Intracranial abscesses are uncommon, serious, life-threatening infections. They include brain abscess and subdural or extradural empyema and are classified according to the anatomical location or the etiologic agent. The term brain abscess is used in this article to represent all types of intracranial abscesses.[1] Intracranial abscesses can originate from infection of contiguous structures (eg,otitis media, dental infection, mastoiditis, sinusitis) secondary to hematogenous spread from a remote site (especially in patients with cyanotic congenital heart disease), after skull trauma or surgery, and, rarely, following meningitis. In at least 15% of cases, no source can be identified.[2] In recent years, the complex array of etiologic agents that cause brain abscess has become better understood.

Brain abscess is caused by intracranial inflammation with subsequent abscess formation. In at least 15% of cases, the source of the infection is unknown (cryptogenic). Infection may enter the intracranial compartment directly or indirectly via 3 routes. Contiguous suppurative focus (45-50% of cases) Direct extension may occur through necrotic areas of osteomyelitis in the posterior wall of the frontal sinus, as well as through the sphenoid and ethmoid sinuses.[3]This direct route of intracranial extension is more commonly associated with subacute and chronic otitic infection and mastoiditis than with sinusitis.[4] Frontal or ethmoid sinus infections generally spread to the frontal lobes. Odontogenic infections can spread to the intracranial space via direct extension or a hematogenous route. These infections also generally spread to the frontal lobe. The frequency of brain abscesses resulting from ear infections has declined in developed countries. However, abscesses complicating sinusitis has not decreased in frequency.[5] Contiguous spread could extend to various sites in the central nervous system, causing cavernous sinus thrombosis; retrograde meningitis; and epidural, subdural, and brain abscess. The valveless venous network that interconnects the intracranial venous system and the vasculature of the sinus mucosa provides an alternative route of intracranial bacterial entry. Thrombophlebitis originating in the mucosal veins progressively involves the emissary veins of the skull, the dural venous sinuses, the subdural veins, and, finally, the cerebral veins. By this mode, the subdural space may be selectively infected without contamination of the intermediary structure; a subdural empyema can exist without evidence of extradural infection or osteomyelitis. Intracranial extension of the infection by the venous route is common in paranasal sinus disease, especially in acute exacerbation of chronic inflammation. Chronic otitis media and mastoiditis generally spread to the inferior temporal lobe and cerebellum, causing frontal or ethmoid sinus infection and dental infection of the frontal lobe.[6] Trauma (10% of cases) Trauma that causes an open skull fracture allows organisms to seed directly in the brain. Brain abscess can also occur as a complication of intracranial surgery, and foreign body, such as pencil tip, lawn dart, bullets, and shrapnel. Occasionally brain abscess can develop after trauma to the face.

is associated with a high mortality rate (up to 80%). Because the main predisposing cause of subdural empyema in young children is bacterial meningitis.Hematogenous spread from a distant focus (25% of cases) These abscesses are more commonly multiple and multiloculated and are frequently found in the distribution of the middle cerebral artery. such as CT scanning and MRI. International Brain abscesses are rare in developed countries but are a significant problem in developing countries. skin infections.[10] The frequency of fungal brain abscess has increased because of the frequent administration of broad-spectrum antimicrobials. Rupture of a brain abscess. Age Brain abscesses occur more frequently in the first 4 decades of life. parietal. the mortality rate has decreased to less than 5-15%. Epidemiology Frequency United States Before the emergence of the AIDS pandemic. abscess. cerebellar.000 hospital admissions. and occipital. temporal. The frequency of neurological sequelae in persons who survive the infection varies from 2079% and is predicated on how quickly the diagnosis is reached and antibiotics administered. The most common effected lobes (in descending frequency) are the fontal. a decrease in meningitis due to the Haemophilus influenzae vaccine has reduced the prevalence in young children History . however.[2] The prevalence of brain abscess in patients with AIDS is higher. brain abscesses were estimated to account for 1 per 10. pulmonary arteriovenous malformations. so the overall rate has thus increased.[9] and HIV infection.[7] These infections are associated with cyanotic heart disease (mostly in children). and corticosteroids.[8] esophageal dilatation. immunosuppressive agents. bronchiectasis). transplantation. neutropenia. injection drug use. empyema.[11] Sex Brain abscesses are more common in males than in females. The predisposing factors vary in different parts of the world. chronic lung infections (eg. endocarditis. or 1500-2500 cases annually. Mortality/Morbidity With the introduction of antimicrobics and the increasing availability of imaging studies. abdominal and pelvic infections.

symptoms are present for 2 weeks or less. Most symptoms are a result of the size and location of the space-occupying lesion or lesions. The frequency of common symptoms and signs is as follows:[1] Headache .65% Fever . Brain abscess usually manifests as symptoms of a space-occupying lesion.50% Seizures .25% Papilledema .25-35% Nausea and vomiting .40% Nuchal rigidity .65% Focal neurologic deficits . The clinical course ranges from indolent to fulminant. is often associated with rupture of the abscess.25% A suddenly worsening headache. and focal neurologic deficit occurs in less than half of patients. The triad of fever. followed by emerging signs of meningismus.70% Mental status changes (may indicate cerebral edema) . The symptoms and signs include the following: Low-grade or high-grade fever Persistent headache (often localized) Drowsiness Confusion Stupor General or focal seizures Nausea and vomiting Focal motor or sensory impairments Papilledema . Physical The clinical manifestations of brain abscess are initially nonspecific. which can lead to delay in diagnosis. headache (often severe and on the side of the abscess).In about two thirds of patients.

hemiparesis with unilateral motor signs.[12. and younger infants may exhibit bulging fontanels. . 13.Neck rigidity In the initial stages of the infection. site of primary infection. vomiting. ipsilateral aphasia (if in the dominant hemisphere). Papilledema may develop in older child and adults. and the patient's immune status. Changes in mental status (lethargy progressing to coma) suggest severe cerebral edema. and hemiparesis Frontal abscess . 14. 15] Oral flora anaerobes generally originate from infected ears and sinuses and abdominal anaerobes (Bacteroides fragilis group) reach the intracranial cavity through bacteremia. 13] Anaerobic and microaerophilic cocci and gram-negative and gram-positive anaerobic bacilli are the most important isolates. vomiting. ataxia. The headache associated with brain abscess can gradually develop or suddenly emerge and is often localized to the abscess' side. an abscess can manifest as a nonspecific form of encephalitis accompanied by signs of increased intracranial pressure. mental status deterioration. inattention. A ruptured brain abscess may produce purulent meningitis associated with signs of neurologic damage. A significant number of brain abscesses are polymicrobic.Ataxia Hemiparesis Neck stiffness Localized neurologic signs are eventually found in most patients. fever.Facial weakness. Vomiting commonly develops in association with increased intracranial pressure. Cerebellar abscess . and visual defects Occipital abscess.Headache. and dysmetria Brainstem abscess .[12.Headache. Causes The etiology depends on the patient's age.Nystagmus. motor speech disorder. Specific clinical symptoms are characteristic of some pathogens. This is a late expression of cerebral edema. and grand mal seizures Temporal lobe abscess . The signs and/or symptoms are a direct function of the intracranial location of the abscess. drowsiness. dysphagia. headache. It is often severe and is not relieved by mild pain medications.

actinomycetemcomitans. Curvularia pallescense. Trypanosoma cruzi. and microaerophilic streptococci. Candida. Bipolaris. including alpha-hemolytic streptococci and Streptococcus anginosus (milleri) group (Streptococcus anginosus. Exophiala dermatitidis. Ochronosis gallopava. including methicillin-resistant[16] Aerobic. Ramichloridium mackenziei) Protozoa (eg. and Proteus species) Pseudomonas species Other anaerobes (Veillonella. and Streptococcus intermedius) Prevotella and Fusobacterium species and B fragilis Enterobacteriaceae (Klebsiella pneumoniae. Histoplasma capsulatum. Mucorales. Actinobacillus. Streptococcus constellatus. Cryptococcus. Coccidioides. Blastomyces dermatitidis. and Salmonella species) Actinobacillus actinomycetemcomitans Actinomyces Nocardia asteroides Mycobacterium species Fungi (eg. Taenia solium) T gondii Pseudallescheria boydii The following organisms are associated with certain predisposing conditions:[17] . Toxoplasma gondii. anaerobic. Aspergillus. Eubacterium) Less common causes include the following: H influenzae Streptococcus pneumoniae Neisseria meningitidis Haemophilus aphrophilus Other Enterobacteriacae (Enterobacter species. Escherichia coli.The predominant organisms include the following: Staphylococcus aureus. Schistosoma. Entamoeba histolytica. Paragonimus) Helminths (eg.

Nocardia.Citrobacter[20] Urinary tract-Pseudomonas. Pseudomonas. microaerophilic streptococci (mainly Streptococcus milleri). Bacteroides). and Enterobacteriaceae Pulmonary infections . 9. Aspergillus. 6. Enterobacter Transplantation . Pseudomonas. 2. anaerobic gramnegative bacilli. microbial flora of brain abscesses is far from being fully known and is differentially distributed depending on the abscess etiology. Bacterial meningitis Brain cancer (primary or metastatic) Cryptococcosis Cysticercosis Epidural Abscess Focal encephalitis Mycotic aneurysm Septic cerebral emboli causing infarction Septic dural sinus thrombosis . Clostridium Neurosurgical procedures-S aureus. Cryptococcus. Actinomyces. Fusobacterium).[24] Differential Diagnoses 1.Aerobic and microaerophilic streptococci. T gondii. Enterobacteriaceae)[14] Ear infections (including mastoiditis) .Aerobic and anaerobic streptococci. Fusobacterium. 22. aerobic streptococci. Therefore. Enterobacteriaceae.T gondii[8] Immunocompromised .Sinus and dental infections . Mycobacterium. Enterobacteriaceae. 3. 8. including 44 not previously described in brain abscess. Mucorales[21. Prevotella. Nocardia.Aspergillus. 5. Candida. Nocardia asteroids. Prevotella. Coccidioides immitis.Aerobic and anaerobic streptococci. 7.Aerobic and anaerobic streptococci. Bacteroides. S aureus Congenital heart disease . Listeria monocytogenes. Cryptococcus. Porphyromonas.Propionibacterium acnes[19] Neonates . 4. Enterobacter.Aerobic gram-negative bacilli. Porphyromonas. S aureus Liver abscess or diabetes mellitus (reported in Southeast Asia) -Klebsiella pneumoniae[18] Penetrating trauma -S aureus. Mucorales. Haemophillus. Haemophillus. Candida. anaerobic gram-negative bacilli (eg.Alpha hemolytic streptococci. L monocytogenes[10] Al Masalma et al performed a 16S rDNA-based metagenomic analysis of cerebral abscesses and identified 80 distinct bacterial taxa. Cryptococcus. Nocardia[9] Endocarditis . 23] HIV infection -T gondii. S aureus. anaerobic gram-negative bacilli (eg.

almost obsolete. consisting of an elevated protein level. pneumoencephalography. A lumbar puncture is mostly of value to rule out other disease processes. ventriculography. CSF polymerase chain reaction [PCR] for Toxoplasma) Blood cultures (at least 2. Serum sodium levels may be low because of inappropriate antidiuretic hormone production.000/µL or higher when the abscess ruptures into the ventricle. It reaches 100. a normal glucose level.[26] The white blood cell count is generally high. CT imaging or MRI scanning prior to lumbar puncture is absolutely indicated upon the presence of any focal neurologic finding or papilledema.Laboratory Studies Routine tests CBC count with differential and platelet count Erythrocyte sedimentation rate (ESR. Cerebrospinal fluid [25] A lumbar puncture is rarely warranted and is contraindicated if increased intracranial pressure is present because of the potential for CNS herniation and death. anaerobic. CT is not as sensitive as MRI but is easier to perform. The results are usually unrewarding. and the ESR and CRP level are generally elevated. elevated in up to two thirds of patients) Serum C-reactive protein (CRP) or Westergren sedimentation rate Serological tests for some pathogens (eg. such as angiography. and the CSF lactic acid level is then elevated to more than 500 mg. . and radionuclide brain scanning. and sterile cultures.[27] Abscess aspirate (obtained via stereotactic CT or surgery) [2] Culture aspirates of abscesses for aerobic. and acid-fast organisms and fungi Gram stain. Many red blood cells are generally observed at that time. preferably before antibiotic usage) Moderate leukocytosis is present. acid-fast stain (for Mycobacterium). serum immunoglobulin G antibodies. especially bacterial meningitis. modified acid-fast stain (forNocardia). pleocytosis with variable neutrophil count. methenamine silver. Platelet counts may be high or low. mucicarmine) Serology anti-anticysticercal antibodies for the diagnosis of neurocysticercosis Histopathological examination of the brain tissue Imaging Studies CT scanning has made other tests. and special fungal stains (eg.

It allows for accurate diagnosis and excellent follow-up of the lesions because of its superior sensitivity and specificity. However. Rarely. and T2-weighted images can demonstrate the edema zone around the abscess. preferably with contrast administration. MRI offers a better ability to detect cerebritis. See the image below. greater contrast between cerebral edema and the brain. and earlier detection of satellite lesions and the spread of inflammation into the ventricles and subarachnoid space. As the abscess forms.[29] . T1-weighted images enhance the abscess capsule. CT scan of a brain abscess. to localize the lesion. In the earlier cerebritis stages. and the location of abscesses. After encapsulation. CT scan results can lag behind clinical findings.CT scanning. a well-organized abscess wall fails to generate such ring enhancement. and to monitor the progression after treatment. provides a rapid means of detecting the size. the enhancement ring. and the cerebral edema around the abscess. CT scans show nodular enhancement with areas of low attenuation without enhancement. CT scans characteristically show the brain abscess as a hypodense center with a peripheral uniform enhancement ring. and it has become the mainstay of diagnosis and follow-up care. Contrast enhancement with gadolinium diethylenetriaminepentaacetic acid (a paramagnetic agent) helps differentiate the abscess. contrast enhancement is observed. Compared with CT scanning. This method is used to confirm the diagnosis. Many authorities consider MRI to be the first diagnostic method in the diagnosis of brain abscess. See the image below. the number.[28] After the injection of a contrast material. the contrast material cannot help differentiate the clear center and the CT scan is similar in appearance to those obtained during the early cerebritis stage. MRI of a brain abscess.

while others advocate repeated aspirations as indicated. Other Tests ECG occasionally reveals a focus of high voltage with slow activity.[33] Once an abscess has formed. special immunochemical tests can be used to detect the organism or its antigens. This is the least accurate procedure in the diagnostic evaluation. Some neurosurgeons advocate complete evacuation of the abscess. is essential in monitoring .[30] Susceptibility-weighted phase imaging showed evidence of paramagnetic substances in agreement with the presence of free radicals from phagocytosis in a study of 14 patients with brain abscesses.Diffusion-weighted (magnetic resonance) imaging (DWI) can be used to differentiate between ring-enhancing lesions caused by brain abscess (hypertensive on DWI) from a malignant lesion (hypotensive on DWI). An early effort at making a microbiologic diagnosis is important in planning appropriate antimicrobial therapy. The introduction of CT-guided needle aspiration may provide this important information.[32] Medical Care Before the abscess has become encapsulated and localized. surgical excision or drainage combined with prolonged antibiotics (usually 4-8 wk) remains the treatment of choice. repeated aspirations are preferred to complete excision. and number of abscesses using contrast CT scanning or MRI. Since the advent of CT scanning and MRI.5 cm or which are at the cerebritis stage are aspirated for diagnostic purposes only. the case-fatality rate has decreased by 90%. while those smaller than 2. antimicrobial therapy. In patients with toxoplasmosis. is essential.[34] The first step is to verify the presence. size. accompanied by measures to control increasing intracranial pressure. Procedures Biopsy of cerebral lesion: Hyphae and type of branching can assist in ion diagnosis of specific fungal infections. and the lesion becomes gradually surrounded by a fibrotic capsule. High-dose antibiotics for an extended period may be an alternative approach in this group of patients. A brain-touch technique using immunofluorescence monoclonal antibodies against the organism can also provide rapid diagnosis. Abscesses larger than 2. Staging The early stage of the infection (first 7-14 d) is called cerebritis and is associated with edema. Frequent scanning. It is nonspecific and rarely of value in confirming the diagnosis. In cases of multiple abscesses or in abscesses in essential brain areas. at least once per week.[31] This technique may provide additional information that is valuable in the characterization of pyogenic brain abscesses.5 cm are excised or aspirated. Emergent surgery should be performed if a single abscess is present. Necrosis and liquefaction occur after 2-3 weeks.

while abscesses larger than 2.5 cm generally respond to antimicrobial therapy. and any effect of steroid therapy on the course of the disease are unknown. Because of the difficulty involved in the penetration of various antimicrobial agents through the blood-brain barrier. When used to reduce cerebral edema.5 wk) and complete resolution in 1-11 months (average. Patients treated with medical therapy alone usually demonstrate clinical improvement before significant changes in the CT scan are observed.5 cm have failed to respond to such treatment.5 mo). and a lessening of the enhancement ring. a decrease in accompanying edema. CSF. may prevent the progress from cerebritis to abscess. Steroid therapy can also produce a rebound effect when discontinued. 2.[35] Corticosteroid use is controversial. The initial course is through an intravenous route. therapy should be of short duration. Improvement on CT scans is generally observed within 1-4 weeks (average. Abscesses smaller than 2. increase necrosis. The appropriate dosage.[35] The length of therapy is guided by continuous assessment of the clinical course and followup imaging studies. Numerous factors should be considered when trying to decide the appropriate approach to therapy. the choice of antibiotics is restricted. selected patients may respond to antibiotics alone.treatment response. A shorter course (3-4 wk) may be adequate in patients who underwent surgical drainage. Steroids can retard the encapsulation process. Although surgical intervention remains an essential treatment. the proper timing. Initial empiric antimicrobial therapy should be based on the expected etiologic agents according to the likely predisposing conditions. CT scanning and MRI should eventually show a decrease in the size of the lesion. when no evidence of an expanding mass lesion exists. The antimicrobial therapy is continued until a clinical response occurs and CT or MRI findings show resolution. and alter the appearance on CT scans because of contrast reduction. abscess. and the . the primary infection source. or other normally sterile sites is essential because it allows for the most appropriate selection of antimicrobial agents. Antibiotic therapy during the early stage. The duration of the symptoms before diagnosis is an important factor. often followed by additional 2-6 months of appropriate oral therapy. Patients who have symptoms for less than a week have a more favorable response to medical therapy than patients with symptoms persisting longer than 1 week. Corticosteroids are used when a significant mass effect is visible on imaging and the patient’s mental status is depressed. However. 3. This finding alone is not an indication to continue antimicrobial therapy or for surgical drainage. The antimicrobial treatment of the brain abscess is generally long (6-8 wk) because of the prolonged time needed for brain tissue to repair and close abscess space. Knowledge of the etiologic agent or agents by recovery from blood. reduce antibiotic penetration into the abscess. Bacterial abscess in the brain is preceded by infarction and cerebritis. increase the risk of ventricular rupture. because the abscess site may show persistent enhancement for several months. and maximal doses are often necessary.

and daptomycin (6 mg/kg IV qd). Antimicrobial that are alternatives to vancomycin include linezolid (600 mg IV or PO bid). and its activity against anaerobic gram-positive anaerobes may be suboptimal. However. Patients with HIV infection may require therapy for toxoplasmosis. When abscess specimens are available. and the addition of rifampin has been shown to be of benefit in staphylococcal meningitis. Chloramphenicol penetrates well into the intracranial space and is also active against Haemophilus species. or sinus origin. or following neurosurgery or penetrating trauma). oxacillin. However. trimethoprim-sulfamethoxazole (5 mg/kg q8-12h). ceftriaxone).presumed pathogenesis of abscess formation. methicillin. staining of the material can help guide selection of therapy. Because of the risk of methicillin-resistant S aureus (MRSA) infection they should only be administered to treat culture proved MSSA . the parenteral cephalosporin of choice is a forth generation cephalosporin (ceftazidime or cefepime). Aminoglycosides do not penetrate well into the CNS and are relatively less active because of the anaerobic conditions and the acidic contents of the abscess. Specific antibiotics [37] Penicillin penetrates well into the abscess cavity and is active against non–beta–lactamaseproducing anaerobes and aerobic organisms. vancomycin (effective against methicillin resistance S aureus) is administered. it is only active against strict anaerobic bacteria. If pseudomonads are isolated or anticipated. the initial empiric therapy can be adjusted to specifically treat the isolated bacteria. cefotaxime plus metronidazole). and most obligate anaerobes. Beta-lactamase–resistant penicillins (eg.[16] . Limited data regarding their use in brain abscess are available. their penetration into the CNS is less than penicillin. Its use has been curtailed dramatically in most US centers because of the availability of other equally efficacious and less toxic antimicrobial combinations (ie. This choice is appropriate for the treatment of an abscess of oral. When S aureus is suspected (a hematogenic origin. However. Metronidazole penetrates well into the CNS and is not affected by concomitant corticosteroid therapy. the emergence of beta–lactamaseproducing organisms limits it use. cefotaxime. Vancomycin is most effective against MRSA and Staphylococcus epidermidis as well as aerobic and anaerobic streptococci and Clostridium species. Cefepime or ceftazidime is administered to treat gram negative aerobic bacteriaPseudomonas aeruginosa infection. gram-negative bacilli). otogenic.[36] Coverage for streptococci can be attained by a high dose of penicillin G or a third-generation cephalosporin (eg. nafcillin) provide good coverage against methicillin-sensitive S aureus (MSSA). Third-generation cephalosporins (eg. cefotaxime. However. they may be considered in instances in which vancomycin is ineffective or can not be used. Whenever proper cultures are taken and organisms are isolated and their susceptibility is determined. Metronidazole is included to cover penicillinresistant anaerobes (ie. S pneumoniae. ceftriaxone) generally provide adequate therapy for aerobic gram-negative organisms as well as microaerophilic and aerobic streptococci. Metronidazole may be added to cover anaerobic bacteria.

The administration of beta-lactamase–resistant penicillin or vancomycin (if methicillinresistant staphylococci are isolated) for the treatment of S aureus is generally recommended. Imipenem has been associated with an increased risk of seizures in patients with brain abscess. If not recognized early. Management of subdural empyema requires prompt surgical evacuation of the infected site and antimicrobial therapy. . because high doses of these agents may be associated with seizure activity. Emergent surgery is needed if neurologic signs related to a mass lesion progress. data are limited regarding their use in treating brain abscesses. It is repeated if the patient fails to respond to therapy. voriconazole for Aspergillus and P boydii infections. Although fluoroquinolones have good penetration into the CNS. Surgical Care Surgical drainage provides the most optimal therapy. and instillation of antibiotics into the abscess after drainage is not needed. Needle aspiration is the preferred and the most commonly used procedure and is often performed using a stereotactic procedure with the guidance of ultrasound or CT scanning. Injection of antibiotics into the abscess cavity was advocated in the past in an effort to sterilize the area before operation. most of the anaerobic pathogens isolated are sensitive to penicillin. and meropenem. Caution should be used in administering carbapenems and beta-lactamases in general. chloramphenicol. Therapy with penicillin should be added to metronidazole to cover aerobic and microaerophilic streptococci. Porphyromonas species. empiric therapy should include agents effective against them that can also penetrate the blood-brain barrier. Cryptococcus. Because these penicillin-resistant anaerobic organisms predominate in brain abscesses.[38] Ventricular drainage combined with administration of intravenous and/or intrathecal antimicrobials is used to treat brain abscesses that rupture into the ventricles. imipenem. However. Craniotomy is generally performed in patients with multiloculated abscesses and in those whose conditions fail to resolve.[34] For optimal results. and Mucoralesinfections. These procedures are also diagnostic and provide material that can guide antimicrobial therapy. These include metronidazole. ticarcillin plus clavulanic acid.With the exception of the Bacteroides fragilis group and some strains of Prevotellaspecies. Aspiration is especially preferred if the speech. motor or sensory cortex area are involved or the patient is comatose. The procedures used are aspiration through a bur hole and complete excision after craniotomy. T gondii infection is treated with pyrimethamine and sulfadiazine. many antimicrobials penetrate brain abscess cavities fairly well. this is usually performed prior to the initiation of antibiotic therapy. both subdural empyema and brain abscess can be fatal. Antibiotics have improved the outlook. Amphotericin B is administered for Candida. and Fusobacterium species. Failure to perform surgical drainage can lead to a higher mortality rate.

A delay in surgical drainage and decompression can be associated with high morbidity and mortality. and/or a progressively growing abscess.Vancomycin. mastoiditis. increased intracranial pressure. Excision is also indicated even after initial aspiration or drainage in patients with depressed sensorium.Vancomycin plus gentamicin in prosthetic valve. periodontal abscess) by an oral surgeon or dentist. cefepime or ceftazidime. Other specialists may be consulted as required by the patient's condition.Vancomycin plus a third-generation cephalosporin Postsurgical .Penicillin plus metronidazole and a sulfonamide (forNocardia infections) Congenital heart disease . This includes drainage of an infected sinus by an otolaryngologist or treatment of a dental infection (eg. no clinical improvement within 7 days. The risk of repeating aspiration is that the procedure may cause bleeding. Excision is clearly indicated in posterior fossa or multiloculated abscesses. and metronidazole . 2 surgical approaches are available: stereotactic-guided aspiration and excision. Optimal therapy of fungal brain abscess generally requires both medical and surgical approach. Patients who do not meet the criteria for medical therapy alone require surgery. and those that reaccumulate following repeated aspirations.Nafcillin or vancomycin plus cefepime or ceftazidime Penetrating trauma . Recent studies illustrate that brain abscess in the early phase of cerebritis may respond to antimicrobial therapy without surgical drainage.Third-generation cephalosporin with metronidazole or ampicillinsulbactam Endocarditis . Consultations The management of a patient in whom a brain abscess is suspected or present involves cooperation among neurologists. and sinusitis . neurosurgeons. those caused by unencapsulated lesions due to fungal or helminthic infection. ampicillin plus gentamicin or third-generation cephalosporin plus vancomycin in natural valve Intravenous drug abuse . Predisposing factors include the following:         Otitis.Penicillin plus metronidazole or amoxicillin-sulbactam Pulmonary infections . Surgical drainage may be necessary in many patients to ensure adequate therapy and complete resolution of infection. those associated with traumatic brain injury (to remove foreign material). Drainage may be delayed or avoided if the infection is at the cerebritis stage or the lesion is at a vital or inaccessible region.Although proper selection of antimicrobial therapy is most important in the management of intracranial infections.Combination of metronidazole or ampicillin-sulbactam plus a third-generation cephalosporin (in those with a predisposing condition) Dental infection . surgical drainage may be required. The primary source of the infection may require the attention of specialists. and infectious disease specialists. Medication Summary The choice of combinations of empiric therapy must cover a broad spectrum of both aerobic and anaerobic bacterial pathogens. Currently. Needle aspiration is generally preferred to surgical excision because it results in fewer sequelae.

View full drug information Cefotaxime (Claforan) Third-generation cephalosporin that has broad gram-negative spectrum. View full drug information Ceftazidime (Fortaz. View full drug information Ampicillin (Marcillin. Antibiotics Class Summary Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting. lower efficacy against gram-positive organisms. and instillation of antibiotics into the abscess after drainage is not needed. and higher efficacy against resistant organisms. View full drug information Chloramphenicol (Chloromycetin) Binds to 50S bacterial ribosomal subunits and inhibits bacterial growth by inhibiting protein synthesis. gram-negative activity.Metronidazole. Alternative to amoxicillin when unable to take medication orally. The anti-inflammatory effects of corticosteroid therapy can decrease cerebral edema. and vancomycin  Neonates. and higher efficacy against resistant organisms. it arrests bacterial cell wall synthesis and inhibits bacterial growth. By binding to 1 or more of the penicillin-binding proteins. it prevents resistance from bacterial subpopulations and provides additive or synergistic effects. higher efficacy against resistant organisms. . View full drug information Ceftriaxone (Rocephin) Third-generation cephalosporin that has broad gram-negative spectrum. or a third-generation or fourth-generation cephalosporin Vancomycin may be required where MRSA is suspected. lower efficacy against gram-positive organisms. Arrests bacterial growth by binding to 1 or more penicillin-binding proteins.third-generation cephalosporin. Complications of meningitis in infants and children . Injection of antibiotics into the abscess cavity was advocated in the past in an effort to sterilize the area before operation. 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. However. Omnipen) Bactericidal activity against susceptible organisms. the use of antibiotic monotherapy is then recommended. vancomycin. In addition. Antibiotic combinations are usually recommended for serious gram-negative bacillary infections. reducing intracranial pressure. Tazidime) Third-generation cephalosporin with broad-spectrum.third-generation cephalosporin and ampicillin  No predisposing condition or the immunocompromised . many antimicrobials penetrate brain abscess cavities fairly well. it arrests bacterial cell wall synthesis and inhibits bacterial growth. Ceptaz. Effective against gram-negative and gram-positive bacteria. By binding to 1 or more of the penicillin-binding proteins. Once organisms and sensitivities are known. This approach ensures coverage for a broad range of organisms and polymicrobial infections. lower efficacy against grampositive organisms. ampicillin.

A sequela of periapical abscess. View full drug information Meropenem (Merrem) Bactericidal broad-spectrum carbapenem antibiotic that inhibits cell wall synthesis. View full drug information Metronidazole (Flagyl) Imidazole ring-based antibiotic active against various anaerobic bacteria and protozoa. Intracranial complications of sinusitis in children. Dexasone) Corticosteroid of choice for reducing intracranial pressure. Used in treatment of inflammatory diseases. 3. View full drug information Vancomycin (Vancocin) Potent antibiotic directed against gram-positive organisms and active againstEnterococcus species. Levy RM. Brain abscess. Jan-Feb 1982. Useful in the treatment of septicemia and skin structure infections. [Medline]. May be absorbed into the cells. Mathisen GE. Use creatinine clearance to adjust dose in patients with renal impairment.91(1 Pt 1):41-3.5 h prior to next dosing. [Medline]. . 2. [Medline]. Used in combination with other antimicrobial agents (except for C difficile enterocolitis). May decrease inflammation by suppressing migration of polymorphonuclear leukocytes and reversing increased capillary permeability. Brain abscess and subdural empyema. Corticosteroids Class Summary These agents have anti-inflammatory properties and cause profound and varied metabolic effects. Has slightly increased activity against gram-negative organisms and slightly decreased activity against staphylococci and streptococci compared to imipenem. View full drug information Dexamethasone (Decadron. quiz 7801.7(3):2238. Oct 1997. To avoid toxicity. and the intermediate-metabolized compounds that bind DNA are then formed and inhibit synthesis. View full drug information Cefepime (Maxipime) Fourth-generation cephalosporin with good gram-negative coverage. Corticosteroids modify the body's immune response to diverse stimuli. Jun 1994. Friedman EM. References 1. Clin Infect Dis.25(4):763-79. Johnson JP. Effective against most gram-positive and gram-negative bacteria.View full drug information Imipenem plus 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. current recommendation is to assay vancomycin trough levels after third dose drawn 0. Curr Opin Neurol. Similar to third-generation cephalosporins but has better gram-positive coverage.Ann Otol Rhinol Laryngol. Brook I. Indicated for patients who cannot receive or have failed to respond to penicillins and cephalosporins or have infections with resistant staphylococci. causing cell death.

10(4):283-8. 18.42(5):405-12.[Medline]. Characteristics of brain abscess with isolation of anaerobic bacteria. 9. NY: Academic Press. [Medline]. Chandra RK. Brain abscess in 142 patients: factors influencing outcome and mortality. Al Masalma M. Springfield: CC Thomas. Corral O. et al. Jun 2006. 7. discussion 876-7. Intracranial complications of pediatric sinusitis. [Medline]. Tseng MY.[Medline]. [Medline]. Cerebellar aspergillosis: case report and literature review. Lu CY. Surg Neurol. Brook I. Spring 2002. Brook I. Sanchez-Portocarrero J. Pomeroy SL. Jan 2007.50(4):874-6. Int J Pediatr Otorhinolaryngol. Pediatrics. Otogenic intracranial complications: a review of 28 cases. Transpl Infect Dis. Balow's infections of the central nervous system. 23. Singh N. Lee PI. 19. [Medline].125(8):819-22. Drancourt M. et al. et al. Finegold SM. 21. Ronsyn M. J Child Neurol. [Medline]. 16. Grollier G.66(6):793-5. 5.73(9):1183-6. Aug 2005. [Medline]. Otolaryngol Head Neck Surg. Jan 2012. Oct 2009. Metagenomic analysis of brain abscesses identifies specific bacterial associations. Sep 2009. 20. Kranick SM. Celasun B. 10. Duvdevani S. Neurosurgery. Ann Hematol. 2004. Propionibacterium acnes brain abscess appearing 10 years after neurosurgery. Swartz MN. Roche PH. Pradhan SK. Update on the treatment of cerebral aspergillosis. The central nervous system and infection by Candida species. Brook I. May 2006. discussion 562. Kolson DL. Arch Neurol. 24. Bensalem MK. Diagn Microbiol Infect Dis. [Medline]. Naesens R. Goodkin HP. Lonjon M. Husain S. Retrospective analysis of 49 cases of brain abscess and review of the literature. HIV and the central nervous system. J Med Microbiol. Anaerobic Bacteria in Human Disease.28(1):23-33. Infect Dis Clin North Am. [Medline]. Sep 2000. 15. Glickstein JS. Berger JR. [Medline]. Jun 2004.113(6):1765-70. Richet H. 8. Thiel E. Stapleton S. Apr 2002. Migirov L.134(5):733-6. Dufour H. Arpaci F. . In: Anaerobic Bacteria: Role in Disease.4. Le Moal G. Clin Infect Dis.[Medline]. 6. Thompson JW. Compr Ther. Microbiology and epidemiology of brain abscess and subdural empyema in a medical center: a 10-year experience.37(3):169-79. Schwartz S. Intracerebral abscess in children: historical trends at Children's Hospital Boston.65(6):557-62. Arch Otolaryngol Head Neck Surg. 11. Acta Otolaryngol. Jul 1995. et al.16(3):589-605. [Medline]. 12. Landron C. Scand J Infect Dis. Brain abscess in children: microbiology and management. J Microbiol Immunol Infect. Microbiology and antimicrobial treatment of orbital and intracranial complications of sinusitis in children and their management. Jun 2009.131(11):1017-9. Nov 2005.2(3):101-11. New York. Holliman R. [Medline]. Kronenberg J. Sep 2009. Druwe P. 22. et al. Erdogan E. Carpenter J. [Medline]. Harper MB. Central nervous system infections in injection drug users. [Medline]. Microbiology of intracranial abscesses and their associated sinusitis. Beyzadeoglu M. [Medline].83 Suppl 1:S42-4.35(5):318-21. 13. 1977. Central nervous system invasion by communityacquired meticillin-resistant Staphylococcus aureus. Perez-Cecilia E. Tunkel AR. Jul 2000. 14. Karchmer AE.54(2):202-10. Eur J Clin Microbiol Infect Dis. Tsou TP. Sep 2002. Infections of the central nervous system in transplant recipients. Vinnard C. [Medline]. 2003.26(1):1-11. 17. 1974:309-25. [Medline].58(Pt 9):1247-51. Tseng JH.

[Medline]. Brain abscess: an overview. Jan 2004.58(6):395-402. Dec 2002. The penetration of antibiotics into cerebrospinal fluid and brain tissue. May-Jun 1981. . Computerized tomographic. Nov 2004.31(1):69-71.25. Adv Tech Stand Neurosurg. Nov 1999. [Medline]. [Medline]. Chuang TC. Yogev R. Livraghi S.4(6):448-56. et al. 29. Bar-Meir M. 38. Jan 26 2012. Iwai Y. The management of brain abscesses. 34. Goel A. Honda H. Britt RH. 2011. Rev Infect Dis. Management of brain abscesses in children. Diffusion-weighted MR imaging in the preoperative assessment of brain abscesses. Wippold FJ 2nd. Crit Rev Comput Tomogr.4(3):203-27. Warren DK. Li JY. 26.52(5):445-8. Intracranial pyogenic abscess: imaging diagnosis utilizing recent advances in computed tomography and magnetic resonance imaging.23(3):609-23. [Medline]. 32. [Medline]. Bernardini GL. et al. Clinical stages of human brain abscesses on serial CT scans after contrast infusion. J Neurosurg. 33. 2004. [Medline]. Nakajima H. Feb 2004.22(4):72430.3(3):470-8. neuropathological. Selkon JB. Chung HW. 36.59(6):972-89. Sep 2009. Apr 1988. Muzumdar D. [Medline]. Sener RN. Curr Neurol Neurosci Rep. and clinical correlations. Stephanov S. May 1978. Surg Neurol.28:285-313. J Neuroradiol. Neurosurgery.[Medline]. Yamanaka K. [Medline]. Weng MJ. 30. Black BR.5T: Characteristics of the Abscess Capsule. Diagnosis and management of brain abscess and subdural empyema.9(2):13644. [Medline]. The importance of lactic acid levels in body fluids in the detection of bacterial infections. Oswood MC. [Medline]. Chang HC. 37. et al. et al. Pediatr Infect Dis J. Successful treatment of brainstem abscess with stereotactic aspiration. Brook I. AJNR Am J Neuroradiol. Surg Neurol.[Medline]. Diffusion MRI findings in neonatal brain abscess. Barling RW. [Medline]. Susceptibility-Weighted Imaging in Patients with Pyogenic Brain Abscesses at 1. Jhawar S. [Medline]. Antunes JL. 27. Surgical treatment of brain abscess. 31. Leimkuehler MM.45(3):181-224. Int J Surg. Leuthardt EC. Infect Dis Clin North Am. Central nervous system infections: meningitis and brain abscess. J Antimicrob Chemother. Lai PH. discussion 402. 35. 2003. 28. Enzmann DR. Nguyen JB. Dec 1983. Melancia JP.23(2):157-9.

Sign up to vote on this title
UsefulNot useful