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Respiratory Distress Syndrome

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Etiology

Type two alveolar cells produce surfactant and do not develop until the 25th to the 28th week of
gestation, in this, respiratory distress syndrome is one of the most common respiratory disease in
premature infants. Furthermore, surfactant deficiency and pulmonary immaturity together leads
to alveolar collapse. Predisposing factors that contribute to poorly functioning type II alveolar
cells in a premature baby are if the child is a preterm male, white infants, infants of mothers with
diabetes, precipitous deliveries, cesarean section performed before the 38th week of gestation.
Surfactant synthesis is influenced by hormones, this ranges form insulin and cortisol. Insulin
inhibits surfactant production, explaining why infants of mothers with diabetes type 1 are at risk
of development of respiratory distress syndrome. Cortisol can speed up maturation of type II
cells and therefore production of surfactant. Finally, in the baby delivered by cesarean section are
at greater risk of developing respiratory distress syndrome because the reduction of cortisol
produced because the lack of stress that happens during vaginal delivery, hence cortisol increases
in high stress and helps in the maturation of type II cells of the alveoli that cause surfactant.

Respiratory Distress Syndrome


Pathophysiology
At birth the pressure needed to expand the lungs requires high inspiratory pressure. In the
presence of normal surfactant levels the lungs retain as much as 40% of the residual volume after
the first breath and thereafter will only require far lower inspiratory pressures. In the case of
deficiency of surfactant the lungs will collapse between breaths, this makes the infant work hard
and each breath is as hard as the first breath. If this goes on further the pulmonary capillary
membranes become more permeable, letting in fibrin rich fluids between the alveolar spaces and
in turn forms a hyaline membrane. The hyaline membrane is a barrier to gas exchange, this
hyaline membrane then causes hypoxemia and carbon dioxide retention that in turn will further
impair surfactant production.

Treatment
Today to prevent respiratory distress syndrome are animal sources and synthetic surfactants, and
administrated through the airways by an endotracheal tube and the surfactant is suspended in a
saline solution. Treatment is initiated post birth and in infants who are at high risk for respiratory
distress syndrome.

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