Postoperative SSIs are believed to occur via bacterial inoculation at the time of surgery or as a result of bacterial contamination of the wound via open pathways to the deep tissue layers.1–3 The probability of SSI is reflected by interaction of parameters that can be categorized into three major groups.2 The first group consists of factors related to the ability of bacteria to cause infection and include initial inoculation load and genetically determined virulence factors that are required for adherence, reproduction, toxin production, and bypassing host defense mechanisms. The second group involves those factors related to the defense capacity of the host including local and systemic defense mechanisms. The last group contains environmental determinants of exposure such as size, time, and location of the surgical wound that can provide an opportunity for the bacteria to enter the surgical wound, overcome the local defense system, sustain their presence, and replicate and initiate local as well as systemic inflammatory reactions of the host. The use of iodine impregnated skin incise drapes shows decreased skin bacterial counts but no correlation has been established with SSI. However, no recommendations regarding the use of skin barriers can be made (see this Workgroup, Question 27).
Alijanipour P, Karam J, Llinás A, et al. Operative environment. J Orthop Res 2014;32(suppl 1):S60–S80.