Do Obese Children Require Inpatient Monitoring After Adenotonsillectomy?

Journal of Clinical Sleep Medicine, Vol. 13, No. 6, 2017 Obesity is one of the major risk factors for obstructive sleep apnea (OSA). Adenotonsillectomy (AT) is considered the first line of treatment in children with OSA, even among obese children.1 AT is generally a safe procedure, but it carries increased risk in certain populations. The postoperative complications from AT can be classified into two categories: nonrespiratory (hemorrhage) and respiratory complications (worsening of apnea, hypoxemia, and pulmonary edema). The mortality and major morbidity of AT are primarily related to respiratory complications.2 Unforeseen serious respiratory complications, including deaths, have been reported in children.3,4 The guideline from the American Academy of Pediatrics indicates increased risk for postoperative respiratory complications following AT in children younger than 3 years and children with severe OSA, obesity, craniofacial anomalies, and neuromuscular disorders.1 There are several reports showing increased respiratory complications during perioperative and postoperative periods following AT in obese children, although these reports are retrospective and observational studies.5-8 Two prospective studies evaluating polysomnographic findings immediately after AT yielded conflicting results.9,10 Both studies failed to specifically assess obese children. In this issue of the Journal of Clinical Sleep Medicine, De et al. reported significant residual OSA on the first surgical night following AT in obese children.11 This is the first study to evaluate this issue in obese children. In this prospective study of 20 obese subjects, 85% of patients had abnormal polysomnographic studies on the night following surgery similar to baseline (obstructive apnea-hypopnea index: 27.1 ± 22.9 events/h [pre] versus 27.0 ± 34.3 events/h [post]). In addition, the degree of oxygen desaturation associated with respiratory events was significant on the postoperative night (80.1 ± 7.9% [pre] versus 82.0 ± 8.7% [post]). The authors also found changes in sleep architecture including increased stage N2 sleep and decreased rapid eye movement sleep. It is unclear from this study whether obesity itself or severity of OSA was associated with significant residual OSA the night following AT. Most subjects (75%) in this study had severe OSA, with only a few subjects with mild to moderate OSA. Significant residual postoperative OSA could be related to severity of OSA at baseline. The lack of control (nonobese) COMMENTARY