The rate of sudden infant death syndrome (SIDS) has plateaued, more than a decade after widespread efforts began to modify infant sleep environments to reduce risk, suggesting contributing factors beyond breathing blockage, according to a study published online December 2 in Pediatrics.
Richard D. Goldstein, MD, from the Dana-Farber/Boston Children's Cancer and Blood Disorders Center and Harvard Medical School, Boston, Massachusetts, and colleagues compared postneonatal mortality from SIDS with the rate of death from other causes, including neglect, circumstantial respiratory diagnoses, congenital malformations, and chromosome abnormalities.
More than half of the approximately 4000 infant deaths in the United States each year are attributed to SIDS, with more than 90% occurring postneonatally. Because biomarkers for SIDS are unavailable, diagnosis is typically made on the basis of a forensic analysis of the circumstances and elimination of medical explanations.
From 1992 to 1996, SIDS prevalence fell by 38% after "Back-to-Sleep" initiatives to encourage infant sleep in the supine position. In their analysis, the researchers used US Mortality Multiple Causes Records from the National Center for Health Statistics for 1983 to 2012, which includes the start of Back-to-Sleep.
The decline in SIDS prevalence stopped a decade after Back-to-Sleep began, but the plateau could reflect a "diagnostic shift," as medical examiners began to replace "SIDS" with such descriptive terms as "accidental suffocation and strangulation in bed." At the same time, increasing use of antenatal steroids and surfactant in premature babies further reduced SIDS incidence.
Because SIDS persists, optimizing sleeping position must not be the only contributing factor, the researchers hypothesize. The Triple Risk Model, which coauthor Hannah C. Kinney, MD, proposed with J. J. Filiano in 1994 ( Biol Neonate. 1994;65:194-197), suggests that SIDS can stem from interaction of an underlying intrinsic sensitivity with extrinsic factors present during a critical period in development.
Specific intrinsic risk factors have yet to be identified, but influences may be genetic (male sex, gene variants more prevalent in certain populations), developmental, or environmental (maternal smoking or alcohol use). Extrinsic factors include bed-sharing, excess bedding, and prone position. In some infants, the intrinsic vulnerability in a risky extrinsic environment disrupts homeostasis, interfering with normal responses to hypoxia, excess carbon dioxide in the blood, heat, or other autonomic stresses during sleep.
The researchers developed the Cumulative Unexplained Infant Death Composite to identify SIDS cases. Then they projected mortality rates from SIDS, assuming they changed in step with changing rates for non-SIDS infant deaths (such as those resulting from congenital malformations and deformities, pregnancy complications, bacterial sepsis, respiratory distress in the newborn, neonatal hemorrhage, and circulatory diseases), and compared them with actual rates. The study included a group of low-birth-weight infants who survived the neonatal period but died of SIDS.
If the changes in incidence of SIDS deaths paralleled those for other causes, especially since the Back-to-Sleep movement, then the same homeostatic disruption that causes other deaths might also contribute to SIDS, the researchers reasoned.
The study included 947,156 infant deaths. Cluster analysis revealed that changes in SIDS rates over the period most closely resembled those resulting from congenital malformations and deformities, chromosomal abnormalities, respiratory distress of the newborn, and circulatory diseases.
SIDS rates declined 71.3% during the 30-year period, mostly from 1994 to 1996, with wide implementation of Back-to-Sleep. "As hypothesized, however, we also found substantial concordance between SIDS rates and that of all other causes of postneonatal mortality," the researchers write. They cite several factors contributing to the decrease in intrinsic risk factors for SIDS: decrease in maternal smoking, increase in breast-feeding, use of antenatal steroids to reduce respiratory distress, and improved prenatal care.
Risk for mortality among low-birth-weight infants in the postneonatal period did not change during the 30-year period. Birth-weight-specific mortality rates were consistent with overall trends in mortality.
A limitation of the study is that use of specific-cause mortality as a proxy for intrinsic SIDS risk is novel and reveals concurrence, not causation.
Rachel Y. Moon, MD, and Fern R. Hauck, MD, from the Department of Pediatrics and the Department of Family Medicine at the University of Virginia School of Medicine in Charlottesville, point out in an accompanying commentary that the article counters the idea that all SIDS deaths are accidental, and therefore preventable. In fact, they write, the rate of postneonatal mortality from all causes has not declined since the late 1990s, and the risk factors underlying different causes are remarkably similar.
The commentators conclude, "If we are to further impact infant mortality rates and eliminate SIDS, focus on the sleep environment will continue to be important but will likely be insufficient. Public health efforts will need to also focus on decreasing intrinsic risk through the promotion of smoking cessation, elimination of in utero drug and alcohol exposure, and increasing rates of breastfeeding and access to high-quality prenatal care."
The researchers and commentators have disclosed no relevant financial relationships.
Pediatrics. Published online December 2, 2015.
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Cite this: SIDS Incidence Influenced by Multiple Contributing Factors - Medscape - Dec 02, 2015.
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