Osteomyelitis

Introduction

Osteomyelitis is infection of bone, usually pyogenic but occasionally granulomatous, which may involve the marrow cavity, cortex and periosteum. It can be acute, evolving over days, or chronic, persisting or relapsing over months to years despite treatment.¹

It matters clinically for two reasons. First, it can be indolent: pain and low-grade systemic upset may be the only features, particularly in chronic disease or in patients whose sensation or immune response is impaired, so the diagnosis is easily missed or delayed. Second, untreated infection causes progressive, often irreversible bone destruction - in children this can damage the growth plate and cause a permanent limb length discrepancy or deformity, and in any age group it can progress to chronic infection that is very difficult to eradicate.

It is a frequent exam topic for exactly these reasons: the child who will not weight-bear, the classic but nuanced sickle cell/Salmonella pairing, the diabetic foot ulcer that probes to bone, and the principle that MRI - not X-ray - is the imaging investigation of choice.

Pathophysiology and classification

Bone becomes infected by one of two routes, and the dominant route differs by age and by underlying risk factors. This classification is worth learning explicitly, because it predicts the typical patient, the typical site, and the likely organism.²

Haematogenous osteomyelitis

Bacteraemia seeds bone directly from the bloodstream. This is the dominant pattern in children, and it characteristically affects the highly vascular metaphysis of long bones - most often the distal femur and proximal tibia. The metaphyseal capillaries form sharp loops before draining into venous sinusoids, and blood flow through them is slow and turbulent; this peculiar circulation allows circulating bacteria to settle and evade clearance, and the sinusoidal vessels lack an effective phagocytic lining, further favouring establishment of infection.

In adults, haematogenous spread more often affects the vertebral bodies - vertebral osteomyelitis, frequently with contiguous discitis - because the vertebral end-plate circulation shows a comparable pattern of slow flow. Risk factors include intravenous drug use, older age, diabetes, immunosuppression and haemodialysis, and there is often an identifiable distant source of bacteraemia such as a urinary tract or skin infection, or an infected intravascular line.³

Contiguous spread and direct inoculation

Infection reaches bone directly from an adjacent focus rather than via the bloodstream: an adjacent soft tissue infection, an open fracture, orthopaedic surgery or implanted prosthetic material, or a penetrating injury. This is the dominant pattern in adults, and the classic example is the diabetic foot ulcer, where chronic skin breakdown allows organisms to track directly into underlying bone. Because the route is via an already colonised or contaminated wound, infection is frequently polymicrobial.

Organisms

Staphylococcus aureus is the commonest cause of osteomyelitis overall, across essentially every patient group and both routes of infection, because it expresses surface proteins that bind readily to bone matrix.

• Staphylococcus aureus - the commonest organism overall, including in haematogenous disease in children and adults, and a major contributor to contiguous infection
• Salmonella species - classically associated with osteomyelitis in sickle cell disease, thought to relate to bowel wall ischaemia allowing translocation, splenic dysfunction impairing clearance, and infarcted bone providing a niche for seeding
• Pseudomonas aeruginosa - associated with puncture wounds through the sole of a shoe or trainer, because the organism is a common coloniser of the rubber sole
• Polymicrobial infection, including anaerobes and Gram-negative organisms alongside Staph aureus, is typical in diabetic foot osteomyelitis owing to chronic wound colonisation
• Coagulase-negative staphylococci (e.g. Staphylococcus epidermidis) - implicated in infection around prosthetic orthopaedic material, reflecting biofilm formation on implant surfaces
• Mycobacterium tuberculosis - consider in vertebral osteomyelitis in patients from or with travel to a TB-endemic area, or with other risk factors for TB (Pott's disease); typically insidious, with a lower-grade systemic picture than pyogenic vertebral infection
• Kingella kingae and Group B streptococcus - important causes in young children and neonates respectively, alongside Staph aureus

Risk factors

• Diabetes mellitus, especially with peripheral neuropathy and peripheral vascular disease - the diabetic foot
• Immunosuppression, including corticosteroid use, chemotherapy, HIV and other causes of impaired host defence
• Intravenous drug use - a recognised risk factor for haematogenous osteomyelitis, particularly vertebral
• Sickle cell disease
• Recent orthopaedic surgery or implanted prosthetic material
• Open fracture
• Peripheral vascular disease, which also impairs wound healing and antibiotic delivery to tissue
• Chronic skin ulceration, whether diabetic, venous or pressure-related
• Older age

Clinical features

The core acute picture is localised bone pain with swelling, warmth and tenderness over the affected bone, and reduced use of the limb. Systemic upset with fever is common but can be subtle or entirely absent, particularly in chronic disease, in contiguous infection, and in patients whose ability to mount a febrile response is blunted by age or immunosuppression - a normal temperature does not exclude the diagnosis.

In young children, osteomyelitis may present with refusal to weight-bear or refusal to use the affected limb, sometimes with remarkably few other localising signs - a picture described as pseudoparalysis. A young child who has stopped using a limb, is limping, or will not weight-bear should always prompt consideration of osteomyelitis or septic arthritis, even before a clearly localised, swollen or hot area is apparent.

In contiguous disease, particularly the diabetic foot, systemic features are often minimal and the picture can be dominated by a chronically non-healing or worsening ulcer, sometimes with surprisingly little pain because of coexisting neuropathy. In chronic osteomyelitis, an overlying discharging sinus may be the presenting feature, sometimes long after the original acute episode was thought to have resolved.

Vertebral osteomyelitis typically presents with insidious, worsening back pain, often with spinal tenderness and a raised inflammatory marker profile, but with fewer overt systemic features than the pyogenic source might suggest. Any new neurological deficit in this context - limb weakness, sensory change, or bladder or bowel disturbance - raises the possibility of an associated epidural abscess and needs urgent imaging.

Investigations

Bloods

• FBC - leucocytosis is common in acute disease but may be absent, especially in chronic or contiguous infection
• CRP and ESR - sensitive but non-specific markers of inflammation; both are useful for monitoring response to treatment, with a falling trend supporting adequate therapy
• Blood cultures - positive in a meaningful proportion of haematogenous cases and should always be taken before antibiotics where possible, since they may obviate the need for a more invasive sample
• HbA1c - relevant context in suspected diabetic foot osteomyelitis

Imaging

Plain X-ray is often normal for the first 1-2 weeks of infection, because it takes time for bone destruction to become radiographically visible - a normal X-ray early in the illness does not exclude osteomyelitis. Later changes include periosteal reaction and lytic lesions, and in established chronic disease a sequestrum (a fragment of necrotic, avascular bone) and involucrum (a sleeve of new periosteal bone forming around it) may be seen.

MRI is the imaging investigation of choice. It is the most sensitive modality for detecting the earliest marrow oedema of osteomyelitis, often positive within days of symptom onset, and it defines the anatomical extent of both bone marrow and soft tissue involvement - information that is essential for surgical planning.¹

Bone biopsy and aspiration

Bone biopsy or aspiration for culture and histology is the definitive way to identify the causative organism and its antibiotic sensitivities, and should be obtained, where the patient is clinically stable enough to allow it, before starting antibiotics or without unduly delaying treatment in an unwell patient. Image-guided percutaneous biopsy is preferred where feasible; open biopsy is reserved for cases where percutaneous sampling is not possible or has been non-diagnostic. Sensitivity results from biopsy allow empirical antibiotic therapy to be rationalised to a narrower, targeted regimen.

Management

Management combines prolonged antimicrobial therapy with surgery where indicated, and addressing any underlying source of infection. Treatment decisions should follow local microbiology and orthopaedic protocols, and involve the multidisciplinary team early.

Antibiotics

Treatment is typically started empirically to cover Staph aureus, then rationalised once culture and sensitivity results are available. A common pattern is several weeks of intravenous antibiotics, followed by a switch to a prolonged course of oral antibiotics once the patient is clinically improving and results allow a suitable oral option - the total duration is usually measured in weeks rather than days, and chronic or vertebral disease may require longer courses still.⁷

Surgical debridement

Surgery is indicated where there is:

• An abscess requiring drainage
• Dead or necrotic bone (a sequestrum), which will not be sterilised by antibiotics alone and acts as a nidus for persistent infection
• A chronic discharging sinus
• Failure to respond to antibiotic therapy alone

Treating the underlying source

Definitive management also addresses the process that allowed infection to establish or persist. In diabetic foot osteomyelitis this may mean revascularisation where there is significant peripheral vascular disease, meticulous wound care and pressure offloading, and optimising glycaemic control.⁵ Where infection surrounds orthopaedic hardware, removal of the infected implant is often necessary for cure, particularly in chronic or relapsing infection, since bacteria form biofilm on implant surfaces that antibiotics penetrate poorly.

Chronic osteomyelitis

Chronic osteomyelitis is established, persistent bone infection, often following inadequately treated acute disease, and it is notoriously difficult to eradicate - relapse can occur years after apparently successful treatment, sometimes precipitated by trauma or a period of reduced host resistance.

The hallmark pathological pattern is a sequestrum - a fragment of dead, avascular bone that has separated from viable bone and acts as a persistent focus of infection because antibiotics cannot reach it through blood flow - surrounded by an involucrum, a sleeve of new, viable periosteal bone that the body lays down around the dead segment. This combination is often visible on plain X-ray or CT in chronic disease and is a strong indicator that surgical removal of the sequestrum will be required for cure.

Brodie's abscess

A Brodie's abscess is a localised, subacute or chronic intraosseous abscess, classically found in the metaphysis of a long bone in a child or young adult. It represents a walled-off, low-grade infection rather than the more florid picture of acute osteomyelitis, and patients may have relatively mild, intermittent pain over weeks to months rather than an acute febrile illness. Radiologically it can appear as a well-defined lucent lesion, sometimes with a surrounding sclerotic rim, and it can mimic a bone tumour - a point worth remembering when a lytic metaphyseal lesion is being worked up, since the differential should always include infection alongside neoplasia.

Differential diagnosis

• Cellulitis or soft tissue infection without bone involvement - overlapping local signs, but without deep bone tenderness or the systemic/imaging features of bone infection; failure to respond to antibiotics for presumed cellulitis should prompt reconsideration of underlying osteomyelitis
• Septic arthritis - can coexist with osteomyelitis, especially in infants, where the metaphysis lies within the joint capsule in certain joints (classically the hip), allowing infection to spread directly between bone and joint
• Bone tumour, particularly Ewing sarcoma, which can mimic infection both clinically (pain, swelling, systemic upset, raised inflammatory markers) and radiologically (permeative bone destruction, periosteal reaction)
• Fracture, including stress fracture, which can cause localised bone pain and tenderness without infection
• Avascular necrosis, which can cause bone pain and characteristic imaging changes without an infective cause
• Charcot arthropathy in diabetic patients - progressive joint and bone destruction from loss of protective sensation, which can closely mimic osteomyelitis clinically and radiologically and is a well-recognised diagnostic pitfall in the diabetic foot

Complications

• Chronic osteomyelitis - persistent or relapsing infection, as above
• Growth plate damage in children, causing limb length discrepancy or angular deformity if the physis is involved
• Pathological fracture through bone weakened by infection
• Chronic discharging sinus
• Squamous cell carcinoma arising in a chronic sinus tract (Marjolin's ulcer) - rare, but a recognised late complication of a long-standing discharging sinus that should prompt biopsy of any new change in a chronic wound
• Amyloidosis (AA amyloid) - a rare consequence of long-standing chronic infection and sustained inflammation

Red flags