Abstract
Study objectives
Because dexmedetomidine (DEX)-induced sedation mimics non-rapid eye movement (NREM) sleep, its utility in sedating children with REM-predominant disease is unclear. We sought to determine the effectiveness of pediatric drug-induced sleep endoscopy (DISE) using DEX and ketamine for children with REM-predominant OSA, specifically whether or not at least one site of obstruction could be identified.
Methods
A retrospective case series of children without tonsillar hypertrophy undergoing DISE at a tertiary pediatric hospital from 10/2013 through 9/2015 who underwent subsequent surgery to address OSA with polysomnography (PSG) before and after.
Results
We included 56 children, mean age 5.6±5.4 years, age range 0.1–17.4 years, mean BMI 20.3±7.4 kg/m2 (76±29 percentile). At least one site of obstruction was identified in all patients, regardless of REM- or NREM-predominance. The mean obstructive apnea-hypopnea index (oAHI) improved (12.6 ± 10.7 to 9.0 ± 14.0 events/h) in children with REM-predominant (P = 0.013) and NREM-predominant disease (21.3 ± 18.9 to 10.3 ± 16.2 events/h) (P = 0.008). The proportion of children with a postoperative oAHI < 5 was 53% and 55% for REM- and NREMpredominant OSA, respectively. Unlike children with NREM-predominant disease, children with REM-predominant disease had significant improvement in the mean saturation nadir (P < 0.001), total sleep time (P = 0.006), and sleep efficiency (P = 0.015).
Conclusions
For children with OSA without tonsillar hypertrophy, DISE using DEX/ketamine was useful to predict at least one site of obstruction, even for those with REM-predominant OSA. DISE-directed outcomes resulted in significant improvements in mean oAHI, total sleep time, sleep efficiency, saturation nadir, and the proportion with oAHI < 5, after surgery for some children with REM-predominant disease.
Keywords: Obstructive sleep apnea, Persistent, Pediatric, Infant, OSA, Drug-induced sleep endoscopy, DISE, Outcomes, REM-predominant, Rapid eye movement sleep
Introduction
The pathophysiologic mechanisms that lead to obstructive sleep apnea (OSA) in children involve a complex interplay of anatomic and neuromuscular abnormalities. These abnormalities, as well as resultant neuromuscular compensation, must be taken into account when considering diagnostic and treatment options. Although airway narrowing can explain some cases of pediatric OSA, it does not explain all patterns of airway collapse encountered in affected children [1]. This is particularly relevant during rapid eye movement (REM) sleep, when airway collapse is attributed to paroxysmal decreases in pharyngeal dilator activity due to central REM sleep processes [1]. Given that upper airway obstruction is more common during REM sleep in children, this is a significant concern.
In order to determine the sites of collapse associated with upper airway obstruction during sleep, various diagnostic techniques such as drug-induced sleep endoscopy (DISE), have been developed. First described by Croft and Pringle [2], DISE has been demonstrated to be a safe and dependable tool for the identification of upper airway obstruction in children [3–5]. Surgical management addressing sites of obstruction identified during endoscopy has been shown to result in improvement in both subjective and objective measures of sleep [4, 6]. DISE is used most frequently for the evaluation of children with persistent OSA after adenotonsillectomy (AT) and less commonly to evaluate infants with OSA.
Dexmedetomidine (DEX) is a highly selective α−2 adrenoreceptor agonist that provides sedation in children with less concern for cardiorespiratory instability that is more likely to occur with the use of other anesthetic agents such as inhalational gases or propofol [7–10]. In light of this, DEX is often used for pediatric DISE [11] in combination with other anesthetics, such as ketamine. Although ketamine can produce negative sequelae, such as bronchial secretions and laryngospasm [12], its’ use does not disrupt cardiovascular stability, preserves spontaneous respiration, and maintains protective airway reflexes [13, 14]. Because electroencephalogram (EEG) output during DEX-induced sedation mimics non-rapid eye movement (NREM) sleep [15], it is unclear if DEX is useful for children with REM-predominant disease. The aim of our study was, therefore, to determine the effectiveness of pediatric DISE using DEX and ketamine (including identification of sites of obstruction) for children with REM-predominant OSA. Our primary outcome was whether at least one site of obstruction could be identified in REM-predominant patients undergoing DISE. Secondary outcomes for this study included changes in PSG parameters (oAHI, total sleep time (TST), sleep efficiency, and oxygen saturation nadir) and their comparison to outcomes for children with NREM-predominant disease.
Methods
Study participants
We performed a retrospective case series of children who underwent DISE-directed surgery from October 2013 through September 2015. We included children who: (1) were diagnosed with persistent OSA after previous AT or OSA without tonsillar hypertrophy, (2) had DISE videos available for review, and (3) had completed polysomnography (PSG) both before and after surgery. Children were excluded from this study if they were 18 years of age or older or had a preoperative obstructive apnea-hypopnea index (oAHI) of < 1 event/h or were using REM suppressant medications. We included infants with OSA who had not received AT as they were determined not to have tonsillar hypertrophy. Demographic data, physical exam findings, including body mass index (BMI), medical history and comorbidities, and PSG results, including overall oAHI, total sleep time (TST), sleep efficiency, and oxygen saturation nadir, were obtained from the electronic medical records of all study participants. This study was approved by the Institutional Review Board at Cincinnati Children’s Hospital Medical Center (CCHMC).
Polysomnography
All study participants underwent an initial diagnostic PSG before DISE within 6 months of the surgical intervention and again within 6 months after surgical intervention at CCHMC. Standard sleep study parameters were evaluated, including pulse oximetry, chest movement, nasal airflow, electrocardiogram, end-tidal carbon dioxide (ETCO2) levels, EEG, electromyogram, and electrooculogram. All variables were recorded with the Twin® digital acquisition system (Grass Technologies, Pleasanton, CA). All sleep studies were scored according to the pediatric scoring criteria of the American Academy of Sleep Medicine (AASM) [16].
After completion, studies were scored by a registered sleep technician and read by board-certified pediatric sleep physicians. Mild, moderate, and severe OSA were defined as an oAHI of 1 to < 5 events/h, ≥ 5 to < 10 events/h, and ≥ 10 events/h, respectively [17–19]. The oxygen (O2) saturation nadir was defined as the lowest oxygen saturation reading during an obstructive respiratory event. OSA was defined as REM-predominant when the ratio of the REM oAHI divided by the NREM oAHI was > 2 [20–22]. The following parameters were obtained from the Twin® digital acquisition system: the TST in minutes, sleep efficiency as percent of sleep during the total study time, the percent of time that ETCO2 measurements were higher than 50 mmHg, and arousal index (arousals/h sleep).
Drug-induced sleep endoscopy
All children underwent DISE as part of our standard evaluation to determine the site(s) of upper airway obstruction. DISE was performed in the operating room with cardiopulmonary anesthetic monitoring, with children in the supine position. Children received a specific combination of medication to simulate a sleep-like state. For children who could not tolerate placement of an intravenous catheter prior to anesthesia, anesthetic induction was carried out with inhaled sevoflurane, which was immediately discontinued once the catheter was secured. No further inhalational agents were used during the administration of DEX and ketamine, allowing appropriate time for wash-out of these anesthetics. DEX was infused, starting with a loading dose of 3 μg/kg over 10 min, followed by a 2 μg/kg infusion. Ketamine was also given at a dose of 1 to 2 mg/kg at the start of the DEX loading dose. We did not use decongestants or topical anesthetics during the procedure in order to avoid altering the natural state of the upper airway. At the completion of the DEX loading dose, a soft nasal suction catheter was placed in the bilateral nasal cavities to clear secretions and confirm appropriate depth of sedation. The flexible fiberoptic endoscope was then introduced into one side of the nasal cavity. As the scope was passed through the upper airway, specific anatomic regions were assessed for size, obstruction, and the presence of anatomic abnormalities. The levels that were assessed included the internal nasal valve, nasal septum, inferior turbinates, nasopharynx (including adenoid tissue), palate orientation, velum, oropharynx, tongue base, lingual tonsils, epiglottis, supraglottis (including the false vocal cords, arytenoids and aryepiglottic folds), and the true vocal folds. Obstruction was recorded as none, partial, or complete (> 90%).
Surgical intervention
Based upon the levels of obstruction identified during DISE, we performed one or more surgical interventions, either concurrently or at the time of a subsequent surgical encounter. Surgical interventions performed in this cohort included lingual tonsillectomy, revision adenoidectomy, partial midline glossectomy, hyoid suspension, genioglossal advancement, lateral expansion pharyngoplasty, and inferior turbinate reduction.
Statistical analyses
The changes in PSG parameters before and after upper airway surgeries were analyzed, including oAHI, ETCO2, sleep efficiency, TST, and saturation nadir. The primary outcome was successful identification of site of obstruction on DISE. Analysis was carried out with Wilcoxon signed rank tests, paired t tests, and Mann-Whitney U tests. Quantitative results were presented as mean ± standard deviation. Differences were considered significant when the P value was < 0.05. Statistical analysis was carried out using Stata 12.0 (StataCorp LP, College Station, TX).
Results
Fifty-six children (32% female) without tonsillar hypertrophy were included in our study. Fourteen (25%) had prior AT and 45 (80%) had REM-predominant disease (Table 1). Overall, the mean age was 5.6 ± 5.4 years (range 0.1–17.4 years) and 19 (34%) were infants. The mean BMI was 20.3 ± 7.4 kg/m2 (76 ± 29 percentile), and 49% had public insurance. Seventy-seven percent of participants identified as white, and 14% identified as black. The mean age for children with REM-predominant OSA was 4.9 ± 5.2 years compared to 8.6 ± 5.4 years for those with NREM-predominant disease (P =0.038). As shown in Table 1, there was no significant difference in gender (P = 0.71), race (P = 0.54), public insurance status (P = 0.11), or BMI (P = 0.28) between the two groups. The time between PSG was 9.5 ± 9.2 months.
Table 1.
Demographic data for subjects who underwent DISE for infant or persistent OSAwith and without rapid eye movement (REM)-predominance during sleep on polysomnography
| Total (N = 56) | NREM-predominant (N = 11) | REM-predominant (N = 45) | P value | |
|---|---|---|---|---|
| Gender, female, n (%) | 38 (67.9) | 8 (72.7) | 30 (66.7) | 0.71 |
| Age, mean ± SD, (range), years | 5.6 ± 5.4 (0.1–17.4) | 8.6 ± 5.4 (0.91–16.9) | 4.9 ± 5.2 (0.1–17.4) | 0.038 |
| Race, n (%) | 0.54 | |||
| White | 43 (76.8) | 8 (72.3) | 35 (77.8) | |
| Black | 8(14.3) | 1(9.1) | 7(15.6) | |
| Other/unknown | 5 (8.9) | 2 (18.2) | 3 (6.7) | |
| Comorbidities, n (%) | ||||
| Laryngomalacia | 24 (43.6) | 6 (54.6) | 18 (40.9) | 0.42 |
| Down syndrome | 23 (41.8) | 4 (36.4) | 19 (43.2) | 0.69 |
| Pierre robin | 7 (12.7) | 2 (18.2) | 5 (11.4) | 0.55 |
| Reactive airway disease/asthma | 11 (20.0) | 1 (9.1) | 10 (22.7) | 0.32 |
| BMI, mean ± SD, (range), kg/m2 | 20.3 ± 7.4 (12.1–43.4) | 22.5 ± 10.4 (13.5–43.4) | 19.8 ± 6.5 (12.10–40.6) | 0.28 |
| BMI percentile mean ± SD, (range) | 76.1 ± 28.7 (1.8–99.7) | 64.7 ± 36.3 (1.8–99.7) | 80.5 ± 24.7 (4.6–99.7) | 0.16 |
| oAHI > 5, n (%) | 43 (84.3) | 9 (81.8) | 34 (85.0) | 0.80 |
N number, SD standard deviation, oAHI obstructive apnea-hypopnea index, BMI body mass index, REM rapid eye movement, NREM non rapid eye movement
t test used to compare groups
Also, at baseline, a similar proportion of the children with REM-predominant disease had an oAHI > 5 events/h (85.0%) as compared to those with NREM-predominant disease (81.8%, P = 0.80) (Table 1). Additionally, there was no significant difference between these 2 groups in comorbidities, including laryngomalacia (P = 0.42), Down syndrome (P = 0.69), Pierre Robin sequence (P = 0.55), or reactive airway disease (P = 0.32). Overall, 17 (89.5%) infants had laryngomalacia, while 7 (18.9%) of the 37 older children had laryngomalacia. Only 3 (5.4%) children had no comorbidities.
At least one site of obstruction was identified in all children, regardless of REM- or NREM-predominant status (Fig. 1). Surgeries performed can be seen summarized in Fig. 2. As seen in Tables 2 and 3, the mean oAHI improved from 12.6 ± 10.7 to 9.0 ± 14.0 events/h for children with REM-predominant disease (P = 0.013) and from 21.3 ± 18.9 to 10.3 ± 16.2 events/h for those with NREM-predominant disease (P = 0.008). The percentage of children with REM- vs NREM-predominant OSA found to have a postoperative oAHI< 5 was 53% and 55%, respectively. Children with REM-predominant disease also had a significant improvement in their mean saturation nadir (P < 0.001), TST (P =0.006), and sleep efficiency (P = 0.015). However, children with NREM-predominant disease showed no significant improvement in the mean saturation nadir (P = 0.068), TST (P =0.59), or sleep efficiency (P = 0.45). There was no significant difference in the amount of total sleep time before or after surgery between groups. PSG results for the entire cohort can be found in Table 4.
Fig. 1.

REM- or NREM-predominant status
Fig. 2.

Surgeries performed
Table 2.
Polysomnographic data before and after DISE-directed surgery for subjects who underwent evaluation for infant or persistent OSA with rapid eye movement (REM)-predominant disease
| Before surgery | After Surgery | P value | |
|---|---|---|---|
| oAHI, events/h | 12.6 ± 10.7 (1.7–47.7) | 9.0 ± 14.0 (0.1–76.5) | 0.013 |
| OSA Disease Severity, n (%) | <0.001 | ||
| No OSA (oAHI < 1) | 0 (0) | 8 (17.8) | |
| Mild (oAHI 1− < 5) | 6 (13.3) | 16 (35.6) | |
| Moderate (oAHI 5− < 10) | 21 (46.7) | 11 (24.4) | |
| Severe (oAHI > 10) | 18 (40.0) | 10 (22.2) | |
| ETCO2 > 50 mmHg, mean ± SD, (range), % TST | 10.4 ± 17.3 (0–57.8) | 11.1 ± 20.5 (0–80.1) | 0.12 |
| Saturation nadir, mean ± SD, (range), % | 83.0 ± 7.9 (67–92) | 86.5 ± 6.9 (61–95) | <0.001 |
| Total sleep time, mean ± SD, (range), minutes | 397 ± 70 (243–517) | 428 ± 81 (161–541) | 0.006 |
| Sleep efficiency, mean ± SD, (range), % | 79.0 ± 10.4 (76–82) | 82.4 ± 12.9 (79–86) | 0.015 |
| Arousal index, mean ± SD, (range), arousals/h | 17.1 ± 6.4 (7–33) | 17.3 ± 9.4 (6–51) | 0.39 |
| Stage 1 sleep, mean ± SD, (range), % TST | 3.4 ± 1.8 (1–9) | 2.8 ± 1.4 (1–6) | 0.12 |
| Stage 2 sleep, mean ± SD, (range), % TST | 43.8 ± 8.6 (27–61) | 46.3 ± 8.4 (28–69) | 0.063 |
| Stage 3 sleep, mean ± SD, (range), % TST | 28.7 ± 8.3 (16–44) | 27.3 ± 7.9 (11–51) | 0.67 |
| Stage REM sleep, mean ± SD, (range), % TST | 27.8 ± 11.3 (13–53) | 28.1 ± 10.4 (12–62) | 0.17 |
N number, SD standard deviation, oAHI obstructive apnea-hypopnea index, ETCO2 end tidal carbon dioxide levels, TST total sleep time,
Wilcoxon signed-rank test for pre- and post-tests
Table 3.
Polysomnographic data before and after DISE-directed surgery for subjects who underwent evaluation for infant or persistent OSA with non-rapid eye movement (NREM)-predominant disease
| Before surgery | After Surgery | P value | |
|---|---|---|---|
| oAHI, events/h | 21.3 ± 18.9 (1.3–61.4) | 10.3 ± 16.2 (0.7–55.5) | 0.008 |
| OSA Disease Severity, n (%) | 0.027 | ||
| No OSA (oAHI < 1) | 0 (0) | 1 (9.1) | |
| Mild (oAHI 1− < 5) | 3 (27.3) | 5 (45.5) | |
| Moderate (oAHI 5− < 10) | 0 (0) | 1 (9.1) | |
| Severe (oAHI > 10) | 8 (72.7) | 4 (36.4) | |
| ETCO2 > 50 mmHg, mean ± SD, (range), % TST | 6.4 ± 11.1 (0–33.1) | 3.7 ± 7.7 (0–24.4) | 0.048 |
| Saturation nadir, mean ± SD, (range), % | 84.6 ± 5.7 (77–93) | 88.4 ± 8.4 (67–95) | 0.068 |
| Total sleep time, mean ± SD, (range), minutes | 376 ± 81 (277–471) | 377 ± 94 (254–503) | 0.59 |
| Sleep efficiency, mean ± SD, (range), % | 73.1 ± 14.7 (56–94) | 75.5 ± 15.5 (51–95) | 0.45 |
| Arousal index, mean ± SD, (range), arousals/h | 19.3 ± 13.5 (6–52) | 14.6 ± 11.0 (5–44) | 0.075 |
| Stage 1 sleep, mean ± SD, (range), % TST | 5.7 ± 3.5 (2–13) | 3.9 ± 2.5 (0–9) | 0.18 |
| Stage 2 sleep, mean ± SD, (range), % TST | 49.7 ± 14.9 (30–89) | 50.5 ± 12.3 (35–82) | 0.82 |
| Stage 3 sleep, mean ± SD, (range), % TST | 25.6 ± 9.4 (1–37) | 26.8 ± 7.8 (8–33) | 0.45 |
| Stage REM sleep, mean ± SD, (range), % TST | 18.9 ± 8.6 (5–31) | 18.9 ± 8.5 (6–32) | 0.68 |
N number, SD standard deviation, oAHI obstructive apnea-hypopnea index, ETCO2 end tidal carbon dioxide levels, TST total sleep time,
Wilcoxon signed-rank test for pre- and post-tests
Table 4.
Polysomnographic Data before and after DISE-directed surgery for all subjects who underwent DISE for OSA without tonsillar hypertrophy
| Before surgery | After Surgery | P value | |
|---|---|---|---|
| oAHI, events/h | 14.9 ± 13.5 (1.3–61.4) | 10.3 ± 16.2 (0.1–76.5) | 0.0015 |
| OSA Disease Severity, n (%) | <0.0001 | ||
| No OSA (oAHI < 1) | 0 (0) | 10 (18) | |
| Mild (oAHI 1− < 5) | 9 (16) | 21 (38) | |
| Moderate (oAHI 5− < 10) | 20 (36) | 10 (18) | |
| Severe (oAHI > 10) | 27 (48) | 15 (27) | |
| ETCO2 > 50 mmHg, mean ± SD, (range), % TST | 2.5 ± 4.5 (0–18.7) | 2.6 ± 5.4 (0–19.0) | 0.14 |
| Saturation nadir, mean ± SD, (range), % | 82.5 ± 10.3 (26–93) | 86.1 ± 9.6 (38–95) | 0.0002 |
| Total sleep time, mean ± SD, (range), minutes | 405 ± 73 (243–565) | 430 ± 75 (161–542) | 0.018 |
| Sleep efficiency, mean ± SD, (range), % | 78.7 ± 11.0 (50–96) | 83.8 ± 11.6 (50–98) | 0.0004 |
| Arousal index, mean ± SD, (range), arousals/h | 17.3 ± 8.7 (6–52) | 17.5 ± 11.0 (5–58) | 0.68 |
N number, SD standard deviation, oAHI obstructive apnea-hypopnea index, ETCO2 end tidal carbon dioxide levels, TST total sleep time,
Worsening of the oAHI by at least 1 event/h from the baseline occurred in 12/45 (26.7%) of children with REM-predominant disease and 0/11 (0%) of those with NREM-predominant disease.
Discussion
Using DEX and ketamine, a site of obstruction was identified for all children, including those with REM-predominant disease. This suggests that DISE performed using DEX and ketamine sedation is useful in identifying specific sites of collapse for these patients despite the fact that DEX specifically has been shown to replicate NREM sleep.12 We also found that after DISE-directed surgery, some children with REM-predominant OSA demonstrated significant improvement in their PSG findings, including the oAHI, oxygen saturation nadir, TST, and sleep efficiency. Moreover, surgical success rates for this population of REM-predominant children were similar to those for children with NREM-predominant OSA. This is the first study to show that DISE with DEX and ketamine is useful for a subset of children with REM-predominant disease and that this subset experienced significant improvement in PSG parameters, including oAHI, from procedures directed by DISE.
DEX is a powerful and highly selective α−2 adrenoreceptor agonist that provides sedation in children with less concern for cardiorespiratory instability that is more likely to occur with other anesthetic agents such as inhalational gases or propofol [22]. EEG activity during DEX-induced sedation in adults and children also closely resembles NREM Stage 2 sleep [23, 24]. Using measurements of active and passive critical closing airway pressure (Pcrit), airway responses in children undergoing DEX sedation resemble responses seen during natural sleep [25]. Due to the anesthetic properties and safety profile, DEX is used frequently to conduct dynamic cine magnetic resonance imaging (MRI) in children [26–28]. At our institution, DEX and ketamine are also the preferred anesthetics for both DISE and CINE MRI as part of the diagnostic airway workup for children with OSA without tonsillar hypertrophy. Despite its good safety profile, the inability to replicate REM sleep under sedation raises concerns that DEX specifically may not induce a sleep state with airway resistance patterns that parallel those seen during physiologic sleep in children with REM-predominant disease. This concern served as the basis for our study.
Using several different anesthetic protocols, both subjective and objective outcome measures have demonstrated the effectiveness of DISE in children with OSA. In a previous (2007) study of 26 children with persistent OSA after AT undergoing propofol-induced sleep endoscopy, families of 92% of the children reported symptomatic improvement after DISE-directed surgery [4]. However, this study was limited by the fact that objective improvements in oAHI were not measured as only one patient completed a postoperative PSG [4]. In a more recent (2014) prospective study of children with OSA prior to tonsillectomy, 4 out of 37 children were reported to have anatomic sites of obstruction other than the tonsils and/or adenoids, and these 4 avoided AT or underwent adenoidectomy alone based on this evaluation [29]. For those who had surgery (predominantly AT), the oAHI significantly improved (P = 0.001) after DISE-directed surgery [29]. In our 2017 study of 56 children without tonsillar hypertrophy (both those with persistent OSA and infants with OSA), we demonstrated significant improvements in both postoperative oAHI (P = 0.001) and oxygen saturation nadir (P < 0.001) after DISE-directed surgery [6]. Despite these findings, none of these studies assessed the impact of REM predominance on DISE-directed surgery outcomes.
Although REM-predominant OSA has been identified in both children and adults, little is known about the best diagnostic and therapeutic approaches, or the long-term health consequences, for these patients [30]. OSA appears to occur predominantly in REM sleep in many children and worsen over the course of the night [31]. Nevertheless, its impact is unclear, as an analysis of over 5000 adults enrolled in the Sleep Heart Health Study found that REM-predominant disease was not independently associated with daytime sleepiness or self-reported sleep disruption [32]. In the current study, the average postoperative oAHIs for children with REM- and NREM-predominant OSA were 9.0 and 10.3 events/h. In this population, the number of children with persistent REM- and NREM-predominant disease with an oAHI > 5 was similar. Interestingly, children with REM-predominant disease did not have improvement in the amount of study time spent with an ETCO2 above 50 mmHg, unlike those children with NREM-predominant disease. This data would suggest that either the identified site of obstruction was not complete or accurate or that other pathophysiologic changes occur in children with REM-predominant disease which are not necessarily best treated with surgical intervention. More work should be done to better understand the differences and phenotypes of responders and nonresponders in those children with REM-predominant disease. The current study is one of the first to explore management options and outcomes for children with REM-predominant disease.
Our study has several limitations. As is characteristic of retrospective studies, there is the potential for selection bias; more specifically, it is likely that children with moderate or severe OSA were more likely to be included than those with mild OSA. In addition, our sample size was not large enough to perform subgroup analysis by disease severity. Although we included infants with OSA who had not received AT as they were determined not to have tonsillar hypertrophy, tonsil size was not routinely collected. In addition, it is unclear what factors worsen the oAHI for the subset of children in the REM-predominant group who experienced this change. This should be addressed in future studies. As mentioned in the results section above, the lapsed time between PSGs was approximately 9 months. In a group of 464 children with OSA recruited to the CHAT study [33], early AT was beneficial for reducing symptoms and improving PSG findings. However, normalization of PSG findings occurred in 45% of healthy children who underwent watchful waiting for 7 months. These data suggest that improvement in symptoms and PSG findings may have occurred in some of the children included in our study regardless of the surgical intervention. In addition, children included in this study had comorbidities which limits generalization to otherwise healthy children. In addition, determination of common sites of obstruction in patients with REM versus NREM disease cannot be assessed with this limited data set but should be a topic of future research. Lastly, the selection of surgical procedures based upon DISE is subjective, depending on the judgment of the individual practitioners. As such, the procedures or approaches for any given DISE finding were not standardized among practitioners and this study was not designed to assess the efficacy or efficiency of surgical procedures based on DISE although we think this should be the subject of future studies. Despite these limitations, we feel that this study is important, as it demonstrates that obstructive sites can be consistently identified during DISE for children with REM-predominant OSA.
Conclusions
DISE was useful in predicting at least one site of obstruction for all children with REM-predominant disease. Outcomes based upon this evaluation revealed significant improvements in oAHI, proportion with oAHI< 5, TST, sleep efficiency, and saturation nadir after surgery in a subset of patients with REM-predominant disease. DISE using DEX and ketamine as an anesthetic agent is a useful technique for the evaluation of upper airway obstruction in children with REM-predominant OSA without tonsillar hypertrophy. Larger prospective studies are needed to better understand which of these patients would be best served by DISE evaluation and why specific patients with REM-predominant disease respond when others do not.
Abbreviations
- AASM
American academy of sleep medicine
- BMI
Body mass index
- CCHMC
Cincinnati children’s hospital medical center
- DEX
Dexmedetomidine
- EEG
Electroencephalography
- ETCO2
End-tidal carbon dioxide
- kg
Kilogram
- mg
Milligram
- MRI
Magnetic resonance imaging
- NREM
Non-rapid eye movement
- oAHI
Obstructive apnea hypopnea index
- OSA
Obstructive sleep apnea
- O2
Oxygen
- Pcrit
Critical closing airway pressure
- PSG
Polysomnography
- REM
Rapid eye movement
- SD
Standard deviation
- TST
Total sleep time
- μg
Microgram
Footnotes
Institution where work was performed: Cincinnati Children’s Hospital Medical Center
This abstract was presented as an oral presentation at the Triological Society Combined Sections Meeting on January 20, 2017.
Current Knowledge / Study Rationale: Drug-induced sleep endoscopy (DISE) is performed for infant obstructive sleep apnea (OSA) or children with persistent OSA after adenotonsillectomy. However, results of DISE-directed surgery have not been compared between those with REM- versus non-REM (NREM)-predominant OSA. Given the effects of certain anesthetics, it is important to determine the utility of DISE for children with rapid eye movement (REM)-predominant OSA.
Study Impact: While dexmedetomidine and ketamine induce NREM-like sleep, identification of a site of obstruction was possible for all of the children with REM-predominant OSA and some had significant improvement in their postoperative oAHI, saturation nadir, total sleep time, and sleep efficiency. This group also had surgical success rates similar to children with NREM-predominant OSA. Here, we demonstrate that DISE using dexmedetomidine and ketamine is useful to evaluate airway obstruction in some children with REM-predominant OSA. Larger studies are needed to better understand more about the specific patients that would be best served by DISE evaluation.
Conflict of interest The authors’ declare that they have no conflict of interest.
Financial disclosures No off-label or investigational use of drugs/materials. The authors have no other disclosures to report.
Ethical approval This article does not contain any studies with human participants performed by any of the authors.
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