Non-cardiogenic pulmonary oedema and diffuse lung inflammation, typically secondary to an underlying illness, occurring within 7 days of the onset of a lung injury
Aetiology
Pulmonary: pneumonia (most common cause), chest sepsis, aspiration, inhalation injury, pulmonary contusion, and transfusion-related lung injury
Non-pulmonary causes: sepsis from a non-pulmonary source, acute pancreatitis, disseminated intravascular coagulation, and drug overdose
Pathophysiology
ARDS involves a diffuse bilateral alveolar injury, as a result of inflammation mediated by inflammatory mediators such as TNF-α, IL-1 and IL-8
Pathological features: diffuse alveolar damage with hyaline membrane formation
The resulting endothelial injury activates neutrophils in the pulmonary capillaries, releasing reactive oxygen species and proteases that damage the alveolar endothelium and type 2 alveolar cells
As a result, the vascular permeability increases and the lung surfactant is lost
Fluid accumulation in the alveoli causes pulmonary oedema and subsequently hypoxaemia
It is not secondary to cardiogenic pulmonary oedema, pleural effusion or atelectasis
ARDS is not the same as neonatal respiratory distress syndrome, which is due to inadequate lung surfactant production caused by prematurity
Clinical features
Symptoms
Acute onset respiratory failure which fails to improve with supplemental oxygen, the symptoms of which include severe dyspnoea, confusion, and presyncope
Signs
Elevated respiratory rate
Bilateral lung crackles (but no other features of heart failure)