UNIVERSITY OF MEDICINE AND PHARMACY OF TÂRGU – MUREȘ Differences in neonatal outcomes among preterm neonates born in a level III maternity unit… [603919]

UNIVERSITY OF MEDICINE AND PHARMACY OF
TÂRGU – MUREȘ

Differences in neonatal outcomes among preterm
neonates born in a level III maternity unit versus referrals

Scientific advisor : Professor Pușcașiu Lucian,MD
Student: [anonimizat]

2018

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CONTENTS

INTRODUCTION …………………………………………………………… ……………. 4
CHAPTER I. – GENERAL PART ……………………………… …………… …………… 5
I.1. Epidemiology ………………………………….……………………………………. 5
I.2. Causes of premature birth …………………………………………………………… 5
I.2.1. Premature labor ……………………………………………………………….. 5
I.2.2. Preeclampsia ………………………………………………………………….. 5
I.2.3. P remature rupture of membrane ……………………………………………… 6
I.3.4. Transverse position …………………………………………………………… 6
I.2.5. Placenta previa ………………………………………………………………… 7
I.2.6. Placenta abruption ……………………………………………………………. 7
I.3. Neonatal outcome ……………………………………………………………………. 7
I.3.1. Premature lung ………………………………………………………………… 7
I.3.2. Respiratory distress syndrome ………………………………………………… 8
I.3.3. Bronchopulmonary dysplasia ………………………………………………… 9
I.3.4. Intraventicular hemorrhage …………………………………………………… 9
I.3.5. Patent ductus arteriosus ………………………………………………………. 10
I.3.6. Necrotizing enterocolitis ……………………………………………………… 10
I.3.7. Hypothermia ………………………………………………………………….. 11
I.3.8. Retinopathy of prematurity …………………………………………………… 11
I.4. Treatment…………………………………………………………………………….. 11
I.4.1. Delivery room intervention …………………………………………………… 11
I.4.2. Corticosteroids ………………………………………………………………… 11
I.4.3. Surfactant ……………………………………………………………………… 12
I.4.3.1. Combination of corticosteroids and surfactant ……………………………… 13
I.4.4. Ventilation ……………………………………………………………………. 13
I.4.4.1 Continues positive airway pressure …………………………………………… 13
I.4.4.2. Intermittent positive pressure ventilation …………………………………… 14
I.4.4.3. Endotracheal intubation ………………………………………………………. 14

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CHAPTER II. – THE PERSONAL CONTRIBUTION………………… …………… ……. 16
II.1. Introduction ……………………………………………………… …………… …… 16
II.1.1. Choosing the topic . ……………………………………… …………… ……… 16
II.1.2. Hypothesis ………………………… ……………………… …………….. …… 16
II.2. Material and methods …………………………………………… ……………. …… 16
II.2.1. Study population …………………………………………… ……………. …… 17
II.2.2. Statistical analyses ……………………………………… ……………. ……… 18
II.3. Result ……… ……………………………………….………… …………… ……… 18
II.4. Discussion ……………………………………………………… …………… ……. 31
II.4.1 Interpretation of the results ………………………………………………… …….. 31
II.4.2. Confirmation of hypothesis ………………………………………………… ……. 32
II.4.3. Improvement of the study or for future studies …………………………….…… 33
II.5. Conclusion ……………………………………………………… ……………… ….. 33
BIBLIOGRAPHY …………………………………………………………..……………… 35

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INTRODUCTION

The main goal of this study analysis was to evaluate neonatal care admission to hospital
type (tertiary neonatal intensive care unit and pediatric hospitals – facility and referral ) in
Romania. Determination of neonatal outcome with administrat ion of antenatal corticosteroid to
mothers in prior to delivery and type of delivery (vaginal or cesarean section) in association with
morbidity and mortality up to 28 days of life, by using neonat es charts to collect the data. The
study also included the differences between inborn and outborn that were administrated
surfactant with CPAP or intubation and outc omes of neonates .
Retrospective cohort study comparing outcomes of neonates in delivered in facilities with
neonates in referring hospital. We studied live births of 246 of neonates delivered between
Janua ry 2016 to December 2017 in hospital with neonatal intensive care and 55 delivered in
referral hospital s. Evaluate the severity of developing intraventricular hemorrhage grade 1 to 4 in
relationship to corticosteroid administration and mortality in neonates between 24 and 34 weeks
of gestation and 35 week with low birth weight/very low birth rate (LBW/VLBW) with no
congenital anomalie s. Mothers that exhibited obstetrical complications as premature rupture of
membrane, preterm labor, transverse position, preeclampsia, placenta abruption and previa were
included in study. The association between obstetrical complications and anten atal steroids
administration were compared in the study.
The study showed that neon ates in different facilities had different outcomes, which may
be due to different management according to location s of delivery. Neonates transported to
tertiary facility had higher mortality rate compared to neonates born in tertiary intensive care
unit.
Mothers to inborn neonates were more likely to receive ant enatal corticosteroids
compared to outborn mothers. Outborn neonates transferred to NICU had higher risk of
developing intraventriuclar hemorrhage grade s 1 to 4 than inborn neonates. The significant
difference may be due to less administration of corticost eroids to mothers of outborn neonates
compared to inborn mothers that receive d more often steroids in prior to delivery .
There was a significance between inborn and outborn treated with surfactant and CPAP
or intubation . Inborn received more surfactant and CPAP compared to outborn that were more
likely to be administrated surfactant and endotracheal intubation .

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CHAPTER I
GENERAL PART

I.1. Epidemiology
Premature birth is defined as birth before 37th completed weeks from first day of last
menstrual cycle. Therefore premature birth is any delivery that occurs between 20 and 37
gestation week, regardless of birth weight. Premature birth can be cause of preterm labor,
spontan eously or induced or cesarean section due to complications to mother or fetus. Labor
before 24 GW is considered not sufficiently developed to survive outside the uterus. Before
28GW is extremely preterm, 28 -30 GW is very preterm and 32 -36 is mild preterm.
The average weight at birth according to Preemie growth chart in 24 -25 weeks of
gestation (GW) is 651 -737g, 26 -37 GW is 827 -936g, 28 -29GW is 1061 -1204g, 30 -31 GW is
1373 -1546g, 32 -33 GW is 1731 -1956g and 34 -35 GW is 2187 -2413g.
Risk factors for preterm labor include race, age, socioeconomic status and body mass index
(BMI) . [1]
Other causes are environmental (poor nutrition, use of substance, alcohol or smoking and
psychosocial causes) and gene tic such a s polymorphism in tum or necrotic factor alpha (TNF -a).

1.2. Causes of premature birth
I.2.1. Premature labor
Intrauterine infections, placental aruption, cervical incompetence, premature memb rane rupture,
multiple pregnancies , intrauterine death, metal and uterine abnormalities and chorioamniontis .
[1]
1. Infection
Infection might activate the biochemical pathways that can lead to cervical ripening and
uterine contractions.
2. Chorioamnionitis
Overgrowth in maternal lower genital tract, with presence of organism in uterine cavity
(decidua) of lower segment followed by inflammation reaction that lead to decid uitis, chorionitis
and extending through amnion into amniotic cavity and further to fetus by aspiration and

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swallowing of the infected amniotic fluid. The most c ommon m icrobial are: Bacterial vaginosis
and Trichomonas vaginalis are associated with p reterm birth . [1]
3. Cervical incompetence
Cervical incompetence is found in woman with inherent weakness in cervix or
compromised cervix due to surgical procedures such as mechanical cervical dilation at time of
termination of pregnancy and surgical evacuation of conception products.
4. Multiple pregnancies
Multiple pregnancies are associated with over distension of uterus that leads to preterm
labor.
5. Genetics
Previous p reterm pregnancies can cause preterm labor.

I.2.2. Preeclampsia
Preeclampsia develops during third trimester. It is believed the problem occurs during
development of placenta due to narrowed blood supply and different responses to hormonal
signals. A factor that may play role is also women with h istory of preterm birth are more likely
to develop preeclampsia with p reterm birth in second preterm birth. Infants are likely to be born
early in presence of maternal preeclampsia. In severe cases a labor might be induced by cesarean
delivery.

I.2.3. Premature rupture of membrane
It refers to rupture of fatal membrane in absence of uterine contractions , prior to onset of
labor of preterm below 37 week s of gestation . It is either spontaneous or induced within 12 to 24
hours. Risk factors for preterm rupture membrane are intra -amniotic infection, decidual
hemorrhage (placent al abruption), and previous history of preterm rupture of membrane.

I.3.4. Transverse position
Fetus is lying in longitudinal axis and perpendicular to long axis of uterus. Fetal non –
vertex position at delivery is a complication of preterm premature rupture of membrane
(PPROM). Fetus in transverse position decrease with increased gestational age. Any
prolongation of transverse position will harm the fetus . Extrinsic causes include mechanical

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compression, amniotic band constriction or dir ect birth trauma. Intrinsic causes include
hypercoagulable state of the neonate leading to arterial or venous thrombosis . [2]
I.2.5. Placenta previa
Placenta previa is a risk for preterm delivery and is necessary to perform urgent cesarean
section. Early delivery could have been a cause of infections or inflammation. Placenta previa is
recurren ce of pregnancy complication. [3]

I.2.6. Placenta abruption
Placental abruption leads to preterm labor by stimulation of myometrial contraction
through release of thrombin. Release of thrombin and chorioamninitis is result of decidua
hemorrhage. Placenta abruption increase mortality rate in fetus with risk factors of perinatal
asphyxia, Intraventricular hemorrhage (IVH) and cerebral palsy .

I.3. Neonatal outcome
Gestational age plays important role in s urvival of preterm infants but also level of
neonatal ca re in delivery room and nursery . Infants that survive are at risk of short -term and
long-term morbidity. Some c onditions are acute and are susceptible to treatment, while others are
long-term disability such as cerebral pals y and respiratory dis orders. Due to preterm infants has
it difficult to adjust to extrauterine due to immature orga n system, following may occur :
1. Respiratory – apnea, hyaline membrane disease, bronchopulmonary dysplasia (BPD ).
2. Neurologic – perinatal depression, intraventricular hemorrhage
3. Cardiovasc ular- hypotension, patent ductus arteriosus
4. Hematologic – anemia,hyperbilirubinemia
5. Gastrointestinal – Necrotizing enterocolitis
6. Temperature regulation – hypothermia
7. Ophthalmologic – retinopathy

I.3.1. Premature lung
The respiratory system in premature infant is incompletely developed and risk of
respiratory morbidity is associated with immature lung structures . The proportions of
diaphragmatic slow -twice muscle fibers are resistant to oxidation and fatigue (Type 1) which are

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smaller by 10% than fast – twitch which tires easily (Type 2 ). Chest of premature infants have
poor ossification of ribs and sternum due to intercostal muscles are not fully functional. During
inspiration the diaphragm work more in order to maintain constant tidal volume. This
phenomenon contributes to accelerating the respiratory functional exhaustion to which low birth
-weight infant with respiratory distress are subject to . [4]
Surfactant synt hesis begins in saccular stage ( 30th gestational week (GW) ) and infants
born before third trimester are at risk for respiratory failure due to surfactant deficiency due to
high surface tension and unstable alveoli. Unstable al veoli causes alveolar collapse ( atelectasis)
in which it results in intrapulmonary shunt that will present poor oxygenation. The collapsed
airspac e demand high ventilatory pressure to the immature distal airways and gas exchange. Due
to absence of surfactant that prevent s collapse distal air space, expansion of the lungs must be
repeated with each breath.
During canalicular (between 16 -26 GW) and saccular stages (between 24 -38GW), the
airways have little smooth muscles in their wall, epithelium is immature and weakened cell
adhesion. Increased deficiency of smooth muscles and the weak cell adhesion in immature
airway increases the risk to injury by elevated pressure and volumes that are important for
effective ventilation. Preterm infants have less compliance of airways, which explain why they
need higher airway pressure. Elevate volume is necessary to inflate the collapsed gas exchange
regions. The lung development of terminal respiratory sacs and alveoli continues un til 34 -36
weeks gestation.

I.3.2. Respiratory distress syndrome
Premature infants presenting these characteristics will develop respiratory distress
syndrome (RDS). 50-60% in infants, who are born before 30 weeks of gestation , presents RDS .
[1]
Acceleration of lung immaturity is done by administration of hormones, such as
glucocorticoids before premature delivery. Antenatal corticosteroids, as Betamethasone or
Dexamethasone will accel erate maturation of alveolar type 2 epithelial cells, a source of
pulmonary surfactant. Therefore, mothers wit h preterm delivery between 24 -34 weeks of
gestation are treated with glucocorticoids. To increase the lung compliance after birth, infusion

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of sur factant will be required. Once the surfactant reaches the lung, surface tension will be
reduced, alveoli will be stabilized and improvement of oxygenation and gas exchange.
Ventilatory induced lung injuries in premature infants due to mechanical ventilations.
These injuries can occur as a result of airway pressure (barotrauma), lung volume (valotrauma)
and the concentration of inspired oxygen (oxygen toxicity). Volutrama after birth can happen as
result of over -inflation elevates that microvascular permeability and cause the release of
inflammatory mediator from leucocytes in lung, which will lead to alveolar flooding. Alveolar
flooding is linked inactivation of surfactant that is associated wit h atelectasis and decrease in
lung compliance. Supplemental oxygenation therapy for extended period of time will result in
increase in lung volutrauma and lung injury may progress to chronic lung disease.
Chronic lung disease is related to need for high i nspired oxygen, high peak inspiratory pressure
and high quantity of fluid intake. Chronic lung disease is found in preterm infants between 23 -26
weeks of gestation and weight less than 1000g.

I.3.3. Bronchopulmonary dysplasia
Bronchopulmonary dysplasia (BPD) is most frequent cause in preterm infants that
survived prolonged mechanical ventilation. BPD is diagnosed in preterm infants that did not
recover from respiratory distress syndrome. Bronchopulmonary dysplasia involves parenchymal
and small airway comp onents. Risk factors for BPD are:
Gestationa l age at birth, low birth weight, pre eclampsia, premature rupture of membrane and
chorioamnionitis.
Postnatal risk fac tors: patent ductus arteriosus and pneumothorax . Administration of antenatal
corticosteroids to women at risk of premature labo r can reduce risk of developing BPD.
Frequency of disease has reduced in premature neonates that were managed with nasal
continuous positive airway pressure (CPAP) than those th at received mechanical ventilation.
The common theme appears to be that nasal CPAP permits alveolar formation, whereas
mechanical ventilation arrests alveolar formation . [1]
Severity of chronic lung disease is less common today due to better understanding of
lung development and improvement in management of preterm infants, such as the use of nasal
CPAP.

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I.3.4. Intravent ricular hemorrhage
Intravent ricular hemorrhage (IVH) is a complication of prematurity that develops in first
48 hours of life . IVH in preterm infants is bleeding into areas as ventricles, due to fragility of
germinal matrix vasculature and disturbance in cerebral blood flow. Highest risk of bleeding
occurs in infants born 10 weeks earlier. IVH is more common in preterm infants with respiratory
distress syndrome. It reduces survival of premature infants and enhances risk of neurological
complications. There are four types of IVH and are usually called grades and are based on degree
of bleedi ng. Grade one and two involve small amount of bleeding with risk of developmental
disabilities. Grade three and four are more severe bleeding. On grade three blood presses on and
on grade four it involves brain tissues. Blood clots can develop and cause bl ockage of flow of
cerebrospinal fluid in which it leads to increase fluid in brain (hydrocephalus), cerebral palsy and
mental retardation. Stabilization is done by blood transfusion . Neonate outcome depends on how
a premature infant was at birth and the grade of hemorrhage . Pregnant woman with high risk of
preterm delivery sho uld receive corticosteroids, whic h can reduce the risk of infant develop IVH.

I.3.5. Patent ductus arteriosus
Patent ductus arteriosus (PDA ) in premature infants depends on gestatio nal age and
respiratory status after birth. PDA depends on magnitude of left to right shunt that
cause increased pulmonary venous pressure and pulmonary congestion . [5]
Due to left side volume overload and ductal phen omenon, it wil l worsen systemic
perfusion in extremely low birth weight (ELBW ) and very low birth weight (VLBW ) infants.
Infants between 500 -1500g are at high risk of persistent PDA. Failure of PDA closure in
preterm infants with respiratory distress syndrome results in a left to right shunt across the duct
which may lead to pulmonary congestion and deterioration in respiratory status . [5]
PDA closure is expected in ELBW neonates at 2 to 6 days and VLBW neonates within
first years of life. Majority o f preterm infants younger than 28 weeks of gestation receive
medical o r surgical therapy to prevent respiratory decompensation, h eart failure, intraventricular
hemorrhage, bronchopulmonary dysplasia, necrotising enterocolitis and death . [1]
PDA is managed by increased oxygen supplement.

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I.3.6. Necrotizing enterocolitis
Necrotizing enterocolitis (NEC ) is common gastrointestinal emergency in premature
infants related to morbidity and mortality in NICU. Most frequent risk factor is prematurity and
low birth weight of less than 1000g, infants that required resuscitation at delivery or mec hanical
ventilation or neonates were delivered prematurely due to placental abruption.

I.3.7. Hypothermia
Hypothermia is body temperature below 36 , 5 degree. Preterm infant with low birth
weight and absence of subcutaneous fat put preterm infants at risk of hypothermia. Hypother mia
is associated with hypoglyc emia, metabolic acidosis and increased mortality rate . Hypothermia is
associated with increased risk of mortality and morbidity in preterm infants during first hours. To
reduce the heat loss in preterm it’s mandatory to transfer the infant to neonatal intensive unit
with use of incub ator. Procedures (intubation and umbilical line catheterization) are most often
performed in the first hours and can potentially lead to hypothermia . [6]
Prevention of heat loss include using powered radiant warmers, warm blankets , hats,
thermal mattress and wrap to cover body of preterm infant.

I.3.8. Retinopathy of prematurity
Disorder vascularisation of retinal blood vessels that disrupt s the vascular growth and
cause retinopathy. Loss of maternal -fetal interaction and hyperopia will suppress growth factors
and will res ult arrest in retinal vascularis ation (phase 1) . Due to poor r etinal vascularis ation it
will lead to hypoxia of retina and stimulation of growth factor (phase 2) that will lead to
detachme nt to retina. In preterm infants receiving oxygen supplement might reduce the risk of
retinopathy.

I.4. Treatment
I.4.1. Delivery room intervention
Preparation for delivery and care for preterm infant is important and may influence the
outcome for the infant. At the time of delivery, resuscitation equipment should be identified and
checked for working order. Room temperature should be 25-26 of degree in order to prevent
hypothermia. Oxygen, bag and mask ventilation devices that is necessary for newborn

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resuscitation. Suction syringe, functional laryngoscope with sized blades, endotracheal tube and
pulse oximetry. Epinephrine should be prepared for potential use.

I.4.2. Corticosteroids
Mothers that receive cor ticosteroids prior to delivery lower ris k of fatal lung
development. Use of steroids in presence of premature rupture of membrane reduced mortality
rate and morbidity (RDS, IVH and NEC ). According to American congress of obstetricians of
gynecology , it is recommended that pregnant woman between 24 we eks -0 days and 33 weeks -6
days of gestation to receive corticosteroids with risk of preterm delivery within 7 days.
Corticosteroids is effective by increasing production of surfactant from type 2 alveolar cells,
increasing the expression of epithelial so dium channels that will allow the alveoli to convert flip
secretion to sodium and fluid absorption with reduction of fatal lung fluid that will lead to
development of lung structure and reduced risk of RDS.
Types of antenatal corticosteroids are Betameth asone (administrated I.M) and
Dexamethasone (administrated I.V) . There are no differences between the two groups.
According to Cochrane trial, they demonstrated that D examethasone reduced the risk of IVH. In
another research of National institute of child health and human development (NICHD) it was
documented that infants with weight of 401 -1500g exposed to B etamethasone had less risk for
neonatal death. While usage of Dexamethasone therapy to pr event BPD in first days of life were
associated with cerebral palsy and neurodevelopment outcome, which may b e due to high dosage
that caused toxicity .

I.4.3. Surfactant
Preterm lung changes occur between 23 and 34 weeks of ges tation. The changes include
stage of lung development (according to gestational age), surfactant deficiency, surfactant
inactivat ion that results in leakage into airway and injury . Surfactant is rich in phospholipids,
proteins and carbohydrates that reduce the alveolar radius and surface tension will fall and will
prevent collapse of small alveolus. Surfactant therapy for respiratory distress syndrome in
preterm infants has decreased incidences of pneu mothorax, pulmonary interstitial emphysema
and mortality rate. Surfactant should be administrated as soon as infant present signs of RDS.
Treatment before any sign of RDS has disadvantages, such as infant may be not developing RDS

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and high volume of surfactant may interfere with resuscitation. Synth etic surfactant is
administered slowly in order to prevent accumulation and obstruction on endotracheal tube
leading to complications as cyanosis and bradycardia. Preterm with respiratory distress syndrome
treated earlier with surfactant and CPAP needed le ss of mechanical ventilation and presented less
complications such as pneumothorax, bronchopulmonary dysplasia or other complications
Today surfactant can be administrated in combination of CPAP, by less invasive surfactant
administration (LISA) with use of small catheter instead of endotracheal tube and surfactant
administration through stiff vascular catheter (MIST). LISA techniques lead to increase in end
expiratory lung volume and oxygen supply to preterm infants receiving CPAP.

I.4.3.1. Combination o f corticosteroids and surfactant
Cortico steroids an d surfactant combination result in improvement of lung compliance.
There is a possibil ity that corticosteroids enhanced alveolarization, by increasing lung gas
volume which re sult improved ventilation and better response to surfactant therapy . [1]

I.4.4. Ventilation
Whenever deciding what type of treatment a neonates needs, clinician must choice one
therapy with better outcome for that neonate . These are some of types of ventilation that are
options for preterm infants.

I.4.4.1 Continues positive airway pressure
Continues positive airway pressure (CPAP) is used non -invasive continuous distending
airway pressure used in neonatal care. CPAP is a simple form of respiratory support to preterm
infants with sufficiency lung to be stabilize d. Early benefits of using n CPAP includ e reduced
risks of infections, chronic lung disease and BPD .
The duration of using CPAP is influenced by:
1. Infants gestational week, weight and respiratory function .
2. Gradual reduction of lower pressure, to allow respiratory muscle adjustment before
discontinuing

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3. NCPAP does not improve ventilation and give adequate oxygenation with FiO2 more
than 0.6; infant should be intubated and administrated surfactant or treating large mouth leakage
and increasing pressure that might cause CPAP to fail.
CPAP is delivered by use of flow -inflating & T -piece resuscitator. An advance of using CPAP is
when administrati ng surfactant with no requirements of endotracheal intubation.
Risk factors for using CPAP are air leakage and high volu mes that impair the ventilation. Apnea
and progressive respiratory acidosis are main reason t o why CPAP fail .

I.4.4.2. Intermittent positive pressure ventilation
Intermittent positive pressure ventilation (IPPV) is frequently used in order to avoid
intubation and invasive ventilation. Self inflation bag, flow -inflating bags and T -piece are used
for ventilation . T-piece resuscitators is more accurately with consist delivery of inspiratory
pressures and PEEP .
Ventilation is provided by sized face mask, endotracheal tube or laryngeal mask airway.
In one study of mask ventilation of preterm infants it was documented that 2 5% of breaths had
airway obstruction and 75% has a mask leakage. Provider has difficult to judge tidal volume that
is delivered or amount of leakage at ventilation . Respiratory function monitor is detecting airway
obstruction and mask leak in delivery room. Ventilation rates between 40 -60 breaths/minute.
Fast rate should be av oided to prevent stack breaths with high risk of developing pneumothorax.
Disadvantage of using IPPV is following :
 Complications of endotracheal tube, subglottic stenosis associat ed with intubation
(duration, endotracheal tube size,occurence of traumatic intu bation). Prolonged
intubation causes subglottic cyst
 Infections (pulmonary and systemic)
 Acute and chronic lung damage due to valotrauma, barotr auma and shear stress with
inflation.

I.4.4.3. Endotracheal intubation
In order to use endotracheal intubation it will depend on gestational week of infa nt, degree of
respiratory depression and the experience to perform it in order to prevent complications.
Accurate size of laryngoscope and correct position of inserting endotracheal tube are very

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important for effective delivery of oxygen . Endotracheal intubation is used in NICU in extremely
premature infants with lower Apgar score. Surfactant administrated by intubation and short
period of mechanical ventilation will be spread to lungs regularly when it administrated rapidly
and with higher volumes t o give infant enough ventilator support and quicker clearance of
airways from fluids.
Neonates above 24 weeks of gestation that are intubated immediately after delivery shall
receive surfactant in less than 2 hour s after birth. Infants that are treated with non invasive
ventilation and develop complications as apnea or hypercarbia will be administrated surfactant
and to be intubate d. Prolonged mechanical ventilation can be avoid ed in preterm infants, if
INtuba te- SURfactant -EXtubate to CPAP (INSURE) technique is employed.
Complications are usually associated to incorrect insertion of ETT due to short trachea.
Complications are foll owing:
 Pulmonary atelectasis
 Pneumothorax
 Unequal surfactant administration
 Bronchopulmonary dysplasia
 Nosocomial respiratory infection

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CHAPTER II
PERSONAL CONTRIBUTION

II.1 Introduction
The aim of the study is to compare the survival rate in neonates born in tertiary
centre (inbor n) at County hospital in Targu M ures – neonatal intensive care unit (NICU) with
neonates that are transferred (outborn) to tertiary unit for further treatment at 24 to 34 or 35
weeks of gestation and were followed up to 28 days of life . The study will use data to determine
the improvement of survival rate in preterm neonates and relationship between administrations of
corticosteroids to mothers before the delivery.
Secondary aim is t o study the complications neonates developing such as intraventricular
hemorrhage. Documentation of surfactant administration with use of supplementary respirat ion
aids (CPAP and endotra cheal intubation ) based on gestational age and weight at birth .

II.1.1. Choosing the topic
I cho ose to write about this topic because of the unique opportunity to learn more about
neonates in different facilities based intensive care level III and perinatal care level I or II in
developing country as Romania . No previous study has be en made in Romania that compared
between facility based and referral neonates at 24 to 35 weeks of gestation.
Neonatal care in level III maternity unit with management ant tre atment to neonates that
have prolong ed life span for th ose that receive therapy compared with those that do not receive
therap y. To be able to identify the type of therapy that were offered to facility and perinatal care
and which one had the best outcome s for mothers and neonates

II.1.2. Hypothesis
We hypothesized that survival rate was improve d in neonates born in facility neonatal
intensive care unit compared with referral neonates by medical care as admi nistration of
corticosteroids, postnatal surfactant and respiratory support with a significant difference of
neonatal outcomes between inborn and outborn neonates. Our hypothesis was to characterize the
rate of exposure of antenatal steroids , postnatal surfactant and types of ventilations among

17
neonates with LBW and VLBW and improvement of neonatal outcomes. Can mortality rate can
be reduced if outborn neonates are admitted in time to level III maternity units .

II.2. Material and methods
We completed a retrospective population cohort study that remained anonymous on
mother and neonates from birth to discharge or death up to 28 days following birth , based on
charts from m edical records . Discharge was defined as discharge d from intensive care unit. The
study was conducted by reviewing charts from County hospital in Targu Mures (including
tertiary NICU) and infants born outside perinatal centre (Level I or II ) and were transferred to
County hospital.

II.2.1. Study population
The study included live births between January 2016 to December 2017of (n=301)
preterm infants born between 24 and 34 weeks of gestation and 35 week with low birth
weight/very low birth rate (LBW/VLBW) transferred to NICU and outcome as neonatal death
was included in the stu dy. Neonate s were subdivided based on gender, gestational ag e at birth
and birth weight . The therapy infants received at NICU, type of ventilations, complications
neonates developed such as intraventriuclar hemorrhage grades 1 -4, and survival and neonatal
death in first 7 days of life and death from 8 to 28 days of life were comprised in study.
Inclusion criteria for mothers were administration of corticosteroids, independently of
complete or incomplete dosage and type of delivery as caesarean section or vaginal delivery .
Evaluat e the association between early administration of corticosteroids to mothers and mortality
rate in neonates.
Mothers that exhibite d obstetrical complications as premature rupture of membrane , preterm
labor, transverse lie position , preeclampsia, placenta abruption and previa were included in study
and mothers presenting other complications other than mentioned were excluded from the study .
The following exclusions were applied, 4.740 were excluded from the study with infants that did
not need neonatal care , above 34th or 35th weeks of gestation , died before 24th week of gesta tion
or infants weighing below 450g at birth. Morbidities as respiratory distress syndrome, chronic
lung disease , necrotizin g enterocolitis and patent ductus arteriosus were excluded from the study.

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II.2.2. Statistical analysis
The data collection was done on an excel spreadsheet containing location of de livery
(inborn versus outborn), gender, gestational week, weight at birth, type of delivery (vaginal or
caesarean), admission at NICU, types of ventilation (nCPAP or endotracheal intubat ion),
therapeutic categories ( antenatal corticosteroids and postnatal surfactant ), developm ent of IVH
and mortality up to 28 days. The analyses were performed to describe the characteristic
association between administra tion of corticosteroids before delivery with location of delivery,
type of delivery (vaginal or cesarean) and causes of premature deliver y. Association between
surfactant administration and types of ventilation neonates received. Association between
corticosteroids administration, development of IVH and mortality rate neonates developed in
NICU .
Study was conducted by p ercentage comparison between groups, Odds ratio with 95 %
confidence interval and chi square were calculated to compare between two groups to exhibit
result s. Tests were 2 – sided and P <0.05 that were considered statistically significant .

II.3. Results
The study was conducted in County hospital – NICU from 2016 to and study populations
of a total of 301 premature infants born were registered in the study. The studies were
categorized into groups: comparing administration of antenata l corticosteroids to mothers of
inbor n and outborn infants , administration of surfactant and the risk of mortality rate and
comparing neonates that received corticosteroids and surfactant with those who did not receive .

19

Figure nr.1 – Antenatal steroid administration to mothers by location of delivery

Table nr.1 – Location of delivery, administration of steroid and mortality rate
Survival 0-7days 8-28days Total
Inborn Corticosteroid Count 113 4 6 123
No corticosteroids Count 113 9 1 123

Outborn Corticosteroid Count
18 0 0 18
No corticosteroids Count 32 1 4 37 020406080100120140
Corticosteroids No corticosteroids Inborn
Outborn

20
Results from ( Table nr.1, Figure nr1 and Figure nr.2 ) obtained that 55 outborn were
transferred from perinatal care to Count y Hospital, NICU and 246 were born in maternity unit
level III . 46.8% (n=141) of our population that received antenatal corticosteroids in prior to
delivery,
50% (n=123) were inborn and 32.7% (n=18 ) were outb orn (OR 0.486;95C%CI,0.262 to
0.90; P= 0.02) wi th outborn being less likely to receive corticosteroids compared to inborn and
with significance association between antenatal corticosteroids and location of delivery. 8.1% of
inborn that recei ved corticosteroids before delivery died and 32.7% of outborn neonates that
received corticosteroids before delivery survive d.
Mortality rate was highest in neonates that did not receive corticosteroi ds in prior to
delivery with 8.1 % of inborn and 13.5% of outborn with (OR= 1.76 ;95%CI,0.563 to 5.53; P=
0.33) indicating that that outborn were more likely to die than inborn neonates with no
significant association between groups.
For outborn infant s that were transported to NICU, 9.1% (n=5) of neonates that died in
NICU in less th an 28 days, compared with 8.1% (n=20) of inborn infants that died in NICU.
The association between mortality rate and location of delivery (Outborn versus inborn)
(OR=1.13;95%CI,0.405 to 3.16; P= 0.81) imply that outborn neonates are expected to die in le ss
than 28 days than inborn with no significant association between location of delivery and
mortality rate in neonates.

21

Figure nr.2 – Mortality rate according to location of delivery

Results from ( Table nr.1 and Figure nr.2 ) indicated that mortality rate in inborn
neonates in first 7 days was 3.3% (n=4) in neonates that received steroids before delivery and
mortality rate after 7 days was 4.9% (n=6). Mothers to inborn neonates that did not receive
corticosteroids resulted 7 .3% (n=9) death in first 7 days and 0.8% (n=1) of deaths were after 7
days. No deaths were documented in outborn mothers that were administrated therapy before
delivery. Outborn neonates mothers that did not received steroids before delivery resulted 2.7%
(n=1) death in first 7 days of life and 10.8% (n=4) in death after 7 days of life.

02468101214
Inborn OutbornNumber of infants
Location of deliveryMortality 0 -7 Days
Mortality 8 -28 Days

22
Table nr.2 – Mortality and morbidity rate s among infants admitted to NICU
*P<0.05

Obtained results from ( Table nr2. and Figure nr.3 ) suggested a significant association of
antenatal corticosteroids and subdivision of gestational week between 26 -27 and 34 -35. There
was an association between corticosteroids and caesarean section delivery between 2 8-29 GW.
Ventilations as noninvasive nCPAP with 85% were most used in neonates at 30 to 31
weeks of gestation while intubation was highest with 64% at 26 to 27 weeks of gestation. Gestational week 24-25
weeks 26-27
Weeks 28-29
weeks 30-31
weeks 32-33
weeks 34-35
weeks
Neonates, n n=20 n=28 n=55 n=60 n=63 n=75
Antenatal
corticosteroids, n(% of
total) 12(60%) 20(71%)* 30(55% ) 33(55 %) 31(49% ) 15(20% )*
Caesarean section
delivery, n(%of total) 9(45%) 10(35.7 %) 38(69 %)* 36(60 %) 33(52.4 %) 41(54.7 %)
Surfactant
administration, n(% of
total) 18(90%) 19(68%) 25(45%) 9(15%) 6(9.5%) 2(2.7 %)
CPAP,n(% of total) 8(40%) 10(36% ) 35(64 %) 51(85%) 52(83 %) 66(88 %)
Intubation,n(% of total) 12(60%) 18(64 %) 20(36%) 9(15%) 11(17 %) 9(12%)
Intraventricular
hemorrhage, n(%of total) 7(35%) 3(10.7% ) 3(5.5 %) 8(13.3% ) 6(9.5% )
5(6.7 %)

Death at NICU, n(%of
rates by live birth) 7(35%) 5(17.9 %) 3(5.5 %) 4(6.7% ) 2(3.2 %)
4(5.3 %)

Alive at discharge, n(%
of live births) 13(65 %) 23(82 %) 52(94 %) 56(93 %) 61(97 %)
71(95 %)

23
74% of neonates between 24 -35 weeks of gestation received noninv asive CPAP and 26%
of neonates received endotracheal int ubation.
Preterm at 24-25 weeks gestation were 6. 6% (n=20) , 60% that received antenatal therapy, 45%
of deliveries were caesarean and live at discharge were 65%.
Preterm born at 26-27 wee ks of gestation were 9.3% (n=28) , 71% received antenatal
therapy, 35.7% of deliveries were caesarean section and live at discharge were 82%.
Preterm between 28 -29 weeks of gestation were 18.3% (n=55) , 55% received antenatal
therapy, 69% of deliveries were caesar ean section and live at discharge were 94%.
Preterm between 30 -31 week s of gestation were 19.9% (n=60) , 55% received antenatal
therapy, 60% of deliveries were caesarean section and live at discharge were 93%
Preterm between 32 -33 weeks of gestation were 20.9% (n=63) , 49% received antenatal therapy,
52.9% of deliveries were caesarean section and live at discharge were 97%.
Preterm between 34 -45 weeks of g estation were 24.9% (n=75), 20% received antenatal
therapy, 54.7% of deliveries were caesarean section and live at discharge were 95% .

Figure nr.3 – Mortality rate by gestational age (weeks)
Results from ( Figure nr.3 ) indicates that death at NICU was highest with 35% (n=7)
among neonates at 24 -25 weeks of gestation and lowest in neonates at 32 -33 weeks of gestation
with 3.2 % (n=2) .
0%5%10%15%20%25%30%35%40%
24-25 26-27 28-29 30-31 32-33 34-35Death at NICU

24
Table nr. 3 – Mortality rate according to birth weight
Birth weight Death OR(95%CI) Chi-square P-value
<500g 4(0) 1.19(0.06 -22.6) 0.9
500-999g 65(15) 6.78(2.87 -15.97) 23.7 0.0001*
1000 -1500g 97(4) 0.37(0.12 -1.12) 3.28 0.07*
>1500g 135(6) 0.35(0.13 -0.92) 4.79 0.03*
*P value <0.05

Therefore, r esult from (Table nr. 3 and Table nr.5 ) implies that 1.3% (n=4) neonates
weight at birth was less than 500g, with no documentation of death. 21.5% (n=65) of neonates
weight at was between 500 -999g, with 23% of neonates that died at NICU.
32.2% (n=97) of neonates weight at birth was between 1000 -1500g and 4.1% of neonates
in this category died.
44.9% (n=135) of neonates’ weight at birth above 1500g and 4. 4% were recorded dead at
NICU.

Table nr.4 – Corticosteroid administration, morbidity and mortality rate
Location/Grade IVH 1 IVH 2 IVH 3 IVH 4
Inborn, n (%). N=22 9(41%) 3(14%) 7(32%) 3 (14%)
– Antenatal corticosteroid, n(%) 5(5.5%) 2(1.5%) 2(28.6 %)
 Death due to IVH, n(%) 1(11%) 1(33.3%) 1(17.3%)
Outborn, n (%). N=10 5(50%) 3(30%) 1(10%) 1(10%)
– Antenatal corticosteroid, n(%) 1(20%)
 Death due to IVH, n(%)

25

Figure nr. 4 – Corticosteroids administration and development of intraventricular
hemorrhage

Results from ( Table nr.4) implied that 18.2% (n=10) of outborn neonates developed IVH
and 8.9% (n=22) of inborn dev eloped IVH grade 1 to 4 (OR=2.38;95%CI,1.06 to 5.37; P= 0.03 )
with outborn more likely to develop IVH than inborn and strong significance association
between location of deliver y and development of IVH.
41% of inborn neonates that developed IVH, had received steroids before delivery and
out of those neonates 13.6 % died. 18 .2% of outborn develope d IVH and out of those 10% had
received steroids before delivery and no neonate died from IVH. 21.9% (n=7) of neonates that
developed intraventricular hemorrhage (with or without therapy) died at NICU.
Corticosteroid administration and development of IVH (OR=0 .478;95%CI,0.21 to 1.05 ;
P=0.06) with significance association between administration of corticosteroids and development
of IVH.
Development of IVH and mortality rate (OR= 1.16;95%CI,0.33 to 4.12; P= 0.8 ) with
significance association between developing IVH and dying from it.
0%5%10%15%20%25%30%35%40%45%
Inborn OutbornNumber of infants

26

Figure nr.5 – Intraventricular hemorrhage according to gestational age (week )

Most common grades of IVH according to gestational age according to (Figure nr.2 and
Figure nr.5) Results indicate s that 35% of preterm at 24 -25GW had developed IVH grade
(2,3&4).
10.7% of preterm at 26 -27 GW had developed IVH grade (1, 2&4).
5.5% of preterm at 28 -29 GW that developed IVH grade (1,3& 4).
13.3% of preterm at 30 -31 GW that developed IVH grade (1&2).
9.5% of preterm at 32 -33 GW that developed IVH grade (1&4) and 6.7% of preterm at
34-35 GW that developed IVH grade (1&4).

27
Study compared neonates th at received surfactant therapy and survived to disc harge with
those received surfactant and died . Results obtained from ( Figure nr.5 ) indicate d that i nborn th at
received surfactant were 27.2% (n=67 ) and out of those that received the therapy 14.9 % (n=10)
did not survive. While outborn th at received su rfactant were 22% (n=12) and 2 5% (n=3) of those
that received the therapy did not surviv e. The inborn neonates that received surfactant had lower
mortality rate than outborn neonates.
Differences between location of delivery and admini stration of surfactant
(OR=0. 757;95%CI,0.37 to 1.49; P= 0.41 ) indicates that inborn received more surfactant that
outborn neonates with a negative association betwee n two groups.
34% (n=27 ) of neonates that were administrated surfactant by C PAP and 66 % (n=52 ) of
neonates that were administrated surfa ctant by endotracheal intubation.

Figure nr.6 – Surfactant admini stration by location of delivery

28
Table nr.5 – Obstetric complications and categories in relation to premature infants
Gestational week 24-25
weeks 26-27
weeks 28-29
weeks 30-31
weeks 32-33
weeks 34-35
weeks
N=20 N=28 N=55 N=60 N=63 N=75
Preterm labo r 3(15%) 5(17.9%) 6(11%) 11(18%) 6(9.5%) 9(12%)
PPROM 4(20%) 7(25%) 8(14.5%) 17(28%) 20(31.7%) 13(17.3%)
Transverse
positions 3(15%) 1(3.6%) 7(13%) 4(6.7%) 3(4.8%) 3(4%)
Placental
abruption 1(5%) 3(10.7%) 8(14.5) 8(13%) 9(14.3%) 5(6.7%)
Placenta previa 1(3.6%) 2(3.6%) 2(3.3%) 5(7.9%) 11(14.7%)
Preeclampsia 2(3.6%) 2(3.3) 2(3.2%) 4(5.3%)
Other 9(45%) 11(39%) 22(40%) 16(26.7%) 18(28.6%) 30(40%)
Vaginal delivery,
n(%of total) 11(55%) 18(64.3% ) 17(31% ) 24(40% ) 30(47.6% ) 34(45% )
<500 2(10%) 2(7.1%)
500-999 18(90%) 23(82%) 12(21.8%) 7(11.7%) 4(6.3%) 1(1.3%)
1000 -1500 3(10.9%) 41(74.5%) 27(45%) 11(17.5%) 15(20%)
>1500 2(3.6%) 26(43%) 48(76.2%) 59(78.7%)
Female 13(65%) 13(46%) 28(51%) 25(41.7%) 28(44%) 31(41.3%)

Results from ( Table nr.5 ) included 65% (n=195) of mothers that presented with obstetric
complication that led to early delivery and 35% of mothers presented other complications . 11.%
of mothers presented with placenta abruption, 23 % presented with preterm rupture of membrane,
7% presented wit h transverse position, 13 % prese nted with premature labor and 3 % presented
with preeclampsia.

29
Table nr.6 – Corticoste roids administration according to obstetric complications
Gestational
week N 24-25
weeks 26-27
weeks 28-29
weeks 30-31
weeks 32-33
weeks 34-35
weeks P
value
Premature
Labor
N=40 1(2.5%) 1(2.5%) 4(40%) 5(12.5%) 2(5%) 2(5%) 0.20
PROM N=69 3(4.3%) 7(10%) 6(8.7%) 11(16%) 7(10%) 6(8.7%) 0.03*
Placenta
Abruptio n N=34

1(2.9%) 3(8.8) 4(11.8%) 5(14.7%) 4(11.8%) 2(5.8%) 0.2
Preeclampsia N=10
1(10%) 1(10%) 1(10%) 0.3
Transverse
position N=21
1(4.8%) 1(4.8%) 4(19%) 1(4.8%) 2(9.5%) 0.7
Placenta
Previa N=21
1(4.8%) 1(4.8%) 2(9.5%) 0.08*
*P<0.05

Result obtained from ( Table nr.6 and Figure nr. 7) indicates a significance difference
between administrations of cortico steroids to mothers in prior to deliver y and obstetrical
complications. A association between PPROM and cortico steroids before delivery and with
mothers presenting with placenta previa .
Corticos teroids administration depended on most frequent obstetrics complications;
At 24 to 25 GW, 4.3% of mothers with PROM and 4.8% with transverse position received
steroids before delivery.
At 26 -27 GW, 10% of mothers with PROM and 8.8% with placenta abruption received
steroids.
At 28 to 29 GW, 40% of mothers with preterm labor and 19% with transverse position
received steroids.
At 30 to 31 GW, 16% of mothers with PROM and 14.7% with placenta abruption
received steroids.

30
At 32 to 33 GW, 11.8% of mothers with placenta abruption and 9.5% with placenta
previa received steroids.
At 34 to 35 GW, 8.7% of mothers with PROM and 5% with pr emature labor received
steroids.
18% of mothers did not receive corticosteroids was due to placenta abruption that lead to
emergency vaginal delivery.

Figure nr.7 – Antenatal corticosteroid administration according to causes of preterm delivery

0%5%10%15%20%25%30%35%40%45%
24-25 26-27 28-29 30-31 32-33 34-35
Gestational age(week)Premature labor
PPROM
Transverse position
Placental abruption
Placenta previa
Preeclampsia

31
II.4. Discussion
Regionalization indicates the development of complexity of maternal facility and
perinatal care of each hospital that is ca pable of providing best qualities for neonates. With
advanced technology , antenatal steroids therapy and improvement of delivery rooms that are able
to stabilize premature infants in maternity level III compared to neonates in perinatal care (Level
I or II) with limited resources . Neonates are at risk of morbidity and morta lity that are increased
with reduced gestational age (week) and reduced weight at birth (VLBW/LBW) .

II.4.1. Interpretation of results
The results from our study suggested that preterm infants were managed differently
according to location of delivery. This might indicate that management of neonates that varied
between units.
Antenatal corticosteroids administration implied a reduced variation in morbidity and
mortality that affected inborn and outborn . We could document that 50% of inborn neonates’
mothers received corticosteroids before delivery , compared to 32.7% of outborn neonates’
mothers that received steroids before delivery . Mothers that did not receive corticosteroids
before delivery resulted that neonates were at highest risk of mortality with 8.1% in inborn
neonates and 13.5% in outborn neonates. Mortality rate was influence by factors such as birth
weight, gestational age, type of therapy that were offered and complications neonates might ha ve
developed and have led to death. The study was observing the mortality rate up to 28 days of life,
due to any later death would not have affected the variables since its rarely neonates between
24th to 34th or 35th (with VLBW) weeks of gestation that die later than 28 days. The
retrospective study had limitation and causes of neonatal death could not be accurately being
persistent for many newborns that resulted in non comparable death except death due to IVH.
Death at NICU was highest in premature between 24 to 25 weeks of gestation with 35%
and lowest mortality rate was documented with 3.2% in premature between 32 to 33 weeks of
gestation.
Effective interventions as surfactant administration and nCPAP or intu bation exhibited a
significant difference between inborn and outborn neonates . 26% of total neonates were
administrated surfactant , 34% of those neonates received surfactant by CPAP and 66 % of
neonates received surfactant by endotracheal intubation. Outborn infants from perinatal clinics

32
and very preterm infants were probable to be intubated with 83% in delivery room f or
administration of surfactant compared to inborn were that were ventilated with 45% with early
CPAP than being intubated immediately .
The weight at birth was a parameter for analyzing outcome s in neonates such as type of
ventilation that was suitable and mortality rate. 44% of neonates weighing between 500 to 999g
needed intubation and 55 % of neonates weighing more than 1500g that needed CPAP .
1.3% of neonates weight at birth was less than 500g, with no documentation of death.
21.5% of neonates weight at birth between 500 -999g with 23% of neonates that died at NICU.
32.2% of neonates weight at birth was between 1000 -1500g and 4.1% of neonates that died.
44.9% of neonates’ weight at birth above 1500g and 4.4% were recorded dead at NICU.
Preterm neonates that were transferred to NICU were more li kely to develop IVH with
20.3% compared to inborn with 9.3%. The significant difference ma y have be due to less
administration of corticos teroids with 32.7% to mothers of outborn neonates , compared to 50 %
of inborn mothers that receive more often steroids in prior to delivery. IVH grade II was most
frequent and cause of death with 33.3% in neon ates. Neonates born at hospital with NICU and
were not exposed to transportation were less likely of developing IVH, compared to outborn
neonates.
Analysis regarding type of delivery and obstetric complications indicated that 45% of
mothers gave birth by vaginal delivery and 55% gave birth by caesarean delivery.
23% of mothers presented with PPROM, 11% with placenta abruption, 13% with
premature labor and 7% with transverse position . Mothers that were offered corticosteroids in
prior to delivery with 8.7% of mothers with premature labor, 20.5% of mothers with PPROM,
9.7% of mothers with placenta abruption, 1.5% of mothers with preeclampsia, 4.6% of mothers
with transverse position and 2% of mothers with placenta previa

II.4.2 . Confirmation of hypothesis
Based on our study we can confirm that our hypothesis was matching the results.
Neonates born in developed facultie s such as NICU with better management of therapy to
mothers and neonates had better outcomes compared to neonates born in perinatal care level I or
II with limited equipment and interventions that affected the neonates . Differences can include
absence of adequate facilities for outborn infants; unable to perform proper resuscitation and

33
stabilization of infant after birth, delay in therapy that mothers and neonate s may be in need of
such as type of ventilation, antenatal corticosteroids or surfactant administration. Mothers to
inborn were more likely to receive corticosteroids before delivery that caused reduced in
development of IVH compared to mothers to outborn neonates. Outborn were more likely to
receive surfactant administration by intubation while inborn were a dministrated surfactant by
nCPAP that may explain the less use of surfactant and intubation in inborn neonates and due to
benefits of early use of nCPAP on neonates. Prolonged use of CPAP may delay hospit alization
time.

II.4.3 . Improvement of the study or for future studies
In order to have better outcome s for neonatal outcomes monitor the mothers status
repeatedly in order to be able to prevent any complications mother may present with or to start
early interventions of administrating corticosteroids and postnatal surfactant, type s of
ventilations that ar e suitable for neonates and type of delivery are important in order to reduce
morbidity and mortality rate.
However, further research with larger sample size are required in order to determ ine the
association between antenatal corticosteroids, location of delivery, morbidities and mortality rate
in neonates. Another type of study to include type of corticosteroid mother s receives before
delivery and how soon a mother should receive steroids. Or a study regarding the transferred
neonates to maternity, type of transfer that were offered, how long it lasted and what are the
complications that neonates can develop during exposure of referral.

II.5. Conclusion
Our conclusions are that reduced in gestational age and extremely low birth weight
neonates present with highest morbidity and mortality rate. The high mortality among outbor n
neonates may be due to limited equipment that necessary to obtain survival in neonates.
We can conclude th e efficiency of antenatal corticosteroids , surfactant administration,
live births and survival rate increased with gestational age.
One disadvantage of this study was that a small number of outborn infants that were
included in our study probably due to extremely prematurity , severely ill or were not considered
in need to be transferred to NICU . Premature neonates requires a s pecialized medical care,

34
intensive care unit for hi gher survival rate with help of antenatal steroids, surfactant and
ventilator supports .
The country should strengthen lower level units in order to reduce neonatal mortality rate
and complications that can occur during transport.

35
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