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Assessment of in utero hypoxia and risk of sudden infant death syndrome

  • Germaine M. Buck
  • , Diane L. Cookfair
  • , Arthur M. Michalek
  • , Philip C. Nasca
  • , Susan J. Standfast
  • , Lowell E. Sever
  • SUNY Buffalo
  • Roswell Park Cancer Institute
  • New York State Department of Health
  • Centers for Disease Control and Prevention

Research output: Contribution to journalArticlepeer-review

17 Scopus citations

Abstract

Summary. Few data are available on the role of hypoxia in sudden infant death syndrome (SIDS). The purpose of this study was to assess whether 10 antenatal factors consistent with in utero hypoxia were associated with an increased risk of SIDS. Cases and two sets of controls were chosen from the Upstate New York Live Birth Cohort for 1974 (n= 132 948). One hundred and forty‐eight SIDS cases were identified, along with 114 dead controls made up of all other sudden deaths. Randomly selected live controls were frequency‐matched to cases on mother's age, race, residence, parity, and infant's birthdate (n=355). Data were collected from vital certificates (97% response), hospital delivery records (89%), and autopsy reports (100%). Odds ratios and 95% confidence intervals were calculated using Mantel‐Haenszel techniques and logistic regression. Abnormal uterine bleeding was the only statistically significant (P<0.05) risk factor observed when dead controls were used (OR=5.4). When live controls were used, statistically significant increases in risk were found for: placenta praevia (OR=21.8), abruptio placentae (OR=3.7), multiple birth (OR=29.6), pregnancy interval ≤12 months (OR=3.8), sexually transmitted disease (OR=6.4), and eclampsia (OR=17.7). These results lend support to a possible hypoxic aetiology of SIDS; however, differences by control group suggest that some factors are not specific to SIDS alone but may be risk factors for infant mortality in general.

Original languageEnglish
Pages (from-to)157-173
Number of pages17
JournalPaediatric and Perinatal Epidemiology
Volume3
Issue number2
DOIs
StatePublished - Apr 1989

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