Continence Coach: Understanding the Underactive Bladder
Individuals facing bladder contractility problems may experience symptoms such as urinary frequency that ironically mimic overactive bladder. Actually, the issue is an underactive bladder or underactive detrusor muscle. Detrusor underactivity (DU) is defined by the International Continence Society (ICS)1 as a contraction of reduced strength and/or duration resulting in prolonged bladder emptying and/or failure to achieve complete bladder emptying within a normal time span.
Very little is understood about the pathophysiology or epidemiology and prevalence of the condition. The aging process can contribute to a gradual weakening of detrusor muscles, causing decline in contractility, not unlike an elastic band that eventually loses its “spring” after being stretched and rebounded time and time again. Other operative factors also may cause a bladder to lose its full ability to contract and empty itself of urine when the brain is alerted that the bladder is more than half full and signals the bladder to take action. In essence, there are two possible causes: myogenic — ie, referring to a contraction initiated by the myocyte cells in the muscle itself — and neurogenic, referring to a contraction originating from a stimulus in the nervous system such as nerve innervation.
No effective pharmacologic agent is available to boost the bladder’s ability to contract as desired. Symptom management is frustrating at best for the patient, who is usually left with little hope. The condition is most often coded diagnostically as 788.20 (“unspecified retention of urine”), 788.21 (“incomplete bladder emptying”), or 788.29 (“other specified retention of urine”), or with even greater vagueness using ICD-9-CM 596.59, where it is defined as “other functional disorder of the bladder.” Such fumbling with explanations illustrates the rudimentary nature of our collective understanding of the condition.
In 2010, a small group of interested ICS members met in Bristol, England2 to discuss what is known about the condition with the goal of framing future research to help providers do a better job of assessing and treating DU. The paper presented at ICS the following year recommended developing novel animal models and new noninvasive tests to improve assessment. The clinicians advocated use of existing evaluation algorithms utilizing standard testing to refine diagnosis. The paper also called for epidemiological studies to quantify the magnitude of the problem to support industry’s investment in the development of new treatment and curative modalities. In the interim, nurses and physicians are well-served by becoming more knowledgeable about how to recognize and definitively diagnose the symptoms, the multifactorial causes of DU, and what strategies may be offered to the patient and family members affected by the symptoms.
As men age, their prostate gland naturally enlarges. At some juncture, men may notice it takes time to initiate the voiding stream, because the force of their urine flow weakens and urination frequency increases because the bladder fails to fully empty. Although an enlarged prostate may appear to be the obvious culprit, 25% to 30% of men with decreased flow are clinically found not to be obstructed.3 Instead, elevated postvoid residual (PVR) urine has been shown to be more indicative of an underactive bladder failing to fully contract than of outlet obstruction.4 Thus, it could be that of the 17 million men who researchers estimate to have bladder outlet obstruction, as many as 5.1 million actually have DU. In fact, one study found that 50% of unobstructed men with lower urinary tract symptoms had an “elevated” PVR, while up to one fourth of severely obstructed men did not.3 Meanwhile, women also may present with symptoms of a weak stream and PVR urine in the case of pelvic organ prolapse or pelvic mass. However, like men, obstruction may not be the causal factor, even in the presence of physiological diagnoses. Of men and women >60 years of age living independently in the community, 22.1% and 10.8%, respectively, report difficulties with bladder emptying.5
The detrusor muscle itself may be normal, but the nerves supplying messages to and from the brain to the bladder may not be normal, as in the case of a neurological disease such as multiple sclerosis (MS). Under normal circumstances, the kidneys filter the body’s wastes and produce urine, which in turn is sent to the bladder for storage. The brain is alerted subconsciously and subsequently consciously that the bladder is full and needs emptying. When appropriate, the brain signals the bladder to contract and simultaneously tells the other pelvic muscles to relax to permit the release of urine from the body’s outlet. In persons with MS, for example, messages between the brain and pelvic region are interrupted due to nerve fiber damage caused by the disease, causing a slowed or erratic response to the need for voiding. Sphincter contractions are ill-timed and may coincide with contraction of the bladder, known as dyssynergia. Muscles, including the bladder itself, become weakened, causing chronic urine retention. Nerve damage from diabetes mellitus, radiotherapy, cerebral stroke, pelvic surgery, or spinal cord injuries at or below the sacral voiding center can similarly result in urine retention and an underactive bladder.2
The aging process can exacerbate circumstances; an older bladder can lose its ability to hold the same volume of urine as a younger bladder. The muscle itself may have weakened, like all of the body’s muscles, and thus be less able to contract to squeeze out the urine it is holding. Much remains to be unearthed regarding how the bladder is precisely affected by the aging process, including decreased bladder sensations, leaving the provider with a complex picture.
Urodynamic studies assessing the filling, storage, and voiding phases are the most definitive tests and thus the gold standard to best determine the etiology of voiding dysfunction and lower urinary tract symptoms.6 Still, the sophisticated algorithms driving the quantification of study results were developed in men and have been validated only in men. Simple tests such as urinary flow rate and PVR volume as indicators of issues fall short in the scope of assessment and accuracy of diagnosis that urodynamic studies offer.
There is no known means of curing or reversing subnormal contractility of the detrusor muscle. No Food and Drug Administration (FDA)-approved medications for symptoms of substandard bladder contractility and urine retention are available. Clinicians have attempted to manage a slow urine stream by addressing flow with offlabel use of adrenoreceptor antagonists such as tamsulosin (Flomax®, Astellas Pharma, Japan) and doxazosin (Cardura XL®, Pfizer, Collegeville, PA). They work by relaxing the smooth muscle of the bladder neck. These can help, particularly in the case of dyssynergia. To aid contraction of the bladder specifically, bethanechol (Urecholine®, Merck Frosst, Canada) has been prescribed,7 although no support for its effectiveness appears in the literature. In general, analyses demonstrate little beneficial effects and unfavorable side effects from these drugs.
In the last decade or so, minimally invasive medical devices have been approved by the FDA to help regulate erratic neurological signals, including office-based percutaneous tibial nerve stimulation (Urgent® PC, Uroplasty, Minnetonka, MN) treatments and a sacral neuromodulation implant (Interstim®, medtronic, Minneapolis, MN). Interstim has labeling approved by the FDA directing its use for treating urinary retention, in addition to approved use for urge incontinence and significant symptoms of urgency-frequency.
Management: Living with Symptoms
One of the biggest challenges facing individuals with DU is the risk of chronic urinary tract infections, either because of the residual urine that can leak into the urethral channel to the body’s outlet and pick up bacteria or from the introduction of bacteria from the use of catheters, including suprapubic catheters, for managing a bladder that has lost virtually all contractility. Nurses must be particularly helpful in coaching patients on this front, relying on resources such as www.nafc.org on topics such as: 1) bathroom behavior, 2) the use of cranberry products and water hydration, 3) proper hygiene in caring for the urethral area, 4) ensuring lubrication to the vagina and urinating immediately after sexual intimacy, 5) using vaginal estrogen (if female), and 6) proper cleansing and storing of catheters, especially with indwelling suprapubic catheters. This greatly reduces the risk of infection.
As a specialty nurse who understands both the complexity and the importance of quality continence care, your job is to identify patients who need to have a definitive diagnosis so intervention can be properly directed.
Dr. Muller is the Executive Director, National Association For Continence (NAFC). The NAFC is a national, private, nonprofit organization dedicated to improving the quality of life of people with incontinence. The NAFC’s purpose is to be the leading source for public education and advocacy about the causes, prevention, diagnosis, treatments, and management alternatives for incontinence. This article was not subject to the Ostomy Wound Managment peer-review process.