Respiratory Behavior in Near-Miss Sudden Infant Death Syndrome

PEDIATRICS ◽  
1982 ◽  
Vol 69 (6) ◽  
pp. 785-792
Author(s):  
Joan E. Hodgman ◽  
Toke Hoppenbrouwers ◽  
Susan Geidel ◽  
Anthony Hadeed ◽  
Maurice B. Sterman ◽  
...  

Seventeen infants with unexplained prolonged apnea that has been designated near-miss sudden infant death syndrome were monitored for sleep and cardiorespiratory variables during a 12-hour, all-night recording session. Infants were matched for gestational age, sex, and age at recording with control infants. Respiratory variables studied included respiratory rate, respiratory variability, apnea duration, apnea density, and periodic breathing. No statistically significant differences were found in sleep state or respiratory variables between near-miss and control infants. Eight infants (47%) had no recurrence of prolonged apnea, whereas three (17.6%) had recurrent apneic episodes for six weeks to eight months following the original episode. No clinical or polygraphic finding predicted which infant would exhibit recurrent apnea. None of the infants was monitored at home. All infants were developing normally when examined at 1 to 2 years of age.

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.


PEDIATRICS ◽  
1982 ◽  
Vol 70 (1) ◽  
pp. 128-131
Author(s):  
Dorothy H. Kelly ◽  
Joseph Twanmoh ◽  
Daniel C. Shannon

Victims of sudden infant death syndrome (SIDS) have been shown to have pathologic abnormalities consistent with chronic hypoxia.1-7 Two groups of infants at high risk of dying of SIDS, near miss infants and subsequent siblings of SIDS victims, have been studied in attempts to demonstrate physiologic abnormalities that could account for these pathologic findings. Investigators have found abnormalities in breathing pattern and the respiratory control system in the former consisting of prolonged sleep apnea, excessive short apnea, periodic breathing, hypoventilation, and depressed response to hypercarbia.8-13 However, studies in the SIDS sibling group have demonstrated varying results of excessive periodic breathing in the home14 and decreased apnea in the laboratory.15


PEDIATRICS ◽  
1979 ◽  
Vol 63 (3) ◽  
pp. 355-360
Author(s):  
Dorothy H. Kelly ◽  
Daniel C. Shannon

Twelve-hour nocturnal home recordings of respiration and heart rates were obtained during sleep in 32 infants with near-miss sudden infant death syndrome (SIDS) and in 32 control infants, and the recordings were analyzed for periodic breathing. An episode of periodic breathing was defined as three or more apneic pauses of three or more seconds. The duration of respirations interrupting the pauses was 20 seconds or less. Analysis revealed a statistically significant difference (P < .001) between the two groups, using criteria of percent of periodic breathing episodes, number of periodic breathing episodes/100 min of recorded sleep time, average duration of all episodes, and duration of the longest episode of periodic breathiflg. It is concluded that periodic breathing is present in excessive amounts during sleep in infants with near-miss sudden infant death svndrome.


PEDIATRICS ◽  
1982 ◽  
Vol 70 (1) ◽  
pp. 69-74 ◽  
Author(s):  
Paul Duffty ◽  
M. Heather Bryan

Electronic monitors were used at home to detect apnea in 134 infants who were considered to be at risk for sudden infant death syndrome (SIDS). Seventy-two infants had idiopathic apnea at a mean age of 2.2 ± 1.4 (± 1 SD) months. Of these, 31 subsequently had prolonged apnea (> 20 seconds) with the last spell occurring at 6.2 ± 3.2 months of age. Fourteen infants required vigorous stimulation on at least one occasion and 14 had more than ten separate episodes. Eighteen infants with awake apnea had a significantly smaller chance of subsequent spells (P < .05). Ten additional term infants had apnea during the first week of life but none had subsequent episodes. Of 52 siblings of SIDS victims, only seven had had apnea before monitoring started. Sixteen had prolonged apnea while on a monitor; seven required vigorous stimulation on at least one occasion and one infant died despite cardiopulmonary resuscitation. The first documented spell in these 16 infants was at 2.6 ± 2.1 months and the last at 7.2 ± 2.7 months of age. Ten infants had more than ten subsequent spells. A tendency to clustering of spells was noted. Preceding events, especially a mild upper respiratory tract infection, were noted in 36 of the 47 infants who had apnea on the home monitor.


PEDIATRICS ◽  
1978 ◽  
Vol 62 (5) ◽  
pp. 686-691
Author(s):  
June P. Brady ◽  
Ronald L. Ariagno ◽  
John L. Watts ◽  
Steven L. Goldman ◽  
Fe M. Dumpit

To find out whether there is any relationship between the ventilatory response to hypoxia and the sudden infant death syndrome (SIDS), we studied the effects of mild induced hypoxia (PIO2, 120 mm Hg = 17% oxygen) in 16 infants aged 2 weeks to 6 months. Eight had recurrent apneic spells (apnea group) (five had aborted SIDS and three had recurrent apnea in the intensive care nursery) and eight were "well" preterm infants about to fly in a pressurized airplane (PIO2, 120 mm Hg) (control group). Mean birth weights were 2,245 and 1,400 gm and mean gestational ages were 35 and 30 weeks. Postconceptual ages (41.8 and 41.3 weeks) were almost identical. Heart rate was obtained from an ECG, and respiratory rate and pattern were obtained from a pneumogram. In addition, end-tidal PCO2 and PN2 or PO2 were obtained with a nasal catheter and gas analyzers. In the apnea group with inhalation of 17% oxygen, we observed an increase in periodic breathing and an increase in both rate and total duration of respiratory pauses. In the control group there were no significant changes. Heart rate and PCO2 did not change in either group. Our findings suggest that infants prone to apnea may have unique respiratory responses to mild induced hypoxia.


PEDIATRICS ◽  
1973 ◽  
Vol 51 (4) ◽  
pp. 755-755
Author(s):  
David S. Bachman

The article on prolonged apnea and the sudden infant death syndrome (SIDS) by Steinschneider1 is very exciting in that it suggests the possibility of identifying infants at risk from SIDS before the final event. Obviously, it is of great importance to learn the mechanism causing the preceding apneic episodes. Do they represent vagal overactivity? Stimulation of the intact vagus nerve in the unanesthetized monkey causes apnea, as well as bradycardia and even arrhythmias.2 In fact, we have seen myocardial myocytolysis secondary to vagal stimulation.3


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.


1982 ◽  
Vol 101 (6) ◽  
pp. 911-917 ◽  
Author(s):  
Kristine McCulloch ◽  
Robert T. Brouillette ◽  
Anthony J. Guzzetta ◽  
Carl E. Hunt

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