Progress in ARDS research: a protection racket?

The acute respiratory distress syndrome in adults (ARDS) may complicate a wide variety of serious medical and surgical conditions, not all of which involve the lung directly.1 The pathogenesis remains unclear, but involves neutrophil recruitment to the alveoli and inflammatory pathway activation leading to increased permeability of the alveolar-capillary membrane and disordered vascular control, manifest clinically as pulmonary oedema formation and refractory hypoxaemia. Compliance is reduced and work of breathing is increased to the extent that most patients require endotracheal intubation and mechanical ventilatory support.2 Despite the recent publication of within-centre studies showing a fall in mortality,3 4 some 40–60% of patients with ARDS fail to survive with most of the deaths being attributable to multiple organ system failure.

It has been appreciated for some years that mechanical ventilation can itself exacerbate pre-existing alveolar injury. This may develop directly as a result of barotrauma and so called “volutrauma”, or indirectly through the adverse effects of increasing the inspired oxygen concentration to obviate hypoxaemia. Thus, studies in experimental animals have suggested that injury rises markedly above an end inspiratory (or plateau) pressure of 35 cm H₂O.5 Secondly, computed tomographic scanning in patients with ARDS subjected to varying levels of positive end expiratory pressure (PEEP) has shown that dependent consolidated areas of lung tend to remain poorly compliant and underventilated, and the application of conventional tidal volumes of the order of 10 ml/kg can overdistend the spared functioning regions.6Consequently, the last decade has seen the emergence of ventilation …