Formerly known as adult respiratory distress syndrome. A form of acute respiratory failure in which a variety of diﬀerent disorders give rise to lung injury by what is thought to be a common pathway. The condition has a high mortality rate (about 70 per cent); it is a complex clinical problem in which a disproportionate immunological response plays a major role. (See IMMUNITY.)
The exact trigger is unknown, but it is thought that, whatever the stimulus, chemical mediators produced by cells of the immune system or elsewhere in the body spread and sustain an inﬂammatory reaction. Cascade mechanisms with multiple interactions are provoked. CYTOTOXIC substances (which damage or kill cells) such as oxygen-free radicals and PROTEASE damage the alveolar capillary membranes (see ALVEOLUS). Once this happens, protein-rich ﬂuid leaks into the alveoli and interstitial spaces. SURFACTANT is also lost. This impairs the exchange of oxygen and carbon dioxide in the lungs and gives rise to the clinical and pathological picture of acute respiratory failure.
The typical patient with ARDS has rapidly worsening hypoxaemia (lack of oxygen in the blood), often requiring mechanical ventilation. There are all the signs of respiratory failure (see TACHYPNOEA; TACHYCARDIA; CYANOSIS), although the chest may be clear apart from a few crackles. Radiographs show bilateral, patchy, peripheral shadowing. Blood gases will show a low PaO2 (concentration of oxygen in arterial blood) and usually a high PaCO2 (concentration of carbon dioxide in arterial blood). The lungs are ‘stiﬀ’ – they are less eﬀective because of the loss of surfactant and the PULMONARY OEDEMA.
Causes The causes of ARDS may be broadly divided into the following: