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Canadian Journal of Anesthesia, Vol 19, 309-318, Copyright © 1972 by Canadian Anesthesiologists' Society
1 Department of Anaesthesia, Vancouver General Hospital and Department of Anaesthesia, Faculty of Medicine, University of British Columbia
Progressive respiratory insufficiency is known to be a disturbing complication following initial therapy for shock or trauma. The syndrome has been divided into four clearcut phases, with initial hypocapnia and associated metabolic acidosis. In the end stage, hypercapnia is present as well, and death is due to asystole secondary to anoxia.
Radiological findings are non-specific. Pathologically oedema, hyaline and fibrinous deposits, haemorrhage and hyperplasia of alveolar lining cells may be seen.
The major pathophysiological features include persistent hyperventilation, metabolic alkalosis progressing to metabolic acidosis secondary to tissue hypoxia, an increased alveolar-arterial oxygen gradient with greatly increased shunting through the lungs. Some of the proposed mechanisms for shunting are discussed, including surfacant depletion.
The pathogenesis of the syndrome is unknown, but several aetiological factors have been proposed. These include fluid overload, fat embolism, platelet aggregation and disseminated intravascular coagulation, aspiration, inadequate position changes, oxygen toxicity and bacterial colonization.
Prevention of the syndrome is more successful than its therapy. Early recognition and treatment of respiratory problems are important.
Management tends to be supportive and often empirical. Avoidance of overtransfusion, adequate ventilation with careffully-controlled inspired oxygen concentrations, strict asepsis, diuretics and corticosteroids may play a role. In spite of our best efforts, the mortality of respiratory insufficiency follwing shock or trauma remains high.
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