A cohort of 53 patients (age range 1-9-16-5 years) with sickle celi disease (49 homozygous SS and four S,0-thalassaemia) was studied for evidence of sleep To determine the prevalence of sleep related UAO and hypoxaemia, as well as its response to treatment, we studied prospectively a cohort of patients with sickle cell disease, utilising overnight sleep recordings in addition to clinical assessment. As the normal data for these studies were based on pulse oximetry values obtained in healthy children with light skin colour, we also compared recordings in black and white control children.
Subjects and methods
PROTOCOL FOR INVESTIGATIONThe protocol included (i) documentation by a haematologist of signs and symptoms of UAO, (ii) overnight multichannel respiratory recordings and clinical assessment performed by a paediatric respiratory unit, (iii) examination and intervention by an ear, nose, and throat surgeon, followed by postoperative physiological recordings, and (iv) a blinded, case-controlled analysis of oxygenation from the overnight physiological recordings.
ABSTRACT. The pathogenesis of bradycardias in preterm infants is poorly understood. Because their pathogenesis may involve both apnea and hypoxemia, we set out to analyze the proportion of bradycardias that were associated with an apneic pause and/or a fall in arterial oxygen saturation (Sao2), and the temporal sequence of the three phenomena, in overnight tape recordings of Saol (Nellcor NlOO in beat-to-beat mode), breathing movements, nasal airflow, and ECG in 80 preterm infants at the time of discharge from hospital. A bradycardia was defined as a fall in heart rate of 233% from baseline for 2 4 s, an apneic pause as a cessation of breathing movements and/or airflow for 2 4 s, and a desaturation as a fall in Sao2 to 580%. A total of 193 bradycardias were found in 46 (58%) of the recordings (median, three per recording; range 1-18). There was a close relationship between bradycardias, apneic pauses, and desaturations: 83% of bradycardias were associated with apneic pauses and 86% with desaturations. Where all three phenomena occurred in combination, the time from the onset of apnea to the onset of the fall in Sao2 was shorter (median interval, 0.8 s; range -4.9-+11.5 s) than that from the onset of apnea to the onset of bradycardia (median, 4.8 s; range -4.0-+14.0 s). Hence, most bradycardias (86%) commenced after the onset of the fall in Sao2. We conclude that bradycardia, apnea, and hypoxemia are closely linked phenomena in preterm infants. (Pediatr Res 34: 144-147, 1993)
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 680% 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 (¢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.
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