To the Editor:—
Regarding the article by Wilder et al. ,1this research is an important step in the right direction to either prove or disprove the association of learning disabilities with multiple exposures to anesthesia in the early years of life possibly caused by anesthetic agent–induced neuroapoptosis. The authors are to be congratulated for making a stab at this complex issue, and not connecting the dots directly but rightfully pointing out that many factors might contribute to their findings that are unrelated to anesthesia. However, one important factor that seems to have been overlooked is that the majority of these children were likely anesthetized before the routine use of pulse oximetry and capnography (1976–1982) became our standard of care. We do not know what happens to a child who is excessively ventilated for prolonged periods of time, resulting in severe hypocapnia and possibly reduced areas of cerebral perfusion. Nor do we know how many of these children experienced prolonged or repeated short episodes of hypoxemia that were either unrecognized or only recognized late in the event, when the child developed bradycardia that could have resulted in subtle neurologic insults. In the early years when capnography was first being advocated but not yet a standard of care, in a prospective study of 331 children, we found an 11% incidence of hypocapnia (expired carbon dioxide value ≤ 30 mmHg) in intubated children, with a very high incidence in children younger than 1 yr.2Likewise, in two randomized blinded studies involving 554 children, we found 94 major desaturation events (oxygen saturation measured by pulse oximetry ≤ 85% for 30 s or longer) in 67 children with a higher incidence by a factor of 2 in those whose anesthesiologist did not have the oximeter data available. These studies suggested that the oximeter allowed early recognition and intervention, thus preventing a minor desaturation event from progressing to a major desaturation event.3,4We also found a higher incidence of these major desaturation events in children younger than 2 yr. I do not know whether it is possible for Wilder et al. to go back and examine the anesthesia records from the 144 children in their cohort who had two or more anesthetic exposures to determine whether hypoxic events were recorded, but it might be a useful endeavor. I suggest that we need to look at other issues beyond simple exposure to anesthetic agents as possible contributory factors and look forward to more wonderful work from the Mayo group.
Harvard Medical School, Mass General Hospital for Children, Massachusetts General Hospital, Boston, Massachusetts. email@example.com