Intracranial Epidural Abscess

Intracranial epidural abscess (IEA) was first described in 1760 by Sir Percival Pott, who also documented the associated scalp swelling, known as Pott puffy tumor. IEAs are less common than intraparenchymal brain abscesses and subdural empyemas. 

An intracranial epidural abscess (IEA) is a suppurative infection of the epidural space, which refers to the space between the dura mater and the inner table of the skull (see the image below). As the dura adheres tightly to the skull and provides a barrier to the spread of the infection, IEAs tend to appear well-circumscribed radiologically, and may progress subacutely. There is often associated osteomyelitis of the overlying bone.[1, 2]  IEAs most commonly are associated with sinusitis and otologic infections, although with modern antibiotic treatment, the incidence has declined. IEAs may also occur as a complication of neurosurgical procedures (ie,. iatrogenic IEAs) or as a sequale of head trauma.[3] As many as 1%–3% of craniotomies result in an IEA, in particular those with frontal sinus breaches.[4, 5] In approximately 10% of cases, an IEA is associated with a subdural empyema, a pyogenic infection between the dura and arachnoid mater, which is more rapidly progressive and carries a poorer prognosis. At autopsy, however, 81% of patients with IEAs have been found to have evidence of subdural extension of the infection, 35% of patients with meningitis, and 17% with intraparenchymal abscess.

IEAs most commonly result from direct, contiguous spread of an infection from the paranasal sinuses (eg, frontal sinus), middle ear (eg, from otitis media), orbit, or mastoids (eg, from mastoiditis). Direct contamination may result from penetrating trauma, contamination of the wound perioperatively, or direct spread from associated osteomyelitis. Less commonly, IEAs result from septic emboli entering via emissary veins, or via hematogenous spread.[6]

The most common causative organisms among non-neurosurgical IEAs are streptococci and anaerobes, particularly when associated with sinusitis. Among traumatic and neurosurgical-associated IEAs, staphylococci (in particular S. aureus) are the most common pathogens, and less commonly gram-negative bacteria.

Once the organism enters the epidural space, hyperemia and fibrin deposition occurs, followed by collection of purulent material and development of chronic granulation and fibrous tissue. Dural attachments, especially at sutures, help to contain the infection. However, when this barrier is compromised because of trauma or surgery, further spread of the infection may ensue, resulting in complications such as osteomyelitis of the bone flap, subdural empyema, dural sinus or coritcal vein thrombosis, purulent leptomeningitis, and intraparenchmyal brain abscess. Virulence of the organism, immune resistance of the host (eg, in immunocompromised patients), and prompt treatment influence the outcome of this condition significantly.

Frequency

Intracranial epidural abscess (IEA) is an uncommon cause of focal intracranial infections; in fact, 90% of epidural abscesses occur in the spine. Because of early and adequate treatment of bacterial middle ear and sinus infections, particularly in children,[7]  IEAs have become less common. Most iatrogenic IEAs after neurosurgical procedures are associated with a superficial surgical site infection (SSIs). Although the incidence of SSIs has been on the decline with more standardized use of perioperative antibiotics and sterile operating room procedures, SSIs still occur in 1%–6% of cases.[8] IEAs complicate 1%–3% of craniotomies overall, although at a significantly higher rate in cases of frontal sinus breaches and reoperations.[9, 10, 4, 5]

Mortality/Morbidity

Mortality from IEAs was 100% in the pre-antibiotic era. With advanced imaging techniques, more effective antibiotics, and prompt surgical treatment, the mortality rate has declined to 6%–20%.

The outcome of patients with IEAS is influenced by neurological status on presentation (eg, presence of altered mental status), whether neurological deterioration occurs, age, comorbid conditions (eg, diabetes, immunocompromised states), virulence of the organism, and delays in beginning appropriate treatment. The primary causes of poor outcome among patients with IEAs are mass effect of the lesion resulting in brain herniation, and extension of the infection into the venous system, which may lead to venous thrombosis and fulminant cerebral edema and leptomeningitis. In an older study, Harris et al. reported 31 cases of localized central nervous system infection over a 7-year period in their community hospital.[11]  The authors found subdural empyemas in 6 cases (20%) and IEAs in 2 cases (6%). Although all patients with cranial subdural empyema and cranial epidural abscess survived, half had severe residual neurologic deficits. With the advent of new antibiotics, improved surgical techniques, and aggressive surgical approach, prognosis has significantly improved.

Germiller et al. report a consecutive sample of 25 children and adolescents treated for 35 intracranial complications associated with intracranial complications of sinusitis.[12] Epidural abscess was most common (13 complications) followed by subdural empyema (n = 9), meningitis (n = 6), encephalitis (n = 2), intracerebral abscess (n = 2), and dural sinus thrombophlebitis (n = 2). Only 1 death occurred from sepsis secondary to meningitis (mortality 4%) and only 2 patients had permanent neurologic sequelae. In another study of the pediatric population by Lundy et al., the authors identified 16 children, 14 of whom had subdural empyemas and 2 who had IEAs only. Although all children with subdural empyemas had neurological manifestions of the disease, those with only IEA did not. One child in the series died. The authors noted that delays in treatment were in part due to delays in obtaining appropriate imaging.[7]

Sex- and age-related demographics

IEAs occurs with greater frequency in boys and men compared to girls and women (ratio of 1:0.56, respectively).[13]

Non-iatrogenic IEAs are more common in older children, adolescents, and younger adults, primarily due to the higher incidence of otologic infections and sinusitis. Iatrogenic IEAs, however, may occur at any age, in particular among the elderly with comorbidities that may comprise immune response and/or wound healing.[13, 14]

If identified and treated promptly before neurological deterioration occurs, the prognosis for intracranial epidural abscess (IEA) is very good. 

Because of the insidious onset of symptoms, neuroimaging by CT scanning and MRI as well as the availability of strong antibiotics have resulted in decreased morbidity and mortality from this condition in recent years.

Signs associated with an excellent prognosis include the following:

• Young age

• No altered mental status

• Absence of severe neurologic deficit on initial presentation

• Absence of neurologic deterioration during initial management

• No comorbid factors (eg, immunocompromised)

Poorer prognosis is often associated with the following:

• Signs of herniation present on initial presentation, when the mortality rate exceeds 50%

• Failure to obtain a brain CT scan in patients with altered mental status, headache, or new neurologic deficit

• Failure to address family concerns about unusual patient behavior, especially when other symptoms indicative of intracranial epidural abscess are present

Early and accurate diagnosis of this potentially deadly but treatable disease is of paramount importance.

Pradilla et al. report that prognosis for both spinal epidural abscesses and intracranial epidural abscesses worsens if there is delayed diagnosis and intervention, and that prognosis largely depends on the neurologic status at the time of diagnosis. Increased clinical awareness can help achieve an earlier diagnosis, and hopefully improve outcomes.[13]

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]

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.

See the list below:

• External evidence of infection (eg, surgical-site infection, purulent drainage from sinuses or ears)
• Evidence of head trauma
• Fever
• Nausea, vomiting
• Signs of meningeal irritation (eg, stiff neck)
• Altered mental status progressing to obtundation
• Focal neurological signs (eg, hemiparesis, cranial nerve palsies)
• CSF rhinorrhea or otorrhea

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.

Prompt recognition of the aformentioned signs and symptoms of an intracranial epidural abscess (IEA) in a high-risk population is essential, so as not to delay diagnosis and appropriate treatment. 

After a performing a history and physical exam (focusing on a neurological and head and neck exam), and checking vital signs (including temperature) to determine stability, relevant laboratory studies should be ordered (see below). 

Findings from routine laboratory tests are not diagnostic for intracranial epidural abscess (IEA) but are essential in the preparation of the patient for operation. These tests may reveal polymorphonuclear (PMN) leukocytosis, and/or an elevated erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and procalcitonin. Note that certain inflammatory markers are normally elevated in the postoperative period. 

In addition, the provider should send at least two sets of blood cultures, which may reveal the organism. 

Hyponatremia has been reported in approximately 30% of cases.

Preoperative lab work (eg, coagulation studies, type and screen) should also be sent in case the patient requires surgery. 

Neuroimaging is key to narrowing down the potential diagnosis and enabling prompt empirical therapy until a specific microbiological diagnosis is made.

An initial CT head scan without contrast is an appropriate, low-cost screening tool for a suspected intracranial lesion. Intracranial epidural abscesses (IEAs) generally appear as a lentiform area of low or intermediate density (see the image below). CT scanning can also show bony destruction and fragmentation in patients with underlying mastoiditis. When contrast is administered, the convex inner side of the low-density lesion often enhances due to inflamed dura.

Historically, plain radiography of the skull could demonstrate the responsible sinusitis, mastoiditis, or osteomyelitis. Before the advent of CT scanning, cerebral angiography was often required. Cerebral angiography would demonstrate an avascular mass displacing the dural sinuses away from the inner table of the skull.

In the setting of a positive CT head scan and/or clinically suggestive signs and symptoms, the provider should obtain an MRI of the brain with and without gadolinium contrast. As an MRI is free from bony artifacts, it can easily demonstrate fluid collections in and outside the brain, and as a result is the diagnostic procedure of choice for an IEA.

Epidural fluid of an IEA is generally crescentic or lentiform in shape, restricts diffusion (on DWI sequence), and has higher signal intensity than CSF on both T1- and T2-weighted MRI. IEAs may have gadolinium enhancement on T1 peripherally, including enhancement of the dura. A hypointense medial rim, representing the displaced dura is very characteristic of an IEA. An MRI may visualize small fluid collections missed on CT, associated cerebral edema, and may help narrow down the radiological differential diagnosis, such as differentiating IEA from acute or subacute epidural hematomas, tumors, and arachnoid cysts. Most significantly,  MRI helps differentiate an IEA from a subdural empyema, which carries a poorer prognosis and requires immediate treatment. See images below:

The vein of Labbé may rarely masquerade as the hypointense rim of an epidural abscess.[19]  Recognition of the vein of Labbé on imaging is therefore essential for the appropriate management of otological and neurotological disease.

Lumbar puncture should generally be avoided, as it carries the risk of precipitating herniation in the setting of increased ICP due to larger intracranial epidural abscesses (IEAs) and/or associated cerebral edema. A lumbar puncture may be appropriate, however, to diagnose patients with primarily meningitic signs and only a small epidural abscess, without mass effect and without clinical symptoms of increased ICP. Risks and benefits should always be carefully weighed before a decision is made to proceed with a spinal tap.

Findings on CSF studies can often be unremarkable, and may show glucose and protein levels within normal limits. CSF pressure may be normal or increased. CSF may contain excess cells that are usually polymorphonuclear cells. The cell count is usually less than 200 cells, but it can be as high as 7000/mm3. Protein may be elevated as much as 100 mg/dL and the glucose level is often within the reference range unless associated meningitis is present, in which case it may be decreased.

Early diagnosis and treatment of intracranial epidural abscess (IEA) cannot be overemphasized, as neurologic outcome mainly depends on the patient’s neurologic status immediately prior to surgery.

Prehospital management

Rapid transport and early stabilization (airway, breathing, and circulation) are essential in the prehospital setting. This may include intubation if necessary. 

Initial management

Initial management depends on the severity and type of clinical presentation.

After initial evaluation and stabilization, relevant laboratory studies should be drawn, including blood cultures, basic labs, coagulation studies, and type and screen. Neuroimaging (beginning with CT of the head) should be obtained as soon as the patient is adequately stable. 

Patients with signs of increased ICP, particularly those with cerebral edema and/or large IEAs, should be given mannitol or hypertonic saline as a temporizing measure. The presence of seizures and focal neurological deficits may require emergent intubation, anticonvulsant therapy, and hemodynamic stabilization before proceeding with diagnostic tests. Patients with sepsis should be treated appropriately, including with fluid resuscitation and pressors if necessary.

Neurologic status should be monitored closely.

Antibiotic therapy

In clinically stable patients without significant neurological deficits, antibiotics should be held until after blood cultures and cultures from the operating room are drawn. Until the culture and sensitivity report of the infectious agent becomes available, the choice of empiric antibiotic therapy should be based on the underlying etiology. For example, when an intracranial abscess is thought to be due to extension of infection from paranasal sinuses involving staphylococcal, aerobic, and anaerobic bacteria, more than one antibiotic is necessary. Likewise, an antistaphylococcal agent would be an appropriate choice for infection occurring after a neurosurgical procedure. A reasonable broad-spectrum regimen is vancomycin, ceftazidime, and metronidazole. Depending on local pathogens and antibiotic resistance patterns, other combinations including meropenem, ertapenem, or linezolid, or possibly antifungal agents, may be considered. 

Once cultures have been finalized, the antibiotic regimen can then be narrowed to treat the cultprit organism. The length of therapy is determined by the patient's clinical response to treatment and by radiological resolution of the epidural abscess on follow-up imaging. Generally, antibiotic therapy should be continued for a minimum of 8 weeks if surgery is not undertaken, and for at least 4 weeks if the abscess is drained. In general, follow-up CT scanning or MRI should be obtained 2 weeks after antibiotic therapy has been discontinued.

Seizure therapy

Prophylactic seizure therapy is not generally recommended, but the provider should have a low threshold to administer AEDs if there is any clinical suspicion. If the IEA is not associated with a subdural empyema, seizures are unlikely to ensue. Patients who present with seizures should be given AEDs and then placed on video EEG postoperatively. Neurology consultation should be obtained to determine an appropriate weaning or taper of the AED, which generally would occur over months. Patients with a prior history of seizures who currently take AEDs should continue taking them. 

Steroid Therapy

Steroids (eg, dexamethasone) may be considered in certain patients, particularly those with meningitic signs and symptoms.

The goal of surgical care is to eliminate the source of infection and to prevent further complications. Surgical evacuation, decompression, and debridement, along with antibiotic therapy, are the mainstays of effective treatment in most patients with intracranial epidural abscesses (IEAs). Medical management alone (with antibiotics) may occasionally be considered in patients who are clinically stable, have no neurological deficits, and have a small IEA with no evidence of other radiological sequelae (eg, subdural empyema, cerebral edema, cerebritis). 

Surgery should be performed promptly, particularly in neurologically deteriorating patients. Depending on the location and etiology of the IEA, neurosurgical as well as otolaryngological consultations may be required. 

The type of surgery for an IEA depends on the size and location of the lesion as well as on involvement of the overlying bone.

• A craniotomy is commonly performed, which involves creating a sufficiently sized bony opening over the IEA, evacuating the purulent material, sending cultures, irrigating copiously with antibiotics, and re-attaching the bone with plates and screws. In cases where a subdural empyema is suspected, the dura should be opened so as to visualize the subdural space. If the dura appears infected, it should be removed and replaced with a dural substitute. 

• If the bone appears infected (eg, from imaging or from visualization at the time of the surgery), a craniectomy is performed, in which the bone is discarded and sent to the pathologist for examination. The surgeon may replace the bone electively (cranioplasty) after 6–8 weeks of antibiotics and resolution of the infection. The bone is replaced with artificial materials, which may be 3D printed. If there is a significant cranial defect after the craniectomy, the patient may be advised to wear a helmet when out of bed until the cranioplasty is performed. 

• For patients who are presenting with an IEA as a complication of a craniotomy, the bone flap is often discarded if it appears infected. In most cases there is an overlying superficial surgical site infection, which may be closed by a plastic surgeon.

• For smaller IEAs, or those in more difficult locations, minimally invasive burr holes may be attempted to drain the purulent material, although the limited visualization provided by a burr hole may limit sufficient inspection and drainage of the infection.

• ENT consultation is frequently required, such as in the setting of an IEA associated with frontal sinusitis 

• An endoscopic endonasal approach may be considered with ENT for IEAs secondary to sinusitis in the anterior skull base, as described by Eviator et al.[20]  

• In the setting of an associated CSF leak, a lumbar drain may be placed intraoperatively, and then drained at 10–20 cc/hr over a period of 3–5 days. 

Aerobic and anaerobic cultures with gram stain, India ink, and acid-fast bacilli (AFB) of the purulent material should be sent from the operating room.

Noggle et al. report that frontal, supraorbital IEAs of the anterior and middle cranial fossa can be adequately and safely debrided via a minimally invasive supraciliary ("eyebrow") craniotomy. This approach has a cosmetic benefit and may decrease approach-related morbidity.[21]

Postoperatively, most patients should be admitted to the Neuro-Intensive Care Unit (or similar) for close Q1 hour neurological checks. A CT head non-contrast should be performed immediately after surgery. Broad spectrum antibiotics should be started.

Immediate neurosurgical consultation is highly warranted.

A multidisciplinary approach involving an otolaryngologist may be necessary if the patient presents with concurrent paranasal sinusitis.

Infectious disease consultation may prove useful as well. 

Complications of intracranial epidural abscess can include the following:

• Subdural empyema
• Cerebritis
• Cerebral edema
• Cerebral venous sinus thrombosis
• Cortical vein thrombosis
• Osteomyelitis
• Intraparenchymal brain abscess
• Cerebral edema
• Stroke
• Seizures
• Intracranial hypertension and brain herniation
• CSF leak
• Coma
• Death

Antibiotic therapy

In clinically stable patients without significant neurological deficits, antibiotics should be held until after blood cultures and cultures from the operating room are drawn. Until the culture and sensitivity report of the infectious agent becomes available, the choice of empiric antibiotic therapy should be based on the underlying etiology. For example, when an intracranial abscess is thought to be due to extension of infection from paranasal sinuses involving staphylococcal, aerobic, and anaerobic bacteria, more than one antibiotic is necessary. Likewise, an antistaphylococcal agent would be an appropriate choice for infection occurring after a neurosurgical procedure. A reasonable broad-spectrum regimen is vancomycin, ceftazidime, and metronidazole. Depending on local antibiotic resistance patterns, other combinations including meropenem, ertapenem, or linezolid may be considered. 

Once cultures have been finalized, the antibiotic regimen can then be narrowed to treat the cultprit organism. The length of therapy is determined by the patient's clinical response to treatment and by radiological resolution of the epidural abscess on follow-up imaging. Generally, antibiotic therapy should be continued for a minimum of 8 weeks if surgery is not undertaken, and for at least 4 weeks if the abscess is drained. In general, follow-up CT scanning or MRI should be obtained 2 weeks after antibiotic therapy has been discontinued.

Seizure therapy

Prophylactic seizure therapy is not generally recommended, but the provider should have a low threshold to administer AEDs if there is any clinical suspicion. If the IEA is not associated with a subdural empyema, seizures are unlikely to ensue. Patients who present with seizures should be given AEDs and then placed on video EEG postoperatively. Neurology consultation should be obtained to determine an appropriate weaning or taper of the AED, which generally would occur over months. Patients with a prior history of seizures who currently take AEDs should continue taking them. 

Steroid Therapy

Steroids (eg, dexamethasone) may be considered in certain patients, particularly those with meningitic signs and symptoms.

Class Summary

For patients presenting in the ED with intracranial epidural abscess, empiric antibiotics are the first-line pharmacologic therapy. These antibiotics must cover a broad spectrum of both aerobic and anaerobic bacterial organisms.

Penicillin G (Pfizerpen)

Along with chloramphenicol, constitutes first-line regimen for empiric treatment of intracranial epidural abscess in the ED. Provides coverage for anaerobes and streptococci.

Chloramphenicol

Constitutes the other half of classic first-line empiric regimen. Enhances anaerobic coverage to include Bacteroides fragilis, Enterobacteriaceae, and Haemophilus species infections.

Cefotaxime

In combination with metronidazole, can replace penicillin G and chloramphenicol. In this regimen, cefotaxime covers streptococci, staphylococci, Haemophilus species, and Enterobacteriaceae. Third-generation cephalosporin with broad gram-negative spectrum, lower efficacy against gram-positive organisms, and higher efficacy against resistant organisms. Arrests bacterial cell wall synthesis and inhibits bacterial growth by binding to one or more of the penicillin-binding proteins.

Metronidazole (Flagyl)

Second half of alternative regimen to penicillin/chloramphenicol. Imidazole ring-based antibiotic active against various anaerobic bacteria and protozoa. Has proved especially effective in otogenic intracranial epidural abscesses.

Nafcillin

Should be added to either regimen mentioned above if S aureus is strongly suspected. Treats infections caused by penicillinase-producing staphylococci. Used to initiate therapy when patients are suspected of having penicillin G resistant staphylococcal infection. Do not use for treatment of penicillin G susceptible staphylococci. Use parenteral therapy initially in severe infections. Very severe infections may require very high doses. Change to PO therapy as condition improves. Because of occasional occurrence of thrombophlebitis associated with parenteral route (particularly in elderly individuals), administer parenterally only for a short period (24-48 h) and change to PO route if clinically possible.

Vancomycin

Replaces nafcillin in patients who are allergic to penicillin and in patients who are suspected to have MRSA as an etiologic agent. Potent antibiotic directed against gram-positive organisms and active against enterococci species. Also useful in treating septicemia and skin structure infections.

Ceftazidime (Fortaz, Tazicef)

Should be added to empiric regimens if pseudomonads are suspected. Third-generation cephalosporin that has broad gram-negative spectrum, lower efficacy against gram-positive organisms, and higher efficacy against resistant organisms. Arrests bacterial cell wall synthesis and inhibits bacterial growth by binding to one or more of the penicillin-binding proteins.

Meropenem

A broad-spectrum carbapenem antibiotic, meropenem inhibits cell wall synthesis and has bactericidal activity. It is effective against most gram-positive and gram-negative bacteria. Meropenem has slightly increased activity against gram-negative organisms and slightly decreased activity against staphylococci and streptococci compared with imipenem.

Class Summary

Anti-inflammatory effects of steroid therapy can decrease associated cerebral edema, reducing ICP. These benefits are offset somewhat by the fact that steroid use decreases antibiotic penetration into the abscess and may slow encapsulation of the abscess site.

Dexamethasone (Decadron, Hemady)

Corticosteroid of choice for reducing ICP. Used in treatment of inflammatory diseases. May decrease inflammation by suppressing migration of polymorphonuclear leukocytes and reversing increased capillary permeability.