INTRODUCTION
Immobility is the enemy of function. Much of physiatric treatment revolves around movement and its antithesis, immobility. This concept applies equally to generalized immobility (progressive functional decline in senior citizens as a result of cumulative effects of pain, fear of falling, and muscle weakness), forced immobility (bed rest during hospitalization or experienced by astronauts in microgravity), and immobilization of discrete body parts (range-of-motion [ROM] restriction caused by spasticity, contracture, or splinting or casting of fractures).
Rehabilitation marshals the body’s ability to change, adapt, and grow in response to stimuli. This is as true for neuroplasticity in a stroke patient as it is for strengthening of the rotator cuff muscles in a patient with chronic tendinopathy. Immobility is not a null state in which bodily functions remain in physiologic equilibrium. Like movement and exercise, immobility is also a condition that stimulates physiologic adaptation, leading to rapid changes in cardiovascular, pulmonary, musculoskeletal, and neurologic function that ultimately decrease our ability to interact with the world around us. The cause and effects of immobility in patients should always be examined and reexamined. These factors have great bearing on an individual’s function, independence, safety, and emotional well-being.
BED REST & IMMOBILIZATION
Throughout the history of medicine, enforced immobilization or bed rest has been a staple of treatment for both illness and injury. Conditions that historically have been or currently are treated with enforced rest include acute low back pain, heart attack, tuberculosis, fracture, and critical illness (eg, sepsis).
Actual and theoretical justifications for bed rest include reducing metabolic demands of the body, thus “conserving” these resources for recovery. Reduction of oxygen consumption by muscles—both skeletal and cardiac—decreases oxygen demand by all tissues, resulting in less mechanical ventilation, lower Fio2, and less risk of ventilator-induced lung injury. Other perceived benefits include decreased cardiac stress, improved central nervous system perfusion, bone healing, and pain control (eg, in the immobilization of an injured appendage for comfort). Additional perceived benefits apply to safety: maintenance of intravenous access and artificial airways, fall prevention, and prevention of occupational injuries to nursing staff.
Specialists in physical medicine and rehabilitation work in the borderland between mobility and immobility. Patients with spinal cord injury, neuropathy, stroke, or peripheral nerve injury with sensory impairment do not experience the same discomfort that would prompt a neurologically intact person to shift position or treat a wound or laceration. Physiatrists also treat patients who are protectively immobilized in splints or casts for fractures, ligament tears, or tendon injury. They often encounter and treat the effects of self-imposed or functional immobility of joints due to stiffness and pain.
Muscle mass drops by 1.5–2% per day in the first 2–3 weeks of bed rest. A muscle completely at rest therefore loses 10–15% of its strength each week, resulting in a loss of roughly 50% after 3–5 weeks of complete immobilization. The lower limb and truncal antigravity muscles (hip extensors, knee extensors, ankle plantar flexors, and paraspinals) are preferentially affected.
Decrease in muscle mass is driven by atrophy. Individual muscle fibers decrease in size, resulting in loss of tension-generating ability and proportional loss of torque. In one study of nine healthy male volunteers exposed to absolute, horizontal bed rest, the cross-sectional area of the gastrocnemius–soleus (ankle plantar flexor) complex decreased by 12% as measured on magnetic resonance imaging. The same muscles lost 26% of strength as measured by dynamometer. Notably, the ankle dorsiflexors (not an antigravity muscle in normal function) did not show significant decrease of area or strength in this study.
Neurogenic muscle immobility resulting from central or peripheral nerve injury has even more dire consequences. Peripheral nerve injury causes flaccid paralysis, and the affected muscles can lose up to 95% of their bulk. If the denervation is irreversible (ie, neurotmesis), the muscle fibers are replaced by fatty atrophy and connective tissue. In spastic paralysis caused by upper motor neuron injury (eg, stroke or spinal cord injury), the antigravity muscles can lose 30–40% of their bulk.
Contraction of a muscle to 20% of maximal tension for several seconds a day will prevent loss of strength. However, this does little to counteract the multitude of other physiologic effects of bed rest.
Disuse myopathy may be reversed with exercise. However, the recovery of strength occurs at a rate of only 6% per week at submaximal (65–75% max) exercise. Thus, for every day of hospital bed rest, the patient must pay back 2–3 days of exercise to return to baseline muscle strength. This figure does not account for the recovery time from other, nonmuscular physiologic effects of bed rest, nor from the illness that resulted in hospitalization in the first place.
A contracture is a fixed joint deformity resulting from immobilization of the joint. The immobilization itself may be caused by splinting or casting of a fracture, or by other disruptors of dynamic tension, such as spasticity from an upper motor neuron lesion (active opposition) or denervation with flaccid paralysis (lower motor neuron lesion, which results in no opposition). Other factors include bed positioning or intrinsic muscle and soft tissue changes caused by burns or connective tissue disease, such as scleroderma.
Groups at highest risk include those with joint disease or paralysis of a muscle group, the frail and elderly, the cognitively impaired, and the very passive, including those with mental illness and catatonia. Muscles at highest risk of contracture during immobilization are those that cross two joints, such as the hamstrings, back muscles, tensor fascia lata, rectus femoris, gastrocnemius, and, in the upper limb, the biceps brachii.
Ligaments are often viewed as relatively fixed, stable structures. In reality, they are dynamic, complex structures that actively respond to the presence or absence of mechanical forces. Thus, joint immobilization can lead to physiologic changes of both the ligamentous insertion and the ligament body itself.
Collagen fibers in areas of movement develop loose alveolar connective tissue, and frequent stretching maintains length. In the absence of movement, the collagen develops into a dense mesh of interconnected sheets and will shorten if not stretched frequently. This can progress to intraarticular fibrofatty infiltration and persistent adhesions.
A series of animal studies investigated the results of 8 weeks’ immobilization in a total body cast. At the end of the trial, knee ligament stiffness decreased to 69% of normal, maximum load at failure decreased to 61% of normal, and energy absorption decreased to 68% of normal. Of note, at 1 year followup, the ligaments had still not returned to their premorbid condition.
Contractures caused by immobility inevitably lead to more severe and prolonged impairment unless aggressive and persistent intervention is undertaken. Contractures interfere with positioning in bed and in wheelchairs, and may bring pressure-sensitive areas into contact with surfaces that increase the risk of deep tissue injury. For example, an immobilized patient with hip flexion contractures may be unable to maintain a supine or semisupine position in bed, have a reduced turning schedule, and develop trochanteric pressure wounds. Contractures also interfere with activities of daily living and the administration of nursing care and hygiene. Left untreated, spastic contracture promotes moisture, fungal infection, maceration and breakdown of the skin, and potentially cellulitis, sepsis, and death.
In the realm of active movement, contractures interfere with normal biomechanics and may prevent or impede safe transfers and ambulation. Even if they allow safe ambulation, lower limb contractures may shorten step length, destabilize stance, and increase overall energy consumption, thus decreasing activity tolerance. Upper limb contractures may prevent effective use of assistive devices or generate mechanical disadvantage in functional tasks or tool use that confounds accommodative or adaptive techniques.
Prevention is essential. It is easier to prevent a contracture than to correct one, though it does require time, labor, and attention to detail. A consulting physiatrist is in a position to assist in the prevention of contractures in the acute care setting by recommending and implementing active and passive ROM exercise programs, static and dynamic bracing (eg, resting splints, functional bracing), serial casting if trained personnel are available, bed and chair positioning, and referral for surgical release when appropriate.
If a joint must be immobilized it should be done in the stretched position if possible, to decrease muscle atrophy, degree of contracture, and loss of tensile strength. If immobilization in stretch is impossible, an alternative is to immobilize in the neutral position to balance length and tension of opposing muscles. Early active immobilization after stabilization is beneficial, if permitted by the nature of the surgical repair.
Established contractures should be assessed for underlying etiology (bony deformity versus spastic paralysis), hard versus soft end point, degree of pain or discomfort both at rest and when stretched, and degree of impact on function. Contractures may be treated with deep heating to 40–45° C, passive ROM, and terminal stretch for 25–30 seconds. Chemoneurolysis with botulinum toxin or phenol, serial casting, splinting, or use of other devices (eg, hinged, locking knee brace; dynamic splint; or continuous passive motion device) may be prescribed when appropriate. Care must be taken with frail or chronically immobilized patients (eg, the elderly or those with spinal cord injury) to prevent insufficiency fractures. Table 5–1 lists contraindications to aggressive ROM programs for contracture.
Like the musculoskeletal system, the heart and blood vessels will actively adapt to prolonged bed rest, as anyone who has attempted to ambulate a patient in the intensive care unit can attest. Studies have shown that heart rate increases by 7–10 beats per minute after 7–14 days of bed rest. Concomitantly, the elevated heart rate decreases systolic ejection and diastolic filling time, rendering the heart less able to meet increased metabolic demands. Table 5–2 summarizes these and other cardiovascular changes associated with prolonged bed rest.
Orthostatic hypotension can occur after 3 weeks of bed rest, or even shorter periods in elderly individuals. The mechanism is multifactorial and involves pooling of blood in the venous circulation of the lower limbs, decreased circulating blood volume, loss of sympathetic tone, and increased heart rate with decreased ventricular diastolic filling.
In a classic 1968 study by Saltin and colleagues, 24 young, healthy male volunteers were subject to 20 days of strict bed rest. The experiment produced a 27% decrease in maximal oxygen uptake, a 25% decrease in stroke volume, and a 20% increase in heart rate. These effects may be exacerbated in the frail and elderly, and in those with preexisting cardiovascular impairment, as well as causing more significant functional consequences in these groups.
Bed rest removes the normal benefits that gravity and activity exert on the digestive system. Esophageal and gastric transit times are prolonged in the esophagus and stomach, up to 66% slower in the supine position. This effect extends to the colon, where stasis leads to excessive reabsorption of water, constipation, and fecal impaction. Furthermore, in the seated (upright) position, stool exerts pressure on the anal sphincter creating the urge to defecate. In the supine position the effect is absent. Bed rest in hospital settings, particularly in cases of trauma, is often accompanied by opioid pain medications, which slow gut motility. This is potentiated by NPO status and lack of dietary fiber and oral hydration.
The loss of normal positioning also allows acidic gastric secretions to collect in the upper stomach and exert pressure against the lower esophageal sphincter. Coupled with the decreased gastric bicarbonate secretion occurring in bed rest, which lowers stomach pH, this may increase symptoms of gastroesophageal reflux and cause or exacerbate preexisting dysphagia.
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