Neonatal respiratory distress syndrome (NRDS), or surfactant deficiency disorder, is a lung disorder in infants that is caused by a deficiency of pulmonary surfactant. It is most common in preterm infants, with the incidence and severity decreasing with gestational age. Surfactant deficiency causes the alveoli to collapse, resulting in impaired blood gas exchange. Symptoms manifest shortly after birth and include tachypnea, tachycardia, increased breathing effort, and/or cyanosis. Suspected diagnosis is based on clinical features and confirmed by evaluating the extent of atelectasis via an x-ray of the chest. Blood gases show respiratory and metabolic acidosis in addition to hypoxia. Treatment primarily involves emergency resuscitative measures, including nasal continuous positive airway pressure (CPAP) and the stabilization of blood sugar levels and electrolytes. Intratracheal surfactant should be administered if infants require an increased FiO2 to maintain a sufficient oxygen saturation despite receiving noninvasive positive pressure ventilation.Intratracheal surfactant should be administered if ventilation alone is unsuccessful. Most cases resolve within 3–5 days of treatment. However, complications such as hypoxemia, tension pneumothorax, bronchopulmonary dysplasia, or sepsis may still occur. In rare cases, NRDS may lead to neonatal death.NRDS can be prevented by administering antenatal glucocorticoids to the mother if premature delivery is expected.
- Premature birth
- 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
- Pulmonary surfactant is a mixture of phospholipids and proteins produced by lamellar bodies of . These phospholipids reduce alveolar surface tension, preventing the alveoli from collapsing.
- Surfactant deficiency is most likely to occur in preterm infants, because:
Surfactant deficiency → little or no reduction of alveolar surface tension → increased alveolar collapse → atelectasis → decreased lung compliance and functional residual capacity → hypoxemia and hypercapnia
- Hypoxemia and hypercapnia → vasoconstriction of the pulmonary vessels (hypoxic vasoconstriction) and respiratory acidosis → intrapulmonary right-to-left shunt → increased permeability due to alveolar epithelial damage → fibrinous exudation within the alveoli → development of hyaline membranes in the lungs (hyaline membrane disease)
- Maternal history of premature birth
- Onset of symptoms: usually immediately after birth but can occur up to 72 hours postpartum
Signs of increased respiratory effort
- 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
- Physical examination: see “Clinical features” above
- Maternal history: previous preterm birth
- X-ray chest
- Blood gas analysis
Amniocentesis for prenatal testing of NRDS: screening for markers of fetal lung immaturity
Lecithin-sphingomyelin ratio < 1.5 (≥ 2 is considered mature)
- The amount of sphingomyelin in the amniotic fluid remains relatively consistent during pregnancy.
- 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.
- Foam stability index < 0.48
- Low surfactant-albumin ratio
- Lecithin-sphingomyelin ratio < 1.5 (≥ 2 is considered mature)
- Histological findings 
- Underdevelopment of the lungs characterized by a decreased number of alveoli and small airways and reduced lung volumes in one or both lobes
- Results in impaired gas exchange and severe respiratory distress that may require intubation
- Associated with left-sided), oligohydramnios, and Potter sequence (usually
- Neonatal pneumonia
|Overview of NDRDS and its differential diagnoses|
Neonatal respiratory distress syndrome
|Apnea of prematurity (AOP)||Transient tachypnea of the newborn (wet lung disease) ||Persistent pulmonary hypertension of the newborn (PPHN) ||Meconium aspiration syndrome |
|Etiology|| || || || |
|Onset of symptoms|| || || || || |
|Complications|| || |
The differential diagnoses listed here are not exhaustive.
- Ventilation 
- Endotracheal administration of artificial surfactant within 2 hours postpartum
- Supportive measures: IV fluid replacement; stabilization of blood sugar levels and electrolytes
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
- Treatment: controlled oxygenation, diuretics, rarely glucocorticoids
- (the persistently low partial pressure of oxygen in the blood contributes to PDA)
- Cardiovascular arrest
- Neonatal sepsis
- Complications of O2 inhalation: , bronchopulmonary dysplasia, intraventricular hemorrhage
We list the most important complications. The selection is not exhaustive.
- Mortality rate: < 10% 
- Most cases resolve within 3–5 days if treated promptly