A 30-year-old woman presented to her physician with complaints of vaginal discharge that persisted for a year and required use of two to three pads per day. What was the cause?
DB, a 30-year-old woman, presented to her physician with complaints of vaginal discharge that persisted for a year and required use of two to three pads per day. Wet prep and urine culture were negative. At her next visit, she was evaluated for vesicovaginal fistula, but instillation of 100 mL of methylene blue through a Foley catheter was negative. The physician suspected urinary incontinence and referred the patient to a urogynecologist.
When DB presented to our office, she complained of urine leakage while coughingevidence of stress incontinenceand frequency, urgency, and incomplete emptying, which suggested urge incontinence. Her physical exam was unremarkable, with a nonmobile urethra, normal neurologic examination, and negative supine stress test. To rule out a persistent vaginal discharge, we had the patient do a pyridium pad test at home, and in fact, she did have daily urinary incontinence, which we attempted to treat with timed voiding and vaginal cones. Several months later, however, when DB presented with worsening urge incontinence, we placed her on anticholinergic medication. Scheduling conflicts prevented her from returning for several months, but when she did return, she again complained about increasing urge incontinence. We found hematuria but urine culture was negative.
To definitively diagnose the urinary incontinence, we had DB return for urodynamic testing. Cystometrography revealed a first sensation at 59 mL, urgency at 121 mL, and strong desire at 145 mL. At 151 mL, we observed a detrusor contraction with strength of 30 cm H2O. Because of DB's persistent hematuria, we scheduled a cystoscopy in the office, which uncovered a 1 x 2 x 0.5-cm bladder calculi (Figure 1). We attempted to extract the stone in the office, but stopped the procedure because of patient discomfort.
DB subsequently underwent outpatient operative cystoscopy under general anesthesia for removal of the "stone," which turned out to be a segment of the balloon from a Foley catheter (Figure 2)!
Six weeks later, at her follow-up appointment, DB reported that her symptoms had dramatically improved, and over the next several months, the condition resolved. At 1 year follow-up, she had minimal stress urinary incontinence (SUI) with coughing, which was not bothersome, and no further complaints of urge incontinence.
Urge incontinence refers to involuntary urine loss immediately after experiencing the urge to void, most often caused by detrusor instability (involuntary contractions of the detrusor muscle). Women with detrusor instability present with frequency (voiding >7 times per day), nocturia (waking up to void two or more times per night), urgency, and urge incontinence. Occasionally, they may also experience enuresis and incontinence during orgasm. Involuntary detrusor contractions may be triggered by specific events, such as hand washing in cold water or putting the key in the door, or they can occur without warning. It may be caused by neurologic diseases, such as Parkinson's disease, dementia, and multiple sclerosis; continence surgery; inflammation; pelvic organ prolapse; psychosomatic disorder; certain types of medications; and detrusor hyperreflexia with impaired contractility. However, there is no recognizable cause or abnormality in more than 90% of women with detrusor instability. When involuntary detrusor contractions are associated with neurologic lesions, the condition is known as detrusor hyperreflexia.
Differential diagnosis for urge incontinence includes severe SUI, overflow incontinence, uninhibited urethral relaxation, suburethral diverticulum, urinary tract fistula, cystitis, urethritis, and a foreign body, such as a bladder stone or neoplasm.
History and physical. When evaluating a woman with urge incontinence, always begin with a detailed history and physical examination. The primary focus of the history is to determine whether the incontinence is due to detrusor instability and its possible cause or to other conditions. Also include in the history a list of current medications: anticholinergic medications, anticonvulsants, phenothiazines, ganglionic blockers, antidepressants, and alpha-adrenergic agonists have been associated with frequency, hesitancy, urinary retention, irritative bladder symptoms, and overflow incontinence. Parasympathomimetics have also been linked to urge incontinence. Caffeine can irritate the bladder and may make symptoms worse among women whose bladder function is borderline.
Focus the physical examination on finding a specific cause for urge incontinence. Examine the anterior vaginal wall for urethral hypermobility, support defects, a midline mass, urethral tenderness, and abnormal elevation. Perform a focused neurologic examination to assess whether the sensory and motor components of S2 to S4 are intact. The sensory component is assessed by determining whether the sharp and dull sensations in the perineum, buttocks, and the inner thighs are intact. The motor component is assessed by testing the strength of the woman's lower extremities and the presence or absence of bulbocavernosus and cough reflexes, and anal wink. If the examination is normal, the patient does not have CNS neuropathy. If you detect a significant abnormality, refer her to a neurologist for consultation. If you fail to elicit the three sacral reflexes, do not assume pathology, since they are absent in approximately 20% of neurologically intact women.
Diagnostic testing. Begin diagnostic testing by obtaining a urine specimen to analyze for leukocytes and erythrocytes, and culture and sensitivity. Perform a wet prep and gonorrhea and chlamydia cultures if the patient has symptoms suggestive of vaginitis or urethritis, leukocytes and erythrocytes in her urine, and a negative urine culture. The next step is simple cystometry to assess the woman's voiding, detrusor function during bladder filling, and urethral sphincter competency. After the patient voids, the postvoid residual (PVR) is measured through a red rubber catheter. Then, attach the catheter to a 60-mL wide-mouth syringe and gradually fill the bladder to its maximum capacity, remove the catheter, and ask the woman to stand and cough. A positive stress test (the loss of small spurts of urine simultaneous with cough) suggests genuine SUI. Reduced bladder capacity, fluctuation of the water column in the syringe during bladder filling, prolonged or delayed urine loss after coughing, and a negative stress test all suggest detrusor instability.
A PVR less than 50 mL indicates adequate bladder emptying whereas a volume greater than 200 mL can be considered inadequate emptying. The significance of a PVR between 50 and 200 mL is less clear and should be considered in context of other clinical findings. If PVR is elevated, always repeat the test after the woman has voided in a private and relaxed setting.
A patient who has persistent erythrocytes and leukocytes in the urine and a negative wet prep and cultures should undergo a cystoscopic examination and IV urography to look for a foreign object or neoplasm before treatment is initiated or other diagnostic studies are done. Painless hematuria and irritative lower urinary tract complaints are the two most common presenting symptoms for bladder neoplasm.
Selecting therapy. Detrusor instability is usually managed conservatively. Commonly prescribed treatments include timed voiding (also known as bladder drill), anticholinergic medications, functional electrical stimulation, and topical estrogen. Available data suggest that timed voiding is the most effective conservative treatment. Randomized controlled trials have shown that it is significantly more effective than anticholinergic medications in managing detrusor instability.1,2 Interestingly, most studies have found that the efficacy of timed voiding is not increased by adding anticholinergics.3-5 Both anticholinergic medications and functional electrical stimulation are more efficacious than placebo in managing detrusor instability.6,7 However, neither was shown to be more effective than other forms of treatment, and thus, should be considered as second-line therapy.8 The two commonly prescribed anticholinergics, oxybutynin and tolterodine, are about equally effective.6,9-12 Oxybutynin is slightly more effective in managing incontinence symptoms and tolterodine has slightly less side effects.13 There are no objective data to suggest that topical estrogen is effective in relieving any of the symptoms associated with detrusor instability.14,15
If a woman's incontinence fails to respond to these conservative measures, refer her for multichannel urodynamic study. A patient who has severe refractory detrusor instability but no associated conditions, such as co-existing cystocele and SUI, may be considered for bladder denervation, an augmentation procedure, or sacral root neuromodulation.
Bladder denervation (selective sacral neurectomy, transvaginal infiltration of pelvic plexus, selective blockade of sacral pelvic nerves, and transvaginal partial denervation) is infrequently performed because of the high failure rate and significant complications. In bladder augmentation, the small or large bowel is used to increase bladder capacity and decrease overactivity. The procedure often cures detrusor instability but impairs voiding function. Postoperatively, patients have to void by straining and performing the Crede maneuver or by clean intermittent self-catheterization.
In sacral root neuromodulation, an implanted device sends electrical impulses to the sacral nerves that control bladder function. The reported cure rate ranges from 40% to 50% at 36 to 48 months.16,17 Another 13% to 45% of patients experience significant symptomatic improvement. Sacral root neuromodulation has fewer complications than bladder augmentation or denervation. The other advantage of the procedure is the ability to try stimulation over several days and assess the effect of neuromodulation before the implant is made permanent.
The problem seems to occur most frequently after continence procedures. Long-term studies have shown that approximately 9% to 42% of women develop detrusor instability after Burch colposuspension and the incidence is similar after a suburethral sling.18-20 Possible causes include local irritative lesions created by the surgery, urethral outlet obstruction, and disruption of sensory afferent nerves.
A woman who develops symptoms suggestive of detrusor instability postoperatively should always be assessed for urinary retention and cystitis. If leukocytes and erythrocytes or infection persist despite adequate antimicrobial therapy, the patient should be cystoscoped to determine whether the surgeon inadvertently put a suture through the bladder.
Detrusor instability is significantly more likely to occur if the continence procedure overcorrects the posterior urethrovesical junction and creates a partial outflow obstruction.21-23 Examination often reveals an overly elevated anterior vaginal wall, a negative Q-tip test (deviated downward from the horizon), decreased urine flow rate, and increased PVR. The initial treatment is similar even though detrusor instability resulting from a continence procedure tends to be more resistant to conservative management. If a woman's symptoms are severe and refractory to conservative management, the continence procedure may have to be taken down surgically and revised. There is no evidence at the present time to directly link nerve injury with the postoperative onset of detrusor instability.
It's rare to see urge incontinence that's been brought on by a foreign body. Recently, a postmenopausal woman presented to our office with severe lower urinary tract symptoms suggestive of detrusor instability. Her history and physical examination were unremarkable but she had persistent leukocytes and erythrocytes in her urine despite negative urine and urethral cultures. Cystoscopic examination revealed a bladder calculus. I suspect that the woman in the case presented here also had persistent leukocytes in her urine as well as erythrocytes and negative cultures. Therefore, I would have proceeded directly to cystoscopy to rule out a foreign object or neoplasm in the bladder before initiating treatment or performing multichannel urodynamic studies, but things are always clearer in hindsight.
I agree with Dr. Porter's suggestion that we should consider all causes when evaluating women with urge incontinenceand inspect all Foley catheters after removal. Evaluation is most easily accomplished by following a specific diagnostic pathway when evaluating urge incontinence, such as the one described here. It allows the physician to arrive at the correct diagnosis with minimal delay and avoid unnecessary diagnostic tests and treatments.
In unexplained or recalcitrant urinary incontinence, a clinician has to consider all causes, including a foreign body in the bladder. Another caveat is to inspect all Foley catheters after removal.
REFERENCES
1. Colombo M, Zanetta G, Scalambrino S, et al. Oxybutynin and bladder training in the management of female urinary urge incontinence: a randomized study. Inter Urogynecol J. 1995;6:63-67.
2. Jarvis JG. A controlled trial of bladder drill and drug therapy in the management of detrusor instability. Br J Urol. 1981;53:565-566.
3. Szonyi G, Collas DM, Ding YY, et al. Oxybutynin with bladder retraining for detrusor instability in elderly people: a randomized controlled trial. Age Aging. 1995;24:287-291.
4. Wiseman PA, Malone-Lee J, Rai GS. Terolidine with bladder retraining for treating detrusor instability in elderly people. BMJ. 1991;302:994-996.
5. Moore KH, Hay DM, Imrie AE, et al. Oxybutynin hydrochlorine (3 mg) in the treatment of women with idiopathic detrusor instability. Br J Urol. 1990;66:479-485.
6. Drutz HP, Appell RA, Gleason D, et al. Clinical efficacy and safety of tolterodine compared to oxybutynin and placebo in patients with overactive bladder. Int Urogynecol J Pelvic Floor Dysfunct. 1999;10:283-289.
7. Brubaker L, Benson JT, Bent A, et al. Transvaginal electrical stimulation for female urinary incontinence. Am J Obstet Gynecol. 1997;177:536-540.
8. Smith JJ 3rd. Intravaginal stimulation randomized trial. J Urol. 1996;155:127-130.
9. Abrams P, Freeman R, Anderstrom C, et al. Tolterodine, a new antimuscarinic agent: as effective but better tolerated than oxybutynin in patients with an overactive bladder. Br J Urol. 1998;81:801-810.
10. Malone-Lee J, Shaffu B, Anand C, et al. Tolterodine: superior tolerability than and comparable efficacy to oxybutynin in individuals 50 years old or older with overactive bladder: a randomized controlled trial. J Urol. 2001;165:1452-1456.
11. Appell RA, Sand P, Dmochowski R, et al. Prospective randomized controlled trial of extended-release oxybutynin chloride and tolterodine tartrate in the treatment of overactive bladder: results of the OBJECT study. Mayo Clin Proc. 2001;76:358-363.
12. Van Kerrebroeck, Kreder K, Jonas U, et al. Tolterodine once-daily: superior efficacy and tolerability in the treatment of overactive bladder. Urology. 2001;57:414-421.
13. Harvey MA, Baker K, Wells GA. Tolterodine versus oxybutynin in the treatment of urge urinary incontinence: a meta-analysis. Am J Obstet Gynecol. 2001;185:56-61.
14. Cardozo L, Rekers H, Tapp A, et al. Oestriol in the treatment of postmenopausal urgency: a multicenter study. Maturitas. 1993;18:47-53.
15. Jackson S, Shepherd A, Brookes S, et al. The effect of oestrogen supplementation on postmenopausal urinary stress incontinence: a double-blind placebo-controlled trial. Br J Obstet Gyneacol. 1999;106:711-718.
16. Bosch JL, Groen J. Sacral nerve neuromodulation in the treatment of patients with refractory motor urge incontinence: long-term results of a prospective longitudinal study. J Urol. 2000;163:1219-1222.
17. Siegel SW, Catanzaro F, Dijkema HE, et al. Long-term results of a multicenter study on sacral nerve stimulation for treatment of urinary urge incontinence, urgency-frequency, and retention. Urology. 2000;56(6 suppl 1):87-91.
18. Enzelsberger H, Helmer H, Schatten C. Comparison of Burch and Lyodura sling procedures for repair of unsuccessful incontinence surgery. Obstet Gynecol. 1996;88:251-256.
19. Dietz HP, Wilson PD. Colposuspension success and failure: a long-term objective follow-up study. Int Urogynecol J Pelvic Floor Dysfunct. 2000;11:346-351.
20. Herbertsson G, Iosif CS. Surgical results and urodynamic studies 10 years after retropubic colpourethrocystopexy. Acta Obstet Gynecol Scand. 1993;72:298-301.
21. van Geelen, Theeuwes AG, Eskes TK, et al. The clinical and urodynamic effects of anterior vaginal repair and Burch colposuspension. Am J Obstet Gynecol. 1988;159:137-144.
22. Langer R, Ron-El R, Newmann M, et al. Detrusor instability following colposuspension for urinary stress incontinence. Br J Obstet Gynaecol. 1988;95:607-610.
23. Bombieri L, Freeman RM, Perkins EP, et al. Why do women have voiding dysfunction and de novo detrusor instability after colposuspension? BJOG. 2002;109:402-412.
William Porter, Eddie Sze. Diagnostic Puzzler: What caused this woman's incontinence? Contemporary Ob/Gyn Sep. 1, 2003;48:103-108.
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