Incidence Of Sudden Infant Death Syndrome Research Articles

Predicting the Risk for Sudden Infant Death Syndrome From Obstetric Characteristics: A Retrospective Cohort Study of 505011 Live Births

We sought to develop a simple robust method for assessing the risk for sudden infant death syndrome (SIDS) on the basis of obstetric characteristics. A population-based retrospective cohort study was conducted of data from the linked Scottish Morbidity Record, Stillbirth and Infant Death Enquiry and General Registrar's Office database of births and deaths, encompassing births in Scotland between 1992 and 2001. All women who had a singleton live birth between 24 and 43 weeks' gestation and for whom data were available (n = 505,011), divided into model development and validation samples, were studied. The main outcome measure was death of the infant in the first year of life as a result of SIDS. The risk for SIDS was modeled in the development sample using logistic regression with the following predictors: maternal age, parity, marital status, smoking, and the birth weight and the gender of the infant. When the model was evaluated in the validation sample, the area under the receiver operating characteristic curve was 0.84 and the incidence of SIDS was 0.7 per 10,000 (95% confidence interval: 0.3-1.4) among 126,253 women in the lower 50% of predicted risk and 29.7 per 10,000 (95% confidence interval: 23.4-37.2) among the 25,250 women in the top 10% of predicted risk. A logistic-regression model then was developed for the whole population, and the output was converted into adjusted likelihood ratios. These are tabulated and provide a simple method for assessing the risk for SIDS associated with any combination of obstetric characteristics. A model that uses maternal characteristics and outcome at birth is predictive of the risk for SIDS. This model is presented in a simple form that allows calculation of the individual risk for SIDS.

Policy Targets Lowering SIDS Incidence

WHILE NOTING THE REDUCtion in the incidence of sudden infant death syndrome (SIDS) by more than half in recent years, the American Academy of Pediatrics (AAP) believes even better results can be achieved. To that end, the AAP on October 10 released an updated policy statement calling for several changes parents can incorporate into their infant care to further reduce SIDS risk (Pediatrics. 2005;116:12451255). But some of the recommendations have raised concerns among certain parenting groups. The updated AAP recommendations stress placing infants only on their backs for sleep, a shift from recommendations issued in 1992 that suggested either a supine or a side-sleep position. The change was made because studies published after 1992 indicated that SIDS risk for infants is higher with side-sleep positioning compared with supine sleeping.

Putting Babies “Back to Sleep”: Can We Do Better?

The American Academy of Pediatrics first recommended in 1992 that infants be placed on their backs for sleep to reduce the risk for sudden infant death syndrome (SIDS). Since that time, there has been a national drop in the incidence of SIDS of more than 40 percent. Unfortunately, many parents and other caregivers are still receiving inconsistent information and observing varying practices regarding infant sleep position. This article emphasizes the role of the health care professional in both teaching and modeling these potentially life-saving practices consistently and unambiguously. Available literature is reviewed regarding attitudes and beliefs about infant sleep positioning, and specific concerns are addressed in order to allow for better tailoring of educational programs.

Sudden infant death syndrome: The colon connection

The etiology of sudden infant death syndrome (SIDS) is not known. Various maternal and infant risk factors have been identified. Adoption of the non-prone position has reduced the incidence of SIDS but has not eliminated the problem. Some sulfate reducing bacteria in the colon produce hydrogen sulfide (H2S) which is as toxic as hydrogen cyanide. Normally, the colonic mechanism for metabolizing and detoxifying H2S is very effective and no H2S appears in the exhaled breath although small amounts are present in the flatus. We are putting forth the hypothesis that in some cases of SIDS colonocytic mechanism for detoxifying H2S may not have matured by the age of 3 months and H2S may be absorbed resulting in SIDS. The hypothesis can be tested by in vitro evaluation of colonic tissue from SIDS cases for its ability to detoxify H2S.

Cytokine responses and sudden infant death syndrome: genetic, developmental, and environmental risk factors

Despite the success of the campaigns to reduce the risk of sudden infant death syndrome (SIDS), it still remains the major cause of postneonatal mortality. The incidence of SIDS is higher among ethnic groups in which there are also high incidences of serious infectious diseases. The risk factors for SIDS parallel those for susceptibility to infection, and recent data have provided evidence to support the mathematical model of the common bacterial toxin hypothesis. One current hypothesis for the etiology of SIDS is that the deaths are a result of overwhelming proinflammatory responses to bacterial toxins; as in inflammatory responses to sepsis, cytokines, induced by bacterial toxins, cause physiological changes leading to death. The genetic, developmental, and environmental risk factors for SIDS are reviewed in relation to colonization by potentially harmful bacteria and the inflammatory responses induced in the nonimmune infant to microorganisms or their products.

Abnormalities of the Brainstem Serotonergic System in the Sudden Infant Death Syndrome: A Review

INTRODUCTION Sudden infant death syndrome (SIDS) is the sudden death of an infant younger than 1 year that remains unexplained by a complete autopsy, death scene investigation, and review of the clinical record [1]. There has been an almost 50% decrease in the incidence of SIDS in the United States after a 1992 national recommendation for the supine sleep position. Nevertheless, SIDS remains a leading cause of postneonatal infant mortality. Its overall incidence is 0.6 per 1,000 live births [2]; approximately 6 infants die per day from SIDS in this country alone. Risk factors for SIDS other than the prone sleeping position are well recognized. Environmental risk factors include maternal cigarette smoking and alcohol intake during pregnancy [3–5]. Genetic risk factors include polymorphisms in the serotonin transporter (SERT) [6–8] and cytokine interleukin-10 [9]. Such risk factors appear to be independent of the prone sleeping position and are certainly more difficult to modify. Thus, SIDS remains a major public health problem, thus mandating further research into the underlying cause(s) and mechanism(s) to develop specific strategies to eradicate all SIDS deaths. Moreover, risk reduction messages are likely to be more compelling to families and health care workers and, hence, more successful when they are based on biologically established or plausible mechanisms. This report presents a review of findings related to brainstem serotonergic (5-HT) abnormalities in a subset of SIDS cases. From 1990 to 2003, my colleagues and I published a series of reports concerning 6 neurotransmitter systems in step tissue sections of the same SIDS and control brainstems [5,10–15]. Our overall conclusion was that the 5-HT system in the medulla oblongata, i.e., the so-called medullary 5-HT system, is abnormal in at least 50% of SIDS cases [16]. We focused on brainstem systems involved in the control of respiration, autonomic function, sleep, and arousal because of an increasing body of prospective studies involving infants who subsequently died of SIDS that indicate subtle abnormalities in respiratory and/or autonomic control during sleep and arousal patterns before death [17–19]. Moreover, studies in normal preterm and term infants have indicated that the period of *Corresponding author, e-mail: hannah.kinney@childrens.harvard.edu Pediatric and Developmental Pathology 8, 507–524, 2005 DOI: 10.1007/s10024-005-0067-y a 2005 Society for Pediatric Pathology

Sudden Unexpected Child Deaths: Forensic Autopsy Results in Cases of Sudden Deaths During a 5-year Period

The aim of the present study was to determine the incidence of various causes of sudden unexpected child deaths (SUCD) and to assess the importance of an autopsy in predicting the likelihood of finding a cause of death. A retrospective analysis of autopsy findings in 97 cases of SUCD between the ages of 0--11 years was undertaken at the Council of Forensic Medicine, Ankara during a 5-year period (1995--2000). Cases were classified as explained causes (80.42 per cent) and sudden infant death syndrome (SIDS) (19.58 per cent). A total of 25.77 per cent of the deaths occurred in the neonatal period, 45.31 per cent of them in the first year of life and the remaining 28.86 per cent after 1 year of life. The causes of neonatal deaths were respiratory pathology (five cases), birth complications (four cases), gastrointestinal pathology (one case), homicide (10 cases), and SIDS (five cases). The incidence of SIDS in the newborn period was 33 per cent. The incidence of unexplained causes of deaths in the postneonatal period was 31 per cent and the causes of deaths were respiratory pathology (15 cases), aspiration (five cases), gastrointestinal pathology (four cases), SIDS (14 cases), and other causes (four cases). The study of an entire population provides more reliable data regarding causes of sudden unexpected child deaths than does the study of small groups and it is also recommended that in addition to a through evaluation, a detailed autopsy must be performed for each case in experienced centers.

Occipital Plagiocephaly

After the “Back to Sleep” campaign, promoted in 1992 by the American Academy of Paediatrics to prevent the Sudden Infant Death Syndrome (SIDS), it was recommended to place babies in a supine sleeping position. The incidence of SIDS has fallen dramatically since 1992, whereas there has been a major increase in the incidence of occipital plagiocephaly (OP). We report the data relative to the OP cases observed in the Paediatric Department of Padua Hospital between 1998 and 2003. 122 (63%) of the 194 cases of craniosynostosis observed presented OP. The 64 children that took part to the study were contacted and underwent neurological examination with an evaluation of skull shape and previous radiograms. We proposed to parents a questionnaire to define the risk factors and estimate the skull deformity over time. 58 of the 64 children presented positional plagiocephaly (PP), six had synostotic plagiocephaly (SP). Since 1998 there has been a progressive increase in cases of PP. There is a male prevalence (65%), but no side prevalence. Firstborns accounted for 33 (51%), whereas 11 were preterm infants (17%). 82% had a gestational age between the 38th and 40th week. The mean value of the Apgar Index was 8 at the first minute and 9 at the 5th minute. At birth the clinical presentation was: occipital flattening already present at birth in 23 children, preferential head orientation in 18, congenital torticollis in 12, ear asymmetry in 12, frontal bossing in ten. We noticed a mild developmental delay in 8 children (13%). The maximum degree of cranial asymmetry was observed in two peaks in cases of PP: at the third and fourth months (34 cases) and then at the sixth and seventh months (13 cases). The SP presented a progressive exacerbation of the deformity until surgery (done at the sixth to seventh months). PP improved by hygienic postural norms in six months; only three patients required surgery for aesthetic reasons. We observed a strict correlation between side of flattening and sleep head position ( χ2 test, p-value=2,256e-09) and a higher degree of occipital flattening at birth in patients with associated congenital torticollis (Mann-Whitney test, p-value=0.002744). In conclusion, OP is a common condition but essentially benign; it does not cause medical consequences but aesthetic problems. It is necessary to recognize the mild deformity in the newborns so as to intervene early with hygienic postural norms that can correct the asymmetry. The diagnosis is largely clinical and only in case of doubt are radiological examinations required (ultrasonography for sutures, 3D CT scans).

Modifiable risk factors for SIDS in Germany: Results of GeSID

The incidence of sudden infant death syndrome (SIDS) has been falling in Germany over the last decade. However, little is known about the prevalence and the importance of well-known risk factors in Germany since a local prevention campaign in 1992. A 3-y, population-based, case-control study was conducted in half of Germany, consisting of 333 cases. All sudden and unexpected deaths in infancy, if they fitted the inclusion criteria, were included in the study. Parental interview was carried out soon after the death, and three living control infants, matched for age, gender, region and sleep time, were recruited. The prevalence of placing infants prone to sleep was only 4% in the control group, but this was associated with a markedly increased risk of SIDS (adjusted odds ration, aOR=6.08). Other modifiable risk factors for SIDS were: maternal smoking during pregnancy, breastfeeding for less than 2 wk (aOR=1.71) and co-sleeping (aOR=2.71), while using a pacifier during the last sleep reduced the risk (aOR=0.39). Previously recognized risk factors for SIDS also occur in Germany. Despite knowledge about the major modifiable risk factors for SIDS, these factors are still present in Germany. To reduce the incidence of SIDS in Germany, a continued effort is needed to inform all parents about preventable risk factors for SIDS.

First-time mothers' selection of infant supine sleep positioning.

The incidence of Sudden Infant Death Syndrome (SIDS) has decreased dramatically since the inception of the "Back to Sleep" campaign initiated by the American Academy of Pediatrics in 1992. However, that decrease has leveled off and many new parents cease to follow the recommendation to place their infants in the supine position for sleep between 1 and 3 months of age, the peak age for the incidence of SIDS. Shortened hospital stays for new mothers and the overwhelming amount of required patient teaching dictate the need to find the best method of instruction. The purpose of this study was to determine if a one-on-one teaching intervention improved the effectiveness of patient education and led to an increase in the desired behavior of placing the infant to sleep in the supine position. A quantitative experimental approach was used to examine the difference in compliance of supine infant positioning. Participants were drawn from a convenience sample of 61 primiparous women between the ages of 18 and 35 years with random assignment to either the experimental or control group. Compared to mothers in the control group, mothers in the experimental group demonstrated greater compliance in selecting supine sleep position in the first week home from the hospital and on the day of follow-up 6 weeks later. However, no difference in "usual position" was reported at 6 weeks and for the night previous to follow-up.

Investigation of sudden infant deaths in the State of Maryland (1990–2000)

The Office of the Chief Medical Examiner (OCME) has recorded a significant decline in the deaths of sudden infant death syndrome (SIDS) in the state of Maryland since 1994. However, infants who died of accidental or non-accidental injuries remained consistent during the same time period. This report focuses on the epidemiological characteristics and scene investigation findings of infant victims who died suddenly and unexpectedly in Maryland between 1990 and 2000. A retrospective study of OCME cases between 1990 and 2000 yielded a total of 1619 infant fatalities. 802 infant deaths were determined to be SIDS, which represented 50% of the total infant deaths in our study population. Five hundred and twenty-three (31.8%) deaths were due to natural diseases, 128 (7.9%) deaths were accidents, and 74 (4.6%) were homicides. The manner of death could not be determined after a thorough scene investigation, review of history and a complete postmortem examination in 92 (5.7%) infants. SIDS deaths most often involved infants who were male and black. The peak incidence of SIDS was between 2 and 4 months of age. The majority of SIDS infants (60%) were found unresponsive on their stomach. Among SIDS infants, 269 (33.4%) were found in bed with another person or persons (bed sharing). Of the bed-sharing SIDS cases, 182 (68%) were African–American. In the past 11 years, 52 infants died of asphyxia due to unsafe sleeping environment, such as defective cribs, ill-fitting mattresses, inappropriate bedding materials. Of the 74 homicide victims, 53 (70%) involved infants less than 6 months of age. Twenty (27%) exhibited the classical abuse syndrome characterized by repeated acts of trauma to the infants.

Cannabinoid receptor expression in peripheral arterial chemoreceptors during postnatal development.

Prenatal exposure to tobacco smoke increases risk of sudden infant death syndrome (SIDS). Marijuana is frequently smoked in conjunction with tobacco, and perinatal exposure to marijuana is associated with increased incidence of SIDS. Abnormalities in peripheral arterial chemoreceptor responses during sleep may be operative in infants at risk for SIDS, and nicotine exposure adversely affects peripheral arterial chemoreceptor responses. To determine whether marijuana could potentially affect the activity of peripheral arterial chemoreceptors during early postnatal development, we used in situ hybridization histochemistry to characterize the pattern and level of mRNA expression for cannabinoid type 1 receptor (CB1R) in the carotid body, superior cervical ganglia (SCG), and nodose-petrosal-jugular ganglia (NG-PG-JG) complex in newborn rats. We used immunohistochemistry and light, confocal, and electron microscopy to characterize the pattern of CB1R and tyrosine hydroxylase protein expression. CB1R mRNA expression was intense in the NG-PG-JG complex, low to moderate in the SCG, and sparse in the carotid body. With maturation, CB1R gene expression significantly increased (P < 0.01) in the NG-PG-JG complex. CB1R immunoreactivity was localized to nuclei of ganglion cells in the SCG and NG-PG-JG complex, whereas tyrosine hydroxylase immunoreactivity was localized to the cytoplasm. Exposure to marijuana during early development could potentially modify cardiorespiratory responses via peripheral arterial chemoreceptors. The novel finding of nuclear localization of CB1Rs in peripheral ganglion cells suggests that these receptors may have an, as yet, undetermined role in nuclear signaling in sensory and autonomic neurons.

Second-trimester maternal serum levels of alpha-fetoprotein and the subsequent risk of sudden infant death syndrome.

Unexplained stillbirth and the sudden infant death syndrome (SIDS) share some features. A raised maternal serum level of alpha-fetoprotein during the second trimester of pregnancy is a marker of placental dysfunction and a strong predictor of the risk of unexplained stillbirth. It is unknown whether alpha-fetoprotein levels also predict the risk of SIDS. We linked a prenatal-screening database for women in western Scotland with databases of maternity, perinatal death, and birth and death certifications to assess the association between second-trimester levels of maternal serum alpha-fetoprotein and the subsequent risk of SIDS. Among 214,532 women with singleton births, there were 114 cases of SIDS (incidence, 2.7 per 10,000 births among women with alpha-fetoprotein levels in the lowest quintile and 7.5 per 10,000 births among those with levels in the highest quintile). When the lowest quintile was used as a referent, the unadjusted odds ratios for SIDS for the second through fifth quintiles were 1.7 (95 percent confidence interval, 0.8 to 3.5), 1.8 (95 percent confidence interval, 0.9 to 3.7), 2.5 (95 percent confidence interval, 1.3 to 4.8), and 2.8 (95 percent confidence interval, 1.4 to 5.4), respectively (P for trend = 0.001). The risk of SIDS varied inversely with the birth-weight percentile and the gestational age at delivery; after adjustment for these factors, the odds ratios for SIDS were 1.7 (95 percent confidence interval, 0.8 to 3.5), 1.7 (95 percent confidence interval, 0.8 to 3.5), 2.2 (95 percent confidence interval, 1.1 to 4.4), and 2.2 (95 percent confidence interval, 1.1 to 4.3), respectively (P for trend = 0.01). There is a direct association between second-trimester maternal serum alpha-fetoprotein levels and the risk of SIDS, which may be mediated in part through impaired fetal growth and preterm birth.

Mortality due to sudden infant death syndrome in Northern Italy, 1990–2000: a baseline for the assessment of prevention campaigns

The aim of this paper is to estimate the infant mortality rate and the incidence of sudden infant death syndrome (SIDS) in Lombardy, Northern Italy, in the period 1990-2000 and to provide basic information for a subsequent comparison of the SIDS incidence before and after the risk-intervention campaign. A retrospective epidemiological study was carried out using all deaths of resident infants occurring up to 1 year of age as recorded by the health districts mortality registries of the Lombardy region, between 1990 and 2000. The infant mortality rate was 4.1 per 1000 live births, with a significant decreasing trend. This decrease is mainly due to the fall in mortality for congenital malformations and perinatal diseases. The SIDS incidence rate was 0.13 per 1000 live births; the annual incidence of SIDS during the study period decreased significantly by 60% from 0.20 to 0.08 deaths per 1000 live births (P = 0.001). When 'possible SIDS deaths', not directly labelled as SIDS, were also considered, the rate of SIDS was 0.54 per 1000 live births. The incidence of SIDS in Northern Italy appears much lower than anticipated. SIDS remains the single leading cause of death in the first year of life after the early neonatal period.

Air pollution and sudden infant death syndrome: a literature review.

Although the rate of sudden infant death syndrome (SIDS) has been reduced with the 'Back to Sleep' campaign, SIDS is still a common cause of death in infancy. A range of environmental factors may interact to contribute to the adverse health conditions conducive to SIDS. Nine studies have evaluated the association between exposure to air pollution and the incidence of SIDS. The available evidence is inadequate to come to any conclusion about a relationship between air pollution and SIDS, although the body of evidence appears to suggest that air pollution (especially particles and some gaseous pollutants) may play a certain role in the occurrence of SIDS. We suggest that future studies should focus on the research design, role of indoor air quality and the effect of smaller particles, particularly those in the ultrafine range.

Interleukin-10 and sudden infant death syndrome

Uncontrolled pro-inflammatory responses to infections or bacterial toxins have been suggested to play a role in triggering the physiological events leading to sudden infant death syndrome (SIDS). We tested the hypothesis that these uncontrolled responses might be due to interactions between the gene polymorphisms inducing low levels of IL-10 and exposure to cigarette smoke. In vitro, the IL-10 (G-1082A) polymorphism was associated with low IL-10 levels and the –1082G allele was associated with high levels. The first objective was to assess the distribution of this polymorphism among SIDS infants, parents of SIDS infants and controls, and two ethnic groups: Aboriginal Australians who have a high incidence of SIDS; and Bangladeshis who in Britain have a low incidence of SIDS compared with Europeans. The second objective was to assess effects of human recombinant IL-10 on interleukin-6 (IL-6) and tumour necrosis factor-α (TNF-α) responses of human leukocytes to staphylococcal toxins implicated in SIDS. The third objective was to assess IL-10 responses to endotoxin and toxic shock syndrome toxin (TSST) from leukocytes of smokers and non-smokers in relation to the IL-10 (G-1082A) polymorphism. There were major differences in the distributions of these polymorphisms between Europeans and Bangladeshis ( p=0.00) and between Europeans and Aboriginal Australians ( p=0.00); however, they were similar for the Bangladeshi and Aboriginal Australian subjects. There were no significant differences in the distribution of these polymorphisms among SIDS infants or parents of SIDS infants compared to control groups. IL-10 significantly reduced IL-6 and TNF-α responses to TSST and staphylococcal enterotoxins A and C. At 50 ng ml −1, IL-10 significantly increased TNF-α but not IL-6 responses to TSST and enterotoxin A. Although IL-10 responses to endotoxin were lower from leukocytes of smokers who were homozygous for the G allele, the differences were not significant; however, significantly lower IL-10 responses were found for smokers who were homozygous for the A allele ( p=0.01) and heterozygotes ( p=0.04). The pooled data found smokers had significantly lower levels of IL-10 responses to TSST, but there were no significant differences for smokers compared with non-smokers for the three genotypes. The high incidence of SIDS and serious respiratory infections among Aboriginal Australian infants and the low incidence of these conditions among Bangladeshi infants might be explained in part by our findings of differences in IL-10 responses between smokers and non-smokers. The lowest levels of IL-10 responses were observed among smokers who were homozygous for the A allele which is most prevalent among the Aboriginal Australians (83%) and Bangladeshis (84%). The major difference between the risk factors for SIDS in these two groups is the level of exposure of infants to cigarette smoke associated with maternal smoking.

Interleukin 1-β responses to bacterial toxins and sudden infant death syndrome

We tested the hypothesis that significantly higher IL-1β responses to toxic shock syndrome toxin (TSST) noted for parents of sudden infant death syndrome (SIDS) infants might be due in part to genetic factors such as the IL-1β (C-511T) and IL-1RN (T + 2018C) single nucleotide polymorphisms (SNP). The first objective was to assess the distribution of these polymorphisms among SIDS infants, parents of SIDS infants and controls, and two ethnic groups: Aboriginal Australians who have a high incidence of SIDS; and Bangladeshis who in Britain have a low incidence of SIDS compared with Europeans. The second objective was to assess IL-1β responses to endotoxin and toxic shock syndrome toxin (TSST) from leukocytes of smokers and non-smokers in relation to these polymorphisms. There were major differences in the distributions of the IL-1β (C-511T) SNP between Europeans and Bangladeshis ( p=0.00) and between Europeans and Aboriginal Australians ( p=0.00); however, they were similar for the Bangladeshi and Aboriginal Australian subjects. The allele frequency distribution of the IL-1RN (T + 2018C) SNP for the Aboriginal Australians was statistically different from the European group ( p=0.00), but it was not different from the Bangladeshi group ( p=0.09). Compared with controls of European origin, there were no significant differences in the distribution of these polymorphisms among SIDS infants or parents of SIDS infants. For the IL-1β (C-511T) SNP, the highest IL-1β responses to endotoxin were obtained with leukocytes of non-smokers with the heterozygous CT genotype. Smokers had significantly lower levels of IL-1β in response to endotoxin ( p=0.01) and these differences were significant for donors with the wild type CC ( p=0.00) and CT ( p=0.03) genotypes. Similar patterns were observed for IL-1β responses to TSST, but the differences were not significant. For the IL-1RN (T + 2018C) SNP, the highest IL-1β responses to endotoxin were obtained with leukocytes from non-smoker donors with the wildtype TT genotype and significantly lower responses were found with leukocytes from donors with the TC genotype ( p=0.02). The responses of smokers were lower but the differences were significant only for donors with the TT genotype ( p=0.00). Similar patterns were observed for IL-1β responses to TSST, but the differences were not significant. IL-1β responses to both endotoxin and TSST were increased for the small number of smokers with the TT genotype of the IL-1β (C-511T) SNP. The TT genotype of the IL-1β (C-511T) was found predominantly among Aboriginal Australian and Bangladeshi individuals but only a small proportion of Europeans. Smokers with the AA genotype of the IL-10 (G-1082A) SNP which is found predominantly among these two groups had significantly lower levels of IL-10 responses. If cigarette smoke enhances pro-inflammatory responses and reduces anti-inflammatory responses in individuals with these genotypes, this might partly explain the increased susceptibility of Aboriginal Australian infants to infections and SIDS.

Higher incidence of SIDS at weekends, especially in younger infants

Background: An increased incidence of sudden infant death syndrome (SIDS) at weekends has been previously noted, although it has not been found in all studies. Where a weekend effect has...

Heat stress and sudden infant death syndrome incidence: a United States population epidemiologic study.

To determine the role of heat stress in sudden infant death syndrome (SIDS) by examining the SIDS rates during periods of extreme environmental temperatures in a period when most infants were placed prone for sleep. A retrospective study of SIDS rates and mortality rates attributable to excessive environmental heat in relationship to climatologic temperature was performed. Data were collected for each of 454 counties in 4 states (Arkansas, Georgia, Kansas, and Missouri) from May 1 to September 30, 1980, and were then summed to yield the mortality rates for each 5 degrees F (2.8 degrees C) temperature range. chi2 analyses revealed significant relationships for heat-related mortality rates and both the maximal daily temperature and mean daily temperature but demonstrated no such relationships for SIDS rates. No association between SIDS rates and heat-related mortality rates was found with Spearman's ranked correlation, for either the maximal daily temperature or the mean daily temperature. On the basis of our findings of no significant association between SIDS and either measure of temperature during periods of high heat stress-related death rates, it seems unlikely that the heat stress associated with the combination of prone sleep positions and elevated environmental temperatures has a significant role in the development of SIDS.

Maternal and obstetric risk factors for sudden infant death syndrome in the United States.

The objectives of this study were to 1). study the incidence of sudden infant death syndrome (SIDS) among singleton births in the United States and 2). identify maternal and obstetric risk factors for SIDS. A cohort of all live births in the United States from 1995 to 1998, formed the source population (n = 15627404). The data were obtained from the National Centers for Health Statistics Linked Births and Infant Deaths File. A nested case-control study was used to examine risk factors for SIDS. From this birth cohort, all SIDS deaths (n = 12404) were first identified (case group). From the remaining non-SIDS births, a 4-fold larger sample (n = 49616) was randomly selected as a control group. The overall incidence of SIDS was 81.7 per 100000 live births. More mothers in the case group than in the control group were reported to have placenta previa (odds ratio [OR]: 1.70; 95% confidence interval [CI] 1.24, 2.33), abruptio placentae (OR 1.57; 95% CI 1.24, 1.98), premature rupture of membranes (OR 1.48; 95% CI 1.33, 1.66), or small for gestational age (OR 1.40; 95% CI 1.30, 1.50 for the 10th percentile). SIDS cases were also more likely to be male. Mothers of cases were more likely to be younger, less educated, and nonwhite, and more of them smoked during pregnancy and did not attend prenatal care. This analysis confirms the importance of several well known demographic and lifestyle risk factors for SIDS. In addition, placental abnormalities were risk factors for SIDS. II-2