New Clues to Sudden Infant Death Syndrome

A study has indicated that hypoxemia, rather than hypercarbia, may contribute to sudden infant death syndrome (SIDS) in infants sleeping with their faces covered by soft porous bedding. Conducted by researchers at the University of Washington School of Medicine (St. Louis, MO, USA), the study was published in the December 2001 issue of the Journal of Applied Physiology.

Although the incidence of SIDS has decreased markedly since recommendations were made to place infants in a nonprone position when sleeping, SIDS is still the leading US cause of infant death beyond the neonatal period. Also, there is still debate as to the cause of SIDS in prone infants. One theory is that a face-down infant rebreathes expired air caught in the porous bedding, resulting in carbon dioxide in the blood, or hypercarbia.

However, increased CO2 while biologically significant is unlikely to cause nonspecific reversible depression of neuronal excitability or rapid death, according to the researchers. Hypoxemia, or subnormal oxygenation of arterial blood, has been noted in animal models of rebreathing. Complex interactions of gas exchange between infants and their environment may influence the degree of hypercarbia and hypoxia that can develop. Therefore, the researchers evaluated four specific aspects of gas exchange in a study of 21 infants five to 24 weeks old, of whom four slept prone, four slept supine or on the side, and 13 slept supine.

The results showed that there are often hidden air channels around an infant's face while sleeping face-down, which allow gas exchange. Slight movements of the infant's head can increase or decrease the flow through these channels. Two important factors affecting gas concentrations were a variable seal between bedding and the infant's face, and gas gradients in the bedding beneath the infants. The researchers found that minute ventilation increased significantly during rebreathing because of an increase in tidal volume, not frequency. The measured drop in O2 was significantly greater than the accompanying rise in inspired CO2, apparently due to the respiratory exchange ratio and differential tissue solubilities of CO2 and O2 during unsteady conditions.




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