We wished to estimate the incidence of surgical-site infection (SSI) after total hip replacement (THR) and hemiarthroplasty and its strength of association with major risk factors. The SSI surveillance service prospectively gathered clinical, operative and infection data on inpatients from 102 hospitals in England during a four-year period. The overall incidence of SSI was 2.23% for 16,291 THRs, 4.97% for 5769 hemiarthroplasty procedures, 3.68% for 2550 revision THRs and 7.6% for 198 revision hemiarthroplasties. Staphylococcus aureus was identified in 50% of SSIs; 59% of these isolates were methicillin-resistant (MRSA). In the single variable analysis of THRs, age, female gender, American Society of Anesthesiologists (ASA) score, body mass index, trauma, duration of operation and pre-operative stay were significantly associated with the risk of SSI (p < 0.05). For hemiarthroplasty, the ASA score and age were significant factors. In revision THRs male gender, ASA score, trauma, wound class, duration of operation and pre-operative stay were significant risk factors. The median time to detection of SSI was eight days for superficial incisional, 11 days for deep incisional and 11 days for joint/bone infections. For each procedure the mean length of stay doubled for patients with SSI. The multivariate analysis identified age group, trauma, duration of operation and ASA score as significant, independent risk factors for SSI. There was significant interhospital variation in the rates of SSI. MRSA was the most common pathogen to cause SSI in hip arthroplasty, especially in patients undergoing hemiarthroplasty, but coagulase-negative Staph. aureus may be more important in deep infections involving the joint.

No abstract

In the three years between November 1989 and October 1992, an outbreak of methicillin-resistant Staphylococcus aureus (MRSA) affected 990 patients at a university hospital. The distribution of patients with carriage, colonization or infection was investigated prospectively. Nosocomial acquisition was confirmed in at least 928 patients, 525 of whom were identified from clinical specimens as being infected (n = 418) or colonized (n = 107) by MRSA. An additional 403 patients were identified from screening specimens, of whom 58 subsequently became infected and 18 colonized. Screening of the nose, throat and perineum detected 98% of all carriers. Of the 580 infections in 476 patients, surgical wound, urinary tract and skin infections accounted for 58% of the infections. Of the 476 infected patients, death was attributable to MRSA infection in 13%. Colonization with MRSA was found in 127 patients and 42% of 165 colonized sites were the skin. Auto-infection from nasal carriage or cross-infection, probably via staff hands, seemed to be the most common mode of acquisition of MRSA infections.

In hospital outbreaks of methicillin-resistant Staphylococcus aureus (MRSA) many patients are initially colonized without infection. The reasons why some progress to infection while others do not are not known. A cohort of 479 hospital patients, initially only colonized with MRSA, was followed prospectively for the development of MRSA infection. Risk factors for progression to infection were assessed using Cox proportional hazards survival analysis. Fifty-three patients (11 .l%) developed 68 MRSA infections. Intensive care setting, administration of three or more antibiotics, ulcers, surgical wounds, nasogastric or endotracheal tubes, drains, and urinary or intravenous catheterization were all associated with increased rates of MRSA infection. Multivariate analysis showed that intensive care patients, compared with medical natients. had a higher rate of develoning MRSA infection within the first' four days of admission, with a hazard ra;o of 26.9 (95% CI 5.7-126). Surgical wounds, pressure ulcers and intravenous catheterization were also independent risk factors, with hazard ratios (and 95% CI) of 2.9 (1.3-6.3), 3.0 (1.6-5.7) and 4.7 (l+15.6), respectively. These findings suggest that, during an MRSA outbreak, clinical infection would be reduced if surgical and intensive care patients received priority for the prevention of initial colonization with MRSA. Prevention of pressure ulcers, and strict aseptic care of intravenous catheters and surgical wounds would also reduce the development of MRSA infection. Since early treatment with vancomycin is known to reduce the mortality, patients colonized with MRSA who also have one or more of these risk factors may warrant empirical vancomycin therapy at the earliest suggestion of infection.

No abstract