Abstract
Treatment approaches to pediatric obstructive sleep apnea (OSA) have remarkably evolved over the last two decades. From an a priori assumption that surgical removal of enlarged upper airway lymphadenoid tissues (T&A) was curative in the vast majority of patients as the recommended first-line treatment for pediatric OSA, residual respiratory abnormalities are frequent. Children likely to manifest persistent OSA after T&A include those with severe OSA, obese or older children, those with concurrent asthma or allergic rhinitis, children with predisposing oropharyngeal or maxillomandibular factors, and patients with underlying medical conditions. Furthermore, selection anti-inflammatory therapy or orthodontic interventions may be preferable in milder cases. The treatment options for residual OSA after T&A encompass a large spectrum of approaches, which may be complementary, and clearly require multidisciplinary cooperation. Among these, continuous positive airway pressure (CPAP), combined anti-inflammatory agents, rapid maxillary expansion, and myofunctional therapy are all part of the armamentarium, albeit with currently low-grade evidence supporting their efficacy. In this context, there is urgent need for prospective evidence that will readily identify the correct candidate for a specific intervention, and thus enable some degree of scientifically based precision in the current one approach fits all model of pediatric OSA medical care.
Highlights
There is little doubt that hypertrophy of upper airway lymphadenoid tissues constitutes the most common factor underlying the presence of obstructive sleep apnea (OSA) in children, a condition that was formally identified as a singular disease only in 1976 by Guilleminault and colleagues [1]
Since 2006 when we initially described the relatively high prevalence of residual OSA after T&A [11,12], confirmation and realization that, the severity of OSA will routinely improve after surgery, it can persist in a significant proportion of patients has definitely settled in [13,14,15,16]
We subsequently identified the presence of increased expression and activity of cysteinyl leukotriene receptors within lymphadenoid tissues of OSA children, and these could even be detected in exhaled condensate, serum, circulating white blood cells, or in urine [61,62,63,64,65,66,67,68,69,70]
Summary
Outside the risk factors delineated above, there are few, if any, studies that have focused on the pathophysiology of residual OSA after T&A. Improved understanding of such elements and their corresponding contributions to any specific child manifesting PSG-based residual OSA after surgery is of paramount importance to formulate a intervention strategy that is efficacious but is precisely aligned to counteract the effects of such risk factors—in other words, personalized medicine. There are three major categories that are implicated in the emergence of residual OSA: (i) anatomical (mal)development; (ii) upper airway tissue deposition or infiltration; and (iii) increased airway collapsibility. Obesity is one of the obvious risk factors for persistent OSA, and the current worldwide obesity epidemic, not just in developed and in developing countries, will likely further increase the proportion of children after T&A who manifest residual disease. Volume increases in the nasopharynx and oropharynx were apparent after T&A, substantial amounts of lymphadenoid tissues were still impinging on the airways along with increases in the volume of the soft palate, tongue and head and neck subcutaneous fat
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