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Time course of severe respiratory syncytial virus infection in mechanically ventilated infants

Respiratory syncytial virus (RSV) is the major cause of viral respiratory tract infection in infants and children (1). Clinical manifestations range from mild upper respiratory tract infections in the majority to severe apnea or lower respiratory tract disorders requiring intensive care management in about 8% of infants and young children (2). The highly contagious nature of the virus means that essentially all children have been infected with RSV by 2 to 3 years of age. Since this is precisely the age group from which comes 50% of all admissions of children with impending or actual respiratory failure to paediatric intensive care units (PICU), such units deal with RSV-induced respiratory failure very frequently. However, despite this frequency there is only sparse information on the pathophysiological and radiological pulmonary changes which occur during the acute stage of this illness. In this issue, Tasker and his colleagues (3) have described two different radiological presentations in infants with RSV-induced respiratory failure characterized either by diffuse consolidation without hyperinflation or gross hyperinflation without consolidation. Recently, with the advent of suitable tests of respiratory function for infants and young children (4), it has been demonstrated that there are two characteristic and distinctly different patterns of lower respiratory disease in infants with RSV-induced respiratory failure. The first pattern is predominantly that of obstructed small airways with a moderate degree of parenchymal or restrictive disease (5). The majority of infants with RSV-triggered respiratory failure suffer from this disorder, which is more traditionally referred to as bronchiolitis. The pulmonary function abnormalities include increased respiratory resistance, reduced maximal expiratory flows and air trapping (5). These are the pathophysiological changes resulting from small airway obstruction due to bronchial mucosal edema and peribronchial inflammation. Lung volumes and compliance are moderately reduced, which is explained anatomically by the presence of atelectatic lung regions. The radiographic changes of hyperinflation and atelectasis in one of the groups described by Tasker et al. (3) are entirely consistent with this obstructive pathophysiology. In contrast, the second pattern is that of severe restrictive parenchymal lung disease with a small increase in airways resistance (6). This is usually referred to as pneumonia and affects about 25–30% of infants with RSV-induced respiratory failure. Typically, respiratory compliance and lung volumes are markedly decreased without significant airway obstruction or air trapping (6). The group of patients with alveolar consolidation as the main radiographic feature described by Tasker et al. (3) is completely consistent with the severe restrictive pulmonary function pattern. It is also noteworthy that these particular infants also fulfill the clinical criteria of acute respiratory distress yndrome (ARDS) that were recently promulgated by an American-European Consensus Committee (7). These criteria are: acute disease onset, PaO 2/Fi 2 ratio 200 mmHg, and bilateral infiltrates on chest radiograph in the absence of left atrial hypertension. The lung function results obtained in our patients with RSVassociated respiratory failure due to restrictive disease (6) are also in agreement with current concepts of respiratory mechanics and lung volume alterations in older children and adults with ARDS (8, 9). Hence, it appears likely that the group of 9 of the 44 patients in the prospective part of the Tasker study, who had alveolar consolidation with severe gas-exchange anomalies, were suffering from pneumonia/ARDS. Further evidence for this is the prolonged length of mechanical ventilation in this subgroup (15–39 days; mean 17) versus the relatively short (4–8 days; mean 7) those 35 patients with the obstructive or bronchiolitic pattern of RSV-associated respiratory failure. While RSV infections are said to vary not only between years but also geographically, these numbers reported from Europe are surprisingly similar to those reported in North America by Hammer et al. for ARDS (6) and Stretton and co-workers for bronchiolitis (2) (see Table I). In their current paper, Tasker et al. (3) used mean airway pressure (MAP) and alveolar-arterial oxygen differences (AaDO2) to identify suitable gas-exchange severity criteria. A MAP >10 cm H2O and an AaDO2 mmHg 400 mmHg correctly identified 9 out of 10 four-quadrant alveolar consolidation patients with no false positives in the first 24 h of mechanical ventilation. For the second 24 h, the same MAP criterion with an AaDO2 300 mmHg correctly identifi d all 10 consolidation patients although there was one false positive. Using both sets of criteria, all consolida-