IMMEDIATE NEONATAL OUTCOMES IN EARLY TERM BIRTH IN TERTIARY CARE HOSPITAL
TIRUNELVELI MEDICAL COLLEGE AND HOSPITAL
DISSERTATION SUBMITTED TO
In partial fulfillment of the requirement for the degree of (Branch VII) M. D. (PAEDIATRIC MEDICINE)
REGISTRATION NO. : 201817358 of
THE TAMIL NADU DR. M. G. R MEDICAL UNIVERSITY CHENNAI- 600032
DEPARTMENT OF PAEDIATRIC MEDICINE TIRUNELVELI MEDICAL COLLEGE
TIRUNELVELI- 11 MAY 2020
BONAFIDE CERTIFICATE
This is to certify that the dissertation entitled “IMMEDIATE NEONATAL OUTCOMES IN EARLY TERM BIRTH IN TERTIARY CARE HOSPITAL–TIRUNELVELI MEDICAL COLLEGE AND HOSPITAL” is a bonafide original work done by Dr.T.PALANIVELRAJA, post graduate in Department of Pediatric Medicine, Tirunelveli Medical College Hospital, Tirunelveli, in partial fulfillment of the requirement for the award of M.D. Degree Branch – VII (Pediatric Medicine) under the Tamilnadu Dr. M.G.R Medical University, Chennai.
Professor &Head of the Department,
Department of Pediatric Medicine Tirunelveli Medical College,
Tirunelveli.
Unit chief
Department of Pediatric Medicine Tirunelveli Medical College,
Tirunelveli.
CERTIFICATE
This is to certify that the Dissertation “IMMEDIATE NEONATAL OUTCOMES IN EARLY TERM BIRTH IN TERTIARY CARE HOSPITAL–TIRUNELVELI MEDICAL COLLEGE AND HOSPITAL” presented herein by Dr.T.PALANIVELRAJA, is an original work done in the Department of Pediatric Medicine, Tirunelveli Medical College Hospital, Tirunelveli for the award of Degree of M.D.
(Branch VII) Pediatric Medicine Under my guidance and supervision during the academic period of 2018 -2020.
The DEAN
Tirunelveli Medical College, Tirunelveli - 627011.
DECLARATION
I solemnly declare that the dissertation titled“IMMEDIATE NEONATAL OUTCOMES IN EARLY TERM BIRTH IN TERTIARY CARE HOSPITAL–TIRUNELVELI MEDICAL COLLEGE AND HOSPITAL” is done by me at Tirunelveli Medical College Hospital, Tirunelveli, under the guidance and supervision of Prof.
Dr.C.Krishnamurthy, Professor and Head of Department of Pediatric Medicine,Tirunelveli Medical College,Tirunelveli. The dissertation is submitted to The Tamilnadu Dr.M.G.R.Medical University, Chennai towards the partial fulfilment of requirements for the award of M.D. Degree (Branch VII) in Pediatric Medicine.
Place: Tirunelveli Date:
Dr.T.PALANIVELRAJA Registration No. : 201817358
Postgraduate Student, M.D Pediatric Medicine, Department of Pediatric Medicine,
Tirunelveli Medical College Tirunelveli.
CERTIFICATE – II
This is to certify that this dissertation work titled “IMMEDIATE NEONATAL OUTCOMES IN EARLY TERM BIRTH IN TERTIARY CARE HOSPITAL–TIRUNELVELI MEDICAL COLLEGE AND HOSPITAL” of the candidate Dr.T.PALANIVELRAJA with registration Number : 201817358 for the award of M.D.,Degree in the branch of PAEDIATRIC MEDICINE (VII). I personally verified the urkund.com website for the purpose of plagiarism check. I found that the uploaded thesis file contains from introduction to conclusion page and result shows 0 %percentageof plagiarism in the dissertation.
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ACKNOWLEDGEMENT
I am grateful to our Dean Prof. Dr. S. M. Kannan M.S., M.Ch., Tirunelveli Medical College for permitting me to carry out the study and for allowing me to utilize the facilities at the hospital.
It is with a deep sense of gratitude that I acknowledge my indebtedness to my HOD and guide, Dr. C. Krishnamurthy M.D., Professor & HOD, Department of Pediatric Medicine, Tirunelveli Medical College for his guidance, valuable suggestions and constant mentoring throughout this study.
I would like to express my humble thanks to my Professors, Dr. T. R. R. Ananthy Shri M.D., Dr. A. S. Babukandhakumar, MD., DCH., DNB., M.N.A.M.S., Dr. C. Baskar M.D., DCH., Dr. R.
Padmanabhan, MD.,DCH., Dr. R. Venkata Subramanian,MD., for their constant support, encouragement and suggestion.
I express my sincere thanks to my PG registrar Dr. B. Naresh M.D., Department of Paediatrics.
I would like to thank my teachersDr. G. Jeyanthi M.D., DCH., Dr.
M. Muthuramasubramaniyan M.D., Dr. A. Maheshwari M.D.,DCH., Assistant Professors, Department of paediatrics. I thank all my friends,
postgraduate colleagues, my seniors and my dear juniors for their co- operation and help in preparing this dissertation.
I also thank all the neonates and their parents who participated in this study without whom this would not have been possible. I dedicate this work to my parents, wife, children and my family members, who have been a source of constant support and inspiration to me. And finally, I thank the almighty for giving me this opportunity.
CONTENTS
SL.NO CONTENTS PAGE.NO
1 INTRODUCTION 1-2
2 AIMS AND OBJECTIVES 3
3 REVIEW OF LITERATURE 4-43
4 MATERIAL AND METHODS 44-47
5 ANALYSIS 48
6 RESULTS 49-68
7 DISCUSSION 69-74
8 CONCLUSION 75
9 BIBLIOGRAPHY
10 ANNEXURE
I. PROFORMA II. CONSENT FORM III. MASTER CHART
LIST OF ABBREVIATIONS
1 ACOG American College of Obstetricians and Gynecologists 2 APH Antepartum haemorrhage
3 BIND Bilirubin Induced Neurological Dysfunction
4 BSA Body Surface Area
5 CFTR Cystic Fibrosis Transmembrane Conductance Regulator 6 CPAP Continuous Partial Airway Pressure
7 CPD Cephalopelvic disproportion
8 DIVC Disseminated Intravacular Coagulation 9 FRC Functional Residual Capacity
10 GA Gestational Age
11 GDM Gestational Diabetes Mellitus 12 KMC Kangaroo Mother Care
13 LSCS Lower segment Caesarean Section 14 MAS Meconium Aspiration Syndrome 15 MSAF Meconium Stained Amniotic Fluid 16 PIH Pregnancy-Induced hypertension
17 PPHN Persistent Pulmonary Hypertension of the Newborn 18 PROM Premature Rupture of Membranes
19 PVR Pulmonary Vascular Resistance 20 RDS Respiratory Distress Syndrome 21 TCB Trans Cutaneous Bilirubin
22 TTN Transient Tachypnoea of Newborn
23 VD Vaginal Delivery
LIST OF TABLES
Table 1 Sex distribution of early term babies in the study 49 Table 2 Distribution of early term babies in the study by
Gravida
51 Table 3 Distribution of early term babies in the study by
mother's age at the time of delivery
52 Table 4 Distribution of early term babies in the study by mode
of delivery
53 Table 5 Distribution of early term babies in the study by birth
weight
54 Table 6 Distribution of early term babies in the study by
gestational age
55 Table 7 Distribution of early term babies in the study by
maternal complications
56 Table 8 Prevalence of morbidity outcome (any) in early term
babies
57 Table 9 Distribution pattern of various morbidity outcome in
early term babies
58 Table 10 Distribution pattern of composite respiratory
morbidity in early term babies
60 Table 11 Distribution pattern of various morbidity outcome in
early term babies by gestation age
61 Table 12 Association of overall neonatal morbidity with Sex of
the early term babies
63 Table 13 Association of overall neonatal morbidity with
gestational age of the early term babies
64 Table 14 Association of overall neonatal morbidity with
mother’s gravidity of early term babies
65 Table 15 Association of overall neonatal morbidity with
maternal complications during early term birth
66 Table 16 Association of overall neonatal morbidity with mode
of delivery during early term birth
67 Table17 Association of Composite respiratory morbidity with
socio-clinical characteristics of early term babies
68
LIST OF FIGURES
Figure Name Page no
1 Definitions of Late Preterm and Early Term 4
2 Epithelial Na (sodium) absorption in the fetal lung near delivery
7
3 Sex Distribution of Study Subjects 50
4 Distribution of early term babies in the study by Gravida
51 5 Distribution of early term babies in the study by
mother's age at the time of delivery
52 6 Distribution of early term babies in the study by mode
of delivery
53 7 Distribution of early term babies in the study by birth
weight
54 8 Distribution of early term babies in the study by
gestational age
55 9 Distribution of early term babies in the study by
maternal complication
56 10 Prevalence of morbidity outcome (any) in early term
babies
57 11 Distribution pattern of various morbidity outcome in
early term babies
59 12 Distribution pattern of composite respiratory morbidity
in early term babies
60 13 Distribution pattern of various morbidity outcome in
early term babies by gestation age
62 14 Association of overall neonatal morbidity with sex of
the early term babies
63 15 Association of overall neonatal morbidity with
gestational age of the early term babies
64 16 Association of overall neonatal morbidity with mother’s
gravidity of early term babies
65 17 Association of overall neonatal morbidity with maternal
complications during early term birth
66 18 Association of overall neonatal morbidity with mode of
delivery during early term birth
67
1
Introduction
Early term babies are those that are delivered between 37 0/7 to 38 6/7 weeks of gestational age. Early term births are assuming importance due to their increase in number in the recent years, thereby contributing substantially to an overall decrease in gestational age at delivery.1 Though the risks associated with preterm and early term births have been recognized during the last decade, neonatal morbidity due to physiological immaturity has been studied primarily in preterm infants less than 37 weeks. As neonatal morbidity decreases with delivery at later gestation ages, babies born between 37 0/7 to 38 6/7 weeks gestation are at increased risk of morbidity when compared to babies delivered beyond 38 weeks. In fact, the category early-term was introduced to highlight the increased risk for morbidity in babies born between 37 0/7 to 38 6/7 weeks of gestation (compared with babies delivered beyond 39 weeks of gestational age) for focused intervention.2
Accumulating evidence suggests that infants born early term between 37 0/7 to 38 6/7 weeks of gestation have higher neonatal morbidity with frequent admissions and respiratory complications when compared with infants delivered beyond 39 weeks.3,4 The morbid conditions associated with early term births include transient tachypnoea of the new born, respiratory distress syndrome, hypothermia, sepsis, hypoglycaemia and
2
neonatal hyperbilirubinemia.4 These risks at birth have an influence across the life course also.1 Hence, understanding these morbidity risks among early term infants will be helpful for new-born care providers to deliver focused interventions.
Given the importance of early neonatal period which accounts for very high morbidities and mortalities (most of which are preventable), necessary interventions and strategies targeting early neonatal period (birth to <7 days) have been emphasized. Thus, it becomes crucial to understand the morbidity risks of early term births especially in their early neonatal period so that the new-born care providers can develop standard operating protocols to anticipate and manage potential morbidity during the birth hospitalization (that coincides with early neonatal period) and earlier follow-up after hospital discharge. Information on morbidity risks of early term births in their early neonatal period will also be helpful to prevent such morbidities through early anticipation and identification during the birth hospitalization. Therefore, we decided to follow up early term babies delivered between 37 0/7 to 38 6/7 weeks of gestation for the first 7 days of life (that is the early neonatal period) to study the morbidity outcome and its pattern.
3
Aims and Objectives
To study the morbidity outcome and its pattern in early term babies delivered in Tirunelveli Medical College, Tamil Nadu
4
Review of Literature
Depending upon the gestational age, newborns are classified as preterm and term.
PRETERM – newborns delivered before 36 6/7 weeks of gestation Preterm newborns are further classified as5,6 :
1. Late preterm -babies born between 34 0/7 to 36 6/7 2. Early preterm - babies born between 32 0/7 to 33 6/7 3. Very preterm - babies born less than 32 weeks
4. Extremely preterm -babies born less than 28 weeks
TERM – newborns delivered between 37 0/7 to 41 6/7 weeks of gestation Term newborns are further classified as5,6 :
1. Early term - babies born between 37 0/7 to 38 6/7 2. Full term - babies born between 39 0/7 to 41 6/7
Figure 1: Definitions of Late Preterm and Early Term
5 PATHOPHYSIOLOGY :
Respiratory
Early term infants have higher morbidity and mortality when compared to full term infants. Many early term infants have respiratory distress immediately after birth. This is defined as a sustained respiratory distress for more than two hours after birth and may be accompanied by tachypnea, retractions, nasal flaring, grunting, and need for supplemental oxygen. Early term infants have fivefold increase in risk of respiratory distress when compared to babies born between 39 to 40 weeks of gestation.
The incidence of respiratory distress significantly increased with every week of gestation less than 39 weeks. Early preterm infants have delayed transition of respiration and transient tachypnoea, the course of respiratory distress still being unpredictable. Due to their more mature appearance, the initial presentation of early term newborns may be misleading and the severity of illness may not be recognized, resulting in delay in diagnosis and treatment. Pulmonary hypertention is more likely to occur in early term infants who develop respiratory distress syndrome than infants born before 32 weeks of gestation. The reason behind this is increased smooth muscle in pulmonary vessels resulting in increase in shunt from right to left and ventilation - perfusion mismatch.
6
Early term infants have mature surfactant profile but these infants may develop respiratory distress because of the delay in clearing lung fluid.
Throughout gestation, lung secretes fluid into the alveolar spaces through chloride channels. Fluid secreted in the lung plays an important role in keeping the alveoli distended and also promotes its growth.
During delivery, lung fluid is cleared, marking the beginning of gas exchange. For effective gas exchange to occur, alveolar fluids must be cleared off and pulmonary blood flow must increase to match ventilation with perfusion.
If either of this is inadequate, there will be difficulty in the transition from fetal to neonatal life, resulting in respiratory distress.
During fetal development, many abnormalities interfere with the normal production of pulmonary fluid. These include pulmonary artery occlusion and uterine compression of the chest from chronic leaking of amniotic fluid.
7
Figure 2: Epithelial Na (sodium) absorption in the fetal lung near delivery
Na enters through the cell via alveolar type I and type II cells through amiloride sensitive epithelial Sodium channels (ENaC), both highly selective and non-selective channels and cyclic nucleotide-gated channels (Figure 2). Electroneutrality is conserved with chloride movement through CFTR (Cystic Fibrosis Transmembrane Conductance Regulator) or through chloride channels in alveolar cells. Thus increase in sodium concentration inside the cells stimulates Sodium Potassium ATPase channels in basolateral cell membrane. The net ion movement from apical surface to the interstitium leads to an osmotic gradient which inturn directs H2O transport in the same direction either by diffusion or by aquaporins.7
Although small amounts of pulmonary fluid is cleared by vaginal squeeze, amiloride sensitive sodium transport via epithelial Sodium Channels is an important event in the trans-epithelial movement of alveolar fluid.8
8
The disruption of epithelial sodium channels results in transient tachypnoea of newborn and respiratory distress syndrome.
Late preterm and some early term infants have lower expression of these channels resulting in decreased fluid clearance from the alveoli.9
Higher doses of Glucocorticoids stimulate the transcription of epithelial sodium channels and increase the available channels by decreasing its degradation and increase activity of existing channels.
And it also enhances the responsiveness to thyroid hormones and beta adrenergic agents.
Several other factors also contribute to the overall burden of respiratory problem. These include inaccurate estimation of GA , elective induction & caesarean delivery.
It is recommended to do fetal lung maturity testing before elective Lower Segment Caesarean Section deliveries but because of high risk of complications this is not done frequently. Recent studies show that early term babies born by caesarean delivery before the onset of labour have respiratory distress despite having a mature surfactant profile. ACOG recommends scheduling deliveries at 39 weeks of gestation by Caesarean.
9
Studies show that antenatal administration of steroids reduces the need for substantial respiratory support during the first 72 hours after birth, reduces respiratory morbidity and also reduces the length of stay in hospital.
Transient tachypnoea of newborn:
It is a benign, self-limited process usually and it is due to delay in clearance of fetal lung fluid. It is characterized by signs of mild respiratory distress with tachypnoea, decreased O2 saturation and resolves by providing supplementary oxygen with fraction of oxygen less than 40 percent.
During transition from fetal to neonatal life, the respiratory epithelium must switch over to absorptive mode from a secretary mode. This transition is influenced by maternal hormonal changes including surge in catecholamines and glucocorticoids, physiological changes at the end of pregnancy and during spontaneous labour.
Amiloride sensitive Sodium channels play an important role during transition phase . Adrenergic stimulation and other factors lead to passive transport of Sodium through basolateral membrane via Na+/K+ ATPase channels followed by passive movements of water and chloride through intercellular and para cellular pathways. This fluid collected into interstitial area is cleared off by the lung lymphatics and pulmonary capillaries. Delay in clearance of lung fluid results in transient edema (pulmonary edema).
10
Compression of airway by fluid leads to airway obstruction , trapping of air and ventilation perfusion mismatch resulting in reduced functional residual capacity (FRC). Risk factors for Transient tachypnea of the newborn are caesarean delivery, precipitious labour (lack of hormonal changes that accompany spontaneous labour), maternal Diabetes, macrosomia and multiple gestation.
Transient tachypnoea of newborn usually presents within 6 hours of birth with tachypnea and mild to moderate respiratory distress with nasal flaring, grunting, retraction and cyanosis and responds to supplemental oxygen therapy with Fio2 less than 40 percent. Respiratory failure and mechanical ventilation are rare.
Chest X-ray shows sun burst appearance (prominent perihilar streaking due to engorgement of lymphatics). Coarse fluffy densities may appear due to alveolar edema. Hyperinflation and widening of inter costal spaces are seen. These changes improve over 12 to 18 hours and resume after 48 to 72 hours. This resolution differentiates this entity from pneumonia and meconium aspiration.
Treatment is mainly supportive with supplemental oxygen and severe cases respond to CPAP (continuous positive airway pressure) and intravenous fluids.
11
Complications are prolonged hospital stay leading to decreased parental bonding and initiation of direct breast feeds and air leak syndrome associated with CPAP.
Respiratory distress syndrome
It is due to insufficient surfactant in pulmonary alveoli. Surfactant is a complex mixture of phospholipids and surfactant proteins that is synthesized by type II alveolar epithelial cells. Surfactant reduces surface tension in alveoli and prevents alveolar collapse. Surfactant deficiency and absence is due to developmental immaturity of type II alveolar cells, spontaneous inactivation, inactivation by inflammation, inherited mutations of surfactant proteins or lung injury resulting in high surface tension and atelectasis. Baby develops tachypnea, retractions, grunting, flaring of alae nasi and cyanosis.
Chest X-ray shows low lung volume with micro atelectasis that appear as ground glass opacities. It may also show air bronchogram highlighted by surrounding microatelectasis. Antenatal corticosteroids are effective in preventing respiratory distress syndrome.
A complete course of Dexamethasone 6mg , 12th hourly, 4 doses and Betamethasone 12mg, 24 hour apart, 2 doses are useful. Treatment is mainly CPAP (continuous partial airway pressure).
12
Neonates with good spontaneous respiratory efforts but manifesting respiratory distress should be started on nasal CPAP at 5 cm of H2O and titrated to achieve target Spo2 between 90-95%.
Continuous positive airway pressure is used to prevent the collapse of alveoli with marginal stability, thus increasing the FRC (Functional residual capacity). Continuous positive airway pressure results in recruitment of alveoli and prevents its collapse.
Components of CPAP system:
Gas source: This gives continuous source of humidified warm and blended gases (air and oxygen)
Pressure generator: To create positive pressure in the circuit. The pressure can be generated by continuous flow devices and variable flow devices.10 In continuous flow devices, desired continuous positive airway pressure is usually generated by obstruction by a valve or water column. In variable flow devices, desired CPAP level is generated by varying the flow
Patient interface: Devices used for CPAP delivery system include nasal prongs, nasal cannula and nasal mask
Common indications for Continuous positive airway pressure are Respiratory distress syndrome, Trasient tachypnoea of newborn, Apnea of
13
prematurity. Rest include post extubation states, pneumonia, meconium aspiration, pulmonary edema .
Contraindications of CPAP:
- Progressive respiratory failure with partial pressure of CO2 levels more than 60 mmHg or partial pressure of O2 less than 50
- Choanal atresia, cleft palate, trachea- esophageal fistula, congenital diaphragmatic hernia and other congenital malformation of airway - Severe cardiavascular compromise
- Air leak and poor respiratory drive not improved by continuous positive airway pressure
Monitoring during Continuous positive airway pressure:
- Heart rate, Respiratory rate, saturation and the severity of respiratory distress serially assessed by Downes or Silverman score.
- Perfusion – capillary refilling time, blood pressure, urine output and peripheral pulses
- Abdominal girth and nasal injury - Arterial blood gas analysis
Complications of CPAP ventilation
1. Local – Nasal irritation, damage to the nasal septum, nasal injury.
A scoring system is helpful to monitor the skin and septal integrity.
14
These can be prevented by the use of appropriate size nasal prongs and instillation of saline nasal drops. Adequate humidity and temperature decrease nasal injury.
2. Over distention of alveoli leads to inadequate tidal volume, hypercarbia, ventilation perfusion mismatch and poor venous return sufficient to reduce cardiac output
3. Under distention: Failure to maintain FRC results in prolonged need for O2
4. Gastric distention leads to CPAP Belly syndrome. These can be prevented by routine orogastric tube insertion.
5. Air leak11
Initial settings for CPAP will be pressure of 5 cm of H2O and Fi O2 of 40 to 50 %. If there is no improvement, increase the pressure upto 7 to 8 H2O and increase the pressure upto a maximum of 60%
Failure of CPAP: Worsening of respiratory distress and/or hypoxemia, hypercarbia despite CPAP pressure of 7 to 8 cm and Fio2 of maximum 50- 60%
Weaning from CPAP: When there is no respiratory distress and saturation is normal, reduce FiO2 in steps of 5-10% ,then decrease the pressure in steps of 1-2 cm of H2O until 3-4 cm of H2O. If FiO2 requirements exceed 40%
early rescue surfactant therapy by INSURE technique is indicated.
15
Also intubation and mechanical ventilation can be considered when there is hypercapnia, partial pressure of CO2 more than 60mm Hg, acidosis, decreased respiratory drive or if surfactant replacement is planned.
Meconium aspiration syndrome
Hypoxia either acute or chronic and infections may result in passage of meconium in utero. In this condition, gasping respiration of fetus or newborn babies can cause aspiration of meconium stained aminiotic fluid.
The incidence of MSAF is 10-15% of deliveries. Most babies with meconium aspiration are those that are delivered beyond 37 weeks of gestation. 3-4% of babies with Meconium stained amniotic fluid (MSAF) can develop meconium aspiration syndrome. Of this thirty to fifty percent of infants need continuous positive airway pressure and mechanical ventilation.
Meconium is a sterile, thick, greenish black, odourless material that results from accumulation of debris in the fetal intestine. Components are water 70-80%, desquamated cells from the intestinal tract, intestinal secretions, lanugo hair and vernix caseosa.
Fetal stress, gasping respiration at term before, during or immediately after delivery result in meconium aspiration. It causes chemical pneumonitis and obstructs the airways like ball & valve mechanism resulting in air
16
trapping and air leakage. Meconium induces release of cytokines and vasoactive substances.
Aspirated meconium leads to vasospasm and pulmonary arterial muscle hypertrophy that results in pulmonary hypertension. One third of newborns with meconium aspiration syndrome develop persistent pulmonary hypertension of newborn.
Steroid component and enzymatic activity of meconium disrupts the surfactant and results in surfactant deficiency.
For vigorous newborns delivered with meconium stained amniotic fluid, routine oro-nasal and endotracheal suctioning is not advised. For non- vigorous babies, entotracheal suctioning was done earlier. Now there is lack of evidence to support this intervention in improving neuro developmental and respiratory outcomes. Thus, this procedure is no longer recommended.
Management is mainly supportive by oxygen therapy. CPAP ventilation may be used but there is a chance of air trapping and hyperinflation.
Mechanical ventilation is indicated when partial pressure of carbondioxide is more than 60 mmHg or partial pressure of oxygen is less than 50 mm Hg.
17
In these infants, mechanical ventilator settings needed higher tidal volumes and high peak inspiratory pressures, approximately 30-35cmH2o, and peak end expiratory pressure usually of 4-6cm H2o. These settings provide adequate expiratory time to prevent air trapping. Usually start with 20-24 breaths / min and inspiratory time of 0.4 to 0.5 seconds. ECMO may be need for babies with refractory respiratory failure.
Hypoglycaemia
Hypoglycaemia is defined as blood glucose level of less than 45 mg/dl. It is often missed in late preterm and early term infants due to early admission to the well-baby care or transfer to mother’s room in order to establish early bonding.
Developmental immaturity leads to various problems, including feeding difficulties and decreased glycogen stores.
Another cause of hypoglycaemia is antenatal steroid administration leading to maternal hyperglycaemia.12 Severe hypoglycaemia leads to adverse neuro-developmental outcomes.13
Early recognition and treatment is more important in neurodevelopmental outcomes and long-term outcome of infants. Standard glucose screening for high risk infants (i.e, Large for gestational age, infant of Diabetic mother and small for gestational age babies) is mandatory.
18
Hypoglycaemia does not occur in utero, because of constant supply of glucose from mother via the placenta. After delivery of the baby, glucose supply abruptly stops. The newborn depends on hepatic gluconeogenesis and glycogenolysis. The uprise of catecholamines, corticosteroids, glucagon and decrease in insulin secretion, plays an important role in maintaining euglycaemia.
The demand increases when baby has associated sepsis, cold stress and birth asphyxia, placing them at a higher risk of hypoglycaemia.
Treatment in early term is based on the underlying cause of hypoglycaemia and correcting it along with symptomatic management.
Time schedule for screening
There is paucity of data regarding the optimal timing and interval of glucose monitoring.
Lowest Blood glucose levels are seen at 2 hours of life. Infants of diabetic mother frequently experience asymptomatic hypoglycaemia very early viz, 1 to 2 hours of life.
Late preterm and early term infants may develop hypoglycaemia when feeding is not established.
19
For at risk infants, the interval of monitoring is as follows - 2,6,12,24,48,72 hours of life. 72-hour monitoring can be omitted if feeding has been established well.
Parents should be counselled regarding the symptoms and risk of hypoglycaemia in their infants and the need for optimal feeding and blood testing at regular intervals.
Methods of Blood glucose estimation
Reagent strips using Glucose oxidase method is widely used for glucose estimation. They are mainly used for screening purposes. When blood glucose levels are less than 40 and 45, values should be confirmed by laboratory testing. Treatment should be started before laboratory results arrive.
It is important to consider variations between capillary, blood, plasma and stored samples. Whole blood sugar values are 15% less than that of plasma. And blood glucose values fall by 14-18 mg/dl per hour in samples that await analysis.
Signs & Symptoms of hypoglycaemia: A greater proportion of babies are asymptomatic. Only a smaller proportion of babies develop symptomatic hypoglycaemia.
20
Signs & symptoms of hypoglycemia are classified into Neuroglycopenic and neurogenic. Neurogenic symptoms occur due to autonomic discharges triggered by hypoglycaemia and include both adrenergic and cholinergic responses. Neuroglycopenic symptoms are due to decreased supply of glucose to brain cells.
For the treatment of asymptomatic hypoglycaemia, direct breast feeding is the best option as it promotes ketogenesis. Ketones are alternative fuels to the brain.
For all symptomatic infants, a bolus of 2 ml per kg of 10% glucose (200mg per kg) should be given. Followed by a rapid bolus, start infusion of glucose at an initial rate of 6mg/kg/min. Recheck blood glucose after 30 mins and then every 6 hours till blood glucose levels are greater than 50mg/dl.
If blood glucose levels are less than 50/mg/dl, glucose infusion rate should be increased in steps of 2mg/kg/min every 15-30 mins until a maximum of 12 mg/kg/min.
If blood glucose value is>50mg/dl, the infusion is tapered off at a rate of 2mg/kg/min. Once glucose infusion rate reaches 4mg/kg/min and blood glucose levels are consistently more than 50 and oral intake is adequate, infusion can be stopped.
21
When glucose concentration is more than 12.5%, central venous access is needed because of risk of thrombophlebitis in peripheral vein.
If infants fail to maintain blood glucose levels within normal limits despite a maximum of 12mg/kg/min or stabilization is not achieved after 7 days of treatment, consider resistant (or) recurrent hypoglycaemia.
Hyperbilirubinemia
In late preterm and early term newborns, it is the most common condition requiring admission. It is also the most common cause of readmission in first week of postnatal life.14
Neonatal hyperbilirubinemia in early term and late preterm is more prevalent and more pronounced than late term infants. The reason for increased bilirubin is due to immature metabolic pathways for bilirubin and immature gastrointestinal motility and function.
Late preterm and some early term infants have increased risk of developing Kernicterus when compared to term infants.15
Kernicterus is a chronic, disabling and devastating condition characterized by neural hearing loss, choreoathetoid cerebral palsy, vertical gaze palsy and dental enamel abnormalities.16
AAP recommends universal pre-discharge measurement of hyperbilirubinemia either by blood sampling or by transcutaneous
22
bilirubinometer. This likely prevents severe hyperbilirubinemia by early phototherapy.
This finding emphasises close monitoring of early term and late preterm babies, in particular the babies of mothers who do not adequately breastfeed. Early discharges are not advisable until proper feeding is established.
Jaundice in neonates is visible in eyes and skin when total serum bilirubin is 5 to 7mg/dl. Increased Bilirubin results from increased production from degraded RBC, decreased clearance by the immature hepatic mechanism and reabsorption by enterohepatic circulation. High bilirubin causes BIND (Bilirubin induced neurological dysfunction).
Physiological jaundice is due to physiological immaturity to handle increased bilirubin production. In early term and late preterm babies, peak level occurs between 3 to 7 days of age whereas in term infant, peak level is on day 3 of age.
Pathological jaundice is considered when visible jaundice occurs in the first 24 hours of life and serum bilirubin rises by more than 0.2 mg/dl/hour or more than 5 mg/dl in 24 hours, if serum bilirubin levels are more than 95th percentile as per age specific bilirubin normogram, signs of bilirubin encephalopathy, clinical jaundice persisting beyond 3 weeks in preterm and 2 weeks in term are present.
23
Visual inspection of jaundice is done by examining the baby without clothing in bright natural light and in absence of yellow background.
Neonates at higher risk of hyperbilirubinemia should be identified at birth and kept under enhanced surveillance for occurrence and progression of jaundice.
Inadequacy of breast feeding is a common cause of exaggerated jaundice during initial few days. Breast feeding problems such as improper positioning and attachment, cracked or sore nipple and engorgement result in reduced milk transfer to the baby, thereby enhancing enterohepatic circulation and increased serum bilirubin.
Multiple counselling is needed to educate the mother regarding positioning and attachment and adequate measures need to be taken to address breast feeding problems in mother.
Measurement of serum bilirubin by transcutaneous bilirubinometry reduces the need for venous sampling by 30%. Transcutaneous bilirubinometry is not reliable in infants less than 35 weeks of gestation, during initial 24 hours of life, TCB more than 15 mg/dl and babies under phototherapy.
TCB value more than 12 to 14 mg/dl should be confirmed by total serum bilirubin.
24
Methods to measure total serum bilirubin include Vandinbergh reaction and by high performance liquid chromatography (HPLC).
Therapeutic options for jaundice in neonates are phototherapy, IV hydration, exchange transfusion and intravenous immunoglobulin.
Phototherapy converts insoluble bilirubin to soluble isomers that are excreted by urine and feces.
Types of phototherapy are compact fluorescence lamps, high intensity LED and fibreoptic units.
For magnifying the efficiency of phototherapy, the irradiance of phototherapy units should be measured periodically to maintain a minimum level of 30μw/cm2/nm in a wavelength of 460-490 nm. Cover the eyes and genitals by diaper. Maintain a distance of 30-45 cm between the baby and light and ensure optimum breast feeding.
Monitor temperature every 2 to 4 hours. Measure total serum bilirubin every 12 to 24 hours. Discontinue phototherapy if serum bilirubin falls by 2 below the age specific cut offs.
Exchange transfusion is indicated when total serum bilirubin levels exceed age specific cut off or infant shows signs of bilirubin encephalopathy.
25
Intravenous Immunoglobulin reduces hemolysis and thereby reduces hyperbilirubinemia in Rh iso-immunisation and ABO incompatibility.
Nutrition:
Feeding problems is one of the primary reasons for delay in the discharge of late preterm and early term infants from hospital. Late preterm and early term infants often have poor coordination of sucking and swallowing due to neuronal immaturity, decreased oromotor tone and inability to generate adequate intraoral pressures during sucking.17
Breastfeeding is also difficult for early term or late preterm infants compared to full-term infants. These problems can lead to dehydration and poor caloric intake. These problems are combined by the differences in practice and nutritional management of these infants, given the paucity of established guidelines. Studies have shown that issues such as poor feeding and hypoglycemia contributed to early term and late preterm babies requiring intravenous (IV) fluids, compared with only 5% of their full-term counterparts. In the view of poor enteral intake, parenteral nutrition may be indicated. It also forms an important therapy in the care of early term and late preterm infant but is often delayed in anticipation of a quick recovery.18 The challenge is then providing adequate nutrition to support growth and also equating the energy expenditure that can occur when the infant faces issues such as hypothermia, sepsis, and respiratory distress, which are often
26
seen in late preterm and early term infants. The energy expenditure of nongrowing low birth weight infants (birth weight less than 2500 g) is 45 to 55 cal/kg per day. These calories are derived from various sources in parenteral nutrition, including lipids and amino acids.18
Late preterm and early term infants soon adapt at handling amino acids, thus permitting the protein content in parenteral nutrition to be started at 2 g/kg per day. With a protein intake of 2.5 to 3 g/kg per day (with adequate caloric intake), a late preterm infant will be able to gain weight similar to that of a human milk fed full-term infant . More controversial is the use of IV lipids in late preterm infants. Of the late preterm and early term infants with respiratory distress , there are two subgroups (1) those with signs of PPHN or increased PVR (2) infants with parenchymal lung disease without increased PVR. The main issue over the use of lipids in the late preterm and early term infant with lung disease is that adult studies have showed failure to clear infused lipids with resultant adverse effects on gas exchange in the lungs. Contrary to the above findings, preterm neonates randomized to different lipid infusion rates did not have any effect on alveolar–arterial oxygen gradient, arterial blood pH, or oxygenation when randomly assigned to modest doses of lipids (0.6 to1.4 g/kg per day) in the first week of life.18 Thus the recommendation is that infants with respiratory disease, but not increased pulmonary vascular resistance, should receive adequate
27
amounts of lipids to prevent fatty acid deficiency.In infants with elements of PPHN , administration of lipids during the critical phase of their illness should be avoided.
Infections
Due to their immunological immaturity, early term infants are more prone for infections. Depending on the onset, infections are categorized as congenital, early onset and late onset sepsis.
Congenital infections are acquired before delivery, early onset sepsis is acquired at the time of delivery and late onset sepsis is often acquired from the hospital and manifest after 72 hours of life.
Congenital infections include Rubella, Herpes simplex virus and Human Immunodeficiency virus. The severity depends upon the time at which the infection occurred. In Herpes simplex and HIV (Human immunodeficiency virus), maternal to fetal transmission more commonly occurs at the time of delivery. A high viral load is important for transmission of Human immunodeficiency virus.19
In early onset sepsis, maternal vaginal colonization of group -B- Streptococcus, E.coli and Candida are the main causes. Additional risks factors are prolonged chorioamnionitis, prolonged rupture of membranes (more than 18 hours) and maternal fever.20
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Late onset sepsis is mainly due to nosocomial infections like Staphylococci, Enterococci and Candida species. Although mortality is low in early term infants, it prolongs hospital stay and increases complications.
Sepsis screening in high risk infants and neonates presenting with respiratory distress, hypothermia, hypoglycaemia will be helpful for management.
Early neonatal sepsis is a clinical syndrome characterized by signs and symptoms of infection with or without associated bacteremia. It encompasses systemic infections such as septicemia, pneumonia, arthritis, meningitis urinary tract infection and osteomyelitis.
In early onset sepsis, neonates present with respiratory distress and pneumonia. The source of infection is usually from maternal genital tract.
Maternal conditions that increase the risk of early onset sepsis are 1) Rupture of membrane>18 hours
2) Single unclean or three sterile pervaginal examinations during labour
3) Foul swelling liquor 4) Prolonged labour
5) Spontaneous prematurity
6) Perinatal asphyxia /APGAR score (<4 at 1 min)
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If neonates have 2 risk factors, it warrants sepsis screening. Foul smelling liquor or 3 or more risk factors warrant antibiotics. If sepsis screening is negative but there is a high suspicion of sepsis, repeat sepsis screening after 12 to 24 hours.
Late onset sepsis manifests after 72 hours. It can be hospital acquired or community acquired. It presents with meningitis or pneumonia or sepsis.
Factors that predispose to an increased risk of nosocomial infections are admission in intensive care unit, prematurity, mechanical ventilation, invasive procedures, administration of intravenous fluids and use of stock solutions.
Factors that are associated with community acquired late onset sepsis are poor hygiene, bottle feeding, poor cord care and prelacteal feeds.
Clinical signs and symptoms of sepsis include hypothermia (or) hyperthermia, lethargy, refusal of feeds prolonged capillary refilling time, bradycardia/tachycardia, respiratory distress/apnea, hypoglycemia and metabolic acidosis. Specific signs related to various systems are :
Central nervous system: Bulging anterior fontanelle, irritability, seizure
Cardio vascular system: Hypotension, poor perfusion
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Gastrointestinal system: Feed intolerance, abdominal distention, vomiting, paralytic ileus.
Hepatic: Hepatomegaly, direct hyperbilirubinemia Haematological: Bleeding, purpura, petechiae
Skin changes: Multiple pustules, umbilical redness & discharge sclerema, abscess
Renal: Acute Kidney injury Investigations
Sepsis screening: All infants suspected to have sepsis should have sepsis screen: These include
1) Absolute neutrophil count<1800 cells/μL 2) Immature to total neutrophil more than 0.2
3) Micro Erythrocyte sedimentation rate more than 15 mm.
4) C-reative protein more than 1mg/dl
It two or more parameters are abnormal, it is considered as a positive screen and neonate should be started on antibiotics. Blood culture is the gold standard for diagnosis of sepsis.
Procalcitonin is a prohormone that is produced by thyroid C cells as precursor of calcitonin. It is an acute phase reactant protein secreted by various stimuli such as cytokines and lipopolysaccharide that act as a chemo
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attractant on blood monocytes. However, if clearly stated there is a need for further studies for evaluating cut offs for early onset/late onset sepsis.
Lumber puncture should be done if meningitis is suspected. The clinical feature for sepsis and meningitis often overlap.
Management of sepsis is mainly supportive along with antimicrobial therapy. Baby should be kept in thermoneutral environment. O2 saturation to be maintained within normal range. If baby is hemodynamically unstable, volume expansion with intravenous crystalloids and inotropes are essential to maintain blood pressure and tissue perfusion.
Indications for starting antibiotics:
The indications for starting antibiotics in neonates at risk of early onset sepsis include any one of the following:
(a) Strong clinical suspicion of sepsis.
(b) Presence of <= 2 risk factor (s) and a positive septic (c) Presence of >=3 risk factors for early onset sepsis and (d) Presence of foul smelling liquor
The indications for starting antibiotics in late onset sepsis include:
(a) Positive septic screen and / or (b) Strong clinical suspicion of sepsis
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Choice of antibiotics: Empirical antibiotic therapy should be specific and determined by the prevalent spectrum of etiological agents and their antibiotic sensitivity pattern. Antibiotics once started should be modified according to the sensitivity reports.
Thermoregulation
Compared to term infants, early term infants are susceptible to hypothermia. It is difficult to assess if baby is sent to mother’s room or infant is not observed closely.
Before birth, the baby is warm and well insulated in the aqueous uterine environment. Fetal temperature is slightly higher than the maternal temperature with a gradient of heat flow from the fetus to the mother.
From this environment, baby comes out naked and wet in the labour room environment, which is maintained at a temperature range for the comfort of the mother, which might not be suitable for newborn’s metabolic needs.
Infant loses heat by
1. Evaporation 2. Radiation 3. Conduction 4. Convection
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Babies respond to cold by muscular activity and metabolic thermogenesis. When baby is exposed to cold, baby cries and makes some movement of limbs but the effort is not sustained.
Non-shivering thermogenesis, as a result of metabolism of the brown adipose tissue, is the important source of heat production in the newborn.
It is distributed at the nape of the neck, interscapular region, axilla, groin, around kidneys and adrenals.
The quantity of brown adipose tissue is directly related to gestational age and birth weight. Brown adipose tissue is characterized by a round nucleus with granular cytoplasm and large number of mitochondria and fat globules.
The brown adipose cells have increased vascularity and rich supply of nerve fibers. The stimulus for activation is cold and their main function is heat production, while white adipose tissue has poor vascularity and very few nerve fibre & mitochondria.The main stimulus for activation is starvation and their function is nutrition.
When the skin of the baby becomes cold, afferents reach the heat regulating centre in the pre-optic anterior hypothalamic VMN (Ventro Medial Nucleus) area near third ventricle and neurogenic efferents, reaching the brown fat releases nor adrenaline leading to oxidation of triglyceride
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into glycerol and fatty acid. Around 30% of non-esterified fatty acids are locally consumed for generation of heat and 10% released into the circulation, 60% are re esterified
The areas of brown adipose tissue become warm and heat is distributed throughout the body via blood stream. Baby needs extra oxygen and glucose for this process.
The narrow range of environmental temperature at which a baby can maintain normal body temperature with minimal oxygen is called thermoneutral temperature. This is the ideal temperature at which babies should be nursed to achieve optimal somatic and brain growth.
Hypothermia is defined as a skin temperature less than 36.5ºC or core temperature less than 36.0ºC.
Causes for heat loss:
Cold environment
Wet or naked baby
Cold linen
During transport and various procedures
Low humidity leads to evaporative heat loss
Increased airflow currents lead to convective heat losses
35 Poor ability to conserve heat loss are due to
Relatively large surface area
Poor insulation
Paucity of fat
Poor muscle tone and inability to assume flexed posture to reduce the effective body surface area.
Severity of Hypothermia
Cold stress has a core temperature between 36.0 and 36.5ºC. The difference between core and peripheral temperature is more than 1.5ºC.
Despite adequate feeding and being free from infection, these babies have poor growth velocity because glucose is wasted for thermogenesis.
Moderate hypothermia is diagnosed when core temperature is between 30.0 and 35.9ºC
Severe hypothermia is designated as core temperature less than 32.0ºC
Clinical manifestations of hypothermia: Initially babies are uncomfortable restless and cry to generate heat by muscular activity. And when unattended at this stage, neonates become sluggish and inactive and skin becomes cold and mottled due to vasoconstriction. All vital functions are depressed and there is bradycardia, shallow breathing, apnea and
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hypotension. Immunological dysfunction leads to infections, septicemia, sclerema and DIVC.
Hypothermic babies are more vulnerable to develop bilirubin encephalopathy due to elevation of free fatty acid and acidemia.
Prevention of hypothermia
The goal of care is to maintain temperature between 36.8 to37.3ºC The following guidelines and recommendations should be implemented to prevent hypothermia
High risk mother should be identified during antenatal period and referred to higher centre for good obstetrical care and neonatal care
If baby cried after birth, baby should be placed on mothers abdomen .Dry the baby using warm blanket and cut the cord after 1-2 minutes and facilitate breast crawl. Place the baby between mothers breasts.
The delivery room temperature should be maintained between 28ºC ± 2ºC. The warmer should be pre-warmed before delivery for at least 20 to 30 minutes
Baby should be effectively covered with cap, socks and mittens
Whatever comes in close contact with the baby should be prewarmed.
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Take special care to prevent hypothermia during procedures and transport.
Application of oil and liquid paraffin can reduce evaporation and heat loss from skin
Skin to skin contact provides excellent source of biologically controlled heat. Apart from providing warmth it promotes breast feeding and bonding
The mothers and health care workers should be provided adequate knowledge and skills for assessment of baby’s temperature and prevention of hypothermia
Kangaroo mother care is mainly for preterm and low birth weight babies.
Physiological benefits of KMC:
Infant and mother bonding
Stability of vital signs with effective temperature control and reduced risk of apneic attacks
Promotion of breastfeeding with improved secretion of milk
Babies sleep better, cry less and have better neuro-behavioural outcomes
Adequate weight gain and reduction in the hospital stay
38 Management of hypothermia
The baby should be immediately transferred to an incubator and slowly warmed to achieve the normal core temperature in 4 to 6 hours.
Hypoglcemia and hypoxia should be prevented by giving adequate oxygen support and intravenous glucose. Antibiotics are administered after taking blood culture sensitivity.
Late preterm and early term infants are susceptible to thermal instability due to their immaturity in thermoregulation, which is dependent on white and brown adipose tissue and on BSA (Body Surface Area).
Late preterm and some early term infants have decreased brown adipose tissue stores and hormones responsible for brown adipose tissue metabolism are less.
Late preterm and early term infants are relatively smaller in size when compared to term infants and it leads to increased body surface area resulting in hypothermia.
Appropriate monitoring and triaging is important in these infants, who are susceptible to temperature instability. This can avoid unnecessary workups, interventions and decrease morbidity and prolonged hospitalization.
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Fetal lungs and brain are among the last to develop and are more prone for injury. Even healthy late preterm and early term newborns are at risk of delayed milestones (developmental delay) through first five years of life.
During the last few weeks of GA, many aspects of brain maturity is still incomplete. These are increasing neuronal arborization and maturation of oligodendroglia. Neurotransmitter system maturation and continued growth of the brain occur during final few weeks of gestation.21
The brain of early term and late preterm is still immature and can grow until 2 years of age when it reaches 80% of adult brain. The cortex is still smooth and gyri & sulci are not fully formed. Inter-neuronal connectivity and myelination are still incomplete.
Discharge Criteria
Because of high risk of morbidities and complications in late preterm and early term infants they should not be discharged before 48 hours from birth.
During the hospital stay, baby should be monitored for vital signs such as heart rate of 100 to 160/beats/per minute, respiratory rate less than 60/min and temperature below 36.5ºC to 37.5ºC with appropriate clothing.
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Adequate urine output, passage of one stool spontaneously and successful feeding with adequate coordination of sucking & swallowing and respiration during feeding should be established.
Weight loss should not exceed 7% in first 48 hours or more than 3%
per day.
Transcutaneous bilirubin level check >12 will warrant serum bilirubin levels.
HBV vaccine should be given or an appointment should be made for its administration.
Patient should be educated for umbilical cord care and skin care. And educate about signs & symptoms of sickness.
Post discharge medical care should be arranged, with a follow-up visit scheduled at 24-48 hours after discharge. A home visit by a village health nurse in the first 72 hours after discharge is also encouraged. If the infant is discharged after about 7 days of age or longer and has met all discharge criteria and all medical issues are resolved, a follow up visit within 7 days of discharge may be recommended.22
Follow-Up After Discharge
After hospital discharge, the newborn baby receives most of the medical care in two main settings: the primary care physician’s office and
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the emergency department. To avoid fragmented care by multiple emergency department visits and to allow an early assessment of the baby, it is recommended that the late preterm and early term babies should be brought for a check-up to the paediatrician within 24 to 48 hours after discharge from the hospital.
In addition, these infants should be assessed frequently to ensure that all milestones are achieved appropriately because of the risk of developmental delay in these babies and that early intervention is in place, if needed, which includes physical therapy, occupational therapy, speech therapy. Early developmental testing can also be useful in determining any cognitive delays, which can then be addressed with individualized educational programs.
The late preterm and early term infants are susceptible to many of the problems of smaller preterm infants. Because of the multiple factors discussed in our study, close monitoring and intense management provided to smaller premature infants are often lacking in early term neonates. In addition, the discharge criteria is more lenient, which sets them (and their parents) up for failure and eventually full-term infants; early, late, and post- neonatal mortality rates were six-fold, three-fold, and two-fold higher respectively. The relative risk of death increased for every decreasing week of less than 40 weeks gestational week. The mortality rate is 30% higher
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even for infants born between 37 and 39 weeks’ gestation (early term).
These emphasize the fact that infants born just a few weeks early are at much greater risk of morbidity and death than those born at full term gestation.
Perinatologists argue that this reduction in fetal demise is directly related to close monitoring of the fetus and early intervention (delivery) when needed.
Recommendations
Admission Criteria: With many deliveries taking place and healthcare teams might not always be equipped to assess and manage the needs of a late preterm and early term infants, it becomes increasingly important to establish measures for the screening, identification, and appropriate triaging of these patients. Hence recommendation for the care of late preterm and early term newborn is essential. On the basis of these guidelines and the potential complications associated with late preterm and early term infants, it is recommended that all infants born before 35 weeks’ gestation and/or weighing less than 2300 g should be admitted to a transitional newborn unit where the infant can be monitored closely until there has been adequate time to assess the baby’s vital signs, feeding abilities, and thermoregulation, among other issues, before the baby is sent to the mother’s room. Neonates becoming sick who require intensive care obviously will need to receive higher levels of care. In addition, each nursery should establish their
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guidelines for the frequency of monitoring vital signs, sepsis assessment and antibiotics usage, and the use of supplemental oxygen. It is also important to determine a threshold (based on comfort level, staff training, and available resources) for transferring the newborn to a tertiary care center when the disease process associated with the late preterm and early term infant continues to progress or worsen.
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Materials And Methods
Study Design:
A prospective observational cohort study Study setting:
Hospital-based Study Site:
The study was conducted in Tirunelveli Medical College. The SNCU attached to the Department of Paediatric Medicine in Tirunelveli Medical College is the nodal centre for neonatal care for the entire south Tamil Nadu beyond Madurai. The department has a busy neonatal care unit with more than 80 neonates under care per day
Study period:
October 2018 - September 2019 (12 months) Study subjects:
All inborn babies delivered between 37 0/7 and 38 6/7 weeks of gestation at Tirunelveli Medical College were included in the study.
45 Inclusion criteria:
All new-born babies born between 37 0/7 to 38 6/7 weeks of gestation in Tirunelveli Medical College and whose parents gave informed consent were enrolled for the study.
Exclusion criteria:
1) Babies with Congenital Heart disease 2) Babies with other congenital anomalies Sample size and sampling:
All the consecutively born babies delivered in Tirunelveli Medical College Hospital satisfying the inclusion criteria were enrolled in the study.
A final total of 197 early term live born babies delivered in Tirunelveli Medical College with 7-days follow-up data were included for final analysis.
Study variables:
The following study variables were included and monitored in the present study:
46 1) Gravida
2) Gestational age 3) Mode of delivery 4) Sex
5) Birth weight
6) Need for initial resuscitation
7) Difficulty in initiating breast feeding 8) Hypoglycemia
9) Hypothermia 10) Neonatal jaundice
11) Transient tachypnea of newborn (TTN) 12) Respiratory distress syndrome (RDS) 13) Birth asphyxia
14) Meconium aspiration syndrome (MAS) 15) Sepsis
All the study variables were defined and recorded as per the Department’s standard operating protocol.
47 Methods and Data collection:
This study was approved by the ethical committee of Tirunelveli Medical College. Informed consent was obtained from the parents of study subjects before enrollment. A pre-structured proforma was used to collect information on the study variables. Data on birth order, gestational age, sex, mode of delivery, need for initial resuscitation and difficulty in initiating breast feeding were obtained from hospital records followed by confirmation form mothers (wherever applicable and possible).
Data on parameters like need for initial resuscitation, difficulty in initiating breast feeding, Hypoglycaemia, Hypothermia, Icterus, Transient tachypnoea of newborn, Respiratory distress syndrome, Birth asphyxia, Meconium aspiration syndrome and Sepsis were obtained from postnatal follow up assessment that were recorded for 7 days.
Those early term new-born babies who were discharged before 7 days were called for follow up assessment in the well-baby clinic on 7th day of life. For those parents who could not turn up on 7th day of follow up, an attempt was made to contact them through the telephone to enquire about the status of the baby.
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Data Analysis
Data were entered into Microsoft Excel Vers.15 (2013) and analyzed using STATA 11.0 (Statacorp LP, College Station, TX 77845, USA).
Descriptive statistics was used to summarize the study variables and describe the sample characteristics.
Study outcome variables like difficulty in initiating breast feeding, Hypoglycaemia, Hypothermia, Icterus, Transient tachypnoea of newborn, Respiratory distress syndrome, Birth asphyxia, Meconium aspiration syndrome and Sepsis were dichotomised as “present” or “absent”. The overall morbidity was defined as a dichotomous variable with present indicating presence of any of the above-mentioned outcome variable and absent indicating absence of all of the above-mentioned variable.
Socio-demographic and clinical characteristics, and overall morbidity (immediate outcome) were computed as proportions for categorical variables and median and Interquartile range for continuous variables. The pattern of morbidity outcome was assessed using relative proportional distribution of the outcome variables.
Chi-square test was used to assess the distribution of overall morbidity with Socio-demographic characteristics. P<0.05 was considered as statistically significant.
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Results
Of the 214 early-term births enrolled for the present study, 197 early- term births had completed data on 7-days follow up. parents of 17 early- term births who ere discharged before 7 days did not turn up for 7th day follow up and they could not be contacted through telephone even after two attempts. Thus, the overall response rate is 92.06%.
Socio-clinical Characteristics of study subjects
Table 1 shows the sex distribution of study subjects. Among 197 early-term births in the study, majority of them were boy babies (52.28%).
The girl babies in the study were 47.72% (Figure 3).
Table 1: Sex distribution of early term babies in the study
Sex Frequency Percentage (%)
Boy 103 52.28
Girl 94 47.72
Total 197 100
