Obstructive sleep apnea: decision making and treatment algorithm

Published on 05/05/2015 by admin

Filed under Otolaryngology

Last modified 22/04/2025

Print this page

rate 1 star rate 2 star rate 3 star rate 4 star rate 5 star
Your rating: none, Average: 0 (0 votes)

This article have been viewed 1885 times

Chapter 7 Obstructive sleep apnea: decision making and treatment algorithm

2 DEFINITIONS OF DISEASE

Sleep-disordered breathing can be viewed as a continuum from normal non-obstructed breathing at one end to a patient with sleep apnea and Pickwickian syndrome at the other (Table 7.1). The level of disease in an individual patient can improve or worsen, moving the patient up or down this continuum both over time and on a night-to-night basis. For instance, a normal patient who gains a significant amount of weight may begin to snore, develop arousals during the night and begin to move into a disease state. With additional weight gain, this patient may develop increased airway resistance or sleep apnea. A patient who consumes alcohol on a given night can also move on the scale in a similar fashion; as muscle tone decreases, obstruction increases. Similarly, a patient with sleep apnea who loses weight may develop less severe airway resistance, simple snoring, or even achieve a normal state of breathing at night. Thus, the number generated on a polysomnogram must be viewed in the context of the patient’s overall disease and night-to-night variation of their sleep-disordered breathing.

Table 7.1 The continuum of sleep disordered breathing

image

Although there are numerous metrics to measure the severity of obstructive sleep apnea, disease severity is generally described in terms of the number of apneas plus hypopneas per hour of sleep, or via the Apnea Hypopnea Index (AHI) and O2 saturation as measured on an overnight sleep study, or polysomnogram. The polysomnogram represents a snapshot in time which may not reflect a patient’s level of disease over a long period of time, but it is still the best measure of disease severity available at present.

Using polysomnography as our standard of determining disease severity, obstructive sleep apnea is represented by an AHI of greater than five events per hour and obstructive sleep apnea syndrome is defined as an AHI of greater than five events per hour with daytime and/or nighttime symptoms such as choking, gasping, snoring and daytime sleepiness. Patients can be further divided into a group with mild apnea with an AHI between five and 15, moderate apnea in patients with an AHI of 15 to 30, and severe apnea in patients who have an AHI of greater than 30. Many use O2 desaturation nadir to modify the description of severity in sleep-disordered breathing. For instance, a patient with an AHI of 12 and O2 desaturation to 70% may be referred to as a patient with moderate OSA. Similarly, a patient with an AHI of 25 and significant desaturation may be called a patient with severe apnea. Other factors on the sleep test such as the presence or absence of REM sleep, the presence or absence of delta sleep (Stage III and IV sleep), and the percentage of time spent with oxygen saturation below 90% may also be important as well. They may help explain the patient’s symptoms and may serve as a guideline as to the success of a procedure if these parameters are improved post treatment.

Lastly, a respiratory effort-related arousal (RERA) is an event that occurs when a patient develops an arousal on electroencephalogram in conjunction with increasing inspiratory effort during sleep. RERAs can be added to apneas and hypopneas to create the Respiratory Disturbance Index (RDI) which many use to guide treatment.2

3 EFFECTS OF SLEEP APNEA AND TREATMENT THRESHOLDS

There are three principal manifestations of sleep-disordered breathing: physiological, behavioral and social.

The physiological manifestations are important and principally relate to cardiovascular consequences of OSA, though there are other physiological effects of disordered breathing during sleep, such as alterations in inflammatory biomarkers, which also occur. Cardiovascular consequences include associations with stroke, hypertension and myocardial infarction and are being studied rigorously in the Sleep Heart Health Study, which is longitudinally tracking a cohort of OSA patients with measures of OSA and medical outcomes.3

The behavioral effects of sleep disruption are commonly evident. These may manifest as tiredness in the morning or daytime, falling asleep in permissive situations such as watching TV or reading a book, an increased incidence of motor vehicle accidents, and losses of concentration and productivity. A simple patient self-report scale, the Epworth Sleepiness Scale, was designed to quantify this level of tiredness4 though there are also objective measures of alertness such as the psychomotor vigilance test.5 The behavioral effects of OSA can be variable among patients where a patient with snoring may have significant tiredness whereas a patient with an elevated AHI and greater nighttime obstruction may not display tiredness. This discrepancy appears to make behavioral measurement alone insufficient to fully characterize the disease or its treatment.

Lastly, social effects are principally related to snoring which may disrupt social harmony by disturbance of bedpartners and others in the home. Subjective measures are commonly used to measure this feature of the disease, such as bedpartner scoring. Snoring is a common reason why patients seek medical attention for obstructive sleep apnea, as it is one of the most obvious and disruptive outward manifestations of obstruction during sleep.

In light of the variability in the manifestation of OSA in patients and the gaps in our knowledge as to which patients will suffer cardiovascular consequences of this disease, significant controversy exists with respect to selection of patients for OSA treatment. In a review article on OSA, Ward Flemons writes, ‘In the majority of patients without coexisting conditions … the primary reason to test for and treat sleep apnea is the potential to improve the quality of life.’1 Studies vary in determining the magnitude of effects of mild to moderate OSA on hypertension and cardiovascular consequences. However, ongoing studies of large cohorts of patients such as the Sleep Heart Health Study are yielding important data that will provide guidelines for treatment in the future.6 With information on physiological consequences of OSA such as effects on inflammatory and other biomarkers as well as data from the Sleep Heart Health Study emerging, our threshold and circumstances for intervention will certainly evolve.

Nevertheless, physicians are faced today with patients needing treatment and decisions must be made. The best available evidence is synthesized to assist with these decisions, and treatment thresholds developed. In an attempt to help delineate a treatment threshold, one oft-quoted study determined that patients with an Apnea Index (AI) of >20 were at increased cardiovascular risk.7 Many use the cut-off of an AHI of 20 as the threshold for treatment (note the original cut-off of AI >20 has been subsequently adopted as AHI >20). While virtually all admit that patients with an AHI of >30 should be treated regardless of co-morbidity or behavioral effects, rigorous evidence for treatment of patients with an AHI of <30 is lacking.2 However, patients with AHI <30 with significant co-morbidity or behavioral effects (e.g. tiredness, loss of concentration) are also considered candidates for treatment of OSA.

It is the opinion of the author that all patients with an AHI >30 should be treated for OSA and symptomatic patients with an AHI <30 should be treated. Patients with an AHI <30 may have other factors that bring them to treatment including medical co-morbidities or other parameters on the polysomnogram that mandate treatment (e.g. low oxygen saturation, arrhythmias).

4 EVALUATION FOR OSA

Proper evaluation and diagnosis of patients with OSA are critical for determining a suitable treatment plan. Clearly a patient whose depression is misdiagnosed as OSA, or conversely, a patient whose OSA is misdiagnosed as depression will receive a treatment plan inappropriate for the clinical condition. In the evaluation of a patient with suspected sleep-disordered breathing, the history and physical examination, various adjunctive studies and consultations are helpful to properly diagnose and therefore treat the patient.

5 TREATMENT OPTIONS

There are three categories of treatment options available to treat patients with OSA: behavioral modification, devices that can be worn and surgical options. Every patient should be informed of the options available in each category and the treating physician and patient should review the appropriateness of treatments in each category based on individual considerations. Various brochures and informational material can be reviewed with the patient to insure that all treatment options are presented to the patient while providing an opportunity for questions to be answered.

5.1 BEHAVIORAL MODIFICATION

In general, all patients should be informed of behavioral modifications that can reduce or eliminate OSA without the need for medicines, device use, or surgery. In patients with moderate or severe OSA, these maneuvers are not likely to be effective as stand-alone therapy; however, they can help to mitigate some effects of OSA in these patients and can also assist in education of the patient in the pathogenesis of their disease (e.g. with regard to weight loss or sleep position).

Behavioral modifications include principally sleep position therapy, weight loss where appropriate, and avoidance of sedatives, alcohol, or large meals before bedtime. In sleep position therapy, the patient sleeps on their side or stomach as opposed to on the back, as most patients obstruct more in the supine position. Pillows or positioners can be helpful to assist in this type of postural therapy. Patients should be encouraged to lose weight if they are overweight or obese, as weight loss reduces the bulk of tissue in the neck which narrows the airway, and reduces airway collapse. As surgical intervention for obesity has become safer and more refined, recommendations for surgical treatment of obesity are becoming more common.10 Patients should be counseled to avoid sedatives, including alcohol and other medications prior to bedtime, as sedatives may be important in causing loss of muscle tone and causing airway collapse during sleep. Eating a large or fatty meal or one replete with carbohydrates before bedtime can have the same effect by reducing muscle tone during sleep and should be avoided.

5.2 DEVICES THAT CAN BE WORN

Two devices are available to help maintain airway patency and reduce the incidence of sleep-disordered breathing. These include positive airway pressure (PAP) and an oral appliance (OA).

Positive airway pressure (PAP)

Positive airway pressure is recognized as the most effective treatment for OSA in patients who can tolerate wearing the device, particularly moderate to severe OSA.

The delivery of positive airway pressure is available in many forms, such as continuous positive airway pressure (CPAP), bilevel positive airway pressure, automatically titrating positive airway pressure, and demand positive airway pressure. A description of each is beyond the scope of this chapter, but suffice it to say that each provides posi-tive pressure to the airway through a device worn on the face, and serves as an internal pneumatic splint for the airway. CPAP, which is the most commonly used form of PAP, typically uses between 5 and 15 cm of water pressure to maintain airway patency. These devices have the advantage of a high rate of effectiveness in the laboratory setting in reversing sleep-disordered breathing. Unfortunately, not all patients are able to wear the device regularly in the home setting, making compliance a significant issue. Additionally, patients frequently misrepresent their PAP use as being more compliant, necessitating close follow-up and the use of covert monitoring that is integrated into the device.11 Issues with regard to use of PAP such as desensitization of the patient to mask use at night, comfort and leaking at the mask interface, and claustrophobia must be reconciled and may require working with the patient intensively.

It is appropriate for every patient with moderate or severe OSA to gain exposure to PAP before undergoing surgical therapy. This allows them experience with a treatment option that is typically effective, reversible, associated with few side effects and widely available. As the effects of PAP are dependent on wearing the device during sleep and no ‘training’ of the airway occurs, compliance with wearing the device nightly is necessary and is the principal obstacle to use. If a patient can tolerate the device, it can sometimes provide diagnostic information as well. Relief of symptoms with PAP can help determine which symptoms are caused by OSA. Patients who tolerate the device for even one full night often awake more refreshed than they have for many years and realize the magnitude of the negative cognitive and behavioral effects sleep-disordered breathing has had. When patients feel the beneficial effects of normal sleep in the absence of sleep-disordered breathing there can be a positive change in their attitude towards treatment of the disease and to PAP as well. The prospect of lifelong use is typically less palatable in young patients who are faced with the prospect of wearing PAP for the remainder of their lives, but even in these patients, even short-term use of PAP can be enormously helpful to highlight the behavioral physiologic effects of OSA.

Oral appliances

Oral appliances, principally a mandibular repositioning device, can also be used for sleep-disordered breathing.12 Mandibular repositioning devices advance the mandible anteriorly, which brings forward the tongue and other muscles of the oropharynx and hypopharynx. The position of the palate is also changed with the mandibular repositioning device, likely through action of the palatoglossus muscle, and airway patency is typically improved. It is used principally for patients with simple snoring and mild apnea and has reduced effectiveness in patients with more severe disease.12 Patients with pre-existing disorders of the temp-oromandibular joint and edentulous patients are not considered to be good candidates for this device. As with PAP, no training of the airway occurs, therefore nightly use is necessary for treatment effect.

5.3 SURGICAL THERAPY FOR OSA

Surgical therapy for OSA can be classified in three categories. The first category includes procedures on the upper airway which may improve PAP use and compliance. The second category includes surgery that improves OSA without surgically altering the upper airway such as tracheotomy and bariatric surgery. The third category includes surgery that directly alters the upper airway to reduce obstruction of breathing during sleep.

Non-upper airway surgery for OSA

Despite its efficacy in bypassing upper airway obstruction, tracheotomy is rarely considered as a sole treatment for patients with OSA.14 More commonly, tracheotomy is used on a temporary basis in the perioperative period for patients undergoing upper airway surgery for OSA. The need for an opening in the neck with its associated hygiene and social burdens appropriately limits its routine use. Tracheotomy is typically reserved for morbidly obese patients who are unable to tolerate PAP, morbidly obese patients with Pickwickian syndrome who require upper airway bypass and nocturnal ventilation, and patients who are unable to tolerate PAP with significant co-morbidities in whom other treatment options have failed.14

Since a significant number of patients with OSA are obese and obesity is a major cause of OSA, bariatric surgery has the potential to significantly reduce a patient’s weight and improve sleep-disordered breathing. Bariatric surgery should be considered in patients with a BMI >40 or patients with a BMI >35 with significant medical co-morbidities.10 Patients who fall into this category should preferably be referred to an appropriate center for bariatric surgery for evaluation. This therapy has the significant advantage of treating other co-morbidities associated with obesity such as diabetes and cardiovascular disease in addition to OSA.10

Upper airway surgery for OSA

In selecting patients for surgical treatment in obstructive sleep apnea, one needs to take into account: (1) OSA severity; (2) individual patient anatomy; (3) the patient’s desires; and (4) associated co-morbidities. Specific recommendations for evaluating site of obstruction and procedure choice are discussed elsewhere in this book. General guidelines for application of these procedures follow.

Patients with a higher AHI are generally in greater need for intervention, as the severity of the disease is greater. Individual anatomy plays a significant role in formulating recommendations for treatment of OSA as specific surgical treatments are targeted at areas of obstruction. In discussing the surgical options with the patient, patient expectations and desires should be explicitly discussed, including the patient’s feelings on cure of their snoring, apnea and symptoms of tiredness that they might have. Lastly, patients with OSA may have significant medical co-morbidities such as cardiovascular issues which must be taken into account when considering a patient for upper airway surgery. As in all surgical procedures, a frank discussion of the surgery including the types of surgery that are available, pain, complication rates, expected consequences, morbidity and costs should be undertaken so that the patient has a full understanding of the treatment plan. The need for evaluation of the patient after the surgical procedure and possible need for subsequent surgeries should be discussed as well, as these are commonly important parts of the treatment plan. As noted above, first-line treatment for patients with moderate or severe OSA is PAP for the reasons stated.

6 ALGORITHM FOR TREATMENT OF OSA AND TREATMENT GOALS

Decision making by the patient and physician is predicated on a thorough history and physical examination. Individual anatomy, disease severity and patient preferences play a central role in the selection of treatment, as not all treatments can be effectively applied to all patients. The choice of treatment and degree of invasiveness of the treatments chosen remain in the hands of doctor and patient.

The goal for treatment for OSA is to alleviate sleep-disordered breathing completely when possible manage the disease if complete cure is not possible. Re-evaluation after a treatment has been instituted is critical to determining treatment success. If one cannot normalize a patient completely, one attempts, at minimum, to move the patient into a less severe disease state through behavioral treatments, application of positive airway pressure, or surgery.

Disease severity*
Mild (5<AHI<15)
No symptoms
Behavioral modification
Symptoms
Behavioral modification

Moderate (15<AHI<30) No symptoms Behavioral modification Symptoms Behavioral modification PAP Surgical intervention for PAP failures • Consider oral appliance Severe (AHI >30) Symptoms or no symptoms Behavioral modification (rarely sufficient alone) PAP Surgical intervention for PAP failures

* Additional parameters from the polysomnogram, such as oxygen desaturation nadir, RERAs, and time spent below oxygen saturation of 90% can also be used to guide treatment, as these can shift a patient in to a higher category of disease severity.

REFERENCES

1. Flemons WW. Obstructive sleep apnea. N Engl. 2002;347(77):498-504.

2. Loube DI, Gay PC, Strohl KP, Pack AI, White DP, Collop NA. Indications for positive airway pressure treatment of adult obstructive sleep apnea patients: a consensus statement. Chest. 1999;115(3):863-866.

3. Quan SF, Howard BV, Iber C, et al. The Sleep Heart Health Study: design, rationale, and methods. Sleep. 1997;20(12):1077-1085.

4. Johns MW. A new method for measuring daytime sleepiness: the Epworth Sleepiness Scale. Sleep. 1991;14(6):540-545.

5. Canisius S, Penzel T. Vigilance monitoring – review and practical aspects. Biomed Tech (Berl). 2007;52(1):77-82.

6. Shahar E, Whitney CW, Redline S, et al. Sleep disordered breathing and cardiovascular disease: cross-sectional results of The Sleep Heart Health Study. Am J Respir Crit Care Med. 2001;163(1):19-25.

7. He J, Kryger MH, Zorick FJ, Conway W, Roth T. Mortality and apnea index in obstructive sleep apnea. Experience in 385 male patients. Chest. 1988;94(1):9-14.

8. Croft CB, Pringle M. Sleep nasendoscopy: a technique of assessment in snoring and obstructive sleep apnoea. Clin Otolaryngol Allied Sci. 1991;16(5):504-509.

9. Ahmed MM, Schwab RJ. Upper airway imaging in obstructive sleep apnea. Curr Opin Pulm Med. 2006;12(6):397-401.

10. Crookes PF. Surgical treatment of morbid obesity. Annu Rev Med. 2006;57:243-264.

11. Kribbs NB, Pack AI, Kline LR, et al. Objective measurement of patterns of nasal CPAP use by patients with obstructive sleep apnea. Am Rev Respir Dis. 1993;147(4):887-895.

12. Ferguson KA, Cartwright R, Rogers R, Schmidt-Nowara W. Oral appliances for snoring and obstructive sleep apnea: a review. Sleep. 2006;29(2):244-262.

13. Zonato AI, Bittencourt LR, Martinho FL, Gregorio LC, Tufik S. Upper airway surgery: the effect on nasal continuous positive airway pressure titration on obstructive sleep apnea patients. Eur Arch Otorhinolaryngol. 2006;263(5):481-486.

14. Kim SH, Eisele DW, Smith PL, Schneider H, Schwartz AR. Evaluation of patients with sleep apnea after tracheotomy. Arch Otolaryngol Head Neck Surg. 1998;124:996-1000.