Sudden Infant Death Syndrome Deaths Research Articles

Sudden infant death syndrome (SIDS): are common bacterial toxins responsible, and do they have a vaccine potential?

Despite extensive research, no unifying concept has satisfactorily explained the cause of the sudden infant death syndrome (SIDS). The details are briefly outlined of some of the evidence supporting the hypothesis that common bacterial toxins are important in the aetiology of SIDS. These bacterial toxins act as triggers to initiate a biochemical cascade resulting in death. Data from four research groups, each working independently, indicated that the bacteria Clostridium perfringens, Escherichia coli, Staphylococcus aureus, Streptococcus spp. and Enterococcus spp. were present in higher numbers in infants who had suffered SIDS than in control infants. Certainly more detailed studies need to be performed on the role of bacterial infections in infants. There are many implications arising from this work, particularly the use of vaccination as a means of reducing infections, and consequently the number of SIDS deaths.

Prevalence of medium-chain acyl-coenzyme A dehydrogenase deficiency in the sudden infant death syndrome

Disorders of fatty acid beta-oxidation have been suggested as playing a significant role in the sudden infant death syndrome (SIDS). To elucidate the role of medium-chain acyl-coenzyme A dehydrogenase (MCAD) deficiency in SIDS, we identified all cases of SIDS occurring in Los Angeles County between January 1986 through December 1991. A total of 1304 SIDS deaths were identified; tissue samples were collected in 1236 cases (94.8%). Extraction of DNA was successful in 1224 tissue samples (93.9%), which were examined for the presence of the G985 mutation, identified as occurring in more than 88% of affected cases of MCAD deficiency. Three heterozygotes and no homozygotes were identified; this incidence does not differ from that reported in the general population. Review of the pathologic specimens from the identified heterozygotes and from 18 ethnic-, age-, and sex-matched control subjects revealed significant fatty infiltration of all organs examined in one of the three heterozygotes and in none of the control subjects. We conclude that MCAD deficiency does not play a significant role in the causation of SIDS.

Smoking and the Sudden Infant Death Syndrome

Maternal smoking has been shown to be a risk factor for sudden infant death syndrome (SIDS). The effect of smoking by the father and other household members has not previously been examined. A large nationwide case-control study. Four hundred eighty-five SIDS deaths in the postneonatal age group were compared with 1800 control infants. Infants of mothers who smoked during pregnancy had a 4.09 (95% confidence interval [CI] = 3.28, 5.11) greater risk of death than infants of mothers who did not smoke. Infants of mothers who smoked postnatally also had an increased risk of SIDS compared with infants of nonsmokers and, furthermore, the risk increased with increasing levels of maternal smoking. Smoking by the father and other household members increased the risk (odds ratio [OR] = 2.41, 95% CI = 1.92, 3.02 and OR = 1.54, 95% CI = 1.20, 1.99, respectively). Smoking by the father increased the risk of SIDS if the mother smoked, but had no effect if she did not smoke. In analyses controlled for a wide range of potential confounders, smoking by the mother and father was still significantly associated with an increased risk of SIDS. Passive tobacco smoking is causally related to SIDS.

Relationship of Sudden Infant Death Syndrome to Maternal Smoking During and After Pregnancy

Sudden infant death syndrome (SIDS) is associated with maternal smoking during pregnancy. However, the relationship between tobacco exposure during infancy and SIDS is unknown. The examination of infants whose mothers smoked only after pregnancy will help determine the relationship between passive cigarette exposure during infancy and SIDS risk. This case-control analysis used data on normal birth weight (> or = 2500 g) infants included in the National Maternal and Infant Health Survey, a nationally representative sample of approximately 10,000 births and 6000 infant deaths. Infants were assigned to one of three exposure groups: maternal smoking during both pregnancy and infancy (combined exposure), maternal smoking only during infancy (passive exposure), and no maternal smoking. SIDS death was determined from death certificate coding. Logistic regression was used to adjust for potentially confounding variables. Infants who died of SIDS were more likely to be exposed to maternal cigarette smoke than were surviving infants. Among black infants the odds ratio was 2.4 for passive exposure and 2.9 for combined exposure. Among white infants the odds ratio was 2.2 for passive exposure and 4.1 for combined exposure. After adjustment for demographic risk factors, the odds ratio for SIDS among normal birth weight infants was approximately 2 for passive exposure and 3 for combined exposure for both races. These data suggest that both intrauterine and passive tobacco exposure are associated with an increased risk of SIDS and are further inducement to encourage smoking cessation among pregnant women and families with children.

Sleeping Prone and the Risk of Sudden Infant Death Syndrome

To critically analyze reports that show a relationship between sudden infant death syndrome (SIDS) and the prone sleeping position in infants. Peer-reviewed articles, published letters, book chapters, and local and national health statistics were used, without time or language restrictions. These studies represented three races, four continents, and seven countries; none was published in North America. No studies were ignored, but only those with case controls were reviewed in detail; we regarded a recent cohort analytic (prospective) study as particularly strong, in addition to six before-and-after (intervention) trials. Hill's criteria for decision making were used to assess the quality and validity of the data. Without exception, all studies demonstrated an increased risk for SIDS associated with the prone sleeping position. The published likelihood ratios (relative risk or odds ratio) for SIDS in the prone position compared with SIDS in any other position ranged from 3.5 to 9.3 in seven studies. Publicity against the use of the prone position has been associated with reduction of SIDS by 20% to 67%, paralleling the reduction in use of the prone position, with no increase in deaths from aspiration or in other diagnostic categories. We recommended avoidance of the prone sleeping position for infants in the first 6 months of life unless there is a specific medical indication for it. Reports from the Netherlands, Great Britain, Australia, and New Zealand indicate that avoiding the prone position for infants in the first 6 months of life could reduce the number of SIDS deaths by as much as 50%. Unfortunately, these findings have received little attention in North America. We offer here an analysis of these reports so that physicians can assess the evidence and advise parents accordingly.

Sleep State Organization in Normal Infants and Victims of the Sudden Infant Death Syndrome

Infants at increased risk of the sudden infant death syndrome (SIDS) show abnormal patterning of sleep-waking states. It was hypothesized that infants who were to die of SIDS would show abnormalities of sleep state distribution prior to their deaths. Twenty-two 12-hour recordings were obtained from infants who subsequently died of SIDS, and sleep state patterns were compared in these records and 66 records of age-matched control infants. Each 1-minute epoch was classified as quiet sleep, rapid eye movement (REM) sleep, waking, indeterminate state, or artifact-contaminated. Victims of SIDS showed less waking and more sleep than control infants during the early-morning hours. Victims of SIDS younger than 1 month of age showed significantly more epochs classified as REM sleep across the night and significantly fewer epochs contaminated by artifacts relative to control infants. Further analysis indicated that the increased number of REM epochs resulted from fewer artifact-contaminated epochs, suggesting reduced motility during REM sleep in the SIDS victims compared with the control infants. The finding of decreased waking time during the early morning is of particular importance since most SIDS deaths occur during this portion of the day. The findings of altered sleep patterns in SIDS victims suggest that central neural changes are associated with SIDS risk.

Space time clustering of births in SIDS: do perinatal infections play a role?

The aetiology of sudden infant death syndrome (SIDS) remains uncertain; many causal pathways have been proposed. In this paper we have examined firstly the variation in the risk of SIDS with age, month of death and month of birth; and secondly the space time clustering of SIDS deaths, and, separately, space time clustering of their births. Data were obtained from the Office of Populations, Censuses and Surveys on all certified SIDS deaths in the period; children were assigned grid references for the address of birth and of death. Data on number of births were abstracted from published material. A log-linear modelling technique was used to investigate the separate effects of age, month of death and month of birth on the risk of SIDS. The Knox method was used to investigate space time clustering of deaths and of births of children who died of SIDS. Separate, statistically significant effects were found for age, month of death and month of birth. There was minor space time clustering of SIDS births and deaths at large time and space intervals, and a marked space time clustering of births in short space time intervals in the first quarter of the year. The finding of an effect of month of birth on the risk of SIDS, and of space time clustering of births suggest that a perinatal hazard--possibly of infectious origin--may play a role in the aetiology of SIDS.

The risk of sudden infant death from gastroesophageal reflux

Gastroesophageal reflux (GER) has been a suspected cause of infant deaths and sudden infant death syndrome (SIDS). We examined our 10-year experience with 499 consecutive infants 6 months of age or less who had extended (18 to 24 hours) esophageal pH monitoring performed to evaluate for GER. The data extracted from the esophageal pH records included the pH score, the pattern of GER (type I, II, or III), and the mean duration of reflux during sleep (ZMD). All infants were followed to determine the occurrence and cause of death during the first year of life. Of the 19 deaths found in the series, three were classified as SIDS and two were in-hospital deaths caused by reflux-induced aspiration. All five of these infants who died had a prolonged ZMD (> 3.8 minutes) and received either basic medical (n = 4) or no (n = 1) antireflux therapy. Four infants also had the type I pattern of GER. There was a 9.1% ( 4 44 ; 95% confidence limits, 2.5% to 21.7%) incidence of reflux-related or SIDS deaths in infants with type I GER and a prolonged ZMD who were treated nonoperatively, compared with none ( 0 83 , P = .03) in the same group of infants treated with antireflux surgery. The incidence of SIDS was higher in infants with type I GER and a prolonged ZMD who were treated nonoperatively ( 3 44 , 6.8%) compared with all other infants treated nonoperatively ( 0 265 , o%; P = .003). Infants with type I GER and a prolonged ZMD had a lower incidence of SIDS when treated with antireflux surgery ( 0 83 , 0%) than when treated nonoperatively ( 3 44 , 6.8%; P = .04). In conclusion, GER appears to be a significant cause of infant death and SIDS. Infants at the highest risk for death can be identified with extended esophageal pH monitoring and the definitive elimination of GER can prevent some SIDS deaths.

Sleep Apnea in Infants Who Succumb to The Sudden Infant Death Syndrome

Previous studies have shown the frequency of respiratory pauses to be altered in groups of infants at risk for the sudden infant death syndrome (SIDS). In this study, we assess the frequency of apneic pauses during quiet sleep and rapid eye movement sleep in control infants and infants who subsequently died of SIDS. Sleep states were identified in 12-hour physiological recordings of SIDS victims and matched control infants, and the number of respiratory pauses from 4 to 30 seconds in duration was computed for quiet sleep and rapid eye movement sleep. SIDS victims 40 to 65 days of age showed significantly fewer apneic pauses than did age-matched control infants across the two sleep states. Fewer short respiratory pauses accounted for most of the reduction in number of apneic events in the SIDS victims during both sleep states. During the first month of life, SIDS victims did not differ significantly from control neonates on this measure. The finding that this respiratory difference exists during the second month of life, just before the period of maximal risk for SIDS, but not earlier, may have implications for the etiology of SIDS deaths.

Sudden Death in an Infant with Central Nervous System Abnormalities

Some deaths during the first year of life are classified as sudden infant death syndrome (SIDS), the diagnosis of which requires a complete autopsy without adequate explanation for the death. We report a 1-month-old infant whose clinical history was fairly typical for SIDS. Postmortem examination was remarkable in revealing clinically unsuspected central nervous system (CNS) abnormalities, including lobar holoprosencephaly, absence of the olfactory tracts and grooves (arhinencephaly), subependymal gray matter heterotopias, and delayed myelination. Although the CNS findings do not adequately explain the patient's sudden death, this case illustrates the need for a complete autopsy to include careful CNS evaluation, especially in any presumed SIDS death.

Natural Death as Viewed by the Medical Examiner: A Review of 1000 Consecutive Autopsies of Individuals Dying of Natural Disease

A study of 1000 consecutive autopsies of individuals dying of natural disease was conducted. Cardiovascular disease was responsible for 60.9% of all deaths with coronary artery disease--not only the main cause of cardiovascular death but also the main cause of all natural deaths--accounting for 45.1% of such cases. Diseases of the central nervous and respiratory systems accounted for 8.7 and 8.6%, respectively, of the natural deaths. Seizure disorders and pneumonia were the main causes of death in these organ systems. There were 124 deaths of children less than one year in age, 91 of which were due to sudden infant death syndrome (SIDS). All of the SIDS deaths were in children less than 10 months old.

Sudden infant death syndrome in infants of substance-abusing mothers

A population-based study was performed to determine whether substance abuse during the perinatal period may be a risk factor for sudden infant death syndrome (SIDS). The incidence of SIDS was studied in 2143 infants of substance-abusing mothers (ISAM) born in Los Angeles County during 1986 and 1987 who were reported to the Los Angeles County Department of Health Services because of a history of drug exposure or positive urine test results in the mother, infant, or both. By comparing the ISAM birth reports with records of autopsy-proven SIDS in Los Angeles County, we found 19 SIDS cases in the population of 2143 ISAM, a SIDS rate of 8.87 cases per 1000 ISAM (95% confidence interval 5.3 to 13.8). This was significantly higher than the SIDS rate for the non-ISAM general population: 396 SIDS deaths among 325,372 live births, an incidence rate of 1.22 cases per 1000 births, p less than 0.00001. The age of ISAM at death was 99 +/- 63 (mean +/- SD) days compared with 91 +/- 52 days for the non-ISAM population (not significant). The incidence of SIDS was significantly greater in male infants, during the winter months, in black infants, and in non-Hispanic white infants in the non-ISAM population. Such differences were not observed in the ISAM group. A greater incidence of symptomatic apnea was reported before SIDS for the ISAM than for the non-ISAM population (22% vs 5.4%, p = 0.022). We conclude that ISAM have a higher incidence of SIDS than the non-ISAM general population. However, it was not possible to separate maternal substance abuse from other confounding variables that may also have had an impact on SIDS risk in the ISAM group.

Preventing the sudden infant death syndrome

Current efforts in the US to prevent the sudden infant death syndrome (SIDS) are largely based on pneumocardiogram screening and home apnoea monitoring. This technology does not prevent most SIDS deaths because the screening procedures lack the sensitivity and specificity needed to identify most high risk infants. In the UK the largest efforts to prevent SIDS have been based on infant health surveillance. These efforts appear to have been ineffective and along with the US failures highlight the need for new strategies to prevent SIDS. One strategy might be to develop methods to avoid known risk factors for SIDS. Prominent among these risk factors are cigarette smoking and the use of psychotropic drugs during pregnancy, overheating and infections in infants. Possible approaches to avoid these and other risks are described in the present paper.

Postneonatal mortality in south New Zealand: necropsy data review.

Three southern New Zealand health districts had a postneonatal mortality rate of 8.1 per 1000 livebirths and a postneonatal sudden infant death syndrome (SIDS) mortality rate of 6.3 per 1000 livebirths for the period 1979-1984. This is one of the highest reported rates of SIDS. The 429 postneonatal deaths occurring during the period were assigned to one of four groups: unpreventable (n = 52), possibly preventable non-SIDS (n = 45), SIDS with minor abnormalities at necropsy or premorbid symptoms (n = 167), and SIDS with no abnormalities at necropsy or documented premorbid symptoms (n = 165). These groups were related to obstetric and perinatal data. For those infants classified as SIDS, the winter peak of deaths was particularly marked if death occurred after 3 months of age. These older SIDS deaths had more minor abnormalities at necropsy, a longer interval between time last seen or heard alive and found dead and more thymic petechiae.

Sudden infant death syndrome as a socially determined cause of death.

The background characteristics of infant deaths which have been certified by physicians as due to Sudden Infant Death Syndrome (SIDS) are examined. Two alternative models for explaining SIDS deaths are considered. The first views SIDS solely in medical/biological terms, while the second emphasizes the role played by social and cultural factors, either as contributing conditions or as factors in the misattribution of SIDS as the cause of death where other conditions are actually present. Data are based on linked birth and death certificates for the 1980-82 cohort of live births in Florida, which have been merged with NCHS reports of multiple cause of death. Analysis suggests a pattern of SIDS reporting which varies inversely with maternal education, prenatal care, and race/ethnicity. This pattern suggests either that social factors affect the etiology of the syndrome to a greater degree than would be expected from the medical/biological model or that deaths to infants of lower socioeconomic status are attributed to SIDS more often than warranted.

The pineal gland in sudden infant death syndrome: preliminary observations.

Sudden infant death syndrome (SIDS) affects infants between 1 month and 1 yr of age, has no known cause, and is diagnosed by exclusion of all other causes of death. The primary mechanism of death in SIDS is considered to be irreversible respiratory cessation during sleep. In a small sampling at necropsy we have observed a statistically significant (P less than .005; determined morphometrically) reduction in the anatomic size of the pineal gland in SIDS infants, as compared to age-matched controls. Whether correspondingly altered pineal glandular function is present in SIDS is as yet unanswered.

Sudden infant death syndrome (SIDS): the Metropolitan Dade County experience, 1979-1983.

A study of Sudden Infant Death Syndrome (SIDS) or ‘crib death’ cases was performed on the case files of the office of the Medical Examiner of Metropolitan Dade County in Miami, Florida, during the years 1979 to 1983. One hundred and thirty-nine cases were collected and analysed according to: the rate per thousand live births; racial and ethnic variation in this rate; the age distribution of the victims; the race and sex of the victim; the location of the terminal incident; and the scene circumstances. The rate of occurrence of SIDS in Dade County has decreased overall in the five years studied—more so in white and Spanish-surnamed individuals than in blacks. The victim is most commonly from eight to nine weeks of age or three to six months of age. Most victims were black males. The most common scenario was being found dead after a feeding in a bed at home. Other SIDS deaths in the family were not common. The mother of the decedent most frequently found the victim and fire rescue intervention (cardiopulmonary resuscitation) occurred approximately half the time.

Statistics and Sudden Infant Death Syndrome

To the Editor.— The recent cohort study by Oren et al1 examined risk factors for sudden infant death syndrome (SIDS) in infants with prolonged unexplained sleep apnea with color change (severe apnea of infancy). This analysis revealed three possible risk factors for SIDS death: having a subsequent monitored apnea episode needing resuscitation or vigorous stimulation, being a sibling of a SIDS victim, or developing a seizure disorder after monitoring began. Unfortunately, there are two serious problems with the authors' analysis: the misrepresentation of relative risk and the use of the χ2 statistic to test associations in small subgroups.

Sibling Grief in Reaction to Sudden Infant Death Syndrome

Much of the literature that exists regarding psychologic outcomes of sudden infant death syndrome (SIDS) has focused on parental grief or family response; at least two studies suggest that a SIDS death also affected siblings. It is believed that children who experience the death of a sibling due to SIDS do grieve. Factors related to bereavement are the child's age at the time of the sibling's death, special circumstances of the SIDS death, and explanations and grieving response of the parents. However, no information currently exists that characterizes the course of the grief response of these children. Studies have indicated that about 1 year is a normal grieving period for adults. This study was conducted to evaluate the time frame of children's grief response to the death of a sibling from SIDS. A questionnaire was designed that incorporated child grieving behaviors from several sources; 151 questionnaires were distributed to families in which a SIDS death had occurred in the past 16 years in Iowa and Illinois. Information was obtained from 43 families for 50 children who were older than 2 years of age at the time of the sibling's death. With respect to the length of children's grief response, 54% were reported to have grieved longer than 1 year and only 40% were reported to have grieved less than 6 months. Thus, it appears that the length of the grieving response for these children is similar to that described for adults.

Thiamine deficiency--a neglected problem of infants and mothers--possible relationships to sudden infant death syndrome.

An unexpectedly high incidence of biochemical thiamine deficiency (erythrocyte transketolase) was found in groups of mothers and infants, selected for apparent health from a westernized Caucasian community in Australia. Deficiency was common in mothers at term but not their infants, and in apparently healthy older infants but not their mothers. These findings can be explained by preferential delivery of thiamine to the fetus, at the expense of the pregnant mother; after delivery the mother recovers, and the infant becomes depleted. The incidence of thiamine deficiency was high in 'near-miss' sudden infant death syndrome (SIDS) infants and their mothers, and in siblings of SIDS. The thiamine deficient infants had a high familial incidence of SIDS deaths. These 'high risk families' might reflect poor nutrition or genetic defects of thiamine uptake and metabolism. Since apparently thriving infants with thiamine deficiency can sometimes die unexpectedly, thiamine status deserves more attention in clinical practice and research.