Abstract

Supportive care with mechanical ventilation continues to be an essential strategy for managing severe neonatal respiratory failure; however, it is well known to cause and accentuate neonatal lung injury. The pathogenesis of ventilator-induced lung injury (VILI) is multifactorial and complex, resulting predominantly from interactions between ventilator-related factors and patient-related factors. Importantly, VILI is a significant risk factor for developing bronchopulmonary dysplasia (BPD), the most common chronic respiratory morbidity of preterm infants that lacks specific therapies, causes life-long morbidities, and imposes psychosocial and economic burdens. Studies of older children and adults suggest that understanding how and why VILI occurs is essential to developing strategies for mitigating VILI and its consequences. This article reviews the preclinical and clinical evidence on the pathogenesis and pathophysiology of VILI in neonates. We also highlight the evidence behind various lung-protective strategies to guide clinicians in preventing and attenuating VILI and, by extension, BPD in neonates. Further, we provide a snapshot of future directions that may help minimize neonatal VILI.

Highlights

  • Respiratory morbidities and respiratory failure continue to be serious problems in preterm neonates [1,2,3]

  • These findings suggest the importance of avoiding hypoxia and hyperoxia, both of which can cause oxidative stress, during the neonatal period

  • randomized controlled trials (RCTs) comprising more than 1000 infants reported that the volume targeted ventilation (VTV) reduced the primary outcome of death or bronchopulmonary dysplasia (BPD) at 36 weeks postmenstrual age (PMA) and the secondary outcomes of pneumothorax, mechanical ventilation (MV) duration, and the incidence of hypocarbia, severe intraventricular hemorrhage (IVH), and periventricular leukomalacia (PVL) [36]

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Summary

Introduction

Respiratory morbidities and respiratory failure continue to be serious problems in preterm neonates [1,2,3]. The mainstay of management for severe neonatal respiratory failure is supportive care with mechanical ventilation (MV). MV by itself may inflict and accentuate lung injury [3,4,5]. This secondary lung damage caused by MV is often called ventilator-induced lung injury (VILI) [6]. The use of MV as an initial modality to mitigate respiratory failure in ELBW infants has substantially declined over the past decade [9]. Some reports indicate that up to ninety-five percent of surviving ELBW infants will be exposed to MV at some point during their NICU stay [10] and 30–80% of them require MV during the first few days of life [11,12], signifying a substantial failure rate of non-invasive respiratory support in the early life of ELBW infants. There is a need to be aware of lung-protective ventilation strategies

Pathology
Risk Factors and Pathogenesis
Volutrauma
Barotrauma
Atelectrauma
Oxidative Stress
Lung Immaturity
Preexisting Lung Disease
Nutrition
Consequences of VILI
Lung-Protective
Open Lung Ventilation Strategy
Preventing Volutrauma
High-Frequency Ventilation
Preventing and Reversing Atelectrauma
Noninvasive Respiratory Support
Conclusions
Findings
Future
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