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Brain Abscess


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Brain Abscess...

M.C. Brouwer and Others

Clinical Pearls

What is the epidemiology of brain abscesses?

Severe immunocompromise, resulting from immunosuppressive therapy in patients who have undergone solid-organ or hematopoietic stem-cell transplantation or from HIV infection, is often associated with tuberculosis or nonbacterial causes of infection, such as fungi or parasites. HIV infection is associated with brain abscess caused by Toxoplasma gondii, but HIV infection also predisposes patients to infection with Mycobacterium tuberculosis. Patients who have received solid-organ transplants are at risk not only for nocardial brain abscess but also for fungal abscess (e.g., resulting from infection by aspergillus or candida species). Abscess formation may occur after neurosurgical procedures or head trauma. In these cases, infection is often caused by skin-colonizing bacteria, such as Staphylococcus aureus and S. epidermidis, or gram-negative bacilli. Brain abscess due to contiguous spread from parameningeal foci of infection (e.g., the middle ears, mastoids, and sinuses) is frequently caused by streptococcus species, but staphylococcal and polymicrobial abscesses (including those caused by anaerobes and gram-negative bacilli) also occur. Staphylococcus and streptococcus species are often identified in brain abscesses after hematogenous spread. The microbial flora of brain abscesses resulting from paranasal sinus or dental infection are often polymicrobial.

What is the typical presentation of a patient with a brain abscess?

The most frequent clinical manifestation of brain abscess is headache; fever and altered level of consciousness are frequently absent. Neurologic signs depend on the site of the abscess and can be subtle for days to weeks. Behavioral changes may occur in patients with abscesses in the frontal or right temporal lobes. Patients with abscesses in the brain stem or cerebellum may present with cranial-nerve palsy, gait disorder, or either headache or altered mental status owing to hydrocephalus. Up to 25% of patients present with seizures.
Morning Report Questions

Q. What are the most appropriate diagnostic tools in cases of suspected brain abscess?

A. Cranial imaging should be performed in all patients with suspected brain abscess. Computed tomographic (CT) scanning with contrast enhancement provides a rapid means of detecting the size, number, and localization of abscesses. Magnetic resonance imaging (MRI), combined with diffusion-weighted and apparent-diffusion-coefficient images, is a valuable diagnostic tool in differentiating brain abscess from primary, cystic, or necrotic tumors. One prospective study involving 115 patients with 147 cystic brain lesions, which included 97 patients with brain abscess, showed that diffusion-weighted imaging had a sensitivity and specificity for the differentiation of brain abscesses from primary or metastatic cancers of 96% (positive predictive value, 98%; negative predictive value, 92%). Cultures of blood and cerebrospinal fluid identify the causative pathogen in approximately one quarter of patients. Cultures of cerebrospinal fluid may be valuable in patients with coexisting meningitis. However, the risk of brain herniation must be considered in these patients.

Figure 3. Imaging Studies of Brain Abscess.

Q. How should a brain abscess be managed?

A. Since 27% of brain abscesses are polymicrobial, broad-spectrum antimicrobial therapy is advised until the results of culture of the abscess itself are known or until repeated aerobic and anaerobic cultures from blood or other sites of infection show no other pathogen. An abscess size of more than 2.5 cm in diameter has been recommended as an indication for neurosurgical intervention, but data from comparative studies are lacking, and this size cannot be regarded as a definitive indication for aspiration. Anticonvulsant treatment is not routinely indicated in patients with brain abscess. Focal neurologic deficits may develop in response to abscess growth or surrounding edema. Adjunctive glucocorticoid therapy may reduce cerebral edema and is used in about half of patients with brain abscess. Since data from randomized studies are lacking and glucocorticoids may reduce passage of antimicrobial agents into the central nervous system, their use should be limited to patients with profound edema that is likely to lead to cerebral herniation.
Despite advances in imaging techniques, laboratory diagnostics, surgical interventions, and antimicrobial treatment, brain abscess remains a challenging clinical problem with substantial case fatality rates. Brain abscess can be caused by bacteria, mycobacteria, fungi, or parasites (protozoa and helminths), and the reported incidence ranges from 0.4 to 0.9 cases per 100,000 population.

Rates are increased in immunosuppressed patients.

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