Respiratory system Flashcards
RDS
*AKA: hyaline membrane disease
*premature infants
*pathophysiology:
premature birth disrupts vascular endothelial growth factor signaling which is necessary for alveolar development. Surfactant formation begins in the canalicular period of lung development and increases in the final weeks of gestation, in premature infants, type 2 pneumocytes do not produce sufficient surfactant; surfactant reduces surface tension at the air-water interface, it also plays a role in immunomodulation.
*CF: tachypnea is the commonest presenting sign, grunting, intercostal retractions, and other signs of labored breathing.
*chest x-ray: hypoexpansion, air-bronchograms, and ground-glass opacities
ABG to assess hypoxemia and acidosis
CBC and blood cultures to rule out infections
*pathology:
lung biopsy shows eosinophilic hyaline membranes lining the alveoli
*Ddx:
TTN
congenital heart disease
infection
meconium aspiration
Tr:
prenatal steroids
surfactant replacement
oxygen and CPAP
*the arrested development of respiratory vasculature increases the risk of pulmonary hypertension
*complications:
prolonged use of oxygen/ventilatory support increases the risk of retinopathy of prematurity and brunchopulmonary dysplasia (most common cause of chronic lung disease in infants), survivours have long-term airway obstruction sequelae similar to emphysema
*physiology:
surfactant is made of proteins and phospholipids; phosphatidylcholine is the major phospholipid
*surfactant can also be affected in adult lung diseases, for example, pseudomonas produces elastases that degrade the lung surfactant
*A course of prophylactic antenatal
betamethasone therapy is given to accelerate fetal lung maturity in women at risk of preterm delivery. Corticosteroids accelerate the development of type 2 pneumocytes. Timing of therapy is key; infants delivered >7 days after; steroids need at least 48 hrs to work
antenatal corticosteroids have a greater need for respiratory support.
