Perioperative Gentamicin Prophylaxis in Robot-Assisted Prostatectomy: Are Surgical Confounders Adequately Addressed?

The study’s most fundamental design feature – a chronological before-after split with gentamicin administered from January 2020 to June 2021 and cefuroxime from July 2021 to December 2022 – introduces a temporal confound that is not addressed in the analysis. Although the authors describe the design as a “matched case-control study,” the groups are in fact sequential cohorts separated by the antibiotic policy change. This distinction is critical because multiple time-dependent variables may have co-evolved with the antibiotic switch. Over a period of nearly 3 years, institutional practices inevitably evolve: anesthesia protocols may be refined, intraoperative fluid management strategies may shift, perioperative monitoring standards may be updated, and familiarity with the nuances of pneumoperitoneum management in robotic cases may deepen [2]. The authors state that anesthesia protocols were consistent across both groups, yet this assertion is not substantiated with quantitative data. Without adjustment for temporal trends or a formal assessment of period effects – for instance, by including the date of surgery as a covariate or by performing an interrupted time-series analysis – it remains uncertain whether the observed difference in AKI rates reflects the antibiotic switch alone or a composite of concurrent changes in perioperative care.

The authors themselves hypothesize that prolonged exposure to elevated intra-abdominal pressure during dissection of larger prostates may impair renal perfusion and potentiate gentamicin accumulation in the renal parenchyma. This is a physiologically compelling mechanism. However, neither total console time, total operative duration, nor the specific duration of the 20 mm Hg high-pressure phase was recorded or included in the multivariable model. The finding that prostate weight emerged as an independent predictor of AKI (OR: 1.024 per gram) may therefore act as a surrogate for prolonged pneumoperitoneum rather than representing an intrinsic renal risk factor. If operative duration were incorporated into the regression model, it is conceivable that part of the variance currently attributed to gentamicin could be redistributed to surgical duration, thereby attenuating the reported odds ratio. We believe that reporting console and pneumoperitoneum times – data routinely captured in robotic surgery logs – and including them in the multivariable analysis would substantially strengthen the causal inference.

The authors note that no restrictive fluid strategy was employed and that anesthesia protocols were consistent across groups, but these assertions are not supported by quantitative data. Mean arterial pressure trends, episodes of intraoperative hypotension, total crystalloid and colloid volumes, estimated blood loss, and use of vasopressors are all established modulators of perioperative renal perfusion [3]. In a study where the primary outcome is AKI, the absence of these variables from both descriptive statistics and the regression model constitutes a notable gap.

Despite these reservations, we agree with the authors’ broader message that PAP protocols require procedure-specific validation rather than blanket adoption across surgical modalities. Current guidelines from both the American Urological Association [4] and the European Association of Urology [5] do not provide RARP-specific antibiotic prophylaxis recommendations. The development of robotic surgery-specific antibiotic stewardship protocols – informed by prospective studies that control for operative duration, pneumoperitoneum parameters, and intraoperative hemodynamics – would represent a meaningful advance. We would encourage the authors, who have access to this institutional cohort, to consider a supplementary analysis incorporating operative time data from their robotic console logs, which may help disentangle the relative contributions of pharmacological nephrotoxicity and surgical hemodynamic stress.

In summary, while the study by Glietsch et al. [1] raises an important clinical signal, the current evidence may not yet be sufficient to conclusively attribute the observed AKI risk solely to gentamicin. Addressing the confounders outlined above would allow for a more definitive conclusion and would provide a stronger foundation for the guideline revisions the authors rightly advocate.

The authors have no conflicts of interest to declare.

This study was not supported by any sponsor or funder.

A.M.B. conceived the idea and drafted the manuscript. B.İ. contributed to the critical review of the original article and revised the manuscript. Both authors approved the final version of the manuscript.

No new data were generated or analyzed in this letter.