“Respiratory Distress in the Newborn” by Megan Connelly for OPENPediatrics


Respiratory Distress in the
Newborn by Dr. Megan Connelly. Learning Objectives. By the end of this
video, the viewer will understand the
differential diagnosis for newborn respiratory
distress and will learn the epidemiology,
pathophysiology, presentation, diagnosis, and management for
the most common etiologies. You are paged to the
nursery to examine a newborn described as being
in respiratory distress. Immediately, you start running
through the differential diagnosis in your head. What history do you need to
know to guide your thinking? History that you’ll find
useful to know includes, how old is the baby? What is the gestational age? Was the delivery vaginal
or via Cesarean section? Is this a preterm, term,
or postterm infant? Were there any
sepsis risk factors? Was mother well
prior to delivery? Was mother Group B Strep
positive or negative? Did mother receive any
antibiotics while in labor? Was the amniotic fluid
clear or meconium-stained? For an infant to transition
to life outside the uterus, multiple physiologic changes
must occur very rapidly. His alveoli must transition from
being filled with fluid to air. He must begin to breathe
in a regular pattern. He must decrease his
pulmonary vascular resistance so that pulmonary blood
flow is increased. Most infants are able
to do this with no aid, but approximately 10% will
require assistance at birth. The differential diagnosis
for respiratory distress in the newborn is long. But with a basic
history, you are able to better narrow
down the diagnoses and determine the
appropriate treatment path. Transient Tachypnea
of the Newborn, TTN, is the most
common etiology, accounting for 60% of cases
of respiratory distress. TTN is due to excess
fluid in the lungs due to impaired clearance of
the fetal lung fluid at birth. Risk factors for
TTN include infants born at less than
39 weeks of age, as well as infants born
via Cesarean section without labor, male
infants, and infants born to mothers with
gestational diabetes. Most commonly, these
infants present within the first
few minutes to hours after birth with tachypnea
which, in an infant, is a respiratory rate
greater than 60 breaths per minute, nasal flaring,
grunting, and retractions. On auscultation, lung
fields may be clear or crackles may be appreciated. Frequently, these infants
have some cyanosis, but very rarely do they need
more supplemental oxygen than 40% FiO2. TTN is a clinical diagnosis,
but on chest X-ray, you can often see
fluid in the interlobar fissure as well as
hyperexpanded lungs with flattened diaphragms,
prominent vasculature in a sunburst
pattern, and sometimes alveolar edema appearing
as fluffy densities. In most infants, the
respiratory symptoms will resolve by 48
to 72 hours of life. If the respiratory
distress resolves within the first two to
six hours after birth, these symptoms may be due to
a brief delay in lung fluid absorption and is often termed
“delayed transition” instead. Neonatal Pneumonia. Neonatal pneumonia
accounts for 11% of cases of neonatal
respiratory distress. Pneumonia is more commonly seen
in infants born prematurely. Other risk factors include
maternal chorioamnionitis and rupture of membranes
of greater than 18 hours. Early-onset pneumonia,
which occurs within three days of
birth, is vertically transmitted from the
mother via aspiration of infected amniotic fluid or
transplacental transmission of organisms via the
placental circulation. Common pathogens of
early onset pneumonia include Group B Strep, which
is the most common, as well as E. coli, Klebsiella,
and Herpes Simplex Virus. Symptoms of
early-onset pneumonia include respiratory distress,
poor feeding, apnea, tachycardia, and poor perfusion. Diagnosis of
neonatal pneumonia is made via laboratory finding
suggestive of infection, such as an elevated
white blood cell count, and characteristic
findings on chest X-ray which often shows bilateral
alveolar densities with air bronchograms. The empiric treatment
of early-onset pneumonia is often with ampicillin
and gentamicin. Late-onset pneumonia is
often hospital-acquired, with a major risk factor being
receipt of respiratory support. Another possible etiology
of late-onset pneumonia is chlamydia trachomatis, which
has a very long incubation period and causes pneumonia
at two to four weeks of life. Respiratory Distress Syndrome. Respiratory Distress
Syndrome, RDS, is a disease most commonly
seen in premature infants with the frequency decreasing
significantly after 37 weeks’ gestational age. RDS is due to the deficiency
of pulmonary surfactant in the immature lung. Surfactant is a
phospholipid that decreases the alveolar
surface tension, which helps with alveolar
expansion and decreases risk of atelectasis. Not all infants may appear
ill immediately after birth, but if RDS is untreated, they
will progressively worsen over the first 48 hours of life. Symptoms include tachypnea,
nasal flaring, grunting, retractions, and cyanosis. In particular,
infants with RDS often grunt in order to
generate positive pressure to keep alveoli open. Chest X-ray typically
demonstrates low lung volumes as well as a classic diffuse
ground glass appearance with air bronchograms. Many studies have
demonstrated that RDS is both less common
and less severe if corticosteroids
are administered to the mother prior to
a pre-term delivery. All neonates at
risk for RDS should receive respiratory support that
reduces alveolar atelectasis, most commonly CPAP. If persistent severe
respiratory distress is noted, infants are intubated
and surfactant is given via the endotracheal tube. Meconium Aspiration Syndrome. In 4% to 9% of infants born
through meconium-stained amniotic fluid, Meconium
Aspiration Syndrome, MAS, is diagnosed. Affected infants are frequently
small for gestational age or post-term. Infants pass meconium
in utero due to stress, most commonly fetal hypoxia. The pathophysiology of MAS
is a complex combination of many factors. These include the
release of cytokines and other pro-inflammatory
factors following the aspiration of
sterile meconium into the lungs as well as
obstruction of the airways, leading to distal gas trapping
with subsequent alveolar rupture and the
deactivation and decreased synthesis of surfactant. These infants
frequently have marked tachypnea, retractions,
grunting and flaring, as well as cyanosis. Their respiratory symptoms
develop immediately after birth. The chest X-ray typically
shows hyperinflation with flattened
diaphragms as well as diffuse patchy
densities alternating with areas of expansion. Treatment consists primarily
of respiratory support. Some infants will be ill enough
to require Extracorporeal Membrane Oxygenation, or ECMO. Other less common etiologies
of newborn respiratory distress include persistent
pulmonary hypertension of the newborn, pneumothorax,
congenital heart disease, congenital
diaphragmatic hernias, and pulmonary
congenital defects. Case Study. You arrive at the warmer and
see a three-hour old infant born at 37 weeks. He’s breathing 60 to
80 breaths per minute, with mild nasal flaring and
intercostal retractions. Pulse oximetry is
reading 90% on room air. His mother was negative
for Group B Strep and the infant was born via
scheduled repeat Cesarean section with
rupture of membranes at the time of delivery. On auscultation, he has
good air entry bilaterally, but scattered crackles
are appreciated. His heart rate is regular
and no murmur is appreciated. He is pink and well perfused. Your differential
diagnosis includes TTN, RDS, and, much less likely,
a pneumothorax or pneumonia. You place him on 30% FiO2 with
normalization of his oxygen levels to greater than 95% and
improvement in his tachypnea and nasal flaring. A chest X-ray is
obtained that shows fluid in the interlobar fissure
and mildly hyperexpanded lungs. You feel confident,
given his response to minimal respiratory support
as well as the X-ray findings, that this infant has
TTN and should improve over the next day or two.

9 thoughts on ““Respiratory Distress in the Newborn” by Megan Connelly for OPENPediatrics

  1. Not only was the explanation super clear, but the added case study at the end helped so much in testing my understanding. Thank you!

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