BackgroundSurgeons play a pivotal role in combating the opioid crisis that currently grips the United States. Changing surgeon behavior is difficult, and the degree to which behavioral science can steer surgeons toward decreased opioid prescribing is unclear.MethodsThis was a single‐institution, single‐arm, pre‐ and postintervention study examining the prescribing of opioids by urologists for adult patients undergoing prostatectomy or nephrectomy. The primary outcome was the quantity of opioids prescribed in oral morphine equivalents (OMEs) after hospital discharge. The primary exposure was a multipronged behavioral intervention designed to decrease opioid prescribing. The intervention had 3 components: 1) formal education, 2) individual audit feedback, and 3) peer comparison performance feedback. There were 3 phases to the study: a pre‐intervention phase, an intervention phase, and a washout phase.ResultsThree hundred eighty‐two patients underwent prostatectomy, and 306 patients underwent nephrectomy. The median OMEs decreased from 195 to 19 in the prostatectomy patients and from 200 to 0 in the nephrectomy patients (P < .05 for both). The median OMEs prescribed did not increase during the washout phase. Prostatectomy patients discharged with opioids had higher levels of anxiety than patients discharged without opioids (P < .05). Otherwise, prostatectomy and nephrectomy patients discharged with and without opioids did not differ in their perception of postoperative pain management, activity levels, psychiatric symptoms, or somatic symptoms (P > .05 for all).ConclusionsImplementing a multipronged behavioral intervention significantly reduced opioid prescribing for patients undergoing prostatectomy or nephrectomy without compromising patient‐reported outcomes.

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The purpose of this study is to determine the effects of pudendal nerve stimulation (PNS) on reflex bladder activity and develop an animal model of underactive bladder (UAB). In six anesthetized cats, a bladder catheter was inserted via the urethra to infuse saline and measure pressure. A cuff electrode was implanted on the pudendal nerve. After determining the threshold intensity (T) for PNS to induce an anal twitch, PNS (5 Hz, 0.2 ms, 2T or 4T) was applied during cystometrograms (CMGs). PNS (4-6T) of 30-min duration was then applied repeatedly until bladder underactivity was produced. Following stimulation control CMGs were performed over 1.5-2 hours to determine the duration of bladder underactivity. When applied during CMGs, PNS (2T and 4T) significantly (p<0.05) increased bladder capacity while PNS at 4T also significantly (p<0.05) reduced bladder contraction amplitude, duration, and area under contraction curve. Repeated application of 30-min PNS for a cumulative period of 3-8 hours produced bladder underactivity exhibiting a significantly (p<0.05) increased bladder capacity (173±14% of control) and a significantly (p<0.05) reduced contraction amplitude (50±7% of control). The bladder underactivity lasted more than 1.5-2 hours after termination of the prolonged PNS. These results provide basic science evidence supporting the proposal that abnormal afferent activity from external urethral/anal sphincter could produce central inhibition that underlies non-obstructive urinary retention (NOUR) in Fowler's syndrome. This cat model of UAB may be useful to investigate the mechanism by which sacral neuromodulation reverses NOUR in Fowler's syndrome.

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Background Although previous studies show that vitamin A deficiency is associated with incident tuberculosis disease, the direction of the association has not been established. We investigated the impact of vitamin A deficiency on tuberculosis disease progression. Methods We conducted a longitudinal cohort study nested within a randomized clinical trial among HIV+ adults in Haiti. Among incident tuberculosis cases, we measured vitamin A levels in stored blood samples obtained 90-365 days before tuberculosis diagnosis. We compared these to vitamin A levels in controls matched on age, gender, follow-up time, and time to antiretroviral therapy initiation using a modified Poisson generalized estimating equation. We also evaluated histopathology, bacterial load, and immune outcomes in tuberculosis infection in a guinea pig model of dietary vitamin A deficiency. Results Among 773 participants, 96 developed incident tuberculosis during follow-up, 62.5% (60) of whom had stored serum samples obtained 90-365 days before tuberculosis diagnosis. In age- and sex- adjusted and multivariate analyses respectively, incident tuberculosis cases were 3.99 times (95% confidence interval [CI] 2.41-6.60) and 3.59 (95% CI 2.05-6.29) more likely to have been vitamin A deficient than matched controls. Vitamin A deficient guinea pigs manifested more extensive pulmonary pathology, atypical granuloma morphology, and increased bacterial growth after experimental tuberculosis infection. Reintroduction of dietary vitamin A to deficient guinea pigs after established tuberculosis disease successfully abrogated severe disease manifestations and altered cellular immune profiles. Conclusion Human and animal studies support the role of baseline vitamin A deficiency as a determinant of future tuberculosis disease progression.