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Katlyn Carter

Respiratory Conditions in the Newborn

Meconium Aspiration Syndrome (MAS)


Definition & Pathophysiology: MAS happens when fluid stained with meconium is aspirated in
the lungs of the fetus/neonate. Approximately 8-20% of all live-born, late pre-term, near or term
infants are born through meconium stained amniotic fluid. One-third of these newborns will
develop MAS. The presence of meconium in the lungs may produce the following:

 Mechanical obstruction of the airways and air is allowed in but not exhaled causing
alveoli to overdistend
 Chemical pneumonitis which may lead to the development of secondary bacterial
pneumonias
 Inactivation of natural surfactant
Alternative names: none
Causes & Clinical Manifestations:

 when a neonate is born through meconium-stained amniotic fluid and aspirates


 when the fetus experiences an episode of fetal hypoxia in utero a few days or a few
minutes before birth, indicated by a sudden increase in fetal movement followed by
diminished activity, slowing FHR or weak or irregular heartbeat, loss of FHR variability,
and meconium staining of the amniotic fluid
 presence of signs of distress at birth such as:
o pallor
o cyanosis
o apnea
o slow heart beat
o low APGAR scores (below 6) at 1 and 5 mins
 exhibit respiratory depression at birth and require resuscitation
Symptoms:

 many infants require mechanical ventilation at birth due to immediate signs of distress
o generalized cyanosis
o tachypnea
o severe retractions
 an overdistended, barrel-shaped chest with increased anteroposterior diameter
 auscultation reveals diminished air movement with prominent rales and rhonchi
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 abdominal palpation may find a displaced liver (from over expansion of the lungs)
 yellowish/pale green staining of the skin, nails, and umbilical cord
Differential diagnoses:

 Sepsis
 Pneumonia
 Delayed transition from fetal circulation
 Pneumothorax
 Pulmonary edema
 Blood aspiration
 Pulmonary hypertension
 Congenital heart disease

Management (alternative treatments, other measures/procedures)

 If the infant is vigorous, no further treatment necessary


 If the infant is absent or depressed respirations, heart rate less than 100 bpm or poor
muscle tone, direct tracheal suctions is indicated (with DeLee)
 Transfer is indicated with further resuscitative efforts

(Davidson, et al., p. 826-827, 2016)

Infant Respiratory Distress Syndrome (RDS)


Definition & Pathophysiology: an inappropriate respiratory adaptation to extrauterine life; results
of a primary absence, deficiency, or alteration in the production of pulmonary surfactant, a
substance produced in the lungs that keeps lungs from collapsing on expiration; occurs most
often in premature Caucasian infants (and twice as often in males). The resulting lung instability
causes the biochemical problems of hypoxia, hypercarbia, and acidemia, which further increases
pulmonary vasoconstriction and hypoperfusion.
Alternative names: hyaline membrane disease (HMD)
Causes: Main factors include the following:

 Prematurity- all preterm newborns (and especially infants of diabetic mothers)


o Any maternal and fetal factors that result in preterm labor and birth,
complications of pregnancy, indications for cesarean birth, and familial tendency
are ALL associated with RDS
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 Surfactant deficiency disease-disease that causes alterations in surfactant quantity,


composition, function, or production
Symptoms:

 The neonate must expend increasing amounts of energy to reopen the collapsed alveoli
with every breath, so each breathe becomes more difficult than the last
 Progressive symptoms
o Cyanosis
o Apnea
o Tachypnea
o Nasal flaring
o Shallow breathing
o Grunting
o Retractions
Differential diagnoses:

 Congenital heart failure


 Bilateral pneumonia
 Alveolar hemorrhage
 Pulmonary edema
Management (alternative treatments, other measures/procedures)

 Prevent preterm birth!


 Transfer in the event of preterm birth or s/s
 Administer steroids to enhance fetal lung development
o Reduce the incidence and severity of RDS and improve survivability of the 24-34
weeks’ gestation and extremely low birth weight newborns
o Postnatal surfactant replacement therapy is given as a prophylaxis or rescue
treatment
 Ventilatory therapy
 Blood gas monitoring
 Pulse ox monitoring
 Correction of acid-base imbalance
 Environmental temperature regulation
 Adequate nutrition
 Protection from infection
(Davidson, et al., p. 817-820, 2016)
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Transient Tachypnea of the Newborn


Definition: progressive respiratory distress that can resemble classic RDS that affects some
newborns, primarily large for gestational age (LGA), term, and late preterm infants. Other risk
factors include maternal diabetes and asthma, male neonates, macrosomia, cesarean delivery
(especially elective without spontaneous labor).
alternative names: none

Pathophysiology & Causes: The neonate may have had intrauterine or intrapartum asphyxia due
to maternal oversedation or poor uterin profusion, maternal bleeding, prolapsed cord, or breech
presentation. The newborn then fails to clear the airway of lung fluid, mucus, and other debris or
an excess of fluid in the lungs due to aspiration of amniotic or tracheal fluid.
Symptoms:

 Often the newborn experiences little or no difficulty at the onset of breathing


 Shortly after birth the symptoms may occur:
o Expiratory grunting
o Flaring of the nares
o Subcostal retractions
o Desaturation
o Mild cyanosis
o Increasing anteroposterior diameter of the chest
o Tachypnea is usually present by 6 hours of age with rates consistently greater than
60 breaths per min, possibly reaching 80-100 breaths/minute
o Mild respiratory and metabolic acidosis may be present in the first 6 hours
 Clinical signs usually improve 12 to 24 hours but may continue for 48 to 72 hours when
more severe and possibly last up to 1 week
Differential diagnoses
Management (alternative treatments, other measures/procedures)

 Same as RDS

(Davidson, et al., p. 822-823, 2016)

Persistent Pulmonary Hypertension (PPHN)


Definition, Cause & Pathophysiology: PPHN is a serious disorder that affects primarily term,
near term, and postterm newborns. The fetus late in gestation needs to increase the pulmonary
expression of nitric oxide synthases and soluble guanylate cyclase, so that normal pulmonary
vasodilation occurs. If the pulmonary circulation does not dilate, it results in Right to Left
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shunting of blood away from the lungs and through the fetal ductus arteriosus and patent
foramen ovale, thus bypassing the lungs and the ability to be oxygenated, causing worsening
hypoxia and acidosis. The hypoxia and acidosis are the most potent stimulants of pulmonary
vasoconstriction and increased vascular resistance. This creates its own cycle that is self-
perpetuating and is hard to interrupt. There is often rapid deterioration.
alternative names: none
Symptoms:

 Signs of respiratory distress which usually occur in the first 12-24 hours of life
o Grunting
o Nasal flaring
o Tachypnea
o Increasing diameter of the anteroposterior diameter of the chest
o cyanosis
Differential diagnoses:

 everything noted above


Management (alternative treatments, other measures/procedures)

 neonates with PPHN are critically ill and require intense care and very careful monitoring
with limited stimulation
(Davidson, et al., p. 828, 2016)

References:
Davidson, M., London, M., & Ladewig, P. (2016). Olds’ maternal-newborn nursing & women’s
health across the lifespan. Boston: Pearson.

King, T. L., Brucker, M. C., Kriebs, J. M., & Fahey, J. O., Gegor, C. L., Varney, H.
(2015). Varney's midwifery. Jones & Bartlett Learning.

Marshall, J. E., Raynor, M. D. (2015). Myles textbook for midwives. Philadelphia, PA: Elsevier
Ltd.
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