Evaluation of urinary incontinence.

Abstract

The safe and efficacious treatment of urinary incontinence (UI) requires correct identification of the underlying cause of this syndrome. UI is a symptom, not a disease or disorder, and may be caused by any of several pathophysiological mechanisms or a combination of mechanisms. Accurate diagnosis of that mechanism, or a reasonable diagnostic hypothesis that separates obstructive and neurogenic causes from other causes, is essential for an appropriate trial of pharmacological therapy. To a lesser extent, it is helpful in enabling the efficient choice of a behavioral therapy. Therefore, a review of normal urinary tract anatomy and neurophysiology will provide the necessary background knowledge on which to build an understanding of the pathologies that cause UI, the diagnostic process, and management options. ANATOMY/PHYSIOLOGY OF MICTURITION The simple anatomy of the male and female urinary tract is presented in Figure 1. The kidneys make urine at a rate that is dependent on many factors. Fluid intake patterns, posture, cardiac output, and renal blood flow are important determinants of rate of urine production. The renal collecting system at the renal pelvis and the ureters form a conduit to transfer urine from the kidneys into storage in the bladder. Micturition is a complex and dynamic process that involves both voluntary and involuntary central nervous system mechanisms. The brain receives afferent stimulation from the urinary tract and sends efferent impulses to the urinary tract via the spinal cord, pelvic ganglia, and peripheral nerves. Higher centers in the cortex are inhibitory to micturition, inputting ethnological and social influences on voiding. The brain stem is facilitatory. Normal micturition depends on a coordinated response to nerve impulses from these higher centers by relaxation of the sphincter mechanism of the bladder to allow urine flow and by the detrusor muscle of the bladder wall, which contracts to evacuate urine. During the low-pressure filling phase of the bladder, autonomic (involuntary) central nervous system stimulation maintains contraction of a proximal component of the urethral sphincter, maintaining continence. As the bladder reaches capacity and stretch receptors send afferent messages to the brain, the voluntary nervous system causes contraction of a distal or external urethral sphincter mechanism. When micturition is consciously desired, the sphincter mechanism must be inhibited in coordination with contraction of the detrusor muscle, which causes unobstructed bladder emptying. The urethra serves as a conduit from the bladder out of the body. The male urethra passes adjacent to and through the prostate gland and along the ventral surface of the penis to the urethral meatus. With advancing age, the prostate gland often hypertrophies and may cause irritative symptoms or obstruction to urine flow. Benign prostatic hypertrophy (BPH) may begin as early as age 25 or 30 years in males and by age 60 years can be found in more than 50% of males. Ninety percent of those aged 85 years have significant BPH. 1 Chronic