Physicians must ensure that patients receive continuous medical follow-up when deciding to discontinue CPAP treatment.
By Allen Boone, RPSGT
Consider this situation: a patient with a diagnosis of obstructive sleep apnea (OSA) arrives for a follow-up appointment. While speaking with the sleep specialist, the patient announces that continuous positive airway pressure (CPAP) therapy is no longer wanted or needed. This problem arises in the offices of sleep specialists every day.
When is it acceptable for the patient to stop using CPAP? There are a number of parameters that must be explored before that decision can be made. For example, the specialist needs to ascertain
- what prompted the initial evaluation for OSA,
- what significant events have occurred since CPAP therapy began, and
- why the patient wants to end CPAP treatment.
The details of the initial diagnosis should also be part of this evaluation. In a sleep disorders center, there are several factors that contribute to the diagnosis of OSA-hypopnea syndrome (OSAHS). The first is a respiratory disturbance index (RDI) of 20 or more events per hour of sleep, as displayed during a diagnostic polysomnographic recording.
The second factor is obesity. While it is not present in all cases, it can place extraneous pressures on the pulmonary system. Pharyngeal fatty deposits increase the instability of the upper airway, leading to an increased risk of OSAHS. The reduction of the patient’s overall body-fat percentage has a positive impact on OSAHS, leading to the resumption of more normal flow characteristics.1
Third, as the body grows older, it loses tone in pharyngeal muscles as well as skeletal muscles. As patency of the upper airway depends on the condition of this area, loss of tone results in a compromise of airflow during sleep.
Excessive diurnal somnolence is the fourth factor. It has long been established that, in the presence of OSAHS, there is conjoint excessive diurnal somnolence. Many sleep specialists believe that the arousal index during polysomnography need be only at the level of 10 events per hour to warrant intervention; over an 8-hour period, the patient would be aroused 80 times for a minimum of 3 seconds per event. Furthermore, sustained sleep deprivation could precipitate a shift in the patient’s circadian cycle.
Fifth, use of tobacco and alcohol greatly affects sleep quality. According to Sanders et al,2 patients who smoke are at a four to five times greater risk for sleep-impaired breathing. Moreover, these patients display greater difficulty in initiating and maintaining sleep, thus increasing the potential for excessive diurnal somnolence (in addition to the lung-compromising effects of smoking). Alcohol, on the other hand, has a dual effect. First, it is a respiratory suppressant that decreases airway patency. Second, it impairs normal sleep-stage transitioning, thus affecting sleep architecture.
What conditions would indicate that the patient could discontinue CPAP? First and foremost, the patient’s polysomnogram would need to display an RDI of fewer than five events per hour, with an equal or lower arousal index. Second, the patient should have lost sufficient weight to fall within the guidelines for a normal body mass index (BMI).
While the aging process itself cannot be reversed, it is possible to reverse some of its effects. Initiating and sustaining an exercise program can help slow or reverse the loss of muscular tone. OSAHS is not the only sleep pathology to result in excessive diurnal somnolence, so any other causes for daytime sleepiness (such as narcolepsy, periodic limb movement syndrome, and idiopathic hypersomnolence) need to be ruled out as part of the evaluation. Last, but not least, the patient needs to have eliminated or drastically reduced indulgence in tobacco and alcohol. Unfortunately, the percentage of patients who qualify for CPAP cessation using this algorithm is exceedingly small; in no small part, that qualification is based on the patient’s past CPAP tolerance and compliance.
Some patients, however, want to stop therapy not because they do no longer need it, but because they feel unable to tolerate it. The pattern of CPAP use (or nonuse) is established shortly after the initiation of home therapy.2 Unfortunately, there is no correlation between disliking the therapy and ceasing to need it. As Sanders3 has stated, “Patients must actively participate in their own treatment or CPAP will not provide effective therapy.” Fortunately, there are more therapeutic options available now than at any point in the development of sleep medicine.
In the event that the patient is unable to tolerate CPAP therapy, there are newer systems on the market for positive–airway-pressure delivery. For example, bilevel and autoadjusting units have been shown to help patients tolerate the effects of higher pressures.4 If the unit can provide different inspiratory and expiratory pressures, patients often feel relief from overexertion during the exhalation cycle.
Autotitrating CPAP, on the other hand, improves the stability of the upper airway during the physiological changes that occur during sleep. One of the hallmarks of rapid-eye-movement (REM) sleep is the body’s skeletal-muscle atonia. This is frequently demonstrated during a diagnostic recording in which apneas become more pronounced during REM. Autotitrating CPAP makes the minor adjustments necessary to compensate for added or reduced pressure requirements.
Rather than looking at the pressure-producing device, many manufacturers have examined the pressure’s point of delivery. When CPAP first became available, the only option for its point of delivery was a nasal mask sold in one style and a few sizes. Today’s options are much more plentiful; they include various masks, as well as different point-of-delivery styles for those masks. For example, the patient’s alternatives include nasal prongs, full-face masks, and tiny masks that seem to cover only the nares.
One manufacturer has taken a completely different approach: the mouth. This company has developed a point-of-delivery device that uses a dentist-fitted bite block that accepts the tubing from a CPAP or bilevel unit.5 The patient wears the mouthpiece much as an athlete would wear a mouth guard. Mechanically, it splints the soft palate back toward the dorsal pharyngeal wall in order to maintain the open airway. In contrast, CPAP operates under the principle of splinting the soft palate toward the genioglossus. Further, as the diameter of the oropharynx is greater than that of the combined nares, the patient may need less pressure to stabilize the airway; this decreased pressure may, in turn, be easier to tolerate. The mouthpiece also offers the secondary assistance of a mandibular advancement device, but it is custom-made by a dentist, adding another clinician to the therapeutic process and increasing overall costs.
There are approximately 30 oral appliances used specifically to decrease the occurrence of sleep-related breathing disturbances. All are designed to reposition the mandible to maximize the diameter of the oropharynx. Much like CPAP therapy, these devices have their own titration process, but it is conducted by altering the distance of mandibular advancement and/or the amount of tongue suppression. The use of these devices should be preceded by polysomnographic and imaging evaluations.
The American Academy of Sleep Medicine6 recommends the use of oral appliances for patients who are being treated for primary snoring and/or mild apnea (with an RDI of less than 20) and for patients who have severe OSAHS but are noncompliant with CPAP therapy and are poor candidates for surgery. Oral appliances are considered lifelong therapies.
While there is no magic-bullet cure for OSAHS, surgery is, for many patients, a viable option. Obviously, one must weigh the discomfort of the surgical procedure against the individual patient’s degree of comfort with CPAP, remembering that a CPAP mask can be changed or removed, but surgery is permanent. When one recalls that the original apnea surgery was tracheostomy, it becomes clear that the medical community has made major advances in the treatment of OSAHS.
The evaluation of surgical options is a serious matter. An assessment targeting airway occlusion takes priority in this evaluation; it will determine the surgical technique to be used. In order to define the targeted area, the sleep specialist and the otolaryngologist review several key areas: neck circumference, BMI, cephalometric analysis, fiber-optic pharyngoscopy findings, and the results of the most recent polysomnographic data. The combined evaluation of these areas can often help to determine whether the obstruction is generalized in the nose, palate, tongue base, or pharyngeal wall.
There are many procedures (and combinations of procedures) that can reduce the occurrence of OSAHS. Tracheostomy was largely replaced by CPAP, but it is still the therapy of choice for patients with an RDI of more than 70, morbid obesity, severe facial deformity, hypoxemia, or significant cardiac arrhythmias. The point of this procedure is to stabilize the patient using the most readily available airway.
Nasal reconstruction is often dictated when obstruction is caused by excessive tissue in the turbinates or by a deviated septum. Patients with these problems are not only highly intolerant to nasal CPAP, but have a generalized tendency to autorotate the mandible backward while in the supine position. This combination results in OSAHS.
Pharyngeal reconstruction has proved to be one of the most popular techniques to date. It is often referred to as uvulo-palatopharyngoplasty (UPPP). The procedure involves removing a portion of the soft palate, the uvula, and any residual tonsillar tissue. Unfortunately, the procedure creates an estimated reduction in respiratory events of only 20% to 50%.7 In the event that the patient needs to return to CPAP therapy after surgery, however, a pressure reduction is often possible.
Other forms of surgery available include a uvulopalatal flap procedure, laser-assisted uvuloplasty (LAUP), mandibular osteotomy with genioglossus advancement, maxillomandibular advancement osteotomy, radiofrequency volumetric tissue reduction, and tonsillectomy-adenoidectomy. The evaluation of the obstructing area of the upper airway determines which of these surgical techniques is used. The goal of all of the procedures is to create greater tension and expansion room for the tongue, thus allowing an increase in the space available for the flow of air. Each procedure, however, is accompanied by its own degree of invasiveness and complexity. For example, maxillomandibular advancement osteotomy is considered a phase-II surgical procedure; repositioning the midface and mandible is generally considered an option only after simpler techniques (such as LAUP and radiofrequency volumetric tissue reduction) have failed. The primary focus is on ameliorating the degree of residual hypopharyngeal obstruction, making this technique most appropriate for patients in whom OSAHS cannot be resolved by any other means.
In contrast, LAUP is less invasive and is frequently performed on an outpatient basis over the course of three to four visits to the surgeon. The rationale for the procedure is the reduction of snoring by means of partial amputation of the uvula through laser incision.
Radiofrequency volumetric tissue reduction is a technique that involves inserting a thermistor-tipped probe into the targeted tissue. The probe is then activated via radio frequency, generating a heated area of 40ÞC to 90ÞC. The surrounding tissue is obliterated; as the body absorbs the dead tissue, the roof of the soft palate raises. The level of snoring and the residual RDI indicate the number of repetitions of this procedure needed to alleviate (or markedly reduce) the pathology. The radiofrequency volumetric tissue reduction technique offers the surgeon the ability to use the device for more than one physiologic area; for example, the unit can be used to reduce the turbinates, tonsils, adenoids, and the base of the tongue. The device can also be used in tandem with other procedures, such as UPPP. If surgical techniques fail to provide relief, the patient’s only available option is the resumption of positive airway pressure therapy.
OSAHS is usually considered a lifelong condition, and the patient who drops out of medical care constitutes a worst-case scenario for sleep specialists. Data on unresolved OSAHS have shown the medical community what adverse physiological effects can occur. Furthermore, the patient’s quality of life is detrimentally affected by untreated OSAHS, and treatment cessation increases the odds of a return to pathology.
The OSAHS patient needs continuous medical follow-up to ensure the efficacy of therapy. Clinicians must remember that the patient did not acquire the disorder overnight; likewise, resolution of the condition will be, at best, a long-term proposition. With this in mind, CPAP therapy should be encouraged and supported.
Allen Boone, RPSGT, is assistant director, Sleep Sciences Inc, Institute of Sleep Medicine, Birmingham, Ala.
1. Bassiri AG, Guilleminault C. Clinical features and evaluation of obstructive sleep apnea—hypopnea syndrome. In: Kryger M, Roth T, Dement W, eds. Principles and Practice of Sleep Medicine. 3rd ed. Philadelphia: WB Saunders; 2000:869-878.
2. Sanders MH, Strollo PJ Jr, Stiller RA. Positive airway pressure in the treatment of sleep-related breathing disorders. In: Chokroverty S, ed. Sleep Disorders Medicine. Boston: Butterworth Heineman; 1999:355-384.
3. Sanders MH. Medical therapy for obstructive sleep apnea—hypopnea syndrome. In: Kryger M, Roth T, Dement W, eds. Principles and Practice of Sleep Medicine. 3rd ed. Philadelphia: WB Saunders; 2000:879-893.
4. Grunstein R, Sullivan C. Continuous positive airway pressure for sleep breathing disorders. In: Kryger M, Roth T, Dement W, eds. Principles and Practice of Sleep Medicine. 3rd ed. Philadelphia: WB Saunders; 2000:894-912.
5. Open Airway Inc page. Available at: http://www.opap.com. Accessed August 14, 2000.
6. Lowe AA. Oral appliances for sleep breathing disorders. In: Kryger M, Roth T, Dement W, eds. Principles and Practice of Sleep Medicine. 3rd ed. Philadelphia: WB Saunders; 2000:929-939.
7. Riley RW, Powell NE, Li KK, Guilleminault C. Surgical therapy for obstructive sleep apnea—hypopnea syndrome. In: Kryger M, Roth T, Dement W, eds. Principles and Practice of Sleep Medicine. 3rd ed. Philadelphia: WB Saunders; 2000:913-928.