Atypical forms of osteomyelitis

Brodie's intraosseous abscess

Brodie's abscess (Brodie's abscess) is a localized intraosseous purulent process in which an area of cancellous bone undergoes necrosis with cavity formation.

• Etiology and pathogenesis: It develops due to a low-virulence staphylococcal infection against the background of reduced bodily reactivity. The cavity usually contains purulent, serous, or bloody fluid.
• Clinical presentation: It proceeds without general symptoms of intoxication (fever, chills). Characteristic features include pain that worsens at night, after physical exertion, or with weather changes. Examination sometimes reveals moderate thickening in the metaphyseal zone and reactive changes in the adjacent joint. The course is recurrent: remissions alternate with exacerbations.
• Radiological diagnosis: The classic localization is the proximal metaphysis of the tibia. The radiograph shows an isolated rounded or oval cavity (2–2.5 cm) surrounded by a clear rim of osteosclerosis. Obvious sequestra and pronounced periosteal reaction are absent (very small cancellous sequestra are occasionally present).
• Treatment: Primarily surgical. Bone trepanation is performed, the walls of the cavity are curetted, and primary closure is applied (muscle plasty is used for large defects).

Garré's sclerosing osteomyelitis

Garré's osteomyelitis (Garré's sclerosing osteomyelitis) is a non-purulent form of primary chronic inflammation affecting the diaphyses of long tubular bones.

• Clinical presentation: The disease lasts for years. Purulent fistulas and paraosseous phlegmons are practically absent. Patients are bothered by nocturnal pain in the limb. Laboratory findings reveal moderate leukocytosis and an elevated ESR.
• Radiological diagnosis (key signs): Marked sclerosis (compaction) of the bone tissue and fusiform thickening of the diaphysis over a considerable extent are observed. The cortical plate forms a massive hyperostosis. The medullary canal is severely narrowed or completely sclerosed. The most crucial sign is that destruction foci, cavities, and sequestra are not detected.
• Treatment: Based on conservative therapy: long courses of antibiotics (lincomycin, fusidic acid), UHF therapy, trypsin electrophoresis. Surgical treatment is rarely used, mainly to remove multiple small foci of inflammation.

Albuminous and tumor-like osteomyelitis

Ollier's albuminous osteomyelitis A specific form in which the process stops at the exudation stage without progressing to suppuration. Instead of pus, serous or mucous fluid rich in proteins (albumins) or mucin accumulates in the bone cavity. This is attributed to high immune defense and extremely low virulence of the microflora. The disease proceeds with mild clinical manifestations: local hyperemia and soft tissue infiltration are minimal. Treatment aims at surgical debridement of the focus.

Tumor-like osteomyelitis An extremely rare form simulating a malignant bone neoplasm (most commonly osteogenic sarcoma).

• A dense tumor-like soft tissue infiltrate is present, tightly fused to the bone.
• Persistent night pains are present.
• Phlegmons, fistulas, and sequestration are absent.

Radiologically, the pathology is difficult to distinguish from sarcoma due to specific periosteal layering. The diagnosis is confirmed only by biopsy results and prolonged dynamic follow-up.

Special forms: antibiotic and post-typhoid

These two forms are distinguished based on a specific medical history preceding the onset of inflammation:

1. Antibiotic osteomyelitis. Occurs in patients who took antibiotics for a prolonged period before the development of bone pathology. The infection immediately assumes an obliterated, sluggish character. Pain syndrome and hyperemia are practically absent, and paraosseous phlegmons do not form. Radiographs show multiple small foci with alternating zones of sclerosis and osteoporosis.
2. Post-typhoid osteomyelitis. Develops shortly after severe infections (typhoid and typhus fevers, paratyphoid fevers, less commonly influenza and scarlet fever). Notably, the causative agent is not a specific infection, but conventional pyogenic microflora with reduced activity. It is characterized by an extremely torpid course.

Class and exam questions

What else to study on this topic

• Radiological criteria for the differential diagnosis of Garré's osteomyelitis and bone sarcomas
• Surgical technique of muscle plasty for bone defects in Brodie's abscess
• The role of low-virulence staphylococcal flora in the pathogenesis of primary chronic osteomyelitis
• Changes in the body's immune reactivity as a factor in the formation of albuminous osteomyelitis
• Regimens of conservative antibacterial therapy in sclerosing bone lesions

Other topics from the section "CHAPTER 11. SURGICAL INFECTION (PURULENT-INFLAMMATORY DISEASES)"

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