Respiratory Distress Syndrome

Respiratory distress syndrome (RDS) of the newborn, formerly termed hyaline

membrane disease, most often occurs in preterm infants, infants of diabetic mothers, infants born
by cesarean birth, or those who for any reason have decreased blood perfusion of the lungs, such
as occurs with meconium aspiration (Raab, 2007) !he pathologic feature of RDS is a hyaline"
li#e (fibrous) membrane formed from an e$udate of an infant%s blood that begins to line the
terminal bronchioles, alveolar ducts, and alveoli !his membrane prevents e$change of o$ygen
and carbon dio$ide at the alveolar&capillary membrane !he cause of RDS is a low level or
absence of surfactant, the phospholipid that normally lines the alveoli and reduces surface
tension to #eep the alveoli from collapsing on e$piration 'ecause surfactant does not form until
the ()th wee# of gestation, as many as (0* of low"birth"weight infants and as many as +0* of
very"low"birth"weight infants are susceptible to this complication
Etiology
,n premature infants, respiratory distress syndrome develops because of impaired
surfactant synthesis and secretion leading to atelectasis, ventilation"perfusion (-./) ine0uality,
and hypoventilation with resultant hypo$emia and hypercarbia 'lood gases show respiratory
and metabolic acidosis that cause pulmonary vasoconstriction, resulting in impaired endothelial
and epithelial integrity with lea#age of proteinaceous e$udate and formation of hyaline
membranes (hence the name)
!he relative deficiency of surfactant decreases lung compliance (see the image below)
and functional residual capacity, with increased dead space !he resulting large -./ mismatch
and right"to"left shunt may involve as much as 10* of the cardiac output 2ypo$ia, acidosis,
hypothermia, and hypotension may impair surfactant production and.or secretion ,n many
neonates, o$ygen to$icity with barotrauma and volutrauma in their structurally immature lungs
causes an influ$ of inflammatory cell, which e$acerbates the vascular in3ury, leading to
bronchopulmonary dysplasia ('4D) 5ntio$idant deficiency and free"radical in3ury worsen the
in3ury
6pon macroscopic evaluation, the lungs of affected newborns appear airless and ruddy
(ie, liverli#e) !herefore, the lungs re0uire an increased critical opening pressure to inflate
Diffuse atelectasis of distal airspaces along with distension of distal airways and perilymphatic
areas are observed microscopically 4rogressive atelectasis, barotrauma or volutrauma, and
o$ygen to$icity damage endothelial and epithelial cells lining these distal airways, resulting in
e$udation of fibrinous matri$ derived from blood
2yaline membranes that line the alveoli (see the image below) may form within a half
hour after birth ,n larger premature infants, the epithelium begins to heal at (7"72 hours after
birth, and endogenous surfactant synthesis begins !he recovery phase is characteri8ed by
regeneration of alveolar cells, including type ,, cells, with a resultant increase in surfactant
activity !he healing process is comple$
5 chronic process often ensues in infants who are e$tremely immature and critically ill
and in infants born to mothers with chorioamnionitis, resulting in '4D ,n e$tremely premature
infants, an arrest in lung development often occurs during the saccular stage, resulting in chronic
lung disease termed 9new9 '4D
Pathophysiology
2igh pressure is re0uired to fill the lungs with air for the first time and overcome the
pressure of lung fluid :or e$ample, it ta#es a pressure between )0 and 70 cm 22; to inspire a
first breath but only <+ to 20 cm 22; to maintain 0uiet, continued breathing ,f alveoli collapse
with each e$piration, as happens when surfactant is deficient, forceful inspirations re0uiring
optimum pressure are still re0uired to inflate them =ven very immature infants release a bolus of
surfactant at birth into their lungs from the stress of birth 2owever, with deficient surfactant,
areas of hypoinflation begin to occur and pulmonary resistance increases 'lood then shunts
through the foramen ovale and the ductus arteriosus as it did during fetal life !he lungs are
poorly perfused, affecting gas e$change 5s a result, the production of surfactant decreases even
further !he poor o$ygen e$change that results leads to tissue hypo$ia, which causes the release
of lactic acid !his, combined with the increasing carbon dio$ide level resulting from the
formation of the hyaline membrane on the alveolar surface, leads to severe acidosis 5cidosis
causes vasoconstriction, and decreased pulmonary perfusion from vasoconstriction further limits
surfactant production >ith decreased surfactant production, the ability to stop alveoli from
collapsing with each e$piration becomes impaired !his vicious cycle continues until the
o$ygen&carbon dio$ide e$change in the alveoli is no longer ade0uate to sustain life without
ventilator support
Assessment
?ost infants who develop RDS have difficulty initiating respirations
at birth 5fter resuscitation, they appear to have a period of hours or a day when they are free of
symptoms because of an initial release of surfactant During this time, however, subtle signs may
appear@
A Bow body temperature
A Casal flaring
A Sternal and subcostal retractions
A !achypnea (more than 70 respirations per minute)
A Dyanotic mucous membranes
>ithin several hours, e$piratory grunting, caused by closure of the glottis to create a prolonged
e$piratory time, can be heard 5 partially closed glottis this way is helpful as it increases the
pressure in the alveoli on e$piration, helps to #eep the alveoli from collapsing, and ma#es
o$ygen e$change more complete =ven with this attempt at better o$ygen e$change, however, as
the disease progresses, infants become cyanotic and their 4;2 and o$ygen saturation levels fall
in room air ;n auscultation, there may be fine rales and diminished breath sounds because of
poor air entry 5s distress increases, an infant may e$hibit@
A Seesaw respirations (on inspiration, the anterior chest wall retracts and the abdomen protrudesE
on e$piration, the sternum rises)
A 2eart failure, evidenced by decreased urine output and edema of the e$tremities
A 4ale gray s#in
A 4eriods of apnea
A 'radycardia
A 4neumothora$
!he diagnosis of RDS is made on the clinical signs of grunting, central cyanosis in room air,
tachypnea, nasal flaring, retractions, and shoc# 5 chest radiograph will reveal a diffuse pattern
of radiopa0ue areas that loo# li#e ground glass (ha8iness) 'lood gas studies (ta#en from an
umbilical vessel catheter) will reveal respiratory acidosis 5 F"hemolytic, group ' streptococcal
infection may mimic RDS, as this infection is so severe in newborns that the insult to the lungs is
enough to stop surfactant production Dultures of blood, cerebrospinal fluid, and s#in may be
obtained to rule out this condition 5n antibiotic (penicillin or ampicillin) and an aminoglycoside
(gentamicin or #anamycin) may be started while culture reports are pending
Therapeutic Management
RDS can be largely prevented by the administration of surfactant through an endotracheal
tube at birth for an infant at ris# because of low gestational age
Surfactant Replacement
5s a preventive measure, synthetic surfactant is sprayed into the lungs by a syringe or
catheter through an endotracheal tube at birth while an infant is first positioned with the head
held upright and then tilted downward ,t is important an infant%s airway not be suctioned for as
long a period as possible after administration of surfactant to avoid suctioning the drug away
5lthough there are almost no unfavorable reactions to surfactant administration, some, such as
mucus plugging from the solution, do occur 5n infant who is receiving surfactant and then is
placed on a ventilator needs close observation because lung e$pansion can improve rapidly
5nticipate the need to ad3ust ventilator settings to prevent e$cessive lung pressure
Oxygen Administration
5dministration of o$ygen is necessary to maintain correct 4;2 and p2 levels
Dontinuous positive airway pressure (D454) or assisted ventilation with positive end e$piratory
pressure (4==4) will e$ert pressure on the alveoli at the end of e$piration and #eep the alveoli
from collapsing (2o et al, 200G) !his greatly improves o$ygen e$change 5 possible
complication of o$ygen therapy in the very immature or very ill infant is retinopathy of
prematurity
Ventilation
Cormally, on a ventilator, inspiration is shorter than e$piration, or there is an
inspiratory.e$piratory ratio (,.= ratio) of <@2 ,t is difficult to deliver enough o$ygen to stiff,
noncompliant lungs in this usual ratio, however, without forcing the air into the lungs at such a
high pressure and rapid rate that a pneumothora$ becomes a constant concern (Snow H 'randon,
2007) ,nfant ventilators are therefore available with a reversed ,.= ratio (2@<) !hese are
pressure"cycled to control the force with which air is delivered 2igh"fre0uency, oscillatory, and
3et ventilation are other methods of introducing o$ygen to infants with noncompliant lungs
!hese systems maintain airway pressure and then intermittently I3etJ or oscillate at a rapid rate
()00&700 times a minute) an additional amount of air to inflate alveoli Domplications of any
type of ventilation are possible, such as pneumothora$ and impaired cardiac output because of
decreased blood flow through the pulmonary artery from lung pressure !here is also a possible
ris# of increased intracranial and arterial pressure and hemorrhage from changing blood pressure
'eing certain that infants are not overhydrated is important to help prevent increased blood
pressure and increased pulmonary artery pressure ,ndomethacin or ibuprofen may be used to
cause closure of a patent ductus arteriosus, ma#ing ventilation more efficient (Don8e, Smith, H
'ryows#y, 2007) ,ndomethacin has been associated with adverse effects such as decreased renal
function, decreased platelet count, and gastric irritation Carefully monitor urine output and
observe for bleeding, especially at puncture sites, if this is prescribed.