Model Answer
0 min readIntroduction
Respiratory Distress Syndrome (RDS), also known as Hyaline Membrane Disease, is a significant cause of morbidity and mortality in premature infants. It arises from a deficiency of pulmonary surfactant, a complex mixture of lipids and proteins essential for reducing surface tension in the alveoli. This deficiency leads to alveolar collapse, impaired gas exchange, and subsequent respiratory distress. The incidence of RDS is inversely proportional to gestational age, with the highest risk in infants born before 37 weeks of gestation. Understanding the pathogenesis of RDS is crucial for effective prevention and management.
Normal Lung Function & Surfactant
The lungs are lined with alveoli, tiny air sacs responsible for gas exchange. Alveolar surface tension, caused by the cohesive forces of water molecules lining the alveoli, tends to cause alveolar collapse, especially during expiration. Pulmonary surfactant, produced by Type II pneumocytes, reduces this surface tension, preventing alveolar collapse and reducing the work of breathing. Surfactant’s key components include dipalmitoylphosphatidylcholine (DPPC), phosphatidylglycerol (PG), and surfactant proteins A, B, C, and D.
Pathogenesis of RDS
1. Surfactant Deficiency: The Primary Cause
The primary cause of RDS is insufficient production of surfactant. This is particularly common in premature infants because:
- Immature Type II Pneumocytes: These cells are responsible for surfactant synthesis, and their development is incomplete in premature infants.
- Lack of Corticosteroid Stimulation: Maternal administration of corticosteroids before delivery stimulates fetal lung maturation, including increased surfactant production. Without this stimulation, surfactant levels are lower.
- Surfactant Compositional Abnormalities: Even if some surfactant is present, its composition may be abnormal, lacking sufficient DPPC or PG, reducing its effectiveness.
2. Alveolar Collapse & Reduced Lung Compliance
Due to surfactant deficiency, surface tension increases, leading to:
- Alveolar Collapse: Alveoli collapse at end-expiration, reducing the functional surface area for gas exchange.
- Reduced Lung Compliance: The lungs become stiffer, requiring greater inspiratory effort to inflate them.
- Increased Work of Breathing: The infant must expend significantly more energy to breathe, leading to fatigue and respiratory failure.
3. Physiological Consequences
The alveolar collapse and reduced lung compliance result in several physiological disturbances:
- Hypoxemia: Reduced alveolar surface area impairs oxygen transfer to the blood, leading to low blood oxygen levels.
- Hypercapnia: Inefficient gas exchange leads to a buildup of carbon dioxide in the blood.
- Acidosis: Hypercapnia causes respiratory acidosis, further exacerbating the respiratory distress.
- Pulmonary Vasoconstriction: Hypoxia causes pulmonary vasoconstriction, increasing pulmonary artery pressure and potentially leading to persistent pulmonary hypertension of the newborn (PPHN).
4. Hyaline Membrane Formation
The term "Hyaline Membrane Disease" originates from the formation of a protein-rich membrane lining the collapsed alveoli. This membrane is composed of fibrin, cellular debris, and surfactant components. While historically considered a primary pathological feature, it is now understood to be a secondary consequence of alveolar injury and edema.
Risk Factors for RDS
- Prematurity: The most significant risk factor.
- Maternal Diabetes: Can delay lung maturation.
- Multiple Gestation: Increases the risk of prematurity.
- Perinatal Asphyxia: Can cause lung injury and surfactant inactivation.
- Cesarean Delivery without Labor: Lack of labor-induced cortisol release may delay lung maturation.
Conclusion
Respiratory Distress Syndrome is a complex condition stemming from surfactant deficiency, leading to alveolar collapse and impaired gas exchange. Understanding the pathogenesis – from the role of Type II pneumocytes to the physiological consequences of hypoxemia and acidosis – is vital for effective management. Prophylactic corticosteroid administration to mothers at risk of preterm delivery and postnatal surfactant replacement therapy have significantly improved outcomes for infants with RDS. Continued research focuses on optimizing lung maturation strategies and minimizing the long-term respiratory complications associated with this condition.
Answer Length
This is a comprehensive model answer for learning purposes and may exceed the word limit. In the exam, always adhere to the prescribed word count.