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Review Article

Obstructive Sleep Apnea Hypopnea Syndrome – Indian scenario

Year : 2014 | Volume : 1 | Issue : 1

C N Prasad
Department of Pulmonary Medicine,
Prathima Institute of Medical Sciences, Karimnagar, AP.

Address for correspondence : Dr. C N Prasad, Professor, Department of Pulmonary Medicine,Prathima Institute of Medical Sciences, Karimnagar, AP.



Obstructive sleep apnea syndrome is far more common than generally believed. The Indian population where obesity rates are also increasing also has a very large population with undiagnosed OSAHS. The association of OSAHS with cardiovascular abnormalities further complicates the disease. Understanding the pathophysiology of OSA in obese and non-obese persons helps in evaluation, diagnosis and management in the individual group. With wider availability of PSG tests and newer treatment modalities, diagnosis and management of OSAHS has become easier. Increasing awareness regarding OSA and OSAHS among the general population and clinicians, wider availability of PSG studies and decreasing the costs of diagnostic tests and treatment can go a long way in identifying and treating these patients.

Key words:  Obstructive sleep apnea hypopnea syndrome, Obstructive sleep apnea, Polysomnography, Obese.


Obstructive sleep apnea hypopnea syndrome (OSAHS) is a disease characterized by snoring, disrupting the sleep, repeated episodes of complete or partial pharyngeal obstruction during sleep resulting in nocturnal hypoxemia, frequent arousals leading to cardiac abnormalities and excessive daytime sleepiness1. OSAHS is a far more prevalent disease than generally believed. The global prevalence varies from 0.3 % to 5.1% in general population.2 In Indian studies obstructive sleep apnea (OSA) varied from 4.4% to 13.7% and OSAHS varied from 2.4% to 2.8%3.OSA in Indian males varied from 4.4 % to 19.7% and in females it was between 2.5% to 7.4% from various studies. OSAHS was observed in males from 2.4% to 7.5% and in females it was 1% to 2.1%3. The new classification of OSA given by the American Association of Sleep Medicine is 4

  1. Obstructive and central sleep apnea syndromes.
  2. Sleep related hyperventilation/hypoxic syndromes due to congenital, idiopathic or medical conditions and
  3. Other unspecified sleep related breathing disorders

OSA: Five or more apneas per hour of sleep, each apnea being ≥ 10 seconds duration.5

OSAHS: OSA with daytime sleepiness is called as OSAHS.

Hypopnea: 50 % reduction in flow with 4% decrement in oxygen saturation.6

Respiratory related arousals (RERA): Detectable changes in EEG are for more than 3 seconds. This term also includes microarousals.7,8


The gold standard test for OSAHS is overnight in laboratory multichannel Polysomnography (PSG).2,9 This test includes surface leads for Electroencephalography (EEG), Electrooculography (EOG), Electromyography (EMG), Electrocardiography (ECG), nasal pressure transducer (or a thermistor) for detection of nasal airflow, thoracic and abdominal impedance belts for respiratory effort, Pulse oximetry, tracheal microphone for snoring and sensors for leg and body positions.

Factors leading to obstructive sleep apnea include10
  1. A compromised often completely closed extrathoracic upper airway (obstructive event).
  2. Marked reduction or cessation of brain stem respiratory center motor output (central event)
  3. A combination of obstruction and central events

These events produce intermittent hypoxemias leading to arousals from sleep, sleep fragmentation and further causing over compensatory responses of autonomic nervous system. The common sites of obstruction are retropalatal, retropharyngeal and hyypopharyngeal areas. Bony abnormalities like reduced mandibular body length, inferiorly positioned hyoid bone, retroposition of maxilla, increased vertical length of the upper airway 10 can lead to OSA. An enlarged soft palate and tongue would reduce the anteroposterior diameter where as enlarged pharyngeal walls reduces the lateral plane.

Obesity and OSA: Obesity indirectly contributes to upper airway narrowing during sleep because the lung volumes are markedly reduced by increased abdominal fat mass and decreased lung volumes in recumbent position. Obesity also gives rise to fat free muscle tissue. Leptin, an adipocyte derived factor affecting respiratory stimulant action and abnormalities in leptin signalling pathway can affect the respiratory pattern.11,12 Many adipose tissue released inflammatory mediators like TNF-α, IL-6 are elevated in OSA and decreases with treatment with continuous positive airway pressure(CPAP).13,14 The disease is also more common in supine position 15, REM sleep, alcohol intake or sedative usage at bed time. 16 Pregnant females also have a high snoring percentage, which was 13.5% in an Indian study conducted in pregnant females, also showed a high sleep disordered breathing (SDB) of 9.5%.17 Incidence of preeclampsia, meconium stained liquor, lower appearance, pulse rate, reflexes, activity, respiratory rate (APGAR) score, lower birth weight was observed in third trimester females on follow up in New Delhi. Abnormal lung function tests (spirometry) are also common in OSA patients. Decrease in (FVC), FEV1/FVC, ratio of forced expiratory volume in first second and forced vital capacity, forced expiratory flow (FEF) 25-75%, PIFR and a ratio of the peak inspiratory flow rate and peak expiratory flow rate PIFR/PEFR ≥ 1was observed in 92% of Indian OSA patients. A negative correlation was observed in daytime arterial PaO2 and respiratory distress index (RDI), and arousal index.18 The effects of OSA include systemic hypertension, pulmonary arterial hypertension, hypercapnea, coronary artery disease, cardiac arrhythmias. Daytime systemic hypertension as a consequence of severe OSA can be explained by enhanced chemoreceptor sensitivity causing excessive sympathetic vasoconstrictor activity on vessels.10 Risk Factors: Obesity, male sex, age, heritable factors, craniofacial anatomic predisposition are the risk factors. Approximately 60-70% of OSA are obese. The occurrence of OSA in non obese exhibits different characteristics. In Indian children Adenoids and tonsillar enlargement (72%) were the causes for snoring, whereas disproportionate upper airway anatomy at multiple levels like long thick soft palate (62%), long and edematous uvula (62.8%), webbing of tonsillar pillars (40%) were the causes.19 Incidence of OSA increases with age from 2% at age 30 for females to 28% at 60 years and from 4% at age 30 to 67% at 60 years of age for males.12 Elderly meconium stained liquor, lower appearance, pulse rate, reflexes, activity, respiratory rate (APGAR) score, lower birth weight was observed third trimester females on follow up in New Delhi. Abnormal lung function tests (spirometry) are also common in OSA patients. Decrease in (FVC), FEV1/FVC, ratio of forced expiratory volume in first second and forced vital capacity, also have high snoring and high excessive daytime sleepiness (EDS), with 27% being habitual snorers.20 The prevalence of obesity is increasing in Asians.21 The increase in prevalence from 2.3% to 19.6% occurred over a period of a decade up to 1998 and rate further increased when a lower cutoff value of 23- 25kg/M2 was given for Asians. The national family health survey India (NFHS) report shows that 12.1% of men and 14.8% of women in India are overweight or obese.22 According to a study in industrial workers in a city in India 30.9% of men and 32.8% of women are obese.


Evaluation should include a comprehensive questionnaire regarding Snoring, intensity of snoring, choking during sleep, witnessed breathing pauses during sleep, recurrent awakenings. Prior medical history, drug usage, alcohol consumption and smoking history, history regarding cardiovascular status should be carefully looked into because higher incidence of coronary artery disease, diastolic dysfunction, left ventricular dysfunction, pulmonary arterial hypertension arrhythmias and coronary artery plaques were observed in Indian patients with OSA in a study conducted in 2009.23 A comparative study between obese and non-obese OSA patients in Lucknow revealed that obese had more smokers, alcoholics, diabetics, hypertensives and snorers.24

LV dysfunction was also observed in 46.8% of OSA patients by R Paul in another Study.25 Increase in both systolic and diastolic hypertension was observed with increasing severity of OSA in a study conducted in Mumbai.26 Measurements of Body mass index, neck circumference, thyromental distance and estimation of Mallampati score must also be done

OSAHS in Indian studies

Majority of PSG centers and institutes where studies on OSA or OSAHS in Indian population are being done, are in big cities in India. Prevalence of sleep disordered breathing (SDB) and OSAHS in middle aged urban. Indian men were studied in a two phased cross sectional study by ZA Udwadia in Mumbai.27 SDB was found in 19.5 %, OSA in 7.5% and EDS in 22%.The snorers had high body mass index (BMI), neck girth, waist girth and hip girth compared to non snorers. Obese individuals also had higher desaturation index, higher arousal index, 86.6% of obese individuals had SDB, 6.6% RERA’s,80% had OSA and OSAHS in 37.5%.25,28 In another study in Mumbai SDB was found in 3.42% of general population with habitual snoring in 6.4%.29 In New Delhi, snoring was seen in 39.5% ( males 49.5% and females 29%) with habitual snoring in 28.2%, SDB in 4.3%, EDS in 48.6% and a high BMI of 13.7%.30 EDS increased with increasing severity of Bronchial Asthma (30.8% in asthmatics vs 11% in nonasthmatics) was observed by AG Ghoshal.31A study in paediatric group in New Delhi showed 12.7% of school children being snorers with SDB in 4.8% and EDS in 24.3%. In children with snoring and mouth breathing, 60% on PSG showed severe SDB and 30% moderate SDB.32

Acceptance of nasal CPAP in Indian OSA patients is low, cost being the major impediment. Discontinuation of CPAP was observed in 25% with leakage from the nasal mask being the major cause.33 Oral appliances were successful in CPAP uncomfortable patients as observed by B Jayan.34 Children with OSA responded better to appropriate surgery after careful selection of patients. 35


Sleep related disorders are high in Indian population but accessibility for diagnosis and treatment is still at a very low level due to various reasons. Increasing awareness regarding OSA and OSAHS among the general population and clinicians, wider availability of PSG studies and decreasing the costs of diagnostic tests and treatment can go a long way in identifying and treating these patients.

  1. McNicholas WT. Diagnostic criteria for sleep apnea syndrome: Time for consensus. Eur Resp J 1996; 9: 634-5.
  2. Young T, Peppard PE, Gottlieb DJ. Epidemiology of obstructive sleep apnea: a population health perspective. Am J Respir Crit Care Med 2002; 165:1217-39.
  3. . Sharma SK, Ahluwalia G. Epidemiology of adult obstructive sleep apnea syndrome in India. Indian J Med Res 2010; 131: 171-5
  4. . American Academy of Sleep Medicine. International Classification of sleep disorders, 2nd edition. Westchester III: American academy of sleep medicine ; 2005.
  5. Michelle TC, Christian G, Clete AK. Clinical features and evaluation of obstructive sleep apnea and upper airway resistance syndrome. In, Kryger MH, Roth T, Dement WC(ed). Principles and Practice of Sleep Medicine, 5th edition. St. Louis, Missouri, Elsevier, 2011; 1206- 18.
  6. Redline S, Kapur VK, Sanders MH, Quan SF, Gottlieb DJ, Rapoport DM et al. Effects of varying approaches for identifying respiratory disturbances on sleep apnea assessment. Am J Respir Crit Care Med 2000; 161:369-74.
  7. Christian G, Riccardo S, Stephen D. Snoring Daytime Sleepiness in Regular Heavy Snorers. Chest 1991; 99:40-8.
  8. Bonnet M, Carley D. EEG Arousals: Scoring rules and examples. A preliminary report from Sleep Disorders Atlas taskforce of ASDA. Sleep1992; 15:173–84.
  9. American Association of Respiratory Care-Association of Polysomnography Technologists clinical practice guideline, Polysomnography. Respir Care 1995; 40:1336-43.
  10. Dempsey JA, Veasey SC, Morgan BJ, O'Donnell CP. Pathophysiology of Sleep Apnea. Physiol Rev 2010; 90: 47–112.
  11. O'donnell CP, Schaub CD, Haines AS, Berkowitz DE, Tankersley CG, Schwartz AR et al. Leptin prevents respiratory depression in obesity. Am J Respir Crit Care Med 1999; 159:1477-84
  12. Phipps PR, Starritt E, Caterson I, Grunstein RR. Association of serum leptin with hypoventilation in human obesity. Thorax 2002; 57:75-6.
  13. Minoguchi K, Tazaki T, Yokoe T, Minoguchi H, Watanabe Y, Yamamoto M et al. Elevated production of tumor necrosis factor-alpha by monocytes in patients with obstructive sleep apnea syndrome. Chest 2004 ; 126:1473-9.
  14. Yokoe T, Minoguchi K, Matsuo H, Oda N, Minoguchi H, Yoshino G et al. Elevated levels of C-reactive protein and interleukin-6 in patients with obstructive sleep apnea syndrome are decreased by nasal continuous positive airway pressure. Circulation 2003 ; 107:1129-34.
  15. Neill AM, Angus SM, Sajkov D, McEvoy RD. Effects of sleep posture on upper airway stability in patients with obstructive sleep apnea. Am J Respir Crit Care Med 1997 ; 155:199-204.
  16. Mitler MM, Dawson A, Henriksen SJ, Sobers M, Bloom FE. Bedtime ethanol increases resistance of upper airways and produces sleep apneas in asymptomatic snorers. Alcohol Clin Exp Res 1988 ; 12: 801-5.
  17. Aggarwal M, Suri JC, Suri S, Sen MK. Maternal and Fetal outcomes of sleep disordered breathing in pregnancy. Indian J Sleep Med 2008;3.1: 25-29
  18. Suri JC, Sen MK. Pulmonary functions in OSAHS in a cohort of patients attending a tertiary sleep center. Ind J of Sleep Med.2007; 2.1: 21-7.
  19. Agarwal K, Mehta C, Sen MK, Suri JC. Evaulation & workup to detect regions of disproportionate anatomy and its subsequent management in patients of snoring and OSA. Indian J Sleep Med 2006; 1.1: 45-9
  20. Suri JC, Sen MK, Ojha UC, Adhikari T. Epidemiology of sleep disorders in the elderly – A questionnaire survey. Indian J Sleep Med 2009; 4.1:12-8
  21. World Health Organisation: Global Health Observatory (GHO) .Available at: Accessed September 21st , 2013.
  22. National Family Health Survey (NFHS-3). National Fact Sheet. INDIA (Provisional data). International Institute for Population Sciences, Mumbai. Ministry of Health and Family Welfare. Government of India. 2005-2006
  23. Sachdev SS, Suri JC, Jain AK, Khalid A, Isser HS, Mittal MK. Cardiovascular morbidity in subjects with Obstructive sleep apnea and Its correlation with the severity of disease. Indian J Sleep Med 2009; 4.2:49-60
  24. 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.
  25. Paul R, Dey R, Barooah N, Nag S, Maji S, Bhattacharyya P. Prevalence of left ventricular diastolic dysfunction in OSA patients: a retrospective study. Indian J Sleep Med 2011; 6.2:50-3.
  26. Mody KR, Athavale AU, Bhaskar MA, Mohan R, Salgia K. Association of Sleep Disordered Breathing with Systemic hypertension – The Indian perspective. Indian J Sleep Med 2008; 3.4, : 138-43.
  27. 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 Jan 15; 169:168-73.
  28. Gupta YK, Jaiswal A, Gupta R, Jain AK, D. Behera D. Pattern of sleep disordered breathing in obese Indians. Indian J Sleep Med 2009; 4.1:19-31.
  29. Saxena S, Gothi D, Joshi JM. Prevalence of symptoms and risk of sleep disordered breathing in Mumbai (India). Indian J Sleep Med 2006; 1.1: 27-31
  30. Suri JC, Sen MK, Adhikari T. Epidemiology of Sleep Disorders in the Adult Population of Delhi: A Questionnaire Based Study. Indian J Sleep Med 2008; 3.4 :128-137.
  31. Ghoshal AG, Sarkar S, Mondal P, Bhattacharjee SK, Shamim S. A Study of Excessive Day time Sleepiness in Asthma. Indian J Sleep Med 2008;3.3: 93-6.
  32. Bhool S, Suri JC, Sen MK, Venkatachalam VP. Clinical, radiological and polysomnographic evaluation of sleep disordered breathing in children. Indian J Sleep Med 2008; 3.3: 85-92.
  33. Suri JC, Sen MK, Ojha UC. Acceptance and Compliance issues of nasal CPAP amongst Indian patients of obstructive sleep apnea. Indian J Sleep Med 2006; 1.4: 197-203.
  34. Jayan B, Prasad BNBM, Rajput AK, Bhattacharrya R, Dhiman RK, Thampi PS. Management of Obstructive Sleep Apnea with Oral Appliances: Our Experience. Indian J Sleep Med 2006; 1.4: 204-7.
  35. Gupta N, Suri JC, Venkatachalam VP, Sen MK. Evaluation of Polysomnographic Patterns with Reference to Various Treatment Modalities in the Management of Patients with Upper Airway Obstruction. Indian J Sleep Med 2006; 1.2: 97-100.

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