Encephalitis Treatment & Management

  • Author: David S Howes, MD; Chief Editor: Barry E Brenner, MD, PhD, FACEP   more...
 
Updated: Jan 6, 2012
 

Emergency Department Care

With the important exceptions of HSE and varicella-zoster encephalitis, the viral encephalitides are not treatable beyond supportive care. Treatments for T gondii and cytomegalovirus (CMV) encephalitis are available but generally not initiated in the ED.

The goal of treatment for acutely ill patients is administration of the first dose or doses of acyclovir, with or without antibiotics or steroids, as quickly as possible. The standard for acute bacterial meningitis is the initiation of treatment within 30 minutes of arrival. Consider instituting an ED triage protocol to identify patients at risk for HSE.

Collect laboratory samples and blood cultures before the start of IV therapy. Even in uncomplicated cases of encephalitis, most authorities recommend a neuroimaging study (eg, magnetic resonance imaging [MRI] or, if that is not available, a contrast-enhanced head computed tomography [CT] scan) before lumbar puncture (LP).

Management of hydrocephalus and increased intracranial pressure

In patients with hydrocephalus and increased intracranial pressure (ICP), general measures include management of fever and pain, control of straining and coughing, and prevention of seizures and systemic hypotension.

In otherwise stable patients, elevating the head and monitoring neurologic status usually are sufficient. When more aggressive maneuvers are indicated, early use of diuresis (eg, furosemide 20 mg IV, mannitol 1 g/kg IV) may be helpful, provided that circulatory volume is protected. Dexamethasone 10 mg IV q6h helps in managing edema surrounding space-occupying lesions. Hyperventilation (arterial CO2 tension [PaCO2] 30 mm Hg) may cause a disproportional decrease in cerebral blood flow (CBF), but it is used to control increasing ICP on an emergency basis.

Intraventricular ICP monitoring is controversial. Some authorities believe that dangerous focal edema with a pressure gradient between the temporal lobe and the subtentorial space usually is not detected by the monitor and that this failure of detection can lead to a false sense of security. In fact, monitor placement may potentially aggravate a pressure gradient.

Treatment of systemic complications

Look for and treat systemic complications (eg, hypotension or shock, hypoxemia, hyponatremia, and exacerbation of chronic diseases), particularly in herpes simplex encephalitis (HSE), eastern equine encephalitis (EEE), Japanese virus encephalitis (JE).

Empiric treatment of HSV meningoencephalitis and VZV encephalitis

Empiric adult emergency treatment for herpes simplex virus (HSV) meningoencephalitis and varicella-zoster virus (VZV) encephalitis consists of acyclovir 10 mg/kg (infused over 1 h) q8h for 14-21 days. Give acyclovir 10-15 mg/kg IV q8h for neonatal HSV; for HSV encephalitis in the pediatric population, give acyclovir 10 mg/kg IV q8h.

In HIV-positive patients, consider foscarnet, given the increased incidence of acyclovir-resistant HSV and herpes zoster virus (HZV).

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Approach Considerations

Prehospital care

In the prehospital setting, evaluate and treat for shock or hypotension. Administer crystalloid infusion in patients with evidence of circulatory compromise. Consider airway protection in patients with an altered mental status. Seizure precautions are indicated. Treat seizures according to usual protocols (ie, lorazepam 0.1 mg/kg given intravenously [IV]). All patients should receive oxygen and have intravenous access secured en route to the emergency department (ED). See the following for more information:

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Contributor Information and Disclosures
Author

David S Howes, MD  Professor of Medicine and Pediatrics, Emergency Medicine Residency Program Director Emeritus, Head, Phemister Society, University of Chicago Division of the Biological Sciences, The Pritzker School of Medicine

David S Howes, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Physicians-American Society of Internal Medicine, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

Marjorie Lazoff, MD  Editor-in-Chief, Medical Computing Review

Marjorie Lazoff, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Emergency Physicians, American Medical Informatics Association, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

Barry E Brenner, MD, PhD, FACEP  Professor of Emergency Medicine, Professor of Internal Medicine, Program Director, Emergency Medicine, Case Medical Center, University Hospitals, Case Western Reserve University School of Medicine

Barry E Brenner, MD, PhD, FACEP is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Chest Physicians, American College of Emergency Physicians, American College of Physicians, American Heart Association, American Thoracic Society, Arkansas Medical Society, New York Academy of Medicine, New York Academy of Sciences, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Additional Contributors

Steven A Conrad, MD, PhD Chief, Department of Emergency Medicine; Chief, Multidisciplinary Critical Care Service, Professor, Department of Emergency and Internal Medicine, Louisiana State University Health Sciences Center

Steven A Conrad, MD, PhD is a member of the following medical societies: American College of Chest Physicians, American College of Critical Care Medicine, American College of Emergency Physicians, American College of Physicians, International Society for Heart and Lung Transplantation, Louisiana State Medical Society, Shock Society, Society for Academic Emergency Medicine, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Robin R Hemphill, MD, MPH Associate Professor, Director, Quality and Safety, Department of Emergency Medicine, Emory University School of Medicine

Robin R Hemphill, MD, MPH is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

J Stephen Huff, MD Associate Professor of Emergency Medicine and Neurology, Department of Emergency Medicine, University of Virginia School of Medicine

J Stephen Huff, MD is a member of the following medical societies: American Academy of Emergency Medicine, American Academy of Neurology, American College of Emergency Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Todd Pritz, MD Intensivist, St Anthony's Medical Center and St John's Mercy Medical Center

Todd Pritz, MD is a member of the following medical societies: Massachusetts Medical Society and Society of Critical Care 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 Reference Salary Employment

References

  1. Final 2008 West Nile Virus Activity in the United States. Centers for Disease Control and Prevention. Available at http://bit.ly/fATcE1. Accessed April 26, 2009.

  2. MacDonald RD, Krym VF. West Nile virus. Primer for family physicians. Can Fam Physician. Jun 2005;51:833-7. [Medline].

  3. Yao K, Honarmand S, Espinosa A, Akhyani N, Glaser C, Jacobson S. Detection of human herpesvirus-6 in cerebrospinal fluid of patients with encephalitis. Ann Neurol. Mar 2009;65(3):257-67. [Medline].

  4. Bloch KC, Glaser C. Diagnostic approaches for patients with suspected encephalitis. Curr Infect Dis Rep. Jul 2007;9(4):315-22. [Medline].

  5. [Guideline] Tunkel AR, Glaser CA, Bloch KC, Sejvar JJ, Marra CM, Roos KL, et al. The management of encephalitis: clinical practice guidelines by the Infectious Diseases Society of America. Clin Infect Dis. Aug 1 2008;47(3):303-27. [Medline].

 
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Table. Cerebrospinal Fluid Findings by Type of Organism
CSF Finding (Normal)Bacterial MeningitisViral Meningitis*Fungal Meningitis
Pressure (5-15 cm water)
  • Increased
  • Normal or mildly increased
  • Normal or mildly increased in most fungal and tuberculous CNS infections
  • Patients with AIDS and cryptococcal meningitis are at increased risk of blindness and death unless pressure maintained at < 30 cm
Cell counts, mononuclear cells/µL



Preterm (0-25)



Term (0-22)



6 mo+ (0-5)



  • Normal cell count excludes bacterial meningitis
  • Typically thousands of polymorphonuclear cells, but counts may not change dramatically or even be normal (classically in very early meningococcal meningitis or in extremely ill neonates)
  • Lymphocytosis with normal CSF chemistry results observed in 15-25% of patients, especially if counts < 1000 or if patient is partially treated
  • About 90% of patients with ventriculoperitoneal shunts and CSF WBC count >100 cells/µL are infected, though CSF glucose level often normal, and bacteria often less pathogenic
  • Cell count and chemistry levels normalize slowly (days) with antibiotics
  • Usually < 500, nearly 100% mononuclear
  • < 48 hours, clinically significant polymorphonuclear pleocytosis may be indistinguishable from early bacterial meningitis, particularly with EEE
  • Nontraumatic RBCs in 80% of patients with HSV meningoencephalitis, though 10% have normal CSF results
  • 100s of mononuclear cells
Microorganisms (none)
  • Gram stain 80% effective
  • Inadequate decolorization may cause Haemophilus influenzae to be mistaken for gram-positive cocci
  • Pretreatment with antibiotics may affect stain uptake, causing gram-positive species to appear to be gram-negative and decrease culture yield by an average of 20
  • No organism
  • India ink 80-90% effective for detecting fungi
  • AFB stain 40% effective for TB; increase yield by staining supernatant from at least 5 mL of CSF
Glucose†



Euglycemia (>50% serum)



Hyperglycemia (>30% serum)



  • Decreased
  • Normal
  • Sometimes decreased
  • In addition to fulminant bacterial meningitis, TB, primary amebic meningoencephalitis, and neurocysticercosis cause low glucose levels
Protein



Preterm (65-150 mg/dL)



Term (20-170 mg/dL



6 mo+ (15-45 mg/dL)



  • Usually >150 mg/dL
  • May be >1000 mg/dL
  • Mildly increased
  • Increased >1000 mg/dL, with relatively benign clinical presentation suggestive of fungal disease
*Some bacteria (eg, Mycoplasma, Listeria, Leptospira, Borrelia burgdorferi [Lyme disease]) cause alterations in spinal fluid that resemble the viral profile. An aseptic profile is also typical of partially treated bacterial infections (>33%, especially those in children, are treated with antimicrobials) and of the 2 most common causes of encephalitis—the arboviruses and the potentially curable HSV.



† Wait 4 hours after glucose load.



AFB—acid-fast bacillus; CSF—cerebrospinal fluid; EEE-eastern equine encephalitis; HSV—herpes simplex virus; RBC—red blood cell; TB—tuberculosis; WBC—white blood cell.



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