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The acute respiratory distress syndrome (ARDS) was first reported in a case series from Denver in 1967.1 Forty-five years later, the syndrome was reborn: the ‘Berlin’ definition captures patients with a mortality of 24% rising to 48% in the group of patients with the most severe respiratory failure.2 Survivors commonly suffer from muscle weakness and neuropsychiatric problems, such that fewer than 50% have returned to work 12 months after leaving intensive care.3 ARDS is important both clinically and financially. It is a not uncommon contributor to the deaths of critically ill patients of all ages4 and survivors commonly suffer from muscle weakness and neuro-psychiatric problems, such that fewer than 50% have returned to work 12 months after leaving intensive care.3 ,5
The onset of ARDS can be ascribed to two processes resulting from acute inflammation or injury at the lung's gas exchange surface: the alveolar–capillary membrane. These processes increase the permeability of the membrane associated with the recruitment of neutrophils into the airspace. The resulting acute inflammatory exudate inactivates surfactant, leading to collapse and consolidation with progressive loss of functioning lung. This would be well tolerated physiologically if the inflammatory process did not paralyse the lung's means of preventing ventilation–perfusion mismatch: hypoxic pulmonary vasoconstriction. The combination of these factors causes profound hypoxaemia accompanied by pulmonary oedema. The latter mechanism accounts for the fact that as a rule patients with ARDS are considerably more hypoxaemic than those with heart failure with similar radiographic appearances.
Since its recognition, much has been learnt about …
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