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Textbook/Neurosurgery/Subdural empyema
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Subdural empyema

Recognise pus spreading in the intracranial subdural space, distinguish it from parenchymal abscess and subdural haematoma, and coordinate urgent imaging, drainage, microbiology and source control.

27 min full readUK scopeSources checked 13 Sept 2026Clinical review pending
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A rapidly progressive intracranial infection

Fever, severe headache, seizure, altered consciousness or focal deficit after sinusitis, otitis, trauma or cranial surgery can indicate subdural empyema spreading over the cerebral convexity or falx with oedema, venous infarction and mass effect.

Action: Call neurosurgery, infection/microbiology, anaesthesia and ENT when relevant immediately; stabilise, treat seizures, obtain urgent contrast MRI with diffusion imaging or CT if faster, avoid lumbar puncture, and prepare surgical drainage plus antimicrobial treatment.

Open the sections you need. The overview is shown first.
01Core principlesThe concepts and mechanisms needed to understand the subject.

Intracranial subdural empyema is a purulent collection between dura and arachnoid. Unlike a parenchymal brain abscess, it can track widely because the subdural space has few anatomical barriers. Neurological injury arises from mass effect, inflammatory cortical injury, cerebritis, seizures, cortical thrombophlebitis and venous infarction. It is a medical and surgical emergency rather than a variant of chronic subdural haematoma.

Route and age matter. Paranasal sinusitis is a prominent source in adolescents and young adults, spreading through bone or valveless veins; otitis and mastoiditis also cause contiguous infection. In infants, empyema may complicate bacterial meningitis and follows a different diagnostic and treatment context. Trauma, infected subdural blood or effusion, cranial surgery and prior burr-hole drainage create postoperative disease with different organisms and implant or bone-flap considerations.

Headache, fever, vomiting, meningeal irritation, focal deficit, seizure and altered consciousness are typical but variable. A patient may deteriorate over hours after apparently routine sinusitis, and early imaging can be misleading. Examine GCS components, pupils, focal motor and language function, visual fields and meningism, while looking for orbital, sinus, ear, mastoid, wound and systemic sepsis findings. Repeat the examination; tempo is as important as the first deficit.

Contrast-enhanced MRI with diffusion-weighted imaging best delineates thin convexity and interhemispheric pus and associated cerebritis or venous injury. Contrast CT is faster and identifies mass effect and sinus disease, so it remains the first rescue image when MRI access would delay care. An equivocal CT is not a rule-out test in a worsening patient. Lumbar puncture is unhelpful for locating subdural pus and can precipitate harmful pressure shift.

Urgent drainage and antimicrobials are the usual combination. Craniotomy can provide wider exposure and break loculations; burr holes may suit selected accessible, fluid collections or particular age/anatomy contexts. Evidence is largely observational and does not create a universal approach for every empyema. Operative pus should be sent for aerobic and anaerobic cultures, Gram stain and host/source-directed tests; culture can be negative after prior treatment.

The empirical regimen depends on likely source, age, prior antimicrobials, allergy, immune status and whether disease is community, traumatic or postoperative. Source control can require sinus surgery, mastoid treatment, dental care, wound debridement or management of infected bone/hardware. Published duration practices vary and extend with osteomyelitis, residual collection or inadequate source control; use infection-specialist and local guidance rather than importing the 6–8-week ESCMID parenchymal-abscess rule.

Seizures are common at presentation and can recur later; treat acute seizures and obtain specialist advice on continued therapy. Monitor for venous sinus thrombosis or infarction when headache, seizure and deficits are disproportionate or imaging suggests venous disease. Rehabilitation may be needed for motor, cognitive, language and seizure-related consequences even after infection clears.

Key points

  • Subdural empyema is pus between dura and arachnoid, not pus within brain parenchyma; the continuous subdural space permits rapid spread over convexity and falx.
  • Sinus and ear disease dominate many community presentations in older children and young adults; infant post-meningitic and postoperative/traumatic empyemas are different populations and microbiological contexts.
  • Contrast MRI with DWI is most sensitive, especially for small or interhemispheric collections; urgent contrast CT is appropriate when MRI would delay rescue, and persistent suspicion after equivocal CT requires MRI or repeat imaging.
  • Lumbar puncture does not diagnose the collection and may be dangerous when mass effect or raised pressure is present.
  • Most patients require urgent craniotomy or burr-hole drainage plus antimicrobials; operative strategy depends on thickness, loculation, location, mass effect, age and prior surgery.
  • Send pus for aerobic and anaerobic culture and context-directed tests, treat the contiguous or postoperative source, and individualise antimicrobial regimen and duration—brain-abscess and meningitis schedules do not transfer automatically.
02Mechanisms and patternsImportant relationships and how to distinguish them.
Sinogenic deteriorationRed flag

New severe headache, fever, seizure, focal deficit or confusion during sinusitis is an intracranial-complication signal, especially in adolescents and young adults.

Spreading subdural syndromeRed flag

Rapidly evolving focal signs, seizures and reduced consciousness reflect spread over cortex and associated oedema or venous injury rather than a single parenchymal focus.

Infant disease

Post-meningitic subdural infection in infants is a separate population; irritability, seizures, enlarging head or persistent fever needs paediatric neurosurgical and infection input.

Postoperative diseaseRed flag

Fever, wound change, seizure or new deficit after cranial surgery or subdural drainage suggests direct inoculation or infected residual fluid and requires the operating service.

Haematoma mimic

A crescentic collection can be mistaken for subdural blood or hygroma; fever, source history and diffusion restriction support pus, while aspiration may establish the diagnosis.

Pressure and venous complicationsRed flag

Midline shift, pupil change, falling GCS, cortical venous thrombosis and venous infarction increase urgency and may explain abrupt worsening.

Red flags requiring action

  • New focal deficit, seizure, confusion, drowsiness or rapid deterioration during or soon after sinusitis or another head-and-neck infection.
  • Severe progressive headache with fever, vomiting, meningism or focal signs, especially in a child, adolescent or young adult.
  • Falling GCS, pupil change, posturing, abnormal breathing or marked midline shift indicates dangerous intracranial pressure and possible herniation.
  • Fever, seizure or new neurological deficit after cranial trauma, craniotomy or subdural-haematoma drainage raises postoperative empyema.
  • An initially normal or non-specific CT does not exclude early or interhemispheric empyema when clinical suspicion persists.
  • Cortical venous thrombosis, venous infarction, cerebritis, abscess and septic shock can coexist and worsen despite initial therapy.
03Interpreting evidenceInformation, measurements and their limitations.
Reasoning sequence

Consider the information, its meaning and its limitations before deciding what follows.

  1. 01
    Contrast MRI brain with DWI
    Why
    Define thin convexity or interhemispheric pus, loculations, cerebritis, abscess, venous injury and mass effect.
    Interpretation and limitations
    Restricted diffusion within a crescentic or parafalcine collection supports empyema. Negative or equivocal early imaging does not overrule progressive clinical suspicion; repeat or alternative imaging may be required.
  2. 02
    Contrast CT head
    Why
    Rapidly identify a subdural collection, enhancement, midline shift and sinus or mastoid source when MRI would delay emergency care.
    Interpretation and limitations
    CT may under-detect small, early or interhemispheric empyema. Proceed to MRI or repeat imaging when the syndrome remains concerning.
  3. 03
    Operative pus and tissue microbiology
    Why
    Identify pathogens and permit narrowing of therapy.
    Interpretation and limitations
    Send aerobic and anaerobic cultures and Gram stain, adding molecular, fungal or mycobacterial studies by context. Prior antibiotics can produce a negative culture.
  4. 04
    Blood cultures and inflammatory profile
    Why
    Detect systemic infection and create a response baseline.
    Interpretation and limitations
    Take cultures before treatment when no delay results. White-cell count and CRP support but do not exclude or localise empyema, particularly in immune compromise.
  5. 05
    ENT, dental and postoperative source assessment
    Why
    Identify a contiguous focus or direct inoculation requiring source control.
    Interpretation and limitations
    Review sinuses, orbit, ears, mastoids, teeth, scalp wound, bone flap and implants according to context; source treatment proceeds alongside cranial drainage.
  6. 06
    Venous imaging when indicated
    Why
    Detect cortical or dural venous thrombosis and venous infarction.
    Interpretation and limitations
    Add CT or MR venography when symptoms or MRI suggest venous involvement. Antithrombotic decisions are individual because intracranial infection and surgery alter bleeding risk.
04Applied reasoningWorked examples connecting principles to decisions.
01Worked case: sinus complicationSeizure and weakness after sinusitisA teenager treated for frontal sinusitis develops fever, severe headache, focal seizure and unilateral weakness.
  1. 1Recognise possible subdural empyema with cortical involvement, stabilise airway and circulation, treat the seizure and activate neurosurgery, infection and ENT teams immediately.
  2. 2Obtain urgent contrast MRI with DWI; use immediate contrast CT if MRI would delay rescue, and avoid lumbar puncture.
  3. 3Take blood cultures if this does not delay treatment, start the locally approved source- and age-appropriate empirical regimen and prepare urgent drainage.
  4. 4Send pus for aerobic and anaerobic culture plus directed studies, and coordinate sinus source control rather than treating the cranial collection alone.
  5. 5Monitor serial neurology, seizures, inflammatory response and imaging, reassessing for residual loculations, venous complications or need for repeat surgery.
02Imaging pathwayClinical suspicion persists after CTInitial CT is normal or non-specific but focal signs or deterioration continue.
  1. 1Do not close the diagnosis: re-examine and escalate the persistent neurological or septic trajectory to neurosurgery and neuroradiology.
  2. 2Obtain contrast MRI with DWI urgently because it is more sensitive for small and interhemispheric collections.
  3. 3If MRI is temporarily impossible and deterioration continues, repeat or escalate CT-based imaging while emergency specialist management proceeds.
03Compartment pathwayName anatomy and acquisition settingImaging shows an extra-axial purulent collection.
  1. 1Distinguish subdural empyema from cranial epidural abscess, parenchymal brain abscess, infected subdural haematoma and device-associated infection.
  2. 2Classify sinogenic, otogenic, infant post-meningitic, traumatic or postoperative context because likely organisms and source control differ.
  3. 3Select drainage, specimens, antimicrobial plan and source intervention for the actual compartment and population.
05Checking understandingVerify the reasoning, revisit uncertainties and apply feedback.
  • Repeat GCS components, pupils, power, language and seizure assessment frequently; new deterioration requires immediate imaging and surgical reassessment.
  • Trend temperature, haemodynamics, blood cultures and inflammatory markers while interpreting them alongside clinical and imaging response.
  • Monitor regimen-specific renal, hepatic, haematological and interaction toxicity under microbiology or infection-specialist guidance.
  • Repeat MRI or CT to assess residual or recurrent empyema when recovery is incomplete or deterioration occurs; do not rely on CRP alone.
  • Plan seizure follow-up and neurological, cognitive, language and physical rehabilitation after acute control.
06Special situationsVariants, exceptions and circumstances that change the usual approach.

The space changes behaviour

Subdural pus can spread widely over cortex, so a small entry source can produce multifocal signs, seizures and venous complications.

CT can be too early

A non-specific first CT does not close the pathway when deterioration continues; diffusion MRI is more sensitive.

Drain both problems

Cranial evacuation without sinus, ear, dental or wound source control leaves the route of infection active.

Age predicts context, not certainty

Infant post-meningitic and adolescent sinogenic disease are useful patterns, but trauma and surgery can occur at any age.

Abscess duration is not empyema duration

Parenchymal ESCMID treatment durations are not automatically transferable to subdural, postoperative or osteomyelitic infection.

07Common pitfallsFrequent interpretation and management errors.
  1. 01

    Calling a crescentic collection chronic subdural haematoma without integrating fever, source history and diffusion imaging.

  2. 02

    Performing lumbar puncture despite focal mass effect or a suspected subdural collection.

  3. 03

    Accepting a normal early CT despite continuing seizure, focal deficit or deterioration.

  4. 04

    Treating antimicrobials as a substitute for urgent neurosurgical source-control assessment in a symptomatic collection.

  5. 05

    Draining intracranial pus while ignoring sinus, mastoid, dental, wound or implant source control.

  6. 06

    Using one antibiotic duration for infant post-meningitic, community sinogenic and postoperative empyema.

Practice

Two practice questions

Question 1 of 20 correct
NeurosurgeryOriginal SBA

Neurological decline during sinusitis

A 17-year-old with frontal sinusitis develops fever, a focal seizure and unilateral weakness. Which action is most appropriate?

Sources and review status3 sources · checked 13 Sept 2026 · clinical review pending
Sources

Sources and review status

National guidance is shown before implementation-dependent detail. Apply principles in context and verify current guidance when a decision affects care. Source check completed 13 Sept 2026; clinical approval remains outstanding.

  • NCBI Subdural Empyema clinical reviewUpdated 6 October 2024; complete aetiology, presentation, imaging, management and complication body read 13 September 2026. Used for intracranial subdural anatomy, rapid deterioration, MRI/DWI, LP danger and combined drainage/antimicrobial principles; narrative review rather than a UK guideline, so drug and duration details were not universalised.
  • Contemporary subdural empyema cohortRetrospective tertiary-centre series published 2022; methods, clinical presentation, imaging, operative management and outcomes read 13 September 2026. Supports real-world surgical and source patterns but is single-centre Nigerian evidence and cannot define universal regimens or approaches.
  • ACR sinonasal disease criteriaACR Appropriateness Criteria 2021 update; intracranial-complication imaging sections read 13 September 2026. Supports contrast MRI for suspected intracranial extension including subdural empyema and abscess; US radiology guidance, not antimicrobial or surgical policy.
Authoring stateComplete draftClinical stateAwaiting reviewJurisdictionUnited Kingdom