Summary
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 surfactant 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 over-transfusion, adequate ventilation with carefully-controlled inspired oxygen concentrations, strict asepsis, diuretics and corticosteroids may playa role. In spite of our best efforts, the mortality of respiratory insuffiCiency following shock or trauma remains high.
Résumé
II est bien établi que l’insuffisance respiratoire progressive est une complication fréquente qui s’installe après la phase aiguë du choc ou des grands traumatismes. Ce syndrome se divise en quatre phases bien distinctes. Au début nous sommes en présence d’une hypocapnie et d’une acidose métabolique. Nous voyons apparaître par la suite une hypercapnie et une mort par asystolie anoxique.
Les signes radiologiques ne sont pas spécifiques. A l’autopsie, on trouve de l’œdème, des dépots hyalins et fibrineux. Des hémorragies et une hyperplasie des cellules alvéolaires peuvent être rencontrées.
Les principaux faits pathophysiologiques sont une hyperventilation persistante, une alcalose métabolique qui se change en acidose à la suite de l’anoxie tissulaire, une différence alvéolo-artérielle qui grandit à cause du shunt au niveau pulmonaire. Les mécanismes de ce shunt ont été discutés, la disparition du surfactant inclusivement.
La pathogénèse de ce syndrome est inconnue, cependant plusieurs causes ont été proposées. Elles incluent la surcharge liquidienne, les embolies graisseuses, l’aggrégation plaquettaire, la coagulation intravasculaire disséminée, l’aspiration, l’immobilisation, la toxicité de l’oxygème et la colonisation bactérienne.
La prévention de ce syndrome a plus de succès que son traitement. L’élimination des surcharges transfusionnelles, la ventilation adéquate avec des concentrations contrôlées d’oxygène, une asepsie stricte, les diurétiques et les corticoïdes sont bénéfiques. Malgré les soins les plus attentifs, la mortalité par insuffisance respiratoire à la suite du choc ou des grands traumatismes demeure élevée.
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Dowd, J., Jenkins, L.C. The lung in shock: A review. Canad. Anaesth. Soc. J. 19, 309–318 (1972). https://doi.org/10.1007/BF03161793
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DOI: https://doi.org/10.1007/BF03161793