Phillip P. Smith

Aging and the underactive detrusor: A failure of activity or activation?†‡

To examine the known and potential contributions of motor, sensory, and biomechanical dysfunctions to the clinical problems of detrusor underactivity and detrusor hyperactivity/impaired contractility.

Pad weight testing in the evaluation of urinary incontinence.

To present the teaching module “Pad Weight Testing in the Evaluation of Urinary Incontinence.” This teaching module embodies a presentation, in combination with this manuscript. This manuscript serves as a scientific background review; the evidence base made available on ICS website to summarize current knowledge and recommendations.

Detrusor expulsive strength is preserved, but responsiveness to bladder filling and urinary sensitivity is diminished in the aging mouse.

The prevalence of urinary symptoms increases with age and is a significant source of distress, morbidity, and expense in the elderly. Recent evidence suggests that symptoms in the aged may result from sensory dysfunction, rather than abnormalities of detrusor performance. Therefore, we employed a pressure/flow multichannel urethane-anesthetized mouse cystometry model to test the hypothesis that in vivo detrusor performance does not degrade with aging. Secondarily, we sought to evaluate sensory responsiveness to volume using pressure-volume data generated during bladder filling. Cystometric data from 2-, 12-, 22-, and 26-mo-old female C57BL6 mice were compared. All 2- and 12-mo-old mice, 66% of 22-mo-old mice, and 50% of 26-mo-old mice responded to continuous bladder filling with periodic reflex voiding. Abdominal wall contraction with voiding had a minimal contribution to expulsive pressure, whereas compliance pressure was a significant contributor. Maximum bladder pressure, estimated detrusor pressure, detrusor impulse (pressure-time integral), as well as indices of detrusor power and work, did not decrease with aging. Bladder precontraction pressures decreased, compliance increased, and nonvoiding contraction counts did not change with increasing age. Intervoid intervals, per-void volumes, and voiding flow rates increased with age. Calculations approximating wall stress during filling suggested loss of bladder volume sensitivity with increasing age. We conclude that aging is associated with an impaired ability to respond to the challenge of continuous bladder filling with cyclic voiding, yet among responsive animals, voiding detrusor contraction strength does not degrade with aging in this murine model. Furthermore, indirect measures suggest that bladder volume sensitivity is diminished. Thus, changes in homeostatic reserve and peripheral and/or central sensory mechanisms may be important contributors to aging-associated changes in bladder function.

Detrusor underactivity and the underactive bladder: Symptoms, function, cause-what do we mean? ICI-RS think tank 2014.

Impaired bladder emptying is a well‐recognized cause of lower urinary tract symptoms. However, the symptoms produced do not always relate to voiding, and may include frequency, urgency and incontinence. Conversely, the etiology of symptoms of disturbed voiding is not necessarily dependent upon objectively impaired voiding. Terms including underactive bladder, detrusor underactivity, and impaired contractility describe aspects of these problems, and have been used somewhat interchangeably. It is possible that the present lack of effective therapy in many cases relates to both etiologic and diagnostic uncertainty stemming from terminologic imprecision. Detrusor underactivity has a standardized definition, unlike underactive bladder and impaired contractility. The relationships of symptoms, function, and cause were the focus of a 2014 ICI‐RS Think Tank entitled Does Detrusor Underactivity Exist, and if so it is neurogenic, myogenic, or both? This review presents a summary of the problem and the Think Tank conclusions. A terminologic hierarchy and specific research goals are presented. Neurourol. Urodynam. 35:312–317, 2016.

Transobturator tape, bladder perforation, and paravaginal defect: a case report

Transobturator midurethral slings (TOT) have been shown to have less risk of vascular and visceral injury than tension-free midurethral slings. Routine cystoscopy has therefore not been felt to be necessary. A case of bladder perforation unrecognized at the time of TOT placement is presented. Findings at sling removal suggested that a clinically nonapparent paravaginal defect may have been instrumental in the injury. Consideration should be given to routine cystoscopy at the time of transobturator sling placement.

Current trends in the evaluation and management of female urinary incontinence

Despite its common occurrence and often seemingly obvious causes, female urinary incontinence requires a thorough and thoughtful evaluation for its proper diagnosis and treatment. With rare exceptions, urinary incontinence is the result of failure of the sphincter mechanism to resist bladder pressures encountered during daily activities. This may be the result of sphincter failure, overactivity of the bladder detrusor muscle or both. In uncomplicated cases, the diagnosis is usually based on an evaluation in the office. Urodynamic and cystoscopic study may be helpful in complex, resistant and recurring cases of urinary incontinence of any cause. Most cases of incontinence may be classified as stress, urge or mixed urinary incontinence. Treatment of stress urinary incontinence focuses on supplementing the urethral continence mechanisms, particularly the urethral supports and periurethral striated muscle function. The current paradigm for the treatment of urge incontinence centres on pharmacologic therapy, primarily by correcting detrusor overactivity with antimuscarinic drugs. Other therapies aimed at altering sensorimotor function may be used in resistant cases. The treatment of mixed urinary incontinence requires consideration of the contribution of each of its components. With proper diagnosis, effective treatment is possible for most patients.

Pathophysiology and animal modeling of underactive bladder

AbstractWhile the symptomology of underactive bladder (UAB) may imply a primary dysfunction of the detrusor muscle, insights into pathophysiology indicate that both myogenic and neurogenic mechanisms need to be considered. Due to lack of proper animal models, the current understanding of the UAB pathophysiology is limited, and much of what is known about the clinical etiology of the condition has been derived from epidemiological data. We hereby review current state of the art in the understanding of the pathophysiology of and animal models used to study the UAB.

Continuous uroflow cystometry in the urethane-anesthetized mouse.

In vivo animal cystometry represents an accepted methodology for the study of lower urinary tract physiology. A particular advantage of the mouse model is the availability of genetically modified strains, offering the possibility of linking individual genes to relevant physiological events. However, small voided volumes complicate the ability to obtain reliable pressure‐flow data by gravimetric methods, due to non‐continuous drop formation and release during voiding. We investigated the feasibility of a simple non‐gravimetric continuous urine collection system during cystometry under urethane anesthesia, and compared urethane‐anesthetized with awake cystometry.

Does defective volume sensation contribute to detrusor underactivity

The urodynamic finding of detrusor underactivity (DU) in neurologically intact unobstructed patients may relate to impaired volume sensations rather than detrusor contractile defects. We hypothesized that DU patients would demonstrate higher volumes but similar wall stress at sensation thresholds, and similar voiding contractility, compared to other groups.

Evidence of central modulation of bladder compliance during filling phase.

Bladder compliance is one expression of the pressure and volume relationship as the bladder fills. In addition to passive elements, autonomous micromotional detrusor activity contributes to this relationship. In the mouse cystometric model, compliance pressure contributes to voiding expulsive pressure. During attempts to isolate the detrusor contractile component of this filling pressurization, we found that compliance reversibly diminishes under conditions which remove central control from the micturition cycle.