The effects of sleeping position, maternal smoking and substance misuse on the ventilatory response to hypoxia in the newborn period

Rossor, Thomas; Ali, Kamal; Bhat, Ravindra; Trenear, Rebecca; Rafferty, Gerrard F.; Greenough, Anne

doi:10.1038/s41390-018-0090-0

Cited by 8 publications

(3 citation statements)

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“…These studies have shown that prone sleep position may alter the autonomic control of the infant cardiovascular system, particularly at 2 to 3 months of age, and may result in decreased cerebral oxygenation [3,4]. Prone position was also shown to decrease cardiac output, mean arterial pressure, oxygen saturation, minute ventilation, and arousal responses to various stimuli [5][6][7][8].…”

Section: Resultsmentioning

confidence: 99%

Effect of sleep position in term healthy newborns on sudden infant death syndrome and other infant outcomes: A systematic review

Balachander

Sankar

2022

J Glob Health

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Background Though recommended by numerous guidelines, adherence to supine sleep position during the first year of life is variable across the globe. Methods This systematic review of randomized trials and observational studies assessed the effect of the supine compared to non-supine (prone or side) sleep position on healthy newborns. Key outcomes were neonatal mortality, sudden infant death syndrome (SIDS), sudden unexpected death in infancy (SUDI), acute life-threatening event (ALTE), neurodevelopment, and positional plagiocephaly. We searched MEDLINE via PubMed, Cochrane CENTRAL, EMBASE, and CINAHL (updated till November 2021). Two authors separately evaluated the risk of bias, extracted data, and synthesised effect estimates using relative risk (RR) or odds ratio (OR). The GRADE approach was used to assess the certainty of evidence. Results We included 54 studies (43 observational studies and 11 intervention trials) involving 474 672 participants. A single study meeting the inclusion criteria suggested that the supine sleep position might reduce the risk of SUDI (0-1 year; OR = 0.39, 95% confidence interval (CI) = 0.23-0.65; 384 infants), compared to non-supine position. Supine sleep position might reduce the risk of SIDS (0-1 year; OR = 0.51, 95% CI = 0.42-0.61; 26 studies, 59332 infants) and unexplained SIDS/severe ALTE (neonatal period; OR = 0.16, 95% CI = 0.03-0.82; 1 study, 119 newborns), but the evidence was very uncertain. Supine sleep position probably increased the odds of being 0.5 standard deviation (SD) below mean on Gross Motor Scale at 6 months (OR = 1.67, 95% CI = 1.22-2.27; 1 study, 2097 participants), but might have little to no effect at 18 months of age (OR = 1.16, 95% CI = 0.96, 1.43; 1 study, 1919 participants). An increase in positional plagiocephaly at 2-7 months of age with supine sleep position is possible (OR = 2.77, 95% CI = 2.06-3.72; 6 studies, 1774 participants). Conclusions Low- to very low-certainty evidence suggests that supine sleep position may reduce the risk of SUDI (0-1 year) and SIDS (0-1 year). Limited evidence suggests that supine sleeping probably delays short-term ‘gross motor’ development at 6 months, but the effect on long-term neurodevelopment at 18 months may be negligible.

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Section: Resultsmentioning

confidence: 99%

Effect of sleep position in term healthy newborns on sudden infant death syndrome and other infant outcomes: A systematic review

Balachander

Sankar

2022

J Glob Health

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“…Regarding the nature of the respiratory stressor causing the SIDS, our experiments indicate that the combination of low O 2 with high CO 2 results more deleterious than hypoxia or hypercapnia separately since by themselves they did not induce sudden death; this is likely because the disturbances in the generation of ETBs worsen arterial O 2 saturation; thus, a defective generation of ETBs, like are those previously reported defects in sighs, arousals, and gasping (Garcia et al, 2013 ), would be considered as a physiological biomarker of susceptibility in SIDS. Abnormalities of breathing control may cause SIDS either by hyporesponsive chemoreflexes that may allow hypoxia to persist without an adequate response or by destabilizing hyperresponsive chemoreflexes (Cummings et al, 2011 ; Gauda et al, 2007 ; Rossor et al, 2018 ) as seem to be the case of the Cx36KO mice. In the stereotyped cascade of events leading to the respiratory arrest in the neonatal Cx36KO mice, we have identified two pathophysiological determinants not previously reported: the early collapse in the generation of EBTs, which accelerates heart rate and worsens the O 2 saturation, and the generation of a paroxysmal clonic‐tonic generalized motor discharge that provokes the definitive cessation of eupneic rhythm and the starting of gasping respiration, and precipitates the collapse of heart rate.…”

Section: Discussionmentioning

confidence: 99%

Respiratory disturbances and high risk of sudden death in the neonatal connexin‐36 knockout mouse

Pérez-Atencio

Casarrubios

Ibarz

et al. 2021

Physiological Reports

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Neural circuits at the brainstem involved in the central generation of the motor patterns of respiration and cardiorespiratory chemoreflexes organize as cell assemblies connected by chemical and electrical synapses. However, the role played by the electrical connectivity mainly mediated by connexin36 (Cx36), which expression reaches peak value during the postnatal period, is still unknown. To address this issue, we analyzed here the respiratory phenotype of a mouse strain devoid constitutively of Cx36 at P14. Male Cx36‐knockout mice at rest showed respiratory instability of variable degree, including a periodic Cheyne–Stokes breathing. Moreover, mice lacking Cx36 exhibited exacerbated chemoreflexes to normoxic and hypoxic hypercapnia characterized by a stronger inspiratory/expiratory coupling due to an increased sensitivity to CO2. Deletion of Cx36 also impaired the generation of the recurrent episodes of transient bradycardia (ETBs) evoked during hypercapnic chemoreflexes; these EBTs constituted a powerful mechanism of cardiorespiratory coupling capable of improving alveolar gaseous exchange under hypoxic hypercapnia conditions. Approximately half of the homo‐ and heterozygous Cx36KO, but none WT, mice succumbed by respiratory arrest when submitted to hypoxia‐hypercapnia, the principal exogenous stressor causing sudden infant death syndrome (SIDS). The early suppression of EBTs, which worsened arterial O2 saturation, and the generation of a paroxysmal generalized clonic‐tonic activity, which provoked the transition from eupneic to gasping respiration, were the critical events causing sudden death in the Cx36KO mice. These results indicate that Cx36 expression plays a pivotal role in respiratory control, cardiorespiratory coordination, and protection against SIDS at the postnatal period.

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“…These differences remained significant when adjusting for differences in birthweight, age and sex (20,21). Furthermore, maternal smoking and substance abuse particularly impair the response to hypoxia in the prone position (22). This maladaptive response can be explained by the infant's chronic exposure to fetal hypoxia, leading to persistent, inappropriate activation of the respiratory neural network underlying the biphasic ventilatory response (21,23).…”

Section: Physiological Abnormalities In Infants Of Mothers Who Smokedmentioning

confidence: 99%

The Role of Maternal Smoking in Sudden Fetal and Infant Death Pathogenesis

2020

Self Cite

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Maternal smoking is a risk factor for both sudden infant death syndrome (SIDS) and sudden intrauterine unexplained death syndrome (SIUDS). Both SIDS and SIUDS are more frequently observed in infants of smoking mothers. The global prevalence of smoking during pregnancy is 1.7% and up to 8.1% of women in Europe smoke during pregnancy and worldwide 250 million women smoke during pregnancy. Infants born to mothers who smoke have an abnormal response to hypoxia and hypercarbia and they also have reduced arousal responses. The harmful effects of tobacco smoke are mainly mediated by release of carbon monoxide and nicotine. Nicotine can enter the fetal circulation and affect multiple developing organs including the lungs, adrenal glands and the brain. Abnormalities in brainstem nuclei crucial to respiratory control, the cerebral cortex and the autonomic nervous system have been demonstrated. In addition, hypodevelopment of the intermediolateral nucleus in the spinal cord has been reported. It initiates episodic respiratory movements that facilitate lung development. Furthermore, abnormal maturation and transmitter levels in the carotid bodies have been described which would make infants more vulnerable to hypoxic challenges. Unfortunately, smoking cessation programs do not appear to have significantly reduced the number of pregnant women who smoke.

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The effects of sleeping position, maternal smoking and substance misuse on the ventilatory response to hypoxia in the newborn period

Abstract: The altered response to hypoxia in the prone position of infants whose mothers substance-misused and smoked in pregnancy may explain their increased vulnerability to SIDS.

Cited by 8 publications

References 25 publications

Effect of sleep position in term healthy newborns on sudden infant death syndrome and other infant outcomes: A systematic review

Effect of sleep position in term healthy newborns on sudden infant death syndrome and other infant outcomes: A systematic review

Respiratory disturbances and high risk of sudden death in the neonatal connexin‐36 knockout mouse

The Role of Maternal Smoking in Sudden Fetal and Infant Death Pathogenesis

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