Osteomyelitis

(8-Mark Question - MBBS Standard)

Definition

Causative Organisms

• Neonates: Group B Streptococcus and Escherichia coli predominate due to immature immune defences.
• Older children: Gram-positive organisms, predominantly S. aureus; H. influenzae was historically important but is now rare due to vaccination.
• Adults: S. aureus remains predominant; gram-negative rods (E. coli, Pseudomonas) are seen after urinary tract infections, IV drug use, or post-surgical contamination.
• Sickle cell disease patients: Salmonella species and other gram-negative organisms are most frequent, because areas of bone infarction act as a nidus for seeding and loss of splenic function impairs the immune response.
• Diabetic foot osteomyelitis: Polymicrobial infections involving gram-negatives and anaerobes are common.
• Vertebral osteomyelitis (Pott's disease): Mycobacterium tuberculosis accounts for up to 40% of cases in endemic regions.
• Post-traumatic / implant-related: Staphylococcus epidermidis (coagulase-negative staphylococci) and S. aureus including MRSA. Panton-Valentine leukocidin (PVL)-positive S. aureus is associated with severe invasive disease and increased morbidity.

Clinical Features

• Systemic features: High-grade fever, rigors, malaise, irritability, and toxaemia. Septicaemia may be present.
• Local features: Severe, constant, throbbing pain over the affected bone. The child refuses to use the limb ("pseudoparalysis" in infants). There is point tenderness over the metaphysis, local swelling, warmth, and erythema of the overlying skin. A sympathetic joint effusion may accompany metaphyseal infection, making differentiation from septic arthritis difficult.

• Persistent or recurrent low-grade aching pain over the affected bone.
• A draining sinus tract through the skin discharging pus and occasionally small fragments of dead bone (sequestrum).
• Surrounding skin thickening, scarring, and pigmentation.
• Periods of apparent quiescence punctuated by acute flare-ups sometimes after years of dormancy.
• Muscle wasting and limb deformity if growth plate damage has occurred in children.

Investigations

• Full blood count (FBC): White cell count is elevated (neutrophilia) in acute infection, though it is normal in up to 35% of cases of chronic osteomyelitis; anaemia may be present in chronic disease.
• Erythrocyte sedimentation rate (ESR): Elevated in most patients and is a useful monitor of response to treatment.
• C-reactive protein (CRP): Elevated in most patients; more rapidly responsive to treatment than ESR and thus a better short-term monitoring tool.
• Blood cultures: Positive in up to 50% of haematogenous cases in children; should always be obtained before starting antibiotics. They provide the organism and its antibiotic sensitivities.
• Bone biopsy and culture: The gold standard for identifying the causative organism. Specimens must be taken from bone, not just from sinus discharge (which reflects surface colonisation, not the true infecting organism). Microbiological cultures plus histopathology are both performed.
• PCR assays: Increasingly used for organism identification, particularly in culture-negative cases.

• Plain radiograph (X-ray): The initial investigation, but changes appear only 10-21 days after infection onset. Early films may be normal. Later features include periosteal reaction, bone lysis (lytic focus), sclerosis, and the classic "bone-within-bone" appearance of sequestrum surrounded by involucrum in chronic disease.
• Ultrasound: Useful in children to detect subperiosteal collections and joint effusions early; can guide aspiration or drainage.
• Technetium-99m bone scan (radionuclide scan): Shows increased uptake ("hot spot") within 24-48 hours of infection onset, making it more sensitive than plain X-ray in early disease. However, it lacks specificity.
• MRI (Magnetic Resonance Imaging): The most sensitive and specific imaging modality for osteomyelitis. It identifies early marrow oedema, cortical destruction, periosteal reaction, subperiosteal abscess, soft tissue extension, and sinus tracts. It is the investigation of choice when the clinical diagnosis is uncertain or when surgery is planned.
• CT scan: Useful for guiding bone biopsy, delineating sequestra, and surgical planning, especially in complex chronic osteomyelitis.
• Sinogram (fistulogram): Injection of radiopaque contrast into a sinus tract under fluoroscopy helps locate the underlying focus of infection in chronic osteomyelitis.

Management

• Rest and splintage of the affected limb to relieve pain and prevent pathological fracture.
• Adequate analgesia.
• Nutritional support and correction of underlying conditions (e.g. optimising blood sugar in diabetes, treatment of sickle cell disease).

• Empirical choice: Flucloxacillin (or cloxacillin) IV is the first-line agent for methicillin-sensitive S. aureus (MSSA) in most regions.
• MRSA suspected / confirmed: Vancomycin IV is used. Teicoplanin or linezolid are alternatives.
• Neonates: Ampicillin + gentamicin (to cover group B streptococcus and gram-negatives).
• Sickle cell patients: A fluoroquinolone or ampicillin-sulbactam to cover Salmonella.
• Mycobacterial (TB) osteomyelitis: Standard anti-tuberculosis combination therapy (rifampicin, isoniazid, pyrazinamide, ethambutol) for at least 6-9 months.

• Drainage of pus: Percutaneous aspiration or surgical incision and drainage of subperiosteal abscesses.
• Sequestrectomy: Removal of dead bone (sequestrum) in chronic osteomyelitis; the surrounding involucrum is preserved as it becomes the new cortex.
• Saucerisation (saucerisation debridement): Removal of all necrotic bone and infected soft tissue creating an open saucer-shaped defect; this is packed or managed with local antibiotic delivery systems.
• Local antibiotic delivery: Antibiotic-laden polymethyl methacrylate (PMMA) or calcium sulphate beads are placed into the dead space created by debridement to deliver high local concentrations of antibiotics.
• Bone stabilisation: External fixators, intramedullary nails, or plates are used to maintain bone stability during and after radical debridement.
• Soft tissue reconstruction: Flap coverage (free or rotational muscle/fasciocutaneous flaps) by a plastic surgeon is often required for large soft tissue defects.
• Bone grafting / bone transport (Ilizarov technique): Used in a staged manner to reconstruct segmental bone defects after radical resection.

Complications

• Septic (suppurative) arthritis: Spread of infection into an adjacent joint, especially at sites where the metaphysis is intracapsular (e.g. hip, shoulder). This causes articular cartilage destruction and permanent disability. It is particularly common in neonates (in whom the proximal femoral osteomyelitis and septic arthritis of the hip are essentially the same condition) because epiphyseal blood vessels penetrate the growth plate.
• Chronic osteomyelitis: The most important local complication. Inadequate treatment leads to persistence of infection, with sequestrum formation, involucrum, and draining sinuses. Chronic infection is characterised by periods of acute flare-ups superimposed on a background of low-grade indolent disease.
• Pathological fracture: Bone destruction and cortical weakening predispose to fracture through the infected segment.
• Sequestrum and involucrum formation: Dead cortical bone (sequestrum) becomes enclosed in a shell of new periosteal bone (involucrum). The sequestrum acts as a focus of persistent infection as antibiotics cannot penetrate it adequately.
• Growth disturbance: Infection involving the physis (growth plate) in children causes premature growth plate closure, leading to limb length discrepancy, angular deformity, and shortening.
• Avascular necrosis: Elevation of the periosteum by a subperiosteal abscess interrupts the periosteal blood supply and contributes to cortical bone necrosis. In the femoral head, this can result in permanent avascular necrosis.
• Draining sinus formation: Periosteal rupture leads to soft tissue abscess that tracks to the skin, creating a chronically draining sinus.

• Septicaemia / bacteraemia: Untreated acute osteomyelitis may progress to systemic sepsis, multi-organ failure, and death.
• Secondary (reactive) amyloidosis (AA amyloidosis): Chronic osteomyelitis with persistent antigenic stimulation leads to deposition of AA-type amyloid protein in kidneys, liver, and spleen, causing organ dysfunction.
• Endocarditis: Haematogenous seeding of heart valves from a chronic bone focus, particularly with S. aureus.
• Squamous cell carcinoma (Marjolin's ulcer): Long-standing chronic draining sinuses undergo malignant transformation into squamous cell carcinoma, typically after decades of disease. This is a well-recognised but uncommon complication.
• Sarcoma: Rarely, sarcoma (osteosarcoma or fibrosarcoma) can arise within chronically infected bone.