SIDS and Other Sleep-Related Infant Deaths: Updated 2016 Recommendations for a Safe Infant Sleeping Environment

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doi:10.1542/peds.2016-2938

Cited by 294 publications

(141 citation statements)

References 22 publications

(26 reference statements)

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“…An American Academy of Pediatrics Policy Statement clearly states “Do not use home cardiorespiratory monitors as a strategy to reduce the risk of Sudden Infant Death Syndrome (SIDS),” noting that there are no data that commercial devices designed to monitor infant vital signs reduce the risk of SIDS. 4 In select populations, including premature infants at high risk of recurrent apnea, bradycardia, and hypoxemia, physiologic monitoring may be indicated. In those populations, monitoring devices with form factors like those in Table 1 may eventually be of value, but only if their safety, accuracy, and effectiveness are demonstrated.…”

Section: Indicationsmentioning

confidence: 99%

The Emerging Market of Smartphone-Integrated Infant Physiologic Monitors

Bonafide

Jamison

Foglia

2017

JAMA

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In the past 2 years, a new class of infant physiologic monitors marketed to parents for use in the home has emerged. Smartphone applications (apps) integrated with sensors built into socks, onesies, buttons, leg bands, and diaper clips have the capability to display infants' respirations, pulse rate, and blood oxygen saturation, and to generate alarms for apnea, tachycardia, bradycardia, and desaturation (Table ). Despite the lack of publicly available evidence supporting the safety, accuracy, effectiveness, or role of these monitors in the care of well infants, sales of these products are brisk and the market is expanding. For example, the makers of a "smart sock" monitor (Owlet Baby Care) that claims to alert parents if their infant stops breathing 1 recently reported sales of 40 000 units at $250 each. 2

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Section: Indicationsmentioning

confidence: 99%

The Emerging Market of Smartphone-Integrated Infant Physiologic Monitors

Bonafide

Jamison

Foglia

2017

JAMA

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“…In 1992, the AAP recommended [76]: “The weight of evidence implicated the prone position as a significant risk for SIDS,” but “there are still good reasons for placing certain infants prone.” In the USA, 54% of all infants and 75% of those second- and thirdborn were put to sleep prone in 1995 [77], and the SIDS rate was 0.87 per 1,000 live births [78]. As late as 2016, the AAP recommended among 18 other measures [79]: “Back to sleep for every sleep.”…”

Section: Risk Reduction Campaignsmentioning

confidence: 99%

Cot Death: History of an Iatrogenic Disaster

Obladen

2017

Neonatology

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Since antiquity, cot death has been explained as accidental suffocation, overlaying, or smothering. Parents were blamed for neglect or drunkenness. A cage called arcuccio was invented around 1570 to protect the sleeping infant. Up to the 19th century, accidents were registered as natural causes of death. From 1830, accidental suffocation became unacceptable for physicians and legislators, and “natural” explanations for the catastrophe were sought, with parents being consoled rather than blamed. Two assumed causes had serious consequences: thymus hyperplasia was irradiated, causing thyroid cancer, and the concept of central apnea was widely accepted, which led to home monitors and distracted from epidemiological evidence. Prone sleeping originated in the 1930s and from 1944, it was associated with cot death. However, from the 1960s, many authors recommended prone sleeping for infants, and many countries adopted the advice. A worldwide epidemic followed, peaking at 2‰ in England and Wales and 5‰ in New Zealand in the 1980s. Although epidemiological evidence was available by 1970, the first intervention was initiated in the Netherlands in 1989. Cot death disappeared almost entirely wherever prone sleeping was avoided. This strongly supports the assumption that prone sleeping has the greatest influence on the disorder, and that the epidemic resulted from wrong advice.

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“…Second, otherwise healthy infants can have abnormal breathing rhythms if their respiratory circuit is not fully developed (Abu-Shaweesh & Martin, 2008). An immature respiratory circuit can cause apneas of prematurity (AOP) (Abu-Shaweesh & Martin, 2008;Poets, 2010;Zhao, Gonzalez, & Mu, 2011) and is a primary risk factor for sudden infant death syndrome (SIDS) (Goldstein, Trachtenberg, Sens, Harty, & Kinney, 2016;Moon, Horne, & Hauck, 2007;SYNDROME, 2016). AOP and SIDS are most prevalent in newborns and premature infants, but AOP often self-resolves with age and, likewise, the risk for SIDS declines when infants mature.…”

Section: Introductionmentioning

confidence: 99%

Development of the brainstem respiratory circuit

Heijden

Zoghbi

2019

WIREs Developmental Biology

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The respiratory circuit is comprised of over a dozen functionally and anatomically segregated brainstem nuclei that work together to control respiratory rhythms. These respiratory rhythms emerge prenatally but only acquire vital importance at birth, which is the first time the respiratory circuit faces the sole responsibility for O2/CO2 homeostasis. Hence, the respiratory circuit has little room for trial‐and‐error‐dependent fine tuning and relies on a detailed genetic blueprint for development. This blueprint is provided by transcription factors that have specific spatiotemporal expression patterns along the rostral‐caudal or dorsal‐ventral axis of the developing brainstem, in proliferating precursor cells and postmitotic neurons. Studying these transcription factors in mice has provided key insights into the functional segregation of respiratory control and the vital importance of specific respiratory nuclei. Many studies converge on just two respiratory nuclei that each have rhythmogenic properties during the prenatal period: the preBötzinger complex (preBötC) and retrotrapezoid nucleus/parafacial nucleus (RTN/pF). Here, we discuss the transcriptional regulation that guides the development of these nuclei. We also summarize evidence showing that normal preBötC development is necessary for neonatal survival, and that neither the preBötC nor the RTN/pF alone is sufficient to sustain normal postnatal respiratory rhythms. Last, we highlight several studies that use intersectional genetics to assess the necessity of transcription factors only in subregions of their expression domain. These studies independently demonstrate that lack of RTN/pF neurons weakens the respiratory circuit, yet these neurons are not necessary for neonatal survival because developmentally related populations can compensate for abnormal RTN/pF function at birth. This article is categorized under: Nervous System Development > Vertebrates: Regional Development

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SIDS and Other Sleep-Related Infant Deaths: Updated 2016 Recommendations for a Safe Infant Sleeping Environment

Cited by 294 publications

References 22 publications

The Emerging Market of Smartphone-Integrated Infant Physiologic Monitors

The Emerging Market of Smartphone-Integrated Infant Physiologic Monitors

Cot Death: History of an Iatrogenic Disaster

Development of the brainstem respiratory circuit

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