Polysomnography in obese children with a history of sleep-associated breathing disorders

Authors

  • Dr. Jean M. Silvestri MD,

    Corresponding author
    1. Rush Medical College of Rush University, Rush-Presbyterian St. Luke's Medical Center, Department of Pediatrics, Chicago, Illinois
    • Center for SIDS Research and Disorders of Respiratory Control in Infancy and Childhood, Rush Presbyterian-St. Luke's Medical Center, 1653 West Congress Parkway, Chicago, IL 60612
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  • Debra E. Weese-Mayer MD,

    1. Rush Medical College of Rush University, Rush-Presbyterian St. Luke's Medical Center, Department of Pediatrics, Chicago, Illinois
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  • Michelle T. Bass,

    1. Rush Medical College of Rush University, Rush-Presbyterian St. Luke's Medical Center, Department of Pediatrics, Chicago, Illinois
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  • Anna S. Kenny CRTT,

    1. Rush Medical College of Rush University, Rush-Presbyterian St. Luke's Medical Center, Department of Pediatrics, Chicago, Illinois
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  • Susan A. Hauptman RRT,

    1. Rush Medical College of Rush University, Rush-Presbyterian St. Luke's Medical Center, Department of Pediatrics, Chicago, Illinois
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  • Sheilah M. Pearsall RN

    1. Rush Medical College of Rush University, Rush-Presbyterian St. Luke's Medical Center, Department of Pediatrics, Chicago, Illinois
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Abstract

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 ⩾200% IBW and adenotonsillar enlargement, elevated PetCO2 and the presence of hypoxemia (SaO2<90%) for ⩾5% of the total sleep time (TST) were correlated, unlike in patients of similar weight but without adenotonsillar enlargement. Individual symptoms did not correlate with the severity of PSG abnormalities. By discriminant analysis, using three variables (IBW, presence of adenotonsillar tissue, and presence of ⩾5 symptoms), we could predict PSG abnormalities with up to 81% reliability. Our findings indicate that in obese children, particularly those with %IBW ⩾200 and adenotonsillar hypertrophy, with sleep-disordered breathing evaluation by polysomnography should be considered. Pediatr Pulmonol. 1993; 16:124–129. © 1993 Wiley-Liss, Inc.

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