General
- Empyema is a collection of pus within a normal anatomical space therefore a collection in the subdural space is deemed an empyema
- Frontal most
Epidemiology (Osborn and Steinberg, 2007).
- It occurs most commonly in the second decade of life
- M:F, 3:1
- Less common than cerebral abscess (ratio of abscess:empyema is ≈ 5:1).
- Found in 32 cases in 10,000 autopsies.
Pathology
- Subdural empyema has the propensity to spread rapidly due to lack of fibrin capsule and anatomical barriers in the subdural space
- Anaerobes
- Concomitant (Osborn and Steinberg, 2007)
- Cerebral abscess may occur in 6– 22%
- Epidural abscess in 9– 17%
- Location
- 70–80% are over the convexity,
- 10–20% are parafalcine.
Pathogen
- Most monomicrobial
- The causative microorganisms vary according to the primary source of infection.
- Paranasal sinuses
- Polymicrobial infections (Nathoo et al., 1999).
- Mastoiditis or sinusitis
- Aerobic and microaerophilic Streptococci (Miller et al., 1987).
- Postoperative and post- traumatic subdural empyema
- Immunocompetent: Staphylococcus aureus
- Immunocompromised: Klebsiella pneumonia (Greenlee et al., 2003).
- Other causative microorganisms that have been reported include Escherichia coli and Salmonella species (Munusamy and Dinesh, 2015).
- The success rate for culturing bacteria from surgically evacuated subdural pus ranges from 54% to 81% (Mauser et al., 1987; Nathoo et al., 1999).
- Low culture positivity due to
- Use of broad- spectrum antibiotics as empirical treatment for infection before sampling
- Difficulties in culturing anaerobic organisms.
Aetiology (Munusamy and Dinesh, 2015).
- Otitis media, mastoiditis
- Most common
- Aerobic and anaerobic streptococci
- S. aureus was not a common pathogen in sinusitis-related SDE
- Postcraniotomy infection
- Staphylococci and Gram-negative species
- CSDH evacuation
- Craniotomy > burr hole drainage.
- Presumably, the relatively simple and limited procedure minimizes tissue trauma and reduces the extent of bacterial inoculation.
- Propionibacterium acnes, a ubiquitous skin commensal can rarely be implicated with an indolent clinical presentation and course of progression (Gritchley and Strachan, 1996)
- Posttraumatic (penetrating injuries)
- Staphylococci and Gram-negative species
- Paranasal sinusitis
- Hematogenous dissemination
- Osteomyelitis of calvarium
- Purulent bacterial meningitis
- Organisms in SDE associated with sinusitis
- Sterile cultures occur in up to 40% (some of which may be due to fastidious anaerobes and/or previous exposure to antibiotics).
Organisms | % |
Adult cases | ㅤ |
Aerobic streptococcus | 30–50 |
Staphylococci | 15–20 |
Microaerophilic and anaerobic strep | 15–25 |
Aerobic Gram-negative rods | 5–10 |
Other anaerobes | 5–10 |
Childhood | ㅤ |
Organisms are similar to meningitis for the same age group. Antibiotics choice is the same as for meningitis | ㅤ |
Complication
- Cerebral abscess (seen in 20–25% of imaging studies in patients with SDE),
- Cortical venous thrombosis with risk of venous infarction
- Localized cerebritis.
Clinical presentation
- SDE should be suspected in the presence of meningismus + unilateral hemisphere dysfunction.
- Fever, headache, and altered mental state >>> rapid neurological deterioration.
- Focal neurologic deficit and/or seizures usually occur late.
- Seizures
- occur in up to 63% of patients (Cowie and Williams, 1983).
- The median time from the onset of symptoms to diagnosis is two days (French et al., 2014).
- Marked tenderness to percussion or pressure over affected air sinuses is common.31
- Forehead or eye swelling (from emissary vein thrombosis) may occur.
- Symptoms are due to mass effect, inflammatory involvement of the brain and meninges, and thrombophlebitis of cerebral veins and/or venous sinuses.
- Progression into an expanding mass lesion → raised ICP.
- Disruption of cerebral blood flow or CSF flow. → Cerebral oedema and hydrocephalus
- Direct spread or septic emboli → Thrombosis of the cortical veins or dural venous sinuses → venous hypertension → may progress to cerebral infarction.
- Other presenting symptoms will depend on underlying aetiology for example sinusitis, mastoiditis, otitis media, meningitis, postoperative wound infection, systemic infection, or head trauma.
- Findings on presentation with SDEᵃ
- ᵃfrom a review of multiple articles
Finding | % |
Fever | 95 |
H/A | 86 |
Meningismus (nuchal rigidity...) | 83 |
Hemiparesis | 80 |
Altered mental status | 76 |
Seizures | 44 |
Sinus tenderness, swelling or inflammation | 42 |
Nausea and/or vomiting | 27 |
Homonymous hemianopsia | 18 |
Speech difficulty | 17 |
Papilledema | 9 |
Evaluation
LP
- ❌ potentially hazardous (risk of herniation).
- Organisms are usually present only in cases originating from meningitis.
- If no meningitis, usually see findings consistent with a parameningeal inflammatory process
- Moderate sterile pleocytosis (150–600 WBC/mm3) with PMNs predominating;
- Glucose normal;
- Opening pressure is usually high;
- Protein is usually elevated (range: 75–150mg/dl)
Radiological
- Radiological features
- Crescent shaped collection
- Dense enhancement of medial membrane
- Crosses suture lines
- On the surface of the brain
- Below the cranial vault or adjacent to the falx or tentorium
- Fq is rim enhancement with administration of contrast media.
- CT
- May miss small lesions.
- Lesion is hypodense (but denser than CSF)
- Images
- CT+C
- If CT+C show no enhancement due to chronic empyema forming well- organized subdural pus (Moseley and Kendall, 1984; Munusamy and Dinesh, 2015)
- MRI
- Low signal on T1WI
- High signal on T2WI
- MRI+C
- More sensitive than CT+C in detecting
- Chronic organized empyema
- Empyema located at the skull base, in the posterior fossa, or along the falx cerebri.
- MRI+DWI: DIffusion restriction
- High signal intensity on DWI
- Low signal intensity on ADC maps
- Can reliably distinguish subdural empyema from subdural hematoma or reactive subdural effusion that may also occur after trauma, surgery, or meningitis (Wong et al., 2004).
Treatment
- Almost all need Surgery
- Antibiotic penetration into subdural space is poor.
- Nonsurgical management has been reported but rarely done,
- Indicated if
- Minimal neurologic involvement,
- Limited extension
- Limited mass effect
- Early favorable response to antibiotics
- Time to treatment
- <72HRs disability 10%
- >72 hrs disability 70%
- Goal of treatment
- Bacteriological identification
- Eradication of the primary foci of infection
- Adequate antibiotic therapy (Miller et al., 1987).
- Surgical options
- Indicated for
- Non-viscous empyema
- Non-loculated empyema
- Early in the course, the pus tends to be more fluid and may be more amenable to burr hole drainage; later, loculations develop which may necessitate craniotomy
- Critically ill patients with localized SDE
- Advantage
- Avoid potential surgical complications associated with longer duration or more complex surgery.
- If Post CSDH Burrhole just reopen and washout but if this is insufficient conversion to craniotomy is mandatory.
- Usually inadequate if loculations are present
- Repeat procedures may be needed, and up to 20% will later require a craniotomy
- Indicated for
- Thicked organized empyema (Munusamy and Dinesh, 2015)
- Craniotomy to debride and, if possible, drain.
- A wide craniotomy is often required because of septations.
- The dura appears white because of pus underneath.
- Open and wash out subdural space.
- Do not try to remove material adherent to cortex (may cause infarction)
- Indicated for
- Thicked organized empyema with significant brain swelling
- In postoperative setting if there is intraoperative suspicion of osteomyelitis of the bone flap which may act as a devascularized nidus of ongoing infection.
- Results of all three have been shown to be comparable as long as effective drainage of purulent material and relief of mass effect was achieved (Bok and Peter, 1993).
- Early studies indicated a better outcome with craniotomy than with burr holes.
- Recent studies show less difference
Burr hole
Craniotomy
Craniectomy
Burrhole vs craniotomy vs craniectomy: which one is the best
- Treat primary source
- Exploration and drainage of the primary source (Otologic or extracranial)
- Anticonvulsants
- Usually given prophylactically
- Mandatory if seizures occur
- Antibiotic
- Initiation of empirical antibiotic therapy without delay is recommended if the patient is septic and clinically unwell from the subdural empyema.
- Further antimicrobial therapy should be targeted against the causative microorganisms revealed by
- Gram stain or special bacterial stains,
- Positive bacterial culture result
- Knowledge of the bacterial profile at the primary site of infection.
- Duration: 4– 6 weeks
- Depending on the clinical and radiological response (Leys et al., 1986).
Outcome
- Outcome depends on factors such as age, comorbidities, primary organism, and prompt diagnosis and treatment.
- Mortality rate of up to 20% and morbidity rate of 50% despite intervention (Le Beau et al., 1973; Nathoo et al., 1999)
- Fatal cases may have associated venous infarction of the brain.
- Neurologic deficits
- Tend to improve following treatment,
- But were present in 55% of patients at the time of discharge from the hospital.
- Poor prognostic factors
- Age≥ 60 years,
- Obtundation or coma at presentation,
- SDE related to surgery or trauma (rather than sinusitis)
- Burr-hole drainage may be associated with a worse outcome than with craniotomy,
- Might be confounded by the poorer condition of these patients.
- Outcome with SDE
Outcome | % |
Persistent seizures | 34 |
Residual hemiparesis | 17 |
Mortality | 10–20 |
- Compares patient mortality with level of consciousness at presentation.
- Those patients presenting awake and alert (grade I) have the greatest chance of survival and those presenting unresponsive to pain (grade IV) are least likely to survive.
- Patients who are drowsy and disoriented (grade II) or responsive only to painful stimuli (grade III) have intermediate survival statistics.
- Of the survivors, decreased level of consciousness at presentation correlates with more severe neurologic sequelae (4,7,8).
- Association of level of consciousness with mortality in SDE
- I = awake and alert; II = drowsy and disoriented; III = responsive to painful stimuli; IV = unresponsive to pain.
Reference | Grade I (No., Deaths) | Grade II (No., Deaths) | Grade III (No., Deaths) | Grade IV (No., Deaths) |
Bradley and Shaw (1) | 20, 0 | 18, 9 | 0, 0 | 5, 5 |
Mauser et al. (4) | 16, 1 | 36, 5 | 22, 6 | 24, 10 |
Hodges et al. (7) | 0, 0 | 5, 0 | 7, 0 | 2, 2 |
Khan and Griebel (8) | 2, 0 | 8, 0 | 4, 1 | 1, 1 |
Hockley and Williams (9) | 7, 1 | 22, 1 | 0, 0 | 13, 5 |
Bannister et al. (12) | 22, 2 | 30, 10 | 6, 1 | 8, 6 |
Dill et al. (18) | 13, 0 | 12, 0 | 5, 2 | 2, 1 |
Morgan and Williams (27) | 1, 1 | 4, 1 | 0, 0 | 2, 2 |
Total | 81, 5 | 135, 26 | 44, 10 | 57, 32 |
% Deaths | 6% | 19% | 23% | 56% |