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Editor—Dargaville et al 1 suggest that infants with severe bronchiolitis exhibit surfactant deficiencies. This has exciting implications for treatment in an illness in which active treatment is essentially supportive. However, the conclusions drawn from their pilot study are limited by the inclusion of unmatched controls.
Most controls were not premature (median gestational age 39 weeks) compared with the infants with bronchiolitis, who were (median gestational age 34 weeks, including one infant born at 24 weeks). At the time of study, the median age of control infants was 1.5 months, whereas the corrected median age of the bronchiolitic infants made them the equivalent of term babies. Weights were also correspondingly different.
Preterm neonates are more likely to have been ventilated before, and to have underlying lung disease, such as bronchopulmonary dysplasia. It is not stated how many of the bronchiolitics had ongoing lung disease and oxygen dependency before they developed infection. Surfactant indicators would be expected to differ in this group compared with the controls, even in the absence of bronchiolitis.
The effect of ventilation and barotrauma on surfactant production needs to be considered before attributing differences top infection. Those with bronchiolitis had been ventilated for a median of 18.5 hours before the first tracheal aspirate was taken. Controls, electively intubated for surgery, would most likely have been ventilated for a much shorter period before the first sample.
Lastly, the term “acute viral bronchiolitis” is a generalisation. The diagnosis of bronchiolitis should include viral identification. If surfactant differences are to be attributed to infection, it is important to distinguish the viral groups. The type of virus responsible for infection may determine clinical symptoms, pronosis, and even surfactant abnormalities.
Further research into surfactant in bronchiolitis, its deficiency, and the role of surfactant administraion in severely infected infants is essential, but must be supported by adequate controls, a larger study group, and viral identification.
Dr Dargaville et al reply: Infants who require mechanical ventilation during an episode of acute viral bronchiolitis (AVB) are very likely to have been premature, and occasionally to have the residua of ventilator induced lung injury.1-1 Nine of the 12 infants with AVB in our study were premature (less than 37 weeks of gestation at birth); of these, four required ventilation in the immediate neonatal period, and two had ongoing evidence of bronchopulmonary dysplasia. We agree with Dr Nelson that age matched controls with a similar profile of premature delivery would be most suitable for comparison with the AVB group. But such infants are only rarely intubated for elective surgery, and sequential samples through a period of mechanical ventilation can almost never be obtained from this group of infants except in the setting of intercurrent pulmonary disease. It is our contention, therefore, that while the control group in our study is imperfect, it at least provides an indication of surfactant concentration in tracheal aspirate samples from the normal infant lung.
With regard to the disparity in the length of time under ventilation before sampling in the two groups, it should be appreciated that articificial ventilation enhances surfactant secretion in the normal lung.1-2 On this basis, one might have expected increased concentrations of surfactant in tracheal aspiratein the infants with AVB sampled after 18 hours of ventilation, compared with the controls sampled soon after intubation. The converse was, in fact, the case, with surfactant concentrations being substantially lower in the AVB group when first sampled. This result, and the context in which it was obtained, led us to conclude that infants with AVB are surfactant deficient at the height of their disease. The substantial improvement seen in the surfactant indicators as the lung disease resolved, adds considerable weight to this conclusion. As stated in our study, 11 of the 12 infants with AVB were infected with respiratory syncytial virus. In all cases the illness was a first presentation, with the typical clinical and radiographic features of AVB.
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