In burn-inhalation injury patients, what is a major contributor to ARDS development?

• A. Hypovolemia
• B. Low tidal volume ventilation
• C. Inhalation injury and sepsis increasing alveolar-capillary permeability
• D. Hyperglycemia

Answer: (C)

The key idea is that ARDS in burn–inhalation injury arises from inflammation-driven disruption of the alveolar–capillary barrier. Inhalation injury causes direct chemical and thermal damage to the airways and lung tissue, triggering a strong local inflammatory response. When sepsis is present, systemic inflammatory mediators amplify this response, activating neutrophils and damaging the capillary endothelium throughout the lung. The result is increased alveolar–capillary permeability, allowing protein-rich fluid to flood the airspaces, forming edema and hyaline membranes that impair gas exchange and reduce lung compliance. This noncardiogenic pulmonary edema and diffuse alveolar damage are the hallmark of ARDS in this setting, making the combination of inhalation injury and sepsis a major contributor.

Hypovolemia affects perfusion and overall circulation but doesn’t directly drive the permeability changes that produce ARDS. Low tidal volume ventilation is a protective strategy to prevent ventilator-induced lung injury, not a cause of ARDS. Hyperglycemia is a metabolic issue after burns and does not explain the lung permeability changes that lead to ARDS.