Changes in Human Body Structure and Function Due to Prolonged Immobilization

Reinita Arlin Puspita 030.08.202

Medical Faculty of Trisakti University Jakarta, 2011

CONTENT ABSTRACT .... 3 INTRODUCTION ... 4 DISCUSSION . 6 CARDIOVASCULAR CHANGES WITH IMMOBILIZATION MUSCULOSKELETAL CHANGES WITH IMMOBILIZATION PULMONARY CHANGES WITH IMMOBILIZATION HORMONAL CHANGES WITH IMMOBILIZATION EFFECTS OF BED REST ON THE NEUROLOGICAL SYSTEM EFFECTS OF BED REST ON THE GASTROINTESTINAL SYTEM EFFECTS OF BED REST ON THE GENITOURINARY SYSTEM EFFECTS OF BED REST ON THE BODY COMPOSITION, METABOLISM AND NUTRITION EFFECTS OF BED REST ON THE SKIN CONCLUSION .

I. ABSTRACT
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Bed rest and immobilization has been routinely and often casually prescribed, during a period of injury or recovery. However, bed rest results in profound deconditioning of the body.(1) Prolonged immobilization can caused lots of problems due to decreased body function and structure. Prolonged bed rest and immobilization causes a generalized deconditioning of the body function, involving most of the physiological systems of the body, including the cardiovascular, pulmonary, gastrointestinal, genitourinary, hormonal,

musculoskeletal, neurological, systems. Even more, prolonged bed rest and immobilization can cause the imbalance of body composition, metabolism, and nutrition which can make the patient more suffer each day. It is important for clinicians to recognize these negative consequences of prolonged bed rest and immobilization, which can be explained independent of disease or disorder. With this in mind, bed rest can be minimized as much as possible and early ambulation and physical activity may be prescribed to limit the deconditioning effects of bed rest.(1)

II.

INTRODUCTION Bed rest and immobilization is a long standing treatment for managing acute and chronic injury and illness. It may have started with Hippocrates, the father of

medicine, who suggested that In every movement of the body, whenever one begins to endure pain, it will be relieved by rest.(1) However, in the 20th century, physicians and scientists became increasingly aware of the harmful effects of prolonged bed rest. Classic bed rest studies following World War II documented the deconditioning that occurs following bed rest. Allen et al. conducted an exhaustive search of the medical literature from 1966 to 1998, which provided additional evidence for the harm of bed rest for any medical condition.(2) In 15 trials that investigated bed rest as a primary treatment for a variety of conditions, no outcomes improved significantly and nine worsened significantly (including acute low back pain, labor, proteinuric hypertension during pregnancy, myocardial infarction, and acute infectious hepatitis). In 24 trials that investigated bed rest after a medical procedure, no outcomes improved significantly, and eight worsened significantly (including lumbar puncture, spinal anesthesia, radiculography, and cardiac catheterization).(2) The resultant physiological adaptations negatively affect most organ systems of the body (1). This paper focuses on the effects of immobilization on the cardiovascular, muscular, and skeletal systems, other organ systems that exhibit the most pronounced deconditioning.
III. DISCUSSION 4

Prolonged bed rest and immobilization inevitably lead to complications. Such complications are much easier to prevent than to treat. Musculoskeletal complications include loss of muscle strength and endurance, contractures and soft tissue changes, disuse osteoporosis, and degenerative joint disease. Cardiovascular complications include an increased heart rate, decreased cardiac reserve, orthostatic hypotension, and venous thromboembolism. Respiratory complications include decreased ventilation, atelectasis, and pneumonia. Decreased basal metabolic rate, increased diuresis, natriuresis, and nitrogen and calcium depletion affect metabolism. Genitourinary problems include renal stones and more frequent urinary tract infections. Glucose intolerance, anorexia, constipation, and pressure sores might develop. Central nervous system changes could affect balance and coordination and lead to increasing dependence on caregivers.(5) III.1. EFFECTS OF BED REST ON THE CARDIOVASCULAR SYSTEM The cardiovascular system functions optimally while counteracting gravity in an upright position (1). A coordinated interaction between the cardiovascular and nervous systems ensures adequate blood perfusion to the brain and other organs. When the body assumes a horizontal position for an extended period of time during bed rest, deconditioning of the cardiovascular system occurs (1).
Maximal oxygen consumption ( V O2max) commonly is used to assess cardiovascular function in both health and disease. Bed rest decreases V O2max, and the extent of the loss depends on the length of the bed rest, with V O2max decreasing approximately 0.9% per day over 30 days of bed rest. The decrease in V O2max

during bed rest appears to be independent of gender and age. However, more fit
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 individuals may experience a greater absolute decrease in V O2max compared to less

fit individuals. (1)

The decrease in V O2max following bed rest can be attributed to both cardiac and

peripheral effects, although cardiac effects predominate (Figure 1).

Figure 1.

Cardiovascular mechanisms affecting V O2max following bed rest.

(Abbreviations: NE, norepinephrine; RBC, red blood cells). Figure modified from Convertino (1).
A 26% decrease in V O2max in five men after 20 days of bed rest was

accompanied by a similar 26% decline in cardiac output. Similarly, a 17% decrease

in V O2max following 10 days of bed rest in 12 men resulted from a 23% reduction

in cardiac output. (1) A change in heart rate is not responsible for the decreased cardiac output following bed rest. In fact, both resting and maximum heart rate have been observed to increase following bed rest. The increase in resting heart rate may be due to a decrease in vagal tone, and the increase in maximum heart rate may be caused by an increased release of norepinephrine and an increased sensitivity of cardiac
adrenergic receptors. The primary cause of decreased cardiac output and V O2max

following bed rest is a reduction in stroke volume. The reduction in stroke volume is not caused by a change in contractility. In fact, contractility and ejection fraction appear to increase following bed rest due to increased sensitivity of cardiac adrenergic receptors. Instead, the primary mechanism for the reduction in stroke volume following bed rest is decreased preload due to a reduction in plasma volume. Rapid diuresis occurs within the initial 24-48 h of bed rest, resulting in a 10-20% reduction in plasma volume. Additionally, venous compliance increases by 20-25% with bed rest, which results in venous pooling in the lower extremities when an upright posture is resumed and a reduction in stroke volume (1).
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Although decreased stroke volume and cardiac output are the primary causes of
the diminished V O2max following bed rest, peripheral factors may also contribute

(Figure 1). Prolonged bed rest resulted in a 9% decrease in red blood cell mass, compromising the oxygen-carrying capacity of the blood, and perhaps contributing to
the reduced V O2max(18). Furthermore, decreased capillarization and muscle blood flow following bed rest also may diminish V O2max (1). In addition to reduced V O2max, bed rest results in additional complications with

the cardiovascular system, including alterations in orthostatic tolerance, and increased frequency of venous thrombi. III.1.1. Orthostatic Hypotension Orthostatic hypotension is believed to occur when the

cardiovascular system does not adapt normally to an upright posture. When it happens, there is an excessive pooling of blood in the lower extremities and a decrease in circulating blood volume. This along with rapid heart rate, results in diminished diastolic ventricular filling and a decline in cerebral perfusion.(3) The circulatory system is unable to restore a stable pulse and blood pressure level. III.1.2. Venous Thromboembolism This complication may develop as a result of venous stasis, increased blood viscosity and hypercoagulability caused by the decline in plasma volume while red blood cell mass remains unchanged.

Most patients are fail to demonstrate any clinical signs such as pain, tenderness, swelling, venous distension, palor, cyanosis, redness. And even though venography is the gold standard of modality, more than 50% patients have no evidence on it.(3) Venous collaterals are generally so well developed that the thrombi must be quite extensive to clog the veins or cause vessel wall inflammation.(3) Venous thromboembolism can be a serious complication of bed rest. Patients with venous thrombi have a 50% chance of

developing pulmonary emboli, and the mortality from untreated pulmonary embolism is 20-35%.(1) III.2. MUSCULOSKELETAL CHANGES WITH IMMOBILIZATION III.2.1. Muscle weakness and atrophy The most obvious effect of prolonged immobilization is loss of muscle strength and endurance.(3) A muscle at complete rest loses 10 15 % of its strength each week. Nearly half of normal strength is lost within 3 5 weeks of immobilization. Patients immobilized in bed find the first muscles to become weak and atrophy and experienced greater loss of strength than other skeletal muscles with inactivity are those of the lower extremities (e.g. gastrocnemius soleus) and trunk that normally resist gravity.(3)

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As would be expected, the decrease in muscle mass following bed rest is accompanied by a decrease in muscle strength(1) (Table 1). Table 1. Change in maximal muscle strength following bed rest.
Number of Days 30 Muscle Group Knee flexors Knee extensors 35 35 Plantar flexors Plantar flexors Dorsi flexors Knee flexors Knee extensors Elbow flexors % Change -6 -19 -26 -25 -8 -8 -19 -7 LeBlanc Gogia Reference Dudley

The greatest decreases in strength are in the antigravity muscles. Maximal strength of the knee flexors (-6%) and knee extensors (-19%) decreased following 30 days of bed rest (28). Thirty-five days of bed rest caused decrements in maximal strength of the ankle plantar flexors (-25%), ankle dorsi flexors (-8%), knee flexors (-8%), knee extensors (-19%), and elbow flexors (-7%) (29). Similarly, maximal strength decreases of 26% were observed in the ankle plantar flexors after 35 days of bed rest. (1). Generalized muscle weakness hampers people in the activities of daily living, work, climbing stairs, and even walking. Local muscle weakness results from local immobilization when fractured bones or injured joints are set in casts. The implication of immobilization can be worse for patients with
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severe orthopedic and neurologic disorders and for persons who are voluntarily inactive (many of the elderly). (3) Unfortunately the rate of recovery from disuse weakness is slower than the rate of loss. Disuse weakness is reversed at a rate of only 6 % per week using submaximal exercise (65 75% of maximum). Muscle strength can be maintained without loss or gain with daily muscle contractions of 20% or more of maximal tension for several second each day. (3) Complete rest will also result in decreased endurance though a reduction in muscle strength, metabolic activity, and circulation. Decreased endurance levels that cause a sense of fatigue and reduced patient motivation set up a vicious circle of greater inactivity and further fatigue (both as a contributing factor to and a result of). (3) Combined muscle atrophy, decreased strength, and limited endurance may be a significant concern because they leads to poor coordination of the movements of the extremities and could affect the patients ability to perform the activities of daily living.(2) In the first few days after returning from space, astronauts exhibit increased postural sway, gait changes, and impaired kinesthetic sense. These factors also contribute to an increased risk of falls in the elderly.(1) Importantly, the lost bone mass is not regained for some weeks or months after muscle mass and strength have returned to normal, further contributing to the risk of fracture. Those who enter a period of bed rest with
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subnormal muscle and bone mass, especially the elderly, are likely to incur additional risk of injury upon reambulation. (6) III.2.2. Contractures and soft tissue changes Contracture defined as fixed deformities of joints as a consequence of immobilization.(3). It occurs most commonly at the lower limb with involvement of muscles that cross two joints in the hips, knees, and ankle while in the upper limb, the shoulders, elbows, wrists, and fingers are more susceptible. (5) Contracture occurs because of the dynamic nature of connective tissue and muscle in the body. Connective tissue is constantly being removed, replaced, and reorganized. In areas of little or no motion (e.g. immobilized muscles), collagen eventually is laid down as a dense mesh of sheets. But the worst part is collagen fibers maintain their length if their frequently stretched but shorten if immobilized.(3) This is why immobilization can caused a lack of full active or passive range of motion.(5) Ligaments are also affected in immobilized patient in both bony ligament insertions and the ligament substance itself. Stiffness of the ligaments may occur as the impact of prolonged immobilization. Immobilization can cause fibrofatty infiltration in joints that can mature into strong adhesions within the joints and might destroy the cartilage.
(3)

In periarticular connective tissue, new type I collagen has been abnormally

deposited and contributes to contracture of the joints.

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III.2.3. Disuse osteoporosis Disuse osteoporosis is the loss of bone density because of the unbalanced of the resorption and the formation on the bone mass caused by lack of stimulus. Disuse osteoporosis is more marked in subperiosteal section.(5) Immobilization leads to bone mass loss in association with hypercalciuria and negative calcium balance. Bone loss during long term immobilization tends to occur in stages. (Table 2).(1) Stages First Second Third Bone Loss Rapid bone loss Beginning at 12 weeks, slower but more prolonged bone loss Stabilization at 40% to 70% of original mass.

Table 3. Stages of Bone Loss during Immobilization(1) Decreases in bone mass following immobilization, coupled with decreases in muscle strength, significantly increase the risk of bone fractures with even minor trauma or falls (6). Osteoporosis can only be prevented by weight bearing standing. A tilting table or a standing frame may be used in patients who are unable to stand unsupported.(5) III.2.4. Degenerative joint disease Contracted capsule and joint immobilization in a fixed position can cause prolonged compression of the cartilage contact sites and their subsequent
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degeneration. Continuous passive motion had a beneficial biologic effect on the healing of full thickness defects in articular cartilage.(3) III.3. PULMONARY SYSTEM CHANGES IN IMMOBILIZATION III.3.1. Decreased Ventilation Immobilized supine patients find it difficult to accomplish a full inspiration because the strength of their respiratory muscles are also affected. Deconditioning of respiratory muscles, a restrictive impairment, overall decrease muscle strength and failure to fully expand the chest wall results in a 25 50 % decrease in respiratory capacity and it compensated by the increase of respiratory rate but the perfusion may not be as effective as in normal patient.(4) III.3.2. Atelectasis and Pneumonia Immobilization can result markedly impaired ability to clear secretions.(4) In the supine patient, mucus secretions accumulate in the dependent segments (i.e. posterior) while the non dependent respiratory segments might be dry and the mucocilliary mechanism becomes ineffective in order to clear the secretions.(5) Secretions then accumulate in the lower part of bronchial tree, blocking airways and eventually causing atelectasis and hypostatic pneumonia.(4) III.4. ENDOCRINE CHANGES WITH IMMOBILIZATION Prolonged bed-rest has significant effects on parameters of endocrine and metabolic function, some of which are related to, or counteracted by physical activity.(7)
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III.4.1. Cortisol secretion One of the major complications of prolonged bedrest is a progressive loss of muscle mass. Known as sarcopaenia, this condition is made worse by changes in the levels of the adrenal glucocorticoid hormones. After physical injury or starvation, the stress hormone cortisol is released. It acts as a natural antiinflammatory and promotes the generation of glucose derivatives from proteins and fat, a process known as gluconeogenesis.(8) When patients are confined to bed, after an injury or a surgical intervention, cortisol secretion increase. This hypercortisolaemia promotes skeletal muscle breakdown and the release of amino acids into the blood.(8) Prolonged bedrest also sensitises skeletal muscles to the catabolic effects of cortisol, further accelerating the rate of muscle atrophy.(8) III.4.2. Metabolic changes It is widely accepted that inactivity and immobility lead to a progressive drop in the metabolic rate. Research has shown that the basal metabolic rate begins to fall after as little as 10 hours of immobility, with a progressive drop in metabolism of around 6.9% after 10-24 hours in bed.(8) These initial drops in basal metabolism are probably related to reduced muscle activity, as thyroid hormones that regulate cellular metabolism do not seem to change much during periods of immobility and bedrest. The metabolic
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rate continues to fall in patients who remain sedentary, probably reflecting the progressive decline in lean muscle mass caused by disuse. (8) Interestingly, a reduced metabolism does not usually lead to weight gain, with most patients confined to bed maintaining a fairly stable body weight. It has been speculated that any potential weight gain that may be expected because of reduced basal metabolism is offset by reduced lean muscle mass and consuming fewer calories because appetite is poor. (8) Several studies have shown that, while lean body mass decreases; there is a simultaneous increase in fat storage within the adipose tissues.(8) III.4.5. Glucose intolerance and the insulin response Immobility, or even just a sedentary lifestyle, have been linked to the onset of insulin resistance, impaired glucose tolerance and the subsequent development of type 2 diabetes. The loss of appetite and reduced calorific intake associated with prolonged bed rest can potentially trigger a condition known as starvation diabetes. (8) The number of insulin receptors expressed in skeletal muscles increases in proportion to physical activity. When a person is active and exercising regularly, expression of insulin receptors is high. (8) Immobility and reduced food intake are associated with a reduction in the expression of insulin receptors in the skeletal muscles. When patients confined to
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bed eat carbohydrate-rich meals, the sensitivity of the skeletal muscles to the effects of insulin is much lower, resulting in lower glucose uptake and a higher blood glucose concentration. The reduced sensitivity of skeletal muscles to the effects of insulin typically results in overproduction and secretion of insulin by the pancreatic islets, leading to hyperinsulinaemia. (8) III.4.6. Renin-angiotensin-aldosterone cascade The renin-angiotensin-aldosterone cascade plays a key part in the longterm control of blood pressure. When blood pressure drops, the kidneys release the enzyme renin, which catalyses the conversion of the plasma protein angiotensinogen into angiotensin I. Angiotensin I is rapidly converted into angiotensin II by the angiotensin-converting enzymes (ACE) in the lungs. Angiotensin II is a potent vasoconstrictor, increasing blood pressure and also stimulating the adrenal glands to release the hormone aldosterone. Aldosterone increases sodium reabsorption in the kidney, increasing blood sodium levels, blood volume and pressure. (8) In those confined to bed, plasma volume falls significantly, largely as a result of increased urine output. This loss of blood volume, together with sodium loss during diuresis, initiates the renin-angiotensin-aldosterone cascade, which can be seen in increased plasma renin activity and increased plasma aldosterone levels. This hyperaldosteronism, seen during prolonged bedrest, stimulates the kidneys to reabsorb greater amounts of sodium, helping to maintain blood volume and arterial pressure. (8)
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III.4.7. Mineral and electrolyte concentrations The diuresis associated with long periods of bedrest has been shown to promote the loss of nitrogen, sodium, potassium, zinc, phosphorus, sulphur and magnesium. (8) Inactivity results in loss of nitrogen from the whole body. Average nitrogen loss through the urine could reach 2 gr/day. This nitrogen loss is due to an increase in protein catabolism and a concurrent decrease in protein synthesis. Nitrogen loss peaks during second week of immobilization. A negative nitrogen balance might be accentuated by starvation, trauma, infection, or inflammation and reach up to 12 gr/day. (4) Sodium loss occurs rapidly in the early stages of bedrest, primarily due to reductions in the level of anti-diuretic hormone, which trigger increased urine output and lead to a drop in total body sodium.(8) This sodium loss can be progressive due to increased aldosterone secretion. Immobilized patient lose calcium because of the rate of bone formation falls below the rate of bone mineral absorption or demineralization. (4) III.5. EFFECTS OF BED REST ON THE NEUROLOGICAL SYSTEM Patients confined to bed in hospital often experience a reduction in environmental stimuli because of severely limited opportunities for being mobile outside their immediate environment and social interaction.
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This restriction is sometimes referred to as sensory deprivation and it can have a knock-on effect on human behaviour. For example, information to the brain normally comes from two main sources: outside the body and within the body. External information constantly competes with internal information for the individuals attention. When the external environment is relatively quiet, it means increased attention is paid to information coming from within the body. Niven (2006) explained how people who perceive their occupation as boring and dull report more physical symptoms and take more medication than people with interesting, absorbing jobs. Sensory and social deprivations have both been linked to changes in brain neurochemistry which may be associated with altered sensory perception, disorientation and confusion. Major neurotransmitters, including dopamine, noradrenalin and serotonin, are all reported to drop after periods of inactivity. The sensory isolation experienced by people when confined to bed is often associated with restlessness, increased aggression, insomnia and a reduced pain threshold. When bedrest is imposed on patients, it often leads to perceptions of uncertainty and unpredictability, which may, in turn, lead to anxiety. The related mental state of perceived uncontrollability or hopelessness is associated with depression.

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Uncertainty and unpredictability may reflect a lack of information, knowledge or education on patients part about the reasons for and consequences of bedrest. This is why providing information and patient education about bedrest are important anxietyreducing factors of hospital treatment. Patients confined to bed in hospital may become increasingly dependent, often relying on medical staff to help with even trivial tasks. This dependency has previously been referred to as learned helplessness syndrome and it is often reinforced by the wellmeaning support of medical staff. According to the theory of learned helplessness, people exposed to uncontrollable events initially react against the stressor (in this case enforced bedrest) by expressing anger and frustration. On realising that their expressions of anger and frustration are futile, they eventually lapse into a state of apathy marked by feelings of helplessness, decline in cognitive function (such as memory lapses and difficulties with simple problem-solving) and a marked loss in motivation. It is also important for clinicians to keep in mind that perceptions are based on personal experiences and are likely to vary between patients. This explains why patients who experience similar conditions, such as a long period of bedrest, sometimes react in very different ways. It is also worth remembering that anxiety and depression are normal and reversible responses to stressful situations but that they can lead to serious disabling effects when experienced in intense or prolonged situations.
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The complications associated with psychosocial deprivation can be partly alleviated by encouraging social interaction, exercise and early mobility .(8) III.6. EFFECTS OF BED REST ON THE GASTROINTESTINAL SYTEM Bedrest is often associated with a reduced sense of taste, smell and a loss of appetite. The resulting drop in food intake leads to progressive disuse of the gastrointestinal tract. This can have a major impact on gut structure and function, including atrophy of the mucosal lining and shrinkage of glandular structures. (8) Swallowing is more difficult for people confined to bed and it has been shown that non-viscous substances pass through the oesophagus more slowly when the body is supine. It also takes longer for food to pass through the stomach 66% more slowly in recumbent patients than in upright ones. (8) Increased transit times slow the movement of faeces through the colon and rectum, increasing water reabsorption(8). As a result, stools progressively harden causing constipation which is a common problem in immobilized patient.(4) Decreased perstaltis and constrictive sphincters also takes a part in causing constipation in patien with immobilization.(4) Constipation is often associated with faecal impaction, which, if severe, may need mechanical intervention for removal.(8) In an upright person, gravity causes stools within the rectum to exert pressure on the anal sphincter, but this effect of gravity is negated in supine patients, reducing the urge to defecate. If constipation becomes chronic, the build-up of faecal material can exert significant pressure on the wall of the colon, increasing the chance of diverticuli. (8)
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The risk of constipation can be reduced by ensuring that patients get enough dietary fibre, which should help to speed up gut transit times. Patients should also be encouraged to take regular drinks of fresh water, which will be soaked up by fibre within the gut, increasing faecal bulk and softening the stools. During bedrest, gastric bicarbonate secretion may also decrease, increasing acidity within the stomach. When patients are in the supine position, these gastric secretions can collect and press against the lower oesophageal (cardiac) sphincter, causing irritation. Patients confined to bed can experience symptoms associated with gastro-oesophageal reflux disease (GORD), such as regurgitation and heartburn.(8) III.7. EFFECTS OF BED REST ON THE GENITOURINARY SYSTEM III.7.1. Reproductive system In both men and women, prolonged bedrest is associated with falling levels of circulating sex hormones. Lack of physical activity in men reduces both the level of circulating androgens (testosterone and testosterone-like hormones) and

spermatogenesis. Regular physical activity is linked to a healthy libido in both men and women.(8) In women it has been shown that an active sex life is associated with a stable and regular menstrual cycle. Conversely, prolonged bedrest in women can lead to significant disruption to the menstrual cycle. A recent study revealed a general lengthening of the menstrual cycle during bedrest, potentially due to a delay in ovulation because of changes in secretion of luteinizing hormone.(8) III.7.2. Urinary System
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III.7.2.1. Urine distribution In the upright position, gravity plays a major role in draining urine away from the kidneys through the ureters to the bladder. In the supine position, urine is still transported from the kidneys into the bladder by peristaltic waves generated within the walls of the ureters. (8) However, the renal calices rely entirely on gravity to drain fully and, when the body is in a recumbent position, urine collects in the lower portions of the renal calices, where it may form small static pools. (8) III.7.2.2. Urinary retention In the upright position, urine collects in the lower portion of the bladder under the influence of gravity. As the bladder fills, pressure is exerted on the bladder wall, neck and urinary sphincter, stimulating the urge to urinate. In the supine position, the effects of gravity are negated and the urge to urinate is greatly reduced. (8) Similarly, in an upright body, gravity causes the internal abdominal organs to press downwards and exert pressure on the bladder. In those confined to bed, the abdominal organs undergo a shift towards the thorax and the pressure exerted on the bladder is reduced. This can significantly decrease the urge to urinate even when the bladder is full. (8)

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It is often difficult to completely empty the bladder into a bedpan or urine bottle when in the supine position. Patients often feel uncomfortable and embarrassed about having to use bedpans, further increasing the chances of urine retention. (8) An over-distended bladder stretches the smooth muscle layer within the bladder wall and, over a period of time, the stretch receptors (which monitor bladder filling) can lose sensitivity, reducing the urge to urinate. (8) III.7.2.3. Renal calculi and urinary tract infections Prolonged bedrest also increases the risk of precipitation and crystalisation of urinary solutes, which can lead to renal calculi (kidney stones). (8) One of the major detrimental effects of prolonged bedrest is a gradual demineralisation of bone tissue. The major minerals lost from bones are ionic calcium and phosphate, which accumulate in the blood and are subsequently excreted in the urine and faeces. Excess calcium in the glomerular filtrate greatly increases the chances of renal calculi forming in the static urine pools within the renal calices. (8) Urine retention and stasis encourage the growth of urea-splitting bacteria such as Proteus sp. These organisms can work their way up through the urinary tract, and increase the pH of the urine to make it more alkaline,

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encouraging the precipitation of calcium and contributing further to the formation of renal calculi.(8) Research suggests the chances of kidney stones can be reduced by light bed exercises and by using bisphosphonate medications.(8) III.8. EFFECTS OF BED REST ON THE SKIN III.8.1. Pressure Sores Pressure sores or decubitus ulcers are localized areas of cellular necrosis. They are usually found over bony prominences subjected to external pressure for prolonged periods(4) of immobilization. Patients at particular risk for pressure sores are those who are comatose, obese, or have burns or ill fitting casts. Patients older than age 70 have more than 70% of all pressure sores. The longer the duration and the greater the magnitude of pressure, the greater chance of necrosis. The complications of grade 3 and 4 pressure sores can be life threatening. However, the most common problem is infection. III.8.2. Dependent Edema Dependent edema can predispose to cellulitis. Preventive measures include adequate mobilization and elevation, use of elastic stockings or gloves, pressure gradient compression and massage.(5) III.8.3. Subcutaneous Bursitis

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Subcutaneous bursitis occurs when there is excessive pressure on the bursae (usually prepatellar or elbow bursae). It can be prevented by removal of aggravating pressure on the bursae. Treatment measures include use of non steroidal anti inflammatory drugs, percutaneus drainage, corticosteroid injections, and surgery in refractory cases.(5)

IV. CONCLUSION From the available research, it is clear that prolonged bed rest has adverse physiological effects on the most systems of human body. This deconditioning can be explained independent of disease or disorder. Many of the negative effects begin within days of confinement, but their consequences can last much longer. It is important for clinicians to recognize these deleterious effects, and to limit immobilization as much as possible. Furthermore, it is important to realize that early ambulation and physical activity may help to limit the deconditioning effects of immobilization.

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V. REFERENCES
1. Stuempfle, KJ, Drury, DG. The Physiological Consequences of Bed Rest.

JEPonline 2007;10(3):32-41.
2. Allen C, Glasziou P and Del Mar C. Bed rest: a potentially harmful treatment

needing more careful evaluation. Lancet 1999;354:1229-1233.

3. Teasel, R, Dittmer, DK. Complications of immobilization and bed rest. Part

1: Musculoskeletal and cardiovascular complications. Can Fam Physician. 1993 June; 39: 1428-32, 1435-7.

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4. Teasel, R, Dittmer, DK. Complications of immobilization and bed rest. Part

2: Other complications. Can Fam Physician. 2007 Mar 31; 39: 1440-2, 1445-6.
5. Tan, Jackson, T. Practical Manual of Physical Medicine and Rehabilitation 2nd

Edition. Saint Louis, MO. 2006.

6. Bloomfield S. Changes in musculoskeletal structure and function with prolonged

bed rest. Med. Sci. Sports Exerc. 1997;29:197-206.

7. DL, Belayy, et al. The effects of bed rest and counter measure exercise on the

endocrine system in male adults - evidence for immobilization induced reduction in SHBG levels. J Endocrinol Invest. 2011 Mar 21. 8. Knight, J. et al Effects of bedrest 2: gastrointestinal, endocrine, renal, reproductive and nervous systems. Nursing Times. 2009; 105; 22, early online publication.

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