Silvestri J M, Weese-Mayer D E, Bass M T, Kenny A S, Hauptman S A, Pearsall S M
Rush Medical College of Rush University, Rush-Presbyterian-St. Luke's Medical Center, Department of Pediatrics, Chicago, Illinois 60612.
Pediatr Pulmonol. 1993 Aug;16(2):124-9. doi: 10.1002/ppul.1950160208.
We hypothesized that obese children with a history of breathing difficulty during sleep would demonstrate (1) evidence of complete and partial obstructive sleep apnea (OSA) with hypercarbia and/or hypoxemia; and (2) correlation between symptoms, degree of obesity, adenoid and tonsil size, and polysomnography (PSG) results. We evaluated 32 obese children [% ideal body weight (IBW), 196 +/- 45%] with a sleep history questionnaire, airway radiographs, electrocardiograms (ECG), and PSG. By history, we found snoring (100%), difficulty breathing (59%), sweating (44%), restlessness (53%), arousals (41%), apnea (50%), worsening with upper respiratory infection (URI) (81%), hypersomnolence (59%), and mouth breathing (59%). We found adenoid and/or tonsil enlargement on 75% of airway x-ray pictures. ECGs were abnormal in 5 patients. Among all patients, mean sleep study oxyhemoglobin saturation (SaO2) was 85 +/- 16% and mean end-tidal CO2 (PetCO2) was 51 +/- 7 torr; 84% had paradoxical inward movement of the chest on inspiration, 59% had OSA, and 66% had partial OSA. In those with > or = 200% IBW and adenotonsillar enlargement, elevated PetCO2 and the presence of hypoxemia (SaO2 < 90%) for > or = 5% of the total sleep time (TST) were correlated, unlike in patients of similar weight but without adenotonsillar enlargement. Individuals symptoms did not correlate with the severity of PSG abnormalities. By discriminant analysis, using three variables (IBW, presence of adenotonsillar tissue, and presence of > or = 5 symptoms), we could predict PSG abnormalities with up to 81% reliability. Our findings indicate that in obese children, particularly those with %IBW > or = 200 and adenotonsillar hypertrophy, with sleep-disordered breathing evaluation by polysomnography should be considered.
我们假设，有睡眠期间呼吸困难病史的肥胖儿童会表现出：（1）伴有高碳酸血症和/或低氧血症的完全性和部分性阻塞性睡眠呼吸暂停（OSA）的证据；以及（2）症状、肥胖程度、腺样体和扁桃体大小与多导睡眠图（PSG）结果之间的相关性。我们通过睡眠病史问卷、气道X光片、心电图（ECG）和PSG对32名肥胖儿童[理想体重（IBW）百分比，196±45%]进行了评估。通过病史，我们发现打鼾（100%）、呼吸困难（59%）、出汗（44%）、烦躁不安（53%）、觉醒（41%）、呼吸暂停（50%）、上呼吸道感染（URI）时加重（81%）、嗜睡（59%）和张口呼吸（59%）。在75%的气道X光片上发现腺样体和/或扁桃体肿大。5例患者心电图异常。在所有患者中，平均睡眠研究氧合血红蛋白饱和度（SaO2）为85±16%，平均呼气末二氧化碳（PetCO2）为51±7托；84%的患者吸气时胸部有矛盾性向内运动，59%的患者患有OSA，66%的患者患有部分OSA。在那些IBW≥200%且腺样体扁桃体肿大的患者中，PetCO2升高和低氧血症（SaO2<90%）持续总睡眠时间（TST）≥5%是相关的，这与体重相似但没有腺样体扁桃体肿大的患者不同。个体症状与PSG异常的严重程度无关。通过判别分析，使用三个变量（IBW、腺样体扁桃体组织的存在以及≥5种症状的存在），我们可以以高达81%的可靠性预测PSG异常。我们的研究结果表明，在肥胖儿童中，尤其是那些IBW%≥200且腺样体扁桃体肥大的儿童，应考虑通过多导睡眠图进行睡眠呼吸障碍评估。
