Urinary incontinence is when the normal process of storing and passing urine is disrupted. This can happen for several reasons. Certain factors may also increase your chance of developing urinary incontinence. Some of the possible causes lead to short-term urinary incontinence, while others may cause a long-term problem. If the cause can be treated, this may cure your incontinence. Stress incontinence is when the pressure inside your bladder as it fills with urine becomes greater than the strength of your urethra to stay closed. Your urethra is the tube that urine passes through to leave the body. Any sudden extra pressure on your bladder, such as laughing or sneezing, can cause urine to leak out of your urethra if you have stress incontinence. Your urethra may not be able to stay closed if the muscles in your pelvis (pelvic floor muscles) are weak or damaged, or if your urethral sphincter – the ring of muscle that keeps the urethra closed – is damaged. Problems with these muscles may be caused by: The urgent and frequent need to pass urine can be caused by a problem with the detrusor muscles in the walls of your bladder. The detrusor muscles relax to allow the bladder to fill with urine, then contract when you go to the toilet to let the urine out. Sometimes the detrusor muscles contract too often, creating an urgent need to go to the toilet. This is known as having an overactive bladder. The reason your detrusor muscles contract too often may not be clear, but possible causes include:
Overflow incontinence, also called chronic urinary retention, is often caused by a blockage or obstruction affecting your bladder. Your bladder may fill up as usual, but because of an obstruction, you will not be able to empty it completely, even when you try. At the same time, pressure from the urine that's left in your bladder builds up behind the obstruction, causing frequent leaks. Your bladder can be obstructed by: Overflow incontinence may also be caused by your detrusor muscles not fully contracting, which means your bladder does not completely empty when you urinate. As a result, the bladder becomes stretched. Your detrusor muscles may not fully contract if:
Total incontinence is when your bladder cannot store any urine at all. It can mean you either pass large amounts of urine constantly, or you pass urine occasionally with frequent leaking in between. Total incontinence can be caused by:
Some medicines can disrupt the normal process of storing and passing urine or increase the amount of urine you produce. These include: Stopping these medicines, if advised to do so by a doctor, may help resolve your incontinence. In addition to common causes, some things can increase your risk of developing urinary incontinence without directly being the cause of the problem. These are known as risk factors. Some of the main risk factors for urinary incontinence include:
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Twenty-four-hour urine volume was studied in 80 determinations from 12 patients with chronic renal failure (creatinine clearances between 7.1 and 38.9 L/d) hospitalized on a metabolic ward. Urine volume ranged from 0.91 to 4.51 L/d. Various components of urine that might affect urine output, ie, osmolar excretion, sodium excretion, urea nitrogen excretion, free water clearance, and potassium excretion, were correlated with urine volume to determine their relative effects. Total osmolar excretion correlated highly with urine output (r = .92, P < .001), while correlation with free water clearance was weak. Of the three osmotic components, total urea nitrogen excretion correlated best with urine volume (r = .86, P < .001), while the correlation with sodium excretion was less pronounced (r = .75, P < .001). The relatively greater impact of urea excretion on urine volume was confirmed by multiple regression analysis. However, total cation excretion (sodium plus potassium) gave nearly as good a regression with urine volume (r = .83, P < .001). Our findings confirm that total osmolar excretion is a major determinant of urine volume in chronic renal failure and suggest that urea excretion may play the most important role in determining output.
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Supported in part by a grant from the National Institutes of Health (AM 16281). DOI: https://doi.org/10.1016/S0272-6386(87)80179-8 © 1987 National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved. |