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This is the most recent scientific information of chronic complications in SCI available in May 2011.
INTRODUCTION Spinal cord injury (SCI) is a common event; in the United States, the incidence of traumatic SCI is about 40 per million persons per year, with approximately 250,000 living survivors of traumatic SCI in July 2005. The prevalence of nontraumatic SCI is unknown, but it is estimated that it is three to four times greater than traumatic SCI. SCI produces a wide variety of changes in systemic physiology that can lead to a number of complications, which rival the neurologic deficits in their impact on function and quality of life.
Medical complications after SCI are both common and severe. In the Model Spinal Cord Injury Systems Database, rehospitalizations occurred in 55 percent of patients in the first year after SCI and continued at a stable rate of about 37 percent per year over the next 20 years. Genitourinary and respiratory complications and pressure ulcers were the most common reasons for hospitalization. Increased patient age and severity of the spinal cord lesion also impacted on the risk of complications requiring hospitalization.
This topic reviews the management of common complications of chronic SCI, whether due to trauma or other conditions.
LIFE EXPECTANCY Life expectancy is reduced among survivors of spinal cord injury (SCI). Mortality rates are highest in the first year. For patients surviving at least one year after traumatic SCI, life expectancy is approximately 90 percent of normal. Higher neurologic level and severity of injury and older age at the time of SCI negatively impact survival.
The most common causes of death after traumatic SCI are diseases of the respiratory system followed by cardiovascular events. In earlier decades (prior to 1972), urinary complications were the leading cause of death. The risk of suicide is also increased among patients with SCI.
CARDIOVASCULAR COMPLICATIONS
Autonomic dysreflexia Spinal cord injuries (SCI) above T6 may be complicated by a phenomenon known as autonomic dysreflexia, a manifestation of the loss of coordinated autonomic responses to demands on heart rate and vascular tone. Uninhibited or exaggerated sympathetic responses to noxious stimuli lead to diffuse vasoconstriction and hypertension. A compensatory parasympathetic response produces bradycardia and vasodilation above the level of the lesion, but this is not sufficient to reduce elevated blood pressure. SCI lesions lower than T6 do not produce this complication, because intact splanchnic innervation allows for compensatory dilatation of the splanchnic vascular bed.
The estimated frequency of this complication is quite variable, ranging from 20 to 70 percent of patients with SCI lesions above T6. Autonomic dysreflexia is unusual within the first month of SCI but usually appears within the first year.
Typical stimuli include bladder distention, bowel impaction, pressure sores, bone fracture, or occult visceral disturbances. Sexual activity can be a trigger. Autonomic dysreflexia can also complicate medical procedures, as well as labor and delivery.
Common clinical manifestations are headache, diaphoresis, and increased blood pressure. Flushing, piloerection, blurred vision, nasal obstruction, anxiety, and nausea may also occur. Bradycardia is common; however, some patients have tachycardia instead. The severity of attacks ranges from asymptomatic hypertension to hypertensive crisis complicated by profound bradycardia and cardiac arrest or intracranial hemorrhage and seizures. The severity of the SCI influences both the frequency and severity of attacks.
Management of acute attacks includes:
- Measuring and monitoring blood pressure.
- Immediately sitting the patient upright to orthostatically lower blood pressure.
- Removal of tight-fitting garments.
- Searching for and correcting noxious inciting stimuli. Bladder distension and fecal impaction are the most common precipitants. Bladder catheterization and evaluation for urinary tract infection should be undertaken; indwelling catheters should be checked for obstruction, and a rectal examination should be performed.
- Prompt reduction of blood pressure with a rapid-onset/short-duration agent, depending on the severity of attack and response to above measures. Medications often used in this setting include nitrates (1 inch, 2 percent nitropaste), nifedipine (10 mg PO or SL), sublingual captopril (25 mg), intravenous hydralazine (10 mg), and intravenous labetalol (10 mg). Nitrates should be avoided in patients who may be using sildenafil for erectile dysfunction.
- Recognition and avoidance of inciting stimuli are important in preventing attacks. Nifedipine, prazosin, and terazosin have been reported to prevent an attack when administered prophylactically.
Coronary artery disease With improved long-term survival, coronary artery disease (CAD) has become an increasingly important complication in SCI. CAD risk factors, such as adverse lipid profile (low levels of high-density lipoproteins, elevated low-density lipoprotein cholesterol) and abnormal glucose metabolism (impaired glucose tolerance, insulin resistance, and diabetes) are more prevalent in chronic SCI patients than the able-bodied population [13]. Factors that contribute to the development of these disorders include decreased muscle mass, increased fat, and inactivity. Studies suggest that the prevalence of CAD is 3 to 10 times higher in SCI patients compared with the general population.
CAD mortality also appears to be higher among SCI patients. One contributing factor may be that SCI lesions above the T5 level may lead to atypical presentations for cardiac ischemia; manifestations may include autonomic dysreflexia or changes in spasticity rather than typical chest pain.
Risk factor management and treatment for CAD are similar to that of able-bodied individuals.
Exercise options for SCI patients include hand-crank ergometry, hand cycling, swimming, and functional electrical stimulation of muscles. Body weight-supported treadmill training has been reported to improve glucose regulation in incomplete SCI. However, diminished sympathetic responses, reduced cardiac output, impaired ventilation, and decreased muscle mass lead to reduced exercise capacity in chronic SCI [13]. Physiologic responses to exercise, including increased heart rate, increased cardiac contractility, and vasoregulation, are also impaired with higher-level SCI.
Others The autonomic nervous system dysfunction that results from SCI disrupts normal cardiovascular hemostasis. With SCI above the T6 level, baseline blood pressure is usually reduced, and baseline heart rate may be as low as 50 to 60 beats per minute. This is generally not a clinical problem, but may contribute to hemodynamic instability and exercise intolerance.
Orthostatic hypotension due to peripheral vasodilatation is more common in the first several months of SCI and tends to dissipate with the development of muscle tone in the lower extremities. However, it may also occur in chronic SCI, especially with excessive bed rest and diminished fluid intake. Gradual position changes, compression stockings, and abdominal binders decrease venous pooling and may improve orthostatic tolerance. Occasionally, increased salt intake, alpha adrenergic agonists (midodrine), or mineralocorticoid agents (fludrocortisone) may be required.
Acute cervical SCI is associated with a risk of cardiac arrhythmia due to excess vagal tone, as well as complicating hypoxia, hypotension, and fluid and electrolyte imbalances. Arrhythmias are much less frequent in chronic SCI. However, patients with complete cervical SCI appear to have an ongoing risk of cardiopulmonary arrest.
PULMONARY COMPLICATIONS Cervical and high thoracic spinal cord injury (SCI) affect respiratory muscles. The severity of ventilatory failure and requirement for assisted ventilation depends on the level and severity of the SCI. Lesser degrees of ventilatory failure may produce dyspnea and exercise intolerance.
Because of impaired cough and difficulty mobilizing lung secretions, patients after SCI are also at increased risk for pneumonia. Although the incidence of pneumonia is highest in the first year following SCI, these patients remain at increased risk over their lifetime. Older patients are at higher risk than younger patients. Efforts to prevent pneumonia include chest physiotherapy and vaccination.
Deep venous thrombosis and pulmonary embolism remain common early complications of SCI despite advances in awareness and treatment. Prophylactic use of low-molecular-weight heparin is the treatment of choice for most patients with SCI. While there are no good clinical trial data to guide duration of treatment, we suggest that it should be continued in paralyzed patients for at least three months after SCI, after which the risk appears to approximate that of the general population [21]. Specific regimens are discussed separately.
URINARY COMPLICATIONS Spinal cord injury (SCI) produces bladder dysfunction, often referred to as the neurogenic bladder. Other complications can result from this, including infections, vesicoureteral reflux, renal failure, and renal calculi.
Urologic evaluation with regular follow-up is recommended for patients after SCI. Complications such as vesicoureteral reflux, renal failure, and nephrolithiasis may not produce symptoms, and if untreated, can have serious consequences. The frequency and specific testing involved (serum creatinine, cystoscopy, urodynamic studies, renal ultrasound) are not well defined but depend in part on the nature of the patient's urologic problems and other risk factors.
Bladder dysfunction SCI disrupts the two major functions of the bladder, storage and emptying of urine. Bladder control is a complex activity requiring the coordinated function of the cerebral cortex, pontine and sacral micturition centers, and peripheral nervous system. In SCI, the sensation for bladder fullness as well as motor control of bladder and sphincter function are impaired. Depending on the acuity, level, and completeness of the spinal cord lesion, a number of problems can result:
- Bladder or detrusor hyperactivity produces reflexive bladder emptying. Patients may be troubled by bladder spasms as well as urgency and frequency, often with incontinence. Over time, this can lead to decreased capacity of the bladder.
- Sphincter hyperactivity can impair complete emptying of the bladder.
- Detrusor sphincter dyssynergia, a combination of detrusor and sphincter hyperactivity, can lead to bladder contractions against a closed sphincter, leading to elevated bladder pressures and vesicoureteral reflux.
- Bladder flaccidity is produced in lower motor neuron injuries affecting the cauda equina or conus medullaris as well as with acute upper motor neuron injuries (spinal shock). This leads to chronic urinary retention with overflow incontinence and incomplete emptying.
- Most patients with incomplete SCI and all patients with complete SCI, regardless of the level of the lesion, require assistance with bladder function. Although there are no clinical trials that guide the long-term management of bladder dysfunction in SCI, accumulated clinical experience has led to some management strategies. The efficacy of these approaches may be manifest by the declining incidence of urinary tract-related morbidity and mortality in SCI patients.
The goal of a SCI bladder program is to preserve renal function while eliminating urine at regular and socially acceptable times, avoiding high bladder pressures, retention, incontinence, and infection. This should begin as early as possible after SCI, with removal of the indwelling Foley catheter.
Clean technique intermittent catheterization (CIC) has a lower infection rate compared with the use of indwelling catheters [20]. CIC is performed at regular intervals, usually every four hours. A bladder volume of less than 500 cc of urine is targeted in order to avoid bladder distention, excessive intravesicular pressure, and reflux, as well as to reduce the incidence of infections. The timing of CIC and the amount of fluid intake is adjusted to reach this goal. A fluid intake restriction of two liters a day is common for patients with SCI. If present, a sensation of fullness and attempt at voluntary voiding is encouraged prior to CIC, since some incompletely injured persons will regain normal voiding function.
Intermittent urinary incontinence is expected. Condom catheters (for men) and adult diapers are important short-term interventions. After ruling out an infection and adjusting the frequency of CIC and fluid intake, medications are considered. Urodynamic studies should be considered to assess physiology and guide pharmacologic intervention:
- Anticholinergic medications (eg, oxybutynin, tolterodine) decrease bladder tone, suppress bladder contractions, and may reduce urinary frequency and incontinence. Tricyclic antidepressants such as imipramine have the added side effect of increasing urethral resistance tone.
- Alpha adrenergic medications (ephedrine and phenylpropanolamine) can increase bladder storage in patients with pathologic relaxation of the sphincter.
- Cholinergic medications (bethanechol) may help complete bladder emptying in those with hypotonic bladders.
- Alpha-blockers (eg, prazosin, terazosin) help sphincter relaxation, lowering bladder pressures during contraction. These can be prescribed for treatment of detrusor sphincter dyssynergia, but may aggravate hypotension.
Most patients are managed with a combination of CIC and oral anticholinergic medications.
For patients unable to perform CIC and without available caregivers, a chronic indwelling catheter may be necessary. This is associated with an increased risk of urinary tract infection (UTI) compared with CIC. The indwelling catheter is changed every month to minimize infections. Oxybutynin chloride (5 mg bid) can decrease catheter-induced bladder spasms. With indwelling catheters, there is an increased risk of prostatitis, epididymitis, and urethral stricture. Suprapubic tube placement can help minimize the risks of infection and stricture. A cystoscopy every two years is recommended to monitor for the increased incidence of bladder cancer and stone development.
Studies of detrusor injections of botulinum toxin A in patients with detrusor hyperactivity suggest that this treatment is safe and highly effective in controlling symptoms and improving quality of life. However, the optimal dose has not been determined and long-term efficacy is unknown. This is not yet an FDA-approved indication for botulinum toxin. There have been no comparative studies with anticholinergic agents. The use of botulinum toxin for the treatment of non-neurogenic lower urinary tract dysfunction is discussed separately.
Studies of implanted sacral nerve modulators show promise as a treatment for urinary incontinence following SCI.
For patients with unsatisfactory response to medical and catheter management, other treatments, bladder augmentation, urinary diversion, sphincterotomy, urethral stent, and electrical implantation devices can be considered in selected cases.
Urinary tract infection Urinary tract infections (UTI) are common in SCI, with an incidence of 2.5 episodes per patient per year. The urinary tract is the most frequent source of septicemia in SCI patients and has a high mortality rate (15 percent). UTI is more common in women than men. Low-frequency and high-volume catheterization increase the risk of UTI, as do indwelling catheters and assisted (as opposed to self) intermittent catheterization.
Symptomatic UTI as manifest by fever, autonomic dysreflexia, increased spasticity, foul-smelling urine, incontinence, frequency, or dysuria warrants prompt antibiotic treatment to avoid septicemia and other complications.
Asymptomatic UTIs are not generally treated; nor is there a role for routine use of prophylactic antibiotics to prevent UTI in SCI patients, despite the fact that asymptomatic bacteriuria is common after SCI and is associated with a higher risk of symptomatic UTI. A meta-analysis of published literature found that antibiotic prophylaxis in patients with SCI reduced asymptomatic bacteriuria but not symptomatic infections, and was associated with a twofold increase in the risk of drug-resistant bacteria. However, some individuals with recurrent UTI may benefit from prophylactic antibiotic treatment, depending on the frequency and clinical severity of the infections. In particular, the combination of frequent UTI and vesicoureteral reflux is associated with a high risk of renal failure.
Other methods of reducing the incidence of UTI are under investigation and include colonization of the urinary tract with inert bacterial strains. Cranberry juice is believed to reduce bacterial adherence to the uroepithelium and thereby prevent UTI. However, its efficacy is unproven, and the associated fluid and caloric intake may be problematic in individuals with SCI. In two small clinical trials, a cranberry supplement was found ineffective in reducing bacteriuria, pyuria, or UTI in patients with SCI.
Urinary calculi Calculi in the kidney, ureter, or bladder are increased after SCI, especially in patients who have recurrent UTIs, indwelling catheters, and immobilization hypercalciuria. (See 'Bone metabolism' below.) Because of altered bladder sensation, there may not be pain to alert the clinician to ureteral obstruction. Other clinical symptoms such as increased limb spasticity and episodes of autonomic dysreflexia should suggest this as a possible diagnosis (see 'Autonomic dysreflexia' above).
Vesicoureteral reflux Impaired function of the vesicoureteral insertion may result from high bladder pressures and recurrent UTI. The estimated incidence of this complication in SCI patients is as high as 25 percent. Because persistent reflux is associated with a higher risk of pyelonephritis and renal dysfunction, it represents a treatment imperative. If reflux persists despite the use of anticholinergic drugs and increased frequency of catheterization, placement of an indwelling catheter or a surgical procedure may be necessary. The use of oxybutynin may reduce phasic increases in bladder pressure caused by bladder spasms with an indwelling catheter.
Renal insufficiency The cumulative incidence of renal insufficiency increases with time since SCI and is as high as 25 percent at 20 years. Indwelling urethral catheters, vesicoureteral reflux, and advanced age are associated with the development of renal failure.
SEXUAL DYSFUNCTION Consequences of spinal cord injury (SCI) on sexual function include decreased libido, impotence, and infertility.
- Male impotence occurs in 75 percent of patients with SCI. Patients with complete as opposed to incomplete injuries have the greatest incidence and severity of this complication. There are a variety of treatment options for erectile dysfunction, including medications, assistive devices, and surgically implanted prostheses. Sildenafil, vardenafil, and tadalafil have documented efficacy in SCI, but are contraindicated (as are other phosphodiesterase-5 inhibitors) if there is comorbid coronary artery disease.
- The prevalence of male infertility in SCI is high as a consequence of erectile dysfunction, ejaculatory dysfunction, and/or poor sperm quality [23,46]. In general, male reproduction after SCI requires artificial insemination.
- Sexual responses in women may also be impaired after SCI, but ovulation and fertility are generally unaffected [22,46]. The lower pregnancy rates among women with SCI as compared with the general population are felt to reflect personal choice. Pregnancy in women with SCI is generally categorized as high risk because of a high rate of complications including infections and autonomic dysreflexia.
GASTROINTESTINAL COMPLICATIONS Bowel dysfunction is common and disabling after spinal cord injury (SCI) and significantly affects functional and quality of life outcomes. A multi-dimensional program is frequently necessary to obtain the best results.
Two patterns of bowel dysfunction may occur. With injuries above the conus medullaris, neural connections between the spinal cord and bowel are maintained, resulting in hyperreflexic pelvic muscle contraction and inability to voluntarily relax the external anal sphincter. This causes constipation and fecal retention. A lower motor neuron or areflexic bowel occurs with injuries below the conus medullaris, leading to slower transit, decreased sphincter tone, and constipation with frequent incontinence.
Because few studies have evaluated the management of this problem, recommendations are based on clinical experience and expert opinion. With a goal of predictable and timely bowel evacuation that avoids fecal incontinence and impaction, a consistent, structured regimen is integrated into the patient's lifestyle as early as possible after SCI, using their preinjury bowel pattern as a guide. A typical routine may begin at a regular time point each day (eg, 30 minutes after a meal) with insertion of a chemical stimulant rectal suppository. After several minutes, digital stimulation with slow, gentle rotation of the finger for 15 to 60 seconds is repeated every 5 to 10 minutes, until stool evacuation is complete. Abdominal massage, deep breathing, Valsalva maneuver, and forward-leaning position may assist evacuation.
Oral bowel medications (stool softener, docusate sodium; bowel stimulants, senna and bisacodyl; bulking agents, psyllium) are often used during the initial phase of establishing a regular bowel pattern, and are then slowly eliminated. Chronic use of stimulant laxatives is associated with a number of side effects.
A regular diet is an important feature of the bowel program and should include adequate fiber intake (30 g) and relatively lower amounts of dairy products and fat content. Targets for fluid intake are often dictated by the patient's bladder status, but if possible, should be high enough to produce 2 to 3 liters of urinary output each day.
If constipation or impaction develops, a trial of enemas, laxatives, or bulk-forming agents may be considered. Abdominal x-rays should be considered to screen for evidence of obstruction. Diseases not related to the SCI, particularly colorectal cancer, should be excluded. Prokinetic medications (eg, cisapride, metoclopramide) are reserved for persistent, severe constipation that is unresponsive to modifications of the bowel program. Some patients with severe bowel dysfunction require a colostomy. Uncontrolled observational studies suggest that regular transanal irrigation can reduce constipation and fecal incontinence and improve quality of life in some patients with chronic bowel dysfunction following SCI. A new therapeutic technology, sacral electrical stimulation, is under investigation and appears promising.
Hemorrhoids can be increased by the interventions (suppositories, enemas, digital stimulation) commonly used in bowel programs for SCI. Treatment includes stool softeners, minimizing trauma, topical anti-inflammatory creams, and suppositories. Hemorrhoids causing persistent bleeding, pain, or autonomic dysreflexia warrant surgical consultation.
Serious abdominal complications (cholecystitis, upper gastrointestinal bleeding, pancreatitis, or appendicitis) account for 10 percent of deaths following SCI, with the most significant risks during the first few months after injury. There is an increased prevalence of gallstones in patients with chronic SCI, perhaps in relationship to denervation. Sensory deficits resulting from SCI contribute to a delay in diagnosis and increased mortality associated with these complications. Vague or nonspecific symptoms such as nausea, anorexia, or autonomic dysreflexia should raise concern for occult abdominal processes.
The superior mesenteric artery syndrome is an unusual complication of SCI, usually in patients with cervical cord injuries. Weight loss leads to loss of the mesenteric fat pad and compression of the duodenum by the superior mesenteric artery, leading to symptoms of small bowel obstruction.
BONE METABOLISM
Osteoporosis After spinal cord injury (SCI), osteoporosis affects bones below the level of the injury and increases the risk of lower extremity fractures. In one series of 41 men, after a median of 15 years after SCI, 61 percent had osteoporosis and 34 percent had had a fracture.
The pathogenesis of osteoporosis is unknown; neural factors as well as disuse are believed to play a role. Biomarkers of bone resorption are increased, beginning as early as the first week after injury, while markers of bone formation are normal or only minimally elevated. Some studies suggest that about two years after SCI, a new steady state level between bone resorption and formation is reestablished. Older age, higher spinal level of injury, lesser degrees of spasticity, and longer chronicity of the injury have been inconsistently associated with higher degrees of observed bone loss. Rates of osteoporosis among men and premenopausal women with SCI are similar; too few postmenopausal women with SCI have been included in studies to know whether this population is at additional risk.
Occasionally, symptomatic hypercalcemia and hypercalciuria complicate early resorption of bone mass within the first few months of SCI. Manifestations can include nausea, vomiting, anorexia, lethargy, and polyuria. There is an increased risk of nephrolithiasis [68]. Treatment is graded to severity of symptoms. Intravenous pamidronate has been used for acute immobilization hypercalcemia after SCI.
Over time, patients with SCI develop a specific pattern of bone abnormalities, with marked loss of bone density in the proximal tibia and femur, and relatively less bone loss in the spine. The impact of weight-bearing on the spine during sitting and wheelchair use may contribute to this discrepancy [68]. Patients with quadriparesis may also experience bone loss in the distal forearm.
In small observational and open-label, randomized studies, treatment with bisphosphonates such as tiludronate, etidronate, pamidronate, and alendronate has been shown to attenuate bone loss in patients with SCI. In one small, double-blind, randomized trial (31 patients), alendronate (70 mg weekly) was also shown to prevent bone loss at the hip when administered within 10 days of acute SCI. Functional electrical stimulation has shown minimal and largely unsustained benefits in improving bone density.
Heterotopic ossification Heterotopic ossification refers to the deposition of bone within the soft tissue around peripheral joints. This occurs in up to half of SCI patients, beginning at a mean of 12 weeks after injury. Although heterotopic ossification is common after SCI, only 10 to 20 percent of patients have clinical symptoms, with decreased range of motion and inflammatory symptoms in the affected joints. The large joints below the level of injury are typically affected, most commonly the hip. The pathogenesis of this phenomenon is incompletely understood, but it is believed to originate from osteoprogenitor stem cells lying dormant within the affected soft tissues. With the proper stimulus (as with hip surgery, spinal cord injury, and stroke), these stem cells may differentiate into osteoblasts that form osteoid and eventually bone.
Deep venous thrombosis, cellulitis, infection, hematoma, and tumor should be considered as alternative diagnoses for localized pain in SCI patients. Because calcification may not appear for weeks after clinical presentation, plain radiographs are of limited use in the early diagnosis. An elevated serum alkaline phosphatase level can help differentiate early heterotopic ossification from other conditions, but is not a specific finding. The triple phase bone scan is the most reliable test for diagnosis.
Early administration of NSAIDs (indomethacin 75 mg daily for three weeks or rofecoxib 25 mg daily for four weeks) after SCI appears to reduce the incidence of heterotopic calcification according to a 2010 systematic review that included two randomized trials. Further research is required to identify which patients will benefit from this intervention. Warfarin and pulse low-intensity electromagnetic field therapy may also be useful in the prevention of heterotopic ossification, but a clinical role for these modalities for this indication is not yet established.
The initial treatments of heterotopic ossification are passive range-of-motion exercise, with the goal of maintaining joint mobility, and nonsteroidal anti-inflammatory drugs (NSAIDS). Bisphosphonates may also be useful. According to uncontrolled case series, etidronate (given intravenous for three days, followed by six months of oral therapy) reduced swelling and retarded or halted progression of heterotopic ossification, particularly if it was administered early, when bone scans were positive, but radiographs remained normal. Radiotherapy also appeared to limit progression in one case series of 52 patients with heterotopic ossification after SCI. For refractory cases, surgery is a treatment option to allow functional range of movement; however, the majority of patients experience recurrence after surgery. A small retrospective study found that intravenous pamidronate (a bisphosphonate) prevented recurrent heterotopic ossification in patients undergoing excision surgery. Reports of early resection in combination with drug and radiation treatment also appear promising.
MUSCULOSKELETAL COMPLICATIONS After spinal cord injury (SCI), muscle contractures can result from reorganization of the collagen tissue matrix that occurs when the muscle lies in the shortened position for an extended period of time. Both immobility and spasticity contribute to this occurrence. Preventive management is extremely important and should begin immediately after a SCI and continue for long-term care:
- Positioning. While in bed, the patient should be positioned, using pillows to minimize flexion at the hip and knee, and adduction and internal rotation at the shoulder. Wheelchair positioning should maintain normal lumbar lordosis. Frequent repositioning prevents skin breakdown as well as contractures; these complications often co-exist.
- Range-of-motion exercise. Paretic extremity joints should be exercised 5 to 20 minutes daily. The intensity of exercises needed to prevent deformity varies among individuals, but the goal is maintenance of full range. Any limitation warrants investigation for heterotopic ossification, fracture, hematoma, infection, or thrombosis.
- Splinting. Upper extremity flexion contractures and ankle plantar-flexion contractures can be prevented with resting night splints or bivalve (removable) casting. The fitting and timing of splints must be adjusted based on skin and pain tolerance.
The goal of these interventions is to induce prolonged muscle stretching of vulnerable muscles; however, their efficacy in preventing contractures has not been documented. Established contractures may require surgical treatment.
Certain contractures can facilitate function. Patients with SCI at C6 level may gain improved functional hand tenodesis with finger flexion contractures that enhance prehension with wrist extension. A slight elbow flexion contracture can improve the mechanical advantage of a weakened biceps muscle.
Repetitive over-use injuries in the upper extremities are common in SCI patients, related to transfers and wheelchair use. Rotator cuff and other tendon injuries, carpal tunnel syndrome, bursitis, and osteoarthritis are common sequelae. The shoulders are most often affected (75 percent), followed by wrists, hands, and elbows (53, 43, and 35 percent, respectively). Specific exercise programs to minimize injuries and preserve joint function can be helpful, as can the use of power wheelchairs and ergonomic assessments.
PRESSURE ULCERS Pressure ulcers result from tissue damage due to unrelieved pressure that typically occurs over bony prominences. Shear, friction, poor nutrition, and changes in skin physiology below the level of the lesion also contribute to the development of pressure ulcers. Prevalence rates for pressure ulcers in chronic spinal cord injury (SCI) are difficult to obtain, but have been estimated at approximately 30 percent at 20 years following SCI. Both the level and severity of SCI impact significantly on the risk of developing a pressure ulcer.
Multiple pressure ulcers occur in more than one-third of patients. The most common locations of pressure ulcers in the SCI patient are:
- Ischium 31 percent
- Trochanter - 26 percent
- Sacrum - 18 percent
- Heel - 5 percent
- Malleolus - 4 percent
- Feet - 2 percent
Preventative strategies include:
- Examining skin over areas most vulnerable to ulcer formation daily
- Avoiding immobility and excess moisture in susceptible regions
- Use of pressure-relieving wheelchairs, cushions, and other devices
- Maintenance of adequate nutritional intake and weight
- Comprehensive treatment includes assessment of health status and status of the ulcer. An ulcer treatment plan consists of cleansing, debridement, nutritional support, and management of tissue loads. The prevention and treatment of pressure ulcers are discussed in detail separately.
SPASTICITY Spasticity is believed to result from disruption of descending inhibitory modulation of the alpha motor neurons, producing hyperexcitability, which is manifest as increased muscle tone and spasms. Negative effects of spasticity include pain, decreased mobility, contractures, and muscle spasms, all of which can interfere with sleep and activities of daily living. At the same time, spasticity has some positive aspects: increased tone can facilitate some functional activities, including standing and transfers. Increased muscle tone may also promote venous return, minimizing deep venous thrombosis and orthostatic hypotension.
Abolishing spasticity is difficult and not necessarily desirable. Treatment should be directed at minimizing spasticity as it relates to functional impairment and should follow a graded approach, starting with the least invasive approach. Nonpharmacologic treatments include physical therapy. Regular stretching and use of braces can help maintain range of movement and prevent contractures. (See 'Musculoskeletal complications' above.)
Oral medications Though often prescribed for spasticity, the evidence of efficacy for commonly used oral medications is not substantial, side effects are often dose limiting, and the relative benefit of these treatments has not been established. With all medications, slow dose escalation may mitigate against adverse side effects, which include sedation, dry mouth, dizziness, and weakness.
- Baclofen, a GABA-B agonist, is the most commonly used oral medication for spasticity, despite the paucity of evidence-based support for its efficacy. Although adverse effects of sedation and weakness can be dose-limiting, baclofen is safe for long-term use, without evidence of tolerance. Abrupt discontinuation of baclofen is advised against because of potential withdrawal symptoms.
- Tizanidine, a centrally acting alpha-2 adrenergic agonist, was compared with placebo in one of the largest studies of spasticity treatment in spinal cord injury (SCI) patients. Among the 78 of 124 randomized patients who completed the study, tizanidine produced a significant reduction in spasticity, but had no effect on activities of daily living and other functional assessments. Sedation was the most common limiting side effect.
- Diazepam, a GABA-A agonist, is the most commonly used benzodiazepine for spasticity, often in conjunction with baclofen or tizanidine. Sedation, confusion, hypotension, and gastrointestinal symptoms can be dose-limiting. Diazepam or clonazepam may be particularly useful in controlling nighttime spasms.
- Dantrolene sodium differs from other medications discussed in that it acts peripherally, inhibiting calcium release from sarcoplasmic reticulum of the muscle. More than the other agents used, it produces weakness of both affected and unaffected muscles [106]. Its potential for hepatotoxicity requires liver function test monitoring every three to six months.
- Less commonly used oral medications used for spasticity include clonidine, gabapentin, cannabinoids, and cyproheptadine.
Intrathecal baclofen Baclofen is centrally acting, but crosses the blood brain barrier ineffectively, limiting its bioavailability when taken orally. Intrathecal baclofen allows for four-times the amount of baclofen to be delivered to the spinal cord with 1 percent of the oral dose. Treatment is administered by a surgically implanted, computer-programmed infusion pump with a catheter extending into the intrathecal space. In general, patients undergo a trial of intrathecal baclofen infusions prior to pump implantation. Although systemic side effects of baclofen are generally avoided with this approach, complications of intrathecal baclofen therapy can include spinal fluid leaks, hemorrhage, infection, catheter dislodgement, and pump failure.
Two double-blind crossover studies compared intrathecal baclofen infusion with saline placebo in patients after SCI. Patients treated with intrathecal baclofen had both reduced spasticity and improved disability. This approach may also reduce pain associated with spasticity.
Injection techniques Chemodenervation provides a localized treatment of spasticity within a muscle or muscle group. Although systemic side effects associated with medications are avoided, the large number of muscles involved in SCI limit the use of this approach for these patients. However, in some patients, targeted relief of spasticity in certain muscle groups can improve ambulation and other specific functions. Agents include botulinum toxin, phenol, and alcohol.
Botulinum toxin acts at the neuromuscular junction, preventing acetylcholine release. Treatment effects last a few months, requiring repeated injections. Side effects include muscle weakness and injection-site reactions, but in general this treatment is safe and effective. One randomized study compared botulinum toxin injections to tizanidine for upper limb spasticity following stroke or traumatic brain injury. Botulinum toxin treatments were more effective in reducing tone and were associated with fewer adverse effects than tizanidine. However, spasticity is not as yet an FDA-approved indication for botulinum toxin.
The US Food and Drug Administration has issued a warning about the possibility of life-threatening systemic adverse effects from local botulinum toxin injections. The warning was based on reports of severe difficulty swallowing or breathing in several patients and occurred mostly in children with cerebral palsy receiving local injections for limb spasticity. Some of these complications appear be caused by inadvertent overdosing, because potency determinations expressed in "units" varied among botulinum toxin products. In response, the FDA mandated changes in drug names that were designed to emphasize these differences in drug potency and prevent medication errors. Providers should be alert for the potential of systemic effects, including dysphagia, dysphonia, weakness, or dyspnea, occurring up to several weeks after treatment.
Phenol and ethanol nerve blocks essentially superimpose a lower motor neuron lesion on the upper motor neuron deficit. Weakness, injection site pain, phlebitis, permanent nerve damage, and sensory dysesthesia can be problematic complications of this procedure.
Surgery Surgical destructive procedures, rhizotomy, myelotomy, cordotomy, and cordectomy are reserved for refractory cases. Orthopedic procedures involving the muscle or tendon can be used to treat established contractures.
PAIN SYNDROMES A significant number of patients develop a chronic pain syndrome several months to years after spinal cord injury (SCI). Reported prevalences vary considerably. On average, two-thirds of patients suffer chronic pain and about one-quarter to one-third of patients have severe pain that significantly affects quality of life.
Neurogenic pain after SCI can be both spontaneous and stimulus-evoked, is often poorly localized, and is often described as burning, stabbing, or electrical in quality. Hyperesthesia is a common component. These qualities can help distinguish neurogenic from musculoskeletal pain (usually dull, aching, and well-localized) that can result from a number of complications common to SCI patients. (See 'Musculoskeletal complications' above.)
Although neurogenic pain appears to be associated with neuronal hyperexcitability, mechanisms are poorly understood. Two types of neurogenic pain syndromes are recognized: at-level pain (ie, pain in segments at the level of SCI) and below-level pain. These are believed to have different neuroanatomic and pathophysiologic bases, with injury to nerve roots and dorsal gray matter causing at-level pain, and injury to spinothalamic tracts and/or thalamic deafferentation responsible for below-level pain. Development of at-level pain should provoke an evaluation for post-traumatic syringomyelia, with which it is associated. (See 'Syringomyelia' below.)
Medical treatments are often unsatisfactory; antidepressant, antiepileptic, and standard analgesic medications are tried, often in combination:
- Antiepileptic drugs are believed to improve neuropathic pain by suppressing abnormal neuronal hyperexcitability. Only a few randomized trials have studied some of these medications (lamotrigine, gabapentin, valproate) in SCI; most do not support their efficacy [121-124]. One randomized study of pregabalin (150 to 600 mg daily) among 137 patients after SCI found improvements in blinded assessments of pain scores as well as disturbed sleep and anxiety [125].
- Antidepressant medications are also used in a variety of central and peripheral neuropathic pain syndromes. Randomized trials of trazodone and amitriptyline in SCI have not demonstrated efficacy.
- Opiates may provide relief in anecdotal reports, but side effects, tolerance, and dependence are significant issues.
- It is reasonable to believe that non-oral routes of administration may provide better efficacy with fewer side effects; however, evidence supporting these therapies is somewhat limited in SCI. Therapies have included intrathecal administration of morphine, clonidine, and baclofen.
Invasive treatments, including deep brain stimulation, motor cortex stimulation, cordotomy, and dorsal root entry zone lesions have been tried, again without substantive evidence of success. In the absence of good therapies, it is not unreasonable to also consider nontraditional treatments such as acupuncture and biofeedback.
Details regarding dosing regimens, side effects, and other aspects of chronic pain management are discussed separately.
NEUROLOGIC DETERIORATION
Syringomyelia A delayed progressive intramedullary cystic degeneration complicates 3 to 4 percent of traumatic spinal cord injury (SCI) as well as other acute myelopathies. The interval since SCI can vary from several months to many years. Postulated mechanisms include scarring with obstruction of CSF flow and altered tissue compliance leading to expansion of the central canal and compression of surrounding cord tissue [133]. Symptoms are consistent with a progressive myelopathy and include worsening motor, sensory, bowel, and bladder deficits and pain. Arachnoiditis, cord compression and/or a narrowed spinal canal, and bony deformity, especially kyphosis, seem to be risk factors for progressive enlargement of the cyst and neurologic deterioration.
An asymptomatic syrinx is a common incidental finding on neuroimaging in SCI patients. This entity usually has a benign prognosis, and likely represents a focal area of liquefaction necrosis of cord tissue.
Treatment is aimed at reducing expansile intracystic pressure and improving CSF flow. Surgical approaches include shunt placement, lysis of subarachnoid adhesions, cyst fenestration, and dural augmentation. Extradural decompression is anecdotally reported to be helpful when there is significant bone deformity and compression of the spinal canal with restriction of spinal fluid circulation. Unfortunately, long-term treatment benefits are seen in less than half of patients, and shunt failure is common. Pain may be more responsive to intervention than are motor symptoms.
Progressive posttraumatic myelomalacic myelopathy Also known as the marshy cord syndrome, progressive posttraumatic myelomalacic myelopathy is a less frequent complication of SCI and is characterized pathologically by microcysts, reactive gliosis, and meningeal thickening. Adhesions and cord tethering appear to be causally related; surgical untethering and duraplasty with expansion of the subarachnoid space can lead to clinical improvement.
PSYCHIATRIC COMPLICATIONS Psychosocial complications associated with spinal cord injury (SCI) include depression, suicide, drug addiction, and divorce.
Between 20 to 45 percent of patients are depressed after traumatic SCI. This symptom often emerges early on, within the first month after SCI, and is not closely tied to the severity of injury. Patients with SCI have a four to five times higher rate of suicide compared to age-matched population samples. Suicide is a leading cause of death in traumatic SCI patients younger than 55 years; 75 percent of suicides occur within the first five years of injury. Similar rates of depression and suicide are observed after transverse myelitis.
Because of its high prevalence and serious consequences, patients with SCI should be regularly screened for symptoms of depression. High levels of pain and lack of social support identify patients at high risk for depression and suicidality.
Depression and anxiety following SCI should be treated; it should not be assumed that symptoms are a "normal" reaction to the circumstances and do not require treatment. Recommended interventions include psychologic counseling, pharmacologic intervention, and peer support groups.
THERMOREGULATORY DYSFUNCTION Disrupted autonomic pathways following spinal cord injury (SCI) can lead to impaired vasomotor and sudomotor responses in regions of insensate skin, reduced thermoregulatory effector response for a given core temperature, and loss of skeletal muscle pump activity from paralyzed limbs. Consequences can include hyperthermia during exercise or high ambient heat and hypothermia in lower ambient heat. There can be a blunted fever or a hypothermic response to infection. Others have noted episodes of hyperthermia or hypothermia in the absence of infection or environmental temperature change in SCI patients.
FUNCTIONAL DEFICITS The level and completeness of the spinal cord injury (SCI) are the principal determinants of the needs, goals, and expectations in functional abilities. Age, general health, body habitus, concurrent injuries, spinal instrumentation, intelligence, and motivation also influence recovery.
Functional recovery after a SCI begins in the acute care setting as soon as the patient is medically stable with range-of-motion and resistive exercise, upright positioning, and transfer work. In the inpatient rehabilitation setting, physical and occupational therapists experienced in SCI rehabilitation develop individualized programs that emphasize strengthening, joint protection, and compensatory strategies, combined with creative use of assistive devices and equipment to maximize function. Despite evolving technological advances, the simplest traditional approaches are often the best.
The general expectations for functional recovery based on motor level are outlined in the Table (table 2) [150]. These assume an uncomplicated, complete SCI followed by appropriate rehabilitation interventions in a healthy, motivated individual.
SUMMARY AND RECOMMENDATIONS Medical complications after spinal cord injury (SCI) are both common and severe, contributing to a high rehospitalization rate and decreased life expectancy. (See 'Life expectancy' above.)
- Autonomic dysreflexia can complicate SCI above T6. This is an exaggerated sympathetic response characterized by headache, diaphoresis, and increased blood pressure that occurs with noxious stimuli such as pain from bladder distension, constipation, or pressure sores. (See 'Autonomic dysreflexia' above.)
- Patients with SCI also have an increased incidence of CAD. Hemodynamic instability and cardiac arrhythmias can be problematic in the acute and subacute SCI and are less frequent problems in chronic SCI. (See 'Cardiovascular complications' above.)
- The severity of ventilatory failure and requirement for assisted ventilation depends on the level and severity of the SCI. Lesser degrees of ventilatory failure may produce dyspnea and exercise intolerance. (See "Respiratory complications of spinal cord injury", section on 'Ventilatory failure' and "Respiratory physiologic changes following spinal cord injury".)
- An increase risk of pneumonia is highest in the first year following SCI, but patients remain at increased risk over their lifetime. (See "Respiratory complications of spinal cord injury", section on 'Pulmonary infection'.)
- Prophylactic use of low-molecular-weight heparin to prevent deep venous thrombosis and pulmonary embolism should be continued for at least three months after SCI, after which the risk appears to approximate that of the general population. (See "Prevention of venous thromboembolic disease in surgical patients".)
- SCI produces bladder dysfunction, often referred to as the neurogenic bladder. Other complications can result from this, including infections, vesicoureteral reflux, renal failure, and renal calculi. Clean intermittent catheterization, supplemented by medications as needed is the usual initial treatment. Some patients require a chronic indwelling catheter. Botulinum toxin and sacral nerve modulators are being investigated as alternative treatment options. (See 'Urinary complications' above.)
- Sexual dysfunction after SCI can include decreased libido, impotence, and infertility. Erectile dysfunction may respond to treatment with a phosphodiesterase-5 inhibitor. (See 'Sexual dysfunction' above.)
- Bowel dysfunction after SCI usually requires treatment with a bowel evacuation protocol and a multi-dimensional approach. A regular diet that includes adequate fiber is an important part of management. (See 'Gastrointestinal complications' above.)
- Osteoporosis affects bones below the level of the SCI and increases the risk of fracture. The role of bisphosphonates in this setting is under investigation. (See 'Bone metabolism' above.)
- Positioning and mobilization can help ameliorate contractures and pressure ulcers after SCI. (See 'Musculoskeletal complications' above and 'Pressure ulcers' above.)
- Spasticity is common after SCI and has positive as well as negative effects. Treatment is empiric and is aimed at minimizing pain while maximizing function. Options include oral medication, intrathecal baclofen, botulinum toxin, and nerve blocks. Refractory spasticity may require surgery. (See 'Spasticity' above.)
- Neurogenic pain after SCI is often refractory but may respond to standard analgesic therapy, antiepileptic drug therapy, and/or antidepressant therapy. (See 'Pain syndromes' above.)
- Depression frequently complicates SCI; patients are at high risk for suicidality and should be monitored. (See 'Psychiatric complications' above.)
- Functional neurologic deficits are determined by the level and completeness of the SCI and are ameliorated by appropriate rehabilitation interventions. If patients experience neurologic decline, neuroimaging is indicated to exclude syringomyelia, posttraumatic myelomalacic myelopathy, or other neurologic pathology. (See 'Functional deficits' above and 'Neurologic deterioration' above.)
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