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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)

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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

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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).

 O2max) commonly is used to assess


Maximal oxygen consumption ( V

 O2max, and
cardiovascular function in both health and disease. Bed rest decreases V

 O2max decreasing
the extent of the loss depends on the length of the bed rest, with V

 O2max
approximately 0.9% per day over 30 days of bed rest. The decrease in V

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

fit individuals. (1)

 O2max following bed rest can be attributed to both cardiac and


The decrease in V

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

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Figure 1.  O2max following bed rest.
Cardiovascular mechanisms affecting V

(Abbreviations: NE, norepinephrine; RBC, red blood cells). Figure modified from

Convertino (1).

 O2max in five men after 20 days of bed rest was


A 26% decrease in V

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

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

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 β

 O2max
adrenergic receptors. The primary cause of decreased cardiac output and V

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 β

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

 O2max following bed rest, peripheral factors may also contribute


the diminished V

(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

 O2max(18). Furthermore, decreased capillarization and muscle blood


the reduced V

 O2max (1).
flow following bed rest also may diminish V

 O2max, bed rest results in additional complications with


In addition to reduced V

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.

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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 Muscle Group % Change Reference

30 Knee flexors -6 Dudley

Knee extensors -19

35 Plantar flexors -26 LeBlanc

35 Plantar flexors -25 Gogia

Dorsi flexors -8

Knee flexors -8

Knee extensors -19

Elbow flexors -7

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 patient’s 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 Bone Loss

First Rapid bone loss


Second Beginning at 12 weeks, slower but more
prolonged bone loss
Third 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 anti-

inflammatory 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 long-

term 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 individual’s 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 anxiety-

reducing 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 well-

meaning 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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