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 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
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
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
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
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
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
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.
Maximal oxygen consumption (VO2max) 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 VO2max 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.
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.
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.
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
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
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
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”).
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.
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.
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
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 (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 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.
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.
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
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).
| Term | Definition |
|---|---|
Nociception Hyperalgesia Allodynia Dysesthesia Paresthesia Epicritic sensations Protopathic sensations Visceral pain Somatic pain Acute pain Chronic pain | The neural process of encoding and processing noxious stimuli An increased sensitivity or response to a painful stimulus A painful response to a normally nonpainful stimulus An unpleasant or painful sensation that occurs spontaneously A sensation of a tingling or numbness of the skin or region of the body that occurs spontaneously Nonpainful sensations such as light touch, vibration, and position sense, transmitted through low-threshold, large-diameter myelinated nerve fibers Painful sensations transmitted through high-threshold, small-diameter unmyelinated nerve fibers Pain generated through internal nocioceptors as a result of internal organ damage Pain generated from peripheral nocioceptors within the skin, muscle, soft tissue, and bone Pain associated with an acute event, generally lasting less than 30 d A pain syndrome lasting beyond 3–6 mo or pain that extends beyond the expected period of healing |
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.
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.
Related posts:
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
