84–8 Community integration after spinal cord injury. Each neurologic group included patients with the American Spinal Injury Association scale A, B, and C.

(Adapted with permission from Whiteneck G, Tate D, Charlifue S: Predicting community integration after spinal cord injury from demographic and injury characteristics. Arch Phys Med Rehab 80:1485-1491, 1999.)

In general, the analysis of demographic data indicates that survivors of SCI with less severe neurologic injury, of younger age, of Caucasian ethnicity, and more education will achieve greater community integration.