a case of acute encephalitis

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CARE CHAPTER

A CASE OF ACUTE ENCEPHALITIS SYNDROME

Dr. GNANDAS BARMAN

PATIENT PARTICULARS

• Name-DIPTANU DAS• Age: 7years• Sex : Male• Address - GOHAT , HOOGLY.• DOA-14/5/15

CHIEF COMPLAINTS

• Fever for six days

• Convulsions for one day

History of present illness

• Patient developed high grade non remittent fever 6 days prior to admission

• Fever was associated with chill and rigor.

• Not associated with rash or any bleeding, headache , burning micturation or catarrhal symptom.

• Patients developed sudden onset convulsion on the sixth day of fever with loss of consciousness and up rolling of eyes.

• Initially on left side of the body with involvement of face.• Subsequently multiple episodes without gaining

consciousness affecting the whole body , tonic clonic type at the height of fever.

• Not associated with vomiting , loose stool or recent vaccination.

• No history of any fall or head injury.

• Past history- no similar history in past• Family history- Nothing significant• Birth history-nothing significant• Developmental history-class two student with

average school performance.• Socioeconomic history-lower middle class

GENERAL EXAMINATION(on admission)• Patient having active convulsion with very depressed sensorium.• GCS-E2 V1 M3

• VITALS: • Pulse-123/min. Volume –normal.• RR-32/min.• BP-104/67• SpO2-90%• Afebrile• Pallor-present. • Facies –normal• Eyes-closed • CBG-102

ANTHROPOMETRY

• WT-20 kg[15th percentile]• HT-118cm[15th -50th percentile]• HC-53 cm

CNS EXAMINATION

• Higher functions- unconscious.• Cranial nerves – No abnormality on cranial nerves

examination was found with normal oculocephalic reflex.

• However, pupils are mid dilated and sluggishly reacting to lights.

• Fundus –normal.• Cough reflex-present

• Muscle mass-normal.• MUSCLE TONE- Increased in all four limbs.• REFLEXES-• Superficial reflexes-abdominal reflex-absent plantar reflex-equivocal.• Deep tendon reflexes- present and exaggerated• Meningeal signs-absent

• SENSORY SYSTEM: abnormal flexion response to pain.

OTHER SYSTEMS

• WNL

PROVISIONAL DIAGNOSIS

ACUTE ENCEPHALITIS SYNDROME

INITIAL MANAGEMENT[on admission in PICU]

• Moist O2.• IVF[60%]• Inj. Midazolam stat then continuous infusion@4

ug/kg/min• Inj. Phenytoin-loading and maintenance • Inj. Valproate-loading and maintenance• 3% NS infusion @1ml/kg/hr• Inj. Ceftriaxone • Inj. Vancomycin • Inj. Aacylovir

INVESTIGATION

• ABG-Ph 7.42, Pco2-41, Pco2-89, HCO3-22.6 Na/K-138/4.6 Ca-1.1 Hb-8.5

CT SCAN OF BRAIN[PLAIN]14/5/15

• SMALL CSF ATTENUATION AREA WITH OUT APPRECIABLE MASS EFFECT SEEN IN RIGHT CENTRUM SEMIOVALE

• IMPRESSION-FOCAL GLIOSIS IN RIGHT CENTRUM SEMIOVALE

Even after receiving midazolam, phenytoin, valproate patient having convulsion of this type.

• Increase midazolam infusion@10 ug/kg/min• Subsequently convulsion controlled.

• Patient was intubated and put on mechanical ventilation in Controlled mode.

• CBC-Hb-8.9 TLC8000, N62 L34 B4. Platelets -2L• LFT-N• CRP-<0.8

• MP,MPDA-NR

• WIDAL-NR

• DENGUE-NR.

0n 15/5

• Patient having multifocal clonic type of seizures in all four limbs and occasional generalisation

• Added inj. Levetiracetum and Tab Clonazepam.

• CSF examination csf pressure- normal, clear. Cell count-10/cmm Cell Type-all mononuclear protein/sugar-16/75 Gram stain-N Indian ink-N ZN smear-N

• JE SEROLOGY • HSV SEROLOGY • CSF CBNAAT send.

• ABG- Normal• PRBC transfusion done

16/5/16• Patient have no GCTS but focal seizures in

different areas persist.• Started Syr. Oxcarbamazepine.• Phenytoin omitted• Sensorium improved, spontaneous eye

opening and localisation of pain present.• Opthalmoscopy-fundus normal.

Clinically improving, occasional focal seizures; more on right side which was controlled by

increasing the dose of valproate and levetiracetam.

Patient extubated[18/6/15]

INVESTIGATION REPORTS[19/6]

• JE serology-NR• HSV IgM-NR• CSF CBNAAT-NR• MEASLES IgG- NORMAL• CSF culture- no growth.• Blood and urine c/s-neg.• Blood count and ABG –normal

20/5/16

• Patient clinically improving.• On OG feeding started.• AEDs Medications through OG.• Able to talk but disoriented.• Focal seizures continued with choreoathetotic

movements.• Plan for-MRI , EEG • NEUROLOGIST OPINION.

MRI OF BRAIN(25/5)-Normal

• EEG [1/6/15]-DIFFUSE ENCEPHALOPATHY.• Ceruloplasmin level, anti NMDA receptor antibody VGKC ANTIBODY[LGI-1, CASPR-1] THYROID ANTIBODY ANA send

6/6/15

• The patient walking with support• Talking irrelevantly, excessively • But poor short and long term memory.• Aggressive behaviours• Abnormal movements persist even during

sleep.• Pulse Inj. methyl prednisolone

30mg/kg/day for 5days.

7/6/15

• Transfused IV IG @2gm/kg over 3 days.

• Ceruloplasmin-normal• Anti NMDA[NR1]-Negative• THYROID antibody-neg.• Tab SERTRALINE added.

10/6/15

• VGKC ANTIBODY-NEGATIVE.

• Abnormal movements-abolished.• CAN WALK WITH OUT SUPPORT.• Memories regaining.• Can draw and write• Abnormal behaviours persists.

15/6

• No more seizures or abnormal movements.• Patient is well oriented.• Some behavioural abnormality present.• Aggressive behaviours subsiding but present.

• Patient is now on oral medications.

• Syr valproate• Syr levetiracetam• Syr oxcarbamazepine• Tab clonazepam• Tab sertraline

• EEG[27/6/15]-NORMAL

DISCUSSION• Acute encephalitis is one of the common

neurological illnesses requiring admission of children in the intensive care unit.

• In developing countries, acute encephalitic presentation in children often results from various infections including viral, bacterial, fungal and protozoal.

• With the advent of better diagnostic modalities and advances in critical care management, more cases of encephalitis beyond infection have been identified.

• Autoimmune encephalitis, acute disseminated encephalomyelitis, vasculitis, paraneoplastic, toxin mediated and metabolic disorders are the non-infectious causes that attribute for encephalitis and encephalopathy in children.

• Early identification and treatment of these disorders can lead better neurological outcome.‡

‡ Yoganathan S et al . Acute Encephalitis;Beyond Infection.J Pediatr Crit Care.April-June 2015;2(2):41-49

• Even after extensive evaluation, the etiology of encephalitis was not established in more than half of the cases.

• Autoimmune encephalitis had surpassed the viral etiologies.

• Acute disseminated encephalomyelitis (ADEM) is the most common immune mediated cause for encephalitis followed by anti N methyl D aspartate receptor (NMDAR) encephalitis.†

†Gable MS et al. The frequency of autoimmune NMDAR encephalitis surpasses that of individual viral etiologies in young individuals enrolled in the California Encephalitis Project. Clin Infect Dis. 2012;54:899–904

Autoimmune panencephalitis seronegative for VGKC-complex, NMDAR, and GAD autoantibodies is a subtype of autoimmune encephalitis that can present with pure neuropsychiatric features and a normal brain MRI.

Delay in starting immune therapy can lead to permanent neuropsychiatric sequelae. ¥

¥ Nijjar S et al. Neuropsychiatric autoimmune encephalitis without VGKC-complex, NMDAR, and GAD autoantibodies.Cogn Behav Neurol. 2013 Mar;26(1):36-49

FINAL DIAGNOSIS

AUTO IMMUNE ENCEPHALITIS

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