Sudden infant death syndrome. Many infants move from position in which they are put to sleep.
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Humans↗
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Sudden infant death syndrome and infant apnea: current questions, clinical management, and research directions.
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Apnea↗
Project LID (lower infant deaths). Lessons learned from a local infant mortality review project.
Project LID (Lower Infant Deaths) is an infant mortality review project conducted by the Minneapolis Department of Health and Family Support and the Saint Paul-Ramsey County Department of Public Health. Infant death occurs when a live-born infant dies before age 1. Multidisciplinary teams reviewed 112 infant-mother cases involving infant death using vital and medical records. Open-ended maternal interviews were conducted for approximately half of the cases. This combination of quantitative and qualitative data provided insights into the contributing social, medical, and environmental factors experienced by some families in Hennepin and Ramsey counties. Case review teams developed recommendations to address factors identified in each case. Recommendations are directed to health care providers, professional societies, health systems, government organizations, policymakers, and community- and school-based organizations. This article describes findings from the project and presents recommendations for Minnesota physicians with practices in obstetrics, family medicine, and pediatrics.
Adolescent↗
Polygraphic features of a victim of sudden infant death syndrome and of infants with apparent life-threatening event.
We analyzed a polygram of a victim of sudden infant death syndrome (SIDS) which had been taken five weeks prior to his death. The findings are discussed in association with the serial polygraphic observations of four infants who had suffered from apparent life-threatening event (ALTE), and twenty neurologically normal infants. Frequencies of respiratory pauses were high in SIDS, and average durations of respiratory pauses showed higher values in ALTE than in the controls. Normal paradoxical motions between chest and abdominal wall during active sleep period (AS) were completely abolished in the records of SIDS and of one ALTE. Normal developmental decreases of localized movements (LMs) on mental muscle with age were insufficient in ALTE. The numbers of twitch movements (TMs) were low in SIDS and in two of ALTE, while those of gross movements in the subjects were identical with those in the controls. Dissociation indexes (ratio of the number of TMs against the sum of the numbers of TMs and LMs) were low in SIDS and in two of ALTE. These findings seemed to be the physiological reflection of the impairment of arousal responsiveness and of the developmental disturbance of the brainstem in SIDS and ALTE. Polygraphic evaluations on the respiratory pattern during AS and the dissociation state of TMs from LMs may be helpful in the early detection of SIDS and/or ALTE in asymptomatic infants.
Brain↗
Unnatural causes of sudden unexpected deaths initially thought to be sudden infant death syndrome.
The aim of this clinicopathological study was to determine the frequency of infant deaths due to unnatural causes among cases of sudden and unexpected infant death. Nine institutes of legal medicine in Germany that took part in the German study on Sudden Infant Death Syndrome (GeSID), representing 35% of the German territory, investigated in a 3-year period (from 1998 to 2001) 339 cases of infant death that were not expected to be due to unnatural causes from the first external examination. All cases were investigated by complete, standardised, post-mortem examination including death scene investigation, autopsy, histology, toxicology and neuropathology. The frequency of unnatural deaths was 5.0% (n=17). The causes of death were head injury (n=7), suffocation (n=5), poisoning (n=2), neglect (n=2) and septicaemia due to aspiration of a foreign body (n=1). Two deaths were unsuspected accidents and 12 were due to infanticide. In 3 cases, it was not possible to differentiate between accidental death and infanticide. A complete postmortem examination including an analysis of the clinical history, death scene investigation, autopsy, histology, toxicology, and neuropathology is mandatory to differentiate sudden and unexpected deaths due to natural causes (e.g. SIDS) and cases of unnatural death.
Autopsy↗
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.
Humans↗
Cortisol levels and control of inflammatory responses to toxic shock syndrome toxin-1 (TSST-1): the prevalence of night-time deaths in sudden infant death syndrome (SIDS).
There is evidence that inflammatory responses have been induced in the tissues and body fluids of many SIDS infants. We suggested that some of these deaths are due to uncontrolled inflammatory responses to infectious agents and possibly cigarette smoke. The majority of SIDS deaths occur during the 2-4 month age range when infants have decreasing levels of maternal antibodies to infectious agents. Most deaths occur during the early hours of the morning. Adults are more susceptible to inflammatory responses at night due to lower levels of cortisol associated with circadian rhythm patterns. Infants develop these patterns between the ages of 7 weeks and 4 months, at which time their night-time cortisol levels drop dramatically. The objective of this study was to use an in vitro model system to assess the effects of different cortisol levels on proinflammatory cytokine production in response to the staphylococcal toxic shock syndrome toxin-1 (TSST-1) which has been identified in a significant number of SIDS infants. Levels of cortisol present in infants at night and during the day before and after the development of the circadian rhythm pattern were examined. Human buffy coats (n = 9) were stimulated with TSST-1 and responses assessed over 72 hours by a bioassay for tumour necrosis factor-alpha (TNF-alpha) and an enzyme linked immunosorbent assay (ELISA) for interleukin-6 (IL-6). Cortisol levels present in an infant at night after development of circadian rhythm (< or = 5 microg dl(-1)), did not significantly increase or decrease production of either TNF-alpha or IL-6. Concentrations of cortisol greater than 5 microg dl(-1) usually found in infants during the day or at night prior to the physiological change significantly decreased production of TNF-alpha at 12 hours and of IL-6 at 12 and 16 hours. Only cortisol levels greater than 5 microg dl(-1) significantly decreased production of the pro-inflammatory cytokines by human buffy coats stimulated with TSST-1. If the switch to the circadian rhythm pattern occurs in an infant when maternal antibodies are still present or after they have developed their own active immunity, the infant could neutralise common viruses, toxins or bacteria: however, if this switch occurs in an infant when antibody levels are low, this could be a window of vulnerability during which infants are at an increased risk of death if uncontrolled inflammatory responses are induced by infectious agents or their products.
Bacterial Toxins↗
Can risk factors for over-heating explain epidemiological features of sudden infant death syndrome?
Sudden infant death syndrome is characterized by a number of epidemiological features that have defied simple explanation. Overheating is believed to play a role in its causation. Overheating can be caused by changes in heat production, changes in insulation of the infant, or changes in the external environmental temperature. Risk factors may influence any of these variables. A model is proposed which links risk factors for overheating to the epidemiological distribution of sudden infant death syndrome. This model might account for the frequently reported association between formula-feeding and sudden infant death syndrome.
Body Temperature Regulation↗
[LHRH in the human hypothalamus. Immunohistochemical mapping in normal newborn infants or in sudden death infants].
The topographical distribution of neurons containing LHRH has been investigated in newborn hypothalamus using the peroxidase anti-peroxidase technique. In control subjects, LHRH immunoreactive (LHRH-IR) perikarya have been mainly observed essentially in the infundibular nucleus. The preoptic region displayed a moderate density of LHRH-IR cell bodies. High LHRH innervation was observed in the anterior hypothalamus in the lamina terminalis and in the mediobasal hypothalamus in the median eminence, and in the peri- and paraventricular regions. In sudden death infant syndrome, a comparable mapping was observed, except a low density in the mediobasal peri- and paraventricular areas.
Brain Mapping↗
Sleep position and bed-sharing in sudden infant deaths: an examination of autopsy findings.
OBJECTIVE: To determine the effect of sleep position, sleep location, and bed-sharing on the incidence of sudden unexpected death in infancy and the frequency of significant autopsy findings. METHODS: We evaluated the cause of death in infants <1 year of age who died during sleep from January 1, 1986, through September 30, 1999. This retrospective series was compiled from log books and files of the Medical Examiner Office, Palm Beach County, Florida. RESULTS: The incidence of sudden unexpected infant death decreased 50% over the study period (P <.01). Of the 217 infants that fit the study criteria, 62.7% were sleeping prone (on the stomach), 9.7% were supine (on the back), 5.5% were on their side, 22.1% were in an unknown position, and 40.1% were bed-sharing. Significant autopsy findings that could explain death were documented by autopsy in 37.5% of all supine and side sleeping infants and only 14.0% of all prone sleeping infants (P <.001). Deaths of supine and side sleeping infants were more likely to be classified as a natural disease process other than sudden infant death syndrome (P <.01). Significant autopsy findings that could explain death were found in 47.6% of the infants sleeping alone in the supine or side position (P <.01), 18.2% of infants bed-sharing in the supine or side position, 16.5% of infants sleeping alone while prone, and 9.3% of infants bed-sharing while prone. CONCLUSIONS: Infant deaths associated with the prone position were less frequently explained by illness or disease than infant deaths associated with non-prone sleeping positions. Bed-sharing appears to increase the proportion of unexplained deaths, regardless of the position of the infant. The "Back to Sleep" campaign appears to be effective in reducing the incidence of unexpected sleeping infant deaths regardless of the certified cause of death.
Female↗
Near-miss sudden infant death syndrome in eight infants with sleep apnea-related cardiac arrhythmias.
Eight full-term infants between 3 and 8 weeks of age, who had had 24 to 48 hours of vague problems involving a congested upper airway and/or irritability, had a life-threatening respiratory episode at home, called a near-miss for sudden infant death syndrome event. Polygraphically monitored mixed apneas occurred in clusters during non-rapid eye movement (NREM) sleep with significant cardiac arrhythmias, predominantly sinus arrest. The cardiorespiratory problems continued during sleep in the following 8 to 12 weeks but did not recur after that time, and there were no long-term sequelae when the children were studied again 4 to 7 years later.
Arrhythmias, Cardiac↗
Effects of heavy maternal smoking on intrauterine growth patterns in sudden infant death victims and surviving infants.
UNLABELLED: Sudden infant death (SID) is associated with both intrauterine growth retardation and maternal smoking during pregnancy. Here, we investigated if the statistical association between maternal smoking and SID is direct or mediated through the well-known growth retarding effects of heavy maternal smoking on the fetoplacental unit. We analysed data from a population-based prospective cohort study (181 cases, total newborn population 227,791 births) within the Westphalian Perinatal Inquiry in Germany between 1990 and 1994. SID victims whose mothers did not smoke had a normal mean birth weight (mean 3415.5 vs 3431.5 g), length (mean 51.46 vs 51.66 cm), and body mass index (BMI) (mean 12.8 vs 12.8 kg/m2) when compared to surviving children. In contrast, SID victims of mothers who smoked heavily (> ten cigarettes per day) had a significantly lower birth weight (2911.21 g vs 3148.34 g), length (48.98 vs 50.39 cm), and BMI (11.8 vs 12.4 kg/m2) when compared to surviving children whose mothers smoked heavily. Stratification for gestational age revealed that these differences are mainly caused by preterm SID infants. CONCLUSION: The statistical association between maternal smoking and SID mainly results from effects of tobacco smoke on the fetoplacental unit which, in later SID victims, appears to be more susceptible to the growth retarding effects of cigarette smoking.
Birth Weight↗
Arousal responses in near-miss sudden infant death syndrome and in normal infants.
Hypercarbic and hypoxic arousal responses were measured in 22 normal and 11 near-miss sudden infant death syndrome infants during natural sleep. End-tidal PCO2, (PACO2), transcutaneous PO2, electrocardiogram and heart rate, and thoracic and abdominal circumference were continuously recorded. The essential behavioral criteria for arousal were eye opening and crying. For each hypercarbic arousal test, step increases in FICO2 were made until arousal occurred or until PACO2 reached 65 mm Hg. For each hypoxic arousal, step decreases in FIO2 were made until arousal occurred or until FIO2 = 0.15 had been maintained for 20 minutes. The hypercarbic arousal threshold was significantly higher in near-miss SIDS than in normal infants, 54.9 +/- 2.3 vs 48.4 +/- 1.4, respectively ((P less than 0.05). An arousal response to hypoxia occurred in only 9% of near-miss SIDS infants compared to 70% of normal infants (P less than 0.01). The level of respiratory chemostimulation required to produce an arousal response from sleep is significantly greater in near-miss SIDS than in normal infants. We speculate that deficient arousal responsiveness, especially to hypoxia, may prevent potential SIDS victims from responding appropriately to apneic asphyxia.
Arousal↗
Incongruent cerebral growth in sudden infant death syndrome.
Sudden infant death syndrome remains a leading cause of post-neonatal mortality in developed countries. Its etiopathogenic mechanisms are unknown. In this neuropathologic study, we noticed that the weights of the brains of infants who died from sudden infant death syndrome (n = 97) were invariably heavier in comparison with those of a group of age-matched controls (n = 23) issuing from the same local population. Brain edema was not a major element, and there were no significant microscopic or macroscopic cerebral anomalies in the brains from either of the study groups. Head circumference did not show a parallel increase in infants with sudden infant death syndrome. The excessive brain weight might reflect abnormal cerebral development and could be detrimental to vital neural control. In a previous study, we disclosed cytokine overexpression in the brains of these victims. Whether increased brain weight is linked to cytokine up-regulation remains, however, a moot case and merits further exploration.
Brain↗
Gender differences in parental psychological distress following perinatal death or sudden infant death syndrome.
BACKGROUND: Stress responses of bereaved parents (mothers 194, fathers 143) who experienced infant loss were compared with parents (mothers 203, fathers 157) with a live born child. METHOD: Psychological distress using scales of anxiety, depression and alcohol use was compared at 2, 8, 15 and 30 months post-loss. RESULTS: Bereaved mothers showed significantly more anxiety/depression than controls at all four interviews. For bereaved fathers, anxiety/depression differed significantly from controls only at two months. Heavy alcohol use was significantly more prevalent at 2 and 30 months. Relative risks showed significant gender differences between bereaved parents at all four interviews for anxiety/depression. When this outcome was extended to include heavy drinking in addition to anxiety/depression, these differences diminished and were significant only at 2 and 8 months. CONCLUSION. Female responses are longer lasting and reflected by elevated levels of anxiety/depression. Male responses equally involve anxiety, depression and heavy alcohol consumption.
Adult↗
Trends in postneonatal aspiration deaths and reclassification of sudden infant death syndrome: impact of the "Back to Sleep" program.
OBJECTIVE: The introduction of the "Back to Sleep" campaign for the prevention of sudden infant death syndrome (SIDS) brought with it concern that there might be an increase in the incidence of aspiration-related deaths. The objective of this analysis was to describe the trends in postneonatal mortality and proportionate mortality ratios for the United States for the years 1991 to 1996 for aspiration-related deaths and other causes to which a SIDS death could conceivably be reclassified. METHODS: Linked birth and infant death vital statistic files for the United States were used for the years 1991, 1995, and 1996. US Vital Statistic Mortality files for the years 1992, 1993, and 1994 were used because of the absence of linked files for those years. RESULTS: The overall postneonatal mortality rate between 1991 and 1996 declined 21.9%, whereas the SIDS rate declined 38.9%. The proportion of the postneonatal mortality (PNPMR) contributed by SIDS declined from 37.1% in 1991 to 28.8% in 1996. There was no significant increase in the PNPMR for aspiration, asphyxia, or respiratory failure. There was, however, a significant increase in the PNPMR for suffocation in bed or cradle from 0.9 to 1.3. CONCLUSIONS: These data show no evidence of an increased risk of death from aspiration as a result of the "Back to Sleep" program. Although there has been an increase in the proportion of postneonatal mortality attributable to suffocation, this represents a very small proportion of postneonatal mortality and thus potentially a very small number of SIDS deaths reclassified as suffocation.
Adult↗
Clostridium botulinum and sudden infant death syndrome: a 10 year prospective study.
It has been proposed that sudden and unexpected death in infants due to intestinal infection with Clostridium botulinum may mimic the clinicopathological features of sudden infant death syndrome. Between 3.3 and 3.8% of infants in some series have had this neurotoxin-producing bacterium isolated on faecal culture. Prospective screening of 248 infants presenting with the sudden infant death syndrome to the Adelaide Children's Hospital over a 10 year period from 1981 to 1990 was conducted. Faecal samples were obtained from both small and large intestines and cultured specifically for C. botulinum. No samples were positive. The results of this study suggest that routine post-mortem culture of faeces for C. botulinum has been of limited use within the South Australian infant population over the last decade, and that occult botulism has not been a significant factor in the causation of sudden death.
Botulism↗
The VIIIth ESPID Conference (European Society for the Study and Prevention of Infant Death), the International Conference on Prevention of Infantile Apnea and Sudden Infant Death on the Verge of the Millenium. Jerusalem, Israel, May 30-June 3, 1999. Abstracts.
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Humans↗