Obstructive Sleep Apnea Starts Early in Cystic Fibrosis

Abstract

Spicuzza L, Sciuto C, Leonardi S, et al. Early occurrence of obstructive sleep apnea in infants and children with cystic fibrosis. Arch Pediatr Adolesc Med. 2012; 166(12): 1165-1169; doi: 10.1001/archpediatrics.2012.1177Investigators from the University of Catania in Italy sought to determine the occurrence of sleep-disordered breathing (SDB) and nocturnal hypoxemia among children with cystic fibrosis (CF). They enrolled children from their CF unit who were in stable clinical condition, defined as a stable forced expiratory volume in one second (FEV1) and the absence of respiratory symptoms such as increased cough, sputum production, and/or increased dyspnea. They also enrolled healthy age-matched controls.Each CF and control child had a daytime oxygen saturation (SpO2) recorded, was evaluated by an otolaryngologist to assess upper airway abnormalities, and underwent a nocturnal polysomnogram. All children ≥6 years old also underwent standard spirometry. Primary outcomes assessed were differences between CF and control children in awake and asleep SpO2, nocturnal hypoventilation (SpO2 <90% for >5% of the night), and apnea-hypopnea index (AHI). AHI was calculated as the number of apneas (absence of airflow for ≥2 respiratory cycles) and hypopneas (decreases of ≥50% in oronasal flow and a concurrent arousal and/or a decrease of ≥3% in SpO2 from baseline) per hour of sleep. Secondary outcomes were the occurrence of obstructive sleep apnea (OSA), defined as an AHI >2, and a characterization of sleep architecture, measured by number of arousals and sleep efficiency (total sleep time divided by the total polysomnogram time).A total of 58 children participated in the study – 40 children with CF and 18 controls. The CF group included children who were aged 6 months to 11 years; 58% were male. The CF group had mean values of FEV1 and forced vital capacity that were significantly lower than controls (P < .001). None of the controls had upper airway abnormalities, while 35% in the CF group had chronic rhinosinusitis and 25% had adenotonsillar hypertrophy.Although the mean awake SpO2 was similar between the CF and control groups, the mean SpO2 fell significantly during sleep for those with CF compared to controls (94.7% vs 97.0%, P < .001). No children in the CF or control group had nocturnal hypoventilation. The mean AHI was significantly higher in the CF group (7.3 vs 0.5, P < .001) and 70% in the CF group had OSA. The highest AHI and lowest mean nocturnal SpO2 occurred in children aged 5 to 6 years. Children in the CF group also had more arousals (mean 11.0 vs 8.2, P < .001) and reduced sleep efficiency (mean 80% vs 88%, P < .001).The authors conclude that SDB occurs in an early stage of life in children with CF and mild lung disease in stable clinical condition.Since OSA is primarily a disturbance of the upper airway, its association with CF is not well understood, particularly among younger children with CF in stable condition. The results of the current study strengthen this observation. In a similar study, Ramos et al1 found that 57% of children and adolescents (age 2 to 14 years) with CF and a clinical suspicion of SDB had an AHI ≥1. Naqvi et al2 found sleep complaints to be common among the 24 children with CF they studied; 44% reported problems with sleep onset, 39% reported sleep maintenance problems, 74% reported daytime sleepiness, and sleep efficiency was significantly reduced.2Reduced sleep efficiency has been noted among adults with CF and it has been shown that adult CF patients with severe lung disease have impaired neurocognitive function and daytime sleepiness, which is partly related to chronic sleep disruption.3,4 With the addition of the current study to the literature, it seems reasonable to suggest that patients with CF be evaluated by a sleep specialist and be considered for a nocturnal polysomnogram, since SDB can occur in CF patients with mildly impaired lung function and without significant respiratory symptoms.5