Neonatal Respiratory Distress Syndrome: Epidemiology and Pathophysiology

00:00 Welcome.

00:02 Today we delve into one of the most frightening conditions a preterm infant and their parents can face, respiratory distress syndrome.

00:09 Respiratory distress syndrome is a condition of preterm infants caused by insufficient pulmonary surfactant leading to alveolar collapse, impaired gas exchange, and respiratory distress shortly after birth.

00:21 So let's begin this talk by discussing the epidemiology of neonatal RDS.

00:27 The key point is that the risk of neonatal respiratory distress syndrome rises as gestational age falls.

00:33 So babies born before 28 weeks carry the highest burden.

00:37 Among preterm infants, white males are overrepresented for reasons not yet fully understood.

00:42 Overall, RDS remains a leading driver of morbidity and mortality in premature newborns, underscoring why every extra day in utero matters.

00:51 All right, let's now try to understand the pathophysiology behind neonatal respiratory distress syndrome.

00:57 And we'll do this by setting the stage with the big picture.

01:00 Healthy newborn lungs stay open and stretchy because they're coated with a detergent we call surfactant.

01:05 Without it, those tiny air sacs behave like wet balloons, which makes them incredibly inefficient for gas exchange, which leads to the collapse of the alveolus.

01:15 So first things first, what's inside the surfactant? In the skin, roughly 85% of surfactant is phospholipid.

01:24 The headliner is DPPC, dipalmitoylphosphatidylcholine, a mouthful we often shorten to lecithin.

01:32 Close behind is phosphatidylglycerol, which really ramps up by about 35 weeks gestation, so much so that we use it as a lab marker of lung maturity.

01:42 A sprinkling of unsaturated phosphatidylcholines rounds out the lipid roster.

01:48 Shifting gears, about 10% of the cocktail is made of four slick little apoproteins, SPA, SPB, SPC, and SPD.

01:56 Think of these as the pit crew that positions, stabilizes, and recycles the lipid film.

02:03 And finally, cholesterol sneaks in as a neutral lipid to tweak fluidity.

02:08 Now, you should be wondering, how do we build the stuff? The answer is in the rough endoplasmic reticulum of a type 2 alveolar cell.

02:17 Here, we stitch together those phospholipids.

02:20 Next, the product rides the elevator to the Golgi apparatus, where final tweaks happen.

02:25 From there, it's packed into tidy lamellar bodies, little surfactant suitcases waiting by the door.

02:30 Once those suitcases open, proteins and phospholipids merge into surfactant lipoprotein complexes and spill onto the alveolar surface.

02:39 Here's the payoff.

02:41 That glossy film slashes surface tension, preventing alveoli from imploding every time the infant exhales.

02:47 Now, imagine we're dealing with a preterm infant whose lungs are still surfactant poor.

02:54 As soon as he gets born, since he does not have enough surfactant, the baby must generate Herculean negative pressures just to pry the alveoli open.

03:03 But of course, this is close to impossible in these conditions.

03:06 What's the result? End expiratory collapse, low lung volumes, and really stiff lungs.

03:12 Because collapsed segments don't ventilate but still receive blood, we create a nasty ventilation-chots perfusion, or VQ, mismatch.

03:21 Consequently, oxygen plummets, carbon dioxide climbs, and acidosis sets in.

03:27 Those chemical alarms trigger pulmonary vasoconstriction, reopening fetal shunts, blood flow falls, alveoli become ischemic, and an inflammatory cascade floods them with protein-rich edema, ratcheting pulmonary vascular resistance back up when it should be low.

03:44 That vicious spiral is the essence of neonatal respiratory distress syndrome, RDS.

03:50 And now that you understand all that, take a glance at the following table to see the major etiologic factors that tip an infant toward RDS.

04:00 First, we have prematurity, where type 2 alveolar cells are still immature, leaving the lung with too little and too weak surfactant to keep the tiny air sacs open.

04:12 Moving on, surfactant inactivation comes into play when meconium or blood leaks into the alveoli, or when oxidative and mechanical stress from ventilation strip away the surfactant film that is already there.

04:24 Next, consider maternal diabetes.

04:27 The mother's high blood glucose drives fetal hyperinsulinemia, and that excess insulin blunts the cortisol surge that normally kickstarts surfactant production, delaying lung maturation.

04:37 After that, cesarean delivery without labor matters, because in the absence of labor, the fetus misses both the hormonal burst, especially cortisol, and the mechanical squeeze that clear lung fluid.

04:48 The result is a wetter lung and slower surfactant release.

04:53 Finally, conditions that cause fetal acidosis, such as perinatal asphyxia, sepsis, intrapartum hypovolemia, or hypotension, injure type 2 cells and hamper both the synthesis and function of surfactant.

05:08 All of these pathways converge on a single problem, insufficient or ineffective surfactant, setting the stage for neonatal respiratory distress syndrome.