IS THERE A ROLE FOR INHALED NITRIC-OXIDE IN PEDIATRIC ARDS

Despite advances in ventilator management and use of extracorporeal lu ng support, mortality related to ARDS in pediatric patients has not be en reduced over the past 20 years. Progressive respiratory failure, du e to evolution of the primary illness or to complications of ventilato r therapy, significantly contributes to poor outcome. ARDS is characte rized by severe ventilation-perfusion mismatch and by pulmonary hypert ension. Because of their side effects which affect systemic hemodynami c status or worsen intrapulmonary shunting, intravenous vasodilator tr ials have been of limited interest. Nitric oxide (NO) has been recogni zed as a gas with vasodilator properties. In neonates studies have sho wn that inhaled NO may have an important role in the therapy of persis tent pulmonary hyptertension. Inhaled NO in adults with severe ARDS ha s been shown to reduce pulmonary hypertension without producing system ic vasodilation. This reduction of pulmonary vascular resistances may reduce pulmonary edema formation, decrease vasoconstrictor response to cardiotonic agents, and improve biventricular function. In addition, arterial oxygenation seems to be increased by improved matching of ven tilation with perfusion. Improvement of oxygenation with inhaled NO su ggests that use of lower tidal volumes and FIO2 may be more successful . Until now, there are no published studies regarding NO administratio n in ARDS affecting nonneonatal pediatric patients. However, the resul ts obtained in adults and newborns suggest that inhaled NO may be a us eful adjuvant therapy of ARDS in children, possibly in association wit h other therapies. Even in adults it remains unclear whether therapy w ith inhaled NO can reduce morbidity and mortality. Prospectives and ra ndomized studies are essential to assess the real utility of inhaled N O in ARDS. Moreover, these studies may be helpful to clarify remaining concerns regarding potential toxicities, including methemoglobinemia and lung injury due to NO2. (C) 1995 Wiley-Liss, Inc.