SIDS Deaths Research Articles

SIDS — a developmental neurological perspective

Most SIDS deaths occur between 2 and 4 months of age. Neural transformations may be important in SIDS. Evidence of delayed myelination has been found in SIDS victims. However a simple neuro-developmental model is insufficient to explain SIDS. The age of death profile is reportedly similar for pre-term and full-term SIDS victims. Another developmental change is that IgG levels are lowest when SIDS risk peaks, and there is data linking SIDS and infections. Prone position may also increase risk. While a developmental model emphasizing neural transformation is useful, other factors affect risk also.

Counseling issues related to maternal substance abuse and subsequent sudden infant death syndrome in offspring

Recent reports linking maternal prenatal drug use to SIDS in offspring raise six specific issues related to professional intervention: (1) blaming addicted parents compounds the normal guilt experienced after SIDS; (2) low self-esteem often underlies drug usage; (3) punitive intervention by child protective agencies may lead to parental mistrust of health professionals, reducing access to help; (4) society's increasing tendency to criminalize drug use during pregnancy may expose women to prosecution if a SIDS death occurs; (5) the debate over monitoring “at risk” infants is further complicated if caretakers use drugs; and (6) recent articles have suggested that the majority of “SIDS deaths” may be the result of homicide, neglect, environmental hazards, etc. For addicted parents, a SIDS death increases the risk of social fragmentation and poses challenges to professional interventions.

84 HYPOXIA PPRECEDES DEATH IN SIDS. POSSIBLE TRIGGER MECHANISMS

Hypoxanthine (Hx) is formed from hypoxic degradation of AMP and is thus a marker of hypoxia. Results of Hx measurements in vitreous humor in 112 SIDS cases and in 21 infants and children suffering sudden violent death, were corrected according to the expected postmortem Hx increase. The corrected median Hx level of the SIDS group was 232 μmol/l, (range 0-668 μmol/l), which is significantly higher than the control group; 0 μmol/l, (range 0-91 umol/l), (p<0.01). The finding confirms that death in SIDS is preceded by a period of hypoxia in most cases. Increased numbers of IgM-cells in the tracheal wall, IgA-cells in the duodenal mucosa and IgA-, IgM- and IgG-cells in the salivary gland in SIDS-victims, suggest an overstimulation of the mucosal immune system in SIDS - perhaps caused by microbial factors. Such peripheral immune stimulation leads to release of cytokines which can induce immunostimulation in vital brain centres creating a vicious circle inducing hypoxia and death in infants at risk. Retrograde axonal transport might be a link to centres of the brain.

Child abuse and cot deaths

A search was made of the Child Protection Register for children with siblings who died of SIDS. The Child Health Department in Southern Derbyshire Health Authority (population 522,000; 7,100 births per year) undertakes confidential inquiries into all child deaths and registered SIDS deaths are noted. This study looked at all children born between January 1, 1984 and June 30, 1988 whose names appeared on the the Child Protection Register as victims of abuse or who were considered to be at risk for abuse. From a cohort of 288 children on the Child Protection Register, one in 30 of the children on the Register had a sibling whose death was registered as caused by SIDS. In Southern Derbyshire there is an association between child abuse and about 10% of deaths of children diagnosed as SIDS.

International trends in postneonatal mortality.

Trends in mortality in the age groups 1-5 and 6-11 months from 1966 to 1987 for Australia, Canada, England and Wales, New Zealand, and Sweden were examined. Mortality rates for ages 1-5 months differed appreciably between countries, with Sweden lower than all other countries examined. Rates have decreased in Australia, Canada, and England and Wales, but increased in New Zealand and Sweden. Mortality reported as due to the sudden death syndrome (SIDS) increased dramatically in all countries, although much of the increase was probably due to diagnostic transfer from respiratory diseases. Over 80% of SIDS deaths occurred in the age group 1-5 months and SIDS accounted for about half of all deaths in this age group. For developed countries total mortality in those aged 1-5 months was an indirect measure of SIDS mortality. A real increase in SIDS has thus occurred in Sweden and New Zealand and possibly in other countries as well. Mortality in the age group 6-11 months has approximately halved in all countries examined over the study period.

Intrathoracic petechial hemorrhages: a clue to the mechanism of death in sudden infant death syndrome?

(1) Intrathoracic petechiae are characteristic of most SIDS cases, and tend to be more numerous in these cases than in deaths from other causes, including mechanical asphyxia. (2) Their localization suggests that intrathoracic negative pressure plays a role in their genesis. (3) Several human and animal studies suggest that petechiae arising from the pulmonary circulation may differ from those originating from systemic vessels in the thorax. (4) Experimental studies suggest that vigorous respiratory efforts are responsible for their formation. This would seem to exclude respiratory paralysis as a mechanism for most SIDS deaths. (5) These petechiae are not consistent with cardiac arrest or failure as the primary agonal event in SIDS. (6) The fact that petechiae are more prominent in SIDS than in other deaths adds to the evidence that SIDS is not a "wastebasket" diagnosis, despite the imperfection of existing diagnostic criteria. (7) These petechiae do not prove that the final mechanism of most SIDS deaths is upper airway obstruction. However, they do provide substantial support for that thesis.

Sudden infant death syndrome: 1987 perspective

The pathophysiology of SIDS remains unknown. Although a multifactorial cause appears plausible on the basis of available data, new data are needed to determine which components of this multifactorial hypothesis are most important and whether other factors need to be added. We need to better understand control of breathing in the newborn infant and the manner in which maturation of cardiorespiratory control progresses during infancy. The unique period of vulnerability for SIDS, in which risk is less in the neonate than at 2 to 6 months of age, remains unexplained. Is there a worsening in some aspect of cardiorespiratory control in infants destined to die of SIDS? An improved understanding of the increased risk in black infants, preterm infants, and infants with intrauterine drug exposure, although only a small percentage of all SIDS deaths, should contribute substantially to our understanding. Appropriately designed and well-controlled prospective studies are needed in asymptomatic infants at risk, to determine the true contemporary nonintervention rate of SIDS and the extent to which any assessment or intervention lowers this rate. Prospective pneumogram screening studies have demonstrated significant group differences in respiratory patterns in normal infants compared with later SIDS victims, but have failed to achieve sufficient sensitivity and specificity to be useful for populationwide prospective screening. To assess aspects of brainstem cardiorespiratory control in addition to those assessed by a conventional pneumogram, future studies will need to be based on an expanded or modified technology. On the basis of both physiologic considerations and available technology, addition of an oxygen saturation channel offers the most promise for providing a more comprehensive assessment of cardiorespiratory control. If there is an underlying deficiency in asphyxic arousal responsiveness, for example, with or without other respiratory control deficits, continuous monitoring of oxygen saturation as part of a second-generation pneumogram system currently has the greatest promise for providing a modified pneumogram assessment of greater clinical use. The use of continuous oxygen saturation as a home monitoring technique should also be investigated. Power spectrum analysis of cardiorespiratory variability also appears to have potential advantages over conventional pneumogram analyses, and needs to be evaluated in prospective studies. The following statements summarize our current knowledge regarding SIDS, apnea, pneumograms, and home monitors: The cause(s) of SIDS remains unknown.(ABSTRACT TRUNCATED AT 400 WORDS)

Effects of birth weight and ethnicity on incidence of sudden infant death syndrome

Sudden infant death syndrome occurs with increased frequency in low birth weight infants and in black infants. The degree to which the higher LBW rate among blacks might explain this higher SIDS rate is unknown. To address this question, we analyzed the 1233 SIDS deaths that occurred among 252,376 neonatal survivors in Cook County from 1975 to 1980, using computer-coded matched infant birth and death records. Birth weight and ethnic group were identified. The overall SIDS rates in blacks, Hispanics, and whites were 5.1, 1.2, and 1.3/1000 neonatal survivors, respectively. Within each ethnic group, the SIDS rates increased progressively with decreasing birth weight. Within the less than or equal to 1500 gm birth weight groups, the SIDS rates were 16.4, 3.9, and 5.5/1000 neonatal survivors in blacks, Hispanics, and whites. Using direct standardization, we found that 27% of the SIDS rate disparity between blacks and whites could be explained by the higher LBW rate in blacks (14% vs 6% in whites). The good outcomes in both LBW and SIDS rates for the Hispanic population were unexpected because, like blacks, Hispanics are socioeconomically disadvantaged. Findings for this group suggest that the remaining 73% of the increased SIDS rate in blacks cannot be attributed in a straightforward manner to differences in income or educational attainment.

Is shock the mode of death in SIDS?

Sequential morphological changes as found in the organs of 179 SIDS infants are described. Detailed examination of macroscopic and microscopic heart lesions reveal extensive myocardial lesions which can be best described as selective focal anoxic muscle fibre necrosis at different developmental stages. Varying from case to case the myocardial lesions present themselves in an acute and subacute phases, and in most cases both phases are present at the same time. These lesions are shown to be identical with the myocardial lesions as encountered in shock and many other conditions observed in clinical cases and in experimental laboratory animals. Lesions in other organs are consistent with the effects due to cardiogenic shock. A conclusion is reached that cardiogenic shock leading to acute cardiac failure is the primary final cause of death in all SIDS infants.

Histopathology of the conduction system in the sudden infant death syndrome.

The cause of the sudden infant death syndrome (SIDS, crib death, or cot death) is unknown. Current hypotheses include lability of heart rate and/or rhythm as a pathogenetic factor. The conduction system of 50 infants coming to autopsy were examined by serial sections; the infants were from newborn to two years of age. Twenty-six were SIDS deaths and 24 were explained deaths (ED). The frequency of histologic abnormalities of the specialized tissue was almost identical in both groups of infants. Hemorrhage in or around different parts of the conduction system was present in 27% SIDS and 29% ED. There was no evidence of cell death or degeneration of conduction fibers, nor obstructive lesions of the atrioventricular (A-V) arteries. Apparent moulding of A-V node and His bundle was a universal finding in both SIDS and ED, and consisted of irregular interdigitation of A-V node and His bundle fibers with the myxoid central fibrous body (CFB). Isolated bundles of conduction fibers residing in CFB and membranous ventricular septum were seen in two SIDS, but no direct contact between these fibers and the working myocardium could be identified in serial sections in either case. Without corroborating antemortem electrophysiologic data, the functional significance of morphologic findings in the conduction system of SIDS must remain conjectural.