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PubMed1995

Accidental death or sudden infant death syndrome?

OBJECTIVE: To describe the reasons why it is difficult to decide whether to attribute some infant deaths to accidents or to SIDS. METHODOLOGY: To extract from infant deaths data in South Australia those where the cause of death is debatable. RESULTS: The risks associated with rocking cradles, bed sharing, bedclothes, couch sleeping, unsafe cots or beds and the prone position are presented. CONCLUSIONS: Uniform worldwide death scene investigations for all infant deaths should help identify unsafe sleeping conditions for infants.

Accidents, Home↗
PubMed1982

Sudden infant death syndrome in infants with bronchopulmonary dysplasia.

The association between bronchopulmonary dysplasia and sudden infant death syndrome was studied retrospectively in low-birth-weight infants discharged from the neonatal program at Harvard Medical School. The incidence of sudden infant death syndrome was seven times greater in infants with bronchopulmonary dysplasia when compared with a group of control infants without bronchopulmonary dysplasia. Confounding factors, including birth weight, sex, multiple birth, socioeconomic status, and apnea were evaluated. The results indicate that there is an association between bronchopulmonary dysplasia and sudden infant death syndrome.

Apnea↗
PubMed1995

Cytokines may give insight into mechanisms of death in sudden infant death syndrome.

There are a number of postulated causes of sudden infant death syndrome, including bacterial toxins, defects in thermoregulation and hypersensitivity. This paper formulates the hypothesis that analysis of cytokine profiles in suspected sudden infant death syndrome victims may give an insight into mechanisms of death. These cytokine profiles may also help to identify specific causes of sudden infant death syndrome or indicate that different causes act in concert in individual cases.

Allergens↗
PubMed1997

Risk status at discharge and cause of death for postneonatal infant deaths: a total population study.

OBJECTIVES: To obtain population-based, clinical information regarding potentially modifiable factors contributing to death during the postneonatal period (28 to 364 days), we examined all postneonatal infant deaths in four areas of the United States to determine: (1) the cause of death from clinical and autopsy data rather than vital statistics, (2) whether death occurred during initial hospitalization or after discharge, and (3) the portion of postneonatal mortality attributable to infants who left the hospital with identified high-risk medical conditions. DESIGN AND SETTING: Retrospective medical record review of all postneonatal infant deaths with birth weights greater than 500 g (total N = 386) born to mothers residing in: (1) the city of Boston (1984 and 1985, N = 55), (2) the city of St Louis and contiguous areas (1985 and 1986, N = 123), (3) San Diego County (1985, N = 112), and (4) the state of Maine (1984 and 1985, N = 96). Deaths were identified using linked birth and death vital statistics, and medical record audits of infants' and mothers' charts were performed. Causes of death were obtained from medical record review in conjunction with autopsy if performed (72%, N = 278), medical record alone (17%, N = 67), or vital statistics if no other source was available (11%, N = 41). The medical conditions at the time of discharge for each infant were reviewed and, if judged to confer an increased risk of morbidity or mortality, were classified as high risk. RESULTS: The causes of death were sudden infant death syndrome (47%, N = 181), congenital conditions (20%, N = 77), prematurity-related conditions (11%, N = 43), infections (9%, N = 34), external causes (including injuries, drownings, ingestions, and burns) (7%, N = 25), and other (6%, N = 23). In 24% of congenital and 25% to 44% of prematurity-related deaths, infection was the acute or associated cause of death. Infants born to black mothers were more likely than those born to white mothers to die during the postneonatal period of all major causes of death (7.3 per 1000 vs 3.0 per 1000). Overall, 18% (N = 68) of deaths occurred to infants who never left the hospital; 79% (N = 305) of the infants were discharged before death; and discharge status was unknown in 3% (N = 13). Eighty-one percent of all infants with prematurity-related postneonatal deaths were never discharged, and of the total infants who were initially discharged, only 1% (N = 4) subsequently died of prematurity-related causes. Of all postneonatal deaths, only 16% (N = 62) left the hospital with identified high-risk medical conditions. CONCLUSIONS: These findings suggest that the etiology of postneonatal mortality is heterogeneous, with significant complexity in attributing specific causes of death and making designations of "preventability." The vast majority of infants who died of prematurity-related postneonatal causes never left the hospital, and only a small percentage of all infants that left the hospital before death were identified as being at high medical risk. Therefore, strategies for further decreasing postneonatal mortality must link high-risk follow-up programs to more comprehensive strategies that address risk throughout pregnancy and early childhood.

Cause of Death↗
PubMed1978

Liberalized abortion in Oregon: effects on fertility, prematurity, fetal death, and infant death.

An analysis of Oregon Vital Statistics data from 1965 to 1975 was conducted to assess the impact of Oregon's 1969 abortion legislation, which substantially increased the number of reported medically induced abortions. This increase was associated with a slight increase in the age-adjusted 1970 fertility rate and there was no decrease in births to women in the age groups obtaining proportionately the most abortions. A significant and persistent 11 per cent reduction in premature births to women over age 20 (p less than .001) and a 22 per cent reduction in spontaneous fetal deaths (p less than .05) were associated with liberalized abortion. Decreases in neonatal and postneonatal infant mortality were observed, but were indistinguishable from an ongoing trend toward improved infant health. A gradual 25 per cent decline in the age-adjusted fertility rate occurred between 1969 and 1975, but the increase in the number of reported abortions could account for only one-fourth of this decrease. A seven-fold increase in the use of family planning clinics between 1970 and 1973 and more liberalized laws regarding provision of family planning service appeared to account for a much higher proportion of the decreased fertility than did liberalized abortion.

Abortion, Legal↗
PubMed1983

Relationship between infant death and maternal age. Comparison of sudden infant death incidence with other causes of infant mortality.

The high incidence of sudden infant death syndrome in infants born to teenage mothers prompted us to search for epidemiologic clues that might relate to SIDS causation. The death rate for SIDS was compared with that of other major causes of infant mortality in two maternal age groups (younger than 20 years and 30 to 34 years). In the neonatal period, a significantly greater overall mortality occurred in infants born to the younger mothers. This difference was primarily related to an excess of low-birth-weight infants dying from diseases of early infancy. "Weight-specific" mortality, however, was similar for the two groups. In the postneonatal period, when most SIDS occurs, the incidence was 5.2 per 1000 among infants of teenage mothers, compared with 1.0 in infants of the older mothers. A similar maternal-age-related incidence was observed for death from infections, accidents, and "other causes." By contrast, death from congenital anomalies was unrelated to maternal age in both periods. We conclude that many postneonatal deaths are influenced by environmental factors, including the age and maturity of the mother.

Adolescent↗
PubMed1986

Sudden infant death syndrome in infants evaluated by apnea programs in California.

Home apnea/bradycardia monitoring is frequently used in the management of infants at increased risk for sudden infant death syndrome (SIDS). However, some infants have died despite evaluation by infant apnea programs, and the benefits of home monitoring remain unproven. To determine the SIDS rate and risk factors of infants evaluated by infant apnea programs, 31 apnea programs and ten home monitor vendors in California were surveyed. Eleven (35%) of the apnea programs and four (40%) of the vendors responded. Information was obtained on 26 infants who died. Thirteen (50%) deaths were due to SIDS. Abnormal sleep studies did not predict death. Fifteen infants died despite a recommendation for home monitoring. Seven deaths occurred in association with technical errors or noncompliance with monitoring. Four deaths were due to nonaccidental trauma. The apnea programs evaluated 3,406 infants during a 5-year period; 1,841 had monitoring recommended. Term infants with apnea, subsequent siblings of SIDS victims, and infants evaluated at referral centers were more likely to have monitoring recommended than premature infants with apnea or infants evaluated at nonreferral centers (P less than .0001). Infants who had monitoring recommended were at equal risk of dying of SIDS as those who did not.

California↗
PubMed1995

Comparison of [125I]iodomelatonin binding sites in infant cerebellum of sudden infant death syndrome and non-sudden infant death syndrome.

[125I]Iodomelatonin bindings sites in human infant cerebellum were studied by radioligand receptor binding assay and in vitro quantitative autoradiography. The binding sites characterized in membrane preparations revealed saturable, reversible and highly specific binding sites with a Kd value of 21.2 +/- 8.33 pM and a Bmax value of 2.02 +/- 0.52 fmol/mg protein. 10 microM of GTP gamma S significantly reduced the binding capacity, suggesting the possible G-protein coupling of the binding sites. Autoradiographic study showed that the labelling was mainly located in the cerebellar cortex. On comparison of the binding parameters from cerebellum of sudden infant death syndrome (SIDS) and non-SIDS infants, no significant change in binding capacity and binding affinity was detected. These findings suggest that the binding sites in cerebellum may not be related to the etiology of SIDS.

Analysis of Variance↗
PubMed1986

Identification of a high-risk group for sudden infant death syndrome among infants who were resuscitated for sleep apnea.

Of the 1,153 infants who completed monitoring by Aug 1, 1984, through our program at Massachusetts General Hospital, 76 infants had an initial apnea spell during sleep which was characterized by a change in tone and color, was unresponsive to repeated vigorous stimulation, and was terminated only after mouth to mouth resuscitation. The infants were hospitalized for observation and evaluation, and no cause could be identified. All were discharged on a home apnea or cardiorespiratory monitor, and subsequent episodes of apnea and/or bradycardia were reviewed. We grouped infants based on the intervention used to terminate subsequent episodes: Group 1, resuscitation; group 2, vigorous stimulation; and group 3, neither resuscitation or vigorous stimulation. There was no significant difference in clinical features or in the results of the initial evaluation in groups 1 and 2, compared with group 3. However, the mortality rate was significantly higher in group 1 (4/13) and group 2 (3/12) than in group 3 (3/51) (P less than .007). Siblings of victims of sudden infant death syndrome (n = 8) were at a significantly higher risk of an adverse outcome (two deaths and four resuscitations) than nonsiblings (P less than .02). A seizure disorder that developed during monitoring was associated with a high mortality (4/11 v 6/65, P less than .02). We conclude that these relatively rare infants who have sleep-onset apnea that responded only to resuscitation and have a subsequent similar episode or are siblings of victims of sudden infant death syndrome or develop a seizure disorder during monitoring have a very high risk of dying (31%, 25%, and 36% respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Bradycardia↗
PubMed2005

Unexpected perinatal death and sudden infant death syndrome (SIDS): anatomopathologic and legal aspects.

This work intends to be a review of the recent histopathological findings elicited by research into sudden and unexpected perinatal death and sudden infant death syndrome (SIDS) that have dictated a novel approach to the inherent problems by pathologists, especially those entrusted with forensic medical authority. The new approach stems from the recent advances made in the understanding of neuro- and/or cardiac-conduction-system diseases present in unexpected perinatal death and SIDS. These demand that an accurate morphologic examination be performed of these structures, which modulate respiratory, cardiovascular, digestive, and arousal activities, in all victims of sudden death. A histopathologic study of an ample register of cases of victims of sudden death, either perinatally or in early infancy, has demonstrated frequent alterations both of the autonomic nervous system (especially hypoplasia of the arcuate nucleus) and of the cardiac conduction system (accessory atrioventricular pathways). The present research provides an in-depth study of the many still-controversial aspects underlying perinatal unexpected death and SIDS and is recommended for professionals working in the forensic field, whose greater insight into this problem will allow more complete medicolegal documentation.

Autonomic Nervous System↗
PubMed1993

Numbers of infant deaths in Scotland, with special reference to sudden infant death syndrome.

There has been an increased interest during 1992 in the numbers of deaths from Sudden Infant Death Syndrome, because of reports of reductions in the numbers in several countries where changes in advice on infant care had been made. Numbers of infant deaths in general and of those due to the syndrome in particular are described and analysed by some of the variables which are provided at the time of registration. The decline in the number of deaths from the syndrome reported recently by the Scottish Cot Death Trust is supported by the full figures for 1991. This decline probably started about the latter part of 1990, well before the official letters giving advice on infant care that had been associated with a decline elsewhere. It was more marked in some areas of Scotland than others. There appears to be a cyclical pattern in the time-series of the numbers of deaths from the syndrome. Further investigation, both of the cyclical movement and of the recent decline in relation to other variables, would be worthwhile. Deaths in the neonatal period from the syndrome and those from other causes have both declined markedly during 1990 and 1991, after several years when the movements in their numbers seemed to be in opposite directions.

Age Factors↗
PubMed1988

Deaths from sudden infant death syndrome on public holidays and weekends.

Deaths from sudden infant death syndrome (SIDS) between 1979 and 1984 were tabulated by month for weekdays, weekends and public holidays. Examination of deaths by day of the week showed the weekend had more deaths than the weekdays (chi 2 = 26.3, df = 6, p = 0.0002) and that this pattern occurred in both the under three months and three-11 months age group. There were 40 deaths on the 78 public holidays in the six years under study. Modelling the data showed that there was no difference between the number of deaths on holidays compared to weekends.

Holidays↗
PubMed1989

Sudden infant death and chronic infant disorders: the N.E.S.T. model versus the lethal Cot-death syndrome hoax.

The Cot-death Syndrome is an out-moded model which is bizarre and unique in medical history for it enables a certificate of cause of death to be issued only if no medical cause can be found. It rewards incompetence. Apart from being a placebo for bereaved parents and a lucrative source of research funds it is unsupportable, lethal nonsense and it must be discarded. There are studies which prove that most infant death and chronic infant illnesses are linked and are primarily associated with environmental stress. The infant death problem is not a medical problem except where the stress trauma is of medical origin. The N.E.S.T. (Non-disease Environmental Stress Trauma) perspective provides a model which has elements of causation, prediction and prevention. It requires that intense investigation be carried out in an unbiased manner that is not hindered by a convenience syndrome barrier to truth. Unfortunately twenty years of adherence to the medical profession's Cot-death Syndrome hoax has meant that the evidence pin-pointing specific, causative environmental stress factors has been denigrated and disregarded. This has permitted the asthma convenience syndrome to thrive. Still-birth or infant death that is not due to disease or inherited causation can only be caused by environment stress trauma. Identifying and preventing such stress trauma is the key to healthy birth and to avoiding infant death and chronic infant disorders.

Environment↗
PubMed1988

Risk of sudden infant death syndrome among infants with in utero exposure to cocaine.

To determine whether the risk of sudden infant death syndrome (SIDS) among infants exposed to cocaine in utero may be elevated, we assessed the risk for SIDS in a large, well-described, prospective cohort of infants whose mothers had or had not used cocaine during pregnancy. Of 996 women consecutively enrolled while registering for prenatal care, 175 used cocaine during pregnancy. Only one infant of the mothers who used cocaine died of SIDS, a risk of 5.6 in 1000, compared with four infants among the 821 nonexposed infants, a risk of 4.9 in 1000. The relative risk for SIDS among infants whose mothers used cocaine during pregnancy compared with those whose mothers did not use cocaine was 1.17 (95% confidence interval 0.13, 10.43), suggesting that there is no increased risk of SIDS among infants exposed in utero to cocaine.

Adult↗