Treatment of Residual OSA in Children

Adenotonsillectomy (i.e., total removal of the adenoids and tonsils) is often a first-line treatment for obstructive sleep apnea (OSA) in children two years or older with enlarged adenoids and tonsils and cures OSA in most of these children. However, research now indicates that an estimated 13%-29% of children have residual OSA after adenotonsillectomy, but among children who are overweight/obese, up to 75% have residual OSA after adenotonsillectomy.^1-4 

Residual OSA can be problematic because continued OSA-related arousals can contribute to poor school performance, difficulty concentrating, irritability and behavioral problems and other symptoms. Therefore, treatments that could further reduce or eliminate residual OSA are needed. Various treatments are increasingly being researched to relieve residual OSA, such as positive airway pressure (PAP), myofunctional therapy, orthodontic devices, weight loss and drug therapy, and some findings have been promising.

In OSA, upper airway muscles relax excessively during sleep, which allows structures supported by the muscles to collapse into and block (i.e., obstruct) the upper airway, which restricts airflow. The blood oxygen level consequently decreases. To compensate for the reduced oxygenation, a person makes increasingly strong efforts to breathe. Despite this effort, the airway obstruction remains. When the oxygen level falls to a certain point, the respiratory center in the brain triggers a brief arousal, during which the upper airway muscle tone is restored, opening the airway. At this point, the person is able to take some deep, quick breaths to restore the blood oxygen level.

The most common treatment for OSA in children is PAP therapy. In this treatment, slightly pressurized air is blown through a mask that fits over the nose or nose and mouth. The pressure of the air pushes against upper airway tissues to prevent their collapse into the airway, thereby preventing OSA and sleep disruption.

For children with OSA and enlarged adenoids and tonsils, removing these tissues totally or partially is often curative. However, adenoidectomy alone (i.e., without tonsillectomy) is not recommended for treating OSA in children because residual OSA is more likely after the procedure and many children who undergo adenoidectomy ultimately have to undergo a total tonsillectomy.⁵

In adenotonsillectomy, the adenoids and the tonsils are fully removed. In denotonsillotomy, most of the adenoids and tonsils are removed. Total adenoidectomy has the risks of post-surgery bleeding, pain, eustachian tube injury and velopharyngeal incompetence (i.e., abnormal movement of the lateral and posterior pharyngeal walls and soft palate caused by injury to the cranial nerves that innervate the adenoids and tonsils), whereas these complications are less frequent with adenotonsillotomy. Various studies have indicated that adenotonsillotomy is effective and safe for children with obstructive sleep apnea syndrome (OSAS).^6,7 However, a drawback of adenotonsillotomy, particularly in younger children,¹ is regrowth of the adenoids and tonsils and the consequent recurrence of OSA. When adenoid or tonsil regrowth occurs, a total tonsillectomy may be needed to resolve OSA.^1,7

The success rate of adenotonsillectomy in obese children with OSA is less than that of nonobese children with OSA (24%-46% versus 80%).^3,8 However, the characteristics that increase the risk of residual OSA after adenotonsillectomy are unknown and have been a recent research focus.

Some research indicates that the maxilla of children with OSA is often narrower than normal.^4,9 In addition, a small mandible (i.e., jawbone) similarly has been noted in children and adults with OSA.⁴ However, whether an abnormal facial structure is a predisposing factor for the residual OSA after adenotonsillectomy is unclear. To investigate whether a link exists, Maeda and colleagues⁴ examined the oropharyngeal structure of Japanese children diagnosed with OSA. All children underwent a polysomnographic study before and after adenotonsillectomy. The average apnea-hypopnea index (AHI) dropped by 75% after adenotonsillectomy, but 85% of the children had residual OSA (i.e., AHI >1 event/hour). Maeda noted that children with residual OSA had smaller than normal mandibles and suggested that this factor may need to be taken into consideration before adenotonsillectomy or adenotonsillotomy.

If a child continues to have residual OSA after adenotonsillectomy, adenotonsillotomy or PAP treatment, the child may benefit from other treatments such as myofunctional therapy, orthodontic devices, weight loss and drug therapy.

Myofunctional Therapy

Myofunctional therapy involves the use of various oropharyngeal exercises with the goal of improving lip closure and tone, promoting nasal breathing, and improving the tone and position of the tongue and orofacial muscles. Examples of exercises are as follows:

1. With lips closed, press the right index finger on the right nostril and inhale gently through the left nostril. At the end of inhalation, remove the right index finger from the right nostril, press the left index finger on the left nostril, and exhale through the right nostril. Alternate these actions five times. This exercise encourages nasal breathing, which can help stabilize the airway during sleep.
2. Stick out the tongue as far possible. While looking at the ceiling, try to touch the chin with the tongue, hold this position for 10-15 seconds and then relax. Repeat five times. This exercise increases tongue tone and strength.
3. Press the tip of the tongue on the top of the front teeth (i.e., incisors). Slowly slide the tongue tip backward across the hard palate, and then relax. This exercise strengthens the tongue and throat muscles.

Oropharyngeal exercises have few complications and are easily learned. However, performing the exercises consistently may be more problematic for children.

Rapid Maxillary Expansion

For some children, an orthodontic device such as the rapid maxillary expander (also called rapid palatal expander) may help relieve OSA events. A rapid maxillary expander fits into the roof of a patient's mouth. Two arms of the expander are glued to the inside of the upper molars. The center of the expander contains a screw that is turned once daily for a few weeks. Each turn gradually pushes the arms away from each other, thereby widening the maxilla. A wider maxilla creates more room in the upper airway, which may improve airflow during sleep and reduce OSA events. Pirelli and colleagues¹⁰ demonstrated that rapid maxillary expansion in children at a normal weight without enlarged adenoids reduced the AHI to normal (from approximately 12 events/hour to <1 event/hour) at four months after beginning the treatment. They suggested that rapid maxillary expansion may be useful for treating abnormal breathing during sleep. However, literature reviews^11,12 note that, although the use of orthodontic devices to expand the upper airway has been shown to reduce OSA in children, insufficient studies exist to definitively support using oral appliances to treat OSA in children.

Weight Loss

Weight loss can improve OSA, even before adenotonsillectomy, and may be a treatment option for children with obesity with residual OSA after adenotonsillectomy.^13,14 In a recent study, Andersen and colleagues¹⁴ studied the effects of weight loss management on the resolution of sleep-related respiratory events in children who are obese with OSA. They found that, with weight loss, breathing was normalized by the end of the study (12 months) in 44% of the children. They further found that children with enlarged tonsils achieved the same effect with weight loss as did children without enlarged tonsils. Andersen proposes that obesity treatment should be considered among the first-line treatments for OSA in children and adolescents who are overweight/obese.

Drug Therapy

People with OSA tend to have a low-grade chronic inflammatory state,¹⁵ which may contribute to increased adenotonsillar size in children with OSA. Therefore, some research has focused on treating OSA by using drug therapy to reduce inflammation.

Nasal Corticosteroid Therapy

In people with OSA, adenoids and tonsils have an increased number of glucocorticoid receptors.^16,17 Glucocorticoids are corticosteroids that reduce the number of leukocytes and macrophages and indirectly block the production of leukotrienes, thereby reducing inflammation. Glucocorticoid treatment has had encouraging results. Brouillette and colleagues¹⁸ treated children with OSA with a six-week course of intranasal fluticasone (a glucocorticoid receptor agonist) or a placebo. Fluticasone significantly reduced the number of respiratory events by approximately 46%, whereas the number of respiratory events increased by approximately 16% in the placebo group; the AHI decreased in 92% of the treated group but in only 50% of the placebo group; and arousals decreased to a greater extent in the treated group. An interesting finding was that changes in tonsillar size and adenoidal size from the baseline size were not significantly different between the two groups. Brouillette suggests that corticosteroids may help ameliorate OSA in children.

In another study, Kheirandish-Gozal et al.¹⁷ demonstrated that corticosteroid drugs reduced cellular proliferation and proinflammatory cytokine production in tonsil and adenoid tissues (retrieved during adenotonsillectomy) that were placed in a medium that contained fluticasone, budesonide (a glucocorticoid receptor agonist) or dexamethasone (a glucocorticoid). All children had been diagnosed with OSA before the surgery. Corticosteroid drugs increased cellular death and substantially reduced the concentrations of inflammatory substances (e.g., tumor necrosis factoralpha). Kheirandish-Gozal suggests that anti-inflammatory treatment with corticosteroid drugs could potentially be used to reduce adenotonsillar size in children with OSA.^16,17

Leukotriene Receptor Antagonist Drug Therapy

Leukotrienes are produced by white blood cells and are released in response to an allergen. Leukotriene receptors are increased in the tonsillar tissues of children with OSA.¹⁹ Blocking the actions of leukotrienes reduces the inflammatory response.

Monteklast, a leukotriene receptor antagonist, has successfully reduced OSA events in children. Goldbart and colleagues²⁰ treated children with sleep-disordered breathing with monteklast daily for 16 weeks. Before and after treatment, the size of the adenoids were measured. Adenoid size and respiratory-related sleep disturbances were significantly reduced after treatment. These effects did not occur in a group of children with sleepdisordered breathing who did not receive this treatment.

For now, scientists remain uncertain regarding which factors could be used to predict residual OSA in children. Some risk factors appear to be overweight/obesity and certain features of the craniofacial structure (e.g., small oropharynx, narrow maxilla, small mandible),^8,21 but more research is needed to clarify this. More research is also needed to determine which treatment approach (e.g., myofunctional exercises, orthodontic devices, drug therapy) would be best for a child with residual OSA. With greater clarity on these issues, physicians could tailor OSA treatment in children to reduce the likelihood of residual OSA.

References

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