Acute Osteomyelitis In Children

Acute osteomyelitis is infection of bone, usually from haematogenous bacterial spread. Metaphyseal regions of rapidly growing long bones are most often affected because their vascular architecture favours bacterial seeding.

Staphylococcus aureus is the dominant pathogen; Kingella kingae is increasingly important in children 6 to 48 months, while Salmonella should be considered in sickle cell disease.

Delayed treatment risks subperiosteal abscess, bone necrosis, pathological fracture, growth plate damage and chronic osteomyelitis.

Presentation is often acute with fever and focal bone pain. Young children may simply refuse to walk or use the affected limb.

• Localized bone tenderness, swelling and warmth
• Limp or refusal to weight bear
• Reduced movement of the adjacent joint because of pain
• Fever, irritability and reduced activity
• Pseudoparalysis in infants
• Back pain or neurological symptoms with vertebral disease

Persistent bacteraemia, severe systemic illness or rapidly increasing swelling should raise concern for abscess formation or aggressive S. aureus infection.

• Blood cultures should be obtained before antibiotics when this does not delay treatment. Positive blood cultures can establish the organism without invasive bone sampling.

• FBC, CRP and ESR support diagnosis and provide useful baselines. CRP is particularly useful for monitoring early treatment response, but normal inflammatory markers do not completely exclude early disease.

• Plain radiographs are useful initially to exclude fracture, tumour or another bone lesion, but may remain normal during the first 1 to 2 weeks.

• MRI with contrast is the imaging investigation of choice where the diagnosis is uncertain, symptoms are severe, or abscess, pyomyositis, joint involvement or spinal disease is suspected.

• Ultrasound can identify a subperiosteal collection but does not adequately assess marrow disease.

• Aspirate or biopsy bone or adjacent abscess for Gram stain, culture and susceptibility where blood cultures are negative, disease is complicated, or unusual organisms are suspected.

• Start empirical therapy active against S. aureus after cultures are obtained. Where methicillin resistant S. aureus prevalence is low, cefazolin 50 mg/kg IV every 8 hours, maximum 2 g per dose, or an antistaphylococcal penicillin such as flucloxacillin is appropriate.

• Where clinically significant community acquired MRSA is prevalent, use clindamycin 10 to 13 mg/kg IV every 8 hours, maximum 900 mg per dose, if local clindamycin susceptibility is reliable; otherwise use vancomycin approximately 15 mg/kg IV every 6 hours, adjusted using therapeutic drug monitoring and renal function.

• Narrow therapy once cultures identify the pathogen. For susceptible MSSA, beta lactam therapy is preferred over vancomycin.

• Clinical improvement, resolution of fever and falling CRP allow transition to an active oral agent such as cefalexin approximately 25 mg/kg PO every 6 hours, maximum 1 g per dose, for MSSA.

• Uncomplicated acute haematogenous osteomyelitis generally requires approximately 3 to 4 weeks total antimicrobial therapy. Longer treatment is required for virulent organisms, delayed response, abscess, extensive bone destruction or complications.

• Drain significant subperiosteal or intramuscular abscesses and obtain urgent orthopaedic input where source control is required.