Neonatal seizures
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Transcript of Neonatal seizures
Neonatal Seizures
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Dr. Kalpana MallaMD Pediatrics
Manipal Teaching Hospital
INTRODUCTION
• Not uncommon•Always due to some underlying cause•25% cases cause – unknown•Often first sign of neurological disorders•Powerful predictors of long term cognitive and developmental impairement
Pathophysiology
1.Large group of neurons undergo excessive, synchronized depolarization which results from –
a) Increase in excitatory neurotransmitters (glutamate)
b) Decrease in inhibitory neurotransmitters (gamma amino butyric acid- GABA
PROBABLE MECHANISMS
c. Disruption of ATP – dependent resting membrane potentials - Failure of Na
- K pump – flow of sodium into the
neuron & potassium out of neuron d. Membrane alteration - Increased
Na permeability
Incidence
• 1 in 200 healthy newborns• 0.5 -0.8% Term babies• 6-12% <1.5 kg (1 in 4 premature and
LBW• Many seizures are very subtle – go
undetected
SEIZURE PATTERN1. Subtle seizure: 50%of seizures- Tonic horizontal deviation of
eyes, staring look,Repetitive blinking / fluttering of eyelids
- Oro- buccal movements-chewing, lip smacking, sucking, yawning
- Tonic posturing of a limb - Apnea- Swimming/ bycycling
movements
SEIZURE PATTERN
2.Clonic - Focal / Multifocal – twitching migrate haphazardly from one limb to another, occur due to HIE & birth trauma
3.Generalised seizure - rare
SEIZURE PATTERN
4. Focal clonic – Localized & often assoc with loss of
consciousness They are signs of bilateral c’bral disorder Common in metabolic disorder, birth
trauma and c’bral infarction
SEIZURE PATTERN
5. Tonic seizure – - Stiffening similar to decerebrate posture but with eye signs and heavy breathing - Often associated with apnea - Seen in IVH, preterm and Kernicterus
SEIZURE PATTERN
6.Myoclonic seizures• Rare in newborns• Single/multiple flexion movements,
slow and jerky• Seen in developmental defects and
anencephaly
Features Jitteriness Seizure
Stimulus sensitive
++ _
Cessation Passive flexion Gentle grasp
-
Rhythmicity
Rhythmic oscillation
Fast & slow components
Features Jitteriness
Seizure
Frequency of jerks
5-6 / sec
2-3 / sec
Abnormal gaze-Eye movement
Nil Present
Autonomic disturbance
Nil Increase HR, BP)
EEG Normal Abnormal
ETIOLOGY
A.Perinatal causes 1. Neonatal encephalopathy -
20- 40% of seizures2. Intracranial hemorrhages-
CNS trauma, SAH, PVH,
B. METABOLIC CAUSES
• Hypoglycemia • Hypocalcemia – most common
metabolic cause for NNS• Hypomagnesemia• Hypo / Hypernatremia• Pyridoxine dependency • IEM - Disorders of amino acid
metabolism
C. Infections
• Intracranial - Meningitis - encephalitis – herpes, coxachie, echo,
CMV, - Toxoplasmosis
Extracranial – septicemia - Tetanus - Severe rep distress
D. Developmental defects
–Cerebral Dysgenesis–Hydrocephalus–Microcephaly–Neuronal migration defects-
Lissencephaly,pachygyria,schizencephaly
Others
E. Drugs- prolonged maternal administration
- Vit B6-pyridoxin dependancy - Narcotic withdrawal - TheophyllineF. PolycythemiaG. Focal infarcts
Others
H .Hypertensive encephalopathy
I . Benign familial epilepsy – does not continue after neonatal period
J .Unknown(Idiopathic : 3-25%
Diagnosis – time of onset
• 1st day – birth asphyxia (HIE) - C’bral trauma - Pyridoxin dependancy - Narcotic withdrawal - IEM
Diagnosis – time of onset
• 1-3 days – - ICH - Hhypocalcemia - Hypoglycemia - Hypo & hypernatremia - Pyridoxin deficiency - Cong C’bral malformations - Narcotic withdrawal
Diagnosis – time of onset
• 4-7 days – - Meningitis - Encephalitis - Hypomagnesemia - TORCH infection - Developmental malformations - Kernicterus - IEM - Pyridoxin dependancy - Tetanus
Refractory seizures
• IEM – • Developmental defects of CNS• Narcotic withdrawal• Pyridoxin dependancy• Kernicterus• Benign familial seizures
Investigations
• CBC• Blood – glucose, calcium, electrolytes, Mg,
bilirubin, ABG• CSF analysis• Blood C/S , urine C/S• Cranial USG
Second line investigations
• TORCH screening• IEM screening – urine organic acids• - S. amino acid assay• Imaging – CT scan - MRI - EEG brain
Management
• Collect all samples • IV line• Thermoneutral environment• Glucose 10% - 2-4ml/kg as bolus followed by
10% glucose as drip @ 8mg/kg/min• IV calcium – gluconate 2ml/kg
ANTICONVULSANTS
Phenobarbitone 15 - 20mg / kg IV loading dose 3.5 - 5mg / kg / day maintenance dosePhenytoin 15 - 20 mg / kg IV at 1mg / kg / min 4 - 8 mg / kg day maintenance doseMidazolam 0.02 - 0.4 mg/kg IM
0.02 - 0.1mg/kg IV0.06 - 0.4mg/kg/hr
Others Lorazepam, diazepam, Paraldehyde
ANTICONVULSANTS
• Phenobarbitone ↓↓• Phenytoin
↓↓• Lorazepam, midazolam drip – 48 hrs
↓↓
ANTICONVULSANTS
↓↓• Barbiturate coma – pentobarbital& thiopental
on ventilator – try to wean every 24 hrs
↓↓• GA with isoflurane or halothane +
neuromuscular blockade (muscle paralysis)
TREATMENT1. Optimise ventilation Maintain CO, BP, Serum electrolytes & pH2. Treat underlying diseases- Metabolic abnor malities,meningitis,Narcotic withdrawal3. Pyridoxine dependency- 50mg IV, repeat every 10 min till control- maintenance dose – 5mg/kg PO daily6. Hyperbilirubinemia –phototherapy, exchange transfusion
Benign familial neonatal seizure
• Typically occur in first 48- 72 hrs of life• Disappear by age 2-6 months• A family history seizures is usual• Development - normal
Benign idiopathic NNS
• Typically Presents at day 5 of life• Also called 5th day fits• Multifocal in type• No cause detected
FOLLOW UP - ANTICONVULSANTS
1. Stop all others except maintenance PB2. Maintenance PB : 2wks - 2months3. Risk of recurrence Little: transient metabolic abnormalities
30-50% : HIE High : Cortex malformations
PROGNOSISNormal Outcome: 56%Neurological sequelae: 30 - 40%Death : 15-25%Chronic seizure disorder: 15-20%
Outcome depends on1. Level of maturity2. Etiology3. Neurological examination4. EEG / Imaging studies
GOOD PROGNOSIS
• Uncomplicated hypoglycemia• Narcotic withdrawal• SAH
POOR PROGNOSIS
• Low APGAR score ≤ 6 at 5min• Onset o seizures within 24 hrs of life• Presence of myoclonic attacks• Abnormal EEG• 3 or more days of uncontrolled seizures
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