Some aspects of development of infectious complications in arthroplasty

Endoprosthetics of the hip joint took the leading place in the surgical treatment of severe forms of hip joint pathology. This operation eliminates or significantly reduces the pain syndrome, restores movement in the joint, ensures limb bearing ability, improves gait and, as a result, significantly improves the patient's quality of life. But it's no secret that any surgical treatment can carry a number of complications, one of which is an infection. According to the literature, the orthopedic center, engaged in endoprosthetics of large joints and performing at least 100 operations per year, for the first year can get the number of infectious complications - 17%, in the second year this amount is reduced by 5%, for the third by 3% and on average can be 4%.

The problem of infectious complications in endoprosthetics of large joints is becoming more important day by day, despite the active use of antibiotic prophylaxis and modern methods of surgical antiseptics. This is due to the growing number of institutions practicing arthroplasty, the difficulty in identifying the causative agent of the infection, the complexity of treatment and the severity of the consequences. All this eventually leads to a deterioration in the results of the intervention, an increase in the cost and timing of postoperative rehabilitation of patients.

The problem is caused by the general status, especially the elderly patient, in which the organism is extremely difficult to fight with the infection. The immunosuppressive state is caused by induced secondary immunodeficiency after a highly traumatic prolonged operation and the entry into the blood of tissue destruction products, as well as the age-related features of the immune system in elderly patients.

The increase in the number of arthroplasty along with the high rehabilitation potential is accompanied by an increase in the number of cases of deep infection in the field of surgical intervention, accounting for 0.3% to 1% for primary and foreign patients, and 40% or more for the revision. Treatment of such infectious complications is a long process, requiring the use of expensive medications and materials. Once it was considered absolutely unacceptable to implant an endoprosthesis in the area affected by the infection. However, the development of an understanding of the pathophysiology of infection associated with implants, as well as progress in surgical technique, made it possible to successfully undergo endoprosthetics in these conditions.

Most surgeons agree that removing the components of the endoprosthesis and careful surgical treatment of the wound are an important initial stage in the treatment of the patient. 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.

[1], [2], [3]

Stages of biofilm formation

Stage 1. Reversible attachment to the surface. Most often, microorganisms exist in the form of freely floating masses or single (eg, planktonic) colonies. However, under normal conditions, most microorganisms tend to attach themselves to the surface and, ultimately, form biofilms.

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

Stage 3. Formation of mucous protective matrix / biofilm. Once firmly attached, the bacteria begin to form an exopolysaccharide surrounding matrix, known as the extracellular polymeric substance. This is a protective matrix or "slime" (EPS-matrix). Small bacterial colonies then form the original biofilm. The composition of the matrix mucus varies according to what microorganisms are present in it, but mainly it includes polysaccharides, proteins, glycolipids and bacterial DNA. A variety of proteins and enzymes contribute to more durable adhesion of biofilms to the wound bed. Completely formed (mature) biofilms permanently lose plankton bacteria, microcolonies and fragments that can dissipate and adhere to other parts of the wound bed or to surfaces of other wounds, forming new colonies of biofilms.

How quickly does the biofilm form?

Experimental laboratory studies have shown that plankton bacteria, for example, staphylococci, streptococci, pseudomonas, E. Coli are usually:

1. join each other within a few minutes;
2. form firmly attached microcolonies for 2-4 hours;
3. produce extracellular polysaccharides and become much more tolerant to biocides, for example, antibiotics, antiseptics and disinfectants, for 6-12 hours;
4. are involved in full colonies of biofilms that are very resistant to biocides and lose plankton bacteria within 2-4 days depending on the species of bacteria and growth conditions;
5. quickly recover after mechanical failure and again form a mature biofilm for 24 hours. These facts suggest that several successive wounds can be treated for a short time, for example, less than 24 hours, during which antimicrobial treatment is most effective against both plankton microorganisms and intra-biofilm cells of the pathogen in the wound.

Can I see a microbial biofilm?

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

[4], [5], [6], [7], [8], [9], [10]

Can biofilms be found in the scab?

The wound corpse is described as a thick yellow, relatively dark layer of the wound bed, whereas biofilms found in the wounds look more gel-like and lighter. Nevertheless, there may be a connection between the biofilms and the scab. Biofilms stimulate inflammation, which increases vascular permeability, the formation of wound exudate and the formation of fibrin scab. Thus, the presence of a scab can indicate the presence of a biofilm in the wound. However, such a connection between a scab and a biofilm in chronic wounds should be studied more thoroughly.

Currently, the most reliable method of confirming the presence of microbial biofilm is a special microscopy, for example, confocal laser scanning microscopic examination.

[11], [12], [13], [14]

Classification

The use of effective classification is important for choosing a rational method of treatment and comparing its results. With all the variety of proposed classification systems, there is no single international accepted system for the diagnosis and subsequent treatment of para- endoprosthetic infection, i.e. Treatment of infectious complications after endoprosthetics is not standardized.

The most common is the classification of a deep infection after complete hip arthroplasty 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 and co-authors supplemented this classification with type IV, defined as a positive intraoperative culture. This type of para- endoprosthetic infection means asymptomatic bacterial colonization of the endoprosthesis surface, which manifests itself in the form of positive intraoperative sowing of two or more specimens with the isolation of the same pathogenic organism. Positive cultures 2-5 intraoperative specimens. Depending on the type of infection, the authors recommended a certain therapeutic tactic.

Classification of deep infection after complete 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 a year
4. Positive intraoperative culture - a year or more later

So, at type I of infection it is considered reasonable to audit with nekrektomiey, replacement of polyethylene liner and preservation of other components of endoprosthesis. In type II infection, revision with mandatory necrosectomy requires the removal of an edentulous prosthesis, and in patients with type III para-endoprosthetic infection an attempt is possible to preserve the endoprosthesis. 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.

Paraendoprosthesis infection is a special case of implant-associated infection and regardless of the pathways of the pathogen, the time of development and the severity of clinical manifestations is specific for endoprosthetics. The leading role in the development of the infectious process is assigned 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 - a dispute. The basis of pathogenicity of microbes that cause para-endoprosthetic infections is their ability to form special biofilms (biofilms) on the surfaces of implants. Understanding this fact is extremely important for determining rational therapeutic tactics.

Bacterial colonization of the implant can be carried out through two alternative mechanisms. By direct non-specific interaction between the bacterium and the artificial surface, which is not covered by the host proteins, due to the forces of the electrostatic field, surface tension forces, the Vaander-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 occurs better to the polymer parts of the endoprosthesis, and strains of St. Aureus - to metal.

In the second mechanism, the material from which the implant is made is coated with host proteins that act as receptors and ligands that bind together the foreign body and the microorganism. It should be noted that all implants undergo so-called physiological changes, as a result of which almost instantaneous coating of the implant with plasma proteins, mainly albumin, occurs.

[15], [16]

How do biofilms interfere with the healing process?

During the release of the wound surface from the biofilm, the latter stimulates a chronic inflammatory response. This reaction leads to the appearance of a large number of neutrophils and macrophages surrounding the biofilm. These inflammatory cells form a large number of reactive oxidants and proteases (matrix metalloproteinases and elastases). Proteases contribute to disruption of biofilm attachment to tissues, removing it from the wound. However, these reactive oxidants and proteases also destroy healthy and healing tissues, proteins and immune cells, which worsens the quality of treatment.

A chronic inflammatory response does not always lead to a successful removal of the biofilm, and a hypothesis has been advanced that such a response is "beneficial" to the biofilm. By inducing an ineffective inflammatory response, the biofilm protects the microorganisms that form it and enhances the production of exudate, which in turn is a source of nutrition and a means of preserving the biofilm.

Are there conditions that promote biofilm formation in the wound?

It is not known whether conditions exist that promote the formation of biofilms in the wound. However, the basic conditions that weaken the immune system or reduce the action of antibiotics can contribute to the development of biofilms in the wounds (eg, tissue ischemia or necrosis, poor nutrition).

[17], [18], [19], [20], [21], [22],

What are the principles of biofilm management?

Even if there is a high probability that the wound has biofilm, there is no one-step treatment. The optimal can be the use of a combined strategy based on the elements of the preparation of the wound bed and serves to remove the mass of biofilms, preventing the reconstruction of biofilms. This approach is sometimes called "biofilm-based wound care" (treatment of wounds with biofilm).

How do I know if the biofilm was removed?

Absence of severe symptoms and well-established laboratory methods for the determination of microbial communities does not allow us to specify the moment of wound release from biofilm. The most revealing is the progressive healing of the wound, characterized by a decrease in exudate exudation and rejection of the scab. Until accurate guidance is developed, clinicians will be asked to decide for themselves how to treat wounds with biofilms in each case. For example, when treatment is successful, it may be necessary to change the method or frequency of wound treatment or to decide whether it is necessary to use local antimicrobial agents. The issues of additional necessary measures to stimulate the wound healing process should be addressed taking into account the patient's health condition and be directed to support his immune system. Thus, biofilms affect the course of chronic inflammatory diseases, and recent findings suggest that they also play a significant role in disturbing the course of healing processes of chronic wounds. Biofilms have a high level of tolerance to antibodies, antibiotics, antiseptics, disinfectants and phagocytes. Current methods of treating wounds with biofilms include the mandatory frequent wound cleaning together with the use of wound coatings and antimicrobial agents to prevent wound reinfection and suppression of biofilm reforming.

When considering the issue of etiopathogenesis of wound infection, it should be borne in mind that any local infectious focus from a microbiological point of view should be considered as a pathological biocenosis. This means that any microbiota present in a given outbreak can actively participate 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 provision, in turn, serves as the basis for subsequent conclusions. If the original pathogenicity of the pathogen is high enough, and the natural mechanisms of the host's anti-infective protection are insufficient or weakened by any background pathological process, the formation of a pathological biotope may result from the gradual development of the infectious process itself.

Candidate of Medical Sciences Garilullov Hamil Gakilievich. Some aspects of development of infectious complications in arthroplasty // Practical medicine. 8 (64) December 2012 / volume 1