The incidence of sleep apnea in the pediatric patient population is approximately 1% to 3%. The most common level of obstruction of the airway during rest is at the base of the tongue and soft palate.³ OSA in children is most commonly associated with enlarged tonsils and adenoids. The degree of hypertrophy does not correspond clinically with the severity of OSA. However, OSA is a multifactorial disorder and is also associated with craniofacial anomalies as well as syndromes that cause decreased pharyngeal tone such as Down Syndrome.⁴ Shwengel et al,⁴ in a review, describe the pediatric OSA patient population as having a peak at 2 to 6 years of age, no gender predominance, and a weak association with obesity in decades past. However, with childhood obesity on the rise, the association of pediatric OSA with obesity has grown. There are numerous physiologic consequences of OSA in children (Table 51-1). Surgical excision of the enlarged tonsils and adenoids is generally definitive therapy in this population. However, obese children can still be at risk for OSA even after adenotonsillectomy.⁴

Clinicians with a responsibility for airway management are most likely to encounter a child with OSA when he/she presents for adenotonsillectomy. However, one may be required to care for a child with undiagnosed OSA in other settings as well, including other operative procedures. Hence, for elective pediatric procedures requiring sedation or airway management, a thorough airway examination and questioning about nighttime snoring are warranted. Snoring is a sensitive marker for OSA in children. Pediatric patients have very little oxygen reserve at baseline and patients with OSA even less so. Preoxygenation is one of the key strategies for a safe induction of anesthesia (Table 51-2). In pediatric patients with adenotonsillar hypertrophy and therefore suspected OSA, it has been shown that lateral positioning in combination with chin lift and jaw thrust provide improved airway patency for anesthetized children.⁵

OSA is far more common in adults than in children (Figs. 51-1, 51-2, 51-3, 51-4, 51-5, 51-6, 51-7, 51-8, 51-9, 51-10 and 51-11). This disorder has an incidence in the adult population of approximately 1 in 4 men and 1 in 10 women.⁶ Only a small percentage of these patients carry an official polysomnographic diagnosis of OSA. Most of the adults with OSA are undiagnosed. Therefore, the undiagnosed OSA patient will be the one most frequently encountered preoperatively. In the perioperative setting, these patients will present for all types of surgery, not solely airway surgery. In the elective situation, a high index of suspicion for OSA will serve the clinician well, as well as the judicious use of OSA-specific questionnaires. OSA is strongly associated with obesity, and the more obese the patient the more likely the incidence of OSA. Obesity results in fatty deposits in the tongue and upper airway,
which reduce lumen diameter and increase the likelihood of obstruction of the upper airway.⁶ There are anatomical differences in the pharyngeal airway between OSA patients and controls. OSA patients have increased total fat volume surrounding the pharyngeal airway and greater airway collapsibility.⁷ Additionally, nonobese OSA patients may have a shorter mandible, inferior hyoid, and retrognathic maxilla.⁸ CT and MRI studies have shown OSA patients have a smaller airway lumen than controls. Neck circumference, male gender, and craniofacial anomalies also predispose the patient to OSA (Table 51-3). Snoring is a very sensitive but nonspecific indicator of OSA.