EET 6/03
Epidural Abscess
Key Points:
• Think of this diagnosis in patients with a predisposing factor (IVDU, immunosuppression) who
present with fever and back pain or weakness
• On physical exam, check for saddle anesthesia or a sensory level, diminished rectal tone, and any
evidence of motor weakness
• Emergent neuroimaging (with an MRI) is the standard of care
• Definitive therapy almost always involves surgical decompression and a prolonged course of
antibiotics
I.
Pathogenesis: May occur as result of either local extension of vertebral osteomyelitis/diskitis
or hematogenous spread of bacteria from distant site of infection or endocarditis. Damage to
the cord occurs either by direct compression, vein thrombosis, arterial interruption, or toxins.
II.
Epidemiology:
• Common in IV drug users (median age 35), but may also occur after trauma, spinal surgery,
or spontaneously (median age 50)
• 50% of patients have some form of underlying immunosuppression (DM, HIV)
III. Microbiology: Overwhelmingly S. aureus (2/3 of cases); also gram-negative rods, other
staph and strep spp. Less common: anaerobes, TB.
IV.
Clinical Manifestations: Symptoms usually progress in a typical sequence of:
a. Back pain (71%): may be reproducible on palpation
b. Fever (66%)
c. Progresses to neuropathic/radicular pain
d. With time, may progress to neurologic compromise, including:
i. Decreased rectal tone or bladder dysfunction
ii. Saddle anesthesia, or sensory “level”
iii. Motor weakness and, eventually, paralysis which may become quickly
irreversible
V.
Diagnosis: Once you suspect an epidural abscess, you are obligated to obtain emergent
neuroimaging – and this is one of the things the MRI team will come in for on a weekend, in
the middle of the night, whenever.
• MRI of the spine is the diagnostic test of choice; if unavailable order CT with contrast
• Blood cx should be drawn, and you will likely need to sample the abscess to guide therapy .
Positive cultures from abscess=90