eMedicine Specialties > Neurology > Neurological Infections

Subdural Empyema

Author: Segun T Dawodu, MD, JD, MBA, FAAPMR, FAANEM, CIME, DipMI(RCSed), Former Clinical Instructor, Mount Sinai Medical School; Current Director, Pain and Injuries Rehabilitation Services, PMRehab Pain and Sports Medicine Associates
Coauthor(s): Nicholas Y Lorenzo, MD, Chief Editor, eMedicine Neurology; Consulting Staff, Neurology Specialists and Consultants
Contributor Information and Disclosures

Updated: Mar 11, 2009

Introduction

Background

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 chapter 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.

Pathophysiology

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.

Frequency

United States

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.

Race

No documented race differences have been found, although geographical differences do exist.

Sex

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.

Age

Subdural empyema can occur at any age, but about two thirds of patients are aged 10-40 years.

Clinical

History

A patient with subdural empyema could present with any of the following symptoms:

• Fever - Temperature above 38°C (100.5°F)
• Headache - Initially focal and later generalized
• Recent history (<2 wk) of sinusitis, otitis media, mastoiditis, meningitis, cranial surgery or trauma, sinus surgery, or pulmonary infection
• Confusion, drowsiness, stupor, or coma
• Hemiparesis or hemiplegia
• Seizure - Focal or generalized
• Nausea or vomiting
• Blurred vision (amblyopia)
• Speech difficulty (dysphasia)
• History of intracerebral abscess (recent or in the past)

Physical

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

Causes

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, 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.

• Paranasal sinusitis -Staphylococcus aureus, alpha-hemolytic streptococci, anaerobic streptococci, Bacteroides species, Enterobacteriaceae
• Otitis media, mastoiditis - Alpha-hemolytic streptococci, Pseudomonas aeruginosa, Bacteroides species, S aureus
• Trauma, postsurgical infection -S aureus, Staphylococcus epidermidis, Enterobacteriaceae
• Pulmonary spread -S pneumoniae, Klebsiella pneumoniae
• 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.

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