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 1. Clonic   Focal Multifocal characteristics slow rhythmic jerky movements approximately 1-3 seconds involves upper or lower extremities on one side of body.
Mainly involves neck or trunk. Infant is conscious during event.

may migrate from one part of the body to other. Movements may start at other times. extension/stiffening movements. extension of all four limbs ( similar to decerebrate rigidity) Upper limbs are maintained in a stiffy flexed position sustained posturing of limbs, Asymmetric posturing of trunk or neck. 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. rapid jerks that involve flexor muscle group.
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2. Tonic  Generalized  Focal

3. Subtle

4. Myoclonic

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

  

Focal Multifocal Generalized

involves upper extremity flexor muscle group. asynchronous twitching of several parts of the body. 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.

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

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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.
Neeta Rajesh Bhide, (M.Sc.N., M.A. Psyco., M.C.F.H., M.D.F.M. Page 3

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.

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

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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.
Neeta Rajesh Bhide, (M.Sc.N., M.A. Psyco., M.C.F.H., M.D.F.M. Page 5

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.

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

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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.

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

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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).

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

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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.
Neeta Rajesh Bhide, (M.Sc.N., M.A. Psyco., M.C.F.H., M.D.F.M. Page 9

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.

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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
Neeta Rajesh Bhide, (M.Sc.N., M.A. Psyco., M.C.F.H., M.D.F.M. Page 11

  

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, Edition6th, 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. 2. 3. 4. 5. 6. 7.

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

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