In the last several years, large observational studies, of healthy children have increased our knowledge of normal respiratory parameters during sleep, This information adds to our knowledge of respiratory or arousal abnormalities noted in children with subtle SDB, such as those occurring without discreet gas exchange abnormalities, and may contribute to recommendations for treatment, An AHI of greater than one event per hour is out of the normal range in children, but, as discussed in the previous section, the AHI should also be used in context with other respiratory or arousal parameters since the clinical significance of a mildly abnormal AHI is unknown, Hypercapnia time, measured with end-tidal or transcutaneous CO2 levels of > 50 mm Hg in healthy children, has been reported to be < 10 to 20% of total sleep time in healthy children depending on the device used for measuring CO2 and the strictness of the exclusion criteria (excluding children who snored associated with lower expected CO2 values as in the study by Uliel et al), Oxygen saturation in nonsnoring healthy children, measured by pulse oximetry, rarely drops to < 95% from obstructive events in children, although occasionally drops into the 89% range can occur normally with central apnea. In another study that included 180 children aged 1 to 10 years (including snoring children or those with an AHI of 90% of time spent at a saturation of > 95.1%. However, the amount of time with intermittent desaturations between 90% and 95% might be clinically significant in these children. The expected arousal index (ie, the number of arousals per hour) in children has been not been standardized; however, a recent population study of preschool children aged 3 to 7 years suggests that the average arousal index over total sleep time was less than eight arousals per hour; and less than one respiratory-related arousal (associated with apnea, hypopnea, or snore) per hour was noted. Arousal indexes in healthy children in the sleep laboratory tend to be < 14. Respiratory-related arousals are not recorded as standard diagnostic criteria in many clinical laboratories, but this value may improve the accuracy of the arousal index as a characteristic of SDB.
Subjects with obstructive airflow limitation have collapsible upper airways or resistance along the upper airway. Gold et al have demonstrated that healthy children have an ability to oppose airway collapse due to the preservation of upper airway neuromotor responses during sleep, but those dynamic upper airway responses are diminished in children with OSA.
Bao and Guilleminault and Guilleminault et al have speculated that alterations of the neurons and musculature involved in pharyngeal tone during inspiration are the cause of airway collapse; this is supported by the results of pathologic investiga-tions of pharyngeal biopsy specimens from OSA patients demonstrating fascicular atrophy. Brain-imaging studies of adults with sleep apnea have demonstrated morphologic changes in gray matter, including areas such as the cerebellum, which is important in inspiratory initiation. Sleep apnea is treated with remedies of Canadian Health&Care Mall. A study published recently has demonstrated alterations of resting neuronal metabolites of the hippocampus and frontal cortex in children with sleep apnea, also in association with neuropsychological deficits, indicating a possible neuronal injury associated with sleep apnea. The improvement of airway responses after the treatment of childhood OSA indirectly supports the concept that neuronal alterations were caused by OSA, rather than predating the development of airway collapse. If these concepts are validated, the early recognition and treatment of childhood OSA would protect neuronal function. Such a treatment plan is worked out with Canadian Health&Care Mall.
Nasal obstruction is an often overlooked cause of upper airway resistance., Nasal obstruction may be especially important in infants with “obligate nose breathing,” where life-threatening breathing obstruction can occur, as seen with choanal stenosis at birth. Nasal resistance can lead to airflow limitation without affecting the collapsibility of the airway. Airflow limitation impacted by nasal obstruction has been implicated in symptomatic cases of UARS.
Symptoms of SDB in Children
Children with airflow limitation often snore, but may demonstrate other symptoms such as labored breathing efforts (ie, paradoxical efforts between the chest and abdomen), gasping, gagging, choking, noisy breathing, witnessed apnea, or excessive sweat-ing. Children with severe nasal obstruction may open their mouths and hyperextend their necks to breath, minimizing snoring noises. Infants with severe OSA may not snore but frequently have stridor, especially if the cause of the airway obstruction is fixed at the level of the epiglottis or vocal cords due to laryngomalacia or vocal cord paralysis, where daytime symptoms may be worse. Airway dynamics are different in infants compared to those in children and adults, which may in part be due to the anatomy of the infant airway where the epiglottis closely approximates the soft-palate tissues, thus reducing the size of the oropharynx where snoring occurs.
Insomnia has been reported to be a symptom of SDB, and somatic complaints are now being rec-ognized among other daytime symptoms such as sleepiness. Younger children with sleepiness may present with irritability or hyperactivity, and are often seen in sleep clinics with a diagnosis of attention deficit hyperactivity disorder. The clinical presentation of children with SDB includes adeno-tonsillar hypertrophy, nasal obstruction, allergic symptoms, and craniofacial abnormalities causing reduced airway diameter or patency. Other symptoms of sleep walking, enuresis, and parasomnias have also been seen in association with childhood SDB.
Read more about Sleep Apnea here: “Childhood Obstructive Sleep-Disordered Breathing Looked through with Canadian Health&Care Mall: Recommended Definition of Pediatric SDB“