Development of respiratory system [except nose]

Tracheo-esophageal fistula-types

Tracheo-esophageal fistula-types

Development of trachea

Tracheomalacia and bronchomalacia Abnormal cartilage development ‘floppy’ airways Collapse during inspiration [if extra thoracic] or expiration [if intra thoracic] Presents early in infancy with cough, tachypnea, stridor and wheeze May be associated with cardiac or respiratory abnormalities [TEF]

Development of bronchi and lungs

Maturation of lungs

Stages in lung development

Embryonic- 26 days to 6 weeksS Respiratory diverticulum arises as a ventral outpouching of foregut endoderm and undergoes three initial rounds of branching, producing the primordia successively of the two lungs, the lung lobes, and the bronchopulmonary segments; the stem of the diverticulum forms the trachea and larynx. Pseudoglandular 6 to 16 weeks  Respiratory tree undergoes 14 more generations of branching, resulting in the formation of terminal bronchioles

Canalicular 16 to 28 weeks Saccular 28 to 36 weeks Each terminal bronchiole divides into two or more respiratory bronchioles. Respiratory vasculature begins to develop. Blood vessels come into close apposition with the lung epithelium. The lung epithelium also begins to differentiate into specialized cell types . Saccular 28 to 36 weeks Respiratory bronchioles subdivide to produce terminal sacs (primitive alveoli). Terminal sacs continue to be produced until well into childhood

Alveolar- 36 weeks to term Alveoli mature

the respiratory distress syndrome The primary cause of this syndrome in premature infants (pulmonary insufficiency accompanied by gasping and cyanosis) is an inadequate production of surfactant threatens the infant with immediate asphyxiation

increased rate of breathing and mechanical ventilation required to support the infant's respiration can also damage the delicate alveolar lining This allows fluid and cellular and serum proteins to exude into the alveolus.

Continued injury may lead to detachment of the layer of cells lining the alveoli, a condition called hyaline membrane disease. In mothers with a high risk for premature delivery, the fetus can be treated antenatally with steroids to accelerate lung maturation and the synthesis of surfactant

Moreover, amniocentesis can be done in late pregnancy to assess fetal lung maturity. the sample of amniotic fluid is analyzed with thin-layer chromatography to determine the lecithin-sphingomyelin ratio (L/S; greater than 1.9 = mature; less than 1.5 =immature) and to detect phosphatidylglycerol (presence indicates lung maturity).

Critically ill newborns were first successfully treated with surfactant replacement therapy-the administration of exogenous surfactant-in the late 1970s. A variety of surfactant preparations are now used for this purpose, some derived from animal lungs or human amniotic fluid, others synthetic.