Hypoxaemia in infants with respiratory tract infections.

Nineteen infants who were graduates from special care baby units underwent two overnight tape recordings of oxygen saturation (SaO2) and breathing movements; one during an upper (n = 12) or lower (n = 7) respiratory tract infection and the other when free of infection. Baseline SaO2 was lower during infection (median 99.6 vs 100%, p less than 0.01), with four patients having values (84.3-95.5%) below the normal lower limit for full-term infants (97%). The median number of apnoeic pauses was also lower during respiratory tract infection (4.7 vs 15.7/h, p less than 0.02). The median number of episodic desaturations (SaO2 less than or equal to 80%) did not change significantly (1.3 vs 1.9/h, p greater than 0.05), with the exception of one patient who had extremely increased values during infection for both apnoeic pauses (63/h) and desaturations (112/h). No infant, however, was considered clinically hypoxaemic. Clinically unsuspected hypoxaemia may thus occur during respiratory tract infection in a proportion of infants graduating from special care baby units. Such hypoxaemia may have potentially deleterious effects.

Arterial oxygen saturation in preterm infants at discharge from the hospital and six weeks later.

To obtain normal data on arterial oxygen saturation (SaO2) in preterm infants and to study early developmental changes in SaO2, we obtained overnight tape recordings of SaO2 and breathing movements in 160 preterm infants at their discharge from three special care baby units (mean gestational age at birth 33 weeks; at time of study, 37 weeks). One hundred ten infants (69%) underwent a second recording 6 weeks later. Median baseline SaO2 during regular breathing was 99.5% (range 88.7% to 100%) at discharge, and 100% (range 95.3% to 100%) at follow-up (p less than 0.001). The number of episodes of desaturation, defined as a fall in SaO2 to less than or equal to 80% for at least 4 seconds, corrected to the mean duration of recording (12.2 hours), decreased from a median of 3 (0 to 355) to 0 (0 to 17) (p less than 0.001). The median duration of each episode of desaturation remained unchanged (5.2 (4.0 to 22.7) vs 5.5 (4.2 to 24.0) seconds). At discharge, a small minority of infants had a clinically unrecognized low baseline SaO2 (lowest, 88.7%; 5th percentile, 95.7%) or a high number of desaturation episodes (the highest was six times the 95th percentile value). At follow-up, all outlying values had normalized. Follow-up recordings made between 42 and 47 weeks of gestational age (n = 53) were compared with similar recordings from 67 term infants at the same gestational age. The preterm infants had a significantly higher baseline SaO2 and no more desaturation than the infants born at term. Knowledge of normal ranges of oxygenation and their changes with age may be of value in identifying clinically undetected hypoxemia in preterm infants at discharge from the hospital. The potential influence of such hypoxemia on clinical outcome remains to be determined.

Oxygen saturation and breathing patterns in infancy. 1: Full term infants in the second month of life.

Overnight 12 hour tape recordings were made of arterial oxygen saturation (SaO2, pulse oximeter in the beat to beat mode) and abdominal wall breathing movement on 67 healthy, full term infants between the ages of 29 and 54 (median 39) days. The median baseline SaO2 during regular breathing was 99.8% (range 97.0-100%). Fifty four infants (81%) had shortlived episodes during which SaO2 fell to 80% or less (desaturation); the median rate was 0.9 desaturations/hour, and the median duration of each desaturation was 1.2 seconds. The 97th centile value for the duration of all episodes in which SaO2 fell to less than or equal to 80% was 4.0 seconds. The frequency of desaturations was significantly higher, and their duration significantly longer, when the breathing pattern was non-regular rather than regular. The percentage of apnoeic pauses (greater than or equal to 4 seconds in duration) followed by a desaturation was higher during non-regular than regular breathing; it was particularly high during periodic breathing. A knowledge of normal variability of baseline measurements of oxygenation and of the relationship between oxygenation and breathing patterns in infants is essential to the use of pulse oximetry in clinical practice.

Oxygen saturation and breathing patterns in infancy. 2: Preterm infants at discharge from special care.

Overnight 12 hour tape recordings of arterial oxygen saturation (SaO2, pulse oximeter in the beat to beat mode), breathing movements, and airflow were made on 66 preterm infants (median gestational age 34 weeks, range 25-36) who had reached term (37 weeks) and were ready for discharge from the special care baby unit. No infant was given additional inspired oxygen during the study. The median baseline SaO2 was 99.4% (range 88.9-100%). Eight infants had baseline SaO2 values below 97%, the lowest value observed in a study on full term infants. All but one infant had short-lived falls in SaO2 to less than or equal to 80% (desaturations), which were more frequent (5.4 compared with 0.9/hour) and longer (mean duration 1.5 compared with 1.2 seconds) than in full term infants. There was no evidence that gestational age at birth influenced the frequency or duration of desaturations among the preterm infants. The frequency of relatively prolonged episodes of desaturation (SaO2 less than or equal to 80% for greater than or equal to 4 seconds), however, decreased significantly with increasing gestational age (0.5, 0.4, 0.2, and 0.1 episodes/hour in infants at less than or equal to 32, 33-34, 35, and 36 weeks' gestational age, respectively). Analysis of the respiratory patterns associated with such episodes showed that 5% occurred despite both continued breathing movements and continuous airflow. Five infants had outlying recordings: three had baseline SaO2 values of less than 95% (88.9, 92.7, and 93.8%), and two had many prolonged desaturations (14 and 92/hour; median for total group 0.2, 95th centile 2.3). None of these five infants had been considered clinically to have dis order of oxygenation. Although these data are insufficient to provide information about outcome, we conclude that reference data on arterial oxygenation in preterm infants are important to enable the identification of otherwise unrecognized hypoxaemia.

QT interval measurements before sudden infant death syndrome.

Standard electrocardiogram recordings were performed on a total of 7254 newly born infants from two maternity hospitals. Fifteen recordings were obtained on 15 infants who subsequently suffered sudden infant death syndrome. None showed lengthening of QT intervals sufficient to warrant the description of 'long QT syndrome'. When the QT intervals corrected for heart rate of cases with sudden infant death syndrome were compared with controls in age matched groups or after individual matching for postnatal age, hospital of birth, and weight at birth, no significant differences could be identified.

Prolonged apnea and cardiac arrhythmias in infants discharged from neonatal intensive care units: failure to predict an increased risk for sudden infant death syndrome.

Twenty-four hour recordings of respiratory wave form and ECG were made on low-birth-weight and/or premature infants within one week of discharge from eight neonatal intensive care units. Eight infants (0.7%) had episodes of apnea greater than 30 seconds in duration, all of which were accompanied by bradycardia less than 100 beats per minute; 25 infants (2.3%) had a total of 36 apneic episodes between 20 and 30 seconds in duration, 29 of which were accompanied by bradycardia less than or equal to 100 beats per minute; and 19 infants (1.7%) had episodes of bradycardia less than or equal to 50 beats per minute without prolonged apnea (as shown by a lack of breathing movement). Five infants had ventricular premature beats (including one with ventricular tachycardia). Eleven infants had supraventricular premature beats (including two with supraventricular tachycardia and one with preexcitation). Four infants had both supraventricular and ventricular premature beats. Two infants had preexcitation. Eleven infants who underwent 24-hour recordings died. Five infants were victims of sudden infant death syndrome. One infant death was sudden and unexpected and was attributed to bronchopneumonia. Two deaths were associated with congenital heart disease and three were associated with major cerebral disorders. None of the six babies who died suddenly and unexpectedly had apnea greater than or equal to 20 seconds, bradycardia less than or equal to 50 beats per minute, or cardiac arrhythmias on their 24-hour recordings.

Prolonged QT interval and cardiac arrhythmias in two neonates: sudden infant death syndrome in one case.

Two neonates with arrhythmias and the long QT syndrome are described. The arrhythmias were detected in utero and both infants were apparently well after birth. The first infant, although well, had a bradycardia for the first 9 days of life. A normal heart rate was documented at 10 days but a prolonged QT interval was not appreciated on the ECG. He was discharged from hospital but died suddenly and unexpectedly 3 days later. A post-mortem examination failed to find a cause for his death which therefore fell into the category of the sudden infant death syndrome (SIDS). A retrospective analysis of the perinatal electrocardiogram showed a probable junctional rhythm with 2:1 conduction to the ventricle; the QT interval was prolonged at 0.52 seconds (QTC = 0.63). The second infant had a QT interval of 0.52 seconds (QTC = 0.54) and frequent ventricular premature beats on a 24-hour electrocardiogram. She was treated with propranolol and remains well 2 years later. Sudden infant death has often been described in the siblings of children with the long QT syndrome and one other report described a case of SIDS which was said to have had a prolonged QT interval on the perinatal ECG. This report, however, provides unquestionable evidence, in one case, of an association between the long QT syndrome and SIDS.

Clinical and subclinical vitamin D deficiency in Bradford children.

A survey of the vitamin D status of Bradford schoolchildren was carried out in April 1973, employing conventional biochemistry, radiology, and measurement of 25-hydroxycholecalciferol levels. Biochemical evidence of rickets was present in 45% of the Asians. When re-examined in September, several children showed spontaneous biochemical resolution; nevertheless, radiological abnormalities were present in 12% of the original sample. No evidence of rickets was detected in the smaller White sample. Minor biochemical abnormalities were present in 9 of the 40 West Indian children. A study of admissions of Bradford hospitals in the 4 years 1969-1972 inclusive confirmed that clinical vitamin D deficiency was confined to Asians except for a few cases of infantile rickets in White children. The probability that one Asian child in 40 may require admission during the period from birth to adolescence emphasizes the urgent need for the introduction of prophylactic measures.

Comparison of treatments for congenital nonobstructive nonhaemolytic hyperbilirubinaemia.

A patient with Crigler-Najjar disease has survived with the help of phototherapy to the age of 2 years without neurological damage. Because long periods of phototherapy are a threat to normal development, a search was made for supplementary treatments. Cholestyramine and a high fat diet were effective, and possibly also aspartic acid. Maintenance therapy with cholestyramine allowed the amount of phototherapy given to be reduced.