Acute Respiratory Distress Syndrome (ARDS)

Acute respiratory distress syndrome (ARDS) is a oxidative respiratory disease48 which is a problem in critically ill patients who are admitted to the intensive care unit (ICU)9. ARDS currently has a mortality rate of 20-40%9,11 which is associated with a high morbidity rate42,32. The original definition of ARDS was given in 1967 and was generalised as respiratory failure from non-cardiogenic pulmonary oedema which requires mechanical ventilation due to breathing difficulties and arterial hypoxemia33.Then the 4 point definition was used which the degree of hypoxemia, the level of positive end expiratory pressure (PEEP), the statics respiratory compliance and the extent of radiographic infiltrates to diagnose ARDS33. From 2012 the Berlin definition

The more risk factors an individual has the increase in the likelihood of ARDS if a severe trauma is sustained33. Some of the major or most common causes of ARDS are pneumonia, a non-pulmonary septic infection, inhalation of the gastric contents or a major physical trauma33,9,32. Less common causes of ARDS include acute pancreatitis, transfusion and drug reactions and fungal or parasitic lung infections33. There are also risk factors associated with variation in genes for regulating inflammation, reactive oxygen species levels, endothelium function and regulation of apoptosis33. For example, a variation in the Fas gene for apoptosis can lead to a change in the promoter region of the Duffy antigen. This change leads to a greater risk of mortality during ARDS for people of African American

There are two phases to ARDS pathogenesis; the acute phase and the resolving phase49. The acute phase is activated by DAMPS (danger associated molecular patterns) and begins the unregulated infiltration of the tissue by inflammatory cells causing accumulation of these cells49,33. These inflammatory cells produce oxidants and proteolytic enzymes49 leading to alveolar epithelial and endothelial injury which alters the permeability of the alveolar barrier33. They also produce cytokines which contribute to the uncontrolled activation of coagulation pathways33 which cause the lungs to become heavier due to protein rich oedema fluid, areas of haemorrhage12 and cellular debris filling the lungs33. The resolving phase in the pathogenesis of ARDS is includes phagocytosis of cellular debris and dead cells, repair of alveoli and resorption of oedema fluid49,12. If the patient survives ARDS they may recover with the full restoration of the alveolar structure, however, some patients develop fibrosis of the