Physical exam findings
Adenotonsillar hypertrophy, obesity, enlarged tongue (broad tongue base, scalloping), increased neck circumference, nasal septal deviation, enlarged nasal turbinates, craniofacial abnormalities, swollen mucous membranes, deviated nasal septum, adenoid facies (elongated midface, mouth-breathing, and infraorbital darkening), high-arched palate, dental overjet, posterior buccal cross-bite, crowded oropharynx, midface hypoplasia, micrognathia, retrognathia, African American race, male sex
Comorbid medical disease
Neuromuscular disease, genetic syndromes, exposure to tobacco, environmental allergies, asthma, GERD, hypertension, enuresis, bruxism
Nighttime features
Snoring, witnessed apneas, gasping/choking arousals, increased work of breathing, mouth-breathing, restless sleep
Daytime features
Nasal congestion, excessive daytime sleepiness, morning headaches, waking with a dry mouth, attentional difficulties, hyperactivity, aggressive behavior, poor school performance
The etiology of excessive daytime sleepiness is often multifactorial, and it is important to address all potential factors that could contribute to sleep fragmentation or reduced sleep quality. For this particular patient, the factors that are contributing to his daytime symptoms include obstructive sleep apnea, a circadian rhythm delay, and poor behavioral sleep practices (often referred to as “sleep hygiene”). Attention to a circadian phase delay should not be overlooked, as sleep apnea and circadian delay tendencies are often comorbid in this patient population, and symptoms of daytime fatigue and sleepiness will not be adequately treated if all aspects of the patient’s sleep disorder are not addressed. Please see the chapter on circadian disorders in adolescents for a full discussion on identification and management of shifts in the internal body clock.
Prior to performing an overnight sleep study, it is prudent to institute sleep hygiene recommendations to increase the likelihood that an adequate duration of sleep will be able to be obtained on the night of the study. Both the American Academy of Pediatrics (AAP) and the American Academy of Sleep Medicine (AASM) recommend routine use of the PSG for diagnosis of sleep apnea, being that the sensitivity and specificity of the history and physical examination are poor, and tonsillar size is not necessarily predictive of the presence of OSA [1, 2]. For example, the sensitivity and specificity of witnessed apneic events as a predictor of OSA ranges anywhere from 47–88 % and 17–90 %, respectively. The sensitivity and specificity of tonsillar hypertrophy (grade 3+ to 4+) as a predictor of OSA ranges anywhere from 12–93 % and 35–89 %, respectively [3]. There are no screening tests or combined metrics that have yet been validated for reliable diagnosis of OSA, and polysomnography remains the gold standard. A potential source of confusion for clinicians is that the surgical guidelines issued by the American Academy of Otolaryngology-Head and Neck Surgery (AAO-HNSF) allow for tonsillectomy to be performed without a preoperative PSG unless the need for surgery is uncertain, reported symptoms are out of proportion to tonsillar size, or certain other clinical criteria are present; including obesity , Down syndrome, craniofacial abnormalities, neuromuscular disorders, sickle cell disease, or mucopolysaccharidoses [4].
At our institution, preoperative polysomnography prior to adenotonsillectomy is usually considered in adolescents for several reasons. (1) Determining the severity of OSA is useful in guiding perioperative and postoperative management (day surgery vs inpatient vs ICU admission), risk stratifying for perioperative complications, estimating the likelihood of residual disease, and guiding the decision whether to obtain follow-up polysomnography. Preoperative PSG can also allow for avoidance of unnecessary or ineffective surgery in patients with primarily non-obstructive events.
In less-severe cases of sleep apnea in adolescents, it is not clear whether to apply pediatric criteria or “adult” criteria for a diagnosis of OSA. According to the ICSD-3, pediatric scoring criteria (obstructive AHI > 1 event per hour or a pattern of obstructive hypoventilation) may be used until age 18, although between ages 13 and 18 there is an option to use adult criteria (obstructive AHI > 5 events per hour) [5]. This decision depends on the clinical context of the individual patient.
Patients with mild or moderate degrees of sleep apnea (less than 10 events per hour) may be at acceptable risk to undergo day surgery. Patients with severe OSA, defined as AHI > 10 events per hour, or severe gas exchange abnormalities (oxygen saturation nadir <80 % or significant hypoventilation), are at higher risk for postoperative complications and should be monitored at least overnight in an inpatient setting. The most common complications associated with adenotonsillectomy are pain and poor oral intake, with more severe complications including hemorrhage, infection, and respiratory decompensation. Risk factors for pulmonary complications following adenotonsillectomy in the adolescent age group include severe OSA (AHI > 10 events per hour, SpO2 nadir <80 %, or significant hypoventilation), morbid obesity , neuromuscular disease, pulmonary hypertension, Down syndrome, craniofacial abnormalities, asthma, sickle cell disease, congenital heart disease, or a history of respiratory compromise. Respiratory decompensation is associated with higher baseline AHI, higher BMI z-score, and lower O2 saturation nadir [6].
Following adenotonsillectomy, all patients should be reassessed clinically for residual symptoms. A follow-up PSG is indicated when there was moderate-to-severe disease preoperatively, or factors associated with an increased risk of residual OSA, which are outlined in Table 4.2. The ideal timing of a follow-up study is 2–3 months, to allow an appropriate postoperative recovery period, but also protect the patient from prolonged periods of untreated apnea in the event of residual disease.
Table 4.2
Factors associated with high risk of residual OSA in adolescents
High preoperative AHI (AHI > 10/h) |
Obesity (BMI > 30) |
Underbite, overbite, crossbite |
Severe allergic rhinitis (hypertrophic turbinates, regrown adenoids) |
Neuromuscular weakness |
Glossoptosis |
Craniofacial syndromes |
Lingual tonsillar hypertrophy |
Occult laryngomalacia |
Age-related increased upper airway collapsibility |
Adenoid facies |
Micrognathia |
Age of adenotonsillectomy > 7 years |
Pitfalls
Snoring is often not the presenting complaint in adolescents with concern for obstructive sleep apnea, and evaluation should include assessment for subtle signs of sleep disordered breathing.
Failure to recognize and address the comorbid circadian factors, poor sleep hygiene, and sleep restriction is not unusual in this age group. Often, both OSA and a delayed circadian sleep phase can coexist and contribute to excessive daytime sleepiness.
Learning Points
There are no physical exam features or screening metrics that can reliably rule-in or rule-out a diagnosis of obstructive sleep apnea and clinical assessment does not predict the severity of the underlying OSA. In-lab polysomnography remains the gold standard.
Even with a high suspicion of obstructive sleep apnea, preoperative PSG should still be performed prior to adenotonsillectomy , as knowledge of disease severity is important for risk stratification and perioperative management.
If there is evidence for severe sleep apnea (based on a high index of events per hour, or substantial gas exchange abnormalities), then inpatient postoperative monitoring is indicated due to the high rates of pulmonary complications.
Clinical Case 2
Peter is an obese 16-year-old boy (BMI 31 kg/m 2 ), presenting with reports of loud snoring, witnessed apneas, and excessive daytime sleepiness. Physical examination revealed a Mallampati class II airway, with 2+ tonsillar hypertrophy. The nasal septum was midline, without significant turbinate hypertrophy. He underwent diagnostic polysomnography and was found to have severe obstructive sleep apnea with AHI of 40 events per hour, and O 2 saturation nadir 87 %. He underwent adenotonsillectomy, tolerated the procedure well, had an uneventful postoperative recovery, and was discharged to home the following day.
In 2-month follow-up, his mother noted that he continued to snore, and his symptoms of daytime sleepiness had not improved. His weight had increased from prior, to BMI 32.5 kg/m 2 . On follow-up PSG, he had a high residual AHI of 22 events per hour. CPAP was titrated from 5–12 cm H 2 O, with 8 cm H 2 O appearing optimal to relieve obstruction. He was started on therapy with CPAP 8 cm H 2 O, recommended to sleep in non-supine positioning, and encouraged to focus on weight loss. He was also referred for otolaryngology evaluation, and there were no clear sites of anatomic obstruction observed on flexible nasolaryngoscopy in the clinic.
At his follow-up visit one month later, he had good compliance with CPAP, with use on more than 80 % of nights, and reported improvement in his daytime energy levels. A plan was made to continue CPAP therapy, in conjunction with efforts at weight loss.
Discussion
Rates of residual obstructive sleep apnea following adenotonsillectomy vary depending on the AHI threshold used, but have been reported as high as 73 % when including obese patients and adolescents and using the more stringent cutoff of AHI ≥ 1 per hour, underscoring the importance of follow-up testing. Factors associated with residual OSA following adenotonsillectomy were discussed above.
OSA in adolescents is thought to result from a combination of enlargement in lymphoid tissue, obesity , and reduction in neuromuscular tone and neuromotor reflexes. The P crit, or pharyngeal closing pressure (a measure of upper airway collapsibility), becomes less negative in adolescents as upper airway motor neuron reflexes decline, and differences in neuromuscular responsiveness between individuals might explain why some obese adolescents develop sleep apnea and others do not [7]. An important question in the adolescent population is whether the pathophysiology of obstructive sleep apnea is more similar to children, with hypertrophic lymphoid tissue being the primary etiologic factor (in the absence of craniofacial structural abnormalities), or whether the abnormality is more similar to adults, with obesity-related anatomic risk factors (enlargement of the parapharyngeal fat pads, tongue, lateral pharyngeal walls, and total upper airway soft tissue volume). Although tonsils typically regress in children beginning around age 8, tonsillar tissue has been shown to continue to increase in size in the presence of snoring. An MRI-based study comparing anatomic features of obese adolescents (age 12–16 years) with sleep apnea to both obese controls without sleep apnea and to lean controls, demonstrated that lymphoid hypertrophy (rather than soft tissue enlargement) is the predominant anatomic risk factor [8]. There is a tendency in clinical practice to underestimate the contribution of the tonsils to obstructive sleep apnea in the adolescent age group and move directly to CPAP without first performing adenotonsillectomy . It is important to recognize that tonsillar hypertrophy might still be contributing significantly despite the presence of obesity, and that adenotonsillectomy remains first-line treatment. It should be noted that adenotonsillectomy has been associated with short-term weight gain, likely due to changes in hormonal regulation [9–11].

Stay updated, free articles. Join our Telegram channel

Full access? Get Clinical Tree

