Abstract
Introduction
Inguinal hernia mesh infection (IHMI) is a rare but a significant problem. The aim of this study was to determine whether etiopathogeneses of early-onset and late-onset IHMIs differ in terms of the origin of infectious agents, and route of dissemination.
Patients and methods
This was a retrospective cohort study with prospective data collection of patients operated on from 2013 to 2015. Early-onset IHMI was defined as symptoms developed within one year after the index surgery, whereas late-onset IHMI was defined as infection developed later than a year after the index surgery. Age, gender, ASA score, BMI, time from index surgery, isolated infectious agents and possible pathogeneses were analyzed.
Results
During the study period, 1438 patients underwent inguinal hernia repair. Sixteen patients (1.1%) had IHMI, of whom nine were early-onset and seven late-onset. The groups were comparable for age (p = .54), gender (p = 1.0), BMI (p = .79), and ASA score (p = 1.0). The most common infectious agent in early-onset IHMI was St. aureus, whereas Enterococci and Enterobacter prevailed in late-onset IHMI. The possible pathogenesis of IHMI in seven patients with early-onset IHMI was primary exogenous infection, whereas in patients with late-onset IHMI the pathogenesis might be hematogenous or contact spread. All patients with IHMI underwent mesh removal. In two patients (one from each group), partial mesh removal was performed previously and IHMI recurred.
Conclusions
Early-onset hernia mesh infection is mostly caused by St. aureus through exogenous contamination, whereas its late-onset counterpart might be a result of hematogenous or contact spread of intestinal flora.
Acknowledgements
Ethical approval: This study was approved by the Ethics Committee of Vladimir City Clinical Hospital of Emergency Medicine with an expedited pathway due to its observational design.
Informed consent: Informed consent was obtained from all included patients.
Presentations: Podium Presentation, American College of Surgeons Clinical Congress, Oct 24, 2018; Boston, MA, USA.
Author’s contributions
All authors have contributed to the following: intellectual conception and design of the work; acquisition, analysis, or interpretation of data for the work; drafting the work or revising it critically for important intellectual content; final approval of the version to be published.
Disclosure statement
No potential conflict of interest was reported by the authors.