Encephalitis

Brief information about encephalitis

1. Encephalitis Presented by: Dr. Mona Mohammed Ali 1

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3. Introduction: Encephalitis, an inflammation of the brain parenchyma, presents as diffuse and/or focal neuropsychological dysfunction. Although it primarily involves the brain, the meninges are frequently involved (meningoencephalitis). From an epidemiologic and pathophysiologic perspective, encephalitis is distinct from meningitis It is also distinct from  cerebritis . Cerebritis describes the stage preceding abscess formation and implies a highly destructive bacterial infection of brain tissue, whereas acute encephalitis is most commonly a viral infection with parenchymal damage varying from mild to profound. 3

4. Etiology : B acterial , fungal, and autoimmune disorders can produce encephalitis, but most cases are viral in origin. The cause of encephalitis is usually infectious in nature. Viral agents, such as HSV types 1 and 2 (the latter much more common in neonates than adults), VZV, EBV, measles virus (PIE and SSPE), mumps virus, and rubella virus, are spread through person-to-person contact. Human herpes virus 6 may also be a causative agent. 4

5. Etiology: The CDC has confirmed that WNV( West Nile Virus) can be transmitted by means of organ transplantation and via blood transfusions. Important animal vectors for some types of encephalitis include: 1- mosquitoes and ticks, which spread the arbovirus group . 2- warm-blooded mammals, which are vectors for rabies and lymphocytic choriomeningitis (LCM). Bacterial pathogens, such as  Mycoplasma  species and those causing rickettsial disease or catscratch disease, are rare and invariably involve inflammation of the meninges out of proportion to their encephalitic components. Noninfectious causes include the demyelinating process in acute disseminated encephalitis. 5

6. Pathophysiology : In general, the virus replicates outside the CNS and gains entry to the CNS either by hematogenous spread or by travel along neural pathways (e.g., rabies virus, HSV, VZV).  Once across the blood-brain barrier, the virus enters neural cells, with resultant disruption in cell functioning, perivascular congestion, hemorrhage, and a diffuse inflammatory response that disproportionately affects gray matter over white matter . 6

7. Pathophysiology (continued): Regional tropism associated with certain viruses is due to neuron cell membrane receptors found only in specific portions of the brain, with more intense focal pathology in these areas. A classic example is the HSV predilection for the inferior and medial temporal lobes. In contrast to viruses that invade gray matter directly, acute disseminated encephalitis and postinfectious encephalomyelitis (PIE), most commonly due to measles infection and associated with Epstein-Barr virus (EBV) and CMV infections, are immune-mediated processes that result in multifocal demyelination of perivenous white matter. 7

8. C/F The viral prodrome typically consists of fever, headache, nausea and vomiting, lethargy, and myalgias. Manifestations associated with specific types of encephalitis include the following: Encephalitis caused by varicella-zoster virus (VZV), Epstein-Barr virus (EBV), cytomegalovirus (CMV), measles virus, or mumps virus: Rash, lymphadenopathy, hepatosplenomegaly, and parotid enlargement. St Louis encephalitis: Dysuria and pyuria. West Nile encephalitis (WNE): Extreme lethargy. 8

9. C/F The classic presentation is encephalopathy with diffuse or focal neurologic symptoms, including the following: Behavioral and personality changes, with decreased level of consciousness. Neck pain, stiffness. Photophobia. Lethargy. Generalized or focal seizures (60% of children with California virus encephalitis [CE ]). Acute confusion or amnestic states. Flaccid paralysis (10% of patients with WNE). 9

10. C/F The signs of encephalitis may be diffuse or focal. Typical findings include the following: Altered mental status. Personality changes (very common ). Focal findings (e.g., hemiparesis, focal seizures, and autonomic dysfunction ). Movement disorders (e.g., St Louis encephalitis, eastern equine encephalitis, and western equine encephalitis). Ataxia. Cranial nerve defects. Dysphagia, particularly in rabies. Meningismus (less common and less pronounced than in meningitis ). Unilateral sensorimotor dysfunction (postinfectious encephalomyelitis.) 10

11. C/F Findings of herpes simplex virus (HSV) infection in neonates may include the following: Herpetic skin lesions over the presenting surface from birth or with breaks in the skin, such as those resulting from fetal scalp monitors. Keratoconjunctivitis. Oropharyngeal involvement, particularly buccal mucosa and tongue. Encephalitis symptoms (e.g., seizures, irritability, change in attentiveness, and bulging fontanels). Additional signs of disseminated, severe HSV include jaundice, hepatomegaly, and shock. 11

12. C/F Encephalitis may be associated with a number of complications, including the following: Seizures. Syndrome of inappropriate secretion of antidiuretic hormone (SIADH ). Increased intracranial pressure (ICP ). Coma. 12

13. Diagnosis: Blood and urine tests that may be helpful include the following: Complete blood count (CBC ). Serum electrolyte levels. Serum glucose level. Blood urea nitrogen (BUN) and creatinine levels. Urine electrolyte levels. Urine or serum toxicology screening. 13

14. Diagnosis : A lumbar puncture (LP) should be performed in all cases of suspected viral encephalitis. Studies that may be ordered to identify the infectious agent include the following: HSV cultures of suspicious lesions and a Tzanck smear. Viral cultures of CSF, including HSV. Blood cultures for bacterial pathogens. Complement fixation antibodies to identify arbovirus. Heterophile antibody and cold agglutinin testing for EBV. Serologic tests for  Toxoplasma. 14

15. Diagnosis : CSF analysis is essential. Parameters to be evaluated include the following: Pressure. Cell counts. Microorganisms. Glucose. Protein. Brain biopsy is the diagnostic standard (96% sensitivity, 100% specificity). 15

16. Diagnosis: Imaging modalities that may be helpful include the following: CT MRI EEG 16

17. Management: Management in the prehospital setting includes the following: Evaluation and treatment for shock or hypotension. Airway protection (in patients with altered mental status ). Seizure precautions. Oxygen and IV access secured en route to the hospital (all patients ). 17

18. Management : In the emergency department (ED), beyond supportive care, viral encephalitides are not treatable, with the exceptions of HSV and VZV encephalitis. Important initial measures include the following: 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 initiation of treatment within 30 minutes of arrival. Consideration of an ED triage protocol to identify patients at risk for HSV encephalitis. Collection of laboratory samples and blood cultures before the start of IV therapy. Neuroimaging (e.g., MRI or, if that is unavailable, contrast-enhanced head CT) before LP. 18

19. Management Additional treatment considerations include the following: Management of hydrocephalus and increased ICP. Treatment of systemic complications (e.g., hypotension or shock, hypoxemia, hyponatremia, and exacerbation of chronic diseases.) Empiric treatment of HSV meningoencephalitis and VZV encephalitis. 19

20. Management Medication Summary: The goals of pharmacotherapy are to reduce morbidity and prevent complications . Antivirals are used to manage treatable viral encephalitides . Corticosteroids may be considered for postinfectious or noninfectious encephalitis . 20

21. Management Antiviral: The goal of the use of antivirals for herpes simplex encephalitis (HSE) and varicella-zoster encephalitis is to shorten the clinical course, prevent complications, prevent the development of latency and/or subsequent recurrences, decrease transmission, and eliminate established latency. Acyclovir ( Zovirax): Acyclovir has demonstrated inhibitory activity directed against both herpes simplex virus type 1 (HSV-1) and HSV-2, and infected cells selectively take it up . Foscarnet (Foscavir): may be used. 21

22. Management Corticosteroids: Corticosteroids are anti-inflammatory agents used for treatment of postinfectious encephalitis and acute disseminated encephalitis. These drugs are commonly presented as treatment alternatives, though supporting data are limited. Dexamethasone : Dexamethasone is used to treat various allergic and inflammatory diseases. It may decrease inflammation by suppressing migration of polymorphonuclear leukocytes and reversing increased capillary permeability. 22

23. Management Diuretics: These agents are used in patients with hydrocephalus and increased intracranial pressure (ICP) when more aggressive diuresis is desired . Furosemide (Lasix) is an example. 23

24. Management Mannitol (Osmitrol ): Mannitol may reduce pressure in the subarachnoid space by creating an osmotic gradient between cerebrospinal fluid in the arachnoid space and plasma. This agent is not intended for long-term use. Initially assess for adequate renal function in adults by administering a test dose of 200 mg/kg, given IV over 3-5 minutes. This should produce a urine flow of at least 30-50 ml/h of urine over 2-3 hours. In children, assess for adequate renal function by administering a test dose of 200 mg/kg, given IV over 3-5 minutes. This should produce a urine flow of at least 1 mL/kg over 1-3 hours. 24

25. Management Benzodiazepines: These agents are used to treat seizures associated with encephalitis . Lorazepam (Ativan) is an example. 25

26. Prognosis: The prognosis is dependent on the virulence of the virus and the patient’s health status. Extremes of age (< 1 y or >55 y), immune-compromised status, and preexisting neurologic conditions are associated with poorer outcomes. Untreated HSE has a mortality of 50-75%, and virtually all untreated or late-treatment survivors have long-term motor and mental disabilities. 26

27. Prognosis : The mortality in treated HSE averages 20%, and the neurologic outcome correlates with the neurological disability present at the time of the first dose of acyclovir or comparable antiviral agents. Approximately 40% of survivors have minor-to-major learning disabilities, memory impairment, neuropsychiatric abnormalities, epilepsy, fine-motor-control deficits, and dysarthria. 27

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