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Clinically Unsuspected Hypoxia During Sleep and Feeding in Infants With Bronchopulmonary Dysplasia


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and Feeding

in Infants





Garg, MD, Sharon

I. Kurzner,

MD, Daisy B. Bautista,


and Thomas

G. Keens,


From the Division of Neonatology and Pediatric Pulmonology, Childrens Hospital of Los Angeles, and Department of Pediatrics, University of Southern California School of Medicine, Los Angeles

ABSTRACT. Infants with bronchopulmonary dysplasia

have a high incidence of sudden, unexplained death in

the postneonatal period; yet the cause of these deaths is unknown. It was hypothesized that infants with bron-chopulmonary dysplasia, thought to be well oxygenated based on awake Pao2 values, would have clinically un-suspected arterial oxygen desaturation during sleep

and that these would correlate with the severity of pul-monary function abnormalities. The infants studied were 14 with bronchopulmonary dysplasia, 15 who were preterm, had no bronchopulmonary dysplasia, but

did have neonatal respiratory distress syndrome, and

eight who were full term and used for control at 37 to 45 weeks postconception. Continuous noninvasive

mon-itoring of oxygenation (arterial oxygen saturation

[Sao2, pulse oximetry] and transcutaneous oxygen ten-sion was performed during sleep, wakefulness, and

feeding. Greater than 80% of each recording was free

of artifact for Sao2. Preterm infants with

bronchopul-monary dysplasia and respiratory distress syndrome spent greater time at Sao2 < 90% than control infants.

Most desaturations occurred during feeding and to a lesser extent during wakefulness, active sleep, and quiet sleep. Episodes of desaturation (Sao2 < 90%)

lasted 15 to 20 seconds and were not associated with apnea, bradycardia, cyanosis, or changes in transcu-taneous Po2. Only infants with bronchopulmonary dys-plasia showed severe desaturations (Sao2 < 80%). Total

desaturation in those infants correlated with airway

resistance (body pressure plethysmography). Abnormal pneumographic findings did not predict abnormal de-saturations. It was concluded that clinically

unsus-pected oxygen desaturation occurs frequently in pre-term infants with and without bronchopulmonary dysplasia, and profound hypoxemia may be responsible for sudden unexplained deaths in these infants.

Pedi-Received for publication May 18, 1987; accepted Aug 3, 1987. Reprint requests to (T.G.K.) Division of Neonatology and Pe-diatric Pulmonology, Childrens Hospital of Los Angeles, 4650 Sunset Blvd, Los Angeles, CA 90027.

PEDIATRICS (ISSN 0031 4005). Copyright © 1988 by the American Academy of Pediatrics.

atrics 1988;81:635-642 hypoxia, preterm infant,

bron-chopulmonary dysplasia, airway resistance, pneumo-gram, sudden infant death syndrome.

Bronchopulmonary dysplasia is a common

Se-quela for babies born prematurely with respira-tory distress syndrome treated with supplemental oxygen and mechanically assisted ventilation.’5

Improvements in the neonatal intensive care of

these babies has resulted in increased survival prior to neonatal intensive care unit discharge.

However, the incidance of sudden unexpected

deaths following discharge is increased.68 The cause or causes of these “late” deaths are not well understood. It is possible that unrecognized

hy-poxic episodes play a role, but these infants with

bronchopulmonary dysplasia often have accepta-ble arterial oxygen tension values as determined by arterial blood gas determinations while awake and have not been observed to be cyanotic, apneic, or bradycardic.

The adequacy of oxygenation in infants with

bronchopulmonary dysplasia is often assessed by

one-time determination of Pao2 by invasive or

noninvasive means while the infant is awake or

crying. Supplemental oxygen would generally not

be recommended if the Pao2 is greater than 55

mm Hg and the infant has not been observed to

be cyanotic. Previous studies of adults with

chronic obstructive lung disease and children and adolescents with cystic fibrosis and asthma have

shown marked hypoxemia during sleep,

espe-cially during rapid eye movement sleep.9’2 We


previous studies of continuous noninvasive mon-itoring of these infants who were thought to be well oxygenated.

The high incidence of postneonatal deaths of in-fants with bronchopulmonary dysplasia and the likelihood that they would have intermittent

hy-poxia were motivations for this study. We

hy-pothesized that infants with bronchopulmonary

dysplasia thought to be well oxygenated based on awake Pao2 values, would have clinically unsus-pected arterial oxygen desaturation during sleep and that these would correlate with the severity

Of pulmonary function abnormalities.

Further-more, unsuspected and unrecognized hypoxia may

result in sudden death in infants with broncho-pulmonary dysplasia.


Study Group

We studied 14 infants with bronchopulmonary dysplasia, 15 preterm infants without

broncho-pulmonary dysplasia who were treated for

neo-natal respiratory distress syndrome and eight age-matched full-term control infants. The bron-chopulmonary dysplasia group was defined as in-fants who were born prematurely, had respiratory

distress syndrome, were treated with supplemen-tal oxygen and/or mechanically assisted ventila-tion for at least 28 days, and had radiographic evidence of stage III or stage IV bronchopulmon-ary dysplasia.3 The respiratory distress syndrome group was defined as infants born prematurely,

had respiratory distress syndrome, but who

re-quired supplemental oxygen and/or mechanically assisted ventilation for no more than seven days, and who did not have clinical or radiographic signs ofchronic lung disease. Control infants were full-term infants without any cardiac or

respira-tory disease. Infants were excluded from any

group if they had cardiac malformations (other than a patent ductus arteriosus which had closed by the time of study), grade III or IV intraven-tricular hemorrhage, necrotizing entrocolitis complicated by short gut syndrome, ventilatory muscle weakness, or abnormalities in neurologic control of breathing. Infants were studied near term. Informed consents were obtained from par-ents prior to study. The study was approved by the Committee on Clinical Investigations

(insti-tutional review board) of Childrens Hospital of

Los Angeles.


Oxygenation was studied by continuous

non-invasive monitoring for three to four hours to

include periods of wakefulness, sleep, and feed-ing. Arterial oxygen saturation (Sao2) by pulse oximetry (Neilcor N100, Nellcor, Hayward,

CA),’3”4 the pulse signal from the pulse

oxime-ter, transcutaneous oxygen tension and carbon

dioxide tension (SensorMedics Transend Cutan-eous Gas System with electrode heated to 44#{176}C, SensorMedics),’5”6 ECG, and heart rate, respi-rations by chest wall impedence, and

electroocu-logram were continuously recorded on a Gould

eight-channel strip chart recorder. The heart

rates determined from ECG and the pulse oxi-meter were compared and Sao2 signals rejected as artifact if the difference was greater than five beats per minute. Wakefulness, sleep state, and feeding were determined by direct observation and behavioral

The portion of each recording without accurate pulse detection by the pulse oximeter was disre-garded because the Sao2 signal is artifactual. Sig-nificant oxygen desaturation was defined as any episode in which Sao2 decreased to less than 90%.

Severe oxygen desaturation was defined as any

episode in which Sao2 decreased to less than 80%. The total number and duration of significant and severe desaturations were quantitated for wake-fulness, quiet sleep, active sleep, feeding, and total recording time and expressed as a percent-age of total artifact-free time for each activity state.

Pulmonary mechanics were measured in the

bronchopulmonary dysplasia and respiratory dis-tress syndrome groups using an infant body

pres-sure plethsymograph (Erich Jaeger, mc,

Wurz-berg, Federal Republic of Germany). The volume ofthe plethysmograph is 114 L. The leak to permit stabilization for temperature effects is set at a time constant of 4.35 seconds. There is less than 5% deviation of pressure amplitude at “respira-tory rates” of 15 to 150 breaths per minute, with less than 3% phase shift in box pressure. Prior to each study, the plethysmograph was calibrated and air in a rebreathing bag was humidified and ventilated. Infants were studied while asleep in the supine position 30-minutes after feeding. Mild sedation using chloral hydrate (40 mg/kg) was ad-ministered prior to the study. Infants were mon-itored for heart rate, respiratory rate, skin

tem-perature, and transcutaneous oxygen tension

during the study. Minute ventilation, tidal

vol-ume, and respiratory frequency were measured

during an average of at least 20 breaths during quiet breathing using an oronasal mask. The door

of the body plethysmograph was closed, and the

infant breathed room air from the box. When

ther-mal equilibrium had been achieved, the


mask, connected to a heated body temperature, pressure, saturation rebreathing bag and a heated

pneumotachograph and shutter, was sealed over

the infant’s nose and mouth. The mask was

checked for leakage both visually and by the ap-pearance of the oscilloscope tracings. All mea-surements were corrected for apparatus dead space (46 mL) and resistance (1.8 cm H20 per liter per second). Thoracic gas volume at functional re-sidual capacity and airways resistance were mea-sured by the method of DuBois et al,’8”9 suitably modified for infants.20’2’ The maximal coefficient of variation for airways resistance in our labo-ratory is 6.7 ± 1.7%. Specific airways conductance was calculated as the reciprocal of the functional capacity and airways resistance divided by

tho-racic gas volume. The maximal coefficient of

variation for specific airways conductance in our laboratory is 6.2 ±


After the conclusion of plethysmographic mea-surements, the infant was repositioned in a right

lateral position. An esophageal balloon (1.0 cm

diameter and 5.0 cm long) containing 0.5 mL of

air was passed until it was positioned in the lower third of the esophagus, according to the method

of Beardsmore et al.22 Dynamic pulmonary

com-pliance was then measured. The maximal

coeffi-cient of variation for dynamic pulmonary compli-ance in our laboratory is 8.7 ± 4.3%.

For each infant, a pneumogram (recording of

chest wall impedance respirations and ECG) was

recorded for 12-hours overnight on magnetic tape using an infant monitor (Healthdyne 16000 infant

monitor, Healthdyne Corporation, Marietta, GA)

and recorder (Oxford Medical Systems, Abingden,

England). Alarms were set to sound for apnea

greater than 20 seconds and bradycardia less than 80 beats per minute. The tape was analyzed using a Pediatric Diagnostic Services computerized ana-lyzer.23 A hard copy of respirations and R-R in-terval heart rate was obtained from the entire 12-hours and displayed on paper at a speed of 25 mm! mm. From each recording, total sleep time, long-est apnea, periodic breathing, and apnea density were calculated as previously described.2427 For purposes of this study, an abnormal pneumogram

was defined as one or more of the measured

pa-rameters greater than 2 SD from the mean

ob-tamed from 94 control infants recorded at home

in southern California.27’28 These criteria include any apnea greater than 15 seconds in duration,

apnea density greater than 1.0% of total sleep

time, and total duration of periodic breathing greater than 4.5% of total sleep time.

Unless otherwise specified, all data are ex-pressed as group means and standard errors of the

mean. Values were compared between study

groups by analysis of variance and independnt t

tests. The relationship between variables was ex-pressed as the correlation coefficient using linear regression analysis by least squares method. The

number and duration of desaturations were

com-pared between activity states by analysis of var-iance and paired t test and between study groups by analysis of variance and independent t test.29


Fourteen infants with bronchopulmonary

dys-plasia, 15 infants with respiratory distress syn-drome, and eight full-term control infants were studied. Clinical variables ofthe study groups are shown in Table 1. Infants with bronchopulmonary dysplasia had significantly lower birth weight and gestational age than control infants or those with respiratory distress syndrome. Infants with bronchopulmonary dysplasia spent significantly

more time requiring mechanically assisted

yen-tilation and supplemental oxygen than infants with respiratory distress syndrome. No control in-fant required any mechanically assisted ventila-tion or supplemental oxygen in the neonatal pe-nod. All infants were studied at greater than 37 weeks postconceptional age. There was no signif-icant difference in age at study between control infants and those with bronchopulmonary dyspla-sia, but infants with respiratory distress

syn-drome were slightly younger. Infants with both

forms of lung disease had similar body weight at the time of study, but control infants were sig-nificantly heavier.

Pulse oximetry is sensitive to movement that

results in an artifactual Sao2 reading. In this study, tracings were judged to be free of artifact if the pulse rate from the pulse oximeter agreed within five beats per minute of the heart rate

de-termined by ECG. Tracings from infants with

bronchopulmonary dysplasia were free of artifact 83.3 ± 3.0% of the total recording time. This was not significantly different from respiratory dis-tress syndrome tracings (86.2 ± 2.1%) or control infants (81.4 ± 3.2%).

Both bronchopulmonary dysplasia and

respi-ratory distress syndrome groups ofinfants showed

periods of oxygen desaturation (Sao2 less than

90%) (Table 2). Control infants showed only brief

periods of Sao2 less than 90%. Infants with

bron-chopulmonary dysplasia had significantly more




Activity Bronchopulmonary Dysplasia

(n - 14)

15.7 ± 5.6” 6.0 ± 2.3”

Respiratory Distress Syndrome

(n - 15)

3.9 ± 1.8

3.4 ± 1.3a

Control (n = 8)

0.2 ± 0.2

0.2 ± 0.2 Sleep

Active 3.6 ± 1.7 2.2 ± 1.0#{176} 0.1 ± 0.0

Quiet 1.2 ± 0.6 1.3 ± 0.7 0.0 ± 0.0


Total recording time

2.5 ± 1.2 6.8 ± 2#{149}4d

2.1 ± #{216}#{149}7C 2.7 ± #{216}#{149}9C

± 0.0 0.1 ± 0.1

* Results are percentages of time ± SD. .05; b < .02; C < .01; d p < .005.

Significant differences from controls: a p <

TABLE 1. Profile of Study Group

Variable Bronchopulmonary Dysplasia

(n = 14)

Respiratory Distress Syndrome

(n = 15)

Control (n = 8)

Age (wk)

Gestational, at birth Postconceptual, at study

28.9 ±

41.0 ± 0.8’

32.9 ± 0.5

37.3 ± 0.4

40.5 ± 0.5

42.8 ± 0.8



At birth 1,180 ± 82#{176} 1,708 ± 139 3,454 ± 193

At study

Duration of supplemental 02 (d)

Duration of mechanically assisted ventilation (d)

2,300 ± 100

53.4 ± 6.9’

48.8 ± 7.2”

2,100 ± 100

6.1 ± 1.0

4.6 ± 1.0

3,800 ± 300

0 0

* All variables for infants with bronchopulmonary dysplasia and those with respiratory distress syndrome were

significantly different from control infants. (P < .001), except postconceptional age at the time of study for bron-chopulmonary dysplasia. Bronchopulmonary dysplasia was significantly different from respiratory distress syn-drome: ap < .005; bp <


TABLE 2. Duration of Arterial Saturation Less Than 90%*

during wakefulness, active sleep, and quiet sleep. These desaturations were not clinically apparent because they did not coincide with apnea, brady-cardia, or cyanosis. Because the mean duration of each episode ofdesaturation was 15 to 20 seconds, transcutaneous oxygen tension often did not de-crease during these episodes.

Infants with bronchopulmonary dysplasia and

respiratory distress syndrome experienced 13.2 ±

4.6 and 5.7 ± 1.7 episodes ofdesaturation to Sao2 less than 90% per 60 minutes of total recording period, respectively. Infants in both groups ex-perienced significantly more events of desatura-tion when compared with control infants who had 0.6 ± 0.4 episodes per 60 minutes of total record-ing period (P < .02 for bronchopulmonary dys-plasia, P < .01 for respiratory distress syndrome).

Both groups of infants showed periods of severe arterial oxygen desaturation with Sao2 less than 80%, but this was not seen in control infants (Table 3). Infants with bronchopulmonary dyspla-sia spent 1.9 ± 0.6% of total recording time at Sao2 less than 80% compared with 0% for control infants (P < .01). Infants with respiratory distress syndrome spent 0. 1 ± 0. 1% oftotal recording time at Sao2 less than 80%, but this was not

signifi-cantly different from control infants. Most severe

desaturations occurred during feeding and to a

lesser extent during wakefulness, active sleep, and quiet sleep in infants with bronchopulmonary dysplasia. Again, these severe desaturations were not clinically apparent because they did not

co-incide with apnea, bradycardia, or cyanosis.

Again, transcutaneous oxygen tension often did

not reflect these episodes of hypoxia because of their short duration.

The normal range for arterial oxygen

desatur-ation in infants was defined as the mean plus 2

SD for the controls in this study. Control infants had a small number ofshort desaturation episodes with Sao2 less than 90%. No control had any Sao2 less than 80%. The normal range for desatura-tions in infants is shown in Table 4.

Pneumograms were recorded from 12 infants

with bronchopulmonary dysplasia and 13 with

respiratory distress syndrome. Cardiorespiratory

abnormalities were observed in five with

bron-chopulmonary dysplasia (42%) and five with res-piratory distress syndrome (38%). The

pneumo-gram results are shown in Table 5. Of these 25


0 Normal Pneumogram

0 Abnormal Pneumogram

kfants With Abnormal

Oxygen Desaturatlon



(12) (13)

(NS) (NS)

Figure. Abnormal pneumogram results did not

pre-dict abnormal oxygen desaturations in infants with

bronchopulmonary dysplasia (BPD) and respiratory distress syndrome (RDS). Proportion ofinfants with

ab-normal percentages of oxygen desaturation is plotted

on ordinate.

TABLE 3. Duration of Arterial Saturation Less Than 80%

Activity Bronchopulmonary Respiratory Control

Dysplasia Distress (n = 8)

(n = 14) Syndrome

(n = 15)

Feeding 4.0 ± 1.8 0.7 ± 0.5 0

Awake 0.9 ± 0.6 0.1 ± 0.1 0


Active 0.9 ± 0.5 0.1 ± 0.1 0

Quiet 0.1 ± 0.1 00 0

Total 0.6 ± 0.4 0.1 ± 0.1 0

Total recording time 1.9 ± 0.6k’ 0.1 ± 0.1 0

* Results are percentages of time ± SD.

Significant differences from controls: a p <


b P <

TABLE 4. Arterial Oxygen Desaturation for Control Infants*

Activity % of Time at Arterial 02 Saturation <90% Mean ± SD Normal Range

Feeding 0.22 ± 0.46 0-1.14

Awake (excludes feeding) 0.23 ± 0.44 0-1.11 Sleep

Active 0.06 ± 0.17 0-0.40

Quiet 0.02 ± 0.05 0-0.12

Total 0.04 ± 0.08 0-0.20

Total recording time 0.12 ± 0.20 0-0.52

* Normal range is mean+2 SD for the control infants in this study. No control infant

had any value <80%.

TABLE 5. Pneumogram Results

Bronchopulmonary Respiratory Dysplasia Distress Syndrome

(n=12) (n=13)

Total sleep time (mm) 531 ± 12 532 ± 15

Longest apnea (s) 8.3 ± 1.1 8.9 ± 1.2

Apnea density (% total sleep time) 0.16 ± 0.04 0.77 ± 0.30

Periodic breathing (% total sleep time) 0.3 ± 0.1 2.7 ± 1.3

Sustained bradycardias (No. of episodes) 1.4 ± 0.6 0.6 ± 0.3

Abnormal recordings (%) 42 38

* Data are expressed as means ± SEM.

abnormal arterial oxygen desaturations. Six of seven infants with bronchopulmonary dysplasia

(86%) with normal pneumogram results had

ab-normal oxygen desaturations, whereas only two

of five infants with bronchopulmonary dysplasia

(40%) with an abnormal pneumogram result had

abnormal oxygen desaturation. Similarly, five of eight infants with respiratory distress syndrome

(63%) with normal pneumogram findings had

ab-normal oxygen desaturation, whereas four of five infants with respiratory distress syndrome (80%)

with an abnormal pneumogram result had

ab-normal oxygen desaturation (Figure). Therefore,

pneumograms were not predictive ofabnormal

de-saturation by



Assessment of pulmonary mechanics in both


TABLE 6. Pulmonary Mechanics

Bronchopulmonary Respiratory Dysplasia Distress Syndrome

(n=14) (n=13)

Respiratory rate (breaths/mm) 60.8 ± 3.8 65.8 ± 2.8

Tidal vol (mL/kg) 12.0 ± 0.6 12.2 ± 0.4

Mm ventilation (mL/kg/min) 661.4 ± 55.4 729 ± 41.3

Thoracic gas vol (mL/kg) 28.8 ± 1.5 27.5 ± 1.4

Airways resistance (cm H2O/L/s) 42.8 ± 2.7 43.4 ± 4.1

Specific airway conductance (1/cm H2O/L/s) 0.39 ± 0.04 0.48 ± 0.06

Dynamic pulmonary compliance (mL/cm H2O) 2.1 ± 0.2 2.3 ± 0.3

resistance was increased and dynamic compliance was decreased in both groups. In infants with

bronchopulmonary dysplasia, time at Sao2 less

than 90% correlated with airway resistance (r =

.582; P < .05). However, dynamic pulmonary com-pliance did not correlate with time at Sao2 less than 90% (r = - .510). Thus, desaturation

ap-pears to occur more commonly in infants with

bronchopulmonary dysplasia and high airway



Pulse oximetry was used as the measure of ox-ygenation in this study. Pulse oximetry has been shown to be an accurate and simple, noninvasive measurement of Sao2 in infants.’3”4’3134 Sao2 is measured by analyzing the differential absorb-ance of two wavelengths of light by the vascular bed in synchrony with the peak systolic arterial pulsation.’3”4 Therefore, accuracy of the reading depends on the ability of the oximeter to detect that arterial pulse. Vigorous body movements, such as kicking and squirming, can interfere with

pulse detection. In this study, we accepted oxygen saturation values only when the pulse rate from the pulse oximeter was within five beats per mm-ute of the heart rate measured by simultaneous

ECG. Greater than 80% of all recordings yielded

accurate oxygen saturation values using these


This study showed that preterm infants with

bronchopulmonary dysplasia and those with

res-piratory distress syndrome but no bronchopul-monary dysplasia experience significant and se-vere hypoxemia, which is clinically unsuspected and unrecognized by usual means of clinical as-sessment. Because normal control infants did not show this hypoxemia, these desaturations are

ab-normal. The hypoxemia seen in the preterm

infants occurred in the absense of apnea,

brady-cardia, or clinical cyanosis. Our data are in

agreement with observations of Loughlin et al35

showing unsuspected hypoxia during sleep in in-fants with bronchopulmonary dysplasia who were

well oxygenated while awake. In this study

de-saturations were observed during wakefulness, quiet sleep, active sleep, and feeding. Therefore,

these infants demonstrated hypoxic episodes in

behavioral states other than active sleep as pre-viously observed in adults and children with chronic obstructive pulmonary disease, cystic fi-brosis, and asthma.9’2 In these adults and older

children, desaturation during rapid eye

move-ment sleep is due to alveolar hypoventilation and ventilation/perfusion mismatch.9’36 Previous studies in preterm infants showed that general-ized motor activity causes irregular respirations,

decreased minute ventilation, and a decrease in

transcutaneous Po2.37 In this study, we did not measure minute ventilation, but the desatura-tions we observed during wakefulness may be ex-plained by these mechanisms.

The highest incidence ofdesaturation in infants

with bronchopulmonary dysplasia and those with

respiratory distress syndrome occurred during

feeding. Wilson et al38 found interruption of

res-piratory flow associated with spontaneous

non-feeding swallows due to airway closure in infants. Sucking movements precede swallowing during feeding, which further inhibits inspiration.39 The breathing pauses during sucking and swallowing

may decerease Pao2, causing the observed

desa-turations. Obstructive apnea, although not

ob-served clinically, may have been missed by our

monitoring techniques.

Decreased dynamic pulmonary compliance and

increased airway resistance were observed in both groups in this study. In infants with

bronchopul-monary dysplasia, high airways resistance

cor-related with desaturation, but no such relation-ship was seen in the respiratory distress syndrome

group. The airways resistance measurement may

be affected by mild sedation which was used in


desaturation in the two groups did not correlate with gestational age at birth, birth weight,

du-ration of supplemental oxygen, or duration of

me-chanically assisted ventilation.

Preterm infants, and especially infants with

bronchopulmonary dysplasia, are at increased

risk for sudden infant death syndrome (SIDS).68

Therefore, increasing numbers ofpreterm infants

are undergoing evaluation for apnea and are

being treated with home apnea-bradycardia

mon-itoring.40’4’ However, sleep studies and

pneumo-grams do not predict clinical outcome and are not

correlated with death or SfflS.842 In this study,

pneumograms did not correlate with abnormal

oxygen desaturation in preterm infants. These

episodes of hypoxemia did not occur in

conjunc-tion with events measured by pneumograms, such

as central apneas or bradycardia. Furthermore,

Naeye and co-workers43 and Valde-Dapena

have described tissue markers of chronic

hypox-emia in a majority of SIDS victims. It is possible that clinically unsuspected hypoxemia, similar to that described in this study, occurs frequently in

preterm infants and that profound hypoxemia

may be responsible for a majority ofsudden

unex-plained deaths in these infants.


This study was supported, in part, by the Los Angeles

County, Orange County, Kern County, and Inland Em-pire Chapters of the Guild for Infant Survival.

The authors thank Charles W. Sargent, BS, BME,

for technical assistance; Anna Basile, Lydia A. Tina-jero, Albert M. Lau, Caroline E. Chan, and Justin Yang

for assistance with data reduction; and Paul Lucas for

preparation of the manuscript.


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32. Deckhardt R, Stavard DJ: Non invasive arterial hemo-globin oxygen saturation versus transcutaneous oxygen

tension monitoring in preterm infants. Grit Care Med


33. Jennis MS, Peabody JL: Pulse oximetry: An alternative method for the assessment of oxygenation in newborn in-fants. Pediatrics 1987;79:524-528

34. Monaco F, Feaster WW, McQuitty JC, et al: Continuous non invasive oxygen saturation monitoring in sick new-borns, abstracted. Respir Care 1983;28:1362

35. Loughlin GM, Allen RP, Pyzik P: Sleep related hypoxemia in children with bronchopulmonary dysplasia (BPD) and adequate oxygen saturation awake, abstracted. Sleep Res


36. Leitch AG, Cloney LI, Leggett RJE: Arterial blood gas tensions, hydrogen ion and electroencephalogram during sleep in patients with chronic ventilatory failure. Thorax


37. Abu-Osba YK, Brouillette RT, Wilson SL, et al: Breathing

pattern and transcutaneous oxygen tension during motor activity in preterm infants. Am Rev Respir Dis 1982; 125:382-387

38. Wilson SL, Thach BT, Brouillette RT, et al: Coordination of breathing and swallowing in human infants. J Appl

Physiol: RespirEnviron ExercisePhysiol 1981;50:851-858 39. Prechtl HFR, Faragel JW, Weinmann HM, et al: Postures,

motility and respirations oflow risk preterm infants. Dev

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44. Valde-Dapena MA: Sudden infant death syndrome: A re-view of the medical literature 1974-1979. Pediatrics






Henry Adams (1838-1918), grandson of John Quincy Adams, the sixth

President of the United States, claimed in his autobiography that his edu-cation was defective, despite the best Boston schools could offer.

In his autobiography, privately printed (1907) and posthumously published (1918) Adams wrote about his dislike of school as follows.’

In any and all forms, the boy [Adamsi detested school, and the prejudice became deeper with years. He always reckoned his school days, from ten to sixteen years old

as time thrown away . . . Indeed, had his father kept the boy at home, and given him

half an hour’s direction every day, he would have done more for him than school ever

could do for him. . . . Most school experience was bad. . . . Books remained as in the

eighteenth century, the source of life, and as they came out-Thackeray, Dickens, Bulwer, Tennyson, Macaulay, Carlyle, and the rest-they were devoured; but as far

as happiness went, the happiest hours of the boy’s education were passed in summer lying on a musty heap of Congressional Documents in the old farmhouse at Quincy,

reading Quentin Durward, Ivanhoe, and The Talisman, and raiding the garden at intervals for peaches and pears. On the whole he learned most then.


Noted by T.E.C., Jr, MD




Meena Garg, Sharon I. Kurzner, Daisy B. Bautista and Thomas G. Keens

Bronchopulmonary Dysplasia

Clinically Unsuspected Hypoxia During Sleep and Feeding in Infants With


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Meena Garg, Sharon I. Kurzner, Daisy B. Bautista and Thomas G. Keens

Bronchopulmonary Dysplasia

Clinically Unsuspected Hypoxia During Sleep and Feeding in Infants With


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