Gerald C. Mingin

Salvage of bilateral asynchronous perinatal testicular torsion.

PURPOSE Current management strategies for prenatal torsion include observation alone, delayed contralateral orchiopexy and emergent contralateral orchiopexy. Bilateral torsion is now being reported with more frequency and approximately a third of these patients have asynchronous torsion. We highlight the role of scrotal exploration in neonates diagnosed with bilateral asynchronous testicular torsion. MATERIALS AND METHODS We reviewed the clinical experience from 2000 to present of 2 senior pediatric urologists to identify cases of bilateral perinatal testicular torsion. Asynchronous torsion was identified by the varying physical findings of each testicle at exploration. A literature review was done to evaluate the evolving management of perinatal testicular torsion. RESULTS Six cases of bilateral perinatal torsion were identified since 2000. In 3 of the 6 cases extravaginal torsion of the contralateral testis was incidentally identified at surgical exploration. All 3 testes had normal Doppler flow before exploration. Testicular salvage was not successful in the 2 patients with bilaterally absent blood flow on newborn ultrasound. The 3 cases of incidentally diagnosed contralateral torsion and 1 of preoperatively diagnosed contralateral torsion were successfully salvaged. Thus, 4 of 6 patients with bilateral torsion were left with 1 viable testis. CONCLUSIONS Physical examination findings and radiography can be inaccurate to assess the contralateral testis in males born with prenatal torsion. We have adopted the strategy of emergent surgical exploration in cases of prenatal torsion. Using this approach anorchia was minimized in patients with bilateral asynchronous torsion.

Endoscopic ablation of longitudinal vaginal septa in prepubertal girls: A minimally invasive alternative to open resection

INTRODUCTION Vaginal septation is a congenital defect seen in patients with persistent cloaca, urogenital sinus and disorders of Müllerian duct aplasia. Rarely, these patients present with symptoms in infancy and childhood with the exception of hydrocolpos. Treatment traditionally consists of surgical excision of the vaginal septum. We present our experience with minimally invasive endoscopic ablation of vaginal septa. MATERIALS AND METHODS We reviewed retrospectively the management of four patients with vaginal septae: Herlyn-Werner-Wunderlich syndrome (1), cloacal malformations (2), and urogenital sinus (1). All were prepubertal (aged 2-9 years). The first patient presented with hydrocolpos. The others were asymptomatic and identified during definitive reconstruction. All four underwent endoscopic ablation in ≤30 min, using a pediatric resectoscope. RESULTS One of the cloacal patients developed a postoperative perineal/vestibular infection leading to urethral stenosis and currently requires intermittent catheterization. There were no other complications. Endoscopic examination under anesthesia at 6 months in all patients revealed no septal scarring or vaginal stenosis. CONCLUSION The advantage of endoscopic ablation over traditional open repair is that it is minimally invasive and can be easily performed as an outpatient procedure or at the time of definitive reconstruction. Our results suggest that endoscopic ablation should be considered as the primary approach for correction of vaginal septa.

Social stress induces changes in urinary bladder function, bladder NGF content, and generalized bladder inflammation in mice

Social stress may play a role in urinary bladder dysfunction in humans, but the underlying mechanisms are unknown. In the present study, we explored changes in bladder function caused by social stress using mouse models of stress and increasing stress. In the stress paradigm, individual submissive FVB mice were exposed to C57BL/6 aggressor mice directly/indirectly for 1 h/day for 2 or 4 wk. Increased stress was induced by continuous, direct/indirect exposure of FVB mice to aggressor mice for 2 wk. Stressed FVB mice exhibited nonvoiding bladder contractions and a decrease in both micturition interval (increased voiding frequency) and bladder capacity compared with control animals. ELISAs demonstrated a significant increase in histamine protein expression with no change in nerve growth factor protein expression in the urinary bladder compared with controls. Unlike stressed mice, mice exposed to an increased stress paradigm exhibited increased bladder capacities and intermicturition intervals (decreased voiding frequency). Both histamine and nerve growth factor protein expression were significantly increased with increased stress compared with control bladders. The change in bladder function from increased voiding frequency to decreased voiding frequency with increased stress intensity suggests that changes in social stress-induced urinary bladder dysfunction are context and duration dependent. In addition, changes in the bladder inflammatory milieu with social stress may be important contributors to changes in urinary bladder function.

Social stress in mice induces urinary bladder overactivity and increases TRPV1 channel-dependent afferent nerve activity

Social stress has been implicated as a cause of urinary bladder hypertrophy and dysfunction in humans. Using a murine model of social stress, we and others have shown that social stress leads to bladder overactivity. Here, we show that social stress leads to bladder overactivity, increased bladder compliance, and increased afferent nerve activity. In the social stress paradigm, 6-wk-old male C57BL/6 mice were exposed for a total of 2 wk, via barrier cage, to a C57BL/6 retired breeder aggressor mouse. We performed conscious cystometry with and without intravesical infusion of the TRPV1 inhibitor capsazepine, and measured pressure-volume relationships and afferent nerve activity during bladder filling using an ex vivo bladder model. Stress leads to a decrease in intermicturition interval and void volume in vivo, which was restored by capsazepine. Ex vivo studies demonstrated that at low pressures, bladder compliance and afferent activity were elevated in stressed bladders compared with unstressed bladders. Capsazepine did not significantly change afferent activity in unstressed mice, but significantly decreased afferent activity at all pressures in stressed bladders. Immunohistochemistry revealed that TRPV1 colocalizes with CGRP to stain nerve fibers in unstressed bladders. Colocalization significantly increased along the same nerve fibers in the stressed bladders. Our results support the concept that social stress induces TRPV1-dependent afferent nerve activity, ultimately leading to the development of overactive bladder symptoms.

Development of stress-induced bladder insufficiency requires functional TRPV1 channels

Social stress causes profound urinary bladder dysfunction in children that often continues into adulthood. We previously discovered that the intensity and duration of social stress influences whether bladder dysfunction presents as overactivity or underactivity. The transient receptor potential vanilloid type 1 (TRPV1) channel is integral in causing stress-induced bladder overactivity by increasing bladder sensory outflow, but little is known about the development of stress-induced bladder underactivity. We sought to determine if TRPV1 channels are involved in bladder underactivity caused by stress. Voiding function, sensory nerve activity, and bladder wall remodeling were assessed in C57BL/6 and TRPV1 knockout mice exposed to intensified social stress using conscious cystometry, ex vivo afferent nerve recordings, and histology. Intensified social stress increased void volume, intermicturition interval, bladder volume, and bladder wall collagen content in C57BL/6 mice, indicative of bladder wall remodeling and underactive bladder. However, afferent nerve activity was unchanged and unaffected by the TRPV1 antagonist capsazepine. Interestingly, all indices of bladder function were unchanged in TRPV1 knockout mice in response to social stress, even though corticotrophin-releasing hormone expression in Barringtons Nucleus still increased. These results suggest that TRPV1 channels in the periphery are a linchpin in the development of stress-induced bladder dysfunction, both with regard to increased sensory outflow that leads to overactive bladder and bladder wall decompensation that leads to underactive bladder. TRPV1 channels represent an intriguing target to prevent the development of stress-induced bladder dysfunction in children.

Acute management of neonatal respiratory failure due to crossed ectopic obstructed megaureter in a duplicated pelvic kidney

Respiratory distress due to urinary tract obstruction can be a urologic emergency. We describe the diagnostic and surgical management of severe respiratory distress in a neonate due to a crossed ectopic obstructed megaureter in a duplicated pelvic kidney.