• Clinical science

Osteomyelitis

Abstract

Osteitis and osteomyelitis are infections of the bone and bone marrow, respectively. Because these terms are often used interchangeably in clinical settings, both conditions will be referred to as osteomyelitis here. Staphylococcus aureus accounts for the majority of acute osteomyelitis cases; however, there are a number of other pathogens associated with this condition. How the pathogen enters the bone determines the type of osteomyelitis: hematogenous and exogenous forms exist. Hematogenous osteomyelitis is caused by seeding from a remote source and is most common among IV drug users and children. Exogenous osteomyelitis is more common in adults and results from direct inoculation through trauma (posttraumatic osteomyelitis) or contiguous spread from infected adjacent tissue (contiguous osteomyelitis due to, e.g., diabetic foot, contaminated prosthetic device). Osteomyelitis may be either acute or chronic and presents with general signs of local inflammation, including swelling, pain, redness, and warmth. Systemic signs, such as fever and chills, are more indicative of an acute infection. Diagnosis of clinically suspected cases is supported via laboratory tests, biopsy, and/or imaging. The treatment of choice for hematogenous osteomyelitis is IV antibiotics. Surgery may be necessary to remove necrotic bone, abscesses, infected foreign bodies, or fistulae. While osteomyelitis in adults often assumes a chronic course and requires prolonged treatment, children typically make a quick and full recovery.

Definition

  • Osteitis: general term for inflammation of the bone
  • Osteomyelitis: infection of the bone marrow
    • Acute form: develops within days or weeks
    • Chronic form: develops slowly (over months or years) and is associated with avascular bone necrosis and sequestrum formation within the bone

Epidemiology

  • Hematogenous osteomyelitis:
    • More common in children and adolescents (> 50% of cases occur in children ≤ 5 years)
    • Vertebral osteomyelitis (a form of hematogenous osteomyelitis) occurs mainly in adults aged > 50 years
  • Exogenous osteomyelitis: more common in adults

References:[1][2][3][4]

Epidemiological data refers to the US, unless otherwise specified.

Etiology

Routes of infection

  • Hematogenous osteomyelitis: most commonly due to a single pathogen
    • Hematogenous dissemination of pathogen
  • Exogenous osteomyelitis: usually due to multiple pathogens
    • Posttraumatic: infection following deep injury (penetrating injury, open fractures, severe soft tissue injury)
    • Contiguous: spread of infection from adjacent tissue
      • Secondary to infected foot ulcer in diabetic patients
      • Iatrogenic (e.g., postoperative infection of a prosthetic joint implant)

Risk factors

Pathogens

Pathogens Commonly affected groups
Staphylococcus aureus
  • Children and adults
Staphylococcus epidermidis
  • Diabetic patients with foot ulcers and pressure ulcers
  • Patients with prosthetics
Streptococci
Pseudomonas aeruginosa
  • IV drug users
  • Plantar puncture wounds (especially if wearing rubber-soled footwear)
Enterobacteriaceae Salmonella
Klebsiella
  • Patients with UTIs or a history of UT instrumentation
Fungal pathogens
Mycobacterium tuberculosis

References:[4][5][6][1][2][3][7][8][9]

Clinical features

Acute osteomyelitis

  • Onset: usually gradual, over several days
  • Chief complaint: pain at the site of infection, possibly related to movement
  • Possible localized findings: point tenderness, swelling, redness, warmth
  • Possible systemic findings: malaise, fever, chills
  • Common localization of hematogenous osteomyelitis:
    • Infants: long bone metaphysis, joints
    • Children: long bone metaphysis, joint infection very rare
    • Adults: vertebral involvement is most common In adults, involvement of the long bones is uncommon. However, if a long bone is involved, there is also a risk of joint involvement because blood vessels of the metaphysis also perfuse the epiphysis, which is ossified.

Chronic osteomyelitis

  • Onset: usually following a prior episode of osteomyelitis; may last for months
  • Chief complaint: recurrent pain
  • Possible findings
    • Swelling, redness
    • Local sinus tract formation, perhaps draining pus

References:[4]

Subtypes and variants

Vertebral osteomyelitis

  • Definition: osteomyelitis of the vertebrae
  • Pathophysiology: hematogenous seeding of a distant infectious focus → infection of the vertebral bone → contiguous spread to the intervertebral discs (and adjacent vertebrae)
    • Discitis refers to the infection of the vertebral disc
  • Classification according to the underlying pathogen
  • Clinical features: often latent, nonspecific symptoms
    • Chief complaint: back/neck pain
      • Not relieved with rest
      • Worse with activity and at nights
    • Tenderness over the spinous process of the affected vertebra (even on light touch)
    • Possibly fever
    • Protective posture, increased muscle tone → extension contracture
  • Diagnostics
    • Assess patient for clinical features and history suggestive of vertebral osteomyelitis
    • Initial work-up: see flowchart
      • Blood cultures
      • Inflammatory markers
      • X-ray imaging (anterior-posterior and lateral views)
        • Often inconclusive in the first 2 weeks of infection
        • Initial narrowing of intervertebral spaces and end plate sclerosis
        • Progressive kyphosis, vertebral body squaring, and development of block vertebra
    • Contrast-enhanced MRI: the most sensitive diagnostic study; for vertebral osteomyelitis
      • Findings
        • Disruption of vertebral structure, fusion of vertebral bodies and discs
        • Contrast enhancement
    • Gallium bone scan if MRI is contraindicated (metal foreign body implants) → detects sites of infection
    • CT-guided needle aspiration biopsy (confirmatory test): culture and histology
      • Indicated if clinical and radiographic tests support the diagnosis but blood cultures are negative
      • Enables appropriate antibiotic selection based on the culture results.
      • Not recommended in patients with neurologic compromise or sepsis.
  • Treatment
    • Bed rest and immobilization of the affected vertebral segment; spinal orthosis required in severe cases
    • Antibiotic treatment (IV administration, for weeks or months)
      • Immediate empiric therapy if the patient presents with signs of neurologic compromise and/or sepsis
      • Pathogen-directed therapy once blood culture results are available (see “Treatment” below)
    • Tuberculosis treatment: if mycobacterium tuberculosis is the underlying pathogen
    • CT-guided catheter drainage of paravertebral abscess
    • Surgery
      • Indications: spinal instability, neurological deficits, cord compression, large epidural or paravertebral abscess, refractory osteomyelitis
      • Debridement; stabilization of collapsed vertebrae/spinal instabilities with or without interbody fusion
  • Complications
    • Abscess formation
    • Vertebral collapse and spinal instability → cord compression → paraplegia
    • Complications of tuberculous spondylitis
      • Pott's paraplegia is primarily a phenomenon of the past; cases have become very rare as a result of improved treatment regimens.
      • Gibbus deformity

Brodie abscess

  • Definition/Pathophysiology: an intraosseous abscess secondary to chronic hematogenous osteomyelitis that appears in immunocompetent children
    • Osteomyelitis due to pathogens of low virulence may be contained locally in the form of an abscess.
  • Localization: most commonly the metaphysis and epiphysis of long bones (especially in the distal femur and proximal tibia)
  • Clinical features: frequently asymptomatic or only mild symptoms; pain
  • Treatment: surgical drainage

References:[3][10]

Diagnostics

Clinical approach

  • Suspect osteomyelitis in patients with focal symptoms (point tenderness) accompanied by nonspecific signs and symptoms of inflammation.
  • Initial work-up includes blood cultures, inflammatory markers, and x-ray imaging.
  • Rule out possible primary sources of infection and/or sites of dissemination (e.g., dental infection, furuncle, and urinary tract infections)!

Laboratory tests

Imaging

  • X-ray:
    • Early stages (< 2 weeks of symptoms onset): typically no pathological findings
    • Later stages: bone destruction, sequestrum formation, periosteal reactions
  • MRI: the most sensitive diagnostic study; shows signs of inflammation ≤ 5 days after onset of infection → cortical destruction, bone marrow inflammation, soft tissue involvement
  • Skeletal scintigraphy: visualizes areas of bone with increased bone turnover
  • Radionuclide-labeled leukocyte scintigraphy: detects sites of infection or inflammation
  • Sonography: assess soft tissue involvement

Early stages of osteomyelitis are not visible on x-ray!

Biopsy (confirmatory test)

  • Bone biopsy: MRI/CT-guided needle or open biopsy + gram staining, culture, and histology
    • Indication: should be performed whenever feasible, before administering antibiotics
    • Detects both osteonecrosis and the pathogen → confirms the diagnosis and helps guide more specific therapy

References:[11][10][4]

Differential diagnoses

The differential diagnoses listed here are not exhaustive.

Treatment

Conservative

  • Bed rest and immobilization of the affected extremity
  • Antibiotic treatment
Initial empiric antibiotic treatment
Patient group Regimen
In adults
In children < 3 months of age
> 3 months of age
Pathogen-directed IV antibiotics (according to bone biopsy findings)
Pathogen Regimen
Methicillin-susceptible S. aureus (MSSA)
MRSA or S. epidermidis
Gram-negative pathogens (including Pseudomonas)
Special cases
Secondary osteomyelitis (e.g., prosthetic joints or foreign bodies) Rifampicin in addition to the antibiotic regimen

Treatment of osteomyelitis should not be delayed, especially in children! Osteomyelitis can have detrimental effects on bone development, resulting in severe long-term complications.

Surgical

  • Indication
    • Osteomyelitis refractory to antibiotic treatmentdebridement of necrotic bone and tissue
    • Abscess → drainage
    • Post-traumatic osteomyelitis → debridement and fracture management (e.g., external fixator)
    • Infected prosthetic joint or foreign body → removal
    • Revascularization in case of poor wound healing due to Peripheral artery disease

References:[12][11][9][3][5][4][13]

Complications

  • Infectious
    • Abscess
    • Sequestrum
    • Pyarthrosis: infiltration of nearby joints
  • Mechanical
  • Course: recurring/chronic cases
  • In children: growth impairment

References:[9][3][2][4][1][11][13]

We list the most important complications. The selection is not exhaustive.

Prognosis

  • Acute osteomyelitis
    • Quick, full recovery is common in children receiving appropriate antimicrobial treatment → > 95% of cases resolve completely.
    • Acute osteomyelitis in adults often relapses and transforms into chronic osteomyelitis.
  • Chronic osteomyelitis
    • Difficult to cure, often requires repeated surgical and antibiotic treatment (over years to decades)
    • In patients with diabetes or vascular insufficiency, the probability of complete resolution is particularly low.

References:[9][11][6]