The diagnosis of ARDS should meet a three-criteria system, including chest radiograph, oxygenation score, and exclusion of cardiogenic causes. Some of the main indications of ARDS are PaO2/FiO2 ≤ 300, bilateral infiltrates with pulmonary edema, and no clinical evidence of left atrial hypertension. Chest pain, dyspnea, cough, bilateral crackles, tachypnea, tachycardia, and the use of accessory muscles are all some of the symptoms that are developed in patients with ARDS.[2]

ARDS occurs as a result of an inflammation of the pulmonary capillary endothelium and alveolar epithelium which increases the permeability of these tissue layers, therefore, leads to an injury of the lung parenchyma that ultimately ends up with leakage of the protein-rich plasma out of the capillary into the interstitial space then into the alveolar space. ARDS has generally been characterized into three stages. The first stage is an early exudative stage arising from diffuse alveolar destruction and endothelial injury. The second stage is a proliferative period that follows approximately 7-14 days after injury, integrating reconstruction of the damaged alveolar structure and restoration of the barrier function along with proliferation of fibroblasts. The last stage is a fibrotic phase with chronic inflammation and fibrosis of the alveoli that follows in some patients.[3]


In conclusion, acute respiratory distress syndrome (ARDS) is an acute life threatening inflammatory lung injury that is characterized by refractory hypoxemia and stiff lungs due to increased pulmonary vascular permeability, and it is associated with a high mortality rate, consequently, almost always requiring immediate mechanical ventilation support.