1. NEONATAL SEIZURES
SHINU K ANTONY
1ST YEAR MSc NURSING

2. DEFINITION
Neonatal seizures are the seizures
that occur within the first 4 weeks
of life and are most commonly seen
within the first 10 days.

3. INCIDENCE
 57.5/1,000 in infants with birth
weights <1,500g
 2.8/1,000 in infants weighing
between 2,500 and 3.999g have
seizures.
 1 in 200 healthy newborns
 Many seizures are very subtle – go
undetected

4. MECHANISM
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

5. MECHANISM
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

6. HYPOTHESIS
 Inhibitory neurons are selectively
damaged and remaining principal
excitatory neurons became hyper
excitable
 Aberrant excitatory circuits are formed as
a part of re organization after injury

7. In neonates
 Immature brain has more excitatory
neurons than matured (excitatory
glutamate containing circuits)
 GABA has a paradoxical excitatory nature
in immature brain
 Additionally GABA sensitive substantia
nigra pars reticulata neurons play a part
in preventing seizures, but in neonates it
is immature

8. ETIOLOGY
PERINATAL ENCEPHALOPATHY
METABOLIC
INBORN ERRORS OF METABOLISM

9. ETIOLOGY……
INFECTIONS
DEVELOPMENTAL DISORDERS
DRUG ASSOCIATED SEIZURES

10. ETIOLOGY…….
THROMBOTIC DISORDERS
BENIGN FAMILIAL NEONATAL SEIZURES
HYPERTENSIVE ENCEPHALOPATHY

11. ETIOLOGY……
UNKNOWN OR
IDIOPATHIC

12. HYPOXIC ISCHEMIC
ENCEPHALOPATHY
Primary neuronal injury: intracellular
energy failure occurs, resulting in
immediate cell death by necrosis
Secondary neuronal injury occurs
hours or days after the orginal insult

14. FOCAL CLONIC SEIZURES
 Localized clonic jerking of one limb with
no loss of consciousness.
 The electroencephalography is unifocally
abnormal .
 Prognosis good.
 Metabolic disturbances like hypocalcemia,
cerebral contusion, focal infarct, or
subarchinoid hemorrhage.

15. MULTIFOCAL CLONIC SEZURES
 More in term infants.
 Characterized by random clonic
movements of limbs. Many muscle groups
are involved simultaneously.
 The EEG is multifocally abnormal.
 The prognosis is variable
 metabolic abnormalities like
hypoglycemia,and hypoxic-ischemic
encephalopathy

16. TONIC SEIZURES
 Seen in preterm neonates.
 May mimic decerebrate or decorticate
posturing. They are often associated with eye
deviation, clonic movements or apnea.
 The EEG is multifocally abnormal with a
burst,suppression pattern or can have
extremely attenuated amplitude.
 The prognosis is generally poor.
 With diffuse cns disease or intraventricular
hemorrhage

17. MYOCLONIC SEIZURES
 Synchronous single or multiple jerks of
upper or lower limbs.
 Involves distal muscle groups.
 The EEG shows burst-suppression pattern
or focal sharp transient waves leading to
hyporrhythmia.
 Diffuse cns pathology,and development
defects like anencephaly.
 The prognosis is poor.

18. SUBTLE SEIZURES
 Most common type (>50%)of neonatal
seizures.
 They can be varied in nature and manifest
variously
 The EEG is often not associated with an
epileptiform or hypersynchronous EEG.
 They are now considered to be brainstem
release phenomenon and not seizures.

20. Clinical seizure with a
consistent EEG event
Clinical seizures with
inconsistent EEG events
Electrical seizures with absent
clinical seizures

21. BENIGN SEIZURES
‘fifth day
seizures’
Benign familial
neonatal
seizures
Benign sleep
myoclonus
These are seizures occurring in well
babies and all investigations are
negative. Causes are

22. SL
NO
:
CLINICAL
FEATURES
JITTERNESS SEIZURES
1 Abnormal gaze or eye
movement
Nil Present
2 Movements Exquisitely stimulus-
sensitive
Spontaneous
3 Movements cease Passive flexion or
gentle restraint
On their own
4 Predominant movement Tremor Clonic jerking
5 Fast and slow components Absent Present
6 EEG Normal Abnormal
7 Rate or jerks 5 to 6 per second 2 to 3 per second
8 Blood pressure, heart rate Normal Increased

23. HISTORY
 ANTENATAL
 INTRANATAL
 POSTNATAL
 FAMILY HISTORY OF SEIZURES OR
NEONATAL DEATHS
 NEUROCUTANEOUS MARKERS

24. Investigations
 CBC
 Blood – glucose, calcium, Na, K, Mg,
bilirubin, ABG, LFT
 CSF analysis
 Blood C/S , urine C/S
 Cranial USG

25. Second line investigations
 TORCH screening
 IEM screening – urine organic acids
- S. amino acid assay
 Metabolic disorders – s.ammonia, ABG

26. Investigations….
 Imaging – CT scan
- MRI
- EEG brain:Routinue neonatal
EEG recording, Amplitude integrated EEG
(aEEG)

27. 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

28. Management…..
If significant seizures persists,
 midazolam 0.15mg/kg IV bolus followed
by IV infusion 0.1-0.4mg/kg/hr (0.2-
0.6mcg/kg/min).
 sodium valporate IV is the usual next drug
in case of resistant seizure (20-
25mg/kg/day).
 Vigabatrin (50mg/kg/day) and topiramate
(3mg/kg) are experimental at present.

29. Further management
 Maintenance dose of anticonvulsants is started
12hours after loading.
 Initial maintenance doses are given as intravenous
and later switched over to oral.
 If on multiple anticonvulsants and seizures free for
2-3 days then try to taper on to monotherapy
 If controlled with calcium gluconate, start
maintenancce dose
 If the baby is seizures free after 1 or 2 episodes
and with normal neurological status or there is a
known cause for seizures then anticonvulsant may
be stopped on discharge.
 If the baby had difficult to control seizures or if
baby is neurologically abnormal then
anticonvulsants may be continued and consider a
neurology consultation

30. ANTICONVULSANT DRUG DOSES
DRUG INITIAL DOSE MAINTENANCE
Phenobarbital 20mg/kg IV. Consider further 5-10mg/kg
increments to a total of 40mg/kg
Check drug levels may not
need further doses for many
days 3-4 mg/kg/day
Phenytoin 20mg/kg IV. Fosphenytoin 20mg /kg IV 3-4mg/kg/day divide bid to
qid
benzodiazepines Lorazepam 0.05-0.1 mg/kg IV. Diazepam
0.3mg/kg IV

31. INITIAL MANAGEMENT OF ACUTE
METABOLIC DISORDERS
Hypoglycemia Dextrose10%2-3ml/kgIV
Hypocalcemia Caciumgluconate5%(50mg/ml),100-200mg/kgIV10%
(100mg/ml)50-100mg/kgIVifinadequatetimefordilation
Hypomagnesemia Magnesiumsulphate12.5%(125mg/ml)50-100mg/kgIV
Hyponatremia Furosemide1mg/kgIV.3%NaCl1-3ml/kgover15to30mts

32. PROGNOSIS AND OUTCOME
 Level of maturation
 Metabolic abnormalities
 Severe grades of IVH and congenital
malformations
 Seizure pattern
 EEG

33. National Collaborative Perinatal
Project
 Apgar <=6 at 5 minutes or longer
 The need for positive pressure ventilation > 5
minutes after birth
 Early onset of seizures within 24hrs
 Hypotonia at 5mts or longer following birth
 3 or more days with uncontrolled seizures
 Presence of tonic or myoclonic seizures
 Seizures lasting longer than 30mts
 Need of more than one anticonvulsant drug
for control of seizures

35. NURSING ASSESSMENT
Health history
Physical examination

36. NURSING DIAGNOSIS
 Decreased intracranial adaptive capacity
related to compression of brain tissue due
to increased intracranial pressure
resulting from brain injury
 Risk for ineffective (cerebral;) tissue
perfusion related to increased ICP
alteration in blood flow secondary to
hemorrhage, vessel malformation or
edema

37. NURSING DIAGNOSIS……..
 Risk for injury related to altered level of
consciousness, weakness, loss of muscle
coordination secondary to seizure activity
 Disturbed sensory perception related to
presence of neurologic leisions or
pressure on sensory or motor nerves
secondary to increased ICP as evidenced
by nystagmus, loss of response to stimuli

38. NURSING DIAGNOSISI……
 Risk for infection related to surgical
interventions, trauma to brain, stasis of
pulmonary secretions and urine
 Imbalanced nutrition less than body
requirement related to vomiting and
difficulty feeding

39. BIBLOGRAPHY
 John Cloherty P, Eric Eichenwald C, Annie, Hansen R, Ann Stark.
Manual of neonatal care.7th ed. South Asia: Lippincott, Williams
and Wilkins; 2012
 Santhosh Kumar A. manual of newborn care. 2nd ed. Newdelhi:
Paras medical publishers; 2011
 Dipak Guha K. Guha’s Neonatology: Principles and Practice. 3rd
ed.Jaypee publication.
 Dorothy Marlow R, Barbara Redding A. Text Book of Paediatric
Nursing. 6th ed. Elsevier publication.
 David Wilson, Marilyn Hockenberry J.Wong’s Clinical Manual of
Paediatric Nursing. 8th ed. Elsevier publication.
 Kliegman, Stauton, Geme S T, Schor, Behrman. Nelson’s Textbook
of Pediatrics.Vol II 19th ed. Philadephia:Elsevier publishers.2012
 Maggie Meeks, Maggie Hallsworth, Helen Yeo. Nursing the
Neonate. 2nd ed. Wiley Blackwell publication.
 Terrikyle, Susan Carmar. Essentials of Pediatric Nursing. 2nd ed.
Phiadephia: Wolters Kluwer Health publishers.2010