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You are here : > Health Centers > Clinical Obstetrics and Gynecology > Urinary Incontinence > Overflow Incontinence

Overflow Incontinence

Overflow Incontinence

Christopher M. Tarnay, MD, & Narender N. Bhatia, MD


Overflow incontinence is defined as the involuntary loss of urine associated with bladder overdistention in the absence of detrusor contraction. This condition classically occurs in men who have outlet obstruction secondary to prostatic enlargement that progresses to urinary retention. In women this is a relatively uncommon cause of urinary incontinence. When it does occur, it can be from increased outlet resistance from advanced vaginal prolapse causing a "kink" in the urethra or after an anti-incontinence procedure which has overcorrected the problem. Additionally, it can result from bladder hyporeflexia from a variety of neurologic causes (Table 45-9).


Overflow incontinence most often occurs due to postoperative obstruction if the bladder neck is overcorrected, or with a hyporeflexic bladder due to neurologic disease or spinal cord injury. The normal act of voiding is controlled centrally by sacral and pontine micturition centers. Impaired emptying can be the result of disruption of either central or peripheral neurons mediating detrusor function. Failure to identify the cause early may lead to permanent dysfunction and may lead to injury to the detrusor muscle or compromise in the parasympathetic ganglia in the bladder wall.

Urinary Incontinence


Usually symptoms are loss of urine without awareness or intermittent dribbling and constant wetness. Suprapubic pressure or pain may be associated. Patients will often note a sensation of a full bladder and the need to strain in order to empty or apply suprapubic pressure to void. Patients are at risk for urinary tract infection secondary to persistent residual urine in the bladder, which acts as a medium for bacterial growth. It is commonly seen after a bladder neck suspension. Complaints of poor urinary stream and sense of incomplete emptying combined with having to strain or apply hand pressure to void are likely.

Evaluation should always include a postvoid residual and, if the diagnosis is questionable, voiding pressure flow studies. An imaging study of the upper urinary tract to evaluate the ureters and kidney should follow, because persistent high-volume retention can lead to reflux and hydroureter or hydronephrosis and renal injury if left unchecked.


Bladder drainage to relieve retention is the first priority. Self-intermittent or prolonged catheterization may be necessary, depending on resolution of the inciting cause. In cases of postoperative urinary retention, bladder function can be evaluated by serial postvoid residual urine determinations. Although no normal volume for residual urine is universally accepted, it less than 100 mL is generally considered to be within normal limits and greater than 150 mL is considered abnormal. More than one value is needed because persistently high residual volumes will require prolonged catheterization.

When urinary retention occurs in the setting of neurologic disease, diabetes, or stroke, correction of the underlying cause is often impossible; therefore, the goal is to prevent injury or damage to the upper urinary tract. Intermittent self-catheterization is preferable to an indwelling catheter, which may predispose to infection, bladder spasms, or erosion.

Medical therapy may assist in the care of these patients. Acetylcholine agonists can stimulate detrusor contractions in patients that have vesical areflexia. α -Adrenergic blockers can facilitate bladder emptying by relaxing tone at the bladder neck.

Behavior modification in the form of timed voiding on a preset schedule to empty regardless of urge will prevent accumulation of excess urine. Usually a voiding pattern of every 2-3 hours is preferable. In bladder areflexia, manual pressure or abdominal splinting may facilitate emptying.







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