Approach

Spinal epidural abscess (SEA) is often difficult to diagnose in the early stages, and late diagnosis is common.[2][28]​ The classic clinical triad is focal back pain, fever, and neurological deficit, but neurological deficit is a late presentation, and only around 10% of patients present with all three symptoms.[2][9][28]

A four-phase sequential evolution has been described, with the following symptoms:

  • Localised spinal pain

  • Radicular pain and paraesthesias

  • Motor weakness, sensory loss, and sphincter dysfunction

  • Paralysis.

Early diagnosis is the major prognostic factor for a favourable outcome of SEA.[29]

Management is multidisciplinary and should include the internist or family physician, an infectious disease specialist, and neurological or orthopaedic surgeons. Early laboratory studies (e.g., erythrocyte sedimentation rate [ESR], C-reactive protein [CRP], and full blood count [FBC]) can aid in the differential diagnosis.

History and examination

Medical history should include recognition of risk factors for SEA. These include intravenous drug use, diabetes mellitus, HIV infection, recent bacteraemia (particularly due to Staphylococcus aureus) or invasive procedures (e.g., previous spinal surgery or trauma, previous neuraxial anaesthesia associated with indwelling [intrathecal/epidural] catheter placement), chronic kidney disease and renal failure, malignancy, alcohol misuse, and obesity. Existing conditions (e.g., infective endocarditis, chronic liver disease, or urinary tract infection) may be a source of infection by haematogenous spread. Any focus of pre-existing local infection should also be ascertained, as direct extension from vertebral osteomyelitis, a psoas abscess, or a retropharyngeal abscess may be the source.[9][17][18][19]​ While the presence of one or more predisposing factors should heighten suspicion for SEA, their absence in appropriate settings such as new severe back pain should not be used to exclude this diagnosis, because up to 20% to 50% of patients with SEA have no preisposing factors. 

Back or neck pain is the most common symptom of SEA, occurring in 70% to 100% of patients.[2][12][30] Most patients with SEA report severe localised back pain.[2][30] Cervical SEA may result in neck pain rather than back pain. Pain is increased with weight-bearing and is not relieved by rest. Some patients present with chest or abdominal pain, which can masquerade as cardiac or intra-abdominal pathology.[31]

On examination, the patient may have fever, often accompanied by sweats or rigors. However, up to 50% of patients are afebrile.[2][12][30]

Signs and symptoms of neurological deficit should be sought. When present, this prompts urgent further investigations and imaging to confirm SEA, as neurological deficit may progress rapidly. In early SEA, weakness of extremities is common and may indicate impending motor weakness. The average time to paralysis, once weakness is present, is 24 hours. Up to 34% of patients have overt motor weakness.[12] Sensory disturbance, abnormal reflexes (ranging from hyperreflexia to reduced or absent responses), and isolated sphincter dysfunction may also be seen.

Laboratory investigations and imaging

All patients with suspected SEA should undergo laboratory testing for ESR, CRP, and FBC with differential to measure white blood cell count. ESR and CRP are elevated in most patients with SEA, and many have leukocytosis on FBC.[2]​ Procalcitonin appears to have a lower sensitivity than CRP in patients with spinal infection.[28][32]

In all patients with suspected SEA, magnetic resonance imaging (MRI) of the whole spine with and without gadolinium enhancement should be carried out to confirm or exclude abscess or other mass lesion.[9][33] Gadolinium-enhanced, diffusion-weighted MRI is the most sensitive, specific, and accurate imaging method for SEA.[2] Comparison with pre-contrast MRI is used to confirm areas of suspected abnormality.[33][34] The degree of thecal sac compression is prognostic: compression more than 50% increases the incidence of progressive neurological injury and late recurrences.[35] Some patients will have non-contiguous SEAs that span across different anatomical levels.[3] Computed tomography with and without contrast may be used if MRI is contraindicated, but is less sensitive.[2][9][33]

All patients should have blood cultures before antibiotic therapy. The most common pathogen in patients with SEA is S aureus, with MRSA increasingly reported. Other causative organisms include Pseudomonas species; other gram-negative bacteria; Mycobacterium tuberculosis; and Streptococcus species. Fungal and parasitic pathogens less commonly cause SEAs. However, no causative organism is identified in up to 25% of cases.[9][20][21]

Ideally specimens should be obtained by local aspiration of purulent material for culture, before initiation of antibiotic therapy.[36]​ Purulent material should undergo Gram stain and aerobic and anaerobic cultures.[36]​ Nucleic acid amplification tests for suspected organisms, especially M tuberculosis, may be considered. Antibiotic therapy can be started after blood cultures are obtained; the impact of antibiotic treatment on organism yield from subsequent invasive procedures may not be significant.[37]

Lumbar puncture should not be performed in any patient with suspected SEA, as it carries a risk of spreading bacteria into the subarachnoid space with consequent meningitis.[2][38] If enhanced MRI of the lumbar and thoracic spine is negative, lumbar puncture may be considered to identify alternative diagnoses.[11][18]

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