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PubMed2002

Epidemiological investigation of sudden infant death syndrome infants--recommendations for future studies.

In recent years the study of infant care practices within the sleeping environment has proved to be the single most important set of observations for reducing the risk of Sudden Infant Death Syndrome (SIDS). To further reduce the number of deaths and resolve the debate on safe infant care practice, a closer scrutiny of this environment is required. However, anecdotal observation from uncontrolled death-scene investigations and a reluctance to diagnose SIDS because of adverse social conditions or circumstantial evidence at the time of death is undermining future research. To investigate SIDS now means investigating the wider umbrella of all Sudden Unexpected Deaths in Infancy (SUDI) because of the potential for misdiagnosis. In trying to find out why SIDS infants die we have increasingly been forced to search for why infants survive in the first few months of life and it is this comparative component of epidemiological observation that has saved so many lives. A death-scene investigation is vital to any planned future investigation of SIDS but equally essential is a sleep-scene investigation of surviving infants to put any findings into context. SIDS infants are no longer scattered across the social strata and the cot is not the only environment in which they are found, social deprivation and use of the parental bed are now more discernable. Future studies should therefore reflect these changes with a second control group of surviving infants more closely matched to the type of environment in which SIDS infants might be found.

Case-Control Studies↗
PubMed1983

'Near-miss' for sudden infant death syndrome infants: a clinical problem.

Three hundred six infants were referred for evaluation of "near-miss" sudden infant death syndrome (SIDS) from 1973 to 1980. Following the hospitalization and medical evaluation, there were 156 infants (115 term and 41 preterm) for whom there was no explanation for the presenting event and who were considered near-miss infants; 88% of these infants were seen during the first 3 months of life. A repeat near-miss event was reported in 63% (term) and 83% (preterm) infants. Twelve percent of term infants and 17% of the preterm infants had ten or more repeat events. A home apnea/cardiac monitor was prescribed for 88% of the infants for an average duration of 5.6 months in term infants and 3.5 months in preterm infants. Monitoring had been discontinued in 69% of the infants by 7 months of age. One full-term infant was later a SIDS victim. The risk of a repeat near-miss event is concluded to be sufficiently great to demand immediate hospitalization, medical evaluation, home monitoring when there is no specific treatment, and close clinical follow-up. Follow-up studies are needed to determine whether there is any long-term morbidity for infants who have had near miss events.

Age Factors↗
PubMed1986

Small upper airway in near-miss sudden infant death syndrome infants and their families.

6 infants (index cases) from five different families had a near-miss sudden infant death syndrome event between 3 and 12 weeks of age and had polygraphically documented apnoeas during sleep. 4 of their siblings had died of SIDS. The index cases, their 4 living siblings, 10 parents, and 8 grandparents underwent respiratory studies during sleep. All the adults and 3 index cases had cephalometric X-rays. 2 index cases underwent volume computerised tomographic scans when awake and during sleep. Index cases had mixed and obstructive sleep apnoea. Several family members had obstructive sleep apnoea; cephalometric X-rays also showed small upper airways, particularly behind the base of the tongue. A small posterior airway at the level of the tongue may be a familial risk factor for apnoea of infancy.

Adult↗
PubMed1979

Neurologic abnormalities in near miss for sudden infant death syndrome infants.

As part of the Sudden Death Research Project at Stanford University School of Medicine, we have performed systematic neurologic examination of 41 near miss infants, 7 normal siblings of babies who died a sudden infant death, and 21 normal control infants. Many infants were examined longitudinally until 2 years of age. We found that near miss infants under 3 months of age had consistent abnormalities of muscle tone, particularly shoulder hypotonia. These abnormalities disappeared with maturation, but only 60% of older infants who had suffered near miss episodes of neurologically and developmentally normal. In addition, only one of the seven apparently normal siblings had an entirely normal neurologic examination when first seen. Thus, infants who present with near miss episodes may have an underlying central nervous system abnormality or may acquire some abnormality as a result of the episode.

California↗
PubMed2000

Changing concepts of sudden infant death syndrome: implications for infant sleeping environment and sleep position. American Academy of Pediatrics. Task Force on Infant Sleep Position and Sudden Infant Death Syndrome.

The American Academy of Pediatrics has recommended since 1992 that infants be placed to sleep on their backs to reduce the risk of sudden infant death syndrome (SIDS). Since that time, the frequency of prone sleeping has decreased from >70% to approximately 20% of US infants, and the SIDS rate has decreased by >40%. However, SIDS remains the highest cause of infant death beyond the neonatal period, and there are still several potentially modifiable risk factors. Although some of these factors have been known for many years (eg, maternal smoking), the importance of other hazards, such as soft bedding and covered airways, has been demonstrated only recently. The present statement is intended to review the evidence about prone sleeping and other risk factors and to make recommendations about strategies that may be effective for further reducing the risk of SIDS. This statement is intended to consolidate and supplant previous statements made by this Task Force.

Cause of Death↗
PubMed1993

Child abuse, sudden infant death syndrome, and unexpected infant death.

There is now evidence, from a variety of approaches, that indicate that between one tenth and one fifth of children currently diagnosed as cases of sudden infant death syndrome are not natural deaths. There is also equally strong evidence, where the possibility of filicide has been explored, that the majority of children diagnosed as cases of sudden infant death syndrome do die of natural causes.

Child Abuse↗
PubMed2004

Sudden infant death syndrome and unclassified sudden infant deaths: a definitional and diagnostic approach.

The definition of sudden infant death syndrome (SIDS) originally appeared in 1969 and was modified 2 decades later. During the following 15 years, an enormous amount of additional information has emerged, justifying additional refinement of the definition of SIDS to incorporate epidemiologic features, risk factors, pathologic features, and ancillary test findings. An expert panel of pediatric and forensic pathologists and pediatricians considered these issues and developed a new general definition of SIDS for administrative and vital statistics purposes. The new definition was then stratified to facilitate research into sudden infant death. Another category, defined as unclassified sudden infant deaths, was introduced for cases that do not meet the criteria for a diagnosis of SIDS and for which alternative diagnoses of natural or unnatural conditions were equivocal. It is anticipated that these new definitions will be modified in the future to accommodate new understanding of SIDS and sudden infant death.

Humans↗
PubMedDate not supplied

Neck extension and rotation in sudden infant death syndrome and other natural infant deaths.

It has been hypothesized that some cases of sudden infant death syndrome (SIDS) are a result of neck extension and/or rotation that causes vertebral artery (VA) compression and brain stem ischemia. There is a paucity of relevant literature on this topic. Therefore, our aim was to compare neck rotation and extension in SIDS and other natural infant deaths. Cases of SIDS and other natural infant deaths within the San Diego SIDS Research Project database were analyzed retrospectively with respect to neck and body position as reported by the trained, experienced scene investigators and/or the caretakers who discovered the infants. Information was used from 246 SIDS cases and 56 cases of other natural deaths. Simultaneous neck extension and rotation was not reported in either group. When data regarding neutral/flexed/extended position and rotation of the neck were combined, no significant differences were found between the two groups (P = 0.94); 40% of the SIDS cases and 41% of the other natural death cases were found with the neck either extended or rotated (odds ratio [OR] 0.97, [reference group = neck either neutral or flexed, and not rotated], 95% confidence interval [CI] 0.45, 2.11). There were also no significant differences between the groups when neck rotation and neck extension were analyzed independent of one another. Neck rotation among cases found in the prone position was common and was not significantly different between the two groups (49% of 146 SIDS cases, 58% of 24 other natural death cases, P = 0.38, OR 0.68, 95% CI 0.28, 1.62). Neck rotation among infants found in the supine position occurred one-third as often in the SIDS group (9% of 33 cases) as in the other natural death group (29% of 14 cases); however, the difference was not significant (P = 0.17; OR 0.25, 95% CI 0.05, 1.31). Although our analysis does not exclude VA compression and brain stem ischemia in some cases of SIDS, we found no evidence to affirm its importance. This study demonstrates the importance of meticulous scene descriptions, including neck position.

Female↗
PubMed2003

A comparison of respiratory symptoms and inflammation in sudden infant death syndrome and in accidental or inflicted infant death.

Upper respiratory infection and pulmonary inflammation are common in sudden infant death syndrome, but their role in the cause of death remains controversial. Controlled studies comparing clinical upper respiratory infection and inflammation in sudden infant death syndrome with sudden infant deaths caused by accidents and inflicted injuries (controls) are unavailable. Our aim was to compare respiratory inflammation and upper respiratory infection within 48 hours of death and postmortem culture results in these two groups. A retrospective analysis of upper respiratory infection and pathologic variables in the trachea and lung of 155 infants dying of sudden infant death syndrome and 33 control infants was undertaken. Upper respiratory infection was present in 39% of sudden infant death syndrome cases and 40% of control cases. Upper respiratory infection was more likely to have occurred in association with more severe lymphocytic interstitial pneumonitis when sudden infant death syndrome cases and control cases were combined ( P=.04). Proximal and distal tracheal lymphocytic infiltration was more severe in control cases than in sudden infant death syndrome cases ( P=.01 and.01, respectively). Lymphocytic infiltrations of the bronchi, bronchioles, and pulmonary interstitium were similar between groups. Bronchial associated lymphoid tissue was more prominent in control cases ( P=.04). Cultures were positive in 80% of sudden infant death syndrome cases, 78% of which were polymicrobial. Among control cases, 89% were positive, with 94% being polymicrobial. This study confirms that microscopic inflammatory infiltrates in sudden infant death syndrome are not lethal.

Accidents↗
PubMed1994

Sudden infant death syndrome and infant mortality in aboriginal and non-aboriginal infants.

The aim of this study was to investigate sudden infant death syndrome (SIDS) in the context of total infant mortality for Aboriginal and non-Aboriginal infants. Deaths for infants born in Western Australia from 1980 to 1988 inclusive were ascertained from a total population data base. Infant mortality rates and rates by period and cause of death were calculated for both populations. Aboriginal infants had a mortality rate three times that for non-Aboriginal infants (23.6 cf. 7.9 per 1000 live births) and both populations showed a similar rate of decline in mortality over the study period. There were differences in the proportion of deaths occurring neonatally and postneonatally in the two populations. In terms of SIDS, 21% of the deaths in Aboriginal infants occurred neonatally compared with 7% for non-Aboriginal infants. The overall cause of infant death distribution differed significantly between the two populations (P < 0.001). During the study period, Aboriginal infants showed a significant increase in deaths due to SIDS and a significant decrease in those due to birth defects and low birthweight. These results suggest it would be useful to review the pathology and diagnosis of sudden unexplained death in infancy.

Cause of Death↗
PubMedDate not supplied

The sudden infant death syndrome and infant botulism.

Fecal and serum specimens taken from 30 cases of sudden infant death and from eight cases of nonsudden infant death that were diagnosed at a single facility in King County, Wash., were examined for the presence of Clostridium botulinum organisms and toxin. Organisms, but not toxin, were recovered from a fecal specimen in one case of sudden infant death, results that parallel those from studies previously reported by investigators in California. Studies made in our laboratory of a nonfatal case of infant botulism revealed that an estimated 366,000 mouse minimal lethal doses of toxin were excreted in feces collected by purging the infant. Organisms and toxin were excreted for at least 15 days after the infant was hospitalized. Observations made in our laboratory of atypical responses in mice to both fecal and serum extracts, coupled with recently described experiments in which mice were used as an animal model for infant botulism in humans, provide a biologically plausible foundation for the hypothesis that C. botulinum may be implicated etiologically in some sudden infant deaths. Additional microbiologic, physiologic, and toxicologic data are needed to adequately test this hypothesis.

Botulinum Toxins↗