Paul F. Pasquina, Caitlin L. McAuliffe, and Kevin F. Fitzpatrick
The goal of rehabilitation is to maximize an individual’s physical, cognitive, and psychological recovery from a disease, injury, or traumatic event. An interdisciplinary team of professionals applies fundamental rehabilitation principles with the objective of preventing secondary injury, achieving optimal pain control, employing therapeutic exercise to meet established goals, utilizing appropriate assistive technology (AT), and providing education and counseling to the patient and family. While the first priority in treating a trauma patient is to preserve life and limb, early initiation of rehabilitation can have a significant impact on recovery, length of stay, reintegration into the community, and, ultimately, quality of life.
Trauma patients, especially those with spinal cord injury (SCI), traumatic brain injury (TBI), burns, and amputations, are particularly vulnerable to secondary complications and multisystem problems that are best treated if recognized early. In order to most appropriately address these unique needs, transfer to a specialized rehabilitation facility should be considered as soon as possible after the acute medical and surgical issues are addressed. The optimal timing for transfer is largely dependent on the condition of the patient and comfort level of the providers at both the discharging and receiving institutions, but generally occurs when the emphasis of care transitions from the acute medical and surgical issues to recovery. It is not uncommon for patients who require additional medical or surgical procedures to transfer back to the acute care hospital from the rehabilitation facility in order to facilitate optimal recovery.
As in other areas of medicine, subspecialty designation within the rehabilitation field is common. Many physicians, therapists, nurses, and counselors receive subspecialized training and board certification in areas such as spinal cord medicine, neurological impairments, limb loss, and cognitive rehabilitation. Rehabilitation facilities themselves receive special accreditation by the Commission on Accreditation of Rehabilitation Facilities (CARF), which helps to ensure quality.1 The National Institute on Disabilities and Rehabilitation Research (NIDRR) also recognizes excellence in rehabilitation institutions with their Models Systems Programs for Burns, SCI, and TBI.2
Trauma providers should not wait until the resolution of all medical and surgical issues before engaging in rehabilitation; rather, it should be an integral part of every trauma patient’s care starting from initial hospitalization. Trauma professionals should also recognize that the medical and surgical care they provide during the acute phase of treatment may have long-lasting implications for a trauma patient’s overall health, recovery, and quality of life.
EFFECTS OF IMMOBILITY
The fundamental principles of rehabilitation are founded on mitigating and preventing (when possible) the effects of immobility. The physiological and psychological effects of immobility lead to adverse organ system changes that may complicate healing and recovery. Therefore, a thorough understanding of these potential consequences will help optimize any treatment plan.
Muscle Atrophy and Weakness
Muscle responds to alterations in loading conditions. While increased activity leads to muscle fiber hypertrophy, less may result in disuse atrophy. The muscles most affected by such disuse atrophy during bed rest or immobilization are the antigravity muscles of the lower limbs and trunk. Thus, muscles with different functional roles atrophy at different rates during unloading.3 During immobilization, the rate of protein synthesis declines while proteolysis increases. The resulting loss in total body protein is accompanied by a significant remodeling of muscle architecture, including a loss of sarcomeres both in series and in parallel; this leads to reduced muscle thickness and length.4Muscle atrophy occurring from immobilization results in diminished force production and a loss of strength of 10–15% per week.5,6Interestingly, muscle strength decreases at a faster rate than muscle size, indicating that, in addition to atrophy, other factors contribute to muscle weakness.7 Immobilization also leads to a decrease in density of mitochondrial volume, reducing muscle oxidative capacity and leading to a loss of endurance—an early trigger of anaerobic metabolism.8
Bone, like muscle, is sensitive to loading stresses. Bone mass increases under mechanical stress and decreases in the absence of muscle activity or gravitational force. An unloaded skeleton during bed rest results in a decrease in bone formation with little to no impact on rates of bone reabsorption. Thus, disuse osteoporosis occurs because of a mismatch between bone growth and bone loss, resulting in a 1–2% reduction in bone mineral density each month.9 Bed rest also leads to an increased excretion of compounds released during bone degradation such as hydroxyproline, pyridinoline, and deoxypyridinoline complexes.10 Greater calcium excretion in the urine, combined with decreased intestinal absorption, results in the negative calcium balance characteristic of loss of bone minerals.11 Patients with preexisting osteopenia, osteoporosis, or SCI are especially susceptible to an increase in bone turnover during immobilization and have a higher risk of osteoporotic-related fractures.
A contracture is defined as a shortening of muscle, characterized by flexion that prevents movement through the normal range of motion. Joint contractures are classified according to etiology as either myogenic or arthrogenic. Myogenic contractures are caused by changes in muscle, tendon, or fascia. While reduction in muscle length clearly contributes to the formation of a myogenic contracture, remodeling of intramuscular connective tissue during immobilization also plays a significant role. Such changes have only been observed, however, when the muscle is immobilized in a shortened position, suggesting that limb position plays a direct role in connective tissue properties.5,12 Arthrogenic contractures are caused by changes in bone, cartilage, synovium/subsynovium, capsule, or ligaments. Proliferation of intra-articular connective tissue, adaptive shortening of the capsule, and increases in cross-linking of collagen fibrils promote this type of contracture formation.13
Prevention and Treatment
The best way to prevent the deleterious effects of immobility on the musculoskeletal system is to keep bed rest or immobilization to a minimum. Strength, endurance, and flexibility programs are integral to both the prevention and treatment of musculoskeletal damage. Physical therapists (PTs), occupational therapists (OTs), and the nursing staff should promote activities as soon as determined to be safe by the medical and surgical team. Resistance exercise has been shown to both maintain muscle protein synthesis and increase bone mass, reducing the incidence of muscle atrophy and disuse osteoporosis during immobilization.4 Electrical stimulation may also be helpful by passively contracting skeletal muscle and maintaining muscle oxidative capacity.14 Daily stretching has been shown to prevent serial sarcomere loss and reorganization of tissue components,12 leading to a reduced risk of muscle atrophy and contracture formation. Daily range of motion, flexibility, and muscle strengthening exercises help maintain the appropriate balance of muscles across joints and can be used to both prevent and treat muscle atrophy, disuse osteoporosis, and contracture formation.
Shift of Body Fluids
Lying in a supine position eliminates the gravitational gradient normally present with standing, causing a fluid shift of approximately 1 L from the legs to the thorax. The resultant increase in pressure within the heart’s ventricles leads to an increase in diastolic filling and stroke volume. Volume regulatory mechanisms within the heart react to the increase in volume of intrathoracic fluid and trigger urinary excretion and reduced thirst, resulting in a resetting of the cardiopulmonary baroreflex and a reduction in plasma volume.15,16
Skeletal muscles generally compress major veins, forcing blood upwards and ensuring its return to the heart. The loss of skeletal muscle during bed rest impairs this venous return, compounding the reduction in blood volume and leading to decreases in diastolic pressure and stroke volume. To counteract this decrease in stroke volume and maintain sufficient cardiac output, heart rate increases. After 4 weeks of bed rest, the resting heart rate is typically increased by approximately 10 beats/min. The heart rate after exercise is increased by almost 40 beats/min, and this places greater demand on the heart. Similar to skeletal muscle, cardiac muscle is also plastic in response to stress. Therefore, as stroke volume decreases, the heart is required to do less work and begins to atrophy. The resulting decrease of cardiac mass and myocardial thinning reduce the effectiveness of the cardiac pump.17,18
Immobilized patients have a reduction in blood volume, venous return, and stroke volume. These factors in conjunction with cardiac deconditioning and myocardial thinning lead to the development of orthostatic hypotension.17Orthostatic hypotension is characterized by an excessive fall in stroke volume on assuming an upright position and has been reported after as little as 20 hours of bed rest.19,20Orthostasis is magnified for patients with SCI as a loss of sympathetically mediated vasoconstriction compounds venous pooling in the abdomen and lower limbs and leads to a decrease in arterial blood pressure. This results in dizziness, lightheadedness, or loss of consciousness when assuming an upright position. Symptoms of orthostatic hypotension may significantly interfere with a patient’s ability to perform activities of daily living (ADLs) or participate in therapy.
Maximal oxygen consumption (VO2max) is a measure of cardiovascular fitness and has been shown to decrease during bed rest in proportion to the duration of immobilization.21 Both peripheral (muscular) and central (cardiovascular) factors play a role in the decrease in VO2max resulting from immobility.8 Individuals with preexisting cardiovascular disease, therefore, present a higher risk for cardiac complications when recovering from a traumatic event and will require clear cardiovascular guidelines for participation in therapy. Typical guidelines include not exceeding a greater than 10–15 mm Hg rise in systolic blood pressure or greater than 60–65% maximal heart rate. Perceived exertion scales such as the Borg scale are often used to help monitor effort, and, when needed, supplemental oxygen and monitoring with pulse oximetry should be used during therapy.
Venous Thrombosis and Pulmonary Embolus
The incidence of deep venous thrombosis (DVT) after major trauma has been reported to be as high as 58%.22,23 Without prophylaxis, its incidence after a motor complete SCI may be as high as 72%.24Typical features of DVT include swelling, erythema, and pain in the affected extremity. A pulmonary embolism (PE) is a potentially fatal consequence of a DVT, caused by part of the clot breaking away from the vein wall and lodging in a pulmonary artery. Typical symptoms include tachycardia, dyspnea, and chest pain. Unfortunately, both DVT and PE may manifest silently without producing any traditional symptoms, especially in patients with paralysis, sensory loss, or impaired consciousness.25 Computed tomographic pulmonary angiography (CTPA) has emerged as the preferential test in diagnosing a PE, due to its high accuracy, ease of use, and ability to provide alternate diagnoses.26 Other common tests for DVT and PE include ultrasound, lung ventilation perfusion scans, and blood tests including D-dimer.
Prevention and Treatment
Minimizing the effects of cardiovascular deconditioning is achieved by reintroducing activities as soon as possible during the initial care of an injured patient. Management of orthostatic hypotension begins with preventing venous pooling in the abdomen and lower limbs by using abdominal binders and lower limb compression stockings. If necessary, the use of medications such as midodrine or florinef may also be helpful in treating or preventing episodes of orthostatic hypotension.27 The incidence of DVT can be reduced to 7–10% with appropriate prophylaxis.24 The current recommendation for the prevention of DVT and PE following trauma is to initiate pharmacological anticoagulation within 72 hours of the injury, provided no contraindications exist (e.g., bleeding, ongoing surgical procedures, or progressive changes in the brain on computed tomography [CT]). Anticoagulation may be accomplished with low-molecular-weight heparin or adjusted dose unfractionated heparin. In addition to pharmacological prophylaxis, use of mechanical prophylaxis such as compression hose or intermittent compression boots should be initiated as soon as possible and continued for at least 2 weeks. If contraindications to pharmacological prophylaxis exist, strong consideration should be given to insertion of a vena cava filter to prevent PE. Duration of pharmacological prophylaxis is dependent on the extent of trauma and continued risk as follows: (1) until hospital discharge for those with uncomplicated motor incomplete SCI; (2) 8 weeks for those with uncomplicated motor complete SCI; and (3) 12 weeks for those with complicated SCI (e.g., lower limb fracture, age >70, or history of thrombosis, cancer, heart failure, or obesity).28 Lifestyle modifications including avoiding immobility and dehydration, stopping smoking, and maintaining normal blood pressure can also help prevent DVT/PE.
Lung Volume and Structural Changes
Patients take fewer deep breaths when lying down due to decreased respiratory muscle strength during immobilization. This decreased tidal volume (amount of air inhaled or exhaled during normal respiration) contributes to a 25–50% decrease in total respiratory capacity. A similar reduction in the diameter of the airways leads to a decrease in functional residual capacity (the amount of air left in lungs after expiration), which can restrict airways and decrease gas exchange.29 Further complicating respiratory function, bed-ridden patients have difficulty clearing secretions leading to accumulation of mucous in the air passages and secondary atelectasis and pneumonia.30,31
Prevention and Treatment
Promoting deep inspiration with an incentive spirometer is important for all trauma patients. Chest physiotherapy, vibration, and postural drainage techniques can be administered by a respiratory therapist and should be considered for any patient with acquired pneumonia while on bed rest. Clearing secretions is especially challenging for patients with paralysis from an SCI. Special coughing techniques, such as the “quad cough,” should be utilized and taught to the patient and family members by a trained therapist.31,32
Urinary System Effects
Urinary Retention/Stones/Urinary Tract Infection
The urge to urinate is often lessened when supine, even when the bladder is full, and this contributes to urinary retention. An overdistended bladder may cause the stretch receptors to lose sensitivity, further reducing the urge to urinate. The aforementioned bone loss due to immobilization results in hypercalciuria, increasing the risk of forming bladder and renal stones. Urinary retention also encourages the growth of bacteria that raise the pH of urine and increase the risk of infection as well as precipitation of calcium that exacerbates stone formation.33,34
Prevention and Treatment
For most trauma patients, an indwelling catheter is placed to ensure adequate emptying of the bladder, prevent fluid stasis and subsequent infection, and prevent a high-pressure system that may lead to hydronephrosis and renal damage. An indwelling catheter also allows the trauma team to monitor fluid output and assess fluid status. Indwelling catheters should be removed as soon as medically possible to prevent urethral or bladder damage and to avoid reducing bladder compliance and storage capacity. After removing an indwelling catheter, it is important to monitor initial postvoid residual bladder volumes (PVR) to ensure adequate emptying. A PVR greater than 50–100 cm3usually mandates replacement of the indwelling catheter and urological consultation.35 Patients with neurogenic bladders from an injury to the central or peripheral nervous system should be on a bladder program as soon as the indwelling catheter is removed (see Section “Spinal Cord Injury”).
Appetite and Gastric Transit Time
Bed rest negatively impacts taste acuity, leading to a reduction in food intake.36 In addition, immobilization results in structural and functional changes of the gastrointestinal tract, including atrophy of the mucosal lining and reduced glandular capacity.37 Gastric transit time is prolonged during bed rest, also. A decreased rate of evacuation from the stomach may cause symptoms of gastroesophageal reflux, regurgitation, and heartburn. The rate of peristalsis and of food absorption is slowed during bed rest, as well.38 Longer transit time increases water reabsorption through the gut, which can lead to constipation and fecal impaction.34
Minimizing immobility, promoting activity, and ensuring adequate hydration are essential components of proper bowel management. The use of a bedside commode or bathroom toilet rather than a bedpan is encouraged. Bowel management should be targeted to the specific dysfunction that is present. Effective bowel programs include techniques such as timed stooling, dietary modifications, timing evacuation about 30 minutes after a meal to take advantage of the gastrocolic reflex, and manual disimpaction, especially for individuals with neurogenic bowel dysfunction from an SCI. If further treatment is required, medications such as bulk-forming agents (e.g., Colace), enemas, colonic irritants (e.g., Dulcolax), and intestinal motility agents (e.g., senna) may be used. The ability of the patient to independently perform manual disimpaction or self-administer enemas or suppositories will depend on his or her level of impairment. A surgical colostomy may be necessary to provide continence in certain patients, and appropriate colostomy care should be taught to the patient or caregiver.
Integumentary System Effects
Decubitus Ulcers (Pressure Sores)
Immobilization is strongly associated with the formation of decubitus ulcers. Bony prominences such as the occiput, shoulder blades, sacrum, and heels are of greatest risk for supine patients.39 Ulcerations that occur over the ischial tuberosities are generally attributable to increased seating pressure. As immobilized patients are unable to make natural postural changes that alleviate pressure on susceptible body parts, blood flow to tissues can become obstructed, leading to necrosis of soft tissue and skin.40 Patients with impaired cognition or sensation are particularly susceptible to the formation of pressure ulcers and between 25% and 80% of patients with an SCI eventually develop them, with up to 8% developing fatal complications.31 In addition, urinary and fecal incontinence may lead to excessive skin maceration and subsequent breakdown.41 When present, pressure ulcers can have a significant negative impact on successful rehabilitation, recovery, and quality of life.42
Frequent skin inspection, appropriate hygiene, achieving urinary and fecal continence, proper fitting of orthotics, and avoiding excessive pressure through a regular turning schedule are all critical aspects of caring for the skin of a trauma patient. Providers should remain particularly attentive to the pressure-sensitive areas of the body and the placement of devices such as cervical collars and multipodus boots. The utilization of specialty beds and seating cushions is encouraged but should not replace vigilant medical and nursing care. Many trauma centers have a dedicated skin and wound care team. These professionals should be consulted at the earliest signs of skin breakdown and should be involved in continuous education of the medical, nursing, and therapy staff. The primary treatment of pressure ulcers should focus on prevention through frequent position changes by a caregiver or the patient. This may require education of caregivers and patient as well as specialized equipment such as wheelchairs with appropriate cushioning and adjustable tilting features.
UNIQUE COMPLICATIONS OF TRAUMA PATIENTS
Heterotopic ossification (HO) is the formation of mature lamellar bone in tissue that is not normally ossified. It commonly develops in patients with TBI, SCI, burn injury, or blast-related amputations. The most common site of HO following SCI is the hip, but it may also occur in the elbow, shoulder, and knee.43 For patients with burns, 92% of cases occur in the elbow,44,45 and up to 80% of patients who sustain an amputation from a blast injury may develop HO.46 The clinical presentation of HO may include a decrease in range of motion and erythema and swelling about the involved joint. It is important to distinguish HO from a DVT, which may involve a similar clinical presentation. Studies such as x-rays, bone scans, and monitoring of serum alkaline phosphatase levels can aid in the diagnosis. Prophylaxis with etidronate, nonsteroidal anti-inflammatory drugs (NSAIDs), and local irradiation may prevent HO.47Treatment of HO involves active and passive range of motion to prevent worsening; in severe cases, surgical excision may be required to improve functional outcomes.43,48 Even when treated aggressively, HO may still result in significant restrictions in range of motion and subsequent disability.
Spasticity is defined as a velocity-dependent increase in muscle tone that occurs following injury to upper motor neurons. Typically, it is associated with increased deep tendon reflexes and other signs of upper motor neuron disease. Spasticity occurs frequently in patients with TBI and SCI and may significantly impede successful rehabilitation if not treated appropriately. During the acute stage, however, a patient with SCI may have diffusely diminished reflexes below the level of injury. This period of hypotonicity and hyporeflexia is referred to as spinal shock. In the weeks following SCI, reflexes return and gradually increase while spasticity develops. The incidence of spasticity following SCI at 1 year is estimated to be 65–78%.49 Spasticity can result in significant pain, difficulty with transfers, and increased risk of skin breakdown. In certain circumstances, spasticity may be of benefit to the patient, particularly when lower limb tone is used to aid in transfers. Therefore, the decision to treat spasticity should be based on improving patient function, hygiene, or care.
Conservative treatment of spasticity begins with positioning, stretching, splinting, and range of motion exercises. Medications used for spasticity include GABA agonists (e.g., baclofen), centrally acting alpha-2 agonists (e.g., tizanidine), and medications that inhibit skeletal muscle contraction (e.g., dantrolene). The appropriate choice of medication should be based on the patient’s response as well as the presence of adverse side effects. Botulinum toxin or phenol injections may also be helpful in spasticity management. Implanted pumps may be used to deliver highly concentrated doses of medications directly to the spinal cord through an intrathecal catheter, which minimizes systemic side effects, and surgical treatment of spasticity may be required to correct fixed deformities.49
Inadequate pain control is associated with delayed healing, increased complications, prolonged hospitalization, poor sleep, and diminished quality of life.50 It has also been shown to be a significant cause for hospital readmission.51Therefore, aggressive pain management should be a priority for any trauma team. Unfortunately, many patients who present to the emergency department (ED) with acute pain are undertreated for their pain.52 Multiple professional organizations, including the American Pain Society (APS) and the Agency for Healthcare Research and Quality (AHRQ), have developed and disseminated clinical practice guidelines to address the insufficient treatment of pain in America’s health care delivery system.53 In addition, the Joint Commission on Accreditation of Healthcare Organizations (JCAHO) introduced new standards for pain assessment and management, advocating pain management as a patient right and requiring health care organizations to employ effective pain management policies.54 Despite these initiatives, significant challenges still remain in changing clinical practice.55
Postoperative pain is a significant problem for most hospitals and demands special attention from the trauma team.56 While a multitude of pain interventions currently exist, numerous barriers prevent patients from receiving optimal care.57 Expecting it as part of the surgical process, patients often underreport their level of pain or are reluctant to ask for pain medication. Pain medications prescribed on an “as-needed” basis can cause a lag in treatment and a “peak and trough” pain pattern of analgesia. Such poor pain management may lead to significant anxiety, poor sleep, and loss of appetite. Given the difficulty in treating established pain, preventative measures such as around-the-clock analgesia represent the best way to ultimately prevent severe pain. In addition, uncontrolled or protracted acute pain may lead to chronic pain states, which may have long-term negative implications on function, return to work, and quality of life.58,59
Providers traditionally underestimate a patient’s level of discomfort. Therefore, it is important to establish a standardized method of communication between the patient and provider. To determine pain levels, most health care organizations utilize a visual analog scale (VAS) typically ranging from 0 (no pain) to 10 (worst imaginable pain). In addition to communicating pain levels, this tool may also be used to assess the effectiveness of pain interventions, and establish therapeutic goals for each patient. Determining pain levels for children or individuals with cognitive impairment may be challenging. In such cases, providers may use the FACES scale, in which images of faces ranging from smiling to grimacing reflect pain scores.60 A speech language pathologist (SLP) may be of great assistance to the patient and treatment team by developing an effective communication system for more challenging communication barriers. Family members should also be engaged with the treatment team to help provide feedback on the patient’s nonverbal expression of pain and response to therapeutic interventions.
Terminology and Pathophysiology
While a detailed discussion is beyond the scope of this chapter, the proper treatment of pain requires a basic understanding of common pain terminology and a familiarity with nervous system physiology (Table 51-1).
TABLE 51-1 Common Pain Terminology
Pain management strategies should target the suspected source of nociception (Fig. 51-1). Issues such as positioning, poor sleep, anxiety, and depression may augment the perception of pain. In addition, chronic underlying conditions such as migraine headaches, diabetic neuropathy, osteoarthritis, or other musculoskeletal injuries may be exacerbated by trauma, adding to a patient’s discomfort. Therefore, a thorough history and physical examination is critical in evaluating every trauma patient. It is also possible that other injuries may have been overlooked during the initial trauma screen; therefore, a tertiary survey is necessary in injured patients. Pain management strategies should be readily discussed among the trauma team and a pain specialist should be consulted for patients with complex pain problems. Treatment strategies generally include both pharmacological and nonpharmacological approaches.
FIGURE 51-1 Afferent nociception pathway: demonstrates pain signals originating from a peripheral noxious stimulus, traveling along sensory afferents through the dorsal root ganglion and into the spinal cord, where both excitatory (red) and inhibitory (green) neurotransmitters modulate impulses before the signal is perceived within the brain.
• Opioids are the most common analgesic drug used during acute care of the trauma patient and may be administered orally, intramuscularly, or intravenously. Meperidine’s active metabolite, normeperidine, has a prolonged half-life and may cause seizures, limiting its use especially in the elderly or those with renal impairment. Morphine is the opioid of choice because of its clear analgesic, amnestic, and sedative effects, and it is also readily available and cost-effective. Fentanyl may also be used, but has a shorter half-life, produces weaker sedation, and costs more.61 Patients on chronic opioids may be safely treated with intravenous opioid bolus dosages up to 20% of their total daily use.62
• NSAIDs can be very helpful in relieving peripherally generated pain by blocking cyclooxygenase and the subsequent formation of prostaglandins, which promote pain and inflammation. There are two isomers of cyclooxygenase (COX-1 and COX-2), each involved in a range of physiological functions. For example, the prostaglandins produced by COX-1 also protect the stomach and support platelet aggregation. Therefore, nonselective COX inhibitors should be used with caution in the injured patient to avoid the possible side effects of peptic ulceration and dyspepsia. Ketorolac is the only NSAID in the United States available in an injectable form. Its administration, either intravenously or intramuscularly, has analgesic effects similar to morphine. Unlike morphine, however, it has a maximum dose of 60 mg and cannot be dose adjusted.
• Antiseizure medications such as gabapentin, pregabaline, carbamazepine, valproic acid, or oxcarbazepine are often used to help treat neuropathic pain and may be effective in treating phantom limb pain for those with amputations, also. These medications act as membrane stabilizers to the axons in the central and peripheral nervous systems.
• Antidepressant medications have long been used to help augment pain management, particularly for neuropathic pain. Tricyclic antidepressants (TCAs) are effective, but have sedative effects. They also have anticholinergic properties, which may lead to secondary problems such as confusion and urinary retention, especially in the elderly. Therefore, side effects should be monitored and the dose of medication adjusted accordingly. Duloxetine is an antidepressant medication with fewer side effects than TCAs and is approved for the treatment of diabetic nerve pain. Although the effect of selective serotonin reuptake inhibitors (SSRIs) on acute or chronic pain is unclear, these medications should be considered to treat depression or anxiety, which may be a contributing factor to the patient’s pain.
• Continuous infusion analgesia and anesthesia may be achieved with intravenous patient-controlled anesthesia (PCA) or with regional anesthesia through a peripherally placed catheter. Intravenous opioid administration through a PCA helps to avoid the “peak and trough” phenomenon of inadequate pain management. Continuous infusion of an anesthetic agent through a catheter in the region of a peripheral nerve or plexus offers outstanding pain control for limb injuries and avoids the secondary cognitive effects of systemic opioids. Regional anesthesia catheters should be monitored for effectiveness as well as signs of infection and have been reported to be safe for up to 34 days in combat-related injuries.63
• Sympathetic blockade may be helpful in patients with sympathetically mediated complex regional pain syndrome (CRPS). CRPS should be suspected if the pain in an extremity persists long after what would be normally expected in patients with similar injuries. Symptoms typically include regional pain, allodynia, hyperalgesia, swelling, and local dysautonomia (sweating, discoloration, or temperature changes). As prolonged immobility may be a precursor to CRPS, early rehabilitation may prevent its occurrence. When CRPS is suspected, a pain specialist consultation is recommended.
• Modalities such as heat or ice may provide effective pain relief for injured patients and should be made available as needed. Caution should be observed when using these modalities for patients with injuries to the central or peripheral nervous system or those with cognitive impairment. Lack of protective sensation or awareness my lead to a significant skin injury or burn.
• Interventions such as acupuncture, desensitization techniques, self-hypnosis, biofeedback, and music therapy may also provide some pain relief for injured patients. Such therapies are generally well received and can be administered without fear of side effects or adverse interaction with other medications.
FUNCTIONAL IMPROVEMENT THROUGH INTERDISCIPLINARY TEAM CARE
As already stated, the early application of rehabilitation principles helps prevent secondary injury and facilitates patient recovery. Consultation with rehabilitation specialists should be considered for every injured patient. An interdisciplinary rehabilitation team employs a variety of specialists from physiatry, physical therapy, occupational therapy, mental health, and speech language pathology. For patients with cognitive impairment, a neuropsychologist may offer invaluable assistance in identifying cognitive deficits and formulating management decisions. In addition to providing holistic care, these providers will spend additional time with the patient and his or her family to determine premorbid and current functional levels as well as to help develop short- and long-term goals for functional improvement.
• Physical medicine and rehabilitation (PM&R) specialists (physiatrists) are board-certified physicians who specialize in neuromusculoskeletal disorders and rehabilitation. They are skilled at integrating medical and surgical treatment plans with the rehabilitation team. Physiatrists are also helpful in establishing safety precautions for the patient, managing pain and bowel/bladder issues, and aiding in appropriate discharge planning and disposition. Subspecialty certifications currently exist in spinal cord medicine, TBI, and pain management.
• PTs help assess motor function and mobility. This includes assessing range of motion of joints and motor strength as well as a patient’s balance and ability to sit, stand, transfer, or walk independently or with an assistive device. Treatment should begin early during the acute care hospitalization and continue until goals are met. PT assessments are very helpful in guiding appropriate discharge planning. It is important for the trauma physician to provide the therapist with guidance on appropriate weight bearing, range of motion, or activity precautions.
• OTs help assess a patient’s ADLs and instrumental ADLs (IADLs). ADLs include feeding, toileting, dressing, and hygiene. IADLs refer to activities beyond basic personal care, typically requiring devices such as a telephone, kitchen utensils, or appliances. Examples of IADLs include managing finances, preparing meals, and doing laundry. A patient’s independence in ADLs and IADLs will help determine appropriate discharge planning. OTs are also skilled at helping those with extremity trauma or nervous system injury regain both gross and fine motor hand function.
• SLPs help assess, diagnose, and treat patients with difficulties related to speech, language, swallowing, or cognitive–communication deficits. Since adequate nutrition is necessary for tissue healing and recovery, assessing a patient’s ability to swallow safely may help guide appropriate interventions to ensure adequate caloric intake. Additionally, the SLP may help develop ways to improve the necessary communication between the treatment team and the patient.
• Orthotists and prosthetists (O&P) are certified in evaluating, fabricating, and custom fitting orthopedic braces (orthotics) and artificial limbs (prostheses). Orthotics are devices used to align, support, protect, or improve the function of a body part. Examples of orthotics used in trauma casualties include halo cervical traction splints, ankle foot orthotics (AFO), and thoracolumbosacral orthotics (TLSO). Orthotics may be either static (rigid) or dynamic (assist with desired motion). Prostheses may be utilized for upper or lower limb amputations, and are composed of a socket, suspension, joint(s), shank, and terminal device (hook, hand, or foot). Early prosthetic fitting may enhance acceptance and functional recovery.
• Mental health professionals should be a part of any interdisciplinary team. Traumatic events have a significant psychological impact on the patient, family members, and caregivers. Nearly all survivors of a major traumatic event will exhibit stress-related symptoms and up to 40% may have a psychiatric disorder at 1 year following trauma.64 For combat casualties, rates of comorbid post-traumatic stress disorder (PTSD) have been reported to be 16.7%.65Fear of isolation, lack of wholeness, and concerns about the future are common, but can be eased by supportive family members and caregivers. A preventative medicine approach to psychiatry helps to decrease stigmatization, foster acceptance of mental health care, and prevent the development of a disabling psychiatric disorder after trauma.66 Special consideration should also be made when introducing children to a parent who suffered limb loss or other disfiguring injury.
• Rehabilitation engineers/AT specialists specialize in the development, fitting, and training of AT devices. AT devices provide essential support for individuals with disabilities, allowing them to perform ADLs and return to work, sports, and recreational activities. They include manual and powered wheelchairs, seating systems, standing systems, adaptive vehicles, augmentative communication systems, electronic aids, and assistive robotics. As technology becomes more sophisticated, expertise is needed in these areas. The Rehabilitation Engineering and Assistive Technology Society of North America (RESNA) currently provides credentialing to suppliers, health care providers, and engineers to ensure quality in products and service delivery.
• Peer support visitors are trauma survivors who receive training to provide support to patients and their families. Peer visitors generally have suffered a similar life-changing injury as the patient and are able to exemplify successful recovery by adapting and returning to community participation. Peer support visitors are especially beneficial for individuals with paralysis, vision loss, disfiguring scars, or limb loss. The Amputee Coalition of America (ACA) offers a peer support training program, which may be helpful for individuals or institutions interested in initiating such a program.
• Vocational rehabilitation specialists interview patients and match career goals with functional capacity, AT, and professional talents. Community reintegration and return to vocation should be in the long-term goals of all trauma patients. Although controversy exists as to the optimal timing of intervention, discussing vocation during early hospitalization may facilitate engagement in rehabilitation and hasten recovery.
• Case managers and social work services are essential to adequately address discharge planning, transfer to the next level of care, coordinate equipment needs, and provide patient and family education. Therefore, these professionals should be an integral part of the trauma treatment team.
SPECIAL CONSIDERATIONS FOR SPECIFIC TRAUMATIC INJURIES
Spinal Cord Injury
Injury to the spinal cord results in impaired motor strength and sensation below the level of injury, and bowel and bladder function, sexual function, and autonomic control are frequently impaired, also. Approximately 12,000 SCIs occur nationally each year, and approximately 259,000 SCI survivors are living in the United States. Males account for approximately 80% of all injuries, and motor vehicle accidents account for 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 up to $3 million per patient.67
SCIs are classified by their severity and level of injury, using the American Spinal Injury Association (ASIA) Standard Neurological Classification Worksheet.68 This worksheet 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.
Functional Outcomes after Spinal Cord Injury
The expected level of independence and functional capacity after 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 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.69
Acute Management of Spinal Cord Injury
Treatment of acute SCI in a trauma center has a significant positive impact on survival and long-term functional recovery.70 Immediate spinal stabilization is essential to prevent further neurological compromise. While not all patients require surgery after SCI, animal models have shown that surgical treatment relieving spinal cord compression can prevent further neurological deterioration. The National Acute Spinal Cord Injury Study recommended that high-dose methylprednisolone be administered for 24–48 hours following acute SCI. These guidelines had been widely followed by the international community.71 Because of concerns over infection, gastrointestinal bleeding, and steroid myopathy, trauma centers came to question the efficacy and safety of this protocol. Therefore, the use of steroids following SCI is currently considered a treatment option rather than the standard of care.
Complications after SCI
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 should be identified. Noxious stimuli often result from tight or constricted clothing, pressure on the skin, bladder distension, or bowel impaction. 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 jelly to prevent a further noxious stimulus. If symptoms persist, manual fecal disimpaction should be performed using lidocaine jelly. If blood pressure remains elevated, pharmacological management may include the use of nitroglycerin paste (which can be easily removed to prevent rebound hypotension) and 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.27,72
• Hypercalcemia as a result of upregulation in osteoclast activity may occur in individuals with SCI, especially adolescent 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.73
• 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 may also 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 (e.g., 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 bladder emptying. 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.74
• 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.75 Both incontinence and failure to empty may result (see 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.
Traumatic Brain Injury
TBI is the leading cause of death and disability in young adults in the United States. Over 1.4 million individuals sustain a TBI annually, with approximately 90,000 injuries resulting in a permanent disability.76 In addition, it is estimated that up to 20% of service members who are deployed sustain a concussion or mild TBI.77 TBI can occur from multiple mechanisms of injury including blunt trauma, penetrating trauma, or blast. Additionally, hypovolemia, anoxia, and metabolic changes after trauma may result in significant brain damage. Injury to the brain 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 a helpful diagnostic tool and should complement a thorough evaluation of mental status and physical examination.78
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).79 The Ranchos Los Amigos Scale is also often used to describe a patient’s level of awareness, cognition, behavior, and interaction with the environment after a TBI (Table 51-3).80 Patients who are mobile, but confused or agitated, will likely require a secured inpatient setting.
TABLE 51-2 Traumatic Brain Injury Classification
TABLE 51-3 Ranchos Los Amigos Scale
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.81 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.82 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. 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.83
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. For those with impairments that prohibit participation in an acute care rehabilitation facility, transfer to a skilled nursing facility (SNF) may be necessary. Patients who sustain significant extremity trauma, but deny TBI or cognitive difficulties, may still 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.84
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.85
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 >65.86Management 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 orthopedic injuries, TBI, SCI, or amputations. Severe disability, altered body image, and numerous physical and medical complications often lead to a diminished quality of life among survivors of burns.87 Burn injuries account for 40,000 hospital admissions annually in the United States and are the fifth most common cause of unintentional death. 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.88,89
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. 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.88,90
• 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.91 In addition to exercise programs, treatment with anabolic agents such as oxandrolone has been observed to reduce or prevent weakness in a burn population.92
• Heat intolerance: The ability to regulate and tolerate heat is often decreased following burn injury.93 The mechanism for heat intolerance may be rooted in changes in central and peripheral thermoregulation; however, studies have suggested still yet unknown factors.94 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 injury88 (see Section “Pain Management”).
• 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.88 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. Depression occurs with an incidence of 17% during the 12 months following burns.95 While no studies specifically investigate the treatment of depression following burns, standard cognitive and pharmacological treatments are often implemented. Hypertrophic scarring often causes facial and limb disfigurement, which can lead to significant body image dissatisfaction and difficulty with community reintegration. PTSD has been reported to occur in 13–25% of patients with burn injuries.88 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.96 The recognition and treatment of psychological complications of burn injuries is crucial to the design and implementation of a successful rehabilitation program.
The incidence of traumatic amputation continues to decline in the United States because of improved safety standards, along with advances in surgical techniques to salvage severely injured limbs. Despite these improvements, however, trauma still remains a significant contributor to pediatric and upper limb amputations. In fact, 68.6% of all traumatic amputations occur in the upper limb. Major limb loss presents numerous physical, psychological, and functional challenges, which may be even further magnified by the presence of other comorbid injuries, paralysis, or cognitive deficits.
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 postinjury, there are no significant functional outcome differences between those who undergo limb salvage surgery and those who undergo amputation, although limb salvage patients are more likely to have longer hospital stays, more operative procedures, and a higher complication rate in the short term. Long-term follow-up of both groups demonstrates a lower quality of life compared with age-matched controls. Patients who need an amputation are also at a higher risk for pain syndromes (phantom and residual limb pain), skin problems in the residual limb, overuse injuries of intact limbs, as well as cardiovascular disease and glucose intolerance. For children, psychological acceptance, altered self-image, and the common development of bony overgrowth of the amputated limb are of particular concern.97,98
For a comprehensive review of amputee care, the reader is referred to the Textbook of Military Medicine: Care of the Combat Amputee.99 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 (e.g., reaching, standing, walking). It is also important to introduce play, sport, and recreational activities with appropriate adaptive equipment to help facilitate socialization and reintegration into the community.
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 also occur as a complication of medical care. Improper bed positioning, compressive casts, poor fitting orthotics, excessive pressure during surgery, or inadvertent needle sticks may lead to injury to a peripheral nerve. 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 critical illness neuropathy or critical illness myopathy may also 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 typically has an excellent prognosis for recovery; on the other hand, 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 per day or 1 in per month.
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 clarified 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 pressure-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 position changes. Special attention is also required when placing casts or external fixation devices. The use of ultrasound to guide interventional procedures may also help to avoid inadvertent iatrogenic injuries.
1. Commission on Accreditation of Rehabilitation Facilities. Available at: www.carf.org. Accessed February 1, 2010.
2. National Rehabilitation Information Center. Landover, MD. Available at: www.naric.com/research/pd/intro.cfm. Accessed February 8, 2010.
3. Dittmer DK, Teasell R. Complications of immobilization and bed rest, part 1: musculoskeletal and cardiovascular complications. Can Fam Physician. 1993;39:1428–1432, 1435–1437.
4. Ferrando AA, Lane HW, Stuart CA, et al. Prolonged bed rest decreases skeletal muscle and whole body protein synthesis. Am J Physiol. 1996; 270(4):E627–E633.
5. Williams PE. Use of intermittent stretch in the prevention of serial sarcomere loss in immobilized muscle. Ann Rheum Dis. 1990;49(5): 316–317.
6. Halar EM, Bell KR. Immobility and inactivity: physiological and functional changes, prevention, and treatment. In: DeLisa JA, eds. Physical Medicine and Rehabilitation: Principles and Practice. Vol. 2. 4th ed. Philadelphia: Lippincott Williams & Wilkins; 2005:1447–1467.
7. de Boer MD, Seynnes OR, di Prampero PE, et al. Effect of 5 weeks horizontal bed rest on human muscle thickness and architecture of weight bearing and non-weight bearing muscles. Eur J Appl Physiol. 2008;104 (2):401–407.
8. Ferretti G, Antonutto G, Denis C, et al. The interplay of central and peripheral factors in limiting maximal O2 consumption in man after prolonged bed rest. J Physiol. 1997;501(3):677–686.
9. Ehrlich PJ, Lanyon LE. Mechanical strain and bone cell function: a review. Osteoporos Int. 2002;13(9):688–700.
10. Holick MF. Perspective on the impact of weightlessness on calcium and bone metabolism. Bone. 1998;22(5 suppl):105S–111S.
11. Bikle DD, Halloran BP. The response of bone to unloading. J Bone Miner Metab. 1999;17(4):233–244.
12. Williams PE, Goldspink G. Connective tissue changes in immobilized muscle. J Anat. 1984;138(2):343–350.
13. Trudel G, Uhthoff HK. Contractures secondary to immobility: is the restriction articular or muscular? An experimental longitudinal study in the rat knee. Arch Phys Med Rehabil. 2000;81(1):6–13.
14. Needham DM, Truong AD, Fan E. Technology to enhance physical rehabilitation of critically ill patients. Crit Care Med. 2009;37 (10 suppl):S436–S441.
15. Perhonen MA, Zuckerman JH, Levine BD. Deterioration of left ventricular chamber performance after bed rest: “cardiovascular deconditioning” or hypovolemia? Circulation. 2001;103(14):1851–1857.
16. Spaak J, Montmerle S, Sundblad P, et al. Long-term bed rest-induced reductions in stroke volume during rest and exercise: cardiac dysfunction vs. volume depletion. J Appl Physiol. 2004;98(2):648–654.
17. Knight J, Nigam Y, Jones A. Effects of bedrest 1: cardiovascular, respiratory, and haematological systems. Nurs Times. 2009;105(21): 16–20.
18. Dorfman TA, Levine BD, Tillery T, et al. Cardiac atrophy in women following bed rest. J Appl Physiol. 2007;103(1):8–16.
19. Levine BD, Zuckerman JH, Pawelczyk JA. Cardiac atrophy after bed-rest deconditioning. Circulation. 1997;96(5):517–525.
20. Gaffney FA, Nixon JV, Karlsson ES, et al. Cardiovascular deconditioning produced by 20 hours of bedrest with head-down tilt (−5°) in middle-aged healthy men. Am J Cardiol. 1985;56:634–638.
21. Capelli C, Antonutto G, Kenfack MA, et al. Factors determining the time course of VO2max decay during bedrest: implications for VO2max limitation. Eur J Appl Physiol. 2006;98(2):152–160.
22. Paffrath T, Wafaisade A, Lefering R, et al. Venous thromboembolism after severe trauma: incidence, risk factors, and outcome. Injury. 2010;41(1): 97–101.
23. Geerts WH, Code KI, Jay RM, et al. A prospective study of venous thromboembolism after major trauma. N Engl J Med. 1994;331(24): 1601–1606.
24. Merli GJ, Crabbe S, Paluzzi RG, Fritz D. Etiology, incidence, and prevention of deep vein thrombosis in acute spinal cord injury. Arch Phys Med Rehabil. 1993;74(11):1199–1205.
25. Manganelli D, Palla A, Donnamaria V, et al. Clinical features of pulmonary embolism. Doubts and certainties. Chest. 1995;107(1 suppl): 25S–32S.
26. Kuriakose J, Patel S. Acute pulmonary embolism. Radiol Clin North Am. 2010;48(1):31–50.
27. Krassioukov A, Eng JJ, Warburton DE, et al. A systematic review of the management of orthostatic hypotension after spinal cord injury. Arch Phys Med Rehabil. 2009;90(5):876–885.
28. Paralyzed Veterans of America/Consortium for Spinal Cord Medicine. Prevention of Thromboembolism in Spinal Cord Injury. 2nd ed. Washington, DC: Paralyzed Veterans of America (PVA); 1999.
29. Dean E. Effect of body position on pulmonary function. Phys Ther. 1985;65(5):613–618.
30. Corcoran PJ. Use it or lose it—the hazards of bed rest and inactivity. West J Med. 1991;154(5):536–568.
31. Teasell R, Dittmer DK. Complications of immobilization and bed rest, part 2: other complications. Can Fam Physician. 1993;39:1440–1442, 1445–1446.
32. Brown R, DiMarco AF, Hoit JD, et al. Respiratory dysfunction and management in spinal cord injury. Respir Care. 2006;51(8):853–868.
33. Hwang TIS, Hill K, Schneider V, et al. Effect of prolonged bedrest on the propensity for renal stone formation. J Clin Endocrinol Metab. 1988; 66(1):109–112.
34. Knight J, Nigam Y, Jones A. Effects of bedrest 2: gastrointestinal, endocrine, renal, reproductive and nervous systems. Nurs Times. 2009;105(22):24–27.
35. Lukacz ES, DuHamel E, Menefee SA, et al. Elevated postvoid residual in women with pelvic floor disorders: prevalence and associated risk factors. Int Urogynecol J Pelvic Floor Dysfunct. 2007;18(4):397–400.
36. Ritz P, Maillet A, Blanc S, et al. Observations in energy and macronutrient intake during prolonged bed-rest in a head-down tilt position. Clin Nutr. 1999;18(4):203–207.
37. Bortz WM. The disuse syndrome. West J Med. 1984;141(5):691–694.
38. Thomas DC, Kreizman IJ, Melchiorre P, et al. Rehabilitation of the patient with chronic critical illness. Crit Care Clin. 2002;18(3):695–715.
39. Winkelman C. Bed rest in health and critical illness: a body systems approach. AACN Adv Crit Care. 2009;20(3):254–266.
40. Lyder CH. Pressure ulcer prevention and management. JAMA. 2003; 289(2):223–226.
41. Reddy M, Gill SS, Rochon PA. Preventing pressure ulcers: a systematic review. JAMA. 2006;296(8):974–984.
42. Regan MA, Reasell RW, Wolfe DL, et al. A systematic review of therapeutic interventions for pressure ulcers after spinal cord injury. Arch Phys Med Rehabil. 2009;90(2):213–231.
43. van Kuijkk AA, Geurts ACH, van Kuppevelt HJM. Neurogenic heterotopic ossification in spinal cord injury. Spinal Cord. 2002;40(7):313–326.
44. Chen HC, Yang JY, Chuang SS, et al. Heterotopic ossification in burns: our experience and literature reviews. Burns. 2009;35(6):857–862.
45. Peterson SL, Mani MM, Crawford CM, et al. Postburn heterotopic ossification: insights for management decision making. J Trauma. 1989; 29(3):365–369.
46. Potter BK, Burns TC, Lacap AP, et al. Heterotopic ossification in the residual limbs of traumatic and combat-related amputees. J Am Acad Orthop Surg. 2006;14(10):S191–S197.
47. Banovac K. The effect of etidronate on late development of heterotopic ossification after spinal cord injury. J Spinal Cord Med. 2000;23(1):40–44.
48. Tsionos I, Leclercq C, Rochet JM. Heterotopic ossification of the elbow in patients with burns: results after early excision. J Bone Joint Surg Br. 2004;86(3):396–403.
49. Adams MM, Hicks AL. Spasticity after spinal cord injury. Spinal Cord. 2005;43(10):577–586.
50. Ferrell BR. The impact of pain on quality of life. A decade of research. Nurs Clin North Am. 1995;30(4):609–624.
51. Grant M, Ferrell BR, Rivera LM, et al. Unscheduled readmissions for uncontrolled symptoms. A health care challenge for nurses. Nurs Clin North Am. 1995;30(4):673–682.
52. Wilson JE, Pendleton JM. Oligoanalgesia in the emergency department. Am J Emerg Med. 1989;7(6):620–623.
53. Agency for Healthcare Research and Quality. Acute Pain Management: Operative or Medical Procedures and Trauma, Clinical Practice Guideline. Rockville, MD: Agency for Healthcare Research and Quality; 1992. Available at: www.ahrq.gov/clinic/medtep/acute.htm#acutefind. Accessed January 15, 2010.
54. Berry PH, Dahl JL. The new JCAHO pain standards: implications for pain management nurses. Pain Manag Nurs. 2000;1(1):3–12.
55. Todd KH, Ducharme J, Choiniere M, et al. Pain in the emergency department: results of the pain and emergency medicine initiative (PEMI) multicenter study. J Pain. 2007;8(6):460–466.
56. Sherwood GD, McNeill JA, Starck PL, et al. Changing acute pain management outcomes in surgical patients. AORN J. 2003;77(2): 377–380, 384–390.
57. Neighbor ML, Honner S, Kohn MA. Factors affecting emergency department opioid administration to severely injured patients. Acad Emerg Med. 2004;11(12):1290–1296.
58. Coderre TJ, Katz J, Vaccarino AL, et al. Contribution of central neuroplasticity to pathological pain: review of clinical and experimental evidence. Pain. 1993;52(3):259–285.
59. Howard RF. Current status of pain management in children. JAMA. 2003;290(18):2464–2469.
60. Belville RG, Seupaul RA. Pain measurement in pediatric emergency care: a review of the faces pain scale—revised. Pediatr Emerg Care. 2005; 21(2):90–99.
61. Zohar Z, Eitan A, Halperin P, et al. Pain relief in major trauma patients: an Israeli perspective. J Trauma. 2001;51(4):767–772.
62. O’Connor AB, Zwemer FL, Hays DP, et al. Outcomes after intravenous opioids in emergency patients: a prospective cohort analysis. Acad Emerg Med. 2009;16(6):477–487.
63. Clark ME, Bair MJ, Buckenmaier CC, et al. Pain and combat injuries in soldiers returning from Operations Enduring Freedom and Iraqi Freedom: implications for research and practice. J Rehabil Res Dev. 2007;44(2): 179–194.
64. O’Donnell ML, Creamer M, Pattison P, et al. Psychiatric morbidity following injury. Am J Psychiatry. 2004;161(3):507–514.
65. Koren D, Norman D, Cohen A, et al. Increased PTSD risk with combat-related injury: a matched comparison study of injured and uninjured soldiers experiencing the same combat events. Am J Psychiatry. 2005; 162(2):276–282.
66. Wain HJ, Grammer GG, Stasinos JJ. Psychiatric intervention for medical and surgical patients following traumatic injuries. In: Ritchie EC, Watson PJ, Friedman MJ, eds. Interventions Following Mass Violence and Natural Disasters: Strategies for Mental Health Practice. New York, NY: The Guilford Press; 2007:278–298.
67. National Spinal Cord Injury Statistical Center. Facts and Figures at a Glance 2009. Available at: https://www.nscisc.uab.edu/public_content/facts_figures_2009.aspx. Accessed January 20, 2010.
68. American Spinal Injury Association. Available at: http://www.asia-spinalinjury.org/. Accessed February 23, 2010.
69. Kirshblum SC, Priebe MM, Ho CH, et al. Spinal cord injury medicine. 3. Rehabilitation phase after acute spinal cord injury. Arch Phys Med Rehabil. 2007;88(3 suppl 1):S62–S70.
70. Bracken MB, Shepard MJ, Collins WF Jr, et al. A randomized, controlled trial of methylprednisolone or naloxone in the treatment of acute spinalcord injury. Results of the Second National Acute Spinal Cord Injury Study. New Engl J Med. 1990;322(20):1405–1411.
71. Krassioukov A, Warburton DE, Teasell R, et al. A systematic review of the management of autonomic dysreflexia after spinal cord injury. Arch Phys Med Rehabil. 2009;90(4):682–695.
72. Paralyzed Veterans of America/Consortium for Spinal Cord Medicine. Acute Management of Autonomic Dysreflexia: Individuals with Spinal Cord Injury Presenting to Health-Care Facilities. 2nd ed. Washington, DC: Paralyzed Veterans of America (PVA); 2001.
73. Maynard FM. Immobilization hypercalcemia following spinal cord injury. Arch Phys Med Rehabil. 1986;67(1):41–44.
74. Samson G, Cardenas DD. Neurogenic bladder in spinal cord injury. Phys Med Rehabil Clin N Am. 2007;18(2):255–274.
75. Correa GI, Rotter KP. Clinical evaluation and management of neurogenic bowel after spinal cord injury. Spinal Cord. 2000;38(5):301–308.
76. Langlois JA, Rutland-Brown W, Thomas KE. Traumatic Brain Injury in the United States: Emergency Department Visits, Hospitalizations, and Deaths. Atlanta, GA: Department of Health and Human Services, Centers for Disease Control and Prevention; 2004.
77. US Department of Defense. Casualty Update Webpage. Available at: http://www.defenselink.mil/news/casualty.pdf. Accessed January 1, 2010.
78. Van Boven RW, Harrington GS, Hackney DB, et al. Advances in neuroimaging of traumatic brain injury and posttraumatic stress disorder. J Rehabil Res Dev. 2009;46(6):717–757.
79. Ahmed S, Bierley R, Shelkh JI, et al. Post-traumatic amnesia after closed head injury: a review of the literature and some suggestions for further research. Brain Inj. 2000;14(9):765–780.
80. Rancho Los Amigos National Rehabilitation Center. Family Guide to the Rancho Levels of Cognitive Functioning. Downey, CA. Available at: www.rancho.org/patient_education/bi_cognition.pdf. Accessed February 2, 2010.
81. Perel P, Edwards P, Wentz R, et al. Systematic review of prognostic models in traumatic brain injury. BMC Med Inform Decis Mak. 2006;6:38.
82. Hall RCW, Hall RCW, Chapman MJ. Definition, diagnosis, and forensic implications of postconcussional syndrome. Psychosomatics. 2005; 46(3):195–202.
83. National Institute of Neurological Disorders and Stroke. Traumatic Brain Injury CDE Standards. Available at: http://www.nindscommondataelements.org.
84. Jaffee MS, Helmick KM, Girard PD, et al. Acute clinical care and coordination for traumatic brain injury within the Department of Defense. J Rehabil Res Dev. 2009;46(6):655–666.
85. Chew E, Zafonte RD. Pharmacological management of neurobehavioral disorders following traumatic brain injury—a state-of-the-art review. J Rehabil Res Dev. 2009;46(6):851–879.
86. Frey LC. Epidemiology of posttraumatic epilepsy: a critical review. Epilepsia. 2003;44(suppl 10):11–17.
87. Rosenberg M, Blakeney P, Robert R, et al. Quality of life of young adults who survived pediatric burns. J Burn Care Res. 2006;27(6): 773–778.
88. Esselman PC. Burn rehabilitation: an overview. Arch Phys Med Rehabil. 2007;88(12 suppl 2):S3–S6.
89. Pruitt BA, Goodwin CW, Mason AD. Epidemiological, demographic, and outcome characteristics of burn injury. In: Herndon DN, ed. Total Burn Care. 2nd ed. New York, NY: WB Saunders; 2002:16–30.
90. Larson DL, Abston S, Evans EB, et al. Techniques for decreasing scar formation and contractures in the burned patient. J Trauma. 1971;11(10): 807–823.
91. Esselman PC, Thombs BD, Magyar-Russell G, et al. Burn rehabilitation: state of the science. Am J Phys Med Rehabil. 2006;85(4):383–413.
92. Hart DW, Wolf SE, Ramzy PI, et al. Anabolic effects of oxandrolone after severe burn. Ann Surg. 2001;233(4):556–564.
93. Ben-Simchon C, Tsur H, Keren G, et al. Heal intolerance in patients with extensive healed burns. Plast Reconstr Surg. 1981;67:499–504.
94. Austin KG, Hansbrough JF, Dore C, et al. Thermoregulation in burn patients during exercise. J Burn Care Rehabil. 2003;24(1):9–14.
95. Fauerbach JA, Lawrence L, Haythornthwaite J, et al. Preburn psychiatric history affects posttrauma morbidity. Psychosomatics. 1997;38(4): 374–385.
96. Rose S, Bisson J, Wessely S. A systematic review of single-session psychological interventions (“debriefing”) following trauma. Psychother Psychosom. 2003;72(4):176–184.
97. Dillingham TR, Pezzin LE, MacKenzie EJ. Limb amputation and limb deficiency: epidemiology and recent trends in the United States. South Med J. 2002;95(8):875–883.
98. MacKenzie EJ, Bosse MJ. Factors influencing outcome following limb-threatening lower limb trauma: lessons learned from the Lower Extremity Assessment Project (LEAP). Am Acad Orthop Surg. 2006;14(10): S205–S210.
99. Pasquina PF, Cooper RA, eds. Care of the Combat Amputee. Washington, DC: Borden Institute; 2010. Textbook of Military Medicine Series.