Febrile encephalopathy

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Febrile encephalopathy

  1. 1. D KALPANAAddl. Professor of Pediatric Neurology,Medical College, Thiruvananthapuram
  2. 2.  Definition of terms Differential diagnosis Points from history/epidemiology Investigations Supportive management Specific management Autoimmune encephalitis
  3. 3. ENCEPHALOPATHY• Diffuse disturbance of brain function without inflammationENCEPHALITIS• Dysfunction of brain associated with inflammationFEBRILE ENCEPHALOPATHY• a/c onset of fever (<1wk)+alteration of consciousness >12 hrs
  4. 4. Febrile inflammation ENCEPHALOPATHY Temp >380C Cellular CSF Seizures Alteration of cerebral Imaging /EEG function suggestive ofFocal neurological signs inflammation
  5. 5.  Clinically, a case of Acute Encephalitis Syndrome (AES) is defined as a person of any age, at any time of year with the acute onset of fever and at least one of: a) change in mental status (including symptoms such as confusion, disorientation, coma, or inability to talk); b) New onset of seizures (excluding simple febrile seizures. ( A simple febrile seizure is defined as a seizure that occurs in a child aged 6 months to less than 6 years old, whose only finding is fever and a single generalized convulsion lasting less than 15 minutes, and who recovers consciousness within 60 minutes of the seizure)Bull World Health Organ 2008, 86(3):178-186.
  6. 6.  INFECTIONS DEMYELINATION - ADEM AUTOIMMUNE ENCEPHALITIS DRUGS/TOXINS COLLAGEN VASCULAR DISORDERS SEIZURES –NON CONVULSIVE STATUS METABOLIC ICSOL
  7. 7.  Viral encephalitis  Herpes simplex type 1. type2  Varicella zoster  HHV6  Epstein Barr virus  Arboviruses – JE,West Nile,Dengue, Chikun gunya,  Rhabdoviruses-rabies  Orthomyxo –H1N1  Paramyxo –measles  HIV
  8. 8.  Bacterial  Meningitis  Brain abscess  Sepsis associated encephalopathy  Leptospirosis  Typhoid  M. tuberculosis  Rickettsial (scrub typhus) Parasitic  Cerebral malaria  Toxoplasma
  9. 9.  Features of infection Evidence of CNS involvement Features of raised intracranial tension Signs and symptoms of meningeal irritation
  10. 10. • HSV is sporadic epidemiology • JE epidemicsh/o animal bites • Rabies • JEMosquito bites • Dengue • Chikun GunyaWorking/playing • Leptospirosis in dirty waterContact withTB • TBM
  11. 11. •Maculopaular •Petechiae/purpura Fever with rash •Vesicles •Eschar •Herpes labialis Respiratory • H1N1 symptoms • enterovirusesDiarrhoea,vomiting • Polio • Mumps Parotitis • EB virus • HIV • DengueMyalgia,arthralgia • leptospirosis
  12. 12. Abnormal Ataxia ADEMbehaviour/psychosis VZV HSV Entero virus Limbic encephalitis NCSE Lower cranial nerveOpisthotonic posture palsies TBMChoreoathetosis VASCULITISJE,autoimmune Brainstem encephalitis JE,west nileMeningeal signs MENINGITIS Visual loss ADEM Optic neuritis meningoencephalitis Hypertensive encephalopathyAsymmetric signs andsymptoms Encephalitis Papilloedema ICSOL TBM Hydrocephalus –TBM ADEM Hypertensive encephalopathy
  13. 13. • EB viruslymphadenopathy • leptospira Hypotension • dengue • Chikungunya shock • leptospira • EBVIRUS • dengue organomegaly • Lepto • HIV • COLLAGEN
  14. 14. management
  15. 15. SHOCK SEPSISINTRCRANIAL SEIZUREINFECTION • STATUS EPILEPTICUS• ENCEPHALITIS • NON CONVULSIVE STATUS• MENINGITIS• TBMRAISED ICT METABOLIC• PAIPPEDEMA • HYPOGLYCEMIA• GCS<8 • HYPERAMMONEMIA• ASYMMETIC PUPILS • ACIDOSIS • DKA• POSTURING • DRUGS• ABSENT DOLL’S EYE
  16. 16. CSF STUDY EEG IMAGING
  17. 17. CONTRAINDICATIONS IMAGING BEFORE LP IN RAISED ICTEMPIRICAL ANTIBIOTICS +ACYCLOVIR IF DELAY OFSEVERAL HRS IS EXPECTED
  18. 18.  NOTE THE OPENING PRESSURE CELLS GRAM STAIN,CULTURE PROTEIN SUGAR VIROLOGICAL STUDIES –PCR,IgM TBPCR LACTATE
  19. 19. BACTERIAL • PMN MENINGITIS • High protein, low sugar, gram stain • Few lymphocytes ASEPTIC • Normal protein MENINGITIS • Normal sugar • lymphocytic VIRAL • Normal sugar, normal to slightlyENCEPHALITIS raised protein • Opalescent, cob webTUBERCULOUS • Lymphocytic MENINGITIS • High protein. Low sugar
  20. 20.  Take at least 5 ml of CSF Be sure that it is not mixed with blood Sensitivity and specificity are relatively good Can be negative very early in HSV and after 10 days of treatment Never stop Acyclovir before repeating once more after 72hrs – if clinical history, EEG and imaging are suggestive Serum/CSF Ig M antibodies useful in JE Paired samples – 4 fold rise in titre
  21. 21.  MRI is preferable to CT scan- CTis advised in unstable patients, delirious children who cannot be kept still for 30 min
  22. 22. JE
  23. 23. RABIES
  24. 24.  Diffuseslowing suggests encephalopathic process PLEDS in HSE Triphasic waves in metabolic encephalopathy Non convulsive status epilepticus
  25. 25.  Should be suspected in confusion, stupor, unarousable coma Subtle features like eye blinking, nystagmus, perioral twitching, automatisms may be seen May follow convulsive seizures EEG is the only diagnostic clue Response to diazepam can be demonstrated in simultaneous EEG recording Generalised/complex partial
  26. 26.  Maintain  Normothermia  Normoglycemia  Normal electrolyte balance  Normotension Management of raised ICT  minimal stimulation  Head end elevation  Avoid hypotonic fluids  3% saline  Mannitol 20% solution  hyperventilation
  27. 27.  Management of seizures/status epilepticus Identify SIADH and manage Rapid correction of hyponatremia may lead to central pontine myelinolysis
  28. 28.  Abnormal /psychotic behaviour – haloperidol+ phenergan Choreoathetosis – dopa blockers Dystonia - tetrabenezine, anticholinergics, muscle relaxants
  29. 29.  HSE –ACYCLOVIR I/V 10 mg/kg/dose 8 hrly x 14 -21 days. (500 mg/m2)Neonates 20 mg/kg/dose Oral acyclovir has very low bioavailability Oral valacyclovir can be used  Very costly Empirical acyclovir Repeat LP after 72 hrs if initial PCR is negative – and stop Acyclovir after that. Other drugs effective - foscarnet
  30. 30.  Varicella zoster – acyclovir HHV 6 - foscarnet +gancyclovir CMV – gancyclovir H1N1- oseltamivir Rickettsia – doxycycline Mycoplasma – azithromycin Leptospira – penicillin Bacterial meningitis – ceftriaxone+ vancomycin ADEM – steroids, IVIG Autoimmune encephalitis - immunosuppressants
  31. 31.  Even in best centres a definite diagnosis of encephalitis is reached only in 42% of cases (Granerod et al) ADEM in 21% 1% autoimmune encephalitis 37% no definite diagnoses  Undiagnosed viral infections  Autoimmune causes  Unidentified metabolic causes
  32. 32.  Poorly understood CNS condition Manifests lethargy –delirium Pathogenesis  bacterial invasion of brain  endotoxins  derangement of neurotransmitter and  amino acid and microvascular changes Prognosis---serious May be seen in patient with 1. mechnical ventilation 2.critical ill patient in micu (sedatives, neuromuscular blocking agents, dyselectrolytemia,hepatic failure may contribute)
  33. 33.  MANIFESTATION MAY BE HIV VIRUS ITSELF OR ITS NEUROLOGICAL COMPLICATION D/T OPPORTUNISTIC INFECTION LIKE 1. CNS tuberculosis 2. cytomegalo virus encephalitis 3. toxoplasmosis 4. cryptococcal meningitis 5.syphilis 6.tumours (primary CNS lymphoma )or drug related complications
  34. 34.  The potentially fatal complication of falciparum malaria ( most important cause of unarousable coma in febrile patients in endemic area ) SUSCEPTIBILITY - childrens - pregnant women - non – immune adults 20 % all severe falciparum malaria requires ICU admission
  35. 35.  Selective cytoadherence and sequestration of parasitized RBC’S in cerebral venules and toxin release at schizont rupture are possible pathological mechanism Systemic complications like hypoglycemia may contribute to development of coma Diagnosis – PS for MP Treatment – artesunate is better than quinine
  36. 36.  often presents with fever behavioural abnormalities psychosis movement disorders seizures/status May be paraneoplastic – teratoma ovary in young females Often no tumour is identified Antibodies to NMDA ,VGKC receptors Treatment – IVIG, plasmapheresis
  37. 37. ???
  38. 38.  A variety of infective and non infective conditions in children can present as acute febrile encephalopathy Stabilisation of patient and supportive management helps a lot in reducing morbidity and mortality Identification of specific etiology helps in institution of specific therapy Awareness of Autoimmune encephalitis is important – another treatable cause like ADEM In a significant proportion of cases aetiology is yet to be identified

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