Kiran encephalitis (2)
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This document provides information on the management of acute encephalitis. It begins by defining encephalitis, meningoencephalitis, and acute encephalitis syndrome. It then discusses the causes of AES which can be viral encephalitis, acute pyogenic meningitis, tuberculosis meningitis, cerebral malaria, or acute disseminated encephalomyelitis. The document outlines the evaluation and management process in 6 steps: rapid assessment and stabilization, clinical evaluation, investigations, empirical treatment, supportive care and treatment, and prevention of complications. It provides details on specific viral, bacterial, and non-infectious causes as well as recommendations on prevention and vaccination.
Kiran encephalitis (2)
- 1. Management of Acute Encephalitis Dr. Kiran Rajput Guide - Dr. Pradeep Pazare 1
- 2. 2 DefinitionDefinition • Encephalitis is an acute inflammatory process involving brain tissue with dysfunction of brain(diagnosis is strictly histopathological but clinical/imaging markers may provide evidence of inflammation) • Meningoencephalitis is an acute inflammatory process involving the meninges and, to a variable degree, brain tissue. • They are often found associated together.
- 3. 3 EncephalopathyEncephalopathy Encephalopathy describes a clinical syndrome of altered mental status, manifesting as reduced consciousness or altered behaviour without inflammation.
- 4. 4 Acute Encephalitis SyndromeAcute Encephalitis Syndrome (AES) Clinically, a case of acute encephalitis syndrome is defined as a person of any age, at any time of year with the acute onset of fever and a 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)
- 5. 5 Causes of AESCauses of AES • Viral encephalitis, • Acute Pyogenic Meningitis, • TBM, • Cerebral Malaria, • Acute Disseminated Encephalomyelitis (ADEM).
- 6. 6 Non-infective causes of epidemic AESNon-infective causes of epidemic AES • Plant toxins • Heat stroke, • Reye’s syndrome.
- 7. 7 Causes of Encephalitis • Infectious causes: – Viral – Bacterial (TBM) – Ricketssial, – Fungal, – Parasites (pl falciparum) • Non-infectious causes.
- 8. 8 VIRAL CAUSES • Arboviruses: e.g. Japanese-B Encephalitis which is more common during summer months. • Herpesvirus. • Enteroviruses • CMV. • EBV. • Mumps. • RSV, Rubeola, Rubella or Rabies (Occasionally).
- 9. 9 Viral CausesViral Causes (continued)(continued) • Dengue Virus, • Measles virus, • Chandipura virus: – Outbreak: AP 2003, GJ 2004, Nagpur 2005 & 2007. – Sporadic: AP 2005-2006.
- 10. 10 Viral EncephalitisViral Encephalitis • Direct viral infection: – Primary Viral Encephalitis. • Indirect immune mediated mechanism: – Post-infectious viral encephalitis.
- 11. 11 Viral EncephalitisViral Encephalitis • Epidemic: – Japanese Encephalitis, – Dengue virus. • Sporadic: – Herpes simplex Encephalitis, – Enterovirus (EV71), – Chandipura virus, – Nipah virus, – Chikangunya virus.
- 12. 12 Other virus causing sporadic encephalitis • Varicella zoster virus, • Mumps, • Human herpesvirus 6 & 7, • EB virus, • Herpes simplex virus.
- 13. 13 Emerging viral agentsEmerging viral agents • Human parvovirus 4, • West Nile virus, • Bagaza virus, • Coxsackie virus.
- 14. 14 Non-Infectious Causes 1.Acute Disseminated Encephalomyelitis (ADEM), 2.Antibody-associated encephalitis, 3.Allergy: Post Vaccine. 4.Heat Hyperpyrexia.
- 15. 15 Signs & Symptoms of Encephalitis • Fever, • Headache, • Lethargy, • Vomiting,
- 16. 16 Clinical FeaturesClinical Features (continued) • Behavioural changes, • Impairment of consciousness, • Focal neurological signs, • Seizures.
- 17. 17 Encephalitis associated with GIT symptoms • Enteroviruses, • Rotavirus, • Parechovirus.
- 18. 18 Encephalitis associated with respiratory illness • Influenza viruses: • Paramyxoviruses, • Bacteria.
- 19. 19 Clue on physical examinationClue on physical examination • Pallor: – Cerebral Malaria, – Intracranial bleed. • Icterus: – Leptospirosis, – Hepatic Encephalopathy, – Cerebral Malaria.
- 20. 20 CluesClues (continued)(continued) • Skin rash:Skin rash: – Meningococcemia, – Dengue, – Measles, – Varicella, – Rickettsial diseases, – Arboviral diseases, – Enteroviral encephalitis.
- 22. 22 CluesClues (continued)(continued) • Petechiae: – Meningococcemia, – Dengue, – Viral Hemorrhagic Fever, • Parotid swelling: – Mumps.
- 23. 23 CluesClues (continued)(continued) • Orchitis: – Mumps • Labial herpes in young children: – Herpes simplex virus encephalitis.
- 24. Etiological agent based on clinical presentation • DEMENTIA Measles HIV • Cerebellar ataxia VZV • Retinitis CMV • Lymphadenopathy HIV EBV CMV Measles Rubella • Extrapyramidal manifestations: Japanese B virus, West Nile virus, Nipah virus • Diarrhea: Enterovirus • Poliomyelitis like flaccid paralysis :Japanese B virus poliovirus enterovirus West Nile virus Tick-borne encephalitis virus • Respiratory tract infection : H1N1 24
- 25. DIFFERNTIAL DIAGNOSIS: • Autoimmune Encephalitis • Sjogren Syndrome • Hashimoto’s Thyroiditis • SLE • ADEM • Vasculitis Of CNS • Reye’s Syndrome • Metabolic and Toxic diseases • Nonconvulsive status • Primary and metastatic brain tumors 25
- 26. LUMBAR PUNCTURE CONTRAINDICATIONS Imaging Before LP In Raised ICT
- 28. 28 ImagingImaging • CT Scan: – Normal. • MRI: – Localized areas of inflammation, – Diffuse brain swelling.
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- 31. 31 Problems encountered in managemntProblems encountered in managemnt • Paucity of data about the regional epidemiology and etiology of viral encephalitis. • Lack of easily available, low-cost microbiological testing for agents of viral encephalitis. • Lack of specific treatment for majority of etiological agents.
- 32. 32 ProblemsProblems (continued) • High incidence of mimickers: – Pyogenic meningitis, – Cerebral malaria, – TBM, – Acute Disseminated Encephalomyelitis (ADEM). • Lack of facility for intensive care in periphery.
- 33. 33 ProblemsProblems (continued) • Lack of facility for neuroimaging in periphery. • Patient delay in seeking health care. • Delay/not performing lumbar puncture. • Inappropriate supportive care.
- 34. 34 ProblemsProblems (continued) Inappropriate response during epidemic: • What samples to take? • How to store? • Whom to inform?
- 35. 35 Steps of evaluationSteps of evaluation and managementand management
- 36. 36 6 steps6 steps • Step 1: Rapid assessment and stabilization. • Step 2:Step 2: Clinical evaluation: – History & Physical Examination. • Step 3:Step 3: Investigations. • Step 4:Step 4: Empirical Treatment • Step 5:Step 5: Supportive care and treatment. • Step 6:Step 6: Complications and Rehabilitation.
- 37. 37 1 2 3 4 5 6 Eyes Does not open eyes Opens eyes in response to painful stimuli Opens eyes in response to speech Opens eyes spontaneously N/A N/A Verbal No verbal response Inconsolable, agitated Inconsistently inconsolable, moaning Cries but consolable, inappropriate interactions Smiles, orients to sounds, follows objects, interacts N/A Motor No motor response Extension to pain decerebrate response Abnormal flexion to pain for an infant decorticate response Infant withdraws from pain Infant withdraws from touch Infant moves spontaneously or purposefully GCSGCS
- 38. 38 Step 1: Rapid Assessment & StabilizationStep 1: Rapid Assessment & Stabilization • Maintain ABC. • Intubate SOS (children with GCS < 8). • Oxygen. • Ventilation. • Establish IV line and take samples. • Fluid bolus (RL/NS 20 ml/kg) SOS.
- 39. 39 Step 1Step 1 (continued)(continued) •Treat/Prevent hypoglycemia. •Identify signs of cerebral herniation and raised ICP. •Manage fever. •Control seizure. •Correct acid-base and electrolyte imbalance, if any.
- 40. 40 Step 2Step 2 • Clinical evaluation: – History including environmental details and – Thorough Physical Examination.
- 41. 41 HistoryHistory • Onset & duration, • Fever, headache, vomiting, diarrhoea, irritability, seizures, and rash. • Contact with TB, Chicken Pox, Mumps, • Place of residence – Endemic for JE? – Near rice-field? – Cattle, Pigs?
- 42. 42 Physical ExaminationPhysical Examination • Vitals, GPE, and Systemic, • Thorough CNS evaluation, • GCS,GCS, • Pupil: – size, shape, symmetry, and response to light.
- 43. 43 Clue!Clue! Unilateral pupillary dilatation in the comatose patient should be considered as evidence of 3rd Nerve compression from ipsilateral uncal herniation, unless proved otherwise.
- 44. 44 Bickerstaff Brain-Stem EncephalitisBickerstaff Brain-Stem Encephalitis Symptoms of progressive symmetrical external ophthalmoplegia suggest Bickerstaff brainstem encephalitis in association with M. pneumoniae, and can serve as a clue to the diagnosis, especially when associated with ataxia.
- 45. 45 Herpes simplex encephalitis (HSE)Herpes simplex encephalitis (HSE) • Personality changes, confusion, and disorientation. • Herpes labialis, • Focal seizures, • Unilateral neurological findings, • Normal CT in first 4-6 days. • MRI and FLAIR more reliable. • Positive CSF PCR.
- 46. 46 FundusFundus • Papilloedema, • Haemorrhage (Clue for CM)
- 47. 47 Look for!Look for! • Hepato-splenomegaly, • Myocarditis – (An important complication of EV 71 encephalitis)
- 48. 48 Step 3: InvestigationsStep 3: Investigations • CSF, • Blood/Serum, Urine, • Throat Swab, Nasopharyngeal Swab, • MRI (if available), avoid sedation.
- 49. 49 Basic InvestigationsBasic Investigations • CBC including platelet count, • Blood Glucose, • Serum Electrolytes, • Liver & Kidney Function Test, • Blood C/S, • ABG, • P/S for MP.
- 50. 50 CSFCSF • Gross appearance: colour, transparency • Chemistry including CSF: Blood Sugar, • Cytology, • C/S, • Latex Agglutination, • PCR for HSV 1 & 2, • IgM antibodies for JE & Dengue.
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- 53. Investigation in immunocompromised patients with altered consciousness • CSF PCR for HSV, CMV, EBV, VZV,HHV- 6and-7 Influenza, ParvovirusB19 • CSF AFB staining for M. tuberculosis • CSF culture for L. monocytogens • Blood culture • Indian ink staining and if positive cryptococcal antigen testing in CSF • Antibody testing and if positive CSF PCR for T. gondii • Antibody testing of serum and if positive CSF for syphilis 53
- 54. 54 Step 4: Empirical TreatmentStep 4: Empirical Treatment • Do not wait for report, start treatment immediately. • Ceftriaxone + Acyclovir + Artesunate (stop artesunate if P/S and RDT are negative).
- 55. 55 Step 5: Supportive Care & TreatmentStep 5: Supportive Care & Treatment 1. Maintain airway, breathing and circulation. 2. Control of seizures. 3. Treatment of raised ICT. 4. Manage fever ((Never give aspirin)Never give aspirin).. 5. Maintain fluid & electrolyte balance. 6. Maintain blood-sugar level. 7. Feeding: NPO initially then NG Tube Feeding. 8. Specific Treatment. 9. Methylprednisolone or dexamethasone must be given to children with suspected ADEM.
- 56. 56 Features of raised ICPFeatures of raised ICP
- 57. 57 5th centile of systolic BP Neonate= 60 mmHg 1mo-1yr = 70 mmHg 2-10yr =70+age(yr)x2 >10 yr = > 90 mmHg
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- 62. 62 Specific Treatment • Until a bacterial cause is excluded, parenteral antibiotics therapy should be administered: – Age 0 to 3 months: • Inj. Cefotaxime + Inj. Ampicillin. – Age 3 months to 12 years: • Inj. Ceftriaxone/Inj. Cefotaxime/Inj. Ampicillin + Inj. Chloramphenicol. • T/T for HSV: – 3month to 12 yr Inj. Acyclovir 500 mg/m2 8 hrly – >12yrs 10mg/kg 8 hrly Duration Confirmed cases for 14 to 21 days iv treatment and minimum 21 days for those aged 3month-12yr
- 63. 63 Role of Antibiotics • Under most situations, it may be nearly impossible to rule out a bacterial infection. • Incidence of super-added bacterial infection is high. • Therefore, a good antibiotic shield is recommended.
- 64. 64 Dosage • Inj. Chloramphenicol: – 100 mg/kg/day in 4 divided doses for 10 days. • Inj. Ceftriaxone: – 100 mg/kg/day in 2 divided doses for 10 days. • Inj. Cefotaxime: – 200 mg/kg/day in 3-4 divided doses for 10-14 days.. • Inj. Ampicillin: – 300 mg/kg/day in 4 divided doses for 10 days.
- 65. 65 Step 6: Prevention/Treatment ofStep 6: Prevention/Treatment of complications and rehabilitationcomplications and rehabilitation • Physiotherapy, posture change, prevent bed- sore and exposure keratitis. • Prevent complications: aspiration pneumonia, nosocomial infection, coagulation disturbances. • Nutrition: early feeding. • Psychological support to patient and family.
- 66. 66 Prognosis • Mortality: 10 – 70%, • Mortality highest in age 5 – 9 yrs. • Sequelae: 5 - 70%.
- 68. 68 Control Measures a. Vector Control: 1. Fogging. ULV 1. Indoor mosquito spray b. Vaccination.
- 69. 69 Personal Protection • Avoid mosquito bites: – Use mosquito-net – House Screening – Mosquito Repellents. – Avoid evening outdoor exposure. – Cover body with clothing • Vaccination
- 70. 70 IAP RecommendationIAP Recommendation • JE vaccine not recommended for routine use. • Needed only for individuals living in endemic area.
- 71. 71 VaccinesVaccines • Inactivated Mouse Brain Vaccine (JE-VAXJE-VAX), not in India • Inactivated Primary Hamster Kidney Cells-P3-China, • Live Attenuated Primary Hamster Kidney (PHK) Cells- SA14-14-2SA14-14-2 strain – China: Marketed for both domestic use and for use in Nepal, S. Korea, Sri Lanka and India. • Inactivated Vero Cell Culture Derived SA-14-14-2 JE vaccine (IC51)-(IXIARO)
- 72. 72 Live Attenuated SA-14-14-2 Vaccine • The IAP thinks there is a need of a second dose of the vaccine to provide more complete and sustained protection. • 1st dose at 9 months along with Measles vaccine. • 2nd dose at 16 to 18 months at the time of 1st booster of DPT vaccine.
- 73. 73 Dosage (SA-14-14-2)Dosage (SA-14-14-2) • Amount: 0.5 ml • Route: SC • Single dose between 1 and 15 years of age. • UIP: 16 – 18 months with 1st booster of DPT. • Store at 80 C • Protect from sunlight • Efficacy- 94.5%
- 74. 74 Inactivated Vero Cell culture-derived Kolar strain, 821564XY, JE Vaccine (JENVAC) • JENVAC is a Vero Cell culture-derived, inactivated, adjuvanted and thiomersal containing vaccine. • The original virus strain used in the vaccine was isolated from a patient in the endemic zone in Kolar, Karnataka, India.
- 75. 75 JENVAC (Kolar Strain)JENVAC (Kolar Strain) • Lacks the experience of multinational trials, • 2 doses of the vaccine, 0.5 ml IM at 4 weeks interval for the primary immunization for children ≥≥ 1 year of age. • Need of booster dose at later stage (further study required for exact timing).
- 76. IN A NUTSHELL • Inadequately investigated and managed • MRI and CT mandatory. PCR testing attempted. • Supportive therapy mainstay. • Treatable DD should always be considered. • Acyclovir should be given empirical therapy. • Once etiological agent of encephalitis identified antimicrobial therapy targeted to that infectious agent. 76
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- 78. Thank You 78