Pathogenesis and Stages of Development
The process always begins in the bone marrow with signs of serous inflammation (edema and hyperemia), which rapidly transforms into purulent infiltration. Further dynamics of the osteomyelitic focus include the following stages:
- Bone marrow phlegmon. Thrombosis of the nutritive vessels develops, leading to local ischemia and necrosis of bone tissue (the compact layer is affected — ostitis).
- Subperiosteal abscess. Pus spreads outward through Haversian canals (osteonal canals), penetrates the bone layer, and strips the periosteum, causing periostitis.
- Paraossal (intermuscular) phlegmon. The periosteum melts, and pus breaks through into the surrounding soft tissues.
- Subcutaneous abscess and fistula. The inflammation involves the subcutaneous tissue and skin. Following spontaneous opening of the abscess, a fistula forms.
If the process is not arrested, pronounced periostitis develops within 1.5–3 weeks, and sequestra (dead areas of bone) surrounded by an involucrum appear within 1–2 months. This is a sign of transition to the secondary chronic form.
Clinical presentation
Three clinical forms are distinguished based on severity: local, toxic, and septicopyemic. The latter is characterized by bacteremia with the formation of new foci and a high probability of a fatal outcome.
Systemic Manifestations:
- Systolic heart murmur.
- Enlargement of the liver and spleen (hepatosplenic syndrome).
- Vomiting, intestinal paresis.
- Lower back pain (positive Pasternatsky's sign).
Local Symptoms (first 24 hours): The limb is in a forced semi-flexed position. All movements in the nearest joint are severely restricted due to pain. A characteristic sign is pronounced tenderness upon gentle tapping over the bone (percussion on the heel causes pain along the entire axis of the limb). The focus is usually localized in one of the metaepiphyses. At later stages, edema increases (limb circumference grows), skin hyperemia, local hyperthermia, and fluctuation appear. In an unfavorable course, a pathological fracture may occur within 3–4 weeks due to osteonecrosis.
Diagnostic methods
Laboratory findings reveal marked leukocytosis (up to $20.0 \times 10^9/\text{L}$) with a left neutrophil shift, elevated ESR, and dysproteinemia (decreased albumin, increased $\alpha_1$- and $\alpha_2$-globulins). Protein, casts, and leukocytes are detected in the urine.
Instrumental Studies:
- Radiography: of low diagnostic value at the onset of the disease. Reliable signs (thickening of the periosteum, "blurring" of the structure, cavity formation) appear only by days 10–14.
- Early Diagnosis: radioisotope scintigraphy shows a focus of radiopharmaceutical hyperfixation as early as days 2–3. Thermography is also used.
- Osteoperforation (bone puncture): performed with a special needle in the metaphyseal zone. The recovery of turbid serosanguineous fluid with fibrin or pus, as well as an elevation of intraosseous pressure up to 300–400 mm H₂O, confirms the diagnosis.
Differential diagnosis
Acute hematogenous osteomyelitis must be differentiated from trauma, typhoid fever, and the following conditions:
- Rheumatism: inflammation involves several small joints, effusion is serous in nature, the focus is in the epiphysis, and there is a prodromal period. In osteomyelitis, a single joint is affected, effusion is purulent, and the metadiaphysis is involved.
- Bone Tuberculosis: proceeds with muscle atrophy. Radiography shows the "melting sugar" sign. In osteomyelitis, areas of osteoporosis alternate with cavities, followed later by sequestra.
Principles of treatment
Therapy must be comprehensive and include both conservative and surgical methods.
The main factor for a successful outcome is early decompressive drainage of the medullary canal with active debridement of the purulent focus. Strict immobilization of the affected limb is mandatory.
Medical treatment includes intensive infusion therapy (povidone, electrolytes, dextran for detoxification; plasma and albumin for protein replacement). Specific (toxoid, bacteriophage) and nonspecific (methyluracil, lysozyme) immunotherapy, as well as desensitizing agents, are used.
For differential diagnosis with rheumatism, remember the osteomyelitis rule "1-P-M": affected 1 joint, effusion is Purulent, localization is Metadiaphysis.
Class and exam questions
Why is radiography unsuitable for early diagnosis?
Reliable radiographic changes (periostitis, destruction) appear no earlier than 10–14 days from the onset of inflammation. For early diagnosis (first 2–3 days), scintigraphy or thermography is preferred.
What happens during a bone puncture in a patient with osteomyelitis?
During osteoperforation, pus or turbid serosanguineous fluid is aspirated from the medullary canal. Osteotonometry demonstrates a sharp increase in intraosseous pressure up to 300–400 mm H₂O.
What are the signs of transition from an acute process to a secondary chronic form?
The main criteria for chronicity are the formation of a sequestrum (dead bone), the development of a granulating involucrum around it, and the presence of purulent fistulas.
What else to study on this topic
- Pathogenesis of sequestrum formation and their types (cortical, total, central)
- Non-hematogenous forms of osteomyelitis (post-traumatic, gunshot)
- Clinical forms of acute hematogenous osteomyelitis (toxic, septicopyemic, local)
- Secondary purulent arthritis as a complication of metaepiphyseal osteomyelitis
- Specific and nonspecific osteomyelitis: classification principles
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