Osteomyelitis Flashcards
What is ostromyelitis?
Infection of the bone marrow
Epidemiology?
Incidence increasing or decreasing? Why?
Age distribution?
Incidence is increasing due to an increase in the prevalence of predisposing conditions such as diabetes, peripheral vascular disease.
Bimodal age distribution - 80% children due to haematogenous spread
Adults and teenagers get contiguous osteomyelitis often associated with direct trauma
Increased risk in elderly as increased risk of DM, PVD, arthroplasties and joint replacements which increase the risk.
Describe the 3 routes of infection Direct inoculation Contiguous spread Haematogenous spread Risk factors for haematogenous spread
Direct inoculation
- Bacteria directly into bone due to trauma
Contiguous spread
- Infection to bone from adjacent soft tissues and joints, polymicrobial or monomicrobial.
- More common in those with DM, older adults, arthroplasty etc.
Haematogenous seeding
- Children (85%) in long bones > vertebra (as long bones are growing so there is a large blood supply making it easier for bacteria to get to joint)
- Adults over 50 (vertebrae > clavicle/pelvis»_space;long bones) - vertebrae get more vascular as we age making bacterial seeding of the vertebral endplate more likely
- Monomicrobial
Risk factors for HS
- IVDU users - younger more often clavicle and pelvis
- People with risk factors for bacteraemia (central lines, dialysis, sickle cell disease, urethral catheterisation, UTI)
Describe the histopathology of osteomyelitis
- Inflammatory exudate in marrow
- Increased intra-medullary pressure
- Extension of exudate into the bone cortex
- Rupture through the periosteum
- Interruption of periosteal blood supply causing necrosis
- Leaves pieces of separated dead bone
- New bone forms here
Acute vs chronic changes in osteomyelitis?
Acute: inflammatory cells present causing oedema, vascular congestion and small vessel thrombosis
Chronic: neutrophil exudates, lymphocytes and histocytes and necrotic bone sequestra with new bone formation - involcrum.
How do we make a diagnosis of osteomyelitis?
Use microbiology and histology
Bone biopsy - 2 specimen showing inflammation and osteonecrosis
Positive blood cultures
Treatment of osteomyelitis
Surgical debridement and replacement of any prosthetic joint for eg.
Antimicrobial therapy: tailored to antibiotic sensitivity findings, use broad spectrum while waiting for results.
Required prolonged duration as abx penetration to bone is unreliable.
Minimum 6 weeks IV currently, sometimes switch to oral.
Stop treatment based on ESR and CRP and if failure to respond, re-image.
Host risk factors for OM
- Risk of trauma
- Vascular supply
- Arterial disease
- DM
- Sickle cell
- Pre-existing bone or joint problems
- Inflammatory arthritis
- Prosthetic material
- Immune deficiency
- Immunosuppressive drugs
Microbial risk factors for OM
- Microbial surface components adhere to matrix molecules
- Key example is S aureus which binds host proteins fibronectin, fibrinogen and collagen and can survive intracellularly in cultured macrophages
Common
- Staph aureus
- Coagulase-neg staphylcocci
- Streptococci and enterococci
- Aerobic gram neg bacilli (30%)
- Fungi, mycobacterium TB in immunocompromised
- Salmonella in sickle cell as they can sequester iron