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Obstructive Sleep Apnea


Kingman P. Strohl

, MD, Case School of Medicine, Case Western Reserve University

Last full review/revision Sep 2020| Content last modified Sep 2020
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Obstructive sleep apnea (OSA) consists of episodes of partial or complete closure of the upper airway that occur during sleep and lead to breathing cessation (defined as a period of apnea or hypopnea > 10 seconds). Symptoms include excessive daytime sleepiness, restlessness, snoring, recurrent awakening, and morning headache. Diagnosis is based on sleep history and polysomnography. Treatment is with nasal continuous positive airway pressure, oral appliances, and, in refractory cases, surgery. Prognosis is good with treatment. Most cases remain undiagnosed and untreated and are often associated with hypertension, atrial fibrillation and other arrhythmias, heart failure, and injury or death due to motor vehicle crashes and other accidents resulting from hypersomnolence.

In at-risk patients, sleep destabilizes patency of the upper airway, leading to partial or complete obstruction of the nasopharynx, oropharynx, or both.

Obstructive sleep hypopnea occurs when breathing is diminished, even if it is not absent.

The prevalence of obstructive sleep apnea is 2 to 9% in adults; the condition is under-recognized and often undiagnosed even in symptomatic patients. Obstructive sleep apnea is up to 4 times more common among men and 7 times more common among people who are obese (ie, body mass index [BMI] > 30). Severe OSA (apnea-hypopnea index [AHI] > 30/hour) increases the risk of death in middle-aged men.

Obstructive sleep apnea is the leading medical cause of excessive daytime sleepiness (sometimes called wake-time sleepiness), increasing risks of automobile crashes, loss of employment, and sexual dysfunction. Relationships with bed partners and roommates and/or housemates may also be adversely affected because affected people may also have difficulty sleeping.

Long-term cardiovascular sequelae of untreated OSA include poorly controlled hypertension, heart failure, and atrial fibrillation (even after catheter ablation) and other arrhythmias (1). OSA also increases the risk for nonalcoholic fatty liver disease, likely due to intermittent nocturnal hypoxia and sleep disruption (2).

General references

  • 1. Zinchuk AV, Jeon S, Koo BB, et al: Polysomnographic phenotypes and their cardiovascular implications in obstructive sleep apnoea. Thorax 2018 73(5):472–480, 2018. doi: 10.1136/thoraxjnl-2017-210431

  • 2. Musso G, Cassader M, Olivetti C, et al: Association of obstructive sleep apnoea with the presence and severity of non-alcoholic fatty liver disease. A systematic review and meta-analysis. Obes Rev 14:417–431, 2013.

Etiology of Obstructive Sleep Apnea

Anatomic risk factors for obstructive sleep apnea include

  • An oropharynx “crowded” by a short or retracted mandible

  • A prominent tongue base or tonsils

  • A rounded head shape and a short neck

  • A neck circumference > 43 cm (> 17 in)

  • Thick lateral pharyngeal walls

  • Lateral parapharyngeal fat pads

Anatomic risk factors are common among obese people.

Other identified risk factors include postmenopausal status, aging, and alcohol or sedative use. A family history of obstructive sleep apnea is present in 25 to 40% of cases, perhaps reflective of heritable factors affecting ventilatory drive or craniofacial structure. The risk of OSA in a family member is proportional to the number of affected family members.

Acromegaly, hypothyroidism, and sometimes stroke can cause or contribute to OSA. Disorders that occur more commonly in patients with OSA include hypertension, stroke, diabetes, hyperlipidemia, gastroesophageal reflux disease, nocturnal angina, heart failure, and atrial fibrillation or other arrhythmias.

Because obesity is a common risk factor for both obstructive sleep apnea and obesity-hypoventilation syndrome, the conditions frequently coexist.

Inspiratory efforts against a closed upper airway cause paroxysms of inspiration, reductions in gas exchange, disruption of normal sleep architecture, and partial or complete arousals from sleep. These factors interact to produce morbidity and mortality through hypoxia, hypercapnia, and sleep fragmentation (1).

OSA is an extreme form of sleep-related upper airway resistance. Less severe forms that do not cause oxygen desaturation include

  • Upper airway airflow resistance causing noisy inspiration but without sleep arousals

  • Upper airway resistance syndrome, characterized by crescendo snoring terminated by respiratory effort-related arousals (RERAs)

Patients with upper airway resistance syndrome are typically younger and less obese than those with OSA, and they complain of daytime sleepiness more than do patients with primary snoring. Frequent arousals occur, but strict criteria for apneas and hypopneas may not be present. Symptoms, diagnostic evaluation, and treatment of snoring and upper airway resistance syndrome are otherwise the same as for obstructive sleep apnea.

Etiology reference

  • 1. Zinchuk AV, Jeon S, Koo BB, et al: Polysomnographic phenotypes and their cardiovascular implications in obstructive sleep apnoea. Thorax 73(5):472–480, 2018. doi: 10.1136/thoraxjnl-2017-210431

Symptoms and Signs of Obstructive Sleep Apnea

Although loud disruptive snoring is reported by 85% of patients with obstructive sleep apnea, most people who snore do not have OSA. Other symptoms of obstructive sleep apnea may include

  • Choking, gasping, or snorting during sleep

  • Restless and unrefreshing sleep

  • Difficulty staying asleep

Most patients are unaware of these symptoms (because they occur during sleep) but are informed of them by bed partners, roommates, or housemates. In the morning, some patients have a sore throat, dry mouth, or a headache.

During daily activities, patients may experience intrusive sleepiness, fatigue, and impaired concentration. The frequency of sleep complaints and the degree of daytime sleepiness do not correlate well with number of events or arousals from sleep.

Diagnosis of Obstructive Sleep Apnea

  • Symptom criteria

  • Sleep studies

The diagnosis of obstructive sleep apnea is suspected in patients with identifiable risk factors, symptoms, or both.

Questionnaires, such as STOP-Bang, Berlin, and Epworth Sleepiness Scale, can be used to assess risk . However, when compared to the more accurate results of sleep studies, these questionnaires have low specificity and thus high false-positive rates (1, 2). The multimodal STOP-BANG and the Berlin Questionnaire are more specific than the Epworth Sleepiness Scale (3).

Criteria for diagnosis consist of daytime symptoms, nighttime symptoms, and sleep monitoring that documents ≥ 5 episodes of hypopnea and/or apnea per hour with symptoms, or ≥ 15 episodes per hour in the absence of symptoms. Specifically, in regard to symptoms, there should be ≥ 1 of the following:

  • Daytime sleepiness, unintentional sleep episodes, unrefreshing sleep, fatigue, or difficulty staying asleep

  • Awakening with breath holding, gasping, or choking

  • Reports by a bed partner of loud snoring, breathing interruptions, or both in the patient’s sleep

The patient and any bed partners, roommates, or housemates are all sources for clinical risk assessment.

Although OSA is the most common medical disorder causing excessive daytime sleepiness, the differential diagnosis is broad and includes

  • Reduced quantity or quality of sleep due to poor sleep hygiene

  • Sedation or mental status changes due to drugs, chronic diseases (including cardiovascular or respiratory diseases), or metabolic disturbances and accompanying therapies

  • Depression, which often also confounds OSA recognition

  • Alcohol or drug abuse

  • Narcolepsy and other primary hypersomnolence syndromes

  • Other primary sleep disorders (eg, restless legs syndrome, periodic limb movement disorder)

An extended sleep history should be taken in all patients who

Most patients who report only snoring, without other symptoms or cardiovascular risks, do not need an extensive evaluation for obstructive sleep apnea.

Studies that classify patients into clinical groups based on symptoms and comorbidities is an area of ongoing interest as it will lead to individualized approaches to OSA (4–8).

The physical examination should include anatomic evaluation (for nasal obstruction, tonsillar hypertrophy, and pharyngeal structure) and identification of clinical features of hypothyroidism and acromegaly.

Polysomnography is ideal for confirming the diagnosis of obstructive sleep apnea and quantifying the severity of OSA. Polysomnography includes continuous measurement of breathing effort by plethysmography, airflow at the nose and mouth using flow sensors, oxygen saturation by oximetry, sleep architecture by EEG, chin electromyography (looking for hypotonia), and electro-oculography to assess the occurrence of rapid eye movements. Polysomnography records and helps classify stages of sleep and the occurrence and duration of apneic and hypopneic periods. The patient is also observed by video, and ECG monitoring is used to determine whether arrhythmias occur in conjunction with the apneic episodes. Other variables evaluated include limb muscle activity (to assess nonrespiratory causes of sleep arousal, such as restless legs syndrome and periodic limb movements disorder) and body position (apnea may occur only in the supine position).

The apnea-hypopnea index (AHI), which is the total number of episodes of apnea and hypopnea occurring during sleep divided by the hours of sleep time, is the common summary measure used to describe respiratory disturbances during sleep and thus the severity of sleep apnea. AHI values can be computed for different sleep stages. Sleep apnea may be classified as

  • Mild: AHI between 5 and 15

  • Moderate: AHI between 15 and 30

  • Severe: AHI > 30

The respiratory disturbance index (RDI), a similar measure, describes the number of episodes of certain arousals related to respiratory effort (called respiratory effort-related arousals or RERAs) plus the number of apnea and hypopnea episodes per hour of sleep.

An arousal index (AI), which is the number of arousals per hour of sleep, can be computed if EEG monitoring is used. The arousal index may be correlated with the apnea-hypopnea index or respiratory disturbance index, but about 20% of apneas and desaturation episodes are not accompanied by arousals, or other causes of arousals are present.

An apnea-hypopnea index> 5 is required for the diagnosis of obstructive sleep apnea; a value > 15 indicates a moderate level of sleep apnea, and a value > 30 indicates a severe level of sleep apnea. Snoring loudly enough to be heard in the next room confers a 10-fold increase in the likelihood of having an apnea-hypopnea index > 5. The arousal index and respiratory disturbance index correlate only moderately with a patient’s symptoms. However, a recent study that linked outcomes to both clinical and polysomnographic data suggested that a composite of variables (not just AHI) influence mortality (9).

Portable diagnostic tools (home sleep testing) are being used more often to detect the presence of apnea and determine severity . Portable monitors can measure heart rate, pulse oximetry, effort, position, and nasal airflow to provide fair estimates of respiratory disturbances during self-reported sleep, thereby estimating AHI/RDI over the time the monitor is worn. If sleep did not occur during the study, the frequency and severity of sleep-disordered breathing will be underestimated. Portable diagnostic tools are often used in combination with questionnaires (eg, STOP-Bang, Berlin Questionnaire) to calculate patients’ risk (the sensitivity and specificity of the test depend on pretest probability). When portable tools are used, coexisting sleep disorders (eg, restless legs syndrome) are not excluded. Follow-up polysomnography may still be needed to determine AHI/RDI values in the different stages of sleep and with changes in position, especially when surgery or therapy other than positive airway pressure is being considered.

Measurement of thyroid-stimulating hormone can be done based on clinical suspicion. No other adjunctive testing (eg, upper airway imaging) has sufficient diagnostic accuracy to be recommended routinely.

Diagnosis references

  • 1. Chung F, Yegneswaran B, Liao P, et al: STOP questionnaire: A tool to screen patients for obstructive sleep apnea. Anesthesiology2008;108:812–821, 2008.

  • 2. Netzer NC, Stoohs RA, Netzer CM, et al: Using the Berlin Questionnaire to identify patients at risk for the sleep apnea syndrome. Ann Intern Med 131(7):485–491, 1999.

  • 3. Luo J, Huang R, Zhong X, et al: STOP-Bang questionnaire is superior to Epworth sleepiness scales, Berlin questionnaire, and STOP questionnaire in screening obstructive sleep apnea hypopnea syndrome patients.Chin Med J (Engl) 127(17):3065–3070, 2014.

  • 4. Keenan BT, Kim J, Singh B, et al: Recognizable clinical subtypes of obstructive sleep apnea across international sleep centers: a cluster analysis. Sleep 41(3):zsx214, 2018. doi: 10.1093/sleep/zsx214

  • 5. Kim J, Keenan BT, Lim DC, et al: Symptom-based subgroups of Koreans with obstructive sleep apnea. J Clin Sleep Med 14(3):437–443, 2018. doi: 10.5664/jcsm.6994

  • 6. Keenan BT, Kim J, Singh B, et al: Recognizable clinical subtypes of obstructive sleep apnea across international sleep centers: A cluster analysis. Sleep 41(3):zsx214, 2018. doi: 10.1093/sleep/zsx214

  • 7. Keenan BT, Kirchner HL, Veatch OJ, et al: Multisite validation of a simple electronic health record algorithm for identifying diagnosed obstructive sleep apnea. J Clin Sleep Med 16(2):175–183, 2020. doi: 10.5664/jcsm.8160

  • 8. Mazzotti DR, Keenan BT, Lim DC, et al: Symptom subtypes of obstructive sleep apnea predict incidence of cardiovascular outcomes. Am J Respir Crit Care Med 200(4):493–506, 2019. doi: 10.1164/rccm.201808-1509OC

  • 9. Zinchuk AV, Jeon S, Koo BB, et al: Polysomnographic phenotypes and their cardiovascular implications in obstructive sleep apnoea. Thorax 73(5):472–480, 2018. doi: 10.1136/thoraxjnl-2017-210431

Prognosis for Obstructive Sleep Apnea

Prognosis of obstructive sleep apnea is excellent if effective treatment is instituted.

Untreated or unrecognized obstructive sleep apnea can lead to cognitive impairment as a result of sleeplessness, which, in turn, can lead to serious injury or death caused by accidents, especially motor vehicle crashes. Sleepy patients should be warned of the risks of driving, operating heavy machinery, or engaging in other activities during which unintentional sleep episodes would be hazardous.

Adverse effects of hypersomnolence, such as loss of employment and sexual dysfunction, can affect families considerably.

In addition, perioperative complications, including cardiac arrest, have been attributed to OSA, probably because anesthesia can cause airway obstruction after a mechanical airway is removed. Patients should therefore inform their anesthesiologist of the diagnosis before undergoing any surgery and should expect to receive continuous positive airway pressure (CPAP) when they receive preoperative drugs and during recovery.

Treatment of Obstructive Sleep Apnea

  • Control of risk factors such as obesity, hypertension, alcohol use, and sedative use

  • Continuous positive airway pressure (CPAP) or oral appliances

  • For anatomic encroachment or disease that does not respond to devices, surgery, or nerve stimulation

The aim of treatment is to reduce episodes of hypoxia and sleep fragmentation; treatment is tailored to the patient and to the degree of impairment. Success is defined as a resolution of symptoms with AHI reduction below a threshold, usually 10/hour.

Treatment is directed at both risk factors and at obstructive sleep apnea itself. Specific treatments for obstructive sleep apnea include continuous positive airway pressure (CPAP), oral appliances, and airway surgery.

Control of risk factors

Initial treatment aims at optimal control of modifiable risk factors for obstructive sleep apnea, including obesity, hypertension, alcohol and sedative use, hypothyroidism, acromegaly, and other chronic disorders. Although modest weight loss (15%) may result in clinically meaningful improvement, weight loss is extremely difficult for most people, especially those who are fatigued or sleepy. Bariatric surgery frequently reverses symptoms and improves AHI in morbidly obese (BMI > 40) patients; however, the degree of these improvements may not be as great as the degree of weight loss. Weight loss, with or without bariatric surgery, should not be considered a cure for OSA.

Continuous positive airway pressure (CPAP)

Nasal continuous positive airway pressure is the treatment of choice for most patients with OSA and subjective daytime sleepiness; adherence is lower in patients who do not experience sleepiness. CPAP improves upper airway patency by applying positive pressure to the collapsible upper airway segment. Effective pressures typically range from 3 to 15 cm water. Disease severity does not correlate with pressure requirements. Many CPAP devices monitor CPAP efficacy and titrate pressures automatically, according to internal algorithms. If clinical improvement is not apparent, CPAP efficacy should be reviewed and patients should be reassessed for a second sleep disorder (eg, upper airway obstruction) or a comorbid disorder. If necessary, pressure can be titrated manually during monitoring with repeat polysomnography. Regardless of improvement in the AHI, CPAP will reduce cognitive impairment and improve quality of life, and it may reduce blood pressure. If CPAP is withdrawn, symptoms recur over several days, though short interruptions of therapy for acute medical conditions are usually well tolerated. Duration of therapy is indefinite (1–4).

Adverse effects of nasal CPAP include dryness and nasal irritation, which can be alleviated in some cases with the use of warm humidified air, and discomfort resulting from a poorly fitting mask. However, newer mask designs have improved comfort and ease of use.

Failures of nasal CPAP are common. Attention should be given to improving adherence by overcoming inherent bias, early attention to problems and mask fit, and close follow-up by a committed caretaker. There is also a need to recognize and address the decreased long-term CPAP adherence among patients who are not obese but have low respiratory arousal sleep threshold and the related propensity for increased arousals and irregular breathing (5).

CPAP can be augmented with inspiratory assistance (bilevel positive airway pressure) for patients with comorbid obesity-hypoventilation syndrome to increase their tidal volumes.

Oral appliances

Oral appliances are designed to advance the mandible or, at the very least, prevent retrusion during sleep. Some appliances are also designed to pull the tongue forward. Use of these appliances to treat both snoring and mild to moderate obstructive sleep apnea is gaining acceptance. Comparisons of appliances to CPAP show equivalence in mild to moderate obstructive sleep apnea, but results of cost-effectiveness studies are not available.


Surgical procedures to correct anatomic factors such as enlarged tonsils and nasal polyps contributing to upper airway obstruction (called anatomic procedures) should be considered. Surgery for macroglossia or micrognathia is also an option. Surgery is a first-line treatment if anatomic encroachment is identified. However, in the absence of encroachment, evidence to support surgery as a first-line treatment is lacking.

Uvulopalatopharyngoplasty (UPPP) was the most commonly used procedure. It involves resection of pharyngeal tissue. UPPP has been largely replaced by less aggressive approaches that might stabilize the lateral walls of the pharynx and/or enlarge the velopharyngeal area without altering speech or swallowing. Equivalence with CPAP was shown in one study using CPAP as a bridge to surgery, but the interventions have not been directly compared. UPPP may not be successful in patients who are morbidly obese or who have anatomic narrowing of the airway. Moreover, after UPPP, recognition of sleep apnea is more difficult because of a lack of snoring. Such silent obstructions may cause apneic episodes as severe as those occurring before surgical intervention.

Other surgical procedures include midline glossectomy, hyoid advancement, and mandibulomaxillary advancement. Mandibulomaxillary advancement is sometimes offered as a 2nd-stage procedure if UPPP is not curative. The optimal multistage approach is not known.

Tracheostomy is the most effective therapeutic maneuver for OSA but is done as a last resort. It bypasses the site of obstruction and is indicated for patients most severely affected (eg, those with cor pulmonale).

Hypoglossal nerve stimulation

A nonanatomic procedure is upper airway stimulation. In upper airway stimulation, an implanted device is used to activate a branch of the hypoglossal nerve (6). This therapy can be successful in highly selected patients with moderate to severe disease who are unable to tolerate CPAP therapy and those in whom mandibulomaxillary advancement is contemplated (7). Experience with this line of therapy is growing, but using appropriate selection criteria is crucial for success.

Adjunctive treatments

Adjunctive treatments are commonly used but have no proven role as first-line treatment for obstructive sleep apnea.

Modafinil can be used for residual sleepiness in OSA in patients who are effectively using CPAP.

Supplemental oxygen improves blood oxygenation, but a beneficial clinical effect cannot be predicted. Also, oxygen may provoke respiratory acidosis and morning headache in some patients.

A number of drugs have been tried (eg, tricyclic antidepressants, theophylline, dronabinol, combined atomoxetine plus oxybutynin) but cannot be routinely advocated because of limited efficacy, a low therapeutic index, or absence of replication of results (8–11). Better methods to recognize sleep apnea subtypes will permit interpretation of successes and failures with this line of treatment.

Nasal dilatory devices and throat sprays sold OTC for snoring have not been studied sufficiently to prove benefits for OSA.

Laser-assisted uvuloplasty, uvular splints, and radiofrequency tissue ablation have been promoted as treatments for loud snoring in patients without obstructive sleep apnea. Although they may transiently decrease snoring loudness, efficacy declines over months to years.

Patient education and support

An informed patient and family are better able to cope with a treatment strategy, including tracheostomy. Patient support groups provide helpful information and effectively support timely treatment and follow-up.

Treatment references

  • 1. McEvoy RD, Antic NA, Heeley E, et al: CPAP for prevention of cardiovascular events in obstructive sleep apnea. N Engl J Med 375(10):919–931, 2016. doi: 10.1056/NEJMoa1606599

  • 2. Gottlieb DJ, Punjabi NM, Mehra R, et al: CPAP versus oxygen in obstructive sleep apnea. N Engl J Med 370(24):2276–2285, 2014. doi: 10.1056/NEJMoa1306766

  • 3. Chirinos JA, Gurubhagavatula I, Teff K, et al: CPAP, weight loss, or both for obstructive sleep apnea. N Engl J Med 370(24):2265–2275, 2014. doi: 10.1056/NEJMoa1306187

  • 4. Pépin JL, Tamisier R, Barone-Rochette G, et al: Comparison of continuous positive airway pressure and valsartan in hypertensive patients with sleep apnea. Am J Respir Crit Care Med 182(7):954–960, 2010. doi: 10.1164/rccm.200912-1803OC

  • 5. Zinchuk A, Edwards BA, Jeon S, et al: Prevalence, associated clinical features, and impact on continuous positive airway pressure use of a low respiratory arousal threshold among male United States veterans with obstructive sleep apnea. J Clin Sleep Med 14(5):809–817, 2018. doi: 10.5664/jcsm.7112

  • 6. Baptista PM, Costantino A, Moffa A, et al: Hypoglossal nerve stimulation in the treatment of obstructive sleep apnea: Patient selection and new perspectives. Nat Sci Sleep 12:151–159, 2020. doi: 10.2147/NSS.S221542

  • 7. Woodson BT, Soose RJ, Gillespie MB, et al: Three-year outcomes of cranial nerve stimulation for obstructive sleep apnea: The STAR Trial. Otolaryngol Head Neck Surg154(1):181–188, 2016. doi: 10.1177/0194599815616618

  • 8. Taranto-Montemurro L, Messineo L, Sands SA, et al: The combination of atomoxetine and oxybutynin greatly reduces obstructive sleep apnea severity: A randomized, placebo-controlled, double-blind crossover trial. Am J Respir Crit Care Med 199(10):1267–1276, 2018. doi: 10.1164/rccm.201808-1493OC

  • 9. Carley DW, Prasad B, Reid KJ, et al: Pharmacotherapy of apnea by cannabimimetic enhancement, the PACE Clinical Trial: Effects of dronabinol in obstructive sleep apnea. Sleep 41(1):zsx184, 2018. doi: 10.1093/sleep/zsx184

  • 10. Taranto-Montemurro L, Messineo L, Azarbarzin A, et al: Effects of the combination of atomoxetine and oxybutynin on OSA endotypic traits. Chest 2020 Jan 30. pii: S0012-3692(20)30135-5. doi: 10.1016/j.chest.2020.01.012 [Epub ahead of print]

  • 11. Taranto-Montemurro L, Messineo L, Wellman A: Targeting endotypic traits with medications for the pharmacological treatment of obstructive sleep apnea. A review of the current literature. J Clin Med 8(11):1846, 2019. doi: 10.3390/jcm8111846

Key Points

  • Obesity, anatomic abnormalities in the upper airway passages, family history, certain disorders (eg, hypothyroidism, stroke), and use of alcohol or sedatives increase the risk of obstructive sleep apnea (OSA).

  • Patients typically snore, have restless and unrefreshing sleep, and often feel daytime sleepiness and fatigue.

  • Most people who snore do not have OSA.

  • Disorders that occur more commonly in patients with OSA include hypertension, stroke, diabetes, gastroesophageal reflux disease, nonalcoholic steatohepatitis, nocturnal angina, heart failure, and atrial fibrillation or other arrhythmias.

  • Confirm the diagnosis by polysomnography or, if uncomplicated OSA, home sleep testing.

  • Control modifiable risk factors and treat most patients with continuous positive airway pressure and/or oral appliances designed to open the airway.

  • Consider surgery for abnormalities causing airway encroachment or if the disorder is intractable.

More Information

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