Subdural empyema (ie, abscess) is an intracranial focal collection of purulent material located between the dura mater and the arachnoid mater. About 95% of subdural empyemas are located within the cranium; most involve the frontal lobe, and 5% involve the spinal neuraxis. This article focuses on the intracranial type, which causes clinical problems through extrinsic compression of the brain by an inflammatory mass and inflammation of the brain and meninges.
Subdural empyema is a life-threatening infection that was first reported in the literature about 100 years ago. It accounts for about 15-22% of focal intracranial infections. The mortality rate approached 100% before the introduction of penicillin in 1944 and has declined since that time. Because the symptoms might be very mild initially, rapid recognition and treatment are important; the early institution of appropriate treatment gives the patient a good chance of recovery with little or no neurological deficit.
Subdural empyema is a primarily intracranial infection located between the dura mater and the arachnoid mater. It has a tendency to spread rapidly through the subdural space until limited by specific boundaries (eg, falx cerebri, tentorium cerebelli, base of the brain, foramen magnum). The subdural space has no septations except in areas where arachnoid granulations are attached to the dura mater. Subdural empyema is usually unilateral.
With progression, subdural empyema has a tendency to behave like an expanding mass lesion with associated increased intracranial pressure and cerebral intraparenchymal penetration. Cerebral edema and hydrocephalus also may be present secondary to disruption of blood flow or cerebrospinal fluid (CSF) flow caused by the increased intracranial pressure. Cerebral infarction may be present from thrombosis of the cortical veins or cavernous sinuses or from septic venous thrombosis of contiguous veins in the area of the subdural empyema.
In infants and young children, subdural empyema most often occurs as a complication of meningitis. In such cases, subdural empyema should be differentiated from reactive subdural effusion (ie, sterile collection of fluid due to increased efflux of intravascular fluids from increased capillary wall fenestrations into the subdural space). In older children and adults, it occurs as a complication of paranasal sinusitis, otitis media, or mastoiditis.
Infection usually enters through the frontal or ethmoid sinuses; less frequently, it enters through the middle ear, mastoid cells, or sphenoid sinus. This often occurs within 2 weeks of a sinusitis episode, with the infection spreading intracranially through thrombophlebitis in the venous sinuses. Infection also may extend directly through the cranium and dura from an erosion of the posterior wall of the mastoid bone or frontal sinus. Direct extension also could be from an intracerebral abscess. Rarely, infection spreads hematogenously from distant foci, most commonly from a pulmonary source or as a complication of trauma, surgery, or septicemia. The sphenoid sinus also could be a source of infection.
Subdural empyema accounts for 15-22% of focal intracranial infections. Sinusitis is the most common predisposing factor in the developed world.
International
Frequency is similar to that in the Unites States. However, otitis media and mastoiditis are the most common predisposing conditions.
Mortality/Morbidity
In the pre-antibiotic era, the mortality rate approached 100%; this still may be the case in developing countries.
In the developed world, the mortality rate has improved tremendously: it is about 6-35% (variance depending on areas and hospitals); however, about 55% of patients have neurological deficits at the time of hospital discharge.
The mortality rate has continued to decline because of early diagnosis and treatment, more accurate localization with head CT scan, early sinus drainage, and recognition of the prominent role of anaerobes in the disease.
The high incidence of morbidity (ie, neurological deficits) is attributed to the short follow-up period and low mortality rate. Very ill patients who would have died in the past now survive with deficits.
Sex- and age-related demographics
Subdural empyema is more common in males, who can account for up to 80% of cases. The reason for this predominance is unknown. One theory is that the normal development of the paranasal sinuses in males results in anatomic differences that predispose them to recurrent sinusitis.
Subdural empyema can occur at any age, but about two thirds of patients are aged 10-40 years.
A patient with subdural empyema may show some of the following signs:
Mental status changes - Confusion, drowsiness, stupor, and coma
Meningismus or meningeal signs
Hemiparesis or hemisensory deficits
Aphasia or dysarthria
Seizure
Sinus tenderness, swelling, or inflammation
Papilledema and other features of increased intracranial pressure, such as nausea/vomiting, mental status changes, and gait disturbance
Homonymous hemianopsia
Palsies of cranial nerves III, V, or VI, especially if the abscess is near a petrous portion of the temporal bone, causing facial pain and lateral rectus muscle weakness
Fixed, dilated pupil on the ipsilateral side due to compression of cranial nerve III
The most common cause is extension from paranasal sinusitis, especially from the frontal and ethmoidal sinuses. It could also arise as a complication of otitis media, mastoiditis, septicemia, subdural hematoma,[2] cranial trauma or surgery, or recent sinus surgery; by spread or extension from an intracerebral abscess; by hematogenous spread from pulmonary sources; or from septic thrombosis of cranial veins. Common causative organisms are anaerobes, aerobic streptococci, staphylococci, Haemophilus influenzae,Streptococcus pneumoniae, and other gram-negative bacilli.
Meningitis (infant or child) -S pneumoniae,H influenzae,Escherichia coli,Neisseria meningitidis
Neonates - Enterobacteriaceae, group B streptococci, Listeria monocytogenes
Others include hematogenous spread from skin postsurgery (eg, abdominal surgery). Spread from a focus of tuberculosis infection could also occur. A case of subdural empyema developing after infection with Plasmodium falciparum malaria.
Cranial MRI is now the imaging study of choice, being superior to cranial CT scan in outlining the extent of subdural empyema and demonstrating the convexity and interhemispheric collections.
MRI also shows greater morphological detail than CT scan.
The sensitivity of MRI is improved by using gadolinium contrast medium. See the image below.
View Image
MRI scan of a subdural empyema in the left parietal area.
Cranial CT[3] scan was the standard technique for quick diagnosis before the advent of MRI. The use of high-resolution, contrast-enhanced CT scan increases diagnostic yield, although it sometimes gives equivocal or normal results.
On CT scan, subdural empyema shows as a hypodense area over the hemisphere or along the falx; the margins are better delineated with the infusion of contrast material. Cerebral involvement also is visible.
Cranial osteomyelitis may be seen.
CT scan is the modality of choice if the patient is comatose or critically ill and MRI is not possible or is contraindicated. See the image below.
View Image
CT scan of a subdural empyema in the left temporal/parietal area.
Cranial ultrasound[4] has been helpful in differentiating subdural empyema from anechoic reactive subdural effusion in infants with meningitis accompanied by complex features (eg, increased echogenicity in the convexity collections, presence of hyperechoic fibrinous strands or thick hyperechoic inner membrane, and increases in echogenicity of the pia-arachnoid).
Lumbar puncture is currently contraindicated because of possible cerebral herniation from increased intracranial pressure.
Lumbar puncture may be performed in the course of a workup to rule out meningeal infection when increased intracranial pressure has been excluded.
CSF examination[5] is an adjunctive test in the diagnosis of subdural empyema and may be obtained in addition to the other diagnostic tests previously outlined. CSF findings include the following:
WBC count (predominantly polymorphonuclear neutrophils) is increased. A significant increase (>50/µL) may be seen, although a slightly elevated cell count of 5-20/µL (reference range, 0-5/µL) does not rule out the possibility of subdural empyema.
Increased protein level greater than 100 mg/dL may be seen (reference range, 20-40 mg/dL), although less substantial elevations (50-90 mg/dL) do not rule out the possibility of subdural empyema.
Decreased glucose levels of 40 mg/dL or less usually are seen (reference range, 50-80 mg/dL). CSF glucose levels should be normalized with a blood glucose level obtained concurrently.
Occasionally, the CSF is normal and sterile in these cases.
The specific CSF findings should be compared with the accepted normal values of the treating physician's laboratory.
Maintain an adequate airway and ensure breathing and circulation by supportive care (eg, oxygen). Establish an intravenous line with adequate monitoring while en route to the emergency department.
Emergency department care
Continue supportive treatment (ie, ABCs) directed toward stabilizing the patient. Request necessary imaging studies and laboratory tests. Commence antibiotic therapy as soon as possible with broad coverage for anaerobes, staphylococci, and aerobic streptococci.
The neurosurgical team should be involved; thoracic surgery and otolaryngology teams also should be consulted if necessary.
Other
Antibiotic therapy[6] alone may be adequate for small subdural empyema (ie, < 1.5 cm diameter). Because of the aggressive nature of this disease, however, this option is not widely utilized.[7] This is an option for patients with major contraindications to surgery or significant mortality risks.
Other medical interventions may include medications for seizure treatment or prophylaxis. Treatment for increased intracranial pressure also has been advocated.
Immediate neurosurgical drainage[8] of the subdural empyema should be considered. The primary surgical option is craniotomy, which allows wide exposure, adequate exploration, and better evacuation of the purulent collection than other procedures. Stereotatic burr hole placement with drainage and irrigation is another option but is less desirable because of decreased exposure and possible incomplete evacuation of the purulent material.[9]
Drainage and debridement of the primary source of infection may be necessary. Samples should be collected for Gram staining, culture, and sensitivity tests.
Patients with contraindications to surgery or significant mortality risks may receive antibiotic therapy alone.[10]
Other surgical interventions may be required to debride or evacuate the primary source of infection. Such efforts may require an otolaryngologist for paranasal sinusitis (eg, bilateral antral washout, mastoidectomy for recurrent chronic mastoiditis, grommets for recurrent otitis media) or a thoracic surgeon for a chronic lung abscess.
Neurosurgery, otolaryngology, and thoracic surgery consultations
Physical medicine and rehabilitation for physical therapy, gait and balance training, occupational therapy, and speech therapy
Clinical psychologist for treatment of any residual cognitive deficit
Ophthalmology or optometry consult if a visual defect is present, especially in patients with palsies of cranial nerves III, V, or VI, or visual field defects (eg, homonymous hemianopsia)
Home care aides and social work for issues after discharge (About 55% of patients have neurological deficits on discharge.)
Clinical Context:
Third-generation cephalosporin with broad-spectrum activity including gram-negative organisms; lower efficacy against gram-positive organisms; higher efficacy against resistant organisms. Arrests bacterial growth by binding to 1 or more penicillin-binding proteins.
Clinical Context:
Beta-lactamase-stable antistaphylococcal agent. Use parenteral therapy initially in severe infections. Change to oral therapy as condition warrants.
Because of risk of thrombophlebitis, particularly in elderly patients, administer parenterally only for short term (1-2 d); change to oral route as clinically indicated.
Clinical Context:
Indicated for patients who cannot receive or have not responded to penicillins and cephalosporins or have infections with resistant staphylococci. Used in conjunction with gentamicin for prophylaxis in penicillin-allergic patients undergoing GI or genitourinary procedures.
To avoid toxicity, current recommendation is to assay vancomycin trough levels after third dose drawn 0.5 h prior to next dosing. Use CrCl to adjust dose in patients diagnosed with renal impairment.
Clinical Context:
Third-generation penicillin with bactericidal activity against susceptible organisms. Alternative to amoxicillin when unable to take medication orally.
Appropriate antibiotics always should be given in addition to any surgical intervention. While awaiting the results of the Gram stain and culture and sensitivities, empirical antibiotic therapy should be instituted against anaerobes, aerobic streptococci, and staphylococci. The antibiotics should be given for a period of 3-6 wk with close monitoring of clinical status.
Recurrence of subdural empyema requires immediate surgical evacuation. If a burr hole was the initial surgical procedure, a craniotomy flap should be considered.
Complications such as seizures and subdural effusion may require more aggressive treatment modalities.
Assess and treat residual neurological deficits. Inpatient rehabilitation (either subacute or acute) may be necessary.
Education should emphasize compliance with medication. Urge patients to follow the advice and instructions of rehabilitation programs. The following should be emphasized:
The need to complete the full course of antibiotics
Regular intake of antiseizure medication, if prescribed
A helmet to protect the area of craniotomy
Home exercise program
For excellent patient education resources, visit eMedicineHealth's Brain and Nervous System Center and Infections Center. Also, see eMedicineHealth's patient education articles Brain Infection and Antibiotics.
Segun Toyin Dawodu, JD, MD, MS, MBA, LLM, FAAPMR, FAANEM, Attending Interventional Physiatrist, Wellspan Health
Disclosure: Nothing to disclose.
Coauthor(s)
Nicholas Lorenzo, MD, MHA, CPE, Co-Founder and Former Chief Publishing Officer, eMedicine and eMedicine Health, Founding Editor-in-Chief, eMedicine Neurology; Founder and Former Chairman and CEO, Pearlsreview; Founder and CEO/CMO, PHLT Consultants; Chief Medical Officer, MeMD Inc; Chief Strategy Officer, Discourse LLC
Disclosure: Nothing to disclose.
Specialty Editors
Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Received salary from Medscape for employment. for: Medscape.
Florian P Thomas, MD, PhD, MA, MS, Chair, Neuroscience Institute and Department of Neurology, Director, National MS Society Multiple Sclerosis Center and Hereditary Neuropathy Foundation Center of Excellence, Hackensack University Medical Center; Founding Chair and Professor, Department of Neurology, Hackensack Meridian School of Medicine at Seton Hall University; Professor Emeritus, Department of Neurology, St Louis University School of Medicine; Editor-in-Chief, Journal of Spinal Cord Medicine
Disclosure: Nothing to disclose.
Chief Editor
Niranjan N Singh, MBBS, MD, DM, FAHS, FAANEM, Adjunct Associate Professor of Neurology, University of Missouri-Columbia School of Medicine; Medical Director of St Mary's Stroke Program, SSM Neurosciences Institute, SSM Health
Disclosure: Nothing to disclose.
Additional Contributors
Edward L Hogan, MD, Professor, Department of Neurology, Medical College of Georgia; Emeritus Professor and Chair, Department of Neurology, Medical University of South Carolina
){kind=link}
){kind=link}