Neonatal seizure2

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NEONATAL NEONATAL SEIZURES SEIZURES Soumya Ranjan Parida Basic B.Sc. Nursing 4 th year Sum Nursing College

Transcript of Neonatal seizure2

NEONATAL NEONATAL SEIZURESSEIZURES

Soumya Ranjan ParidaBasic B.Sc. Nursing 4th year

Sum Nursing College

INTRODUCTIONINTRODUCTION

IT IS A MEDICAL EMERGENCY COMMONLY OBSERVED NEUROLOGICAL

PROBLEM IN NEW BORNS MAY AFFECT FUTURE NEUROLOGICAL &

MENTAL DEVELOPMENT INCIDENCE - TERM 0.2-0.8%

PRE TERM 15-20%

DEFINITIONDEFINITION

PAROXYSMAL ALTERATION OF NEUROLOGICAL FUNCTIONS

MOTOR BEHAVIOUR AUTONOMIC• DEFINITION INCLUDES EPILEPTIC SEIZURES – CLONIC NON-EPILEPTIC SEIZURES – SUBTLE,

GENERALISED TONIC EEG SEIZURES

CLASSIFICATIONCLASSIFICATION

SUBTLE [FRAGMENTARY] – 48%CLONIC – 32%MYOCLONIC –13%TONIC – 7%APNOEA* NON-EPILEPTIC MOVEMENTS –

JITTERINESS OR TREMORS, NORMAL MOVEMENTS SEEN IN PRETERM

Type Frequency Clinical Manifestations EEG

Subtle 48% (PT>Term)

Eyelid fluttering, eye deviation, fixed open stare, chewing, sucking, tongue thrusting, cycling, boxing, pedaling limb movements, tachycardia, apnoea*.

Variable

Clonic 32% Rythmic jerking (1-4/sec.), having a fast and slow component. Conciousness is usually not preserved. (i) Focal (ii) Multifocal

Present Absent

Myoclonic 13% Sudden jerky movements (Single or multiple slow jerks of upper or lower limb) produced by episodic contraction of a group of muscle.

Absent

Tonic 7% Sustain flexion or extension of axial or appendicular muscle groups : (i) Generalised – Decebrate/Decorticate(ii) Focal

Absent Present

JITTERINESS OR TREMORSJITTERINESS OR TREMORS Fast Movement (4 – 6 per second) Absence of fast and slow components. Stimulus sensitive. Frequency is more. Symmetrical tremors of limbs/extremities. Abolish by sucking or flexion of limb. Not associated with chewing movements, Tongue

thrusting and eye movements. Not associated with physiological (HR, RR,

SaO2)/Autonomic changes and EEG correlates.

NORMAL MOVEMENTS NORMAL MOVEMENTS COMMONLY SEEN IN PRETERMSCOMMONLY SEEN IN PRETERMS

Benign neonatal sleep myoclonus in REM sleep in preterm with normal EEG.

Fragmentary myoclonic jerks. Eye movements – Roving or dysconjugate

eye movements with occasional non- sustained nystagmoid jerks.

CAUSESCAUSES

AGE

FIRST DAY

BETWEEN 1-3 DAYS

BETWEEN 4-14 DAYS

BETWEEN 2-8 WEEKS

CAUSES

HIE, HYPOCALCEMIA, PYRIDOXINE DEPENDENCY

ICH, HYPOGLYCEMIA, INBORN ERRORS OF METABOLISM

INFECTION, METABOLIC, KERNICTERUS, TETANY

INFECTION, HEAD INJURY, IBM, BENIGN

COMMON CAUSES OF COMMON CAUSES OF NEONATAL SEIZURESNEONATAL SEIZURES

HIE Commonest cause of seizures in neonates. Secondary to Perinatal asphyxia. Constituting 50-65% of all neonatal seizures. Seizures of HIE starts within 12 hours. Onset within 24-48 hrs. Subtle seizures are commonest.

ICH Seizures due to SAH, intra parenchymal hemorrhage or SDH

occur more often in term babies. Intraventricular hemorrhage more common in preterm babies. Mostly occur within 2-7 days.

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COMMON CAUSES OF COMMON CAUSES OF NEONATAL SEIZURESNEONATAL SEIZURES

Hypoglycemia – Screening is indicated in VLBW (<1500 gm) Preterm (<35 weeks) IUGR (SGA) Infants of diabetic mother Large for gestational age Infants with Rh haemolytic disease Infants born to mothers receiving therapy (terbutaline/

propanolol/oral hypoglycaemic agents) Neonates with perinatal birth asphyxia/ polycythemia/

sepsis/shock/RDS/hypothermia Neonates on IV fluid and TPN

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COMMON CAUSES OF COMMON CAUSES OF NEONATAL SEIZURESNEONATAL SEIZURES

Hypocalcemia – Screening is indicated in :

1. Early onset (within first 3 days) Prematurity Infants of diabetic mother Birth asphyxia

2. Late onset (presents at end of first week) Hypomagnesemia Increased phosphate load (cow’s milk) Hypoparathyroidism Vitamin D deficiency

MANAGEMENTMANAGEMENT

INCLUDES DIAGNOSIS AND TREATMENT

DIAGNOSIS

- HISTORY TAKING

- GENERAL PHYSICAL EXAMINATION

- SYSTEMIC EXAMINATION

INVESTIGATIONSINVESTIGATIONS

FIRST LINE INVESTIGATIONS - CBC, ELECTROLYTES [Ca+2, PO4, Na+1, Mg+2],

BLOOD SUGAR, BILIRUBIN, VENOUS pH AND BASE EXCESS

- CSF & BLOOD CULTURE - EEG & CRANIAL USG SECOND LINE INVESTIGATIONS - CT SCAN / MRI - TORCH / VDRL - AMMONIA / ABG / LACTATE / PYRUVATE LEVELS - BABY’S METABOLIC SCREENING

EEG (Electroencephalography)EEG (Electroencephalography)

Both Diagnostic and Prognostic. Ictal EEG is useful for Diagnosis of suspected

seizures and in neonates receiving muscle relaxant therapy.

Interictal EEG is useful for long term prognosis. Abnormal EEG indicates high risk for

neurological sequalae. Persistently abnormal EEG increases the risk of

seizure recurrence.

TREATMENTTREATMENT

VENTILATION, CIRCULATION & CEREBRAL METABOLISM (TABC)

SPECIFIC THERAPY TARGETED FOR UNDERLYING ETIOLOGY

ANTIEPILEPTIC DRUGS [AED]

ALGORITHM FOR MANAGEMENT ALGORITHM FOR MANAGEMENT OF NEONATAL SEIZURESOF NEONATAL SEIZURES

ABNORMAL MOVEMENTS

SEIZURES JITTERINESS

CLINICAL EVALUATION

PRIMARY MANAGEMENT DRAW BLOOD FOR

[TABC] INVESTIGATIONS

RBS [RANDOM BLOOD SUGAR]

CONTD....

RBS [RANDOM BLOOD SUGAR]

>40mg/dl <40mg/dl (hypoglycaemia) Injection dextrose 10% 5ml/Kg IV stat followed by dextrose infusion (treat as hypoglycaemia protocol)

S. Calcium

>7 mg/dl(Ionised > 4 mg/dl)

< 7 mg/dl (hypocalcemia) (Ionised <4 mg/dl)

Inj. Calcium gluconate 10% 2ml/kg with 1:1 dilution slowly over 10 min. under CCM (treat as hypocalcemia protocol)

Seizures persist Seizures persist

S. Magnesium

Contd..... >1.5 Meq/lt. <1.5 Meq/lt (Hypomagnesemia) Injection MgSO4 (50%) 0.2ml/kg IM q 12 hr 3 days

Seizures persist

Inj. Phenobarbitone (20 mg/kg. I.V. loading dose)

Seizures persist after 20-30 min. Seizures stopped(Maintenance Phenobarbitone 3-5 mg/kg/day in divided dose)

Repeat 10 mg/kg./IV

Repeat 10 mg/kg./IV (Total 40 mg/kg.)

Seizures persist

Injection phenytoin (20 mg/kg. IV loading dose)

Repeat 10 mg/kg./IV Seizures stopped (maintenance therapy)

Repeat 10 mg/kg./IV (Total 40 mg/kg.)

Seizures persist

Contd.....

Seizures persist

Pyridoxine 100 mg / IV Bolus

Seizures persist Seizures stopped(may required maintenance pyridoxine)

Continuous IV infusion – Midazolam/Diazepam/Lorazepam

Seizures persist (Resistant Seizures)

Newer AED (Vigabatrin, Primidone, Lamotrigine), Paraldehyde, Lidocaine, Thiopental, Formic acid, general anesthesia

ANTIEPILEPTIC THERAPY ANTIEPILEPTIC THERAPY [AED][AED]

PHENOBARBITONE

DOSE – 20 mg/kg. IV Bolus Stat

40 mg/kg. IV Maximum Cumulative PHENYTOIN

DOSE – 20 mg/kg. IV Bolus Stat

40 mg/kg. IV Maximum Cumulative FOSPHENYTOIN

BENZODIAZEPINESBENZODIAZEPINES

DIAZEPAM Dose : 0.1 – 0.3 mg./kg. IV Slowly stat &

Infusion of 0.3 mg./kg./hr. MIDAZOLAM Dose : 0.15 mg/kg. IV stat followed by 0.1

mg/kg./hr. by infusion LORAZEPAM Dose : 0.10 mg/kg. over 2-5 minutes IV

OTHER THERAPIES OTHER THERAPIES PYRIDOXINE Dependency should be suspected in refractory

seizures, positive family history & if there is history of in utero fluttering

EEG typically shows generalized burst of spikes of 1-4 Hz.

Pyridoxine dependency requires a dose of 50 mg. per day & deficiency 5 mg./day

EXCHANGE TRANSFUSION Indicated in life threatening metabolic disorders,

accidental injection of LA, Transplacental transfer of maternal drugs & kernicterus

MAINTENANCE & DURATION OF AEDMAINTENANCE & DURATION OF AED

MAINTENANCE – Monotherapy is preferred. Wean the baby to only phenobarbitone.

DURATION – determined by the cause, neurological examination & EEG.

Newborn on anticonvulsant therapy

Wean all AED except phenobarbitone once seizures controlled

Perform neurological examination prior to discharge

Normal Abnormal

Stop Phenobarbitone prior to discharge(Over 1-2 Weeks)

Continue phenobarbitone for 1 month

Repeat neurological examination at 1 month

Normal examination at 1 month Abnormal examination

Evaluate EEG

Taper drugs over 4 Weeks Normal EEG Taper Drugs over 4 Weeks Abnormal EEG Continue drugs reassess after 3 months

WEANING & DURATION OF AEDWEANING & DURATION OF AED

PROGNOSISPROGNOSIS

NORMAL OUTCOME – 50-60%NEUROLOGICAL SEQUALAE – 30-40%

(C.P., M.R., SEIZURES) MORTALITY – 15-20% PROGNOSIS DEPENDS UPON

ETIOLOGY, SEIZURE PATTERN & EEG BACKGROUND

VARIABLE NORMAL DEVELOPMENT

ETIOLOGYLATE ONSET HYPOCALCAEMIAPRIMARY SAHIDIOPATHICHIE, BACT. MENINGITIS, HYPOGLYCEMIA AND EARLY ONSET HYPOCALCAEMIACNS DEVELOPMENTAL DEFECTS

100%90%75%50%

0%

SEIZURE PATTERNFOCAL CLONICGENERALIZED, SUBTLE AND TONICMULTIFOCAL MYOCLONIC

100% (T) / 30% (PT)50% (T) / 40% (PT)30% (T) / 30% (PT)0% (T) / 0% (PT)

EEG BACKGROUNDNORMALMODERATE ABNORMALITY(VOLTAGE ASYMMETRY)SEVERE ABNORMALITY (BURST SUPPRESSION PATTERN, MARKED VOLTAGE SUPPRESSION AND ELECTROCEREBERAL SILENCE)

>90%50%

<10%

THANKS