eMedicine Specialties > Emergency Medicine > Infectious Diseases

Brain Abscess

Lisa Elizabeth Thomas, MD, Staff Physician, Harvard Affiliated Emergency Medicine Residency, Brigham and Women's Hospital and Massachusetts General Hospital
Joshua N Goldstein, MD, PhD, FAAEM, Assistant Professor of Surgery (Emergency Medicine), Harvard Medical School; Attending Physician, Department of Emergency Medicine, Massachusetts General Hospital

Updated: Sep 25, 2008

Introduction

Background

Although rare in developed countries, brain abscess is a serious, life-threatening emergency. Once having a dire outcome, morbidity and mortality have decreased because of advances in diagnostic modalities, antibiotic regimens, and earlier surgical interventions.^1,2 However, changes in epidemiology, including new disease pathogens and predisposing factors, have renewed concern about the diagnosis and treatment of this condition.

Pathophysiology

Brain abscess is a focal infection, which begins when organisms are inoculated into the brain parenchyma, usually from a site distant from the central nervous system (CNS). Abscess formation occurs through several stages. Inflammation during the "early cerebritis" stage evolves into a necrotic collection of pus, eventually surrounded by a well-vascularized capsule after 2 weeks.^3,4

The 3 mechanisms of entry into the brain are as follows:^2,5,6

• Direct extension: Infections stemming from the sinuses, teeth, middle ear, or mastoid may gain access to the venous drainage of the brain via valveless emissary veins that drain these regions. Because of improved antibiotic therapy for ear infections, this mechanism is decreasing in incidence, accounting for only approximately 25% of cases.²
• Hematogenous: Seeding of the brain occurs from distant infection sites and often results in multiple brain abscesses.⁷ This remains an important cause of brain abscess.
• Following penetrating head injury or neurosurgery: Previously low in incidence, more brain abscesses are developing after head trauma and neurosurgical procedures. A recent case series found that 37% of brain abscesses were associated with head penetration.^2,8

Up to 25% of abscesses are cryptogenic and have no clear source.^2,7

Frequency

United States

Brain abscess is rare in the general population; however, immunocompromised patients have increasing incidence of brain abscess, often with fungal or protozoan organisms.

In the United States, 1500-2500 cases are reported per year.⁷

Mortality/Morbidity

• The mortality rate from brain abscess is currently approximately 10%.^1,2,9
• However, if the abscess ruptures into the ventricular system, the mortality rate may be 80%.²
• Morbidity in survivors is generally due to residual neurologic defects, increased incidence of seizures due to scar tissue foci, or neuropsychiatric changes.⁷

Race

No compelling evidence exists for racial differences in the incidence of brain abscess.

Sex

Brain abscess occurs twice as often among men than women.^2,4,10,11

Age

Traditionally, brain abscesses were disproportionately diagnosed in the young. However, with changes in vaccination practices, treatment of pediatric infections, and the AIDS pandemic, current literature suggests a shift in peak incidence toward the third to fifth decades of life.^2,11,12

Clinical

History

• Headache is the most common presenting symptom of brain abscess (50-90% of cases).^2,11
• Focal neurologic deficit (50%) may correlate with the local region of infection.⁶
• Classic triad of headache, fever, and focal neurologic deficit is rarely seen (<5% of cases in a recent case series).²
• Seizure (40%) and mental status changes (50%) are common.^2,11
• Nausea, vomiting, or stiff neck may be reported with increased cerebral edema due to the mass lesion.⁶
• Sudden worsening of a preexisting headache accompanied with meningismus may be indicative of a catastrophic event—rupture of the abscess into the ventricular space.⁶

Physical

• Fever is typically low grade, but presence or absence of fever does not aid in diagnosis, as it is present in less than half of all cases.^6,11
• Altered mental status ranges from subtle personality changes through drowsiness to full-blown coma.¹¹
• Nuchal rigidity occurs in about 25% of cases.¹¹
• Focal neurologic findings are commonly present^6,11 and can signal increasing cerebral edema around the abscess.⁴
• Seizures are typically generalized.¹¹
• Papilledema indicates the disease process is well advanced and increased intracranial pressure is present.¹¹
• Bulging fontanelles, irritability, and enlarging head circumference may be noted in infants.⁵

Causes

A wide variety of organisms can cause brain abscess, depending on the portal of entry, and up to one third may be polymicrobial.^3,6  

• Direct extension - Sinus, odontogenic, and otogenic sources are common.
  • Streptococcus species (aerobic and anaerobic) are most frequently isolated.
  • Other organisms include Bacteroides, Enterobacteriaceae, Pseudomonas, Fusobacterium, Prevotella, Peptococcus, and Propionibacterium.
• Hematogenous spread - Pathogens depend on predisposing source. Some common examples are listed below.
  • Endocarditis -Streptococcus viridans, Staphylococcus aureus
  • Pulmonary infections -Streptococcus, Fusobacterium, Corynebacterium, and Peptococcus species
  • Cardiac defects with right-to-left shunt -Streptococcus species
  • Intra-abdominal infections -Klebsiella species, E coli, other Enterobacteriaceae, Streptococcus species, anaerobes
  • Urinary tract infections - Enterobacteriaceae, Pseudomonas species
  • Wound infection -S aureus
• Penetrating head trauma, postoperative⁸
  • S aureus is most commonly isolated.
  • Enterobacteriaceae, other gram-negative bacilli, S epidermidis, Clostridium species, anaerobes, and Pseudomonas species may also be found.
  • Opportunistic infection is an increasing cause of brain abscess, as there are more patients with organ transplant, HIV, and immunodeficiencies. Common organisms include Toxoplasma gondii andNocardia, Aspergillus, and Candida species.^4,5,6 Cases of Nocardia are increasing even in immunocompetent patients and have high mortality.^2,4,13
  • Other predisposing risk factors include intravenous drug use, cardiac abnormalities (ie, prosthetic valve, septal defect), cyanotic congential heart disease (most common cause of multiple brain abscesses in children), diabetes, chronic steroid use, alcoholism, and neoplasm.^2,7,11
  • Case reports of near drowning, foreign body aspiration, application of dental braces, and esophageal dilatation have also been associated with brain abscess.^14,15,16,17
  • When there is no obvious source (up to 25% of cases), upper respiratory tract flora and anaerobes are often isolated.² Several sources have identified a patent foramen ovale by echocardiogram in these cases and propose this as a possible mechanism for seeding oral flora to the brain.¹⁸
  • Several cases of community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA) causing brain abscess have been reported recently, so this must be considered when initiating empiric therapy in patients presenting with neurologic symptoms who also have risk factors for CA-MRSA.^19,20

Differential Diagnoses

Other Problems to Be Considered

Cerebellopontine angle tumor
Extradural abscess
Pediatric AIDS
Subdural empyema
Cranial osteomyelitis 

Recent evidence suggests that a strong statistical association of pulmonary arteriovenous malformation (PAVM) and brain abscess exists. To date, no evidence of a causal relationship between the two exists, but if a patient is known to have PAVM, an increased level of suspicion should exist for brain abscess if symptoms suggest the diagnosis. Conversely, some have called for screening for PAVM in all patients with brain abscess in order to avoid missing this potentially life-threatening disorder.¹⁰

Workup

Laboratory Studies

Laboratory tests are rarely helpful in establishing a diagnosis of brain abscess.^2,7

• Elevated white blood cell (WBC) count or erythrocyte sedimentation rate (ESR) is not reliably found.^6,21
• Blood culture results may only be positive in 30% of patients^2,22 but should always be obtained. Hematogenous spread may be the source as noted above, and a positive blood culture result may help guide therapy, especially if empiric antibiotics are started and abscess fluid culture yields no growth.^6,2
• Culture specimen from any other suspected focus of infection should also be collected, as this may also give clues for possible distant sources.¹¹

Imaging Studies

• CT imaging of the brain (with and without contrast) is the most readily available study for establishing diagnosis of brain abscess in the ED. 
  • Early in the course, abscess appears as a low-density, irregular zone that does not enhance in the presence of intravenous contrast (early cerebritis).
  • Classically, as the disease progresses, a distinctive "ring enhancement" appears on contrast-enhanced CT, as the abscess wall thickens.
  • Rarely, a well-organized abscess wall fails to generate such ring enhancement. Such false-negative results should not have an impact on ED care or disposition; they have more implications for inpatient care, where the timing of surgical intervention may be dictated by response to preliminary intravenous antibiotics and subsequent organization of the abscess wall.²³  
• CT is generally sufficient to make the preliminary diagnosis, which mandates neurosurgical consultation and admission to the hospital.^2,3,6
• However, MRI is increasingly being used for further evaluation.
  • MRI is more sensitive in detecting early cerebritis.²
  • Posterior fossa lesions may not be identified on CT scan and may require MRI to make the critical diagnosis.^2,4
  • A ring-enhancing lesion on CT scan may give rise to a differential diagnosis including abscess versus primary tumor or metastasis. Gadolinium-enhanced MRI is helpful in characterizing these lesions. On diffusion-weighted imaging, pyogenic abscesses have a hyperintense signal, whereas nonpyogenic lesions will have a hypointense or mixed signal. Although not readily available in the emergency department, proton magnetic resonance spectroscopy may also be used to differentiate abscesses.^24,25

See Brain, Abscess for images.

Other Tests

• Ultrasonography: As ultrasonography is becoming widely used in the emergency department, bedside ocular ultrasonography may be performed to assess for increased intracranial pressure.²⁶

Procedures

• Lumbar puncture (LP)
  • LP results are generally not helpful in the diagnosis of brain abscess. Performing this procedure in the emergency department is generally indicated only in cases highly suspicious for bacterial meningitis, with a careful balance between any potential change in management and the risk of CNS herniation.^4,11
  • The suspicion of brain abscess, presence of any focal neurologic finding, or of papilledema is an absolute indication for CT imaging prior to LP.²⁷
• In cases where LP had been performed, the findings were nonspecific and cultures were rarely positive.²
• Abscess aspiration: Culture of the abscess fluid is the most important microbiological study to ensure appropriate targeted therapy. As a result, urgent or emergent neurosurgical consultation is necessary.^2,3

Treatment

Prehospital Care

Rapid transport is the key component of prehospital care for suspected intracranial abscess.

Emergency Department Care

• The initial evaluation is dictated by the severity of the patient's condition.
• Emergent intubation using a cerebroprotective rapid sequence induction regimen is often necessary in patients with obtundation, inability to protect the airway, and suspected herniation.
• Stable patients whose presentation suggests the diagnosis should undergo rapid neuroimaging after initial evaluation.² ,³ ,⁷ Close monitoring of neurologic status is essential and having at least one nurse or advanced provider in attendance while the patient is undergoing imaging is probably advisable.
• Antibiotics should be administered as early as possible in the patient's course in the ED. These may be given prior to imaging in cases where the diagnosis is very strongly suspected.¹¹
• Seizures should be treated aggressively to decrease the risk of sustained increases in intracranial pressure. Prophylactic anticonvulsants are often used given the relatively high frequency of seizures in this population.³

Consultations

• Once the diagnosis is clear, immediate neurosurgical consultation is mandatory.^2,3
• Infectious disease consultation may be necessary to optimize antibiotic therapy, especially in immunocompromised hosts.^2,4
• Neurology consultation is helpful in guiding both immediate and long-term management.

Medication

In the early phase of abscess formation, cerebritis, patients may respond to antibiotic therapy alone.^7,5

However, in almost all cases, definitive treatment of brain abscess requires surgical drainage.^2,3

Since seizures are a frequent complication of brain abscess, anticonvulsants for seizure prophylaxis are often recommended at the initial time of diagnosis and for a prolonged period of time, often greater than 1 year.^3,7

Antibiotics

In the ED, empirical regimens of antibiotic therapy are the first-line pharmacologic treatment of brain abscess based on presumed source:³  

• Direct extension from sinuses, teeth, middle ear - Penicillin G + metronidazole + third-generation cephalosporin
• Hematogenous spread or penetrating trauma - Nafcillin + metronidazole + third-generation cephalosporin
• Postoperative - Vancomycin (concern for MRSA) + ceftazidime or cefepime (concern for Pseudomonas)
• No predisposing factor - Metronidazole + vancomycin + third-generation cephalosporin

Imipenem or meropenem can also be used for broad-spectrum coverage when other drug toxicities are unacceptable, but imipenem has been associated with seizures in patients with brain abscess.⁴

Additional targeted therapy may also be initiated in suspected fungal or protozoan infections, especially in immunocompromised patients.²

Ceftriaxone (Rocephin)

Third-generation cephalosporin with broad-spectrum, gram-negative activity; lower efficacy against gram-positive organisms; higher efficacy against resistant organisms. Bactericidal activity results from inhibiting cell wall synthesis by binding to one or more penicillin-binding proteins. Exerts antimicrobial effect by interfering with synthesis of peptidoglycan, a major structural component of bacterial cell wall. Bacteria eventually lyse due to the ongoing activity of cell wall autolytic enzymes while cell wall assembly is arrested.
Highly stable in presence of beta-lactamases, both penicillinase and cephalosporinase, of gram-negative and gram-positive bacteria.

Dosing

Adult

2 g IV q12-24h, max 4 g/d

Pediatric

100 mg/kg/d IV divided q12h

Interactions

Probenecid may increase ceftriaxone levels; coadministration with ethacrynic acid, furosemide, and aminoglycosides may increase nephrotoxicity

Contraindications

Documented hypersensitivity; hyperbilirubinemic neonates, particularly those who are premature

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Adjust dose in severe renal insufficiency (high doses may cause CNS toxicity); superinfections and promotion of nonsusceptible organisms may occur with prolonged use or repeated therapy; caution in breastfeeding women; may displace bilirubin from albumin binding sites increasing the risk of kernicterus; caution with gallbladder, biliary tract, liver, or pancreatic disease; caution in patients with history of colitis or penicillin hypersensitivity

Cefepime (Maxipime)

Fourth-generation cephalosporin. Gram-negative coverage comparable to ceftazidime but has better gram-positive coverage (comparable to ceftriaxone). Covers Pseudomonas.

Dosing

Adult

2 g IV q8-12h

Pediatric

Neonates: 30 mg/kg IV q12h
>2 months: 50 mg/kg IV q8h (max 2 g/dose)

Interactions

Probenecid may increase effects of cefepime; aminoglycosides increase the nephrotoxic potential of cefepime

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Dosage adjustments (adult adjustments)
CrCl (mL/min) 80-50: 0.5-2 g q12-24h
CrCl 50-10: 0.5-2 g/d
CrCl <10: 0.25-0.5 g/d
HD: As for CrCl <10, with an extra 0.25 g after HD
During peritoneal dialysis: 1-2 g q48h
High doses may cause CNS toxicity; prolonged use of cefepime may predispose patients to superinfection

Imipenem and cilastatin (Primaxin)

For treatment of multiple organism infections in which other agents do not have wide spectrum coverage or are contraindicated due to potential for toxicity.

Dosing

Adult

500-750 mg IV q6h; in healthy young adults with excellent renal function, doses of 1 g q6h may be necessary (max dose: 4 g/d)

Pediatric

Infants >3 months and children <12 years: 15-25 mg/kg/dose IV q6h
Fully susceptible organisms: Not to exceed 2 g/d
Infections with moderately susceptible organisms: Not to exceed 4 g/d
>12 years: Administer as in adults

Interactions

Coadministration with cyclosporine may increase CNS side effects of both agents; coadministration with ganciclovir may result in generalized seizures

Contraindications

Documented hypersensitivity; known hypersensitivity to amide local anesthetics; children with CNS infections (increased seizure risk); children <30 kg with renal impairment (lack of data)

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Adjust dose in renal insufficiency (adult adjustments)
CrCl (mL/min) 80-50: 0.5 g q6-8h
CrCl 50-10: 0.5 g q8-12h
Hemodialysis (HD): 0.25-0.5 g after HD, then q12h
Adjust dose in renal insufficiency; avoid use in children <12 y with CNS infections
Caution with history of seizures, hypersensitivity to penicillins, cephalosporins, or other beta-lactam antibiotics

Meropenem (Merrem IV)

Bactericidal broad-spectrum carbapenem antibiotic that inhibits cell-wall synthesis. Effective against most gram-positive and gram-negative bacteria. Has slightly increased activity against gram-negatives and slightly decreased activity against staphylococci and streptococci compared with imipenem.

Dosing

Adult

1-2 g IV q8h

Pediatric

<3 months: Not established
>3 months: 40 mg/kg IV q8h (max dose 2 g/dose)

Interactions

Probenecid may inhibit renal excretion of meropenem, increasing meropenem levels

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Dosage adjustments (adult adjustments)
CrCl (mL/min) 10-50: 0.5-1 g q12h
CrCl <10: 0.5 g/d
HD: As for CrCl <10, with an extra 0.5 g after HD
Pseudomembranous colitis and thrombocytopenia may occur, requiring immediate discontinuation of medication

Penicillin G (Pfizerpen)

May be used as first-line regimen for empiric treatment of brain abscess in ED. Provides coverage for anaerobes and streptococci. Penetrates well into abscess cavity.

Dosing

Adult

6 million U IV q6h

Pediatric

<14 kg (30 lb): 600,000 U IV q6h
14-27 kg (30-60 lb): 900,000-1,200,000 U IV q6h
>27 kg (>60 lb): Administer as in adults

Interactions

Probenecid can increase effects; tetracyclines can decrease effects

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in impaired renal function

Metronidazole (Flagyl)

First line. Imidazole ring-based antibiotic active against various anaerobic bacteria and protozoa. Has proved especially effective in otogenic brain abscesses.

Dosing

Adult

500-750 mg IV q6h

Pediatric

30 mg/kg/d IV

Interactions

May increase toxicity of anticoagulants, lithium, and phenytoin; cimetidine may increase toxicity; disulfiram reaction may occur with orally ingested ethanol

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Adjust dose in hepatic disease; monitor for seizures and development of peripheral neuropathy

Cefotaxime (Claforan)

First line. Covers streptococci, staphylococci, and Haemophilus and Enterobacter species. This third-generation cephalosporin has broad gram-negative spectrum, lower efficacy against gram-positive organisms, and higher efficacy against resistant organisms than earlier generation cephalosporins. Arrests bacteria cell wall synthesis and inhibits bacterial growth by binding to 1 or more penicillin-binding proteins.

Dosing

Adult

2g IV q4-6h

Pediatric

Neonates: 50-200 mg/kg/d IV
Infants and children: 200 mg/kg/d IV divided into q6h-q8h

Interactions

Probenecid may increase levels; coadministration with furosemide or aminoglycosides may increase nephrotoxicity

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Adjust dose in severe renal impairment; has been associated with severe colitis

Nafcillin (Unipen)

Treats infections caused by penicillinase-producing staphylococci. Used to initiate therapy when penicillin G-resistant staphylococcal infection suspected. 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 oral therapy as condition improves. Because of occasional occurrence of thrombophlebitis associated with parenteral route (particularly in elderly persons) administer parenterally only for short term (24-48 h) and change to oral route if clinically possible.

Dosing

Adult

2g IV q4h

Pediatric

Neonates:
1200-2000 g, <7 days: 50 mg/kg/d IV divided q12h
>2000 g and <7 days or 1200-2000g and >7 days: 75 mg/kg/d IV divided q8h
>2000 g, >7 days: 100-140 mg/kg/d IV divided q6h
Children: 200 mg/kg/d in divided doses q4-6h

Interactions

Associated with warfarin resistance when administered concurrently; effects may decrease with bacteriostatic action of tetracycline derivatives

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

To optimize therapy, determine causative organisms and susceptibility; >10 d treatment needed to eliminate infection and prevent sequelae (eg, endocarditis, rheumatic fever); take cultures after treatment to confirm that infection is eradicated

Vancomycin (Vancocin)

Replaces nafcillin in both penicillin-allergic patients and those in whom MRSA is suspected as etiologic agent. Potent antibiotic directed against gram-positive organisms and active against enterococci. Also useful in treating septicemia and skin structure infections. Adjust dose as needed in patients with renal impairment. Check trough level after third dose (30 min prior to next dose) to avoid toxicity.

Dosing

Adult

1 g IV q12h or loading dose of 15 mg/kg IV q8-12h
Dose for peaks 25-40 mcg/mL, troughs 5-10 mcg/mL

Pediatric

60 mg/kg/d IV in divided doses q6h

Interactions

Erythema, histamine reactionlike flushing, and anaphylactic reactions may occur when administered with anesthetic agents; concurrent aminoglycosides may increase risk of nephrotoxicity above that with aminoglycoside monotherapy; concurrent nondepolarizing muscle relaxants may enhance effects of neuromuscular blockade

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in renal failure, neutropenia; adjust dose in patients with renal impairment; red man syndrome caused by too rapid IV infusion (ie, dose given over a few min) but rarely happens when dose given as 2-h infusion or by PO or IP route; red man syndrome not allergic reaction

Ceftazidime (Fortaz, Ceptaz)

Add 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 than many agents. Arrests bacteria cell wall synthesis and inhibits bacterial growth by binding to 1 or more penicillin-binding proteins.

Dosing

Adult

6 g/d IV

Pediatric

Not established

Interactions

Nephrotoxicity may increase with aminoglycosides, furosemide, or ethacrynic acid; probenecid may increase levels

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Adjust dose in renal impairment

Corticosteroids

Use of steroids is controversial. The anti-inflammatory effects of steroid therapy can decrease cerebral edema, reducing intracranial pressure (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. Therefore, many authors recommend steroids only in cases of massive cerebral edema with impending herniation.^3,11

Dexamethasone (Decadron, Dexasone)

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.

Dosing

Adult

Loading dose: 10-12 mg IV
Maintenance dose: 4 mg IV q6h

Pediatric

Loading dose: 1-2 mg/kg/dose IV once
Maintenance dose: 1-1.5 mg/kg/d IV
Not to exceed 16 mg/d divided q4-6h for 5 d; taper dose for 5 d and discontinue

Interactions

Effects decrease with coadministration of barbiturates, phenytoin, or rifampin; decreases effect of salicylates and vaccines used for immunization

Contraindications

Documented hypersensitivity, active bacterial or fungal infection

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Increases risk of multiple complications, including severe infections; monitor for adrenal insufficiency when tapering drug; abrupt discontinuation may cause adrenal crisis; possible complications include hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections

Follow-up

Further Inpatient Care

• A combined medical and surgical approach is used for most brain abscesses to eradicate the invasive organism.
• Duration of antibiotic treatment is unclear and is dictated by clinical response. Traditionally 6-8 weeks of intravenous antibiotics has been used followed by oral antibiotics for another 4-8 weeks to prevent relapse.^2,4,7,28 A recent series reported clinical resolution in some patients with only 2 weeks of intravenous therapy,² indicating that some patients may not need extended parenteral treatment.
• Surgery is the only way to precisely isolate the causative organism and tailor antibiotic therapy. One study concluded that antibiotic pretreatment for up to 10 days does not alter culture positivity of intracerebral specimen.¹¹ At present, most neurosurgeons use nonoperative management (ie, prolonged courses of parenteral antibiotics) only in rare cases, such as an abscess at an inoperable site or multiple abscesses.^2,3
• Surgical options include aspiration, incision and drainage, or excision depending on the location, size, number of sites, and other characteristics of the abscess as well as the patient's clinical status.^2,3 The specific choice of surgical technique is less important than the basic principle of removing the pathogen.³
• Many abscesses that were once inoperable can now be reached by stereotactic aspiration guided by precision mapping of the lesion's location by CT or MRI.^3,28 Stereotactic aspiration is widely preferred to open craniotomy because it is minimally invasive, has low morbidity/mortality, and allows rapid drainage.^2,6 Reports of magnetic resonance fluoroscopy to guide aspiration also exist.²⁹
• Some interest exists in the possible role of hyperbaric oxygen as an adjunct therapy to the initial phase of treatment with intravenous antibiotics. Reports in children³⁰ and in adults³¹ suggest that such adjunct therapy may reduce the length of inpatient stay by decreasing the duration of antibiotics needed for clinical improvement; however, the number of cases studied to date is small.

Further Outpatient Care

Interval CT scans are recommended for inpatients and outpatients to followup for complications and resolution of abscess,³ ,⁴ as there is a risk of abscess reaccumulation or failure to resolve in some cases requiring reaspiration.²

Transfer

Lack of neurosurgical availability is an indication for transfer to a medical center that has such support.

Complications

• Uncal or tonsillar herniation due to increased intracranial pressure (ICP)²¹
• Rupture of abscess into ventricles or subarachnoid space is a complication. This is often lethal. High-risk features for this complication include an abscess that is deep seated, multiloculated, and/or close to the ventricular wall.³²
• Recurrence of abscess²
• Long-term neurologic sequelae in up to 50% of patients (ie, hemiparesis, seizures)^4,6,11,22

Prognosis

• Survival rates for brain abscess are excellent.
• Characteristics associated with an excellent prognosis include the following:
  • Young age¹¹
  • Absence of severe neurologic defect on initial presentation^11,33
  • Absence of neurologic deterioration during initial workup^11,33
  • Absence of comorbid disease^11,33
• Worse prognosis of brain abscess is associated with the following:
  • Signs of herniation on initial presentation (Mortality rate exceeds 50%.¹¹ )
  • Extent of brain lesion on radiology (ie, increased size, critical location, more lesions, increasing edema/midline shift)³⁴
  • Short duration of symptom-onset before diagnosis⁴
  • Gram-negative infection³⁵
  • Nocardial abscess (Mortality rate is 3 times that of bacterial abscess and can reach fatality rates as high as 50% in immunocompromised patients.¹³ )

Patient Education

• For excellent patient education resources, visit eMedicine's Infections Center, Brain and Nervous System Center, and Brain and Nervous System Center. Also, see eMedicine's patient education articles Brain Infection, Antibiotics, and Brain Infection.

Miscellaneous

Medicolegal Pitfalls

• Failure to obtain emergency neuroimaging in patients with headache and new neurologic defect
• Discharging a patient without explaining a new neurologic finding
• Failure to heed family concerns about unusual patient behavior when other symptoms suggestive of brain abscess are present.

References

1. Alderson D, Strong AJ, Ingham HR, et al. Fifteen-year review of the mortality of brain abscess. Neurosurgery. Jan 1981;8(1):1-6. [Medline].

2. Carpenter J, Stapleton S, Holliman R. Retrospective analysis of 49 cases of brain abscess and review of the literature. Eur J Clin Microbiol Infect Dis. Jan 2007;26(1):1-11. [Medline].

3. Lu CH, Chang WN, Lui CC. Strategies for the management of bacterial brain abscess. J Clin Neurosci. Dec 2006;13(10):979-85. [Medline].

4. Mathisen GE, Johnson JP. Brain abscess. Clin Infect Dis. Oct 1997;25(4):763-79; quiz 780-1. [Medline].

5. Sáez-Llorens X. Brain abscess in children. Semin Pediatr Infect Dis. Apr 2003;14(2):108-14. [Medline].

6. Bernardini GL. Diagnosis and management of brain abscess and subdural empyema. Curr Neurol Neurosci Rep. Nov 2004;4(6):448-56. [Medline].

7. Mamelak AN, Mampalam TJ, Obana WG, et al. Improved management of multiple brain abscesses: a combined surgical and medical approach. Neurosurgery. 1995;36(1):76-85. [Medline].

8. Yang KY, Chang WN, Ho JT, et al. Postneurosurgical nosocomial bacterial brain abscess in adults. Infection. Oct 2006;34(5):247-51. [Medline].

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Keywords

brain abscess, intracranial abscess, intracerebral abscess, cerebritis, cerebral abscess

Contributor Information and Disclosures

Author

Lisa Elizabeth Thomas, MD, Staff Physician, Harvard Affiliated Emergency Medicine Residency, Brigham and Women's Hospital and Massachusetts General Hospital
Lisa Elizabeth Thomas, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, and Phi Beta Kappa
Disclosure: Nothing to disclose.

Coauthor(s)

Joshua N Goldstein, MD, PhD, FAAEM, Assistant Professor of Surgery (Emergency Medicine), Harvard Medical School; Attending Physician, Department of Emergency Medicine, Massachusetts General Hospital
Joshua N Goldstein, MD, PhD, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Stroke Association, and Society for Academic Emergency Medicine
Disclosure: CSL Behring Consulting fee Consulting; Genentech Consulting fee Consulting

Medical Editor

Edward Bessman, MD, Chairman, Department of Emergency Medicine, John Hopkins Bayview Medical Center; Assistant Professor, Department of Emergency Medicine, Johns Hopkins University
Edward Bessman, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Barry J Sheridan, DO, Chief, Department of Emergency Medical Services, Brooke Army Medical Center
Barry J Sheridan, DO is a member of the following medical societies: American Academy of Emergency Medicine
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Jonathan Adler, MD, Attending Physician, Department of Emergency Medicine, Massachusetts General Hospital; Division of Emergency Medicine, Harvard Medical School
Jonathan Adler, MD is a member of the following medical societies: American Academy of Emergency Medicine and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

The authors and editors of eMedicine gratefully acknowledge the contributions of previous author, William Ernoehazy, Jr, MD, to the development and writing of this article.

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