In Reply

We thank Dr. Kendall for his repeated interest in our investigations and his valuable comments.

Dr. Kendall’s first concern was our choice of primary outcome (i.e., differences in postvoid residual urine volume rather than the need for bladder catheterization), arguing that the need for bladder catheterization is related to poor outcome.¹  Indeed, bladder catheterization is linked with urinary tract infections and patient discomfort.²  We chose a change in postvoid residual because elevated postvoid residuals are a common reason for bladder catheterization. Therefore, postvoid residual is not only a surrogate of voiding dysfunction, but also directly linked to poor outcomes. Our study was underpowered to assess significance in the rate of urinary tract infections, but this was not the focus of our study. Changes in postvoid residual, however, are a very sensitive value for lower urinary tract function in general and an acknowledged sign of its dysfunction, which was the target of assessment in this randomized clinical trial. The International Consultation on Benign Prostatic Hyperplasia defines a postvoid residual of 50 to 100 ml as abnormal.³  Based on precedent observations⁴  the primary endpoint, change in postvoid residual, indicates a relevant change in lower urinary tract function.

Dr. Kendall also pondered the lack of reporting the need for postoperative bladder catheterization. In the study setting the bladder catheter always was left in place until the postoperative urodynamic investigation. However, we did report that 4 of 19 patients (21%) in the bupivacaine group and 2 of 17 patients (12%) in the ropivacaine group had a maximum flow rate of 0 ml/s postoperatively and were unable to void, which is an absolute indication for catheterization. It is of utmost importance to avoid urinary retention postoperatively because this is a bladder distension beyond the maximum capacity and is associated with bladder ischemia and the resulting bladder dysfunction.⁵ 

Dr. Kendall’s second concern was the lack of information concerning intraoperative pain management. General anesthesia was induced with fentanyl 2 µg/kg and propofol 2 mg/kg. Orotracheal intubation was facilitated with rocuronium 0.6 mg/kg and boluses were given for intraoperative muscle relaxation to maintain no response to train-of-four stimulation. Anesthesia was maintained with desflurane in a mixture of oxygen and air using a closed circuit. The systemic use of fentanyl was limited to the induction, and intraoperative analgesia was performed with the epidural administration of bupivacaine 0.2% at a rate of 6 to 8 ml/h. Dr. Kendall is right when arguing that the anesthetic agents (opioids, halogenated anesthetics, anticholinergics) may influence lower urinary tract function. However, our postoperative urodynamic investigations were performed on postoperative day 2 or 3 depending on patient’s ability to be mobilized more than 1 h (the average duration needed for urodynamic investigations). Because these drugs were only administered intraoperatively, as mentioned in our Results section,¹  their systemic impact is negligible. We previously demonstrated the clinically nonrelevant plasma concentration of epidurally administered fentanyl.⁴ 

We thank Dr. Kendall for his interest in our publication and hope we were able to clarify the issues addressed.