Dr. dr. Tirza Z. Tamin, Sp.KFR-K

Department of Physical Medicine and Rehabilitation, Cipto Mangunkusomo Hospital


            Immobilization is the physical restriction of movement involving a body segment or the entire body. Common cause of immobilization in PM&R include neuromusculoskeletal disorder and injuries (e.g., paralysis due to stroke); orthopedic casts, body jackets, and splints, usually after trauma or fracture; critical illness requiring bed rest (e.g.,  after acute myocardial infarction); and prolonged stays in recumbent position (e.g., chronic low back pain) or sitting position (e.g., wheelchair sitting). Immobilization due to prolonged bed rest result in a clinical entity called deconditioning, which is separate from the original process that led to the immobilization. In decontioning, there is a reduced functional capacity of multiple body systems, especially the musculoskeletal system. It leds to further inactivity and perpetuates the vicious cycle.1

            Patients  with a high level of physical fitness will hava a more rapid decline in physiological function with periods of extended immobility or decreased activity. The changes can be measured after as little as 2 weeks of inactivity.2

An acute hospitalization, older adults patients spend approximately 83% of their hospital stay in bed and 12% of their time in a chair. Prolonged immobility in the hospital has serious consequences on muscle strength, muscle mass, cognitive function, muscle protein synthesis, and functional ability in older adults.3

A.  Definition

Deconditioning syndrome is reduced functional capacity of musculoskeletal and other body systems because of inactivity or immobilization. The often cited 4% to 5% loss of muscle strength for each week of bed rest was derived from studies that involved young healthy test individuals without underlying disease or musculoskeletal conditions. It is likely that the rate of deconditioning is even faster in older adult patients with multiple comorbidities, because ambulatory function and ability to perform basic ADLs have been shown to decline in one third of hospitalized patients over the age of 70 years. Some of the complications of immobility include orthostatic intolerance, skeletal muscle changes, joint contractures, pulmonary atelectasis, urinary stasis, glucose intolerance, and pressure ulcers.4


B.  Funtional Impairments of Disused Muscle

  • Musculoskeletal changes

Contracture is the lack of full active or passive range of motion (ROM) due to a joint, soft tissue, or muscle limitation. Conditions producing limited joint ROM include pain (e.g., trauma, inflammation), muscle imbalance (e.g., paralysis and spasticity), capsular or periarticular tissue fibrosis, primary muscle damage (e.g., muscular dystrophy), or mechanical factors (e.g., improper bed positioning). The muscle fibers and connective tissue which are maintained in shortened position (e.g., for 5 to 7 days), adapt to the shortened length by contraction of collagen fibers and a decrease in mucle fiber sarcomeres. In 3 weeks or more, the loose connective tissue in muscle and around joints gradually change into dense connective tissue, causing contracture on the relaxed side of the joint.1

Muscle weakness and atrophy are usually seen in the antigravity muscles of the lower limbs. With total inactivity, complete immobilization can lead to a 50% decrease in muscle strength in 3 to 5 weeks. Strength that is lost in 1 week may take 4 weeks to regain even with a maximal strengthening program. To prevent disuse weakness, a muscle must exert 20 to 30% of its maximal capacity performed for 1 sec/day is even more effective.1

Disuse (Immobilization) osteoporosis is the loss of bone density due to increased resorption caused by lack of stimulus (e.g., weight bearing) on bone mass. The adverse effects of prolonged immobilization on the endocrine system cause increased urinary excretion of calcium and hydroxyproline and increased excretion of calcium in the stool which contributes to disuse osteoporosis. Disuse osteoporosis is more marked in the subperiosteal region, in contrast to senile osteoporosis, which develops from the marrow outward. Disuse osteoporosis initially involves the cancellous bone at the metaphysis and epiphysis, and later extends to the entire diaphysis. Bone density is reduced by 40 to 45% after 12 weeks of bed rest.1

TABLE 2. Diuse Osteoporosis

  • Cardiovascular changes

Orthostatic (postural) hypotension  is due to the impaired ability of the circulatory system to adjust to the upright position. As the person stands, blood pools in the lower limbs causing an immediate drop in venous return, which reduces stroke volume and cardiac output. Normally, there is immediate vasocontriction and increase in heart rate (HR) and systolic blood pressure (SBP). However, prolonged bed rest causes the person to lose this adaptation which is manifested in the following clinical signs and symptoms: tingling, burning in the lower limbs, dizziness, lightheadedness, fainting, vertigo, increased pulse rate (20 or more mmHg), and decreased pulse pressure.1

Treatment includes early mobilization (ROM exercises, strengthening exercises, ambulation, and calisthenics); abdominal strengthening and isotonic-isometric exercises of the legs (to reverse venous stasis and pooling); providing the wheelchair with elevating leg rests and a reclining back; use of the tilt table (gradual tilt up to 75 degrees for 20 minutes); use of Ace bandage wraps, full length elastic stockings, and abdominal binders; use of sympathomimetic pressor agents (ephedrine, 10-25mg slow IV infusion which may be repeated every 5-10 minutes; or phenylephrine [Neo-Synephrine]; 100-200 µg, IV for severe hypotension or infusion of 20 mg in 250 ml 5% dextrose in water [80µg/ml] at 40-180µg/min [35-160 ml/ hr]); use of mineralocorticoid (fludrocortisone  0.1 mg, po, qd)  to help maintain blood pressure; and maintaining an adequate salt and fluid intake to prevent further blood volume contraction and worsening of hypotension.1

Changes due to cardiac deconditioning take at least as long or twice as long to recover as it took to deteriorate. Hence early mobilization is important.1

  • At rest, cardiac changes caused by deconditioning include increased resting HR by one beat per minute every 2 days for the first 3 to 4 weeks of immobilization; decreased resting stroke volume up to 15% after 2 weeks of bed rest, which is related to a decreased in blood volume by 7% after 20 days of bedrest, decreased cardiac size by 11%; and decreased left ventricular end diastolic volume.1
  • With exercise, cardiac changes caused by deconditioning include increased HR response to submaximal exercise (up to 30-40 beats per minute greater than expected after 3 weeks of bedrest), although maximal HR remains unchanged or slightly increased; decreased stroke volume at submaximal exercise and up to 26% at maximal exercise); decreased maximum oxygen uptake (VO2 max) by 27%, which indicates reduced aerobic fitness; increased arteriovenous oxygen difference at submaximal exercise but not at maximal exercise.1

TABLE 3. Disuse Weakness, Deconditioning, and Cardiovascular Disease

Changes in fluid balance in the recumbent position include increased CO by 24%; increased cardiac work by 30%; shift of 700 ml of blood volume to the thorax; delayed shift of extravascular fluid into the circulation; and compensatory diuresis, which leads to decreased plasma volume with subsequent loss  of plasma mineral and protein.1

Venous thromboembolism may develop due to venous stasis increased blood viscosity, and hypercoagulability (caused by the decline in plasma volume while red blood cell mass remains unchanged).1

  • Respiratory changes due to bed rest are caused by mechanical restriction of breathing (caused in part by reduced chest excursion due to progressive reduction of ROM in the costovertebral and costochondral joints) which subsequently result in rapid, shallow breathing. Pulmonary function parametes, such as tidal volume, minute volume, vital capacity, and maximum voluntary ventilation, are all reduced.1
  • Skin changes

Pressure ulcers

Dependent edema can predispose to cellulitis. Preventive measures include adequate mobilization and elevation, use of elastic stockings or gloves, pressure gradient compression, and massage.1

Subcutaneus bursitis occurs when there is excessive pressure on the bursae (usually prepatellar or elbow bursae).1

  • Gastrointestinal changes include decreased appetite, decreased gastric secretion, atrophy of the intestinal mucosa and glands, slower rate of absorption, distaste for protein-rich food, and constipation due to decreased gastric and intestinal motility.1
  • Genitourinary changes include increased diuresis and mineral excretion, stone formation, and urinary track infection.1
  • Metabolic and nutritional changes include decreased lean body mass, increased body fat, disorder of nitrogen balance, and mineral and electrolytes losses. Hypercalcemia due to immobilization is associated with osteoporosis.1
  • Endocrine changes are due to altered responsiveness of hormones and enzymes. They include glucose intolerance; altered circadian rhythm; altered temperature and sweating responses; and altered regulation of parathyroid hormone (PTH), thyroid hormone, adrenal hormones, pituitary hormones, growth hormones, androgens, and plasma renin activity.1
  • Neurological emotional, and intellectual changes include the effects of sensory deprivation (decreased attention span, confusion and disorientation to time and space, decreased hand-to-eye coordination); decreased intellectual capacity; emotional and behavioral disturbances (e.g., anxiety, lack of motivation); increased auditory threshold and decreased visual acuity; impaired balance and coordination (probably due to neural factors rather than muscle weakness); and compression neuropathies. Preventive measures include encouraging the patient to interact with others, and recreational therapy for psychosocial integration, resocialization, and adjustment to independent functioning.1

C.  Organs Systems affected with prolonged debilitation


– Heart: Increased heart rate (reting tachycardia), decreased stroke volume 15% in 2 weeks, and cardiac muscle mass may decrease.5

– Blood Vessels: Blood pools in the legs. Blood vessels may lose their ability to constrict in response to postural change also decrease in venous return, stroke volume, and blood pressure. Therapy include early mobilization, isometric LE exercise, positioning/gradual tilting, TEDs, fluids, and meds.5

– Fluid balance: Prolonged recumbence leads to volume loss; shifts 700cc to thorax, increase CO by 25%, gradual diuresis (protein loss), and decreased plasma volume 10-15%, hct may increase, then fall as RBC mass decreases.5

– Venous Thrombosis (DVT): Virchow’s triad (stasis, hypercoagulability, vessel trauma) is risk factors for thrombosis. Risk Factors of DVT are: age 40-60 years, history of DVT or PE, malignancy, obesity, immobilization, major surgery, paralysis, trauma, severe COPD, pregnancy or post partum  <1 month, severe sepsis, hypercoagulable state, nephrotic syndrome, leg ulcers, edema, or stasis.5


Includes potential decrease in lung volumes (vital capacity, TLC, residual volume, expiratory reserve, functional residual capacity), A-V shunting, increased respiratory rate, pneumonia, atelectasis.5


Includes progressive decrease in muscle strength / endurance, strength declines 1-3% day. Also fatigability, decrease ATP & glucose stores and ability to use fatty acids; decrease in muscle mass & tension. Body composition also changes as in decreased lean body mass and increased body fat.5

TABLE 4. Mobility and ADL5


Contracture may happen; decrease PROM of joint, with immobility, collagen develops CROSS-LINKS and become less flexible (joint – synovial tightening, connective tissue – loose turns to dense, muscle – decreased sarcomeres). Risk factors for contractures are positioning, pain (e.g., local trauma, infection), muscle imbalance (paralysis/weakness and spasticity). Contracture prevention are bed positioning (extension of neck, hips, knee, ankle neutral, “functional” hand position), BID range of motion exercises (terminal, sustained), splinting, heat (40-43 degrees), surgery, and nerve & MP block.5

D.  Preventive Treatments

Prevention of deconditioning in hospitals during acute illness requires physical therapy, maintenance of nutrition, medical management, and psychological support. Activity and independence should be promoted from the time of admission.6

Exercise programs has been shown to improve lower-limb muscle strength, exercise endurance, balance, speed of walking, and overall levels of physical activity. Practice of specific skills is required if improved muscle strength is to translate into functional benefits. Exercises including a balance component (e.g., tai chi) may be useful in preventing falls. Physical exertion has potential dangers, and exercise programs for older people should be tailored to the needs and capacity of the individual person.6

Restoration of physical function and independence in a frail and deconditioned hospital patient is particularly difficult. Comprehensive clinical, functional, and psychosocial assessment is mandatory. It is important to set measurable, attainable goals and to monitor progress carefully. This is aided by the use of standardized tools to measure important areas such as cognitive function and the ability to perform daily activities. An active multidisciplinary rehabilitation program is essential, and should include nutritional and psychologic support.6

Early mobilization, strengthening exercise, range of motion, maintain skin integrity, DVT prophylaxis, pain management, phychological assessment/treatment, and aggressive respiratory management also needed for preventing treatments.6

E.  Examination for Deconditioning Syndrome

Anamnesis history and duration of disability that caused immobilization, medical condition before and after immobilization, the present of pain, drug use that disrupt mobilization, patient’s psychological and motivation, and environment factor.7

Physical Examination includes general examination and functional capacity

TABLE 5.  Muscle Strength Grading7

Table 5. Ulcus Decubitus Grading7

 F.   Intervention of Deconditioning Syndrome

  1. Communication and Education

Guide the patient’s family and other health care provider to avoid encouraging the patient to overexert or underexert performing activities. Inforn about the physiological benefit of exercise. Understand that period of rest during the day are important for pacing their activities and limiting fatigue. Educate the warning sign, such as increase in respiratory rate and heart rate, fatigue that indicate the need to rest.7

  1. Aerobic Exercise

Exercise for acute care inpatient setting

The primary goal is to improve the patient’s functional abilities to prepare for discharge home or to another health care facilities. Severe deconditioning : sitting upright in bed or chair (standing and walking for short distances [less than 50 feets]). Ambulatory patient: walking exercise program with distance and speed used to progress exercise intensity and monitor exercise tolerance.7

Improved exercise tolerance in hospitalized patients can be adjusted depending on the duration of treatment, the patient’s initial condition, and the level of initial training. A stationary bicycle or arm ergometer can be transported to patient’s room to prolonged endurance exercise. Patient’s may also be able to use the long corridor and stairs of hospital to increase their walking endurance. Upper extremity ROM exercise using light resistance with sets of 12-15 repititions are also recommended.7

General guidelines for stopping an exercise session are as follows :

– Heart rate : A drop below the resting rate or an increase  >20 to 30 beats per minute (bpm) above the resting rate

– Systolic blood pressure : a drop >10 mmHg below  the resting rate

– Oxygen saturation level : below 90%

– Symptoms : angina, significantly increased by dyspnea

Exercise for acute care outpatient setting

The goal of exercise for outpatient setting are improve patient’s functional, vocational, and recreational activities, mantain and improve overall fitness, and often reduce the risk of reccurence of their disease progress.7

Exercise session includes warm up and cool down. Warm periods; can reduce the risk of cardiac arrythmias and ischemia and improve muscle performance. Cool down periods; should be closely monitored because adverse cardiac events are thought to occur most often during this period. It must be long enough to allow the heart rate and BP to return toward the resting level.7

Exercise Intensity

The American College of Sports Medicine (ACSM) recommended beginning exercise program for unfit individuals on 55-65% of estimated maximum heart rate or at 40-50% of the heart rate reserve (HRR). To calculate the target heart rate using the Karvonen method:

= [maximum heart rate- resting heart rate] x goal percentage of HRR ) + resting heart rate

A metabolic equivalent (MET) is another commonly used to measure activity intensity

One MET equivalent to approximately 3.5 ml of oxygen/kg/min.7

TABLE 6. Metabolic Equivalent (MET)7

A deconditioned patient should ideally maintain a low-to-moderate intensity of exercise for 20 to 60 minutes to gain physiological benefits of aerobic training. The ACSM recommends 2 to 5 exercise sessions per week for improving aerobic capacity in deconditioned patients.

  1. Weight Training

A resistive weight training program will improve muscle strength impairment and may improve associated functional limitations. Circuit weight training (CWT) is defined as the performances of 10-15 repetitions using 40-60% of one repitition maximum (1 RM) in continuous fashion and moving from one exercise station or machine to another with short rest periods between stations. CWT has been shown to increase strength by 20-40% after 8-20 weeks training, but aerobic capacity only by 5-10%.7


Due to deconditioning syndrome give a significant impact of decrease in functional ability and in terms of medical and financial. Increased morbidity and mortality associated with thromboembolic disease, pneumonia, and the incidence of falls. Further functional decline may extend the re-hospitalization and treatment of acute patients. Patients with significant functional limitations brought to riskier long-term care facilities7




 Tan JC. Practical Manual of Physical Medicine and Rehabilitation: Diagnostics, Therapeutics, and Basic Problems. 1st ed. Philadelphia. Mosby-Year Book;1998. Chapter 5.1, Deconditioning;p.425.

  1. Elokda AS, Helgeson K. Deconditioning. In: Cameron MH, Monroe LG, editors. Physical Rehabilitation for the physical therapist assistant. Missouri. Elsevier Saunders; 2011.
  2. Clark LV, White PD. The role of deconditioning and therapeutic exercise in chronic fatigue syndrome (CFS). Journal of Mental Health. 2005 June;14(3):237-52.
  3. Bartels M, Prince DZ. Acute Medical Conditions. In: Cifu DX, editors. Braddom’s Physical Medicine & Rehabilitation. 5th ed. Philadelphia. Elsevier Saunders; 2016.
  4. Brown M, Sinacore DR, Ehsani AA, Binder EF, Holloszy JO, and Korht WM. Low-Intensity Exercise As a Modifier of Physical Frailty in Older Adults. Archives of Physical Medicine and Rehabilitation 81 (2000): 960–965.
  5. Bucher DM, Wagner EH. Preventing Frail Health. Clinics in Geriatric Medicine 8 (1992): 1–17.
  6. Kane RL, Ouslander JG, Abrass IB, Resnick B. Essentials of clinical geriatrics. 6th edition. New York: The MCGraw-Hill Companies, Inc.; 2009. Chapter 10, Immobility; P.297-331.











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