Peri-prosthetic Infection Following Total Hip Arthroplasty

Ever since the introduction and clinical establishment of total joint replacement, endoprostheses have helped to improve the quality of life of numerous patients. Nowadays, joint replacement is an indispensable component of modern medicine. Total hip replacement (THR) especially is considered to be one of the most successful performable operations. Approximately 750,000 THRs are performed annually worldwide. Despite aseptic conditions during surgery and peri-operative antibiotic prophylaxis, the implant-associated infection rates are 0.5–2% after primary THR.^1,2 These infections occur more often after revision arthroplasty.³ Due to large implants and immunosuppression by adjuvant radiotherapy and chemotherapy, an infection rate of up to 35% was found in literature⁴ for the endoprosthetic reconstruction after bone resection in case of tumours.

Epidemiology and Pathophysiology
The bacterial peri-prosthetic infection is characterised as follows:¹

• Relatively low bacterial inoculum is being sufficient to trigger an infection.
• Characteristic spectrum consisting of low virulent pathogens from the normal skin flora.
• Inability in many cases to cure the infection without the removal of the foreign body (implant).

It is considered that the minimum forming dose of bacterial pustule is reduced by log¹⁰ in case of presence of a foreign body. ⁵ This reduction of the minimum infection forming dose has also been observed in terms of avital bone and soft tissue.⁶ The so-called race for the surface between human cells and planktonic bacteria, which is crucial for the further fate of the implant, begins directly with the implantation of the biomaterial. ⁷ The fundamental first step of biomaterial-associated infection is bacterial adhesion, triggered by a pathogenetic sequence.⁸ The adhesive colonisation of the biomaterial after the implantation process results in a bacterial resistance against host defence mechanisms and the systemic antibiotic therapy.⁷ This can lead to a transformation of non-pathogenic to pathogenic bacteria resulting in an infection that cannot be cured in numerous cases without the removal of the implant. ¹ To a certain extent, adhesion of bacteria depends on the surface characteristics of the biomaterials. ^9–11 In general, the implant surface exposed to a biological environment is surrounded by a conditioning film. Initially, the surface repels the bacteria as both are anionic. During this phase of bacterial adhesion, physical London-van der Waal’s forces and hydrophobic molecules of bacteria and biomaterial enable an adequate contact time in order to form an irreversible bond.⁷ This initial bond is followed by the proliferation of a biofilm containing bacteria, polysaccharides and ions,¹² which is considered the final stage of infection. By the time of biofilm formation, the bacteria have created a protective environment against host defence mechanisms and antibiotic agents. The biofilm acts as a buffer against the ever-changing influences of the direct environment and simplifies the exchange of nutrients and elimination of waste products.⁹ The ability of biofilm formation and adherence to implant surfaces has been described as an important factor of pathogenicity of bacteria and especially applies to the species of staphylococci.¹¹ Therefore, Staphyloccus aureus and coagulase negative staphylococci, especially S. epidermidis, account for the majority of implant infections (see Table 1 ). ¹ Therefore, S. epidermidis is often found to adhere to polymers, where S. aureus is mainly associated with metallic implant and soft tissue infections.¹³ Furthermore, an increased resistance against antibiotic therapy has been demonstrated for bacteria that colonise medical implants. ^14,15 The implications of a changing pattern of bacterial infections following total joint replacement have been published. ¹⁶ Thereby, a significant increase of multiple-drug resistant pathogens was observed, with methicillin-resistant S. aureus (MRSA) being the most common isolate.¹⁶

In terms of the elapsed ime until implant-associated infection after implantation, an early infection occurs within the first two months, a delayed infection between two to 12 months and a late infection from then onwards. ¹ Specific pathogens are associated with any of these intervals (see Table 2 ). ^1,17 Bacteria may come into contact either with the biomaterial via direct colonisation, per continuitatem or haematogenous and lymphogenous dissemination. Furthermore, it is considered that bacteria causing a peri-prosthetic infection within the first two years after implantation must have reached the host during the operation. If the infection occurs later, a haematogenous or lymphogenous dissemination has to be assumed. ¹⁸

Clinical Diagnostic
A complex diagnostic procedure co-ordinated between clinicians and microbiologists begins, if a peri-prosthetic infection is suspected. The effective functioning of this process has a direct impact on the therapy and hence the prognosis of the patient. ¹

Clinical symptoms and paraclinical parameters of a peri-prosthetic infection are characterised by novel or persisting pain, local reddening or hyperthermia, persisting secretion, tensioned soft tissue, pyrexia, leukocytosis and a novel or persisting elevation of the C-reactive protein (CRP) or erythrocyte sedimentation rate (ESR).¹⁹ A sensitivity of 96% and specificity of 92% in terms of peri prosthetic infections has been described for the CRP and 82 and 85%, respectively, for the ESR. ²⁰ To make a diagnosis, the peri-prosthetic infection score may be used as a diagnostic instrument. A patient with a constant maximum score of five may be considered non-infectious or healed.²¹