Maternal diabetes mellitus: leads to ↑ fetal insulin, which inhibits surfactant synthesis
Hereditary
Cesarean delivery: results in lower levels of fetal glucocorticoids than vaginal delivery, in which higher levels are released as a response to stress from uterine contractions
Hydrops fetalis
Multifetal pregnancies
Male sex
Pathophysiology
Deficiency of pulmonary surfactant in premature infants.
Surfactant is produced by Type II pneumocytes starting around 24-28 weeks gestation, with mature levels achieved after 35 weeks.
Key component of surfactant: Dipalmitoylphosphatidylcholine (DPPC).
Function of surfactant: ↓ alveolar surface tension, which prevents atelectasis at end-expiration.
Onset of symptoms: usually immediately after birth but can occur up to 72 hours postpartum
Signs of increased respiratory effort
Tachypnea
Nasal flaring and moderate to severe subcostal/intercostal and jugular retractions
Characteristic expiratory grunting
Decreased breath sounds on auscultation
Cyanosis due to pulmonary hypoxic vasoconstriction
Diagnostics
X-ray chest
Interstitial pulmonary edema with perihilar streaking
Diffuse, fine, reticulogranular (ground-glass) densities with low lung volumes and air bronchograms
Atelectasis
Prenatal Assessment: Lecithin-to-sphingomyelin (L/S) ratio in amniotic fluid.
L/S ratio < 2.0 indicates lung immaturity.
Presence of phosphatidylglycerol signifies lung maturity.
The amount of lecithin, which is the major component of surfactant, starts increasing after week 26 of gestation.
The lower the lecithin-sphingomyelin ratio, the more likely it is that the lungs are immature.
Complications
Bronchopulmonary dysplasia (BPD)
Definition: chronic lung condition secondary to prolonged mechanical ventilation and oxygen therapy for NRDS
Etiology: Pulmonary barotrauma and oxygen toxicity with subsequent inflammation of lung tissue due to ventilation of the immature lung (ventilation for more than 28 days)
Clinical features
Seen in infants < 32 weeks
Persistence of symptoms similar to NRDS (e.g., tachypnea, grunting, nasal flaring)
Episodes of desaturation
Diagnostics
X-ray chest: diffuse, fine, granular densities, areas of atelectasis interspersed with areas of hyperinflation
Blood gas analysis: respiratory and metabolic acidosis
Histology: atelectasis, fibrosis, emphysematous alveolar changes (decreased number and septation of alveoli)
