Underlying Etiology of Acute Respiratory Distress Syndrome

In our previous blog, we defined acute respiratory distress syndrome (ARDS) and briefly discussed treatment options which include supportive measures and salvage therapies. To access that blog post, click here. In this blog, we will delve into the etiology of ARDS.

In ARDS, inflammatory cells bombard the lungs destroying the endothelial and epithelial borders causing the alveoli to be flooded with inflammatory cells, fluid, protein, and red blood cells. This injury can be intra- or extrapulmonary. Intrapulmonary, or direct, risk factors of ARDS are pneumonia, aspiration, pulmonary contusion, oxygen toxicity, near drowning, and inhalation injury. Extrapulmonary, or indirect, risk factors include sepsis, severe trauma, pancreatitis, multiple transfusions, overdose, and cardiopulmonary bypass1. This cascade results in massive alveolar edema and begins the exudative phase2.(A)

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The next phase is the proliferative phase (B) in which the body tries to repair itself by rebuilding the epithelium and clearing out the excess fluid3.

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The fibrotic stage (C) occurs next but is not clearly understood and does not take place in all patients with ARDS. What is known is that if the proliferative phase is extended or impaired, it leads to lung fibrosis1. Any intervention in this stage would be considered salvage therapy2.

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Prone positioning is indicated for many different types of respiratory disorders. The Pronova-O2TM Automated Prone Therapy System provides a safe and efficient method for placing patients in the prone position. For more information, visit turnmedical.com or call 855-ASK-TURN. Join us for our next blog as we discuss standards of care for ARDS as well as salvage therapies