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Approach To Meningitis and Encephalitis.pptx
- 1. Approach To Meningitis and Encephalitis
- 2. BACTERIAL MENINGITIS Inflammation of meninges, particularly arachnoid and pia mater associated with invasion of bacteria into sub arachnoid space.
- 3. COMMON BACTERIAs… Premature /Neonates (<3 months) Group B streptococci Gram –ve enterics Listeria monocytogenes Children <5 years Haemophilus influenzae B Neisseria meningitidis Streptococcus pneumoniae Adults N.meningitidis S.pneumoniae (80% cases) L.monocytogenes(Risk > 50 yrs)
- 6. Investigations Blood • • • • • • FBC with differential Blood cultures (aerobic and anaerobic) CRP/ESR/procalcitonin HIV Rapid plasma reagent • Serum for acute serology (store for paired convalescent sample in 3 to 4 weeks) Heterophile antibodies (Epstein- Barr virus) Lyme disease tests Rickettsial serologies • • • • CSF • • • Opening pressure Cell count and differential Serum and CSF glucose concentration Protein concentration Stains: Gram, India ink, AFB Cultures: aerobic, anaerobic, acid-fast bacillus, fungal Cytology • • • • • • Antibody testing (arboviral) PCRs: enteroviral, West Nile virus,a herpesvirus types 1 and 2) CSF lactate (posttrauma or neurosurgical) •
- 9. Bacterial meningitis is a neurologic emergency Antimicrobial therapy as soon as possible (Must continue 48-72 hrs as empirical ) Choice of agents for empiric therapy determined by the patient’s age presence of predisposing conditions antimicrobial resistance Antimicrobial therapy should be modified as soon as the pathogen has been isolated and in vitro tests have been performed
- 10. EMPIRICAL THERAPY BASED ON AGE AND PATHOGENS Less than 1 month S.agalactiae (GBS) Gram –ve enterics L.monocytogenes Ampicillin + Cefotaxime OR Ampicillin + Aminoglycoside
- 11. 1-23 months S.pneumoniae N.meningitidis H.influenzae S.agalactiae Vancomycin + 3rd generation cephalosporin (cefotaxime/ceftriaxone)
- 12. 2 years – 50 years N.meningi tidis S.pneumo niae Vancomycin + 3rd generation cephalosporin (cefotaxime/ceftriaxone)
- 13. Above 50 years • N.meningitidis S.Pneumoniae Gram –ve enterics L.monocytogenes • Vancomycin + 3rd generation cephalosporin (cefotaxime/ceftriaxone)
- 16. Encephalitis
- 17. • diagnosis that should only be made if there is tissue confirmation • in practice: –febrile illness, severe headache reduced consciousness –surrogate markers of brain inflammation Encephalitis
- 18. Causes (1)
- 19. Causes (2)
- 20. • HSV- brain parenchyma in the temporal lobes, sometimes with frontal or parietal involvement. • Mumps virus - acute viral encephalitis, or a delayed immune mediated encephalitis. • Measles virus - post-infectious encephalitis, which can sometimes have a acute haemorrhagic leukoencephalitis. • Influenza A virus - diffuse cerebral oedema • Varicella zoster virus (VZV) -vasculitis
- 24. • acute flu-like prodrome, fever, • severe headache • nausea, vomiting • altered consciousness • seizures • focal neurological signs Clinical presentations HSV-1 encephalitis •febrile (91%) •disorientation (76%) •speech disturbances (59%) •behavioural changes (41%) •seizures (33%) •Alterations in higher mental function
- 26. Approach • In the approach to the patient with encephalitis, an attempt should be made to establish an etiologic diagnosis. • Although there are no definitive effective treatments in many cases of encephalitis, identification of a specific agent may be important for: – Prognosis, – Potential prophylaxis, – Counseling of patients and family members, and – Public health interventions
- 27. History • • • • • from family members rashes travel history occupation and recreational activities risk factors for HIV
- 28. Examinations • • • • • • GCS rashes, shingels, scar, bites, sign of immunocompromised state, subtle seizure meningism, and look for focal neurological signs lower cranial neuropathies and myoclonus (rhomboencephalitis or basal meningoencephalitis)
- 29. • Body fluid specimens: • – Cultures and analysis (i.e., antigen detection and nucleic acid amplification tests). • Biopsy of specific tissues: With culture, antigen detection, pcr and histopathologic evaluation, • Serologic testing for specific IgM and acute-and-convalescent- phase IgG antibody titers.
- 30. • MRI of the brain should be performed in all patients, with CT used only if: • MRI is unavailable, unreliable, or cannot be performed. • Neuroimaging findings may also suggest disease caused by specific etiologic agents.
- 31. EEG • usually shows non-specific diffuse high amplitude slow waves of encephalopathy, • subtle epileptic seizures. • Periodic lateralised epileptiform (HSV encephalitis)
- 34. Targeted Treatment Virus Treatment Herpes simplex virus Acyclovir Varicella-zoster virus Acyclovir, ganciclovir can be considered an alternative; adjunctive steroids to be considered Cytomegalovirus the combination of ganciclovir plus foscarnet is recommended. Cidofovir is not recommended (Poor BBB penetration) Epstein-Barr virus Acyclovir is not recommended, the use of corticosteroids may be beneficial Human herpesvirus 6 Ganciclovir or foscarnet B virus valacyclovir is recommended Influenza virus oseltamivir Measles and Nipah virus ribavirin West Nile virus ribavirin is not recommended Japanese encephalitis virus IFN-a is not recommended. St. Louis encephalitis virus IFN-2a can be considered HIV HAART JC virus reversal of immunosuppression (IDSA encephalitis guidelines, 2008) & (BIA encephalitis guidelines, 2012).