Fetal Lung Maturation is Delayed in Diabetic Pregnancies
The most likely reason for IRDS development despite an L/S ratio of 2:1 is that fetal lung maturation is delayed in poorly controlled diabetic patients, particularly affecting the final maturation step of phosphatidylglycerol (PG) synthesis. The absence of PG in this case is the critical finding that should have prompted delay of delivery.
Why Diabetes Delays Lung Maturation
The absence of phosphatidylglycerol represents incomplete lung maturation in diabetic pregnancies, even when the L/S ratio appears mature. 1
Infants who develop chronic lung disease demonstrate delayed appearance of phosphatidylglycerol, a pattern particularly prominent in diabetic pregnancies 1
In the presence of PG, regardless of L/S ratio, only 0.6% of babies develop RDS, while absent PG is associated with an 82.8% incidence of RDS 2
When PG is absent, the incidence of RDS is 16.7% in diabetic pregnancies versus 14.4% in non-diabetics 3
The Critical Interpretation Error
The L/S ratio of 2:1 alone is insufficient to confirm lung maturity in diabetic patients—PG presence is mandatory. 2, 4
When both PG is present AND L/S ratio is mature (>2.0), no babies develop RDS 2
However, when L/S ratio is mature but PG is absent, 3.4% still develop RDS 2
In diabetic pregnancies specifically, surfactant-deficient RDS occurred in 0.95% of tested cases, with all five cases occurring before 34 weeks gestation 4
Why the Other Options Are Incorrect
Option b (fetal urine contamination): This would falsely lower the L/S ratio, not raise it to 2:1, making this explanation inconsistent with the findings 3, 2
Option c (diabetics don't produce sphingomyelin): This is physiologically incorrect—diabetic patients produce sphingomyelin normally; the issue is delayed PG synthesis 3, 2, 4
Option d (maternal blood contamination): Blood contamination would affect the L/S ratio measurement but does not explain the specific absence of PG in the context of diabetes 2
Option e (foam test not performed): The foam test is a screening tool with lower specificity; the definitive tests (L/S ratio and PG) were already performed, making this irrelevant 5
Clinical Implications for Practice
Delivery should have been delayed until PG appeared in the amniotic fluid, regardless of the L/S ratio. 2, 4
At 37 weeks in a poorly controlled diabetic, the absence of PG indicates incomplete surfactant maturation 6
PG appears as the final step in surfactant maturation and is essential for optimal surface-active properties 6
Standard maturity values (L/S >2.0, PG >2-5%) are valid in diabetic gestations, but both must be present 4
The Pathophysiology
Surfactant without PG has inferior surface-active properties and fails to adequately stabilize alveoli in newborns. 6
PG-deficient surfactant contains prominent phosphatidylinositol (PI) instead, which has suboptimal function 6
High alveolar capillary permeability allows serum proteins to leak into airways, further inhibiting the already-compromised surfactant function 1
This leads to widespread atelectasis, impaired gas exchange, and the clinical manifestation of RDS 7, 8
The correct answer is (a): Fetal lung maturation may be delayed in diabetic patients.