Postneonatal Infant Death Research Articles

Catecholamine neurons alteration in the brainstem of sudden infant death syndrome victims.

Sudden infant death syndrome (SIDS) is a leading cause of postneonatal infant death. The pathogenesis of sudden death is still unknown, but an abnormality in the central nervous regulation of breathing during sleep has been suggested. The aim of study is to confirm the brainstem disorder of SIDS victims. In order to do this, it is necessary to investigate the alterations of brain neurotransmitter systems thought to be involved in respiratory control. Neuropathologic study performed on the brainstem of SIDS victims. The disorders of catecholaminergic systems in 22 SIDS victims were examined on the substantia nigra in the midbrain, locus coeruleus in the pons, vagal nuclei, and area reticularis superficialis ventrolateralis with the immunohistochemical method. Immunoperoxidase staining was performed with the antityrosine hydroxylase (TH) and the glial fibrillary acidic protein antibodies. Immunoreactivity was compared with 13 age-matched control infants. For statistical analysis, the chi 2 test and the Student's t test were performed. The main finding was diminished TH immunoreactivity in the vagal nuclei and area reticularis superficialis ventrolateralis of SIDS victims, suggesting that adrenaline and noradrenaline neurons are altered in SIDS. In addition, this decrease in TH was closely correlated with brainstem gliosis. These catecholaminergic changes may be caused by chronic hypoxia or ischemia, and also may underlie alterations in respiratory and cardiovascular control in sleep.

Sudden infant death syndrome (SIDS) in Austria. Socioeconomic risk factors for postneonatal SIDS- and non-SIDS-mortality

Objective: To examine and compare socioeconomic risk factors for SIDS and non-SIDS in postneonatal age in Austria. Methods: We conducted a population-based retrospective cohort study using the govermental linked birth and death certificate file for 1984 to 1993. Our studied population includes all single live-births surviving the neonatal period (n = 880 601). Postneonatal deaths (n = 2989) were divided into SIDS (ICD9 798.0; n = 1070) and all other causes of death (non-SIDS; n = 1919). Mortality rates were expressed as deaths per 1000 infants surviving the neonatal period. Crude and adjusted relative risks of death (RR) and 95 % confidence intervals (CI) were obtained by logistic regression analysis. Social risk factors, demographic risk factors, and birth weight were included as independent variables. Results: Social risk factors turned out to be closely associated both with SIDS and with non-SIDS-mortality. Concerning SIDS, women in the lowest educational group have a RR of 1.45 (CI = 1.16–1.81) compared to highly educated women. For non-SIDS the RR was 1.48 (CI = 1.26–1.74). Immigrant workers (women of Turkish and Ex-Yugoslavian origin) had a much lower risk for SIDS compared to Austrian mothers (RR = 0.33, CI = 0.24–0.47). Living in big cities was associated with a higher risk for SIDS (RR = 1.63, CI = 1.42–1.86), in contrast to a lower risk for non-SIDS (RR = 0.89, CI = 0.80–1.00). Conclusions: When controlling for demographic risk factors and birth weight, unfavourable social conditions still remain an important risk factor for SIDS and non-SIDS in postneonatal age. Attempts to improve these conditions should not be confined to SIDS, but they should be integrated into preventive programs aimed at reducing infant mortality in general.

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

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. 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. 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. 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.

Sudden Infant Death Syndrome (SIDS) in Denmark: Evaluation of the Increasing Incidence of Registered SIDS in the Period 1972 to 1983 and Results of a Prospective Study in 1987 through 1988

To investigate a reported increase, from 0.4 to 1.3 per thousand live births, in the Danish incidence of sudden infant death syndrome (SIDS), a retrospective analysis of SIDS in Denmark from 1972 to 1983 was carried out. Based on data registered with the National Board of Health, a notable regional difference in SIDS rate between the western and eastern parts of Denmark was found. This difference did not correlate with the overall postneonatal mortality by region. Danish law requires medicolegal investigation in all cases of sudden unexpected death. Medicolegal autopsies are performed only in the three forensic institutes which cover all of Denmark. Despite the law and a uniform organization of the forensic medical services, differing application of postmortem examinations and individual interpretation of the history and autopsy in cases of sudden infant death existed. Differences in reporting of respiratory infections, suffocation, and cardiac malformation were found to contribute to the increase and to regional disparities in SIDS incidence. The three Danish forensic institutes examined all cases of sudden infant deaths in Denmark 1987 and 1988. These cases were classified as explained cause of death, pure SIDS, and atypical SIDS; atypical cases were evaluated by consensus. The SIDS incidence (the number of classic SIDS and atypical SIDS per thousand live births) was 1.9 in 1987 and 1.3 in 1988, and it was identical in the eastern and western part of Denmark; however, a higher incidence both of overall postneonatal and SIDS mortality was found in the middle region of Denmark.(ABSTRACT TRUNCATED AT 250 WORDS)

A review of epidemiological studies of sudden infant death syndrome in Southern New Zealand

The rate of sudden infant death syndrome (SIDS) in Southern New Zealand has been very high with an apparent real increase in incidence from the early 1970s. Recent research is reviewed and the results of specific interventions aimed at preventing SIDS summarized. The intervention consisted of strongly advising new parents that their babies sleep on their back or side and that they avoid over-heating, especially during infections. For the Otago area, child-care practice has been documented and prone sleeping of 1 month old babies has declined from 41.8% in 1986 to 2.4% in 1989-90. There is also evidence that parental control of infants' thermal environment has improved, maternal smoking during pregnancy has slightly decreased and the number of babies breast fed at 1 month of age has increased by 11%. In Southern NZ there has been a decline in post-neonatal SIDS mortality from 6.3 deaths per 1000 live births 1979-84 to 1.3 per 1000 live births in 1990. There are grounds for supposing that the intervention has been causative of this change, a possibility being addressed by on-going studies.

Estimates of morbidity and mortality rates for diarrheal diseases in American children

Although the importance of diarrhea as a prime cause of morbidity and death in developing countries is well recognized, the disease burden in the United States has never been thoroughly examined. We have prepared national estimates of the annual number of cases of diarrhea in children less than 5 years of age and of the outcome, measured in terms of visits to a physician, hospitalizations, and deaths. The annual number of diarrheal episodes was estimated by reviewing longitudinal studies of childhood diarrhea conducted in the United States and extrapolating these data to the nation. Estimates of physician visits, hospitalizations, and deaths were prepared from a variety of national data sources. We estimate that 16.5 million children less than 5 years of age have between 21 and 37 million episodes of diarrhea annually. Of these, 2.1 to 3.7 million episodes lead to a physician visit, a total of 220,000 patients are hospitalized, and 325 to 425 children die. The major cost of diarrhea lies in the high numbers and cost of hospitalizations, because approximately 10.6% of hospitalizations in this age group are for diarrhea. Diarrheal deaths occur in relatively small numbers, are more common in the South and among black persons, are potentially avoidable, and could represent as much as 10% of the preventable postneonatal infant death in the United States. These estimates underscore the extensive burden of diarrheal illness in children in the United States and suggest that interventions to prevent disease or decrease its severity could be cost-effective.

Are race and length of gestation related to age at death in the sudden infant death syndrome?

Although race and preterm delivery are known to be associated with sudden infant death syndrome (SIDS), the relationships between age at death from SIDS and these factors have not been well described. To examine these relationships, we used linked infant birth and death records for the cohort of 1,204,375 White and 283,776 Black postneonates who were born from 1979 to 1981 in five states: California, Georgia, Missouri, South Carolina and Tennessee. Deaths attributable to SIDS occurred to 1404 White postneonates and to 696 Black postneonates. Although postneonatal SIDS rate among Black infants was twice that of White infants, the relative risk was smaller among infants with gestations of less than 35 weeks. For White postneonates, the median postneonatal age at death sharply declined for gestations from 28-29 weeks to 36-37 weeks and levelled off for longer gestations. For Black postneonates, the results do not support an association between length of gestation and age at death. The findings suggest that practitioners investigating approaches to avert SIDS need to maintain their interventions to an older age among White preterm infants. Researchers investigating the causes of SIDS need to consider the relationship between length of gestation and age at death from SIDS as well as possible developmental differences between White and Black preterm infants.

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.

Autopsy and Diagnosing SIDS

To the Editor. — Allen et al 1 make one assumption concerning postneonatal sudden infant death with which I do not agree. They assume that sudden infant death syndrome (SIDS) can be verified by autopsy. However, SIDS is an exclusionary diagnosis that requires careful death-scene investigation. 2 There are no shortcuts; the investigation should include an on-site environmental assessment. Unfortunately, the authors did not collect detailed deathscene information on the circumstances surrounding death in the SIDS cases. The source of the SIDS diagnosis in their small study was frequently death certificate data. 3 The Georgia Post-Mortem Examination Act allows medical examiners to perform autopsies and conduct deathscene investigations on infants who die presumptively of SIDS. It is surprising that, with the great advances in neonatal survival in Georgia and with the tremendous cost in the intensive care of critically ill newborns, nearly half of the infants in this study who

Perinatal and infant mortality in Wales: inter-district variations and associations with socio-environmental characteristics.

Stillbirth rates, perinatal death rates, early and late neonatal death rates and (post-neonatal) infant death rates are reported for Wales since local government and NHS reorganization in 1974. The time trends in these rates show declining mortality, in full weight and in low birthweight babies. Analysis of average rates for the period 1974-81 inclusive in the 37 local authority districts within Wales demonstrate wide variations, with PMRs ranging from 11.5 to 22.5 per 1000. Many highly statistically significant associations were evident between socioeconomic characteristics of the districts and stillbirth rates but few with neonatal death rates and none with infant death rates.

The lethal “cot-death syndrome” fallacy

The ammonia factor theory of infant death causation shows how the known, deadly properties of this respiratory poison, potentially present at every inflant's cot are compatible with the known causative relationships found with “cot-death syndrome” infants. It also predicted and demonstrated that a causal relationship existed between cot-death infants and most other post neo-natal infant deaths. The ammonia factor theory is quite incompatible with the medical profession's “cot-death syndrome” model. A critical evaluation of the medical profession's “cot-death syndrome” model shows that it provides no predictive, causative, diagnostic, or preventative dimensions and is used by some of the medical profession as a tool of fear to extract research monies and by others in the profession to placate parents. The “cot-death syndrome” model is a definition of a non-reality and the antithesis of a scientific model. As a mathematical model it is impossible and is supported by statistical gerrymandering. It places diagnosed “cot-death syndrome” parents in legal jeopardy. Its correlation with the reality of infant death is staggeringly improbable. These features are in stark contrast with the ammonia factor theory of infant death causation. The ammonia factor theory shows that the overall infant death rate is preventable through a programme of welfare, as well as through educational, social and environmental improvements. The medically centred “cot-death syndrome” model is a useless, lethal fallacy. It is politically obstructive. It must be discarded.

Changing patterns of perinatal and infant mortality in Western Australia: implications for prevention.

Perinatal and infant mortality rates have fallen dramatically in the developed world this century. A review of perinatal and infant mortality in Western Australia from 1970 to 1981 was undertaken, to examine trends in birthweight-specific and cause-specific rates. The predominant causes of death are now congenital malformation, stillbirth of unknown cause, preterm birth and cot death. Perinatal and infant mortality rates are unlikely to be reduced substantially until the reasons for these four causes of death are elucidated.

Causes of Neonatal Mortality

To the Editor.— In his letter, Causes of Neonatal Mortality, Bader 1 displays data (Table 2) that contain a remarkable finding, in addition to his findings that relate to the role of lethal congenital anomalies in infant mortality but on which his letter does not remark. Specifically, his additional finding is the relationship between birth weight and postneonatal sudden infant death syndrome (SIDS). Of the 690 postneonatal deaths of infants with birth weights of 2,500 g or greater, 59.1% were caused by SIDS. The corresponding SIDS percentages of postneonatal deaths of infants with birth weights of 1,500 to 2,499 g and less than 1,500 g were 48.3% and 27.8%, respectively. (The Bader's data appear to be in conflict with pronouncements by many SIDS researchers, viz, that infants of higher birth weights are at less