Question
What happens in the lungs when a child develops pediatric acute respiratory distress syndrome (PARDS)?
Answer
In a healthy lung, each alveolus contains a layer of surfactant produced by type 2 pneumocytes. This surfactant maintains appropriate surface tension to keep the alveolus inflated. A basement membrane protects the alveolar wall. Capillaries remain close to the alveolar surface, enabling good ventilation-perfusion matching, and alveolar macrophages remain relatively quiescent.
When a patient becomes critically ill and requires mechanical ventilation, the shear forces generated by the ventilator can slough bronchial epithelium, denude the basement membrane, and create stress fractures in alveolar tissue. Interstitial flooding leads to protein-rich edema, which inactivates surfactant. Disrupted apoptosis impairs normal cellular renewal. Fibrin collects within alveolar walls, and gap formations develop in capillary walls under the pressure and volume delivered by the ventilator.
Once blood enters the air spaces or air enters the tissue spaces, an inflammatory cascade is triggered. Activated alveolar macrophages release interleukins and tumor necrosis factor, which act as chemoattractants for neutrophils. Neutrophils migrate into the lung from the bloodstream and, in attempting to contain the injury, release oxidants, leukotrienes, and proteases. The result is the full clinical picture of PARDS.
This Ask the Expert is an edited excerpt from the course, An RT Overview of the Revised PARDS Guidelines from PALICC II, presented by Evan Richards, BSc, RT.
