Rehabilitation
John A. Horton III
Gary N. Galang
I. Introduction
Trauma results in injury that can impact the functioning of those involved. Spinal cord injury (SCI), traumatic brain injury (TBI), and severe multiple trauma are among the most life-altering events. These create a need for rehabilitation services during and after acute care to minimize or avoid impairments that affect the ability to care for themselves, to fulfill customary social roles, and to return to daily activities. Some injuries (e.g., SCI, TBI) affect numerous physiologic, psychological, social, and vocational functions to the degree that the individual loses functional independence. The rehabilitation team is responsible to teach the patient the skills and to provide the necessary equipment to optimize function, maximize the return to independence, and enable a reestablishment of a meaningful existence. Beginning this process in the acute care setting and carrying forward into the post-acute continuum is essential to optimize outcomes and ease the adjustment for the patient.
Prevention of disabling complications during the acute care phase of treatment minimizes required interventions during the rehabilitation phase of treatment. Secondary injury results in decrement in function and complicates care. Commonly, secondary debility is the result of the prolonged immobilization of the patient. Although rarely life threatening, these secondary concerns can limit eventual functional recovery, can delay patient progression and can contribute to total health care cost.
II. General Effects of Neurotrauma and Immobilization After Injury
Cardiovascular deconditioning occurs rapidly with any period of inactivity, with the heart and peripheral vascular mechanisms losing the capacity to respond to stressors. With certain types of injury (e.g., SCI with its associated loss of sympathetic nervous system control), the inability to maintain perfusion pressure with changes in posture can inhibit attempts to mobilize the patient. The most important approach to this problem is to minimize immobility and get the patient upright as soon as possible. Additional benefits from this early mobilization include improved respiratory functioning, with decreased atelectasis and complications.
A recumbency-induced rise in the resting heart rate of 0.5 beats/min/day adds to any stress rate changes. The combined effect of these changes is resting tachycardia and a reduced ability to meet oxygen demands with activity; this effect is persistent for up to 2 months after return to activity.
Many peripheral factors, including decreases in vascular volume, loss of adaptive baroreceptor reflex responses to the upright posture, and increased pooling of blood in lower limb veins, contribute to the intolerance of the patient to an upright posture after immobility.
In healthy individuals, the adaptive response to upright positioning can be totally lost after 3 weeks of complete bed rest. Older patients lose this capacity to respond even more quickly, and return to baseline is slower. Concomitant premorbid disease (e.g., cerebrovascular or cardiovascular lesions) makes older individuals less tolerant of this postural drop in blood pressure.
Increasing periods of sitting with the feet in a dependent position helps reconditioning efforts for those unable to stand. The use of tilt or recline systems on wheelchairs can facilitate the tolerance to this activity. In severe
cases, a tilt table can be used to progressively place the person in an upright position while blood pressure is monitored.
Compressive garments, full-length elastic stockings, (e.g., TED hose, JOBST stockings, Tubigrip stockings, etc.) and abdominal binders may limit venous pooling and provide blood pressure support while adaptation occurs.
Pay attention to nutrition to maintain plasma protein levels, immune system function, and proper hydration to aid combatting hypotension.
In severe cases unresponsive to compression garments, increasing salt intake (up to 1 g PO QID), using sympathomimetic agents (pseudoephedrine, ephedrine, midodrine, or phenylephrine), or giving mineralocorticoids (fludrocortisone) may assist.
In persons with TBI and elevations or fluctuations in intracranial pressure, be careful with aggressive mobilization.
Joint contractures result when a joint is not subjected to frequent passive or active range of motion. Contracture formation is most often a consequence of untreated muscular spasm because of upper motor neuron impairment. Spasticity is defined as a response to velocity-dependent stretch. This involuntary movement causes sustained, uncontrolled muscle tension creating unopposed shortening of the muscles crossing the joint. Muscular tension becomes unbalanced, thereby reducing the mobility of the affected joint. When this limitation of joint range persists, the soft tissues of the joint itself can also become contracted. Remodeling of the connective tissue around the joint contributes to decreased elasticity. The subsequent contracture that is produced is the result of this prolonged shortening and increased stiffness of the soft tissues of the joint.
Contractures contribute to increased morbidity.
Difficulties in positioning the patient can lead to the formation of decubitus ulcers.
Hygiene, particularly in the perineum, palms of the hands, and axillae, is difficult.
Contractures also inhibit functional recovery as motor function or control is regained. This leads to prolonged rehabilitation, potential need for surgical intervention, and higher costs. Contractures may also limit patient long-term functionality, preventing achievement of the full potential for recovery.
Contractures should be prevented.
Fully ranging all joints twice a day is often enough to prevent the formation of these deformities. Active ranging by the patient is preferred when possible as it helps maintain strength and motor control. If weak but voluntary muscle power is present, use active assisted range of motion as the next in preference. In cases of paralysis or coma, use passive range of motion. This may be difficult if severe spasticity or rigidity exist already.
Positioning the patient can help reinforce the gains of therapy after range of motion has been performed. A prone position provides a prolonged stretch to hip flexors. Splinting of the wrists, hands, and ankles is also useful in reinforcement of range of motion gains and prevention of further deformation. Use splints intermittently (not continuously) to avoid skin breakdown in areas of splint contact.
Other physical modalities, in conjunction with range of motion, allow a greater stretch.
Deep heat via use of ultrasound can increase the elasticity of collagen, but may be contraindicated in areas with metallic implants.
Cooling of the muscle helps to decrease the activity of the muscle spindle mechanism, and thus decrease muscle tone.
Serial casting of an extremity is useful to provide a prolonged stretch. A plaster or fiberglass cast is applied, but must be prepared to pad prominences to prevent skin lesion. Stretch is maintained as the cast material cures. The cast is typically left in place for 3 to 5 days before removal. Once desired positioning is achieved through a series of progressive cast applications, the cast can then be cut into halves longitudinally (bivalve) and used as a resting splint.
Focal neurolysis is another tool in the arsenal against contracture formation. Temporary reduction of muscle tone by employment of motor point or peripheral nerve blocks using neurolytic agents (e.g., phenol—approximately 6- to 12-month duration of effect) or neuromuscular blocking agents (e.g., botulinum toxins—approximately 1- to 3-month duration of effect) is useful in cases where tone prevents full range of a joint. These should be performed under EMG, ultrasound, or stimulator guidance and may be required before splinting or serial casting can be successful. Phenol produces a direct neurolysis. Several serotypes of botulinum toxin have been described (A, B, C, D, and E), with only A and B commercially available in the United States.
Anti-spasticity medications are used to reduce hyper-reactivity of the skeletal muscle. This phenomenon is common, although usually delayed in onset, in the head-injured patient and those patients with cerebral vascular accident or SCI. Common medications include baclofen, tizanidine, diazepam, and dantrolene sodium.
Baclofen and diazepam are GABA analogue agents and act to provide improved descending inhibition to otherwise disinhibited pathways in the spinal cord. Both of these agents can produce sedation, and baclofen can lower the seizure threshold. Rapid baclofen withdrawal may result in seizures, hyperthermia, and systemic collapse. In general practice, baclofen is most often employed in patients with SCI and perhaps less valuable in patients with spasticity of cerebral origin.
Tizanidine is an α2-adrenergic agonist, which although sedating, also provides inhibition of descending pathways promoting decreases in muscle tone. Some advocate this for use in more prominent upper extremity tone situations or in decreasing dysesthetic pain. Like baclofen, tizanidine is more often used in SCI patients.
Dantrolene sodium is a peripheral acting agent that acts at the level of the sarcoplasmic reticulum and appears to produce less cognitive disturbance among those with CNS injury. Use cautiously in those with liver disturbance and monitor for hepatic necrosis (serial transaminases).
Decubitus ulcers are a common but preventable complication. Pressure is the primary factor in the development of a skin breakdown. Ulcers occur over bony prominences when the pressure of body weight is unrelieved for prolonged periods. Pressure causes occlusion of perforating blood vessels which results in ischemic damage to the skin and underlying soft tissues. This occurs most commonly at the bone/soft tissue interface. Higher pressures cause breakdown in a shorter time than lower pressures. Evidence of a lesion on the skin surface may only hint at the full extent of the underlying damage which has already taken place.
Multiple factors contribute to the development of these dangerous lesions:
Shear either between the skin and supporting surfaces or within the soft tissues causes ischemia at lower pressures than when shear is not present.
Anemia causes increased risk of ischemic damage due to lack of oxygen availability in the deep tissues.
Excessive skin moisture from perspiration or urine reduces the resistance to skin damage.
Poor nutrition predisposes to poor wound healing and also impaired resistance to skin breakdown due to decreased quality of collagen formation.
Infection can lead to skin breakdown with sepsis increasing capillary leak and impaired blood flow to pressure prone areas.
Lack of sensation and altered mental status also contribute to development of pressure ulcers. The normal protective pain sensation or pain awareness, which would otherwise prompt a position change, is missing and thus the pressure is not alleviated, facilitating the development of a lesion.
Prevention of ulceration must be the goal.
Careful positioning of the patient. Frequent turning, initially on a schedule of a minimum of every 2 hours, is essential. Increased attention to the occiput, scapulae, sacrum, ischial tuberosities, greater trochanters, malleoli, and heels
is key given the frequency of breakdown at these sites. Pillows and foam blocks can relieve pressure over these bony prominences or distribute it to other areas.
Inspection of the skin regularly – at least every shift – is ideal. If signs of breakdown are seen, alleviation of pressure to the area is essential. The earliest sign of damage is an area of non-blanching erythema. Palpation may reveal induration of the underlying soft tissue. If induration is present, more extensive damage may already have occurred, making the situation more critical to treat with increased urgency.
Managing urinary and bowel incontinence to prevent prolonged contact between the skin and urine or feces is important to prevent skin irritation and infection.
For patients at high risk, use of specialized mattresses and seating surfaces are a cost-effective component of a decubitus prevention program.
Heterotopic ossification (HO) is a pathologic process during which new bone is formed within periarticular soft tissue. It is hypothesized that trauma promotes the disinhibition of factors allowing multipotential mesenchymal cells to be converted to osteoclast-like cells. Histologically normal bone develops in the soft tissues surrounding a joint.
This process should be distinguished from traumatic myositis ossificans, in which bone is formed within traumatized muscles, often because of ossification of intramuscular hematoma.
Populations at risk for HO include those with burns, TBI, SCI, and those with prolonged immobilization. Following SCI or TBI, incidence is from 11% to 79%.
Different distributions of ossification and time course occur in spinal cord versus brain injury. In both cases, the lesions develop below the level of the neurologic injury around major joints. The process appears to be more aggressive in limbs with greater spasticity-related muscular tone.
Upper extremity involvement is more common in brain injury. HO tends to be more extensive and persistent following SCI.
The earliest manifestation of HO is painful loss of range of motion. Otherwise, a striking similarity is seen to the clinical presentation of deep venous thrombosis, with a warm, swollen, erythematous limb. HO may also manifest as “fever of unknown origin.”
Diagnostic tools.
Triple-phase bone scan is the earliest, most specific test to confirm the diagnosis. The first and second phases are abnormal in HO.Related posts:
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