scholarly journals 1738 OBSTRUCTIVE SLEEP APNEA IN A 7-YEAR-OLD BOY WHO HAD A NEAR-SUDDEN INFANT DEATH (N-SIDS) EPISODE AT 6 WEEKS

1985 ◽  
Vol 19 (4) ◽  
pp. 400A-400A
Author(s):  
Joan L Caddell
PEDIATRICS ◽  
1984 ◽  
Vol 74 (2) ◽  
pp. 319-320
Author(s):  
CHRISTIAN GUILLEMINAULT

In Reply.— Harpey and Renault postulate a relationship between the uvula, obstructive sleep apnea, and sudden infant death syndrome. Although I believe that obstructive sleep apnea syndrome may be one of the mechanisms leading to sudden infant death syndrome, this speculation is extremely controversial. I do concur with Harpey and Renault that obstructive sleep apnea can trigger esophageal reflux. A segment from a sleep recording of a 9-week-old, full-term infant with near-miss sudden infant death syndrome is presented in the Figure.


Author(s):  
J. Kerz ◽  
P. Schürmann ◽  
T. Rothämel ◽  
T. Dörk ◽  
M. Klintschar

Abstract Background Both obstructive sleep apnea (OSA) and (at least a fraction of) sudden infant death syndrome (SIDS) are associated with impaired respiration. For OSA, an association with several gene variants was identified. Therefore, our hypothesis is that these polymorphisms might be of relevance in SIDS as well. Methods Twenty-four single nucleotide polymorphisms (SNPs) in 21 candidate genes connected to OSA, were genotyped in a total of 282 SIDS cases and 374 controls. Additionally, subgroups based on factors codetermining the SIDS risk (age, sex, season, and prone position) were established and compared as well. Results Two of the analyzed SNPs showed nominally significant differences between SIDS and control groups: rs1042714 in ADRB2 (adrenoceptor beta 2) and rs1800541 in EDN1 (endothelin 1). In the subgroup analyses, 10 further SNPs gave significant results. Nevertheless, these associations did not survive adjustment for multiple testing. Conclusions Our results suggest that there might be a link between SIDS and OSA and its resulting respiratory and cardiovascular problems, albeit this predisposition might be dependent on the combination with other, hitherto unknown gene variants. These findings may encourage replication studies to get a better understanding of this connection.


2002 ◽  
Vol 166 (6) ◽  
pp. 833-838 ◽  
Author(s):  
Thorarinn Gislason ◽  
Johann Heidar Johannsson ◽  
Asgeir Haraldsson ◽  
Berglind Ran Olafsdottir ◽  
Helga Jonsdottir ◽  
...  

2018 ◽  
Vol 56 (7) ◽  
pp. 890-895 ◽  
Author(s):  
Christopher J. Greenlee ◽  
Melissa A. Scholes ◽  
Dexiang Gao ◽  
Norman R. Friedman

Objective:To determine whether nonsupine sleep improves obstructive sleep apnea (OSA) in infants with cleft palate undergoing polysomnography (PSG).Design:Retrospective chart review.Setting:Tertiary care pediatric hospital.Patients:Twenty-seven infants (1 month to 1 year) with cleft palate with or without cleft lip (CP ± L) undergoing PSG testing for suspected OSA were included.Main Outcome Measures:Polysomnography measures included obstructive apnea–hypopnea index (OAHI), central apnea–hypopnea index (CAHI), oxygen saturation (SpO2) nadir, SpO2, and end-tidal carbon dioxide (ETCO2).Results:Twenty-three PSGs with at least 20 minutes of sleep in both the supine and the nonsupine positions were analyzed. The supine OAHI (mean: 16.8 events/hour; standard deviation [SD]: 18.5) and nonsupine OAHI (mean: 12.6 events/hour; SD: 12.6) did not differ significantly ( P = .10). The supine CAHI (mean: 1.9 events/hour; SD: 2.7) and nonsupine CAHI (mean: 3.1 events/hour; SD: 3.7; P = .15), the supine SpO2nadir (mean: 81.2%; SD: 6.3) and nonsupine SpO2nadir (mean: 81.8%; SD: 5.3; P = .70), the supine mean SpO2(mean: 95.5%; SD: 1.9) and nonsupine mean SpO2saturation (mean: 95.3%; SD: 2.4; P = .34), and the supine ETCO2(mean: 45.4 mm Hg; SD: 5.3) and nonsupine ETCO2(mean: 42.5 mm Hg; SD: 10.1; P = .24) were also similar.Conclusions:There were no significant improvements in OSA metrics during nonsupine sleep in infants with CP ± L. Prior to recommending nonsupine positioning which increases infant’s exposure to sudden infant death syndrome risk, we advocate obtaining a PSG to verify an objective improvement in OSA.


PEDIATRICS ◽  
1984 ◽  
Vol 73 (1) ◽  
pp. 71-78
Author(s):  
Christian Guilleminault ◽  
Marianne Souquet ◽  
R. L. Ariagno ◽  
Rowena Korobkin ◽  
F. B. Simmons

Five full-term infants were referred for "near miss" sudden infant death syndrome events, which occurred between 3 and 12 weeks of age. After a complete pediatric evaluation and 24-hour polygraphic monitoring, each infant was monitored at home with a cardiorespiratory monitor. Each was followed regularly (with repeat polygraphic recordings) up to 4 years of age. All five infants developed heavy snoring at night and symptoms of obstrutive sleep apnea syndrome. The diagnosis of obstructive sleep apnea syndrome was confirmed by polygraphic recordings; surgery was recommended. Four of the five children underwent adenoidectomies between 3 and 4 years of age, and this significantly improved their condition. These five cases are the first polygraphically documented histories of the development of obstructive sleep apnea syndrome.


PEDIATRICS ◽  
1979 ◽  
Vol 64 (6) ◽  
pp. 882-891 ◽  
Author(s):  
Christian Guilleminault ◽  
Ronald Ariagno ◽  
Rowena Korobkin ◽  
Lynn Nagel ◽  
Roger Baldwin ◽  
...  

Twenty-nine full-term near miss for sudden infant death syndrome (SIDS) and 30 normal control infants underwent 24-hour polygraphic monitoring. Several types of respiratory events during sleep (eg, central, mixed, and obstructive apnea, periodic breathing) were defined and tabulated. Analysis of these respiratory variables and comparison of groups of near miss and control infants indicated that between 3 weeks and 4½ months of age only one variable was consistently different at a statistically significant level: the number of mixed and obstructive apnea 3 seconds during total sleep time. This study also showed an increase in mixed and obstructive respiratory events during sleep at 6 weeks of age in control as well as in near miss infants.


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