Injury to the spinal cord results in impaired motor strength and sensation below the level of injury. Spinal cord injury is often associated with bowel and bladder dysfunction and may cause sexual impairment as well as dysfunction of the autonomic nervous system, also. Approximately 12,000 SCIs occur nationally each year, and approximately 259,000 trauma survivors are living with SCI in the United States. Males account for approximately 80% of those with SCI, and motor vehicle accidents represent the largest proportion of injuries, followed by falls, violence, and sports injuries. The societal impact of SCI is staggering, resulting in total lifetime costs of between $1 and $4.6 million per patient.76
SCIs are classified by their severity and level of injury, using the American Spinal Injury Association (ASIA) Standard Neurological Classification Worksheet.77 This classification system provides guidelines for measuring key motor levels and sensory examination points that represent function at a given spinal level. According to this method of classification, patients are given two scores, with one based on level and the other on the degree of impairment. The neurological level of injury is defined as the lowest level of normal functioning. The impairment is rated as A, B, C, D, or E. An A is assigned to a patient with a complete injury, with no motor or sensory function in the S4 or S5 levels. B represents an incomplete injury with sensory sparing, but no motor activity below the level of injury. A patient with some motor (nonfunctional) strength below the level of injury is assigned a C, whereas a D classifies a patient with more motor sparing below the level of the lesion, as indicated by antigravity strength in greater than 50% of those muscles spared. A classification of E represents normal strength and sensation.
Treatment of acute SCI in a trauma center has a significant positive impact on survival and long-term functional recovery.78 Immediate spinal stabilization is essential to prevent further neurological compromise. While not all patients require surgery after SCI, current literature suggests that surgical treatment relieving spinal cord compression can prevent further neurological deterioration.79
The use of high-dose methylprednisolone following acute SCI is highly controversial. In 1990, the National Acute Spinal Cord Injury Study recommended that high-dose methylprednisolone be administered for 24–48 hours following acute SCI, and these guidelines were widely followed by the international community.80 Because of concern about infection, gastrointestinal bleeding, and steroid myopathy, however, some trauma centers questioned the efficacy and safety of this protocol.81 Further, the 2013 guidelines of the American Association of Neurological Surgeons and Congress of Neurological Surgeons recommended against the routine use of methylprednisolone following acute spinal cord injury.82 In addition, a recent meta-analysis failed to demonstrate a benefit in functional outcome between those receiving methylprednisolone versus a placebo at both 6-month and 1-year follow-up.83 Therefore, the use of steroids following SCI is currently considered a controversial treatment option, with the need for future research.
When an SCI occurs, the axons of the spinal cord nerves are destroyed and the surrounding oligodendrocytes die. Since the body cannot replace these cells, a functional defect results. Stem cells have become a source of research as a potential way to repair the nerve cells of the spinal cord and surrounding structures. They not only have the theoretical ability to rebuild the physical defect in structure, but they also have anti-inflammatory and immunomodulatory effects that are postulated to have a positive effect following SCI.84,85
In preclinical studies, embryonic stem cells transplanted into rodent models of SCI have demonstrated some recovery of function; however, concerns about the use of embryonic stem cells are both logistical (the plausibility of translating rodent models to humans) and ethical (the use of embryonic tissue).86 Mesenchymal stem cells are found in the bone marrow and may exist in adipose and muscle tissue, also. They are not only easier to isolate, but their usage also has fewer ethical concerns than embryonic stem cells; however, a major concern is the potential for spontaneous malignant transformation.87 Preclinical studies thus far have had mixed success in improvements in functional outcome following the implantation of mesenchymal stem cells into rodent models.88,89 The potential of stem cells to provide a cure for SCI has resulted in many clinical trials over the last decade. Thus far, the question as to their efficacy is still unanswered, and there is no consensus about which type of stem cell will be the most effective therapeutically.90
Functional Outcomes After Spinal Cord Injury
The expected level of independence and functional capacity after a SCI depends largely on the level of injury and the impairment rating. While lifelong mechanical ventilation is typically required for patients with complete injuries at the level of C3 or above, it is often not necessary for those with injuries at C4 or below. An injury at the C5 level is expected to result in independent mobility in an electrically powered wheelchair and driving in a van with appropriate modifications. C7 level injuries allow independence with transfers, weight-shifting maneuvers, and bowel and bladder management. While individuals with thoracic level injuries have full function of the upper limbs, they typically require the use of a manual wheelchair with varying degrees of truncal support. Patients with an L1 or L2 injury also generally require a manual wheelchair, also, but have independent truncal control. Patients with L3 or L4 injuries may be able to ambulate with assistive devices, and those with injuries at L5 or below should be able to independently ambulate.78
New technologies are emerging to assist those with preexisting SCIs to achieve a better functional outcome. In 2014, the first exoskeleton device (the ReWalk Personal System) was approved by the FDA.91 This device allows those with a SCI to stand upright and walk, which not only allows for functional mobility, but also offers cardiovascular, gastrointestinal, and psychological benefits, among others. Several other exoskeletons are currently on the market, as well, and further research is necessary to determine their effectiveness as assistive mobility devices.92 Brain-machine interfaces have also been investigated as a technology to achieve functional restoration of limb movement for those with a spinal cord injury; these devices allow the patient to have control of assistive devices by analyzing brain signals.93 In addition, spinal cord stimulation has been investigated as a way of activating networks to induce locomotor-like movements in the legs, with promising results in preliminary animal models.94
The management of patients with SCI is focused on the prevention of complications that may interfere with successful rehabilitation. The recognition of and attention to these complications is a critical component of a successful rehabilitation program.
Autonomic dysreflexia (AD) is a severe and life-threatening complication of SCI that occurs in patients with lesions at or above T6. AD typically occurs as a result of a noxious stimulus below the level of the injury, which triggers a sympathetic reflex that goes “unchecked” or uncorrected because of injury to the descending inhibitory tracts within the spinal cord. This results in elevated blood pressure, bradycardia or tachycardia, headache, and sweating or piloerection above the level of the injury. If not recognized and treated properly, stroke or death may occur. Once AD is recognized, the patient’s head should be elevated and the noxious stimulus (eg, tight or constricted clothing, pressure on the skin, bladder distension, or bowel impaction) should be identified. If an indwelling catheter is in place, it should be thoroughly examined for constriction or kinks that may cause distension. If replacement is needed, it should be inserted with the use of lidocaine gel to decrease the amount of noxious stimuli. A rectal exam should be performed to assess for fecal impaction and if present, manual disimpaction may be required. If blood pressure remains elevated, pharmacological management may be necessary. Typical first line medications include nitroglycerin paste (which can be easily removed to prevent rebound hypotension) or chewable calcium channel blockers. During the management of AD, blood pressure should be continually monitored, and the patient should be continually reexamined for sources of noxious stimulation.27,95,96
Hypercalcemia as a result of upregulation in osteoclast activity may occur in individuals with SCI, especially adolescents and young adult males. This may result in lethargy, abdominal pain, nausea, vomiting, psychological changes, polydipsia, and polyuria. If hypercalcemia is suspected, serum calcium levels should be monitored and treated appropriately.97
Bladder dysfunction following SCI may lead to incontinence and urinary retention. In a typical upper motor neuron lesion, the bladder will become spastic and inadequately store urine, resulting in frequent episodes of small-volume incontinence. In lower motor neuron lesions, the bladder may become flaccid, resulting in failure to empty and overflow incontinence. Many patients with SCI develop detrusor–sphincter dyssynergia, characterized by a detrusor contraction against an unrelaxed sphincter, leading to failure to empty and a high-pressure urinary system. Management of bladder dysfunction aims to prevent incontinence and urinary reflux and infection, while ensuring adequate voiding at socially acceptable times. Options for bladder voiding include indwelling catheters (eg, Foley catheter or suprapubic catheter) or clean intermittent catheterization (Crede maneuver) in which the patient or a caregiver provides manual pressure to the suprapubic region to facilitate emptying of the bladder. Pharmacological management of a hyperactive bladder consists primarily of anticholinergic medications to relax the detrusor muscle. Intravesical administration of botulinum toxin may also be considered to treat detrusor spasticity. Surgical options include augmentation cystoplasty, cutaneous conduits, and urinary diversions.98
Bowel dysfunction is common after SCI due to a loss of bowel control from the central nervous system, resulting in constipation, delayed gastric emptying, and poor colonic motility.99 Both incontinence and failure to empty may result (see the section “Effects of Immobility”).
Spasticity, orthostatic hypotension, skin breakdown, and HO are also significant problems for patients with SCI. The reader should refer to the previous discussion of these topics.
TBI is the leading cause of death and disability in young adults in the United States, with over 1.4 million individuals presenting to emergency and other acute medical settings each year. Of these, 275,000 require hospitalization and 52,000 cases are fatal.100 In addition, it is estimated that 19–23% of service members who deploy overseas, sustain a concussion or mild TBI.101 Reports estimate that there were approximately 313,816 service members diagnosed with TBI between 2000 and 2014 from the wars in Iraq and Afghanistan.102 TBI may occur from multiple mechanisms including blunt, penetrating, or blast trauma. The presence and severity of TBI may be difficult to diagnose, particularly if the injury was not witnessed. Additionally, secondary effects of trauma, such as hypovolemia, anoxia, and metabolic change may lead to significant brain injury, also. TBI may occur in discrete lesions or more diffusely such as in diffuse axonal injury (DAI). Neuroimaging, including CT, magnetic resonance imaging (MRI), functional MRI (fMRI), and diffusion tensor imaging (DTI), is used to confirm the presence of a mechanical lesion that may require surgical evacuation.103
Much debate surrounds the optimal way to classify TBI. Most trauma centers rely on the Glasgow Coma Scale (GCS) or length of post-traumatic amnesia (PTA) to determine severity of the TBI (Table 51-2). PTA is the time between injury and the development of new memories, demonstrated by the patient’s ability to recall daily events. It may be more formally assessed using tools such as the Galveston Orientation and Amnesia Test (GOAT).104 The Ranchos Los Amigos Scale is often used to describe a patient’s level of awareness, cognition, behavior, and interaction with the environment after a TBI (Table 51-3).105 Patients who are mobile, but confused or agitated, will likely require a secured inpatient setting.
TABLE 51-2Traumatic Brain Injury Classification ||Download (.pdf) TABLE 51-2 Traumatic Brain Injury Classification
|Injury severity ||Glasgow coma scale ||Post-traumatic amnesia |
TABLE 51-3Ranchos Los Amigos Scale ||Download (.pdf) TABLE 51-3 Ranchos Los Amigos Scale
|Cognitive level ||Outcome ||Patient response |
Confused and agitated
Confused and inappropriate
Confused and appropriate
Automatic and appropriate
Purposeful and appropriate
No response to sounds, sights, touch, or movement
Limited response, which is inconsistent and nonpurposeful; responses to sounds, sights, touch, or movement
Inconsistent but purposeful response in a more specific manner to stimuli; may follow simple commands
Confused and often frightened; overreactions to stimuli by hitting or screaming; highly focused on basic needs (eg, eating, toileting); difficulty following directions
Appears alert and responds to commands; easily distracted by the environment; frustrated and verbally inappropriate; focused on basic needs
Follows simple directions consistently; may have some memory but lacks details, attention span of about 30 min
Follows a set schedule; does routine self-care without help; attention difficulty in distracting or stressful situations; problems in planning and following through
Realizes difficulties with thinking and memory; less rigid and more flexible thinking; able to learn new things; demonstrates poor judgment; may need guidance for decisions
Predicting outcomes after TBI is extremely challenging because of imprecise classification systems. In addition, issues such as heterogeneity of injury patterns, premorbid cognitive and physical functioning, family support, and psychosocial factors all play differential roles in recovery.106 Reports indicate that 38–80% of patients experiencing mild TBI will develop postconcussive syndrome (PCS), characterized by headache, fatigue, anxiety, and impaired memory, attention, and concentration.107 The best predictor of outcome after TBI is the patient’s speed of recovery and response to treatment; therefore, monitoring patient performance in multiple functional domains is important. Furthermore, an extended duration of loss of consciousness immediately following TBI has been negatively correlated with long-term rehabilitative potential, also.108 Numerous outcome instruments are currently in practice including the Glasgow Outcome Scale (GOS), Functional Independence Measure (FIM), Community Integration Questionnaire (CIQ), Craig Handicap Assessment and Reporting Technique (CHART), and Disability Rating Scale (DRS). For a more comprehensive reference on TBI outcome tools the reader is referred to the National Institute of Neurological Disorders and Stroke’s Traumatic Brain Injury Common Data Element Standards.109
A comprehensive discussion of treatment strategies for individuals with TBI is beyond the scope of this chapter. Trauma teams should consider the effects of immobility as described above and apply the appropriate rehabilitation principles. Patients with severe TBI should be transferred to a specialized rehabilitation facility as soon a possible. Comprehensive acute inpatient rehabilitation programs provide intensive medical, physical, cognitive, and behavioral therapy regimes, which are coordinated in an inter-disciplinary fashion. Because of the frequent association of other sensory disturbances, these treatment teams are often augmented by highly skilled audiologist, neuropthalmologists, optometrists, and vision rehabilitation specialists. In addition, music and art therapists may be invaluable in not only engaging the patient in therapy, but in improving cognitive and communication therapies. Transfer to a skilled nursing facility (SNF) may be necessary for those with impairments that prohibit transfer to an acute inpatient rehabilitation facility (eg, unable to tolerate a minimum of three hours of rehabilitation per day.110 Patients who sustain severe trauma, but deny TBI or cognitive difficulties, may still be determined to have significant cognitive deficits during formal neuropsychological testing. Common symptoms of TBI include headache, visual and hearing disturbances, balance difficulties, poor sleep, irritability, and impaired cognition.111 Additionally, symptoms of other neuropsychiatric comorbidities such as depression, PTSD, and generalized anxiety disorder often accompany TBI.
Pharmacological interventions for neuroprotection and management of neurobehavioral disorders following TBI continue to lack significant scientific evidence in the medical literature. Neuroprotective agents seek to prevent death of neurons after injury. While some agents have shown promise in animal studies, large clinical trials in humans have not revealed strong evidence in support of a single agent. In addition, numerous medications have been advocated to help facilitate recovery of functional deficits after TBI. Clinicians should consider the following pharmacological management: (1) for arousal, methylphenidate, amantadine, modafinil, and zolpidem; (2) for attention and memory, methylphenidate, dextroamphetamine, amantadine, physostigmine, and donepezil; and (3) for agitation, irritability, and aggression, propranolol, quetiapine, clozapine, valproate, and antidepressants.112
Post-traumatic seizures (PTS)/epilepsy occur in 2–47% of patients with TBI. PTS are typically characterized as immediate (within the first 24 hours), early (within the first week), or late (occurring after the first week). Risk factors for early PTS include intracerebral hematoma, subdural hematoma in children, younger age, severity of injury, and alcoholism, while risk factors for late PTS include early PTS, intracranial bleed, severity of injury, and age more than 65.113 Management of seizures is usually achieved with antiepileptic medications such as carbamazepine and valproate. The use of phenytoin is limited because of the risk of cognitive side effects.
Patients with TBI are also at significant risk for developing HO, DVT/PE, spasticity, bowel and bladder incontinence, and skin breakdown. The reader should refer to discussion of these topics earlier in the chapter.
Burns often occur simultaneously with other traumatic injuries including orthopaedic injuries, TBI, SCI, or amputations (see Chapter 48). Severe disability, altered body image, and numerous physical and medical complications often lead to a diminished quality of life among survivors of burns.114 Burn injuries account for 40,000 hospital admissions annually in the United States and are the fifth most common cause of unintentional death.115 Advances in early resuscitation techniques, topical chemotherapy, early wound excision, isolation practices, infection control, antibiotics, and grafting techniques have contributed to the improved survival rates from severe burns.116,117
Burns are classified by size and thickness. The size of a burn is measured as a percentage of total body surface area, with the rule of nines providing a rough estimation of the area that has been burned in an adult. Using this rule, the head and neck and both upper extremities account for 9% each of the total body surface area, the lower extremities and the anterior and posterior trunk are 18% each, and the perineum and genitalia are 1%. Thus, an estimate of the total body surface area involved in a burn can be quickly calculated. The thickness of a burn is classified as superficial, partial thickness, or full thickness. A superficial burn affects only the epidermis, while a partial-thickness burn extends through the epidermis to part of the dermis. A full-thickness burn affects the epidermis and entire dermis and may also involve underlying muscle, tendon, fascia, or bone.
After acute treatment, the focus of burn care shifts to rehabilitation and restoration of function. Attention to the prevention and treatment of the following complications is an important aspect of burn rehabilitation:
Hypertrophic scarring. Excessive scarring following burns may result in significant joint contractures and disfigurement, negatively impacting functional capabilities and quality of life. Despite little evidence of its efficacy, the most widespread method of preventing excessive scarring is the application of pressure garments. Other preventative measures include splinting, stretching, and range of motion exercises.115,118
Weakness and protein catabolism. Following severe burns, a dramatic increase in protein catabolism results in weakness, decreased exercise tolerance, and functional deficits. Treatment and prevention consists of strength training and endurance exercises, which may be effective in increasing strength and function.119 In addition to exercise programs, treatment with anabolic agents such as oxandrolone has been observed to reduce or prevent weakness in a burn population.120
Heat intolerance. The ability to regulate and tolerate heat is often decreased following burn injury.121 The mechanism for heat intolerance may be rooted in changes in central and peripheral thermoregulation; however, studies have suggested the involvement of still yet unknown factors.122 Despite the uncertainty surrounding the etiology of heat intolerance in burn patients, it must be recognized and incorporated into the rehabilitation program of this population.
Pain after burn injuries. Pain after a burn depends on the depth of the injury. In a partial-thickness burn, nerve endings in the dermis may remain intact, resulting in significant pain. In contrast, pain may be less or absent in areas of full-thickness burns because of loss of nerve endings. Approximately 35% of burn survivors continue to report significant pain more than a year following the injury (see the section “Pain Management”).115
Amputation(s). Despite aggressive limb preservation procedures after a burn, the extent of tissue damage or secondary complications such as infection or ischemia may mandate amputation.115 The combination of comorbid burns and amputation presents unique rehabilitation challenges, especially with regard to the prosthetic socket interface and skin breakdown.
Psychological complications. Following burn injuries, emotional complications including depression, body image dissatisfaction, and PTSD may complicate recovery and rehabilitation. In the one month after a burn injury, 54% of patients report depression, while 43% of patients continue to report emotional distress 2 years post-injury.123 Hypertrophic scarring often causes disfigurement of the face and limbs, which can lead to significant dissatisfaction with body image and difficulty with reintegration into the community. PTSD has been reported to occur in 13–25% of patients with burn injuries.115 While there is little evidence for specific treatment recommendations, it has been established that “debriefing” sessions may actually be harmful or increase the rate of PTSD following traumatic events.124 The recognition and treatment of psychological complications of burn injuries is crucial to the design and implementation of a successful rehabilitation program.
In the United States approximately 2 million people live with limb loss. Demographic projections estimate that by the year 2050, nearly 3.6 million Americans will be living with major limb loss (1:144 persons).125,126 These high estimates are due to vascular occlusive diseases, which have been known to cause approximately 82% of amputations and account for nearly 30,000 new cases annually. The majority (>60%) of these patients have diabetes mellitus, as well.127 Traumatic amputations from war wounds have accounted for nearly 1700 service members losing a major limb from wounds sustained in either Iraq or Afghanistan.128 In addition to their distinct mechanism of injury (blast), these injured service members represent a unique patient population when compared to other civilians with acquired limb loss in terms of demographics, location of amputation, and presence of comorbid injuries.129 Trauma remains the highest contributor to pediatric and upper limb amputations, whether in civilian or military populations. In fact, 68.6% of all traumatic amputations occur in the upper limb. Numerous physical, psychological, and functional challenges accompany major limb loss and create additional challenges for successful rehabilitation and reintegration.
The decision to amputate or salvage a limb depends on the extent of injury and tissue viability. Evidence suggests that at 2 and 7 years post-injury, there are no significant functional outcome differences between those who undergo limb salvage surgery and those who undergo amputation. Limb salvage patients, however, are more likely to have longer hospital stays, more operative procedures, and a higher complication rate in the short term. Additionally, long-term follow-up of both groups demonstrates a lower quality of life compared with age-matched controls.130 Individuals with acquired major limb amputation have a higher lifetime incidence of various pain syndromes (eg, residual limb pain, phantom limb pain, back pain), skin problems in the residual limb, overuse injuries, cardiovascular disease and diabetes mellitus.130 Of particular concern for children with limb loss are psychological acceptance, altered self-image, and the development of bony overgrowth of the amputated limb are of particular concern.
For a comprehensive review of amputee care, the reader is referred to the textbook of Military Medicine: Care of the Combat Amputee. While there have been great advances in the rehabilitation methods and prosthetic devices that are currently available for individuals with major limb amputation, the acute medical and surgical care of these patients has long-lasting implications for community reintegration and quality of life. Decisions such as optimizing limb length, balancing muscles, appropriately managing transected nerves, and achieving adequate soft tissue coverage are fundamental surgical principles that will greatly affect prosthetic fitting and training. Aggressive acute pain management, physical and occupational therapy, and balance and gait training, along with reduction of cardiovascular risk and nutritional counseling, will likely reduce long-term complications. Introduction of a prosthesis early during the course of treatment is essential, especially for individuals with upper limb loss, in order to promote lifelong bimanual activity and help ovoid overuse injuries of the intact limb. Prosthetic fitting and training for children with amputation(s) is especially challenging and should be guided by the child’s developmental milestones (eg, reaching, standing, walking). It is important to introduce play, sport, and recreational activities with appropriate adaptive equipment to help facilitate socialization and reintegration into the community, as well.
Peripheral Nerve Injuries and Complications
Traumatic injuries to the peripheral nervous system may contribute to a significant loss of function and independence, which may not be readily evident during the initial trauma screen. Peripheral nerve injuries may occur as a complication of medical care, also. Reported causes have included improper bed positioning, compressive casts, poor fitting orthotics, excessive pressure during surgery, or inadvertent needle sticks. Common sites of nerve injury include the brachial plexus, ulnar nerve at the elbow, and peroneal nerve at the fibular head.
Cognitive impairment or injury to the spinal cord may limit the ability to fully assess the peripheral nervous system. In addition, confounding conditions such as a critical illness neuropathy or myopathy may contribute to sensory or motor dysfunction especially for patients requiring extended intensive care. Electrodiagnostic testing may be helpful in assessing the presence and extent of peripheral nerve damage as well as establishing the prognosis for recovery. Typically, nerve injuries are classified as either complete or incomplete. Neuropraxia refers to an incomplete injury, characterized by demyelination, and has an excellent prognosis for recovery. Damage to the axon (axonotmesis) signifies a more severe injury with a poorer prognosis. Axon regeneration can be estimated to occur at a rate of 1–5 mm/d or 1 in/mo.
A discussion of repair or grafting for peripheral nerve injuries is beyond the scope of this chapter; however, if repair is undertaken, proper postoperative positioning, splinting, and activity precautions should be explained to the patient and treatment team to help support healing and prevent damage. Peripheral nerve care and injury prevention requires serial neurological examinations, attention to patient positioning, and frequent monitoring of pressusre-sensitive areas. Positioning is particularly important during surgical procedures. Frequent turning by nursing staff may be necessary if the patient’s injuries do not allow independent changes in position. Special attention is required when placing casts or external fixation devices, also. The use of ultrasound to guide interventional procedures may help to avoid inadvertent iatrogenic injuries.