Exploring what happens to the gastrointestinal, endocrine, renal, reproductive and nervous systems, and processes in the body when a person is confined to bed
This article has been updated
The evidence in this article is no longer current
This article is the second in a series discussing the effects of long periods of bedrest on the body. It explores what happens to the gastrointestinal, endocrine and renal systems when a person is confined to bed. The effects on the reproductive and nervous systems are also covered. Part 1 examined the effects on the cardiovascular, respiratory and haematological systems.
Citation: Knight J et al (2009) Effects of bedrest 2: gastrointestinal, endocrine, renal, reproductive and nervous systems. Nursing Times; 105; 22, early online publication.
Authors: John Knight, Yamni Nigam and Aled Jones are lecturers, School of Health Science, Swansea University.
- This article has been double-blind peer-reviewed
The first article in this series examined the adverse effects of immobility and bedrest on the cardiovascular, respiratory and haematological systems. Because the major role of these systems is to deliver oxygen and nutrients to all areas of the body, the detrimental effects of bedrest have a negative impact on every organ system. This article explores how immobility specifically affects digestion, elimination and reproduction, and can interfere with the activities of the endocrine and nervous systems.
Bedrest is often associated with a reduced sense of taste, smell and a loss of appetite (Rousseau, 1993; Bortz, 1984). The resulting drop in food intake leads to progressive disuse of the gastrointestinal (GI) tract. This can have a major impact on gut structure and function, including atrophy of the mucosal lining and shrinkage of glandular structures (Bortz, 1984).
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 (Kaplan, 2005). It also takes longer for food to pass through the stomach – 66% more slowly in recumbent patients than in upright ones (Thomas et al, 2002).
Increased transit times slow the movement of faeces through the colon and rectum, increasing water reabsorption. As a result, stools progressively harden causing constipation, a common problem in patients confined to bed.
Constipation is often associated with faecal impaction, which, if severe, may need mechanical intervention for removal.
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 (Fig 1).
The problem of constipation is particularly troublesome in patients confined to bed receiving opioid-based pain relief medications. Drugs such as morphine dramatically slow down gut motility (Jordan, 2008), exacerbating the effects of immobility.
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 (Bortz, 1984).
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 (Kaplan, 2005), 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.
This can be alleviated by using pillows to prop them up after a meal. This position also encourages the gastric juices to collect in the lower portion of the stomach, reducing the risk of reflux.
Antacid medications can also be given to relieve the sensation of heartburn.
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 (Montague et al, 2005). It acts as a natural anti-inflammatory and promotes the generation of glucose derivatives from proteins and fat, a process known as gluconeogenesis.
When patients are confined to bed, after an injury or a surgical intervention, cortisol secretion increases (Ferrando et al, 1999). This hypercortisolaemia promotes skeletal muscle breakdown and the release of amino acids into the blood.
Prolonged bedrest also sensitises skeletal muscles to the catabolic effects of cortisol, further accelerating the rate of muscle atrophy (Ferrando et al, 1999).
It is widely accepted that inactivity and immobility lead to a progressive drop in the metabolic rate (Withers et al, 1998).
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 (Rousseau, 1993).
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 rate continues to fall in patients who remain sedentary, probably reflecting the progressive decline in lean muscle mass caused by disuse.
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 (Rousseau, 1993).
Several studies have shown that, while lean body mass decreases, there is a simultaneous increase in fat storage within the adipose tissues (Krebs, 1990).
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 (Blanc et al, 2000).
The body’s ability to regulate blood glucose is adversely affected by long periods of bedrest. Studies have shown a progressive development of glucose intolerance that correlates directly to the length of time that patients remain in bed (Takayama, 1974; Rousseau, 1993).
The loss of appetite and reduced calorific intake associated with prolonged bedrest can potentially trigger a condition known as starvation diabetes.
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.
When active people eat a meal rich in carbohydrates, their blood glucose levels will rise, triggering insulin release. Insulin will bind to the abundant receptors within the skeletal muscles, promoting rapid glucose uptake, returning the blood glucose level to within the normal range.
Immobility and reduced food intake are associated with a reduction in the expression of insulin receptors in the skeletal muscles (Rousseau, 1993).
When patients confined to 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 (Blanc et al, 2000).
The problem of glucose intolerance may be helped by encouraging patients to undertake light exercise. This is proven to increase the number of insulin receptors within skeletal muscle (Soman et al, 1979), enhancing the effects of insulin.
The renin-angiotensin-aldosterone cascade plays a key part in the long-term control of blood pressure (Montague et al, 2005).
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.
In those confined to bed, plasma volume falls significantly, largely as a result of increased urine output (see part 1). 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 (Annat et al, 1986; Gharib et al, 1985).
This hyperaldosteronism, seen during prolonged bedrest, stimulates the kidneys to reabsorb greater amounts of sodium, helping to maintain blood volume and arterial pressure.
Mineral and electrolyte concentrations
The diuresis associated with long periods of bedrest has been shown to promote the loss of sodium, potassium, zinc, phosphorus, sulphur and magnesium (Rousseau, 1993).
Sodium loss occurs rapidly in the early stages of bedrest, primarily due to reductions in the level of anti-diuretic hormone (see part 1), which trigger increased urine output and lead to a drop in total body sodium (Rousseau, 1993).
Sodium levels tend to stabilise as hyponatraemia (low blood sodium) and reduced blood volume trigger aldosterone release (see above).
Although increased aldosterone secretion is effective at limiting further sodium losses, at the same time it causes a progressive loss of potassium in the urine (Chobanian et al, 1974).
Plasma calcium levels increase in patients confined to bed, largely because of bone demineralisation associated with immobility (see part 3).
Research has shown that losses in bone density are exacerbated by an increase in the level of parathyroid hormone which is known to stimulate the activity of osteoclasts – specialised cells that break down bone (Montague et al, 2005).
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.
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 (Fig 2).
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 (Montague et al, 2005). In the supine position, the effects of gravity are negated and the urge to urinate is greatly reduced.
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 (see part 1) and the pressure exerted on the bladder is reduced. This can significantly decrease the urge to urinate even when the bladder is full.
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.
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.
The problem of urinary retention can be reduced by encouraging patients to take regular drinks of fresh water and by discouraging the use of bedpans and urine bottles in favour of commodes, or, if possible, regular visits to the toilet.
In patients who are not ambulatory, a catheter may be necessary.
Renal calculi and urinary tract infections
Over-distention of the bladder can cause small cuts or tears to develop in its epithelial lining, providing sites for opportunistic infection.
Prolonged bedrest also increases the risk of precipitation and crystalisation of urinary solutes, which can lead to renal calculi (kidney stones).
One of the major detrimental effects of prolonged bedrest is a gradual demineralisation of bone tissue (see part 3). 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 (Fig 2).
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.
Research suggests the chances of kidney stones can be reduced by light bed exercises and by using bisphosphonate medications (Atsushi et al, 2008).
The effect of immobility on reproductive biology is poorly understood. In both men and women, prolonged bedrest is associated with falling levels of circulating sex hormones (Brown, 2008).
Lack of physical activity in men reduces both the level of circulating androgens (testosterone and testosterone-like hormones) and spermatogenesis (sperm production). Regular physical activity is linked to a healthy libido in both men and women.
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 luteinising hormone (Wade, 2008).
This author speculates that the changes to the menstrual cycle and female sex hormones observed in women confined to bed may contribute to some of the adverse effects of bedrest, including loss of bone mass and reductions in blood volume (Wade, 2008).
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 (Hayes, 2000) 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 deprivation have both been linked to changes in brain neurochemistry which may be associated with altered sensory perception, disorientation and confusion.
Major neurotransmitters, including dopamine, noradrenaline and serotonin, are all reported to drop after periods of inactivity (Norton and Sibbald, 2004).
The sensory isolation experienced by people when confined to bed is often associated with restlessness, increased aggression, insomnia and a reduced pain threshold (Fletcher, 2005; Rousseau, 1993).
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 (Payne and Walker, 2002).
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 and nursing care.
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 (Corcoran, 1991) and it is often reinforced by the well-meaning support of medical staff.
According to the theory of learned helplessness (Seligman, 1975), 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 (Russell, 1999).
It is also important for nurses 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.
The complications associated with psychosocial deprivation can be partly alleviated by encouraging social interaction, exercise and early mobility (Rousseau, 1993).
- Patients confined to bed are prone to gastric reflux and constipation
- They often show a progressive slowing down of metabolic rate and a reduction in insulin sensitivity that may lead to glucose intolerance
- Such patients are prone to urinary retention and have an increased risk of developing urinary tract infections
- Prolonged bedrest often deprives patients of environmental and social stimulation, which may lead to increased anxiety, confusion and depression
Annat, G. et al (1986) Plasma vasopressin, neurophysin, renin and aldosterone during a 4-day head-down bedrest with and without exercise.European Journal of Applied Physiology and Occupational Physiology; 55: 1, 59–63.
Atsushi, O.et al (2008) Risk of renal stone formation induced by long-term bedrest could be decreased by premedication with bisphosphonate and increased by resistive exercise. International Journal of Urology; 15: 7, 630–635.
Blanc, S. et al (2000) Fuel homeostasis during physical inactivity induced by bedrest. The Journal of ClinicalEndocrinology and Metabolism; 85: 6, 2223–2233.
Bortz, W.M. (1984) The disuse syndrome. Western Journal of Medicine; 141: 691–694.
Brown, M. (2008) Skeletal muscle and bone: effect of sex steroids and aging. AdvancedPhysiology Education; 32: 120–126.
Chobanian, A.V. et al (1974) The metabolic and hemodynamic effects of prolonged bedrest in normal subjects.Circulation; 49; 551–559.
Corcoran, P.J. (1991) Use it or lose it – the hazards of bedrest and inactivity. Western Journal of Medicine; 54: 5, 536–538.
Ferrando, A.A. et al (1999) Inactivity amplifies the catabolic response of skeletal muscle to cortisol. The Journalof Clinical Endocrinology and Metabolism; 84: 10, 3515–3521.
Fletcher, K. (2005) Immobility: geriatric self-learning module. MEDSURG Nursing; 14: 1, 35–37.
Gharib, C. et al (1985) Volume regulating hormones (renin, aldosterone, vasopressin and natriuretic factor) during simulated weightlessness. Physiologist; 28: 30–33.
Hayes, N. (2000) Foundations of Psychology. London: Thomson Learning.
Jordan, S. (2008) The Prescription Drug Guide for Nurses. Maidenhead: Open University Press.
Kaplan, R. (2005) Physical Medicine and Rehabilitation Review. Maidenhead: McGraw-Hill Education Europe.
Krebs, J.M. et al (1990) Energy absorption, lean body mass, and total body fat changes during 5 weeks of continuous bed-rest. Aviation, Space and Environmental Medicine; 61: 314–318.
Montague, S.E. et al(2005)Physiology for Nursing Practice. Amsterdam: Elsevier.
Niven, N. (2006) The Psychology of Nursing Care. Basingstoke: Palgrave Macmillan.
Norton, L., Sibbald, G. (2004) Is bedrest an effective treatment modality for pressure ulcers? Ostomy WoundManagement; 50: 10, 40–51.
Payne, S., Walker, J. (2002) Psychology for Nurses and the Caring Professions. Buckingham: Open University Press.
Rousseau, P. (1993) Immobility in the aged.Archives of Family Medicine; 2: 2, 169–177.
Russell, G. (1999) Essential Psychology for Nurses and Other Health Professionals. London: Routledge.
Seligman, M. (1975) Helplessness: On Depression. San Francisco, Freeman.
Soman, V.R. et al (1979) Increased insulin sensitivity and insulin binding to monocytes after physical training. New England Journal of Medicine; 301: 1200–1204.
Takayama, H. et al (1974) The effect of physical exercise and prolonged bedrest on carbohydrate, lipid and amino acid metabolism. Journal of Clinical Pathology; 22: 126–136.
Thomas, D.C. et al (2002) Rehabilitation of the patient with chronic critical illness. Critical Care Clinics; 18: 3, 695–715.
Wade, C. (2008) 60-days of head-down bed rest increases the incidence of menstrual cycle disruption. 37th COSPAR Scientific Assembly. 13–20 July 2008, Montréal, Canada; 3371.
Withers, R.T. et al (1998) Energy metabolism in sedentary and active 49–to–70–yr-old women. Journal of Appliedphysiology; 84: 4, 1333–1340.