## Pathophysiology of Meconium Aspiration Syndrome ### Correct Mechanisms in MAS **Key Point:** MAS results from aspiration of meconium-stained amniotic fluid (MSAF) into the fetal lungs, typically during episodes of intrauterine hypoxia and gasping. ### Three Main Mechanisms of Lung Injury 1. **Chemical Pneumonitis** - Meconium contains bile salts, pancreatic enzymes, and inflammatory mediators - Direct toxic injury to airway epithelium and alveolar lining - Triggers inflammatory cascade with neutrophil infiltration 2. **Mechanical Obstruction (Ball-Valve Effect)** - Meconium particles lodge in small airways - Air enters during inspiration but cannot escape during expiration - Results in air trapping, hyperinflation, and barotrauma - Leads to pneumothorax and pneumomediastinum in severe cases 3. **Surfactant Inactivation** - Meconium components (bile salts, free fatty acids) inhibit surfactant function - Reduces surface tension reduction capacity - ~~Surfactant deficiency~~ (surfactant is present but inactivated) ### Why Option 4 is Incorrect **High-Yield:** The fundamental distinction between MAS and RDS: - **RDS:** Surfactant *deficiency* (immature lungs, prematurity) - **MAS:** Surfactant *inactivation* (present but non-functional due to meconium) MAS occurs in term and post-term infants with adequate surfactant production; the problem is that meconium inactivates it. ### Clinical Correlation **Clinical Pearl:** Meconium passage in utero is a marker of fetal distress and hypoxia. The fetus gasps in response to hypoxia, aspirating meconium-stained fluid into the lungs before delivery. This is why MAS is more common in post-term infants and those with intrauterine growth restriction (IUGR). ### Key Radiologic Features - Bilateral patchy infiltrates ("ball-in-valve" appearance) - Hyperinflation with flattened diaphragms - Pneumothorax (10–40% of severe cases) - Atelectasis alternating with hyperinflated areas [cite:Nelson Textbook of Pediatrics 21e Ch 102]
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