Musculoskeletal · PANCE / PANRE

Osteomyelitis

Infection of bone; acute or chronic; managed with prolonged antibiotics and often surgical debridement.

Also known as: osteomyelitis, bone infection

Overview

Inflammation of bone and bone marrow caused by infection. Classified by mechanism (hematogenous, contiguous, vascular insufficiency), duration (acute vs chronic), and host (Cierny-Mader classification considers host physiology).

Epidemiology

Hematogenous osteomyelitis predominates in children (long-bone metaphysis) and elderly patients (vertebral). Contiguous spread predominates in adults from diabetic foot ulcers, pressure ulcers, postoperative wounds, or trauma. S. aureus (including MRSA) is the most common pathogen across all forms.

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Risk factors

  • Diabetes mellitus (foot osteomyelitis under ulcer)
  • Peripheral vascular disease
  • IV drug use (vertebral, sternoclavicular, sacroiliac)
  • Recent orthopedic surgery, open fracture, prosthetic hardware
  • Pressure ulcers, decubitus wounds
  • Sickle cell disease (Salmonella in addition to S. aureus)
  • Immunosuppression
  • Endocarditis or persistent bacteremia
  • Pediatric: recent infection, blunt trauma to bone

Pathophysiology

Bacteria reach bone via hematogenous seeding, contiguous spread, or direct inoculation. Bacterial proliferation triggers neutrophilic inflammation; rising intramedullary pressure compromises blood supply, producing devitalized bone (sequestrum) that harbors persistent infection. New reactive bone (involucrum) forms around the sequestrum. Biofilms on hardware and necrotic bone make chronic osteomyelitis difficult to eradicate without surgical debridement.

Clinical presentation

Symptoms

  • Acute: fever, chills, focal bone pain, soft tissue swelling
  • Chronic: indolent pain, sinus tract with drainage over weeks to months, non-healing wound
  • Vertebral osteomyelitis: focal back pain, fever (often absent), neurologic deficit if epidural extension
  • Diabetic foot osteomyelitis: non-healing ulcer, exposed bone on probing

Signs / physical exam

  • Warmth, swelling, tenderness over involved bone
  • Sinus tract or exposed bone (probe-to-bone test positive)
  • Limp or refusal to bear weight (children)
  • Spinal tenderness, possibly neurologic deficits

Differential diagnosis

  • Charcot neuroarthropathy — Diabetic neuropathy with destructive midfoot arthropathy; warm swollen foot without ulcer; MRI can mimic osteomyelitis
  • Soft tissue infection / cellulitis — No bone involvement; MRI normal marrow
  • Bone tumor (Ewing sarcoma, osteosarcoma, metastasis) — Periosteal reaction, lytic/sclerotic lesions; biopsy if equivocal
  • Stress fracture — Repetitive activity, focal pain; MRI shows fracture line
  • Avascular necrosis — Risk factors (steroids, sickle, alcohol); MRI 'double-line' sign
  • Septic arthritis with adjacent bone involvement — Joint effusion plus bony edema; treat both
  • Gout / pseudogout — Crystals; can be confused with foot osteomyelitis on imaging

Diagnostic workup

Labs

  • CBC — leukocytosis variable
  • ESR, CRP — elevated; CRP useful to track response
  • Blood cultures × 2 sets (positive in ~50% of acute hematogenous and vertebral cases)
  • Bone biopsy with culture and histopathology — gold standard before starting antibiotics whenever possible
  • Diabetic foot: deep tissue or bone culture preferred over superficial swab

Imaging

  • Plain radiographs — first study; periosteal reaction, lucency, sclerosis, sequestrum; lag 10-14 days behind disease
  • MRI with and without contrast — most sensitive and specific; bone marrow edema, abscess, sinus tracts
  • CT — defines bony sequestrum and surgical anatomy; useful when MRI contraindicated
  • Three-phase bone scan or labeled WBC scan — useful when MRI not feasible or hardware artifact
  • Probe-to-bone test in diabetic foot ulcers — positive test in a high-risk patient nearly diagnostic

Diagnostic algorithm

flowchart TD
  A[Suspected osteomyelitis] --> B[X-ray + ESR/CRP<br/>+ blood cultures x 2]
  B --> C[MRI with contrast<br/>most sensitive]
  C --> D{Stable patient?}
  D -->|Yes| E[Bone biopsy<br/>BEFORE antibiotics]
  D -->|No, sepsis| F[Empiric vanco + GN coverage<br/>cultures ASAP]
  E --> G[Targeted antibiotics<br/>4-6 weeks]
  F --> G
  G --> H{Necrotic bone,<br/>hardware, or abscess?}
  H -->|Yes| I[Surgical debridement /<br/>hardware management]
  H -->|No| J[Antibiotics alone<br/>track CRP response]
Osteomyelitis workup and treatment — biopsy first, antibiotics targeted, surgery for sequestra and hardware.

Complications

  • Chronic osteomyelitis with sinus tracts (squamous cell carcinoma can arise — Marjolin ulcer)
  • Pathologic fracture
  • Growth plate damage with limb-length discrepancy (pediatric)
  • Spinal cord compression from epidural abscess (vertebral osteomyelitis emergency)
  • Sepsis, endocarditis, metastatic infection
  • Amyloidosis (chronic suppurative osteomyelitis)

PANCE pearls

  • Probe-to-bone test in a diabetic foot ulcer combined with elevated CRP/ESR is sufficient to start treatment.
  • ESR >70 in diabetic foot ulcer is a sensitive marker for osteomyelitis.
  • Hold antibiotics for bone biopsy whenever the patient is stable — empiric therapy without culture often produces inadequate treatment of chronic disease.
  • Vertebral osteomyelitis with new neurologic deficit = epidural abscess until proven otherwise — emergent MRI and neurosurgical consult.
  • Sickle cell + osteomyelitis = think Salmonella in addition to staph.

References

  • IDSA 2015 — IDSA Clinical Practice Guideline for the Diagnosis and Treatment of Native Vertebral Osteomyelitis (Berbari et al., Clin Infect Dis 2015)
  • IDSA 2012 — IDSA Clinical Practice Guideline for the Diagnosis and Treatment of Diabetic Foot Infections (Lipsky et al., Clin Infect Dis 2012)
  • OVIVA Trial — Oral versus Intravenous Antibiotics for Bone and Joint Infection (Li et al., NEJM 2019)

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