Biochemical and immunological studies in SIDS victims. Clues to understanding the death mechanism

Rognum, TO; Saugstad, Ola Didrik

doi:10.1111/j.1651-2227.1993.tb12886.x

Cited by 86 publications

(76 citation statements)

References 23 publications

(17 reference statements)

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“…6 Filiano and Kinney referenced a study by Hoffman et al 23 in support of this statement. However, that study had 2 control groups and group B, the one that was matched for birth weight and race, reduced the odds ratio of SIDS for all newborn risk factors, such as Apgars, to nonsignificance.…”

Section: Vulnerable Infantmentioning

confidence: 58%

“…They continued, "together, these risk factors point to a suboptimal intrauterine environment, and suggest that the mechanisms for risk for SIDS develop in fetal life in at least some cases." 6 What follows is a detailed review of these 4 lines of evidence.…”

Section: Vulnerable Infantmentioning

confidence: 99%

“…6 Naeye reported in 1976 significant proliferation of astroglial fibers in the brainstem of half of his SIDS cases 12 ; the other half had no more nor less astrogliosis than did controls who had died of trauma or acute asphyxia. (Because 4 days or more are required to develop astrogliosis, 13 its presence cannot be attributed to a single acute episode ending in death.)…”

Section: Vulnerable Infantmentioning

confidence: 99%

“…More recently, Rognum and Saugstad 6 proposed a "fatal triangle in SIDS," a hypothesis that also involved 3 types of risk factors: 1) a vulnerable developmental stage of central nervous system (CNS) and mucosal immunity, 2) predisposing factors (astrogliosis, genetic make-up), and 3) a trigger event, such as an infection.…”

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confidence: 99%

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The Triple Risk Hypotheses in Sudden Infant Death Syndrome

2002

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ABSTRACT. Sudden infant death syndrome (SIDS) victims were regarded as normal as a matter of definition (Beckwith 1970) until 1952 when Kinney and colleagues argued for elimination of the clause, "unexpected by history." They argued that "not all SIDS victims were normal," and referred to their hypothesis that SIDS results from brain abnormalities, which they postulated "to originate in utero and lead to sudden death during a vulnerable postnatal period." Bergman (1970) Interest in the brainstem of SIDS victims began with Naeye's 1976 report of astrogliosis in 50% of all victims. He concluded that these changes were caused by hypoxia and were not the cause of SIDS. He noted an absence of astrogliosis in some older SIDS victims, compatible with a single, terminal episode of hypoxia without previous hypoxic episodes, prenatal or postnatal.Kinney and colleagues (1983) reported gliosis in 22% of their SIDS victims. Subsequently, they instituted studies of neurotransmitter systems in the brainstem, particularly the muscarinic (1995) and serotenergic systems (2001). The major issue is when did the brainstem abnormalities, astrogliosis, or neurotransmitter changes occur and whether either is specific to SIDS. There is no published method known to us of determining the time of origin of these markers except that the injury causing astrogliosis must have occurred at least 4 days before death (Del Bigio and Becker, 1994). Because the changes in neurotransmitter systems found in the arcuate nucleus in SIDS victims were also found in the chronic controls with known hypoxia, specificity of these markers for SIDS has not been established. It seems likely that the "acute control" group of Kinney et al (1995) died too quickly to develop gliosis or severe depletion of the neurotransmitter systems. We can conclude that the acute controls had no previous episodes of severe hypoxia, unlike SIDS or their "chronic controls." Although the average muscarinic cholinergic receptor level in the SIDS victim was significantly less than in the acute controls, the difference was only 27%, and only 21 of 41 SIDS victims had values below the mean of the acute controls. The study of the medullary serotonergic network by Kinney et al (2001) revealed greater reductions in the SIDS victims than in acute controls, but the questions of cause versus effect of the abnormalities, and whether they occurred prenatally or postnatally, remain unanswered. Hypoplasia of the arcuate nucleus was stated to occur in 5% of their SIDS cases by Kinney et al (2001), but this is a "primary developmental defect" according to Matturri et al (2002) with a larger series, many of whom were stillbirths. These cases should not be included under the rubric of SIDS, by definition.There are difficulties with Filiano and Kinney's (1994) explanation of the age at death distribution of SIDS. They postulate that the period between 1 and 6 months represents an unstable time for virtually all physiologic systems. However, this period demonstrates much less instability than does the...

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Section: Vulnerable Infantmentioning

confidence: 58%

Section: Vulnerable Infantmentioning

confidence: 99%

Section: Vulnerable Infantmentioning

confidence: 99%

mentioning

confidence: 99%

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The Triple Risk Hypotheses in Sudden Infant Death Syndrome

2002

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“…6 This was subsequently formulated as the 'fatal triangle' and 'triple risk' models for SIDS by Rognum and Saugstad , 7 and Filiano and Kinney. 8 Following this lead, it may now be useful to extend this model to provide a conceptual framework for dealing with risk factors for accidental suffocation and unexpected infant death in a shared sleeping situation.…”

Section: The Triple Risk Model For Shared Sleepingmentioning

confidence: 99%

The Triple Risk Model for Shared Sleeping

Byard

2012

J Paediatrics Child Health

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PUTTING BED-SHARING FINDINGS INTO PERSPECTIVEWe read with interest the paper by Weber et al. 1 and suggest that the findings need to be put into context, both in terms of what happens in the surviving infant population and the specific circumstances surrounding bed-sharing deaths. The limitations of the study design and inconsistency in the details available makes such contextual interpretation difficult. Recently, we conducted a population-based case-control study in the south-west of England 2 that can answer both these questions. We too found that over 50% of the sudden infant death syndrome (SIDS) deaths occurred in co-sleeping situations but also a similar situation for 21% of our age-matched controls, suggesting that we would expect a fifth of the SIDS deaths to occur whilst co-sleeping, and this fact may have nothing to do with the causal mechanism of death. Much of the excess risk associated with co-sleeping seems to be associated with recent parental alcohol consumption, illegal drugs and/or using a sofa to co-sleep. The multivariable interaction between co-sleeping and the consumption of drugs and/or alcohol was significant, and the high number of unexplained co-sleeping deaths on a sofa found in Weber's study and ours confirms observations 3 that the only sleeping environment in the UK in which SIDS deaths are increasing is those found co-sleeping on a sofa. Removing these hazardous conditions showed the proportion of co-sleepers was similar (18% vs. 16% controls) and in the opposite direction (6% vs. 10%) if we further removed parents who regularly smoked. Thus, the message we need to get across is not that all parents should avoid co-sleeping, but that all parents should avoid drinking alcohol, taking drugs or smoking if they want to sleep with their baby, and that co-sleeping on a sofa is a far more dangerous practice than using the parental bed.We welcome the recent press announcement by the FSID to actively monitor infant death data and emphasise the importance of including details on recent drug and alcohol consumption, parental smoking and use of sofas. Our study 2 showed that for infants sleeping in a cot, the most common sleeping position both for healthy infants and those who died was supine, which has repeatedly been shown to be the safest sleeping position. In the absence of control data, this finding could have led to entirely incorrect conclusions being drawn. Thus national monitoring should include age-matched data from the surviving infant population to avoid the possibility of misleading anecdotal observations.

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Sudden and Unexpected Deaths in Infants and Sudden Infant Death Syndrome

Bajanowski¹,

Vennemann²

2014

Handbook of Forensic Medicine

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Biochemical and immunological studies in SIDS victims. Clues to understanding the death mechanism

Cited by 86 publications

References 23 publications

The Triple Risk Hypotheses in Sudden Infant Death Syndrome

The Triple Risk Hypotheses in Sudden Infant Death Syndrome

The Triple Risk Model for Shared Sleeping

Sudden and Unexpected Deaths in Infants and Sudden Infant Death Syndrome

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