Traditional medicine

Acute hematogenous osteomyelitis. Acute hematogenous osteomyelitis in children

Clinical picture

Acute hematogenous osteomyelitis in children and adolescents usually begins as a severe general infectious disease, and in the first days general symptoms are so dominant over the locals.

The disease is often preceded by a sore throat, a local purulent process (festering abrasion, boil) or a bruise of a limb.

The disease begins with a sudden rise in temperature to 39-40°C, severe chills, which is accompanied by a sharp deterioration in general health, sometimes delirium. In children younger age profuse vomiting often occurs, making one think about a disease of the gastrointestinal tract. In some cases, the disease is extremely severe, malignant and ends in death with symptoms of fulminant sepsis within a few days.

Simultaneously or several later development severe intoxication, there are complaints of strong bursting, aggravated by movement, shifting, pain in the corresponding bone, but, as a rule, there is no swelling or redness in this area in the first days. There is no pain during palpation, especially on the thigh, where the periosteum is located deep under the muscles. It is especially difficult to detect local symptoms in the first days of the disease. The correct diagnosis is helped by targeted identification of local symptoms, in particular muscle contracture in nearby joints, local pain, pain when loading the limb along the axis, etc.

Only after 7-10 days, when the purulent process spreads under the periosteum, more distinct pain and swelling begins to be detected. A few days after the process spreads into the muscle spaces, the pressure in the lesion drops, as a result of which the pain weakens somewhat. Clinical symptoms characteristic of deep phlegmon are observed. In the future, the pus may break out with the formation of a fistula, after which the acute phenomena may subside.

According to T.P. Krasnobaeva, there are three forms of the clinical course of acute hematogenous osteomyelitis: local (mild), septicopyemic (severe), toxic (adynamic). The clinical course of the disease when different bones are affected is basically the same.

The local (mild) form is characterized by the absence of septic phenomena and the predominance of clinical local changes over violations of the general condition, which can be severe, moderate or close to satisfactory. Intoxication is moderate, the temperature at the beginning of the disease and subsequently is 38-39 degrees. Local inflammatory changes are limited in nature, their clinical manifestations are less pronounced than in the septicopyemic form.

If the subperiosteal abscess is not opened in a timely manner, it breaks into the soft tissue and intermuscular phlegmon forms. Pus can spread through the interfascial spaces and break out far from the bone lesion. After the abscess is emptied, the patient’s condition quickly improves, the temperature drops, and the process takes chronic course.

In the septic-pyemic form, the disease begins suddenly with a rise in temperature to high numbers. In the first hours and days of illness, a serious condition develops due to intoxication, and repeated vomiting is observed.

Local changes are moving quickly. During the first 2 days, localized pain appears; they are of a sharp nature, the limb assumes a forced position (painful contracture), active movements in it are absent, passive ones are sharply limited. Swelling of the soft tissues rapidly increases, which, if the focus is localized in the femur, can spread to the lower leg, anterior abdominal wall, when localized in the brachial

bones - on the chest. The skin over the lesion is hyperemic, tense, shiny, and often has a pronounced venous pattern; there is an increase in local temperature.

The appearance of edema corresponds to the beginning of the formation of a subperiosteal abscess, the development of hyperemia corresponds to the breakthrough of the abscess into the soft tissues and the appearance of fluctuations in their depths.

Sympathetic (reactive) arthritis of one or both adjacent joints often develops, first serous, then purulent.

In the following days of illness, the temperature remains high (39-40 degrees) without noticeable daily fluctuations, and changes in blood composition typical for acute purulent inflammation are noted.

If treatment is ineffective, the patient’s serious general condition worsens, intoxication and dehydration of the body increase, and headache, pain throughout the body, loss of appetite, thirst, anemia.

Metabolic processes are disrupted: metabolic acidosis develops; disorders of water-salt metabolism lead to persistent hyperkalemia and calcemia, hyponatremia and other disorders.

Indicators are getting worse nonspecific factors immunity, blood coagulation system, excessive accumulation of inflammatory mediators (histamine, serotonin, etc.) occurs.

Pronounced phase changes occur in the hemostatic system. During the first 10 days of the disease, hypercoagulation phenomena are observed (phase I), which creates conditions for disseminated intravascular coagulation, sharply aggravating bone destruction.

On days 10-20, hypocoagulation phenomena occur (phase II) with a tendency to transition to the activation phase and an increase in pathological fibrinolysis (phase III). With the septicopyemic form, these changes develop in 90%, with the local form - in 25%.

Hormonal regulation of body functions, myocardial metabolism, antitoxic liver function, kidney function are disrupted, and they are depleted compensatory mechanisms respiratory and circulatory systems.

All these changes develop over 5-10 days and create favorable conditions for the generalization of purulent infection and its hematogenous metastasis. Toxic hemolytic jaundice often develops.

The toxic (adynamic) form occurs in 1-3% of patients. The disease develops at lightning speed. During the first day, symptoms of severe toxicosis increase; hypothermia, meningeal symptoms, loss of consciousness, convulsions followed by adynamia; acute cardiovascular failure develops, blood pressure decreases. Local inflammatory phenomena do not have time to manifest themselves: patients die in the first days of the disease as a result of profound metabolic disorders.

Complications

The most severe complication of acute hematogenous osteomyelitis is sepsis, which often develops with delayed or improper treatment of the disease. When the inflammatory process spreads to the joint, purulent arthritis develops.

In 8-10% of patients (with septicopyemic forms - in 30%), metastatic purulent foci develop in the internal organs with the development of septic pneumonia, purulent pleurisy, pericarditis, brain abscess, etc.

Pathological bone fracture, including epiphysiolysis, occurs as a result of bone destruction, often resulting in a false joint. Epiphyseal and metaphyseal osteomyelitis, due to the close location of the lesion to the growth zone, can lead to growth disturbances and significant bone deformations (curvature, shortening, less often lengthening), pathological dislocation, contracture or ankylosis.

Diagnostics

Laboratory data indicate the presence of a focus of purulent infection in the body (leukocytosis, shift of the formula to the left, etc.).

X-ray data in the first two weeks of the disease are negative ( pathological changes are missing). Subsequently, a faint shadow of exfoliated periosteum appears at first, beginning to produce bone substance (periostitis). Even later, zones of rarefaction and lubrication of the cancellous bone structure appear in the metaphysis. The bone structure becomes uneven. The distinct formation of sequestra (separately lying areas of necrotic bone tissue) and sequestral cavity can be detected only 2-4 months after the onset of the disease, when the process has already become chronic. During this period, in the presence of fistulas, fistulography, as well as tomography, isotope and ultrasound examination, thermal imaging, and radiothermometry help in the X-ray diagnosis of cavities and sequestration.

Treatment of hematogenous osteomyelitis consists of a general effect on the body and a local effect on the source of infection.

a) General treatment

The general principles of treating purulent infections also apply to osteomyelitis.

Complex therapy for acute osteomyelitis includes the following elements.

1. Antibiotic therapy.

From the moment the diagnosis is made, the patient is injected intramuscularly with semisynthetic penicillins, lincomycin or cephalosporins, which usually leads to a sharp improvement in the patient’s condition, a decrease in temperature, a decrease in intoxication and a rapid recovery. If antibiotic treatment is started early, the inflammatory process in bone marrow can be eliminated, and the bone structure disturbed by the purulent process is gradually restored. Use of antibiotics in early stages hematogenous osteomyelitis significantly changed its course and improved treatment outcomes. Endolymphatic administration of antibiotics has proven itself well.

2. Powerful detoxification therapy.

It is carried out from the first days, transfusions of crystalloid solutions and blood substitutes with detoxification effects, as well as blood plasma, are carried out. In severe cases, it is possible to use extracorporeal detoxification methods.

3. Immunocorrection and symptomatic therapy.

Conducted according to general principles treatment of purulent surgical infection.

b) Local treatment

From the very beginning of the disease, rest and immobilization of the diseased limb using a plaster splint are necessary.

Due to the effectiveness of antibiotic treatment, surgery is rarely necessary. Surgical treatment is indicated for advanced processes with the development of intermuscular phlegmon and in cases where conservative treatment does not succeed within several days when the general condition worsens. During the operation in the early stages (before the pus breaks through into the soft tissues), the soft tissues are dissected, burr holes are made through the bone to the cavity of the bone marrow abscess, and drains are installed for flow-through drainage.

When intermuscular phlegmon develops, it is opened with a wide incision, which must be made taking into account the location of the phlegmon, the topography of the vessels, nerves and muscles. In this case, the periosteum is dissected, the underlying bone is carefully inspected, and if there is a bone cavity, the bone is trephinated and constant flow-through drainage is established.

Osteoperforation in children is performed under general anesthesia. After exposing the affected area, the bone is penetrated through its cortical layer into the medullary canal using an electric drill or a triangular awl; Catheters are inserted into the formed holes to drain and wash the bone marrow canal. For the same purposes, you can use two Kassirsky or Dufault needles at a certain distance.

After introducing a 0.25% novocaine solution into the bone marrow canal, about 1 liter of saline is injected into the cavity through flow-through drainage. antibiotic solution. In the next 5-7 days, intraosseous rinsing is repeated 2 times a day with the same amount of solution, but it is carried out drip-wise (90 drops per minute).

Intraosseous lavages promote rapid and complete removal of pus and other decay products from the bone, preventing intoxication, provide a constant high concentration of antibiotics in the bone, remove pathological impulses from the lesion and create conditions for accelerating recovery processes.

It is impossible to expand the scope of surgical intervention to wide trepanation of the bone marrow canal because this can lead to dissemination purulent process and death.

In the postoperative period, treatment is carried out according to the general principles of treating purulent wounds; immobilization is required until the inflammatory process is completely relieved.

CHRONIC HEMATOGENIC OSTEOMYELITIS

Chronic hematogenous osteomyelitis is a disease characterized by the presence of a purulent-necrotic focus in the bone with a fistula (or without it), long-lasting and, as a rule, not prone to self-healing.

Etiopathogenesis

Chronic osteomyelitis is necessarily preceded by an acute stage.

The transition of acute osteomyelitis to chronic occurs on average within a period of 3 weeks to 4 months from the onset of the disease and largely depends on the rate of sequestration.

Due to mechanical and chemical properties of the bone, its dead part, called sequestrum, cannot, under the influence of pus enzymes, either quickly dissolve or quickly separate from living tissue. The sequestration process is very slow and continues for months and sometimes years.

Inflammatory and reparative processes in the circumference of the dead part of the bone occur due to the osteogenic tissue of the endosteum and periosteum, which form a capsule of newly formed bone with a granulation lining inside. As a result, the sequestrum, which has lost its mechanical connection with the surrounding living bone, appears, as it were, immured in a capsule of newly formed bone (sequestration box). Being infected foreign body, sequestration, being extremely slowly dissolved, maintains chronic suppuration for years.

Pus is released through fistulas, which may close periodically. The latter leads to retention of pus and a new outbreak of process activity with corresponding local and general reaction. This condition can last for decades and sometimes leads to severe changes in parenchymal organs (renal and hepatic failure, amyloidosis), which, in turn, can cause death.

Clinical picture

The clinical course is characterized by scant signs: aching pain in the area of the osteomyelitic lesion, the presence of purulent fistulas, and rough postoperative scars. When the process worsens, severe pain, an increase in body temperature to 38-39°C, and skin hyperemia in the area of the osteomyelitic fistula are noted. Exacerbation of chronic osteomyelitis is most often associated with temporary closure of a previously functioning purulent fistula.

In the diagnosis of chronic osteomyelitis, radiography is of leading importance. In this case, thickening of the bone, cavities in it, sequesters, osteosclerosis, narrowing of the bone marrow canal, and thickening of the periosteum are detected. An important place in the diagnosis of fistulous forms is occupied by fistulography, as well as tomography, scintigraphy and especially computed tomography.

Phases of the course of chronic (secondary) osteomyelitis:

The phase of the final transition of an acute process to a chronic one

Remission phase

Relapse (exacerbation) phase of inflammation

As acute hematogenous osteomyelitis transitions to chronic, the patient’s well-being improves, and the pain gradually weakens.

Signs of intoxication decrease or completely disappear; body temperature decreases to normal or low-grade levels, respiratory function and cardiovascular system are normalized; weakness decreases, appetite and sleep improve. Leukocytosis decreases, ESR slows down, white and red blood counts improve; the amount of protein and leukocytes in the urine decreases.

Fistulas finally form in the focal area. The fistula comes from one osteomyelitic focus or from different ones, it can be single or multiple, often several fistulas are connected to each other in the soft tissues, forming a complex network of infected canals. The external opening of the fistula is sometimes located at a considerable distance from the osteomyelitic focus. Suppuration decreases.

In soft tissues inflammatory infiltration gradually decreases as it enters the remission stage.

The process of gradual sequestration over the coming weeks, sometimes months, ends with the complete separation of necrotic areas (sequestra) from healthy bone tissue and the formation of a bone cavity.

The size and shape of sequestration may vary. With all their diversity, the following types of sequesters are distinguished.

Types of sequesters

Cortical (cortical) - with necrotization of a thin bone plate under the periosteum.

Central - with necrosis of the endosteal surface of the bone.

Penetrating - with necrosis of the entire thickness of the compact layer in a circumferentially limited area of the bone.

Total - with necrosis of the tubular bone along its entire circumference, sometimes throughout the entire bone.

Circulatory (coronal) - with necrosis of the diaphysis along the entire circumference, but in a small area along the length (sequestrum in the form of a narrow ring).

Spongy - with necrosis of spongy tissue of long tubular or flat bones.

Central, cortical and penetrating sequestration are more common.

The sequester can be located entirely or partially in the bone cavity or outside it, in soft tissues.

Along with sequestration, a sequestral capsule (box) is formed around the bone cavity, inside which there are usually sequesters and pus; The inner walls of the capsule are covered with granulations.

The sequestral capsule has one or more holes through which pus from the osteomyelitic lesion flows into the fistulous tracts.

The sequesters located in the sequestration box practically do not dissolve, or this process occurs extremely slowly - over decades.

In the remission phase, most patients note the disappearance of pain and improvement in general condition: body temperature returns to normal. The fistulas release a small amount of pus and sometimes close temporarily. By the beginning of this phase, the processes of sequestration and the formation of a sequestral capsule are completely completed.

The duration of remissions can last from several weeks to many years, which depends on the size and number of sequestration, the virulence of microbes, the state of the body's defenses, age, localization of the process, etc.

The relapse phase resembles the onset of acute osteomyelitis, however, inflammatory changes and the degree of intoxication are less pronounced.

Relapse is often preceded by closure of a purulent fistula, which leads first to the accumulation of pus in the capsule, and then to its saturation of the surrounding soft tissues and the development of paraosseous intermuscular phlegmon.

With a relapse, there is an increase in pain in the focal area, tissue swelling, skin hyperemia, local hyperthermia appear, and the function of the limb is further impaired.

At the same time, signs of purulent intoxication appear: appetite worsens, body temperature rises to 38-39 degrees, tachycardia and heavy sweating appear, leukocytosis increases, and ESR accelerates.

If the phlegmon is not opened in a timely manner, new purulent streaks may form and the symptoms of intoxication may intensify.

After the opening of the phlegmon or the breakthrough of pus through the opened fistula, the patient’s condition quickly improves, the local inflammatory process subsides, the exacerbation phase gradually returns to the remission phase

Treatment

The main goal of treatment for chronic osteomyelitis is to eliminate the focus of the purulent-destructive process in bone tissue. This requires a complex effect, combining radical surgery with targeted antimicrobial therapy, detoxification and activation of the body’s immune forces.

The operation is indicated for all patients suffering from chronic osteomyelitis in the stage of remission or exacerbation, in whom radiographs reveal the focus of bone destruction.

In case of radical surgical intervention, all fistulas are excised after preliminary staining with methylene blue. After this, trepanation of the bone is performed with opening of the osteomyelitic cavity along its entire length, sequestrectomy, removal of infected granulations and pus from the cavity, as well as the internal walls of the cavity to normal, unchanged bone tissue. Drains are installed in the area of the trepanned bone and the wound is sutured. The best view drainage is flow-wash.

In the presence of large-scale bone damage, an important stage of surgical treatment is plastic surgery of the bone cavity. The most common method is plastic surgery with a muscle flap on a pedicle from adjacent muscles. Fat grafting is less commonly used bone grafting(preserved demineralized bone, autologous bone), the use of vascularized tissue flaps, memory metals (nickel-titanium), etc.

Atypical forms of chronic osteomyelitis

In some cases, hematogenous osteomyelitis immediately occurs as a chronic process.

There are three main, so-called atypical forms of primary chronic osteomyelitis.

Brody's abscess

The pathogen enters hematogenously into the spongy bone, forming a cavity.

Morphologically, a smooth-walled bone cavity is round in shape, 1.5-5 cm in size, lined with a fibrous capsule, sometimes with parietal granulations, containing purulent or serous fluid. Bone sclerosis develops around the cavity, like a dense capsule.

Clinically, the abscess shows almost nothing. Sometimes patients complain of pain in the limbs, worsening at night. Microbes found in pus are low virulent or are not even detectable.

Diagnosed only by x-ray.

Treatment. Trephination of the cavity, removal of pus, biological

tamponade followed by suturing the wound tightly.

Garre's sclerosing osteomyelitis

Garre's sclerosing osteomyelitis (osteomyelitis scleroticans Garre) was described in 1893. It begins subacutely and is characterized by pain in the limb, often at night, dysfunction, moderate fever, leukocytosis and accelerated ESR.

The causative agent is weakly virulent staphylococcus.

The middle third of the bone diaphysis is most often affected in men aged 20-30 years. X-ray reveals a fusiform thickening of the diaphysis over 8-12 cm due to pronounced dense homogeneous compact periosteal layers.

At the level of the lesion, endosteal bone formation is also detected, due to which the bone becomes denser and the medullary canal narrows.

There is a tendency towards excessive sclerosis of the bone (impregnated with lime salts), somewhat reminiscent of syphilitic osteoperiostitis.

Often the medullary canal becomes obliterated. The process can reach purulent inflammation, most often localized in the femur or tibia. Necrosis, formation of cavities, and fistulas are not observed. Treatment is conservative (physiotherapy, mud therapy); sometimes longitudinal bone resection.

Ollier's albuminous osteomyelitis

Albuminous osteomyelitis Ollier (osteomyelitis albuminosa Ollier) was described in 1864. From the very beginning it occurs with minor local changes on the limb in the form of slight infiltration of soft tissues and mild hyperemia of the skin. In the primary osteomyelitic focus, between the periosteum and cortical layer bones, no suppuration occurs; instead of pus, a serous fluid rich in protein or mucin accumulates in the lesion, from which it is possible to inoculate staphylococcus and streptococcus.

The disease is sometimes complicated by bone destruction with the formation of sequestration or the secondary addition of purulent infection.

Treatment. Incision, scraping with a sharp spoon. In the absence of bone destruction - puncture, suction of the contents, administration of a weak iodine solution.

Complications of chronic osteomyelitis

The main complications of chronic osteomyelitis are:

Deformation of long tubular bones.

Ankylosis of the joints.

Pathological fractures, pseudarthrosis, non-union fractures, bone defects.

Malignization of the walls of osteomyelitic fistulas.

Amyloidosis of internal organs.

RELEVANCE......................................................... ........................................... 2

ETIOPATHOGENESIS................................................................... ..................................... 3

ACUTE HEMATOGENIC OSTEOMYELITIS.................................................... 9

Clinical picture................................................... ...................................... 9

Complications................................................. ........................................................ 12

Diagnostics................................................. ........................................................ 13

Treatment................................................. ........................................................ ....... 13

CHRONIC HEMATOGENIC OSTEOMYELITIS..................................... 16

Etiopathogenesis......................................................... ........................................... 16

Clinical picture................................................... .................................... 17

Treatment................................................. ........................................................ ....... 20

Atypical forms of chronic osteomyelitis.................................................... 21

Ollier's albuminous osteomyelitis.................................................... ............. 22

Complications of chronic osteomyelitis................................................................. ..... 23

List of used literature................................................... 24

In 1831, Raynaud coined the term “osteomyelitis.” Translated, this word means inflammation of the bone marrow. However, isolated purulent bone marrow lesions practically never occur.

Currently, the term osteomyelitis refers to a purulent inflammatory process that affects all elements of the bone as an organ: bone marrow, bone itself and periosteum.

In the vast majority of cases, the soft tissue surrounding the affected bone is involved to some extent in the process.

Purulent osteomyelitis is divided into two large groups, differing significantly in the method of penetration of infectious pathogens into the bone and in pathogenesis. In cases where infectious pathogens enter the bone (bone marrow) through the hematogenous route, osteomyelitis is called hematogenous.

If the bone and its elements become infected during open injury(open fracture), osteomyelitis is called traumatic (with a fracture due to gunshot wound- osteomyelitis is called gunshot; when osteomyelitis develops after surgical treatment - osteosynthesis - it is called postoperative). In addition, this section will discuss the diagnosis and treatment of acute purulent arthritis - inflammation of the joint and acute purulent bursitis- inflammation of the synovial joint capsule.

Hematogenous osteomyelitis is a very serious disease that usually affects children and adolescents, with boys approximately three times more likely than girls. According to various statistics, patients with hematogenous osteomyelitis make up from 3 to 10% of all patients in pediatric surgical departments. Since in some cases the disease, becoming chronic, lasts for many years, and sometimes decades, patients with hematogenous osteomyelitis are often found among adults and even elderly people. In peacetime is the most frequent form osteomyelitis and according to T.P. Krasnobaev, in 75-85% of cases occurs in children. Among the sick, about 30% are children under the age of one year, 45-48% are aged from 6 to 14 years, boys - 65-70%, girls - 30-35%. Adults usually experience exacerbations and relapses of this disease suffered in childhood.

Acute hematogenous osteomyelitis predominantly affects long tubular (80-85%), less often flat (9-13%) and short (6-7%) bones.

The most commonly affected bones are the femur (35-40%), tibia (30-32%) and humerus (7-10%); of the short ones - the bones of the foot; from flat ones - the bones of the pelvis and upper jaw.

When long tubular bones are affected, they are distinguished: metaphyseal, the focus of which affects the marginal zone of the diaphysis or epiphysis (observed in 65% of patients), epiphyseal (25-28% of patients), metadiaphyseal, affecting the metaphysis and more than half of the diaphysis, or total, affecting the diaphysis and both metaphysis (7-10% of patients). Multiple processes are observed in 10-15% of patients.

a) Etiology

The causative agent of hematogenous osteomyelitis in the vast majority of cases is Staphylococcus aureus, somewhat less commonly - streptococcus, pneumococcus and E. coli. Hematogenous osteomyelitis is characterized by monoinfection.

b) Pathogenesis

As the name suggests, hematogenous osteomyelitis must be preceded by bacteremia. The place where the pathogen enters the blood can be a small, sometimes inconspicuous purulent focus (for example, a suppurating abrasion, a boil or an abscess in a lymphoid follicle with a sore throat), which by the time a clinically pronounced process occurs in the bone can be healed and forgotten. At the same time, bacteremia can also be a consequence of severe purulent processes.

Hematogenous osteomyelitis is a disease of the growth period; children aged 7 to 15 years are most often affected.

The occurrence of a hematogenous focus of infection in the bone is associated with the structural features of the child’s bone in the zone of its growth, identified by Lexer in late XIX century. These features are as follows:

In children, the metaphysis at the border with the actively functioning epiphyseal cartilage has an extremely abundant network of vessels, characterized by very wide capillaries with slow blood flow.

The vascular network of the metaphysis does not communicate with the vascular network of the epiphyseal cartilage. Partly as a result of this, many vessels (arterioles) of the metaphysis at the border with the growth cartilage end blindly. They are closed, finite and extend under acute angle, due to which conditions are created for the retention and fixation of microorganisms in them. Then, in adolescence, as the epiphyseal cartilage is reduced, vascular connections between the epiphysis and metaphysis, blindly ending vessels disappear, blood circulation in the metaphysis generally becomes more scarce, which, apparently, corresponds to a decrease in the likelihood of microorganisms fixing here.

In children, the spongy bone contains tender bone beams that are easily melted by pus, a periosteum richly supplied with vessels and loosely connected to the bone, which contributes to the occurrence and progression of osteomyelitic changes.

Pathogens that have entered the capillaries of the child’s metaphysis and become fixed there may not cause the process immediately or may not cause it at all. With an appropriate ratio of the number and pathogenicity of pathogens and the state of resistance of the organism, the following options for the course of the process are possible:

Microorganisms die in the bone marrow, being phagocytosed by macrophages.

Microorganisms immediately cause an outbreak of a purulent process.

Microorganisms remain to exist in the form of a dormant, clinically unmanifested infection, which gives an outbreak with one or another decrease in the local or general resistance of the macroorganism, sometimes years after introduction.

Often, a factor that weakens local resistance to infection is trauma (bruise) to the bone, into which, apparently, pyogenic pathogens were previously introduced by hematogenous means. In almost half of the cases, trauma precedes an outbreak of acute hematogenous osteomyelitis.

Factors that reduce overall resistance in children are childhood infections, influenza, and hypothermia.

c) Pathomorphology

With the development of hematogenous osteomyelitis, a number of consistent changes are observed (Fig. 1).

A small abscess formed at the border of the epiphyseal cartilage in the metaphysis causes necrosis of nearby bone beams and vascular thrombosis. These changes extend in the direction of the diaphysis (epiphyseal cartilage is quite resistant to suppuration).

a - bone marrow abscess;

b - subperiosteal abscess;

c - intermuscular phlegmon

d - fistula formation

The bone marrow becomes necrotic and undergoes purulent melting (a), as a result of which the cortical layer of the bone is deprived of nutrition from the inside.

Through the system of Haversian canals, pus spreads under the periosteum, peeling it off from the bone (in children it is loosely bound) and forming a subperiosteal abscess (b).

Due to this, the bone is deprived of nutrition from the periosteum and becomes necrosis with the formation of a larger or smaller area of osteonecrosis. High pressure of pus inside a closed medullary cavity leads to abundant absorption of toxic products and microorganisms into the blood, which usually causes severe purulent intoxication and even sepsis. High pressure inside the medullary canal also causes severe pain.

Eventually, the pus, melting the periosteum, breaks into the soft tissue, causing the development of intermuscular phlegmon (c). Subsequently, the pus can break out and form a fistula (d).

A breakthrough of pus or surgical drainage of the purulent focus ends acute period, characterized by a severe purulent-necrotic process, involving all the main elements of the bone and accompanied by severe intoxication.

In hematogenous osteomyelitis, the metaphyses of long tubular bones are most often affected, most often the metaphyses adjacent to the knee joint. Diaphyseal lesions are observed three times less frequently than metaphyseal lesions. Of the flat bones, the pelvic bones are most often affected.

Around the foci of inflammation, rapid resorption of bone tissue begins from the first days, subsequently spreading to the entire damaged bone and, with a long course of osteomyelitis, leading to its rarefaction - osteoporosis.

In favorable cases, especially with early use of antibiotics, abscess formation may not occur and the elimination of the source of inflammation occurs even before the formation of sequestration. Liquid part the exudate is absorbed, and the abscess cavity is gradually filled with granulations originating from the non-osteogenic bone marrow stroma. The granulations turn into fibrous connective tissue and are subsequently resorbed to restore the normal structure of the bone marrow.

In place of large inflammatory foci, cysts with fibrous walls can form. If a bone trepanation was performed, the trepanation hole is gradually filled with osteogenic and later bone tissue. In childhood, traces of inflammation may disappear.

In other cases, encapsulation of ulcers in the bones is observed. By the 3-4th week from the onset of the disease with X-ray examination Against the background of rarefication, foci of bone necrosis are determined, since the dead bone does not undergo resorption and retains its previous density. Subsequently, those of them that are located in the very focus of suppuration undergo sequestration.

Sequestration consists of the rejection of dead areas of bone located in the cavity of the abscess from the surrounding bone tissue. In this case, in the case of the formation of a sequester in a compact plate, a sequestral groove appears on its surface in the area of adjacent granulations and gradually deepens, and in the thickness there is an expansion of the Haversian canals and their merging with each other. After all the bone substance in the specified zone has dissolved, the sequester appears freely lying in the cavity of the abscess.

Corticole sequestration can be total or segmental: penetrating, central and external.

The sequesters of the cancellous bone are separated from the rest of it due to the dissolution of the adjacent bone beams located in the granulation zone.

Along with the destructive process in osteomyelitis, a productive process is always observed. The most reactive of all bone elements is the periosteum, which produces bone in the form of periosteal layers. The latter, surrounding the sequestering areas of the bone, form sequestral boxes or capsules.

In more late stages During the course of osteomyelitis, the inflamed areas of the bone become saturated with layers of lime, and bone sclerosis develops. After which recovery may occur.

During chronic osteomyelitis, subsidence and exacerbation of the process are observed.

Exacerbations sometimes occur after the fistula is closed. In this case, acute inflammation occurs in the form of phlegmon, the abscess opens, a fistula forms again, and the inflammatory phenomena subside.

As a result of a long suppurative process, the entire body suffers, especially the kidneys, liver, and heart. Amyloid degeneration can develop in the liver and kidneys, which sometimes kills patients.

Clinically, acute and chronic osteomyelitis are distinguished.

Acute hematogenous osteomyelitis in children and adolescents usually begins as a severe general infectious disease, and in the first days general symptoms prevail over local ones.

The disease is often preceded by a sore throat, a local purulent process (festering abrasion, boil) or a bruised limb.

The disease begins with a sudden rise in temperature to 39-40°C, severe chills, which is accompanied by a sharp deterioration in general health, sometimes delirium. Young children often experience profuse vomiting, which makes them think about a disease of the gastrointestinal tract. In some cases, the disease is extremely severe, malignant and ends in death with symptoms of fulminant sepsis within a few days.

Simultaneously or somewhat later than the development of severe intoxication, complaints of strong bursting pain in the corresponding bone appear, aggravated by movement, shifting, but there is, as a rule, no swelling or redness in this area in the first days. There is no pain during palpation, especially on the thigh, where the periosteum is located deep under the muscles. It is especially difficult to detect local symptoms in the first days of the disease. The correct diagnosis is helped by targeted identification of local symptoms, in particular muscle contracture in nearby joints, local pain, pain when loading the limb along the axis, etc.

The local (mild) form is characterized by the absence of septic phenomena and the predominance of clinical local changes over disorders of the general condition, which can be severe, moderate or close to satisfactory. Intoxication is moderate, the temperature at the beginning of the disease and subsequently is 38-39 degrees. Local inflammatory changes are limited in nature, their clinical manifestations are less pronounced than in the septicopyemic form.

Local changes are moving quickly. During the first 2 days, localized pain appears; they are of a sharp nature, the limb takes a forced position (painful contracture), there are no active movements in it, passive ones are sharply limited. Soft tissue swelling quickly increases, which, if the focus is localized in the femur, can spread to the lower leg, the anterior abdominal wall, or if localized in the shoulder

bones - on chest. The skin over the lesion is hyperemic, tense, shiny, and often has a pronounced venous pattern; there is an increase in local temperature.

Sympathetic (reactive) arthritis of one or both adjacent joints often develops, first serous, then purulent.

If treatment is ineffective, the patient’s serious general condition worsens, intoxication and dehydration of the body increase, headache, pain throughout the body, loss of appetite, thirst, and anemia occur.

Metabolic processes are disrupted: metabolic acidosis develops; disorders of water-salt metabolism lead to persistent hyperkalemia and calcemia, hyponatremia and other disorders.

The indicators of nonspecific immune factors and the blood coagulation system deteriorate, and there is an excessive accumulation of inflammatory mediators (histamine, serotonin, etc.).

The hormonal regulation of body functions, myocardial metabolism, antitoxic liver function, and kidney function are disrupted, and the compensatory mechanisms of the respiratory and circulatory systems are depleted.

All these changes develop over 5-10 days and create favorable conditions for the generalization of purulent infection and its hematogenous metastasis. Toxic hemolytic jaundice often develops.

Pathological bone fracture, including epiphysiolysis, occurs as a result of bone destruction, often resulting in a false joint. Epiphyseal and metaphyseal osteomyelitis, due to the proximity of the lesion to the growth zone, can lead to growth disturbances and significant bone deformations (curvature, shortening, less often lengthening), pathological dislocation, contracture or ankylosis.

Laboratory data indicate the presence of a focus of purulent infection in the body (leukocytosis, shift of the formula to the left, etc.).

X-ray data in the first two weeks of the disease are negative (no pathological changes). Subsequently, a faint shadow of exfoliated periosteum appears at first, beginning to produce bone substance (periostitis). Even later, zones of rarefaction and lubrication of the cancellous bone structure appear in the metaphysis. The bone structure becomes uneven. The distinct formation of sequestra (separately lying areas of necrotic bone tissue) and sequestral cavity can be detected only 2-4 months after the onset of the disease, when the process has already become chronic. During this period, in the presence of fistulas, fistulography, as well as tomography, isotope and ultrasound examination, thermal imaging, and radiothermometry help in the X-ray diagnosis of cavities and sequestration.

Treatment of hematogenous osteomyelitis consists of a general effect on the body and a local effect on the source of infection.

a) General treatment

The general principles of treating purulent infections also apply to osteomyelitis.

Complex therapy for acute osteomyelitis includes the following elements.

1. Antibiotic therapy.

From the moment the diagnosis is made, the patient is injected intramuscularly with semisynthetic penicillins, lincomycin or cephalosporins, which usually leads to a sharp improvement in the patient’s condition, a decrease in temperature, a decrease in intoxication and a rapid recovery. If antibiotic treatment is started early, the inflammatory process in the bone marrow can be eliminated, and the bone structure damaged by the purulent process is gradually restored. The use of antibiotics in the early stages of hematogenous osteomyelitis has significantly changed its course and improved treatment outcomes. Endolymphatic administration of antibiotics has proven itself well.

2. Powerful detoxification therapy.

This is carried out from the first days, transfusions of crystalloid solutions and blood substitutes with detoxification effects, as well as blood plasma, are carried out. In severe cases, it is possible to use extracorporeal detoxification methods.

3. Immunocorrection and symptomatic therapy.

They are carried out according to the general principles of treatment of purulent surgical infection.

b) Local treatment

From the very beginning of the disease, rest and immobilization of the diseased limb using a plaster splint are necessary.

It is impossible to expand the scope of surgical intervention to wide trepanation of the bone marrow canal, since this can lead to dissemination of the purulent process and death.

Chronic osteomyelitis is necessarily preceded by an acute stage.

The transition of acute osteomyelitis to chronic occurs on average within a period of 3 weeks to 4 months from the onset of the disease and largely depends on the rate of sequestration.

Due to the mechanical and chemical properties of the bone, its dead part, called sequestrum, cannot, under the influence of pus enzymes, either quickly dissolve or quickly separate from living tissue. The sequestration process is very slow and continues for months and sometimes years.

Inflammatory and reparative processes in the circumference of the dead part of the bone occur due to the osteogenic tissue of the endosteum and periosteum, which form a capsule of newly formed bone with a granulation lining inside. As a result, the sequestrum, which has lost its mechanical connection with the surrounding living bone, appears as if immured in a capsule of newly formed bone (sequestration box). Being an infected foreign body, the sequester, being extremely slowly dissolved, maintains chronic suppuration for years.

Pus is released through fistulas, which may close periodically. The latter leads to retention of pus and a new outbreak of process activity with a corresponding local and general reaction. This condition can last for decades and sometimes leads to severe changes in parenchymal organs (renal and hepatic failure, amyloidosis), which, in turn, can cause death.

The clinical course is characterized by scant signs: aching pain in the area of the osteomyelitic lesion, the presence of purulent fistulas, rough postoperative scars. With an exacerbation of the process, already pronounced pain, an increase in body temperature to 38-39 ° C, and hyperemia of the skin in the area of the osteomyelitic fistula are noted. Exacerbation of chronic osteomyelitis is most often associated with temporary closure of a previously functioning purulent fistula.

Phases of the course of chronic (secondary) osteomyelitis:

The phase of the final transition of the acute process to the chronic one

· Remission phase (quiescence)

· Relapse (exacerbation) phase of inflammation

As acute hematogenous osteomyelitis transitions to chronic, the patient’s well-being improves, and the pain gradually weakens.

Signs of intoxication decrease or completely disappear; body temperature drops to normal or subfebrile levels, respiratory and cardiovascular functions are normalized; weakness decreases, appetite and sleep improve. Leukocytosis decreases, ESR slows down, white and red blood counts improve; the amount of protein and leukocytes in the urine decreases.

Fistulas finally form in the focal area. The fistula comes from one osteomyelitic focus or from different ones, can be single or multiple, often several fistulas are connected to each other in the soft tissues, forming a complex network of infected canals. The external opening of the fistula is sometimes located at a considerable distance from the osteomyelitic focus. Suppuration decreases.

In soft tissues, inflammatory infiltration gradually decreases as it enters the remission stage.