Breast feeding and the sudden infant death syndrome in Scandinavia, 1992-95

Aims: To assess the effects of breast feeding habits on sudden infant death syndrome (SIDS). Methods: The analyses are based on data from the Nordic Epidemiological SIDS Study, a case–control study in which parents of SIDS victims in the Scandinavian countries between 1 September 1992 and 31 August 1995 were invited to participate, each with parents of four matched controls. The odds ratios presented were computed by conditional logistic regression analysis. Results: After adjustment for smoking during pregnancy, paternal employment, sleeping position, and age of the infant, the adjusted odds ratio (95% CI) was 5.1 (2.3 to 11.2) if the infant was exclusively breast fed for less than four weeks, 3.7 (1.6 to 8.4) for 4–7 weeks, 1.6 (0.7 to 3.6) for 8–11 weeks, and 2.8 (1.2 to 6.8) for 12–15 weeks, with exclusive breast feeding over 16 weeks as the reference. Mixed feeding in the first week post partum did not increase the risk. Conclusions: The study is supportive of a weak relation between breast feeding and SIDS reduction.     

Seasonality of sudden infant death syndrome (SIDS) by age at death

Seasonality of sudden infant death syndrome (SIDS) is a well-established epidemiological finding. The purpose of the study was to determine whether this feature varied significantly with age at death. In total, 13 990 cases of SIDS in Scotland, England and Wales during 1982–1992 were studied by age group at death. Seasonality was established by fitting a sinusoidal curve and for each set of monthly data the peak position in the year and its magnitude were determined. Weighted regression revealed significant differences in peak position and amplitude of seasonal variation between those dying at ≤ 4 months and those aged ≥ 5 months at death. Those infants in the younger age group were more likely to die earlier in the winter months and had a smaller variation in seasonality. The peak (acrophase) months were January for ≤ 4 months and February for ≥ 5 months at death. Weighted regressions of peak position and amplitude on age at death had p-values of < 0.001 and < 0.01, respectively. A log linear model relating SIDS incidence to month of birth, month of death and age was able to explain some of these findings. The findings support the hypothesis that in SIDS there may be more than one infant cohort, each of which passes through a vulnerable developmental window at different ages.     

Breast feeding and the sudden infant death syndrome in Scandinavia, 1992-95.

AIMS: To assess the effects of breast feeding habits on sudden infant death syndrome (SIDS). METHODS: The analyses are based on data from the Nordic Epidemiological SIDS Study, a case-control study in which parents of SIDS victims in the Scandinavian countries between 1 September 1992 and 31 August 1995 were invited to participate, each with parents of four matched controls. The odds ratios presented were computed by conditional logistic regression analysis. RESULTS: After adjustment for smoking during pregnancy, paternal employment, sleeping position, and age of the infant, the adjusted odds ratio (95% CI) was 5.1 (2.3 to 11.2) if the infant was exclusively breast fed for less than four weeks, 3.7 (1.6 to 8.4) for 4-7 weeks, 1.6 (0.7 to 3.6) for 8-11 weeks, and 2.8 (1.2 to 6.8) for 12-15 weeks, with exclusive breast feeding over 16 weeks as the reference. Mixed feeding in the first week post partum did not increase the risk. CONCLUSIONS: The study is supportive of a weak relation between breast feeding and SIDS reduction.     

Comparative epidemiology of sudden infant death syndrome and sudden intrauterine unexplained death

BACKGROUND: Unexplained antepartum stillbirth and sudden infant death syndrome (SIDS) are major contributors to perinatal and infant mortality in the western world. A relation between them has been suggested. As an equivalent of SIDS, only cases validated by post mortem examination are diagnosed as sudden intrauterine unexplained death (SIUD). OBJECTIVE: To test the hypothesis that SIDS and SIUD have common risk factors. METHODS: Registration comprised all stillbirths in Oslo and all infant deaths in Oslo and the neighbouring county, Akershus, Norway during 1986-1995. Seventy six cases of SIUD and 78 of SIDS were found, along with 582 random controls surviving infancy, all singletons. Odds ratios were obtained by multiple logistic regression analysis. RESULTS: Whereas SIUD was associated with high maternal age, overweight/obesity, smoking, and low education, SIDS was associated with low maternal age, smoking, male sex, multiparity, proteinuria during pregnancy, and fundal height exceeding +2 SD. Thus the effects of maternal age were opposite in SIUD and SIDS (adjusted odds ratio 1.39 (95% confidence interval 1.17 to 1.66) per year, p < 0.0005). Heavy smoking, male sex, and a multiparous mother was less likely in SIUD than in SIDS (0.22 (0.06 to 0.83), 0.22 (0.07 to 0.78), and 0.03 (<0.01 to 0.17) respectively). Overweight/obesity and low fundal height were more common in SIUD than in SIDS (7.45 (1.49 to 37.3) and 13.8 (1.56 to 122) respectively). CONCLUSIONS: The differences in risk factors do not support the hypothesis that SIDS and SIUD have similar determinants in maternal or fetal characteristics detectable by basic antenatal care.     

Defining the sudden infant death syndrome

Sudden infant death syndrome (SIDS) is a term that was first proposed in 1969 for a distinctive subgroup of unexpected infant deaths that occur during the postneonatal period with relatively consistent clinical, epidemiological, and pathological features. This term played an important role by focusing attention on a major category of postneonatal infant death, providing support to grieving families, and diminishing the guilt and blame characteristic of these deaths. Unfortunately, the application of this term has become increasingly controversial. Some have applied it too liberally, and others not at all. According to the definition proposed in 1969, despite slight changes suggested in 1989, SIDS remains a diagnosis of exclusion. Although this syndrome has several distinctive features, including age distribution and apparent occurrence during sleep, there has been reluctance to include these features in the definition. The problems created by the lack of an adequate definition are discussed. A 2-tiered approach is suggested, with a more general definition intended primarily for case management and death administration, and a more restrictive one intended primarily for research purposes, which distinguishes those deaths closely fitting the classic SIDS profile from those with one or more less typical features.     

Update on sudden infant death syndrome

PURPOSE OF REVIEW: With the introduction of the Back to Sleep campaign by the American Academy of Pediatrics in 1992, the incidence of Sudden infant death syndrome has decreased by almost 50%. Despite this success, SIDS continues to be the most common cause of unexplained infant death in Western countries. This article will briefly review the definition, etiology, and risk factors of SIDS. Attention will then focus on ways to target specific associated risk factors and at risk populations to promote a continued downward trend in the number of SIDS deaths. RECENT FINDINGS: Recent literature in SIDS research has focused on identifying infants at continued risk for SIDS. Children attending child care centers have an increased risk for SIDS, which is of particular concern as the number of infants in child care continues to rise. The reasons for this, along with strategies to decrease this risk, will be reviewed. In addition, the SIDS rate among black infants continues to be more than twice that of white infants. A review of the reasons for this disparity and ways to intervene through targeted campaigns will be discussed. Recent data has also suggested that the prevention of SIDS should not be an indication for use of home cardiorespiratory monitoring. The use of home monitoring may be warranted for some infants and will be reviewed. SUMMARY: Our jobs as pediatricians should be to ensure that the incidence of SIDS continues to decline. This can be done through parent education at each and every well child visit, lobbying to enforce state law to implement SIDS education campaigns for child care centers and within African-American communities, and continued review of the most current literature in SIDS research to keep ourselves current and well informed.     

Neuronal apoptosis in sudden infant death syndrome

Although evidence shows that victims of sudden infant death syndrome (SIDS) suffer repetitive episodes of hypoxemia, only subtle abnormalities have been found in their brains by light microscopy. The aim of the present study was to determine whether apoptosis, a form of cell death that can be triggered by hypoxemia and that leaves no scarring detectable by light microscopy, would be present in hypoxia-sensitive brain regions of SIDS victims. We looked for the presence of apoptosis with an in situ end-labeling method that detects DNA fragmentation. We studied 29 SIDS victims who were age-matched to nine control cases. We found significant neuronal apoptosis in 79% of the SIDS cases: 55% of the cases positive in the hippocampus and 96% positive in the brainstem. Whereas the distribution of apoptosis in the hippocampus was in hypoxia-sensitive subregions, the distribution in the brainstem was mostly in dorsal nuclei, including those involved with sensation in the face and position of the head (nucleus of the spinal trigeminal tract and vestibular nuclei). The control cases showed no significant apoptosis in the hippocampus and a mild degree in the brainstem in three cases. Our results indicate the occurrence of an acute insult at least several hours before death, an insult from which the infants had apparently recuperated. This suggests that SIDS victims suffered repeated apoptosis resulting in significant neuronal damage and, thus, functional loss in key brain regions. The involvement of specific nuclei in the brainstem may be linked to the fact that prone sleeping is a significant risk factor for SIDS. Enhanced neuronal death by apoptosis may thus have major implications for understanding the sequence of events leading to SIDS.     

Co-sleeping and sudden infant death syndrome]

Bedsharing has recently become a controversial subject. Some authors, mainly from North America, assign to bedsharing a positive effect on the efficacy and duration of breast-feeding. Moreover, it would protect against sudden infant death syndrome (SIDS). Conversely, other studies consider bedsharing as an additional risk factor for SIDS. From the literature data, there is some evidence for an increased risk of SIDS when bedsharing is associated with maternal smoking and alcohol consumption. Bedsharing cannot be recommended as an absolutely safe practice. Breast-feeding mothers should be aware of these potential hazards.     

Simultaneous sudden infant death syndrome in twins

Nine cases of twin infants dying suddenly and simultaneously are described, two of which the author examined personally. A review of this phenomenon described in other literature is also presented. It is hoped that increased awareness of this phenomenon will decrease the profound suspicions of both lay and professional persons that the deaths were due to criminal instrumentality.     

Growth and the sudden infant death syndrome

Objective : To compare the growth curves based on measurements of body weight for male and female infants dying of sudden infant death syndrome (SIDS) with those of male and female controls. Methods : The data were drawn from a large case control study of SIDS carried out in New Zealand between 1987 and 1990. Results : The mean birthweight for the cases was 3049 g and for the controls 3526 g. The mean growth curves for the male and female controls were close to the 50th centile of growth charts used in New Zealand. The growth curve for the male cases diverged from that of the controls, being closer to the 25th percentile. The differences between the female cases and controls were less pronounced. The differences in weekly weight increments derived from the curves for the cases and controls for nine 4-week periods were not statistically significant after taking into account race, manner of feeding and maternal smoking for any 4-week period. Conclusions : SIDS cases were lighter at birth, but their growth velocity was normal postnatally.     

Hypothermia and sudden infant death syndrome.

We recently reported an association between recurrent episodes of severe apnoea requiring vigorous resuscitation for which no cause could be found and episodic hypothermia. Two similar cases are now reported that give further evidence of a link between hypothermia and acute life threatening episodes of apnoea.     

Infant botulism and sudden infant death syndrome

Infant botulism represents a distinct entity of botulism. Ingestion of the ubiquitously present spores of Clostridium botulinum leads to germination of the organism and neurotoxin production in the infant intestine. Symptoms typically develop gradually in contrast to classical food botulism in which an acute onset of symptoms shortly after the ingestion of preformed toxin in a food is characteristic. Microbiologically, the diagnosis is established by identification of Clostridium botulinum organism and toxin in stool specimen. However, positive results in these tests provide only indirect evidence for the clinical relevance of the neurotoxin since asymptomatic carriers have been found. The toxin irreversibly blocks the release of acetylcholin from the motoric end plate which results in muscle weakness and paralysis. Depending on the amount of toxin produced, infant botulism exhibits a broad clinical spectrum ranging from oligosymptomatic forms to a fulminant course with acute respiratory failure within hours leading to sudden death. Unrecognized mild forms or beginning muscle weakness can be a co-factor for other risk factors of sudden infant death (SIDS). In studies analyzing infants who died from SIDS, botulism bacteria or toxin were found in up to 20 % of cases. Infant botulism therefore represents an important differential diagnosis of unexplained and inconclusive muscular hypotonia in the first year of life.