Urinary incontinence: types, causes and nursing management

Detrusor overactivity means the detrusor contracts involuntarily while the bladder is filling. It is not the same thing as incontinence: overactivity is found in healthy, continent older people, so an overactive bladder causes leakage only when the lower urinary tract and the person’s functional compensatory mechanisms also fail. The older distinction between detrusor hyperreflexia, used when a central nervous system lesion such as a stroke or cervical stenosis is present, and detrusor instability, used when no such lesion is found, has become blurred in older patients and rarely changes management. Two variants deserve their own names. Detrusor hyperactivity with impaired contractility, usually shortened to DHIC, combines involuntary contractions with weak emptying, so the patient has urgency and frequency yet an elevated post-void residual without any outlet obstruction. DHIC accounts for most established incontinence in frail older people and is a diagnostic trap: women are misdiagnosed with stress incontinence when the weak contractions are not detected, and men are misdiagnosed with outlet obstruction because urgency, frequency, a poor stream and residual urine look identical in both. A patient with DHIC who is given a bladder relaxant may tip into complete retention, which is why the residual is measured before and during treatment. Less common causes of urge leakage are interstitial cystitis, which produces urgency with otherwise unexplained pelvic pain, and spinal cord injury, which impairs detrusor compliance or produces detrusor–sphincter dyssynergia, a simultaneous contraction of bladder and sphincter.

Behavioural treatment for urge incontinence rests on two principles: void often enough to keep the bladder volume low, and retrain the central and pelvic mechanisms that inhibit detrusor contractions. A cognitively intact patient uses bladder retraining. Timed voiding is set from a written voiding record, starting at the shortest interval the patient currently manages. When a precipitant urge arrives, the patient stands still or sits down, breathes in deeply and lets the breath out slowly, and pictures the urge as a wave that peaks and then falls; once the urge is under control she walks slowly to the toilet rather than hurrying. After two days without leakage the scheduled interval is lengthened by 30 to 60 minutes until voiding every three to four hours is achieved without leakage. Success usually takes several weeks and early failure is common, so reassurance is part of the treatment; biofeedback is a useful teaching adjunct.

For a cognitively impaired patient the methods change shape: habit training bases the interval on the person’s own usual voiding pattern, scheduled voiding offers the toilet every two to three hours, and prompted voiding adds three components — regular monitoring with encouragement to report continence status, prompting to toilet on schedule, and praise when the person is dry and attempts to toilet. Prompted voiding is most likely to work in a patient who voids fewer than four times in twelve daytime hours and toilets correctly more than three quarters of the time in an initial trial.

When behaviour alone fails, bladder-suppressant drugs are added. They usually do not abolish overactivity, but they reduce leakage and frequency. Oxybutynin has both antimuscarinic and musculotropic action; it starts at 2.5 mg two to three times daily, or 5 mg once daily in extended-release form, and is titrated up to a maximum of 20 mg a day. Extended-release oxybutynin allows once-daily dosing with fewer side effects, and tolterodine 2 mg twice daily has similar efficacy with possibly less dry mouth, or 4 mg daily in extended release. Anticholinergic effects limit treatment: constipation and the extra fluid a patient drinks for a dry mouth can both worsen leakage, and a dry mouth predisposes to dental caries. The post-void residual is rechecked if leakage worsens, because a rising residual may mean retention that requires a lower dose. Double voiding, Valsalva’s manoeuvre or Credé’s manoeuvre can improve emptying, and augmentation cystoplasty carries high morbidity and is reserved for profound overactivity.

Pelvic muscle exercises are the cornerstone of non-invasive treatment for stress incontinence because they strengthen the muscular component of the urethral supports. Patients often report that these exercises failed when in fact they were taught or performed incorrectly. The prescription resembles any strength training programme: a small number of isometric contractions at maximal effort, not many weak ones. The conventional starting scheme is three sets of eight to ten strong contractions, each held for six to eight seconds, three to four times a week, with the hold gradually extended towards ten seconds. Instruction must concentrate on isolating the pelvic muscles and on avoiding contraction of the buttocks, abdomen or thighs, which substitutes the wrong muscles. Biofeedback improves teaching and lets the patient see progress. Evidence for electrical or magnetic stimulation and for weighted vaginal cones is less clear.

A pessary can help a woman whose stress leakage is worsened by bladder or uterine prolapse, and systemic or topical oestrogen may reduce both stress and urge leakage in atrophic vaginitis and urethritis. Imipramine, which has alpha-agonist and anticholinergic actions, has been used in mixed stress and urge incontinence, but it can raise the residual, make stress leakage worse, and the evidence for it is thin.

Surgery offers the highest cure rates for stress incontinence at the cost of added morbidity, and the operation must match the defect. When the problem is urethral hypermobility — genuine stress incontinence — bladder neck suspension procedures that repair the urethral supports are preferred; complications include urinary retention and prolapse of the vaginal wall. The abdominal Marshall-Marchetti-Krantz procedure has greater morbidity, and anterior colporrhaphy and needle suspension are less effective and no longer recommended. When the problem is intrinsic sphincter deficiency — from trauma or scarring after anti-incontinence surgery in women or prostatectomy in men, or from severe urethral atrophy — sling procedures using autologous or synthetic material, or periurethral bulking injections of collagen or autologous fat, are preferred, and slings are increasingly used for urethral hypermobility as well. Post-prostatectomy leakage in men is difficult: mild cases may respond to pelvic muscle exercises and bulking injections, while severe cases often need protective garments or a catheter. An artificial sphincter can work but carries reoperation rates up to 40 per cent even in experienced hands.

Overflow incontinence comes from detrusor underactivity, bladder outlet obstruction, or both together. Leakage is small in volume but continual, the post-void residual is high, and the patient reports dribbling, a weak stream, intermittency, hesitancy, frequency and nocturia. Outlet obstruction is the second most common cause of incontinence in older men, although most obstructed men are not incontinent; benign prostatic hyperplasia, prostate cancer and urethral stricture are the usual causes. In women obstruction is uncommon and usually follows anti-incontinence surgery or a large cystocele that kinks the urethra; removing a single suture or performing urethrolysis, which frees adhesions, can restore continence. Detrusor underactivity causes retention and overflow in only five to ten per cent of older people. Its intrinsic form replaces detrusor smooth muscle with fibrosis and connective tissue, typically after years of obstruction. Its neurological form follows peripheral neuropathy, as in diabetes, pernicious anaemia, Parkinson’s disease or alcoholism, or mechanical damage to the spinal afferents by disc herniation, spinal stenosis or tumour.

Treatment of underactivity is supportive: drugs that weaken detrusor contraction or increase urethral tone are reduced or stopped, constipation is treated, and bethanechol is ineffective except possibly in a patient who must remain on anticholinergic medication. Intermittent clean catheterisation can manage the bladder effectively, and sterile intermittent catheterisation is preferred for frailer or institutionalised patients. Credé’s or Valsalva’s manoeuvre during voiding, double voiding and unhurried voiding may improve emptying, and for men with chronic obstruction an intraurethral stent may be preferred to an indwelling catheter.

Indwelling catheters deserve respect. The 1990 Omnibus Budget Reconciliation Act led to more appropriate and less frequent catheter use in long-term care, but the prevalence of incontinence rose. Closed drainage systems reduce bacteriuria and infection, whereas topical meatal antimicrobials, antimicrobial-coated catheters, collection-bag disinfectants and antimicrobial irrigation do not. Routine antibiotics reduce bacteriuria but breed resistant organisms and secondary infection such as Clostridium difficile colitis. Bacteriuria is universal in catheterised patients and is not treated unless there are clear symptoms, and routine cultures are not taken; in a symptomatic patient a culture is taken after the old catheter is removed and a new one inserted. After acute retention, decompression continues for at least seven days, followed by a voiding trial after removal — the catheter is never clamped. Risk factors for blockage include alkaline urine, female gender, poor mobility, calciuria, proteinuria, copious mucin, Proteus colonisation and pre-existing bladder stones; in these patients changing the catheter every seven to ten days may help, while in their absence routine changes are unnecessary as long as monitoring is adequate.