Vertebral Osteomyelitis

Pathogenesis:

1. Hematogenous spread – by far the most common route.  Predisposed due to the fact that vertebral bone in adults has abundant, highly vascular marrow.
2. Contiguous spread from adjacent soft tissue infection – i.e. from infections involving the aorta, esophagus, bowel, etc.
3. Direct inoculation from trauma or spinal surgery

A few key points regarding the pathogenesis:

• The segmental arteries bifurcate to supply two adjacent vertebral bodies; as such, in infectious osteomyelitis, typically two adjacent vertebral bodies and their intervertebral disc are affected.
•  Important point radiographically regarding the above – vertebral metastasess typically affect the vertebral body but spare the disc, as opposed to infection which involves 2 adjacent vertebrae and the intervening disc.
•  The lumbar area is most commonly affected, followed by thoracic, and much less commonly cervical.
•  Infection can extend posteriorly, causing epidural or subdural abscesses and even meningitis.
•  Infection can also extend anteriorly and laterally, leading to paravertebral abscesses, mediastinal abscess, and so forth.  Can even cause thoracic empyemas.
•  The biggest complication of vertebral osteomyelitis is neurological impairment which can occur due to 1) epidural abscess, or 2) bony collapse. 

 

Microbiology:
#1 = Staph aureus - > 50% of cases – most likely to cause acute presentations with systemic toxicity.  The increasingly rates of vertebral osteomyelitis in recent years is due in large part to the increasing use of intravascular catheters/devices etc, which predisposes to S.aureus.
2. Enteric Gram negative rods – especially prone after Urinary tract instrumentation
3. Pseudomonas – predisposition =IV drug use
4. Candida – also in IV drug users
5. Streptococcus – Group B, C, G – especially in diabetics
6. Tuberculosis (Pott’s disease)

 

Clinical presentation: 

Typically, insidious onset of back pain, often worse at night.  In one study, the median duration of symptoms was 48 days.  Fever is an inconsistent finding (<50%).   Exam often shows local tenderness to palpation.  If epidural abscess is present, patients get focal severel back pain with motor and sensory symptoms, which progresses to paralysis. 

 

Labs:

Key point is that the WBC is often normal!!  However, >80% have elevated ESR (often >100) and CRP.  Blood cultures are positive in 50-70% of cases.

 

Imaging:
1) X-rays insentive and nonspecific.  Especially insensitive early on. 

2) CT scan – generally, quite a bit less sensitive than MRI and particularly bad at detecting epidural abscesses; however, helpful if positive and easier to obtain; also helpful for detecting adjacent abscesses (i.e., psoas abscess).

3) MRI with contrast – generally, the best study, and also the test of choice for detecting epidural abscesses.  The main caveat is that it can be falsely negative early on in disease; also, in terms of following response to therapy, early worsening after therapy does not necessarily predict treatment failure.

4) Bone scan – generally, only done if MRI cannot be performed (i.e. due to pacemaker or other metallic implants).
Definitive diagnosis, if blood cultures are not revealing, often involves a CT-guided aspiration/biopsy.

1. Tagged WBC: not sensitive or specific
2. Gallium: quite sensitive and specific (binds to acute phase reactants)
3. Technetium: quite sensitive and specific (affinity for areas of bone turnover)

 

Biopsy:

Percutaneous needle biopsy to isolate organism – key to guide therapy

 

Therapy – involves long-term IV therapy for a minimum of 6 weeks, with serial ESR/CRP measurements.   Note that the CRP falls faster in response to therapy than ESR.  The role of follow-up MRIs is somewhat controversial (see above).

 

 

(Christopher Woo MD, 1/6/11)

(Chanu Rhee MD, 4/1/11)