Neonatal respiratory distress syndrome: Clinical sciences

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Introduction0:00–1:08

Neonatal respiratory distress syndrome, also called neonatal RDS or hyaline membrane disease, is a life-threatening condition characterized by lung immaturity and alveolar surfactant deficiency.
Now, surfactant is a complex of phospholipids and proteins that reduces alveolar surface tension and prevents collapse of the alveoli.
Alveolar cells called type 2 pneumocytes produce surfactant beginning around 24 to 26 weeks of gestation, and it doesn’t reach mature levels until 34 to 36 weeks of gestation, so the incidence of neonatal RDS is inversely related to gestational age at birth.
Surfactant deficiency causes decreased lung compliance, atelectasis, low lung volumes, inflammation, pulmonary edema, and pulmonary arterial vasoconstriction; all of which result in hypoxia, hypercapnia, and acidemia.
Now, if a pediatric patient presents with a chief concern suggesting neonatal RDS, perform an ABCDE assessment to determine if they are stable or unstable.

Unstable patient1:08–2:08

These patients are typically unstable, so begin acute management immediately. First, stabilize their airway, breathing, and circulation; and then provide noninvasive respiratory support, such as nasal continuous positive airway pressure, or nasal CPAP.
If your patient is apneic or has a poor respiratory effort, you may need to perform endotracheal intubation and begin mechanical ventilation.
Next, obtain intravenous or intraosseous access, or consider placing an umbilical venous catheter. Then, start IV fluids; begin continuous vital sign monitoring, including heart rate, blood pressure, pulse oximetry, and respiratory rate; and provide supplemental oxygen to maintain oxygen saturations between 90 and 95 percent.

Focused H&P2:08–7:19

Once you stabilize your patient, perform a focused history and physical examination and obtain pulse oximetry measurements.
History will reveal the onset of respiratory distress within minutes or hours of birth. These patients are typically premature, with the majority being between 23 and 29 weeks of gestational age at birth; or are very low birth weight, which is defined as under 1500 grams.
The prenatal ultrasound is usually normal, but in some cases, the obstetrical history might identify risk factors, such as multiple gestation, biological male, maternal diabetes, fetal distress or asphyxia, C-section delivery without labor, or a family history of neonatal RDS.
The history may also reveal preterm labor without antenatal corticosteroid administration. Here’s a clinical pearl to keep in mind!
Betamethasone is a corticosteroid that’s usually given when labor begins before 34 weeks of gestation to stimulate alveolar surfactant production and reduce the risk of neonatal RDS.
Antenatal corticosteroid administration can also decrease the incidence of intraventricular hemorrhage and necrotizing enterocolitis, and reduce mortality in premature infants.
As for the physical exam, these infants classically demonstrate tachypnea, with a respiratory rate above 60 breaths per minute; as well as signs of labored breathing, such as grunting, nasal flaring, and intercostal and suprasternal retractions.
Lung auscultation often demonstrates poor air movement, and occasionally, audible crackles. Your patient might also appear cyanotic.
In addition, pulse oximetry usually reveals an oxygen saturation below 90%. These findings should lead you to suspect neonatal respiratory distress syndrome, which can often be diagnosed clinically.
Still, in most cases, you’ll want to obtain a chest X-ray to confirm the diagnosis. Now if the X-ray reveals ground glass opacities with air bronchograms and hypoexpansion, diagnose neonatal respiratory distress syndrome.
Here’s another clinical pearl! Other conditions that present with neonatal respiratory distress include transient tachypnea of the newborn, meconium aspiration syndrome, pneumonia, pneumothorax, persistent pulmonary hypertension of the newborn, patent ductus arteriosus, and congenital heart lesions.
These conditions can be differentiated from neonatal RDS using historical clues, as well as pre- and post-ductal oxygen saturations; chest X-ray findings; and echocardiography.
However, because it can be difficult to distinguish pneumonia from neonatal RDS, antibiotics are often administered whenever a neonate presents with respiratory distress.
Once you’ve diagnosed neonatal RDS, you’ll need to provide prompt treatment! For respiratory management, provide warm, humidified oxygen at a concentration that maintains adequate tissue oxygenation while minimizing oxygen toxicity.
In general, this means that you’ll keep your patient’s oxygen saturation between 90 and 95 percent. Next, provide pharmacologic management, as needed, which primarily consists of exogenous surfactant.
If your patient is intubated, administer surfactant directly into the lungs through the endotracheal tube. On the other hand, if your patient is receiving noninvasive respiratory support but has a rising FiO2 requirement to maintain oxygen saturations above 90 percent, administer surfactant using a technique such as Minimally Invasive Surfactant Therapy, or MIST for short, where surfactant is administered via a small catheter placed through the vocal cords while the infant is on nasal CPAP.
Alternatively, you could consider a technique called INtubate SURfactant Extubate, or INSURE for short, where the infant is intubated in order to administer the surfactant through an endotracheal tube, and then extubated and put back on nasal CPAP after the surfactant is delivered.
Because neonatal RDS is a self-limited condition, most patients improve by 3 to 4 days of life, once endogenous surfactant production increases.
Finally, provide general supportive care, which includes maintaining a neutral thermal environment, providing nutritional support, managing fluid and electrolyte balance, and maintaining hemodynamic stability.
Also keep in mind the importance of weaning supplemental oxygen and mechanical ventilation as soon as possible to avoid complications such as oxygen toxicity and ventilator-associated lung injury.
Here’s one last clinical pearl! If a newborn’s respiratory distress continues despite surfactant treatment, be sure to evaluate for another underlying condition, such as patent ductus arteriosus, congenital heart disease, persistent pulmonary hypertension of the newborn, or inherited disorders of surfactant production and function.

Review7:19–8:02

Alright, as a quick recap… Neonatal RDS primarily occurs in premature infants and is characterized by lung immaturity and alveolar surfactant deficiency.
Diagnosis is based on classic clinical features, including the development of respiratory distress shortly after birth, and is supported by characteristic radiographic findings.
Treatment relies on adequate oxygenation; ventilatory support, which could include nasal CPAP or intubation with mechanical ventilation; and exogenous surfactant administration.
Most patients improve by 3 to 4 days of life, once endogenous surfactant production increases.