Correct Answer: D. Surface tension - increased; Compliance - decreased
Respiratory distress syndrome (RDS) in preterm infants at 28 weeks is fundamentally a disease of surfactant deficiency. Pulmonary surfactant, synthesized by type II alveolar cells, begins significant production only after 32–34 weeks of gestation; at 28 weeks, production is minimal. Surfactant's primary role is to reduce surface tension at the air–liquid interface in alveoli. Without adequate surfactant, surface tension remains elevated, making alveolar collapse (atelectasis) inevitable during expiration. This directly impairs compliance (the ease with which the lungs can be inflated). Compliance is inversely related to surface tension and elastic recoil; when surface tension is high, the lungs become stiff and non-compliant. The baby must generate enormous negative intrathoracic pressures to re-expand collapsed alveoli with each breath, leading to the classic signs of RDS: tachypnea, grunting (to maintain positive end-expiratory pressure), intercostal and subcostal retractions, and nasal flaring. In Indian NICUs, surfactant replacement therapy (exogenous surfactant—INSURE or LISA technique) is now standard of care for RDS, which dramatically improves compliance and oxygenation by reducing surface tension. The pathophysiology is clear: high surface tension → low compliance → respiratory distress.
Why the other options are wrong
A. Both surface tension and compliance decreased — This is wrong because it reverses the pathophysiology of RDS. Surfactant deficiency causes surface tension to increase, not decrease. While compliance does decrease (correct), the first part is fundamentally incorrect. This trap may lure students who confuse the effect of surfactant presence with surfactant absence. B. Surface tension - decreased; Compliance - increased — This is completely opposite to the true pathophysiology. It describes a baby with normal or excess surfactant, not a preterm infant with RDS. This option may trap students who know surfactant reduces surface tension but fail to recognize that a 28-week preterm baby has insufficient surfactant, not excess. C. Both surface tension and compliance increased — This is wrong because compliance cannot increase in RDS; it always decreases due to alveolar collapse and increased elastic recoil. While surface tension does increase (correct), the second part contradicts the clinical presentation of RDS. This may trap students who confuse stiffness with increased compliance.
High-Yield Facts
- Surfactant synthesis begins at ~20 weeks but becomes clinically significant only after 32–34 weeks; at 28 weeks, production is minimal and RDS is likely.
- Surface tension is inversely proportional to compliance; high surface tension → low compliance (stiff lungs).
- Surfactant reduces surface tension by ~70% in normal lungs; its absence in RDS leaves surface tension elevated.
- Compliance in RDS is typically 0.5–1 mL/cm H₂O (normal: 100 mL/cm H₂O); this is the hallmark of 'stiff baby syndrome'.
- Exogenous surfactant (INSURE/LISA technique) is the standard of care in Indian NICUs for RDS; it rapidly restores compliance and reduces mortality.
Mnemonics
RDS Pathophysiology: STIFF Surfactant deficiency → Tension ↑ → Inflation difficult → Failing compliance → Flexibility lost. Use this when you see 'preterm + RDS' to lock in the direction of changes. Surfactant = Softener Think of surfactant as a 'lung softener'—without it, lungs become stiff (low compliance). At 28 weeks, the softener factory is barely open; hence stiff lungs and high surface tension.
NBE Trap
NBE pairs 'preterm infant' with 'RDS' to test whether students understand the direction of changes in surface tension and compliance. A common trap is to confuse the effect of surfactant (which reduces tension and increases compliance) with the effect of surfactant deficiency (which increases tension and decreases compliance).
Clinical Pearl
In Indian NICUs, a preterm baby at 28 weeks presenting with RDS will show severe retractions and grunting—clinical signs of the lungs' struggle against high surface tension and low compliance. Immediate surfactant replacement (within 1–2 hours of birth) is life-saving and dramatically improves oxygenation and survival rates, making this a high-yield bedside correlation for NEET PG.
_Reference: Guyton & Hall Textbook of Medical Physiology, Ch. 37 (Pulmonary Ventilation); Harrison's Principles of Internal Medicine, Ch. 246 (Acute Respiratory Distress Syndrome); OP Ghai Essentials of Pediatrics, Ch. 10 (Respiratory Distress Syndrome)_