Research Article: Neurogenic Bladder

Date Published: February 8, 2012

Publisher: Hindawi Publishing Corporation

Author(s): Peter T. Dorsher, Peter M. McIntosh.

http://doi.org/10.1155/2012/816274

Abstract

Congenital anomalies such as meningomyelocele and diseases/damage of the central, peripheral, or autonomic nervous systems may produce neurogenic bladder dysfunction, which untreated can result in progressive renal damage, adverse physical effects including decubiti and urinary tract infections, and psychological and social sequelae related to urinary incontinence. A comprehensive bladder-retraining program that incorporates appropriate education, training, medication, and surgical interventions can mitigate the adverse consequences of neurogenic bladder dysfunction and improve both quantity and quality of life. The goals of bladder retraining for neurogenic bladder dysfunction are prevention of urinary incontinence, urinary tract infections, detrusor overdistension, and progressive upper urinary tract damage due to chronic, excessive detrusor pressures. Understanding the physiology and pathophysiology of micturition is essential to select appropriate pharmacologic and surgical interventions to achieve these goals. Future perspectives on potential pharmacological, surgical, and regenerative medicine options for treating neurogenic bladder dysfunction are also presented.

Partial Text

Normal micturition involves proper function of both the bladder and urethra. A detrusor of normal compliance and a physiologically competent urethral sphincter are both necessary to maintain urinary continence. Any increase in abdominal pressure, which inherently produces an increase in bladder pressure, is normally counteracted by an even greater increase in urethral pressure.

The basic neuroanatomy and neurophysiology of the upper and lower urinary tracts should be understood before considering bladder management issues. Normal voluntary micturition includes bladder filling, storage, and emptying [1]. The kidneys receive nearly 25% of the cardiac output, filtering 180 L per day though only approximately 1 L/day is excreted as urine. This filtrate is transported through the ureters to the bladder. The ureters, which are approximately 25–30 cm in length, pass obliquely through bladder wall at the ureterovesicular junction to form a one-way valve that serves to prevent retrograde reflux of urine to the kidneys during bladder filling and emptying stages. This one-way valve mechanism remains competent only as long as the oblique course of the ureters is maintained thru the bladder wall. The bladder stores urine in a low pressure system with a normal capacity of 400–500 cc. Anatomically, the bladder is divided into the detrusor (aka as “body” or “dome” of the bladder), which consists of smooth muscle, and the base, which includes the trigone and bladder neck that are intimately connected to the pelvic floor. The bladder outlet has two urethral sphincters, the internal (smooth muscle) sphincter in the bladder neck and proximal urethra and the external (striated muscle) sphincter of the membranous urethra. Females have a less complex urinary sphincter mechanism that surrounds a shorter urethra.

Many classifications have been used to group neurogenic bladder dysfunction. Each has their merits and clinical utility. These classifications may be based on urodynamic findings (e.g., Lapides [6], Krane, and Siroky [7]), neurourologic criteria (Hald and Bradley [8], Bors and Comarr [9]), or on bladder and urethral function (International Continence Society [10], Wein [11]).

This evaluation is essential to assess lower urinary tract function.

Management of neurogenic bladder conditions requires patient education and may include interventions such as timed voiding, manual expression, medications, intermittent catheterization, indwelling urinary catheter, and bladder and/or urethral surgical procedures.

When nonpharmacologic and pharmacologic treatments fail to control neurogenic detrusor overactivity, then surgical options including neuromodulation are appropriate treatment options.

Neurogenic bladder dysfunction can be successfully treated to achieve goals of urinary continence, prevention of renal damage from chronically high detrusor pressures, and minimizing risk of urinary tract infections or bladder overdistension. A comprehensive multidisciplinary bladder retraining program can best achieve these goals utilizing patient education, instruction in catheter use/care, medications, and/or bladder or urethral surgical procedures. Experimental works in lumbar-to-sacral nerve rerouting and in regenerative medicine including use of stem cells to mitigate or reverse spinal cord damage producing neurogenic bladder dysfunction are still in their infancy, and more research will be needed to see if the promising results of some small pilot studies are confirmed in larger, controlled studies with long-term followup.

 

Source:

http://doi.org/10.1155/2012/816274

 

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