scholarly journals 1265 Severe Central and Obstructive Sleep Apnea in Teenager with Severe Obesity, Tonsillar Hyper-trophy, and Maxillary Constriction

SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A481-A481
Author(s):  
Mary-Alice Jaeger

Abstract Introduction Obesity in children escalated in the past 50 years. For American children 2-19 years old, Obesi-ty(BMI >= 95th%) increased from 5% in 1971-4 to 19%(13.7 million children)2015-16. Severe Obesity(BMI >=120th% or >35) is less common with prevalences of 1% 1971-4 to 6% in 2015-16(1). Obesity increases risk for physical and mental illness. Sleep apnea risk factors include obesity, maxillary restriction(3), and adenotonsillar hypertro-phy(4). Report of Case 16 yo boy with snoring, gasping during sleep, witnessed apneas, mouth breathing, morning head-aches, EDS, and learning disability requiring an IEP. Past medical history of neonatal snoring, apneas, and reflux. Physical exam revealed severe obesity(BMI 45.3), high arched/narrow palate, Class II bite, large tongue, Mallampati IV, Grade 3-4 tonsils, CricoMental Space +1cm. Inattentive with mildly de-pressed affect. No cardiovascular, pulmonary or neurologic findings. PSG: CAI 31.2, OAHI 23.8. Average O2 sat 97% with 11 minutes<88%. End-tidal CO2 average 50 during sleep and wake. 51% of total sleep time with ETCO2>50 mmHg. CPAP titration: CAI 1.8, OAHI 10.4. Average O2 sat 96% with <1 minute<88%. Events improved with CPAP 14 cm H20 to OAHI 3.5 with >30 minutes of supine REM. Conclusion Severe Central Sleep Apnea with significant obstructive component associated with hypoxia and hypoventilation. With the diurnal hypoventilation, the likely etiology for central apneas is Obesity Hypoventilation Syndrome(5). The central apnea improved with CPAP. His management included CPAP therapy, ENT referral for adenotonsillectomy(5), bariatric referral, and further evaluation for learning/behavior concerns. In retrospect, earlier diagnosis/intervention on behalf of this teenage boy with a history of neonatal snoring presenting now with Severe Obesity, tonsillar hypertrophy and maxillary constriction may have made a significant difference for his cognitive/mental/physical health outcomes.

2012 ◽  
Vol 2012 ◽  
pp. 1-4 ◽  
Author(s):  
L. M. Paulson ◽  
C. J. MacArthur ◽  
K. B. Beaulieu ◽  
J. H. Brockman ◽  
H. A. Milczuk

Introduction. Controversy exists over whether tonsillectomy will affect speech in patients with known velopharyngeal insufficiency (VPI), particularly in those with cleft palate.Methods. All patients seen at the OHSU Doernbecher Children's Hospital VPI clinic between 1997 and 2010 with VPI who underwent tonsillectomy were reviewed. Speech parameters were assessed before and after tonsillectomy. Wilcoxon rank-sum testing was used to evaluate for significance.Results. A total of 46 patients with VPI underwent tonsillectomy during this period. Twenty-three had pre- and postoperative speech evaluation sufficient for analysis. The majority (87%) had a history of cleft palate. Indications for tonsillectomy included obstructive sleep apnea in 11 (48%) and staged tonsillectomy prior to pharyngoplasty in 10 (43%). There was no significant difference between pre- and postoperative speech intelligibility or velopharyngeal competency in this population.Conclusion. In this study, tonsillectomy in patients with VPI did not significantly alter speech intelligibility or velopharyngeal competence.


SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A335-A335
Author(s):  
K Kaplan ◽  
D Spielberg ◽  
L Petitto ◽  
M Musso ◽  
D Glaze

Abstract Introduction Children with down syndrome are at high risk for developing obstructive sleep apnea when compared to typically developing children. Treatment of obstructive sleep apnea is complicated as these children often struggle with traditional therapies such as positive airway pressure. In adult populations it has been shown that head elevation is successful in reducing the severity of OSA (AHI). The hypothesis of this study is that head elevation (30°) would improve OSA in a cohort of pre-pubertal children with down syndrome. Methods Children with down syndrome, aged 4-13, presenting to the sleep clinic at Texas Children’s Hospital were screened for enrollment into the study (n=21; 11 male). Subjects were randomized to begin a diagnostic polysomnogram with either the head of the bed flat (0°) or elevated (30°). Head position was alternated every 2 hours during the study. Studies were performed in an AASM pediatric sleep center by a registered PSG technologist. Studies were scored using AASM pediatric scoring rules. Data was analyzed using paired student t-tests. Each subject served as their own control. Results There was no significant difference in AHI (p=0.71), RDI (p=0.7), O2 nadir (p=0.17), total sleep time (p=0.34), sleep efficiency (p=0.28), time in REM sleep (p=0.94) or arousal index (p=0.14) when the head of the bed was flat (0°) versus elevated (30°). The study shows that head elevation is not successful in significantly reducing obstructive sleep apnea in a pre-pubertal pediatric population of children with down syndrome. Conclusion In children with down syndrome, aged 4-13, referred for a diagnostic sleep study, there is no improvement in OSA due to head elevation (30°) when compared to sleeping flat (0°). These findings were independent of if the subject started with the head of the bed flat or elevated. Other cofounders were eliminated as each subject served as their own control. Support No external funding was utilized for this study.


Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Patricia Tung ◽  
Yamini S Levitzky ◽  
Rui Wang ◽  
Stuart F Quan ◽  
Daniel J Gottlieb ◽  
...  

INTRODUCTION: Prior studies have documented a higher prevalence of atrial fibrillation (AF) in those with obstructive sleep apnea (OSA). OSA has been associated with AF recurrence following cardioversion and ablation, and with prevalent and incident AF in cross-sectional and retrospective studies. Central sleep apnea (CSA) also has been associated with AF in patients with heart failure. However, data from prospective cohorts are sparse and few studies have evaluated the association of CSA with AF in population studies. METHODS: We assessed the association of OSA and CSA with incident AF among 3,420 subjects without a history of AF in the Sleep Heart Health Study (SHHS), a prospective, community-based study designed to evaluate the cardiovascular consequences of sleep disordered breathing. Subjects underwent overnight polysomnography at baseline and were followed over time for the development of incident AF, documented at any time after baseline polysomnogram until the end of follow-up. OSA was defined as an obstructive apnea-hypopnea index ≥ 5 and CSA was defined as a central apnea index ≥ 5. RESULTS: At baseline, the sample include 1499 men (44.4%) with a mean age of 62.4 (±10.9); 1569 (45.9%) subjects met criteria for mild to severe OSA and 54 (1.6%) for CSA. Over a mean follow-up of 8.2 years, 382 cases of incident AF were identified. The prevalence of both OSA and CSA was higher among those who developed AF compared to those who did not (OSA 49% vs 44%, p=0.001 and CSA 5% vs 1.2%, p=0.001). After adjustment for multiple AF risk factors, CSA was associated with an approximately 2-fold increased odds of incident AF (RR=2.38, 95% CI, 1.15-4.94; p = 0.02). The association persisted after exclusion of 258 subjects with a history of heart failure (RR=2.78, 95% CI, 1.28-6.04; p = 0.01). We did not find a significant association of OSA with incident AF (Table). CONCLUSION: In our prospective, community-based cohort baseline CSA was associated with incident AF.


SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A307-A307
Author(s):  
Christine Matarese ◽  
Risa Nakase-Richardson ◽  
Emily Almeida ◽  
John Whyte ◽  
Sagarika Nallu ◽  
...  

Abstract Introduction Recent work has highlighted prevalent obstructive not central sleep apnea following traumatic brain injury (TBI). Treatment of comorbid OSA may facilitate neurologic recovery but widespread screening is limited. Mixed support exists for the presence of dysphagia as a biomarker of OSA in the general population and stroke patients. Dysphagia is common following TBI; however, no study has examined the relation between OSA and dysphagia in this cohort. Leveraging data from a recent six-center clinical trial of OSA and TBI during inpatient rehabilitation, this secondary analysis examined the association between OSA severity indices and proxy measures of dysphagia. Methods Level 1 polysomnography (PSG) was used to assess OSA (AHI ≥ 5 and ≥ 15) during inpatient rehabilitation for the overall sample (N=248; 203 male; 60.6% severe injury) evaluated at a median of 120.6 days post-TBI and subset ≤ 60 days post-injury. Dysphagia was approximated as the presence of a PEG tube and/or a modified texture diet (MTD) on the day of PSG. Chi square and Fisher’s Exact tests were utilized for group comparisons. Results As previously reported, OSA in this cohort was prevalent (68.2% (n=169) at AHI ≥ 5 and 33.5% (n=83) AHI ≥ 15) with predominantly obstructive events. 27.4% (n=68) met criteria for dysphagia combining proxy measures (34 peg; 49 MTD). No significant difference was found for presence of dysphagia across OSA severity cutoffs (AHI ≥ 5 & 15; p=0.1029 & 0.5959). When examining OSA across the individual proxy measures, persons without a peg tube were significantly more likely to have OSA at AHI ≥ 5 (62.5% vs 5.65%; p=0.0003) and AHI ≥ 15 (31.05% vs 2.42%; p=0.0353). When examining participants less than 60 days post-TBI, the group differences remained. Conclusion The incidence of dysphagia in TBI patients, as indexed by a modified diet or presence of a feeding tube, was not elevated in those with OSA. Sample bias (for undergoing Level 1 PSG and improvement facilitating inpatient rehabilitation admission) may have contributed to findings. Finally, future work with more sensitive indices of dysphagia is needed to accurately evaluate this association. Support (if any) PCORI (CER-1511–33005), NIIDLRR (90DPTB0004)


SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A471-A472
Author(s):  
Lauren M Castner ◽  
Mark D Garwood

Abstract Introduction Amyloidoses are a group of systemic diseases characterized by misfolded protein fragment deposition within the organs, including the heart, kidney, liver, gastrointestinal tract, nervous system, pulmonary system, and soft tissues1. Obstructive and central sleep apnea are known to occur frequently in those with cardiac amyloidosis. This case discusses a patient with systemic amyloidosis and chronic hypercarbic, hypoxic respiratory failure. Report of Case A 66 year old female with a history of systemic amyloidosis, non-ischemic cardiomyopathy, hypertension, and obstructive sleep apnea was admitted for acute on chronic heart failure. Despite intravenous diuresis, she remained hypoxemic, requiring 1 liter per minute of oxygen. She was found to have bilaterally reduced diaphragmatic excursion and a restrictive ventilatory defect on spirometry. She had a preceding history of chronic carbon dioxide retention with elevated CO2 levels for greater than a year (52-74 mmHg). Sleep medicine was consulted to assist in evaluation of the patient’s obstructive sleep apnea and hypoxic, hypercarbic respiratory failure. Baseline polysomnogram revealed sleep related hypoventilation with transcutaneous CO2 (TCO2) ranging between 77-86 mmHg without clear obstructive sleep apnea. A bilevel positive airway pressure (BPAP) titration was then performed (TCO2 54-69 mmHg) and while the patient’s obstructive sleep apnea was well treated, sleep-related hypoventilation and central apneas persisted. Average volume assured pressure support (AVAPS) was initiated for management of sleep related hypoventilation. In follow up, the patient is feeling well, off oxygen, with daytime TCO2 38 mmHg. Conclusion This case demonstrates a rare complication of systemic amyloidosis in the setting of respiratory failure attributed to amyloid infiltration of the diaphragm. In the few previously reported cases of neuromuscular respiratory failure in systemic amyloidosis there is rapid progression and high mortality3, which highlights the importance of assessing for sleep disordered breathing and additional causes of respiratory failure in a patient with a complex systemic disease.


2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
P Meurin ◽  
A Ben Driss ◽  
C Defrance ◽  
N Renaud ◽  
R Dumaine ◽  
...  

Abstract Background Although the prevalence of obstructive sleep apnea (OSA) syndrome is high in patients with acute coronary syndrome (ACS), little is known about central sleep apnea (CSA) in these patients, especially if they have no left ventricular dysfunction (indeed, it is well known that heart failure could be a confounding factor as it is an important cause of CSA). Furthermore, central apnea could be promoted by ticagrelor, a relatively new drug, already known to cause dyspnea (which could modify the apneic threshold) in some patients. Purpose To investigate the prevalence of central sleep apnea in patients without left ventricular dysfunction after ACS. Methods Monocentric prospective survey. All consecutive patients within 365 days after ACS were included if they had (1) left ventricular ejection fraction LVEF >45%, (2) no history of heart failure, (3) systolic arterial pulmonary artery pressure <45 mm Hg, and (4) no history of sleep apnea. After inclusion, patients underwent an overnight sleep study with a portable sleep monitor validated to differentiate central and obstructive apneas. Patients were then classified as “normal” patients if they had an AHI (apnea hypopnea index) <15, “CSA patients” if they had an AHI >15 with a majority of central sleep apneas and “OSA patients” if they had an AHI >15 with a majority of obstructive sleep apneas. Results Between January 2018 and January, 2020, we included 115 consecutive patients (age 56.1±10.5, male 84%, mean body mass index 28.4±4.5, LVEF: 56±4%). Sleep study was performed 68±62 days (7–350 days) after ACS on average. All of the patients were receiving a single or (mostly) dual antiplatelet therapy: aspirin (n=114: 99%, ticagrelor (n=80: 69.5%), clopidogrel (n=28: 24%), prasugrel (n=4: 3.5%). Finally 80 patients were taking ticagrelor, while 35 were not. A total of 49/115 patients (42.6%) had a clinically significant (moderate to severe) sleep disordered breathing, with an AHI>15: (CSA: n=27/115: 23.5%, OSA:n=22/115: 19%). Among them, 25/115 patients (22%) had a severe (AHI >30) sleep disordered breathing: CSA 12% OSA: 10%. Among patients receiving ticagrelor, 24/80 (30%) had a CSA with an AHI >15, while, in patients not taking ticagrelor only 3/35 (8.5%) had CSA with an AHI >15 (p=0.04) Conclusion As expected, OSA is frequent after ACS, as in all types of coronary artery disease patients. High prevalence of CSA was less expected and seemed to be correlated with ticagrelor administration. This monocentric survey is a preliminary safety signal. Further studies are needed to investigate the exact incidence, the sustainability and the potential consequences of ticagrelor induced central sleep apnea. Funding Acknowledgement Type of funding source: None


2020 ◽  
pp. 014556132093195
Author(s):  
Nian Sun ◽  
Jingying Ye ◽  
Junbo Zhang ◽  
Dan Kang ◽  
Jun Tai ◽  
...  

Background: Positional obstructive sleep apnea hypopnea syndrome (P-OSAHS) is a distinct OSAHS type. Whether velopharyngeal surgery is efficacious for patients with P-OSAHS remains unclear. Aim/Objective: To investigate the efficacy and factors influencing velopharyngeal surgery for treatment of patients with P-OSAHS, defined as the apnea hypopnea index (AHI) in different body postures (supine AHI ≥2*nonsupine AHI). Materials and Methods: A total of 44 patients with P-OSAHS who underwent velopharyngeal surgery were retrospectively studied. The clinical data of these patients, including polysomnography (PSG), physical examination, and surgical information, were collected for analysis. All patients underwent a PSG about 6 months after surgery to determine the treatment outcomes. Results: The overall AHI of the 44 patients decreased from 40.2 ± 18.7 events/h to 18.5 ± 17.5 events/h after surgery ( P < .001). There were 29 responders (65.9%) according to the classical definition of surgical success. The percentage of sleep time with oxygen saturation below 90% (CT90) was the only predictive parameter for surgical success ( P = .014, odds ratio value = 0.894). There was no significant difference between the change in supine AHI (−55.9 ± 35.2%) and the change in nonsupine AHI (−43.4 ± 74.1%; P = .167), and these 2 parameters were significantly correlated ( r = 0.616, P < .001). Among the 38 patients with residual OSAHS (residual AHI ≥5), 28 had persistent P-OSAHS, and the percentage was as high as 82.4%. Conclusions and Significance: Patients with P-OSAHS with a lower CT90 value are more likely to benefit from velopharyngeal surgery. Positional therapy could be indicated for most of the patients who are not cured by such surgery.


SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A367-A368
Author(s):  
W Powell ◽  
M Rech ◽  
C Schaaf ◽  
J Wrede

Abstract Introduction Schaaf-Yang Syndrome (SYS) is a genetic disorder caused by truncating variants in the MAGEL2 gene located in the maternally imprinted, paternally expressed Prader-Willi syndrome (PWS) region at 15q11-13. The SYS phenotype shares features with PWS, a disorder with known high incidence of central and obstructive sleep apnea (OSA). However the spectrum of sleep-disordered breathing in SYS has not been described. Methods We performed a retrospective analysis of polysomnograms from 22 of the known 115 patients with molecular diagnosis of SYS. Sleep characteristics including total sleep time, latency, efficiency, % sleep stages, apnea-hypopnea index (AHI), obstructive index, central index, and oxygenation were analyzed for the whole group and by truncation location (c.1996dupC variants [n=11] or other locations [n=11]). Only the initial diagnostic study or initial diagnostic portion of a split-night study was used in analysis (analytic n=21). Results We collected 33 sleep study reports from 22 patients, ages 2 months - 18.5 years. Mean analyzed sleep time was 357 minutes (129-589 min) with mean sleep efficiency of 71.45% (45-94%) and sleep latency of 24.8 minutes (0-146 min). The mean apnea-hypopnea index (AHI) was 19.1/hr (0.9 -49/hr) with mean obstructive AHI of 16.3 (0.6-49/hr). Mean central index was 2.8/hr (0-14/hr). 18/21 (86%) were diagnosed with OSA, and 13/21 (62%) with moderate or severe OSA (oAHI &gt;5/hr). Central sleep apnea was diagnosed in 2/21 (9.5%). 15 studies reported periodic limb movement index (PLMI) with mean of 7.8 (0-67/hr) and 4/15 (26%) with PLMI &gt;5. Comparison of genotype groups did not reveal any difference in presence of OSA or severity of OSA. Conclusion OSA is frequently identified on polysomnography in patients with SYS. Central sleep apnea is less common, which is in contrast to PWS. The majority of patients with OSA had moderate or severe OSA, and 47% had severe OSA. Support N/A


2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Agata Gabryelska ◽  
Piotr Białasiewicz

AbstractThe aim of the study was to compare REM-dependent and REM-independent, obstructive sleep apnea syndrome (OSA) patients in relation to their daily sleepiness assessed by Epworth sleepiness scale (ESS). The study included 1863 consecutive patients, who were referred to a sleep centre with a presumed diagnosis of OSA. Following polysomnography, 292 patients fulfilled criteria for either REM-dependent OSA (REM-OSA, n = 102) or REM-independent OSA (nREM-OSA, n = 190). Both study groups were matched regarding sex and age. REM-OSA group had two times lower median apnoea-hypopnea index (AHI) compared to nREM-OSA (p < 0.001), yet day-time sleepiness measured by ESS was similar: median score 9.0 (6.0–11.0) and 8.0 (4.8–11.0), p = 0.109, respectively. Subsequent post-hoc ANCOVA analysis, with covariates (BMI, percent of total sleep time spent in REM stage, percent of total sleep time spent in the supine position), has shown statistically significant difference between study groups regarding AHI (p < 0.001) and no difference regarding ESS score (p = 0.063). Despite two times lower AHI, patients with REM-OSA present with similar day-time sleepiness as those with REM independent OSA. Daily sleepiness may be stronger associated with apneas/hypopneas occurring in REM than nREM sleep.


SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A468-A468
Author(s):  
Talayeh Rezayat ◽  
Melisa Chang

Abstract Introduction Treatment of obstructive sleep apnea (OSA) with positive airway pressure (PAP), mandibular advancement devices (MAD) and oral surgery have been reported to lead to emergent central sleep apnea (CSA). In this case report the emergence of CSA in a Cheyne-Stokes pattern following the use of hypoglossal nerve stimulator as a treatment modality for OSA is discussed. Report of Case A 70-year-old man with a history of hypothyroidism and severe OSA diagnosed via a home sleep apnea test with a respiratory event index (REI) of 38 events/ hr was intolerant of PAP therapy and an MAD did not effectively treat his OSA. He was deemed an appropriate candidate for hypoglossal nerve stimulation following a drug induced sleep endoscopy. Following implantation and activation, he developed a lip droop and was ruled out for a stroke. A polysomnogram was completed which showed significant improvement in his sleep apnea at a voltage range of 1.4-17V. At 1.8V he developed REM- supine central events. When the voltage was further increased to 1.9-2.0V non-REM supine central events arose. These events appeared to have Cheyne-Stoke morphology with a cycle duration of over 50s. He was set to an amplitude of 1.6 V with a positional belt for treatment of his OSA without any emergent CSA. Conclusion This patient developed central sleep apneas with Cheyne-Stoke morphology following treatment of obstructive sleep apnea using a hypoglossal nerve stimulator. The central events began at higher voltage settings (greater than 1.8V). He had no history of heart failure or arrhythmias. This higher voltage may lead to overshoot of the tongue out of the airway resulting in hyperpnea, hypocapnia and central apnea but the underlying pathophysiology for the Cheyne-Stoke pattern in the absence of heart failure remains unknown.


Sign in / Sign up

Export Citation Format

Share Document