This report by the authors was enlightening, because many studies do not go on to ask what alternatives were sought by the patient. Not seeking other treatment is a very important follow-up question to ask in nonresponders to any OSA treatment. Adherence declines over time and is thought to be largely due to temporomandibular joint TMJ problems. Given the literature, TMJ, occlusal changes, excessive salivation, and discomfort are likely to be chief among the reasons for nonadherence to effective OA treatment.
As with all treatment, ineffectiveness is among the most prominent reasons patients do not adhere to treatment. To assess the above mentioned concerns of OA treatment, OSA patients treated with an OA need to return to determine optimal fit and then at 6 months, 1 year, and annually thereafter. This standard is not different from good medical care for any sleep medical treatment eg, prescription medicine, weight loss, CPAP, surgery.
Multiple PSG studies may be required to document a therapeutic response. Home studies seem indicated in these cases, with final verification using a full PSG in the sleep center. Long-term follow up is very important in OA therapy. Insufficient data exist to determine if damage to teeth and joints occur in patients using OA therapy. As noted, adherence data for OA treatment derive from subjective reports, whereas CPAP adherence can be monitored objectively. The development of objective measures of OA treatment would be of benefit in the future for patients and so that assessment of the adherence can be meaningfully compared between OA treatment, CPAP, treatment, and surgical correction over time.
Complications or adverse effects include excessive salivation, dental misalignment with bite change, and tooth movement. Cost may be a barrier to OA therapy. The lack of long-term studies with OA therapy may limit the clinician from choosing it as an option. Check with individual insurance carriers to verify coverage.
Research is needed to clarify design characteristics most beneficial in given patient groups, so that device selection is driven by data that are more precise. Surgical correction of the upper airway UA is still performed but is not considered primary therapy for OSA. The theoretical advantage of surgery is that if the patient is cured, compliance with CPAP or OA therapy is no longer an issue.
However, a primary reason why surgery has not become a standard therapy is the lack of any long-term outcome studies showing that surgical correction continues to be effective 5 or more years after it is performed. Surgery is also indicated in patients who have a specific underlying abnormality that is causing the OSA. Although surgical correction of such an abnormality ie, tonsillectomy can potentially cure OSA, most adult patients do not have such correctible lesions.
In some patients, tracheostomy or CPAP therapy is required in the perioperative period to ensure a safe airway. Functional division of the pharynx into the retropalatal-oropharyngeal region posterior to the soft palate and the retrolingual-hypopharyngeal region posterior to the vertical portion of the tongue has been proposed.
Obstruction in patients with SDB is classified into 3 types according to region. Type I is obstruction in only the retropalatal region. Type II is obstruction in both the retropalatal and retrolingual regions. Type III is obstruction in only the retrolingual region. A full listing of possible surgical procedures for OSA is available elsewhere.
UPPP is resection of the uvula and soft palate. Long term, patients with treatment success often present with a recurrence of symptoms, especially if they continue to gain weight. Craniofacial reconstruction involves advancement of the tongue ie, genioglossus advancement with hyoid myotomy [GAHM] or the maxillomandibular bones ie, maxillomandibular osteotomy [MMO]. These operations should be performed only at centers with expert personnel. Tracheostomy provides definitive correction because it bypasses the obstruction.
Different surgical procedures have been proposed for patients with different levels of obstruction. UPPP may correct type I obstruction. MMO may correct obstruction at all levels. Surgery is indicated only if noninvasive types of therapy have not worked or are rejected by the patient. Because several sites of obstruction may be responsible, a systematic approach for selecting surgery has been developed.
The protocol has 2 phases. Patients who are not adequately treated with phase I surgery are offered phase II surgery. It involves removal of the tonsils if present , the uvula, the distal margin of the soft palate, and the redundant pharyngeal tissue, as well as reshaping of the soft tissues in the lateral pharyngeal walls. Good preoperative evaluation does not guarantee surgical success; the effectiveness of the UPPP is variable, and the procedure should be considered when nonsurgical treatment options, such as CPAP, have been considered.
As such, it is not a recommended surgery alone in the adult OSA patient. This rate is despite preselection of patients with type I obstruction by using imaging and endoscopic studies. This finding highlights the inadequacy of the methods available to identify sites of UA obstruction. Complications from UPPP should be explained to patients in detail, as with all procedures; however, this is particularly true for those patients who use their voice to make a professional living eg, singers, muscicians who play instruments that require maneuvers involving the areas where tissue will be removed.
Change in voice, singing, or the playing of musical instruments that require changes in the soft palate to play. Silent apnea may result post-UPPP. Silent apnea refers to a condition in which the vibration of the tissues that caused snoring during airway collapse remains; thus, OSA persists but snoring does not. The decision to reevaluate OSA postsurgically should not depend on a postive report of snoring.
If the patient still snores, however, this indicates that the surgery was not curative of obstructive sleep-related breathing disturbance see the image below. It may also compromise subsequent CPAP therapy by promoting mouth leaking. In GAHM, the genioglossus muscle is repositioned anteriorly through an inferior mandibular osteotomy genioglossus advancement. This maneuver places the pharyngeal muscles and the base of the tongue on tension and expands the airway. The hyoid is suspended to the superior edge of the larynx and fixed in this position, adding to the effect of genioglossus advancement.
In MMO, the midface, palate, and mandible are moved forward, increasing the space behind the tongue and increasing tension on the genioglossus muscle. This operation is more extensive than any of the others described. It is usually reserved for patients in whom other treatment modalities fail. Tracheostomy is now reserved for patients with severe OSA in whom other medical and surgical treatment modalities fail.
Tracheostomy is also used for airway protection during UA reconstructive surgery. It may cause more scarring than UPPP, and it could potentially worsen apnea. Worsened OSA has been observed in the early postoperative period after laser-assisted uvulopalatoplasty. Laser-assisted uvulopalatoplasty is not recommended for the treatment of OSA until further data are available.
Laser midline glossectomy and lingualplasty are performed to enlarge the retrolingual region by using a laser to remove a portion of the posterior aspect of the tongue. The role of these procedures in the management of SDB has yet to be defined. Nasal surgery includes septoplasty, turbinectomy, and polypectomy and may be useful as an adjunct to other procedures or to improve CPAP adherence. Nasal surgery by itself is rarely effective for the treatment of OSA. Recent interest has been generated in a new technique, pioneered by Powell and associates, [ ] in which radiofrequency RF energy is used to ablate the soft palate.
A midline soft palate submucosal scar is created by using a needle electrode inserted near the border of the hard palate and directing it toward the uvula. Pulses of RF energy are delivered, resulting in tissue necrosis and needle-tract fibrosis over subsequent weeks to months. A study of 22 patients with mild SDB demonstrated reduced palatal tissue volume and improved symptoms in all subjects.
Evidence showed postsurgical improvement in the severity of esophageal pressure swings, indicating that this treatment may be useful in patients with UARS. One study of RF volumetric reduction of the soft palate in 12 patients demonstrated success in treating snoring, but data regarding adequate treatment of SDB are lacking.
RF volumetric reduction appears to decrease morbidity compared with UPPP, laser-assisted uvulopalatoplasty, and lingualplasty. Finally, animal studies of RF volumetric reduction of the tongue have shown volume reduction in tongue tissue after treatment. Results of human studies are pending. Bariatric surgery as therapy for OSA has been investigated in several nonrandomized, uncontrolled studies, with most showing a decrease in the AHI with weight loss.
Unfortunately, studies have not examined presurgery and postsurgery RDI or AHI using a design in which subjects were randomly assigned to a weight-loss surgery group and followed over time. At best, improvements in clinical symptoms have occurred after weight-loss surgery; however, again because no PSG data were available before or after weight-loss surgery and because subjects could not be randomly assigned to a weight-loss surgery group or control group, these data suggest that weight loss reduces OSA symptoms. It is unknown whether this is a placebo effect, as objective reduction in the RDI or AHI as determined by the criterion standard of PSG, was not permitted by the human subjects committee.
In a position paper on the treatment of OSA, the AASM stated that "[b]ariatric surgery should be considered as an adjunct to less invasive and rapidly active first-line therapies such as [positive airway pressure] for patients who have OSA and meet the currently published guidelines for bariatric surgery Consensus. Perioperative management of OSA is of special concern to anesthesiologists, and best practice papers have been published to address these concerns. Factors that increase the likelihood of successful surgery include 1 lower AHI, 2 lower BMI, 3 the location of collapse surgeries targeted specifically to collapse at either the nasopharynx or oropharynx improve outcome , 4 the degree of mandibular protrusion better outcomes are achieved in patients with clear deficiencies , and 5 the presence of fewer comorbidities.
The success of surgical procedures for OSA depends on accurate identification of the site of obstruction in the UA. Modalities available for identifying the site of obstruction include lateral cephalometry, endoscopy, fluoroscopy, computed tomography CT scanning, and magnetic resonance imaging MRI.
The accuracy of these methods in identifying the sites of obstruction is not clear. Data regarding surgical therapy for OSA are mainly from case series. The phased protocol of Riley-Powell-Stanford holds promise for achieving cure in patients with OSA, but further data from controlled clinical trials are needed to decide its role in the overall management of OSA. The success rates quoted are from select centers with surgeons highly skilled in these special procedures. These results cannot be extrapolated to the general population of patients with OSA. In one randomized study comparing temperature-controlled RF tissue ablation of the tongue with CPAP, CPAP was more effective at lowering the AHI but no differences were noted in functional outcome measures such as sleepiness at approximately 1 month of treatment.
In a retrospective cohort study, UPPP was found to be associated with decreased mortality compared with CPAP [ ] over a 3- to 5-year period of follow-up. Some of these patients may not have been "optimally" treated; rather, they were put on a positive pressure setting which, during the sleep disorders center positive airway pressure study, is sufficient to correct OSA. They may not be optimally treated for a number of reasons that need to be considered first, before placing patients in this subgroup of patients.
Positive airway pressure titration may be insufficient to fully treat OSA and snoring. Research suggests that pressures used to correct OSA and snoring are typically lower than those needed to abolish OSA and snoring. Once OSA and snoring are treated, patients may be noted to have complex sleep apnea ie, residual central sleep apneas that do not resolve spontaneously. Complex sleep apnea is beyond the scope of this article. Patients may not be using the positive pressure machine at home sufficiently to obtain adequate benefit to abolish sleepiness during waking hours.
A change in medication may have occurred that may decrease arousal from sleep eg, benzodiazepines , use of alcohol may have changed, or a medication that suppressed rapid eye movement REM sleep percentage was discontinued on the titration night, but once stopped, an increase in REM sleep percentage may be correlated with OSA exacerbation OSA is typically worse in REM sleep. Sildenafil Viagra may be increasing the severity of OSA.
Sildenafil prolongs the action of cyclic guanosine monophosphate cGMP and nitric oxide by inhibiting cGMP-specific phosphodiesterase 5. Nitric oxide promotes upper airway congestion, muscle relaxation, and pulmonary vasodilation and may be the mechanism by which sildenafil exacerbates OSA. A medical disorder that causes excessive sleepiness eg, hypothyroidism, even if subclinical may be present. Only rarely do new CPAP devices not have cards that stores data regarding daily positive airway pressure use.
Another sleep disorder known to have hypersomnia as a major presenting symptom eg, insufficient sleep syndrome, narcolepsy may be present. Consider a diagnosis of sleepiness in addition to OSA eg, narcolepsy. If residual sleepiness after treatment is present, a series of questions must be asked to determine its etiology. The residual sleepiness should never be considered idiopathic until all questions have been answered satisfactorily.
The algorithm used by the author can be found in the image below and the questions that follow it. Is the patient compliant with CPAP? Compliance has been generally defined in the modafinil studies as greater than 4 hours of use, at least 5 nights per week. Patient self-reporting may not be adequate to determine compliance. Objective monitoring with one of the newer CPAP units that measures compliance may be necessary. If identified, work with the patient to improve compliance. Is the titration pressure adequate? This is particularly important in 2 situations.
The first is if the patient had a difficult first titration, resulting in a prescription that may not be adequate to relieve symptoms. The second is if the patient develops symptoms months to years after initial relief, generally due to weight gain. In both cases, repeat titration is recommended. Some authorities advocate autotitration CPAP units in these situations.
Is the patient sleeping sufficiently or performing shift work? Chronic insufficient sleep and shift work are 2 of the more common causes of sleepiness.
In both cases, the patient must be counseled to sleep more. Is the patient on any medications that cause sleepiness. The most common medications causing this are the over-the-counter antihistamines. Other common agents are tricyclic antidepressants, benzodiazepines, narcotics, and many neurologic and psychiatric medications.
Does the patient have evidence of another sleep disorder that could cause sleepiness? A full evaluation by a sleep physician can often determine a second sleep disorder, such as narcolepsy or periodic limb movement disorder. If the above-mentioned potential causes of excessive sleepiness have been excluded, among others that the author may not have considered herein, use of stimulants to treat excessive sleepiness is indicated.
Two medications should be considered for treatment of residual sleepiness: These 2 agents are approved by the FDA for treating residual sleepiness despite optimal treatment of OSA using positive airway pressure therapy. If modafinil does not help at higher doses, the authors then consider armodafinil. Armodafinil reaches a peak plasma level nearly as quickly as modafinil and has a larger area under the curve for a given dose; additionally, the duration of action of armodafinil continues at the higher dosage throughout the day.
Because of this action, armodafinil has more potency and most often requires only once-a-day dosing taken in the morning for daytime workers and in the evening for nighttime workers. FDA approval of modafinil was based on several studies carried out in this patient population. One hundred fifty-seven patients were randomized 77 modafinil, 80 placebo , with completing the study 66 modafinil, 77 placebo.
Both the ESS and daytime sleep latency improved in the modafinil group. No difference was noted in CPAP use between groups. The effectiveness of modafinil in this clinical situation has been confirmed by a randomized, double-blind study of modafinil versus placebo for 12 weeks, which showed that the efficacy of modafinil, as measured subjectively by the ESS and objectively by the maintenance of wakefulness test MWT , does not change over an extended period 12 wk.
One concern clinicians share with the use of modafinil or other stimulants in the management of OSA is whether improvement in alertness with the use of these agents may lead to noncompliance with CPAP therapy. This is an important concern, because stimulants do not control the SDB, resulting in worsening symptom control and potentially increasing the risk of cardiovascular morbidity. Fortunately, this does not appear to be a major problem at present. The 2 largest trials did not show a decrease in CPAP usage with modafinil.
More data are needed to increase assurance that use of stimulants does not lead to noncompliance. The use of stimulant medications such as modafinil and armodafinil should be reserved for patients ideally treated with CPAP and who remain sleepy. However, there is not yet a consensus on the role of stimulant medications to enhance alertness, and research in nonideally treated OSA patients has not been performed to determine to what degree, if any, subjective and objective changes occur when the medications are used for OSA patients not treated ideally with CPAP.
Patients should restrict their body positions during sleep.game.kovalev.com.ua/assets/75.php
Obstructive Sleep Apnea Treatment & Management
SDB is worse in the supine position, and some patients have apnea only in this position. However, these devices are cumbersome and appear to benefit only those patients with mild OSA. Patients with marked obesity may benefit from sleeping in an upright position. Patients should avoid smoking. Smoking increases the risk of snoring and apnea. Smoking cessation appears to decrease the risk.
Individuals who smoke are also more likely than those who do not smoke to report problems with going to sleep, maintaining sleep, and daytime somnolence.
Obstructive sleep apnoea syndrome and its management
Patients should avoid drinking alcohol and using other sedatives known to make apnea worse. Finally, patients should avoid sleep deprivation. All patients with signs or symptoms of OSA should be referred to a sleep disorders center for an evaluation by a sleep physician and a PSG study. Any patient with loud habitual snoring and any other feature of OSA who is being considered for surgery should be referred for a sleep study prior to surgery. This is important to rule out OSA because the surgery is likely to correct the snoring but may not correct the apneas or hypopneas, which are associated with other morbidities.
Patients should also undergo complete evaluation by a dental professional, who should be experienced in OA therapy and should work in close collaboration with the sleep disorders specialist. Most patients are seen within 2 months of initiating CPAP to determine if it has been effective in alleviating symptoms eg, daytime sleepiness is substantially reduced or eliminated , to troubleshoot problems preventing regular use of the CPAP, and to reinforce the importance of daily use. If CPAP has been effective, the patient is generally seen at 6- to month intervals to troubleshoot new problems, to reinforce daily use, and to be certain the CPAP remains effective.
If CPAP has not been effective, problems preventing use are identified, steps are taken to eliminate problems, and the patient is seen at 2- to 3-month intervals until use is regular and the CPAP is alleviating symptoms. Repeat titration may be necessary. Routine repeat PSG is generally not indicated for patients who report improved symptoms. Repeat CPAP titrations are usually performed in patients without effective relief of their symptoms despite intervention or in patients who had relief of symptoms but present months to years later reporting the return of symptoms, generally in association with weight gain.
A study by Kuna et al assessed home monitoring and determined that functional outcome and treatment adherence in patients evaluated using a home testing algorithm was not clinically inferior to the results found among patients receiving standard, in-laboratory PSG. Assess the risk of driving in any patient with OSA. Criteria that increase this risk are as follows:. Immediately warn patients at highest risk of the potential dangers of driving while sleepy—specifically, of the potential personal and social risk. Provide additional counseling depending on other risk factors eg, occupation.
Advise patients to not drive until their OSA is treated adequately. Provide additional counseling to family members as appropriate, and help patients explore alternatives to driving if they are unaware of their sleepiness or if they are unwilling to acknowledge their increased risk. This documentation reinforces the importance of the message to the patient and helps reduce the risk of legal liability for medical personnel. Whether and under what circumstances patients with sleep apnea should be reported to the licensing authority depend on the laws of the state.
Those who take care of patients with OSA must be aware of state statutes or regulations regarding reporting of high-risk drivers. Laws regarding impaired drivers, including those with OSA, vary from state to state. In some states, the clinician is obligated to report patients under specific conditions ie, mandatory reporting statute , whereas other states permit reporting but do not require it ie, permissive reporting statute.
Mandatory statutes take 1 of the 2 following approaches:. With the categorical approach, the clinician is obligated to report patients who have specified medical conditions, such as epilepsy. In these states, the reporting obligation is based on diagnosis alone. Each clinician is obligated to adhere to the requirements of the law in the specific state of practice, even if those laws do not reflect sound public policy or medical evidence. Irrespective of whether statutory reporting is required, clinicians may be liable for damages if a patient with obstructive sleep apnea injures himself or herself or someone else while driving.
American Thoracic Society guidelines on reporting of patients to the appropriate state authorities are as follows [ 74 ]:. Increased occupational exposure to driving or increased occupational risk for an accident of substantial importance to the public may be other indications for reporting. Examples of patients in this situation are truck drivers who are transporting hazardous waste and school bus drivers.
A diagnosis of OSA without additional risk factors for impaired driving should not be the basis for reporting a patient unless required by state law. Categorical reporting may be most appropriate in the context of occupational licenses, but this is arguable. At a minimum, the threshold for suspecting an increased driving risk due to sleepiness should be low given the increased hazard.
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Evidence for lipid peroxidation in obstructive sleep apnea. In addition to risk factors, numerous signs and symptoms can suggest OSA, but polysomnography is the diagnostic standard. Predictive clinical features of OSA include observed gasping during sleep, morning headache, excessive daytime sleepiness, loud snoring, and neck circumference of greater than 16 inches Table 2 lists risk factors for OSA.
Information from references 6 , 19 , and As previously mentioned, men are three times more likely to have OSA, but they are nine times more likely to be referred for polysomnography, which suggests that the diagnosis of OSA may be overlooked in women. There are several screening questionnaires for OSA, although the accuracy of many of them is limited.
Nocturia and snoring are sensitive, but not specific, signs of OSA, although the specificity of snoring increases in proportion to the severity. In addition to large neck circumference and high body mass index, factors predictive of OSA include posterior chin position retrognathia , reduced distance and increased angles from the chin to the thyroid cartilage, and a narrow oropharyngeal opening. Sleep studies performed in a sleep laboratory or in the home can quantify the apnea-hypopnea index, which is required to diagnose OSA. Apnea is a complete obstruction of airflow, and hypopnea is a partial obstruction of airflow; both must last a minimum of 10 seconds.
The apnea-hypopnea index is calculated by adding all apneas and hypopneas and then dividing by total sleep time. An apnea-hypopnea index of 15 or more events per hour, or five or more events per hour in the presence of symptoms or cardiovascular comorbidities, is diagnostic for OSA Table 3. The diagnostic threshold for obstructive sleep apnea is reached when the apnea-hypopnea index reaches five or more events per hour in the presence of symptoms or cardiovascular comorbidities. Information from references 4 , 23 , 24 , 29 , and Overnight polysomnography performed in a sleep laboratory in the presence of an attendant is considered the first-line diagnostic study and is classified as a type-I study.
Diagnosis of obstructive sleep apnea in adults: In general, home sleep apnea tests are considered to be less accurate than type-I studies because of data loss from detached or malfunctioning monitoring equipment. Home sleep apnea tests can be an alternative to type-I studies in patients who are unable to present to a sleep laboratory. These tests are more accurate in identifying patients with a higher pretest probability of OSA and can rule out OSA in low-risk patients. Obesity results in fatty deposits around the neck, which contribute to pharyngeal collapse.
Strategies to avoid the supine position include placing tennis balls in a sock or pocket and pinning or sewing them onto the back of a shirt; wearing vests with posterior bumpers; and using positional alarms, verbal instruction, and pillows. Positive pressure therapies include continuous positive airway pressure CPAP , bilevel positive airway pressure, and auto-titrating positive airway pressure.
CPAP works via pneumatic splinting of the upper airways. Airway pressure may be applied through oral, oronasal, and nasal devices. CPAP has not only been shown to improve quality-of-life and sleep indices in patients with OSA, but also to lower blood pressure and rates of arrhythmia and stroke, to improve left ventricular ejection fraction in patients with heart failure, and to improve the rates of fatal and nonfatal cardiovascular events.
Auto-titrating positive airway pressure automatically adjusts pressure as needed to maintain airway patency and can be used in lieu of a formal CPAP titration study. These devices can be maintained in continuous self-adjustment mode, or a fixed pressure can be set based on information obtained during titration. The two main oral appliance therapies are mandibular advancement devices, which keep the patient's jaw forward to maintain an open airway, and tongue-retaining devices, which splint the tongue in place to keep the airway open.
Newer devices such as oral pressure therapy, which uses a mouthpiece and a vacuum pump to stabilize upper airway tissue, are being studied. CPAP has been shown to be superior to oral appliances in reducing apnea-hypopnea indices, arousal indices, and oxygen desaturation, particularly in patients with moderate to severe OSA, although quality-of-life indices appear to be similar to oral appliances. Numerous surgeries have been proposed and attempted to correct anatomic obstruction in patients with OSA: Surgical implantation of neurostimulators delivers electrical pulses to the hypoglossal nerve to increase tone to upper airway muscles.
A recent study showed that this method may be effective for treating OSA. They have been shown to be effective in reducing snoring but not effective for other sleep parameters. A PubMed search was performed using the key term obstructive sleep apnea. The search included randomized controlled trials, reviews, clinical trials, and meta-analyses. The authors thank Marilyn Daniels for her assistance with this manuscript. This article updates a previous article on this topic by Victor. Already a member or subscriber? At the time the article was submitted, Dr. Floyd was a third-year family medicine resident at Excela Health Latrobe Hospital.
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