Some aspects of the development of infectious complications in arthroplasty

Hip replacement surgery has taken a leading place in the surgical treatment of severe forms of hip joint pathology. This operation eliminates or significantly reduces pain, restores joint movement, provides support for the limb, improves gait and, as a result, significantly improves the patient's quality of life. But it is no secret that any surgical treatment can also have a number of complications, one of which is infection. According to literature, an orthopedic center that performs large joint replacement surgery and performs at least 100 surgeries per year can have a 17% infectious complication rate in the first year, this rate decreases by 5% in the second year, by 3% in the third year and can average 4%.

The problem of infectious complications in endoprosthetics of large joints is becoming more and more urgent every day, despite the active use of antibiotic prophylaxis and modern methods of surgical antisepsis. This is due to the growth in the number of institutions practicing arthroplasty, the difficulty of identifying the pathogen, the complexity of treatment and the severity of the consequences. All this ultimately leads to deterioration of the results of the intervention, an increase in the cost and terms of postoperative rehabilitation of patients.

The problem is also caused by the general status, especially of an elderly patient, in which the body has a very difficult time fighting infection. The immunosuppressive state is caused by induced secondary immunodeficiency after a highly traumatic long-term surgical intervention and the entry of tissue destruction products into the blood, as well as age-related features of the immune system in elderly patients.

The increase in the number of arthroplasties along with a high rehabilitation potential is accompanied by an increase in cases of deep infection in the area of surgical intervention, amounting, according to domestic and foreign authors, from 0.3% to 1% in primary intervention, and up to 40% or more in revision. Treatment of such infectious complications is a long process requiring the use of expensive medications and materials. It was once considered absolutely unacceptable to implant an endoprosthesis in an area affected by infection. However, the development of an understanding of the pathophysiology of infection associated with implants, as well as progress in surgical technique, made successful endoprosthetics possible even in these conditions.

Most surgeons agree that removal of the endoprosthesis components and careful surgical treatment of the wound are an important initial stage of patient treatment. However, there is still no consensus on methods that can restore the functional state of the joint without pain and with a minimal risk of recurrence of infection.

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Stages of biofilm formation

Stage 1. Reversible attachment to the surface. Most often, microorganisms exist as free-floating masses or single (e.g., planktonic) colonies. However, under normal conditions, most microorganisms tend to attach to the surface and, ultimately, form a biofilm.

Stage 2. Permanent adhesion to the surface. As bacteria multiply, they adhere more firmly to the surface, differentiate, and exchange genes, which ensures their survival.

Step 3: Formation of a mucus protective matrix/biofilm. Once firmly attached, bacteria begin to form an exopolysaccharide surrounding matrix known as an extracellular polymeric substance. This is the EPS matrix. Small colonies of bacteria then form the initial biofilm. The composition of the EPS matrix varies depending on the specific microorganisms present, but it generally includes polysaccharides, proteins, glycolipids, and bacterial DNA. A variety of proteins and enzymes help the biofilm adhere more firmly to the wound bed. Fully formed (mature) biofilms continually shed planktonic bacteria, microcolonies, and fragments, which can disperse and adhere to other parts of the wound bed or to other wound surfaces to form new biofilm colonies.

How quickly does biofilm form?

Experimental laboratory studies have shown that planktonic bacteria, such as staphylococci, streptococci, pseudomonas, and E. coli, usually:

1. join each other within a few minutes;
2. form firmly attached microcolonies within 2-4 hours;
3. produce extracellular polysaccharides and become significantly more tolerant to biocides, such as antibiotics, antiseptics and disinfectants, within 6-12 hours;
4. are involved in full-fledged biofilm colonies, which are very resistant to biocides and lose planktonic bacteria within 2-4 days depending on the type of bacteria and growth conditions;
5. rapidly recover from mechanical destruction and re-form a mature biofilm within 24 hours. These facts suggest that several successive wound cleansings may provide a short period of time, for example, less than 24 hours, during which antimicrobial treatment is most effective against both planktonic microorganisms and intra-biofilm pathogen cells in the wound.

Can you see microbial biofilm?

Biofilms are microscopic structures. However, in some situations, when allowed to grow unchecked for an extended period of time, they become so dense that they can be seen with the naked eye. For example, dental plaque can accumulate and become clearly visible within a day. Some bacteria in the phenotype produce pigments that can facilitate visual detection of the entire biofilm. For example, P. aeruginosa, being in the biofilm phenotype, produces the green molecular pyocyanin in the "quorum sensing" system. But even in this case, green staining of the wound does not always indicate the presence of a biofilm formed by Pseudomonas sp.

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Can biofilms be found in scabs?

Eschar is described as a thick, yellow, relatively dark layer of the wound bed, whereas biofilms found in wounds appear more gelatinous and lighter. However, there may be a relationship between biofilms and eschar. Biofilms stimulate inflammation, which increases vascular permeability, wound exudate formation, and fibrin eschar formation. Thus, the presence of eschar may indicate the presence of biofilm in the wound. However, such a relationship between eschar and biofilm in chronic wounds needs to be studied more thoroughly.

Currently, the most reliable method for confirming the presence of microbial biofilm is specialized microscopy, such as confocal laser scanning microscopy.

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Classification

The use of an effective classification is important for choosing a rational method of treatment and comparing its results. Despite the diversity of proposed classification systems, there is no single internationally accepted system for constructing a diagnosis and subsequent treatment of paraendoprosthetic infection, i.e. the treatment of infectious complications after endoprosthetics is not standardized.

The most common classification of deep infection after total hip arthroplasty is by MB Coventry (1975) - RH Fitzgerald (1977). The main classification criterion is the time of infection manifestation (the time interval between the operation and the first manifestation of the infectious process). Based on this criterion, the authors proposed three main clinical types of deep infection. In 1996, DT Tsukayama et al. supplemented this classification with type IV, defined as a positive intraoperative culture. This type of paraendoprosthetic infection means asymptomatic bacterial colonization of the endoprosthesis surface, which manifests itself in the form of positive intraoperative cultures of two or more samples with isolation of the same pathogen. Positive cultures of 2-5 intraoperative samples. Depending on the type of infection, the authors recommended a certain treatment strategy.

Classification of deep infection after total hip arthroplasty (Coventry-Fitzgerald-Tsukayama)

1. Acute postoperative infection - within the first month
2. Late chronic infection - from one month
3. Acute hematogenous infection - up to one year
4. Positive intraoperative culture - after one year or more

Thus, with type I infection, revision with necrectomy, replacement of the polyethylene liner and preservation of the remaining components of the endoprosthesis is considered justified. With type II infection, during revision with mandatory necrectomy, removal of the endoprosthesis is required, and in patients with type III paraendoprosthetic infection, an attempt to preserve the endoprosthesis is possible. In turn, when diagnosing a positive intraoperative culture, treatment can be conservative - suppressive parenteral antibiotic therapy for six weeks.
Features of the pathogenesis of paraendoprosthetic infection.

Paraendoprosthetic infection is a special case of implant-associated infection and, regardless of the pathogen penetration routes, development time and severity of clinical manifestations, is specific to endoprosthetics. In this case, the leading role in the development of the infectious process is given to microorganisms, their ability to colonize biogenic and abiogenic surfaces.

Microorganisms can exist in several phenotypic states: adherent - biofilm form of bacteria (biofilm), free-living - planktonic form (in solution in a suspended state), latent - spore. The basis of the pathogenicity of microbes causing paraendoprosthetic infections is their ability to form special biofilms (biofilms) on the surfaces of implants. Understanding this fact is extremely important for determining rational treatment tactics.

Bacterial colonization of the implant can be accomplished through two alternative mechanisms. By direct non-specific interaction between the bacterium and the artificial surface not covered with host proteins due to electrostatic field forces, surface tension forces, Vander-Wils forces, hydrophobicity and hydrogen bonds (the first mechanism). It has been shown that there is selective adhesion of microbes to the implant depending on the material from which it is made. Adhesion of St. epidermidis strains occurs better to polymer parts of the endoprosthesis, and St. aureus strains - to metal ones.

In the second mechanism, the material from which the implant is made is coated with "host" proteins, which act as receptors and ligands that bind the foreign body and microorganism together. It should be noted that all implants undergo so-called physiological changes, which result in the implant being coated almost instantly with plasma proteins, primarily albumin.

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How do biofilms interfere with the wound healing process?

During the release of the wound surface from the biofilm, the latter stimulates a chronic inflammatory response. This reaction results in the appearance of large numbers of neutrophils and macrophages surrounding the biofilm. These inflammatory cells produce large numbers of reactive oxidants and proteases (matrix metalloproteinases and elastases). Proteases help disrupt the attachment of the biofilm to tissues, removing it from the wound. However, these reactive oxidants and proteases also destroy healthy and healing tissues, proteins, and immune cells, which impairs the quality of treatment.

The chronic inflammatory response does not always lead to successful removal of the biofilm, and it has been hypothesized that such a response is “beneficial” to the biofilm. By inducing an ineffective inflammatory response, the biofilm protects the microorganisms that form it and increases the production of exudate, which in turn is a source of nutrition and a means of maintaining the biofilm.

Are there conditions that promote biofilm formation in a wound?

It is not known whether there are conditions that favor the formation of biofilm in a wound. However, underlying conditions that weaken the immune system or reduce the effects of antibiotics may favor the development of biofilm in wounds (e.g., tissue ischemia or necrosis, poor nutrition).

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What are the principles of biofilm management?

Even if there is a high probability that a wound contains biofilm, there is no single-step treatment. A combination strategy that uses elements of wound bed preparation to remove the biofilm mass and prevent biofilm remodeling may be optimal. This approach is sometimes referred to as “biofilm-based wound care.”

How do I know if the biofilm has been removed?

The lack of clear symptoms and established laboratory methods for identifying microbial communities makes it difficult to pinpoint the moment when a wound is free of biofilm. The most indicative is progressive wound healing, characterized by a decrease in exudate secretion and sloughing of the eschar. Until definitive guidelines are developed, clinicians will have to make decisions about how to treat biofilm-affected wounds on a case-by-case basis. For example, when treatment is successful, it may be necessary to change the method or frequency of wound care or to consider the need for topical antimicrobials. Additional measures to stimulate wound healing should be considered in the context of the patient's health status and should be aimed at supporting the immune system. Thus, biofilms influence the course of chronic inflammatory diseases, and recent data suggest that they also play a significant role in disrupting the healing process of chronic wounds. Biofilms have a high level of tolerance to antibodies, antibiotics, antiseptics, disinfectants and phagocytes. Current treatments for wounds with biofilms include mandatory frequent wound cleaning in combination with the use of wound dressings and antimicrobial agents to prevent wound reinfection and inhibit biofilm reformation.

When considering the etiopathogenesis of wound infection, it should be taken into account that any local infectious focus should be considered as a pathological biocenosis from a microbiological standpoint. This means that any microbiota located in a given focus is capable of actively participating in the infectious process only insofar as it finds optimal conditions for the existence and manifestation of all vegetative functions, including the maximum realization of its pathogenicity for the host organism. Recognition of this position, in turn, serves as the basis for subsequent conclusions. If the initial pathogenicity of the pathogen is high enough, and the natural mechanisms of anti-infective defense of the host are insufficient or weakened by some background pathological process, then the formation of a pathological biotope can be a consequence of the gradual development of the infectious process itself.

Candidate of Medical Sciences Garifullov Gamil Gakilievich. Some aspects of the development of infectious complications during arthroplasty // Practical Medicine. 8 (64) December 2012 / Volume 1