An algorithm can help detect and manage this common problem.
Elim Shih, MD
Center for Specialized Women’s Health, Cleveland Clinic
Heather Hirsch, MD
The Ohio State University Wexner Medical Center, Columbus
Holly L. Thacker, MD, FACP, NCMP, CCD
Director, Center for Specialized Women’s Health, Department of Obstetrics and Gynecology, Cleveland Clinic; Professor, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH
Address: Holly Thacker, MD, Center for Specialized Women’s Health, Cleveland Clinic, 9500 Euclid Avenue, A10, Cleveland, OH 44195; email@example.com
Obesity has become a national epidemic, with more than 68% of Americans found to be overweight or obese according to the National Institutes of Health.21
Several studies found obesity to be an independent risk factor for urinary incontinence. As early as 1946, the British Birth Cohort study found that women ages 48 through 54 who were obese earlier in life had a higher risk of urinary incontinence in middle age, and those who were obese by age 20 were more likely to report severe incontinence.22 Likewise, the Nurses’ Health Study showed that women with a body mass index (BMI) more than 30 kg/m2 had 3.1 times the risk of severe incontinence compared with women with a normal BMI. Also, the Study of Women’s Health Across the Nation and the Leicestershire Medical Research Council (MRC) incontinence study both showed that a higher BMI and weight gain are strongly correlated with urinary incontinence.23,24
Increased intra-abdominal pressure may be the causative mechanism of stress urinary incontinence in obesity. The Korean National Health and Nutrition Examination Survey showed that central adiposity correlated with urgency incontinence.25,26
The MRC study was one of the largest to evaluate the effect of diet on urinary symptoms. Consuming a diet dense in vegetables, bread, and chicken was found to reduce the risk of urinary incontinence, while carbonated drinks were associated with a higher risk.25 These studies and others may point to reducing calories, and thus BMI, as a conservative treatment for urinary incontinence.
Newer data show bariatric surgery is associated with a strong reduction in urinary incontinence, demonstrated in a study that followed patients for 3 years after surgery.27 This encouraging result is but one of several positive health outcomes from bariatric surgery.
The ACP recommends both weight loss and exercise for overweight women with urinary incontinence, and grades this as strong with moderate-quality evidence.
The bladder neck is rich with sympathetic alpha-adrenergic receptors, and the bladder dome is dense with parasympathetic muscarinic receptors and sympathetic beta-adrenergic receptors. When the parasympathetic system is stimulated, the muscarinic receptors are activated, causing detrusor contraction and ultimately bladder emptying.
Agonism of beta-alpha adrenergic receptors and inhibition of parasympathetic receptors are both strategies of drug treatment of urinary incontinence.
Anticholinergic medications function by blocking the muscarinic receptor, thereby inhibiting detrusor contraction.
Six oral anticholinergic medications are available: oxybutynin, tolterodine, fesoterodine, solifenacin, trospium, and darifenacin. These drugs have about the same effectiveness in treating urgency urinary incontinence, as measured by achieving continence and improving quality of life.28 Given their similarity in effectiveness, the choice of agent typically relies on the side-effect profile. Extended-release formulations have a more favorable side-effect profile, with fewer cases of dry mouth compared with immediate-release formulations.29
Overall, however, the benefit of these medications is small, with fewer than 200 patients achieving continence per 1,000 treated.28
Other limitations of these medications include their adverse effects and contraindications, and patients’ poor adherence to therapy. The most commonly reported adverse effect is dry mouth, but other common side effects include constipation, abdominal pain, dyspepsia, fatigue, dry eye, and dry skin. Transdermal oxybutynin therapy has been associated with fewer anticholinergic side effects than oral therapy.30
Contraindications to these medications include gastric retention, urinary retention, and angle-closure glaucoma.
Long-term adherence to anticholinergics is low, reported between 14% to 35% after 12 months, with the highest rates of adherence with solifenacin.31 The most commonly cited reason for discontinuation is lack of effect.32
Caution is urged when considering starting anticholinergic medications in older adults because of the central nervous system side effects, including drowsiness, hallucinations, cognitive impairment, and dementia. After 3 weeks, oxybutynin caused a memory decline as measured by delayed recall that was comparable to the decline seen over 10 years in normal aging.33 There is evidence suggesting trospium may cause less cognitive impairment, and therefore may be a better option for older patients.34
Activation of beta-3 adrenergic receptors through the sympathetic nervous system relaxes the detrusor muscle, allowing the bladder to store urine.
Mirabegron is a selective beta-3 adrenoreceptor agonist that effectively relaxes the bladder and increases bladder capacity. It improves continence, treatment satisfaction, and quality of life.35,36 There are fewer reports of dry mouth and constipation with this drug than with the anticholinergics; however, beta-3 adrenoreceptor agonists may be associated with greater risk of hypertension, nasopharyngitis, headache, and urinary tract infection.37
Duloxetine, an antidepressant, blocks the reuptake of both serotonin and norepinephrine. Consequently, it decreases parasympathetic activity and increases sympathetic and somatic activity in the urinary system.38 While urine is stored, this cascade of neural activity is thought to collectively increase pudendal nerve activity and improve closure of the urethra.
Although duloxetine is approved to treat stress urinary incontinence in Europe, this is an off-label use in the United States.
A meta-analysis39 found that duloxetine improved quality of life in patients with stress urinary incontinence and that subjective cure rates were 10.8% with duloxetine vs 7.7% with placebo (P = .04). However the rate of adverse events is high, with nausea most common. Given its modest benefit and high rate of side effects, physicians may consider starting duloxetine only if there are psychiatric comorbidities such as depression, anxiety, or fibromyalgia.
The ACP recommends against systemic pharmacologic therapy for stress urinary incontinence. For urgency urinary incontinence, pharmacologic therapy is recommended if bladder training fails, and should be individualized based on the patient’s preference and medical comorbidities and the drug’s tolerability, cost, and ease of use.
In 2014, the North American Menopause Society recommended replacing the term “vulvovaginal atrophy” with the term genitourinary syndrome of menopause, which better encompasses the postmenopausal changes to the female genital system.40
Estrogen therapy is commercially available in both systemic and local preparations. The effect of exogenous estrogen on urinary incontinence may depend on whether it is given locally or systemically.
A systematic review41 definitively concluded that all commercially prepared local vaginal estrogen preparations can effectively relieve the genitourinary syndrome of menopause, including not only the common complaints of dryness, burning, and irritation but also urinary complaints of frequency, urgency, and urgency urinary incontinence.41 Additionally, the estradiol vaginal ring for vaginal atrophy (Estring) may have dual effects, functioning like an incontinence pessary by supporting the bladder neck while simultaneously providing local estrogen to the atrophied vaginal tissue.
However, in the Women’s Health Initiative,42 continent women who received either systemic estrogen therapy alone or systemic estrogen combined with progestin actually had a higher risk of developing urinary incontinence, and those already experiencing incontinence developed a worsening of their symptoms on systemic hormone therapy. The mechanism by which systemic hormone therapy causes urinary incontinence is unclear; however, previous studies showed that hormone therapy leads to a reduction in periurethral collagen and increased bladder contractility.43,44
An algorithm can help detect and manage this common problem.
In many cases it can be managed through exercise, lifestyle changes, pelvic stimulation, and sometimes medicine or other treatments.