Spinal Epidural Abscess

Spinal epidural abscess (SEA) is a neurosurgical emergency with potentially devastating consequences. Delayed diagnosis leads to irreversible paralysis, and early recognition in high-risk populations, followed by immediate MRI and emergent decompression, is the only way to preserve neurologic function.

The triad. Fever, spinal pain and neurologic deficit make up the classic triad, but it is complete in only 10-30% of patients at first presentation. Any two elements in a high-risk patient warrant urgent MRI.

Who gets it. The incidence is 0.2-2 per 10,000 hospital admissions worldwide, with a male predominance of 55-70%. Mean age is 50-60 years, but the disease is rising in younger populations of intravenous drug users. The thoracic and lumbar spine are the commonest sites; cervical involvement carries the highest morbidity.

Risk factors. IV drug use and diabetes are the strongest. Patients in the high-risk groups develop SEA at higher rates and progress faster to paralysis.

• Diabetes - microvascular compromise and immune dysfunction
• IV drug use - haematogenous spread from skin flora
• Immunosuppression - steroids, HIV, malignancy
• Recent spinal procedure
• Extension from an infected focus - discitis, osteomyelitis, endocarditis, urinary tract infection

Three routes in. Infection reaches the epidural space by one of three main routes.

1. Haematogenous spread from distant foci (skin, urinary tract, endocarditis), most common in IV drug users and diabetics
2. Contiguous extension from adjacent discitis, vertebral osteomyelitis or a paravertebral abscess
3. Direct inoculation after spinal procedures or trauma

Why it tracks along the spine. The epidural space is a continuous compartment of loose areolar tissue drained by a valveless venous plexus, so infection extends rapidly cephalad and caudad.

Where the pus sits. The posterior epidural space is wider, especially in the thoracic spine, so posterior abscesses predominate. Anterior abscesses often arise from vertebral osteomyelitis. The cord ends at L1-L2, so a lumbar abscess compresses the cauda equina.

How the cord is damaged. Neurological injury in SEA is not purely mechanical. There are two mechanisms, and the second explains why a deficit can be out of proportion to the visible compression and why some patients deteriorate despite a technically adequate decompression.

• Direct mechanical compression of the cord or cauda equina by the abscess, the inflammatory mass and its oedema. This is the component that surgery relieves.
• Vascular compromise: septic thrombophlebitis of the valveless epidural venous plexus, and thrombosis or arteritis of the segmental and radicular feeding vessels, causing ischaemic (often venous) cord infarction.

The vascular component is largely irreversible. It is why rapid, profound neurological loss can occur with only modest compression, and why outcome correlates with the duration and severity of deficit before treatment rather than with abscess size alone.

Microbiology. Staphylococcus aureus dominates, and cultures are negative in up to 30% once antibiotics have been started.

• Staphylococcus aureus - 50-70% of cases, with MRSA rising
• Gram-negative bacilli - 15-20% (E. coli, and Pseudomonas in IV drug users)
• Streptococci and anaerobes - 5-10%
• Polymicrobial - in post-operative and sacral abscesses

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SEA is described by where the collection sits, which shapes the surgical approach, and by the neurological stage it has reached (Heusner), which sets the urgency.

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History. The pain is severe and localised to the back or neck, worse at night and not relieved by rest. Fever or rigors are present in the majority (60-80%) and may be low-grade, but fever may be absent in the immunocompromised. Rapid progression over days is typical, although chronic forms exist in tuberculosis.

Ask directly about the risk factors (IV drug use, diabetes, a recent procedure, endocarditis, urinary tract infection) and about neurologic symptoms: weakness, numbness, bowel or bladder change and gait disturbance.

Examination. Examine for sepsis and its source as well as the neurology.

• Vital signs - fever, tachycardia, possible hypotension if septic
• Spine - localised tenderness, paraspinal spasm, limited range of movement
• Neurology - sensory level, motor weakness, hyperreflexia or areflexia, upgoing plantars
• Sphincters - urinary retention, reduced anal tone, saddle anaesthesia
• Source - skin infection, injection sites, heart murmur

Bloods and cultures first. Take a full blood count, CRP, ESR and three sets of blood cultures immediately. Blood cultures are positive in 50-70% and guide targeted therapy. Inflammatory markers are often elevated but can be normal early or in the immunocompromised, so do not rely on them, and do not wait for them or for the culture results before scanning.

MRI with gadolinium, within 4 hours. Contrast-enhanced MRI is the gold standard, and the only modality that reliably diagnoses the abscess and defines the extent of cord compression. It shows the enhancing epidural collection, cord or cauda equina compression, and any associated discitis or osteomyelitis; sagittal and axial post-contrast T1 sequences are essential. The clinical triad plus risk factors is enough to order the scan.

Image the whole spine. The epidural space is a continuous compartment, so whole-spine MRI is mandatory.

What not to rely on. Plain radiographs are normal early, and CT without contrast misses the abscess, so do not delay for CT if MRI is available. A CT myelogram is the alternative only when MRI is contraindicated: it demonstrates a block to contrast flow and the epidural mass effect, but is less sensitive for soft-tissue detail and associated vertebral infection.

Find the source. Before surgery, an echocardiogram looks for endocarditis, which has a high association with SEA in IV drug users. CT of the chest, abdomen and pelvis identifies a distant source if none is obvious.

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The principle. Emergent surgical decompression plus IV antibiotics is the standard of care. Once the diagnosis is confirmed, do not delay surgery for medical optimisation: neurologic deterioration can occur within hours.

Algorithm

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Indications for decompression. Any one of these is enough:

• Any neurologic deficit: new or worsening motor or sensory loss
• Progressive symptoms
• Bowel or bladder involvement, or cauda equina
• A compressive abscess on MRI or CT myelogram, including a large abscess with cord compression
• Sepsis, or infection uncontrolled despite antibiotics
• Failure of medical therapy

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Antibiotics. Start the empiric regimen immediately after cultures, before or during surgery: vancomycin plus a third-generation cephalosporin (ceftriaxone or cefotaxime), with metronidazole if anaerobic cover is needed. Adjust once sensitivities are known. The course is typically 4-6 weeks IV, longer if osteomyelitis is present.

Non-operative management. A neurologically intact patient may occasionally be treated with antibiotics and close observation, often after CT-guided aspiration to obtain the organism. Failure of medical management is common and can be sudden and catastrophic, so know the independent risk factors for failure:

• Diabetes mellitus
• A high inflammatory burden: CRP greater than about 115 mg/L, white cell count greater than about 12.5
• Positive blood cultures or bacteraemia, especially MRSA
• Age over about 65
• Any neurologic compromise

The more that are present, the lower the threshold for early surgery. A patient managed medically needs a confirmed organism, serial neurological checks and repeat MRI, with immediate decompression at the first sign of deterioration.

When medical therapy has failed. Neurologic deterioration on antibiotics, persistent fever or a rising CRP after 72 hours, or enlargement of the abscess on repeat MRI each mean medical therapy has failed, and the abscess requires surgical drainage.

Approach follows the pus. Do not default to laminectomy for every abscess; the approach must match the collection's position relative to the cord.

• Posterior collection (the majority) → posterior laminectomy and evacuation. This reaches the pus directly and is the default.
• Anterior collection, usually accompanying vertebral osteomyelitis or discitis → laminectomy alone is both inadequate, because it cannot reach an anterior collection, and destabilising, especially if facets are sacrificed. These need an anterior approach (corpectomy, debridement and anterior-column reconstruction with a strut graft or cage) or a posterolateral route (costotransversectomy in the thoracic spine, or transpedicular drainage), often with posterior instrumented stabilisation. In the neck, an anterior cervical abscess requires anterior cervical decompression and fusion.
• Circumferential disease → may require combined anterior and posterior (360-degree) surgery.

Positioning. Prone for posterior thoracic and lumbar abscesses, on a radiolucent table, with Mayfield or Gardner-Wells traction if the abscess is cervical. Lateral decubitus is used for anterior cervical approaches.

Posterior decompression. Laminectomy over the length of the abscess, usually 3-5 levels, allows drainage and decompression of the cord. Preserve the facet joints to avoid instability.

Drainage and cultures. Evacuate all purulent material and send multiple cultures: aerobic, anaerobic, fungal and mycobacterial. Irrigate copiously and avoid retracting the cord. Intraoperative ultrasound confirms complete decompression.

Stabilisation. Instrumented fusion is indicated after an extensive laminectomy, with a pre-existing spondylolisthesis, or where osteomyelitis has destroyed the vertebra; anterior corpectomy with debridement can also leave the spine unstable. Titanium instrumentation may therefore be needed despite active infection, and contemporary series support fusion provided debridement is adequate and antibiotics are appropriate.

Closure. Close in layers over suction drains. IV antibiotics continue post-operatively, guided by cultures, with serial CRP monitoring.

After surgery. Monitor in ICU for 24-48 hours, with hourly neurologic observations initially. Bladder scanning or catheter care, DVT prophylaxis, serial inflammatory markers and early mobilisation once stable complete the post-operative care.

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Permanent neurological deficit. This is the dominant complication, and the outcome that urgent decompression aims to prevent. Established deficit at the time of decompression (motor weakness, sphincter dysfunction, cauda equina syndrome) is the strongest predictor of a poor recovery. A complete deficit present for more than 24-48 hours rarely recovers fully, whereas patients decompressed before or soon after deficit onset do far better.

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The other complications.

• Permanent paralysis in 15-30% of delayed cases, with bowel and bladder dysfunction a common sequela
• Cauda equina syndrome - bladder and bowel dysfunction and saddle anaesthesia from lumbosacral thecal sac compression
• Sepsis and septic shock - bacteraemia and metastatic infection (endocarditis, septic arthritis) may coexist
• Vertebral osteomyelitis or discitis - contiguous infection frequently accompanies the abscess and may cause later deformity or instability
• Recurrence or treatment failure - 5-10% after treatment; incomplete drainage, inadequate or premature cessation of antibiotics, or failure of non-operative management (which carries a real risk of sudden, irreversible deterioration) can lead to recurrence requiring further surgery

Mortality. Mortality was historically very high. With modern MRI, surgery and antibiotics it is roughly 5-15%, driven by sepsis and comorbidity in older, diabetic or immunocompromised patients. Outcomes are poorer with cervical location and delayed surgery.

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No society publishes a dedicated spinal epidural abscess guideline; this table synthesises the IDSA native vertebral osteomyelitis guideline (2015), UK red-flag imaging pathways, and AO Spine infection-management principles as they are conventionally applied to SEA.