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Sudden infant death syndrome: 1987 perspective

Carl E. Hunt*, Robert T. Brouillette

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

135 Scopus citations

Abstract

The pathophysiology of SIDS remains unknown. Although a multifactorial cause appears plausible on the basis of available data, new data are needed to determine which components of this multifactorial hypothesis are most important and whether other factors need to be added. We need to better understand control of breathing in the newborn infant and the manner in which maturation of cardiorespiratory control progresses during infancy. The unique period of vulnerability for SIDS, in which risk is less in the neonate than at 2 to 6 months of age, remains unexplained. Is there a worsening in some aspect of cardiorespiratory control in infants destined to die of SIDS? An improved understanding of the increased risk in black infants, preterm infants, and infants with intrauterine drug exposure, although only a small percentage of all SIDS deaths, should contribute substantially to our understanding. Appropriately designed and well-controlled prospective studies are needed in asymptomatic infants at risk, to determine the true contemporary nonintervention rate of SIDS and the extent to which any assessment or intervention lowers this rate. Prospective pneumogram screening studies have demonstrated significant group differences in respiratory patterns in normal infants compared with later SIDS victims, but have failed to achieve sufficient sensitivity and specificity to be useful for populationwide prospective screening. To assess aspects of brainstem cardiorespiratory control in addition to those assessed by a conventional pneumogram, future studies will need to be based on an expanded or modified technology. On the basis of both physiologic considerations and available technology, addition of an oxygen saturation channel offers the most promise for providing a more comprehensive assessment of cardiorespiratory control. If there is an underlying deficiency in asphyxic arousal responsiveness, for example, with or without other respiratory control deficits, continuous monitoring of oxygen saturation as part of a second-generation pneumogram system currently has the greatest promise for providing a modified pneumogram assessment of greater clinical use. The use of continuous oxygen saturation as a home monitoring technique should also be investigated. Power spectrum analysis of cardiorespiratory variability also appears to have potential advantages over conventional pneumogram analyses, and needs to be evaluated in prospective studies. The following statements summarize our current knowledge regarding SIDS, apnea, pneumograms, and home monitors:o1.The cause(s) of SIDS remains unknown.2.The respiratory control hypothesis regarding SIDS still appears to be the most compelling, but it is incorrect to consider apnea as either the only or the most important component of respiratory control.3.No prospective assessment has sufficient sensitivity and specificity to identify infants destined to die of SIDS. However, failure of the pneumogram as a screening test in asymptomatic infants is not equivalent to failure as a useful test in apnea of infancy.4.All patients with apnea of infancy require intervention, and pneumograms may be helpful in managing these patients.5.The current low incidence of subsequent SIDS in patients with apnea of infancy may be a tribute, at least in part, to the efficacy of intervention, not proof against the relationship between SIDS and apnea of infancy.6.In asymptomatic infants at risk, the controversy regarding pneumograms and home monitors will remain unresolved until appropriately designed prospective controlled studies have been conducted using a modified or expanded technology for cardiorespiratory analysis and for home monotoring.

Original languageEnglish
Pages (from-to)669-678
Number of pages10
JournalThe Journal of Pediatrics
Volume110
Issue number5
DOIs
StatePublished - May 1987

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