Brain Abscess in Emergency Medicine Medication

  • Author: Lisa Elizabeth Thomas, MD; Chief Editor: Rick Kulkarni, MD   more...
 
Updated: May 13, 2010
 

Medication Summary

Selection of appropriate antimicrobials with adequate CNS penetration and coverage of typical anaerobic and aerobic organisms is critical in controlling infection and preventing complications.

In the early phase of abscess formation, cerebritis, patients may respond to antibiotic therapy alone.[5, 9]

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, 9]

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Antibiotics

Class Summary

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 with equal or better cure rates compared to a standard regimen of cefotaxime and metronidazole, 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, 42]

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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.

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Cefepime (Maxipime)

 

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

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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.

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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.

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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.

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Metronidazole (Flagyl)

 

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

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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.

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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.

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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.

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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.

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Corticosteroids

Class Summary

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, 14]

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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.

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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, 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

Specialty Editor Board

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

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.

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

Disclosure: Medscape Salary Employment

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.

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

Rick Kulkarni, MD  Attending Physician, Department of Emergency Medicine, Cambridge Health Alliance, Division of Emergency Medicine, Harvard Medical School

Rick Kulkarni, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine

Disclosure: WebMD Salary Employment

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