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Indian Journal of Otolaryngology and Head & Neck Surgery logoLink to Indian Journal of Otolaryngology and Head & Neck Surgery
. 2024 Aug 1;76(6):5126–5132. doi: 10.1007/s12070-024-04908-0

Analysis of Possible Predictors of Moderate and Severe Obstructive Sleep Apnea in Obese Patients

Silvia Matarredona-Quiles 1,✉, Marina Carrasco-Llatas 1,2, Paula Martínez-Ruíz de Apodaca 1, José Ángel Díez-Ares 3, Elena González-Turienzo 1, José Dalmau-Galofre 1
PMCID: PMC11569310  PMID: 39559156

Abstract

Objectives: To determine if there are clinical or anatomical differences between patients with grade II-IV obesity without obstructive sleep apnea (OSA) or mild OSA and patients with moderate or severe OSA and to assess whether any of these factors are predictive of moderate/severe OSA. Methods: Observational case-control study with consecutive sampling including patients between 18 and 65 years of age with grade II-IV obesity who were candidates for bariatric surgery. An anamnesis regarding OSA symptoms, a physical examination of the upper airway and a cardiorespiratory polygraphy were performed. Results: A total of 124 patients were included in the study, of whom 61.3% did not have OSA or had mild OSA and 38.7% had moderate or severe OSA. Age over 48 years was the only independent factor associated with moderate or severe OSA. Other factors showed a relation with moderate/severe OSA after multivariate analysis: male sex, STOP-BANG questionnaire ≥ 3, weight ≥ 105 kg, thick neck, neck circumference ≥ 41.25 cm, flaccid palate, Mallampati III-IV index, Friedman tongue position III-IV and retropalatal narrowing. Conclusions: The only independent predictive factor related to moderate or severe OSA in patients with morbid obesity was age over 48 years, therefore a sleep study remains essential for its diagnosis.

Supplementary Information

The online version contains supplementary material available at 10.1007/s12070-024-04908-0.

Keywords: Obstructive Sleep Apnea, Bariatric Surgery, Morbid Obesity, Upper Airway

Introduction

Obstructive sleep apnea (OSA) is the most prevalent sleep breathing disorder in the general population, affecting 4-30% of the population between 30 and 69 years of age worldwide [1]. Obesity is its main risk factor [2]. OSA prevalence is estimated in around 63 and 83% of obese patients [3, 4] and for every 10% increase in body weight, the risk of suffering OSA increases six-fold [5]. Individuals with central or visceral obesity, in which fat is deposited in the trunk and neck regions, are at higher risk. In addition, OSA patients develop more sedentary lifestyles due to daytime sleepiness, thus perpetuating this close relationship between OSA and obesity.

Despite its high prevalence, the pathophysiology of OSA in obese patients is still not clearly established. Obesity is thought to contribute to airway collapse by a multifactorial mechanism [6]. Apart from hormonal and metabolic factors [7–9], the local deposit of fat at the neck, pharynx and tongue [10, 11] is one of the factors responsible for OSA in obese patients by reducing the caliber of the upper airway (UA) and increasing its collapsibility [12]. However, there are very few studies in the literature that have studied the anatomy of the upper airway in these patients. Therefore, the main purpose of this study is to determine whether there are clinical or anatomical differences between patients without OSA or mild OSA and those with moderate or severe OSA, and to assess whether any of these factors are predictive of moderate/severe OSA.

Materials and Methods

This study was approved by the Research Ethics Committee (CEIm) at the Research Unit of the Hospital on March 25th, 2020 (CEIm code: 38/20).

Data Sources

Observational case-control study with consecutive sampling including patients aged 18–65 years with obesity grade II (body mass index (BMI) ≥ 35 kg/m2) and hypertension, type 2 diabetes, metabolic syndrome or OSA or obesity grade III or IV (BMI ≥ 40 kg/m2) elective for bariatric surgery (laparoscopic Roux-en-Y gastric bypass (RYGB) or vertical sleeve gastrectomy (VSG)) at the General Surgery department. Patients had to have lost at least 10% of their maximum weight and present a favorable psychiatric evaluation in order to be considered for bariatric surgery. In addition, patients had to voluntarily agree to be part of the study and sign the informed consent form.

As part of the preoperative study, patients were evaluated at the Otolaryngology department with an anamnesis regarding OSA and a physical examination of the UA. A cardiorespiratory polygraphy (CRP) was also requested. The following data were collected in the anamnesis: age, sex, smoking or drinking habits, cardiovascular risk factors, previous diagnosis of OSA, Epworth sleepiness scale [13] and STOP-BANG questionnaire [14]. Features included in the physical examination were: weight (kg), height (m), BMI (kg/m2), neck length and thickness, neck circumference, uvula thickness and length, narrowing at the posterior pharyngeal pillars and the pharyngeal lateral walls, palatal shape, tongue scalloping, Mallampati index (MI) [15], Friedman tongue position (FTP) [16] and the tonsillar size based on Brodsky classification [17]. A flexible fibre-optic endoscopy was also performed, assessing retropalatal or tongue base obstruction, and lingual tonsil size [18]. From the CRP, the following were recorded: number of apneas and hypopneas, apnea hypopnea index (AHI), oxygen desaturation index (ODI), minimum oxygen saturation (SatO2) and time with SatO2 below 90%.

Patients under 18 or over 65 years of age were excluded, as well as those who refused to participate in the study, pregnant women, patients with a score equal to or greater than IV on the American Society of Anesthesiologists (ASA) scale, those who did not attend the pre- or post-surgical Otorhinolaryngology visit or patients that did not undergo the pre or post-surgical CRP or it was not valid (less than 6 h of recording).

Statistical Analysis

Patients were divided in two groups based on the CRP results: no OSA or mild OSA (AHI < 15/h) and moderate or severe OSA (AHI≥15/h). Continuous variables were expressed by mean, median, range and standard deviation and categorical parameters by their frequencies.

ROC curves were used to determine the cut-off value with the highest sensitivity and specificity for predicting success of bariatric surgery in the treatment of OSA, dichotomizing continuous variables. A simple binary logistic regression analysis was performed to analyze factors related a higher risk of moderate/severe OSA (AHI≥15/h), determining the OR and 95% confidence intervals (CI) for non-adjusted association. Most relevant variables (p < 0.05) and possible confounders were selected for a multivariate model and adjusted ORs.

The Statistical Package for the Social Sciences (SPSS Inc., Chicago, IL, USA), 24.0.0.0 version, was used for the analysis. A p value < 0.05 was considered statistically significant.

Results

An anamnesis regarding OSA and a physical examination of the UA were performed on 169 patients. Of these, 45 patients refused to undergo CRP or it was not valid, therefore a total of 124 patients were included in the study.

CRP Metrics

Of the total, 25.8% (n = 32) did not suffer from OSA, 35.5% (n = 44) had mild OSA, 21% (n = 26) moderate, and 17.7% (n = 22) severe OSA.

In the non-OSA or mild OSA group, 76 patients (61.3%) were included, and in the moderate or severe OSA group, 48 patients (38.7%). The results of the CRP in both groups are shown in Table 1.

Table 1.

CRP results of patients without OSA/mild OSA (n = 76) and moderate/severe OSA (n = 48)

No OSA/mild OSA Moderate/severe OSA
AHI (events/h) 6.25 ± 4.33 34.44 ± 16.87
ODI (events/h) 39.29 ± 4.46 41.39 ± 4.96
Minimum SatO 2 (%) 94.597 ± 2.39 92.99 ± 2.65
TSatO2 < 90% (min) 26.53 ± 68.24 70.16 ± 74.61
TSatO2 < 90% (%) 6.28 ± 15.47 16.61 ± 19.31
Number of Apneas 3.42 ± 6.72 68.9 ± 78.05
Number of Hypopneas 39.45 ± 27.21 143.8 ± 77.96

AHI: apnea hypopnea index, CRP: cardiorespiratory polygraphy, ODI: oxygen desaturation index, OSA: obstructive sleep apnea, SatO2 minimum oxygen saturation, TSatO2 < 90%: time with SatO2 below 90%

Demographics

The mean age of patients without OSA or mild OSA was 46.17 ± 10.52 years (range = 19–64 years, median = 47 years), whereas for patients with moderate and severe OSA the mean age was 52.94 ± 7.93 years (range = 35–64 years, median = 54.5 years) (p = 0.000). Individuals over 48 years old had a sensitivity of 77.1% and a specificity of 53.9% for the detection of moderate and severe OSA (AUC = 0.693 (0.6–0.787)).

In the group of patients with moderate and severe OSA there were more men, a higher mean age and higher scores on the STOP-BANG questionnaire (Table 2).

Table 2.

Association between moderate/severe OSA and the patient’s clinical profile: Chi2and the simple binary logistic regression model

Category No OSA/mild OSA Moderate/severe OSA p-value OR (95% CI) p-value
Sex Female 68 (67.3%) 33 (32.7%) 0.004
Male 8 (34.8%) 15 (65.2%) 3.86 (1.49–10.03) 0.005
Age < 48 years old 41 (78.8%) 11 (21.2%) 0.001
≥ 48 years old 35 (48.6%) 37 (51.4%) 3.94 (1.75–8.86) 0.001
Epworth Sleepiness Scale < 12 67 (64.4%) 37 (35.6%) 0.216
≥ 12 5 (45.4%) 6 (54.5%) 2.17 (0.62–7.61) 0.225
STOP-BANG Low risk 25 (89.3%) 3 (10.7%) 0.001
Moderate-severe risk 49 (53.8%) 42 (46.2%) 7.14 (2.01–25.35) 0.002

CI: confidence interval, OSA: obstructive sleep apnea, OR: odds ratio

In the preoperative physical examination, differences in mean weight, BMI, and neck circumference were observed among patients without OSA or mild OSA and those with moderate or severe OSA (Table 3). A weight of 105 kg at the ENT visit had a sensitivity of 65.2% and a specificity of 54% for the detection of moderate or severe OSA (AUC = 0.538 (0.426–0.650). A body mass index (BMI) of 39.3 kg/m2 had a sensitivity of 58.7% and a specificity of 53.6% for the detection of moderate or severe OSA (AUC = 0.619 (0.515–0.723)). A neck circumference greater than 41.25 cm had a sensitivity of 66.7% and a specificity of 65.8% for the detection of moderate and severe OSA (AUC = 0.74 (0.653–0.826)).

Table 3.

Weight, BMI, and mean neck circumference of the non-OSA/mild OSA group vs. moderate/severe OSA: Student’s t-test for independent samples

No OSA/mild OSA Moderate/severe OSA p-value
Weight (kg) 105.14 ± 15.44 113.29 ± 16.19 0.006
BMI (kg/m 2 ) 39.29 ± 4.46 41.39 ± 4.96 0.017
Neck circumference (cm) 40.67 ± 4.07 44.32 ± 4.16 0.000

BMI: body mass index, OSA: obstructive sleep apnea

Of all the anatomical features examined, significant differences were observed in the parameters shown in Table 4. The rest of the features explored are shown in the complementary material.

Table 4.

Association between moderate/severe obstructive sleep apnea and upper airway examination: Chi2and simple binary logistic regression model

Category No OSA/mild OSA Moderate/severe OSA p-value OR (95% CI) p-value
Weight < 105 kg 41 (71.9%) 16 (28.1%) 0.025
≥ 105 kg 35 (52.2%) 32 (47.8%) 2.34 (1.11–4.96) 0.026
Neck thickness Normal 27 (87.1%) 4 (12.9%) 0.001
Thick 49 (53.8%) 42 (46.2%) 5.79 (1.87–17.88) 0.002
Neck circumference < 41.25 cm 50 (76.9%) 15 (23.1%) 0.000
≥ 41.25 cm 26 (44.1%) 33 (55.9%) 4.23 (1.95–9.16) 0.000
Flaccid soft palate No 39 (73.6%) 14 (26.4%) 0.024
Yes 37 (53.6%) 32 (46.4%) 2.41 (1.11–5.22) 0.026
Mallampati Index I-II 50 (70.4%) 21 (29.6%) 0.004
III-IV 15 (41.7%) 21 (58.3%) 3.33 (1.45–7.7) 0.005
Friedman tongue position I-II 28 (75.7%) 9 (24.3%) 0.044
III-IV 48 (56.5%) 37 (43.5%) 2.4 (1.01–5.7) 0.047
Retropalatal space Normal 59 (68.6%) 27 (31.4%) 0.042
Narrow 16 (48.5%) 17 (51.5%) 2.32 (1.02–5.28) 0.044

CI: confidence interval, OSA: obstructive sleep apnea, OR: odds ratio

Risk Factors for Moderate/Severe OSA

Age over 48 years was the only variable that showed a significant association with the development of moderate/severe OSA in the multivariate analysis (Table 5).

Table 5.

Association between moderate/severe OSA and clinical-anatomical characteristics: multivariate regression

Category OR CI 95% p-value
Sex: male 0.065 0.003–1.67 0.095
Age ≥ 48 years old 33.64 1.2–944.44 0.039
STOP-BANG: moderate-high risk 0.426 0.02–9.52 0.59
Weight ≥ 105 kg 4.62 0.33–65.86 0.258
Neck: thick 3.79 0.25–57.76 0.338
Neck circumference ≥ 41.25 cm 6.61 0.29–149.13 0.235
Flaccid palate: yes 2.31 0.22–24.04 0.483
Mallampati index III-IV 1.16 0.07–18.32 0.92
Friedman Tongue position III-IV 3.07 0.21–45.11 0.413
Retropalatal space: narrow 0.73 0.06–8.46 0.803

CI: confidence interval, OR: odds ratio

Discussion

In recent years, several studies have investigated the factors associated with the development of OSA in obese patients, mainly related to male gender, age and BMI [19–23].

In our study, in order to analyze the factors associated with the development of OSA, two groups were differentiated on the basis of pre-surgical CRP: no OSA/mild OSA (AHI < 15/h) and moderate/severe OSA (AHI ≥ 15/h), since AHI ≥ 15/h indicates a clinically significant level of disease [23].

Age over 48 years was the only independent predictor of moderate/severe OSA. The studies of Duarte et al. and Khan et al. also associated age with an increased risk of OSA (OR = 1.078 and OR = 1.4, respectively) [21, 22]. Carneiro et al. [19]. and Dixon et al. [20]. established an age over 36 and 38 years, respectively, as a risk factor for developing OSA, an age lower than that of our study, being this difference probably due to the lower mean age of the population in both studies. However, for Lee et al. age did not prove to be a predictor of OSA [23], also probably due to the fact that their study population had a lower mean age than ours (35.69 ± 9.6 years vs. 48.79 ± 10.12 years). In the general population, age has also been defined as a risk factor for the development of OSA due to its association with increased upper airway resistance, neck adiposity deposit, impaired pharyngeal muscle reflexes, and narrowing of the upper airway of the pharynx [24].

In the simple regression analysis, other factors related to the development of moderate/severe OSA were identified. Male gender was a simple predictor of moderate or severe OSA [4, 20–22]. Several studies have previously noted male gender as a risk factor for OSA [4, 21, 22] or severe OSA [20]. This association of OSA with male sex is probably due to different hormonal and physical factors, including the higher predisposition to fat deposition in the parapharyngeal space in men and the fact that men have a longer and more collapsible upper airway [25], in addition to the fact that testosterone favors the development of OSA whereas estrogens and progesterone are protective factors [26]. In our study, sex was no longer a risk factor for moderate/severe OSA after adjusting for confounding factors such as the difference in age and weight between both sexes. Men had higher weight than women (122.32 ± 16.13 kg vs. 104.53 ± 13.25 kg, p = 0.000), although there were no differences in BMI (40.32 ± 4.9 kg/m2 vs. 39.71 ± 4.61 kg/m2, p = 0.497). Women were younger than men (47.54 ± 10.24 years vs. 53.56 ± 7.44 years, p = 0.000).

The Epworth Sleepiness Scale score was normal in most cases, unrelated to the presence of moderate/severe OSA, as in previous studies [20, 27, 28]. This low sensitivity of the Epworth scale and the lack of association with OSA are possibly due to its subjectivity and low reproducibility.

A score of ≥ 3 on the STOP-BANG scale was associated with moderate/severe OSA. Kositanurit et al. obtained an OR = 16 (95% CI: 6.67–43.49, p < 0.001) for the STOP-BANG score ≥ 3 and the presence of OSA [30]. In the study by Glazer et al. the STOP-BANG questionnaire was the best predictor of moderate and severe OSA [27]. Despite not being a clearly validated questionnaire in obese patients, previous studies have demonstrated it to be a suitable tool for the detection of moderate and severe OSA in this group of patients [28, 29], with greater efficiency in the female gender among severely obese patients (sensitivity and specificity of 71% and 80%, respectively, in women vs. 90% and 12% in men) [28].

After our review of the literature, no studies evaluating the exploration of the upper airway in obese patients with OSA in the Otolaryngology clinic beyond the measurement of the neck circumference have been found, although there are studies that have assessed the upper airway in these patients using measurements obtained on plain lateral radiography [30], magnetic resonance imaging (MRI) [31–33] or computed tomography (CT) [34, 35].

In the present study, a large number of UA characteristics were evaluated in patients with morbid obesity. Significant differences between non-OSA/mild OSA and moderate/severe OSA were observed in weight, cervical thickness, presence of a flaccid palate, Mallampati index (MI), Friedman Tongue Position (FTP) and retropalatal space, with differences mainly observed in weight, cervical thickness and tongue size, consistent with the differences most frequently obtained in previous studies.

Weight was 8.14 kg higher in subjects with moderate/severe OSA, with a weight of 105 kg being the cut-off point with the highest sensitivity and specificity for its detection. Schafer et al. also observed a relationship between weight and AHI, but it was not an independent factor to predict OSA either, same as in our study [36].

In this study, the BMI was 2.1 kg/m2 higher in patients with moderate/severe OSA, but it was not a predictive factor, as in previous studies [19, 22, 23]. In other studies, it has been considered a risk factor for OSA in general [21, 37] and for severe OSA [37, 38], but of all the factors found, it was the least important [37]. This difference in the association of BMI and OSA among the variety of studies may be due to the fact that BMI might not be a good predictor of OSA, since this disease is more associated with central fat distribution and BMI does not reflect such distribution [39]. Proof of this is the study by Dixon et al., in which BMI, one of the predictors of severe OSA included in their logistic regression, was replaced by neck circumference when measures of central weight distribution were added to the analysis [20]. In addition, the mean BMI of our sample was lower than that of most of the compared studies [4, 19, 21–23, 37].

A thick neck was associated with the presence of moderate/severe OSA, with this group having a 3.65 cm greater cervical perimeter. The cut-off point with the highest sensitivity and specificity for the detection of moderate and severe OSA was 41.25 cm, but it was not an independent risk factor. Previous studies also observed thicker necks in patients with OSA [23, 28, 40] and pointed out the measure of 43 cm of neck perimeter as a predictor of OSA [20, 23, 28], being this characteristic an independent risk factor [20, 21, 23]. In other studies, cervical circumference was also not an independent predictor of OSA [22, 37]. Neck circumference, which is a good marker of central obesity, seems to be a good marker of OSA as well. Furthermore, it more directly reflects the accumulation of adipose tissue in the upper airway and it is more closely related to the pathophysiology of OSA than waist circumference [21, 23, 38].

In our study, the variables that evaluated macroglossia were tongue scalloping, MI and FTP, being the latter two partially dependent on the size of the tongue and related to the presence of moderate/severe OSA. Macroglossia has also been associated with OSA in obese patients in previous studies [31, 40].

The presence of a flaccid palate and the retropalatal narrowing were also associated with the presence of moderate and severe OSA, as stated by Feng et al. who observed a smaller retropalatal space measured on MRI in patients with AHI ≥ 15/h after adjusting for gender, age, BMI, and race [33]. This observation may be due to the fact that the adipose tissue in the upper airway, in addition to depositing and infiltrating tissues such as the tongue, also does so in the parapharyngeal space and the soft palate, causing this accumulation to narrow the retropalatal space [32] favoring, as a result, the collapse of the UA and finally OSA, being such reduction of the retropalatal area an important factor for the development of OSA in obese patients.

Limitations

Most of the participants in this study were women (81.5%), as occurs in other cohorts of patients undergoing bariatric surgery, which might have underestimated the real prevalence of moderate and severe OSA in the morbidly obese population, since men suffer from the disease more frequently and severely.

The sleep test performed in all cases was the CRP and not the polysomnography. The CRP test may underestimate the severity of OSA and desaturations by not taking into account actual sleep time but rather recording time.

Only the AHI was used to establish the diagnosis of OSA without considering clinical or other sleep testing criteria, as has been done in the majority of previous studies in the literature to facilitate comparison with other works.

It should be taken into account that the exploration of the UA is subjective and poorly quantifiable. In addition, examination in an awake patient does not allow evaluating parameters beyond anatomy, therefore this work does not analyze how these elements behave during sleep causing the collapse of the UA [41].

Other confounding factors that could be related to the development of OSA in obese patients, such as genetic [40], hormonal, neuromuscular factors [26, 40, 42] or the osseous structural variables of the UA, were not evaluated.

Conclusion

The only independent predictor of moderate or severe OSA in this study was age over 48 years, although this group of patients presented a higher deposit of fat in the neck, tongue, and soft palate, coinciding with previous studies. It is to presume that the anatomical factor is not the only one involved in the development of OSA in patients with morbid obesity and that other characteristics such as neuromuscular, hormonal or genetic factors are probably related and have not been analyzed in the present study. Therefore, with the current knowledge, we believe that there is no reliable predictive factor for diagnosing OSA in patients who are candidates for bariatric surgery, maintaining the sleep study essential for its diagnosis.

Electronic Supplementary Material

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Supplementary Material 1 (101.7KB, docx)

Funding

This research did not receive any specific grant from any funding agency in the public, commercial or not-for-profit sector.

Declarations

Conflict of Interest

The authors have no conflicts of interest to declare.

Footnotes

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References

  • 1.Benjafield AV, Ayas NT, Eastwood PR, Heinzer R, Ip MSM, Morrell MJ et al (2019) Estimation of the global prevalence and burden of obstructive sleep apnoea: a literature-based analysis. Lancet Respir Med 7:687–698. 10.1016/S2213-2600(19)30198-5 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 2.Salzano G, Maglitto F, Bisogno A, Vaira LA, De Riu G, Cavaliere M et al (2021) Obstructive sleep apnoea/hypopnoea syndrome: relationship with obesity and management in obese patients. Acta Otorhinolaryngol Ital 41:120–130. 10.14639/0392-100X-N1100 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 3.Ravesloot MJL, Hilgevoord AAJ, van Wagensveld BA, de Vries N (2014) Assessment of the Effect of bariatric surgery on obstructive sleep apnea at two postoperative intervals. Obes Surg 24:22–31. 10.1007/s11695-013-1023-y [DOI] [PubMed] [Google Scholar]
  • 4.Rao AD, Beng HT, Ramalingam G, Poh AGH (2009) Obstructive sleep apnoea (OSA) patterns in bariatric surgical practice and response of OSA to weight loss after laparoscopic adjustable gastric banding (LAGB). Ann Acad Med Singap 38:587–593. https://pubmed.ncbi.nlm.nih.gov/19652849/ [PubMed] [Google Scholar]
  • 5.Madkikar N, Pandey S, Ghaisas V (2019) Multi Level single stage: Barbed Reposition Pharyngoplasty and nasal surgery in treatment of OSA—Our experience. Indian J Otolaryngol Head Neck Surg 71:309–314. 10.1007/s12070-019-01694-y [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 6.Romero-Corral A, Caples SM, Lopez-Jimenez F, Somers VK (2010) Interactions between obesity and obstructive sleep apnea: implications for treatment. Chest 137(3):711–719. 10.1378/chest.09-0360 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 7.Enriori PJ, Evans AE, Sinnayah P, Cowley MA (2006) Leptin resistance and obesity. Obes (Silver Spring) 14(Suppl 5):254–258. 10.1038/oby.2006.319 [DOI] [PubMed] [Google Scholar]
  • 8.Ong CW, O’Driscoll DM, Truby H, Naughton MT, Hamilton GS (2013) The reciprocal interaction between obesity and obstructive sleep apnoea. Sleep Med Rev 17:123–131. 10.1016/j.smrv.2012.05.002 [DOI] [PubMed] [Google Scholar]
  • 9.Imayama I, Prasad B (2017) Role of leptin in obstructive sleep apnea. Ann Am Thorac Soc 14:1607–1621. 10.1513/AnnalsATS.201702-181FR [DOI] [PubMed] [Google Scholar]
  • 10.Schwab RJ, Gupta KB, Gefter WB, Metzger LJ, Hoffman EA, Pack AI (1995) Upper Airway and Soft tissue anatomy in normal subjects and patients with sleep-disordered breathing. Am J Respir Crit Care Med 152:1673–1689. 10.1164/ajrccm.152.5.7582313 [DOI] [PubMed] [Google Scholar]
  • 11.Wang SH, Keenan BT, Wiemken A, Zang Y, Staley B, Sarwer DB et al (2020) Effect of weight loss on upper airway anatomy and the apnea–hypopnea index the importance of tongue fat. Am J Respir Crit Care Med 201:718–727. 10.1164/rccm.201903-0692OC [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 12.Schwartz AR, Patil SP, Squier S, Schneider H, Kirkness JP, Smith PL (2010) Obesity and upper airway control during sleep. J Appl Physiol 108:430–435. 10.1152/japplphysiol.00919.2009 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 13.Johns MW (1991) A new method for measuring daytime sleepiness: the Epworth sleepiness scale. Sleep 14:540–545. 10.1093/sleep/14.6.540 [DOI] [PubMed] [Google Scholar]
  • 14.Chung F, Subramanyam R, Liao P, Sasaki E, Shapiro C, Sun Y (2012) High STOP-Bang score indicates a high probability of obstructive sleep apnoea. Br J Anaesth 108:768–775. 10.1093/bja/aes022 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 15.Mallampati SR, Gatt SP, Gugino LD, Desai SP, Waraksa B, Freiberger D et al (1985) A clinical sign to predict difficult tracheal intubation; a prospective study. Can Anaesth Soc J 32:429–434. 10.1007/BF03011357 [DOI] [PubMed] [Google Scholar]
  • 16.Friedman M, Ibrahim H, Bass L (2002) Clinical staging for sleep-disordered breathing. Otolaryngol Head Neck Surg 127:13–21. 10.1067/mhn.2002.12 [DOI] [PubMed] [Google Scholar]
  • 17.Lu X, Zhang J, Xiao S (2018) Correlation between Brodsky Tonsil Scale and Tonsil volume in adult patients. Biomed Res Int 6434872. 10.1155/2018/6434872 [DOI] [PMC free article] [PubMed]
  • 18.Friedman M, Yalamanchali S, Gorelick G, Joseph NJ, Hwang MS (2015) A standardized lingual tonsil grading system: Interexaminer agreement. Otolaryngol - Head Neck Surg (United States) 152:667–672. 10.1177/0194599815568970 [DOI] [PubMed] [Google Scholar]
  • 19.Carneiro G, Flório RTB, Zanella MT, Pradella-Hallinan M, Ribeiro-Filho FF, Tufik S et al (2012) Is mandatory screening for obstructive sleep apnea with polysomnography in all severely obese patients indicated? Sleep Breath 16:163–168. 10.1007/s11325-010-0468-7 [DOI] [PubMed] [Google Scholar]
  • 20.Dixon JB, Schachter LM, O’Brien PE (2003) Predicting sleep apnea and excessive day sleepiness in the severely obese: indicators for polysomnography. Chest 123:1134–1141. 10.1378/chest.123.4.1134 [DOI] [PubMed] [Google Scholar]
  • 21.Duarte RLM, Magalhães-da-Silveira FJ, Gozal D (2022) Predictive factors for obstructive sleep apnea diagnosis in bariatric surgery candidates with or without chronic Insomnia complaints. Obes Surg 32(1):33–41. 10.1007/s11695-021-05748-5 [DOI] [PubMed] [Google Scholar]
  • 22.Khan A, King WC, Patterson EJ, Laut J, Raum W, Courcoulas AP et al (2013) Assessment of obstructive sleep apnea in adults undergoing bariatric surgery in the longitudinal assessment of bariatric surgery-2 (LABS-2) study. J Clin Sleep Med 9:21–29. 10.5664/jcsm.2332 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 23.Lee YH, Johan A, Wong KKH, Edwards N, Sullivan C (2009) Prevalence and risk factors for obstructive sleep apnea in a multiethnic population of patients presenting for bariatric surgery in Singapore. Sleep Med 10:226–232. 10.1016/j.sleep.2008.01.005 [DOI] [PubMed] [Google Scholar]
  • 24.Gharibeh T, Mehra R (2010) Obstructive sleep apnea syndrome: natural history, diagnosis, and emerging treatment options. Nat Sci Sleep 2:233–255. 10.2147/NSS.S6844 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 25.Young T, Peppard PE, Gottlieb DJ (2002) Epidemiology of obstructive sleep apnea: a population health perspective. Am J Respir Crit Care Med 165:1217–1239 [DOI] [PubMed] [Google Scholar]
  • 26.Carneiro G, Zanella MT (2018) Obesity metabolic and hormonal disorders associated with obstructive sleep apnea and their impact on the risk of cardiovascular events. Metabolism 84:76–84. 10.1164/rccm.2109080 [DOI] [PubMed] [Google Scholar]
  • 27.Glazer SA, Erickson AL, Crosby RD, Kieda J, Zawisza ADM The evaluation of screening questionnaires for obstructive sleep apnea to identify high-risk obese patients undergoing bariatric surgery. Obes Surg 28:3544–3552. 10.1007/s11695-018-3391-9 [DOI] [PubMed]
  • 28.Horvath CM, Jossen J, Kröll D, Nett PC, Baty F, Brill AK et al (2018) Prevalence and prediction of Obstructive Sleep Apnea prior to bariatric surgery—gender-specific performance of four sleep questionnaires. Obes Surg 28:2720–2726. 10.1007/s11695-018-3222-z [DOI] [PubMed] [Google Scholar]
  • 29.Chung F, Yang Y, Liao P (2013) Predictive performance of the stop-bang score for identifying obstructive sleep apnea in obese patients. Obes Surg 23:2050–2057. 10.1007/s11695-013-1006-z [DOI] [PubMed] [Google Scholar]
  • 30.KavithaGiri NL, Mani MS, Ahamed SYSG (2021) Evaluation of central obesity, increased body Mass Index, and its relation to Oropharyngeal Airway Space using lateral Cephalogram in Risk Prediction of Obstructive Sleep Apnea. J Pharm Bioallied Sci 13:S549–S554. 10.4103/jpbs.JPBS_566_20 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 31.Kim AM, Keenan BT, Jackson N, Chan EL, Staley B, Poptani H et al (2014) Tongue fat and its relationship to obstructive sleep apnea. Sleep. ;37:1639-1648D. https://academic.oup.com/sleep/article/37/10/1639/2416812 [DOI] [PMC free article] [PubMed]
  • 32.Ciscar MA, Juan G, Martínez V, Ramón M, Lloret T, Mínguez J et al (2001) Magnetic resonance imaging of the pharynx in OSA patients and healthy subjects. Eur Respir J 17:79–86. 10.1183/09031936.01.17100790 [DOI] [PubMed] [Google Scholar]
  • 33.Feng Y, Keenan BT, Wang S, Leinwand S, Wiemken A, Pack AI et al (2018) Dynamic upper airway imaging during wakefulness in obese subjects with and without sleep apnea. Am J Respir Crit Care Med 198:1435–1443. 10.1164/rccm.201711-2171OC [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 34.Santiago-Recuerda A, Gómez-Terreros FJ, Caballero P, Martín-Duce A, Soleto MJ, Vesperinas G et al (2007) Relationship between the upper airway and obstructive sleep apnea-hypopnea syndrome in morbidly obese women. Obes Surg 17:689–697. 10.1007/s11695-007-9120-4 [DOI] [PubMed] [Google Scholar]
  • 35.Lahav Y, Adi M, Arberboy E, Halperin D, Shoffel-Havakuk H, Cohen O (2021) Relations between body mass index, laryngeal fat pads, and laryngeal airway configuration in adult men population. Int J Obes 45:288–295. 10.1038/s41366-020-0631-6 [DOI] [PubMed] [Google Scholar]
  • 36.Schäfer H, Pauleit D, Sudhop T, Gouni-Berthold I, Ewig S, Berthold HK (2002) Body fat distribution, serum leptin, and cardiovascular risk factors in men with obstructive sleep apnea. Chest 122:829–839. 10.1378/chest.122.3.829 [DOI] [PubMed] [Google Scholar]
  • 37.Kositanurit W, Muntham D, Udomsawaengsup S, Chirakalwasan N (2018) Prevalence and associated factors of obstructive sleep apnea in morbidly obese patients undergoing bariatric surgery. Sleep Breath 22:251–256. 10.1007/s11325-017-1500-y [DOI] [PubMed] [Google Scholar]
  • 38.Liu Y, Zou J, Qian Y, Xu H, Zhu H, Meng L et al (2021) The association between obesity indices and obstructive sleep apnea is modified by age in a sex-specific manner. Sleep Breath 25:189–197. 10.1007/s11325-020-02083-4 [DOI] [PubMed] [Google Scholar]
  • 39.Martinez-Rivera C, Abad J, Fiz JA, Rios J, Morera J (2008) Usefulness of truncal obesity indices as predictive factors for obstructive sleep apnea syndrome. Obesity 16:113–118. 10.1038/oby.2007.20 [DOI] [PubMed] [Google Scholar]
  • 40.De Sousa AGP, Cercato C, Mancini MC, Halpern A (2008) Obesity and obstructive sleep apnea-hypopnea syndrome. Obes Rev 9:340–354. 10.1111/j.1467-789X.2008.00478.x [DOI] [PubMed] [Google Scholar]
  • 41.Certal VF, Pratas R, Guimarães L, Lugo R, Tsou Y, Camacho M et al (2016) Awake examination versus DISE for surgical decision making in patients with OSA: a systematic review. Laryngoscope 126:768–774. 10.1002/lary.25722 [DOI] [PubMed] [Google Scholar]
  • 42.Berger S, Polotsky VY (2018) Leptin and leptin resistance in the pathogenesis of obstructive sleep apnea: a possible link to oxidative stress and cardiovascular complications. Oxid Med Cell Longev 2018. 10.1155/2018/5137947 [DOI] [PMC free article] [PubMed]

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