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Development of the lower respiratory tract begins on day 22 and continues to form the trachea, lungs, bronchi, and alveoli. The process divides into five stages: embryonic, pseudoglandular, canalicular, saccular, and alveolar stage. Although the process begins early on in fetal development, complete maturation does not take place until the child is approximately 8 years of age. This developmental delay is vital in premature babies where their survival is intricately linked to which developmental stage their respiratory tract has reached at the time of birth.

Reduced pulmonary segments or terminal sacs, commonly known as pulmonary hypoplasia, is due to insufficient lung fluid during gestation. Lung fluid is produced by epithelial cells as early as 6 weeks and plays a vital role in maintaining fetal lung expansion.[7] Once inhaled during fetal breathing movements, peristaltic waves shift this fluid distally resulting in the stretching of the lower airway, subsequently stimulating the release of various growth factors involved in the regulation of lung development. Decreased volumes of lung fluid result in reduced branches in the pulmonary tree and fewer terminal sacs, thus compromising the structural integrity of the lungs. Pulmonary hypoplasia usually occurs secondary to a defect which limits the pleural cavity, consequently reducing lung expansion and adversely affecting development. Commonly associated abnormalities include musculoskeletal defects of the chest wall, congenital diaphragmatic hernia, and oligohydramnios due to renal agenesis.

Reduced pulmonary segments or terminal sacs, commonly known as pulmonary hypoplasia, is due to insufficient lung fluid during gestation. Lung fluid is produced by epithelial cells as early as 6 weeks and plays a vital role in maintaining fetal lung expansion.[7] Once inhaled during fetal breathing movements, peristaltic waves shift this fluid distally resulting in the stretching of the lower airway, subsequently stimulating the release of various growth factors involved in the regulation of lung development. Decreased volumes of lung fluid result in reduced branches in the pulmonary tree and fewer terminal sacs, thus compromising the structural integrity of the lungs. Pulmonary hypoplasia usually occurs secondary to a defect which limits the pleural cavity, consequently reducing lung expansion and adversely affecting development. Commonly associated abnormalities include musculoskeletal defects of the chest wall, congenital diaphragmatic hernia, and oligohydramnios due to renal agenesis. Surfactant deficiency is the most common cause of neonatal respiratory distress syndrome. Pulmonary surfactant production is via type II pneumocytes and is responsible for maintaining lung surface tension. It spreads as a thin layer over the air-liquid barrier of alveoli, thus preventing atelectasis at the end of expiration. Approximately 90% is formed by phospholipids (phosphatidylcholine, phosphatidylglycerol, phosphatidylethanolamine) with the remaining 10% formed by proteins. These are primarily four surfactant proteins (surfactant proteins A-D), each with its particular function; surfactant protein A and D (SP-A, SP-D) function in innate immunity. Hence degradation of these proteins may increase susceptibility to lung inflammation and infection. Surfactant protein B and C (SP-B, SP-C) contribute to the surface properties of surfactant. SP-B and SP-C organize the surfactant protein into tubular myelin, which is essential in reducing surface tension. Production of pulmonary surfactant begins as early as 24 weeks, however the production of sufficient amounts does not occur until late gestation, thus the risk of neonatal respiratory distress syndrome is inversely proportional to gestational age; the risk decreases from 60% at less than 24 weeks gestation to less than 5% for those infants born after 34 weeks [8]. Infants typically present in the first few hours of life, with tachypnoea, hypoxia, hypercapnia, breathing difficulties, cyanosis, and nasal flaring.[6]

Surfactant deficiency is the most common cause of neonatal respiratory distress syndrome. Pulmonary surfactant production is via type II pneumocytes and is responsible for maintaining lung surface tension. It spreads as a thin layer over the air-liquid barrier of alveoli, thus preventing atelectasis at the end of expiration. Approximately 90% is formed by phospholipids (phosphatidylcholine, phosphatidylglycerol, phosphatidylethanolamine) with the remaining 10% formed by proteins. These are primarily four surfactant proteins (surfactant proteins A-D), each with its particular function; surfactant protein A and D (SP-A, SP-D) function in innate immunity. Hence degradation of these proteins may increase susceptibility to lung inflammation and infection. Surfactant protein B and C (SP-B, SP-C) contribute to the surface properties of surfactant. SP-B and SP-C organize the surfactant protein into tubular myelin, which is essential in reducing surface tension. Production of pulmonary surfactant begins as early as 24 weeks, however the production of sufficient amounts does not occur until late gestation, thus the risk of neonatal respiratory distress syndrome is inversely proportional to gestational age; the risk decreases from 60% at less than 24 weeks gestation to less than 5% for those infants born after 34 weeks [8]. Infants typically present in the first few hours of life, with tachypnoea, hypoxia, hypercapnia, breathing difficulties, cyanosis, and nasal flaring.[6] Esophageal atresia is a blind pouch in the esophagus and is commonly associated with an abnormal communication with the trachea known as a tracheoesophageal fistula. This condition occurs when the laryngotracheal tube fails to bud off to form the esophagus dorsal to the trachea. Possible causes include the failure of the esophageal endoderm to proliferate rapidly during the fourth to fifth weeks of embryonic development due to mutations in the SHH signaling pathway. Tracheoesophageal fistulas are commonly associated with polyhydramnios as the abnormal communication with the trachea prevents the fetus from swallowing, thus impairing its ability to return the amniotic fluid to the maternal circulation. Infants typically present with coughing, gagging or choking when attempts to feed are made, and may also have bluish skin.