Chapter 51: Rehabilitation

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 to prevent secondary injury, achieve optimal pain control, employ therapeutic exercise to meet established goals, utilize appropriate assistive technology (AT), and educate and counsel the patient and family. While the first priority in treating trauma patients is to preserve life and limb, early initiation of rehabilitation can have a significant positive impact on recovery, length of stay, community reintegration and 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, early consultation by rehabilitation professionals should be considered while still addressing the acute medical and surgical issues. When considering transfer to an inpatient rehabilitation facility, 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. It is not uncommon for patients on rehabilitation units to continue to need ongoing medical or surgical care.

As in other areas of medicine, subspecialty designation within the field of “rehabilitation” is common. Many physicians, therapists, nurses, and counselors receive subspecialized training and board certification in areas such as spinal cord medicine, neurological rehabilitation, amputee care and TBI. 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. Healthcare professionals should also recognize that the medical and surgical care they provide during the acute phase of treatment may have long-lasting implications for the patient’s overall health, recovery and quality of life.

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. 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 activity may result in disuse atrophy. The muscles most affected by such disuse atrophy during 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 loss of sarcomeres both in series and in parallel, and this leads to reduced muscle thickness and length.⁴ Muscle atrophy occurring from immobilization results in diminished force production and a loss of strength of 10–15% per week.⁵ Interestingly, muscle strength decreases at a faster rate than muscle size, indicating that, in addition to atrophy, other factors contribute to muscle weakness.⁶ 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.⁷

Disuse Osteoporosis

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.^8,9 Patients with preexisting osteopenia or osteoporosis are especially susceptible to an increase in bone turnover during immobilization and, as a result, have a higher risk of osteoporotic-related fractures. In addition, individuals with limb loss, particularly proximal trans-femoral amputation have also been shown to experience significant bone mineral loss, compounded with delayed ambulation.¹⁰ Because of the high rate of bone reabsorption, hypercalcemia may also occur, particularly in young trauma patients, and clinicians should monitor calcium levels on a regular basis.¹¹

Contractures

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 plays a significant role, also. Such changes have only been observed when the muscle is immobilized in a shortened position, and this suggests that limb positioning plays a direct role in connective tissue properties.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 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 activity 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, 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.¹⁵

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.¹⁶

Cardiac Effects

Skeletal muscles generally compress major veins, forcing blood upward and ensuring its return to the heart. The loss of skeletal muscle due to injury or during bed rest impairs this venous return, decreasing diastolic pressure and stroke volume. In order to counteract this effect, heart rate typically increases. In fact, after 4 weeks of bed rest, the resting hear rate may increase by approximately 10 beats/min.¹⁷ 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.¹⁸

Orthostatic Hypotension

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.¹⁷ Orthostatic 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.^19,20 Orthostasis 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 participate in therapy or perform activities of daily living (ADL). Further, these symptoms may persist after a protracted period of time, particularly for elderly patients.

Aerobic Capacity

Maximal oxygen consumption (VO_2max) is a measure of cardiovascular fitness and has been shown to decrease in proportion to the duration of immobilization.²¹ Both peripheral (muscular) and central (cardiovascular) factors play a role in the decrease in VO_2max resulting from immobility.⁸ Individuals with preexisting cardiovascular disease present a higher risk for cardiac complications when recovering from a traumatic event and require explicit 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%.²⁴ Typical 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 assessing the presence of DVT or 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 (eg, 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, a vena cava filter may be inserted to prevent PE. Duration of pharmacological prophylaxis is dependent on the extent of trauma and continued risk of thrombus formation. Guidelines for the management of individuals with SCI suggest the following indications to continue prophylaxis: (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 (eg, 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.²⁹ 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.³⁰ 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.³¹

Prevention and Treatment

Promoting deep inspiration with an incentive spirometer is important for all trauma patients. Chest physiotherapy, vibration, and postural drainage techniques may 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 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 allows the trauma team to monitor fluid output and assess fluid status, also, but 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 (PVR) bladder volumes to ensure adequate emptying. A PVR greater than 50–100 cm³ usually 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 the 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. The resultant decreased rate of evacuation from the stomach may cause symptoms of gastroesophageal reflux, regurgitation, and heartburn. The rate of intestinal peristalsis is slowed during bed rest, also, further delaying intestinal motility, increasing water absorption and may lead to constipation and fecal impaction.^34,38 These effects are likely to be magnified with the use of opioids o r other pharmacological agents that may also slow intestinal motility.

Prevention/Treatment

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 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 (eg, Metamucil), enemas, colonic irritants (eg, Dulcolax), and intestinal motility agents (eg, 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.

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 may 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 may have a significantly negative impact on rehabilitation, recovery and quality of life.⁴²

Prevention/Treatment

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.

Heterotopic Ossification

Heterotopic ossification (HO) is the formation of mature lamellar bone in tissue that is not normally ossified.⁴³ It commonly develops in patients with TBI, SCI, burn injury, or blast-related amputations.^44,45,46 The most common site of HO following SCI is the hip, but it may also occur in the elbow, shoulder, and knee.⁴⁷ For patients with burns, 92% of cases occur in the elbow,^48,49 and up to 80% of patients who sustain an amputation from a blast injury may develop HO.⁵⁰ The clinical presentation of HO may include a decrease in range of motion and erythema and swelling about the involved joint. Radiographs, bone scans, and monitoring of serum alkaline phosphatase levels may aid in the diagnosis. Prophylaxis with bisphosphonates, nonsteroidal anti-inflammatory drugs (NSAIDs), and local irradiation may prevent HO.⁵¹ Treatment of HO involves active and passive range of motion to prevent worsening; however, in severe cases, surgical excision may be required to improve functional outcomes.^47,52 Even when treated aggressively, HO may still result in significant restrictions in range of motion and subsequent disability.

Spasticity

Spasticity is defined as a velocity-dependent increase in muscle tone that occurs following injury to upper motor neurons and 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%.⁵³ Spasticity may result in significant pain, impaired mobility, difficulty with dressing and hygiene, as well as an increased risk of skin breakdown. In certain circumstances, however, 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 must be based on improving patient function, hygiene, and/or care.

Conservative treatment of spasticity begins with positioning, stretching, splinting, and range of motion exercises. Medications used for spasticity include GABA agonists (eg, baclofen), centrally acting α₂-agonists (eg, tizanidine), and medications that inhibit skeletal muscle contraction (eg, dantrolene). Botulinum toxin or phenol injections may also be helpful in the management of spasticity. 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.⁵³ The appropriate choice of medication, however, should be based on the patient’s response as well as the presence of adverse side effects.

Background

Inadequate pain control is associated with delayed healing, increased complications, prolonged hospitalization, poor sleep, and diminished quality of life.⁵⁴ It has been shown to be a significant cause for hospital readmission, also.⁵⁵ Therefore, attentive 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.⁵⁶ 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 healthcare delivery system.⁵⁷ 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.⁵⁸ Despite these initiatives, significant challenges still remain in changing clinical practice.⁵⁹

Postoperative pain is a significant problem for most patients and demands special attention from the trauma team.⁶⁰ While a multitude of pain interventions currently exist, numerous barriers prevent patients from receiving optimal care.⁶¹ Patients may underreport their level of pain, particularly if they expect it as part of their disease process or treatment. 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. In addition, under-treating pain may impair the patient’s ability to participate in rehabilitation. Once severe pain has been established, it is more difficult to treat. Therefore, aggressively treating perioperative pain early with the use of multimodal and around-the-clock analgesia can be very helpful in avoiding the development of more complex pain syndromes. Furthermore, uncontrolled or protracted acute pain may lead to chronic pain conditions, which may have long-term negative implications on function, return to work and quality of life.^62,63

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 healthcare 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.⁶⁴ 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.

Phantom Limb Pain

While pain affects all patients with traumatic injury, phantom limb pain (PLP) is unique to individuals with acquired amputation. PLP is the experience of a painful sensation (eg, cramping, burning, aching, etc) within a missing (phantom) limb. The phenomenon occurs in up to 90% of patients following amputation of a major limb and is thought to be the result of central nervous system reorganization or hypersensitivity. PLP symptoms may occur immediately after limb loss or may be delayed by several weeks. While most individuals experience a gradual decrease in PLP over time, 30–70% of individuals with report persistent symptoms. Most common treatments include medications that are typically used for neuropathic pain (see section below). In addition, mirror therapy has also been shown to be an effective treatment.⁶⁵

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).

Treatment

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 possible that other injuries may have been overlooked during the initial trauma screen due to a distracting injury; therefore, a tertiary survey is necessary for all trauma 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 non-pharmacological approaches.

Pharmacological

• Opioids are the most common analgesic medications 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 often selected because of its clear analgesic, amnestic, and sedative effects, and it is readily available and cost-effective, as well. Fentanyl may be used, but has a shorter half-life, produces weaker sedation, and costs more.⁶⁶ Patients on chronic opioids may be safely treated with intravenous opioid bolus dosages up to 20% of their total daily use.⁶⁷

• 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. The prostaglandins produced by COX-1 protect the stomach and support platelet aggregation, also. 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 (Toradol) 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. The use of all NSAIDs should be cautioned in the presence of complex fractures, particularly those with high propensity for nonunion.⁶⁸

• Antiseizure medications such as gabapentin, pregabaline, carbamazepine, valproic acid, or oxcarbazepine are often used to help treat neuropathic pain and may provide relief from PLP, as well. These medications act as membrane stabilizers to the axons in the central and peripheral nervous systems. In the case of lumbosacral radicular pain, a double-blinded multi-center study demonstrated that epidural steroid injections might offer slight advantages over gabapentin, but the effects were minimal and transient.⁶⁹

• 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 analgesia (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.⁷⁰

• Sympathetic blockade may be helpful in patients with a 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.

Nonpharmacological

• 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 skin injury and/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.

The early application of rehabilitation principles helps prevent secondary injury and facilitates patient recovery. Consultation with rehabilitation specialists should be considered for every trauma 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 also offer invaluable assistance in identifying cognitive deficits and formulating management decisions. In addition to providing holistic care, rehabilitation providers spend additional time with patients and family members to perform a comprehensive functional assessment to determine pre-injury functional capacity as well as current functionality. Rehabilitation professionals will assess any potential barriers that might prevent timely hospital discharge (eg, cognition, mobility, safety, architectural barriers, etc) or independent living with or without assistance, also. Once these barriers are identified, therapeutic interventions may be initiated and appropriate assistive equipment can be ordered in a manner to fit with establishing short and long-term rehabilitation goals.

Physical Medicine and Rehabilitation (PM&R) Specialists (Physiatrists)

Physiatrists are board-certified physicians who specialize in neuromusculoskeletal disorders and rehabilitation. These healthcare providers 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.

Physical Therapists

Physical therapists evaluate 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.

Occupational Therapists

Occupational therapists (OTs) assess a patient’s ADLs and instrumental ADLs (IADLs). ADLs include feeding, toileting, dressing, and hygiene. Instrumental ADLs 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.

Speech-Language Pathologists

Speech-language pathologists (SLPs) 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, evaluating a patient’s ability to swallow safely may help guide appropriate interventions to ensure appropriate caloric intake.

Additionally, the SLP may develop ways to improve the necessary communication between the treatment team and the patient.

Orthotists and Prosthetists

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),⁷¹ 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

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 major traumatic events will exhibit stress-related symptoms and up to 40% may have a psychiatric disorder at 1 year following trauma.⁷² For combat casualties, rates of comorbid post-traumatic stress disorder (PTSD) have been reported to be 16.7%⁷³ with 118,829 cases reported in post-deployment service members between September, 2001, and Q1 2014.⁷⁴ Fear 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 the stigma that is often associated with seeing a behavioral health specialist. Fostering appropriate mental healthcare acutely likely helps to prevent the developing of disabling psychiatric disorders often associated with trauma.⁷⁵ Special consideration should also be made to the children and other family members of those who suffer trauma, particularly those with disfiguring injuries.

Rehabilitation Engineers/Assistive Technology Specialists

Rehabilitation engineers specialize in the fabrication, fitting, and training of AT devices. Assistive technology 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/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, healthcare providers, and engineers to ensure quality in products and service delivery.

Peer Support Visitors

Peer support visitors are trauma survivors who receive training to support other patients and their families. Peer visitors generally have suffered a similar life-changing injury as the patient and demonstrate a 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. Non-for-profit organizations, such as the Amputee Coalition (AC), offer specialized peer support training program, which may be helpful for individuals or institutions interested in initiating such a program.

Vocational Rehabilitation Specialists

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

Case managers 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.

Spinal Cord Injury

Introduction

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

Classification

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.

Acute Management

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.

Regenerative Medicine

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

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 (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.

Traumatic Brain Injury

Introduction

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

Classification

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.

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

Treatment

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.

Burn Injuries

Introduction

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

Classification

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.

Complications

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.

Amputation

Introduction

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.

Treatment

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

Introduction

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.

Prevention/Treatment

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.