1 DIAGNOSIS OF DYSPNEA IN CHILDREN

Polysomnographic diagnosis is usually necessary for adults, in whom clinical symptoms will be presented when there are more than five apneas per hour, or over 30 times in 7 hours of sleep. In the case of children, apnea-like symptoms may be observed even when there is continuous hypoventilation, but not a typical apnea. We measured the esophageal pressure (Peso) to evaluate the respiratory efforts in children with adenotonsillar hypertrophy and OSA, and discovered that the degree of Peso increased even without apnea when in deep sleep (Fig. 64.3). Therefore, because the measurement of polysomnography (PSG) in a child is difficult, and also because of the specific characteristic of children’s OSA, the diagnostic criterion of PSG is still unclear in children, especially in infants.

Fig 64.3

Monitoring oxygen saturation during sleep seems to be valid. The degree of stenosis in airways can be detected by profile roentgen film (Fig. 64.4), or by direct observation under a thin flexible fiberscope. A video camera is nowadays available in many families. A video record is also useful in observing respiratory situations, and even in cases without obvious desaturation, apnea could be found.

Fig. 64.4 Profile roentgen film of upper airway in children pre- and post-adenotonsillectomy.

In 37 children with adenotonsillar hypertrophy, we ­inv estigated the thickness of adenoid, size of the airway space, and the lowest saturation during sleep. The lowest saturation was correlated to neither adenoid thickness nor airway space (Fig. 64.5). The grade of upper airway stenosis by adenoid or tonsillar hypertrophy on profile roentgen films could not predict the severity of apnea during sleep. For precise diagnosis of respiratory severity caused by ­adenoid–tonsillar hypertrophy, video observation with simultaneous SpaO₂ monitoring is necessary. However, this result did not suggest that roentgenic measurement of stenosis is meaningless. When severe hypertrophy of the tonsil and adenoid is recognized, the possible existence of respiratory impairment should be investigated out of caution. Even in cases with moderate hypertrophy, severe apnea could be a possible accompaniment.

Fig. 64.5 Correlation between adenoid thickness, airway space and lowest saturation. No significant relationship was recognized.

On the other hand, the adenoid and tonsil keep growing after birth until around 8 years old. Although the airway space in the pharynx also becomes larger, the ratio of adenotonsillar thickness to airway space reaches its peak at 4–6 years old. A previous study pointed out that children with OSA showed severe hypertrophy at younger ages (less than 3 years), which differed significantly compared to physiological hypertrophy of normal children (Fig. 64.6). Earlier surgical treatments are necessary for these cases.

Fig. 64.6 Adenoid size was already large enough to induce sleep dyspnea in sleep apnea children less than 3 years old compared with a control group (Shintani et al. 1997).

Rights were not granted to include this figure in electronic media. Please refer to the printed book.

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