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Brain Abscess in Emergency Medicine Workup

  • Author: Naomi George, MD; Chief Editor: Jeter (Jay) Pritchard Taylor, III, MD  more...
 
Updated: Jul 20, 2015
 

Laboratory Studies

Although nondiagnostic, patients with suspected brain abscess should have routine laboratory tests drawn to aid in narrowing the differential diagnosis.[68] If surgical intervention appears likely, preoperative laboratory testing should be considered.

CBC count should be obtained. Elevation of white blood cell count is present in 30-60% of patients.[11, 21, 36]

Sedimentation rate and C-reactive protein may be obtained. Elevation of acute phase may be present, but results are nonsensitive, nonspecific findings. In one series, only 47% of patients had elevated erythrocyte sedimentation rate.[36]

Two sets of blood cultures should be obtained, optimally prior to antibiotic administration; positive blood cultures are found in approximately 10% of cases. Brain abscess secondary to L monocytogenes may be more likely to yield positive blood cultures.[8, 69]

When hematogenous spread is suspected, consider obtaining cultures from the suspected primary infection.[42]

In immunocompromised patients, laboratory testing may include tuberculin skin testing and serotesting for toxoplasmal and anticysticercal antibodies in the cerebrospinal fluid (CSF). Background seroprevalence of Toxoplasma immunoglobulin G is high, and more than 97% of HIV/AIDS patients with toxoplasmosis brain abscesses have positive titers. Therefore, a negative test in an HIV/AIDS patient may be helpful in excluding toxoplasmosis from the differential.[70]

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Imaging Studies

Advanced neuroimaging modalities, such as CT and MRI are credited with a substantial reduction in morbidity and mortality of brain abscess[8] ; this is due, in part, to the reduction of diagnostic delay.[71] CT imaging is readily available in most emergency departments and may aid in rapid diagnosis of intracranial lesions; however, findings may vary with the stage of disease.

CT scans should be conducted with and without intravenous contrast. During the early stage of cerebritis, the lesion may appear irregular or hypodense and may be enhancing or nonenhancing with contrast. As the abscess begins to wall-off, CT imaging may reveal a classic ring-enhancing lesion. CT may be insufficient to detect infection during the cerebritis state, as well as for detecting posterior fossa lesions.[72] CT is not 100% sensitive and may miss early lesions or those abscesses that fail to wall-off. Additionally, it cannot reliably distinguish between abscess and other causes of ring-enhancing lesions, such as tumor. Despite these challenges, CT imaging is generally sufficient to mandate admission and further inpatient workup.

MRI is more sensitive than CT imaging and may be used to aid in the diagnosis of brain abscess. MRI should be performed using gadolinium, which can increase the signal intensity of the lesion on T1.[73]

MRI can be particularly useful during the early cerebritis stage or when there is suspicion of a posterior fossa lesion or satellite lesions.[2] Moreover, unlike CT, MRI is capable of distinguishing between pyogenic and nonsuppurative lesions on diffusion-weighted imaging (DWI).[73] On MRI, cerebritis appears as an area of low-signal intensity on T1-weighted imaging and has increased signal intensity on T2-weighted imaging.[74, 75]

DWI is used for differentiating ring-enhancing lesions that are neoplastic in origin, versus infectious causes. Suppurative abscess fluid restricts diffusion, leading to a hyperintense appearance of the lesion on DWI. In contrast, neoplastic lesions are typically hypointense or varied in intensity on DWI.

Neuroimaging aids in the detection of abscess and it plays a critical role in microbiological sampling, disease management, and follow-up. The advent of stereotactic CT-guided aspiration of abscess fluid has allowed for greater yield of abscess fluid and can aid in directing antimicrobial therapy.

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Other Tests

As ultrasonography is becoming widely used in the emergency department, bedside ocular ultrasonography may be performed to assess for increased intracranial pressure.[76]

Abscess aspiration and culture can be performed. Brain abscesses are aspirated by a neurosurgeon. Microbiological findings of the aspirate often help steer antimicrobial therapy.[44] Therefore, patients with suspected brain abscess warrant urgent neurosurgical consultation. Neurosurgical intervention may include brain biopsy for culture and histopathology. The abscess may be accessed by stereotactic CT-guided aspiration, open evacuation of the abscess, or with ultrasound guidance. CT guidance is the most common modality. Abscess fluid is typically evaluated by Gram stain and culture, including aerobes, anaerobes, acid-fast staining for mycobacteria, and modified acid-fast staining for Nocardia. Specific fungal staining, such as methenamine silver or mucicarmine, can be performed on the aspirate. In the case of suspected neurocysticercosis, serology may be obtained for anticysticercal antibodies.

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Procedures

Lumbar puncture

In instances in which meningitis is suspected, a lumbar puncture (LP) may have initially been obtained; however, lumbar puncture without prior CT imaging is contraindicated in the setting of focal neurological deficit or papilledema.[77] Furthermore, if neuroimaging reveals a mass lesion, LP is contraindicated. Occasionally, as is the case with early cerebritis, neuroimaging may not reveal a mass lesion. Although the risk of herniation may be low, CSF sampling to confirm diagnosis of brain abscess is rarely indicated and of very low yield.[78]

CSF findings may include increased or normal cell count, increased polymorphic neutrophils, elevated protein, and normal glucose—findings that are neither sensitive nor specific for brain abscess. Gram stain and cultures of CSF are rarely helpful.[2, 78]

In the case of intraventricular rupture, CSF may show an abundance of red blood cells and leukocytosis. Elevated CSF lactic acid levels have been reported and may aid in diagnosis.[79]

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Contributor Information and Disclosures
Author

Naomi George, MD Resident Physician, Department of Emergency Medicine, Rhode Island Hospital, The Warren Alpert School of Medicine of Brown University

Naomi George, MD is a member of the following medical societies: American College of Emergency Physicians, Society for Academic Emergency Medicine, Emergency Medicine Residents' Association

Disclosure: Nothing to disclose.

Coauthor(s)

Matthew S Siket, MD, MS Assistant Professor of Emergency Medicine, The Warren Alpert Medical School of Brown University; Attending Physician, Department of Emergency Medicine, Rhode Island Hospital and The Miriam Hospital

Matthew S Siket, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Heart Association, American Medical Association, Society for Academic Emergency Medicine, American Stroke Association

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Barry J Sheridan, DO Chief Warrior in Transition 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.

Chief Editor

Jeter (Jay) Pritchard Taylor, III, MD Assistant Professor, Department of Surgery, University of South Carolina School of Medicine; Attending Physician, Clinical Instructor, Compliance Officer, Department of Emergency Medicine, Palmetto Richland Hospital

Jeter (Jay) Pritchard Taylor, III, MD is a member of the following medical societies: American Academy of Emergency Medicine, South Carolina Medical Association, Columbia Medical Society, South Carolina College of Emergency Physicians, American College of Emergency Physicians, American Medical Association, Society for Academic Emergency Medicine

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Chief Editor for Medscape.

Additional Contributors

Edward Bessman, MD, MBA Chairman and Clinical Director, Department of Emergency Medicine, John Hopkins Bayview Medical Center; Assistant Professor, Department of Emergency Medicine, Johns Hopkins University School of Medicine

Edward Bessman, MD, MBA is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Acknowledgements

Joshua N Goldstein, MD, PhD, FAAEM Assistant Professor, 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, Neurocritical Care Society, and Society for Academic Emergency Medicine

Disclosure: CSL Behring Consulting fee Consulting

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.

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Brain abscess.
Sagittal (a) and axial (b) gadolinium-enhanced T1-weighted MRI images from a patient who presented with headache, word-finding difficulties, stuttering speech, and right hand/foot numbness. Note the peripheral enhancement of a lesion in the left insula with surrounding edema.
CT (a) and T2 fluid-attenuated inversion recovery (FLAIR) MRI (b, c) images from the same patient as the first image. Images a and b were obtained at the time of initial diagnosis, and image c was obtained 5 months later following successful treatment.
Diffusion-weighted (a), T2 fluid-attenuated inversion recovery (FLAIR) (b), and post-gadolinium enhanced T1-weighted (c) images from a patient who presented initially with vomiting, followed by fever and coma. Numerous abscesses are demonstrated with coalescence in the right occipital and basal ganglia with surrounding edema and midline shift.
Axial (a) and coronal (b) CT images from the same patient as the third image. Multiple hypodensities with cerebral edema and mass effect are noted.
 
 
 
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