Epidemiology and Risk Factors. Brain abscess is a rare disease in immunocompetent individuals. In adults, otitis media and paranasal sinusitis (frontal, ethmoidal, or sphenoidal sinuses) are the most common predisposing conditions for brain abscess formation. In children, otitis media and cyanotic congenital heart disease are the most common predisposing conditions for brain abscess formation. Individuals with the acquired immunodeficiency syndrome (AIDS) are at increased risk for focal intracranial infections caused by Toxoplasma gondii. Organ transplant recipients are at risk for brain abscesses caused by Aspergillus fumigatus. Patients receiving chronic corticosteroid therapy and those who are immunosuppressed from bone marrow transplantation are at a particular risk for CNS candidiasis manifested as multiple intraparenchymal microabscesses mainly in the territory of the middle cerebral artery. Brain abscesses may develop as a result of cranial trauma, either penetrating brain injuries or neurosurgical procedures, of which the most common is craniotomy. The reported incidence of brain abscess following clean neurosurgical procedures is 6 to 7 per 10,000 cases. y A brain abscess may develop as the result of hematogenous spread of infection from a remote site such as chronic pyogenic lung diseases, wound and skin infections, osteomyelitis,
intra-abdominal and pelvic infections, and endocarditis. Finally, pulmonary arteriovenous malformation is a predisposing condition for brain abscess formation.
Pathogenesis and Pathophysiology. A brain abscess may develop in association with any of the following: (1) direct spread from a contiguous cranial site of infection such as otitis media, odontogenic infections, sinusitis or mastoiditis, or retrograde septic thrombophlebitis from these sites as well as facial and scalp infections; (2) following cranial trauma; (3) hematogenous spread from a remote infection site; and, (4) immunosuppression either from neutropenia, organ or bone marrow transplantation, lymphoma, leukemia or AIDS. Approximately 20 percent of brain abscesses are said to be cryptogenic, with no predisposing factor. The results of animal experiments suggest that in order for brain abscesses to form, there must be a pre-existing area of ischemia, necrosis, or hypoxia in brain tissue. y Intact brain parenchyma is relatively resistant to infection. y Once bacteria have established an infection, brain abscess formation evolves through four stages regardless of the infecting organism. These stages were described in animal models of brain abscesses, and have been shown to correlate with human brain abscess evolution observed by computed tomography (CT) imaging. These stages are early cerebritis, late cerebritis, early capsule formation, and late capsule formation. The early cerebritis stage (days 1 to 3 following intracerebral inoculation with alpha-hemolytic streptococci in dogs) is characterized by perivascular infiltration of inflammatory cells composed of polymorphonuclear leukocytes, plasma cells, and mononuclear cells that surround a central core of coagulative necrosis. Marked cerebral edema surrounds the lesion at this stage. y , y The CT scan reveals a low-density lesion with faint contrast enhancement at its edge. The late cerebritis stage (days 4 to 9) is characterized by a lesion with a necrotic center surrounded by an inflammatory infiltrate of macrophages and fibroblasts. Rapid new vessel formation occurs around the developing abscess. A thin capsule of fibroblasts and reticular fibers gradually develops, and the area is surrounded by cerebral edema. The CT scan image demonstrates a low-density lesion surrounded by a prominent ring of enhancement following contrast administration. In the stage of early capsule formation (days 10 to 13), the necrotic center decreases in size, and the inflammatory infiltrate changes in character and contains an increasing number of fibroblasts and macrophages. Mature collagen evolves from reticulin precursors, forming a capsule that is better developed on the cortical than the ventricular side of the lesion. The CT scan image shows an area of low density, and the diameter of ring-contrast enhancement has decreased in size. The stage of late capsule formation (day 14 and later) is characterized by a well-formed necrotic center surrounded by a dense collagenous capsule. On the CT scan image, the low-density lesion is surrounded by a sharply demarcated, dense ring of contrast enhancement. The above-mentioned description of brain abscess formation may be modified slightly by different microorganisms and altered in the immunocompromised host. Depending on the etiologic organism and the predisposing condition leading to infection, there may be delayed or incomplete encapsulation of the abscess cavity, or the abscess may enlarge more quickly than described earlier. y
Clinical Features and Differential Diagnosis. A brain abscess presents as an expanding focal infectious mass lesion. The most common clinical presentation is headache, either hemicranial or generalized, fever, vomiting, a focal neurological deficit, or focal or generalized seizure activity. The findings on neurological examination are related both to the site of the abscess and to the degree of raised ICP. Patients with increased ICP will have alterations in consciousness ranging from lethargy to irritability, confusion, or coma. There may be papilledema, and deficits of cranial nerves III or VI, or both. If the abscess has ruptured into the ventricular system or if there has been spread of infection to the subarachnoid space, there may be signs of meningitis. The differential diagnosis of this clinical presentation includes herpes simplex virus encephalitis, subdural empyema, cranial epidural abscess, a focal cerebral infarction with edema, a cerebral hemorrhage, a primary neurological tumor, or a metastatic tumor.
Evaluation. The diagnosis of a brain abscess is made through neuroimaging using either a cranial CT or MRI scan that demonstrates a ring-enhancing lesion. Typically, the cranial CT scan demonstrates the abscess as a low- density lesion with a sharply demarcated, dense ring of contrast enhancement surrounded by a variable hypodense region of edema. In the early and late stages of cerebritis, there is often diffusion of contrast medium into the low- density center of the abscess on delayed scans obtained 30 minutes after the administration of intravenous contrast. As the abscess matures, its margin becomes more defined and the enhancement around the abscess become more homogeneous. In the early and late stages of capsule formation, there is no significant inward diffusion of contrast on delayed scans. Cranial MRI scanning is superior to cranial CT scanning in detecting a lesion in the early cerebritis stage. On this type of image, the abscess appears as an area of hypointensity on T1-weighted images and hyperintensity on T2-weighted images with indistinct margins. When the abscess becomes encapsulated, it appears as a lesion of low intensity surrounded by an area of isointensity or hyperintensity on T1-weighted images. The T2-weighted MRI images reveal a hyperintense lesion surrounded by a rim of hypointensity with surrounding area of hyperintensity that represents edema. The T1-weighted MRI images obtained after intravenous gadolinium administration demonstrate ring enhancement of the abscess capsule. y Patients with a brain abscess may have a peripheral leukocytosis or an elevated erythrocyte sedimentation rate; however, in a significant number of patients, the laboratory criteria for infection will be lacking. The serum C-reactive protein (CRP) concentration has been reported to be useful in distinguishing brain abscess from brain tumor. Patients with brain abscesses have an elevated CRP level, whereas those with a brain tumor will have low levels. y , '45' Indium-111-labeled leukocyte scintigraphy may also be useful in distinguishing between a brain abscess and tumor. This scan uses radiolabeled leukocytes to detect areas of active inflammation. False-positive results may occur when there has been leukocytic infiltration into a brain tumor, especially those with severe necrosis. A lumbar puncture is contraindicated in a patient with a brain abscess because of the risk of herniation. The etiological organism is rarely identified from CSF cultures obtained by lumbar puncture,
but it can be identified by CT- or MRI-guided stereotactic aspiration of the abscess. This approach is the procedure of choice for the identification of the infectious organism. All patients should also have a chest roentgenogram. Additionally, a CT scan of the head with bony windows for the evaluation of the paranasal sinuses, middle ear, and mastoids should be done when a contiguous site of infection is suspected as the source of the brain abscess. Blood cultures should be obtained when hematogenous dissemination from a remote site of infection is the likely etiology.
Management. The management of a brain abscess is directed at decreasing the mass effect associated with the abscess, draining the pus, and the use of antimicrobial therapy to treat the abscess and the primary source of infection. [4o] Surgical management of a brain abscess involves either complete extirpation of the abscess or aspiration of the abscess cavity through a burr hole with or without placement of a drainage catheter into the abscess cavity. The purulent material obtained at the time of aspiration allows for the identification of the infecting organism. Aspiration of the contents of an abscess cavity has a lower morbidity and a lower risk of seizures compared with complete excision. Complete excision removes the lesion from the parenchyma of the brain and allows for a rapid decompression but may cause damage to brain parenchyma. Complete excision is recommended when gas is present within the abscess cavity and for some fungal abscesses, particularly Nocardia species.
In the majority of patients with a brain abscess, stereotactic aspiration of the abscess should be performed for Gram's stain and bacterial culture, as well as fungal smear and culture. In patients with AIDS, however, the majority of focal infectious CNS lesions are caused by T. gondii, and in such cases, serum should be sent for antitoxoplasma IgG. The lesions of T. gondii are typically located at the gray-white junction in the cerebral hemispheres, in the deep white matter, and in the thalamus and basal ganglia. With contrast administration, the majority of lesions enhance in a ringed, nodular, or homogeneous pattern and are surrounded by edema. Cranial MRI scanning is superior to CT scanning in detecting the multiple lesions of toxoplasma abscesses. Thallium single photon emission computed tomography imaging may be helpful in distinguishing cerebral toxoplasmosis from primary CNS lymphoma. Focal areas of increased uptake are seen in patients with lymphoma. In patients with a detectable toxoplasma serology and more than one enhancing lesion on neuroimaging, a presumptive diagnosis of toxoplasma encephalitis can be made and a treatment trial with pyrimethamine and sulfadiazine or pyrimethamine and clindamycin can be initiated. The other group of patients that provide an exceptional diagnostic and therapeutic challenge are those not infected with HIV but who have multiple brain abscesses. In these patients, stereotactic aspiration of the largest lesion for purulent material for culture is recommended.
The etiological organism of a brain abscess can be predicted to some degree based on the location of the abscess and the predisposing condition. Streptococci, specifically S. milleri, are the most frequent organisms isolated from frontal lobe abscesses associated with chronic sinusitis. Temporal lobe abscesses are most frequently secondary to chronic infections of the ear, and streptococci (anaerobic or aerobic), Enterobacteriaceae and Bacteroides species are the most commonly isolated bacteria. A brain abscess owing to chronic otitis media frequently yields multiple organisms in culture. The majority of brain abscesses secondary to trauma or craniotomy are caused by S. aureus. [4o] Viridans, anaerobic, and microaerophilic streptococci are the usual organisms isolated from brain abscesses caused by cyanotic congenital heart disease. A brain abscess in an immunocompromised individual may be from Candida species, Nocardia asteroides, Aspergillus, Zygomycetes, Enterobacteriaceae or P. aeruginosa.
A combination of vancomycin (2 g/d intravenously in an adult, 40 to 60 mg/kg/d in a child), a third-generation cephalosporin (cefotaxime, ceftriaxone, or ceftazidime), and metronidazole (500 mg q 6 hr intravenously for an adult and 7.5 mg/kg q 8 hr for a child) is the recommended empirical therapy for immunocompetent patients with brain abscesses. The final culture results and organism sensitivities are used to make the antibiotic coverage more specific. Aspergillosis should be considered in immunosuppressed patients with unremitting fever and multiple brain abscesses. A chest x-ray study may demonstrate pulmonary infiltrates and bronchoscopy may identify the infecting organism in some cases. Fungal brain abscesses are treated with amphotericin B; liposomal amphotericin B should be used for brain abscesses due to Aspergillus species. Corticosteroid therapy is recommended for the treatment of vasogenic cerebral edema that surrounds a brain abscess and to treat any mass effect. Because steroid therapy may decrease the penetration of antibiotics into brain tissue, it should be discontinued when the edema and mass effect improve or resolve. Abscesses that enlarge or do not become smaller during antimicrobial therapy may need repeat aspiration or excision.
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