Search

Data from Missouri for the period 1980 to 1985 suggest a dose-response relationship between smoking during pregnancy and the incidence of sudden infant death syndrome (SIDS). However, data from the National Institute of Child Health and Human Development SIDS Cooperative Epidemiological Study did not support a dose-response relationship. Neither the Missouri data nor the Cooperative Study data support a relationship between the age of occurrence of SIDS and smoking during pregnancy.

A specially designed method for measuring infant mortality among families with subsequent siblings of sudden infant death syndrome (SIDS) victims in the state of Washington, 1969 to 1984, yielded results similar to those from an earlier study in Norway. In both studies the SIDS rates among siblings were substantially lower than prior estimates. The rate of SIDS in siblings of infants who died of SIDS did not differ significantly from the SIDS rate among control infants matched for maternal age and birth order. Total infant mortality rates in the two groups were virtually identical. From the data at hand, it appears that earlier estimates of the risk of SIDS in siblings were inflated and that parents of SIDS victims can be counseled accordingly.

During a 12-year period (1969 through 1980), 431 episodes of sudden infant death syndrome (SIDS) occurred in King County, Washington. Longitudinal analysis of these data confirms the inverse association of SIDS occurrence with maternal age, which has been reported repeatedly from previous cross-sectional analyses. Risk of SIDS increases with increasing birth order, but the inverse maternal age gradient remains constant within each birth-order category. Available evidence suggests that maternal age may be a more important clue to SIDS causation than previously supposed. Assessment of established SIDS risk factors in relation to maternal age deserves further attention. The role of nutrition of pregnancy in relation to maternal age and SIDS risk may also be a productive avenue for future investigation.

All 1998 resident infant deaths in the 1969--1977 King County, Washington birth cohort of 139,132 resident live births comprise the data base for epidemiologic comparisons of the sudden infant death syndrome (SIDS) with eight other major infant mortality components: hyaline membrane disease; respiratory distress syndrome; asphyxia of the newborn; immaturity; birth injury; congenital malformation; infection; and "all other." These components were compared with respect to age at death; sex; race; prior fetal loss; prior live-born, now dead; birth plurality; birth weight; maternal age; birth order; marital status; prenatal care; and season of death in an attempt to determine the uniqueness of these purported SIDS risk factors. Only the age at death distribution unequivocally distinguished SIDS from the other components. The combination of low maternal age and multiparity was demonstrated to be putatively synergistic for risk of SIDS, hyaline membrane disease, and respiratory disease syndrome. Only deaths from infection exhibited seasonal variation similar to SIDS. These observations probably reflect secondary associations with as yet unidentified primary risk factors relatable to maternal experience.

Serum triiodothyronine concentrations in victims of sudden infant death syndrome, when compared with those of both living and dead controls, were found to be elevated to a degree comparable to those found in a previous study. Thyroxine, thyroid-stimulating hormone, and thyroglobulin values were not elevated. Neonatal triiodothyronine and thyroxine values, determined on specimens collected within a few days of birth for most of the sudden infant death syndrome victims, did not differ significantly from those of comparable peers in their birth cohort. These results indicate that hypertriiodothyroninemia may serve as a useful postmortem diagnostic marker for the syndrome but not as a premortem predictor. Parenthetically, thyroid hormones appear to remain stable in either a frozen or dried state for up to two years.

The possible association between diphtheria-pertussis-tetanus (DTP) immunization and the subsequent occurrence of sudden infant death has been examined using data from the National Institute of Child Health and Human Development (NICHD) Sudden Infant Death Syndrome (SIDS) Cooperative Epidemiological Study, a large multicenter, population-based, case-control study. In a preliminary report based on the first 400 eligible singleton SIDS victims and 800 matched living control infants, no temporal association between SIDS and DTP immunization was found. From the final sample of 800 eligible singleton SIDS victims, 95% (n = 757) were defined as definitely or probably having died of SIDS on the basis of pathology data. Data from these 757 case infants and their corresponding control infants (n = 1,514) are presented in this report. Two control infants, both living, were randomly selected for each case infant: an age-matched control A and an age-, race-, and low birth weight-matched control B. Overall, case infants were less likely to have received any DTP immunization. Only 39.8% of case infants had received at least one DTP immunization compared to 55.0% of control A infants and 53.2% of control B infants. Based on maternal interviews and postnatal medical records, 1.8% of case infants (five infants) immunized with DTP died within the first 24 hours following immunization. Similarly, 5.0% of control A infants (n = 21) and 2.2% of control B infants (n = 9) had been immunized within 24 hours of the maternal interview, which represents the comparable time frame for the age-matched control infants. These results confirm the earlier preliminary findings from the NICHD SIDS Cooperative Epidemiological Study and suggest that DTP immunization is not a significant factor in the occurrence of SIDS.

A case-control investigation of the association of Sudden Infant Death Syndrome with a family history compatible with susceptibility to malignant hyperthermia disclosed close agreement with a previously published uncontrolled study from Australia. A definitive investigation of this association will require development of a less invasive and simpler test than is currently available for identifying individuals at risk.

Postmortem heart blood aspirates from 24 consecutive sudden infant deaths and 23 consecutive infant deaths from other causes yielded evidence of erythrocyte transketolase activity (ETKA) in every instance. ETKA measurements from cadaver specimens have not been previously reported. ETKA values did not correlate with the interval from death to sampling or with age at death. Activity coefficients from postmortem material corresponded closely to those from previous studies on living subjects which suggests that the method of Bayoumi and Rosalki yields valid measurements at least for 77 h postmortem. Statistical comparisons of the sudden infant deaths with non-sudden infant deaths revealed no significant differences. This investigation failed to disclose evidence in favor of the hypothesis, advanced by Read, that unsuspected thiamin deficiency may explain some cases of the sudden infant death syndrome.

The hypothesis, advanced by Asch (Mt Sinai J Med NY 35:214-220, 1968), that a majority of sudden infant death syndrome (SIDS) cases are actually infanticides, is addressed by examination of age comparable infant homicide rates (United States, 1950-1974) and consideration of current theory regarding SIDS pathogenesis. The analysis provides no support for the hypothesis.

A unique opportunity to study proven infant apnoea (PIA) and Sudden Infant Death Syndrome (SIDS) occurrences epidemiologically in 12 Counties in north-western Washington State during the same time period during which 180,017 live births were recorded revealed markedly dissimilar distribution patterns. The overall incidence of SIDS exceeded that of PIA by a factor of 3. Five PIA babies subsequently succumbed to SIDS. Statistical analysis reveals that these five events cannot be explained as random coincidences; they represent 3% of 163 PIA cases but only 1% of 503 SIDS occurrences. Infant apnoea is an infrequent precursor of SIDS. These results do not support the view that SIDS and infant apnoea are related conditions caused by a common underlying disorder. Aetiological models other than infant apnoea must be devised if the momentum of SIDS research is to be sustained.

Fecal and serum specimens taken from 30 cases of sudden infant death and from eight cases of nonsudden infant death that were diagnosed at a single facility in King County, Wash., were examined for the presence of Clostridium botulinum organisms and toxin. Organisms, but not toxin, were recovered from a fecal specimen in one case of sudden infant death, results that parallel those from studies previously reported by investigators in California. Studies made in our laboratory of a nonfatal case of infant botulism revealed that an estimated 366,000 mouse minimal lethal doses of toxin were excreted in feces collected by purging the infant. Organisms and toxin were excreted for at least 15 days after the infant was hospitalized. Observations made in our laboratory of atypical responses in mice to both fecal and serum extracts, coupled with recently described experiments in which mice were used as an animal model for infant botulism in humans, provide a biologically plausible foundation for the hypothesis that C. botulinum may be implicated etiologically in some sudden infant deaths. Additional microbiologic, physiologic, and toxicologic data are needed to adequately test this hypothesis.

Data from an earlier study on postnatal growth and the sudden infant death syndrome (SIDS) by Peterson et al. (Am J Epidemiol 1974;99:389-94) were reanalyzed in light of new evidence on the effects of maternal smoking on prenatal and postnatal growth and on the relative risk of SIDS. The data set available for reanalysis consisted of weight and length (crown to heel) measurements at birth and autopsy for 155 babies diagnosed with SIDS in King County, Washington, in 1968-1971. The comparison group consisted of 270 contemporary living peers with weight and length data available. This reanalysis reveals that the retarded growth pattern of SIDS victims is remarkably similar to those of babies born to mothers who smoke during pregnancy. Known and suspected effects of maternal smoking on the fetus and neonate can account for increased susceptibility of death from a variety of causes, including SIDS. The association, if confirmed by further studies, could help clarify the pathogenesis of SIDS in victims with postmortem evidence of antemortem hypoxia with or without a history of periodic apnea.

The diagnosis of sudden infant death syndrome (SIDS) is less than 100% certain in any given instance. Approximately 90% of all SIDS have occurred by age 6 months. A visual aid consisting of 1,000 dots helps in communicating numerical information such as 'rates' to parents (and others as well). The annual and seasonal occurrence patterns are independent of so-called SIDS risk factors. A single, major gene defect cannot account for SIDS but the root cause may be genetic (polygenic). Recent estimates of sibling risk to SIDS indicate that earlier estimates were inflated. Use of apnea monitors to prevent SIDS has no basis in fact but may provide emotional support. DTP immunization does not cause SIDS.

Data from six geographically dispersed metropolitan areas in the United States in which special sudden infant death syndrome (SIDS) surveillance programs for detection and autopsy diagnosis existed during the period 1965 through 1974 reveal considerable diversity in overall ten-year incidence rates as well as in annual rate distribution patterns. A downward trend in SIDS incidence occurred in some areas but not in others. Non-SIDS postneonatal death rates, which were used for comparison, also decreased in some areas. Rate trends for whites and nonwhites were not consistent. During the same period, the fertility rate in the United States decreased by about a third for both whites and nonwhites. To explain the observed trends we postulate that concomitants of the fertility rate decline may have reduced the number of "high mortality risk babies" to a variable degree in different places and at different times.

Knowledge of the likelihood of a repetition of sudden infant death syndrome within a sibship, particularly in the next sibling, is important to parents. Methodologic considerations with respect to the studies of recurrence risk already published indicate that the rates reported are overestimates. This suspicion is confirmed by our study based on 826,162 infants surviving the first week of life on file in the Medical Birth Registry of Norway. A total of 1062 (1.3 per 1,000) infants died of SIDS; five deaths occurred as the second case in a family. The recurrence risk for the nextborn sibling was 5.6 per 1000, and for all subsequent siblings 4.8 per 1000, which would seem encouragingly low from a counseling point of view.

Among Alaskian natives the sudden infant death syndrome (SIDS) occurs at a rate somewhat less than that reported for native Americans indigenous to temperate latitudes. Cases occurred in both the arctic and subarctic regions of the state and among all but one of the ethnically distinct native population groups. No striking male predisposition was evident. These findings are, in general, similar to previously reported accounts from the states of California and Washington. Any theory of SIDS epidemiogenesis must take into account its wide geoethnic and peculiar sex distribution.