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Respiratory Distress in the Newborn

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 Respiratory Distress in the Newborn
Suzanne Reuter, Chuanpit Moser and Michelle Baack
Pediatrics in Review 2014;35;417
DOI: 10.1542/pir.35-10-417

The online version of this article, along with updated information and services, is
located on the World Wide Web at:
http://pedsinreview.aappublications.org/content/35/10/417

Pediatrics in Review is the official journal of the American Academy of Pediatrics. A monthly
publication, it has been published continuously since 1979. Pediatrics in Review is owned,
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 Respiratory Distress in the Newborn
Suzanne Reuter, MD,* Chuanpit Moser, MD,† Michelle Baack, MD*‡
*Department of Neonatal-Perinatal Medicine, Sanford School of Medicine–University of South Dakota, Sanford Children’s Specialty Clinic, Sioux Falls, SD.
†
Department of Pediatric Pulmonology, Sanford School of Medicine–University of South Dakota, Sanford Children’s Specialty Clinic, Sioux Falls, SD.
‡
Sanford Children’s Health Research Center, Sioux Falls, SD.

Educational Gap
Respiratory distress is common, affecting up to 7% of all term newborns,
(1) and is increasingly common in even modest prematurity. Preventive
and therapeutic measures for some of the most common underlying
causes are well studied and when implemented can reduce the burden of
disease. (2)(3)(4)(5)(6)(7)(8) Failure to readily recognize symptoms and
treat the underlying cause of respiratory distress in the newborn can lead
to short- and long-term complications, including chronic lung disease,
respiratory failure, and even death.

Objectives After completing this article, the reader should be able to:

1. Use a physiologic approach to understand and differentially diagnose

the most common causes of respiratory distress in the newborn infant.
2. Distinguish pulmonary disease from airway, cardiovascular, and other
systemic causes of respiratory distress in the newborn.
3. Appreciate the risks associated with late preterm (34–36 weeks’
gestation) and early term (37–38 weeks’ gestation) deliveries, especially
AUTHOR DISCLOSURES Drs Reuter, Moser, by caesarean section.
and Baack have disclosed no financial
relationships relevant to this article. This
4. Recognize clinical symptoms and radiographic patterns that reflect
commentary does not contain information transient tachypnea of the newborn (TTN), neonatal pneumonia,
about unapproved/investigative commercial respiratory distress syndrome (RDS), and meconium aspiration
products or devices.
syndrome (MAS).
ABBREVIATIONS
5. Identify the short- and long-term complications associated with
BPD bronchopulmonary dysplasia
CPAP continuous positive airway pressure common neonatal respiratory disorders, including pneumothorax,
ECMO extracorporal membrane persistent pulmonary hypertension of the newborn, and chronic lung
oxygenation
disease.
Fio2 fraction of inspired oxygen
FRC functional residual capacity 6. Understand management strategies for TTN, pneumonia, RDS, and
GBS group B streptococcus MAS.
MAS meconium aspiration syndrome
MSAF meconium-stained amniotic fluid 7. Implement up-to-date recommendations for the prevention of
PPHN persistent pulmonary hypertension neonatal pneumonia, RDS, and MAS.
of the newborn
PROM prolonged rupture of membranes
RDS respiratory distress syndrome
TTN transient tachypnea of the newborn

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 INTRODUCTION increase. Hypoxemia further increases tachypnea. (16)(18)
Therefore, affected newborns present with marked tachypnea.
Respiratory distress is one of the most common reasons an
Because tachypnea is a nonspecific symptom, additional
infant is admitted to the neonatal intensive care unit. (1)
clinical findings aid in narrowing the cause to a respiratory
Fifteen percent of term infants and 29% of late preterm
disorder.
infants admitted to the neonatal intensive care unit develop
Increased work of breathing results from mismatched
significant respiratory morbidity; this is even higher for
pulmonary mechanics from increased airway resistance
infants born before 34 weeks’ gestation. (2) Certain risk
(DPressure/Volumetric Flow), decreased lung compliance
factors increase the likelihood of neonatal respiratory disease.
(DVolume/ DPressure), or both. Airway resistance increases
These factors include prematurity, meconium-stained amni-
when there is obstruction of air flow. The critical importance
otic fluid (MSAF), caesarian section delivery, gestational
of airway radius is indicated in the equation R ¼ V(8lh/pr
diabetes, maternal chorioamnionitis, or prenatal ultrasono-
(4)), where R is resistance, V is flow, l is length, h is viscosity,
graphic findings, such as oligohydramnios or structural lung
and r is radius. (19) If the airway radius is halved, resistance
abnormalities. (2)(9)(10)(11)(12)(13)(14) However, predicting
increases 16-fold. Nasal flaring is a compensatory symptom
which infants will become symptomatic is not always possible
that increases upper airway diameter and reduces resistance
before birth. Regardless of the cause, if not recognized and
and work of breathing. Retractions, evident by the use of
managed quickly, respiratory distress can escalate to respi-
accessory muscles in the neck, rib cage, sternum, or abdo-
ratory failure and cardiopulmonary arrest. Therefore, it is
men, occur when lung compliance is poor or airway resis-
imperative that any health care practitioner caring for new-
tance is high. Noisy breathing may indicate increased airway
born infants can readily recognize the signs and symptoms of
resistance, and the type of noise auscultated may help
respiratory distress, differentiate various causes, and initiate
localize airway obstruction (Table 1). Stertor is a sonorous
management strategies to prevent significant complications
snoring sound heard over extrathoracic airways that indi-
or death.
cates nasopharyngeal obstruction. Stridor is a high-pitched,
monophonic breath sound that indicates obstruction at the
larynx, glottis, or subglottic area. Wheezing may also be high
DEFINITION, SIGNS, SYMPTOMS
pitched but is typically polyphonic, is heard on expiration,
Respiratory distress in the newborn is recognized as one or and indicates tracheobronchial obstruction. Grunting is an
more signs of increased work of breathing, such as tachypnea, expiratory sound caused by sudden closure of the glottis
nasal flaring, chest retractions, or grunting. (1)(15) Normally, during expiration in an attempt to maintain FRC and pre-
the newborn’s respiratory rate is 30 to 60 breaths per minute. vent alveolar atelectasis. Because lung compliance is worse
Tachypnea is defined as a respiratory rate greater than 60 at very low or very high FRC, achieving and maintaining
breaths per minute. (15) Tachypnea is a compensatory mech- physiologic FRC is essential in the management of respi-
anism for hypercarbia, hypoxemia, or acidosis (both metabolic ratory disorders with poor compliance, such as RDS or TTN.
and respiratory), (16) making it a common but nonspecific On the other end of the spectrum, meconium aspiration
finding in a large variety of respiratory, cardiovascular, met- syndrome (MAS) is an example of lower airway obstruction
abolic, or systemic diseases. Pulmonary disease may incite with air trapping. These newborns often have high lung
tachypnea, especially in neonates. The natural elastic property volumes, which adversely affects their lung compliance.
of the lungs is to deflate. When balanced by the outward recoil Regardless of the cause, it is vital to recognize symptoms
of the chest wall, functional residual capacity (FRC) occurs at and act quickly. If the newborn cannot sustain the extra work
the end of expiration to prevent alveoli from collapsing. The of breathing to meet its respiratory needs, respiratory failure
newborn chest wall, composed primarily of cartilage, is more follows. This failure may manifest as impaired oxygenation
pliable, predisposing neonatal lungs to pulmonary atelectasis (cyanosis) or ventilation (respiratory acidosis). Without prompt
and decreased FRC. (16)(17)(18) Pulmonary compliance refers intervention, respiratory arrest is imminent.
to a given change in volume (DVolume) for every given change
in pressure (DPressure), essentially the ability of the alveoli to
PATHOGENESIS
fill with air under a set pressure. If lung compliance is
decreased, such as with transient tachypnea of the newborn The causes of respiratory distress in a newborn are diverse
(TTN), respiratory distress syndrome (RDS), pneumonia, or and multisystemic. Pulmonary causes may be related to
pulmonary edema, there is a decrease in tidal volume. To alterations during normal lung development or transition to
achieve sufficient minute ventilation, the respiratory rate must extrauterine life. Normal lung development occurs in 5

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TABLE 1. Noisy Breathing Characteristics in Term Infants
TYPE DEFINITION CAUSES

Stertor Sonorous snoring sound, mid-pitched, monophonic, may Nasopharyngeal obstruction—nasal or airway secretions,
transmit throughout airways, heard loudest with congestion, choanal stenosis, enlarged or redundant upper
stethoscope near mouth and nose airway tissue or tongue
Stridor Musical, monophonic, audible breath sound. Typically Laryngeal obstruction—laryngomalacia, vocal cord paralysis,
high-pitched. Types: Inspiratory (above the vocal cords), subglottic stenosis, vascular ring, papillomatosis, foreign
biphasic (at the glottis or subglottis), or expiratory body
(lower trachea)
Wheezing High-pitched, whistling sound, typically expiratory, Lower airway obstruction—MAS, bronchiolitis, pneumonia
polyphonic, loudest in chest
Grunting Low- or mid-pitched, expiratory sound caused by Compensatory symptom for poor pulmonary compliance—
sudden closure of the glottis during expiration TTN, RDS, pneumonia, atelectasis, congenital lung
in an attempt to maintain FRC malformation or hypoplasia, pleural effusion, pneumothorax

FRC¼functional residual capacity; MAS¼meconium aspiration syndrome; RDS¼respiratory distress syndrome; TTN¼transient tachypnea of the newborn.

phases (20) (Table 2). Respiratory disease may result from Thus, after initial resuscitation and stabilization, it is impor-
developmental abnormalities that occur before or after tant to use a detailed history, physical examination, and
birth. Early developmental malformations include trache- radiographic and laboratory findings to determine a more
oesophageal fistula, bronchopulmonary sequestration (abnor- specific diagnosis and appropriately tailor management. A
mal mass of pulmonary tissue not connected to the thorough history may guide in identifying risk factors
tracheobronchial tree), and bronchogenic cysts (abnormal associated with common causes of neonatal respiratory
branching of the tracheobronchial tree). Later in gestation, distress (Table 4). A detailed physical examination should
parenchymal lung malformations, including congenital cystic focus beyond the lungs to identify nonpulmonary causes,
adenomatoid malformation or pulmonary hypoplasia from such as airway obstruction, abnormalities of the chest wall,
congenital diaphragmatic hernia or severe oligohydramnios, cardiovascular disease, or neuromuscular disease, that may
may develop. More common respiratory diseases, such as initially present as respiratory distress in a newborn. Radio-
TTN, RDS, neonatal pneumonia, MAS, and persistent pul- graphic findings can identify diaphragmatic paralysis, con-
monary hypertension of the newborn (PPHN), result from genital pulmonary malformations, and intrathoracic space–
complications during the prenatal to postnatal transition occupying lesions, such as pneumothorax, mediastinal
period. Although mature alveoli are present at 36 weeks’ mass, and congenital diaphragmatic hernia, that can com-
gestation, a great deal of alveolar septation and microvascular promise lung expansion. Significant tachypnea without
maturation occur postnatally. The lungs are not fully devel- increased work of breathing should prompt additional lab-
oped until ages 2 to 5 years. (20)(21) Therefore, developmental oratory investigation to identify metabolic acidosis or sepsis.
lung disease can also occur after birth. Bronchopulmonary Hypoglycemia, hypomagnesemia, and hematologic abnor-
dysplasia (BPD), for example, is a significant lung disease that malities may result in a depressed ventilatory drive or
complicates prematurity due to arrested alveolarization in impaired oxygen transport to the peripheral tissues, so
developing lungs exposed to mechanical ventilation, oxygen, laboratory evaluation should also be considered with these
and other inflammatory mediators before normal develop- clinical findings. Hypermagnesemia may contribute to
ment is complete. As defined by an ongoing oxygen require- respiratory distress and affect a newborn’s capacity to
ment at 36 weeks’ adjusted gestational age, BPD affects up to respond to resuscitation due to hypotonia and a depressed
32% of premature infants and 50% of very low-birth-weight respiratory drive or even apnea.
infants. (22) Cardiovascular disease may be difficult to distinguish
from pulmonary causes of respiratory distress (Table 5).
Most congenital heart defects present with cyanosis, tachy-
DIFFERENTIAL DIAGNOSIS
pnea, or respiratory distress from cardiac failure. Timing
The underlying cause of respiratory distress in a newborn may be an important clue to differentiation because very few
varies and does not always lie within the lungs (15) (Table 3). congenital heart defects present immediately after birth;

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 TABLE 2. Developmental Stages of Lung Development and Respiratory
Disease Pathogenesis
DEVELOPMENTAL
STAGE EMBRYONIC PSEUDOGLANDULAR CANALICULAR TERMINAL SAC ALVEOLAR

Gestation 0–6 weeks 7–16 weeks 17–24 weeks 25–36 weeks >37 weeks
Structural Trachea, bronchi Bronchioles, terminal Respiratory bronchioles, Alveolar ducts, thin- Definitive alveoli
morphogenesis bronchioles, lung primitive alveoli walled alveolar sacs, and mature
circulation increasing type 2 cellsa
functional
type 2 cellsa
Disease Tracheoesophageal Bronchogenic cyst, Pulmonary hypoplasia, RDS, BPD TTN, MAS,
manifestation fistula, pulmonary congenital RDS, BPD, alveolar neonatal
sequestration diaphragmatic capillary dysplasia pneumonia,
hernia, PPHN
congenital cystic
adenomatoid
malformation

BPD¼bronchopulmonary dysplasia; MAS¼meconium aspiration syndrome; PPHN¼persistent pulmonary hypertension of the newborn; RDS¼respiratory
distress syndrome; TTN¼transient tachypnea of the newborn;
a
Type 2 pneumocytes are surfactant-producing cells

more often they present several hours to days after delivery Case 1
as the ductus arteriosus closes. (2) Table 5 aids in this A 3.2-kg female infant is delivered by caesarean section at 38
differentiation. weeks’ gestational age without a trial of labor. Her Apgar
Pulmonary hypertension should be considered in any scores are 9 and 9 at 1 and 5 minutes, respectively. She
infant with respiratory distress and cyanosis. This condition develops tachypnea and subcostal retractions with nasal
results when there is a failure to transition from in utero to flaring at 1 hour of life. Temperature is 97.9°F (36.6°C),
postnatal pulmonary circulation after delivery. Pulmonary pulse is 165 beats per minute, and respiratory rate is 74
vascular resistance remains high, resulting in cyanosis from breaths per minute. Aside from increased work of breathing,
impaired pulmonary blood flow and right-to-left shunting of her physical examination findings are normal. The chest
blood across the foramen ovale and ductus arteriosus. radiograph is shown in Figure 1. She requires supplemental
Shunting further contributes to systemic hypoxemia and oxygen via nasal cannula with a fraction of inspired oxygen
metabolic acidemia—both of which contribute to ongoing (FiO2) of 0.3 for 36 hours. She then weans to room air. Her
increased pulmonary vascular resistance. PPHN may be respiratory rate is 35 breaths per minute, and she has no
primary or secondary to respiratory disease, particularly increased work of breathing.
congenital diaphragmatic hernia, MAS, or RDS. When
Transient Tachypnea of the Newborn
PPHN occurs without concurrent pulmonary disease, dif-
TTN, also known as retained fetal lung fluid syndrome,
ferentiating from cyanotic heart disease is difficult. The
presents with early respiratory distress in term and late-
response to ventilation with 100% oxygen (hyperoxia test)
preterm infants. TTN is a frequent cause of respiratory dis-
can help distinguish the 2 conditions. In some neonates
tress in newborns and is caused by impaired fetal lung fluid
with PPHN, the PaO2 will increase to above 100 mm Hg,
clearance. Normally in utero, the fetal airspaces and air sacs
whereas it will not increase above 45 mm Hg in infants with
are fluid filled. For effective gas exchange to occur after birth,
cyanotic heart defects that have circulatory mixing. (5)(23)
this fluid must be cleared from the alveolar airspaces. Late in
gestation and before birth, the chloride and fluid-secreting
COMMON CASE SCENARIOS
channels in the lung epithelium are reversed so that fluid
Four case scenarios are highlighted to help in identifying the absorption predominates and fluid is removed from the
most common causes of respiratory distress in the newborn lungs. This process is enhanced by labor, so that delivery
followed by discussion about the pathophysiology, risk before labor onset increases the risk of retained fetal lung
factors, prevention, and management strategies for each fluid. (20) Factors that increase the clearance of lung fluid
disorder. include antenatal corticosteroids, fetal thorax compression

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 oxygen, and frequently the distending forces of continuous
TABLE 3. Differential Diagnosis of Respiratory positive airway pressure (CPAP) are necessary to assist in
Distress in the Newborn maintaining alveolar integrity and driving fluid into circula-
tion. Blood gases often reveal a mild respiratory acidosis and
Airway
hypoxemia. The course of TTN is self-limited and does not
Nasal obstruction, choanal atresia, micrognathia, Pierre Robin
usually require mechanical ventilation.
sequence, macroglossia, congenital high airway obstruction
syndrome, including laryngeal or tracheal atresia, subglottic Preventive measures may include avoiding elective cae-
stenosis, laryngeal cyst or laryngeal web, vocal cord paralysis, sarean section before the onset of labor in infants younger
subglottic stenosis, airway hemangiomas or papillomas,
laryngomalacia, tracheobronchomalacia, tracheoesophageal than 39 weeks’ gestation. This is because the most common
fistula vascular rings, and external compression from a neck mass risk factors for TTN include delivery before 39 weeks’
Pulmonary gestation, (1)(2)(3)(9)(25)(26) precipitous delivery, fetal dis-
RDS,a TTN,a MAS,a neonatal pneumonia,a pneumothorax,a PPHN,a tress, maternal sedation, and maternal diabetes. Although it
pleural effusion (congenital chylothorax), pulmonary is well known that premature infants have a higher risk of
hemorrhage, bronchopulmonary sequestration, bronchogenic
respiratory problems, the consequences of early-term deliv-
cyst, congenital cystic adenomatoid malformation or congenital
pulmonary airway malformation, pulmonary hypoplasia, ery (37–38 weeks’ gestation) are underrecognized. Early-
congenital lobar emphysema, pulmonary alveolar proteinosis, term infants have an increased risk of requiring respiratory
alveolar capillary dysplasia, congenital pulmonary
lymphangiectasis, and surfactant protein deficiency support, mechanical ventilation, and neonatal service; deliv-
ery by caesarean section in this population is common and
Cardiovascular
further increases risk. (25) In addition, a single course of
Cyanotic and select acyanotic congenital heart defects,a neonatal
cardiomyopathy, pericardial effusion or cardiac tamponade, fetal antenatal glucocorticoids (2 doses of betamethasone) at least
arrhythmia with compromised cardiac function, and high-output 48 hours before an elective term caesarean delivery de-
cardiac failure
creases respiratory morbidity among infants. (27) On the
Thoracic basis of multiple cohort studies and expert opinion, we
Pneumomediastinum, chest wall deformities, mass, skeletal recommend a careful consideration about elective delivery
dysplasia, and diaphragmatic hernia or paralysis before spontaneous onset of labor at less than 39 weeks’
Neuromuscular gestation and encourage pediatricians to be aware of the
Central nervous system injury (birth trauma or hemorrhage),a increased risk of respiratory morbidity in late preterm and
hypoxic-ischemic encephalopathy,a cerebral malformations, early-term newborns. (1)(2)(3)(9)(25)(26)
chromosomal abnormalities, medication (neonatal or maternal
sedation, antidepressants, or magnesium), congenital TORCH
infections, meningitis, seizure disorder, obstructed Case 2
hydrocephalus, arthrogryposis, congenital myotonic dystrophy, A 2.9-kg male infant is born by vaginal delivery at 39 weeks’
neonatal myasthenia gravis, spinal muscular atrophy, congenital
myopathies, and spinal cord injury gestational age after rupture of membranes for 22 hours.
Other Apgar scores are 8 and 8 at 1 and 5 minutes, respectively. He
requires an FiO2 of 0.4 in the delivery room. He is tachy-
Sepsis,a hypoglycemia,a metabolic acidosis,a hypothermia or
hyperthermia, hydrops fetalis, inborn error of metabolism, pneic and has acrocyanosis. There are coarse rales noted
hypermagnesemia, hyponatremia or hypernatremia, severe bilaterally. Temperature is 98.6°F (37°C), pulse is 144 beats
hemolytic disease, anemia, and polycythemia
per minute, and respiratory rate is 65 breaths per minute.
BPD¼bronchopulmonary dysplasia; MAS¼meconium aspiration syndrome; Despite being given CPAP, his grunting and tachypnea
PPHN¼persistent pulmonary hypertension of the newborn; RDS¼respiratory worsen, and he requires intubation and ventilation for
distress syndrome; TTN¼transient tachypnea of the newborn.
a progressive increased work of breathing, respiratory acido-
Relatively common causes of respiratory distress in the newborn.
sis, and oxygen requirement during the next 6 hours. The
chest radiograph is shown in Figure 1.
with uterine contractions, and a release of fetal adrenaline in
labor, which enhances uptake of lung fluids. (24) Neonatal Pneumonia
Infants with TTN usually present with tachypnea and Respiratory infections in the newborn may be bacterial,
increased work of breathing, which persists for 24 to 72 viral, fungal, spirochetal, or protozoan in origin. Infants
hours. Chest radiographs reveal excess diffuse parenchymal may acquire pneumonia transplacentally, through infected
infiltrates due to fluid in the interstitium, fluid in the inter- amniotic fluid, via colonization at the time of birth, or
lobar fissure, and occasionally pleural effusions (Figure 1). nosocomially. (20) Perinatal pneumonia is the most com-
Management is supportive. Infants may require supplemental mon form of neonatal pneumonia and is acquired at birth.

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 TABLE 4. Perinatal History Associated With Common Respiratory
Diseases in the Newborn Infant
RESPIRATORY DISEASE RISK FACTORS

TTN Caesarian section, precipitous delivery, late preterm or early term, maternal sedation or medication, fetal
distress, gestational diabetes
Neonatal pneumonia Maternal group B streptococcus carrier, chorioamnionitis, maternal fever, PROM, prematurity, perinatal
depression
RDS Prematurity, gestational diabetes, male infant, multiple gestation
MAS MSAF, postterm gestation, fetal distress or perinatal depression, African American ethnicity
Pulmonary hypoplasia Oligohydramnios, renal dysplasia or agenesis, urinary outlet obstruction, premature PROM,
diaphragmatic hernia, neuromuscular disorder (loss of fetal respirations/bell-shaped chest)

MAS¼meconium aspiration syndrome; MSAF¼meconium-stained amniotic fluid; PROM¼prolonged rupture of membranes; RDS¼respiratory distress
syndrome; TTN¼transient tachypnea of the newborn.

Group B streptococcus (GBS) is the most common organ- physiologic features make the newborn at higher risk of
ism that affects term infants. (28)(29) Congenital pneumo- infection. The underdeveloped respiratory cilia and the
nia occurs when the causative organism is passed decreased number of pulmonary macrophages result in
transplacentally to the fetus. The most common pathogens decreased clearance of pathogens from the respiratory sys-
are rubella, cytomegalovirus, adenovirus, enteroviruses, tem. Newborns also have diminished cellular and humoral
mumps, Toxoplasma gondii, Treponema pallidum, Mycobac- immune function, which is even more pronounced in the
terium tuberculosis, Listeria monocytogenes, varicella zoster, premature infant. (28)
and human immunodeficiency virus. (30) Immaturity of the Risk factors for perinatal pneumonia include prolonged
infant’s immune system and the pulmonary anatomical and rupture of membranes (PROM), maternal infection, and

TABLE 5. Differentiation of Cyanotic Heart Disease From Pulmonary

Disease Among Infants in Respiratory Distressa
VARIABLE CYANOTIC HEART DISEASE PULMONARY DISEASE

Previous sibling with congenital heart disease Maternal fever

History Diagnosis of congenital heart disease by prenatal MSAF
ultrasonography Preterm delivery
Cyanosis Cyanosis
Gallop rhythm or murmur Severe retractions
Physical examination Single second heart sound Split second heart sound
Large liver Temperature instability
Mild respiratory distress
Increased heart size Normal heart size
Decreased pulmonary vascularity (except in Abnormal pulmonary parenchyma, such as total
Chest radiograph transposition of the great vessels or total whiteout or patches of consolidation in pneumonia,
anomalous pulmonary venous return) fluid in the fissures in TTN or ground glass
appearance in RDS
Normal or decreased PaCO2 Increased PaCO2
Arterial blood gas
Decreased PaO2 Decreased PaO2
Hyperoxia test PaO2 <150 mm Hg PaO2 >150 mm Hg (except in severe PPHN)
Echocardiography Abnormal heart or vessels Normal heart and vessels

MSAF¼meconium-stained amniotic fluid; PPHN¼persistent pulmonary hypertension of the newborn; RDS¼respiratory distress syndrome; TTN¼transient
tachypnea of the newborn.
a
Reproduced with permission from Aly et al. (23) Copyright 2014 by the American Academy of Pediatrics.

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Figure 1. Case 1: Transient tachypnea of the
newborn is characterized by streaky,
pulmonary interstitial markings and fluid in
the fissure apparent on chest radiograph.
Case 2: Neonatal pneumonia with bilateral
opacities, air bronchograms, and pleural
effusions is apparent. Case 3: Respiratory
distress syndrome is characterized by diffuse,
bilateral, ground glass fields with air
bronchograms secondary to diffuse
atelectasis. Case 4: Meconium aspiration
syndrome causes a chemical pneumonitis,
partial airway obstruction, and a localized
surfactant inactivation that leads to areas of
hyperinflation mixed with diffuse, patchy
infiltrates radiographically.

prematurity. (1) Infants present with increased work of bilateral infiltrates, and a complete blood cell count with
breathing and oxygen requirement. Chest radiography often a differential reveals eosinophilia. Treatment of chlamydial
reveals diffuse parenchymal infiltrates with air broncho- pneumonia or conjunctivitis (even without pneumonia)
grams or lobar consolidation. Pleural effusions may also be requires systemic macrolide antibiotic therapy and ophthal-
seen. In contrast to older infants and children, neonatal mologic follow-up. Regardless of the causal organism, new-
pneumonia is part of a generalized sepsis illness; thus, borns with pneumonia require supportive care in addition
obtaining blood and cerebrospinal fluid cultures and initi- to antibiotics. Many infants will require not only supple-
ating broad-spectrum antibiotic therapy is recommended mental oxygen but also CPAP and mechanical ventilation.
for any symptomatic infant. (31)(32) Other supportive measures include intravenous nutrition
In the newborn with early-onset pneumonia or sepsis, and vasopressors for cardiovascular support. PPHN is
a combination of penicillin and an aminoglycoside are the a common complication of neonatal pneumonia.
preferred initial treatment. (31) For infants who have been On the basis of strong evidence, prevention of neonatal
hospitalized in a neonatal intensive care unit for more than pneumonia and its complications focuses on maternal GBS
4 days, organisms such as methicillin-resistant Staphylococ- screening, intrapartum antibiotic prophylaxis, and appro-
cus aureus and Staphylococcus epidermidis require vancomy- priate follow-up of newborns at high risk after delivery. (4)
cin therapy. Infants who develop pneumonia in the nursery (31)(32)(34) Anyone caring for newborns should be able to
or at home are likely to have infections caused by respiratory recognize at-risk infants and whether appropriate intrapartum
viruses (adenovirus, respiratory syncytial virus, and influ- antibiotic prophylaxis has been administered. They must
enza virus), gram-positive bacteria (streptococcal species also know which infants require additional screening,
and S aureus), and gram-negative enteric bacteria (Klebsiella, observation, and antibiotic initiation after birth. Guidelines
Proteus, Pseudomonas aeruginosa, Serratia marcescens, and have been established by the Centers for Disease Control
Escherichia coli). (30) Infants with pneumonia caused by and Prevention and endorsed by the American Academy of
Chlamydia trachomatis present later in the newborn period Pediatrics and the American College of Obstetrics and
(4–12 weeks of age) with a staccato cough but no wheezing Gynecology for best practice management of at-risk infants.
or fever. (33) Chlamydial conjunctivitis may also be present (4) Infants who require additional attention include those
(5 to 14 days after birth). Chest radiography reveals diffuse born to mothers who are GBS carriers (culture or polymerase

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 chain reaction positive), those with a history of GBS bacteruria, Case 3
those affected by GBS or with an unknown GBS status but A 1.5-kg male is delivered via vaginal delivery because of
who were delivered at less than 37 weeks’ gestation, those preterm labor at 33 weeks’ gestation. Apgar scores are 7 and
with PROM of 18 hours or long, or those with intrapartum 8 at 1 and 5 minutes, respectively. The infant is cyanotic and
fever (‡100.4°F [38°C]). (4)(31) The preferred intrapartum requires CPAP immediately after delivery. He has subcostal
antibiotic for these situations is intravenous penicillin (5 retractions, grunting, and nasal flaring. Auscultation reveals
million units followed by 2.5 million to 3.0 million units decreased air entry in the lung fields throughout. Temper-
every 4 hours) administered at least 4 hours before delivery; ature is 98.2°F (36.8°C), pulse is 175 beats per minute, and
cefazolin may be used for penicillin-allergic women who are respiratory rate is 70 breaths per minute. He requires an
at low risk for anaphylaxis. (4)(31) For severely penicillin- FiO2 of 0.4. His chest radiograph is shown in Figure 1.
allergic women, clindamycin culture sensitivity should be
performed, and if mother’s strain is sensitive (75% of cases), Respiratory Distress Syndrome
clindamycin should be used. Vancomycin is reserved for RDS, also known as hyaline membrane disease, is a com-
severely allergic women with resistant strains. (4)(31) In mon cause of respiratory disease in the premature infant.
addition to intrapartum antibiotic prophylaxis, promising RDS is also seen in infants whose mothers have diabetes in
GBS vaccines are in clinical trials (35) and may be widely pregnancy. RDS is caused by a deficiency of alveolar sur-
accepted by patients (36) but are not yet ready for general factant, which increases surface tension in alveoli, resulting
use. in microatelectasis and low lung volumes. Surfactant defi-
Since widespread implementation of maternal GBS ciency appears as diffuse fine granular infiltrates on radio-
screening and intrapartum antibiotic prophylaxis adminis- graph (Figure 1). Pulmonary edema plays a central role in
tration, the incidence of early-onset GBS infection has the pathogenesis of RDS and contributes to the develop-
decreased from 1.8 cases per 1,000 to 0.3 case per 1,000 ment of air bronchograms. Excess lung fluid is attributed to
live births. (31)(32) However, cases and deaths continue to epithelial injury in the airways, decreased concentration of
occur with GBS as the leading offender. (31)(34)(35) Most of sodium-absorbing channels in the lung epithelium, and
the term infants affected are born to mothers without or a relative oliguria in the first 2 days after birth in premature
with an unknown GBS status but who had PROM or fever infants. (37) Infants typically improve on onset of diuresis by
and did not receive antibiotic administration during labor. the fourth day after birth.
(34) Others are born to women who received inadequate Infants with RDS typically present within the first several
prophylaxis (<4 hours before delivery or macrolide antibi- hours of life, often immediately after delivery. Clinically,
otic use). (31) Many missed opportunities for prevention infants have marked respiratory distress with tachypnea,
increase the burden of disease. (29) nasal flaring, grunting, and subcostal, intercostal, and/or
Thus, it is imperative to appropriately manage any new- suprasternal retractions. Grunting occurs when an infant
born with the aforementioned risk factors cautiously after attempts to maintain an adequate FRC in the face of poorly
birth. According to updated 2010 guidelines, any infant compliant lungs by partial glottic closure. As the infant
who develops signs or symptoms of illness requires a full prolongs the expiratory phase against this partially closed
diagnostic evaluation (including blood and spinal fluid glottis, there is a prolonged and increased residual volume
cultures) and antibiotic initiation. (4)(31)(32) If maternal that maintains the airway opening and also an audible
chorioamnionitis is suspected but the infant has no signs expiratory sound. Infants with RDS have cyanosis and
or symptoms of disease, a limited evaluation (blood culture require supplemental oxygen. Mild cases of RDS may
and complete blood cell count), along with antibiotic therapy respond to the distending pressures of CPAP, but more
initiation for at least 48 hours, is recommended. (4)(31)(32) severe cases require endotracheal intubation and adminis-
Asymptomatic, at-risk infants, who did not receive adequate tration of exogenous surfactant into the lungs. Currently,
antibiotic prophylaxis, require a limited evaluation and obser- there are no universal guidelines that dictate if and when to
vation for 48 hours, but antibiotic initiation is not necessary administer exogenous surfactant. Some institutions advo-
unless clinical suspicion arises. (4)(31)(32) Asymptomatic, at- cate administration of prophylactic surfactant in the first 2
risk infants who received adequate intrapartum antibiotic pro- hours of life for all premature infants younger than 30
phylaxis should be observed for 48 hours. Adherence to these weeks’ gestation. Others begin with noninvasive ventilation
guidelines will decrease the incidence of neonatal pneumonia (CPAP) and reserve intubation and surfactant administra-
and allow for early detection and treatment that may prevent tion only for infants who require more than 35% to 45%
life-threatening complications, such as PPHN or death. oxygen concentration to maintain an arterial PaO2 greater

424 Pediatrics in Review

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than 50 mm Hg. In determining a management strategy, it per minute. Physical examination findings are significant
is important to consider the administration of antenatal for marked increased work of breathing with nasal flaring,
corticosteroids, the clinical presentation, radiographic find- subcostal and suprasternal retractions, a barrel-shaped
ings, and the infant’s oxygen requirements. (38) chest, and coarse rhonchi in bilateral lung fields. Her chest
The course of RDS is self-limited and typically improves radiograph is shown in Figure 1.
by age 3 to 4 days in correlation with the aforementioned
diuresis phase and as the infant begins to produce endog- Meconium Aspiration Syndrome
enous surfactant. (20) Use of mechanical ventilation before MSAF occurs when the fetus passes meconium before birth.
this is supportive and should proceed with caution to avoid Infants born through MSAF are at risk for aspiration of
ventilator-induced lung injury. Infants who do not improve meconium in utero or immediately after birth. Any infant
with surfactant administration should be evaluated for the who is born through MSAF and develops respiratory dis-
presence of a patent ductus arteriosus or other congenital tress after delivery, which cannot be attributed to another
heart disease. The infant who initially improves with admin- cause, is diagnosed as having MAS.
istration of surfactant and subsequently deteriorates should Meconium is composed of lanugo, bile, vernix, pancre-
also be evaluated for nosocomial pneumonia. (20) On atic enzymes, desquamated epithelia, amniotic fluid, and
admission, it is appropriate to initiate antibiotic therapy mucus. Meconium is present in the gastrointestinal tract as
in the newborn with RDS because pneumonia may present early as 16 weeks’ gestation but is not present in the lower
clinically in the same manner and findings on chest radio- descending colon until 34 weeks’ gestation; therefore, MSAF
graphs can be indistinguishable from RDS. is seldom seen in infants younger than 37 weeks’ gestation.
Preventing premature birth will lower the incidence of (41) In the compromised fetus, hypoxia or acidosis may result
RDS. However, attempts to prevent premature births have in a peristaltic wave and relaxation of the anal sphincter,
been largely unsuccessful, with the rate of premature births resulting in meconium passage in utero. Aspiration may
still 11.5% of all births in 2012. To benefit those infants who occur in utero or immediately after birth as the compromised
will deliver prematurely, multiple randomized clinical trials fetus gasps.
strongly support the use of maternal antenatal corticoste- Meconium is toxic to the newborn lung, causing inflam-
roids. Two doses of betamethasone significantly reduce the mation and epithelial injury as it migrates distally. The pH of
incidence of RDS, intraventricular hemorrhage, and mor- meconium is 7.1 to 7.2. The acidity causes airway inflam-
tality in infants age 23 to 29 weeks’ gestation. (5)(39)(40) mation and a chemical pneumonitis with release of cyto-
kines. (41) As meconium reaches the small airways, partial
Case 4 obstruction occurs, which results in air trapping and
A 4.4-kg female infant is delivered via caesarean section at hyperaeration. The typical chest radiograph initially appears
41 weeks’ gestational age because of presumed large for streaky with diffuse parenchymal infiltrates. In time, lungs
gestational age status. The amniotic fluid is stained with become hyperinflated with patchy areas of atelectasis and
thick meconium. She is limp and cyanotic at birth with infiltrate amid alveolar distension (Figure 1). Surfactant is
minimal respiratory effort. Apgar scores are 2 and 7 at 1 and inactivated by the bile acids in meconium, resulting in
5 minutes, respectively. Temperature is 99°F (37.2°C), pulse localized atelectasis, so alternatively, radiographs may
is 177 beats per minute, and respiratory rate is 80 breaths resemble those of RDS with low lung volumes. Although

Figure 2. Common complications of

meconium aspiration syndrome include
pneumothorax (left upper) and persistent
pulmonary hypertension of the newborn
(right upper) characterized by cyanosis with
normal lung fields and decreased pulmonary
vascular markings.

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 air leak syndromes may occur with other respiratory dis- Approximately 13% of all live births are through MSAF.
eases of the newborn, pneumomediastinum, pneumotho- Although the number of cases has decreased during the past
rax, and PPHN are common in MAS (Figure 2). decade, 4% to 5% of these will develop MAS. (30)(41) Pre-
Management is directed at strategies to support the viously, many postterm infants (‡42 weeks’ gestation) devel-
infant. Supplemental oxygen is required, and CPAP and oped MAS. However, a recent meta-analysis provides evidence
mechanical ventilation may also be considered in severe that induction of labor at 41 weeks’ gestation reduces the risk
cases. Replacement with exogenous surfactant is common of MAS and perinatal death without increasing the risk of
practice and reduces the need for extracorporal membrane caesarean section. (7) Therefore, many obstetricians do not
oxygenation (ECMO) and the risk of pneumothorax. (42) allow pregnancies to advance beyond 41 weeks’ gestation. In
Because MAS results in a ventilation-perfusion mismatch addition, advances in fetal heart rate monitoring have iden-
whereby ventilated alveolar units are not perfused by pul- tified compromised fetuses, allowing for timely obstetric
monary blood vessels, severe hypoxemia may result and intervention that may help prevent in utero aspiration of
further increases pulmonary vascular resistance. Echocar- meconium. Amnioinfusion or transcervical infusion of saline
diography helps confirm PPHN by revealing ventricular into the amniotic cavity has been proposed as a practice to
septal wall flattening, tricuspid regurgitation, and right-to- decrease the incidence of MAS. Although amnioinfusion is
left shunting at the patent ductus arteriosus. Inhaled nitric beneficial for the distressed fetus with oligohydramnios, best
oxide is a selective pulmonary vasodilator without systemic evidence does not indicate a reduced risk of moderate to
effects. It is often used with high-frequency ventilation in severe MAS or perinatal death. (49)
severe cases of MAS to maintain adequate oxygenation and
ventilation and reduce the need for ECMO. Initiation of CONCLUSION
broad-spectrum antibiotic therapy is appropriate because
Learning to readily recognize respiratory distress in the
meconium is a growth medium for gram-negative organ-
newborn and understanding physiologic abnormalities as-
isms. Residual pulmonary compromise is common after
sociated with each of the various causes will guide optimal
MAS. As many as 50% of affected infants are diagnosed as
management. Although decreasing the incidence through
having reactive airway disease during their first 6 months of
preventive measures is ideal, early recognition and treat-
life, and persistent pulmonary insufficiency is seen in
ment of the common neonatal respiratory diseases will de-
children as old as 8 years. (43)
crease both short- and long-term complications and related
Because of the significant morbidity associated with
mortality of at-risk infants.
MAS, preventive measures are important. Historically, oro-
pharyngeal and nasopharyngeal suctioning was performed
on the meconium-stained infant after delivery of the head Summary
but before delivery of the shoulders and was initially thought • Respiratory distress presents as tachypnea, nasal flaring,
to be an effective preventive measure. (44) However, a large, retractions, and grunting and may progress to respiratory failure if
multicenter randomized controlled trial in 2004 found that not readily recognized and managed.
this practice does not prevent MAS or decrease the need for • Causes of respiratory distress vary and may not lie within the lung.
mechanical ventilation or hospital length of stay. (45) Con- A thorough history, physical examination, and radiographic and
sequently, routine suctioning on the perineum is no longer laboratory findings will aid in the differential diagnosis. Common
causes include transient tachypnea of the newborn, neonatal
indicated. Endotracheal suctioning immediately after birth
pneumonia, respiratory distress syndrome (RDS), and meconium
was also a routine practice for all meconium-stained infants aspiration syndrome (MAS).
until a large randomized controlled trial found that intubating • Strong evidence reveals an inverse relationship between
and suctioning vigorous infants born through MSAF had no gestational age and respiratory morbidity. (1)(2)(9)(25)(26) Expert
benefit and increased the rate of complications. (46) This opinion recommends careful consideration about elective
finding has been confirmed by additional, well-designed delivery without labor at less than 39 weeks’ gestation.
studies, (47) prompting a change in practice guidelines in • Extensive evidence, including randomized control trials, cohort
2000. Current evidence still supports immediate endotra- studies, and expert opinion, supports maternal group B streptococcus
screening, intrapartum antibiotic prophylaxis, and appropriate follow-
cheal suctioning of the depressed infant as defined by a low
up of high-risk newborns according to guidelines established by the
heart rate (<100 beats per minute), poor muscle tone, and Centers for Disease Control and Prevention. (4)(29)(31)(32)(34)
no spontaneous respiratory effort. (8) Intubation and suc- Following these best-practice strategies is effective in preventing
tioning the vigorous, spontaneously breathing infant is not neonatal pneumonia and its complications. (31)(32)(34)
recommended. (8)(47)(48)

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 13. Adzick NS, Harrison MR, Crombleholme TM, Flake AW, Howell LJ.
Fetal lung lesions: management and outcome. Am J Obstet Gynecol.
• On the basis of strong evidence, including randomized control
1998;179(4):884–889
trials and Cochrane Reviews, administration of antenatal
corticosteroids (5) and postnatal surfactant (6) decrease 14. Bak SY, Shin YH, Jeon JH, et al. Prognostic factors for treatment
outcomes in transient tachypnea of the newborn. Pediatr Int.
respiratory morbidity associated with RDS.
2012;54(6):875–880
• Trends in perinatal management strategies to prevent MAS have
15. Warren JB, Anderson JM. Newborn respiratory disorders. Pediatr
changed. There is strong evidence that amnioinfusion, (49) Rev. 2010;31(12):487–495, quiz 496
oropharyngeal and nasopharyngeal suctioning at the perineum,
16. West JB. Respiratory Physiology: The Essentials. Baltimore, MD:
(45) or intubation and endotracheal suctioning of vigorous
Williams & Wilkins; 2012
infants (46)(47) do not decrease MAS or its complications. Some
research and expert opinion supports endotracheal suctioning of 17. Davis RP, Mychaliska GB. Neonatal pulmonary physiology. Semin
Pediatr Surg. 2013;22(4):179–184
nonvigorous meconium-stained infants (8) and induction of labor
at 41 weeks’ gestation (7) to prevent MAS. 18. Wilmott RW, Boat TF, Bush A, Chernick V, Deterding RR. Kendig
and Chernick’s Disorders of the Respiratory Tract in Children.
Philadelphia, PA: Elsevier Saunders; 2012
19. Magder S. Bench-to-bedside review: ventilatory abnormalities in
sepsis. Crit Care. 2009;13(1):202
References 20. Weisman LE, Hansen TN. Contemporary Diagnosis and Management
1. Edwards MO, Kotecha SJ, Kotecha S. Respiratory distress of the of Neonatal Respiratory Diseases. 3rd ed. Newton, PA: Handbooks in
term newborn infant. Paediatr Respir Rev. 2013;14(1):29–36 Health Care Co.; 2003

2. Hibbard JU, Wilkins I, Sun L, et al; Consortium on Safe Labor. 21. Bancalari E, Polin RA. The Newborn Lung: Neonatology Questions and
Respiratory morbidity in late preterm births. JAMA. 2010;304 Controversies. Philadelphia, PA: Saunders Elsevier; 2008
(4):419–425 22. Bhandari A, McGrath-Morrow S. Long-term pulmonary outcomes
3. Mahoney AD, Jain L. Respiratory disorders in moderately preterm, of patients with bronchopulmonary dysplasia. Semin Perinatol.
late preterm, and early term infants. Clin Perinatol. 2013;40(4): 2013;37(2):132–137
665–678 23. Aly H. Respiratory disorders in the newborn: identification and
4. Verani JR, McGee L, Schrag SJ. Division of Bacterial Diseases, diagnosis. Pediatr Rev. 2004;25(6):201–208
National Center for Immunization and Respiratory Diseases, 24. Elias N, O’Brodovich H. Clearance of fluid from airspaces of
Centers for Disease Control and Prevention. Prevention of perinatal newborns and infants. Neoreviews. 2006;7:e88
group B streptococcal disease: revised guidelines from CDC, 2010.
25. Sengupta S, Carrion V, Shelton J, et al. Adverse neonatal outcomes
MMWR Recomm Rep. 2010;59(RR-10):1–36
associated with early-term birth. JAMA Pediatr. 2013;167(11):
5. Carlo WA, McDonald SA, Fanaroff AA, et al; Eunice Kennedy 1053–1059
Shriver National Institute of Child Health and Human
26. Shapiro-Mendoza CK, Tomashek KM, Kotelchuck M, et al. Effect of
Development Neonatal Research Network. Association of antenatal
late-preterm birth and maternal medical conditions on newborn
corticosteroids with mortality and neurodevelopmental outcomes
morbidity risk. Pediatrics. 2008;121(2):e223–e232
among infants born at 22 to 25 weeks’ gestation. JAMA. 2011;306
(21):2348–2358 27. Jain L, Dudell GG. Respiratory transition in infants delivered by
cesarean section. Semin Perinatol. 2006;30(5):296–304
6. Bahadue FL, Soll R. Early versus delayed selective surfactant
treatment for neonatal respiratory distress syndrome. Cochrane 28. Campbell JR. Neonatal pneumonia. Semin Respir Infect. 1996;11
Database Syst Rev. 2012;11:CD001456 (3):155–162
7. Gülmezoglu AM, Crowther CA, Middleton P, Heatley E. Induction 29. Stoll BJ, Hansen NI, Sánchez PJ, et al; Eunice Kennedy Shriver
of labour for improving birth outcomes for women at or beyond National Institute of Child Health and Human Development
term. Cochrane Database Syst Rev. 2012;6:CD004945 Neonatal Research Network. Early onset neonatal sepsis: the burden
of group B streptococcal and E. coli disease continues. Pediatrics.
8. Bhat R, Vidyasagar D. Delivery room management of meconium-
2011;127(5):817–826
stained infant. Clin Perinatol. 2012;39(4):817–831
30. Flidel-Rimon O, Shinwell ES. Respiratory distress in the term and
9. Gouyon JB, Ribakovsky C, Ferdynus C, Quantin C, Sagot P, Gouyon
near-term infant. Neoreviews. 2005;6:2289–e297
B; Burgundy Perinatal Network. Severe respiratory disorders in
term neonates. Paediatr Perinat Epidemiol. 2008;22(1):22–30 31. Randis TM, Polin RA. Early-onset group B streptococcal sepsis: new
recommendations from the Centres for Disease Control and
10. Williams O, Hutchings G, Hubinont C, Debauche C, Greenough A.
Prevention. Arch Dis Child Fetal Neonatal Ed. 2012;97(4):F291–F294
Pulmonary effects of prolonged oligohydramnios following mid-
trimester rupture of the membranes—antenatal and postnatal 32. Oh W. Early onset neonatal group B streptococcal sepsis. Am J
management. Neonatology. 2012;101(2):83–90 Perinatol. 2013;30(2):143–147
11. Piper JM, Xenakis EM, Langer O. Delayed appearance of pulmonary 33. Nissen MD. Congenital and neonatal pneumonia. Paediatr Respir
maturation markers is associated with poor glucose control in Rev. 2007;8(3):195–203
diabetic pregnancies. J Matern Fetal Med. 1998;7(3):148–153 34. Puopolo KM, Madoff LC, Eichenwald EC. Early-onset group B
12. Jobe AH. Effects of chorioamnionitis on the fetal lung. Clin streptococcal disease in the era of maternal screening. Pediatrics.
Perinatol. 2012;39(3):441–457 2005;115(5):1240–1246

Vol. 35 No. 10 O C T O B E R 2 0 1 4 427

Downloaded from http://pedsinreview.aappublications.org/ at Sanford Health Sciences Library - Bismarck on October 30, 2014
 35. Madhi SA, Dangor Z, Heath PT, et al. Considerations for a phase-III 42. Findlay RD, Taeusch HW, Walther FJ. Surfactant replacement therapy
trial to evaluate a group B Streptococcus polysaccharide-protein for meconium aspiration syndrome. Pediatrics. 1996;97(1):48–52
conjugate vaccine in pregnant women for the prevention of early- 43. Macfarlane PI, Heaf DP. Pulmonary function in children after
and late-onset invasive disease in young-infants. Vaccine. 2013;31 neonatal meconium aspiration syndrome. Arch Dis Child. 1988;63
(suppl 4):D52–D57 (4):368–372
36. Dempsey AF, Pyrzanowski J, Donnelly M, et al. Acceptability of 44. Carson BS, Losey RW, Bowes WA Jr, Simmons MA. Combined
a hypothetical group B strep vaccine among pregnant and recently obstetric and pediatric approach to prevent meconium aspiration
delivered women. Vaccine. 2014;32(21):2463–2468 syndrome. Am J Obstet Gynecol. 1976;126(6):712–715
37. Helve O, Pitkänen OM, Andersson S, O’Brodovich H, Kirjavainen T, 45. Vain NE, Szyld EG, Prudent LM, Wiswell TE, Aguilar AM, Vivas NI.
Otulakowski G. Low expression of human epithelial sodium Oropharyngeal and nasopharyngeal suctioning of meconium-
channel in airway epithelium of preterm infants with respiratory stained neonates before delivery of their shoulders: multicentre,
distress. Pediatrics. 2004;113(5):1267–1272 randomised controlled trial. Lancet. 2004;364(9434):597–602
38. Lista G, Castoldi F. Which clinical markers for appropriate timing of 46. Linder N, Aranda JV, Tsur M, et al. Need for endotracheal intubation and
surfactant therapy?Acta Biomed. 2013;84(suppl 1):15–17 suction in meconium-stained neonates. J Pediatr. 1988;112(4):613–615
39. Hayes EJ, Paul DA, Stahl GE, et al. Effect of antenatal corticosteroids 47. Wiswell TE, Gannon CM, Jacob J, et al. Delivery room management
on survival for neonates born at 23 weeks of gestation. Obstet of the apparently vigorous meconium-stained neonate: results of the
Gynecol. 2008;111(4):921–926 multicenter, international collaborative trial. Pediatrics. 2000;105
40. Abbasi S, Oxford C, Gerdes J, Sehdev H, Ludmir J. Antenatal (1, pt 1):1–7
corticosteroids prior to 24 weeks’ gestation and neonatal outcome of 48. Wiswell TE. Handling the meconium-stained infant. Semin
extremely low birth weight infants. Am J Perinatol. 2010;27(1): Neonatol. 2001;6(3):225–231
61–66 49. Fraser WD, Hofmeyr J, Lede R, et al; Amnioinfusion Trial Group.
41. Yeh TF. Meconium aspiration syndrome: pathogenesis and current Amnioinfusion for the prevention of the meconium aspiration
management. Neoreviews. 2010;11:e503–e51 syndrome. N Engl J Med. 2005;353(9):909–917

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PIR Quiz
1. Which of the following is the strongest risk factor associated with the development of REQUIREMENTS: Learners
transient tachypnea of the newborn (TTN)? can take Pediatrics in
A. Cesarean birth of a 38-week-gestation infant. Review quizzes and claim
B. Hypothermia. credit online only at:
C. Maternal edema. http://pedsinreview.org.
D. Maternal preeclampsia.
E. Small for gestational age. To successfully complete
2. A gravida 3, para 2 mother presents at 38 weeks’ gestation in spontaneous labor from 2014 Pediatrics in Review
home. She reports spontaneous rupture of membranes the previous day (22 hours ago) articles for AMA PRA
that is confirmed on inspection. She has a low-grade temperature of 100.5°F (38.1°C) but Category 1 CreditTM,
has not had any problems during the pregnancy and is group B streptococcus negative. learners must
She is allergic to amoxicillin from which she developed a nonurticarial rash but has no demonstrate a minimum
other known allergies. The obstetrician asks you about the best management to prevent performance level of 60%
neonatal pneumonia. You reply: or higher on this
A. Institute intrapartum antibiotic prophylaxis with intravenous cefazolin. assessment, which
B. Institute intrapartum antibiotic prophylaxis with intravenous penicillin. measures achievement of
C. Institute intrapartum antibiotic prophylaxis with oral azithromycin. the educational purpose
D. Monitor fever and if it persists proceed with a caesarian section. and/or objectives of this
E. Rescreen for group B streptococcus with a nucleic acid amplification test. activity. If you score less
than 60% on the
3. A 3.8-kg female infant is born to the mother presented and managed in question 2. The
assessment, you will be
infant has a heart rate of 180 beats per minute and mild grunting and flaring. She is mildly
given additional
pale and has oxygen saturation of 85% on room air at 20 minutes after birth. The best
opportunities to answer
practice management strategy for this infant is:
questions until an overall
A. Allow the family time to bond with the infant, placing the infant skin to skin with 60% or greater score is
mother. achieved.
B. Stabilize the infant’s respiratory status and observe for 48 hours.
C. Stabilize the infant’s respiratory status and obtain a limited evaluation, including
a complete blood cell count and blood culture.
D. Stabilize the infant’s respiratory status, obtain a limited evaluation that includes
a complete blood cell count and blood culture, and initiate intravenous antibiotic
therapy.
E. Stabilize the infant’s respiratory status, plan a complete evaluation that includes
a complete blood cell count and blood and spinal fluid culture, and initiate
intravenous antibiotic therapy.
4. A 1.1-kg female is born at 29 weeks’ gestation because of preterm labor. She is vigorous at
birth but shows signs of significant respiratory distress evidenced by subcostal retractions,
nasal flaring, and audible expiratory grunting. She is diagnosed as having respiratory
distress syndrome and administered exogenous endotracheal surfactant. At what period
would one expect to observe the diuretic phase of respiratory distress syndrome?
A. Within 1 day after birth.
B. 4 days after birth.
C. 7 days after birth.
D. 10 days after birth.
E. Immediately after birth.
5. A 4.5-kg male infant is born via cesarean section at 41 weeks’ gestation in meconium-
stained amniotic fluid. At birth he is noted to have a low heart rate, poor muscle tone, and
no spontaneous respirations. Which of the following procedures has been found to have
the greatest effect on a favorable outcome in this infant?
A. Amnioinfusion 6 hours before delivery.
B. Antenatal maternal corticosteroids.
C. Endotracheal intubation and suctioning before the infant’s first breath.
D. Oropharyngeal and nasopharyngeal suctioning before delivery of the shoulders.
E. Systemic macrolide antibiotic therapy.

Vol. 35 No. 10 O C T O B E R 2 0 1 4 429

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 Respiratory Distress in the Newborn
Suzanne Reuter, Chuanpit Moser and Michelle Baack
Pediatrics in Review 2014;35;417
DOI: 10.1542/pir.35-10-417

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