The objective of this study was to determine the accuracy and practicality of home testing for pediatric obstructive sleep apnea syndrome (OSAS) secondary to adenotonsillar hypertrophy. Twenty-one children aged 2-12 years and referred for possible OSAS were studied twice, once at home and once in the sleep laboratory. The home test consisted of two parts: 1) a cardiorespiratory recording of saturation (SaO2), pulse rate, pulse waveform, electrocardiogram, and respiratory inductive plethysmography; and 2) an 8-hour videotape recording of the sleeping child. In the laboratory, standard nocturnal polysomnography including electroencephalography was performed. Experiences with another 62 children who underwent home testing alone were also reviewed and are reported. At home, saturation, respiratory, and video data were obtained 96.4 +/- 13.3% (mean +/- SD) 99.4 +/- 1.6%, and 90.0 +/- 78% of the time, respectively. The sleep efficiency was greater at home than in the laboratory, 91.1 +/- 3.9% vs. 86.1 +/- 7.2%, with a mean difference of 5.0% (P < 0.01). The median environmentally induced movement/arousal index was lower in the home than in the laboratory, 0.0 (inter-quartile range, 0.0-0.3 vs. 2.4/hr (inter-quartile range 1.2-4.2), with a median difference of 2.4/h (P < 0.001). Study duration, apnea/hypopnea index, desaturation index, respiratory and spontaneous movement/arousal indices, and oxygen saturation during sleep were similar for home and laboratory studies. Although neither sleep state nor PCO2 (transcutaneous or end-tidal) was measured in the home, this information would have modified patient management in, at most, one case. In the second group of 62 children, exclusively studied at home, all studies were successfully recorded despite a wide range of sleep efficiencies, apnea/hypopnea indices, and desaturation indices. We conclude that home testing, using a simplified cardiorespiratory montage plus video recording, is accurate and of practical use in the routine evaluation of OSAS in patients with adenotonsillar hypertrophy.

No abstract

There is limited information concerning the exercise performance of long-term survivors of bronchopulmonary dysplasia (BPD), and much of what is available pertains to those with relatively mild disease. The present study was undertaken to describe exercise responses in patients with a history of severe BPD, defined as those patients with a clinical and radiographic diagnosis of BPD who required supplemental oxygen at least until they were 44 wk postconceptual age and who were discharged home on oxygen. Fifteen children with a history of severe BPD were matched for gestational age with 15 children who had previously had respiratory distress syndrome but who did not develop BPD (Prem). These Prem control children were subsequently compared with 13 healthy control children born at term (Control) who were of similar postnatal age. Participants underwent pulmonary function testing, progressive exercise testing on a cycle ergometer, and a steady-state exercise test with cardiac output determined by CO2-rebreathing. Despite the patients with BPD having a lower FEV1 than those in the Prem group, who had lower values than the Control group (BPD, 64 +/- 21%; Prem, 85 +/- 11%; Control, 95 +/- 8%), the exercise capacity did not differ between the BPD and the Prem and between the Prem and the Control groups (BPD, 84 +/- 15%; Prem, 81 +/- 17%; Control, 91 +/- 12%). However, the BPD patients used a greater percentage of their ventilatory reserve (VEmax/40 FEV1: BPD, 93 +/- 20%; Prem, 67 +/- 12%; Control, 59 +/- 13%). Of the four patients with BPD who had significant oxygen desaturation with exercise, three had the lowest values for FEV1. Cardiac output was appropriate for oxygen consumption in most patients.

CF children showed evidence of increased oxidative stress with worsening of glucose metabolism. NR may delay the appearance of CFRD.