Annually, several hundred infant deaths occur in sitting devices (eg, car safety seats [CSSs] and strollers). Although American Academy of Pediatrics guidelines discourage routine sleeping in sitting devices, little is known about factors associated with deaths in sitting devices. Our objective was to describe factors associated with sleep-related infant deaths in sitting devices.
We analyzed 2004–2014 National Center for Fatality Review and Prevention data. The main outcome was sleep location (sitting device versus not). Setting, primary caregiver, supervisor at time of death, bed-sharing, and objects in the environment were compared by using χ2 tests and multivariable logistic regression. Descriptive statistics of additional possible risk factors were reviewed.
Of 11 779 infant sleep-related deaths, 348 (3.0%) occurred in sitting devices. Of deaths in sitting devices, 62.9% were in CSSs, and in these cases, the CSS was used as directed in <10%. Among all sitting-device deaths, 81.9% had ≥1 risk factor, and 54.9% had ≥2 risk factors. More than half (51.6%) of deaths in CSSs were at the child’s home. Compared with other deaths, deaths in sitting devices had higher odds of occurring under the supervision of a child care provider (adjusted odds ratio 2.8; 95% confidence interval 1.5–5.2) or baby-sitter (adjusted odds ratio 2.0; 95% confidence interval 1.3–3.2) compared with a parent.
There are higher odds of sleep-related infant death in sitting devices when a child care provider or baby-sitter is the primary supervisor. Using CSSs for sleep in nontraveling contexts may pose a risk to the infant.
Comments
RE: Infant Deaths in Sitting Devices
For the time being and without going into a long-winded defence of the following observations, suffice it to say, that the model referred to below concludes that all SIDS fatalities are attributable solely to the silencing of Na+ cation electrically potentiated neuronal signalling along the abdominal afferential vagal system returning to the NTS. Normally the activation of this pathway results in CAP A1 microarousal signatures appearing in the EEG/PSG recordings during the descending NREM phase of sleep, which then lead to a terminal 'macro' A1 rendition transitioning into the ascending phase, and followed by the A2 and A3 CAP episodes which precede the REM phases.
Accordingly, concentration and dilution of saline in the abdominal lumen, therefore both activates and sustains the regulation of the voltage. Hence the following comment:
The higher odds of sleep-related infant deaths in sitting devices that occur when a child care provider or baby-sitter is the primary supervisor, is a conclusion which not alone informatively adds to th readers' understanding of SIDS and related phenomena, but which also in drawing attention to the provision of care, implicity points to considering the possibility of providers and baby-sitters unwittingly contributing to the fatalities.
In that regard, a theoretical model of sleep and arousal can be applied to show how such fatalities can be directly attributable to care providers performing what would otherwise be regarded as a not unusual commonplace and unremarkable procedure. Namely, providing infants with a 'quick fix' feeding bottle containing some kind of watery concoction such as juice or the like. And which, since it is normally regarded as being harmless and of such little concern, the fact that it has occurred prior to the death of an infant placed in a sitting device, or in a cot or bed ... or anywhere for that matter ... traditionally has been both overlooked, and research-wise disregarded, to the extent that a search of the SIDS death scene literature will fail to evidence even a passing mention of it.
However, and inasmuch as that has been and continues to be the case, the model indicates that the study's conclusion can be applied likewise to the elevated occurrences of infant deaths in parental abodes at weekends and New Year's, to the highly elevated occurrences of SIDS fatalities in various daycare environments, and also to the simultaneous deaths of twins (SSIDS).
The fatalities occurring on New Year's and weekends are believed to be related to parental alcohol consumption, and presumably resulting in their impaired judgment and failing to follow BTS and/or other safe sleeping protocols. ( http://healthland.time.com/2010/12/30/why-do-sids-deaths-spike-on-new-ye... ) However, it's not alcoholic befuddlement that is the real culprit, but rather the 'quick fix' bottle being employed instead of providing the infant with its usual feed.
Keeping infants sleeping permits daycare providers to see to a variety of other concerns, and particularly where there are also older two- and three-year toddlers to look after, keeping the younger infants sleeping is the time-saver. and unwittingly/unintentionally both care providers and 'hungover' parents are contributing to increasing hazards of SIDS. That said, and inasmuch as the care providers are completely and innocently unsuspecting that diluted bottles can cause SIDS, nevertheless, there have been more than a few cases where infants have died after being given cough medicines containing the sedative diphenhydramine (Benadryl) to put them to sleep... ... and there was also a case in Connecticut where melatonin was employed.
So how can water be involved in elevating the SIDS fatalities statistics? To understand the answer we have to go all the way back to the early 1960's, In research during those years electrolytes began to be ruled out of both sleep and SIDS studies as being non relevant. Generally speaking that has continued to be the case, with the exception that in animal models aspiration of water or saline into the airways has been shown to prevent autoresuscitation, and with the implication that infants' aspiration of gastric contents merits consideration as a contributory cause of SIDS. However, the time may have arrived to reconsider the accuracy of the conclusionof non relevance.
For additional information please visit :
https://www.researchgate.net/publication/331161323
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https://www.researchgate.net/publication/331072170_Hypoxemia_cyclic_alte...