this is presentation done for a morning session of dhaka medical college hospital, paediatrics department by dr. tasnuba atique and nur-e-jannat naima. the information was collected from various textbooks and arranged in an easy-to-read manner to conduct a presentation of 45 minutes.

1. DR. TASNUBA ATIQUE
DR. NURE JANNATUN NAIMA
HMO PU-II

2.  Definition
 Pathophysiology
 Classification
 Etiology
 Evaluation
 Treatment
 Prognosis
 Sequelae
 Follow-up
 Prevention

3.  B/O Khaleda, 2 hours old male baby, 37
weeks of gestational age, weighing 2400 g,
presented with
 History of delayed cry after birth
 Several episodes of convulsion

4. ◦ Neonatal Seizures is defined clinically as
a paroxysmal alteration in neurological
function (i.e, behavioral, motor or
autonomic function) either or all three,
occurring within 28 days of age.

5.  Full-term baby : 3 in 1000
 Preterm baby: 60 in 1000
 Infants with birth weights <1500 g:
◦ 57.5/1000
 Infants with birth weights between 2500 and
3999 g:
◦ 2.8/1000

7. 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)

8. 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

9.  Seizures are different from those seen in older
children due to
◦ Neuroanatomic and
◦ Neurophysiologic developmental status
 Decreased seizures threshold
 In the neonatal brain,
◦ Glial proliferation,
◦ Neuronal migration,
◦ Axonal and dendritic contacts
◦ Myelin deposition are incomplete

10.  Overexpression of excitatory amino acid
receptors
 Deficiency of glutamate reuptake transporters
 Delay in Na+K+ ATPase maturation
 AMPA receptor activity (permeability to Ca++)
 Expression of Cl- transporter, NCCK1
Excitability
Upon activation of GABA receptors
Cl- influx into cell
Depolarization

11. 1. Perinatal Asphyxia:
Hypoxic-ischemic encephalopathy
2. Intracranial haemorrhage:
a. Subarachnoid Haemorrhage
b. PeRiventricular or Intraventricular
Haemorrhage
c. Subdural Haemorrhage

12. 3. Metabolic disturbances:
a. Hypoglycemia
b. Hypocalcemia
c. Hyponatraemia
d. Hypernatremia
e. Pyridoxin dependency
f. Amino acid disorders

13. 4. Infections
a. Bacterial : Group b streptococcus,
Escherichia coli
Listeria monocytogenes
b. Non-bacterial: Herpes simplex virus
Cytomegalovirus
Rubella
Coxsackie virus

14. 5. CNS malformation: Lissencephaly
Focal Cortical Dysplasia
6. Inborn Errors of Metabolism
7. Toxin: Local anaesthesia
Drug withdrawal
8. Neonatal Epileptic Syndromes

15.  Pyridoxin dependency
 Nonketotic hyperglycinemia
 Urea cycle defects
 Sulfite oxidase deficiency
 Glutaric aciduria type 2
 Maple syrup urine disease
 Menkes disease
 Mitochondrial disease
 Glucose transporter deficiency

16.  Benign Idiopathic Neonatal seizures
(fifth day fits)
 Benign Familial Neonatal seizures
 Early Myoclonic Encephalopathy
 Early Infantile Epilpetic Encephalopathy
(Ohtahara Syndrome)

17. 41%
16%
15%
5%
5%
1% 5%
1% 1%
10%
Etiology Of Neonatal seizures
Global Cerebral Hypoxia Focal Infarction- Cerbral Hypoxia
Intracranial Haemorrhage CNS infection
Transient metabolic disease Inborn errors of metabolism
Cerebral dysgenesis Neonatal epileptic syndrome
Neonatal abstinence syndrome unknown

18. 48%
40% 40%
10.30%
5.50%
8.50%
0%
10%
20%
30%
40%
50%
60%
Term
Neonate
Preterm
Neonate
both Term
and
Preterm
and
Unknown
Gestation
Hypoxic-Ischemic
Encephalopathy
Hypogycemia
Hypocalcaemia
Central Nervous
System Infections

19. 1. Subtle Seizures:
a. Ocular
b. Oral-facial-lingual movement
c. Limb movement
d. Autonomic phenomena
e. Apnoea
2. Clonic Seizures
3. Tonic Seizures
4. Myoclonic Seizures

21. Jitteriness seizures
Stimulus sensitive ++ _
Ceasation Passive flexion
Gentle grasp
-
Rhythmicity Rhythmic
oscillation
Fast & slow
components
Frequency of jerks 5-6 / sec 2-3 / sec
Abnormal gaze-Eye
movement
Nil Present
Autonomic
disturbance
Nil Increase HR, BP
EEG Normal Abnormal

22. 1-4 Days
 Hypoxic Ischemic Encephalopathy
 Drug Withdrawal
 Drug Toxicity
 Intraventricular Haemorrhage
 Acute Metabolic Disorders
 Inborn Errors Of Metabolism
 Pyridoxin Dependency

23. 4-14 days
 CNS Infection
 Metabolic Disorders
 Drug Withdrawal
 Benign Neonatal Convulsion
 Kernicterus
 Developmental Delay

24. 2-8 weeks
 CNS Infection
 Developmental Malformations
 Head Injury
 Inherited Disorders of Metabolism
 Tuberous Sclerosis
 Sturge-Weber Syndrome

25. a. History
1. Maternal history:
◦ Age, para, gravida, consanguinity
◦ Medical history: diabetes, anaemia, fever and
rash
◦ Medication taken pre-pregnancy and during
pregnancy
2. Family history:
◦ Epilepsy
◦ Neonatal seizures

26. 3. labour and delivery:
◦ Place, mode and duration of delivery
◦ Presentation and cord around the neck
◦ Maternal problem: PROM,
 Obstructed labour,
 Foetal distress,
 PET, eclampsia
 Liquor

27. 4. Baby’s condition at birth:
◦ Delayed cry
◦ Cyanosis
◦ Term or preterm
◦ Resuscitation
◦ 1st feeding

28. b. Neonatal examination :
1. General Examination :
Gestational age
Birth weight and length
Head
OFC
Umbilicus
Eye
Cyanosis
Jaundice
Presence of skin lesions.
Presence of hepatosplenomegaly

29. 2. Neurologic evaluation
 Level of alertness
 Motor function
 Neonatal reflexes
 Fontanelle
 Pupillary size and reaction to light
 Muscle tone
 CBG
 SPO²

31. 1. Metabolic work-up
◦ a. Serum glucose level.
◦ b. Serum sodium level.
◦ c. Serum ionized and total calcium levels.
◦ d. Serum magnesium level.

32. 2. Infection workup
◦ Complete blood cell count with differential
◦ CRP
◦ Culture and sensitivity of
 Blood
 Urine
 Cerebrospinal fluid
◦ TORCH infection screening by
 Serum immunoglobulin M (IgM)

33. 3. Blood gas levels
4. Studies for Inborn Errors of Metabolism
◦ Serum ammonia,
◦ S. lactate, CSF lactate,
◦ Urine organic acids/serum amino acids

34. 1. Ultrasound examination of the head
2. Computed tomography (CT) scan of the
head
3. Magnetic resonance angiography
4. Electroencephalography (EEG)

37. General Management
Control of Convulsion
Treatment of Cause

38. General Management
ABC
A- Airway
1. Opening up the airway
(Head Tilt Chin Lift maneuver)
2. Clearing up the airway secretion,vomitus by
suction
3. Put the child in recovery position
4. Sometimes endotracheal intubation m to
may be necessary to maintain the airway

39. B-Breathing
1. Assess Breathing
2.If the baby has dyspnoea orcyanosis,
Give oxygen by nasal cannula or by headbox
3. If impending respiratory failure,provide
assisted ventilation by bag and mask
ventilation or intubation and mechanical
ventilation

40. C-Circulation
1. Assess circulation
Heart Rate,BP,
Capillary refilling time,
Cardiovascular Examination
2. Secure an IV line and infuse crystalloid fluid
if required
3. If patient in shock
-IV Normal Saline bolus rapidly
-Repeat it if needed
-Inj. Dopamin if necessary

42.  Maintain slight to moderate fluid restriction
 Monitor urine output and the vital signs

43. Maintain normal blood glucose level
 To maintain the glucose level 75-100mg/dl
 To avoid hyperglycemia to prevent
hyperosmolarity

44. Control of convulsion
Seizure continue
IV PB 20mg/kg slowly over 20min @< 1
mg/kg/min
Correct hypoglycaemia or hypocalcaemia if
abnormal and simultaneously load with PB

45. Repeat PB 10mg/kg/dose after 10 mins
Seizure continue
Repeat PB 10mg/kg/dose
Seizure continue

46. Repeat Fosphenytoin 15 mg/kg/dose
Seizures continue
Start Phenytoin 20mg/kg/dose OR Fosphenytoin
30mg/kg/dose
Seizures continue

47. Wean Antiepileptic drug when seizure stops
Seizure Free
Seizure continue
Consider other antiepileptic drug
Seizure continue
Consider Inj.Midazolam/Lidocaine,Pyridoxine,folinic Acid

48. Maintenance therapy is begun after the
loading dose PB (5 mg /kg/day) can be
given IV or IM or per oral in two divided
dose (BD) possible for about within 2 weeks
or before discharge

49. Newborn on anticonvulsant therapy
Wean all antiepileptic drugs except
phenobarbitone once seizure controlled
Perform neurological examination prior to
discharge
Normal Abnormal
Stop phenobarbitone prior to
discharge

50. Abnormal
Continue phenobarbitone for 1 month
Repeat neurological examination at 1 month
Normal
examination
Abnormal examination
Evaluate EEGTaper drugs over 2
weeks
Normal EEG
Taper drugs
over 2 weeks
Abnormal EEG
Continue drug;
reassess at 3
months

51. Hypoglycemia
 Infuse a mini bolus of 2ml/kg10% glucose
solution.Give continuous infusion of glucose
at the rate of 6-8mg/kg/min and increase
the rate as needed to maintain a normal
blood glucose level (>40-60 mg/dl)
 The level should be monitored every 30-60
minutes interval

52. Hypocalcaemia
 Inj.10% Calcium Gluconate 100-200 mg/kg
IV very slowly over 15-20 minutes with
cardiac monitoring
 Maintenance of Inj.10%Calcium Gluconate
45 mg/kg/day

53. Hypomagnesaemia
 Inj.Magnesium Sulphate 25-50 mg/kg/dose
(0.2-0.4 meq/kg/dose) IV every 8-12 hours
for 2-3 doses until magnesium level is
normal
 Maintenance - By Inj.Magnesium Sulphate
0.25-0.5 meq/kg/24 hrs IV

54. Sepsis
 Supportive treatment
 Broad spectrum antibiotic

56. Overall prognosis for survival in neonatal
seizure is around 85%
The range of outcome after neonatal
seizures varies widely with the three major
predictors of long term outcome being
i. Underlying etiology
ii. Electrographic features
iii. Gestational age

57. Etiology Normal outcome (%)
Hypoxia- ischemia 50
Meningitis 50
Hypoglycemia 50
Subarachnoid hemorrhage 90
Early hypocalcaemia 50
Late hypocalcaemia 100
Intra ventricular hemorrhage 10
Dysgenesis 00
Unknown 75

58. Poor Outcome
 Abnormal background of EEG
 Prolonged electrographic seizure10 min/hr
 Multifocal periodic discharge
 Spread of electrographic seizure to
contralateral hemisphere

59.  Neonatal seizure < 32 wks
high mortality up to 80%
 In some studies significantly higher risk
of adverse neurological outcome in
survivors when compare to term infants

61.  Cerebral palsy (spastic)
 Severe or profound mental retardation
 Cortical blindness
 Seizure disorder
 Microcephaly

62.  Optical atrophy : Poor visual outcome
Smaller visual field
Lower visual acuity score
 Hearing disability
 Delayed skill in regarding spelling and
attention
 Death (PNA HIE III :mortality rate 80%)

63. All the babies faced neonatal seizures must have
get a follow up at1month and 3 months of age
 Thorough Neurological Examination
including
Activity
Reflexes
Muscle tone
 Specially assessment of hearing and vision

64.  Regular F/U at CDC-Child Development
Centre (Shishu Bikash Kendro),available in all
Government Medical College Hospital
 Special F/U for assessment of hearing and
vision at BSMMU

65.  Regular antenatal check up
 Treatment of infection during antenatal period
 Correction of anaemia and control of
Gestational HTN
 Control of diabetes
 Training of local DAI or paramedics about
proper delivery and referral system

66.  Raising awareness about institutional delivery
 In a diagnosed case of fetal distress
High concentration of 02
Proper positioning
Initiating operative delivery before severe
fetal injury occurs
 Ensuring proper training of neonatal
resuscitation

67. A Good Co-operation
Among
Obstetricians and Pediatricians
May Give A New Life

68. • Nelson textbook of paediatrics,19th edition, Robert M
Kliegman,Bonita F.Stanton,Joseph W.St.GemeIII,Nina F.
Schor,Richard E.Behrman
• Neonatology(Management,procedure,on call
problems,diseases and drugs) 6th edition, Tricia Lacy
Gomella,M.Douglas Cunningham and Fabien G.Eyal
• Manual of Neonatal Care,6th edition,John P.Cloherty,
Eric C.Eichenwald,Ann R.Stark
• The Essence of Paediatrics,4th edition,Prof. M.R.Khan
Prof M.Ekhlasur Rahman
• Volpe JJ Neonatal seizure,Neurology of the newborn
4th edition,WHO guidelines on neonatal seizures,2011