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Spinal Epidural Abscess — Surgical Decompression

Operative SurgerySpine
SpineAdvancedCore Procedure

Spinal Epidural Abscess — Surgical Decompression

Surgical technique guide for emergency decompression of a spinal epidural abscess — posterior laminectomy for dorsal collections, anterior debridement for ventral pus with vertebral osteomyelitis, indications, instrumentation, complications and post-operative rehabilitation

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Peer-reviewed · 2026-06-20
High-yield overview

Emergency posterior laminectomy and abscess evacuation, or anterior debridement for a ventral collection with vertebral osteomyelitis · advanced

spineSubspecialty
12Key steps
4Danger zones
2–4hDuration
Critical Must-Knows
  • The classic triad of spinal epidural abscess — back pain, fever and progressive neurological deficit — is present in only a minority at first presentation, but when all three coexist the risk of irreversible paralysis rises sharply and urgent decompression is mandatory.
  • Staphylococcus aureus is the causative organism in roughly 50–70% of cases; blood cultures must be drawn before the first antibiotic dose wherever possible, as positive cultures direct targeted therapy and improve outcomes.
  • Posterior laminectomy is the standard approach for dorsal or posterolateral collections; anterior debridement is reserved for ventral collections associated with vertebral osteomyelitis and discitis where the ventral thecal sac is compressed.
  • Neurological deficit or progression of deficit is the key surgical indication — every hour of untreated cord or cauda equina compression increases the likelihood of irreversible paralysis; delay beyond 24 hours of symptom onset correlates with poor recovery.
  • Instrumentation and fusion are not routine but are required when multilevel laminectomy or facet destruction from osteomyelitis creates instability; anterior column reconstruction with a cage and posterior pedicle screw fixation is used in extensive disease.
Clinical Pearls
  • “
    The Heusner staging framework describes a predictable clinical trajectory from localised back pain through radicular pain, motor and sensory deficit, and on to complete paralysis — surgical decompression before stage 3 (motor deficit) gives the best neurological recovery.
  • “
    A neurologically intact patient with a small epidural collection and no neurological progression may be managed with targeted IV antibiotics alone (6–8 weeks) provided neurological status is checked hourly and a repeat MRI is obtained at 48–72 hours — but any deterioration mandates urgent surgery.
  • “
    Diabetes, intravenous drug use, immunosuppression, chronic renal failure and recent spinal procedures are the major risk factors; the patient is often diabetic or immunocompromised and at elevated risk of wound complications.
  • “
    Post-operative antibiotics run 6–8 weeks total: a minimum of 4–6 weeks intravenous followed by oral step-down guided by CRP trends and culture sensitivities — the spine surgeon and infectious diseases team co-manage this phase.

When & Why


The operation. Emergency evacuation of a spinal epidural abscess — most often a posterior laminectomy that unroofs the canal over the full craniocaudal extent of the collection, evacuates the pus, and decompresses the thecal sac — with anterior debridement and reconstruction reserved for ventral collections sitting against vertebral osteomyelitis and discitis. The cord and cauda equina tolerate compression poorly: pus produces direct mechanical compression and ischaemia, and surgical evacuation relieves the mechanical component while giving direct culture and debridement. Confirm the diagnosis first. MRI with gadolinium is the gold-standard investigation (sensitivity and specificity both greater than 90%), showing the collection, any cord or cauda equina compression, and associated osteomyelitis or discitis in a single study. Draw two sets of blood cultures from separate sites before the first antibiotic dose (positive in 50–70%). Both ESR and CRP are typically markedly raised — a CRP greater than 100 mg/L is common, and serial CRP is the most useful marker for monitoring response. ### Absolute indications - Progressive neurological deficit — any new motor weakness, sensory level, or sphincter disturbance attributable to the epidural abscess.

  • Complete or incomplete paralysis — urgent decompression within hours; recovery correlates with speed of intervention.
  • Sepsis or haemodynamic instability from the spinal infection not responding to antibiotics alone.
  • Abscess with cord compression on MRI in a patient deteriorating despite appropriate antibiotics.
  • Ventral collection with vertebral osteomyelitis where anterior debridement and reconstruction are required to decompress the thecal sac and stabilise the spine. ### Relative indications - Large epidural collection (greater than 75% of canal cross-sectional area) with significant thecal sac compression, even in a neurologically intact patient.
  • Failure of antibiotic therapy — persistent fever, rising CRP, or expanding collection on repeat MRI after 48–72 hours of targeted treatment.
  • Patient unable to cooperate with neurological monitoring — intensive care, altered mental state, or language barrier precluding reliable serial exams.
  • Recurrent abscess after previous non-operative management. ### When non-operative management is appropriate A neurologically intact patient may be managed with targeted antibiotics alone provided all of the following hold: a small collection with no significant cord compression on MRI; no clinical deterioration over a minimum of 72 hours of close observation; a reliable patient who can communicate changes; an identified organism with targeted susceptibility; and negative TB and fungal cultures before committing to a long non-operative course. This is high-risk and requires an hourly neurological chart, a repeat MRI at 48–72 hours, and a low threshold to abandon for surgery — any new deficit mandates urgent decompression. No randomised trial has compared surgery with antibiotics alone; the evidence is from case series and retrospective studies.
Neurological status
Surgery — urgent decompression
ANY motor deficit, sensory level, or sphincter disturbance
Antibiotics alone — careful monitoring
Completely intact; no deficit at all
Clinical trajectory
Surgery — urgent decompression
Deteriorating or plateaued with deficit
Antibiotics alone — careful monitoring
Stable or improving with antibiotics
MRI findings
Surgery — urgent decompression
Significant cord or cauda equina compression by collection
Antibiotics alone — careful monitoring
Small collection, no significant compression, no thecal sac deformity
Location
Surgery — urgent decompression
Any level — ventral or dorsal
Antibiotics alone — careful monitoring
Small dorsal or posterolateral collection only
Sepsis
Surgery — urgent decompression
Present or not controlled with antibiotics
Antibiotics alone — careful monitoring
Controlled with antibiotics
Patient reliability
Surgery — urgent decompression
Any patient with deficit
Antibiotics alone — careful monitoring
Reliable, communicative, able to report changes
Monitoring
Surgery — urgent decompression
Post-operative: serial neurological exams, CRP, wound check
Antibiotics alone — careful monitoring
Hourly neurological chart, repeat MRI at 48–72 hours, CRP trending
Antibiotic duration
Surgery — urgent decompression
6–8 weeks total (minimum 4–6 weeks IV then oral)
Antibiotics alone — careful monitoring
6–8 weeks total (minimum 4–6 weeks IV then oral)
Failure to improve
Surgery — urgent decompression
Re-exploration and washout
Antibiotics alone — careful monitoring
ANY deterioration = urgent surgical decompression
Surgical versus non-operative management — decision framework
FactorSurgery — urgent decompressionAntibiotics alone — careful monitoring
Neurological statusANY motor deficit, sensory level, or sphincter disturbanceCompletely intact; no deficit at all
Clinical trajectoryDeteriorating or plateaued with deficitStable or improving with antibiotics
MRI findingsSignificant cord or cauda equina compression by collectionSmall collection, no significant compression, no thecal sac deformity
LocationAny level — ventral or dorsalSmall dorsal or posterolateral collection only
SepsisPresent or not controlled with antibioticsControlled with antibiotics
Patient reliabilityAny patient with deficitReliable, communicative, able to report changes
MonitoringPost-operative: serial neurological exams, CRP, wound checkHourly neurological chart, repeat MRI at 48–72 hours, CRP trending
Antibiotic duration6–8 weeks total (minimum 4–6 weeks IV then oral)6–8 weeks total (minimum 4–6 weeks IV then oral)
Failure to improveRe-exploration and washoutANY deterioration = urgent surgical decompression

Consent specifically for the risk of permanent paralysis or neurological worsening (the patient already has deficit in most cases), infection recurrence, wound dehiscence or infection, CSF leak if a durotomy occurs, instability requiring further surgery, and the need for prolonged antibiotics (6–8 weeks). Pre-operative preparation. Blood cultures (two sets from separate sites) are drawn before the first antibiotic dose wherever possible. The first dose of empiric IV antibiotics (typically vancomycin plus a third- or fourth-generation cephalosporin or meropenem) is given in the anaesthetic room — but administration must not delay surgery. Somatosensory and motor evoked potentials (SSEPs and MEPs) are strongly recommended, particularly for cervical and thoracic abscesses, with baseline traces obtained before and confirmed after positioning.

The Operation


The goal: unroof the canal over the full extent of the collection, evacuate the pus and open every loculation while protecting an inflamed, friable dura, obtain deep cultures before irrigation, and stabilise the segment if the laminectomy or osteomyelitis has destabilised it. The posterior midline exposure is the workhorse and is laid out in full below; a ventral collection with osteomyelitis needs an anterior debridement and reconstruction instead, described afterwards.

Spinal canal epidural space (axial)
Axial view of the spinal canal: an epidural collection around the thecal sac compresses the cord; decompression evacuates the abscess and relieves the cord.Credit: OrthoVellum surgical illustration

Posterior laminectomy and abscess evacuation — dorsal collection

Step 1Positioning and preparation
  • Prone on a radiolucent frame (Jackson table or Wilson frame). Pad every pressure point — chest rolls or gel pads, iliac crests, knees, ankles — and let the abdomen hang free to reduce epidural venous bleeding.
  • Obtain SSEP and MEP baselines before positioning and reconfirm them after positioning, before incision.
  • Fluoroscopy is used to confirm the correct level; the pre-operative MRI is displayed in theatre for reference.
Step 2Fluoroscopic level confirmation
  • Obtain a lateral fluoroscopic image with a metallic marker (needle or clamp) on the skin and correlate with the pre-operative MRI to confirm the intended levels.
  • Mark the midline over the appropriate spinous processes. In the thoracic spine, count up from T12 (the thoracolumbar junction is reliable) rather than down from C7.
Step 3Midline incision and subperiosteal exposure — THE EXPOSURE
  • Make a midline longitudinal incision centred over the planned laminectomy levels.
  • Subperiosteal dissection of the paraspinal muscles from the spinous processes and laminae using a Cobb elevator, working out to the facet joints.
  • Place self-retaining retractors. Achieve meticulous haemostasis with diathermy and bone wax on bleeding bone — in the septic patient bleeding from bone and muscle is often brisk, and early haemostasis saves blood loss and improves visualisation during the epidural decompression.
  • Expose the laminae and facet joints at the planned levels and at least one level above and below the MRI-demonstrated abscess extent — the collection often extends beyond what the MRI shows, particularly into the epidural fat.
Step 4Laminectomy — ligamentum flavum first
  • Remove the spinous processes at the affected levels with a rongeur.
  • Perform a wide laminectomy from the base of one spinous process to the next, removing the laminae and ligamenta flava with Kerrison rongeurs (2 mm and 3 mm footplates). The ligamentum flavum is the first structure removed at each level.
  • The epidural abscess is typically encountered immediately deep to the ligamentum flavum — a yellow-white or grey purulent collection replacing the normal epidural fat, with a capsule that enhances on MRI.
Step 5Collect specimens BEFORE irrigation
  • Before any irrigation, take at least three separate samples of pus and tissue from different sites within the cavity for Gram stain, aerobic culture, anaerobic culture, fungal culture, and TB culture where indicated.
  • Also send a sample for histopathology. Once the field is irrigated, culture yield drops dramatically.
Step 6Evacuate the pus and open loculations
  • Gently evacuate the purulent material using suction and curettes.
  • The capsule may be thick and adherent to the dura — do not attempt to strip the capsule from the dura, which risks a durotomy. Instead, decompress the thecal sac by removing the bulk of the collection and opening any loculations.
Step 7Copious irrigation
  • Irrigate the epidural space with at least 3 litres of warm normal saline using a bulb syringe or pulsatile lavage.
  • This dilutes residual bacteria, removes loose debris, and provides mechanical decompression of the thecal sac. Use gentle pressure — high-pressure irrigation against a thin, inflamed dura can cause a dural tear.
  • After irrigation, suction pooled fluid and re-palpate the thecal sac to confirm it is soft and decompressed throughout the laminectomy extent — irrigant pooling on the wound floor can create the false impression of an adequate decompression.
Step 8Inspect the dura and repair any tear
  • Under magnification, inspect the exposed dura over the entire decompression zone.
  • If a dural tear has occurred, repair primarily with 6-0 Prolene interrupted sutures, reinforce with a dural substitute patch (collagen matrix) and fibrin glue, keep the patient flat for 24–48 hours, and extend antibiotic cover to meningitis organisms.
Step 9Stabilisation decision — fuse if unstable
  • Instrumentation and fusion are not routine, but are required when the laminectomy spans 3 or more levels, when the infection has destroyed facet joints, or when anterior column support is lost.
  • In that case place posterior pedicle screw instrumentation spanning the decompression to prevent post-operative kyphosis and allow early mobilisation.
Step 10Closure — primary versus VAC
  • Primary closure (deep fascia with 0 Vicryl, subcutaneous fat with 2-0 Vicryl, skin with staples, plus a closed suction drain to deep fascia brought out through a separate stab) is appropriate when the infection burden is moderate, debridement is adequate, haemostasis is good, and the patient is not severely immunocompromised. Remove the drain when output is less than 30 mL per 24 hours (typically 48–72 hours).
  • Delayed primary closure or a VAC dressing is preferred in high-risk patients — poorly controlled diabetes (HbA1c greater than 9%), chronic high-dose steroids, dialysis-dependent renal failure, or extensive purulence beyond the epidural space.
Dangers during laminectomy and evacuation
  • Wrong-level surgery: correlate the fluoroscopic image carefully with the MRI — count from T12 in the thoracic spine and note transitional vertebrae, ribs, and the iliac crests.
  • Adherent dura: in chronic infection the dura may be adherent to the ligamentum flavum. Use sharp dissection under magnification to separate the dura before applying Kerrison rongeurs; always advance the Kerrison with the footplate against bone and under direct vision so it does not plunge.
  • Cervical and thoracic cord: lies immediately beneath the lamina with little epidural margin for error — there is far less room than in the lumbar canal.
Expose one level above and below

Always extend the exposure at least one level above and below the MRI-demonstrated abscess extent. The collection can spread further than the scan suggests, particularly in the epidural fat, and finishing the laminectomy only to find residual pus at the margins is the classic avoidable error.

Cultures before you irrigate

Collect at least three separate specimens from different parts of the abscess for aerobic, anaerobic and TB or fungal culture before any irrigation. Be gentle with the capsule — it can be densely adherent to an inflamed dura, and trying to peel it off causes dural tears. Decompress by evacuating pus and opening loculations, then irrigate copiously.

Anterior debridement and reconstruction — ventral collection with osteomyelitis

Step 1Anterior exposure by level
  • Use the standard anterior exposure for the level: anterior cervical (Smith-Robinson) for the cervical spine, transthoracic or thoracoscopic for the thoracic spine, and anterior retroperitoneal or lateral (XLIF/OLIF) for the lumbar spine.
  • Retract and protect the great vessels — aorta and IVC in the lumbar spine; carotid sheath, vertebral artery, recurrent laryngeal nerve, oesophagus and trachea in the cervical spine.
Step 2Debride infected bone and disc to bleeding bone
  • Identify the infected vertebral bodies and disc space. Excise the disc and debride the infected endplates back to bleeding cancellous bone with curettes and rongeurs — any residual necrotic bone will harbour infection and cause recurrence.
  • Send debrided bone and disc specimens for culture and histopathology.
Step 3Evacuate ventral pus under direct vision
  • Debride the ventral epidural abscess from the anterior surface of the dura. Remove the posterior longitudinal ligament at the infected level to access the ventral pus.
  • The key advantage of the anterior approach is that you can see the dura and confirm decompression. Irrigate copiously with at least 3 litres of warm saline.
Step 4Reconstruct the anterior column
  • Reconstruct with a titanium or PEEK interbody cage (or strut graft) packed with autograft or allograft.
  • Ensure the cage contacts healthy, bleeding endplate above and below the debridement zone — cage subsidence into osteoporotic or debrided bone is a recognised failure.
Step 5Fixation and circumferential stability
  • Apply anterior plate fixation (cervical) or anterolateral screw-rod fixation (thoracolumbar).
  • In most cases perform a posterior pedicle screw instrumentation as well (staged or same-day, with separate prone positioning) for circumferential stability while the anterior graft consolidates.
Step 6Closure or VAC
  • Close in layers. Consider a VAC dressing in high-risk patients, as for the posterior approach.
Dangers during anterior debridement
  • Great vessel injury during anterior exposure — the aorta and IVC overlie the anterior lumbar vertebral surface; meticulous dissection and vascular control are essential.
  • Incomplete debridement — debride back to visibly bleeding bone; residual necrotic bone harbours infection and recurs.
  • Dural tear during ventral debridement — the dura may be adherent to the infected posterior longitudinal ligament; sharp dissection under magnification is required.
  • Cage subsidence if placed into osteoporotic or debrided bone with insufficient contact surface — ensure the cage rests on healthy endplate.

Aftercare & Complications


Post-operative antibiotic protocol Post-operative antibiotics run 6–8 weeks total regardless of approach — a minimum of 4–6 weeks intravenous, then an oral step-down guided by culture sensitivities and the CRP trend. The spine surgeon and infectious diseases physician co-manage the course. Antibiotics are not a substitute for adequate surgical debridement: if the source is inadequately controlled, infection recurs regardless of antibiotic duration. - Empiric (before culture results): IV vancomycin (15–20 mg/kg every 8–12 hours, trough 15–20 mcg/mL) PLUS IV ceftriaxone 2 g daily OR IV cefepime 2 g every 8 hours. For penicillin allergy, IV vancomycin PLUS IV meropenem 1 g every 8 hours. Add IV rifampicin 600 mg daily where MRSA risk is high (improves bone penetration for Staph aureus), and add quadruple anti-TB therapy if TB is suspected.

  • Culture-directed: MSSA — switch vancomycin to IV flucloxacillin (better bone penetration). MRSA — continue vancomycin; switch to linezolid or daptomycin if the vancomycin MIC is greater than 2 mcg/mL or if treatment fails despite adequate troughs. Gram-negatives (E. coli, Proteus, Klebsiella) — target by sensitivity.
  • Monitoring: CRP twice weekly during the IV phase (should decline steadily; a rising or plateaued CRP prompts repeat MRI); ESR weekly; clinical wound and neurological checks; repeat MRI at 4–6 weeks if the CRP is not normalising. ### Rehabilitation - Immediate (day 0–3): ICU or high-dependency care for cervical abscess, sepsis, or significant deficit. Hourly neurological observations for the first 48 hours (motor power, sensation, sphincter function). DVT prophylaxis is mechanical immediately and pharmacological (LMWH) once haemostasis is secured at 24–48 hours. Remove the drain when output is less than 30 mL per 24 hours.
  • Mobilisation and bracing: with instrumented fusion, mobilise in a TLSO (thoracolumbar) or Philadelphia collar (cervical) for 6–12 weeks; without fusion, a TLSO is advisable for multilevel laminectomy (3 or more levels) or if any facet was violated. Physiotherapy within 24–48 hours.
  • Neurological recovery: depends on the severity and duration of pre-operative deficit. Motor recovery can continue for 12–18 months, though most occurs in the first 3–6 months. Incomplete pre-operative paralysis (ASIA B, C, D) has a reasonable chance of functional improvement; complete paralysis (ASIA A) for greater than 24–48 hours has a poor motor prognosis, though pain and sphincter function may still improve.
  • Follow-up: 2 weeks (wound check, CRP), 6 weeks (CRP, radiographs if fused), 3 months (CRP, MRI, IV-to-oral decision), 6 months (radiographs, recurrence check), 12 months (final review). Any new back pain with fever or neurological symptoms in a patient with a prior epidural abscess triggers urgent MRI and repeat blood cultures.
Permanent neurological deficit / no recovery
Incidence
10–30% (higher with delayed surgery and complete pre-op paralysis)
Recognition
Persistent motor weakness, sensory deficit, or sphincter disturbance post-decompression; failure to improve over 3–6 months
Prevention and management
Prevention: urgent decompression within 24 hours of deficit onset; intraoperative neurophysiological monitoring. Management: inpatient neurorehabilitation, orthotic bracing, urological review, manage spasticity and neuropathic pain
New iatrogenic neurological deficit
Incidence
less than 5%
Recognition
New weakness, sensory loss, or bowel/bladder dysfunction that was NOT present pre-operatively
Prevention and management
Prevention: neurophysiological monitoring throughout; careful Kerrison technique under direct vision; avoid cord manipulation. Management: urgent repeat MRI; return to theatre for residual collection, haematoma, or hardware compression; high-dose steroids if cord injury suspected
Recurrence of epidural abscess
Incidence
5–15%
Recognition
Return of back pain, fever, raised inflammatory markers, or new deficit weeks to months after treatment
Prevention and management
Prevention: complete evacuation, copious irrigation, culture-directed antibiotics for 6–8 weeks, repeat MRI if CRP not normalised. Management: repeat MRI; return to theatre for repeat decompression and washout; adjust antibiotics on new cultures
Wound infection / dehiscence
Incidence
10–20% (higher in diabetics, immunocompromised)
Recognition
Erythema, warmth, discharge, wound breakdown, exposed hardware; fever; rising CRP after an initial decline
Prevention and management
Prevention: perioperative prophylaxis and 6–8 weeks therapeutic antibiotics; meticulous haemostasis; VAC and delayed closure in high-risk patients (HbA1c greater than 9%, chronic steroids); glycaemic control. Management: wound and deep tissue cultures, debridement and washout, VAC, adjust antibiotics; retain hardware if solid, remove if persistent infection
Post-operative instability / kyphosis
Incidence
5–15% (higher with multilevel laminectomy without fusion)
Recognition
New or progressive deformity on upright radiographs; increasing back pain on mobilisation; mechanical symptoms
Prevention and management
Prevention: instrumented fusion for laminectomy of 3 or more levels; facet-sparing technique; postoperative TLSO if unfused. Management: extend fusion if progressive deformity; anterior reconstruction for progressive kyphosis
CSF leak (post-durotomy)
Incidence
2–5%
Recognition
Clear fluid from wound or drain; postural headache; meningism; wound bulging on Valsalva
Prevention and management
Prevention: careful dural dissection under magnification; primary repair with 6-0 Prolene; dural substitute and fibrin glue; keep patient flat 24–48 hours. Management: bed rest, consider lumbar drain for 48–72 hours, extend antibiotics for meningitis cover; re-explore if persistent
Epidural haematoma
Incidence
1–3%
Recognition
New post-operative deficit (especially first 24–48 hours); severe back pain; wound haematoma; drain blockage
Prevention and management
Prevention: meticulous haemostasis before closure; closed suction drain; reverse anticoagulation pre-operatively. Management: urgent return to theatre for evacuation and haemostasis
Sepsis and systemic complications
Incidence
10–20%
Recognition
Persistent fever, tachycardia, hypotension, organ dysfunction; respiratory failure (cervical); AKI; DVT/PE
Prevention and management
Prevention: early targeted antibiotics; ICU care for cervical abscess or sepsis; DVT prophylaxis; glucose control. Management: ICU support, source control, multidisciplinary organ-failure management
Complications — recognition, prevention, management
ComplicationIncidenceRecognitionPrevention and management
Permanent neurological deficit / no recovery10–30% (higher with delayed surgery and complete pre-op paralysis)Persistent motor weakness, sensory deficit, or sphincter disturbance post-decompression; failure to improve over 3–6 monthsPrevention: urgent decompression within 24 hours of deficit onset; intraoperative neurophysiological monitoring. Management: inpatient neurorehabilitation, orthotic bracing, urological review, manage spasticity and neuropathic pain
New iatrogenic neurological deficitless than 5%New weakness, sensory loss, or bowel/bladder dysfunction that was NOT present pre-operativelyPrevention: neurophysiological monitoring throughout; careful Kerrison technique under direct vision; avoid cord manipulation. Management: urgent repeat MRI; return to theatre for residual collection, haematoma, or hardware compression; high-dose steroids if cord injury suspected
Recurrence of epidural abscess5–15%Return of back pain, fever, raised inflammatory markers, or new deficit weeks to months after treatmentPrevention: complete evacuation, copious irrigation, culture-directed antibiotics for 6–8 weeks, repeat MRI if CRP not normalised. Management: repeat MRI; return to theatre for repeat decompression and washout; adjust antibiotics on new cultures
Wound infection / dehiscence10–20% (higher in diabetics, immunocompromised)Erythema, warmth, discharge, wound breakdown, exposed hardware; fever; rising CRP after an initial declinePrevention: perioperative prophylaxis and 6–8 weeks therapeutic antibiotics; meticulous haemostasis; VAC and delayed closure in high-risk patients (HbA1c greater than 9%, chronic steroids); glycaemic control. Management: wound and deep tissue cultures, debridement and washout, VAC, adjust antibiotics; retain hardware if solid, remove if persistent infection
Post-operative instability / kyphosis5–15% (higher with multilevel laminectomy without fusion)New or progressive deformity on upright radiographs; increasing back pain on mobilisation; mechanical symptomsPrevention: instrumented fusion for laminectomy of 3 or more levels; facet-sparing technique; postoperative TLSO if unfused. Management: extend fusion if progressive deformity; anterior reconstruction for progressive kyphosis
CSF leak (post-durotomy)2–5%Clear fluid from wound or drain; postural headache; meningism; wound bulging on ValsalvaPrevention: careful dural dissection under magnification; primary repair with 6-0 Prolene; dural substitute and fibrin glue; keep patient flat 24–48 hours. Management: bed rest, consider lumbar drain for 48–72 hours, extend antibiotics for meningitis cover; re-explore if persistent
Epidural haematoma1–3%New post-operative deficit (especially first 24–48 hours); severe back pain; wound haematoma; drain blockagePrevention: meticulous haemostasis before closure; closed suction drain; reverse anticoagulation pre-operatively. Management: urgent return to theatre for evacuation and haemostasis
Sepsis and systemic complications10–20%Persistent fever, tachycardia, hypotension, organ dysfunction; respiratory failure (cervical); AKI; DVT/PEPrevention: early targeted antibiotics; ICU care for cervical abscess or sepsis; DVT prophylaxis; glucose control. Management: ICU support, source control, multidisciplinary organ-failure management

Viva & Exam Focus


Mnemonic

ABCESSABCESS — presentation and diagnosis

A
Ask about back pain
The first symptom in over 90% of patients — suspect it in any febrile patient with new back pain and risk factors.
B
Blood cultures before antibiotics
Draw at least two sets from separate sites before the first dose — positive in 50–70% and essential for targeted therapy.
C
CRP and ESR
Both typically markedly raised (CRP often greater than 100 mg/L); useful for diagnosis and for monitoring response.
E
Emergent MRI with gadolinium
The gold-standard investigation — shows the collection, cord compression, osteomyelitis and discitis in one study.
S
Staging (Heusner)
Stages 1 (back pain) through 5 (death); outcomes correlate with stage — operate before motor deficit for best results.
S
Surgery if deficit or deterioration
Neurologically intact patients may be managed conservatively, but any new motor weakness, sensory level, or sphincter disturbance mandates urgent decompression.
Mnemonic

DECOMPDECOMP — intraoperative principles

D
Debride all necrotic tissue
Remove all necrotic tissue, infected bone and pus; send multiple specimens for culture (aerobic, anaerobic, fungal, TB).
E
Expose widely
Wide laminectomy over the full craniocaudal extent of the abscess; leave no residual pocket of pus.
C
Cultures before irrigation
Send at least three specimens from different sites within the abscess for Gram stain and culture before irrigation.
O
Osteomyelitis check
If vertebral osteomyelitis is present, debride the endplates and disc, and consider anterior column reconstruction.
M
Monitor with SSEP and MEP
Check intraoperative somatosensory and motor evoked potentials throughout to detect iatrogenic cord injury.
P
Protect the dura
Infection makes the dura thin and friable; gentle dissection avoids inadvertent durotomy and CSF contamination.
Critical danger structures and exam traps
Delay to surgery — irreversible paralysis

The trap. Waiting for inflammatory markers to normalise, or for an MRI on the next available list, in a patient with a new neurological deficit. Each hour of compression worsens the prognosis. The fix. Any patient with new or worsening motor weakness, sensory level, or sphincter disturbance from a confirmed epidural abscess goes to theatre urgently — draw blood cultures then give the first antibiotic dose, but do not let antibiotics delay surgery. The spinal or neurosurgical team must be contacted immediately.

Neurologically intact — over-treatment

The trap. Taking a neurologically intact patient with a small dorsal collection to theatre when close monitoring and targeted antibiotics would suffice. The fix. A patient who is neurologically intact with a small collection, no cord compression on MRI, and no progression may be managed non-operatively — provided an hourly neurological chart is instituted, antibiotics are culture-directed, and a repeat MRI is performed at 48–72 hours. Any new deficit mandates urgent decompression.

Ventral collection — wrong approach

The trap. Performing a posterior laminectomy for a predominantly ventral collection where the pus compresses the cord from the front, leaving the ventral thecal sac inadequately decompressed. The fix. Ventral collections with associated vertebral osteomyelitis and discitis require an anterior approach (cervical: anterior cervical discectomy or corpectomy; thoracic: transthoracic or thoracoscopic; lumbar: anterior lumbar interbody) with debridement and reconstruction, often supplemented by posterior fixation. Posterior-only approaches cannot adequately decompress ventral pus.

Dural tear — CSF leak and meningitis

The trap. Inadvertent durotomy during laminectomy or evacuation of a collection densely adherent to the dura — particularly after previous spinal surgery or with chronic infection. The fix. Identify the dura before decompressing. If a tear occurs, repair primarily with 6-0 Prolene under magnification, reinforce with a dural substitute and fibrin glue, extend antibiotics to cover meningitis risk, and keep the patient flat for 24–48 hours to reduce CSF leak pressure.

Instability after multilevel laminectomy

The trap. Performing a multilevel laminectomy (3 or more levels) for an extensive abscess without planned instrumented fusion, leading to post-operative deformity, progressive kyphosis, and chronic pain. The fix. If the laminectomy spans 3 or more levels, or if facet joints are violated during debridement, plan concurrent posterior pedicle screw instrumentation. The instability risk is higher in the cervical and thoracic spine, where fusion is more strongly indicated; anterior reconstruction may also be needed.

Diabetic and immunocompromised — wound failure

The trap. Primary wound closure in a patient with poorly controlled diabetes, chronic steroids, or end-stage renal disease, resulting in wound dehiscence and persistent infection. The fix. In high-risk patients (HbA1c greater than 9%, chronic steroid use greater than 10 mg prednisolone daily, dialysis-dependent), consider delayed primary closure or a VAC dressing for 48–72 hours with a planned re-look. Optimise glycaemic control perioperatively and use meticulous layered closure to eliminate dead space.

Clinical Decision Scenarios

Practise clinical reasoning and management decisions out loud

Viva scenarioAdvanced
Clinical prompt

“A 55-year-old man with insulin-dependent diabetes (HbA1c 9.8%) presents with a 5-day history of progressive mid-thoracic back pain, fever, and now difficulty walking. Examination reveals a T10 sensory level, bilaterally hyperreflexic legs, upgoing plantars, and 3/5 power in the hip flexors and knee extensors. MRI shows a dorsal epidural collection from T8 to T11 with cord compression. Blood cultures have been sent but results are pending. What do you do?”

Viva scenarioAdvanced
Clinical prompt

“A 35-year-old intravenous drug user presents with severe lumbar back pain and a fever of 38.9 degrees Celsius. She has no motor weakness, no sensory deficit, and normal bladder and bowel function. MRI shows a posterolateral epidural collection at L3–L4 compressing the thecal sac to about 60% of its normal anteroposterior diameter. Blood cultures are growing MSSA. How do you manage her?”

Viva scenarioAdvanced
Clinical prompt

“You are called to see a 70-year-old woman 4 days after a T12–L1 laminectomy and pedicle screw fixation for a dorsal epidural abscess. She was neurologically improving post-operatively, but today she has new fever (38.5 degrees Celsius), wound erythema, and a serosanguinous discharge from the wound. Her CRP was falling and is now rising again. What is your assessment and management plan?”

Exam day cheat sheet
Spinal epidural abscess decompression — exam-day essentials

Key diagnosis points

  • Classic triad (back pain, fever, deficit) is present in a minority — back pain is universal; suspect it in any febrile patient with new back pain and risk factors
  • Heusner stages: 1 back pain, 2 root pain, 3 motor or sensory deficit, 4 paralysis, 5 death — best outcomes with surgery before stage 3
  • Staph aureus in 50–70%; blood cultures positive in 50–70% — draw before antibiotics
  • ESR and CRP both markedly raised; CRP greater than 100 mg/L is common; serial CRP monitors response
  • MRI with gadolinium is the gold standard; sensitivity and specificity both greater than 90%; image the whole clinically relevant spine
  • Risk factors: diabetes, IV drug use, immunocompromised, chronic renal failure, alcohol, recent spinal procedure, endocarditis

Indications for surgery

  • ANY new or worsening motor weakness, sensory level, or sphincter disturbance equals urgent decompression
  • Complete or incomplete paralysis equals emergency decompression within hours
  • Failure of antibiotics (persistent fever, rising CRP, expanding collection on repeat MRI at 48–72 hours)
  • Sepsis refractory to antibiotics
  • Ventral collection with vertebral osteomyelitis requiring anterior debridement and reconstruction
  • Large collection (greater than 75% of canal cross-section) with significant cord compression, even if intact

Non-operative criteria

  • Neurologically intact, small collection, no significant cord compression on MRI
  • No clinical deterioration over a minimum of 72 hours of observation
  • Identified organism with targeted susceptibility
  • Hourly neurological observation chart by trained nursing staff
  • Repeat MRI at 48–72 hours; CRP trending down
  • ANY new deficit equals immediate surgery; low threshold to abandon non-operative management

Antibiotics

  • Empiric: IV vancomycin PLUS IV ceftriaxone (or cefepime or meropenem)
  • MSSA: switch vancomycin to IV flucloxacillin (better bone penetration)
  • MRSA: continue vancomycin; consider linezolid or daptomycin if high MIC or failure
  • Duration 6–8 weeks total; minimum 4–6 weeks IV then oral step-down
  • Monitor CRP twice weekly; repeat MRI if CRP is not declining

Posterior laminectomy — key steps

  • Prone on a radiolucent table; SSEP and MEP monitoring
  • Fluoroscopic level confirmation — count from T12 in the thoracic spine
  • Midline incision; subperiosteal exposure at least one level above and below
  • Wide laminectomy over the full craniocaudal extent; ligamentum flavum is removed first
  • Identify and protect the dura (may be adherent); sharp dissection under magnification
  • Collect 3 separate specimens from different sites before irrigation
  • Evacuate pus and open loculations; do NOT strip an adherent capsule from the dura
  • Copious irrigation: at least 3 litres of warm saline
  • Fusion if the laminectomy spans 3 or more levels or facets are destroyed
  • Closure: primary with drain (standard risk) or VAC and delayed closure (high risk)

Anterior approach — when and how

  • Indicated for a ventral collection with vertebral osteomyelitis and discitis
  • Cervical: anterior cervical corpectomy with plate; thoracic: transthoracic; lumbar: anterior retroperitoneal or lateral
  • Debride infected bone and disc back to bleeding cancellous bone; send specimens
  • Evacuate ventral pus under direct vision; copious irrigation
  • Reconstruct the anterior column with a cage or strut graft packed with autograft or allograft
  • Supplement with posterior pedicle screw fixation for circumferential stability

Danger zones

  • Delay to surgery in a patient with deficit — every hour of compression worsens prognosis
  • Wrong-level surgery — always fluoroscopic mark and count carefully from a reliable landmark
  • Durotomy from an adherent inflamed dura — sharp dissection under magnification; repair with 6-0 Prolene and a dural substitute
  • Inadequate decompression extent — extend at least one level above and below the MRI collection
  • Posterior approach for a ventral collection — cannot decompress the ventral cord adequately
  • Multilevel laminectomy without fusion — post-operative kyphosis and instability
  • Primary closure in high-risk patients (HbA1c greater than 9%, chronic steroids) — use VAC and delayed closure

Complications

  • Permanent paralysis: 10–30% (higher with delayed surgery and complete pre-op deficit); urgent decompression is the best prevention
  • Recurrence: 5–15%; repeat MRI, return to theatre, adjust antibiotics
  • Wound infection: 10–20% (higher in diabetics); VAC, debridement, culture-directed antibiotics; retain hardware if solid
  • Instability: 5–15% after multilevel laminectomy without fusion; instrumented fusion prevents this
  • CSF leak: 2–5%; primary repair, dural substitute, fibrin glue, flat bed rest 24–48 hours
  • Epidural haematoma: 1–3%; urgent return to theatre for evacuation

Post-operative rehabilitation

  • ICU or HDU for cervical abscess, sepsis, or significant deficit
  • Hourly neurological observations for the first 48 hours
  • Antibiotics 6–8 weeks total (4–6 weeks IV minimum); co-manage with infectious diseases
  • CRP twice weekly during the IV phase; repeat MRI at 4–6 weeks if CRP is not normalising
  • TLSO brace for 6–12 weeks (fused patients); earlier mobilisation with brace support
  • Neurorehabilitation from day 2–3; motor recovery can continue for 12–18 months
  • Follow-up at 2 weeks, 6 weeks, 3 months, 6 months, 12 months with CRP, radiographs, and MRI

Background & Evidence


Epidemiology and risk factors. Spinal epidural abscess is uncommon but rising with an ageing, increasingly immunocompromised population and more spinal procedures. The major risk factors are diabetes mellitus (present in 20–40% of cases), intravenous drug use (especially Staph aureus bacteraemia), immunosuppression (HIV, chemotherapy, chronic steroids, TNF-alpha inhibitors, transplant), chronic renal failure and dialysis, alcohol abuse, a recent spinal procedure or epidural injection, endocarditis, and skin, soft-tissue or urinary tract infection with haematogenous seeding. Up to 20% of patients have no identifiable risk factor at presentation. Organisms. Staphylococcus aureus is the causative organism in 50–70% of cases, including most post-procedural abscesses. Gram-negative rods (E. coli, Proteus, Klebsiella) follow urinary tract seeding, and Mycobacterium tuberculosis causes a chronic granulomatous picture. The valveless Batson venous plexus communicates with pelvic and thoracic veins, explaining haematogenous spread from pelvic, urinary, or IV-drug-use sources. ### Clinical presentation — the Heusner staging framework The clinical course follows a recognisable pattern. The exam answer for when to operate is any patient who reaches stage 3 or beyond; the best outcomes come from decompression before motor deficit develops, but most patients present at stage 2–3.

1
Clinical feature
Localised back pain and tenderness — present in over 90%, often misattributed to mechanical pain
Significance
Earliest stage — best surgical outcomes if decompressed here
2
Clinical feature
Radicular pain from nerve root irritation — bilateral or unilateral, mimics a disc herniation
Significance
Operate here for the best neurological recovery
3
Clinical feature
Motor weakness and sensory deficit — UMN signs in cervical or thoracic; LMN signs in cauda equina; a sensory level may be present
Significance
Absolute surgical indication — outcome worsens with every hour of delay
4
Clinical feature
Paralysis — complete motor and sensory loss below the lesion; sphincter disturbance (retention, loss of anal tone)
Significance
Point of no return for many patients — emergency decompression
5
Clinical feature
Death — from sepsis, respiratory failure (cervical), or complications of prolonged paralysis
Significance
Outcome of delayed or missed diagnosis
Heusner staging of spinal epidural abscess
StageClinical featureSignificance
1Localised back pain and tenderness — present in over 90%, often misattributed to mechanical painEarliest stage — best surgical outcomes if decompressed here
2Radicular pain from nerve root irritation — bilateral or unilateral, mimics a disc herniationOperate here for the best neurological recovery
3Motor weakness and sensory deficit — UMN signs in cervical or thoracic; LMN signs in cauda equina; a sensory level may be presentAbsolute surgical indication — outcome worsens with every hour of delay
4Paralysis — complete motor and sensory loss below the lesion; sphincter disturbance (retention, loss of anal tone)Point of no return for many patients — emergency decompression
5Death — from sepsis, respiratory failure (cervical), or complications of prolonged paralysisOutcome of delayed or missed diagnosis

Common presenting features are back pain (greater than 90%, localised, progressive, worse at night, unresponsive to simple analgesia), fever (50–70%, often absent in the immunocompromised and those already on antibiotics), neurological deficit (30–50% at first presentation), raised inflammatory markers (ESR commonly greater than 50 mm/hr, CRP commonly greater than 100 mg/L), and tenderness on spinal percussion at the affected level. ### Surgical anatomy The epidural space lies between the dura and the vertebral canal (the vertebral-body periosteum and the ligamentum flavum) and contains epidural fat, the valveless Batson venous plexus, lymphatics, and loose connective tissue. It is a true potential space along which infection can spread over several levels — which is why epidural abscesses often extend over multiple segments, and why the laminectomy must span the full craniocaudal extent. - Posterior epidural space (the laminectomy corridor): bounded posteriorly by the laminae and ligamenta flava, anteriorly by the posterior dura. The abscess typically lies immediately deep to the ligamentum flavum. The posterior space is narrowest in the cervical spine and largest in the lumbar spine.

  • Ventral epidural space (the anterior approach target): bounded anteriorly by the posterior longitudinal ligament and vertebral body, posteriorly by the anterior dura. A ventral collection cannot be adequately decompressed from behind without risk of cord manipulation. What is at risk. The anterior spinal artery supplies the anterior two-thirds of the cord (motor and spinothalamic tracts) and is vulnerable to compression and ischaemia; the artery of Adamkiewicz enters between T8 and L4 and its compromise can cause anterior spinal artery syndrome. The thoracic cord (T4–T8) sits in the narrowest canal relative to cord diameter and is at greatest risk. The conus at T12–L1 causes early sphincter disturbance and saddle anaesthesia, while cauda equina compression below L2 produces a lower motor neuron pattern. Ligaments. The ligamentum flavum (C2 to S1, thickest lumbar, high elastin) is the first structure removed at each level during a posterior decompression; in infection it may be oedematous and the dura may be adherent to it. The posterior longitudinal ligament is the barrier between infected bone or disc and the dura during anterior debridement. ### Vertebral osteomyelitis and discitis Haematogenous seeding of the subchondral endplate (rich metaphyseal blood supply) leads to osteomyelitis, which spreads across the disc to the adjacent body (discitis) and then into the anterior epidural space as a ventral abscess. Staph aureus is again the most common organism. The surgical relevance: a ventral abscess with osteomyelitis needs both decompression (anterior) and debridement of infected bone back to bleeding bone, followed by anterior column reconstruction and posterior fixation. ### Key evidence — surgical versus non-operative management The fundamental surgical principle is that the cord and cauda equina tolerate compression poorly. Multiple large case series and the 915-patient Reihsaus meta-analysis show that patients with a pre-operative neurological deficit who undergo early surgical decompression do better neurologically than those managed non-operatively or whose surgery is delayed, and that mortality remains 5–30%. Recovery correlates with the duration of pre-operative deficit — decompression within 24 hours of symptom onset gives the best chance of recovery, and beyond 36–48 hours the prognosis worsens markedly, particularly for complete paralysis. The Pourtaheri review frames the decision: surgery is non-negotiable for any deficit, sepsis refractory to antibiotics, or failure of conservative care, while a highly selected neurologically intact subgroup may be managed non-operatively provided monitoring is rigorous and the threshold to abandon conservative care is low. ### Special situations - Cervical abscess. The narrow cervical canal leaves little margin — a small collection can cause severe cord compression and rapid quadriparesis with respiratory compromise, and patients may need intubation before surgery. Posterior laminectomy and fusion for dorsal collections; anterior corpectomy and reconstruction for ventral; circumferential surgery for extensive disease; rigid collar (Philadelphia or Aspen) for 6–12 weeks.
  • The IV drug user. Commonly Staph aureus (including MRSA) but also Gram-negatives and unusual pathogens; often multilevel disease; hepatitis B, C, and HIV co-infection are common and must be screened. Start MRSA-active empiric cover, liaise early with infectious diseases, addiction medicine, and social work, consider OPAT if reliable, and counsel about the high recurrence risk if drug use continues.

References


Evidence

Bacterial spinal epidural abscess. Review of 43 cases and literature survey

Level III
Darouiche RO, Hamill RJ, Greenberg SB, Weathers SW, Musher DM • Medicine (Baltimore) (1992)
Key Findings:
  • Retrospective review of 43 cases of bacterial spinal epidural abscess at a single institution
  • Staphylococcus aureus was the most common causative organism (roughly two-thirds of culture-positive cases)
  • Patients who underwent early surgical decompression had significantly better neurological outcomes than those with delayed surgery or non-operative management
  • Back pain was present in all patients at presentation; fever was present in roughly two-thirds
Clinical implication: Established the association between early surgical decompression and improved neurological outcomes; highlighted that back pain is the universal presenting symptom and that delay is the single biggest modifiable risk factor for poor outcome.
Source: Medicine (Baltimore) 1992 Nov;71(6):369-85
Verify on PubMed (PMID 1359381)
Evidence

Spinal epidural abscess: a meta-analysis of 915 patients

Level III
Reihsaus E, Waldbaur H, Seeling W • Neurosurg Rev (2000)
Key Findings:
  • Meta-analysis of 915 patients with spinal epidural abscess drawn from approximately 10 years of published case series
  • Reported mortality rates ranging from 5% to 30% depending on patient factors, organism virulence, and speed of treatment
  • Emphasised the importance of early diagnosis with MRI and the poor correlation between inflammatory markers and neurological recovery
Clinical implication: Reinforced that mortality remains significant despite modern antibiotics and surgical techniques; underscores the importance of early MRI in any suspicious case and the primacy of clinical neurological status over laboratory values in guiding surgical timing.
Source: Neurosurg Rev 2000 Dec;23(4):175-204
Verify on PubMed (PMID 11153548)
Evidence

Spinal epidural abscess in clinical practice

Level III
Sendi P, Bregenzer T, Zimmerli W • QJM (2008)
Key Findings:
  • Review article summarising the clinical features, diagnostic workup, and treatment strategies for spinal epidural abscess in adults
  • Described the classical presentation sequence of back pain, fever, and progressive neurological deficit
  • Highlighted that up to 20% of patients had no identifiable risk factor at presentation
  • Advocated MRI as the investigation of choice and emphasised the role of early surgical decompression in patients with neurological deficit
Clinical implication: Provides a comprehensive clinical framework for diagnosis and management; reinforces that absence of risk factors does not exclude the diagnosis and that MRI must not be delayed in clinically suspicious cases.
Source: QJM 2008 Jan;101(1):1-12
Verify on PubMed (PMID 17982180)
Evidence

Cervical epidural abscess after epidural steroid injection

Level III
Huang RC, Shapiro GS, Lim M, Sandhu HS, Lutz GE, Herzog RJ • Spine (Phila Pa 1976) (2004)
Key Findings:
  • Case report of cervical epidural abscess following epidural steroid injection with literature review of post-injection spinal epidural infection
  • Staphylococcus aureus is the most common causative organism, including in post-injection abscesses
  • Cervical abscesses progress rapidly to quadriparesis and respiratory compromise; the narrow cervical canal leaves little margin before cord compression becomes irreversible
  • MRI with gadolinium is the diagnostic study of choice; surgical decompression must proceed urgently once neurological deficit develops
Clinical implication: Highlights that invasive spinal procedures (epidural steroid injection, epidural catheterisation) are a recognised risk factor and that cervical abscess in particular demands emergency decompression — a small collection in the narrow cervical canal produces severe cord compression far earlier than in the lumbar canal.
Source: Spine (Phila Pa 1976) 2004 Jan 1;29(1):E7-9
Verify on PubMed (PMID 14699291)
Evidence

When do you drain epidural abscesses of the spine?

Level III
Pourtaheri S, Issa K, Stewart T, Patel Y, Sinha K, Hwang K, Emami A • Surg Technol Int (2016)
Key Findings:
  • Surgical review of the indications and timing for drainage of spinal epidural abscess
  • Progressive neurological deficit, sepsis refractory to antibiotics, or failure of conservative management are absolute indications for surgical drainage
  • Neurologically intact patients with small collections, no significant thecal sac compression, and an identified organism may be treated with targeted IV antibiotics and close neurological monitoring, with surgery reserved for any deterioration
  • Early surgical decompression is associated with improved neurological recovery; delay beyond 24–36 hours of deficit onset markedly worsens prognosis
Clinical implication: Provides a decision framework for operative timing — surgery is non-negotiable for any neurological deficit, but a highly selected neurologically intact subgroup can be managed non-operatively provided monitoring is rigorous and the threshold to abandon conservative care is low.
Source: Surg Technol Int 2016 Oct 26;29:374-378
Verify on PubMed (PMID 27608748)
Evidence

Long-term outcome after neurosurgically treated spinal epidural abscess following epidural analgesia

Level III
Wang LP, Hauerberg J, Schmidt JF • Acta Anaesthesiol Scand (2001)
Key Findings:
  • Single-centre case series with long-term neurological follow-up after surgical treatment of spinal epidural abscess arising as a complication of epidural analgesia
  • Demonstrated a high rate of residual neurological deficit in patients whose presentation or surgery was delayed
  • Reinforces that epidural catheterisation is a recognised precipitant and that delayed decompression leaves lasting deficit
Clinical implication: Underscores the long-term cost of diagnostic or operative delay in post-procedure epidural abscess, and supports a low threshold for urgent imaging and decompression in any patient with new neurological symptoms after an epidural.
Source: Acta Anaesthesiol Scand 2001 Feb;45(2):233-9
Verify on PubMed (PMID 11167170)
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