Neonatal seizures, neonatal hypoglycemia, neonatal hypocalcaemia,

hypomagnesemia

Neonatal seizures

Introduction
Neonatal convulsion are common life-threatening emergency in the newborn due to cerebral or
biochemical abnormality. Preterm babies are more prone to this problem.

Incidence
Incidence being 0.2-2.7/1000live births in term babies and 57.5-132/1000 live births in preterm
babies.

Definition
A seizure is a paroxysmal behavior caused by hyper synchronous discharge of a group of neurons.
Neonatal seizures are the most common overt manifestation of neurological
dysfunction in the newborn.

It is a paroxysmal spell of altered neurological function (behavior, motor or autonomic function)

occurring during the first 28 days in term infants or 44weeks gestational age in pre-term infants.

Classification of neonatal seizures

Type characteristics

1. Clonic slow rhythmic jerky movements approximately 1-3 seconds

 Focal involves upper or lower extremities on one side of body.

Mainly involves neck or trunk. Infant is conscious during event.

 Multifocal may migrate from one part of the body to other.

Movements may start at other times.

2. Tonic extension/stiffening movements.

 Generalized extension of all four limbs ( similar to decerebrate rigidity)
Upper limbs are maintained in a stiffy flexed position
 Focal sustained posturing of limbs, Asymmetric posturing of
trunk or neck.

3. Subtle May develop in full term or pre-term . common in

preterm Eye deviation (Term)
Blinking, fixed stare (Preterm). Repetitive mouth & tongue
movements, Apnea, Pedaling, tonic posturing of limbs.

4. Myoclonic rapid jerks that involve flexor muscle group.

Neeta Rajesh Bhide, (M.Sc.N., M.A. Psyco., M.C.F.H., M.D.F.M. Page 1

  Focal involves upper extremity flexor muscle group.
 Multifocal asynchronous twitching of several parts of the body.
 Generalized bilateral jerks of upper and lower limbs.

Causes of neonatal seizures

1. Metabolic problems
Hypoglycemia, Hypocalcaemia, Hyponatremia, Hypomagnesaemia, Pyridoxine
Deficiency

2. Developmental neurological problems

Congenital hydrocephalus, microcephaly, cerebral dysgenesis, porencephaly,,
Polymicrogyria, hydraencephaly, lissencephaly, Agenesis of corpus callosum

3. Toxic
Uremia, Bilirubin encephalopathy

4. Prenatal infections
Toxoplasmosis, syphilis, cytomegalovirus, herpes simplex, hepatitis

5. Postnatal complications
Bacterial meningitis, viral meningoencephalitis, sepsis, brain abscess

6. Trauma at birth
Hypoxic brain injury, intracranial hemorrhage, subarachnoid hemorrhage, subdural
hemorrhage, intraventricular hemorrhage

7. Miscellaneous conditions
a. Neonates born to narcotic withdrawal or abstinence syndrome: the babies born to
the mother addicted to heroin alcohol, diamorphine, methadone. May manifest with
characteristic withdrawal symptoms like irritability, high pitched cry, tremors,
hyper tonicity, vomiting diarrhea after 48 hours of birth.
b. Local anesthetics: During paracervical block inadvertent injection of local
anesthetics into fetal scalp may result in intractable convulsion.
c. Hypomagnesaemia
d. Pyridoxine dependency : prolonged maternal administration of vitamin B6during
pregnancy may predispose to this condition.

Benign seizures in neonates

1. Benign neonatal sleep myoclonus: It has onset during first week of life and occur as
synchronous myoclonic jerks during REM sleep. There are no seizures when the baby is
awake. EEG is normal and seizures spontaneously disappear by 2 motnhs of age.
2. Benign familial neonatal convulsions occur as self limiting isolated clonic seizures on
second and third day of life the recovery is within 1-6 months of life.
3. Benign idiopathic “ fifth day seizures” : the multi focal clonic seizures occur on day 5 and
usually disssapear on day 15 the cause is umknown though CSF zinc level is reported in
some cases.

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Age of onset of convulsion
First day: Hypoxic-ischemic encephalopathy, cerebral contusion, first day
hypocalcaemia, pyridoxine dependency accidental injections of local anesthesia
Between 1-3 days: intracranial hemorrhage, hypoglycemia, narcotic withdrawal, inborn
error of metabolism.
Fourth to seventh day : tetany, meningitis, torch infection developmental
malformation,kernicterus.

Investigations
 Family history of convulsion, history of maternal drug addiction and infections are
important aspect of investigation.
 Electroencephalography (EEG) is essential in diagnosis and management of neonatal
seizures.
 Neuroimaging: Imaging the brain is essential in determining the etiology of neonatal
seizures.MRI scanning is very effective for determining the presence and extent of
hypoxic-ischemic injury and of parenchyma brain injury. If MRI scanning is not possible
acutely,
 CT scan is effective for determining the presence of hemorrhage and calcification (e.g.,
congenital infection, cortical dysplasia).
 Blood examination fro calcium, sugar, phosphorus
 Lumbar puncture for CSF study
 Serology for STORCH

Management:

A.Infant should be nursed in thermoneutral environment and special attention should be

given to the baby’s perfusion and ventilation.
B. Stop feeds and start 10%dextrose
C. Treating the primary cause
 Hypoglycaemia – IV 10% dextrose 5ml-10 ml/kg as a bolus is given , then 2ml/kg
dextrose 10% strated. The blood glucose should be maintained between 70-120 mg/dl.
 Hypocalcemia (Ionised Ca <1.1) – IV 10% calcium gluconate 2ml/kg over 10mins
 Hypomagnesemia (<1.0) – IV/IM 50% MgSO4 0.2ml/kg over 10mins
D. Anticonvulsant therapy
Parenteral dose of phenobarbitone 20m/kgis administered slowly intravenously over
20 minute. If no response in 15 minutes additional dose of phenobarbitone 10mg/kg
every 15 minutes is administerd intravenously till seizures are controlled.
If convulsions are still uncontrolled phenytoin is administered intravenously in a
loading dose of 20 mg/kg .
The maintenance therapy with phenobarbitone and phenytoin is started after 12
hours of loading dose and given in a dose of 5mg/kg/day in two divided dose.
If convulsions are intractable and baby is in status convulssicus give lorazepam
50ug/kg IV slowly over 2-5 min. Alternately clonazepam 100-200 ug/kg can be
given IV 30 sec.
Specific situation :
a. Pyridoxine dependent seizures ; give 100mg IV under EEG control and close
observation
b. Exchange blood transfusion; In life threatening metabolic disorder , kernicterus,
accidental injections.
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Nursing management
• Document any fits or abnormal movement in the baby on the fit chart.
• Raise any concerns with the doctors regarding any abnormal movement.
• Do observations as requested.
• Document any concerns which parents have and to inform to the doctors.

Prognosis
The outcome following neonatal seizures depends primarily on the underlying cause. The presence
of both clinical and electrographic seizures in the newborn often indicates some degree of brain
injury and may alter the prognosis of the underlying disorder (e.g., hypoxic-ischemic injury) The
prognosis is good in hypocalcemic convulsions. About one-fourth to 40 percent of neonates with
neonatal convulsions die. Birth trauma and hypoxia are having bad prognosis. Among survivors,
about 25 percent suffer from recurrent convulsions and neurodevelopmental defects.

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 Neonatal HYPOGLYCEMIA

Introduction
Neonatal hypoglycemia is a common metabolic disorder which can cause unexplained death and
high mortality. Incidence and severity can be reduced by initiating appropriate feeding regimen
and timely administration of supplements.

Definition
Hypoglycemia in the newborn baby is termed when the blood glucose level is less than 40 mg/dl,
irrespective of period of gestational age. It may be asymptomatic or symptomatic.

Types
1. Increased or impaired glucose utilization :
Large or normal size infants who appears to suffer from hyperinsulinism, infant born to
women with diabetes, infants with increased metabolic demand such as cold stress, sepsis,
or after resuscitation, infants with enzymatic or metabolic endocrine defects.
2. Decreased glucose stores:
Small or growth restricted infant’s premature infants.

Causes of neonatal hypoglycemia

Transient hypoglycemia
1. Inadequate substrate
i. Premature and SGA infants
ii. Smaller of the twins
iii. Infants of diabetic mothers
2. Relative hyperinsulinism as in infants of diabetic mothers.
Persistent hypoglycemia
1. Hyper insulin states
i. Beta cell hyperplasia
ii. Adenoma of beta cells
iii. Leucine sensitivity
2. Deficiency of hormones such as glucagon ,adrenal and ACTH
3. Deficiency of substrate such as in ketotic hypoglycemia
4. Disorders of carbohydrate metabolism such as glycogen storage disease and fructose
intolerance.
Others
1. May be due to perinatal stress like asphyxia, hypothermia, infection, polycethemia,
respiratory distress and neurological disturbances.
2. Maternal tocolytic therapy like isoxusprine, salbutamol, etc.

Clinical manifestation
The clinical features are associated with release of epinephrine and activation of autonomic
nervous systems which may alter due to anoxia and intracranial injury.
 Cerebral Signs:
Limpness, jitteriness, tremors, twitching, pallor, hypothermia, high pitched cry, lethargy
or irritability, restlessness, convulsions and coma.
 Other signs:
Apnea with cyanosis, tachypnea with irregular breathing, sweating, eye rolling, poor
feeding.

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Screening
Besides monitoring serum blood glucose should be done for all infants at risk.
 Infants who also may need screening include:
 Significant hypoxia, perinatal distress, or five-minute Apgar <5
 Infant with mother on terbutaline, beta-blockers, or oral hypoglycemic agents
 Infant with isolated hepatomegaly (rule out glycogen storage disease [GSD]);
microcephaly; anterior midline defects; gigantism
 Infants with macroglossia or hemi hypertrophy (rule out Beckwith-Wiedemann Syndrome)
 Infants you suspect have an inborn error of metabolism

Management
1. Hypoglycemia should be prevented by early initiation of breast feeding within first hour of
birth.
2. The baby should be nursed in warm or thermo neutral environment with careful
observation of at-risk situation and prevention of hypoxia and hypothermia.
3. In symptomatic infants with convulsions, 25 percent dextrose 2ml/ kg intravenously is
given as bolus. If there is no convulsion, 10 percent dextrose at a rate of 6-8 mg/kg/minute.
4. Blood glucose level to be checked every ½ hourly. Infusion rate to be reduced only if last
two glucose estimation is more than 60mg/dl.
5. Oral feeds are introduced gradually and glucose infusion is tapered off.
6. If blood glucose level is not corrected then bolus administration of dextrose can be
repeated and serum cortisol and insulin level is checked.
7. Glucogen and/or epinephrine, diazoxide may be given to the babies with maternal diabetes
mellitus or erythroblastosis.
8. Asymptomatic case with low blood sugar level should be treated as symptomatic cases.

Nursing management
 Identify infants at risk or with hypoglycemia
 Reduce environmental factors that predispose to hypoglycemia eg cold stress, respiratory
distress.
 Administer IV glucose as prescribed
 Initiate early feedings in healthy infant.
 Ensure adequate intake of carbohydrates ( breast milk or formula).

Prognosis
The prognosis of hypoglycemia is generally poor. Untreated symptomatic neonates usually have
fatal outcome. Among survivors of symptomatic cases, about 50 percent neonates may have
mental retardation or cerebral palsy with convulsions. In asymptomatic hypoglycemic babies of
diabetic mothers the prognosis is usually excellent.

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 Neonatal HYPOCALCEMIA

Introduction
Hypocalcaemia is a common metabolic problem in newborns. Hypocalcemia occurs in 30% of
infants with very low birth weight (<1500 g) and 89% of infants whose gestational age at birth
was less than 32 weeks. A high incidence is also reported in infants of mothers with diabetes
mellitus and in infants with birth asphyxia.

Definition
Hypocalcaemia is defined as total serum calcium <7 mg/dl or ionized calcium < 4mg/dl.

Perinatal metabolism
During pregnancy, calcium is transferred actively from the maternal circulation to the fetus by a
transplacental Ca pump regulated by parathyroid hormone. The majority of fetal Ca accretion
occurs in the third trimester. This process results in higher plasma Ca concentrations in the fetus
than in the mother and leads to fetal hypercalcemia, with total and ionized Ca concentrations of 10
to 11 mg/dL (2.5 to 2.75 mmol/L) and 6 mg/dL (1.5 mmol/L), respectively, in umbilical cord
blood at term After the abrupt cessation of placental transfer of Ca at birth, total serum Ca
concentration falls to 8 to 9 mg/dL (2 to 2.25 mmol/L) and ionized Ca to as low as 4.4 to 5.4
mg/dL (1.1 to 1.35 mmol/L) at 24 hours.. Serum Ca concentration subsequently rises, reaching
levels seen in older children and adults by two weeks of age.

Calcium homeostasis in newborn

Body calcium exists in two major compartments; (a) Skeleton (99%) and (b)
Extracellular fluid (1%).

Both calcium and maternal parathyroid hormone cross the placenta

There is an active transport of calcium and phosphorus to fetus from maternal sources

Fetal concentrations are 1.0mg/dl higher than maternal

Placental transport of calcium takes place during last trimester of pregnancy

Paratharmone & 1,25 dihydroxy vitamin D3 are the principal calcium regulating hormones

Paratharmone mobilizes calcium from bones, increases calcium reabsorption in renal tubules

Serum calcium level falls after birth in preterm babies

Hypocalcaemia occurs during 24-36 hours of age

Due to reduced GFR and defective tubular reabsorption in the newborn kidney is unable to excrete
phosphorus

During first days of life serum calcium falls and phosphorus level rises.

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Types of hypocalcaemia
1. Early onset Neonatal Hypocalcaemia (ENH)
This condition is fairly common and seen within the first 3 days of life.
 Prematurity: Preterm babies born at a gestation £32 weeks are at an increased risk of
ENH in the first 3 days of postnatal life. This may be related to premature termination of
trans-placental supply, exaggeration of the postnatal drop to hypocalcemic levels and
diminished target organ responsiveness to parathyroid hormone.
 Infant of diabetic mother: (gestational and insulin dependent). This may be related to
increased calcium demands of a macrocosmic baby.
 Perinatal asphyxia: Hypocalcaemia and hyperphosphatemia in this condition may be
related to renal insufficiency, metabolic acidosis and diminished parathyroid hormone
secretion.

Screening is recommended in at-risk neonates:

1. Preterm infants (£32 weeks)
2. Infant of diabetic mothers
3. Severe perinatal asphyxia defined as Apgar score <4 at 1 minute of age. Screening for
hypocalcaemia is not needed in small for gestational age (SGA) infants unless additional risk
factors like asphyxia are present.

Time schedule for screening:

At 24 and 48 hours in high-risk babies

Clinical presentation:
 Early onset: jitteriness, apnea, cyanotic, episodes, high pitched cry, abdominal distension.
 Late onset: twitching, tremors, seizures.

Diagnosis
1. Clinical presentation
2. History: abnormal movements and lethargy may precede seizure activity rarely use of
goat’s milk or cow milk may be reported.
3. Laboratory: Total or ionized serum calcium (total <7 mg/dL or ionized <4.0 mg/dL).
Ionized calcium is the preferred mode for diagnosis of hypocalcaemia.
4. ECG

Treatment:

1. Patients at increased risk of hypocalcemia: Preterm infants, sick infants of diabetic mothers
and those with severe perinatal asphyxia should receive 40 mg/kg/day of elemental calcium (4
ml/kg/day of 10% calcium gluconate). Infants tolerating oral feeds may receive this calcium orally
q 6 hourly. Therapy should be continued for 3 days.

2. Patients diagnosed to have asymptomatic hypocalcemia: Infants detected to have

hypocalcemia on screening and who are otherwise asymptomatic should receive 80-mg/kg/day
elemental calcium (8 ml/kg/day of 10% calcium gluconate) for 48 hours. This may be tapered to
50% dose for another 24 hours and then discontinued. Neonates tolerating oral feeds may be
treated with oral calcium (IV preparation may be used orally).

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3. Patients diagnosed to have symptomatic hypocalcemia: These patients should receive a bolus
dose of 2 ml/kg/dose diluted 1:1 with 5% dextrose over 10 minutes, under cardiac monitoring.
This should be followed by a continuous IV infusion of 80-mg/kg/day elemental calcium for 48
hours. Continuous infusion is preferred to IV bolus doses (1ml/kg/dose q 6 hourly).

2. Late onset neonatal hypocalcemia (LNH)

This condition is rare as compared to ENH. It usually presents at the end of the first week It is
usually symptomatic in the form of neonatal tetany.

Causes of late onset hypocalcemia

1. Hypomagnesemia
2. Increased phosphate load: Cows milk
3. Hypoparathyroidism
 Idiopathic, transient
 Hypoplasia, aplasia of parathyroid glands. (DiGeorge’s syndrome)
 Pseudohypoparathyroidism
 Maternal hyperparathyroidism
4. Vitamin deficiency
 Maternal vitamin D deficiency
 Malabsorption
 Maternal anticonvulsant therapy
 Renal insufficiency
 Hepatobiliary disease

Investigations
These should be considered in LNH or if the hypocalcaemia does not respond to adequate
doses of calcium.
 Serum magnesium: Magnesium levels <1.2 mg/dL should be treated
 Serum phosphate (P): Phosphate levels are increased in renal failure, top feeding with
cow’s milk and hyperparathyroidism.
 Alkaline phosphates (ALP): ALP levels are increased in hyperparathyroidism
 PTH levels: PTH is decreased in hyperparathyroidism.
 Urine calcium/ creatinine ratio: Ratio >0.2 is suggestive of hyperparathyroidism
 Chest x-ray
 Maternal calcium, phosphate and alkaline phosphates levels: These would be helpful in
detection of maternal vitamin D deficiency

Treatment of LNH
The treatment of LNH is specific to etiology and may in certain diseases be life-long

1. Hypomagnesaemia: Symptomatic hypocalcaemia unresponsive to adequate doses of IV

calcium therapy is usually due to hypomagnesaemia. It may present either as ENH or later as
LNH. The neonate should receive 2 doses of 0.2ml/kg of 50% MgSO4 injection, 12 8 hours apart,
deep IM followed by a maintenance dose of 0.2 ml/kg/day of 50% MgSO4, PO, 3 days.

2. High phosphate load: These infants have hyperphosphatemia with near normal
calcium levels. Exclusive breast-feeding should be encouraged and top feeding with
cow’s milk should be discontinued.
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3. Hypoparathyroidism: These infants tend to be hyperphosphatemic and hypocalcemic
with normal renal functions. Elevated phosphate levels in the absence of exogenous
phosphate load (cow’s milk) and presence of normal renal functions indicates
parathormone inefficiency. These neonates need supplementation with calcium (50
mg/kg/day in 3 divided doses) and 1,25(OH)2 Vitamin D3 (0.5-1 mg/day). Syrup Shelcal
has 250 mg/5ml of calcium and Vitamin D3 (calcitriol) is available as 0.25 mg capsules.
Therapy may be stopped in hypocalcaemia secondary to maternal hyperparathyroidism
after 6 weeks.

4. Vitamin D deficiency states: These babies have hypocalcaemia associated with

hypophosphatemia due to an intact parathormone response on the kidneys. They benefit
from Vitamin D3 supplementation in a dose of 30-60 mg/kg/day

Nursing management
1. Identify infant at risk or with hypocalcaemia.
2. Provide calm environment to reduce stimuli that might precipitate a seizures or tremors.
3. Administer calcium as prescribed. Observe for sign of acute hypocalcaemia (eg
bradycardia, vomiting)
4. Precautions should be taken while administration of calcium
Bradycardia and arrhythmia are known side effects of bolus IV calcium administration
and bolus doses of calcium should be diluted 1:1 with 5% dextrose and given under
cardiac monitoring.
5. An umbilical venous catheter (UVC) may be used for administration of calcium only after
ensuring that the tip of the catheter is in the inferior vena cava.
6. Hepatic necrosis may occur if the tip of the UVC lies in a branch of the portal vein.
7. Umbilical artery catheter (UAC) should never be used for giving calcium injections.
8. Accidental injection into the UAC may result in arterial spasms and intestinal necrosis.
9. Skin and subcutaneous tissue necrosis may occur due to extravasation. Hence IV sites
where calcium is being infused should be checked at least q 6 hourly to monitor for
extravasation and avoid subcutaneous tissue necrosis.

Neeta Rajesh Bhide, (M.Sc.N., M.A. Psyco., M.C.F.H., M.D.F.M. Page 10

 Neonatal Hypomagnesemia

Introduction
Hypomagnesemia is an electrolyte disturbance in which there is an abnormally low level of
magnesium in the blood. Usually a serum level less than 0.7 mmol/l is used as reference.
Hypomagnesaemia is not equal to magnesium deficiency. Hypomagnesaemia can be present
without magnesium deficiency and vice versa. Magnesium is the second most abundant
intracellular cation and the fourth most abundant cation overall. Almost all enzymatic processes
using phosphorus as an energy source require magnesium for activation

It is resorbed through the small intestine, and to a lesser degree in the colon. The rectum and
sigmoid colon can absorb magnesium Hypomagnesaemia stimulates and hypomagnesaemia
inhibits this absorption. The kidneys regulate the serum magnesium. About 2400 mg of
magnesium passes through the kidneys, of which 5% (120 mg) is excreted through urine. The loop
of Henle is the major site for Mg-homeostasis, and 60% is resorbed.

Definition
Neonatal hypomagnesaemia is defined as total magnesium (TMg) ≤0.65 mmol/L (1.6 mg/dl

Normal plasma magnesium is 1.5-2.3mg/dl. Infants have slightly higher plasma magnesium
concentration than older children.
Human milk contains approximately 35mg/l of magnesium formula contains 40-70mg/l of
magnesium. Small intestine is the major site of magnesium absorption.

Causes
1. Gastrointestinal disorder
Diarrhea, nasogastric suction, emesis, pancreatitis, celiac disease, cystic firbrosis, protein
calorie malnutrition, hypomagnesaemia secondary to hypocalcaemia, chronic kidney
disease.
2. Renal disorders
Acute tubular necrosis, hypocalcaemia, genetic diseases, Bartter syndrome, autosomal
recessive renal magnesemia wasting.
3. Miscellaneous causes
Poor intake, hungry bone syndrome, pancreatitis, exchange transfusion, infant of diabetic
mother, IUGR.

Transient hypomagnesaemia in newborn

Commonly seen in infants of diabetic mother due to maternal depletion from osmotic losses. Other
maternal diseases that cause magnesium losses predispose infants to hypomagnesaemia.
Hypomagnesaemia is more common in infants with intrauterine restriction.hyomagnesemia
develops in infants who require exchange transfusion because of magnesium removal in banked
blood.

Clinical manifestation
 Seizures
 Tetany
 Tremors
 Restlessness at 28 weeks of life due to severe hypomagnesemia

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  Depression
 ECG changes flattening of T waves and lengthening of ST segment
 Arrhythmias may occur

Diagnosis
 Clinical manifestation
 Serum magnesium: low serum magnesium level of < 1.6 mg/dl suggests
hypomagnesaemia.

Management
 Severe hypomagnesaemia treated with parenteral magnesium-
 Magnesium sulphate is given at dose of 25 -50 mg/kg/ 0.05-.1ml/kg og 50% solution
administered as I/V I/M in neonates. Dose is repeated every 8-12 hours in neonates.
 Exchange transfusion

Bibliography

1. Hockenberry J.Marilyn(2005)Wong’s Essentials of Pediatric Nursing, Edition -7th

Missouri: Mosby pp272-282
2. Dutta Parul(2007) Pediatric Nursing, Edition-1st New Delhi:Jaypee Brothers, pp 102-103
3. Marlow R Dorothy & Barbara .A Redding (2001).Textbook of Pediatric Nursing, Edition-
6th, Philadelphia: W.B.Saunders.pp 386-437.
4. Chloherty, Eichenwald,(2008) Manual of neonatal care,edition-6th ,Lippincott Williams &
Wilkins : Philedephia,pp540,551
5. Kleigman, Behrman,(2008),Nelson’s Textbook of Peadiatircs,Edition- 18th ,Volume 2,
Elsevier: Saunders, pp-282
6. Dr.Meharban. Singh, (2004),Care of Newborn,edition-6th ,Sagar
Publications:NewDelhi,pp-351-363

Internet
1. www.uptodate.com/patients/content/topic.do?topicKey=~M0SV9YKC...
2. www.newbornwhocc.org/pdf/Hypoglycemia.pdf
3. www.healthsystem.virginia.edu/uvahealth/peds_diabetes/hyponew.cfm
4. www.healthsystem.virginia.edu/uvahealth/peds_diabetes/hyponew.cfm
5. www.newbornwhocc.org/pdf/Hypocalcemia.pdf
6. www.healthsystem.virginia.edu/uvahealth/peds_hrnewborn/hypocal.cfm
7. www.ucsfhealth.org/childrens/health_professionals/.../48_Seizures.pdf

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