Lung Protective Strategies of Ventilation in the Neonate: What Are They?
- 1 January 2000
- journal article
- research article
- Published by American Academy of Pediatrics (AAP) in Pediatrics
- Vol. 105 (1) , 112-114
- https://doi.org/10.1542/peds.105.1.112
Abstract
* Abbreviations: VILI = : ventilator-induced lung injury • ARDS = : acute respiratory distress syndrome • NIH = : National Institutes of Health • RDS = : respiratory distress syndrome • PEEP = : positive end–expiratory pressure • HFV = : high-frequency ventilation • EEP = : end–expiratory pressure • Fio2 = : fraction of inspired oxygen In the July 1999 issue of the Journal of the American Medical Association, Dr Leonard Hudson proclaims that “the concept of ventilator-induced lung injury (VILI) has come of age.”1 His comments were derived from a report by Ranieri et al2 which shows that a “lung-protective strategy” of respiratory support reduces cytokine levels in both the bronchoalveolar lavage fluid and serum of adult patients with acute respiratory distress syndrome (ARDS). Dr Hudson's enthusiasm is increased by the recent press release from the National Institutes of Health (NIH) ARDS Network Study, reporting positive results of a study evaluating a “lung-protective strategy” in >800 adults with ARDS. The NIH study was stopped early, when the safety monitoring committee noted “25% fewer deaths” among patients receiving small (6 mL/kg) rather than large (12 mL/kg) tidal volumes to support gas exchange. The importance of these observations is that they provide data in support of the hypothesis that VILI can cause biotrauma associated with a “mediator storm” (perhaps cytokines) that is responsible for distal organ dysfunction, subsequent multiorgan failure, and death.3 These adult data unequivocally prove that how we support gas exchange in patients with lung disease markedly affects outcome. Although it has been shown that pulmonary cytokine levels also appear to be elevated in some neonates on assisted ventilation, an exact relationship to neonatal lung injury has not yet been well defined.4–7 Proinflammatory mediators may be elevated because of fetal exposure to maternal inflammatory mediators, postnatal infection, or by release from preterm lungs attributable to ventilator-induced injury.5 The neonatal lung is still in stages of development and growth, therefore cytokine responses and effects may be immature and different from what is seen in adults. Indeed, data from Kwong et al8 ,9 suggests a possible relationship between cytokine signaling and …Keywords
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