Postneonatal Infant Death Research Articles

The correlation between microtubule-associated protein 2 in the brainstem of SIDS victims and physiological data on sleep apnea

Background: Microtubule-associated protein 2 (MAP2), a cytoskeletal protein of the neuron, is a marker of early ischemic neuronal damage. As a chronic hypoxic situation exists in the brains of victims of the sudden infant death syndrome (SIDS), the correlation between MAP2-positive neurons or dendritic spines in the brainstem and sleep apnea was investigated in SIDS, which is still the main cause of postneonatal infant death. Materials and methods: Twenty-seven thousand infants were studied prospectively to characterize their sleep–wake behavior and amongst these, 38 infants died under 6 months of age. They included 26 cases of SIDS. The frequency and duration of sleep apneae were analyzed. The brainstem material was collected and immunohistochemistry of MAP2 was carried out. The density of MAP2-positive neurons, dendrites, and dendritic spines were measured quantitatively. Correlation analyses were carried out between the MAP2-associated pathological data and the physiological data of sleep apnea. Results: One negative correlation between the density of MAP2-positive endrites in the pars compacta of pedunculo-pontine tegmentum nucleus (PPTNc) and the duration of obstructive apnea ( P=0.017) and two SIDS-specific positive correlations between the density of MAP2-positive dendrites in the pars dissipata of pedunculo-pontine tegmentum nucleus (PPTNd) and the duration of central apnea ( P=0.005) and between the dorsal raphe and the frequency of obstructive apnea were found in SIDS victims. The density of MAP2-positive dendritic spines in PPTNc was significantly higher in SIDS than in control ( P=0.034). Conclusions: The significant correlations with the MAP2-positive findings in the midbrain arousal pathway and the characteristics of sleep apnea in SIDS victims were in agreement with the association with apnea and arousal-deficiency in SIDS.

Correlation between the Ki-67 antigen in the brainstem and physiological data on sleep apnea in SIDS victims

Background: The Ki-67 antigen appears in all human proliferating cells during late G1, S, M and G2 phases of the cell cycle, but is consistently absent in the G o phase (noncycling) cells. The correlation between Ki-67 in the brainstem and sleep apnea in victims of the sudden infant death syndrome (SIDS) was investigated to elucidate cell kinetics in the brainstem of this condition, which is still the main cause of postneonatal infant death. Materials and methods: Twenty-six cases of SIDS occurred among 38 infants dying under 6 months of age in a cohort of 27,000 infants studied prospectively to characterize their sleep–wake behavior. All the infants had been recorded during one night in a pediatric sleep laboratory some 3–12 weeks before death. The frequency and duration of sleep apnea were analyzed. At autopsy, brainstem material was collected and immunohistochemistry for Ki-67 was carried out. The density of Ki-67-positive neurons was measured semiquantitatively. Correlation analyses were carried out between the density of Ki-67-positive neurons and the data on sleep apnea. Results: Except in two cases in SIDS victims and in one control, the detection of Ki-67 was negative. No correlation analysis between the Ki-67 and of sleep apnea was found. Conclusions: There were no abnormal cell kinetics detected by the demonstration of Ki-67 antigen in the brainstems of SIDS victims.

α2-Adrenergic receptor subtype alterations in the brainstem in the sudden infant death syndrome

Background: The sudden infant death syndrome (SIDS) is still the main cause of postneonatal infant death. However, the causes and mechanisms of SIDS have never been completely elucidated. Catecholamines, via α2-adrenergic receptor (α2-AR) interactions, are known to influence brainstem autonomic and respiratory activity. Aims: To examine the catecholaminergic system abnormalities in SIDS victims, we investigated the alterations of α2-AR subtypes. Subjects and methods: We examined the developmental changes of α2-AR subtypes in the brainstem, especially in cardiorespiratory nuclei, in 21 SIDS victims and 17 age-matched controls by means of immunohistochemical methods. For statistical analysis, the χ 2-test or Fisher's exact probability test was performed. Results: There was a significant decrease in α2A-AR immunoreactivity in the solitary nucleus and ventrolateral medulla (VLM) in the medulla oblongata in SIDS victims compared with in control cases, but there were no significant differences of the α2B and α2C-AR immunoreactivity in the brainstem between SIDS victims and controls. Conclusion: α2A-AR immunoreactivity was selectively decreased in the solitary nucleus and VLM in the medulla oblongata in SIDS victims, so there was no possibility that it was secondary to chronic hypoxia or repeated ischemia. It may be related to some impairment of the cardiorespiratory neuronal system. Therefore, SIDS victims may be vulnerable to asphyxia, hypoxia, and/or hypercapnia, and fail to exhibit brainstem responses.

Clinicopathological correlation between brainstem gliosis using GFAP as a marker and sleep apnea in the sudden infant death syndrome

Background: Chronic hypoxia, leading to brainstem gliosis, has been postulated as a factor in the sudden infant death syndrome (SIDS), which is still the main cause of postneonatal infant death. Gliosis detected by immunohistochemistry of glial fibrillary acidic protein (GFAP) is a marker of apoptosis. The correlation between GFAP-positive reactive astrocytes in the brainstem and sleep apnea in SIDS was investigated. Materials and Methods: Among 27,000 infants studied prospectively to characterize their sleep–wake behavior, 38 infants died under 6 months of age, including 26 cases of SIDS. The frequency and duration of sleep apnea were analyzed. Brainstem material was collected and immunohistochemistry of GFAP carried out. The density of GFAP-positive reactive astrocytes was measured quantitatively. Correlation analyses were carried out between the data on gliosis and the physiological data of sleep apnea. Results: A SIDS-specific negative correlation between the density of gliosis in the dorsal vagus nucleus in the medulla oblongata and the frequency of obstructive apnea ( p=0.022) was found. Conclusions: A significant SIDS-specific correlation with gliosis in the dorsal vagus nucleus and the characteristics of sleep apnea might invite the cardiorespiratory changes in SIDS.

The relationship between neuronal plasticity and serotonergic neurons in the brainstem of SIDS victims

Background: The sudden infant death syndrome (SIDS) is still the main cause of postneonatal infant death and its cause is still unknown. Recently, the medullary serotonergic network deficiency theory has been proposed and an association between SIDS and neuronal plasticity has also been suggested. The growth-associated phosphoprotein 43 (GAP43) is a marker of synaptic plasticity and is critical for normal development of the serotonergic innervation. Therefore, the characteristics of GAP43-positive elements and their association with serotonergic neurons were here investigated in the brainstem of SIDS victims. Materials and methods: The materials of this study included 26 cases of SIDS and 12 control cases. The brainstem material was collected and the immunohistochemistry of GAP43 and tryptophan hydroxylase (TrypH) carried out. The density of GAP43-positive neurons and dendrites and of TrypH-positive neurons were measured quntitatively. Nonparametric analyses of GAP43 between SIDS and non-SIDS and correlation analyses between GAP43 and TrypH were performed. Results: No significant difference in GAP43-associated findings was found between SIDS and non-SIDS nor any significant correlation between GAP43-associated findings and TrypH-positive neurons. Conclusions:. The results of this study were not in agreement with the association of GAP43 with SIDS and with serotonergic innervation in SIDS.

Correlation between the Ki-67 antigen in the brainstem and physiological data on sleep apnea in SIDS victims

Background: The Ki-67 antigen appears in all human proliferating cells during late G1, S, M and G2 phases of the cell cycle, but is consistently absent in the G o phase (noncycling) cells. The correlation between Ki-67 in the brainstem and sleep apnea in victims of the sudden infant death syndrome (SIDS) was investigated to elucidate cell kinetics in the brainstem of this condition, which is still the main cause of postneonatal infant death. Materials and Methods: Twenty-six cases of SIDS occurred among 38 infants dying under 6 months of age in a cohort of 27,000 infants studied prospectively to characterize their sleep–wake behavior. All the infants had been recorded during one night in a pediatric sleep laboratory some 3 to 12 weeks before death. The frequency and duration of sleep apnea were analyzed. At autopsy, brainstem material was collected and immunohistochemistry for Ki-67 was carried out. The density of Ki-67-positive neurons was measured semiquantitatively. Correlation analyses were carried out between the density of Ki-67-positive neurons and the data on sleep apnea. Results: Except in two cases in SIDS victims and in one control, the detection of Ki-67 was negative. No correlation analysis between the Ki-67 and of sleep apnea was found. Conclusions: There were no abnormal cell kinetics detected by the demonstration of Ki-67 antigen in the brainstems of SIDS victims.

The correlation between ubiquitin in the brainstem and sleep apnea in SIDS victims

Background: The sudden infant death syndrome (SIDS) is still the main cause of postneonatal infant death and its etiology has stimulated many competing theories, among which is the role of hypoxia and brainstem abnormalities. One report claims an increased in ubiquitin in the liver of SIDS victims, ubiquitin being one of the heat-shock proteins. The correlation between ubiquitin in the brainstem and sleep apnea in SIDS was investigated here. Materials and methods: Among 27,000 infants studied prospectively to characterize their sleep–wake behavior, 38 infants died under 6 months of age, including 26 cases of SIDS. All the infants had been recorded during one night in a pediatric sleep laboratory some 3–12 weeks before death. The frequency and duration of sleep apnea were analyzed. Brainstem material was collected at autopsy and examined immunohistochemically for ubiquitin. The density of ubiquitin-positive elements was measured semiquantitatively. Correlation analyses were carried out between the density of ubiquitin-positive elements and the data on sleep apnea. Results: In the victims of SIDS, a statistically significant positive correlation was found between the density of ubiquitin-positive neuronal factors in the pons and the frequency of obstructive apnea ( p=0.001) and statistically significant negative correlations were seen between the density of ubiquitin-positive cells in the ependyma in the pons and the duration of obstructive apnea ( p=0.044) and between the density of ubiquitin-positive cells in the subependyma in the medulla and the frequency of central apnea ( p=0.024). Conclusions: It was found that three significant associations existed between the pathological data referring to ubiquitin and physiological data in SIDS victims. These facts are in agreements with the association of sleep apnea in SIDS.

Serotonergic receptors in the midbrain correlated with physiological data on sleep apnea in SIDS victims

Background: Recently it has been reported that serotonin and related matters are associated with the sudden infant death syndrome (SIDS), which is still the main cause of postneonatal infant death. To further explore this claim, the correlation between serotonin receptors in the brainstem and sleep apnea in SIDS victims was investigated. Materials and methods: Among 27,000 infants studied prospectively to characterize their sleep–wake behavior, 38 infants died under 6 months of age including 26 cases of SIDS. All the infants had been recorded during one night in a pediatric sleep laboratory some 3–12 weeks before death. The frequency and duration of sleep apnea were analyzed. Brainstem material was collected and immunohistochemistry on 5-hydroxy tryptamine 1A (5HT1A) receptor was carried out. The density of 5HT1A receptor-positive neurons was measured quantitatively. Nonparametric analysis of the density of 5HT1A receptor-positive neurons was carried out between SIDS and non-SIDS cases. Correlation analyses were performed between the density of 5HT1A receptor-positive neurons and the data on sleep apnea. Results: There was no correlation between the pathological data on 5HT1A receptors and the physiological data on sleep apnea in SIDS victims. Conclusions: No correlation between pathological findings of serotonin and physiological findings of sleep apnea were not in agreement with the association of sleep apnea in pathophysiology of SIDS.

Pathological data on apoptosis in the brainstem and physiological data on sleep apnea in SIDS victims

The sudden infant death syndrome (SIDS) is still the main cause of postneonatal infant death and its cause is still unknown. A chronic hypoxic situation has been shown to exist in the brains of SIDS victims and apoptosis has been demonstrated in hypoxic situations. In this study, the correlation between apoptotic neurons or glias and sleep apnea in SIDS was investigated in the brainstem of SIDS victims. Materials and methods: In a cohort of 27,000 infants studied prospectively to characterize their sleep–wake behavior, 38 infants died under 6 months of age. They included 26 cases of SIDS. The frequency and duration of sleep apnea were analyzed. The brainstem material was collected and terminal-deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) method was carried out. The density of TUNEL-positive neurons or glias was measured quantitatively. Correlation analyses were carried out between the apoptosis-associated pathological data and the physiological data of sleep apnea. Results: No significant negative or positive correlation between the density of TUNEL-positive neurons or glias and the characteristics of sleep apnea was observed in SIDS victims. No statistically significant differences associated with apoptotic neurons and glias were observed between SIDS and non-SIDS. Conclusions: The pathological findings of apoptosis were not in agreement with the hypothesis refer to apnea and arousal phenomenon in pathophysiology of SIDS.

The correlation between microtubule-associated protein 2 in the brainstem of SIDS victims and physiological data on sleep apnea

Background: Microtubule-associated protein 2(MAP2), a cytoskeletal protein of the neuron, is a marker of early ischemic neuronal damage. As a chronic hypoxic situation exists in the brains of victims of the sudden infant death syndrome (SIDS), the correlation between MAP2-positive neurons or dendritic spines in the brainstem and sleep apnea was investigated in SIDS, which is still the main cause of postneonatal infant death. Materials and methods: 27,000 infants were studied prospectively to characterize their sleep–wake behavior and amongst these, 38 infants died under 6 months of age. They included 26 cases of SIDS. The frequency and duration of sleep apneae were analyzed. The brainstem material was collected and immunohistochemistry of MAP2 was carried out. The density of MAP2-positive neurons, dendrites and dendritic spines were measured quantitatively. Correlation analyses were carried out between the MAP2-associated pathological data and the physiological data of sleep apnea. Results: One negative correlation between the density of MAP2-positive dendrites in the pars compacta of pedunculo-pontine tegmentum nucleus (PPTNc) and the duration of obstructive apnea ( p=0.017) and two SIDS-specific positive correlations between the density of MAP2-positive dendrites in the pars dissipata of pedunculo-pontine tegmentum nucleus (PPTNd) and the duration of central apnea ( p=0.005) and between the dorsal raphe and the frequency of obstructive apnea were found in SIDS victims. The density of MAP2-positive dendritic spines in PPTNc was significantly higher in SIDS than in control ( p=0.034). Conclusions: The significant correlations with the MAP2-positive findings in the midbrain arousal pathway and the characteristics of sleep apnea in SIDS victims were in agreement with the association with apnea and arousal-deficiency in SIDS.

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.

The triple risk hypotheses in sudden infant death syndrome.

The triple risk hypotheses in sudden infant death syndrome.

Infanticide: Is Its Incidence Among Postneonatal Infant Deaths Increasing?

The decline in the incidence of sudden infant death syndrome (SIDS) and recent recommendations regarding the differentiation of SIDS and child abuse has generated speculation that some cases of infanticide were misdiagnosed as SIDS. The aims of this study were to determine the change in incidences and proportions of postneonatal deaths from all causes, SIDS, and infanticide in California over an 18-year interval encompassing years before and after the Back to Sleep campaign. Selected postneonatal mortality data from 1981 through 1998 obtained from the California Department of Health Services were analyzed and graphically displayed. The total postneonatal mortality and incidence of SIDS deaths per 100,000 live births decreased 45% and 66%, respectively, during the study interval; the incidence of infanticide remained low. The ratio of infanticide to SIDS increased from 4.3 per 100 in 1981 to 10.2 per 100 in 1998. Infanticide deaths, as a percentage of the total number of postneonatal deaths, increased slightly from the first to the second half of the study interval but never rose above 3.2%. It is concluded that this increased percentage is due to a decrease in SIDS deaths and not to an actual increase in infanticide deaths.

Postneonatal infant mortality and quality of medical care: a case-control study

OBJECTIVE: To identify the risk factors for postneonatal infant mortality caused by diarrhea and pneumonia in relation to the quality of medical assistance. METHODS: Population-based case-control study of 277 postneonatal infant deaths caused by diarrhea and pneumonia occurring in the metropolitan area of Belo Horizonte, Brazil, between May/1991 and April/1992. The cases were compared with hospitalized controls, and matched by pathology, age and hospital. Information on cases and controls were collected from medical records and through home interviews. Some variables related to the quality of medical care were analyzed. McNemar test and conditional logistic regression were used to define the risk factors for postneonatal deaths. RESULTS: Multiple logistic regression analysis showed the following factors independently associated with increased risk of postneonatal death induced by diarrhea and pneumonia: delayed immunization (OR = 2.48; 95%CI=1.17-5.23), general status (serious) on hospital admission (OR=10.94; 95%CI=4.91-24.34), unaccomplished hospital procedures (OR=10.08; 95%CI = 3.55-20.59) and malnutrition on hospital admission (OR=3.58; 95%CI=1.42-9.07). CONCLUSIONS: The results indicate the low quality of medical assistance as an important risk factor for avoidable causes of postneonatal deaths. The authors highlight the lack of integration between the outpatient clinic and hospital activities as an important determinant of low quality. It is necessary that the performance of health services and their effect on avoidable infant mortality be widely discussed, also taking into consideration the preponderant role of socioeconomic variables

CLINICAL REVIEW ARTICLE: Is changing the sleep environment enough? Current recommendations for SIDS

Sudden infant death syndrome (SIDS or cot death) was the major cause of post-neonatal infant death in many countries in the late 1970s and 1980s. There is now very strong evidence that public intervention campaigns targeting the prone sleeping position, which had been identified by epidemiological studies as a major risk factor, were followed by substantial falls in the rate of SIDS. In the present review we discuss the evidence on which current recommendations for the prevention of SIDS are based. The prone sleeping position is now clearly causally associated with SIDS. Further reductions in SIDS may be produced by recommending the back sleeping position as opposed to the side position. Maternal smoking in pregnancy and bed sharing by infants of mothers who smoke are also strongly associated with SIDS, but have been harder to influence. Paternal smoking has also been implicated, although the magnitude of the reported risk is small. Finally, breastfeeding, pacifier use and having the infant sharing the parents bedroom, but not the bed, may also reduce risk. Continued reductions in SIDS mortality will require innovative public health education to target these major risk factors, while building on the “back to sleep” approach.

The contribution of mild and moderate preterm birth to infant mortality. Fetal and Infant Health Study Group of the Canadian Perinatal Surveillance System.

The World Health Organization defines preterm birth as birth at less than 37 completed gestational weeks, but most studies have focused on very preterm infants (birth at <32 weeks) because of their high risk of mortality and serious morbidity. However, infants born at 32 through 36 weeks are more common and their public health impact has not been well studied. To assess the quantitative contribution of mild (birth at 34-36 gestational weeks) and moderate (birth at 32-33 gestational weeks) preterm birth to infant mortality. Population-based cohort study using linked singleton live birth-infant death cohort files for US birth cohorts for 1985 and 1995 and Canadian birth cohorts (excluding Ontario) for 1985-1987 and 1992-1994. Relative risks (RRs) and etiologic fractions (EFs) for overall and cause-specific early neonatal (age 0-6 days), late neonatal (age 7-27 days), postneonatal (age 28-364 days), and total infant death among mild and moderate preterm births vs term births (at >/=37 gestational weeks). Relative risks for infant death from all causes among singletons born at 32 through 33 gestational weeks were 6.6 (95% confidence interval [CI], 6.1-7.0) in the United States in 1995 and 15.2 (95% CI, 13.2-17.5) in Canada in 1992-1994; among singletons born at 34 through 36 gestational weeks, the RRs were 2.9 (95% CI, 2.8-3.0) and 4.5 (95% CI, 4.0-5.0), respectively. Corresponding EFs were 3.2% and 4.8%, respectively, at 32 through 33 gestational weeks and 6.3% and 8.0%, respectively, at 34 through 36 gestational weeks; the sum of the EFs for births at 32 through 33 and 34 through 36 gestational weeks exceeded those for births at 28 through 31 gestational weeks. Substantial RRs were observed overall for the neonatal (eg, for early neonatal deaths, 14.6 and 33.0 for US and Canadian infants, respectively, born at 32-33 gestational weeks; EFs, 3.6% and and 6. 2% for US and Canadian infants, respectively) and postneonatal (RRs, 2.1-3.8 and 3.0-7.0 for US and Canadian infants, respectively, born at 32-36 gestational weeks; EFs, 2.7%-5.8% and 3.0%-7.0% for the same groups, respectively) periods and for death due to asphyxia, infection, sudden infant death syndrome, and external causes. Except for a reduction in the RR and EF for neonatal mortality due to infection, the patterns have changed little since 1985 in either country. Mild- and moderate-preterm birth infants are at high RR for death during infancy and are responsible for an important fraction of infant deaths. JAMA. 2000;284:843-849

Birth Weight- and Gestational Age-Specific Sudden Infant Death Syndrome Mortality: United States, 1991 Versus 1995

To estimate the changes in birth weight- and gestational age-specific sudden infant death syndrome (SIDS) mortality rates since the publication of the sleep-positioning recommendations by the American Academy of Pediatrics Task Force on Infant Positioning and SIDS. This is a historical cohort study using US vital statistic linked birth and infant death certificate files for the years 1991 and 1995. SIDS deaths were identified as any death attributed to International Classification of Diseases, Ninth Revision code 7980, occurring between the 28th and 365th days of life. There were 4871 deaths attributed to SIDS in 1991 for a postneonatal mortality rate of 1.2/1000 postneonatal survivors compared with 3114 deaths in 1995 for a rate of.8/1000. This represents a 33% drop in the postneonatal SIDS mortality from 1991 to 1995. Between 1991 and 1995, SIDS rates declined 38%, 38%, 35%, and 32% for birth weight groupings of 500 to 999 g, 1000 to 1499 g, 1500 to 2499 g, and >/=2500 g, respectively. There were no SIDS deaths attributed to infants weighing <500 g. The SIDS rates declined 27%, 21%, 40%, and 23% for gestational age groups of <29 weeks, 29 to 32 weeks, 33 to 36 weeks, and >/=37 weeks. The rate of decline did not differ significantly across birth weight- or gestational age-specific categories. There was a significant increase in the black:non-black postneonatal SIDS mortality ratio from 2.00 to 2.28, reflecting a smaller decline in birth weight- and gestational age-specific mortality for blacks than observed for the non-black population. Postneonatal SIDS mortality decreased significantly across all broad birth weight and gestational age categories. If the decline in the prevalence of prone positioning that has been reported since 1992 has occurred across all birth weight and gestational age, these data support the hypothesis that supine or side sleep positioning is effective in preterm/low birth weight infants as well as term infants.

Perinatal and Infant Mortality and Low Birth Weight among Residents near Cokeworks in Great Britain

With growing evidence of the adverse health effects of air pollution--especially fine particulates--investigators must concentrate on the fetus, neonate, and infant as potentially vulnerable groups. Cokeworks are a major source of smoke and sulfur dioxide. In the current study, the authors investigated whether populations residing near cokeworks had a higher risk of adverse perinatal and infant outcomes. Zones of 7.5-km radius around 22 cokeworks in Great Britain were studied, within which the authors assumed that exposure declined from highest levels within 2 km to background levels. Routinely recorded birth and death data for Great Britain during the period 1981-1992 were analyzed. Each individual record had a postcode that referred to a small geographical area of typically 15-17 addresses. The authors calculated expected numbers on the basis of regional rates, stratified by year, sex, and a small-area socioeconomic deprivation score. For all cokeworks combined, the observed/expected ratio (95% confidence intervals within parentheses) within 2 km of cokeworks was 1.00 (0.95, 1.06) for low-birth-weight (i.e., < 2,500 g) infants; 0.94 (0.78, 1.12) for still births; 0.95 (0.83, 1.09) for infant mortality; 0.86 (0.72, 1.03) for neonatal mortality; 1.10 (0.90, 1.33) for postneonatal mortality; 0.79 (0.30, 1.46) for respiratory postneonatal mortality; and 1.07 (0.77, 1.43) for postneonatal Sudden Infant Death Syndrome. Respiratory postneonatal mortality was low throughout the entire 0-7.5-km study area (observed/expected = 0.74 [0.61, 0.88]). There was no statistically significant decline in risk with distance from cokeworks for any of the outcomes studied. The authors concluded that there was no evidence of an increased risk of low birth weight, stillbirths, and/or neonatal mortality near cokeworks, and there was no strong evidence for any association between residence near cokeworks and postneonatal mortality. One must remember, however, the limited statistical power of the study to detect small risks.

Laryngeal basement membrane thickening is not a reliable postmortem marker for SIDS: results from the Chicago Infant Mortality Study.

It has been suggested that laryngeal basement membrane (LBM) thickening is a pathognomonic postmortem marker for sudden infant death syndrome (SIDS) and is not seen in other causes of explained sudden infant death. To test this hypothesis, we evaluated longitudinal sections of the right hemilarynx taken through the midpoint of the true vocal cord from 129 SIDS cases and 77 postneonatal sudden infant death controls. Using a five-point semi-quantitative scale, maximum LBM thickness (LBMT) for SIDS cases and controls was not statistically different (mean, 2.39 + 0.69 and 2.40 + 0.77, respectively). Likewise, scores based on the average thickness along the entire basement membrane (i.e., "average" score), were not found to be different between SIDS cases and controls. Average and maximum LBMT increased with age in both SIDS cases and controls and were not different between SIDS cases and controls within each age interval. Similar trends in the distribution of maximum and average LBMTs were found between black and Hispanic SIDS and controls; the number of white/non-Hispanic infants was too low for meaningful comparisons. Maximum and average LBMTs were not different in SIDS cases and controls exposed to environmental tobacco compared with unexposed infants. The LBMTs also increased significantly with body weight and length in both SIDS cases and controls. Finally, there were no differences in LBMT in infants intubated prior to death compared with those who were not intubated. From these data, we conclude that LBMT is not pathognomonic of SIDS, is present or absent with equal frequency in SIDS and controls, increases with postnatal age, and does not correlate with passive smoke exposure. Therefore, LBMT should not be used to diagnose SIDS.

Influence of increased survival in very low birth weight, low birth weight, and normal birth weight infants on the incidence of sudden infant death syndrome in the United States: 1985-1991.

To examine the relationship between infant survival and the rates sudden infant death syndrome (SIDS) in very low birth weight (VLBW), low birth weight (LBW), and normal birth weight (NBW) infants from 1985 to 1991. The National Center for Health Statistics Birth Cohort Linked Birth/Infant Death Data Sets were used to determine birth weight, age at death, and cause of death for US-born singleton infants with birth weights of 500 g or more. Increasing infant and postneonatal survival rates were greatest in VLBW infants. In contrast, SIDS rates did not change in VLBW infants (3.66 to 3.69; P = .70) but declined in both LBW (3.51 to 3.32; P = .041) and NBW (1.07 to 1.03; P = .008) infants. Postneonatal SIDS rates (per 1000 neonatal survivors) did not change in VLBW (4.93 to 4.58; P = .58) or LBW (3.36 to 3.22; P = .07) infants but declined in NBW infants (1.00 to 0.97; P = .018). Although there were differences among the slopes of survival rates, there was no statistical evidence of differences in the slope of SIDS rates among the three groups. The marked increase in survival of VLBW infants increased the pool of babies at potential risk for SIDS. VLBW infants' SIDS rates have not changed while they have declined in NBW and LBW infants.