Deep Sternal Wound Infections After Cardiac Surgery: A New Australian Tertiary Centre Experience

Abstract

Deep sternal wound infections (DSWI) after cardiac surgery impose a significant burden to patient outcomes and health care costs. The objective of this study is to identify risk factors, microbiological characteristics and protective factors for deep sternal wound infections following cardiac surgery in an Australian hospital. We performed a retrospective study on 1,902 patients who underwent cardiac surgery at Fiona Stanley Hospital, a tertiary hospital in Western Australia from February 2015 to April 2019. Patients were grouped into having either deep sternal wound infections or no wound infections. Of 1,902 patients, 26 (1.4%) patients had DSWI. On multivariate analysis, male gender was associated with DSWI with an adjusted odds ratio of 7.390 (95% CI 1.189-45.918, p=0.032). Increased body mass index (BMI) had an odds ratio of 1.101 (95% 1.03-1.18, p=0.008). Increased length of stay (LOS) had an odds ratio of 1.05 (95% CI 1.02-1.08, p=0.002). Left main disease had an odds ratio of 3.076 (95% CI 1.204-7.86, p=0.019). The presence of hypercholesterolaemia had an odds ratio of 0.043 (95% CI 0.009-0.204, p<0.001). Staphylococcus aureus and Staphylococcus epidermidis were the most common organisms found in deep sternal wound infections (23.1% and 26.9% respectively). Polymicrobial growth occurred in 19.2% of patients. One gram of topical cephazolin was applied in 315 patients. None of these patients developed a deep sternal wound infection (p=0.022). In a large Australian tertiary centre, male gender, increased BMI, presence of left main coronary artery disease, and increased length of hospital stay are significantly associated with the risk of deep sternal wound infections. Staphylococcus aureus and Staphylococcus epidermidis are common organisms in deep sternal wound infections. Topical antibiotics such as cephazolin are useful in preventing deep sternal wound infections. The presence of hypercholesterolaemia is a protective factor and we hypothesise that this is due to long-term statin use.