Context Home monitors designed to identify cardiorespiratory events are frequently
used in infants at increased risk for sudden infant death syndrome (SIDS),
but the efficacy of such devices for this use is unproven.
Objective To test the hypothesis that preterm infants, siblings of infants who
died of SIDS, and infants who have experienced an idiopathic, apparent life-threatening
event have a greater risk of cardiorespiratory events than healthy term infants.
Design Longitudinal cohort study conducted from May 1994 through February 1998.
Setting Five metropolitan medical centers in the United States.
Participants A total of 1079 infants (classified as healthy term infants and 6 groups
of those at risk for SIDS) who, during the first 6 months after birth, were
observed with home cardiorespiratory monitors using respiratory inductance
plethysmography to detect apnea and obstructed breathing.
Main Outcome Measures Occurrence of cardiorespiratory events that exceeded predefined conventional
and extreme thresholds as recorded by the monitors.
Results During 718 358 hours of home monitoring, 6993 events exceeding
conventional alarm thresholds occurred in 445 infants (41%). Of these, 653
were extreme events in 116 infants (10%), and of those events with apnea,
70% included at least 3 obstructed breaths. The frequency of at least 1 extreme
event was similar in term infants in all groups, but preterm infants were
at increased risk of extreme events until 43 weeks' postconceptional age.
Conclusions In this study, conventional events are quite common, even in healthy
term infants. Extreme events were common only in preterm infants, and their
timing suggests that they are not likely to be immediate precursors to SIDS.
The high frequency of obstructed breathing in study participants would likely
preclude detection of many events by conventional techniques. These data should
be important for designing future monitors and determining if an infant is
likely to be at risk for a cardiorespiratory event.
In the 1980s, a leading hypothesis related to sudden infant death syndrome
(SIDS) was that prolonged apnea and bradycardia were markers for the susceptible
infant and preceded the terminal event. The use of home monitoring subsequently
expanded in the hope that timely recognition of apnea or bradycardia would
lead to life-saving intervention.
In 1986, a National Institutes of Health Consensus Conference1 concluded that although the effectiveness of home
cardiorespiratory monitors in reducing infant morbidity or mortality remained
to be established: "cardiorespiratory monitoring or an alternative therapy
is medically indicated for certain groups of infants at high risk for sudden
death. . . . These groups include infants with one or more severe apparent
life threatening events (ALTEs) requiring mouth-to-mouth resuscitation or
vigorous stimulation, symptomatic preterm infants, and siblings of two or
more SIDS victims. . . ." For siblings of 1 SIDS infant, it was stated that
available evidence was inconclusive and "the decision reached will be specific
to the infant." Therefore, premature infants, siblings of infants who died
of SIDS (SIDS-SIBs), and those who experienced an ALTE were commonly monitored
at home because of these recommendations and their reported increased risk
of SIDS (at least 2.5 times the general population, although data were sparse
for infants with an ALTE2-5).
However, it is important to recognize the unproven assumptions implicit in
the following recommendations: (1) infants for whom home monitors are recommended
are at increased risk for episodes of prolonged apnea or severe bradycardia;
(2) such episodes are precursors to SIDS; and (3) home cardiorespiratory monitoring
will warn caregivers in time for successful intervention. The Collaborative
Home Infant Monitoring Evaluation (CHIME) study was designed to address the
validity of the first assumption.
We specifically tested the hypothesis that preterm infants, SIDS-SIBs,
and infants who have experienced an idiopathic ALTE have a greater risk of
cardiorespiratory events than healthy infants, and risk is related to postconceptional
age (PCA). We assessed the frequency and time course of events based on commonly
used or conventional monitor alarm thresholds, but because these events are
often not considered clinically relevant, we also assessed a subset of more
severe events that we termed "extreme events." Although there were no means
to establish the consequences of extreme events a priori, the event criteria
defined a severity more likely to influence clinical management than commonly
used thresholds. We selected a home monitor with extensive memory and one
that also detected obstructed breaths to view the full range of respiratory
abnormalities that might cause apnea.2,5-7
Infants were recruited from 5 clinical sites (see "Acknowledgment")
between May 1994 and February 1998. The institutional review board at each
site approved the study, and the parents of all subjects gave written informed
consent.
For purposes of analysis, infants were divided into 7 groups (Figure 1). Enrollment was relatively balanced
by site, each contributing between 18% and 24% of subjects. The 7 groups of
infants were derived from 4 initial categories of eligibility using stratification
criteria that we thought a priori would influence outcome. These include the
following:
Criteria included: (1) 38 to 42 weeks' gestation at birth; (2) birth
weight, 10th to 90th percentile; (3) 30 days or younger postnatal age; (4)
clinically well (defined as Apgar score >4 at 1 and >7 at 5 minutes, not admitted
to a special care nursery, discharge on or before date of maternal discharge,
no medications, and no apnea or ALTE events based on clinical history or medical
record); (5) no family history of SIDS in siblings; and (6) no other family
history of SIDS in the last 10 years.
Within the previous 30 days, an unexplained sudden episode of color
change (cyanosis or pallor), tone change (limpness, stiffness), or apnea that
required mouth-to-mouth resuscitation or vigorous stimulation.1
Postnatal age had to be at least 12 hours but younger than 6 months when the
ALTE occurred. The index event was identified by caretaker observation and
occurred prior to the use of a home monitor. To establish an ALTE as idiopathic,
an evaluation was performed based on the infants' initial presentation, and
only those infants without an explained cause were enrolled. Based on whether
or not they were born at 37 or less weeks' gestation, the infants with an
ALTE were stratified into term idiopathic ALTE and preterm idiopathic ALTE groups.
Criteria included: (1) full or half sibling of 1 or more previous SIDS
infants (documented by autopsy), and (2) 30 days or younger postnatal age
(<4 weeks after SIDS in a twin but <6 months' postnatal age). Based
on whether or not they were born at 37 or less weeks' gestation, the SIDS-SIB
infants were stratified into: term SIDS-SIB and preterm SIDS-SIB groups.
Ineligible for other groups and (1) 34 or less weeks' gestation at birth,
(2) birth weight less than 1750 g, (3) postnatal age younger than 120 days
at time of discharge from the neonatal intensive care unit, and (4) 2 weeks
or less since discharge. Based on whether staff in the neonatal intensive
care unit observed apnea or bradycardia associated with cyanosis within 5
days of discharge, the preterm group was stratified into asymptomatic preterm and symptomatic preterm
groups.
General Exclusion Criteria
Since our intent was to characterize cardiorespiratory events in infants
for whom the cause was unknown, infants were excluded if they had any of the
following: current pneumonia confirmed by chest x-ray; home treatment with
continuous oxygen, bronchodilators, diuretics, steroids, medications for gastroesophageal
reflux or seizure; congenital heart disease except asymptomatic patent ductus
arteriosus, atrial septal defect, or small muscular ventricular septal defect;
ventricular-peritoneal shunt; congenital brain anomaly that would result in
a non-SIDS diagnosis in the event of sudden death; chromosomal abnormality;
midfacial hypoplasia or cleft palate; inborn error of metabolism; caregiver
currently using illicit drugs; or parental inability to communicate (language
barrier or no telephone).
Following enrollment, each infant had cardiorespiratory waveforms recorded
in the home using the CHIME monitor (NonInvasive Monitoring Systems, Miami,
Fla).8 Rib cage and abdominal movement were
recorded by respiratory inductance plethysmography (RIP) bands, and a third
signal proportional to tidal volume was calculated from the weighted algebraic
sum (sum channel). The monitor recognizes a breath whenever there is an excursion
on the sum channel that is at least 25% of the amplitude determined during
a calibration period (first 5 minutes each time the monitor is turned on).
The monitor continuously measures the time following a breath. During each
period of monitor-defined apnea (when there is no breath for a time exceeding
a specified threshold) there may be (1) effort in which the rib cage and abdominal
excursions are out of phase (consistent with obstruction) or (2) no respiratory
effort (central apnea) (Figure 2).9-11 Heart rate was determined
by an R-wave detection algorithm using standard disposable infant electrocardiogram
electrodes. Hemoglobin oxygen saturation by pulse oximetry (SpO2)12 (Ohmeda Minx pulse oximeter, Ohmeda Corp, Liberty
Center, NJ) and transthoracic impedance signals (Aequitron Inc, Plymouth,
Minn) were also monitored but were not used to define recording or alarm thresholds
in this report.
The monitor had the capability to initiate recording and storage of
physiologic data at a preset duration (threshold) for low heart rate and apnea;
the duration for initiating an alarm was longer and could be set independently.
All events stored in memory included the 75 seconds preceding onset of the
event, the event, and 30 seconds after resolution of the event. The thresholds
for recording physiologic events were identical for all groups of subjects:
apnea (as defined above) at least 16 seconds in duration or a heart rate less
than 80 or 60 beats per minute (bpm) for at least 5 seconds for infants less
than 44 or 44 or more weeks' PCA, respectively.
In contrast to the recording thresholds, we varied the threshold for
alarms. The alarm thresholds in the healthy term group were set at 40 or more
seconds for apnea and less than 40 bpm for heart rate since they had no clinical
indication for the audible alarm. For all other infants, the monitor was set
to sound an audible alarm for apnea of at least 20 seconds (ie, 4 seconds
beyond the threshold for recording), or a heart rate less than 80 bpm for
at least 5 seconds for infants less than 44 weeks' PCA, or 60 bpm for those
at least 44 weeks' PCA (same threshold as for recording). These alarm thresholds
were equivalent to customary practice so that infants who would have been
monitored absent our study received the same level of surveillance.
Families received standardized training and ongoing support of home
monitoring and were instructed to use the monitor whenever the infant was
sleeping or unobserved. Although parents were provided a form on which to
note any observations or interventions related to cardiorespiratory events,
these records were not consistently kept. Accordingly, only the recorded physiologic
data are reported herein. The intended duration of home monitoring was through
66 weeks' PCA for the healthy term and SIDS-SIB groups, 56 weeks' PCA for
the preterm groups, and 16 weeks from enrollment for the ALTE groups. In addition,
infants continued to be monitored until they were free of events exceeding
alarm thresholds for at least 12 weeks.
The memory monitor cartridges were downloaded every 2 to 4 weeks and
waveforms were available for review locally if needed for clinical management.
After infants completed home monitoring, waveforms were analyzed at the data
coordinating and analysis center by technicians unaware of study group or
clinical status. A software tool, which permitted magnification of the signal
amplitude and time scale, was developed to facilitate the scoring procedures
and analyses (Figure 2). We have
previously reported a high level of interrater reliability using this tool.8
For the purposes of data analysis, events were categorized as exceeding,
recording (see above criteria), conventional, or extreme thresholds. Conventional
thresholds were defined as follows: (1) apnea of at least 20 seconds; (2)
if less than 44 weeks' PCA, heart rate less than 60 bpm for at least 5 seconds
or less than 80 bpm for at least 15 seconds; or (3) if 44 weeks' PCA, heart
rate less than 50 bpm for at least 5 seconds or less than 60 bpm for at least
15 seconds. Extreme thresholds were defined as: (1) apnea of at least 30 seconds;
(2) if less than 44 weeks' PCA, heart rate less than 60 bpm for at least 10
seconds; or (3) if at least 44 weeks' PCA, heart rate less than 50 bpm for
at least 10 seconds.
We analyzed the frequency of events exceeding both conventional and
extreme thresholds. For a primary comparison of the risk of at least 1 event
by group, we calculated the time in days from beginning of monitoring to first
event for those with events and the total time in the study (≤180 days)
for those without events. We calculated Kaplan-Meier survival curves and computed
1-minus estimates from these survival curves, thus accounting for variable
days of monitor use.13 The last date that subjects
used the monitor became a censoring date. Cox proportional hazards models
were then used to obtain risk ratios (RRs) (with 95% confidence intervals
[CIs]) of an event in comparison with the healthy term group.14
These models also account for the variable monitoring duration. In the Cox
models, we additionally accounted for variability in monitor use by adding
total hours of actual monitor use to the models. The assumption of proportional
hazards was tested by including a time-dependent variable in the model for
each group.
Since PCA varied widely among groups, we also compared the groups regarding
the number of infants with at least 1 event per 20 000 hours of monitor
use during 4-week PCA periods. We chose 4-week PCA time periods to ensure
that we would observe a sufficient number of infants with events for analysis.
We expressed the rate of events per 20 000 hours of monitor use because
this represents approximately the number of hours that 100 infants would be
expected to use the monitor during a 4-week period (hence an estimate of expected
number of infants with at least 1 event among 100 infants monitored for a
4-week period). We constructed smoothed plots for each group by calculating
a moving average estimate at each week, using the 4-week window beginning
at the week under consideration and the subsequent 3 weeks (eg, for week 35,
we calculated the average of the rates from weeks 35-38). A formal comparison
of the rate at which infants in each group had at least 1 event was conducted
using Poisson regression with repeated observations for selected 4-week periods,
adjusting for the number of hours monitored before the event for those with
an event and the total number of hours monitored for those without events.15,16 The reference rate chosen for these
comparisons was that observed in the healthy term group during the 4-week
PCA period from 42 to 45 weeks, the earliest 4-week PCA observation period
for healthy term infants. Relative rates (and 95% CIs) were calculated for
each group for successive, nonoverlapping 4-week PCA periods (ie, 34-37, 38-41,
42-45 weeks' PCA). From an assessment of data collected during the initial
2 years of the study, we estimated that events exceeding the extreme threshold
would be observed in 1% to 2% of healthy term infants. To achieve a reasonably
precise estimate of the event rate in the healthy term group, we set a goal
of enrollment of at least 300 infants. With a sample of 300 healthy term infants,
the upper 95% confidence limit for an observed rate of 2% is 3.6%.
Table 1 provides the characteristics
of the 1079 infants who participated in the study. Each of the 7 groups included
racial/ethnic diversity and had characteristics representative of the target
populations for this study. Although there were some small differences between
participants and eligible nonparticipants with respect to marital status,
education, and ethnic group, we were unable to discern a meaningful trend.
Six infants died during the study, but none was being monitored at the
time of death. The cases were independently reviewed by an expert panel, which
included the medical examiners or pathologists at each CHIME site. There were
2 SIDS cases, including an infant in the healthy term group who died at 17
weeks and an infant in the preterm group born at 28 weeks' gestational age
who died at 20 weeks. There were 2 cases for which the autopsy and medical
history were consistent with SIDS, but there was no information on the death
scene, including a term infant in the SIDS-SIB group who died at 7 weeks of
age and an infant in the preterm group born at 32 weeks' gestation who died
at 12 weeks of age. One infant in the term ALTE group, who was also a SIDS-SIB,
died suddenly and unexpectedly at 32 weeks of age and was designated "undetermined"
because of uncertainty regarding the SIDS diagnosis. One infant in the preterm
group born at 32 weeks' gestation, who was also a SIDS-SIB, died at 41 weeks
of age, and the cause of death was homicide.
The CHIME monitor was used for a total of 718 358 hours, with wide
differences in usage within and between groups, which necessitated analytic
approaches that accounted for individual time monitored.
Based on CHIME criteria, we analyzed 21 647 events that exceeded
recording thresholds. Of these, 6993 events exceeded conventional thresholds
in 445 (41%) of the 1079 infants, and 653 events exceeded extreme thresholds
in 116 (10%) of the 1079 infants. Because SpO2 values were available
and of sufficient quality for assessment in 84% and 67% of events that exceeded
conventional and extreme thresholds, respectively, we were able to examine
the relationship between these events and hypoxemia (Figure 3). Apnea without bradycardia represented 5258 (75%) of 6993
events exceeding conventional thresholds (≥20 seconds) and 321 (49%) of
653 events exceeding extreme thresholds (≥30 seconds). Bradycardia without
apnea of at least 20 seconds represented 948 (14%) of 6993 events exceeding
conventional thresholds and 144 (22%) of 653 events that exceeded extreme
thresholds. In general, the degree of hypoxemia increased with increasing
duration of apnea or bradycardia. When severe bradycardia coexisted with apnea,
however, there was slightly less hypoxemia, but fewer events with SpO2 values of sufficient quality for assessment. Of all extreme events,
25% were associated with a decrease in SpO2 of less than 10%. Using
RIP, we also assessed the proportion of apnea events that met criteria for
obstructed breaths, which correlate well with obstructed breaths on polysomnographic
studies.9-11 Among
all extreme events with apnea of 30 seconds, 70% included at least 3 obstructed
breaths. Among all conventional events with apnea of at least 20 seconds,
50% of the apneas included at least 3 obstructed breaths.
Table 2 provides RRs for
each study group compared with healthy term infants for the occurrence of
at least 1 event exceeding the extreme threshold and at least 1 event exceeding
the conventional threshold during the first 180 days of monitoring (Cox proportional
hazards model). Only the 4 preterm groups had significantly increased risk
of an extreme event. The 2 highest RRs occurred in the symptomatic and asymptomatic
preterm groups (18.0 and 10.1, respectively), and these 2 RRs declined over
time (P<.01). For example, at day 7 of monitoring,
the RRs were 34 and 17 for symptomatic and asymptomatic preterm infants, respectively,
while by day 28 of monitoring, the RRs had declined to 14 and 8 for symptomatic
and asymptomatic preterm infants, respectively. For both groups, the risk
of at least 1 extreme event remained significantly higher than the healthy
term group for approximately the first 7 weeks of monitoring (ie, up to 43
weeks' PCA). Similarly, the symptomatic and asymptomatic preterm groups also
had the highest RRs for events exceeding conventional thresholds. However,
the occurrence of at least 1 event exceeding conventional alarm thresholds
was very common (cumulative incidence, 43%) in all groups including the healthy
term group. For events exceeding conventional thresholds, as with events exceeding
extreme thresholds, the RRs for the preterm groups declined with time, and
by 7 weeks of monitoring were no longer significantly higher than the healthy
term group.
Risk for Recurrence of Event
We next assessed the pattern of recurrence of extreme events among the
116 infants who had at least 1 extreme event. We combined the groups since,
except for the preterm group, the numbers of infants were too few for separate
analysis. A second extreme event occurred in 60 (51.7%) of the 116 infants,
a third occurred in 35 (57.3%) of the 60, and a fourth was observed in 28
(80%) of the 35. In each case, almost all the subsequent events occurred within
6 weeks of the prior event.
Relationship of Events to PCA
The above analyses assess occurrence of extreme events in relation to
the number of days an infant was monitored at home. However, the PCA at onset
of home monitoring varied considerably. Analyses of the effect of increasing
PCA on occurrence of extreme events in each group of infants (Poisson analyses, Figure 4) indicate the number of infants
in each group experiencing at least 1 extreme event per 20 000 hours
of monitoring during successive 4-week PCA intervals. The likelihood of experiencing
at least 1 extreme event decreased as PCA increased until about 43 weeks'
PCA, after which all groups had similarly low rates of having at least 1 extreme
event. During the 4-week period from 34 to 37 weeks' PCA, only the symptomatic
(Figure 4, point A) and asymptomatic
(point B) preterm infants had a sufficient number and hours of monitoring
for analysis. Compared with the healthy term group at 42 to 45 weeks' PCA,
the number of infants having more than 1 extreme event per 4 weeks of monitoring
time was 19.7 (P<.001) and 10.5 (P = .002) times higher for the 34 to 37 weeks' PCA symptomatic and
asymptomatic preterm groups, respectively. At 38 to 41 weeks' PCA, all 4 preterm
groups also demonstrated significantly higher rates than the reference. At
42 to 45 weeks' PCA and thereafter, no group had a rate that was significantly
higher than the reference rate.
This is the first large, longitudinal study comparing incidence of cardiorespiratory
events among infants monitored at home with that of healthy term infants.
Based on more than 700 000 hours of monitor use, we determined that events
previously described as "pathologic"1 are actually
quite common, even in healthy term infants. Furthermore, we identified groups
that, when compared with healthy term infants, have higher risks of extreme
events that are likely to influence clinical management. Our data indicate
an increased risk of at least 1 extreme event only in preterm infants and
only until about 43 weeks' PCA. Although our choice of RIP for breath detection
limits direct comparison to data based on customary impedance monitoring,
the high frequency of obstructed breaths in our subjects strongly suggests
that many events would have been missed by techniques commonly used in clinical
practice.
There are several aspects of the CHIME study that are important to consider.
First, although the threshold used to define extreme events is much higher
than commonly used, our study does not have the means to delineate the pathologic
nature of extreme events. Because it is not possible to determine a priori
how long apnea or bradycardia can be tolerated without injury, it is only
possible to raise the threshold for detection of events in an iterative fashion.
Second, since many conventional and extreme events caused a monitor alarm,
it is possible that the duration of some events in the risk groups was shortened
by either an alarm-induced auditory arousal or by caretaker intervention.
The use of conventional alarm thresholds in these groups was a design compromise
to be consistent with current practice in infants perceived to be susceptible
to life-threatening events, but they could have resulted in an underestimate
of extreme events in risk groups and hence reduced ability to detect differences
compared with healthy term infants. In addition, subsequent clinical management
of infants who experienced events may have influenced their risk for subsequent
events. Third, our definitions for extreme and conventional events took into
account apnea, bradycardia, and combinations. It is possible that the results
would have been different had we chosen alternative criteria. Fourth, the
procedures, tools, and criteria used for scoring can have a substantial impact
on the events identified. To limit variability in data analysis, high scoring
reliability was attained.8 Furthermore, we
have confirmed a high level of concordance between apnea detected by the monitor
and apnea detected by polysomnogram recordings.9
Fifth, we excluded infants who had diagnoses commonly associated with cardiorespiratory
events, recognizing that the frequency and nature of events thus may have
been different. Sixth, due to limited sample size, 95% CIs for RRs were relatively
wide, especially in the term risk groups. The upper limits of the 95% CI for
term SIDS-SIBs and term infants with idiopathic ALTE, for example, were 8.7
and 9.2, respectively. However, even these upper limits are well below the
RRs observed for the preterm infants.
We considered describing apnea events as obstructive, central, or mixed,
but recognized early that such categorization obscures the wide range of variability
in these events. The high proportion of apnea containing at least 3 obstructed
breaths exemplifies the value of using RIP, which can identify obstructed
breaths.9-11 For
this reason, transthoracic impedance, which detects effort during obstruction,
would not detect many of these apneas, and currently available home monitors
would have detected less apnea than we observed. Thus, the distribution of
events might vary between our subjects and those reported using other technology.17-22
Although detection of bradycardia might provide an alternative opportunity
to detect events, fully half of extreme events had no bradycardia, even when
associated with desaturation.
The CHIME study was not designed to address the important question of
whether infants who experience extreme cardiorespiratory events are more likely
to die of SIDS. The 6 deaths among study participants are too few to derive
conclusions. However, the highest rates of extreme events were observed among
infants who were 43 or less weeks' PCA, whereas the peak incidence of SIDS
generally occurs at older mean PCAs of 44.2, 46.8, and 52.7 weeks for infants
born at 24 to 28, 29 to 32, and 37 weeks, respectively.23
These differences in timing suggest that extreme events are not likely to
be immediate precursors to SIDS, although it does not eliminate the possibility
that they are markers of vulnerability.
The CHIME study was also not designed to determine whether use of a
monitor decreases the rate of SIDS. The finding that preterm infants 43 weeks'
PCA exhibited more extreme events than healthy term infants does not resolve
the debate whether such infants would benefit from monitoring. The observation
that 20% of asymptomatic preterm infants experienced 1 extreme event highlights
the need to determine clinical relevance of extreme events. Until then, however,
it is not possible to refute or support the recommendations of the NIH Consensus
Development Conference that monitoring or an alternative therapy is medically
indicated for symptomatic but not asymptomatic preterm infants.
Controversies regarding who should be monitored notwithstanding, the
CHIME data are responsive to an identified gap in our knowledge by defining
risk of occurrence and timing of extreme events during early postnatal development.1 These data also document a high frequency of obstructed
breathing within events. Our choice of RIP for breath detection does limit
direct comparison to all prior (transthoracic impedance–based) data,
but it is important to note that commercially available monitors would likely
have missed many CHIME events due to the high frequency of obstructed breaths.
These results should be important for designing future monitors and determining
if an infant is likely to be at risk for a cardiorespiratory event.
1. Consensus Statement. National Institutes of Health Consensus Development
Conference on Infantile Apnea and Home Monitoring, Sept 29 to Oct 1, 1986.
Pediatrics.1987;79:292-299.Google Scholar 2.Hunt CE. Sudden infant death syndrome. In: Beckerman RC, Brouillette RT, Hunt CE, eds. Respiratory Control Disorders in Infants and Children. Baltimore, Md:
Williams & Wilkins; 1992:190-211.
3.Malloy MH, Freeman DH. Birth weight- and gestational age-specific sudden infant death syndrome
mortality: United States, 1991 versus 1995.
Pediatrics.2000;105:1227-1231.Google Scholar 4.Guntheroth WG, Lohmann R, Spiers PS. Risk of sudden infant death syndrome in subsequent siblings.
J Pediatr.1990;116:520-524.Google Scholar 5.Leach CE, Blair PS, Fleming PJ.
et al. Epidemiology of SIDS and explained sudden infant deaths.
Pediatrics.1999;104:e43.Google Scholar 6.Kahn A, Blum D, Waterschoot P, Engelman E, Smets P. Effects of obstructive sleep apneas on transcutaneous oxygen pressure
in control infants, siblings of sudden infant death syndrome victims, and
near miss infants: comparison with the effects of central sleep apneas.
Pediatrics.1982;70:852-857.Google Scholar 7.Hoppenbrouwers T, Hodgman JE, Cabal L. Obstructive apnea, associated patterns of movement, heart rate, and
oxygenation in infants at low and increased risk for SIDS.
Pediatr Pulmonol.1993;15:1-12.Google Scholar 8.Corwin MJ, Lister G, Silvestri JM.
et al. and the CHIME Study Group. Agreement among raters in assessment of physiologic waveforms recorded
by a cardiorespiratory monitor for home use.
Pediatr Res.1998;44:682-690.Google Scholar 9.Weese-Mayer DE, Corwin MJ, Peucker MR.
et al. and the CHIME Study Group. Accuracy of the respiratory inductance plethysmography (RIP) Collaborative
Home Infant Monitoring Evaluation (CHIME) monitor in identifying obstructed
breaths.
Am J Respir Crit Care Med.2000;162:471-480.Google Scholar 10.Brouillette RT, Morrow AS, Weese-Mayer DE, Hunt CE. Comparison of respiratory inductance plethysmography and thoracic impedance
for apnea monitoring.
J Pediatr.1987;111:377-383.Google Scholar 11.Tobin MJ, Guenther SM, Perez W, Mador MJ. Accuracy of the respiratory inductive plethysmograph during loaded
breaths.
J Appl Physiol.1987;62:497-505.Google Scholar 12.Hunt CE, Corwin MJ, Lister G.
et al. and the CHIME Study Group. Longitudinal assessment of hemoglobin oxygen saturation in healthy
infants during the first 6 months of age.
J Pediatr.1999;135:580-586.Google Scholar 13.Kaplan EL, Meier P. Nonparametric estimation from incomplete observations.
J Am Stat Assoc.1958;53:457-481.Google Scholar 14.Lawless JF. Statistical Models and Methods for Lifetime Data. New York, NY: John Wiley & Sons; 1980.
15.McCullagh P, Nelder JA. Generalized Linear Models. London, England: Chapman & Hall; 1983.
16.Diggle PJ, Liang KY, Zeger SL. Analysis of Longitudinal Data. Oxford, England: Clarendon Press; 1994.
17.Hunt CE, Hufford D, Bourguignon C, Oess MA. Home documented monitoring of cardiorespiratory pattern and oxygen
saturation in healthy infants.
Pediatr Res.1996;39:216-222.Google Scholar 18.Southall DP, Richards JM, Rhoden KJ.
et al. Prolonged apnea and cardiac arrhythmias in infants discharged from
neonatal intensive care units: failure to predict an increased risk for sudden
infant death syndrome.
Pediatrics.1982;70:844-851.Google Scholar 19.Cote A, Hum C, Brouillette RT, Themens M. Frequency and timing of recurrent events in infants using home cardiorespiratory
monitors.
J Pediatr.1998;132:783-789.Google Scholar 20.Hageman JR, Holmes D, Suchy S, Hunt CE. Respiratory pattern at hospital discharge in asymptomatic preterm infants.
Pediatr Pulmonol.1988;4:78-83.Google Scholar 21.Barrington KJ, Finer N, Li D. Predischarge respiratory recordings in very low birth weight newborn
infants.
J Pediatr.1996;129:934-940.Google Scholar 22.Eichenwald EC, Aina A, Stark AR. Apnea frequently persists beyond term gestation in infants delivered
at 24 to 28 weeks.
Pediatrics.1997;100:354-359.Google Scholar 23.Malloy MH, Hoffman HJ. Prematurity, sudden infant death syndrome, and age of death.
Pediatrics.1995;96:464-471.Google Scholar