SEMINAR ON NEONATAL

SEIZURES,NEONATAL HYPOCALCEMIA,
HYPOGLYCEMIA, HYPOMAGNESAEMIA

PRESENTED BY :
S.A.SASIKALA
MSC(N) II YEAR
 NEONATAL SEIZURES

• SEIZURE is defined clinically as paroxysmal

alteration in neurologic function ie: motor,
behaviour and/or autonomic function.
• Epileptic seizures - phenomenon associated with
corresponding EEG seizure activity. Eg: clonic seizures.
• Non-epileptic seizures - clinical seizures without
corresponding EEG correlate. Eg: subtle and
generalised tonic seizures.
• EEG seizures - abnormal EEG activity with no clinical
correlation.
• Why seizures are common in neonatal period ?
• Seizures are common in neonatal period than any other time
in life due to decreased seizure threshold.
• Transient overdevelopment of excitatory system than
inhibitory system.
• Why generalised seizures are rare in neonates ?
Neonatal brain has reduced connectivity due to incomplete
myelination, so electrical discharges spread incompletely.
 TYPES

• Four types of neonatal seizures

1. Subtle seizures
2. Clonic seizures
3. Tonic seizures
4. Myoclonic seizures
 SUBTLE SEIZURES

Most common form(>50%). It includes :

a) Ocular - tonic horizontal deviation of eyes or sustained eye
opening with ocular fixation or cycled fluttering.
b) Oral facial lingual movements - chewing, tongue thrusting, lip
smacking etc.
c) Limb movements - cycling, paddling, boxing etc.
d) Autonomic phenomena-tachycardia or bradycardia.
e) Apnea may be a rare manifestation of seizure.
 CLONIC SEIZURES

• Rhythmic movements of muscle groups.

• Have both fast and slow movements with frequency
of 1- 3 jerks per second.
• Commonly associated with EEG changes.
• May be unifocal or multifocal.
• Focal clonic has good prognosis.
 TONIC SEIZURES

• Pattern is sustained posture of limbs or asymmetrical

truncal postures.
• cause: diffuse neurological injury or IVH in preterm or
post asphyxial.
• Usually no EEG changes.
• Prognosis is poor except for post asphyxial cases.
 MYOCLONIC SEIZURES

• Non rhythmic lightning fast contraction.

• Seen in diffuse brain damage as in perinatal asphyxia,
inborn errors of metabolism, cerebral dysgenesis.
• Worst prognosis in terms of neuro developmental
outcome and seizure recurrence.
 ETIOLOGY

• 1.Perinatal events:
• Hypoxic ischemic encephalopathy
• Intracranial hemorrhage: Germinal matrix
intraventricular hemorrhage, subdural hemorrhage,
primary subarachnoid hemorrhage (well baby
seizures)
 2.METABOLIC
• Hypoglycemia
• Hypocalcemia
• Early: preterm, asphyxia, IDM
• Late: Top feeding
• Hypomagnesemia
• Hyponatremia / hypernatremia
• Pyridoxine deficiency
• IEM: non-ketotic hyperglycinemia, urea cycle defects, maple syrup disease,
glutaric aciduria, propionic aciduria, methyl malanoic aciduria,
mitochondrial disease.
3.INFECTIONS:
• Bacterial meningitis
• Non-bacterial infections: toxoplasmosis, herpes simplex,
rubella, cytomegalovirus
4.DEVELOPMENTAL PROBLEMS:
• Cerebral cortical dysgenesis
• Neuronal migration disorders
• Pachygyria, polymicrogyria
 5.MISCELLANEOUS
 Passive drug withdrawal
 Accidental injection of local anesthetic into fetal scalp.
 Neonatal epileptic syndromes
 Benign familial neonatal convulsions
 Benign idiopathic neonatal convulsions (fifth day fits)
 Early myoclonic encephalopathy
 Early infantile epileptic encephalopathy (Ohtahara’ssyndrome)
 Malignant migrating partial seizures in infancy( coppola syndrome)
 NEONATAL SEIZURES – TIME OF ONSET
Time of Etiology
onset
<24hrs HIE, severe birth trauma, hypoglycemia, hypocalcemia, drug
withdrawal, congenital CNS anomalies, intracranial hemorrhage

1-3 days All above , subarachnoid hemorrhage, IEM, benign familial neonatal
seizures

>3days sepsis ,meningitis, progressive hydrocephalus, epileptic syndromes,

herpes encephalitis, IEM
 SPECIFIC ETIOLOGIES
• Hypoxic Ischemic Encephalopathy
• Most common cause of neonatal seizures usually in the first 24 hours.

• Intra cranial hemorrhages

• Sub arachanoid hemorrhages cause seizures usually on second day and have a very good outcome.

• Acute metabolic disorders

• Hypoglycemia
• Hypocalcemia
• Hypomagnesemia
• Hypo/Hypernatremia

• Neonatal seizure syndromes

• Benign familial neonatal seizures
• Benign idiopathic neonatal seizures ( fifth day fits )
• Early infantile epileptic encephalopathy ( Ohtahara syndrome )
• Malignant migrating partial seizures ( Coppala syndrome )
 ACUTE MANAGEMENT

Neonate with seizures

•Identify and characterize the seizure • Secure airway and optimize

breathing, circulation, and temperature • Secure IV access and take
samples for baseline investigations

•If hypoglycemic : administer 2 ml/kg of 10% dextrose as bolus

followed by a continuous infusion of 6-8 mg/kg/min • If serum
calcium is abnormal, 2 ml/kg of calcium gluconate (10%) should be
given IV under cardiac monitoring
Seizures persists
 Administer phenobarbitone 20mg/kg IV stat over 20 minutes
Seizures continue
Repeat phenobarbitone in 10 mg/kg/dose aliquots until 40
mg/kg dose is reached
Seizures continue
Administer phenytoin 20 mg/kg IV slowly over 20 minutes under
cardiac monitoring
Seizures continue
Lorazepam: 0.05 mg/kg IV bolus over 2-5 minutes; may be repeated
Midazolam: 0.15 mg/kg IV bolus followed by infusion of 1-7 mcg/kg/min
Clonazepam 0.1mg/kg;Consider ventilation
Seizures continue
 Second line drugs like Lidocaine[4mg/kg f/b 2mg/kg/hr]
Paraldehyde[0.1-0.2ml/kg/dose IM] sodium valproate[20-
25mg/kg f/b 5-10mg/kg/12h] Topiramate(20mg/kg/day)
Levetiracetam(10-30mg/kg/day) Vigabatrin(50mg/kg/day)
Pyridoxine(100mgIVtestdose) exchange transfusion[IEMs,
drug toxicity,bilirubin encephalopathy
Seizures controlled

Wean AEDs slowly to maintenance phenobarbitone

 MAINTENANCE DOSE

• Phenobarbitone or phenytoin after loading dose

maintenance dose 3-5 mg/kg/day in two divided
doses.
• Wean slowly in a way, taper the last given anti
convulsant first and first given phenobarbitone in
last.
 HYPOCALCEMIA

• Children – is defined as a total serum calcium

concentration less than 2.1 mmol/L (8.5 mg/dL).
• Term infants -less than 2 mmol/L (8 mg/dL) or ionized
fraction of less than 1.1 mmol/L (4.4 mg/dL)
• Pre term -less than 1.75 mmol/L (7 mg/dl)
 Normal calcium values

 Cord = 9-11.5 mg/dl

 Newborn, 3-24 hours = 9-
10.6mg/dl
 Newborn, 24-28 hours = 7-12
mg/dl
 Newborn, 4-7 days = 9-10.9 mg/dl
 EPIDEMIOLOGY

• Late onset hypoglycemia –common (developing countries)

• Age related demographics -: -Mostly new borns -older
children : associated with
• critical illness
• acquired hypo-parathyroidism
• mutations in calcium – sensing receptor
• defect in Vit.D supply or metabolism
 ETIOLOGY

In neonates In infants and children

 Early onset neonatal  Hypoparathyroidism,
hypocalcemia  Abnormal vitamin d
 Late onset neonatal Production or action,
hypocalcemia  Hyperphosphatemia
PATHOPHYSIOLOGY
 DIAGNOSTIC FINDINGS
• History collection
• Physical examination
• Lab .findings
 LABORATORY FINDINGS
• Total and ionized serum calcium levels
• Serum magnesium levels
• Serum electrolyte and glucose levels
• Phosphorus levels
• Parathormone levels
• Vitamin D metabolite (25- hydroxyvitamin D and 1,25-
dihydroxyvitamin D) levels
• Urine calcium, magnesium, phosphorus, and creatinine levels
• Serum alkaline phosphatase levels
 ADDITIONAL FINDINGS

• Malabsorption workup
• Total lymphocyte and T-cell subset analyses
• Chest radiography
• Ankle and wrist radiography
• Electrocardiography
• Karyotyping
 MANAGEMENT

• 1 ml of Ca.gluconate (10%) -9 mg elemental ca.

EARLY NEOANTAL HYPOCALCEMIA:
• Patients at increased risk of hypocalcemia
• Patients diagnosed –asymptomatic
• Patients diagnosed – symptomatic
• Patients at increased risk of hypocalcemia
• -pre term + sick (DM) + perinatal asphyxia = 40
mg/kg/day
• -infants (oral feeds) calcium PO=q.6 hrly
• -therapy – continued ---3 days
• Patients diagnosed –asymptomatic
• 80 mg/kg/day elemental calcium – 48 hrs
• Tapered 50% --------
• For an Patients diagnosed – symptomatic Bolus
• 2ml/kgldose -----5% D-----10 min Contin.
Infusion-----80mg/kg/day -----48hrs 50% dropped-----next 24
hrs-----discontinued other 24 hrs
• oral feeds---------PO calcium
 NURSING MANAGEMENT

• Assessment
• Identify the infants at risk
• Administer supp. Ca, vit .D, phos.
• Monitor during infusion
• Nutritional supplementation
 DIAGNOSIS

• Risk for injury r/t seizures secondary to hypocalcemia

• Ineffective airway clearance r/t laryngospasm
secondary to hypocalcemia
• Impaired skin integrity r/t infiltration of calcium
infusion
• Ineffective perfusion r/t rapid infusion of calcium
Hypomagnesaemia
 Hypomagnesemia occurs when serum
concentrations fall below 0.66mmol/L (1.6mg/dL)
 CLINICAL
ETIOLOGY MANIFESTATIONS
• Decreased mg supply • NEONATALPERIOD –
• Magnesium loss • Malabsorption syndrome
• Intractable hypocalcemic
seizures
 Management(medical)

• Should not be treated with Ca.or Vit.D

• Mg. salts ----can be given
• 50% solution of MgSO4, 0.005 to 0.1 mL/kg (0.1 to 0.2 mmol/kg or 2.5
to 5.0 mg / kg ) slow IV 30-60 MIN ……..Repeated doses-q 8-12 hrs
Concominant oral Mg suppl
• If Mal absorption- 1mg/kg/day PO (daily)
• Serum Mg. conc. Measured
• Oral MgSO4 --- are not well absorbed--- diarrhoea
• Well titrated
 NURSING MANAGEMENT
• Assessment • Monitor serum Mg. levels
• fluid balances • Monitor BP
• weight changes • Monitor RR & depth
• skeletal muscle • Monitor deep tendon
strength(weakness)
reflexes
• cardiac rhythm(arrythmia)
• Admin. Drugs
• cerebral func.(LOC)
• Monitor electrolyte balances
• GI func(bowel sounds)
•
• Parent education
neuro muscular excitability
 COMPLICATIONS
• Hypotonia
• Respiratory depression
• Hypotension
• Cardiac arrythmias
HYPOGLYCEMIA
• Neonatal Hypoglycemia is defined as a plasma
glucose level of less than mg/dL ( mmol/L) in the first
24 hrs of life and less than 45 mg/dL (2.5 mmol/L) .
 RISK FACTORS

1.Decreased substrate availability

•Intra-uterine fetal growth restriction
•Glycogen storage disease
•Inborn errors (e.g., fructose intolerance)
• Prematurity
•Prolonged fasting without IV glucose
2.Hyperinsulinemia
 Infant of diabetic mother
 Islet cell hyperplasia
 Erythroblastosis fetalis
 Exchange transfusion
 Beckwith-Wiedemann Syndrome
 Maternal ß-mimetic tocolytic agents
 ”High” umbilical arterial catheter
 Abrupt cessation of IV glucose
3.Other endocrine abnormalities
•Pan-hypopituitarism
•Hypothyroidism
•Adrenal insufficiency
4.Increased glucose utilization
• Cold stress
• Increased work of breathing
• Sepsis
• Perinatal asphyxia
5.Miscellaneous condition
• Polycythemia
• Congenital heart disease
• CNS abnormalities
 CLINICAL MANIFESTATIONS
• Infants ---1 st/ 2nd day of life ------asymptomatic
• Hypotonia
• Lethargy
• Poor feeding
• Jitteriness, seizures
• CHF
• Cyanosis
• Apnea
• Hypothermia
 C/M ---ASSOCIATED WITH ANS

• Anxiety, tremulouness
• Diaphoresis
• Tachycardia
• Pallor
• Hunger, nausea, & vomiting
 C/M ---OF HYPOGLYCORRHACHIA

• Head ache • Dysarrthria

• Mental confusion • Seizures
• Staring • Ataxia
• behavioral changes • Somnolence
• Difficulty concentrating • Coma
• Visual disturbances • Stroke
 Diagnostic findings

• Serum or plasma glucose levels

• Serum insulin
• Urine for ketone bodies
• Screening for metabolic errors
• Angiography
 Management
• Screening-------1,2,4,6,9,12 hrs
• At risk neonates-----2,6,12,24,48,72hrs
• Sick babies, sepsis, asphyxia, shock 6-8 hrs
• Asymptomatic babies ---with BS 20-40 mg/dL
• after 1 hr of oral feed -later q 6 hrs till 48 hrs ( if BS > 50
mg/dl
• with BS levels < 20 mg/dL -after 1 hr of starting IV fluids &
then q hr ----BS
THEORY APPLICATION
 JOURNAL STUDY
Topic: Etiology of neonatal seizures and maintenance therapy use: a 10-year
retrospective study at Toulouse Children's hospital.
Background
• No guidelines exist concerning the maintenance antiepileptic drug to use after
neonatal seizures. Practices vary from one hospital to another. The aim of this study
was to investigate etiologies and to report on the use of maintenance antiepileptic
therapy in our population of full-term neonates presenting neonatal seizures.
Methods
• From January 2004 to October 2014, we retrospectively collected data from all full-
term neonates with neonatal seizures admitted to the Children’s Hospital of
Toulouse, France.
Results
• Two hundred and forty-three neonates were included (59% males, 48% electroencephalographic
confirmation). The frequencies of etiologies of neonatal seizures were: hypoxic-ischemic encephalopathy (HIE)
(n = 91; 37%), ischemic infarction (n = 36; 15%), intracranial hemorrhage (n = 29; 12%), intracranial infection
(n = 19; 8%), metabolic or electrolyte disorders (n = 9; 3%), inborn errors of metabolism (n = 5; 2%), congenital
malformations of the central nervous system (n = 11; 5%), epileptic syndromes (n = 27; 12%) and unknown
(n = 16; 7%). A maintenance therapy was prescribed in 180 (72%) newborns: valproic acid (n = 123),
carbamazepine (n = 28), levetiracetam (n = 17), vigabatrin (n = 2), and phenobarbital (n = 4). In our cohort, the
choice of antiepileptic drug depended mainly on etiology. The average duration of treatment was six months.
Conclusions
• In our cohort, valproic acid was the most frequently prescribed maintenance antiepileptic therapy. However,
the arrival on the market of new antiepileptic drugs and a better understanding of the physiopathology of
genetic encephalopathies is changing our practice
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