Osteomyelitis

The term "osteomyelitis" was proposed to denote inflammation of the bone and bone marrow (from Greek "osteomyelitis" means inflammation of the bone marrow). Currently, this term is understood as an infectious and inflammatory lesion of bone tissue (osteitis), bone marrow (myelitis), periosteum (periostitis) and surrounding soft tissues. Osteomyelitis is also defined as an infection in the bone.

Osteomyelitis is a local inflammatory process that develops in response to the invasion and proliferation of microbial bodies. The main trigger for hematogenous osteomyelitis is the endogenous invasion of microbial bodies into the bone marrow canal; in exogenous osteomyelitis, microbial invasion occurs as a result of trauma to the bone or surrounding tissues. Localization of inflammation serves as a protective reaction of the body, preventing the development of sepsis, which is possible if the mechanisms for limiting the purulent-necrotic process become insolvent. This may be due to the high virulence and pathogenicity of microorganisms, the vastness of the lesion, the duration of the inflammatory process, and the weakening of the protective forces of the macroorganism.

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Epidemiology

Despite the steady progress in understanding the pathogenesis of bone and joint infection and the introduction of modern diagnostic and treatment methods, the number of such patients has not shown a downward trend over the past 30 years.

Acute hematogenous osteomyelitis occurs in 2 out of 10,000 children, chronic osteomyelitis - in 2 out of 10,000 people, and the bones of the lower limbs are affected in 90% of cases. The tibia accounts for 50%, the femur - 30%, the fibula - 12%, the humerus - 3%, the ulna - 3% and the radius - 2% of long bone lesions. Currently, several trends are observed in the epidemiology of long bone osteomyelitis. Changes have occurred in the structure of hematogenous osteomyelitis. In the leading industrial countries, a decrease in the incidence of acute hematogenous osteomyelitis of long bones in children is noted (2.9 new cases per 100,000 population per year) and Staphylococcus aureus as the main causative agent of the disease - from 55 to 31%. In countries with developed infrastructure, these diseases have become quite rare.

In recent years, there has been an increase in the number of patients with post-traumatic osteomyelitis. This is primarily due to the increase in trauma, especially as a result of road traffic accidents, changes in microflora that can cause suppuration, and disorders of the human immune system. The development of bone infection is facilitated by diabetes mellitus, obliterating vascular diseases, tumors, alcoholism and smoking. In adults, the main cause of osteomyelitis is fractures of long bones. The development of this pathological condition depends on many factors, primarily on the location and extent of damage to the bone and soft tissues, impaired blood supply and innervation, timeliness and quality of primary surgical treatment, antibiotic prophylaxis method, choice of osteosynthesis method and plastic wound closure. In this regard, the incidence of osteomyelitis varies widely - from 0.5-2% in surgical treatment of closed fractures and injuries of the upper limb to 50% and higher in open fractures of the leg and thigh with extensive damage to soft tissues.

In modern conditions, the role of purulent complications, including osteomyelitis, after gunshot wounds to the extremities has increased, the main causes of which are the severity of bone and joint injuries, as well as treatment defects made at the stages of medical evacuation. According to the experience of post-war armed conflicts, the incidence of gunshot osteomyelitis is at least 9-20%.

Various types of internal metal osteosynthesis have become widespread in the treatment of fractures worldwide. Unjustified expansion of indications for surgical methods in severe fractures with extensive damage to soft tissues, failure to comply with the timing and technique of performing surgeries, incorrect choice of surgical aid and metal construction lead to severe purulent inflammation of bones and joints. Suppuration around the spokes and rods, as well as "spoke" osteomyelitis remain the most common complications during osteosynthesis with external fixation devices. About 1 million knee and hip replacement surgeries are performed worldwide annually. Therefore, osteomyelitis that occurs after endoprosthetics is becoming a big problem, especially in developed countries.

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Causes osteomyelitis

In 1880, Louis Pasteur was the first to isolate microbes from the pus of a patient with osteomyelitis and called them staphylococci. It was later established that any pyogenic microbes can cause osteomyelitis, and the clinical and morphological picture of the disease can depend on their species composition. Currently, the causative agent of acute hematogenous osteomyelitis of long bones in children is mainly monoflora (up to 95%). This is, as a rule, Staphylococcus aureus, isolated in 50-90% of cases. This microorganism remains the leading causative agent in all cases of osteomyelitis due to its osteochondrotropism and high adaptability, which leads to the development of a large number of various antibiotic-resistant virulent strains and, ultimately, to a decrease in the effectiveness of conservative treatment.

In children under one year of age, Streptococcus agalactiae and Escherichia coli are most often isolated from bone and blood, while in children over one year of age, Streptococcus pyogenes and Haemophilus influenzae are isolated. The incidence of H. influenzae isolation decreases in children over four years of age, which is also associated with the use of a new vaccine against this pathogen.

In patients with acute posttraumatic osteomyelitis, which occurs with open fractures with extensive damage to soft tissues, mixed aerobic-anaerobic associations with a predominance of gram-negative microorganisms, mainly Pseudomonas aeruginosa, are cultured. Microbial contamination in the lesion, as a rule, is 106-108 microbial bodies in 1 g of bone tissue.

In chronic osteomyelitis, the leading etiologic role is played by gram-positive cocci of the genus Staphylococcus, with Staphylococcus aureus predominating, the frequency of seeding of which depends on the stage of the process and ranges from 60 to 85%. In chronic inflammatory processes, staphylococci can be present in monocultures or as part of aerobic-anaerobic associations. Staphylococci are replaced by gram-negative and anaerobic bacteria, which are characterized by a higher resistance to widespread antibacterial drugs than gram-positive bacteria.

Pathogenesis

Osteomyelitis can be caused by hematogenous spread of infection, direct penetration of microorganisms into the bone or from an adjacent, external focus of infection. In posttraumatic osteomyelitis, direct penetration of microbial flora occurs due to tissue damage and disruption of blood supply. The development of this form of osteomyelitis directly depends on the invasion of microorganisms, their quantity, type, virulence and the degree of damage to soft tissues. After adverse effects on the protective and adaptive reactions of the body of various physical, biological factors and concomitant diseases, its ability to show an effective response to contain the infection is reduced, which can contribute to the development of the initial stage of the disease.

Deep, long-term bone infection is maintained by the presence of devascularized cortex surrounded by bacteria. It acts as a foreign body, which is the main cause of osteomyelitis in most open fractures. Posttraumatic osteomyelitis, in addition to the usual pathogenic microorganisms, can also be caused by nonpathogenic staphylococci and anaerobic cocci. At the time of injury, they enter the devitalized areas of the cortex and here, under anaerobic conditions, promote sequestration and the development of osteomyelitis. Such bone infection often develops after open fractures.

A number of systemic and local factors affect the immune response, metabolism, and local blood supply during the development of osteomyelitis. Systemic factors include poor nutrition, impaired renal and hepatic function, diabetes mellitus, chronic hypoxia, immune diseases, malignant diseases, old and senile age, immunosuppression and immunodeficiency, splenectomy, viral infection, alcoholism, and smoking. Local factors such as chronic lymphedema, venous stasis, vascular lesions, arteritis, severe cicatricial changes, fibrosis, small vessel pathology, and neuropathy also contribute to the development of infection.

Acute osteomyelitis is characterized as a purulent infection accompanied by edema, vascular stasis and thrombosis of small vessels. In the acute period of the disease, due to local inflammation, intraosseous and periosteal blood supply is disrupted, large fragments of dead bone (sequesters) are formed. The existence of infected, non-viable tissues and an ineffective response of the macroorganism, as well as inadequate treatment, lead to chronicity of the disease. As the purulent process passes into the chronic stage, a gradual change in the microbial landscape occurs. Low-virulence strains of Staphylococcus epidermidis and Staphylococcus aureus begin to play a dominant role.

Bone tissue necrosis is an important feature of acute posttraumatic osteomyelitis. Dead bone is slowly resorbed by granulation tissue enzymes. Resorption occurs most rapidly and early at the junction of living and necrotic bone. Dead spongy bone in localized osteomyelitis is slowly resorbed. The dead area of the cortical part of the bone gradually separates from the living bone, forming a sequestrum. Organic elements in dead bone are largely destroyed by proteolytic enzymes produced by macrophages or polymorphonuclear leukocytes. Due to impaired blood supply, dead bone visually appears lighter than living bone. Small areas of non-viable spongy bone are resorbed within 2-3 weeks; sequestration of the cortical part may take months.

The morphological features of chronic osteomyelitis are the presence of bone necrosis, new bone formation, and exudation of polymorphonuclear leukocytes, to which large numbers of lymphocytes, histiocytes, and sometimes plasma cells are added. The presence of dead bone often causes fistulas to form, through which pus enters the surrounding soft tissues and eventually emerges on the skin surface, forming a chronic fistula. The density and thickness of the newly formed bone may gradually increase, forming part or all of the new diaphysis under relatively favorable conditions. The two parallel processes develop over many weeks or months, depending on the extent of the necrosis and the degree and duration of the infection. Endosteal bone growths may obscure the medullary canal.

After removal of the sequestrum, the remaining cavity can be filled with new bone. This happens especially often in children. Post-traumatic, secondary osteomyelitis develops as a result of tissue damage caused by trauma, on the one hand, and invasion and development of microorganisms, on the other hand. The lack of sufficient stabilization of the damaged bone leads to the development and spread of purulent infection, the formation of secondary necrosis and sequestra.

Most authors are of the opinion that it is advisable to treat extensive wounds in patients with open fractures without early closure of the wound surface, which creates the problem of combating acute purulent infection. A long period of open management of such wounds is fraught with a real threat of osteomyelitis. Thus, the main causes of post-traumatic osteomyelitis in patients with open fractures should be considered:

• untimely and inadequate surgical treatment of the lesion;
• inadequate, incorrectly chosen method of fixation;
• a long-standing, extensive wound;
• incorrect assessment of the degree of soft tissue damage;
• insufficient postoperative monitoring.

Of great importance for the prevention of osteomyelitis in open fractures is the timely removal of wound exudate during the process of temporary and final closure of the wound surface. The accumulation of wound exudate is also one of the reasons for the development of secondary necrosis.

Analysis of the causes of posttraumatic osteomyelitis development confirms the fact that the factors influencing the frequency of purulent complications in open fractures and osteomyelitis development include immersion metal osteosynthesis. It is known that its use in open fractures with massive damage to soft tissues, especially in the shin, dramatically increases the risk of infection. This pattern is especially clearly seen in gunshot fractures, which determined the opinion of a number of experts on the need to ban the use of immersion osteosynthesis in this type of injury.

Despite the fact that the alloys used to manufacture the fixators are considered immunologically inert, sometimes we have to observe cases of metal "intolerance". In severe cases, the result of such a reaction is a clinical picture of acute inflammation with the formation of fistulas and secondary infection. This process is based on the formation of haptens - substances that arise as a result of the biotransformation of the metal and the bond of its molecules with proteins, which creates the prerequisites for sensitization. The trigger for this process is the superficial destruction of the implant as a result of oxidation by peroxide compounds, phagocytosis or mechanical destruction (in case of disruption of the stability of bone fragments or friction of the fixator elements with each other). Sensitization to metal can exist initially or develop as a result of immersion metal osteosynthesis.

A new stage in deepening knowledge about osteomyelitis is associated with the study of its pathogenesis at different levels of organization: submolecular, molecular, cellular and organ. The study of the main causative agents of osteomyelitis, such as Staphylococcus aureus, made it possible to identify extracellular and intracellular microbial mechanisms of aggression and invasion, with the help of which bacteria cause and maintain infection, directly damage bone tissue cells, disrupt the body's protective immune response, and reduce the effectiveness of antibiotics. In recent years, the role of cytokines, one of the regulators of cellular and humoral immunity, has been actively studied. A new, previously unknown role of bone-producing cells - osteoblasts, capable of causing antigen-specific activation of immune cells and inflammatory mediators in response to intracellular invasion of microorganisms in bone tissue, has also been shown. At the same time, it should be noted that not everything is completely clear in the pathogenesis of osteomyelitis, given the wide range of its manifestations. Many proposed pathogenetic mechanisms are at the hypothetical level.

Symptoms osteomyelitis

A detailed history is often sufficient to diagnose osteomyelitis. Children with hematogenous osteomyelitis may present with acute signs of infection, including fever, irritability, fatigue, weakness, and local signs of inflammation. However, an atypical course is also common. In children with hematogenous osteomyelitis, the soft tissues surrounding the affected bone can localize the infection. The joint is usually not affected by infection. In adults with hematogenous osteomyelitis, vague signs are usually found, including prolonged pain and low-grade fever. High fever, chills, swelling, and hyperemia over the affected bone may also occur. In contact osteomyelitis, there is often localized bone and joint pain, hyperemia, swelling, and exudation around the site of injury. Signs of a severe systemic inflammatory reaction, such as fever, chills, and evening sweats, may be present in the acute phase of osteomyelitis, but they are not observed in the chronic phase. Both hematogenous and contact osteomyelitis can progress to a chronic stage. Chronic stage is characterized by persistent pain, exudation, and low-grade fever. Fistula tracts are often found near the site of infection. If the fistula tract closes, the patient may develop an abscess or acute disseminated soft tissue infection.

Forms

According to the clinical course and duration of the disease, osteomyelitis is traditionally divided into acute and chronic. According to the pathogenetic principle, osteomyelitis is divided into hematogenous and post-traumatic, which can develop as a result of mechanical, surgical, gunshot injury to both bone tissue and surrounding soft tissues. Hematogenous osteomyelitis can manifest itself as a primarily chronic course (Brodie's abscess, Garre's sclerosing osteomyelitis, Ollier's albuminous osteomyelitis).

The clinical and anatomical classification of osteomyelitis of long bones in adults adopted by the University of Texas Medical Department - the Czerny-Mader Classification - seems convenient for practical use. The classification is based on two principles: the structure of bone damage and the patient's condition. According to this classification, structural bone damage is conditionally divided into four types:

• Type I (medullary osteomyelitis) - damage to a large area of the structures of the bone marrow cavity of a long bone in hematogenous osteomyelitis and in suppuration after intramedullary osteosynthesis;
• Type II (superficial osteomyelitis) - damage to only the cortical part of the bone, which usually occurs with direct infection of the bone or from an adjacent source of infection in soft tissues; a septic joint is also classified as superficial osteomyelitis (osteochondritis);
• Type III (focal osteomyelitis) - damage to the cortical part of the bone and the structures of the bone marrow canal. However, with this type of damage, the bone is still stable, because the infectious process does not spread to the entire diameter of the bone;
• Type IV (diffuse osteomyelitis) - damage to the entire diameter of the bone with loss of stability; an example would be an infected pseudoarthrosis, osteomyelitis after an open comminuted fracture.

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