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SEIZURE
LEARNING
OBJECTIVES
To identify the early signs of neonatal seizures
Better understanding of the condition for proper
evaluation and treatment
Understanding of the prognosis to enable to support
the parents
INTRODUCTION
Neonatal seizures are a
neurologic dysfunction in the first
28 days of life in an infant.
Seizures in neonates are
relatively common, with variable
clinical manifestations. The first
sign of neurologic dysfunction
are powerful predictors of long-
term cognitive and
developmental impairment.
PATHOPHYSIOLOGY
A clinical seizure results from excessive synchronized
depolarization of the neurons within the central nervous system
resulting in excessive synchronous electrical discharge. This
excessive depolarization of the neurons might occur remains
unknown. Theories were suggested include the following:
Imbalance between excitatory and inhibitory neurotransmitter
like excessive excitatory amino acid or deficient inhibitory
neurotransmitter.
Failure of energy production due to disruption of ATP
dependent resting membrane potentials resulting in failure of
sodium potassium pump which in turn leading to movement of
sodium into the neuron and potassium out of the neuron.
Neuronal hyper excitability state in the neonatal period, as
evidenced by the extremely low threshold to seizures in
general and that this is the period of highest incidence of
seizures across the life span.
Among the factors that cause increase excitability are
incomplete myelination and neuropeptides particularly
corticotrophin releasing hormone (CRH).
PATHOPHYSIOLOGY
Hypoglycemia
Dextrose 10% 2-3ml/kg IV
Hypocalcaemia
Calcium Gluconate, 5% (50 mg/ml), 100-200 mg/kg IV 10%
(100mg/ml) 50-100 mg/kg IV if inadequate time for dilation
Hypomagnesaemia
Magnesium Sulphate , 12.5% (125 mg/ml) 50-100 mg/kg IV
Hypernatremia
Furosemide 1 mg/kg IV
3% NaCl 1-3 ml/kg over 15 to 30 minutes
CAUSES
• Malformations / structural lesions
Cerebral dysgenesis – severe disorders such as hemimegalencephaly,
lissencephaly and polymicrogyrias.
• Epilepsy Syndromes
Benign familial neonatal convulsions occur in well infants on day 2 or 3
of life. Seizures may be focal clonic or tonic. This disorder is associated
with abnormality of voltage-gated potassium channels usually KCNQ2
and less frequently KCNQ3.
CLINICAL CLASSIFICATIONS
Focal/Multifocal Clonic
Not generalized
Migratory
Not necessarily focal etiology
Focal Tonic
Not usually generalized
Generalized Myoclonic
Subtle (“Hypomotor”)
Motor activity arrest
Apnea
Eye deviation
Autonomic changes
Motor automatisms
Oral-buccal-lingual movements
Swimming
Bicycling
EVALUATION
• Serum electrolytes (Glucose, Calcium, Magnesium,
Sodium)
• CSF
• Head ultrasound
• EEG
• Tox screen
• CT or MRI of brain
• Metabolic screening, congenital infection work up.
MANAGEMENT:
Rule out hypoxia – check ABG, start oxygen, KIV intubate and
ventilate / optimise ventilator settings if already intubated
Check hypocount – if low glucose, give IV D10% (2ml/kg)
Correct electrolyte abnormalities – sodium, calcium, magnesium
Anti-convulsants – (to be discussed on next slides)
Treat Infection – IV CP/Genta, KIV IV acyclovir (HSV encephalitis)
Polycythemia – partial plasma exchange
Hydrocephalus – may need repeat LPs / VP shunt
Close follow up for possible neurologic sequelae and
developmental delay
Refer to pediatric neurologist for recurrent seizures.
TREATMENT OF
SEIZURE
Phenobarbital – limits the spread of seizure activity, possibly by increasing
inhibitory neurotransmission.
Loading dose: 20mg/kg IV, given slowly over 10 to 15 minutes.
Refractory seizures: Additional 5 mg/kg doses, up to a total of 40 mg/kg
Maintenance: 3 to 4 mg/kg per day beginning 12 to 24 hours after the load.
Route: IV slow push,IM, PO, PR
Compatibility: NS, D5%, D10%
Strength: 30mg/ml
Solution:
3800 grams = 3.8 kg
3.8 mg = 3800 mcg
Answer = 2ml/hr
TREATMENT OF
SEIZURE
Midazolam
How to compute for mcg/kg/hr if the doctor asks for Midazolam to
run for 2 ml/hr. Baby’s weight of 3800 grams.
= 493 mg ÷ 6 ml
= 82 mg/ ml or 80 mg/ml
NICU CARE PLAN
Ensure safety and initiate seizure precautions. This includes
having suction set up and working, having an ambu-bag in
the room, padding side rails, not restrain them or putting
anything in their mouth if a seizure occurs, having all side
rails up, and so forth.
Maintain patent airway.
Assess, monitor and document seizure activity. To report
immediately to the physician any early recognition of seizure.
Administer antiepileptics (PRN and scheduled) medications
per orders.
Reevaluate effectiveness of medication given.
Perform daily measurement of head circumference for cases
of intracranial hemorrhage. A rapid increase in HC may
indicate hydrocephalus.
Educate the parents on hospital procedures.
Provide emotional support.
OUTCOME
45 % controlled after either phenobarbital or phenytoin
60 % controlled with both
30% of survivors develop epilepsy
WORSE: HIE, meningitis, dysplasia
REFERENCES
Volpe JJ, ed. Neonatal Seizures in Neurology of the Newborn 5th
ed. Philadelphia: WB Saunders
Silverstein FS, Jensen FE. Neonatal seizures
Leinekugel X, Medina I, Khalilov R, et al. Ca ++ oscillations
mediated by the synergistic excitatory actions of GABA – A and
NMDA receptors in the neonatal hippocampus. Neuron 1997; 18:
243 – 55.
Jensen F E. Neonatal Seizures: An Update on Mechanisms and
Management. Clinics in Perinatology 200; 36 : 881-900.
Prof Isam Zwaini, Neonatal seizures
Fakhraee SH. Neonatal seizures; A review. Iranian Journal of
Child Neurology 2007; 1: 7 – 11.
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