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Acute Viral Encephalitis


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Weekly Wednesday departmental presentation

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Acute Viral Encephalitis

  1. 1. ACUTE VIRAL ENCEPHALITIS Dr. Thomas O. Oricha Department of Medicine, FTH, Gombe 1st February, 2017
  2. 2. Outline • Introduction • Epidemiology • Aetiology • Risk factors • Pathogenesis • Clinical manifestation • Investigations/Diagnosis • Differential diagnosis • Treatment • Sequelae • Conclusion • References
  3. 3. Introduction • Encephalitis is defined as inflammation of the brain parenchyma associated with neurologic dysfunction • Acute encephalitis associated with viral infections includes 2 distinct clinical-pathological diseases. ACUTE VIRAL ENCEPHALITIS Postinfectious encephalomyelitis • Acute viral encephalitis is due to direct effects of acute infections on the brain
  4. 4. Introduction • Definition of terms Panencephalitis Polioencephalitis Leukoencephalitis Rhombencephalitis Meningoencephalitis Meningoencephalomyelitis Meningoencephaloradiculitis Encephalomyeloradiculitis
  5. 5. Introduction WHO Clinical case definition of acute encephalitis syndrome • Person of any age, at any time of year, with • Acute onset of fever AND • Change in mental status (including symptoms such as confusion, disorientation, coma, or inability to talk) AND/OR • New onset of seizures (excluding simple febrile seizures) • Other early clinical findings can include an increase in irritability, somnolence or abnormal behaviour greater than that seen with usual febrile illness
  6. 6. Epidemiology • Acute viral encephalitis is of public health concern worldwide because of its high morbidity and mortality • Incidence of 5-10 per 100 000/year • Commoner in children and the elderly • Slight predominance in males • Paucity of data in Nigerian
  7. 7. Aetiology NOT GEOGRAPHICALLY RESTRICTED (SPORADIC CAUSES) Herpes viruses HSV 1&2, VZV, EBV, CMV, HHV 6&7 Enteroviruses Coxsackie viruses, echoviruses, enteroviruses 70&71, parechovirus, poliovirus Paramyxoviruses Measles virus, mumps virus Others (rarer causes) Influenza viruses, adenovirus, parvovirus, lymphocytic choreomeningitis virus, rubella virus
  8. 8. Aetiology GEOGRAPHICALLY RESTRICTED The Americas WNV, La Cross virus, St Louis encephalitis virus, Rocio virus, Powassan encephalitis, VEEV, EEEV, WEEV, Colorado tick fever virus, dengue virus (DV), rabies virus (RV) Europe/Middle East Tick-borne encephalitis, WNV, Tosana virus, RV, DV, louping ill virus Africa WNV, RVF virus, CCHF virus, DV, chikungunya virus, RV Asia JEV, WNV, DV, Murray Valley encephalitis virus (MVEV), RV, chikungunya virus, Nipah virus Australasia MVEV, JEV, kunjin virus, DV
  9. 9. Risk factors RISK FACTOR POSSIBLE VIRUSES Agammaglobulinemia Enteroviruses Animal contact Bats Rabies virus, Nipah virus Birds WNV, EEEV, WEEV, VEEV, St. Louis encephalitis virus, MVEV, JEV Cats/Dogs Rabies virus Horses EEEV, WEEV, VEEV Rodents EEEV, VEEV, tickborne encephalitis virus, Powassan virus, La Crosse virus Swine JEV, Nipah virus Immunocompromised VZV, CMV, HHV 6, WNV, HSV Transfusion and transplantation CMV, EBV, WNV, HIV, tickborne encephalitis virus
  10. 10. Risk factors RISK FACTOR POSSIBLE VIRUSES Insect contact Mosquitoes EEEV, WEEV, VEEV, St. Louis encephalitis virus, MVEV, JEV, WNV Ticks Tickborne encephalitis virus, Powassan virus Occupation Laboratory workers West Nile virus Physicians and health care workers VZV, HIV, influenza virus, measles virus Veterinarians Rabies virus Recreational activities Camping/hunting All agents transmitted by mosquitoes and ticks Spelunking Rabies virus Swimming Enteroviruses MSP HIV
  11. 11. Pathogenesis Entry • Respiratory/olfactory, GI, GU, skin, conjunctiva, blood Entry into the CNS Hematogenous dissemination Intraneural spread Neurovirulence Direct cytopathic effect Immune-mediated injury
  12. 12. Pathogenesis Histopathologic Changes • Perivascular infiltration of mononuclear inflammatory cells • Reactive astrocytosis • Formation of glial nodules • Neuronophagia
  13. 13. Pathogenesis Immunopathology • Cytotoxic T cells & phagocytic macrophages act as effectors • Interferons (α, β, and γ) and their regulatory transacting proteins may act to limit CNS virus replication • IL-1β, IL-6, and TNF-α are injurious
  14. 14. Pathogenesis • Specific sites of viral predilection Temporal and inferior frontal lobes (HSV) Periventricular areas (CMV) Limbic system (RV) Cerebellum (VZV) Basal ganglia (JEV)
  15. 15. Clinical manifestation • Severity of deficits range from very mild to extreme • Progressive constellation of symptoms evolves over a period of days Acute febrile illness Frequent meningeal involvement (headache, neck stiffness) Brain parenchymal involvement
  16. 16. Clinical manifestation • Seizures, behavioral changes, weakness, altered sensorium  coma • Hallucination, agitation, personality change, frankly psychotic state • Focal findings: aphasia, ataxia, UMN/LMN patterns of weakness, involuntary movements (e.g. myoclonus, tremor), CN deficits • Involvement of hypothalamic-pituitary axis: Temp dysregulation, DI, SIADH
  17. 17. Clinical manifestation • Extraneural features Parotitis (mumps) Pharyngitis & lymphadenopathy (EBV) Dermatomal rash (VZV) Herpangina (Coxsackie virus) Pneumonitis (LCMV)
  18. 18. Case presentation • A 35-year-old man presented to A/E with 3 days of low-grade fever • He awoke at 2:00 AM on the fourth day, got dressed, went to the kitchen, poured cereal onto the kitchen table, added milk, got the car keys, and promptly packed his car across the garage door. At that point, his wife immediately took him to A/E • He had no witnessed seizures • Temp in A/E was 38.5◦C; he was normotensive • On neurologic examination, he had an expressive aphasia • No focal signs of weakness at presentation
  19. 19. Case presentation oComment • This case is a classic presentation for HS encephalitis • It is now the responsibility of the A/E physician or neurologist to define a course of action • First, a working differential diagnosis must be established • Numerous diseases mimic HS encephalitis; most are not treatable • Clearly, the expressive aphasia points to focal neurologic process
  20. 20. Investigations/Diagnosis Investigations • Specific Cerebrospinal fluid analysis Pathogen-specific assays Culture of other body fluid specimens HIV Electroencephalography Neuroimaging studies Brain biopsy • Nonspecific: CBC, E/U/Cr, LFT, coagulation studies, & CXR
  21. 21. Investigations/Diagnosis
  22. 22. Investigations/Diagnosis
  23. 23. Investigations/Diagnosis
  24. 24. Investigations/Diagnosis Diagnostic Criteria for Acute Encephalitis Major Criterion (required): Altered mental status (decreased/altered level of consciousness, lethargy or personality change) ≥24hrs, no alternative cause identified Minor Criteria • 2 for possible encephalitis • ≥3 for probable or confirmed encephalitis
  25. 25. Investigations/Diagnosis Minor Criteria Documented fever ≥38° C within 72hrs before or after presentation Generalized/partial seizures not fully attributable to preexisting seizure disorder New onset focal neurologic findings
  26. 26. Investigations/Diagnosis Minor Criteria CSF WBC count ≥5/mm³ Neuroimaging suggestive of encephalitis either new from prior studies or appears acute in onset Abnormality on EEG consistent with encephalitis and not attributable to another cause
  27. 27. Differential diagnosis
  28. 28. Treatment • 3 “Es”: emergent issues, epilepsy, and etiology Emergent issues ABC of resuscitation Consider admission to ICU Fluid restriction Avoidance of hypotonic intravenous solutions Suppression of fever Management of raised ICP
  29. 29. Treatment Hyperventilation to pCO2 30+/-2mmHg & MAP ≥60mmHg Mannitol 0.25-1g/kg bolus every 4-6 hours Hypertonic saline • Active brain herniation: 23.4% saline (30 mL bolus via CV line) • Maintenance 2%-3% saline (250-500 mL boluses or continuous venous infusion; 3% saline via CV line)
  30. 30. Treatment Seizures Aetiology • Acyclovir, 10 mg/kg IV q 8 hrs x 14-21 days • Oral acyclovir, famciclovir, and valacyclovir (efficacy against HSV, VZV, EBV) have not been evaluated in the treatment of encephalitis either as primary therapy or as supplemental therapy • IV ribavirin 15-25 mg/kg/day in divided doses every 8 hrs
  31. 31. Treatment Algorithm for Mgt of Acute Viral Encephalitis
  32. 32. Treatment Algorithm for Mgt of Acute Viral Encephalitis contd
  33. 33. Sequelae • Behavioural and psychiatric disturbances • Epilepsy • Post-encephalitic parkinsonism • Memory difficulties • Speech disturbances • Permanent home care
  34. 34. Prognosis Factors of bad prognosis • Severe neurologic impairment • Older age • High viral load in CSF • Delay in initiation of therapy
  35. 35. Rehabilitation • Periodic neuropsychiatric evaluation • Speech therapy • Physiotherapy • Occupational rehabilitation
  36. 36. Conclusion • Acute viral encephalitis is frequently devastating • All patients with a febrile illness and altered behaviour or consciousness should be investigated promptly for viral encephalitis • Patients suspected need a lumbar puncture as soon as possible • Early institution of therapy improves prognosis
  37. 37. References • Ftichard T. Johnson, Acute Encephalitis, Clinical Infectious Diseases 1996;23:219-26 • WHO – recommended standards for surveillance of selected vaccine-preventable diseases. Geneva: WHO; 2006: documents/DocsPDF06/843.pdf • DiseaseM.Saminathan, K. Karuppanasamy, S. Pavulraj, A. Gopalakrishnan and R. B. Rai Acute Encephalitis Syndrome - A Complex Zoonotic Int. J. Livest. Res. 2013; 3(2): 174-177 • Tom Solomon, Ian J Hart, Nicholas J Beeching; Viral encephalitis: a clinician’s guide; Practical Neurology 2007;7;288-305 • Allan R. Tunkel et al, The Management of Encephalitis: Clinical Practice Guidelines by the Infectious Diseases Society of America; Clinical Infectious Diseases 2008; 47:303–27 • David Schlossberg, Clinical Infectious Disease 2nd Edition; 2015 Chapter 76
  38. 38. References • Dennis L. Kasper et al, Harrison’s Principles of Internal Medicine, 19th Edition; 2015, p. 893-898 • Venkatesan et al, Case Definitions, Diagnostic Algorithms, and Priorities in Encephalitis: Consensus Statement of the International Encephalitis Consortium; Clinical Infectious Diseases 2013;57(8):1114–28 • Sergio Ferrari et al, Viral Encephalitis: Etiology, Clinical Features, Diagnosis and Management, The Open Infectious Diseases Journal, 2009, 3, 1-12 • Richard J. Whitley, Herpes Simplex Virus Infections of the Central Nervous System, Continuum (Minneap Minn) 2015;21(6):1704–1713 • T. Solomon et al, Management of suspected viral encephalitis in adults- Association of British Neurologists and British Infection Association National Guidelines; Journal of Infection (2012) 64, 347e373