History
An intracranial epidural abscess (IEA) may have a more insidious and subacute onset than a subdural empyema, as symptoms may develop over days to weeks. Symptoms of the initiating infection (eg, sinusitis) may be the patient's chief complaint rather than neurological symptoms.
Critical elements in the patient's history include: current or recent frontal sinus infection, otologic infection (eg, otitis media), osteomyelitis of the skull base (eg, mastoiditis), head trauma with or without known post-traumatic infection, recent intracranial surgery (particularly with surgical site infection), congenital defects of the skull base, and immunocompromising conditions (eg, HIV, diabetes, chemotherapy). [13]
Signs and symptoms
Patients often present with a headache that is either diffuse or localized to one side with scalp tenderness. Headache may be the only presenting symptom. Purulent discharge from the ears or sinuses, periorbital swelling, and edema of the scalp might occur. The patient may have persistent fever that develops during or after treatment for a sinus or middle ear infection. In cases of congenital skull defects or in trauma, the provider should check for signs of cerebrospinal fluid (CSF) leakage, such as CSF otorrhea and rhinorrhea, and ask if the patient has had related symptoms, such as a salty or metallic taste in their mouth.
As IEAs tend to enlarge slowly, neurological deficits usually develop later in the course of the illness, particularly when complicated by a subdural empyema, at which point the patient might present with neck stiffness, nausea, vomiting, lethargy, and hemiparesis. Seizures may also be a presenting symptom in some cases.
As the lesion enlarges, signs and symptoms of increased intracranial pressure (ICP) may occur (eg, nausea, vomiting, altered consciousness, blurry vision, papilledema). Rarely, when the epidural abscess develops near the petrous bone and involves the fifth and sixth cranial nerves, the patient may present with ipsilateral facial pain and weakness of the lateral rectus muscle (Gradenigo syndrome). Often, the patient may have scalp cellulitis, a surgical site infeciton, sinusitis, or a skull fracture.
One should consider the diagnosis of IEA when a patient presents with unresolved frontal sinus symptoms. Also consider this diagnosis in patients with new neurological symptoms after trauma or cranial surgery, even if weeks to months have elapsed since the operation or trauma. The clincial onset may still be acute in some cases, however.
Mittal et al. detail the case of an 11-year-old girl who presented with typical features of meningitis, suggesting that sinusitis can rarely be latent and present directly with intracranial complications. The patient underwent neuroimaging because of slow improvement and concern for a brain abscess. Although no history or examination findings were suggestive of sinusitis, the patient was found to have pansinusitis with intracranial extension causing meningitis and IEA. [15]
Causes
As mentioned, the intracranial epidural space is a potential space, as the dura is generally adherent to the inner table of the skull (particularly in older patients). Intracranial epidural abscess (IEA) most commonly results from an infection that begins more superficially.
The most common etiology is direct, continguous spread from sinusitis (mastoid, ethmoid, sphenoid, and frontal sinusitis), otologic infection (eg, otitis media), or orbital cellulitis. Other causes include trauma (eg, with associated skull fracture), and following neurosurgical procedures (eg, craniotomy, hardware implantation), especially when there is violation of the frontal sinus, an SSI, or if the patient has undergone multiple reoperations. [3, 4] Other etiologies include extension from cranial osteomyelitis, sagittal sinus phlebitis, and mucormycosis. [16] Although hematogenous spread (eg, in the setting of bacteremia) from a remote site of infection is a common cause of spinal epidural abscess, it is a rare cause of IEA. [13]
Mallur et al. reported on 11 children with acute mastoiditis. Complications in these children were as follows: 4 cases of cranial IEA, 4 cases of sigmoid sinus thrombosis, 2 cases of perisigmoid abscess or bony erosion, and 1 case of tegmen mastoideum dehiscence. The authors claim that, although uncommon, intracranial complications of acute mastoiditis may present without clinical signs or symptoms. Computed tomography of the temporal bone with contrast is essential for identifying asymptomatic complications. [17]
Bacteriology
The most frequently isolated pathogens in IEAs are streptococci, Staphylococcus aureus, and S. epidermidis. Less commongly, there are enteric gram-negative bacilli (especially Escherichia coli), Pseudomonas species, Bacteroides species, and other anaerobes. Polymicrobial aerobic and microaerophilic streptococci are usually responsible for infection that has spread from the paranasal sinuses. Rarely, Salmonella species, Eikenella corrodens, and Mucor species have been isolated. After neurosurgical procedures, the most common organisms are S. aureus (including both methicillin-sensitive and methicillin-resistant species), S. epidermidis, and Cutibacterium (formerly P. acnes). [3, 4, 8] Haemophilus influenzae may also be the responsible organism, in addition to Mycobacterium tuberculosis, Proteus penneri, Actinomyces species, Blastomyces species, Aspergillus fumigatus, and Cladosporium species. Although rare in the United States and Europe, Mycobacterium tuberculosis is a common cause of IEA in endemic countries. [13]
In 5%–10% of patients with systemic blastomycosis, central nervous system (CNS) involvement occurs, often associated with worse morbidity and mortality [18] The imaging and clinical features in this case may often suggest an epidermoid tumor. Surgical pathology with isolation of the organism is required to make the diagnosis.
Physical Examination
See the list below:
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External evidence of infection (eg, surgical-site infection, purulent drainage from sinuses or ears)
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Evidence of head trauma
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Fever
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Nausea, vomiting
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Signs of meningeal irritation (eg, stiff neck)
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Altered mental status progressing to obtundation
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Focal neurological signs (eg, hemiparesis, cranial nerve palsies)
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CSF rhinorrhea or otorrhea
Complications
Complications of an untreated intracranial epidural abscess (IEA) include subdural empyema, osteomyelitis, venous sinus or cortical vein thrombosis, and ultimately brain edema and herniation leading to death.
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CT scan showing lenticular-shaped intracranial epidural abscess.
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Intracranial epidural abscess. Enhanced MRI of the brain, axial section, revealing a left temporal epidural abscess with an abscess cavity and a thickened enhancing capsule. Adjacent thickened dura enhances as well. In addition, mass effect is evident.
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Intracranial epidural abscess. A coronal section of the MRI revealing a left temporal epidural abscess with an abscess cavity and a thickened enhancing capsule. Adjacent thickened dura enhances as well. In addition, mass effect is evident.
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Intracranial epidural abscess. MRI of the brain, unenhanced. A T1-weighted image (axial view) showing a left temporal epidural abscess with an abscess cavity, surrounding capsule, and the thickened dura underneath. Mass effect is evident.
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Epidural abscess in the posterior fossa following a suboccipital craniectomy.
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Epidural abscess photo, taken intraoperatively.
