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Sudden infant death syndrome: seasonality and a biphasic model of pathogenesis
A L Ponsonby1, T Dwyer, M E Jones
1Menzies Centre for Population Health Research, University of Tasmania, Clinical School, Hobart, Australia.
Study Objective:
This paper examines the relationship between season, age, and the sudden infant death syndrome (SIDS). It provides a theoretical model for the pathogenesis of SIDS and uses it as a framework to consider risk factor mechanism.
Design:
A case series analysis was used to examine season and age in relation to SIDS and seasonal pattern and age at death distribution of perinatal risk factors.
Setting:
The source population for the SIDS cases in this study was all live births in the state of Tasmania, Australia, 1975 to 1987 inclusive.
Subjects:
Cases were all infants born 1975 to 1987 who died of SIDS on whom birth notification information was available (n = 348). The live birth cohort 1980-87 (n = 55,944) was used as the control population for risk factor identification.
Measurements And Main Results:
The median ages of death for spring, summer, autumn, and winter born infants were 115, 103.5, 91 and 78 days. Spring and summer born infants died at a significantly older median age than winter born infants. The month of birth distribution of SIDS cases did not alter significantly from a uniform, nonseasonal distribution (p greater than 0.25) but month of death was seasonally distributed (p less than 0.01). Premature and low birthweight infants died at an older median age (p less than 0.05) than term and non-low-birthweight infants. An excess of male infant deaths and infant deaths to older mothers occurred during winter (p less than 0.05).
Conclusions:
The pathogenesis of SIDS can be represented as a biphasic model with three pathways of risk factor operation. In this study, season influenced the age at death of SIDS infants. We propose that risk factors with a strong seasonal distribution are likely to be operating in the postnatal period.