Clinical aspects

Description

It is recommended that after diagnosis and treatment of acute spinal cord injury, as well as medical stabilization by a team comprised of a neurosurgeon, orthopedic surgeon, rehabilitation medicine specialist, and neuroradiologist (03; 92; 08; 110), the patient should be transferred to an inpatient rehabilitation facility with experience in the care of those with spinal cord injury. Early intervention by a care team familiar with the particular needs, medical challenges, and increased burden related to care of patients with spinal cord injury is important to prevent complications. The inpatient rehabilitation setting allows for an intense rehabilitation regimen to focus on neurologic gains that are typically most pronounced within the first three months following injury (103). It also allows for education regarding disease process and functional training for the patient and family. The goal is to achieve as much independence as possible after leaving the hospital setting (34; 62).

Functional rehabilitation

The approach to rehabilitation of spinal cord injury is highly dependent on the level and severity of injury. A patient with a high cervical injury can be expected to have very different functional goals than that of a low cervical injury or a patient with dorso-lumbar spinal cord injury. Similarly, a patient who is motor incomplete will have different expectations of recovery compared to someone who is motor complete and may change the goals of rehabilitation (12). For simplicity purposes, the following section will review levels assuming a complete injury (44; 54).

C1- to C4-level injuries. Patients with a complete lesion below C1- to C4-level (pentaplegia) are tetraplegics who are dependent usually on respirators. Patients may maintain shoulder shrug and neck movements. As such, rehabilitation of these patients is focused on patient ventilation, education, self-direction of care, family training, and power wheelchair training. Even patients with high injuries should be able to successfully control a power wheelchair using specialized control systems (such as sip-and-puff breath control, tongue control, chin control, or controls and buttons around their head.) It is also helpful to begin familiarizing these patients with environmental control units or voice-activated phones and smart home systems to better control their environment and communicate more easily (99; 64; 87; 86; 68).

A book written by Dr. Stanley Hoppenfeld is an essential tool to understand the following paragraph (Hoppenfeld 1977):

C5-level injuries. Patients with C5-level injuries have strength in several important muscle groups, allowing for better shoulder control and stronger elbow flexion. With the use of splints and cuffs, these patients may be able to perform more self-care tasks. Gross motor movement can allow for the use of a hand-operated joystick on a power wheelchair. With extremely motivated patients, an ultra lightweight manual wheelchair with special hand-rims may be feasible; however, for other reasons (such as ease of transfers, extra truncal support, and weight shifts), a power wheelchair would probably still be recommended for most (25). Patients with C5-level injury would be expected to feed and groom themselves after set-up with assistive devices.

C6-level injuries. Patients with C6-level injuries are able to learn the tenodesis grip, in which active wrist extension causes the passive flexion of the fingers, making a quasi-hand grip (39). With setup help, these patients can be taught to be independent with many components of self-care, including feeding, grooming, hygiene, and some upper extremity dressing. Patients may be able to assist with transfers using a transfer board. Motivated patients may be trained to use manual wheelchairs, although for longer distances they may require power assist functions or full power wheelchairs.

C7-level injuries. C7 is considered the key level where a highly motivated individual with injury can become independent without aides (25). They can be trained to propel a manual wheelchair and perform level transfers, weight shifts, and most self-care tasks. Tasks that may require assistance or adaptive devices include lower body dressing and bowel training. Independent intermittent catheterization can be accomplished, but it is easier to train men than women due to anatomic differences. A rehabilitation program can include all of these functional and mobility goals.

C8-level injuries. Patients with C8-level injuries can more easily accomplish all of these functional tasks because of added grip strength. Patients with this level of injury can be expected to perform all the tasks mentioned above without assistance.

When planning a rehabilitation program, it is important to remember that patients with complete injuries should expect to gain improved function or sensation 1 to 2 levels below their initial neurologic level over time (63). Therefore, a patient’s functional goals can change if their level improves.

Thoracic paraplegia. With thoracic paraplegia, a patient should be able to become independent with all self-care and mobility using a manual wheelchair. These patients should also be able to transfer into a car and use hand controls to drive. Depending on the level of thoracic injury, the patients may have varying degrees of truncal stability requiring different levels of support from their manual wheelchair (91). Working on truncal balance is an important aspect of rehabilitation in these patients.

Lumbar levels. Patients with lumbar levels of injuries may be able to ambulate with the help of orthoses. Depending on the level of weakness, the patient may require more support at each level. For example, with low lumbar injuries, simple ankle-foot orthoses may be sufficient. With weakness at L3-L4 affecting quadriceps, a knee-ankle-foot orthosis may be necessary (47). This can be explored during the inpatient rehabilitation facility stay.

Cauda equina syndrome (CES) involves compression of some or all of the lumbar and sacral peripheral nerve roots. The following symptoms or signs must be present:

Dual diagnosis. Half of the patients, of more, with traumatic spinal cord injury can present with traumatic brain injury, although 75% of them are mild. It is more common in motor vehicle accidents and falls and less common in spinal cord injury where violence or sports are the etiology. Brain injury is also more common in upper cervical spinal cord injury than in lower cervical or thoracic spinal cord injury (59). Concomitant traumatic brain injury can result in increased length of rehabilitation stay and increased cost of care, and alter discharge planning due to neuropsychological impairments (09).

Other concomitant injuries include limb fractures, and/or chest and abdominal injuries (in blunt or penetrating trauma) (32).

Physical rehabilitation

Physical rehabilitation of patients with spinal cord injury involves strengthening intact muscles, as they will now be performing more duties than previously, and strengthening muscles with some intact motor movement. Having at least a 1/5 on manual muscle testing suggests there are at least some intact fibers; antigravity strength (3/5) demonstrates that a muscle can be used functionally (46). For muscles with no strength, other modalities may be employed, such as functional electrical stimulation and locomotor training (102). Early evidence suggests that complete injuries may still have some ability for small recovery with intensive robotic locomotor training (33). Studies have shown that volitional motor recovery with epidural stimulation is possible in individuals with chronic complete spinal cord injury. This is independent of the cross-section area of spinal cord at C3 and of the length of severe myelomalacia on MRI but is dependent on the relationship of the stimulation paddle to the spinal cord lumbosacral area (65).

Not all those who care for the acute and chronic spinal cord injury patients are happy to implement and implant highly sophisticated expensive devices for spinally-injured people or use recent developments like progress in cellular therapy with mesenchymal stem cells (41), spinal stimulations (66), brain stimulation (58), etc.

There is no real alternative for empathy, comprehensive interdisciplinary approach, education, and reeducation, fighting to enhance more understanding for the needs of those with disabilities, improve accessibility and legislation, and more.

Stretching is another focus in rehabilitation, particularly in developing spasticity or strength imbalances between agonist and antagonist muscle groups. Avoid over-stretching finger extensors, as at least some degree of tautness is required to use a tenodesis grip in those with C6 injuries.

Advancements in robotics and pattern recognition technology have brought new interesting device options for those with spinal cord injury. Several robotic exoskeletons are available to practice ambulation. However, it is somewhat too early to determine whether they promote recovery, although they do allow patients who otherwise would not be able to stand upright and ambulate to do so (51). They may also improve cardiovascular health (38). Brain-computer interfaces are allowing patients with high injuries to control computers and robotic devices with signals from their motor cortex; however, they are still not feasible for use outside of a controlled laboratory setting (23; 16; 17; 60).

Medical rehabilitation

All those who care for spinal cord injury patients should be aware of emergencies (36; 74).

Respiratory system. Special attention must be paid to prevent pulmonary compromise in patients with spinal cord injury. Muscles from the neck down to the abdomen, as well as diaphragmatic innervation at C3-C5, are all important in achieving full lung inspiratory and expiratory volumes. Therefore, the higher the injury, the more difficulty a patient will have with respiration. The net response of respiratory function to spinal cord injury is a reduction in vital capacity, which can approach two thirds in patients with cervical spinal cord injury. Also seen is a reduction in maximum breathing capacity, functional residual capacity, expiratory reserve volume, peak inspiratory and expiratory flow rates, inspiratory capacity, total lung capacity, and rib cage and chest wall compliance accompanied by an increase in diaphragm and abdominal wall compliance. This results in significantly decreased respiratory reserves, which is especially important at times of illness and activity (14). Various strategies may be necessary to protect the lungs, including ventilator support and diaphragm/phrenic nerve pacing (83) for high cervical injuries, chest PT, breathing treatments, and abdominal binders. Management of expiratory weakness seen in patients with weak abdominal muscles with injuries at the T6 level and above may need secretion management techniques or mechanical insufflation/exsufflation for daily management or at times of illness (10; 84; 81).

Sleep-disordered breathing is seen in greater than 60% of cervical and 25% of thoracic spinal cord injured persons, higher in motor complete patients. Although this is most commonly in the form of obstructive sleep apnea, up to 60% of cervical spinal cord injured have clinically significant central apnea (89). This is significant as central apnea requires a backup rate, whereas obstructive apnea can usually be treated effectively with positive pressure. Because the onset of these findings is stable after the first few weeks after spinal cord injury, early evaluation and treatment are important. Home-based evaluation is an effective strategy (06), although more hospital-based centers are being equipped to manage spinal cord injury patients (19).

Cardiovascular system. Patients with spinal cord injuries at a level of T6 or above are at risk for autonomic dysreflexia, a process by which the sympathetic nervous system is put into overdrive. It is characterized by flushing, sweating, tachycardia, and blood pressure higher than 20/10 mmHg above their baseline (55). Autonomic dysreflexia may not present until after the acute period of spinal shock (22). Autonomic dysreflexia is usually caused by noxious stimuli below the level of injury. The most common culprits are full bladder or bowels; however, thromboembolism, fractures, ingrown toenails, or infections should be considered in the differential diagnosis. Treatment involves elevating the head, loosening tight clothing, and rectifying the offending agent; this should include intermittent catheterization, resolving constipation, and alleviating pain if present. The blood pressure may increase to the point of hypertensive urgency or emergency; therefore, vasodilator blood pressure-lowering agents, such as nitropaste or nifedipine, may be necessary (26). Medications used for prevention include prazosin (alpha-1 adrenergic receptor blocker), gabapentin (inhibition of presynaptic glutamate release), tizanidine (targeting descending noradrenergic pathways as an alpha-2 agonist), and botulinum toxin (injected into the bladder muscles to decrease detrusor muscle overactivity and resultant sympathetic afferent activity) (94).

Orthostatic hypotension is common after spinal cord injury due to the combination of spinal shock and the lack of normal sympathetic response (70). Midodrine has demonstrated efficacy in some patients with spinal cord injury (104; 82).

Spinal cord injury results in decreased lean body mass and decreased basal energy expenditure. There is decreased arterial diameter below the level of injury. This, with the overall decrease in systolic blood pressure, contributes to the risk of hyperthermia and hypothermia with changes in ambient temperature. There is impairment of vasomotor and sudomotor responses that impacts overall thermoregulation. Cardiac output is decreased due to decreased cardiac sympathetic innervation impacting heart rate (67).

Late after spinal cord injury, there is significant risk of cardiovascular disease. Patients with tetraplegia have a 16%, and paraplegia a 70%, greater risk of cardiovascular disease compared to the general population. Treatment is further complicated by the high incidence of asymptomatic disease. Metabolic syndrome is twice as prevalent compared to the general population. After the first-year post-injury, elevations in cholesterol and low HDL levels are more commonly seen. Increased inflammatory markers may be present as well. There is decreased physical activity and blunted cardiovascular response to exercise (93; 108; 70; 85).

Deep vein thrombosis risk. Patients with spinal cord injury are at increased risk of developing a deep vein thrombosis and complicating pulmonary embolism. Current guidelines are for adult patients to be treated with low molecular weight heparin at prophylactic dose for at least eight weeks after injury, with longer treatment to at least 12 weeks for patients with coagulopathy, cancer history, or concomitant lower extremity fracture (02).

Neurogenic bladder. Loss of bladder control is also a common sequela of spinal cord injury. In general, those with upper motor neuron injuries may end up losing some or all volitional control of the bladder, often with overactivity of their detrusor muscle, or bladder internal sphincter spasticity. Patients with lower motor neuron bladders will still lack control of their bladder, but this is usually due to detrusor underactivity and the inability to increase pressures enough to initiate voiding.

Regardless of the type of bladder dysfunction, if a patient is unable to void on their own, the rehabilitation program should include teaching the patient or family clean intermittent catheterization, which has less of an infection risk than chronic indwelling Foleys. Patients should adjust fluid intake so that they require catheterization of about 500 cc every 4 to 6 hours.

Detrusor overactivity can be treated with a multitude of agents, such as anticholinergics (oxybutynin and tolterodine, etc.) or antimuscarinics (solifenacin, darifenacin, fesoterodine, mirabegron, etc.). Injecting botulinum toxin into the bladder can be an effective treatment for detrusor overactivity. In general, anticholinergics have more side effects than antimuscarinics, but are usually less expensive. Sphincter spasticity usually requires an alpha blocker, most commonly tamsulosin. Detrusor underactivity can be much more difficult to treat; however, if there is any suggestion the patient has sensation or can initiate a void, a cholinergic medication such as bethanechol may be worth trying (88).

Patients with neurogenic bladder should have urodynamic studies completed after the end of spinal shock and with symptom changes. Patients with lower motor neuron bladders (lumbar and sacral level spinal cord injuries) should have a urodynamic study in the first year. Follow up with a urologist should be on a yearly basis, with urodynamic studies every 1 to 2 years, more frequently in those with detrusor-sphincter dyssynergia or changes in symptoms and less frequently in those who have achieved a low pressure bladder reservoir and are otherwise symptomatically stable (90).

Risk of urinary tract infections is increased in patients with spinal cord injury due to bladder overdistention, high-pressure voiding, vesicoureteric reflux, incomplete bladder emptying, urinary stasis, bladder calculi, indwelling catheter use (suprapubic or urethral) and urinary diversions (29). Preventing urinary tract infections is dependent on preventing bladder wall over distention, which results in ischemia and mucosal disruption of the bladder wall. If this proceeds to chronicity, the resultant bladder wall trabeculation leads to decreased bladder wall compliance, which enhances bladder wall ischemia and risk of urinary tract infection. Improving bladder wall compliance with anticholinergic medications and intravesical botulinum toxin improves bladder wall compliance, decreases bladder wall ischemia, and decreases frequency of urinary tract infection. Asymptomatic urinary tract infections with bladder colonization do not need specific treatment. Symptomatic urinary tract infections with elevated bladder urine bacterial colony counts, pyuria, and change in symptoms do require treatment. Strategies to decrease urinary tract infection frequency include treating kidney stones, bladder acidification with methenamine hippurate, and reducing bacterial adhesion with cranberry extract, although there is only strong evidence of effectiveness for treating kidney stones. The use of prophylactic antibiotics is frowned on as ineffective and leading to resistant strains (29; 56). Judicious treatment of urinary tract infections is furthermore important as urinary tract infection-related antibiotic use increases the risk of clostridium difficile infection in patients with spinal cord injury. Means to mitigate this risk is by testing urine to be sure one is treating an infection rather than colonization and avoiding fluoroquinolones and cephalosporins unless indicated by urine culture as they are more likely to lead to clostridium difficile infection than the use of sulfamethoxazole/trimethoprim or macrodantin (57).

Kidney stones incidence of 8 to 9 per 1000 person-years is more than 10 times that of the able-bodied population. In spinal cord injury, there is an overall risk of 15% for every 20 years. It is most common in the first six months post-injury related to calcium excretion, with a 5-year recurrence rate of 35% to 65%. The most common stone is calcium phosphate (apatite), which represents about 50% of all spinal cord injury–related kidney stones. Magnesium ammonium phosphate (struvite) is also common (18%) as it results from urease-producing bacteria in the GI tract (proteus, providencia, klebsiella, morganella, serratia). Other contributing factors to kidney stone production include hypocitraturia, dehydration, elevated urine pH, and vesicoureteral reflux. On presentation, urgent kidney drainage is required in 13% to 17%. More than two-thirds can be treated conservatively (105).

Neurogenic bowel. Patients with spinal cord injury often lose sensation and volitional control of bowel movements. How the neurogenic bowel presents depends on the level of injury, may not become obvious until after spinal shock, and can be obscured by surgical and opioid-induced constipation. Neurogenic bowel is classified as supraconal (slowed GI transit, anorectal hypertonicity, and hyperreflexia) and conal/caudal (hypotonicity). Although neurogenic bowel makes continence a challenge, there are several techniques used to regulate bowel movements. Assessment includes information about bowel frequency, stool consistency, fecal incontinence, and strategies used for bowel management and their efficacy. Evaluation for medications that significantly impact bowel function is important (antimuscarinics, baclofen, opioids, NSAIDs, and antibiotics). Caffeine, alcohol, and sorbitol soften stool and can contribute to incontinence. The main objective is to have a scheduled time once daily to evacuate all stool at once and avoid incontinence. In patients with upper motor neuron bowel patterns, this timing can be supplemented by using reflexes that generally stay intact, such as the gastrocolic reflex (urge to have a bowel movement after a meal) and the rectocolic reflex (bowel movement when the rectal wall is stretched). Therefore, it is recommended to perform a bowel program after a meal, using a suppository and digital stimulation to induce a bowel movement (24). Stool softeners and other promotility agents are often also used to improve evacuation. For lower motor neuron bowels, fiber is utilized to promote stool bulk, and manual disimpaction is generally recommended and may be required more than once per day. Surgical options include sacral neuromodulation, antegrade continent enema procedure, and elective colostomy (28).

An inpatient rehabilitation facility stay allows the rehab team to evaluate bowel function, address constipation or diarrhea, and begin retraining the bowels to evacuate at the same time every day.

Skin. With decreased mobility and impaired sensation, patients with spinal cord injury are particularly at risk for pressure injuries. Although data have not been conclusive on the clinical benefits of weight shifts and turning while in bed, these are still primary recommendations for preventing pressure ulcers (48; 27). There are several other risk factors for developing pressure ulcers in spinal cord injury, including spasticity, tobacco use, immobility, and urinary incontinence (11).

Pain (somatic or neuropathic). Due to the traumatic nature of most spinal cord injuries, nociceptive pain is often present during the initial rehabilitation stage, particularly at the level of injury where the vertebrae may be fractured. Spinal cord injury may accompany various other musculoskeletal, visceral, or traumatic brain injuries that may warrant treatment as well (97). Although patients often are initially started on strong pain medications, such as opioids, there should be a goal to reduce usage overtime, especially because the side effects of opioid usage can compound with other physiologic compromise in patients with spinal cord injury, such as neurogenic bowel and impaired respiratory strength. The treatment team should consider using medications with the least chance of adverse effects first, such as topical analgesics, modalities, acetaminophen, and tramadol in order to minimize the use of opioid pain medications (31; 50).

Neuropathic pain is common in patients after spinal cord injury (106). It may be seen at the level of the injury as well as below the level of injury. The proposed mechanism is neuroplasticity resulting in peripheral and central neuronal re-organization and maladaptive activation (72). Neuropathic pain is typically characterized as burning, shooting, tingling, or pins-and-needles type pain. Between 40% to 60% of all spinal cord injury patients develop neuropathic pain at or below the level of injury, and half of them report pain levels as moderate to severe that typically becomes chronic (96). It is important to distinguish between nociceptive and neuropathic pain as neuropathic pain may be more effectively treated with certain classes of medications, such as some antiepileptics, tricyclic antidepressants, and serotonin-norepinephrine reuptake inhibitors. Gabapentin, nortriptyline, and duloxetine have all been shown to improve neuropathic pain, although effectiveness above 50% is unusual (106). Pregabalin is the only agent approved by the United States FDA for spinal cord injury-related neuropathic pain (95; 13), although given its higher cost, other agents are usually attempted first. Laboratory and early clinical studies indicate a role of moderate weight bearing exercise and the concomitant proprioceptive and motor activity in attenuating neuropathic pain (72).

Musculoskeletal. Pain related to the musculoskeletal system is noted in more than half of patients with spinal cord injury, although it is much less likely to be considered severe. It is present earlier than other forms of spinal cord injury–related pain with more than one quarter noting musculoskeletal-related pain in the first three months post-injury. The continued prevalence through the first five years after injury indicates the role of degeneration and overuse on persistent musculoskeletal pain in this population (96). Manual wheelchair propulsion and overhead activities more than pressure relief results in significant risk of impingement, with the supraspinatus specifically impacted by propulsion activity (69).

Heterotopic ossification of the hips is the most common location for neurogenic heterotopic ossification after spinal cord injury. Risk factors in adult patients include complete injury, younger age, male sex, post-injury history of urinary tract infection and/or pneumonia, and spasticity. Treatment options include bisphosphonates, nonsteroidal anti-inflammatories, radiation therapy, and surgical excision (101). Clinical presentation is most commonly loss of range of motion, with local swelling being common as well. Patients can present with increased spasticity, pain, and/or autonomic dysreflexia. There is developing literature on the effectiveness of nonsteroidal anti-inflammatory medication in primary prevention (109).

Bone loss due to loss of muscle activity and loss of weight bearing occurs rapidly after spinal cord injury, predominately due to bone resorption increase resulting in relative hypercalcemia with suppression of parathyroid hormone levels. There is a 4% per month loss of trabecular bone mineral loss in the first two years after spinal cord injury, with the rate of loss reaching a lower plateau after. The result is that nearly half of all patients with a chronic spinal cord injury will develop a pathological bone fracture. Risks after fracture include contracture, delayed union, deep vein thrombosis, autonomic dysreflexia, and further loss of function. The risk is greatest at the distal femur and proximal tibia; however, traditional DEXA scans do not test at those levels, and there lacks adequate correlation between hip/lumbar spine measurement and the areas around the knee of greatest concern for patients with spinal cord injury (21). Bisphosphonates decrease resorption but do not improve bone mineral density in persons in the acute/subacute phase after an spinal cord injury. They can statistically prevent bone loss in the total hip, femoral neck, and trochanter at 6 and 12 months after starting treatment, and they can improve bone mineral density of the lumbar spine 12 months after starting treatment. They had no clear effect on serum PINP or serum calcium levels (107). Denosumab maintained bone mineral density and prevented bone loss in the distal femur epiphysis and metaphysis, proximal tibia, and femoral neck in the first 18 months after spinal cord injury (20). Experimental studies on weight bearing and functional electrical stimulation in spinal cord injury show promise in reducing bone loss, but their long-term impact on bone mineral density has not been demonstrated (05). Functional electrical stimulation assisted-rowing did not attenuate bone loss in the distal femur, proximal tibia, or femur metaphysis; however, adding zoledronic acid improved bone strength at the distal femur or femur metaphysis and mitigated bone loss at the tibia (37).

Spasticity. Spasticity is a velocity-dependent increase in muscle tone that is often seen in spinal cord injury as well as part of other upper motor neuron syndromes. Although the pathophysiology is not completely understood, it is thought to be related to the loss of supraspinal inhibition of interneurons (52). Spasticity develops after spinal shock but can vary in when and how severely it presents, from days to months after spinal shock ends (35). For most patients, it results in very tight muscles that can make it more difficult to function and ambulate. Spastic muscles are susceptible to becoming contracted and losing range of motion. The monitoring for spasticity development is an essential component of the rehabilitation plan. After outlining specific functional goals for spasticity management, several options may be explored for treatment. Stretching can be an effective option for minimal spasticity. Beyond that, oral medications such as baclofen, tizanidine, clonidine, and benzodiazepines may be used (01). Unfortunately, they all have sedating properties and, therefore, have a limited therapeutic window. Dantrolene is another oral option that acts at the level of the muscle, but liver function must be monitored with this medication. For global spasticity not adequately treated with oral medications, an intrathecal baclofen pump may be an option (100). For focal spasticity, neurolytic injections with botulinum toxins can be beneficial (61).

Depression. Depression, mental health disorders, and substance use disorders are more common in the spinal cord injury population. In a study of a VA spinal cord injury registry, 20% of patients had a mental health disorder, 12% had a substance use disorder, and 14% had both. Depression was the most common at 27%, whereas tobacco use was common (19%). Increased duration of spinal cord injury was associated with a decreased risk of mental health disorder or substance use disorder. Depression and anxiety remained high in spinal cord injury patients with chronic secondary conditions (04). Cognitive impairment after spinal cord injury may be due to multiple factors including concomitant traumatic brain injury, cerebral injury due to hypoxia, cardiovascular and cerebrovascular dysfunction, medication side effects, untreated sleep apnea, and core temperature dysregulation. Although no difference in working memory or attention was noted, impairment of information processing speed, verbal learning and memory, and verbal fluency is seen in a chronic spinal cord injury population compared to age matched controls and an older control group (18).

Rare complications, premature morbidity, accelerated aging

Long-term follow up of these patients may find rare complications like endocrinological irregularities in males or females (07; 40).

Special care must be given to the pregnant paraplegic (79) and to those who lost limbs during the initial trauma (76).

Our hypothesis, based on clinical observation and literature, is that chronic spinal cord injured patients are prone to premature aging. Physical and mental disabilities and prolonged immobilization change the entire homeostatic mechanisms into a new state. Thus, we feel that this lead to accelerated aging among these chronic handicapped persons (80; 45; 77; 73).

Our findings suggest that individuals with physical disability (including spinal cord injury) and who exhibit high levels of perceived stress may be particularly vulnerable for accelerated cellular aging, suggesting that perceived stress can be used as a valuable target for intervention (50; 49).

Indications

Any patient who has been diagnosed with a spinal cord injury would benefit from a rehabilitation program to some degree. As mentioned above, an inpatient rehabilitation program allows for learning the functional, physical, and medical rehabilitation techniques with an interdisciplinary team. Any suggestion of spinal cord injury-related impairments could benefit from a comprehensive program in order to maximize independence outside of the hospital.

The expected length of time in rehabilitation varies greatly depending on the patient’s injury, progress, medical comorbidities, institution type, and insurance coverage. Of all patients with spinal cord injury, average rehabilitation length of stay is 35 days (71). Due to a changing healthcare ecosystem in the United states, this length of stay has decreased substantially since the 1970s, when 98 days was the norm. It has been noted that inpatient rehabilitation facilities specializing in spinal cord injury may be getting patients discharged more quickly, with stays averaging 23 days in motor-complete tetraplegia. Patients with paraplegia tend to stay for a shorter period of time compared to those with tetraplegia, and patients with motor-incomplete injuries tend to stay for shorter periods than motor-complete injuries.

Contraindications

In some cases, patients may not be ready to undergo an inpatient rehabilitation program with a focus on spinal cord injury rehabilitation. There may be certain temporary orthopedic restrictions that warrant delay in a program. For example, if a patient with paraplegia is non-weightbearing due to an arm fracture, they would be prohibited from performing transfers or any gait training with upper extremities. In this case, it may be reasonable to wait for their arm fracture to heal prior to beginning inpatient rehabilitation. Occasionally, a patient’s pain may be so severe that they would not yet tolerate an intensive rehabilitation program. Similarly, restrictions on cardiac monitoring or need for frequent diagnostic testing may prevent sicker patients from being able to fully participate in inpatient rehabilitation. However, not all rehabilitation specialist physicians will agree with these contraindications.

Special considerations

Spinal cord damage due to cancer or other non-traumatic etiology. Individuals may develop primary or metastasizing tumors to the spine resulting in paralysis. Cancer-related pain, fatigue, and neuropathy make these patients particularly challenging to rehabilitate and treat. Goals of care should be explored based on prognosis as this may affect the rehabilitation goals and length of inpatient stay. In some cases, treatment for a new cancer diagnosis may take precedence over inpatient rehabilitation due to the urgency of the situation. In others, oncologists may want their patients as strong as possible prior to undergoing cancer treatment. Sometimes, treatment and rehabilitation must occur concurrently. Individuals with other nontraumatic spinal cord damage will benefit from rehabilitation treatments and follow up.

Clinical vignette

A 15-year-old young man with no past medical history experienced a diving accident, resulting in a C6 motor-complete spinal cord injury. Following surgical stabilization, the patient was admitted to an inpatient rehabilitation facility. Goals for this patient included transferring independently, using a wheelchair independently, bowel training, and straight-catheterization training.

By the end of rehabilitation, he had done well with self-care and mobility at a manual wheelchair level. With bowel training, he successfully produced one bowel movement per day with no incontinence. Although he was able to master his tenodesis grip, he was unable to easily hold a catheter, and, therefore, needed assistance with catheterization. He eventually developed urinary leakage between catheterizations. He was originally treated for a urinary tract infection, which can worsen bladder spasticity; however, the leakage continued. Several bladder spasticity medications were attempted over the course of three weeks. Ultimately, only an oxybutynin patch was effective. He was recommended for bladder on a botulinum toxin A as an outpatient.

Scientific basis

There are studies and guidelines that establish standard protocols for most aspects of spinal cord injury rehabilitation. Refer to references for more information (30; 92; 43).