Purpose: The purpose of this study was to establish patient mortality following salvage treatment (debridement, retention of prosthesis and antibiotic therapy) for infection of primary joint replacement, performed at the unit.

Method: A series of 89 patients underwent salvage treatment for infected primary total joint replacement (47 hips and 42 knees) between 1998 and 2003. The average age of the patients was 70.3 years (range 31.8 to 89.1). A survival analysis was performed using death as the sole endpoint and there were no patients lost to follow-up.

Results: There were a total of 26 deaths with a mean time to death of 3.3 years (range 0.8 to 7.2). The 7-year cumulative patient survival of was 66% (CI 5, number at risk 21).

Conclusions: The morbidity associated with infected total arthroplasty has been well documented. This study highlights that patients undergoing salvage treatment for this condition have significant mortality, with up to a third of patients potentially dying by 7 years.

Osteomyelitis commonly causes bone destruction and is most frequently due to infection by Staphylococcus aureus. S. aureus is known to secrete a number of surface-associated proteins which are extremely potent stimulators of bone resorption in the mouse calvarial assay system. The precise cellular and humoral mechanisms whereby this stimulatory effect is mediated, in particular whether osteoclast formation or activity is directly promoted by these factors, have not been determined by this study. Surface-associated material (SAM)(0.001ug/ml)obtained from 24 hour cultures of S. aureus was added to cultures of mouse and human osteoclast precursors (RAW 264.7 cells and human peripheral blood mononuclear cells respectively). These cultures were incubated in the presence and absence of receptor activator of nuclear factor kappa B ligand (RANKL) and macrophage colony stimulating factor (M-CSF). It was found that independent of RANKL, SAM was capable of inducing osteoclast formation in cultures of RAW cells and human monocytes. This was evidenced by the generation of tartrate-resistant acid phosphatase-positive multinucleated cells, which formed lacunar resorption pits when these cells were cultured on dentine slices. In cultures where M-CSF, RANKL and SAM were added, osteoclast formation was increased, but did not exceed the osteoclast formation in cultures with M-CSF and RANKL. These findings indicate that S. aureus produces a soluble factor which can promote osteoclast formation. Identification of this factor may help to develop therapeutic strategies for treating bone destruction due to Staphylococcal osteomyelitis.

Study Design: A six-year retrospective analysis of all instrumented spinal fusions performed in the Nuffield Orthopaedic Centre and the John Radcliffe Hospital.

Objective: To assess the incidence of infection following instrumented spinal fusion, the nature of the infecting organisms and their subsequent management.

Subjects: All patients who had undergone removal of spinal metalwork were analysed for evidence of infection. The indications for removal of metalwork included proven deep infection, refractory postoperative pain or planned removal after thoraco-lumbar fracture.

Outcome Measures: Successful treatment of infection was documented when the patient was asymptomatic and inflammatory markers remained within normal limits following cessation of antibiotic therapy. Failure was documented when the patient had recurrent sepsis, refractory pain following removal of metalwork or died.

Results: 80 spinal infections following instrumented fusions were found between 1997 and 2003. 34 of the infecting organisms were propionibacteria, 19 were coagulase negative staphylococcus, 10 were staphylococcus aureus, 8 were methicillin resistant staphylococcus aureus, 3 were coliforms, 2 were proteus, 2 were diphtheroids, 1 was alpha haemolytic streptococcus and 1 was anaerobic streptococcus. 29 of these infections were polymicrobial. Of 55 patients who had metalwork removed secondary to pain, 20 patients had proven infection postoperatively (36.3%). Preoperative inflammatory markers failed to accurately predict the presence of infection for trauma patients. Our management of infection is removal of metalwork with six intraoperative samples sent for culture and histology specimens, followed by administration of at least six weeks of intravenous or oral antibiotic, depending on the organism and its antibiotic sensitivity. Prolonged treatment is used where inflammatory markers remain raised.

Conclusions: Infection of spinal implants presents different management problems to those which follow infected total joint replacement. The lack of specific clinical, laboratory and radiological findings in patients who are subsequently diagnosed as having infections associated with spinal instrumentation presents a challenging clinical problem. We found the most predictive sign of infection following instrumented fusion of scoliotic spines was postoperative pain. CRP and ESR were unreliable as predictors of infection.