Pathogenesis
AO results in one of three ways:
1. haematogenous spread - bacteria reach bone tissue via the blood stream from a 1 o nidus of infection (eg. a boil, or breach in the skin)
2. direct extension of infection into bone from adjacent soft tissue (eg. a cellulitis)
3. direct bone infection from a penetrating wound or open fracture. By far the haematogenous route is the most common.
Pathology
The infective process usually begins in the metaphysis. In children the growth plate is rarely affected since there is minimal vascularity in this region. However in adults, the continuity of the metaphysis with the epiphysis allows extension of infection towards the joint. Pus formed during the necrotic process pushes against the periosteum eventually bursting through it. It then tracks towards the skin via muscle and soft tissue to form a sinus from which the pus is discharged. The infarcted bone is called sequestrum. New periosteal bone surrounding dead bone is called the involucrum, and the pores within the involucrum through which pus tracks are called cloacas.  
 
Clinical Features
Pain is the first and most important symptom. Its onset and exact position are vital clues to a correct diagnosis. If the soft tissues surrounding the bone are affected, then swelling, erythema and /or an abscess may be present. A history of trauma may be present or associated with onset of symptoms.
The lower limb is more often the site than the upper limb. Distal femur and proximal tibia are sites of predilection in children. The crucial physical signs are bony tenderness, loss of limb function and fever. Of importance here is the differentiation between osteomyelitis and septic arthritis. In the latter, absolutely no movement is permitted to the joint, while in the former, minimal function of the adjacent joint remains.
Investigations
· ESR and neutrophil count are often raised. Biochemical parameters are often useful; serum Caz+, P043- and alkaline phosphatase levels are normal in osteomyelitis but may be altered in metabolic bone disease.
· Radiology - mild soft tissue swelling can be detected early but demineralisation and new bone formation can only be observed after day 10.
· CT is not useful. MRI scans may help to visualise spinal disease.
· isotope bone scan - only in equivocal cases; very sensitive but specificity is low. · blood cultures (positive in 50-70% of cases) are essential and must be taken before commencement of antibiotics.
· biopsy - for identification of pathogen (NB. adequate specimens for Mycobacterial and fungal identification have to be taken); antibiotic sensitivities should be performed. A positive culture is seen in 80% of cases. Isolates from discharging sinus tracts may give incorrect results.
Differential Diagnosis
Important diagnoses to consider are:
· septic arthritis
· acute rheumatic arthritis · haemarthrosis
· Ewing's sarcoma
Management
Acute management involves admission into hospital, splinting of the limb, and resuscitation the patient with regard to fluid and electrolyte imbalances. Antibiotic treatment is entirely dependent upon identification of the causal organism and its sensitivities (the regimens given about are merely guides). Usually, intravenous antibiotics are prescribed for 3 weeks, followed by 3 weeks of oral antibiotics. A minimum of 4-6 weeks of antimicrobial therapy has to be instituted for a successful response. This is indicated by a fall in WBC count, ESR, temperature and improvement of local symptoms/signs. Surgical management may be required if improvement is not seen within 36 hours of treatment, as this indicates the presence of pus in the metaphysis and immediate drainage is necessary.
Prognosis
AO is a curable disease if it is diagnosed early and treated appropriately. General complications of AO are:
· septicaemia and metastatic abscesses
· secondary involvement ofthe adjacentjoint
· chronic osteomyelitis
Recurrence rates of AO are higher for lower limb lesions than for upper limb and spine. In particular infection of the metatarsals (50% recurrence) and femur/tibia (25%).
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