1. The basic pathophysiological change of ARDS/ALI is pulmonary edema due to hyperpermeability of vascular endothelial cells and alveolar epithelial cells. The pathogenesis has been studied extensively to date and neutrophils have been found to play a decisive role, but ALI/ARDS can still occur when neutrophils are reduced, so its pathogenesis has not been fully elucidated. In general, the pathogenesis of ARDS is based on the activation of inflammatory cells such as macrophages and neutrophils and the release of chemical mediators such as cytokines through pathophysiological changes underlying the pathogenesis. Activated neutrophils have significantly increased adhesion to endothelial cells and accumulate in the pulmonary vasculature; the aggregated neutrophils are influenced by chemokines produced by alveolar macrophages and travel outside the pulmonary vasculature; the neutrophils that travel outside the pulmonary vasculature reach the interstitium and alveolar lumen and release tissue-damaging substances such as neutrophil elastase, causing pulmonary vascular endothelial cells and alveolar epithelial cells to undergo Severe inflammatory response leads to cellular dysfunction. As a result, pulmonary edema occurs due to increased permeability of the pulmonary vasculature and alveolar epithelium and leakage of plasma-containing exudate into the alveolar cavity; at the same time, microthrombus formation in the pulmonary vasculature due to the dysfunction of the blood coagulation and fibrinolytic system caused by inflammation is also a cause of pulmonary edema. Pathologically, ARDS is a type of lung injury known as diffuse alveolar damage (DAD), especially DAD due to systemic infection, in which intracapillary thrombosis and neutrophil aggregation are more pronounced; alveolar septa are swollen due to interstitial edema, and sometimes fibrin and erythrocyte deposits are seen. The acute phase from the onset to 1 week after the onset of the disease is characterized by interstitial and alveolar edema, hyaline membrane formation, type I alveolar epithelial cell necrosis, intravascular leukocyte aggregation, vascular endothelial cell necrosis, and microthrombosis. The subacute phase was in the 2nd week, with fibroblast proliferation in the interstitial and alveolar membranes, hyaline membrane fibrosis, type II alveolar epithelial cell hyperproliferation, and intra-pulmonary artery thrombus mechanization. 2 weeks later, it entered the chronic phase, with interstitial and alveolar membrane remodeling. Despite long-term research and advances in treatment, ALI/ARDS has an incidence of 79/100,000 and a mortality rate of 40% in the United States, and is one of the major lesions in critical illnesses requiring ICU management. The results of RCTs have been recognized by clinicians as high-grade evidence and have a great impact on the choice of treatment plan. However, it is important to note that even RCTs are subject to various limitations and restrictions, which may affect the results and may incorrectly analyze the RCT results. Several RCTs with new mechanical ventilation modalities and new drugs for ALI/ARDS have been performed, but the results are almost always negative and no new effective treatment options have been identified. When using diagnostic criteria with low credibility, the diagnosis of ALI/ARDS is made or ruled out rather by errors and omissions during observation than by differences in the condition. Thus, the diagnostic criteria of the AECC are too lenient and not rigorous because they take into account the different backgrounds of patients. In addition, the criteria focus only on physiological abnormalities of the lung while ignoring differences in etiology. The abnormalities seen in pulmonary dysfunction that are clinically compatible with the diagnostic criteria of AECC are not specific to ALI/ARDS and are sometimes not distinguishable from cardiogenic pulmonary edema when evaluating pulmonary dysfunction based on oxygenation index, pulmonary compliance, PEEP levels, and the extent of pulmonary infiltrative shadows. Direct pathologic diagnosis is best made using the lung tissue where the lesion occurred, but open-chest lung biopsy is not easily performed clinically, and autopsy is rarely performed, including in patients with ALI/ARDS. 3, imaging examination CT in ALI/ARDS can help to detect shadows and their extent, especially high resolution CT (HRCT) can detect pathological lesions, so it is very helpful to judge the progress of lesions. However, CT in ALI/ARDS is not so-called “diffuse” but heterogeneous in distribution. The imaging changes often vary depending on the etiology and pathophysiological progression. However, there is a difference of about 12 hours between the onset of pulmonary dysfunction and the appearance of shadowing on imaging. Therefore, the severity and stage of the disease at the time of diagnosis do not accurately reflect the progression of pulmonary pathology, but HRCT to determine the progression of pathology can help determine the efficacy. 4. Differential diagnosis As described in the AECC, the etiology of ALI/ARDS is mixed and diverse (Table 2) and needs to be differentiated from the underlying disease. Arroliga et al. reported that direct lung injury accounted for 76%, systemic infection for 18%, and other causes for 6% of ALI/ARDS in adults in Ohio, USA; Bersten et al. from Australia reported that direct lung injury accounted for 57% and indirect lung injury for 43%. Pneumonia was the most common cause of direct lung injury, followed by aspiration and pulmonary trauma; systemic infection of non-pulmonary origin was the most common cause of indirect lung injury; only 7% had both direct and indirect causes of lung injury. Therefore, the etiology of ALI/ARDS is diverse and the clinical course varies. The pathophysiological changes are different between ALI/ARDS of pulmonary origin and ALI/ARDS of non-pulmonary origin, which have been clearly identified so far. According to the diagnostic criteria of AECC, both respiratory failure due to viral pneumonia and respiratory failure due to infectious shock can be diagnosed as ALI/ARDS, but their biochemical, immunological and pathophysiological alterations are completely different.