It’s very common for children with respiratory disorders to suffer from snoring and apnea (pauses in breathing) during sleep, some studies reveal that between a 4% and 10% of the population suffer from sleep apnea.
“The obstructive sleep apnea syndrome (OSAS) in children is a disorder of breathing during sleep characterized by prolonged partial upper airway obstruction and/or intermittent complete obstruction that disrupts normal ventilation during sleep and normal sleep patterns. Childhood OSAS is not simply adult OSAS in little people, and adult definitions and criteria are not applicable to children. Adults with OSAS frequently have fragmented sleep. In contrast, children with OSAS often do not have cortical arousals in response to obstructive apnea, and may therefore have preservation of their sleep architecture. However, few systematic studies of sleep architecture have been performed in children with OSAS, and the effects of different sleep stages on sleep-disordered breathing have not been described in detail. Worsening of respiratory parameters through the night has been described in obstructive sleep apnea in adults, but data are not available for children. This information may shed some light on the understanding of the disease pathophysiology and mechanisms involved in the termination of apnea events in children. We hypothesized that because children with OSAS do not have frequent cortical arousals, sleep architecture would not differ between children with OSAS and control subjects. Further, based on our clinical observations, we hypothesized that obstructive apnea would worsen over the course of the night, with increases in apnea density and apnea-related desaturation.”1
“The etiology of childhood OSAS (obstructive sleep apnea syndrome) is quite different from the adult condition. In adults, OSAS is usually associated with obesity. Obese children are also at risk for OSAS, and the degree of OSAS is proportional to the degree of obesity. However, most children with OSAS are not obese. In fact, they may have failure to thrive. Instead, the vast majority of cases of OSAS in children are associated with adenotonsillar hypertrophy. The peak prevalence of childhood OSAS occurs at 2–8 yr, which is the age when the tonsils and adenoid are the largest in relation to the underlying airway size; endoscopy has shown that the site of collapse is most often at the level of the adenoid; and most children with OSAS improve following tonsillectomy and adenoidectomy (T&A). OSAS also occurs in children with upper airway narrowing due to craniofacial anomalies, or those with neuromuscular abnormalities such as hypotonia (e.g., muscular dystrophy) or muscular incoordination (e.g., cerebral palsy).”2
“Habitual snoring has been associated with cognitive and behavior problems in school-aged children, even when formal polysomnography results are ambiguous or negative. SDB (sleep-disordered breathing) treatment studies have reported encouraging short-term results in school-aged children, but there have been no published randomized clinical trials, and the few natural history studies have yielded mixed results on whether the resolution of snoring yields improved cognitive skills and/or behavior. Little is known about SDB (sleep-disordered breathing) in very young children, even though SDB (sleep-disordered breathing) symptoms spike at ∼2 to 3 years of age, and snoring-related arousals from sleep correlate with early mental development. Without intervention, many very young children continue to snore for years. The impact of persistent snoring on preschool-aged children is unknown; in older children, persistent snoring increases the chances for new or worsening behavior problems over time. Care decisions for preschool-aged children who snore are based on guidelines developed largely for older children and involve weighing the rare but real risks of interventions (eg, adenotonsillectomy) against suspected but unknown risks associated with persistent SDB (sleep-disordered breathing).”3
Snoring is the most common symptom. Parents are not always aware that their child snores and sometimes the snoring is interrupted by apnea. Usually these alterations happen during the REM phase of sleep and can go unnoticed. Some other symptoms are difficulty breathing, intercostal retraction and profuse sweating during sleep.
Some diurnal symptoms are excessive daytime sleepiness, alterations in behavior like extreme shyness, social isolation, hyperactivity, aggression, difficulty in staying focused, etc. In more severe cases, the child may have an important tendency to fatigue quickly, dyspnea on exertion, and even heart failure.
Respiratory disturbances during sleep can also influence the development of certain structures. For instance, there may be problems of dental malocclusion due to negative changes in the development of the lower jaw because of the continuous increase in respiratory effort during sleep. This is important, because some orthodontic treatments, aimed at correcting malocclusion, actually worsen respiratory related sleep disorders, creating a vicious circle.
“The determinants of upper airway stability include anatomical structure, neuromuscular activation of airway dilators, ventilatory control, and the arousal threshold from sleep. During wakefulness, laryngeal and pharyngeal dilator muscles actively sustain airway patency and a stable breathing pattern is maintained. The infant may appear to have labored breathing and stridor, but frank obstructions and gas exchange abnormalities are typically absent unless there is comorbid neuromuscular weakness or marked upper airway narrowing. At sleep onset, there is a reduction in airway and respiratory muscle activity, as well as the emergence of an apneic threshold to CO2 that is approximately 1 mm Hg below eupneic levels. As sleep progresses, there is a gradual recruitment of upper airway dilator muscles and increased respiratory drive in response to hypercapnia and negative luminal pressure. Stable breathing is intermittently achieved provided that the increase in respiratory drive, hypercapnia, and negative luminal pressure remain below the infant’s arousal threshold. Sudden airway opening, as seen during an arousal, promotes a ventilatory overshoot that lowers CO2 below the apneic threshold, thus initiating obstructive cycling. The specific determinants affecting the clinical expression of OSA (obstructive sleep apnea) in infants are discussed in more detail below.”4
“Infants have a highly compliant rib cage resulting in paradoxical respirations, which may persist up to 3 years of age during REM sleep. Because the compliance of the infant lung is similar to that of an adult, the net result is a smaller relaxation lung volume. Breathing at such low lung volume results in increased work of breathing and a decreased pulmonary reserve of oxygen. Consequently, infants actively maintain an end-expiratory volume above the passively determined relaxation volume via expiratory laryngeal closure, post inspiratory diaphragmatic activity, and tachypnea. These mechanisms appear to be intact during non–rapid eye movement (NREM) sleep but are attenuated or absent during REM sleep, resulting in lower lung volumes and a propensity toward oxygen desaturation with normal respiratory pauses. These mechanisms may be impaired in the setting of vocal cord dysfunction or diaphragmatic paralysis, and may lead to respiratory distress in infants. By 6 to 12 months of age, the chest wall compliance has decreased, and large improvements in pulmonary reserve can be expected.”5
“Snoring is observed in most infants diagnosed with OSA (Obstructive Sleep Apnea). However, snoring is also prevalent in the general population, occurring in 11.8% of infants at least 2 days/week, and in 5.3% at least 3 days/week. Risk factors for snoring in infancy include maternal smoking and being overweight. Less than 10% of snoring infants have polysomnographic evidence of OSA (Obstructive Sleep Apnea). Infant OSA (Obstructive Sleep Apnea) is more frequently observed with prematurity, prenatal smoking, bronchopulmonary dysplasia, males, obesity, and in younger babies. Infants with chronic lung disease have an increased incidence of OSA (Obstructive Sleep Apnea) and unsuspected sleep-associated hypoxemia, which may also be associated with poor growth. Infants with Prader-Willi syndrome and who are receiving growth hormone have been observed to develop OSA (Obstructive Sleep Apnea) during upper respiratory infections. Many infants with ALTE (Apparent Life Threatening Event) presentations have documented OSA (Obstructive Sleep Apnea) or eventually develop OSA. In addition, infants with OSA (Obstructive Sleep Apnea) more often have a positive family history of OSA and craniofacial risk factors for OSA. The obstructive sleep-disordered breathing indices of infants with OSA (Obstructive Sleep Apnea) appear to lessen over the first 6–12 months of life.”6
There are a number of situations that predispose children to respiratory related sleep disorders that should alert parents and pediatricians. Some of these factors are:
- Obesity: it’s an important risk factor, although there are many non-obese children with respiratory disorders in sleep.
- Nasal, oropharyngeal or laryngeal abnormalities.
- Genetic malformations such as down syndrome, Arnold Chiari syndrome and myelomeningocele.
- Neurological disorders like cerebral palsy.
If the pediatrician or the child’s parents suspect the presence of obstructive sleep apnea syndrome (OSAS), they should refer them to a sleep specialist to confirm the diagnosis and assess the severity of the disorder.
Video recording prolonged sleep (more than four hours) can be very useful, both in the child’s home and in the sleep clinic.
“A thorough physical examination of a child suspected of having OSA (obstructive sleep apnea) must include evaluation of the child’s general appearance, with careful attention to craniofacial characteristics such as midface hypoplasia, micrognathia, and occlusal relationships. Evaluation for nasal obstruction depends on the child’s age. Septal deviation, choanal atresia, naso-lacrimal cysts, and nasal aperture stenosis must be considered in infants. In older children, nasal polyps and turbinate hypertrophy must be ruled out.”8
“The role of polysomnography in the diagnosis of childhood sleep-disordered breathing remains controversial. Although polysomnography is the current gold standard, authorities cite the lack of reliable sleep laboratories for children, excess cost, and lack of consensus on interpretation of polysomnograms as reasons it is not required for diagnosis.”9
In children with hypertrophy of the adenoids or tonsils and OSAS, the treatment of choice is surgical intervention to remove them. However, sometimes the problem is not completely resolved and new interventions are necessary. In mild cases, or when nasal obstruction is the most important factor, improvements can be achieved by eliminating nasal congestion by using intranasal corticosteroids.
“The overwhelming majority of children with OSAS (obstructive sleep apnea syndrome) will have both symptomatic and polysomnographic resolution following T&A (tonsillectomy and adenoidectomy). OSAS results from the relative size and structure of the upper airway components, rather than the absolute size of the adenotonsillar tissue. Thus, even children with associated medical conditions, such as Down syndrome or obesity, tend to improve following T&A (tonsillectomy and adenoidectomy), although additional treatment may be needed. Children with OSAS are at risk for respiratory compromise postoperatively, due to upper airway edema, increased secretions, respiratory depression secondary to analgesic and anesthetic agents, and postobstructive pulmonary edema. Postoperative respiratory compromise has been reported to occur in 16–27% of children with OSAS. Particularly high-risk children include those younger than 3 yr of age, those with severe OSAS, and those with additional medical conditions; these patients should not undergo outpatient surgery. Postoperative polysomnograms 6–8 wk following surgery are recommended for patients with additional risk factors for OSAS, or those with a high apnea index, to ensure that additional treatment is not required.”10
You can also use a CPAP or BiPAP machine. A CPAP (Continuous Positive Airway Pressure) machine maintains constant positive pressure, while a BiPAP (Bi-level Positive Airway Pressure does not offer continuous airway pressure. Rather, pressure from a BiPAP machine oscillates with the respiratory cycle, so that it is higher with inspiration and lower during expiration. Although the adjustment period is more delicate than in adults, a CPAP machine is usually well tolerated and effective in children.
(1) Sleep Architecture and Respiratory Disturbances in Children with Obstructive Sleep Apnea. Goh, D.Y., Galster, P. & Marcus, C.L. American Journal of Respiratory and Critical Care Medicine. 1999. https://www.atsjournals.org/doi/full/10.1164/ajrccm.162.2.9908058
(2, 10) Sleep-disordered Breathing in Children. Marcus, C.L.American Journal of Respiratory and Critical Care Medicine. 2000. https://www.atsjournals.org/doi/full/10.1164/ajrccm.164.1.2008171
(3) Persistent Snoring in Preschool Children: Predictors and Behavioral and Developmental Correlates. Beebe, D,W., Rausch, J., Byars, K.C., Lanphear, B. & Yolton, K. Pediatrics. 2015. https://pediatrics.aappublications.org/content/130/3/382
(4, 5, 6) Obstructive Sleep Apnea in Infants. Katz, E.S., Mitchell, R.B. & D’Ambrosio, C.M. American Journal of Respiratory and Critical Care Medicine. 2012. https://www.atsjournals.org/doi/full/10.1164/rccm.201108-1455CI
(7, 8, 9) Obstructive Sleep Apnea in Children. Chan J., Edman, J.C. & Koltai, T.J. American Family Physician. 2004. https://www.researchgate.net/profile/Simone_Fagondes/publication/47508428_Obstructive_sleep_apnea_in_children/links/53efc86b0cf26b9b7dcdf32a/Obstructive-sleep-apnea-in-children.pdf