Childhood Obstructive Sleep Apnea: One or Two Distinct Disease Entities?

Abstract

The spectrum of sleep disordered breathing (SDB) encompasses habitual snoring at the low end of severity all the way to frank obstructive sleep apnea (OSA), with upper airway resistance syndrome (UARS) and obstructive alveolar hypoventilation being considered as less severe variants of this condition. SDB occurs in children of all ages, from neonates to adolescents, and is characterized by repeated events of increased upper airway resistance as well as with either partial or complete upper airway obstruction during sleep, all of which may result in disruption of normal gas exchange and sleep integrity [1]. SDB was initially described over a century ago [2] and was then rediscovered in children by Guilleminault in 1976 [3]. However, this complex and relatively prevalent disorder is only now being recognized as a major public health problem. During the initial years since the seminal paper by Guilleminault et al [3], it became apparent that the classic clinical syndrome of OSA in children markedly differed from the OSA seen in adults, in particular with respect to gender distribution, clinical manifestations, polysomnographic findings, and treatment approaches [4,5]. However in more recent years, the epidemic of obesity that affects the pediatric population all over the world has led, in our opinion, to the emergence of a phenotypic variant of OSA in children that closely resembles that of adults with the disease. In this paper, we will review the pathophysiological mechanisms of OSA in children, delineate the clinical manifestations associated with the disease, and provide arguments for our novel and hopefully useful proposition that aims to define 2 types of OSA in children. For the sake of convenience, and in analogy with type I and type II diabetes, we propose to divide pediatric OSA as types I and II.

Figure 1. Habitual snoring in a 4-year old child without any evidence of gas exchange abnormalities or sleep alterations

EOG-electrooculogram; EEG – electroencephalogram; ECG – electrocardiogram; chin EMG – chin electromyograms; Snore – sound channel; LAT – left anterior tibial EMG; RAT – right anterior tibial EMG; Flow – thermistor derived oronasal flow; Chest – chest respiratory excursion; Abd – abdominal respiratory excursion; nP – nasal pressure; SpO2- oxyhemoglobin saturation by pulse oximetry; ETCO2 – end tidal carbon dioxide; PW- pulse waveform from pulse oximeter

Figure 2. Polygraphic tracing in a 7-year old child with upper airway resistance

EOG- electrooculogram; EEG – electroencephalogram; ECG – electrocardiogram; chin EMG – chin electromyograms; Snore – sound channel; LAT – left anterior tibial EMG; RAT – right anterior tibial EMG; nP – nasal pressure; Flow – thermistor derived oronasal flow; ETCO2 – end tidal carbon dioxide; Chest – chest respiratory excursion; Abd – abdominal respiratory excursion; IC-EMG – intercostal EMG; SpO2- oxyhemoglobin saturation by pulse oximetry; PW- pulse waveform from pulse oximeter

Figure 3. Obstructive alveolar hypoventilation in a 8-year old obese child

EOG-electrooculogram; EEG – electroencephalogram; ECG – electrocardiogram; chin EMG – chin electromyograms;; Flow – thermistor derived oronasal flow; nP – nasal pressure; ETCO2 – end tidal carbon dioxide; Chest – chest respiratory excursion; Abd – abdominal respiratory excursion; SpO2- oxyhemoglobin saturation by pulse oximetry; PETCO2 – end-tidal carbon dioxide readings

Figure 4. Obstructive sleep apnea in a 3 year-old child

EOG- electrooculogram; EEG – electroencephalogram; ECG – electrocardiogram; chin EMG – chin electromyograms; Snore – sound channel; LAT – left anterior tibial EMG; RAT – right anterior tibial EMG; Flow – thermistor derived oronasal flow; nP – nasal pressure; Chest – chest respiratory excursion; Abd – abdominal respiratory excursion; SpO2- oxyhemoglobin saturation by pulse oximetry; ETCO2 – end tidal carbon dioxide; PW- pulse waveform from pulse oximeter