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
