Respiratory Distress Syndrome (RDS)

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Respiratory Distress Syndrome (RDS)
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Introduction
Fetal Respiratory Distress Syndrome (RDS), otherwise known as hyaline membrane disease, is
one of the most common respiratory complications among preterm infants. Preterm infants have
structurally immature lungs with low surfactant thus they are prone to atelectasis which is the
cause of the condition. It is diagnosed among any preterm infants with breathing difficulties,
tachypnea, retractions, and grunting. RDS is a serious condition with statistics showing that
40,000 infants in Australia are affected per year. Furthermore, it also contributes to 20% of
deaths in Australia (Tagami, Sakka, & Monnet, 2018, p. 305). Within the framework of this
essay, there will be an analysis of the etiology and pathophysiology of RDS, diagnosis, signs and
symptoms and the embryological development of the disease. There will also be a conclusion to
summarize the main points in the essay
The etiology and pathophysiology of the disease
Several studies agree that the major cause of respiratory Distress syndrome in children is an
inadequate pulmonary surfactant. Pulmonary surfactant, according to Thompson, Chambers, &
Liu, is defined or rather is a composition of lipids and proteins produced by epithelial cells in the
alveolar spaces (Thompson, Chambers, & Liu, 2017, p. 568). The main function is to lower the
surface tension at the air and liquid interface of the lungs. Since the lungs in infants and
structurally immature and low in surfactant, they have a low tendency to both compliance and
the tendency to atelectasis. Other studies also note that low alveolar radius and a feeble chest
wall contribute to atelectasis (Sweet et al., 2016, p. 122). Atelectasis then leads to
hypoventilation in alveolar space and V/Q mismatch in the well perfused but impartially
ventilated sections of the lungs. V/Q mismatch is defined as the imbalance in exchange of air
between the lungs and the environment and the flow of blood in the lungs. This two conditions

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eventually lead to hypoxemia and hypercarbia (Sweeney & McAuley, 2016, p. 2420).
Hypoxemia and systemic hypoperfusion give rise to low oxygen delivery, anaerobic metabolism
and lactic acidosis. Furthermore, the interplay of hypoxemia and acidosis leads to impaired
oxygenation through pulmonary vasoconstriction. This then gives rise to the right-left shunting at
the foramen and ductus arteriosus sections.
(Sweeney & McAuley, 2016, p. 2420).
Studies also elaborate that baro or volutrauma and elevated FIO2 may stimulate the production
of inflammatory cytokines and chemokines leading to more injury to both epithelial and
endothelial cells ("Pediatric Acute Respiratory Distress Syndrome," 2015, p. 432). The injured
cells lead to low production of surfactant and high endothelial permeability causing pulmonary
edema. Permeability of the cells further cause leakage of proteins in the alveolar spaces and this
worsens production of surfactant.