Encephalitis ppt

gen approach of acute encephalitis syndrome

1. Acute Encephalitis syndrome 1 Presenter; Dr. Sachin giri Gen Medicine Moderator; Dr A.C. Shrivastava

2. Definition 2 The Encephalitis is an acute inflammatory process involving brain tissue. Meningoencephalitis is an acute inflammatory process involving the meninges and, to a variable degree, brain tissue. • They are often found associated together.

3. Encephalitis 3 Two Components : Inflammation of brain, and Dysfunction of brain.

4. Encephalopathy 5 Encephalopathy describes a clinical syndrome of altered mental status, manifesting as reduced consciousness or altered behaviour.

5. Causes of Encephalopathy 6 Systemic infection, Metabolic derangement (e.g. DKA), Toxins, Drugs & Poisoning, Hypoxia, Trauma, Vasculitis, CNS infection.

6. Acute Encephalitis Syndrome (AES) 7 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)

7. Causes of AES 8 Infectious cause Viral encephalitis, Acute Pyogenic Meningitis, TBM, Cerebral Malaria, Acute Disseminated Encephalomyelitis (ADE).

8. Causes ….. Srtuctural CNS lesions Hypothalamic lesion Brain stem lesion Intraventricular /SAH Cerebral venous sinus thrombosis

9. Non-infective causes of epidemic AES Plant toxins Neuroleptic malignant syndrome Heat stroke Malignant hyperthermia Reye’s syndrome. Thyrotoxic encephalopathy 10

10. Causes of Encephalitis 11 Infectious causes: Viral Bacterial (TBM) Ricketssial , Fungal Parasites P l . falciparum Protozoal( Naegleria,Acanthamoeba , balamuthia )

11. VIRAL CAUSES 12 • Enteroviruses: More than 80% of all cases . • Arboviruses: e.g. Japanese-B Encephalitis which is more common during summer months. • Herpesvirus. • C MV. • E BV. • Mu m p s . • RSV, Rubeola, Rubella or Rabies (Occasionally).

12. Viral Causes (continued) 13 Dengue Virus, Measles virus, Chandipura virus: – Outbreak: – Sporadic: KFD

13. Viral Encephalitis 14 Direct viral infection: Primary Viral Encephalitis. Indirect immune mediated mechanism: Post-infectious viral encephalitis.

14. Viral Encephalitis 15 Epidemic: Japanese Encephalitis, Dengue virus. Sporadic: Herpes simplex Encephalitis, Enterovirus (EV71), Chandipura virus, Nipah virus, Chikangunya virus.

15. Other virus causing sporadic encephalitis Varicella zoster virus, Mumps, Human herpesvirus 6 & 7, EB V irus , Herpes simplex virus. 16

16. Emerging viral agents 17 Human parvovirus 4, West Nile virus, Bagaza virus, Coxsackie virus.

17. N o n - I n f e c t i ou s C a us e s 18 Acute Disseminated Encephalomyelitis (ADEM), Antibody-associated encephalitis, 3.Allergy: Post Vaccine. 4.Heat Hyperpyrexia.

18. Signs & Symptoms of Encephalitis Fever, Headache, Lethargy, Vomiting, 19

19. 20 C ontinued … Behavioural changes, Impairment of consciousness, Focal neurological signs, Seizures.

20. Encephalitis associated with GIT symptoms 21 E nt e roviru ses , Rotavirus, Parechovirus.

21. Encephalitis associated with respiratory illness Influenza viruses: – Myositis may also be associated. Paramyxoviruses, Bacteria. 22

22. Clue on physical examination 23 Pallor: Cerebral Malaria, Icterus: Leptospirosis, Hepatic Encephalopathy, Cerebral Malaria.

23. Clues (continued) 24 Skin rash: Meningococcemia, Dengue, Measles, Varicella, Rickettsial diseases, Arboviral diseases, Enteroviral encephalitis.

24. Clues (continued) 25 Petechiae: Meningococcemia, Dengue, Viral Hemorrhagic Fever, Parotid swelling: Mumps.

25. Clues (continued) 26 Lymphadenopathy EBV,Leptospira,Lymphoma,TB Orchitis: Mumps Labial herpes in young children: Herpes simplex virus encephalitis.

26. Investigations Routine blood examination Renal function test Liver function test Serum electrolytes PBS for malarial parasites

27. CSF in viral encephalitis 28 Pressure: normal or slightly raised, Sugar: normal, Cells: acellular (no cell) or mild leukocytosis (mostly lymphocytes)

28. I m ag ing 29 CT Scan: Normal. MRI: Localized areas of inflammation, Diffuse brain swelling.

29. Management 30

30. DR. M. S. PRASAD 8 3 Principles of Management Hospitalization. Save Life. Relieve symptoms. Provide specific treatment Prevent neurological residues

31. Steps of evaluation and management 32

32. 6 steps Rapid assessment and stabilization. Clinical evaluation: History & Physical Examination . Investigations. Supportive care and treatment. Empirical Treatment Complications and Rehabilitation. 33 Step 1: Step 2: Step 3: Step 4: Step 5: Step 6:

33. 34 Step 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.

34. Step 1 (continued) 35 • Fluid bolus (RL/NS 20 ml/kg) SOS. • Treat/Prevent hypoglycemia. • Identify signs of cerebral herniation and raised ICP. • Manage fever. • Control seizure. • Correct acid-base and electrolyte imbalance, if any.

35. Step 2 36 Clinical evaluation: History including environmental details and Thorough Physical Examination.

36. History 37 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?

37. Physical Examination 38 Vitals, G eneral physical E xamination , and Systemic examination Thorough CNS evaluation, GCS, Pupil: – size, shape, symmetry, and response to light.

38. Step 3: Investigations 39 Blood/Serum, Urine, Microscopy CXR CSF, Throat Swab, Nasopharyngeal Swab, MRI (if available), avoid sedation.

39. Basic Investigations 40 CBC including platelet count, Blood Glucose, Serum Electrolytes, Liver & Kidney Function Test, Blood C/S, ABG, P/S for MP.

40. C SF 41 • Gross appearance: colour, transparency • Chemistry : Blood Sugar, Protein • Cytology, • C / S, • Latex Agglutination, • PCR for HSV 1 & 2, • IgM antibodies for JE & Dengue.

41. Step 4: Empirical Treatment 42 Do not wait for report, start treatment immediately. Ceftriaxone + Acyclovir + Artesunate (stop artesunate if P/S and RDT are negative).

42. Step 5: Supportive Care & Treatment 43 Maintain airway, breathing and circulation. Control of seizures. Treatment of raised ICT. Manage fever (Never give aspirin). Maintain fluid & electrolyte balance. Maintain blood-sugar level. Feeding: NPO initially then NG Tube Feeding. Specific Treatment. Methylprednisolone or dexamethasone must be given to children with suspected ADEM.

43. 44 Step 6: Prevention/Treatment of complications 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.

44. UK Regimen 45 (till culture-report is available) Aciclovir : 10 mg/kg 8 hrly to cover HSV, 3 rd generation cephalosporin: to cover bacterial cause, Erythromycin /Azithromycin : to cover mycoplasma .

45. Japanese-B Encephali t is 46

46. Jap a n es e E n c e p h a l i t is (J E ) 47 One of the commonest cause of AES. Assam, West Bengal, Uttar Pradesh and Jharkhand.

47. Japanese Encephalitis (JE) 48 Leading viral cause of acute encephalitis syndrome (AES) in Asia. Primarily affects children under age 15. Acute onset, fulminant course, and high mortality & morbidity. 70% of patients either die or survive with long term neurological disability.

48. JE 49 Group-B arbovirus (Flavivirus). Mosquito borne Encephalitis. Transmitted by Culicine (culex) mosquitoes. Zoonotic Disease. Rice or Pig Farming. Peak season: JUN – SEP.

49. V i rus 50 Japanese Encephalitis Virus (JEV), Single stranded RNA virus, Genus: flaviviridae

50. Emerging Problem in West Bengal, Bihar, Assam, Madhya Pradesh, Maharastra, Manipur, Haryana, Odisha, Goa, and P uduche r y . 51

51. S p r e ad 52 Spreads by mosquito bite only, Man is an incidental dead end host, Man-to-man transmission not reported.

52. Life-cycle of virus 53 Pi g M o s qu i to Pig Bird Mosquito Bird MAN IS AN INCIDENTAL “DEAD END” HOST

53. 54

54. HOSTS 55 Infected pigs do not manifest any overt symptoms of illness. AMPLIFIER OF VIRUS. Others: Cattle Buffaloes Horses Birds.

55. Japanese-B Encephalitis 56 Incubation Period: 5-15 days. Ratio of overt disease to unapparent infection = 1:300 to 1: 1000. Cases represent tip of iceberg. Case Fatality Rate: 10 –70%. Incidence: 1- 10/10, 000 population.

56. Pathology 57 Mosquito bite transmission to man JEV multiplies Neurologic invasion enters CNS  JEV replicates in endoplasmic reticulum and Golgi apparatus and destroys them. Changes mainly in gray matter. Growth of the virus across vascular endothelium  mainly thalamus, basal ganglia, brain-stem, cerebellum, hippocampus and cerebral cortex.

57. Pathology outside CNS 58 Hyperplasia of germinal centers of lymph-nodes, Enlargement of malpigian bodies in spleen. Interstitial myocarditis, swelling and hyaline changes in Kuffer’s cells of liver, pulmonary interalviolitis, and focal hemorrhages in kidneys.

58. Clinical Features. 59

59. Japanese-B Encephalitis 60 Sudden onset with high fever, headache, vomiting, Mental Confusion, Irritability, Loss of consciousness. Severe Encephalomyelitis. With Radiculitis. Without Radiculitis.

60. 3 Stages 61 Prodromal Illness [2 - 3 days] Encephalitis stage Acute Stage [3 - 4 days] Sub-acute Stage [7 - 10 days] 1. Convalescence [4 - 7 weeks]

61. Prodromal Stage 62 High grade fever +/- rigor, Headache, General malaise, Nausea and Vomiting. During this stage, a definitive clinical diagnosis is not possible.

62. Encephalitic Stage 63 • • Altered mental status: – Confusion, agitation, coma Generalized weakness, • Hypertonia & Hyper-reflexia, • S e i z u r e s , • Papilloedema and/or Cr anial N erve involvement, • GIT bleed & Pulmonary Hemorrhage.

63. L a t e S tage 64 Stage of convalescence, Recovery, Persistence of signs of CNS injury: – Residual neurological impairments Secondary infections are frequent in this stage.

64. Residual neurological impairments 65 Involuntary movements: – Choreoathetosis or extrapyramidal symptoms, Paralysis & Paresis, Speech disorders. Decorticate or Decerebrate Posturing. Post-Encephalitis Cerebral Palsy.

65. DIA G N O S IS 66 Clinical Manifestations. Epidemiology. CSF: Pleocytosis: Initially Polymorphs then Lymphocytes. Increased protein. Normal sugar. EEG: Diffuse slow-wave activity. CT or MRI: Swelling of the brain parenchyma.

66. Diagnosis (Contd) 67 Virus isolation Detection of viral component (antigen detection) Viral serology

67. Virus Isolation 68 CSF Nasopharynx Faeces Urine

68. Detection of antigen and specific antibody 69 Nucleic Acid Probe PCR RIA ELISA

69. Viral Serology 70 IgM & IgG: IgM appears early within 2 weeks of infection IgG appears later, peaking around 8 weeks.

70. Two Samples 71 Acute Serum (at admission). Convalescent Serum (after at least four weeks).

71. Differential Diagnosis 72 Polio Cerebral Malaria TBM.

72. D/D with Febrile Seizure 73 Age : Febrile seizures limited to age group from 6 months to 6 years. Encephalitis and CM occur at any age. Recovery from unconsciousness : Patients with febrile seizures become fully conscious and alert after control of seizure. Patients with CM or Encephalitis do not gain consciousness even after control of seizures.

73. Suspected JE 74 All cases of Acute Encephalitis Syndrome, i.e. Any presenting with acute onset of fever, and altered state of consciousness with or without seizures. • P atient regains consciousness after control of seizures in simple febrile seizure but continues to have altered state of consciousness in JE.

74. P r oba b l e JE 75 A suspected case that occurs in close geographic and temporal relationship to a laboratory-confirmed case of JE, in the context of an outbreak.

75. 76 Confirmed JE A probable case that has been confirmed by laboratory tests.

76. Management 77

77. Prognosis 78 Mortality: 10 – 70% . Mortality highest in age 5 – 9 yrs. Sequelae: 5 - 70%.

78. Prevention 79

79. Control Measures 80 Vector Control: Fogging. 1. Indoor mosquito spray b. Vaccination.

80. Personal Protection 81 Avoid mosquito bites: Use mosquito-net House Screening Mosquito Repellents. Avoid evening outdoor exposure. Cover body with clothing Vaccination

81. 82 Vaccination Vaccination against JE is advised in endemic areas In s u ch area s, i t i s gi v e n ro u ti n ely to children above 1 year of age,

82. V ac c i n e s 83 • Inactivated Mouse Brain Vaccine ( JE-VAX ), • Inactivated Primary Hamster Kidney Cells-P3 -China, • Live Attenuated Primary Hamster Kidney (PHK) Cells- SA14-14-2 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 )

83. Live Attenuated SA-14-14-2 Vaccine 84 Launched in India in 2006. Single Dose. Efficacy: 94.5% JE Vaccine efficacy: 60% in UP and 70% in Assam Results better in Nepal.

84. Dosage (SA-14-14-2) 85 • Amount: 0.5 ml • Route: S .C • Single dose between 1 and 15 years of age. Store at 8 C • Protect from sunlight

85. 86 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.

86. Vaccination 87 Protective immunity develops in about a month’s time after the second dose. Revaccination after 3 yrs. Best used in inter-epidemic period.

87. THANK YOU….