| Diagnosis of orthopaedic prosthesis infections with radionuclide techniques; clinical application of various imaging methods | ||
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Primary thromboembolic complications have been reported in 1.4%, luxations in 1.4%, infections in 0.9% and evacuated hematomas in 0.6% of operations in the Finnish Arthroplasty Register. Data from the register indicate that the results of replacements are improving. The most common reasons for revision are aseptic loosening (65%), dislocation (9%) and infection (7%). (Paavolainen et al. 1991, Puolakka et al. 2001)
There is evidence to suggest that a significant number of cases of aseptic loosening result from an inflammatory reaction. Histological examinations of failed prostheses show a pseudo-membranous structure that develops at the cement-bone interface, the cellular composition of which varies: histiocytes are seen most frequently (95% of specimens), followed by giant cells (80%) and lymphocytes and plasma cells (25%). Neutrophils are present in less than 10% of cases. It is believed that particulate debris from component fragmentation activates phagocytes around the prosthesis. This debris is resistant to enzymatic destruction, leading to repeated attempts at phagocytosis, which stimulate the secretion of cytokines and proteolytic enzymes that damage bone and cartilage (Peersman et al. 2001, Spangehl et al. 1999, Ure et al. 1998). Tunney et al. (1999) found infiltration of neutrophils, lymphocytes or macrophages into tissue associated with prostheses in 73% of 120 patients undergoing total hip revision surgery.
High rates of infection complicated the early experience of arthroplasty, and infection is still a source of considerable morbidity. In the 1960s, Charnley considered a rate of infection of 7% as unacceptable (Charnley & Eftekhar 1969). More recently, authors have reported infection-related failures in 1% to 2% of primary total hip prostheses and in 2% of knee prostheses. The rate is higher after revision procedures, being about 3% for hip prostheses and 5% for knee prostheses (Spangehl et al. 1998). In a recent review of 6489 total knee replacements carried out between 1993 and 1999, as low an infection incidence as 0.39% was reached in primary operations, while the incidence in revision operations was 0.97% (Peersman et al. 2001).
In a study using immunological and DNA detection methods and culture for the detection of bacteria in the hip prostheses retrieved from 120 patients undergoing total hip revision surgery, bacterial DNA was detected in 72% of samples by PCR amplification techniques. All the culture-positive samples were also positive for bacterial DNA. Bacteria were also detected by immunolabelling and fluorescence microscopy after the prostheses had been subjected to ultrasonic treatment in 62% of the cases. The authors concluded that unrecognised infection is a potential major cause for prosthetic hip failure (Tunney et al. 1999). The question remains open at present.
Although the risk factors for joint prosthesis infections have not been established, there is evidence that at least diabetes and psoriasis increase the risk of joint replacement infections. Long operating time is a considerable risk factor, and it has been shown that an operating time longer than 2.5 hours increases the risk of infection significantly. (England et al. 1990, Peersman et al. 2001, Stern et al. 1989)
In addition to standard aseptic techniques, there are other documented countermeasures available to reduce the incidence of infections. These include the use of ultra-clean air and laminar flow in the operating theatre, the use whole-body exhaust-ventilated suits by the surgeons and antibiotic prophylaxis for the patient.
The effect of ultra-clean air was shown to reduce the incidence of infections to about half, and when whole-body exhaust-ventilated suits were added, the incidence was further reduced to about one quarter of the original incidence in a series of over 8000 operations (Lidwell et al. 1982). In a recent series of over 6000 operations with an especially low incidence of infections, the operations were made in a theatre with vertical laminar flow and with the surgical team using body exhaust suits (Peersman et al. 2001).
The effect of antibiotic prophylaxis was proved in a double-blind, placebo-controlled trial of 2137 patients undergoing hip replacement in nine centres, in which five days of prophylactic treatment reduced the number of infections significantly from 3.3% to 0.9% (Hill et al. 1981). The duration of antibiotic prophylaxis has varied, and in a recent study with excellent results, there was no change in the infection rate when the duration of antibiotic prophylaxis was decreased from 48 to 24 hours after surgery (Peersman et al. 2001).
Staphylococcus epidermidis (31% of cases) and Staphylococcus aureus (20%) are the most common bacteria, whereas Streptococcus viridans (11%), Escherichia coli (11%), Enterococcus faecalis (8%) and group B Streptococci (5%) are less frequently encountered (Davis et al. 1999, Evans et al. 1998, Gaine et al. 2000, Peersman et al. 2001, Segawa et al. 1999, Spangehl et al. 1998). Microorganisms also include anaerobes, gram-negative bacilli, such as Pseudomonas species or, especially in hematogenous infections, Streptococci. Propionibacterium species were isolated in 60% of orthopaedic device infections by using anaerobic bacteriologic practices (Tunney et al. 1999). Propionibacterium species are also the second most frequent contaminant observed in joint aspiration (Widmer 2001).
Understanding of the pathogenesis of biofilm formation facilitates optimal diagnosis and treatment. It also explains why signs and symptoms are relieved by short-term treatment with antimicrobial agents but reoccur soon after withdrawal of treatment. All prostheses undergo physiological changes after implantation. The earliest and probably clinically the most important step is the competition between tissue cell integration and bacterial adhesion to the same surface. Upon contact, body fluids immediately coat all surfaces with a layer of material, primarily serum proteins and platelets. Albumin, the major serum component, is rapidly deposited on foreign material and prevents non-specific neutrophil activation and deposition of matrix proteins on the surfaces. Adherence of Staphylococcus aureus to bioprosthetic materials is mediated by adhesins, such as fibronectin, fibrinogen, fibrin, collagen, laminin, vitronectin, thrombospondin, bone sialoprotein, elastin and matrix-binding proteins, which promote attachment onto polymeric or metallic surfaces by specific receptors. Adherence of microorganisms progresses to aggregation on the surface of the prosthesis, forming a biofilm. As the colonies mature, sessile bacteria detach and disperse as planktonic bacteria. Costerton et al. (1999) defined bacterial biofilms as ”structured communities of bacterial cells enclosed in a self-produced polymeric matrix and adherent to an inert or living surface”. These types of surfaces are frequently present in prostheses. Biofilms grow slowly and resist cellular and humoral immune responses. Moreover, several mechanisms render bacteria protected by biofilm less susceptible to antimicrobial agents than their planctonic counterparts. Clinically established mechanisms include adherence, slime production, and a slow rate of bacterial growth. Bacteria become sessile in the biofilm, their features change considerably, and they become resistant through several mechanisms. Two clinically important mechanisms are the failure of antimicrobial agents to penetrate the biofilm and the stationary phase of growth. In addition, some bacteria form small-colony variants, characterised by a reduced growth rate, diminished exoprotein production, decreased susceptibility to aminoglycosides and, possibly, intracellular persistence. Standard antibiotic therapy typically alleviates symptoms caused by planktonic bacteria released from the biofilm but fails to kill the bacteria in the biofilm. Therefore, successful treatment of prosthesis infections with retention of the implant must incorporate treatment against both planktonic and sessile bacteria. Another possibility is to kill planktonic bacteria by antimicrobial agents and to remove the implant to get rid of sessile bacteria. (Widmer 2001)
A variety of microorganisms develop slime, an amorphous extracellular glycocaliceal substance based on polysaccharide, which promotes intracellular adhesion, captures nutrients and protects microorganisms from the effects of antimicrobial agents. Slime can also block penetration of antibiotics into the bacterial cell and decrease chemotaxis of neutrophil granulocytes. (Widmer 2001)
Bacteria in biofilm do not grow exponentially. They exist in a slow-growing or stationary phase. Studies of orthopaedic device-related infections in an animal model have confirmed the slow growth of Staphylococcus aureus and Escherichia coli. (Costerton et al. 1999)