Expanded use of surfactant replacement therapy
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There are a number of respiratory diseases affecting infants in which there is surfactant dysfunction or deficiency. Surfactant is inactivated by cholesterol, free fatty acids and bilirubin in meconium aspiration syndrome, by haemoglobin and red blood cell lipids in pulmonary haemorrhage and plasma proteins are the culprit in conditions associated with increased alveolar capillary permeability. Surfactant production can be adversely affected by damage to the type 2 pneumocytes by viruses and neutrophil derived reactive oxygen metabolites. Not surprisingly, therefore, the efficacy of exogenous surfactant has been tested, usually in animal models and anecdotal series in “non respiratory distress syndrome” respiratory disorders. Improvements in oxygenation have usually been described. Relatively few randomized trials, however, have been performed, but those undertaken have demonstrated longer term benefits. In term infants with severe respiratory failure, surfactant administration significantly shortened the duration of extracorporeal membrane oygenation and, in those in the early phase of severe respiratory failure or with meconium aspiration syndrome, it significantly reduced the need for extracorporeal membrane oygenation. In meconium aspiration syndrome, a smaller number of surfactant treated patients compared to controls developed airleaks. Surfactant administration was also associated with a reduction in the duration of ventilation and intensive care unit stay in patients with meconium aspiration syndrome or bronchiolitis. Those data are very promising and should encourage studies to identify the optimum type of surfactant, dosage regimen and administration method.
Conclusion Further randomized trials are required to fully assess the efficacy and cost benefit ratio of surfactant treatment in “non respiratory distress syndrome” respiratory diseases.
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