Increasing Comorbidity and Frailty is Not Associated with Early Postoperative Complications among Men Undergoing Artificial Urinary Sphincter or Sling Implantation: A Real-World Application of NSQIP® Data to Reconstructive Urology.

INTRODUCTION: Urologists may be hesitant to surgically treat urinary incontinence in comorbid genitourinary cancer survivors. We assessed the relationship between comorbidities and 30-day perioperative outcomes following artificial urinary sphincter and sling implantation. METHODS: Using the National Surgical Quality Improvement Program, patients with CPT codes for artificial urinary sphincter and sling implantation were identified between 2007 and 2015. The patient's Charlson comorbidity index and Frailty Index scores were calculated based on ICD-9 codes. The primary outcome was presence of perioperative complications. The association between Charlson comorbidity index and Frailty Index and each primary outcome was investigated using multivariate logistic regression models. RESULTS: We queried 1,370 and 1,018 records with artificial urinary sphincter and sling implantation, respectively. The median Charlson comorbidity index for artificial urinary sphincter patients was 4.0 (Q1 3, Q3 5), while for sling patients it was 3.0 (Q1 3, Q3 4). In the artificial urinary sphincter cohort, 47% had 1 Frailty Index condition, whereas 25% had 2 or more Frailty Index conditions. In the sling group, 42% had 1 Frailty Index condition, while 19% had 2 or more Frailty Index conditions. The event rate for overall complications was 5.4% and 3.0% in the artificial urinary sphincter and sling cohort, respectively. After adjusting for covariates in both the artificial urinary sphincter and sling cohort Charlson comorbidity index or Frailty Index was not associated with the odds of having a complication. CONCLUSIONS: The presence of increased comorbidities or frailty is not associated with short-term postoperative complications among men undergoing artificial urinary sphincter or sling implantation.

Bladder decompensation and reduction in nerve density in a rat model of chronic bladder outlet obstruction are attenuated with the NLRP3 inhibitor glyburide.

Bladder outlet obstruction (BOO) leads to progressive voiding dysfunction. Acutely, obstruction triggers inflammation that drives bladder dysfunction. Over time, inflammation leads to decreased bladder nerve density and increased fibrosis, responsible for eventual decompensation and irreversibility. We have previously shown that BOO triggers inflammation, reduced bladder nerve density and increased fibrosis via activation of the NLRP3 inflammasome in an acutely obstructed (12-day) rat model. However, as BOO progresses, the bladder may become decompensated with an increase in postvoid residual volume and decreased voiding efficiency. Currently, we have examined rat bladder function and nerve densities after chronic BOO to determine whether NLRP3 plays a role in the decompensation at this stage. Four groups were examined: control, sham-operated, BOO, or BOO+gly (glyburide; an NLRP3 inhibitor). After 42 days, bladder weight, inflammation (Evans blue), urodynamics, and nerve density were measured. BOO greatly enhanced bladder weights and inflammation, while inflammation was prevented by glyburide. Voiding pressures were increased, and flow rates decreased in BOO and BOO+gly groups, demonstrating physical obstruction. No difference in frequency or voided volume was detected. However, postvoid residual volumes were greatly increased in BOO rats while BOO+gly rats were not different than controls. Moreover, there was a dramatic decrease in voiding efficiency in the chronic BOO rats, which was prevented with glyburide treatment. Finally, a reduction in nerve density was apparent with BOO and attenuated with glyburide. Together the results suggest a critical role for NLRP3 in mediating bladder decompensation and nerve density during chronic BOO.

Magnetic resonance imaging features of pubic symphysis urinary fistula with pubic bone osteomyelitis in the treated prostate cancer patient.

INTRODUCTION: Pubic bone osteomyelitis with pubic symphysis urinary fistula represents a debilitating complication of radiation and ablative treatments for prostate cancer. The definitive radiographic diagnosis of this clinical entity is not described. In this study, we characterize the plain film and magnetic resonance imaging findings of pubic osteomyelitis. MATERIALS AND METHODS: We reviewed a database of prostate cancer survivors with diagnosed pubic osteomyelitis from 2011 to 2015. These patients underwent pelvic plain radiographs and magnetic resonance imaging with T1-weighted and fat-suppressed T2-weighted fast spin echo sequences. Intravenous gadolinium was utilized. The diagnosis was verified with extirpative surgery. 16 patients with diagnosed pubic osteomyelitis from 2011 to 2015 underwent imaging at our institution. RESULTS: All patients demonstrated increased signal on T2- weighted sequences and decreased signal on T1-weighted sequences along the pubic symphysis and the marrow of the involved pubic rami. Inflammatory myositis with diastasis of the pubic symphysis and cortical bone erosion were identified in the majority of patients. Fluid collections were identified in 75% of patients. 63% of conventional radiographs demonstrated no radiographic evidence of pubic osteomyelitis. CONCLUSION: Magnetic resonance imaging of pubic symphysis osteomyelitis in the prostate cancer survivor is characterized by high signal on T2-weighted images and low signal on T1-weighted images of the involved pubic rami, with the majority of patients demonstrating regional myositis. Imaging data combined with clinical assessment should prompt diagnosis and management of pubic osteomyelitis. Conventional radiography is generally insensitive to these findings. We consider magnetic resonance imaging to be the definitive diagnostic modality for this clinical entity.

The Emerging Role of Inflammasomes as Central Mediators in Inflammatory Bladder Pathology.

Irritative voiding symptoms (e.g. increased frequency and urgency) occur in many common pathologic conditions such as urinary tract infections and bladder outlet obstruction, and these conditions are well-established to have underlying inflammation that directly triggers these symptoms. However, it remains unclear as to how such diverse stimuli individually generate a common inflammatory process. Jürg Tschopp provided substantial insight into this conundrum when, working with extracts from THP-1 cells, he reported the existence of the inflammasome. He described it as a structure that senses multiple diverse signals from intracellular/extracellular sources and pathogens and triggers inflammation by the maturation and release of the pro-inflammatory cytokines interleukin-1ß and interleukin-18. Recently, many of these sensors were found in the bladder and the nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3, has been shown to be a central mediator of inflammation in several urological diseases. In this review, we introduce the nucleotide-binding domain, leucine-rich-containing family, pyrin domaincontaining-3 inflammasome, highlight its emerging role in several common urologic conditions, and speculate on the potential involvement of other inflammasomes in bladder pathology.