Diagnostic approach to acute encephalopathy
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DIAGNOSTIC APPROACH TO ACUTE ENCEPHALOPATHY
Paediatric Update 2014Hospital Tawau
Dr. Thay Wee Ying
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ENCEPHALOPATHY 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
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ENCEPHALOPATHY Full consiousness death
› Restless› Agitated› Confused› Delirious› Lethargic› Drowsy› Stuporous› Comatose
Glasgow Coma Scale
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CAUSES OF ACUTE ENCEPHALOPATHY
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
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CAUSES OF ACUTE ENCEPHALOPATHY CNS infection/ Para-
infection
Autoimmune
Metabolic/ Toxins
Seizure related
Hypertensive
Trauma/ hemorrhage
Hypoxic-ischemic
Tumour/ Malignancy
Hydrocephalus/ Other causes of raised ICP
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ACUTE ENCEPHALOPATHY IN CHILDREN
An important paediatric emergency
Involves children of any age
Previously normal children, or children with pre-existing neurological impairment
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ACUTE ENCEPHALOPATHY IN CHILDREN
Associated with significant mortality and long term morbidity in survivors
Good assessment with appropriate investigations identify treatable causes minimize neurological impairment
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ACUTE ENCEPHALOPATHY
Wide range of differential diagnoses
long list of possible investigations
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CLINICAL ASSESSMENT History
Physical examination
Investigations
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HISTORY 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
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HISTORY 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
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EXAMINATION Opportunistic examination and
observation
Vital signs: HR, BP, RR, Spo2, temperature
Mental state, communication, behaviour, orientation, memory etc.
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Examination Neurological examination:
› Focal neurological deficit Motor & sensory Cranial nerves & limbs
› Eyes: nystagmus, ophthalmoplegia, pupils, fundoscopy
› Abnormal movement
Examination of other systems
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INVESTIGATIONS Initial investigations
› Blood glucose› Blood gases› Urea & electrolytes› LFT› Ammonia› FBC & blood picture› Urine FEME
Prompt identification of treatable cause
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INVESTIGATIONS Further tests should be tailored to the
differential diagnoses
Lumbar puncture: CNS infections
Neuro-imaging (Ultrasound, CT, MRI)
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CNS infections / Para-infection
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)
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CNS infection: Investigations
FBC, CRP, ESR
Blood culture
Viral study (blood, throat, urine, stool)
TB work-up
CSF: ME, sugar, protein, C&S, virology, TB, fungus
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CNS infection: Neuro-imaging
CT with contrast: Bacterial meningitis: Subdural effusion, meningeal enhancement, abscess formation
CT with contrast: Brain abscess with ring enhancement
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Neuro-imaging: TB meningitis
Plain CT: Hydrocephalus CT with contrast: Basal enhancement
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Neuro-imaging: Herpes Encephalitis
MRI (T2): Bilateral asymmetric temporal, insular & basifrontal hyper-intensity
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Neuro-imaging: Acute Disseminated Encephalomyelitis (ADEM)
MRI, T2 (Lt), FLAIR (Rt): Multiple hyper-intense foci involving the white matter & deep grey matter
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Neuro-imaging: Acute Necrotising Encephalopathy of Childhood (ANEC)
MRI (T2, FLAIR, DWI): Bilaterally symmetric signal change in the thalami
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Neuro-imaging: Infantile Bilateral Striatal Necrosis (IBSN)
Plain CT: Bilaterally symmetric hypodensity of the caudate nuclei & putamen with mass effect
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Autoimmune Encephalitis & Immune Related Encephalopathy
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
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Autoimmune Encephalitis & Immune Related Encephalopathy
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
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Intracranial Haemorrhage Traumatic
› Accidental › Non-accidental: Child abuse (Shaken baby
syndrome)
Spontaneous› Vascular malformation› Bleeding disorder
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Trauma / Intracranial Haemorrhage
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.
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Trauma / Intracranial Haemorrhage
Blood count (platelet), coagulation profile
Neuro-imaging
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Metabolic Disorders 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
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Metabolic Disorders Investigations
› *Initial investigations› Metabolic work-up› Neuro-imaging, MR spectoscopy
MRI. Leigh syndrome: Bilateral symmetrical T2 high signal in caudate nuclei /putamenand white matter
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Neuro-imaging: MELAS syndrome
(A) CT: Basal ganglia calcification. (B & C) MRI T2: Hyperintense lesion in the left temporo-parieto-occipital regions. (D) MRS: High lactate peak
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Tumour/ CNS Malignancy Suggestive features
› Signs & symptoms of raised ICP› Focal neurological deficit› Seizures› Extra-cranial primary malignancy
Neuro-imaging: 1st line investigation
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Diffuse Intrinsic Brainstem Glioma
Gliablastoma multiformeMedulloblastoma
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Acute Encephalopathy in
ChildrenCase Illustration
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Case1 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
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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
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Urine ME: RBC 5+
ASOT 800
Diagnosis: Hypertensive encephalopathy secondary to post-streptococcus acute gromerulo-nephritis (AGN)
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Brain MRI
Posterior Reversible Encephalopathy Syndrome
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Case 211 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
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Able to talk & walk independently
Activities of daily living: need supervision with some assistance
On anti-epileptic drug, occasional breakthrough seizures
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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
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Case 3
Video EEG: Non-convulsive status epilepticus
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Conclusion 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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Thank you