NEONATAL SEIZURES
SHINU K ANTONY
1ST YEAR MSc NURSING
DEFINITION
Neonatal seizures are the seizures
that occur within the first 4 weeks
of life and are most commonly seen
withi...
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...
MECHANISM
1.Large group of neurons undergo
excessive, synchronized depolarization
which results from –
a) Increase in exci...
MECHANISM
c. Disruption of ATP – dependent resting
membrane potentials - Failure of Na - K
pump – flow of sodium into the ...
HYPOTHESIS
 Inhibitory neurons are selectively
damaged and remaining principal
excitatory neurons became hyper
excitable
...
In neonates
 Immature brain has more excitatory
neurons than matured (excitatory
glutamate containing circuits)
 GABA ha...
ETIOLOGY
PERINATAL ENCEPHALOPATHY
METABOLIC
INBORN ERRORS OF METABOLISM
ETIOLOGY……
INFECTIONS
DEVELOPMENTAL DISORDERS
DRUG ASSOCIATED SEIZURES
ETIOLOGY…….
THROMBOTIC DISORDERS
BENIGN FAMILIAL NEONATAL SEIZURES
HYPERTENSIVE ENCEPHALOPATHY
ETIOLOGY……
UNKNOWN OR
IDIOPATHIC
HYPOXIC ISCHEMIC
ENCEPHALOPATHY
Primary neuronal injury: intracellular
energy failure occurs, resulting in
immediate cell...
FOCAL CLONIC SEIZURES
 Localized clonic jerking of one limb with
no loss of consciousness.
 The electroencephalography i...
MULTIFOCAL CLONIC SEZURES
 More in term infants.
 Characterized by random clonic
movements of limbs. Many muscle groups
...
TONIC SEIZURES
 Seen in preterm neonates.
 May mimic decerebrate or decorticate
posturing. They are often associated wit...
MYOCLONIC SEIZURES
 Synchronous single or multiple jerks of
upper or lower limbs.
 Involves distal muscle groups.
 The ...
SUBTLE SEIZURES
 Most common type (>50%)of neonatal
seizures.
 They can be varied in nature and manifest
variously
 The...
Clinical seizure with a
consistent EEG event
Clinical seizures with
inconsistent EEG events
Electrical seizures with absen...
BENIGN SEIZURES
‘fifth day
seizures’
Benign familial
neonatal
seizures
Benign sleep
myoclonus
These are seizures occurring...
SL
NO
:
CLINICAL
FEATURES
JITTERNESS SEIZURES
1 Abnormal gaze or eye
movement
Nil Present
2 Movements Exquisitely stimulus...
HISTORY
 ANTENATAL
 INTRANATAL
 POSTNATAL
 FAMILY HISTORY OF SEIZURES OR
NEONATAL DEATHS
 NEUROCUTANEOUS MARKERS
Investigations
 CBC
 Blood – glucose, calcium, Na, K, Mg,
bilirubin, ABG, LFT
 CSF analysis
 Blood C/S , urine C/S
 C...
Second line investigations
 TORCH screening
 IEM screening – urine organic acids
- S. amino acid assay
 Metabolic disor...
Investigations….
 Imaging – CT scan
- MRI
- EEG brain:Routinue neonatal
EEG recording, Amplitude integrated EEG
(aEEG)
Management
 Collect all samples
 IV line
 Thermoneutral environment
 Glucose 10% - 2-4ml/kg as bolus followed
by 10% g...
Management…..
If significant seizures persists,
 midazolam 0.15mg/kg IV bolus followed
by IV infusion 0.1-0.4mg/kg/hr (0....
Further management
 Maintenance dose of anticonvulsants is started
12hours after loading.
 Initial maintenance doses are...
ANTICONVULSANT DRUG DOSES
DRUG INITIAL DOSE MAINTENANCE
Phenobarbital 20mg/kg IV. Consider further 5-10mg/kg
increments to...
INITIAL MANAGEMENT OF ACUTE
METABOLIC DISORDERS
Hypoglycemia Dextrose10%2-3ml/kgIV
Hypocalcemia Caciumgluconate5%(50mg/ml)...
PROGNOSIS AND OUTCOME
 Level of maturation
 Metabolic abnormalities
 Severe grades of IVH and congenital
malformations
...
National Collaborative Perinatal
Project
 Apgar <=6 at 5 minutes or longer
 The need for positive pressure ventilation >...
NURSING ASSESSMENT
Health history
Physical examination
NURSING DIAGNOSIS
 Decreased intracranial adaptive capacity
related to compression of brain tissue due
to increased intra...
NURSING DIAGNOSIS……..
 Risk for injury related to altered level of
consciousness, weakness, loss of muscle
coordination s...
NURSING DIAGNOSISI……
 Risk for infection related to surgical
interventions, trauma to brain, stasis of
pulmonary secretio...
BIBLOGRAPHY
 John Cloherty P, Eric Eichenwald C, Annie, Hansen R, Ann Stark.
Manual of neonatal care.7th ed. South Asia: ...
Neonatal seizures
Neonatal seizures
Neonatal seizures
Neonatal seizures
Neonatal seizures
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Neonatal seizures

  1. 1. NEONATAL SEIZURES SHINU K ANTONY 1ST YEAR MSc NURSING
  2. 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. 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. 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. 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. 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. 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. 8. ETIOLOGY PERINATAL ENCEPHALOPATHY METABOLIC INBORN ERRORS OF METABOLISM
  9. 9. ETIOLOGY…… INFECTIONS DEVELOPMENTAL DISORDERS DRUG ASSOCIATED SEIZURES
  10. 10. ETIOLOGY……. THROMBOTIC DISORDERS BENIGN FAMILIAL NEONATAL SEIZURES HYPERTENSIVE ENCEPHALOPATHY
  11. 11. ETIOLOGY…… UNKNOWN OR IDIOPATHIC
  12. 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
  13. 13. 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.
  14. 14. 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
  15. 15. 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
  16. 16. 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.
  17. 17. 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.
  18. 18. Clinical seizure with a consistent EEG event Clinical seizures with inconsistent EEG events Electrical seizures with absent clinical seizures
  19. 19. 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
  20. 20. 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
  21. 21. HISTORY  ANTENATAL  INTRANATAL  POSTNATAL  FAMILY HISTORY OF SEIZURES OR NEONATAL DEATHS  NEUROCUTANEOUS MARKERS
  22. 22. Investigations  CBC  Blood – glucose, calcium, Na, K, Mg, bilirubin, ABG, LFT  CSF analysis  Blood C/S , urine C/S  Cranial USG
  23. 23. Second line investigations  TORCH screening  IEM screening – urine organic acids - S. amino acid assay  Metabolic disorders – s.ammonia, ABG
  24. 24. Investigations….  Imaging – CT scan - MRI - EEG brain:Routinue neonatal EEG recording, Amplitude integrated EEG (aEEG)
  25. 25. 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
  26. 26. 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.
  27. 27. 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
  28. 28. 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
  29. 29. 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
  30. 30. PROGNOSIS AND OUTCOME  Level of maturation  Metabolic abnormalities  Severe grades of IVH and congenital malformations  Seizure pattern  EEG
  31. 31. 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
  32. 32. NURSING ASSESSMENT Health history Physical examination
  33. 33. 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
  34. 34. 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
  35. 35. 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
  36. 36. 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
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