“Look at the patient lying in bed. What a pathetic picture he makes. The blood clotting in his veins, the lime draining from his bones…the spirit evaporating from his soul.”
— Dr. Richard Asher

The Dangers of Going to Bed, 19831

As nurses, we have known for many years that bedrest can have dire consequences. Although we’ve made great strides in getting patients out of bed as quickly as possible, we must remain ever vigilant against potential complications that our patients may suffer from long periods of bedrest and immobility. Preventing iatrogenic complications will most certainly expedite the transition from hospital to home.² We will be more likely to provide proactive interventions for our patients when we have a better understanding of all the changes that occur within the body during prolonged periods of bedrest or immobility. And we will be better able to protect the elderly with underlying preorgan dysfunction secondary to age-related changes, for whom the risks of bedrest are profound.³

Back in time

In the 1950s and 1960s, providers routinely prescribed strict bedrest of two weeks after childbirth, three weeks after a herniorrhaphy, and four weeks after a myocardial infarction.⁴ Although often treated as primary therapy, bedrest itself led to lengthy hospitalizations, soaring health care costs, and secondary complications. Early hospital discharges, which took a foothold in the Diagnosis Related Groups Coding era of the 1980s, and the surgence of clinical pathways have contributed to getting patients up and about as soon as they are hemodynamically stable, reducing the numbers of patients who remain in bed. However, many intermediate and long-term care patients continue to suffer from the adverse effects of bedrest.^2,4

Psychological changes and counter measures

Immobility can wreak havoc on an individual’s emotional state — immobile patients frequently exhibit anxiety, apathy, depression, disorientation, passive/aggressive verbal and nonverbal communication, mood swings, listlessness, withdrawal, social isolation, regression, and altered body perception.⁵

In the late 1960s, NASA studied young healthy males who were confined to bed for five weeks. The men exhibited a significant increase in anxiety, hostility, depression, and sleep disturbances.⁵ Other notable psychological effects of immobility/bedrest included a diminished ability to concentrate, recall sequential events, problem solve, and perform self-care.⁵

While one would imagine that patients on bedrest get more than ample sleep, this is not the case. Patients confined to bed often have more complicated disease processes that require round-the-clock nursing interventions. Disturbances during the night infringe on much needed Rapid Eye Movement (REM) sleep. When patients are deprived of REM sleep, their sleep and wake cycles are disrupted and they report feelings of inadequate rest,⁶ and may exhibit signs of sleep deprivation, which are similar to the psychological manifestations of immobility.

In order to best limit unhealthy psychological responses to immobility, nurses can minimize sensory overload and promote meaningful stimuli: Turn down alarms and protect patients from noxious sounds and odors; provide a stimulating and pleasant environment conducive for rest and relaxation; allow freedom with visitation to meet the patients’ social needs; and schedule activities that allow for a normal routine in day-night activities. Providing patients with items like wall calendars and clocks, newspapers, magazines, radios, and televisions assists with maintaining their orientation to time, place, and daily events. Ensuring that patients have their hearing aids, eyeglasses, dentures, and prostheses gives them the tools they need to deal with their environment.⁷

Deconditioned muscles

The musculoskeletal system is one of the first systems of the body to suffer the far-reaching effects of immobility,⁸ and research has shown that changes not only occur to the muscle fibers but also at a subcellular level in the system.^9-11 The consequences of these changes include the loss of muscle strength and endurance, reduced skeletal muscle fiber size, diameter, and capillarity (atrophy); and contractures, disuse osteoporosis, and degenerative joint disease. The severity of muscle deconditioning is related to the duration and magnitude of the activity limitation. If left unchecked, this muscle wasting can lead to long-term sequelae — muscle atrophy, joint ankylosis, and fibrofatty tissue proliferation, which leads to the formation of adhesions, scar tissue, and contractures — impairing functional capacity and permanently damaging the muscle.^4,12,13

Recent research indicates that bedrest is associated with intervertebral disc changes which may exacerbate lower back pain.¹⁴ Bedrest, once commonly prescribed for back pain, has been replaced with controlled exercise to rebuild strength, flexibility, and coordination.¹⁴

Inactivity elevates lactic acid production and adversely affects adenosine triphosphate (ATP) concentrations, a vital energy source for muscle. Bedrest also diminishes protein synthesis and glycogen, augmenting fat stores, causing a glucose intolerance that requires more insulin for carbohydrate metabolism and resulting in reduced muscle mass and strength and oxidative capacity.^15,16 Although healthy adults normally change positions during sleep every 116 minutes, bedridden patients with weakened muscles may be incapable of moving independently. External pressure from lying in one position compresses the skin’s capillaries and obstructs its circulation, particularly over the bony prominences, leading to skin breakdown and pressure ulcers.^17,18

Immobilization causes loss of normal muscle contraction in the lower extremities and contributes to venous pooling and venous stasis in dependent parts of the body.⁷ Slowing of venous circulation, coupled with constant pressure from the weight of the resting body, compresses capillary vessels and raises their internal pressure above normal, damaging the intimal lining. Venous stasis may also impede the usual clearance of coagulation factors produced by the liver.¹⁹ The combination of venous stasis, pathophysiogenic changes in the vessel walls, and hypercoagulability of the blood is known as Virchow’s Triad. When Virchow’s Triad is activated, these changes lead to deep vein thrombosis, often causing life-threatening pulmonary emboli.^20,21 As many as 13% of bedridden patients develop deep vein thrombosis.¹⁹ DVT was first strongly identified in persons during World War II when they sat for prolonged periods in air-raid shelters. From this, speculation arose targeting sedentary lifestyles and prolonged periods of immobilization, such as air travel, car trips, and even extensive use of computers, as major determinants in the development of immobilization-induced thrombus.¹⁸ In one study, prolonged inactivity was found to be the strongest factor in the development of a DVT.²²

Immobility and diminished weight bearing has also been linked to a disruption in parathyroid functions, calcium metabolism, and bone formation. Resulting osteoporosis places an older adult at risk for pathologic fractures of the vertebrae, hips, pelvis, and shoulder bones.^18,19 Studies on the effects of immobilization have shown that the thickness of cartilage may be reduced as much as 50%. The periarticular muscles also undergo significant atrophy from disuse due to immobilization.²³

The dangers of a sedentary lung

Immobility can also be devastating to lung function. Underused, weakened respiratory muscles can hamper chest wall expansion and impede adequate tidal volume for air exchange. A patient’s cough can become impaired, hindering the effective clearing of pulmonary secretions. As retained secretions occlude air passages, alveoli collapse and atelectasis occurs. Atelectasis partially or completely disrupts the lungs’ ability to exchange oxygen and carbon dioxide secondary to hypoventilation and causes hypoxemia and hypercarbia. As blood flow is shunted by gravity to dependent portions of the lung and the bulk of ventilation takes place at the “top” of the lungs where there is less blood flow, patients may become hypoxemic.^18,19

The supine position is particularly dangerous for the lung, predisposing immobile patients to aspiration, pneumonia, and respiratory infections.⁵ By itself, this position reduces normal functional residual capacity in the lung — the volume of air that remains in the lungs between breaths — by 800 cc causing a decrease in PO2 and O2 saturation,²⁴ and reduces the vital capacity of the lungs by 4%.⁵ However, with additional pressure of the abdominal contents on the diaphragm, inspiratory capacity may become severely handicapped. The anxiety of not being able to move or take a deep breath may cause patients to experience dyspnea. As gravitational forces redistribute blood and fluid shifts in the pulmonary vascular bed, dependent pulmonary edema may result which increases the patient’s risk for severe dyspnea and pulmonary emboli.¹⁹ The likelihood of emboli and thrombophlebitis is heightened as bedrest interferes with normal liver function and coagulation.^18,19

The consequences of compromised ventilation can extend to the cellular levels where a reduction in oxygen impairs normal cellular function. For example, inadequate cellular oxygenation compromises wound healing by inhibiting collagen synthesis that is necessary for tissue repair, and by impeding the control of bacterial growth which increases risk for infection.²⁵

The cardiovascular system on bedrest

Prolonged immobility sets in motion a cascade of damage in the cardiovascular system. Changing positions from upright to supine triggers fluid shifts that raise central venous pressure and activate renal and hormonal receptors to cause diuresis. When the venous pooling in the lower extremities and an often reduced oral intake are added to fluid-shift effects, stroke volume and cardiac output may deteriorate. Orthostatic hypotension and tachycardia may ensue as the heart attempts to compensate for the low stroke volume.^3,17,18 Even a healthy young adult may take several weeks to recover orthostatic function after bedrest.⁵

Consequences for every system

Immobility alters hormonal homeostasis by stimulating an excessive release of epinephrine and norepinephrine from the sympathetic nervous system; triiodothyronine (T3) and thyroxine (T4) from the thyroid; adrenocorticotropic hormone (ACTH) from the pituitary gland; and aldosterone, a prime factor in the renin-angiotension cycle that regulates the excretion of sodium and water.¹⁹

Impaired taste and smell, as well as difficulty in swallowing while in a recumbent position, all contribute to a reduction in appetite and fluid intake. A negative nitrogen balance caused by catabolic processes from immobilization occurs as early as the sixth to the tenth day and can cause anorexia.¹⁷ Diminished peristalsis, associated with inactivity, impaired fluid intake, and physiological fluid shifts, can lead to constipation, nausea and vomiting, or even paralytic ileus, further augmenting the patient’s fluid deficit.¹⁸

Patients on prolonged bedrest, especially the elderly, are susceptible to complications of urinary retention and mineral loss. The supine position hinders drainage of urine from the renal pelvis to the bladder. Patients often have difficulty using a urinal or bedpan because of the supine position or feeling embarrassed. Avoidance of urinating can lead to overdistention of the bladder muscle. As the bladder becomes more distended, patients may lose the sensation to void and experience even more difficulty, resulting in urinary retention, stasis, and infection. Non-weight bearing — particularly not using the longitudinal bones — hastens demineralization of calcium and phosphorous from bones, predisposing the patient to renal calculi.^18,19,26

Mobilizing answers

Patient functional activity and mobility are essential to recovery and minimization of the risks associated with immobility. Using an interdisciplinary team approach (nurses, patient care assistants, physical therapists, occupational therapists) has been successful in increasing awareness and improving the consistency with which patient activity is addressed, thus reducing the incidence of immobility-associated complications.²⁷

Nursing interventions must focus on preventing the untoward physiological changes and general complications of immobility by starting with the basics:

• Provide adequate hydration by offering fresh water and fluids at frequent intervals, and monitor fluid balance by following the patients’ intake and output.
• Enhance nutritional intake by providing an opportunity for mouth care before eating, supplying foods that patients prefer, and assisting them to get out of bed for meals.
• Counter problems of urinary stasis and constipation by assisting patients to use bedside commodes rather than using bedpans and by facilitating early ambulation. Record daily urine consistency and stools and use stool softeners, high-fiber diets, and fruit juices to promote regular bowel habits.¹⁷

Nursing measures that mobilize patients and promote their independence in activities of daily living (ADLs) can prevent musculoskeletal deconditioning and skin complications. Many of these interventions, such as ambulation, benefit several systems at the same time. For example, weight bearing on longitudinal bones not only helps to promote musculoskeletal and cardiovascular tone, but also combats the loss of calcium and phosphorus from bone. Encourage patients to weight bear during bed to chair transfer and to ambulate as soon as possible.⁷

While they are in bed, help patients both to maintain proper body alignment and to routinely perform active and passive range of motion exercises, using the expertise of physical therapists when needed. Exercising, including passive stretching, during bedrest may reduce loss of muscle strength. Devices, such as pneumatic compression boots, elastic stockings, and hand and foot splints are helpful, but need to be periodically discontinued to allow for normal functioning. The administration of prescribed anticoagulants and calcium supplements, plus adequate hydration and nutrition, can further protect the patient progressing towards optimum mobility. Managing a patient’s pain whether it’s the cause or the result of immobility is essential. Effective drug therapy such as opioids and nonopioids, and therapeutic therapy such as heat and cold, and relaxation techniques must be individualized to the patient’s need.

Prevent cardiopulmonary complications by encouraging frequent pulmonary hygiene, maintaining an every-two-hour schedule of deep breathing and coughing exercises with or without incentive spirometry, and frequent repositioning to prevent pooling of pulmonary secretions and collapse of alveoli. Leg exercises and the use of pneumatic compression sleeves that are used to counter musculoskeletal complications can also help prevent the venous stasis frequently associated with bedrest. These basic nursing measures not only prevent calcium loss from the bones, but will promote hemodynamic stability reducing the risk for orthostatic hypotension. Have patients dangle their legs for five to 10 minutes three times a day; rather than lifting the patient from the bed to the chair, encourage progressive weight bearing by having them first stand and pivot to a chair, and eventually ambulate from the bed to the chair. These out-of-bed activities not only prevent complications, but also promote a sense of well-being.^7,17

Patients admitted to hospitals, intermediate, and long-term care facilities need astute nursing assessments and early interventions to prevent permanent disabilities and potential life-threatening complications that can result from bedrest and immobility. Nurses need to initiate consistent interventions to prevent psychological and physical deconditioning, progressive dependence and deterioration, and possible death. We can do this by keeping our patients moving.