Abstract
BackgroundThe most common cause of implant failure is aseptic loosening (AL), followed by prosthetic joint infection (PJI). This study evaluates the incidence of PJI among patients operated with suspected AL and whether the diagnosis of PJI was predictive of subsequent implant failure including re-infection, at 2 years of follow up.MethodsPatients undergoing revision hip or knee arthroplasty due to presumed AL from February 2009 to September 2011 were prospectively evaluated. A sonication fluid of prosthesis and tissue samples for microbiology and histopathology at the time of the surgery were collected. Implant failure include recurrent or persistent infection, reoperation for any reason or need for chronic antibiotic suppression.ResultsOf 198 patients with pre-and intraoperative diagnosis of AL, 24 (12.1 %) had postoperative diagnosis of PJI. After a follow up of 31 months (IQR: 21 to 38 months), 9 (37.5 %) of 24 patients in the PJI group had implant failure compared to only 1 (1.1 %) in the 198 of AL group (p < 0.0001). Sensitivity of sonicate fluid culture (>20 CFU) and peri-prosthetic tissue culture were 87.5 % vs 66.7 %, respectively. Specificities were 100 % for both techniques (95 % CI, 97.9–100 %). A greater number of patients with PJI (79.1 %) had previous partial arthroplasty revisions than those patients in the AL group (56.9 %) (p = 0.04). In addition, 5 (55.5 %) patients with PJI and implant failure had more revision arthroplasties during the first year after the last implant placement than those patients with PJI without implant failure (1 patient; 6.7 %) (RR 3.8; 95 % CI 1.4-10.1; p = 0.015). On the other hand, 6 (25 %) patients finally diagnosed of PJI were initially diagnosed of AL in the first year after primary arthroplasty, whereas it was only 16 (9.2 %) patients in the group of true AL (RR 2.7; 95 % CI 1.2–6.1; p = 0.03).ConclusionsMore than one tenth of patients with suspected AL are misdiagnosed PJI. Positive histology and positive peri-implant tissue and sonicate fluid cultures are highly predictive of implant failure in patients with PJI. Patients with greater number of partial hip revisions for a presumed AL had more risk of PJI. Early loosening is more often caused by hidden PJI than late loosening.
Highlights
The most common cause of implant failure is aseptic loosening (AL), followed by prosthetic joint infection (PJI)
First using a sonication method to remove biofilm bacteria from AL of orthopedic implants, 3 studies have reported positive sonicate-fluid cultures in 9.5, 11.2 and 57.7 % of the patients, respectively [4,5,6]; secondly an association has been found between the degree of osteolysis and sonication cultures in patients with AL of hip and knee implants [6]; and third, the ability of bacterial subpopulations to switch to strains resulting in an unusual morphological appearance called small-colony variants (SCVs), which often remain undetected [7]
Three out of the 24 PJI cases were diagnosed by histopathological findings; 8 had histopathology and positive periprosthetic tissue and sonicate fluid cultures; 8 had positive periprosthetic tissue and sonicate fluid cultures; 4 had histopathology and positive sonicate fluid cultures; and 1 had positive sonicate fluid culture (Fig. 1)
Summary
The most common cause of implant failure is aseptic loosening (AL), followed by prosthetic joint infection (PJI). Infection is a challenging problem associated with orthopedic implants It is projected in the United States that the percentages of deep implant infections for hip and knee arthroplasties will increase from 8.4 to 47.5 % and from 16.8 to 65.5 %, respectively, through 2030 [1, 2]. First using a sonication method to remove biofilm bacteria from AL of orthopedic implants, 3 studies have reported positive sonicate-fluid cultures in 9.5, 11.2 and 57.7 % of the patients, respectively [4,5,6]; secondly an association has been found between the degree of osteolysis and sonication cultures in patients with AL of hip and knee implants [6]; and third, the ability of bacterial subpopulations to switch to strains resulting in an unusual morphological appearance called small-colony variants (SCVs), which often remain undetected [7]
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