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ADULT RESPIRATORY DISTRESS SYN­DROME (ARDS) A form of acute respira­tory failure in which a variety of different disorders give rise to pulmonary injury by what is thought to be a common pathway. It has a high mortality (about 70 per cent).

The exact aetiology is unknown, but it is thought that, whatever the stimulus, activation of neutrophils (which may then be sequestered in the lungs) releases cytotoxic substances -substances that damage or kill cells - such as oxygen-free radicals and proteases which dam­age the alveolar capillary membranes. Once these are damaged protein-rich oedema fluid leaks into the alveoli and insterstitial spaces. surfactant is also lost. This impairs gas ex­change 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, which contrasts with the relative lack of physi­cal signs. There are all the signs of respiratory failure (see tachypnoea, tachycardia, cyano­sis, etc.), though the chest may be clear apart from a few crackles. Radiographs show bilat­eral, patchy, peripheral shadowing sparing the cardio and costophrenic angles. Blood gases will show a low Pa02 (concentration of oxygen in pulmonary arterial blood) and usually a high PaC02 (concentration of carbon dioxide in pulmonary arterial blood). The lungs are 'stiff' - they are less effective because of the loss of surfactant and the non-cardiogenic pulmonary oedema.

Causes The causes of ARDS may be broadly divided into the following: microbiological Pulmonary, distant, or gener­alized infectioaby bacteria, fungi, or viruses activation of host defence Massive iranslu sion, transfusion reaction, bypass, etc., may cause activation of neutro­phils via complement pathways. chemical This includes drugs, inhaled toxic gases and smoke, and metabolic disorders like uraemia and pancreatitis (see pancreas, dis­eases of).

physical Trauma to the lung, aspiration of stomach contents, aspiration of water, etc.

Treatment The principles of management are supportive, with treatment of the underlying condition if that is possible. Oxygenation is improved by increasing inspired oxygen concen­tration and mechanical ventilation of the lungs. Attempts are made to reduce the formation of pulmonary oedema by careful management of fluid balance. Secondary infections are treated if they arise, as are the possible complications of prolonged ventilation with low lung compliance (e.g., pneumothorax). There is some evidence that giving surfactant through a nebulizer or aerosol may help to improve lung effectiveness and reduce oedema. There is little evidence that steroids are of use. Some experimental evidence supports the use of free radical scavengers and antioxidants, but these are not commonly used. In severe cases extracorporeal gas exchange has been advocated as a supportive measure until the lungs have healed enough for adequate gas exchange.

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