changes in human body structure and function due to prolonged immobilization
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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 ………………………………………………………………………….
2
I. ABSTRACT
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)
3
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.
4
III. DISCUSSION
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 ( O2max) commonly is used to assess
cardiovascular function in both health and disease. Bed rest decreases O2max, and
the extent of the loss depends on the length of the bed rest, with O2max decreasing
5
approximately 0.9% per day over 30 days of bed rest. The decrease in O2max
during bed rest appears to be independent of gender and age. However, more fit
individuals may experience a greater absolute decrease in O2max compared to less
fit individuals. (1)
The decrease in O2max following bed rest can be attributed to both cardiac and
peripheral effects, although cardiac effects predominate (Figure 1).
Figure 1. Cardiovascular mechanisms affecting O2max following bed rest.
(Abbreviations: NE, norepinephrine; RBC, red blood cells). Figure modified from
Convertino (1).
6
A 26% decrease in 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 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 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).
Although decreased stroke volume and cardiac output are the primary causes of
the diminished O2max following bed rest, peripheral factors may also contribute
(Figure 1). Prolonged bed rest resulted in a 9% decrease in red blood cell mass,
7
compromising the oxygen-carrying capacity of the blood, and perhaps contributing to
the reduced O2max(18). Furthermore, decreased capillarization and muscle blood
flow following bed rest also may diminish O2max (1).
In addition to reduced 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
8
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)
As would be expected, the decrease in muscle mass following bed rest
is accompanied by a decrease in muscle strength(1) (Table 1).
9
Table 1. Change in maximal muscle strength following bed rest.
Number of Days Muscle Group % Change Reference
30 Knee flexors
Knee extensors
-6
-19
Dudley
35 Plantar flexors -26 LeBlanc
35 Plantar flexors
Dorsi flexors
Knee flexors
Knee extensors
Elbow flexors
-25
-8
-8
-19
-7
Gogia
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
severe orthopedic and neurologic disorders and for persons who are
voluntarily inactive (many of the elderly). (3)
10
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
subnormal muscle and bone mass, especially the elderly, are likely to incur
additional risk of injury upon reambulation. (6)
11
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.
III.2.3. Disuse osteoporosis
12
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
degeneration. Continuous passive motion had a beneficial biologic effect on
the healing of full thickness defects in articular cartilage.(3)
13
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)
III.4.1. Cortisol secretion
14
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
15
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
16
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
17
kidneys to reabsorb greater amounts of sodium, helping to maintain blood volume
and arterial pressure. (8)
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
18
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.
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.
19
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.
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.
20
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.
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)
21
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)
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
22
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
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)
23
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)
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
24
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,
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
25
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
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.
26
Furthermore, it is important to realize that early ambulation and physical activity
may help to limit the deconditioning effects of immobilization.
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.
27
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.
4. Teasel, R, Dittmer, DK. Complications of immobilization and bed rest. Part
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