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Christophe Gaugler, MD
Jean Messer, MD
Pediatrie 2 Departement
Centre Hospitalier Régional Universitaire de Hautepierre
F-67098 Strasbourg, France
Ng et al, in response to our article,1 raise some important points that we feel require additional clarifications.
Their first concern regards the classification of apneas and therefore the type of apnea that olfactory treatment is effectively able to prevent. In our study, we focused on central apneas. Consistent with general acceptation,2,3 apneas were classified as central when "complete cessation of breathing movements" occurred. Indeed, during pure obstructive apnea, thoracic movements still persist, and such events were not further considered in our study. Ng et al are right to outline that some mixed events occur. In a great majority, these events are of central origin, followed by an obstructive component.4 They are effectively more difficult to distinguish from pure central apneas on the basis of thoracic movements, because part of such episodes occurs in the absence of any respiratory effort.4 In consequence, some events that we considered as central may have been in fact central-obstructive apnea. We agree on this point. Nevertheless, the risk of error should be very small. First, because mixed apneas are not so "frequently present" in premature infants, as Ng et al affirmed. Even in the study to which these authors refer4,5 of 4484 apneic episodes that were analyzed, 4241 (95%) were central, 45 (<1%) were obstructive, and only 198 (4%) were mixed. It is true that the proportion of these different types of apneas vary according to the duration of the respiratory pause and that the relative percentage of mixed apnea increases in episodes >20 seconds.5 However, such prolonged episodes were extremely rare (<5%) among the events we considered. Contrary to the affirmation of Ng et al, our definition of central apnea was not limited to the sole "cessation of breathing movements >20 seconds" (in this case, effectively, the proportion of mixed apneas would have been significant). It was clearly mentioned in our article (see "Classification of Apnea and Data Analysis"1(p84)) that shorter periods of apnea were considered when cessations of breathing movements were associated with hypoxia or bradycardia. These short episodes of apnea, during which apneas are quasi-exclusively of central origin, constituted in fact >95% of the events that we retained.
The second concern of Ng et al is that the use of cardiac waveform oscillation coupled with airflow tracing would be helpful to distinguish pure central apnea from central-obstructive apnea, in which breathing movements are sometimes absent. We completely agree on this point. When we designed our study, we first intended to use this technique, with which we were familiar. For 3 reasons, we finally decided not to use this technique in our study. First, because of the small incidence of mixed apnea (4%; see above), the level of error in considering part of such apneas as central seems limited and the gain finally minimal. Second, we are not sure that it is so important to make a fundamental distinction between pure central apneas and mixed apneas. Because in most instances these latter apneas begin as central, both of these kinds of apneas can be controlled successfully with similar treatments (eg, with central respiratory stimulants such as methylxanthines).5 Also, in our study the beneficial effect of olfactory stimulation most probably affected both kinds of apneas. The third and most important reason was an ethical one: we were reluctant to apply a nosepiece to a premature infant for the complete duration of the study. A continuous application during 3 days would have been certainly perceived as invasive by the infant. Note that in the study cited by Ng et al,4 observations lasted <3 hours.
Ng et al's third concern regards the influence of sleep on the incidence of apnea. As mentioned in our article, "because of the absence of clear indicators of sleep/wake states during the first step of this study, it was not possible to provide more details on this potential effect." Nevertheless, additional data on this point will be published soon by our team.
Finally, the last concern of Ng et al is that our study lacked additional testing of the upper airway to assess the risk of upper airway obstruction. We sincerely think that such a supplementary test is absolutely not applicable both as a routine and in the context of experimental research. First, this method is considered to be an invasive procedure, and its use has to be strictly justified. Second, this examination requires a high degree of competency that is not widely available in neonatology departments. Finally, based on our experience in the use of this method,6,7 it seems extremely difficult to estimate the pharynx rigidity in premature infants of 24 to 28 gestational weeks of age. It is well known that malacia increases the risk of upper airway closure, and numerous cases have already been published on this topic. These aspects nevertheless seem very far from the main topic of our article.
Certainly more research should be done to reach consensus in the field regarding optimal classification of apnea of prematurity. We also would like to encourage researchers to conduct additional studies for more effective treatments against apneas of prematurity that are jeopardizing the integrity of the developing brain. We are pleased to be part of that effort.
REFERENCES
Related articles in Pediatrics:
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