Sudden Infant Death Syndrome (SIDS): An Integration of Ontogenetic Pathologic, Physiologic and Epidemiologic Factors¹

Abstract

Sudden Infant Death Syndrome (SIDS) is the most prevalent cause of death in infants between one and six months of age. Epidemiologic pathologic and physiologic data suggest the mechanism of SIDS is complex, characterized by interactions at many levels of the neuraxis, between the organism and the environment and spanning both pre- and post-natal life. Details of one such model are presented here. The model is based on 1) systematic physiological studies of two groups of infants at statistically increased risk for SIDS: subsequent siblings and near-miss for SIDS. 2) An epidemiological study of approximately 800 SIDS in Los Angeles County, and 3) clinical perinatal data and fetal heart rate recordings of a subset of these 800 SIDS. Data from other investigators are incorporated as well.

Factors unique to SIDS are: Age of death, association with sleep, seasonal distribution and increased risk for the second born. The proposed core deficit consists of mild hypoxia, sustained during pre- and post-natal life, for which the majority of infants successfully compensates. Previously not fully appreciated changes between one and three months of age in development and integration of the central nervous system, give rise to increased vulnerability to endogenous and exogenous deleterious influences at this time. Altered sleep state distributions consisting of an increase in Quiet sleep (QS) and a decrease in Active sleep (AS), are temporally and functionally associated with alterations in respiratory and cardiac regulation. Some infants pass through this age period sooner, at a faster rate and with less reserve and thus are more susceptible to additional stress. Although the etiology of the core deficit is unknown, many factors can potentiate an existing mild hypoxia. One such potential mechanism is the influence of ambient pollutants. Other mild deficiencies of varied origin operate as predisposing factors to risk or precipitating events causing death. A large number of infants would be expected to be stressed but only an unfortunate intersection of prior vulnerability and one or more aggravating conditions encountered during a discrete limited age of risk would result in death. Many nonspecific factors associated with SIDS are identical to those associated with perinatal morbidity and mortality. Programs aimed at reducing the latter should substantially reduce the rate of SIDS as well.

Key words

SIDS - Hypoxia - Sleep - Respiration - Apnea - Ambient pollutants