Recent years have witnessed a dramatic course of events where total hip arthroplasty (THA) utilizing metal-on-metal (MOM) bearing surfaces has resulted in a unique failure mechanism involving the interaction of bearing wear debris, metal ions, and the surrounding soft tissues.
Although uncommon, development of adverse local tissue reaction (ALTR) has attracted much media attention and resulted in anxiety to the patients. When present, manifestation of ALTR can be dramatic with impressive destruction of periarticular soft tissues, skeletonization of the proximal femur, and purulent fluid collection. When encountered, distinguishing ALTR from periprosthetic joint infection can be difficult. In the early years and before full recognition of ALTR, I subjected a patient with failure of MOM hip replacement to two-stage exchange arthroplasty as I was concerned about the presence of pus in the joint that we had encountered during revision arthroplasty. The latter challenge still continues. The dilemma for the surgeons treating these patients is to unravel the etiology of failure. Considering the fact that patients with MOM failure are also at a slightly higher risk of periprosthetic joint infection makes this distinction critical.1 On the one hand the treating surgeon does not wish to subject the patient to a two-stage exchange arthroplasty if failure is not due to infection and on the other hand missing diagnosis of PJI can result in a suboptimal outcome and the need for further surgical interventions.
The question is what metric, if any, do we have available that will allow the surgeon to reach appropriate diagnosis for failure of a MOM THA? Current clinical, laboratory, and other diagnostic methods with proven utility identifying PJI in patients with metal on polyethylene implants do not clearly delineate septic from aseptic MOM cases. This presents a challenge in managing the patient with a MOM THA and concerns for failure.
Presenting patient symptoms are myriad and non-specific. Patients with aseptic or septic MOM failure generally present with groin pain, typically exacerbated by weight bearing. However, timing of pain onset may offer insight. Persistent pain with no pain-free interval since index surgery may be more indicative of PJI. A draining osteocutaneous sinus is also suggestive of PJI.2 Although elevated ESR and CRP are the hallmark of diagnosis of PJI, they can also be elevated in aseptic failure and ALTR. Cobalt/Chromium ion levels are inconclusive and are observed in many patients with successful MOM implants. Imaging may assist in the evaluation of component positioning or loosening but provide limited discriminatory evaluation of soft tissues and fluid collections. Analysis of joint aspirate is also problematic. The presence of metal and tissue debris in patients with ALTR does not allow proper automated analysis of the synovial fluid and the result obtained for cell count and neutrophil differential may not be reliable. We have instructed our laboratory to perform a manual count of the synovial fluid in these circumstances. One of the promising diagnostic tools is leukocyte esterase dipstick test.3 As the inflammatory response in ALTR cases is mostly mediated by lymphocytes and much less by neutrophils, the LE test appears to be able to distinguish the septic from aseptic failure (institution data). Another great modality, which does depend on availability of a trained musculoskeletal pathologist, is histological examination of retrieved tissues. Again the predominance of lymphocytes is more indicative of ALTR and less of PJI. The presence of neutrophils, with greater than 5 cells per high power field in more than five fields,2 is strongly suggestive of septic etiology for failure.
Intra-operative findings are also similar in cases of PJI when compared with cases of aseptic ALTR. Purulent-appearing fluid under pressure encountered upon entering the joint capsule and metallosis is not unique to PJI. The latter needs to be taken into account when treating these patients. This highlights the importance of an appropriate work up of these patients and having as many data points as possible so that the treating surgeon does not need to make clinical judgments based on the appearance of intra-articular fluid alone.
The milieu of MOM wear debris, metal ions, and interacting tissues promotes an immune micro-environment that presents a challenge in differentiating ALTR associated MOM THA failure from septic failure. More research is required to develop diagnostic methods in distinguishing septic from aseptic failure in MOM THA.
Javad Parvizi, Professor of Orthopaedic Surgery, and Dr Paul Lichstein, Research Fellow, Rothman institute at Thomas Jefferson University, Philedelphia, USA
References
1. Judd, KT, Noiseux, N. Concomitant infection and local metal reaction in patients undergoing revision of metal on metal total hip arthroplasty. Iowa Orthop J 2011;31:59-63.
2. Parvizi, J, Zmistowski B, Berbari EF, et al. New definition of periprosthetic joint infection: from the Workgroup of the Musculoskeletal Infection Society. Clin Orthop Relat Res 2011;469:2992-4.
3. Parvizi, J, Jacovides C, Antoci V, Ghanem E, et al. Diagnosis of periprosthetic joint infection: the utility of a simple yet unappreciated enzyme. J Bone Joint Surg [Am] 2011;93-A:2242-8.
