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 A syndrome of global brain dysfunction
 Definition (International Pediatric MS
study Group 2007):
› Behavioral change: ...
 Full consiousness death
› Restless
› Agitated
› Confused
› Delirious
› Lethargic
› Drowsy
› Stuporous
› Comatose
 Glasg...
Davies E et.al. Encephalopathy in
children: an approach to
assessment and management.
Arch DisChild. 2012
May;97(5):452-8....
 CNS infection/ Para-
infection
 Autoimmune
 Metabolic/ Toxins
 Seizure related
 Hypertensive
 Trauma/
hemorrhage
 ...
 An important paediatric emergency
 Involves children of any age
 Previously normal children, or children
with pre-exis...
 Associated with significant mortality and
long term morbidity in survivors
 Good assessment with appropriate
investigat...
 Wide range of differential diagnoses
long list of possible investigations
 History
 Physical examination
 Investigations
 Timing and nature of the encephalopathy
 Associated symptoms
› Fever, vomiting, loss of appetite
› Headache, seizures
...
 Pre-existing medical / neurological condition
 Developmental history
 Travel, contact with animals/ insects
 Drug/ to...
 Opportunistic examination and
observation
 Vital signs: HR, BP, RR, Spo2, temperature
 Mental state, communication,
be...
 Neurological examination:
› Focal neurological deficit
 Motor & sensory
 Cranial nerves & limbs
› Eyes: nystagmus, oph...
 Initial investigations
› Blood glucose
› Blood gases
› Urea & electrolytes
› LFT
› Ammonia
› FBC & blood picture
› Urine...
 Further tests should be tailored to the
differential diagnoses
 Lumbar puncture: CNS infections
 Neuro-imaging (Ultras...
 Suggestive features:
› Fever , headache
› Meningism
› Focal neurological deficits
› Seizures
› Primary source of infecti...
 FBC, CRP, ESR
 Blood culture
 Viral study (blood, throat, urine, stool)
 TB work-up
 CSF: ME, sugar, protein, C&S, v...
CT with contrast: Bacterial
meningitis: Subdural effusion,
meningeal enhancement,
abscess formation
CT with contrast: Brai...
Plain CT: Hydrocephalus CT with contrast: Basal
enhancement
MRI (T2): Bilateral asymmetric temporal, insular & basifrontal
hyper-intensity
MRI, T2 (Lt), FLAIR (Rt): Multiple hyper-intense foci involving the
white matter & deep grey matter
MRI (T2, FLAIR, DWI): Bilaterally symmetric
signal change in the thalami
Plain CT: Bilaterally symmetric hypodensity of the caudate nuclei &
putamen with mass effect
 NMDA-receptor antibody encephalitis,
limbic encephalitis, Hashimoto’s
encephalopathy, CNS lupus etc.
 Suggestive featur...
 Investigations:
› Work-up for vasculitic disorders
› Blood or CSF for specific neuronal
antibodies:
 Anti-NMDA receptor...
 Traumatic
› Accidental
› Non-accidental: Child abuse (Shaken baby
syndrome)
 Spontaneous
› Vascular malformation
› Blee...
 Suggestive features:
› History of head trauma
› Sudden onset of encephalopathy ( +seizure) in a
well child
› Signs of ac...
 Blood count (platelet), coagulation
profile
 Neuro-imaging
 Broad category of conditions
 Suggestive features:
› History of development delay / regression, growth
failure, epileps...
 Investigations
› *Initial investigations
› Metabolic work-up
› Neuro-imaging, MR spectoscopy

MRI. Leigh syndrome:
Bila...
(A) CT: Basal ganglia calcification. (B & C) MRI T2: Hyperintense lesion in
the left temporo-parieto-occipital regions. (D...
 Suggestive features
› Signs & symptoms of raised ICP
› Focal neurological deficit
› Seizures
› Extra-cranial primary mal...
Gliablastoma multiformeMedulloblastoma
 7 year old boy, previously well
› Headache & lethargic for 3 days
blurred vision, confusion,
followed by status epilepti...
 On arrival, sedated; pupils-equal &
reactive; fundus-N; no focal neurological
deficit
 Noted hypertension but no bradyc...
 Urine ME: RBC 5+
 ASOT 800
Diagnosis:
Hypertensive encephalopathy secondary to
post-streptococcus acute gromerulo-nephr...
 Brain MRI
Posterior Reversible Encephalopathy Syndrome
11 yr old girl
 Learning disability with history of
recurrent stroke-like episodes & epilepsy
 Diagnosed Mitochondrial
E...
 Able to talk & walk independently
 Activities of daily living: need supervision
with some assistance
 On anti-epilepti...
 Presented with:
› More frequent seizures, 1-2 episodes / day,
for 3 days
› Lost her verbal skills, not interactive
› Poo...
 Video EEG: Non-convulsive status epilepticus
 Acute encephalopathy in children is an
emergency with wide range of
differential diagnoses; significant
morbidity & mort...
Diagnostic approach to acute encephalopathy
Diagnostic approach to acute encephalopathy
Diagnostic approach to acute encephalopathy
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Diagnostic approach to acute encephalopathy

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Encephalopathy

Published in: Health & Medicine
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Diagnostic approach to acute encephalopathy

  1. 1.  A syndrome of global brain dysfunction  Definition (International Pediatric MS study Group 2007): › Behavioral change: confusion, excessive irritability › Alteration in consciousness: lethargy, coma  Acute or insidious onset
  2. 2.  Full consiousness death › Restless › Agitated › Confused › Delirious › Lethargic › Drowsy › Stuporous › Comatose  Glasgow Coma Scale
  3. 3. Davies E et.al. Encephalopathy in children: an approach to assessment and management. Arch DisChild. 2012 May;97(5):452-8. doi: 10.1136/adc.2011.300998. Epub 2011 Dec 27
  4. 4.  CNS infection/ Para- infection  Autoimmune  Metabolic/ Toxins  Seizure related  Hypertensive  Trauma/ hemorrhage  Hypoxic-ischemic  Tumour/ Malignancy  Hydrocephalus/ Other causes of raised ICP
  5. 5.  An important paediatric emergency  Involves children of any age  Previously normal children, or children with pre-existing neurological impairment
  6. 6.  Associated with significant mortality and long term morbidity in survivors  Good assessment with appropriate investigations identify treatable causes minimize neurological impairment
  7. 7.  Wide range of differential diagnoses long list of possible investigations
  8. 8.  History  Physical examination  Investigations
  9. 9.  Timing and nature of the encephalopathy  Associated symptoms › Fever, vomiting, loss of appetite › Headache, seizures  Current/ recent febrile illness  In some cases, the cause is obvious  E.g. acute renal/ liver failure, DM, following head trauma or hypoxic event
  10. 10.  Pre-existing medical / neurological condition  Developmental history  Travel, contact with animals/ insects  Drug/ toxin ingestion  Family history › Neurological/ metabolic disorder; vascular/ bleeding disorder › Parental consanguinity › Early/ unexplained childhood deaths  Social history: non accidental injury
  11. 11.  Opportunistic examination and observation  Vital signs: HR, BP, RR, Spo2, temperature  Mental state, communication, behaviour, orientation, memory etc.
  12. 12.  Neurological examination: › Focal neurological deficit  Motor & sensory  Cranial nerves & limbs › Eyes: nystagmus, ophthalmoplegia, pupils, fundoscopy › Abnormal movement  Examination of other systems
  13. 13.  Initial investigations › Blood glucose › Blood gases › Urea & electrolytes › LFT › Ammonia › FBC & blood picture › Urine FEME  Prompt identification of treatable cause
  14. 14.  Further tests should be tailored to the differential diagnoses  Lumbar puncture: CNS infections  Neuro-imaging (Ultrasound, CT, MRI)
  15. 15.  Suggestive features: › Fever , headache › Meningism › Focal neurological deficits › Seizures › Primary source of infection › Pneumonia (bacteria, mycoplasma, TB), purpuric rash (meningococcemia), mucosal herpetic lesions, cyanotic heart dis. (brain abscess)
  16. 16.  FBC, CRP, ESR  Blood culture  Viral study (blood, throat, urine, stool)  TB work-up  CSF: ME, sugar, protein, C&S, virology, TB, fungus
  17. 17. CT with contrast: Bacterial meningitis: Subdural effusion, meningeal enhancement, abscess formation CT with contrast: Brain abscess with ring enhancement
  18. 18. Plain CT: Hydrocephalus CT with contrast: Basal enhancement
  19. 19. MRI (T2): Bilateral asymmetric temporal, insular & basifrontal hyper-intensity
  20. 20. MRI, T2 (Lt), FLAIR (Rt): Multiple hyper-intense foci involving the white matter & deep grey matter
  21. 21. MRI (T2, FLAIR, DWI): Bilaterally symmetric signal change in the thalami
  22. 22. Plain CT: Bilaterally symmetric hypodensity of the caudate nuclei & putamen with mass effect
  23. 23.  NMDA-receptor antibody encephalitis, limbic encephalitis, Hashimoto’s encephalopathy, CNS lupus etc.  Suggestive features: › Prolonged course & fluctuating symptoms › Unresponsive to anti-microbial drugs › No infectious agent identified › Specific movement disorders › Underlying immune disorder
  24. 24.  Investigations: › Work-up for vasculitic disorders › Blood or CSF for specific neuronal antibodies:  Anti-NMDA receptor antibody  Anti-VGKC antibody e.t.c › Thyroid function, anti-thyroid antibodies
  25. 25.  Traumatic › Accidental › Non-accidental: Child abuse (Shaken baby syndrome)  Spontaneous › Vascular malformation › Bleeding disorder
  26. 26.  Suggestive features: › History of head trauma › Sudden onset of encephalopathy ( +seizure) in a well child › Signs of acute blood loss: Pallor, tachycardia › History or family history of bleeding disorder › Non-accidental injury  Inconsistent / suspicious history, other suspicious body injuries, retinal haemorrhage, e.t.c.
  27. 27.  Blood count (platelet), coagulation profile  Neuro-imaging
  28. 28.  Broad category of conditions  Suggestive features: › History of development delay / regression, growth failure, epilepsy › Relapsing acute encephalopathy / septic-like episodes › Multi-organ impairment › Consanguineous parents, significant family history
  29. 29.  Investigations › *Initial investigations › Metabolic work-up › Neuro-imaging, MR spectoscopy  MRI. Leigh syndrome: Bilateral symmetrical T2 high signal in caudate nuclei /putamenand white matter
  30. 30. (A) CT: Basal ganglia calcification. (B & C) MRI T2: Hyperintense lesion in the left temporo-parieto-occipital regions. (D) MRS: High lactate peak
  31. 31.  Suggestive features › Signs & symptoms of raised ICP › Focal neurological deficit › Seizures › Extra-cranial primary malignancy  Neuro-imaging: 1st line investigation
  32. 32. Gliablastoma multiformeMedulloblastoma
  33. 33.  7 year old boy, previously well › Headache & lethargic for 3 days blurred vision, confusion, followed by status epilepticus › Intubated in district hospital, seizure was aborted with iv diazepam
  34. 34.  On arrival, sedated; pupils-equal & reactive; fundus-N; no focal neurological deficit  Noted hypertension but no bradycardia  Brain CT: Mild cerebral oedema  Wean off sedation but the child remained encephalopathic; Persistent hypertension
  35. 35.  Urine ME: RBC 5+  ASOT 800 Diagnosis: Hypertensive encephalopathy secondary to post-streptococcus acute gromerulo-nephritis (AGN)
  36. 36.  Brain MRI Posterior Reversible Encephalopathy Syndrome
  37. 37. 11 yr old girl  Learning disability with history of recurrent stroke-like episodes & epilepsy  Diagnosed Mitochondrial Encephalomyopathy, Lactic Acidosis, Stroke-like episodes (MELAS) syndrome at 9 yr old, confirmed by gene mutation study
  38. 38.  Able to talk & walk independently  Activities of daily living: need supervision with some assistance  On anti-epileptic drug, occasional breakthrough seizures
  39. 39.  Presented with: › More frequent seizures, 1-2 episodes / day, for 3 days › Lost her verbal skills, not interactive › Poor head control, needed assistance in walking › Drooling of saliva › Urinary incontinence › Unable to eat
  40. 40.  Video EEG: Non-convulsive status epilepticus
  41. 41.  Acute encephalopathy in children is an emergency with wide range of differential diagnoses; significant morbidity & mortality  A systematic approach is essential for early & accurate diagnosis to ensure appropriate & timely treatment

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