Respiratory Distress Syndrome

Respiratory distress syndrome Pathophysiology

(RDS) of the newborn, formerly High pressure is required to fill
termed hyaline membrane the lungs with air for the first
disease, most often occurs in time and overcome the pressure
preterm infants, infants of of lung fluid. For example,
diabetic mothers, infants born by it takes a pressure between 40
cesarean birth, or those who for and 70 cm H2O to inspire a
any reason have decreased first breath but only 15 to 20 cm
blood perfusion of the lungs, H2O to maintain quiet,
such as occurs with meconium continued breathing. If alveoli
aspiration (Raab, 2007). The collapse with each expiration,
pathologic feature of RDS is a as happens when surfactant is
hyaline-like (fibrous) membrane deficient, forceful inspirations
formed from an exudate of requiring optimum pressure are
an infant’s blood that begins to still required to inflate them.
line the terminal bronchioles, Even very immature infants
alveolar ducts, and alveoli. This release a bolus of surfactant at
membrane prevents exchange birth into their lungs from the
of oxygen and carbon dioxide at stress of birth. However, with
the alveolar–capillary deficient surfactant, areas of
membrane. The cause of RDS is hypoinflation begin to occur and
a low level or absence pulmonary resistance increases.
of surfactant, the phospholipid Blood then shunts through the
that normally lines the alveoli foramen ovale and the ductus
and reduces surface tension to arteriosus as it did during fetal
keep the alveoli from collapsing life. The lungs are poorly
on expiration. perfused, affecting gas exchange.
Because surfactant does not form As
until the 34th week of a result, the production of
gestation, as many as 30% of surfactant decreases even further.
low-birth-weight infants and as The poor oxygen exchange that
many as 50% of very-low-birth- results leads to tissue hypoxia,
weight infants are susceptible which causes the release of lactic
to this complication. acid. This, combined
with the increasing carbon • Low body temperature
dioxide level resulting from the • Nasal flaring
formation
of the hyaline membrane on the
alveolar surface, leads
to severe acidosis. Acidosis
causes vasoconstriction, and
decreased CHAPTER 26 Nursing Care of a
pulmonary perfusion from Family With a High-Risk
vasoconstriction further Newborn 725
limits surfactant production. • Sternal and subcostal
With decreased surfactant retractions
production, • Tachypnea (more than 60
the ability to stop alveoli from respirations per minute)
collapsing with each • Cyanotic mucous membranes
expiration becomes impaired. Within several hours, expiratory
This vicious cycle continues grunting, caused by closure
until the oxygen–carbon dioxide of the glottis to create a
exchange in the alveoli is no prolonged expiratory time, can
longer adequate to sustain life be heard. A partially closed
without ventilator support. glottis this way is helpful as it
increases
Assessment
the pressure in the alveoli on
Most infants who develop RDS
expiration, helps to keep
have difficulty initiating
the alveoli from collapsing, and
respirations
makes oxygen exchange
at birth. After resuscitation, they
more complete. Even with this
appear to have a
attempt at better oxygen
period of hours or a day when
exchange,
they are free of symptoms
however, as the disease
because
progresses, infants become
of an initial release of surfactant.
cyanotic and their PO2 and
During this time,
oxygen saturation levels fall in
however, subtle signs may
room air. On auscultation, there
appear:
may be fine rales and diminished
breath sounds because of poor air Cultures of blood, cerebrospinal
entry. As distress fluid, and skin may
increases, an infant may exhibit: be obtained to rule out this
• Seesaw respirations (on condition. An antibiotic
inspiration, the anterior chest (penicillin
wall or ampicillin) and an
retracts and the abdomen aminoglycoside (gentamicin
protrudes; on expiration, the or kanamycin) may be started
sternum rises) while culture reports are
• Heart failure, evidenced by pending.
decreased urine output and Therapeutic Management
edema of the extremities RDS can be largely prevented by
• Pale gray skin the administration of surfactant
• Periods of apnea through an endotracheal tube at
• Bradycardia birth for an infant at
• Pneumothorax risk because of low gestational
The diagnosis of RDS is made on age.
the clinical signs of Surfactant Replacement. As a
grunting, central cyanosis in preventive measure, synthetic
room air, tachypnea, nasal surfactant is sprayed into the
flaring, retractions, and shock. A lungs by a syringe or
chest radiograph will catheter through an endotracheal
reveal a diffuse pattern of tube at birth while an infant
radiopaque areas that look is first positioned with the head
like ground glass (haziness). held upright and then
Blood gas studies (taken from tilted downward. It is important
an umbilical vessel catheter) will an infant’s airway not be
reveal respiratory acidosis. suctioned for as long a period as
A _-hemolytic, group B possible after administration
streptococcal infection may of surfactant to avoid suctioning
mimic RDS, as this infection is the drug away.
so severe in newborns that Although there are almost no
the insult to the lungs is enough unfavorable reactions to
to stop surfactant production. surfactant
administration, some, such as shorter than expiration, or there
mucus plugging from is an inspiratory/expiratory
the solution, do occur. An infant ratio (I/E ratio) of 1:2. It is
who is receiving surfactant difficult to deliver enough
and then is placed on a ventilator oxygen
needs close observation to stiff, noncompliant lungs in
because lung expansion can this usual ratio, however,
improve rapidly. without forcing the air into the
Anticipate the need to adjust lungs at such a high
ventilator settings to prevent pressure and rapid rate that a
excessive lung pressure. pneumothorax becomes a
Oxygen Administration. constant concern (Snow &
Administration of oxygen is Brandon, 2007). Infant
necessary ventilators
to maintain correct PO2 and pH are therefore available with a
levels. Continuous positive reversed I/E ratio (2:1).
airway pressure (CPAP) or These are pressure-cycled to
assisted ventilation with positive control the force with which
end-expiratory pressure (PEEP) air is delivered. High-frequency,
will exert pressure on oscillatory, and jet ventilation
the alveoli at the end of are other methods of introducing
expiration and keep the alveoli oxygen to infants
from with noncompliant lungs. These
collapsing (Ho et al., 2009). This systems maintain airway
greatly improves oxygen pressure and then intermittently
exchange. A possible “jet” or oscillate at a rapid
complication of oxygen therapy rate (400–600 times a minute) an
in the additional amount of air
very immature or very ill infant to inflate alveoli.
is retinopathy of prematurity Complications of any type of
(see discussion later in chapter) ventilation are possible,
or bronchopulmonary dysplasia such as pneumothorax and
(see Chapter 40). impaired cardiac output because
Ventilation. Normally, on a of decreased blood flow through
ventilator, inspiration is the pulmonary artery from
lung pressure. There is also a Doing so allows mechanical
possible risk of increased ventilation to be accomplished
intracranial at lower pressures because there
and arterial pressure and is no normal muscle resistance
hemorrhage from to overcome. The possibility of
changing blood pressure. Being pneumothorax is reduced
certain that infants are not while PO2 is increased.
overhydrated is important to help Obviously infants who have
prevent increased blood no spontaneous respiratory
pressure and increased function because of drug
pulmonary artery pressure. administration
Indomethacin or ibuprofen may need critical observation and
be used to cause closure frequent ABG
of a patent ductus arteriosus, analysis because they totally
making ventilation more efficient depend on caregivers at this
(Donze, Smith, & Bryowsky, point (Playfor et al., 2007).
2007). Indomethacin has The effect of pancuronium
been associated with adverse decreases as the life of the
effects such as decreased renal drug expires; its effect can be
function, decreased platelet interrupted by the administration
count, and gastric irritation. of atropine or injectable
Carefully monitor urine output neostigmine methylsulfate
and observe for bleeding, (Prostigmin Methylsulfate
especially Injectable). For this reason,
at puncture sites, if this is when pancuronium is being
prescribed. administered, both atropine
Additional Therapy. Yet and Prostigmin should be
another method of increasing immediately available. An
pulmonary infant’s
blood flow is by using muscle plan of care should be specially
relaxants. marked to show that
Pancuronium (Pavulon) can be pancuronium therapy is being
administered intravenously used so in the event of a
to the point of abolishing power failure, manual ventilatory
spontaneous respiratory action. assistance can be begun
immediately.