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NEONATAL SEIZURES
DIANA PRASAD
MSc NURSING (Pediatrics)
WESTFORT COLLEGE OF NURSING
 A stereotypic, paroxysmal spell of
altered neurologic function
(behavior, motor,and/or autonomic
function)
DEFINITION
 Neonatal period limited to :
- first 28 days for term infants
- 44 weeks gestational age for
pre-term
 Immature CNS cannot sustain a synchronized, well
orchestrated generalized seizure
Why do neonatal seizures have such
unusual presentations?
A. Perinatal causes
1. Neonatal encephalopathy - 20-
40% of seizures
2. Intracranial hemorrhages- CNS
trauma, SAH, PVH,
ETIOLOGY
 Hypoglycemia
 Hypocalcemia – most common metabolic cause
for NNS
 Hypomagnesemia
 Hypo / Hypernatremia
 Pyridoxine dependency
 IEM - Disorders of amino acid metabolism
B. METABOLIC CAUSES
 Intracranial
- Meningitis
- encephalitis – herpes, coxachie, echo, CMV,
- Toxoplasmosis
Extracranial
– septicemia
- Tetanus
- Severe rep distress
C. Infections
 Cerebral Dysgenesis
 Hydrocephalus
 Microcephaly
 Neuronal migration defects-
Lissencephaly,pachygyria,schizenc
ephaly
D. Developmental defects
H .Hypertensive encephalopathy
I . Benign familial epilepsy – does not
continue after neonatal period
J .Unknown(Idiopathic : 3-25%
Others
Probable Mechanisms of Some Neonatal Seizures
PROBABLE MECHANISM DISORDER
Failure of Na + -K + pump secondary to Hypoxemia, ischemia,
 adenosine triphosphate and hypoglycemia
Excess of excitatory neurotransmitter
(eg.glutamic acid—excessive excitation) Hypoxemia, ischemia
and hypoglycemia
Deficit of inhibitory neurotransmitter Pyridoxine dependency
(i.e., relative excess of excitatory
neurotransmitter)
Membrane alteration—  Na + Hypocalcemia and
Permeability hypomagnesemia
I. Clinical Seizure
 Subtle
 Tonic
 Clonic
 Myoclonic
Classification
1. Subtle
 More in preterm than in term
 Eye deviation (term)
 Blinking, fixed stare (preterm)
 Repetitive mouth and tongue movements
 Apnea
 Pedaling and tonic posturing of limbs
Clinical Classification
2. Tonic
 Primarily in Preterm
 May be focal or generalized
 Sustained extension of the upper and
lower limbs (mimics decerebrate posturing)
 Sustained flexion of upper with extension of
lower limbs (mimics decorticate posturing)
 Signals severe ICH in preterm infants
Clinical Classification
3. Clonic
 Primarily in term
 Focal or multifocal
 Clonic limb movements(synchronous or
asynchronous, localized or often with no anatomic
order of progression)
 Consciousness may be preserved
 Signals focal cerebral injury
Clinical Classification
4. Myoclonic
 Rare
 Focal, multifocal or generalized
 Lightning-like jerks of extremities
(upper > lower)
Clinical Classification
 Certain clinical seizures in the human
newborn originate from electrical seizures
in deep cerebral structures (limbic regions),
or in diencephalic, or brain stem structures
and thereby are either not detected by
surface-recorded EEG or inconsistently
propagated to the surface
Does absence of EEG seizure activity indicate
that a clinical seizure is non- epileptic?
(1) electroencephalogram
(2) blood glucose
(3) serum calcium
(4) serum magnesium
(5) arterial pH
(6) serum sodium
(7) serum urea and creatinine
(8) lumbar puncture
(9) blood culture
(10) cranial ultrasound scan
DIAGNOSIS
 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
Management
ANTICONVULSANTS
Phenobarbitone
15 - 20mg / kg IV loading dose
3.5 - 5mg / kg / day maintenance dose
Phenytoin
15 - 20 mg / kg IV at 1mg / kg / min
4 - 8 mg / kg day maintenance dose
Midazolam 0.02 - 0.4 mg/kg IM
0.02 - 0.1mg/kg IV
0.06 - 0.4mg/kg/hr
Others Lorazepam, diazepam, Paraldehyde
 Phenobarbitone
↓↓
 Phenytoin
↓↓
 Lorazepam, midazolam drip – 48 hrs
ANTICONVULSANTS
TREATMENT
1. Optimise ventilation
Maintain CO, BP, Serum electrolytes & pH
2. Treat underlying diseases- Metabolic abnor
malities,meningitis,Narcotic withdrawal
3. Pyridoxine dependency- 50mg IV, repeat every 10 min till control-
maintenance dose – 5mg/kg PO daily
6. Hyperbilirubinemia –phototherapy,
exchange transfusion
FOLLOW UP -
ANTICONVULSANTS
1. Stop all others except maintenance PB
2. Maintenance PB : 2wks - 2months
3. Risk of recurrence
Little: transient metabolic abnormalities
30-50% : HIE
High : Cortex malformations
PROGNOSIS
Normal Outcome: 56%
Neurological sequelae: 30 - 40%
Death : 15-25%
Chronic seizure disorder: 15-20%
Outcome depends on
1. Level of maturity
2. Etiology
3. Neurological examination
4. EEG / Imaging studies
Uncomplicated hypoglycemia
Narcotic withdrawal
SAH
GOOD 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
POOR PROGNOSIS
THANK YOU

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Neonatal seizures

  • 1. NEONATAL SEIZURES DIANA PRASAD MSc NURSING (Pediatrics) WESTFORT COLLEGE OF NURSING
  • 2.  A stereotypic, paroxysmal spell of altered neurologic function (behavior, motor,and/or autonomic function) DEFINITION
  • 3.  Neonatal period limited to : - first 28 days for term infants - 44 weeks gestational age for pre-term
  • 4.  Immature CNS cannot sustain a synchronized, well orchestrated generalized seizure Why do neonatal seizures have such unusual presentations?
  • 5. A. Perinatal causes 1. Neonatal encephalopathy - 20- 40% of seizures 2. Intracranial hemorrhages- CNS trauma, SAH, PVH, ETIOLOGY
  • 6.  Hypoglycemia  Hypocalcemia – most common metabolic cause for NNS  Hypomagnesemia  Hypo / Hypernatremia  Pyridoxine dependency  IEM - Disorders of amino acid metabolism B. METABOLIC CAUSES
  • 7.  Intracranial - Meningitis - encephalitis – herpes, coxachie, echo, CMV, - Toxoplasmosis Extracranial – septicemia - Tetanus - Severe rep distress C. Infections
  • 8.  Cerebral Dysgenesis  Hydrocephalus  Microcephaly  Neuronal migration defects- Lissencephaly,pachygyria,schizenc ephaly D. Developmental defects
  • 9. H .Hypertensive encephalopathy I . Benign familial epilepsy – does not continue after neonatal period J .Unknown(Idiopathic : 3-25% Others
  • 10. Probable Mechanisms of Some Neonatal Seizures PROBABLE MECHANISM DISORDER Failure of Na + -K + pump secondary to Hypoxemia, ischemia,  adenosine triphosphate and hypoglycemia Excess of excitatory neurotransmitter (eg.glutamic acid—excessive excitation) Hypoxemia, ischemia and hypoglycemia Deficit of inhibitory neurotransmitter Pyridoxine dependency (i.e., relative excess of excitatory neurotransmitter) Membrane alteration—  Na + Hypocalcemia and Permeability hypomagnesemia
  • 11. I. Clinical Seizure  Subtle  Tonic  Clonic  Myoclonic Classification
  • 12. 1. Subtle  More in preterm than in term  Eye deviation (term)  Blinking, fixed stare (preterm)  Repetitive mouth and tongue movements  Apnea  Pedaling and tonic posturing of limbs Clinical Classification
  • 13. 2. Tonic  Primarily in Preterm  May be focal or generalized  Sustained extension of the upper and lower limbs (mimics decerebrate posturing)  Sustained flexion of upper with extension of lower limbs (mimics decorticate posturing)  Signals severe ICH in preterm infants Clinical Classification
  • 14. 3. Clonic  Primarily in term  Focal or multifocal  Clonic limb movements(synchronous or asynchronous, localized or often with no anatomic order of progression)  Consciousness may be preserved  Signals focal cerebral injury Clinical Classification
  • 15. 4. Myoclonic  Rare  Focal, multifocal or generalized  Lightning-like jerks of extremities (upper > lower) Clinical Classification
  • 16.  Certain clinical seizures in the human newborn originate from electrical seizures in deep cerebral structures (limbic regions), or in diencephalic, or brain stem structures and thereby are either not detected by surface-recorded EEG or inconsistently propagated to the surface Does absence of EEG seizure activity indicate that a clinical seizure is non- epileptic?
  • 17. (1) electroencephalogram (2) blood glucose (3) serum calcium (4) serum magnesium (5) arterial pH (6) serum sodium (7) serum urea and creatinine (8) lumbar puncture (9) blood culture (10) cranial ultrasound scan DIAGNOSIS
  • 18.  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 Management
  • 19. ANTICONVULSANTS Phenobarbitone 15 - 20mg / kg IV loading dose 3.5 - 5mg / kg / day maintenance dose Phenytoin 15 - 20 mg / kg IV at 1mg / kg / min 4 - 8 mg / kg day maintenance dose Midazolam 0.02 - 0.4 mg/kg IM 0.02 - 0.1mg/kg IV 0.06 - 0.4mg/kg/hr Others Lorazepam, diazepam, Paraldehyde
  • 20.  Phenobarbitone ↓↓  Phenytoin ↓↓  Lorazepam, midazolam drip – 48 hrs ANTICONVULSANTS
  • 21. TREATMENT 1. Optimise ventilation Maintain CO, BP, Serum electrolytes & pH 2. Treat underlying diseases- Metabolic abnor malities,meningitis,Narcotic withdrawal 3. Pyridoxine dependency- 50mg IV, repeat every 10 min till control- maintenance dose – 5mg/kg PO daily 6. Hyperbilirubinemia –phototherapy, exchange transfusion
  • 22. FOLLOW UP - ANTICONVULSANTS 1. Stop all others except maintenance PB 2. Maintenance PB : 2wks - 2months 3. Risk of recurrence Little: transient metabolic abnormalities 30-50% : HIE High : Cortex malformations
  • 23. PROGNOSIS Normal Outcome: 56% Neurological sequelae: 30 - 40% Death : 15-25% Chronic seizure disorder: 15-20% Outcome depends on 1. Level of maturity 2. Etiology 3. Neurological examination 4. EEG / Imaging studies
  • 25.  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 POOR PROGNOSIS