Mecanismos de injuria pulmonar

Noviembre 2006

 

 

 

Minimising ventilator induced lung injury in preterm infants

 

S M Donn, S K Sinha

 

Arch Dis Child Fetal Neonatal Ed 2006;91:F226–F230.

 

 

Ventilator induced lung injury continues to occur at an unacceptably high rate, which is inversely related to gestational age. Although the ‘‘new BPD’’ may not be entirely avoidable in the extremely premature infant, recognition of risk factors and adoption of an appropriate ventilatory strategy, along with continuous real time monitoring, may help to minimise lung damage. This paper will review the pathogenesis of ventilator induced lung injury and strategies that may mitigate it.

 

Bronchopulmonary dysplasia (BPD) was first described in 1967 by Northway et al, in a group of 13 infants who were mechanically ventilated for respiratory distress syndrome (RDS). These infants ranged from 1474 to 3204 g birth weight and 30 to 39 weeks gestational age. Most had required high concentrations of supplemental oxygen and high airway pressures. Their chest radiographs revealed overinflation and cystic emphysema, and pulmonary histopathology consisted of interstitial and alveolar oedema, small airway disease, extensive inflammation, and fibrosis.

 

Over the ensuing decade, the mechanisms of chronic lung disease (CLD) became better understood. In 1975, Philip described the aetiology of BPD as ‘‘oxygen plus pressure plus time.’’ Over the next 25 years, advances in neonatal medicine extended survival to infants born considerably more immature than those described by Northway et al, and the characteristics of affected infants changed dramatically.

The ‘‘old BPD’’ described by Northway and Philip has been replaced by the ‘‘new BPD’’ described by Jobe. The disorder is now seen primarily in very low birthweight infants requiring modest ventilator support and supplemental oxygen. It is characterised radiographically by diffuse haziness and a fine, lacy pattern, and histopathologically by decreased alveolarisation, minimal small airway disease, and less inflammation and fibrosis. There is no universally accepted definition of CLD, and thus its incidence has been variously reported, generally between 30% and 40% among very low birthweight infants.

 

Although the past quarter century has seen dramatic advances in the treatment of RDS, including sophisticated mechanical ventilators and surfactant replacement therapy, the prevalence of CLD remains quite high. Although the characteristics of CLD have changed, and it may not be entirely avoidable, ventilator induced lung injury remains a significant component of it. Understanding the pulmonary injury sequence is important to the realisation that some lung damage may be minimised by using lung protective strategies. Ventilator induced lung injury itself is multifactorial. Various connotations  have been used to describe its individual components, which may be inter-related and act synergistically. Volutrauma refers to the damage caused by overdistension of the lung by the delivery of too much gas. Barotrauma, or excessive pressure, may damage airway epithelium and disrupt alveoli. Atelectotrauma refers to the damage caused by the continual opening and closing (the cycle of recruitment and subsequent derecruitment) of lung units. Biotrauma is a collective term to describe the injurious effects of infection and inflammation (and oxidative stress) on the developing lung. Rheotrauma refers to injury caused by inappropriate airway flow . If excessive, turbulence, inefficient gas exchange, inadvertent positive end expiratory pressure (PEEP), and lung overinflation may occur; if inadequate, it may lead to flow starvation (air hunger) and increased work of breathing. Lung protective strategies seek to minimise ventilator induced lung injury by avoiding or ameliorating the damaging effects of these components.

 

LUNG PROTECTIVE STRATEGIES

 

Lung protective strategies, in fact, begin even before the institution of mechanical ventilation or continuous positive airway pressure (CPAP). It is now a world wide practice to administer antenatal corticosteroids to women at risk of delivering preterm infants, generally before 32 weeks completed gestation. Antenatal corticosteroid therapy has dramatically reduced the incidence and severity of RDS and thus CLD, although it may be argued that improved survival of extremely preterm infants resulting from this has shifted the overall incidence of CLD. Similarly, there is little doubt about the impact of surfactant replacement therapy on the treatment of RDS resulting in increased survival, but without a concomitant reduction in CLD. Thus it would appear that efforts to bring about improvement in the incidence and severity of CLD must be approached by using appropriate ventilatory strategies aimed at reducing or avoiding ventilator induced lung injury.