Dataset Information

Risk of Hernia Mesh Explantation following Early Versus Late Onset Skin and Soft Tissue Infection.

ABSTRACT: To estimate the relative risk of explantation in patients with skin and soft tissue infection onset within 90 days of hernia surgery, compared with days 91-365 and after 1 year.

Background

Infectious complications occurring after hernia repair with synthetic mesh require prolonged treatment, and eventual mesh explantation. Little is known whether early versus late onset infection is associated with differential risk of mesh removal, and whether treatment with long-term antibiotics or debridement are associated with mesh salvage.

Methods

This was a retrospective observational cohort study. We obtained data on all inguinal, umbilical, and ventral hernia repairs with implanted synthetic mesh performed in Veterans Affairs hospitals during 2008-2015. Participants without a 5-year infection after hernia surgery were excluded. Logistic regression estimated the association of mesh explantation with exposure to mesh-related infection during postoperative days 0-90, versus days 91-365 versus after 1 year. Additional covariates included any subsequent abdominal operation, antibiotic administration, and incision and drainage (I&D) or debridement procedures.

Results

One thousand eight hundred eighty-five patients underwent index hernia repair and developed a skin and soft tissue infection within 5 years. Infection onset during days 91-365 was associated with increased explantation risk (OR, 1.62; 95% CI, 1.04-2.48), as was increased antibiotic use (OR, 1.04; 95% CI, 1.03-1.05) and surgical treatments (OR, 3.74; 95% CI, 3.02-4.67). Subsequent abdominal operation was associated with lower explantation risk (OR, 0.46; 95% CI, 0.33-0.61).

Conclusions

Early infections may be more suitable for conservative management. Later-onset infections have lower probability of mesh salvage and should be considered for earlier explantation to save the patients prolonged courses of antibiotics and surgical interventions.

SUBMITTER: O'Brien WJ

PROVIDER: S-EPMC8694247 | biostudies-literature |

REPOSITORIES: biostudies-literature

ACCESS DATA

Similar Datasets

Project description:BackgroundIn ventral hernia surgery, mesh implants are used to reduce recurrence. Infection after mesh implantation can be a problem and rates around 6-10% have been reported. Bacterial colonization of mesh implants in patients without clinical signs of infection has not been thoroughly investigated. Molecular techniques have proven effective in demonstrating bacterial diversity in various environments and are able to identify bacteria on a gene-specific level.ObjectiveThe purpose of this study was to detect bacterial biofilm in mesh implants, analyze its bacterial diversity, and look for possible resemblance with bacterial biofilm from the periodontal pocket.MethodsThirty patients referred to our hospital for recurrence after former ventral hernia mesh repair, were examined for periodontitis in advance of new surgical hernia repair. Oral examination included periapical radiographs, periodontal probing, and subgingival plaque collection. A piece of mesh (1×1 cm) from the abdominal wall was harvested during the new surgical hernia repair and analyzed for bacteria by PCR and 16S rRNA gene sequencing. From patients with positive PCR mesh samples, subgingival plaque samples were analyzed with the same techniques.ResultsA great variety of taxa were detected in 20 (66.7%) mesh samples, including typical oral commensals and periodontopathogens, enterics, and skin bacteria. Mesh and periodontal bacteria were further analyzed for similarity in 16S rRNA gene sequences. In 17 sequences, the level of resemblance between mesh and subgingival bacterial colonization was 98-100% suggesting, but not proving, a transfer of oral bacteria to the mesh.ConclusionThe results show great bacterial diversity on mesh implants from the anterior abdominal wall including oral commensals and periodontopathogens. Mesh can be reached by bacteria in several ways including hematogenous spread from an oral site. However, other sites such as gut and skin may also serve as sources for the mesh biofilm.