Osteomyelitis Flashcards

1
Q

What is the epidemiology of osteomyelitis?

A

Bimodal age distribution:

  • Acute, haematogenous osteomyelitis occurring mostly in paeds
  • Contiguous osteomyelitis (often associated with direct trauma) is more commonly seen in adolescents and adults
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2
Q

What is the aetiology of osteomyelitis? (risk factors and pathogens)

A

Risk factors:

  • Trauma - open fracture; orthopaedic surgery
  • Prosthetic orthopaedic device
  • DM - especially following foot ulcers; often goes unsuspected/underdiagnosed
  • Peripheral artery disease
  • Chronic joint disease
  • Alcoholism
  • IV drug use
  • Chronic steroid use
  • Immunosuppression
  • TB, HIV/AIDS
  • Sickle cell disease
  • Presence of catheter related blood infection

Pathogens:

  • S.aureus = most common; including MRSA
  • H.influenzae
  • Strep spp.
  • E.coli
  • Proteus spp.
  • Pseudomnas spp.
  • Coagulase-negative Staph spp.
  • Mycobacteria
  • Fungi
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3
Q

What is the pathophysiology of osteomyelitis?

A

An infection of the bone marrow which may spread to the bone cortex and periosteum via Haversian canals

  • Inflammatory destruction of bone
  • Periostium involvement leads to necrosis
  • When dead bone becomes detached from healthy bone = ‘sequestrum’ - a focus for ongoing infection

Haematogenous vs. Direct/contiguous:
- Haematogenous = bacterial ‘seeding’ from remote source; more common in kids as metaphyses of growing bones are highly vascular
Contiguous = direct contact between infectious tissue and bone; signs are often more localised and with multiple organisms involved

Acute vs. chronic:
- Chronic can evolve over months or even years

At the active site of infection, bone remodelling can occur, often with associated deformity

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4
Q

How does long bone haematogenous osteomyelitis present?

A

Classically:

  • Acutely febrile + bacteraemic patient
  • Markedly painful immobile limb
  • Swelling + extreme tenderness exaccerbated by movement +/- erythema +/- warmth

Other:

  • May be mild symptoms including a mild/absence of pyrexia
  • Possible Hx of blunt trauma which may have easily been forgotten e.g. a bump against a hard surface
  • Non-specific systemic malaise attributed to viral illness before localising signs develop later
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5
Q

How does vertebral osteomyelitis present? What is Pott’s disease?

A

Usually insidiously:

  • Following a septicaemic episode
  • Localised erythema + tenderness OR
  • Chronic, unremitting back pain which is worse at rest and at night

Pott’s disease:

  • Vertebral osteomyelitis from haematogenous spread of TB
  • Damage to the bodies of two neighbouring vertebrae leading to vertebral collapse and subsequent abscess formation
  • Pus can track out into adjacent structures leading to systemic symptoms (malaise, fever, night sweats)
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6
Q

How does contiguous osteomyelitis present?

A

Patients present in the classical manner - fever + pain + erythema etc.
- Signs are often better localised

But associated Hx of accidental or surgical trauma i.e. the location of the infection should be more obvious

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7
Q

How do diabetic foot ulcers present with osteomyelitis?

A

In diabetic foot disease, neuropathy and vascular insufficiency complicate Dx:

  • Pain + tenderness may be masked by neuropathy
  • Local erythema, warmth and purulent drainage may be reduced due to poor blood flow

Systemic signs:

  • Fever + chills are also often absent (2/3)
  • Recalcitrant hyperglycaemia is often the only sign
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8
Q

How does chronic osteomyelitis present?

A

Patients may have one or more of the following:

  • Previous acute osteomyelitis (possibly unresponsive to treatment or relapsing)
  • Localised bone pain
  • Erythema and swelling over affected area
  • Decreased ROM in adjacent joints
  • Chronic fatigue
  • Generalised malaise
  • Non-healing ulcer
  • Draining sinus tracts

Sometimes chronic abscess formation may occur in the bone (Brodie’s abscess)

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9
Q

How do you investigate osteomyelitis?

A

Labs:

  • FBC - raised WCC and inflammatory markers
  • Blood cultures - +ve in 60% of cases
  • Any expressed pus should be cultured, as should joint effusions and other potential primary sources e.g. urine
  • Bone cultures are the gold standard for Dx

Imaging:

  • MRI is the modality of choice
  • Plain film XR may be helpful for Dx of chronic (patchy osteopaenia + bony destruction); periosteal reaction cannot be seen until c.7 days and bone necrosis after 10 days
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10
Q

What are the general principles of treatment in osteomyelitis?

A

5 Key principles:

  • Local bone and soft tissue debridement
  • Stabilisation of bone
  • Local Abx
  • Reconstruction of soft tissue
  • Reconstruction of osseous defect zone

Surgical cleaning should be extensive; possible need for removal of implants

Analgesia +/- limb splinting (if long bone involved) = symptom control

Prompt identification + treatment is essential for good outcomes

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11
Q

What antibiotics are used in acute osteomyelitis?

A

Drug:

1) Flucoxacillin +/- fusidic acid or rifampicin for first 2 weeks
- Clindamycin if penicillin allergic
- Vancomycin/teicoplanin if MRSA suspected

High doses are essential to reach suitable concentrations in necrotic avascular bone

  • IV used initially and to cover surgery and up to two weeks after
  • PO switch once clinical condition stabilises, inflammatory markers are down and we know what bugs are growing for certain

Timescale:

  • Acute: 4-6wks Abx
  • Chronic: 3-6 months Abx

Seek specialist advice in chronic infection or prostheses

Increasingly complicated by rising prevalence of MRSA etc.

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12
Q

How does chronic osteomyelitis treatment differ?

A

Usually appropriate to delay treatment until MC+S are obtained, unless severe infection

Standard recommendation:

  • Surgical debridement
  • 6wks parentral ABx but optimal duration unknown
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