Introduction
Osteomyelitis is an infection, typically bacterial, involving bone. It is difficult to treat often requiring long courses of antibiotics with or without surgery. It is particularly prevalent in diabetics or those with peripheral arterial disease.
Epidemiology
- Incidence: 20.00 cases per 100,000 person-years
- Peak incidence: 60-70 years
- Sex ratio: 1:1
| Condition | Relative incidence |
|---|---|
| Cellulitis | 75.00 |
| Gout | 7.75 |
| Bone metastases | 5.00 |
| Osteomyelitis | 1 |
| Avascular necrosis of the hip | 0.13 |
| <1 | 1-5 | 6+ | 16+ | 30+ | 40+ | 50+ | 60+ | 70+ | 80+ |
Aetiology
Risk factors:
Associated conditions
- Haematogenous osteomyelitis is more likely when there is a remote source of infection, such as indwelling vascular catheters or intravenous drug use
- Nonhaematogenous osteomyelitis is associated with direct inoculation of the affected tissues via trauma or medical procedures
- Osteomyelitis is more likely if there is associated vascular insufficiency
Associated conditions
- Diabetes: poorly controlled diabetes with associated peripheral neuropathy and impairs blood supply can lead to the development of non-healing infected ulcers and secondary nonhaematogenous spread of the associated pathogens to bone
- Peripheral arterial disease can also cause osteomyelitis through a similar process to diabetes
- Sickle cell disease can cause infarction of the bone and bone marrow leading to secondary infection
Pathophysiology
Generally bone is very resistant to infection and the pathophysiology of osteomyelitis is not entirely understood.
There are two types of osteomyelitis as defined by their source: haematogenous and nonhaematogenous.
Haematogenous:
Nonhaematogenous:
- Damaged bone (be it traumatic or iatrogenic) is at risk of infection if exposed to a high enough concentrations of a pathogen.
- Staph aureus is the most common causative pathogen in osteomyelitis.
- Studies suggest it is able to adhere to multiple components within the bone matrix.
- It can survive within osteoblasts and seems to become more resistant to antibiotic treatment when it does so - potentially explaining why prolonged courses of antibiotics are needed to adequately treat it.
- In patients with sickle cell disease Salmonella is the most common cause
- Gram negative rods are identified in up to a third of cases
- Other causative pathogens may be seen in intravenous drug users or immunosuppressed patients
- Fungal osteomyelitis may be seen, again usually in patients with immunosuppression
There are two types of osteomyelitis as defined by their source: haematogenous and nonhaematogenous.
Haematogenous:
- More common of the two
- Describes osteomyelitis caused by seeding of microorganisms from another source
- More common in children and as a cause of vertebral osteomyelitis
- The presence of foreign bodies such as vascular catheters or orthopaedic hardware increases risk
- Intravenous drug users are particularly at risk
- May be caused as a sequelae of endocarditis
Nonhaematogenous:
- May be caused as a result of trauma/surgery or as a consequence of adjacent soft tissue infection
- Peripheral neuropathy (due to diabetes, for example) significantly increases risk
- The presence of vascular insufficiency can prevent wound healing, leading to persistent colonisation of associated pathogens
Clinical features
Symptoms vary depending on whether the osteomyelitis is acute or chronic.
Acute osteomyelitis:
Chronic osteomyelitis:
%
Acute osteomyelitis:
- Symptoms tend to develop gradually over a few days
- Pain is the most common symptom, along with warmth, erythema and swelling of the soft tissue surrounding the affected bone
- Osteomyelitis of the proximal joints such as the hips or vertebrae may present only with pain
- Systemic symptoms such as fever and malaise may be present
Chronic osteomyelitis:
- Tends to present only with local symptoms such as swelling, erythema and pain
- Systemic symptoms such as fever are often absent
- A draining sinus tract may be seen - this is pathognomonic of osteomyelitis
- Patients with diabetes or vascular insufficiency may develop osteomyelitis subsequent to foot ulcers without the classic symptoms described above
- May also present as non-healing fractures
- Diabetics with ulcers >2cm2 are very likely to have osteomyelitis, even if no bone is visible
- Some practitioners use a 'probe to bone test' when assessing diabetic foot ulcers - a sterile metal instrument is used to probe the ulcer, with the detection of a hard and gritty surface suggesting osteomyelitis. This may guide the need for further investigation such as imaging or biopsy.
%
Investigations
Osteomyelitis can be difficult to diagnose with simple biochemical testing and plain film imaging alone.
Blood tests:
X-Ray:
Magnetic resonance imaging (MRI):
Computed tomography (CT):
Nuclear studies:
Ultrasound:
Histopathology:
Blood tests:
- Non-specific inflammatory response may be seen in acute osteomyelitis with a raised white cell count and a C-reactive protein (CRP) or plasma viscosity (PV) rise
- White cell count will often be normal in chronic osteomyelitis
- Blood cultures are positive in about half of cases of acute osteomyelitis
X-Ray:
- May be normal for the first two weeks of infection
- Signs include soft tissue swelling, osteopaenia, bone destruction, periosteal reaction, endosteal scalloping and new bone apposition
- Cannot always distinguish between osteomyelitis and fracture or other processes such as Charcot arthropathy
Magnetic resonance imaging (MRI):
- MRI is the imaging modality of choice in suspected osteomyelitis
- Imaging may be abnormal in the first few days of acute infection - initially with evidence of marrow oedema
- Able to identify soft tissue or joint complications
- Contrast does not improve diagnostic sensitivity but can improve imaging quality
Computed tomography (CT):
- Not as good as MRI but better than plain imaging alone where MRI is contraindicated (for example the patient has a pacemaker)
- Cannot detect marrow oedema so may be normal in early osteomyelitis
- Use of contrast improves ability to identify soft tissue abnormalities
Nuclear studies:
- Very sensitive at detecting inflammation
- May be used if CT and MRI are suboptimal (for example due to the presence of prosthetic material that degrades image quality)
- Multiple different modalities may be used
Ultrasound:
- Unable to visualise bone so of little use in the diagnosis of osteomyelitis
- May be used to identify surrounding soft tissue abnormalities such as abscesses or cellulitis
Histopathology:
- Bone biopsy can accurately identify osteomyelitis and its causative organism where imaging/blood analysis is inconclusive
- Not generally needed if there is convincing radiological evidence
- Biopsy sites can heal poorly if there is coexisting vascular insufficiency
Differential diagnosis
There are several differential diagnoses:
Soft tissue infection (e.g. cellulitis):
Charcot arthropathy:
Gout:
Fracture:
Avascular necrosis (AVN):
Soft tissue infection (e.g. cellulitis):
- Most common differential and may progress into osteomyelitis if untreated
- Difficult to differentiate clinically at initial presentation
- Osteomyelitis should be suspected if symptoms fail to respond to conventional short courses of antibiotics
- High risk patients such as diabetics or those with peripheral vascular disease should have a low threshold for imaging
Charcot arthropathy:
- Acute Charot arthropathy may present with similar symptoms to osteomyelitis
- Often co-exists with skin ulcers than can lead to chronic osteomyelitis
- May be differentiated on MRI
- Bone biopsy may be needed if there is diagnostic uncertainty
Gout:
- Much more common than osteomyelitis but with a faster onset
- More likely in a patient without any risk factors for osteomyelitis
- Will generally have no systemic symptoms
Fracture:
- May be difficult to distinguish on initial imaging
- Fractures that fail to heal should raise suspicion for osteomyelitis
- Bone biopsy may be needed to confirm a diagnosis
Avascular necrosis (AVN):
- Symptoms are similar but AVN will usually have a clear trigger such as radiation exposure or a history of bisphosphonate use, otherwise AVN is very unlikely
- May co-exist with osteomyelitis in osteonecrosis of the jaw
Management
Osteomyelitis is treated with antibiotics, usually with surgical debridement. In some patients with diabetic foot osteomyelitis antibiotic treatment alone may be sufficient.
Antibiotic therapy:
Surgery:
Antibiotic therapy:
- Antibiotic therapy should be guided by local microbiology advice
- The BNF recommends flucloxacillin (clindamycin if penicillin allergic), with consideration of the addition of fusidic acid or rifampicin for the first two weeks
- If meticillin-resistant staphylococcus aureus (MRSA) is suspected, vancomycin or teicoplanin is recommended
- If the affected bone is completely removed a short duration of antibiotics may be sufficient
- Otherwise at least 6 weeks of treatment, usually parental via PICC is needed
Surgery:
- For adequate treatment of osteomyelitis any infected necrotic bone must be removed
- Patients with necrotising soft tissue infection or secondary systemic infection from osteomyelitis may need urgent surgical debridement
- A soft tissue envelope must be left over the site of infection to allow healing
- If there is involvement of orthopaedic hardware specialist opinion must be sought as removal may be needed
Prognosis
Prognosis of osteomyelitis is highly variable depending on site of infection and associated comorbidities.
- Success rates for treatment are reported from 60-90%
- Co-existent vascular insufficiency or diabetes will adversely affect treatment outcomes