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Respiratory distress syndrome: Pathology review
0 / 8 complete
|Blood Gases, Serum|
Two people are admitted to the emergency department.
A few hours after delivery, she develops tachypnea, chest wall retractions with nasal flaring, and tachycardia.
Aside from increased work of breathing, her physical examination findings are normal.
A chest x-ray was ordered and it showed diffuse reticulogranular ground glass appearance with air bronchograms.
Now, both people are in respiratory distress.
But first, a bit of physiology.
First, type I pneumocytes are thin, and have a large surface area that that facilitate gas exchange.
More important for the exams are the type II pneumocytes, which are smaller, thicker and have the ability to proliferate in response to lung injury.
They are in charge of making a fluid called surfactant which contains various phospholipids.
Respiratory distress syndrome (RDS) is a respiratory condition in which the alveoli collapse due to the deficiency of the surface-active substance called surfactant. Collapsed alveoli make it difficult to breathe and get enough oxygen. Acute respiratory distress syndrome happens when inflammation causes diffuse alveolar injury and pulmonary edema. This edema can wash away the surfactant coating the alveoli to the point where it causes the alveoli to collapse. There is also neonatal respiratory distress syndrome, which mostly affects premature infants, whose lungs are not fully developed and lack enough surfactant.
Symptoms of respiratory distress syndrome include rapid breathing, grunting, and flaring of the nostrils while breathing, as well as cyanosis (bluish color of the skin) and difficulty feeding. All forms of respiratory distress can lead to respiratory failure and death if not treated promptly. Treatment includes providing respiratory support, and administering surfactants, especially in neonatal respiratory syndrome. The use of corticosteroids before delivery may also be considered to improve lung function in some cases.
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