Pathophysiology of acute respiratory distress syndrome

Hyaline membranes - intermed mag

Acute Respiratory Distress Syndrome (ARDS) is a severe, life-threatening medical condition characterized by rapid onset of widespread inflammation in the lungs. It is a type of respiratory failure marked by fluid buildup in the tiny, elastic air sacs (alveoli) in the lungs. The fluid prevents the lungs from filling with enough air, which means less oxygen reaches the bloodstream. This deprives the organs of the oxygen they need to function. The pathophysiology of ARDS involves complex interactions between various cellular and molecular mechanisms.

Etiology

ARDS can be triggered by various direct and indirect lung injuries. Direct injuries include pneumonia, aspiration of gastric contents, and inhalation injury, while indirect injuries encompass sepsis, severe trauma, and blood transfusions. These initial insults lead to an inflammatory response in the lungs.

Pathogenesis

The pathogenesis of ARDS is characterized by three phases: the exudative phase, the proliferative phase, and the fibrotic phase.

Exudative Phase

The exudative phase occurs within the first week after lung injury and is marked by the development of diffuse alveolar damage. The injury to the alveolar-capillary membrane leads to increased permeability and the leakage of protein-rich fluid into the alveoli, resulting in pulmonary edema and decreased lung compliance. Neutrophils and other inflammatory cells are recruited to the site of injury, releasing inflammatory mediators that further damage the lung tissue.

Proliferative Phase

The proliferative phase typically occurs 1 to 2 weeks after the onset of ARDS. This phase is characterized by the proliferation of type II pneumocytes and fibroblasts, leading to the formation of hyaline membranes and fibrosis within the interstitium and alveolar spaces. This process can result in impaired gas exchange and reduced lung compliance.

Fibrotic Phase

The fibrotic phase can develop in some patients, leading to irreversible lung damage and chronic respiratory failure. This phase is marked by extensive fibrosis, remodeling of the lung architecture, and further decline in lung function.

Clinical Features

Patients with ARDS present with rapid onset of severe dyspnea, hypoxemia, and bilateral infiltrates on chest imaging, without evidence of cardiac failure or fluid overload. The severity of ARDS is classified based on the degree of hypoxemia: mild, moderate, and severe.

Diagnosis

The diagnosis of ARDS is clinical, based on the Berlin Definition, which includes timing of the respiratory symptoms, origin of edema, severity of hypoxemia, and radiological findings.

Treatment

Treatment of ARDS focuses on supportive care, with mechanical ventilation to ensure adequate oxygenation. Strategies such as low tidal volume ventilation, prone positioning, and conservative fluid management have been shown to improve outcomes. In severe cases, extracorporeal membrane oxygenation (ECMO) may be considered.

Conclusion

ARDS is a complex disorder with a high mortality rate, necessitating early recognition and aggressive management. Understanding the pathophysiology of ARDS is crucial for the development of targeted therapies and improving patient outcomes.

‎