Year : 2012 | Volume
: 7 | Issue : 1 | Page : 26--30
A comparative study on the clinical and polysomnographic pattern of obstructive sleep apnea among obese and non-obese subjects
Rajiv Garg, Abhijeet Singh, Rajendra Prasad, S Saheer, P Jabeed, Ramkishun Verma
Department of Pulmonary Medicine, CSM Medical University, UP, Lucknow, India
Department of Pulmonary Medicine, CSM Medical University, Lucknow - 226 003, UP
Objective: This study was designed to compare the pattern of obstructive sleep apnea (OSA) among obese and nonobese subjects regarding clinical and polysomnographic data obtained for a polysomnographic study.
Methods: A cross-sectional retrospective descriptive study was conducted by analyzing polysomnographic data in 112 consecutive patients underwent a sleep study at our sleep laboratory from January 2009 to July 2010. Out of them, 81 were diagnosed to have OSA (apnea-hypopnoea Index ≥5). These patients were classified in two groups with body mass index (BMI) < 27.5 kg/m 2 as nonobese and BMI≥27.5 kg/m 2 as obese. Clinical as well as polysomnographic data were evaluated and compared between the two groups. Patients were also evaluated for other risk factors such as smoking, alcoholism, and use of sedatives. Data were subjected to statistical analysis (χ2 -test, P value <0.05 considered to be significant). The Fisher Exact test was applied wherever the expected frequency for a variable was ≤5.
Results: Of 81 patients with OSA, 36 (44.4%) were nonobese with a mean BMI of 26.62 ± 2.29 kg/m 2 and 45 (55.6%) were obese with a mean BMI of 35.14 ± 3.74 kg/m 2 . Mean AHI per hour was significantly more in the obese than in the nonobese group (50.09 ± 29.49 vs. 24.36 ± 12.17, P<0.001). The use of one or more sedatives was more in nonobese as compared to obese (58.3% vs. 24.4%, P=0.002). The obese group had significantly higher desaturation and arousal index (P<</i>0.001). The minimal oxygen saturation was lower in the obese than the nonobese group (68.5 ± 13.00 vs. 80.3 ± 7.40, P<</i>0.001) and was well below 90% in both groups. Overall, the OSA in nonobese patients was mild-to-moderate as compared to that of the obese and no significant differences were observed between them as regard to age, gender, mean neck circumference, excessive daytime sleepiness, adenoid or tonsillar enlargement, smoking, and remaining polysomnographic parameters.
Conclusion: Obstructive sleep apnea can occur in nonobese persons though with less severity as compared to obese leading to a concept that OSA is not restricted to obese persons only and there is a high demand of its awareness regarding evaluation, diagnosis, and management in such individuals.
|How to cite this article:|
Garg R, Singh A, Prasad R, Saheer S, Jabeed P, Verma R. A comparative study on the clinical and polysomnographic pattern of obstructive sleep apnea among obese and non-obese subjects.Ann Thorac Med 2012;7:26-30
|How to cite this URL:|
Garg R, Singh A, Prasad R, Saheer S, Jabeed P, Verma R. A comparative study on the clinical and polysomnographic pattern of obstructive sleep apnea among obese and non-obese subjects. Ann Thorac Med [serial online] 2012 [cited 2020 May 26 ];7:26-30
Available from: http://www.thoracicmedicine.org/text.asp?2012/7/1/26/91561
Obstructive sleep apnea (OSA) is a disease that is characterized by disruptive snoring, repeated episodes of complete or partial pharyngeal obstruction during sleep resulting in nocturnal hypoxemia, frequent arousals during sleep, and excessive daytime sleepiness (EDS).  It is a serious and potentially life-threatening disorder that is far more common than generally believed. Several risk factors, including obesity, male sex, age, and heritable factors, have been associated with an increased prevalence of obstructive sleep apnea in the general population. Obesity has been considered to be one of the classical risk factor for OSA.  It has become a major health problem worldwide with an increasing prevalence and associated with high comorbidities such as diabetes mellitus, hypertension, cardiovascular disease, dyslipidemia, malignancies, and overall mortality. Results of various studies indicate that approximately 60-70% of patients with OSA are obese. ,,,,,,,,,,,,, The data regarding association of OSA among nonobese patients is scarce and needs great effort as fewer studies have reported magnitude of association. , The occurrence of OSA in nonobese patients may exhibit different characteristics than obese patients with OSA. Therefore, this study was designed to study the pattern of OSA among nonobese Indian subjects coming for the polysomnographic study.
This cross-sectional retrospective study was done by reviewing data from 81 OSA patients consecutively referred to the sleep laboratory of Department of Pulmonary Medicine, Chhatrapati Shahuji Maharaj Medical University, Lucknow, between August 2009 and July 2010. This study was conducted after approval by the local research ethics committee. OSA was diagnosed if there was apnea hypopnoea index (AHI)>5 events/h combined with habitual snoring or EDS. The patients were classified into nonobese (n=36) and obese (n=45) groups if their body mass index (BMI) was <27.5 and ≥27.5 kg/m 2 , respectively, as per the WHO criteria of obesity for Asians.  Clinical and polysomnographic data were evaluated and compared between the two groups. Clinical evaluation was done with the help of sleep questionnaire by recording age, sex, co-morbid illnesses, EDS by Epworth sleepiness scale (ESS), and anthropometric measurements (BMI, neck circumference, thyromental distance, and Mallampati's score). Patients were also evaluated for other risk factors such as smoking, alcohol, and the use of sedative or tranquilizers. Neck circumference was measured with a tape measure at the level of cricothyroid membrane. Thyromental distance was measured horizontally from the thyroid prominence to a perpendicular dropped from the soft tissue mentum. Mallampati's score was measured with mouth wide open, tongue maximally protruded without phonation, and classified into Grades I-IV. However, subjects having age >80 years, tuberculosis, chronic obstructive pulmonary disease (COPD), pregnancy, uncontrolled congestive heart failure (CHF), chronic renal failure (CRF), and neurological disorders were excluded from the study.
All patients with OSA underwent a sleep study consisting of an overnight polysomnographic examination, which included an EEG (C3-A2, C4-A1, O2-A1, and O3-A2), bilateral electrooculogram, chin and lower leg electromyogram, nasal and mouth airflow, thoracic and abdominal respiratory movements, ECG, oxygen saturation measured by finger oximetry, and body position. For this study, S-7000 computerized polysomnography machine (manufactured in the year 2007 by Cogent Technologies EMBLA System Inc., UK) with 20 channel inputs was used. Sleep staging was done with the help of Somnologica Studio software and classified into Awake, nonrapid eye movement (NREM) sleep with Stages I, II, III and IV, and rapid eye movement (REM) sleep. The episodes of apnea were defined as complete cessation of airflow for ≥10 s, and hypopnea consisted of a ≥50% reduction in oronasal airflow accompanied by a reduction in oxygen saturation measured by pulse oximetry of at least 4%. Apnea events were classified as obstructive, mixed, or central, according to the presence or absence of breathing efforts with thoracoabdominal paradox. AHI was determined by the frequency of these events per hour during sleep time based on the results of the overnight polysomnography. Polysomnographic data, including respiratory arousal index, minimal oxygen saturation, total sleep time, and desaturation index, were also collected. Sleep data recorded by the computer was cross checked manually for scoring of sleep stages apneas and hypopnoeas regarding each subject.
Numerical and categorical data were compared between groups using the Student t-test and χ2 -test as appropriate. All statistical analyses were performed using statistical software SPSS version 10.0 (SPSS Inc, Chicago, USA). A P value of <0.05 was considered significant.
There were 81 patients of OSA, among them 36 (44.4%) were non-obese and 45 (55.6%) were obese with a mean BMI of 26.62 ± 2.29 and 35.14 ± 3.74 kg/m 2 , respectively. No significant difference was found in mean age, gender, mean neck circumference, Mallampati grading, ESS, adenoid or tonsillar enlargement, smoking, and other co-morbid conditions. More patients with smoking, alcohol use, snoring, diabetes, and hypertension were found in the obese group [Table 1]. The hypertension was significantly higher in the obese (57.8% vs. 33.3%, P=0.03) than the non-obese patients. The use of sedatives was more common in the non-obese patients than the obese patients (58.3% vs. 24.4%, P=0.002). The nonobese group were also having significantly shorter thyromental distance than the obese group (48.41 ± 10.61 mm vs. 60.54 ± 12.24 mm, P<0.001). Mean AHI was significantly less in the non-obese than in the obese (24.36 ± 12.17/h vs. 50.09 ± 29.49/h, P<0.001). Most of the non-obese patients were having mild-to-moderate severity OSA, as 26 (72.2%) of them were having AHI≤30/h as compared to only 14 (31.1%) obese patients. The obese group had a significance with regard to lower minimal oxygen saturation (68.47 ± 13.00 vs. 80.25 ± 7.40, P<0.001), higher average desaturation index (48.32 ± 13.08 vs. 30.63 ± 15.63, P<0.001), and higher arousal index (28.42 ± 4.99 mm vs. 17.84 ± 5.07 mm, P<0.001). Although there were more number of obese patients than nonobese (25/45 vs. 14/36) having minimum oxygen saturation <90%, but the percentage of nonobese patients showing similar findings were not less (55.6 vs. 38.9, P=0.37). Rest of the polysomnographic parameters were comparable. The data are summarized in [Table 2].
Obese patients with OSA have been observed to show significant severity than the nonobese OSA patients in terms of various parameters such as AHI, average as well as minimal oxygen saturation, arousal and desaturation indices. ,,,, The present study has also shown similar findings and strikingly the minimal oxygen saturation was well below 90% in both the groups. The etiology of OSA in obese has been linked with anatomic alterations that predisposes to upper airway obstruction during sleep. Obesity seems to have two distinct mechanical influences on the pharyngeal airway collapsibility.  First, it increases soft tissue surrounding the pharyngeal airway within limited maxillo-mandibular closure occupying and narrowing its space (pharyngeal anatomical imbalance). It can be considered that elevations in neck circumference and increased deposition of peripharyngeal fat could narrow and compress the upper airway. , Furthermore, increased peripharyngeal fat has been correlated with increased sleep apnea severity. , Second, it increases visceral fat volume that decreases lung volumes such as functional residual capacity (FRC) and expiratory reserve volume (ERV) leading to increased pharyngeal wall collapsibility possibly through decreased longitudinal tracheal retraction. Thus, obesity imposes mechanical loads on both the upper airway and respiratory system that predispose to upper airway narrowing, collapse, and airflow obstruction during sleep. Neural compensation for functioning structural abnormalities operating during wakefulness is also lost during sleep. These effects may be mediated by circulating adipokines, which influence body fat distribution and central nervous system activity. 
In contrast, Sakakibara et al. observed that the etiology of OSA in nonobese patients appears to be somewhat different which includes bony structure discrepancies.  In accordance with this study, we observed shorter thyromental distance in the nonobese patients which signifies that the position of the chin is relatively low with reference to the thyroid cartilage and shorter length of the anterior cranial base.  A retrospective study from Thailand also reported similar findings in 71 nonobese patients.  Nonobese OSA patients tend to present the following anatomical craniofacial characteristics such as caudal hyoid, increased soft palate dimensions, and consequent anteroposterior reductions of the airways at the soft palate level, reduction of anteroposterior region of nasopharynx, and oral pharynx. Obese OSA patients can present with these findings but in addition they have increased volume of tongue and anterior hyoid bone. Lower and anterior position of hyoid bone in obese patients seems to be related to increased fat deposition on the tongue, which increases its volume.  It has been suggested that the discrepancy in these cephalometric measurements may also depend on sex, age, and race. ,,,, OSA in Asian men has been found more frequently in the nonobese patients, despite the presence of severe illness, when compared with white male patients with OSAS. 
The present nonobese subjects were more likely in habit of taking sedatives for sleeping as compared to obese counterpart which is in concordance with study conducted by Ghanem and Mahmood on 102 patients with OSA.  The incidence of hypertension was observed to be more in the obese OSA patients than the non-obese patients. This finding has been supported by several cross-sectional, longitudinal, and treatment studies. ,,,, Obesity and OSA are each very strongly associated with hypertension.  OSA is independently associated with hypertension, independent of obesity. Furthermore, obesity and OSA often co-exist and, in fact, one may be conducive to the other. It is therefore plausible that at least part of the association between obesity and hypertension is related to the presence of OSA and perhaps vice versa. The presence of OSA in the obese patients may further contribute to adverse cardiovascular outcomes including hypertension when compared with each condition in isolation.  OSA probably contributes to or exacerbates the obesity-related hypertension. OSA should be strongly suspected in obese individuals with resistant hypertension, those with the absence of a nocturnal decrease in blood pressure, those with unexplained weight gain or difficulty losing weight, and in those with symptoms suggestive of OSA. The diagnosis of OSA in this context is therefore of considerable clinical importance.
There are some potential limitations to this study. One limitation of the study was that we have considered parameters such asthyromental distance and Mallampati grading for cephalometric analysis as they are easy and cheap to perform in clinical practice and can correlate with severity of OSA. There are multiple imaging techniques to evaluate the upper airway in patients with OSA such as cephalometric radiography, CT, MRI, fluoroscopy, and somnofluoroscopy but these methods are cumbersome and expensive. Cephalometry is a diagnostic procedure to collect information on skeleton abnormalities and soft tissues of patients with OSA, providing support for indication of surgery. This should be based on disease severity and the presence of anatomical alterations of upper airway and of craniofacial skeleton. Another limitation is that the findings of this study need to be confirmed in a large number of samples.
It can be concluded that obstructive sleep apnea is not uncommon in the nonobese persons contrary to earlier concept that OSA is confined to the obese persons. Therefore, whenever a nonobese patient presents with a clinical picture suggestive of OSA, the diagnostic possibility should not be underestimated and should be evaluated thoroughly.
The authors are grateful to all the patients for their co-operation and to Mr. Ravi Verma for his technical help.
|1||Mc Nicholas WT. Diagnostic criteria for the sleep apnoea syndrome: Time for consensus. Eur Respir J 1996;9:634-5.|
|2||Dixon JB, Schacter LM, O'Brien PE. Predicting sleep apnea and excessive daytime sleepiness in the severely obese. Chest 2003;123:1134-41.|
|3||Gislason T, Almqvist M, Eriksson G, Taube A, Boman G. Prevalence of sleep apnea syndrome among Swedish men: An epidemiological study. J Clin Epidemiol 1988;41:571-6.|
|4||Young T, Palta M, Dempsey J, Skaturd J, Weber S, Badr S. The occurrence of sleep-disordered breathing among middle-aged adults. N Engl J Med 1993;328:1230-5.|
|5||Bearpark H, Elliott L, Grunstein R, Cullen S, Schneider H, Althaus W, et al. Snoring and sleep apnea: A population study in Australian men. Am J Respir Crit Care Med 1995;151:1459-65.|
|6||Olson LG, King MT, Hensley MJ, Saunders NA. A community study of snoring and sleep-disordered breathing: Prevalence. Am J Respir Crit Care Med 1995;152:711-6.|
|7||Stradling JR, Crosby JH. Predictors and prevalence of obstructive sleep apnea and snoring in 1001 middle-aged men. Thorax 1997;46:85-90.|
|8||Bixler EO, Vgontzas AN, Lin HM, Ten Have T, Rein J, Vela-Bueno A, et al. Prevalence of sleep disordered breathing in women: Effects of gender. Am J Respir Crit Care Med 2001;163:608-13.|
|9||Duran J, Esnaola S, Rubio R, Iztueta A. Obstructive sleep apnea and related clinical features in a population-based sample of subjects aged 30-70 years. Am J Respir Crit Care Med 2001;163:685-9.|
|10||Ancoli-Israel S, Kripke D, Klaube MR, Mason WJ, Fell R, Kaplan O. Sleep disordered breathing in community dwelling elderly. Sleep 1991;14:486-95.|
|11||Lindberg E, Taube A, Janson C, Gislason T, Svardsudd K, Boman G. A 10-year follow-up of snoring in men. Chest 1998;114:1048-55.|
|12||Ip M, Lam B, Lauder IJ, Tang LC, Ip TY, Lam WK. A community study of sleep disordered breathing in middle aged Chinese men in Hong Kong. Chest 2001;119:62-9|
|13||Young T, Peppard PE, Gottlieb DJ. Epidemiology of obstructive sleep apnea: A population health perspective. AmJ Respir Crit Care Med 2002;165:1217-39.|
|14||Kim J, In K, You S, Kang K, Shim J, Lee S. Prevalence of sleep-disordered breathing in middle-aged Korean men and women. Am J Respir Crit Care Med 2004;170:1108-13.|
|15||Udwadia ZF, Doshi AV, Lonkar SG, Singh CI. Prevalence of sleep-disordered breathing and sleep apnea in middle-aged urban Indian men. Am J Respir Crit Care Med 2004;169:168-73.|
|16||Sharma SK, Kumpawat S, Banga A, Goel A. Prevalence and risk factors of obstructive sleep apnea syndrome in a population of Delhi, India. Chest 2006;130:149-56.|
|17||Sakakibara H, Tong M, Matsushita K, Hirata M, Konishi Y, Suetsugu S. Cephalometric abnormalities in non-obese and obese patients with obstructive sleep apnoea. Eur Respir J 1999;13:403-10.|
|18||Chierakul N, Chaipattarapol C, Ruttanaumpawan P, Nana A, Naruman C, Tangchityongsiva S. Comparison of clinical and polysomnographic characteristics of non-obese and obese patients with obstructive sleep apnea. J Med Assoc Thai 2007;90:48-53.|
|19||Nishida C. Appropriate body mass index for Asian populations and its implications for policy and intervention strategies. Lancet 2004;363:157-63.|
|20||Sakakibara H, Tong M, Matsushita K, Hirata M, Konishi Y, Suetsugu S. Cephalometric abnormalities in non-obese and obese patients with obstructive sleep apnoea. Eur Respir J 1999;13:403-10.|
|21||Ghanem A, Mahmood S. Is obstructive sleep apnoea in non-obese patients a less serious disease than in obese patients? Chest 2005;128:231s-a.|
|22||Davies RJ, Stradling JR. The relationship between neck circumference, radiographic pharyngealanatomy, and the obstructive sleep apnoea syndrome. Eur Respir J 1990;3:509-14.|
|23||Deegan PC, McNicholas WT. Predictive value of clinical features for the obstructive sleep apnoea syndrome. Eur Respir J 1996;9:117-24.|
|24||Sergi M, Rizzi M, Comi AL, Resta O, Palma P, De Stefano A, et al. Sleep apnea in moderate-severe obese patients. Sleep Breath 1999;3:47-52.|
|25||Isono S. Obstructive sleep apnoea of obese adults: Pathophysiology and perioperative airway management. Anesthesiology 2009;110:908-21.|
|26||Katz I, Stradling J, Slutsky AS, Zamel N, Hoffstein V. Do patients with obstructive sleep apnea have thick necks? Am Rev Respir Dis1990;141:1228-31.|
|27||Davies RJ, Stradling JR. The relationship between neck circumference, radiographic pharyngeal anatomy, and the obstructive sleep apnoea syndrome. Eur Respir J 1990;3:509-14.|
|28||Schwab RJ, Gupta KB, Gefter WB, Metzger LJ, Hoffman EA, Pack AI. Upper airway and soft tissue anatomy in normal subjects and patients with sleep-disordered breathing: Significance of the lateral pharyngeal walls. Am J Respir Crit Care Med 1995;152:1673-89.|
|29||Shelton KE, Woodson H, Gay S, Suratt PM. Pharyngeal fat in obstructive sleep apnea. Am Rev Respir Dis 1993;148:462-6.|
|30||Zhang HH, Kumar S, Barnett AH, Eggo MC. Dexamethasone inhibits tumor necrosis factor-alpha-induced apoptosis and interleukin-1 beta release in human subcutaneous adipocytes and preadipocytes. J Clin Endocrinol Metab 2001;86:2817-25.|
|31||Tangugsorn V, Krogstad O, Espeland L, Lyberg T. Obstructive sleep apnea: A canonical correlation of cephalometric and selected demographic variables in obese and non-obese patients. Angle Orthod 2001;71:23-35.|
|32||Yu X, Fujimoto K, Urushibata K, Matsuzawa Y, Kubo K. Cephalometric analysis in obese and non-obese patients with obstructive sleep apnea syndrome. Chest 2003;124:212-8.|
|33||Guilleminault C, Quera-Salva MA, Partinen M, Jamieson A. Women and the obstructive sleep apnea syndrome. Chest 1988;93:104-9.|
|34||Maltais F, Carrier G, Ornier Y, Sériès F. Cephalometric measurements in snorers, non-snorers, and patients with sleep apnea. Thorax 1991;46:419-23.|
|35||Ong KC, Clerk AA. Comparison of the severity of sleep disordered breathing in Asian and Caucasian patients seen at a sleep disorders centre. Respir Med 1998;92:843-8.|
|36||Li KK, Powell NP, Kushida C, Riley RW, Adornato B, Guilleminault C. A comparison of Asian and white patients with obstructive sleep apnea syndrome. Laryngoscope 1999;109:1937-40.|
|37||Li KK, Kushida C, Powell NB, Riley RW, Guilleminault C. Obstructive sleep apnea syndrome: A comparison between Far-East Asian and white men. Laryngoscope 2000;110:1689-93.|
|38||Nieto FJ, Young TB, Lind BK, Shahar E, Samet JM, Redline S, et al. Association of sleep-disordered breathing, sleep apnea, and hypertension in a large community-based study: Sleep heart health study. JAMA 2000;283:1829-36.|
|39||Peker Y, Hedner J, Norum J, Kraiczi H, Carlson J. Increased incidence of cardiovascular disease in middle-aged men with obstructive sleep apnea: A 7-year follow-up. Am J Respir Crit Care Med 2002;166:159-65.|
|40||Peppard PE, Young T, Palta M, Skatrud J. Prospective study of the association between sleep-disordered breathing and hypertension. N Engl J Med 2000;342:1378-84.|
|41||Logan AG, Perlikowski SM, Mente A, Tisler A, Tkacova R, Niroumand M, et al. High prevalence of unrecognized sleep apnoea in drug-resistant hypertension. J Hypertens 2001;19:2271-7.|
|42||Ruttanaumpawan P, Nopmaneejumruslers C, Logan AG, Lazarescu A, Qian I, Bradley TD. Association between refractory hypertension and obstructive sleep apnoea. J Hypertens 2009;27:1439-45.|
|43||Wolk R, Shamsuzzaman AS, Somers VK. Obesity, sleep apnoea and hypertension. Hypertension 2003;42:1067-74.|
|44||Ramar K, Caples SM. Cardiovascular consequences of obese and non-obese obstructive sleep apnea. Med Clin North Am 2010;94:465-78.|