Hyaline Membrane Disease (HMD):Best article 2025


Pathophysiology of HMD

Hyaline Membrane Disease(HMD) arises due to a deficiency in pulmonary surfactant production, which leads to increased surface tension in the alveoli. The key steps in its pathophysiology include:

  1. Surfactant Deficiency:
  • Surfactant is a lipoprotein complex produced by alveolar type II cells starting from 24 weeks of gestation, with sufficient production by 34-36 weeks.
  • Premature newborns (<34 weeks) have immature lungs and insufficient surfactant synthesis.
  1. Increased Alveolar Surface Tension:
  • In the absence of adequate surfactant, alveoli collapse during exhalation (atelectasis), leading to a reduction in functional residual capacity (FRC).
  • This increases the work of breathing and oxygen consumption.
  1. Impaired Gas Exchange:
  • Collapsed alveoli impair ventilation and perfusion matching, causing hypoxemia and hypercarbia (respiratory acidosis).
  • Hypoxemia triggers pulmonary vasoconstriction, further reducing oxygenation.
  1. Inflammatory Response and Hyaline Membrane Formation:
  • Atelectasis and lung injury cause epithelial and endothelial cell damage.
  • Proteinaceous exudate from damaged capillaries combines with necrotic epithelial cells to form “hyaline membranes,” lining alveoli and further impairing gas exchange.
  1. Cycle of Worsening Respiratory Failure:
  • Without intervention, the combination of atelectasis, surfactant deficiency, and inflammation perpetuates respiratory failure.

Strategies to Prevent HMD

Antenatal Strategies:

  1. Antenatal Corticosteroids:
  • Administration of corticosteroids (e.g., betamethasone) to mothers at risk of preterm labor (24-34 weeks) enhances fetal lung maturity.
  • These steroids stimulate surfactant production and improve alveolar stability.
  1. Prevention of Preterm Birth:
  • Tocolytic agents can be used to delay labor in high-risk pregnancies to allow time for corticosteroids to take effect.
  • Optimal prenatal care and management of maternal conditions like hypertension and infections reduce preterm birth risk.

Postnatal Strategies:

  1. Surfactant Replacement Therapy:
  • Exogenous surfactant, delivered via endotracheal tube, reduces surface tension, improves oxygenation, and decreases mortality. It can be used prophylactically or therapeutically.
  • Examples: Poractant alfa, beractant.
  1. Respiratory Support:
  • Continuous Positive Airway Pressure (CPAP): Prevents alveolar collapse and improves oxygenation.
  • Mechanical Ventilation: Required in severe cases but should be used judiciously to minimize lung injury (barotrauma/volutrauma).
  1. Oxygen Therapy:
  • Careful titration of oxygen to avoid hypoxemia and hyperoxia. Pulse oximetry and blood gas monitoring are essential.
  1. Minimizing Ventilation-Associated Injury:
  • Strategies such as permissive hypercapnia and use of non-invasive ventilation are preferred.
  1. Nutritional Support:
  • Early initiation of parenteral or enteral nutrition helps optimize overall recovery and growth.

References:

  • Nelson Textbook of Pediatrics, 21st Edition: Discusses the development of the respiratory system and pathophysiology of HMD.
  • Cloherty and Stark’s Manual of Neonatal Care, 8th Edition: Provides detailed preventive strategies and management of HMD

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