Kin K. Jim, MScMatthijs C. Brouwer,

MD, PhDArie van der Ende, PhDDiederik van de Beek,

MD, PhD

Correspondence & reprintrequests to Dr. van de Beek:d.vandebeek@amc.uva.nl

CME

Subdural empyema in bacterial meningitis

ABSTRACT

Objective: To evaluate the occurrence, treatment, and outcome of subdural empyema complicat-ing community-acquired bacterial meningitis in adults.

Methods: Case series from a prospective nationwide cohort study from Dutch hospitals from2006 to 2011.

Results: Subdural empyema was diagnosed in 28 of 1,034 episodes (2.7%), and was present onadmission in 10 episodes and diagnosed during admission in 18. Predisposing conditions werepresent in 26 patients (93%), and consisted of otitis or sinusitis in 21 patients (75%). In all thesepatients the otitis or sinusitis spread to the subdural space. Twenty-three patients (82%) pre-sented with neurologic symptoms (paresis, focal seizures, dysesthesia contralateral to the empy-ema). Streptococcus pneumoniae was identified in 26 patients (93%) and Streptococcuspyogenes in 1 (3%); 1 patient had negative CSF cultures. Clinical course was frequently compli-cated with seizures (50%), focal neurologic abnormalities (54%), and hearing impairment (39%),causing an unfavorable outcome in 19 episodes (68%). Neurosurgical evacuation of the empy-ema was performed in 5 patients, all with considerable midline shift.

Conclusions: Although rare, subdural empyema must be considered in patients with community-acquired bacterial meningitis and otitis or sinusitis, focal neurologic deficits, or epileptic seizures.S pneumoniae is the predominant causative organism and neurosurgical intervention should beregarded as first-choice therapy in patients with empyema causing midline shift and focal neu-rologic abnormalities or a decreased level of consciousness. Neurology� 2012;79:2133–2139

GLOSSARYADC 5 apparent diffusion coefficient; DWI 5 diffusion-weighted imaging; NRLBM 5 Netherlands Reference Laboratory forBacterial Meningitis.

Bacterial meningitis is a life-threatening disease that requires immediate medical attention. The pre-dominant causative pathogens are Streptococcus pneumoniae and Neisseria meningitidis in adults,causing 80%–85% of all cases, with mortality rates varying from 19% to 37% for S pneumoniaeand 3%–13% for N meningitidis.1–4 Community-acquired bacterial meningitis is associated withserious intracranial complications such as cerebral infarctions, hydrocephalus, subdural empyema, andcerebral abscess, which can be life-threatening and may require neurosurgical treatment.2,3,5–10 Sub-dural empyema has only been reported as an uncommon complication of community-acquiredbacterial meningitis in adults.2–4,9,11,12 We investigated the occurrence, treatment, andoutcome of subdural empyemas in adults with community-acquired bacterial meningitis.

METHODS We included adults (defined as patients older than 16 years of age) who had bacterial meningitis and were listed in the

database of the Netherlands Reference Laboratory for Bacterial Meningitis (NRLBM) from March 2006 to November 2011 in a

nationwide prospective cohort study. The NRLBM receives CSF and blood isolates from approximately 90% of all patients with

CSF culture–positive bacterial meningitis in the Netherlands (population, 16.7 million).2,11,12 The NRLBM provided daily updates

of the names of the hospitals where patients with bacterial meningitis had been admitted in the preceding 2–6 days and the names of

physicians. Physicians were contacted, and informed consent was obtained from all participating patients or their legally authorized

representatives. Physicians could also contact the investigators without report of the NRLBM for inclusion of patients. Episodes

From the Departments of Neurology (K.K.J., M.C.B., D.v.d.B.) and Medical Microbiology (A.v.d.E.) and The Netherlands Reference Laboratoryfor Bacterial Meningitis (A.v.d.E.), Center of Infection and Immunity Amsterdam (CINIMA), Academic Medical Center, University of Amsterdam,Amsterdam, the Netherlands.

Study funding: Funding information is provided at the end of the article.

Go to Neurology.org for full disclosures. Disclosures deemed relevant by the authors, if any, are provided at the end of this article.

© 2012 American Academy of Neurology 2133

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reported by physicians with negative CSF cultures could also be

included if CSF results showed at least one individual predictor of

bacterial meningitis (defined as a glucose level of less than 34 mg/

dL [1.9 mmol/L], a ratio of CSF glucose to blood glucose of less

than 0.23, a protein level of more than 220 mg/dL, or a leukocyte

count of more than 2,000/mL)13 and the clinical presentation was

compatible with bacterial meningitis. Patients were considered

immunocompromised if they used immunosuppressive drugs or

had a history of splenectomy, diabetes mellitus, alcoholism, cancer,

or HIV infection. Patients with hospital-associated meningitis

(defined as meningitis that occurred during hospitalization or

within 1 week of discharge) including neurosurgery patients,

and patients with a neurosurgical device, or neurotrauma within

1 month of the onset of meningitis were excluded.

Case-record forms were used to collect data on patient history,

symptoms and signs on admission, clinical course, and outcome.

Treatment information regarding antimicrobial treatment and

(neuro)surgical interventions was collected. At discharge, all patients

underwent neurologic examination performed by a neurologist, and

the outcome was graded according to the Glasgow Outcome Scale.

The Glasgow Outcome Scale is a well-validated instrument with

good interobserver agreement.14 A favorable outcome was defined

as a score of 5, and an unfavorable outcome as a score of 1–4.

Patients were classified as having subdural empyema if reported

by the treating physician and cranial imaging showed a crescent- or

ellipse-shaped fluid collection in the subdural space. We chose to

classify all subdural fluid collections as empyemas, as subdural effu-

sion is a sterile fluid collection, mostly found in chronic disease.15

The differentiation between subdural empyema and effusion is

difficult even with contrast-enhanced CT or MRI, and therefore

one can also read “subdural empyema or effusion” when we use

“subdural empyema.” Cranial radiologic imaging was collected and

independently re-evaluated by 2 investigators (K.K.J., M.C.B.).

Midline shift was measured, and the volume of the empyema was

calculated using the ABC/2 method.16 To check for underreporting

by physicians, we evaluated 150 consecutive patients who under-

went cranial imaging in whom subdural empyema was not reported.

None of these patients had subdural empyema.

The Mann-Whitney U test was used to identify differences

between episodes with and without subdural empyema with respect

to continuous variables, and dichotomous variables were compared

with use of the x2 test. Pearson correlation test was used to identify

correlations between continuous variables. All tests were 2-tailed

and a p value,0.05 was considered significant. Statistical analyses

were performed with use of IBM SPSS Statistics, version 19.0.0.

Standard protocol approvals, registrations, and patient consents.The study was approved by the ethics committee of the AcademicMed-

ical Center, Amsterdam.

RESULTS From March 2006 to November 2011, weincluded 1,034 patients with bacterial meningitis. Atotal of 678 (66%) episodes were caused by S pneumo-niae, 107 (10%) by N meningitidis, and 165 (16%) byother bacteria. A total of 79 patients had negative CSFcultures but at least one individual CSF marker of bac-terial meningitis. Subdural empyema was diagnosed in28 of 1,034 episodes of bacterial meningitis (2.7%)and in 3.1% of 916 patients in whom cranial imagingwas performed. Subdural empyema was present onadmission in 10 patients (38%). In the remaining18 patients (64%) the empyema was detected dur-ing hospitalization with a median time to detectionof 5 days after admission (range 2–38 days).

The mean age at diagnosis was 58 years (range,25–81; table 1). Predisposing conditions for bacterial

Table 1 Clinical and laboratory features in 28adult bacterial meningitis patients withsubdural empyemasa

Clinical characteristics Values

Mean age, y (SD) 58 (14)

Male 19/28 (68)

Predisposing conditions 26/28 (93)

Otitis or sinusitis 21/28 (75)

Pneumonia 3/28 (11)

Immunocompromised stateb 8/28 (29)

Symptoms and signs on admission

Duration of symptoms >24 h 18/28 (64)

Headache 23/27 (85)

Nausea 10/26 (38)

Neck stiffness 20/28 (71)

Seizures 2/27 (7)

Temperature ‡ 38°C 22/28 (79)

Score on Glasgow Coma Scale (GCS) 10 (8–12)

GCS score <14 indicating alteredmental status

23/28 (82)

GCS score <8 indicating coma 6/28 (21)

Focal neurologic deficits 11/28 (39)

Aphasia 4/14 (29)

Ataxia 1/11 (9)

Paresis 7/28 (25)

Cranial nerve palsyc 3/26 (12)

CSF valuesd

Leukocyte count, cells/mm3 2,133 (415–4,665)

Protein, g/L 3.1 (1.6–5.7)

CSF-blood glucose ratio 0.04 (0.00–0.29)

Microbiologic findings

Positive CSF Gram staine 22/24 (92)

Positive blood culture 20/24 (83)

CSF culture

Streptococcus pneumoniae 26/28 (93)

Streptococcus pyogenes 1/28 (4)

Negative 1/28 (4)

aData are number/number evaluated (%) and continuous valuesare median (interquartile range) unless otherwise stated.b Immunocompromise was defined as the use of immuno-suppressive drugs or a history of splenectomy, diabetesmellitus, alcoholism, cancer, or HIV infection.cOculomotor nerve in 2 patients, abducens and facial nervein 1 patient each.dCSF leukocyte count was determined in 28 patients, CSF-blood glucose ratio in 27 patients, and CSF protein con-centration in 26 patients.eGram-positive cocci in 21 (88%) and Gram-negative rodsin 1 (4%).

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meningitis were present in 26 of 28 patients (93%)and consisted of otitis, sinusitis, pneumonia, or animmunocompromised state. Of the patients with pre-disposing conditions, 21 had otitis or sinusitis (75%).On admission, 23 patients (82%) had an altered men-tal status (defined by a score on the Glasgow ComaScale below 14) and 6 patients (21%) were comatose(Glasgow Coma Scale score,8). Focal neurologic def-icits were present on admission in 11 (39%) patients.The classic meningitis triad of neck stiffness, fever, andaltered mental status was present in 13 patients (46%).Of the 10 patients diagnosed with subdural empyemaon admission, 7 (70%) had a subacute presentationwith symptoms for more than 24 hours. Focal neuro-logic abnormalities were present in 6 of these 10 patients(60%). Twenty-five patients (89%) presented with neu-rologic symptoms (paresis, focal seizures, dysesthesia) onthe contralateral side of the empyema or effusion.Patients with subdural empyema were more likely tohave predisposing conditions on admission (93% vs54%; p , 0.001; table 2), especially otitis or sinusitis(75% vs 31%; p , 0.001), than patients withoutsubdural empyema. Furthermore, they were more likelyto present with a paresis on admission (25% vs 9%;p 5 0.007) than patients without subdural empyema.

Lumbar puncture was performed on admission inall patients. At least one individual CSF finding pre-dictive of bacterial meningitis (a glucose level of lessthan 34 mg/dL [1.9 mmol/L], a ratio of CSF glucoseto blood glucose of less than 0.23, a protein level of

more than 220 mg/dL, or a leukocyte count of morethan 2,000/mm3) was present in all patients withsubdural empyema. Eleven patients deteriorated clin-ically within 8 hours of initial lumbar puncture, buttranstentorial cerebral herniation with pupil dilationand abnormal posturing was not observed. The dete-rioration consisted of (increase in) hemiparesis in 6patients, respiratory failure in 4, and seizures in 4.Cranial imaging was repeated following deteriorationin 10 of 11 patients and did not show radiologic signsof transtentorial cerebral herniation. Gram staining ofCSF was done in 24 patients (86%) and showed pres-ence of bacteria in 22 patients (92%). CSF culturesshowed S pneumoniae in 26 patients, Streptococcuspyogenes in 1 patient, and 1 patient had a negativeCSF culture. The incidence of subdural empyemain patients with pneumococcal meningitis presentingwith otitis or sinusitis was 17 of 224 (8%). Patientswith subdural empyema were more likely to haveS pneumoniae as the causative microorganism com-pared to patients without empyema (93% vs 65%;p 5 0.002). Conversely, patients with pneumococcalmeningitis are more likely to have subdural empyemathan patients with meningitis due to another micro-organism (3.8% vs 0.6%, p , 0.001).

The subdural empyema was located at the left con-vexity in 12 patients, right convexity in 14 patients,and bilateral in 2 patients (figures 1 and 2). Cranialimaging was available for re-evaluation in 25 of 28patients. The median volume of the subdural empy-ema was 16.7 mL (range 1.6–129 mL). The subduralempyema caused a mass effect in 21 of 25 patients(84%), resulting in midline shift in 19 patients (76%).Medianmidline shift measured 3.0 mm (range 1.0–10.7mm), and midline shift over 4 mm occurred more oftenin patients under 60 years (p 5 0.016). The degree ofmidline shift was strongly correlated to the volume of theempyema (coefficient 0.533, p 5 0.02). Cranial MRIwas performed in 7 patients and included diffusion-weighted imaging (DWI) and apparent diffusion coeffi-cient (ADC) imaging in 4. On all these 4 MRIs thesubdural fluid collection showed a DWI hyperintenseand ADC hypointense signal (figure 2). This pattern istypical for subdural empyema, in contrast to subduraleffusions, which are hypointense on DWI.17

Other abnormalities on cranial imaging were sinus-itis or mastoiditis in 23 patients (82%), generalizedcerebral edema in 8 patients (28%), and cerebral abscessand infarction each in 2 patients (7%). Meningioma,sinus thrombosis, hydrocephalus, and intracerebralhemorrhage were each identified in 1 patient (3%). Inall 21 patients with mastoiditis the subdural empyemadeveloped on the same side.

Initial antimicrobial treatment consisted of a combi-nation of amoxicillin/penicillin and third-generationcephalosporins for 9 patients (32%), monotherapy

Table 2 Clinical and laboratory features in adults with and without subduralempyema among 1,034 episodes of bacterial meningitisa

Characteristic

Episodes withsubduralempyema (n 5 28)

Episodes withoutsubduralempyema (n 5 1,006) p Value

Age, y, mean (SD) 58 (14) 57 (18) 0.836

Predisposing conditions 26/28 (93) 548/1,006 (55) ,0.001

Otitis or sinusitis 21/28 (75) 314/1,005 (31) ,0.001

Symptoms and signs onadmission

Headache 23/27 (85) 734/877 (84) 0.836

Focal neurologic deficits 11/28 (39) 283/1,006 (28) 0.197

Paresis 7/28 (25) 87/921 (9) 0.007

Neurologic complications

Focal neurologicabnormalities

15/28 (54) 189/930 (20) ,0.001

Seizures 14/28 (50) 100/1,003 (10) ,0.001

Hearing impairment 11/28 (39) 193/840 (23) 0.045

Causative organism

Streptococcus pneumoniae 26/28 (93) 652/1,006 (65) 0.002

Outcome

Unfavorable outcome 19/28 (68) 383/1,003 (38) ,0.001

aData are number/number evaluated (%).

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ª 2012 American Academy of Neurology. Unauthorized reproduction of this article is prohibited.

penicillin or amoxicillin in 10 patients (36%), mono-therapy with a third-generation cephalosporin in 7patients (25%), and monotherapy carbapenem and acombination of penicillin and carbapenem each in1 patient (4%). All patients received microbiologicallyadequate initial antimicrobial therapy. The medianduration of antimicrobial treatment in survivingpatients was 17 days (range 11–62). The durationof treatment was not associated with the size of theempyema, with the causative microorganism, or withwhether neurosurgical removal of the empyema wasperformed. None of the patients had a relapse ofsymptoms after discontinuation of antimicrobial ther-apy. Adjunctive steroids were administered in 25 pa-tients (89%). Dexamethasone, given 10 mg every 6hours for 4 days started before or with the first dose ofantibiotics, was given in 24 patients (86%).

Nine patients underwent surgical treatment: cra-niectomy for evacuation of subdural empyema in 5patients, mastoidectomy in 4 patients, paracentesisin 3, and 1 patient required an external ventriculardrain for treatment of a hydrocephalus. All 5 patientswho underwent craniectomy survived, of whom 3had neurologic sequelae at discharge. The perfor-mance of craniectomy was associated with the degreeof midline shift (p 5 0.01), but not with the volumeof the empyema (p 5 0.41).

Complications developed during clinical course in27 of 28 patients (96%; table 3). Neurologic compli-cations occurred in all 27 and systemic complicationsin 11. Focal neurologic abnormalities developed in 15patients (54%), seizures in 14 (50%), and hearingimpairment in 11 (39%). In 10 of 11 episodes (91%)that were complicated by hearing impairment, otitis was

Figure 1 CTs of empyema complicating bacterial meningitis

Axial CT of patient with bacterial meningitis with bilateral subdural empyema (A), temporal subdural empyema (B), frontalsubdural empyema adjacent to intracerebral abscess causing brain shift (C), and parafalcine subdural empyema (D).

2136 Neurology 79 November 20, 2012

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diagnosed on admission. Five patients died (18%) and19 had an unfavorable outcome (68%; table 3). A high-er rate of unfavorable outcome was observed in patientswith subdural empyema compared to patients withmeningitis without subdural fluid collection (68% vs38%; p , 0.001). Thirteen of 23 survivors had neu-rologic sequelae on discharge (57%).

DISCUSSION Our study shows that subdural empy-ema complicates 2.7% of adult cases of community-acquired bacterial meningitis but is associated with ahigh rate of unfavorable outcome (68%). Subdural fluidcollection has been reported previously to occur in 1%–

3.4%.3,4,18 Important clues for the diagnosis of empyemawere otitis or sinusitis, focal neurologic deficits, or epi-leptic seizures. For patients with meningitis who developneurologic complications during admission, cranialimaging to detect subdural empyema is indicated.3,19

MRI with DWI remains the preferred imaging modality

for detecting subdural empyema. DWI and diffusion onthe ADC map have proven to be valuable in evaluationof intracranial pyogenic processes (abscess and empy-ema). Furthermore, DWI can distinguish subduralempyema from reactive subdural effusion.17

The incidence of subdural empyema in patients withpneumococcal meningitis presenting with otitis washigh (8%). In all patients with otitis or sinusitis the bac-teria spread from the mastoid or sinus to the adjacentsubdural space causing the subdural empyema. Becauseof the increased risk of empyema in patients with otitisor sinusitis, consultation of an ear, nose, and throatspecialist is warranted early during clinical course inall patients with bacterial meningitis.

Only a minority of patients underwent neurosurgicalevacuation of the empyema. In our series, midline shiftwas associated with the decision to evacuate the empy-ema and increased shift was associated with youngerage rather than thickness or volume of the empyema.

Figure 2 MRIs of empyema complicating bacterial meningitis

Axial (A) and sagittal (B) T1-weighted gadolinium-enhanced MRI of patients with parafalcine subdural empyema (arrows/as-terisks), and diffusion-weighted (C) and apparent diffusion coefficient (D)–weightedMRI of a subdural empyema over the leftconvexity (arrows).

Neurology 79 November 20, 2012 2137

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This may well be explained by age-related cerebral atro-phy. In our study, all 5 patients with subdural empyemawho underwent craniectomy survived, albeit with neu-rologic sequelae at discharge in 3 of them. Nevertheless,neurosurgical intervention should be regarded as first-choice therapy in patients with empyema causingmidline shift and focal neurologic abnormalities ora decreased level of consciousness.

A substantial number of patients deteriorated inthe first 8 hours after lumbar puncture, developingseizures, respiratory failure, and hemiparesis contra-lateral to the empyema. These symptoms may be ex-plained by local expansion of the empyema but couldalso be the result of brain shift following the lumbarpuncture, although no transtentorial cerebral hernia-tion was observed on cranial imaging. Patients withsubdural empyema should be carefully monitored fol-lowing lumbar puncture, as the empyema couldexpand and cause brain shift.

In our study, the median duration of antimicrobialtreatment in surviving patients was only 17 days, and

was not associated with the size of the empyema, mid-line shift, or whether the empyema was neurosurgi-cally evacuated. The optimal duration of antimicrobialtreatment for patients with subdural empyema or effu-sion has not been established in trials or comparativestudies, but general recommendations are to treat pa-tients with empyema for 3–4 weeks if an empyemahas been evacuated, and even longer if the patient isconservatively treated.20 This indicates that subduralempyemas do not trigger Dutch physicians to prolongantimicrobial treatment, but also that relatively shortcourses of antibiotics do not result in microbiologic treat-ment failures in these patients.

Our study has several important limitations. First,cranial imaging was not performed in all patients inthe cohort and cases of subdural fluid collectionmight have been missed. This could have led to anunderestimation of the incidence of subdural empy-ema or effusion. Furthermore, subdural empyemasthat remain subclinical may go undetected, whichmay lead to an overestimation of the severity of thedisorder in our study. Asymptomatic subdural collec-tions may resolve without neurosurgical intervention.Second, culture-negative patients are underrepresentedin our study. Negative CSF cultures occur in 11%–

30% of patients with bacterial meningitis.1,2,4 Thesepatients were only included if the treating physiciancontacted the investigators, which occurred in 11% ofthe episodes.21 Third, the diagnosis subdural effusionor subdural empyema was classified by the treatingphysician, and therefore it is unclear if the differenti-ation between subdural empyema and subdural effusionalways occurred in a similar fashion. To differentiatebetween subdural empyema and subdural effusioncontrast-enhanced cranial imaging is necessary. Somepatients did not undergo contrast-enhanced cranialimaging, and therefore the differentiation betweenempyema and effusion may not have been accurate inall cases.

Although rare, subdural empyema must be consid-ered in patients with community-acquired bacterialmeningitis and otitis or sinusitis, focal neurologic def-icits, or epileptic seizures. S pneumoniae is the pre-dominant causative organism and patients are at highrisk of developing seizures and unfavorable outcome(68%). Therefore, early diagnosis of empyema is nec-essary and neurosurgical intervention should be regardedas first-choice therapy in patients with empyema causingmidline shift and focal neurologic abnormalities or adecreased level of consciousness.

AUTHOR CONTRIBUTIONSKin K. Jim, Matthijs Brouwer, and Diederik van de Beek performed the data

analyses and wrote the manuscript. Arie van der Ende wrote the manuscript.

Diederik van de Beek was the principal investigator of the study and

provided funding.

Table 3 Complications and outcome in 28 adultbacterial meningitis patients withsubdural empyemaa

Clinical characteristics Values

Neurologic complications 27/28 (97)

Impairment of consciousness 19/28 (68)

Focal neurologic deficits 15/28 (54)

Hearing impairment 11/28 (39)

Seizures 14/28 (50)

Cerebrovascular complicationsb 4/28 (14)

Cerebral abscess 2/28 (7)

Hydrocephalus 1/28 (4)

Systemic complications 13/28 (46)

Pneumonia 4/28 (14)

Respiratory failure 7/28 (25)

Otherc 4/28 (15)

Glasgow Outcome Scale

1) Death 5 (17)

2) Vegetative state 0

3) Severe disability 1 (3)

4) Moderate disability 13 (46)

5) Complete recovery 9 (32)

Neurologic sequelaed 13/28 (46)

aData are number/number evaluated (%).bCerebral infarction in 2, sinus thrombosis in 1, and intra-cranial hemorrhage in 1.cOsteomyelitis, hyponatremia, rhabdomyolysis, and deepvenous thrombosis of the arm each occurred in 1 patient.dHemiparesis in 9 patients, sensory change in 7 patients,cognitive impairment in 6, cranial nerve palsy in 6, ataxiaand aphasia both occurred in 1 patient.

2138 Neurology 79 November 20, 2012

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STUDY FUNDINGD.v.d.B. is supported by grants from the Netherlands Organization for

Health Research and Development (ZonMw; NWO-Vidi grant 2010),

the Academic Medical Center (AMC Fellowship 2008), and the Euro-

pean Research Council (ERC Starting Grant 2011).

DISCLOSUREThe authors report no disclosures relevant to the manuscript. Go to

Neurology.org for full disclosures.

Received April 23, 2012. Accepted in final form July 31, 2012.

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