Chronic hematogenous osteomyelitis often develops as an outcome of acute osteomyelitis. becomes low-grade, pain disappears. The affected limb is thickened, swollen, and its function is limited. In the area where a spontaneous breakthrough of pus was produced or occurred, sometimes multiple ones are formed. The external opening of the fistula is small, surrounded granulation tissue. From the fistula constantly discharges into small quantity pus. Fistulas exist for a long time, for years, and close only after removal or release of the sequestration. Sometimes fistulas close temporarily. When pus is retained in the soft tissues, pain appears and body temperature rises; the fistula opens again. Small bone sequestra are sometimes released spontaneously; around large sequestra, a capsule (sequestral box) is formed from the periosteum with an opening (cloaca) leading into fistulous tract(cm. ).

Treatment. All patients with suspected acute hematogenous osteomyelitis are subject to urgent hospitalization. In the hospital, complex treatment is carried out: antibiotics are prescribed, surgical intervention and restoratives are prescribed if indicated. It is necessary to ensure the rest of the affected limb by applying a plaster splint. Immobilization is continued until the inflammatory phenomena completely subside, and when osteomyelitis becomes chronic, until a sequestral capsule is formed, since a pathological fracture is possible. In chronic hematogenous osteomyelitis, treatment is reduced to opening the sequestral box and removing the sequestration that supports suppuration and fistula. After the operation, a blind plaster cast is applied. At the same time, restorative treatment is carried out. In case of exacerbations of the process - antibiotic therapy. Patients with chronic hematogenous osteomyelitis after surgery, as well as patients with recurrent osteomyelitis with fistulas in cases where surgery is not indicated, are treated at mud resorts.

Brody's abscess in the metaphysis tibia.

Brody's Abscess- a kind of primary chronic hematogenous osteomyelitis, in which the inflammatory focus is localized in a limited area, most often in the proximal metaphysis of the tibia (Fig.). It is observed predominantly in males at a young age. The causative agent of the process is aureus or typhus bacillus. Brody's abscess occurs benignly, sometimes unnoticed by the patient and is discovered by chance when done for some other reason. Sometimes there are exacerbations, pain appears, which intensifies with pressure on the lesion, and body temperature rises. Fistulas never form.

Treatment. During exacerbation - antibiotics. Radical treatment surgical. By trepanning the bone, the lesion is opened, and the granulation pyogenic membrane is scraped out with a sharp spoon. If the patient is operated on during an exacerbation, it is better not to suture the wound. Antibiotics are administered intramuscularly for a week.

Rice. 2. Hematogenous osteomyelitis metaphysis femur: 1 - intraosseous abscesses with sequestration of spongy substance; 2 - subperiosteal abscess.

Chronic hematogenous osteomyelitis most often develops as a result of acute hematogenous osteomyelitis. The process is usually localized in the epimetaphyseal region of the long tubular bones, less often in the diaphysis or in flat and short bones. It begins as a diffuse phlegmon of the bone marrow, then the inflammation spreads to the Haversian canals and periosteum (tsvetn. Fig. 2). The inflammation is accompanied by necrosis of the bone marrow and compact lamina and after a few days becomes localized, delimited by a demarcation line, and then by granulations; as a result, an abscess is formed in the bone, containing purulently melted bone marrow and dead areas of the compact plate and spongy substance. Over time, the abscess is surrounded by a pyogenic membrane, and the necrotic, pus-soaked areas of bone located in it undergo sequestration.

The size and shape of sequesters depend on the size of the focus of suppuration: sequesters can be total, subtotal, or represent small fragments of a compact lamina.

Pus from the focus in the bone flows out after the formation of urticaria in the bone and fistulas in the soft tissues, or through surgical incisions, the walls of which quickly become covered with granulations. With the formation of sequesters, inflammation takes a chronic course.

With the development of suppuration, the entire affected bone, especially its sections located closer to the purulent focus, undergoes rarefaction, and in the areas of the periosteum and bone marrow adjacent to the area of ​​suppuration, bone growths appear, forming a sequestral capsule around the abscess and leading to focal eburnation of the bone. The sequestral capsule has one or more openings (cloaca) communicating with fistulas in the soft tissues. Each new exacerbation of the process causes reactive formation bone tissue around the sequestral capsule and in adjacent areas of the periosteum, often with the occurrence of exostoses.

During the course of the disease, bone loss continues, especially in the zone of granulation growth, which leads to the destruction of the compact lamina (“bone beetle”, inflammatory caries). Under the influence of rarefaction and eburnation due to the formation of exostoses, deformation of the affected bone occurs (Fig. 1), and in children and adolescence, its growth may be impaired. Thus, when the lesion is localized in the metaphysis, growth retardation is possible due to the destruction of the growth cartilage, and with diaphyseal osteomyelitis, bone elongation is possible due to irritation of the growth cartilage, which is located in the zone of collateral hyperemia, and possibly due to interstitial bone growth .

Rice. 1. Chronic osteomyelitis of the femur with a large sequestrum, sequestral capsule and massive periosteal bone growths.

Clinical picture and course. When acute osteomyelitis transitions to chronic after the pus breaks out, the general condition improves, the temperature drops to low-grade, and the pain disappears. However, the affected limb remains swollen and its function is not restored. Fistulas are formed that communicate with the bone, from which pus is secreted for a long time and persistently. The external opening of the fistula is small, surrounded by an area of ​​granulation. Sometimes it closes temporarily. In these cases, pus lingers, pain appears, febrile state; then the fistula opens again. Sometimes small sequestra are released through it independently (see Sequester, sequestration). Larger ones do not stand out on their own. The process of sequestration rejection can take several years. With chronic osteomyelitis, repeated outbreaks of infection are possible, i.e., relapses or exacerbations. The intervals between them can be 6-8 years or more.

Epiphyseal osteomyelitis does not have a chronic form.

Garre's sclerosing osteomyelitis is rare and usually occurs in adults. Clinically characterized by a sluggish course without acute manifestations. Pain appears in the later stages of the process. Thickening of the limb gradually develops due to uniform fusiform thickening of the cortical bone layer. Sequestra and fistulas, as a rule, do not form.

Hematogenous osteomyelitis

Acute hematogenous osteomyelitis (osteomyelitis haematogenica) accounts for 7% of all cases of osteomyelitis of the jaws in children; most often develops on the upper jaw when a child is 1-2 years old. Staphylococcus is the main etiological factor that causes hematogenous osteomyelitis of the jaws in early

at his age, biological feature which is high antibiotic resistance. The entrance gates of infection are umbilical sepsis, pustular skin lesions (strepto- and staphyloderma), microtrauma of the mucous membrane oral cavity, chroniosepsis, drank etc.

The process begins acutely, with severe intoxication. In the first 2-3 days local symptoms so small that the diagnosis is usually not made in a timely manner. Symptoms of a general condition disorder predominate and give the pediatrician reason to diagnose acute respiratory disease or sepsis in most cases.

Complaints parents - on the excitement of the child, p.chach, refusal of food, bad dream, increased body temperature.

Clinic. According to the clinical course, there are 3 forms of hematogenous osteomyelitis - toxic, septicopyemic and locally focal. The last V of children practically does not occur.

The toxic form has a rapid course - accompanied by high body temperature and severe intoxication of the body. The examination reveals tachycardia, rapid and shallow breathing. In the blood - a picture of hypochromic anemia, leukocytosis, a shift of the formula to the left, increase in ESR, hypoproteinemia. Against the background of expressed big picture local clinical signs erased. A careful examination can reveal slight swelling of the mucous membrane of the alveolar process and its barely noticeable hyperemia. Symptoms of jaw damage are detected only 4-6 days after the onset of the disease.

The septicopyemic form is characterized by rapid development and a sharp deterioration in the child’s general condition. Unlike the toxic form, local signs grow faster.

If the upper jaw is affected, then swelling in the infraorbital region and infiltration of soft tissues are detected (Fig. 30). Due to inflammation of the orbital tissue, exophthalmos may be observed; chemosis of the conjunctiva is determined, the eye is closed (Fig. 31). After 2-3 days from the onset of the disease, purulent exudate melts the cortical plate of the bone and exits under the periosteum (Fig. 32). The alveolar process of the jaw is deformed on both sides, the transitional fold is smoothed, the mucous membrane is hyperemic and infiltrated. Fluctuation may be detected. The presence of primary infiltrates and fistulas is characteristic (Fig. 33). In case of defeat medial sections upper jaw difficulties are observed nasal breathing due to swelling of the nasal mucosa, discharge of pus from the corresponding nasal passage. Swelling and tissue infiltration in the area of ​​the inner corner of the eye, swelling of the eyelids are determined; the skin of these areas is tense and hyperemic. The mucous membrane of the alveolar process is edematous, hyperemic, the transitional fold is smoothed due to the infiltrate located on the anterior surface of the upper jaw. The process extends to the slope of the nose. Fistulas occur near the inner corner of the eye. Both compact plates of bone may be destructured, in which case there is a breakthrough of pus into the nasal cavity or into the maxillary sinus.

If the lateral parts of the upper jaw (zygomatic process) are affected, nasal breathing is free. An infiltrate appears in the upper part of the cheek, there is a sharp swelling of the eyelids, exophthalmos, the sclera and conjunctiva are hyperemic.

Inflammatory diseases of the maxillofacial area

Now, there is significant mucopurulent discharge on the eyelids. The process spreads to the zygomatic bone, pus breaks out along the lower orbital edge near the outer corner of the eye, and fistulas may form on the alveolar process. The death of the rudiments of temporary teeth occurs.

When the disease passes into the chronic stage, small sequesters are formed already in the 1st-2nd week. Large sequestra usually do not form in the upper jaw. Their appearance may be due to irrational treatment. Follicles permanent teeth can die, sequester and maintain inflammatory process.

It is extremely rare to observe bilateral diffuse lesions of the upper jaw, accompanied by the development of phlegmon in the retrobulbar space. Sometimes damage to the facial bones and long bones develops. The disease is often complicated by the development of septic pneumonia.

If the lower jaw (condylar process) is affected, then 3-4 days from the onset of the disease, inflammatory infiltrates develop in the subzygomatic and parotid-masticatory areas. Purulent exudate spreads towards the external ear canal, which is accompanied by melting of the bones of the latter with the formation of fistulas. Fistulas can occur after the opening of purulent foci along the lower edge of the zygomatic arch.

Damage to the articular process lower jaw In young children, osteomyelitis is masked by a disease of the middle ear, which is why it is often treated inadequately and is detected much later in older children as unilateral or bilateral ankylosis of the temporomandibular joint.

Very rarely, acute hematogenous osteomyelitis of the lower jaw in children turns into a chronic form (Fig. 34), in which medium and large sequestration occurs (2-3 weeks from the onset of the disease). The rudiments of teeth in the zone of inflammation die and are sequestered, the growth zones of the jaws are affected, and purulent osteoarthritis develops. Often the disease becomes chronic and relapsing, and sequestration of new areas of bone is observed. With this course of the disease in children, the indicators decrease cellular immunity(lymphopenia, decrease in the content of active T-lymphocytes).

X-ray examination jaw in the early period (up to 10 days) does not reveal signs of osteomyelitis. Very rarely, on the 6-7th day from the onset of the disease, foci of diffuse lysis and weak signs bone formation. Blood and urine examination reveals signs of acute inflammation (erythropenia, leukocytosis, increase in ESR, shift of the formula to the left, appearance of C-reactive protein; in urine - the presence of protein, erythrocytes, leukocytes).

Diagnosis is based on a thorough examination of complaints ( sharp violation general condition of the child - agitation, refusal to eat, poor sleep, body temperature up to 39-40 "C), data objective examination(swelling of the soft tissues around the upper jaw with hyperemic skin above it, smoothness of the transitional fold and fluctuation during palpation, bilateral thickening of the alveolar process), blood and urine test data (erythropenia, leukocytosis, increased ESR, shift of the formula to the left, C-reactive protein - in blood; protein, erythrocytes and leukocytes - in urine).

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Rice. 30. Child with hematogenous osteomyelitis of the right upper jaw

Rice. 32. Formation of a subperiosteal abscess in the left upper jaw in the same child

Rice. 31. Child with hematogenous osteomyelitis of the left upper jaw, retrobulbar abscess and chemosis of the eyelids

Rice. 33. Child with acute hematogenous osteomyelitis of the left upper jaw and primary fistula on the palate

Rice. 34. Child with chronic hematogenous osteomyelitis of the left half of the lower jaw

Differential diagnosis acute hematogenous osteomyelitis should be carried out with odontogenic osteomyelitis, Ewing's sarcoma, soft tissue abscesses, acute parotitis, inflammatory diseases middle ear, acute inflammatory diseases of the eyes and orbit.

Treatment should be early, comprehensive and carried out only in a hospital setting. General treatment primarily aimed at detoxifying the child’s body. It must be agreed with the pediatrician.

All drug therapy in the first days is carried out exclusively intravenously. To do this, perform venesection or Seldinger venipuncture of the peripheral or subclavian vein. In the future, intramuscular administration of drugs is possible. Among antibiotics, broad-spectrum drugs are prescribed - claforan, kefzol, cefazolin, cephalosporins, thienam and triples for bone tissue; if necessary, two compatible antibiotics are administered.

For detoxification purposes, an isotope solution, glucose, neocomiensan, neogemodez, and reopolyglucin are transfused. Vitamins of group B and C are prescribed. Optimization of the general somatic condition is achieved by passive immunotherapy - transfusion of antistaphylococcal hyperimmune plasma, antistaphylococcal gamma globulin.

Surgical treatment includes adequate opening of abscesses and soft tissue infiltrates, subperiosteal abscesses with further drainage of wounds and their management according to the principles of purulent maxillofacial surgery.

Complications hematogenous osteomyelitis may be transitioned to the chronic stage, sepsis, meningitis, mediastinitis, arthritis, mumps, the formation of abscesses and phlegmons, the spread of inflammation into the orbit, the death of jaw growth zones and the rudiments of permanent teeth.

Consequences hematogenous osteomyelitis: possible secondary deformations of the jaws, bones and soft tissues of the maxillofacial area, cicatricial eversion of the eyelids, adentia, obliteration maxillary sinus, unilateral or bilateral ankylosis of the temporomandibular joint.

Hematogenous osteomyelitis is an inflammatory process of infectious origin, which is characterized by damage to the bones (bone marrow, bone beams, periosteum, as well as the soft tissues that surround them).

In hematogenous osteomyelitis, the pathogen enters the bone structures from the source of infection during blood circulation between tissues.

Manifests itself with general and local symptoms. The disease occurs due to the invasion of pus-forming microbes into the bone marrow. Most often the causative agent of the disease is Staphylococcus aureus, less often - mixed cocci, typhoid, paratyphoid, Escherichia coli and Pseudomonas aeruginosa, Proteus.

Etiology and pathogenesis

There are several theories explaining the disturbance of bone circulation and the occurrence of osteonecrosis. There is a hypothesis that osteomyelitis may occur as a result of embolism, spasm, endovasculitis of bone vessels caused by allergic reaction to the pathogen.

The modern theory is based on data on the structure of bone vessels. The arteries of the spongy substance branch into arterial capillaries, which become venous. In the latter there are local expansions - sinuses.

A slowdown in blood circulation in the sinuses allows the infection to settle and spread paravasally to the osteonic vessels. Edema of paravasal cells and their purulent infiltration lead to a significant increase in intraosseous pressure. As a result, the veins are first compressed, then the arteries, and it is this process that causes the development of ischemic necrosis and progressive bone damage.

Intravascular occlusion (obstruction) that occurs due to spasm, vasculitis, thrombosis or embolism is secondary local manifestation diseases. External vascular occlusion is primary, it prevents the resumption of collateral circulation in the bones.

The result is the appearance of a lesion in the bone tissue, which subsequently becomes a source of infection and participates in the destruction of bone tissue.

In children, the risk of developing the disease increases due to a history of frequent viral diseases, which suppress the body's defenses.

Pathological picture

Hematogenous osteomyelitis can occur at any age, but more often it develops in childhood: from 5 to 16 years.

The incidence of the disease is higher in males. This is explained more frequent injuries and the characteristics of their immune and endocrine status.

IN lately There have been outbreaks of the disease in infants. This is due to decreased immunity in the mother and, as a consequence, in the newborn.

Most often, the pathological focus of hematogenous osteomyelitis is localized in the long bones of the extremities, namely in the femur, tibia, and humerus.

Much less often the disease is diagnosed in short and flat bones– skull, spine, pelvic bones, ribs. However, osteomyelitis of such localization is more “malignant” than in long bones. This is due to the fact that many flat and short bones border on vital organs.

You should be especially careful if hematogenous osteomyelitis has developed in the bones of the skull. Proximity to brain structures that can be affected by the inflammatory process requires a lightning-fast response to the disease.

The development of the disease is divided into several phases:

1. Acute phase of hematogenous osteomyelitis. It begins acutely, with specific symptoms increasing, requiring immediate treatment.
2. Subacute phase of hematogenous osteomyelitis. This phase lasts from 2 to 6 months. Characterized by attenuation of symptoms of the acute phase. Without antibacterial treatment possible appearance of lesions on the skin with purulent contents.
3. Chronic phase of hematogenous osteomyelitis. During this phase of the disease clinical manifestations practically absent, with the exception of periodically appearing aching pains. This phase can last a long time, with periodic relapses occurring.

Due to the deep location of the source of inflammation on initial stages As the disease progresses, symptoms may be blurred or absent.

Classification and symptoms

According to the speed of development and severity of the general condition, acute hematogenous osteomyelitis is divided into several forms:

• The most severe is the septic-toxic form.
• Satisfactory – septic-pyemic form.
• With damage to one bone - local form.
• The atypical form, which practically does not occur at a young age, has acute form: sclerosing and albuminous. This type of osteomyelitis also includes an abscess (intraosseous).

This classification is rather conditional, since often in practice these forms can transform into one another during the development of the disease.

The most understandable classification is according to Shalygin: they determine the etiology of the disease (pathogen), form, stage (acute/chronic), localization in bone tissue, clinical manifestations and complications.

Recently, the clinical picture of the disease has undergone changes. This is due to the development of antibiotic-resistant bacterial strains, which can cause mild forms of the disease, with a gradual transition to a chronic process or provoke more severe course diseases.

Septic-toxic (adynamic) form – complex disease, which begins acutely and has a severe course for the patient:

• Increase in body temperature to critical levels.
• General intoxication of the body, which is accompanied by weakness, loss of consciousness, intense pain all over the body.
• The appearance of convulsive activity, especially in young children.
• The risk of developing dysfunction in the cardiovascular system, respiratory system and genitourinary system.
• When examining blood, pronounced leukocytosis and a sharply increased ESR are observed.

Septic-pyemic form of hematogenous osteomyelitis has the same symptoms as septic-toxic, with the exception of the risk of developing deficiency syndrome from the above body systems. With this form, failure of organs and systems is not observed.

A few days after the onset of the disease, in the septicopyemic form, local signs of osteomyelitis appear, which are localized in the area of ​​the affected bone (usually in the area of ​​the metaphysis of long bones). Symptoms:

• Appearance pain over the affected area of ​​the bone.
• Development of local swelling of soft tissues.
• Hyperemia of the skin with increased temperature at the site of swelling.

Due to swelling, pain in the limbs can transform into joint pain, and contracture develops with limited movement in the joint or limb.

Local form of osteomyelitis flows easily and has favorable prognosis. Clinically, it begins as an acute disease, with increased body temperature and swelling at the site of the lesion. However, the symptoms of intoxication do not increase, and when timely treatment local form of hematogenous osteomyelitis passes without severe consequences and complications.

Diagnostics

Diagnosis of hematogenous osteomyelitis is based on the results of assessing the patient’s complaints, objective examination, clinical data laboratory research and intrascopic imaging methods.

For inflammation of bone tissue, multi-projection radiography and planar tomography are used, with the help of which the development phase and extent of the process are determined.

Conventional radiography of bones is mainly used in two projections - frontal and lateral. Magnetic resonance imaging, computed tomography and nuclear magnetic resonance in this case are not very informative.

CT is prescribed when it is necessary to establish the depth of the pathological focus in the bone tissue, as well as to clarify the condition of adjacent soft formations and determine the degree of bone mineralization.

MRI does not make it possible to evaluate features destructive process in bone tissue, but it is recommended when it is necessary to diagnose inflammation of the bone marrow, to study the condition of soft tissues and the boundaries of the spread of the process.

All radiological diagnostic methods used for hematogenous osteomyelitis must be carried out over time.

In acute hematogenous osteomyelitis, a change in the muscle structures, noticeable already at 1 week of illness. And the phenomena of periostitis can be diagnosed from 3 weeks from the onset of the disease. In the future, X-ray changes will be visualized in the bone tissue, in the area of ​​the metaphysis, with the process spreading to the entire bone.

In chronic hematogenous osteomyelitis, there will be foci of bone destruction at the level of the diaphysis with hyperostosis, which leads to an increase in the bone in transverse size.

If you suspect the appearance of decompensatory elements on the part of other organs and systems (for example, the development of cardiovascular failure), it is necessary to use integrated approach in diagnostics with the involvement of related medical specialists.

Particularly important are the methods early diagnosis diseases when the pathological process is detected in the first two days from the onset of the disease. With this diagnosis, it is possible to block the inflammatory process within the boundaries of the bone marrow canal and prevent the process from spreading to the bone marrow.

Treatment

Treatment of hematogenous osteomyelitis is based on three general principles:

1. Surgical treatment of purulent foci. The cavity with purulent contents is opened, its sanitation and subsequent tamponade are performed. muscle fibers. According to indications, when intraosseous pressure increases, osteoperforation and drainage of the source of infection are performed (using burr holes). At this stage of treatment, it is necessary to limit movement, it is advisable to completely eliminate the activity of the affected limb.
2. Treatment with antibacterial drugs. Required individual selection a drug that will effectively act on the infectious agent. To do this, determine the sensitivity of the microflora, compatibility with other drugs and conduct an assessment - toxicity / benefit, choosing the best option.
3. Symptomatic treatment. Fighting intoxication (detoxification therapy), “launching” homeostasis (various corrective infusion solutions), monitoring normal operation organs and systems (primarily cardiovascular and genitourinary).

Complex treatment of the disease also includes:

• Various physiotherapeutic procedures.
• Immunocorrection is carried out for general strengthening organism and increasing its resistance to infectious invasion.
• The use of multivitamin preparations, which include vitamins E, C and membrane stabilizers, helps cleanse the body and increase its anti-infective resistance.
• Quite a lot important during the rehabilitation period and during chronic phase has diseases spa treatment: use of therapeutic mud.

Which doctor treats

Chronic hematogenous osteomyelitis (CHO) develops after acute illness and is characterized by a long-term course, when periods of exacerbation and remission (relative well-being) alternate. The morphological substrate for such a course of the disease, as a rule, is the area of ​​bone that has died as a result of acute inflammation. Over time, it is rejected by living bone, and a sequestrum is formed, usually located in the bone cavity - the sequestration box. A common component of CHO are purulent fistulas, which are pathological passages in tissues connecting the osteomyelitic cavity with the external environment. Usually the fistula opens on the skin with its external opening and is a kind of drainage that discharges into external environment excess pus that forms. Being an absolute pathology, a fistula, nevertheless, allows the patient to sometimes live for many months and years with minimal manifestations of the inflammatory process. When the fistula closes or it is unable to drain the pathological intraosseous lesion, conditions are created for the exacerbation of the disease. Pain appears or intensifies, the temperature rises, local signs of an acute inflammatory process are observed (swelling, redness, etc.). In the future, paraosseous phlegmon may develop, or a purulent fistula will reopen. As a rule, patients with exacerbation of chronic gastrointestinal tract urgently seek medical care. Untimely assistance in this case carries the danger of spreading purulent process on surrounding tissues, increased intoxication, and development of sepsis.

Diagnosis of chronic hematogenous osteomyelitis

Diagnosis of CHO in most cases does not present any difficulties, since usually patients with such a diagnosis have long been in the field of view of a specialist familiar with the peculiarities of the course of the disease. However, it is possible to judge structural changes in the bone: their nature, severity and prevalence only on the basis of the instrumental examination sick. The examination begins with a survey x-ray, which makes it possible to identify the main pathological changes in bone tissue. However, many details of bone damage may be inaccessible even to an experienced eye. Moreover, their assessment is extremely important when planning surgical intervention, which is the main treatment method for patients suffering from CHO. Multispiral X-ray capabilities computed tomography allow you to objectify and visualize changes in detail bone structures, which is especially important when massive bones are affected, such as, for example, the pelvic bones, sternum, etc. Moreover, modern instrumental diagnostics Osteomyelitis in a significant number of cases requires mandatory computed tomography (CT). In case of CHO, it is absolutely necessary. The presence of a purulent fistula is considered the basis for fistulography. The study involves the introduction of a radiopaque substance into the fistula tract, followed by a series of x-rays. Fistulography is primarily necessary for planning surgical intervention, since all purulent fistulas must be removed. Magnetic resonance imaging in the diagnosis of chronic hematogenous osteomyelitis is of auxiliary value, helping in some cases to identify the extent of damage to the soft tissue surrounding the bone, including purulent leaks in complex anatomical areas, for example, with

Rice. 1. External opening of a purulent fistula in a patient with chronic hematogenous osteomyelitis of the femur. Numerous scars are identified after previous surgical interventions.

Rice. 2. Fistulogram of the same patient. Thickening and deformation are determinedof the femur affected by osteomyelitis. A contrast agent injected into the external opening of the fistula enters the paraosseous and intraosseous purulent cavities.

Rice. 3. CT scan of the same patient. A large osteomyelitic cavity is detected in the femur.

Rice. 4. HGO ulna. The latter is significantly thickened and deformed. A sequester is detected in the bone cavity.

Rice. 5. CT scan of the femur. Transverse section at the level of the distal metaepiphysis. A free-lying bone sequestrum is identified in the osteomyelitic cavity.

Rice. 6. Fistulogram of a patient suffering from CTO of the femur. Multiple purulent fistulas located both in soft tissues and penetrating into the osteomyelitic cavity are contrasted.

Rice. 7. X-ray picture CHO of the femur. Anamnesis of the disease for more than 40 years. Pronounced structural changes in the femur are determined (thickening, deformation, multiple osteomyelitic cavities with sequesters located in them). To clarify the volume and nature of destructive changes, a CT scan is necessary.

Treatment of chronic hematogenous osteomyelitis

The main treatment method for CHO is surgery. Tasks surgical treatment diseases include removal of sequesters and non-viable areas of bone tissue, drainage of the bone cavity. In some cases, there is a need for filling or plastic surgery of the bone cavity. Surgical tactics and technique in the treatment of CGO are determined by the prevalence pathological process, and directly anatomical features affected bone. In the treatment of osteomyelitis, it is important to assess the condition of the surrounding soft tissues, since they are important in the blood supply to the bone. Cicatricial and destructive changes in the soft tissue surrounding the bone significantly complicate the task of surgical treatment of osteomyelitis. In some cases, various ones come to the rescue.

One of the fundamental principles of surgical treatment of chronic gonorrhea is the principle of “do no harm.” This means that an unsuccessful operation for osteomyelitis can significantly worsen both the general condition of the patient (for example, as a result of massive bleeding) and cause serious functional disorders(postoperative fractures, joint contractures, etc.).

Surgical treatment of CHO, along with professional skills, requires the presence of special instruments that make it possible to reach the osteomyelitic focus, which in CHO is often located intraosseously, with minimal trauma, as well as to remove pathologically altered areas without disturbing the blood supply to the remaining bone.

Conservative treatment complements surgical treatment or is the only one if there are contraindications or the patient refuses surgical intervention. Task conservative treatment in these cases it will be reduced to reducing the severity of inflammatory phenomena. It includes antibacterial, detoxification therapy, physiotherapeutic treatment, and washing of fistulas with antiseptic solutions.

Rice. 8. Plain X-ray of a patient suffering from CHO humerus. In the proximal part of the bone, pronounced bone-destructive changes are determined, located on the side of the bone marrow canal, i.e. endosteal.

Rice. 9. Fistulogram of the same patient. Inserted into the fistula contrast agent enters the bone, forming a depot in the osteomyelitic cavity in the area of ​​the proximal metaepiphysis of the humerus.

Rice. 9. X-ray of the same patient after surgical treatment. Trephination of the humerus with osteonecresequestrectomy was performed.

Hematogenous osteomyelitis- the use of antibiotics has revolutionized the treatment of hematogenous osteomyelitis for the better. However, even today it remains one of the most severe and dangerous diseases childhood. The disease affects growing bones, especially during periods of faster growth.

From hematogenous osteomyelitis caused by pyogenic microbes, it is necessary to distinguish between specific osteomyelitis caused by microbes of tuberculosis, syphilis, osteomyelitis due to brucellosis, actinomycosis, typhus, etc.

A special form of osteomyelitis is traumatic osteomyelitis with open fractures and gunshot wounds.

Etiology and pathogenesis Hematogenous osteomyelitis. Studies of pus and blood showed the predominance of golden and white staphylococci (70-90%) - Much less often the presence of streptococci, alone or in combination with other microbes (4-18%) and rarely (2-5%) the presence of other pyogenic microbes - diplococci and etc.

Pathogens enter. into the body from superficial or deeper purulent foci, break through the lymphatic system into the blood and cause bacteremia. Usually the body has enough antitoxins, and the bactericidal nature of the blood is sufficient to destroy microbes. However, virulent pathogens 4 overcome bone marrow resistance.

These microbes exhibit osteotroggaya, that is, a tendency to infect bone, especially the metaphyses of long tubular bones “near the knee, away from the elbow.”

The pathogenesis of hematogenous osteomyelitis is not entirely clear.

The theory of embolism was expressed by A. A. Bobrov (1889) and developed by E. Lexer (1894). Osteomyelitis was considered as a manifestation of septicopyemia. The bacterial embolus settles in one of the terminal vessels, which is facilitated by the narrowness of the terminal arteries and slower blood flow in them. A. O. Vilensky (Wilensky, 1934) further developed the embolic theory and pointed out the importance of thrombophlebitis and thrombarteritis that occur after embolism.

In connection with this theory, the types of blood supply to bone were intensively studied (Nussbaum, N.Y. Anserov, M.G. Prives, etc.) Currently not given special meaning the presence of a main or scattered type of vessel structure and the angle of departure of the feeding arteries of the bone from the main trunk, which was previously used to explain the localization of the disease in the bone.

According to the allergic theory developed by S. M. Derizhanov (1940), the inflammatory process in the bone is caused in a sensitized organism by resolving factors of an endogenous and exogenous nature, similar to the Arthus phenomenon. Such nonspecific irritants can also be injury and cooling.

According to reflex theory, central nervous system plays a leading role in sensitization of the body, in the occurrence of disturbances in the blood supply to the bone (vasospasm) and in creating conditions for the occurrence of osteomyelitis (N. N. Elansky, B. K. Osipov, B. V. Turbin, etc.).

All three theories complement each other.

Course of osteomyelitis: separate acute and chronic stage. Less common is primary chronic hematogenous osteomyelitis.

Acute stage, or acute hematogenous osteomyelitis, is serious illness, with acute onset, high fever, severe general condition, sharp pain And severe inflammation in the area of ​​the affected bone.

According to T.P. Krasnobaev, there are three forms of the disease: toxic, or adynamic, septicopyemic and mild.

Toxic or adynamic, acute osteomyelitis develops rapidly, even at lightning speed. Toxic phenomena predominate. A sick child dies in the first days of the disease. Some authors [Leveuf] consider this form to be staphylococcal sepsis and are not classified as osteomyelitis, since the changes in the bone characteristic of osteomyelitis do not have time to develop.

Characteristic for acute hematogenous osteomyelitis is a septicopyemic form of the disease, in which the phenomena of sepsis are combined with acute inflammation bones. It flows like an acute purulent infection and therefore it is also called infectious hematogenous osteomyelitis.

The inflammatory process begins diffusely, in bone marrow, spreads to the Haversian canals and the periosteum, has the character of phlegmon.

Around the foci of inflammation, bone tissue is reabsorbed from the very beginning and osteoporosis develops.

With early use of antibiotics, suppuration may not occur and the source of inflammation can be eliminated without the formation of sequestration.

The cavity of the abscess is filled with granulations, which turn into fibrous tissue; the tissue is then resorbed and the normal structure of the bone marrow is subsequently restored.

In severe cases, with microbial resistance or lack of proper treatment, the process spreads through the bone marrow cavity, through the Haversian canals it penetrates under the periosteum and a subperiosteal abscess appears. At the same time, blood flow through the vessels of the periosteum stops. Toxic hemolysis and secondary thrombophlebitis occur, spreading to the vessels of the compact layer and periosteum. The result is bone necrosis.

The fleshonous process can spread throughout the bone marrow cavity, even occupying it completely. In this case, necrosis of the entire diaphysis may occur. The pus is looking for a way out. Fistulas are formed, through which pus is emptied and bone sequestra are sometimes released.

From the 3rd week, a periosteal reaction appears in the form of a gentle layer. Then an osteoplastic reaction from the surrounding environment joins connective tissue and endosteum. At the periphery of the lesion, sclerosis appears in the bone as a result of the osteoplastic process. A sequestral capsule is formed.

There is high leukocytosis with a shift in the blood count to the left, accelerated ROE, and a gradual drop in hemoglobin. Blood cultures are usually negative. Data from other laboratory tests, as in acute infections.

X-ray changes are absent in the “reactive negative phase” during the first two weeks; they appear at the beginning of the 3rd week, somewhat earlier or later, depending on the virulence of the infection, the body’s reaction, the age of the child and the treatment performed.

As a result of the resorption of bone tissue, an erased structure first appears at the site of inflammation, the spongiosa beams disappear, at the end of the 2nd week, first a “cotton” structure appears, then foci of clearing and osteoporosis of adjacent areas of the bone. The bone becomes spotted and streaked. By the 3-4th week, foci of necrosis begin to be identified, since they do not undergo resorption, but retain the same density.

X-ray changes when using antibiotics are less pronounced, often erased, and less characteristic.

Recognition of acute hematogenous osteomyelitis can sometimes be difficult.

Toxic or adynamic forms go under the picture of general sepsis and are recognized only during section.

Septicopyemic forms can initially be mistaken for infectious disease. Sometimes hematogenous osteomyelitis is mixed with acute articular rheumatism. In osteomyelitis, the metaphysis of the long tubular bone is affected, and in rheumatism, the inflammation is localized in the joints.

In addition, rheumatism usually affects several joints, while osteomyelitis is predominantly localized in one bone. Multiple localization does not exceed 16% (K. Ya. Lenzberk), moreover, in most of these cases the process begins in one bone.

Pain and swelling in the area of ​​the metaphyses of long bones can sometimes be confused with deep phlegmon, or deep lymphadenitis. Because these diseases are treated similarly, this uncertainty in diagnosis does not have harmful consequences. The course of the disease in the coming days reveals its true nature.

In mild forms of acute hematogenous osteomyelitis, sometimes at the onset of the disease it is difficult to differentiate it from acutely beginning osteoarticular tuberculosis. However, the difference in localization and the characteristic features of both processes already provide valuable indications at the outset.

One disease from another makes it possible to distinguish the characteristics of the blood picture, the results of the Pirquet and Mantoux reactions, and finally, the further course of the disease with a characteristic clinical picture and radiographic changes for each of them.

Treatment of hematogenous osteomyelitis comes down to the use of antibiotics and sulfonamides, immobilization of the affected limb and general restorative treatment. Punctures of the local lesion are performed, and, if necessary, surgical interventions.

The effect of treatment depends on early use antibiotics and sulfonamides. The main antibiotics are penicillin and streptomycin.

Depending on the antibiotic data, it is necessary to resort to various combinations with other antibiotics: tetracycline, biomycin, aureomycin, etc. Often the latter have to be combined with sulfonamides.

Antibiotics must be used in large doses until the temperature is stable normalized within 2-3 weeks. To prevent candidiasis, nystatin is given at the same time.

A puncture is performed with suction of pus and local administration of antibiotics with a 0.5% solution of novocaine, daily, until the inflammation subsides.

Rest of the affected limb is best ensured by a plaster cast with a window for control and production local treatment(punctures). During treatment, massive doses of vitamins and food rich in proteins and vitamins are given.

Acute hematogenous osteomyelitis usually heals without surgical intervention, if treatment is started in the first two days of the disease with large doses of an effective combination of antibiotics intramuscularly and locally and is carried out for a sufficiently long time.

In severe cases, with a delayed start of treatment, with high virulence of microbes and their resistance to antibiotics, extensive necrosis of the bone and surrounding tissue occurs after pus breaks through the periosteum. In such cases, opening of the phlegmon with removal of necrosis and subsequent suturing of the surgical wound is indicated. .

Gentle trepanation necessary in heavy and advanced cases. It is performed with a sharp chisel in a limited area. After removal of soft tissue necrosis, the surgical wound is sutured in layers.

Drainage is not recommended, since this opens the gate for exogenous infection (Levef). In case of accumulation, pus is removed by puncture followed by the administration of antibiotics in accordance with the antibiogram data.