Osteomyelitis

Osteomyelitis is a infection of the bone and bone marrow. It is most commonly a bacterial infection, although fungal infection may occur. It may reach the bone through various routes and may form both acute and chronic infections. It has an annual incidence of 2% every year and has a bimodal distribution with haematogenous infections affecting children predominantly and contiguous infections affecting adults and adolescents mainly.

Pathophysiology

Osteomyelitis are primarily caused by the staphylococcus species of bacteria (with Staphylococcus aureus being the most commonly implicated bacteria).

Infections spread and reach the bone through a variety of mechanisms:

1. Haematogenous spread - it is more common in children and involves the dissemination of bacteria through the bloodstream to the metaphyseal region of long bones as there is slow blood flow with high vasculature - providing a fertile environment for the bacteria to grow. The infection spreads through the Haversian and Volkmann canal systems. It is also more common in intravenous drug users. Vertebral osteomyelitis remains the most common cause of acute osteomyelitis and it spreads haematogenously across all age groups.
2. Direct inoculation - this is when bacteria are introduced directly into the bone. It may occur through trauma, penetrating injuries or surgical procedures (especially after open fractures or in orthopaedic procedures with implanted hardware - it occurs in around 1% of joint replacements).
3. Contiguous spread - this is commonly seen in those with chronic wounds, pressure ulcers or diabetic foot infections. The infection spreads from adjacent soft tissue and joints into the bone. This is more common in adults. It can also be that osteomyelitis spreads contiguously into joints to cause septic arthritis.

Bacteria that enter the bloodstream float freely. These bacteria express adhesins (binding proteins) that bind to host proteins on the bone. Once they attach, they produce a biofilm. Some organisms in the biofilm enter a dormant state where they do not divide much. As such antibiotics that target cell division are rendered minimally effective and the sensitivity of a laboratory culture may not correlate with the theoretical effectiveness of the antibiotic. The biofilm may also Preakness off and form new infection sites in the local area. Bacteria in the biofilm also produce enzymes that degrade immune mediators.

With haematogenous spread, the capillary anatomy in the metaphyseal area contain venous sinusoids that allow stagnation of the bacteria. There is also a lower pH and partial pressure of oxygen near the growth plate that aid bacterial growth.

Chronic osteomyelitis is persistent and often relapsing in nature. It may last for months or years. It forms from an acute osteomyelitis that was not treated appropriately. In chronic osteomyelitis there are necrotic bone fragments known as sequestra which act as a reservoir for bacteria. The body attempts to form new bone around the sequestrum, known as involucrum. The involucrum encapsulates the bacteria and makes it even harder to eradicate.

🦠 Causative agents

• Staphylococcus aureus - this is the most common causative agent in adults. Affects children, adults, IV drug users, prosthesis, vertebral lesions and diabetic patients with foot ulcers/pressure ulcers.
• Staphylococcus epidermidis - affects prosthesis mainly.
• Pseudomonas aeruginosa - affects patients with plantar puncture wounds mainly (especially those wearing rubber-soled footwear).
• Group A streptococcus - most common in children and adolescents.
• Enterobacteriaceae (such as salmonella and klebsiella) - salmonella commonly affects patients with sickle cell disease while klebsiella affects patients with UTIs.
• Mycobacterium tuberculosis - causes Pott’s disease (tuberculous spondylitis).
• Pasteurella multocida - acquired from bites from cats and dogs.
• Fungi (such as candida species) - more commonly affects the immunocompromised and IV drug users.

⚠️ Risk factors

• History of osteomyelitis
• Penetrating injury
• IV drug use
• Diabetes
• HIV and immunocompromised states
• Orthopaedic surgery
• Local/distant infection
• Sickle cell anaemia - due to increased risk of encapsulated bacterial infections (such as salmonella).
• Rheumatoid arthritis
• Chronic kidney disease
• Upper respiratory tract infections in children
• Catheter-related septicaemia

😷 Presentation

• Acute osteomyelitis of the long bone
• It has an acute onset (within days or weeks).
• Patient presents with a painful and immobile limb and a limp. The pain is exacerbated by movement and the patient may be reluctant to weight bear.
• Swelling, tenderness, erythema and warmth are all experienced over the affected area.
• Effusion of neighbouring joints
• Nonspecific malaise symptoms may also be present.
• Acute osteomyelitis of the vertebra
• Back pain
• Fever
• Localised oedema, erythema and associated vascular insufficiency
• If it spreads, it may lead to neurological deficits (such as limb weakness, paralysis, paraesthesia, sensory loss, radiculopathies).
• Chronic osteomyelitis
• The patient will typically have an acute osteomyelitis infection.
• Localised bone pain with erythema and swelling over the affected area. There may be
• Reduced range of motion
• Malaise
• Non-healing ulcer
• Avascular necrosis sequestrum and involucrum formation
• Pathological fractures
• Loosening of implants
• Sinus tract formation with pus draining from it.
• Positive probe-to-bone test - this is when a sterile, blunt probe is inserted into an ulcer. Direct contact of the probe to the bone strongly indicates underlying osteomyelitis (especially in patients with diabetes).
• Patients who have osteomyelitis due to contiguous spread may have an associated history of trauma or surgical procedures.
• Patients with diabetic foot ulcers may have no pain due to neuropathy and few local signs of infection. Often the only sign is intractable hyperglycaemia as stress hormones counteract the effects of insulin further.

🔍 Investigations

Bloods:

• FBC - raised WCC.
• ESR and CRP - CRP is high in 97% of acute cases, and ESR is high in 90% of chronic cases.
• Blood cultures - may be positive, indicating the infecting organism and microbial sensitivities

Imaging:

• 🥇 X-rays of the affected bone (as well as the joint above & the joint below) - they often do not show any changes, particularly in early disease (the first 14 days). They cannot be used to exclude osteomyelitis, but is helpful to exclude other differentials. The potential signs of osteomyelitis on an x-ray are:
• Acute disease - typically no pathological findings
• Subacute/chronic disease - bone destruction, sequestrum formation (devascularised bone that may act as a nidus for inflammation), periosteal reactions, and cloaca.
• CT - effective in identifying necrotic bone and guiding a needle for biopsy.
• 🏆 MRI scans - the best imaging investigation for establishing a diagnosis. If negative, it rules out osteomyelitis. Penumbra sign can be seen on MRI in acute osteomyelitis: T1 shows dark central abscess with bright internal wall and dark external sclerotic rim

🧰 Management

🚨 Complications

• Chronic osteomyelitis
• Pyarthrosis - pus in the associated joint.
• Sinus tract formation
• Sepsis
• Cellulitis
• Progressive bone destruction
• Pathological
• Pseudoarthrosis/nonunion of bone fragments - after injury or surgery.
• Marjolin ulcer formation - a malignant ulcer that develops >25 years after an initial infection.

🚨

Brodie abscess

A Brodie abscess is an intraosseous abscess that commonly affects the distal femur and proximal tibia.

It forms from seeding of distant infections through haematogenous spread leading to subacute/chronic pyogenic infection of the bone. This then leads to fibrous tissue formation around this pyogenic focus which causes a localised abscess.

It presents with localised pain but is frequently asymptomatic.

Brodie abscess is diagnosed on X-ray or MRI as a well-circumscribed, thick-walled, cystic lesion in the metaphysis and epiphysis of long bones.