Respiratory distress

syndrome
∞ Formerly termed hyaline membrane disease
∞ Most often occurs in preterm infants, infants with
diabetic mothers, infants born by cesarean birth,
or those who have decreased blood perfusion of
the lungs
∞ The pathologic feature is a hyaline (fibrous)
membrane formed from an exudate of an infant’s
blood that begins to line the terminal; bronchioles,
alveolar ducts and alveoli

∞ This membrane prevents the exchange of oxygen

and carbon dioxide at the alveolar-capillary
membrane that interferes with effective
oxygenation
∞ The cause is low level or absence of Surfactant,
the phospholipid that normally lines the alveoli and
reduces surface tension to keep the alveoli from
collapsing on expiration
∞ Surfactant does not form until the 34th week of
gestation
 ∞ Most infants have difficulty initiating respirations at
birth Assessment
∞ After resuscitation they appear to have free
symptoms for hours and day because of initial ∞ Difficulty in establishing respirations at birth
release surfactant ∞ The APGAR score is apt to be low
∞ During this time subtle signs may appear such as: ∞ Almost immediately, tachypnea, retractions, and
low body temperature, nasal flaring, sternal and cyanosis begin
subcostal retractions, tachypnea (more than ∞ Tachypnea
60bpm), cyanotic mucous membrane ∞ Retractions – the inflammation of bronchi tends to
∞ Within several hours, expiratory grunting occurs trap air in the alveoli, limiting entrance of oxygen
caused by closure of glottis ∞ This trap air may cause enlargement of the
∞ As distress increases, an infant may exhibit:
seesaw respirations (on inspiration the anterior
chest wall retracts and the abdomen protrudes; on
expiration the sternum rises)
∞ Heart failure evidenced by decreased urine output
edema of the extremities
 Pale gray skin
 Periods of apnea
 Bradycardia
 Pneumothorax

Therapeutic Management
∞ Surfactant replacement (survanta) to restore
naturally occurring lung surfactant to improve lung
compliance
∞ Oxygen administration
∞ Kept warm-reduces the infant’s metabolic oxygen anteroposterior diameter of the chest (barrel
demand chest)

Prevention
∞ Magnesium sulfate – can help prevent preterm
Therapeutic Management
birth ∞ Amnioinfusion can be used to dilute the amount of
∞ Betamethasone – steroids appear to quicken the meconium in the amniotic fluid and reduce the risk
formation of lecithin (24-34 weeks) of aspiration
∞ Deeply stained amniotic fluid – cesarean birth is

Meconium Aspiration
Syndrome
∞ Meconium is present in the fetal bowel as early as
10 weeks gestation
∞ If hypoxia occurs, a vagus reflex is stimulated,
resulting in relaxation of the rectal sphincter
∞ This relaxes meconium into the amniotic fluid
∞ Babies born breech may expel meconium into the
amniotic fluid from pressure on the buttocks
∞ Meconium staining occurs in approximately 10% -
20% of all births and 2 to 4 of these births, infants
will aspirate enough meconium to cause
Meconium Aspiration Syndrome
∞ The infant may aspirate meconium either in the
utero or with the first hour at birth
Meconium can Cause
Respiratory Distress in Three
Ways
∞ It causes inflammation of bronchioles because it is
a foreign substance
∞ It can block small bronchioles by mechanical
plugging
∞ It can cause a decrease in surfactant production
through lung trauma
∞
recommended
After birth and tracheal suctioning, oxygen and
assisted ventilation
∞ Antibiotic therapy to forestall the development of
pneumonia as a secondary problem
∞ If lung compliance is poor, surfactant may be
administered
∞ Observe infants for air trapping in the alveoli
because the alveoli can expand only so far and
then will rupture, sending air into the pleural space
(Pneumothorax)
∞ Warm environment
∞ Chest physiotherapy with percussion and vibration
to encourage removal of remnants of meconium
from the lungs
Sudden Infant Death
Syndrome
∞ Sudden unexplained death in infancy
∞ It occurs at a higher than usual rate in infants of
adolescent mothers, infants of closely spaced
pregnancies and underweight and preterm infants
∞ The peak age of incidence is 2-4months of age
∞ Cause is unknown, in addition to prolonged but
unexplained apnea
Other Possible Contributing ∞ An infant’s liver processes littler bilirubin in utero
because the mother’s circulation does this for an

Factors
∞ Sleeping prone rather than supine
∞ Viral respiratory infection
∞ Exposure to secondary smoke
∞ Pulmonary edema
∞ Brain stem abnormalities
∞ Neurotransmitter deficiencies
∞ Heart rate abnormalities
∞ Distorted familial breathing patterns
∞ Decreased arousal responses
∞ Possible lack of surfactant in the alveoli
∞ Sleeping in room without moving air currents (the
infant rebreathes expired carbon dioxide)
∞ Typically affected infants are well-nourished
∞ Parents may report an infant who had a slight
head cold after being put to bed at night, the infant
is found dead a few hours later
∞ An autopsy often reveals petechiae in the lungs
and mild inflammation and congestion in the
respiratory tract
Recommendations
∞ Put newborns to sleep on their back
∞ Use firm sleep surface
∞ Breastfeeding
∞ Room sharing without bed sharing
∞ Routine immunization
∞ Consideration of using a pacifier
∞ Avoid soft bedding, overheating
∞ Exposure to tobacco smoke, alcohol and elicit
drugs
∞
infant
With birth, exposure to light apparently triggers the
liver to assume this function
∞ Additional light would speed the conversion
potential of the liver
∞ An infant is continuously exposed to specialized
light such a quartz halogen, cool white daylight or
special blue florescent light
∞ The light are placed 12-30 inches above the
newborn’s bassinet or incubator
∞ Term newborns are scheduled for phototherapy
when the total serum bilirubin level rises to 10-12
mg/dl at 24 hours of age
∞ Preterm infants may have treatment begun at level
lower than this
∞ Continuous exposure may be harmful to the
newborn
∞ Infant’s eyes must always be covered while under
bilirubin lights
∞ Check the dressings frequently to be certain they
have not slipped or are causing irritation
∞ Stools are usually bright green because of
excessive bilirubin being excreted as a result of
the therapy
∞ Stools are frequently loose and may irritating to
the skin

Hemolytic Disease of
the Newborn
∞ Also known as hyperbilirubinemia
∞ Hemolytic – latin for destruction (lysis of RBC)
∞ A certain degree of lysis of RBC in the newborn
results from destruction of RBC
∞ Hemolytic disease is present when there is
excessive destruction of RBC, which leads to
elevated bilirubin level (hyperbilirubinemia)
∞ Cord blood has a total serum bilirubin level of 0 to
3 mg/100ml
∞ An increasing bilirubin levels becomes dangerous
if the level rise to 20 mg/dl in a term infant and as
low as 12 mg/dl in preterm infant = brain damage
(invasion of bilirubin into the brain cells)
∞ Liver and spleen may be enlarged
∞ Extreme edema
∞ Anemia
∞ Progressive jaundice occurs within 24 hours

Therapeutic Management
∞ The initiation of early breastfeeding. Bilirubin is
removed from the body into feces. Therefore the
sooner the bowel elimination begins the sooner
bilirubin removal begins

Phototherapy