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NEONATALNEONATAL
SEIZURESSEIZURES
Soumya Ranjan Parida
Basic 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 MOVEMENTSNORMAL 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 OFCOMMON 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.
Continue.....
COMMON CAUSES OFCOMMON 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
Continue.....
COMMON CAUSES OFCOMMON 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 MANAGEMENTALGORITHM 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 THERAPYANTIEPILEPTIC 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 THERAPIESOTHER 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
ETIOLOGY
LATE ONSET HYPOCALCAEMIA
PRIMARY SAH
IDIOPATHIC
HIE, BACT. MENINGITIS, HYPOGLYCEMIA AND EARLY
ONSET HYPOCALCAEMIA
CNS DEVELOPMENTAL DEFECTS
100%
90%
75%
50%
0%
SEIZURE PATTERN
FOCAL CLONIC
GENERALIZED, SUBTLE AND TONIC
MULTIFOCAL
MYOCLONIC
100% (T) / 30% (PT)
50% (T) / 40% (PT)
30% (T) / 30% (PT)
0% (T) / 0% (PT)
EEG BACKGROUND
NORMAL
MODERATE ABNORMALITY
(VOLTAGE ASYMMETRY)
SEVERE ABNORMALITY (BURST SUPPRESSION PATTERN,
MARKED VOLTAGE SUPPRESSION AND ELECTROCEREBERAL
SILENCE)
>90%
50%
<10%
THANKS

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Neonatal seizure2

  • 1. NEONATALNEONATAL SEIZURESSEIZURES Soumya Ranjan Parida Basic B.Sc. Nursing 4th year Sum Nursing College
  • 2. 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%
  • 3. DEFINITIONDEFINITION  PAROXYSMAL ALTERATION OF NEUROLOGICAL FUNCTIONS  MOTOR  BEHAVIOUR  AUTONOMIC • DEFINITION INCLUDES  EPILEPTIC SEIZURES – CLONIC  NON-EPILEPTIC SEIZURES – SUBTLE, GENERALISED TONIC  EEG SEIZURES
  • 4. CLASSIFICATIONCLASSIFICATION SUBTLE [FRAGMENTARY] – 48% CLONIC – 32% MYOCLONIC –13% TONIC – 7% APNOEA* NON-EPILEPTIC MOVEMENTS – JITTERINESS OR TREMORS, NORMAL MOVEMENTS SEEN IN PRETERM
  • 5. 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
  • 6. 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.
  • 7. NORMAL MOVEMENTSNORMAL 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.
  • 8. 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
  • 9. COMMON CAUSES OFCOMMON 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. Continue.....
  • 10. COMMON CAUSES OFCOMMON 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 Continue.....
  • 11. COMMON CAUSES OFCOMMON 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
  • 12. MANAGEMENTMANAGEMENT INCLUDES DIAGNOSIS AND TREATMENT DIAGNOSIS - HISTORY TAKING - GENERAL PHYSICAL EXAMINATION - SYSTEMIC EXAMINATION
  • 13. 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
  • 14. 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.
  • 15. TREATMENTTREATMENT VENTILATION, CIRCULATION & CEREBRAL METABOLISM (TABC) SPECIFIC THERAPY TARGETED FOR UNDERLYING ETIOLOGY ANTIEPILEPTIC DRUGS [AED]
  • 16. ALGORITHM FOR MANAGEMENTALGORITHM 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....
  • 17. 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
  • 18. 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.....
  • 19. 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
  • 20. ANTIEPILEPTIC THERAPYANTIEPILEPTIC 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
  • 21. 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
  • 22. OTHER THERAPIESOTHER 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
  • 23. 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.
  • 24. 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
  • 25. 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
  • 26. VARIABLE NORMAL DEVELOPMENT ETIOLOGY LATE ONSET HYPOCALCAEMIA PRIMARY SAH IDIOPATHIC HIE, BACT. MENINGITIS, HYPOGLYCEMIA AND EARLY ONSET HYPOCALCAEMIA CNS DEVELOPMENTAL DEFECTS 100% 90% 75% 50% 0% SEIZURE PATTERN FOCAL CLONIC GENERALIZED, SUBTLE AND TONIC MULTIFOCAL MYOCLONIC 100% (T) / 30% (PT) 50% (T) / 40% (PT) 30% (T) / 30% (PT) 0% (T) / 0% (PT) EEG BACKGROUND NORMAL MODERATE ABNORMALITY (VOLTAGE ASYMMETRY) SEVERE ABNORMALITY (BURST SUPPRESSION PATTERN, MARKED VOLTAGE SUPPRESSION AND ELECTROCEREBERAL SILENCE) >90% 50% <10%