Obstructive Sleep Apnea Syndrome
Obstructive Sleep Apnea Syndrome
Author: Steven M. Koenig, MD, FCCP, Director, Occupational Lung Disease Program, Director, Outpatient Pulmonary Rehabilitation Program, University of Virginia Health Systems, Charlottesville, VA.
Peer Reviewer: Paul Suratt, MD, John L. Guerrant Professor of Internal Medicine, Division of Pulmonary and Critical Care Medicine; Director of Sleep Disorders Center, University of Virginia, Charlottesville, VA.
Editor’s Note—The classic example of a disorder due to abnormal breathing during sleep is the obstructive sleep apnea (OSA) syndrome. Classically, the OSA syndrome is characterized by repetitive episodes of complete or partial upper airway obstruction during sleep, which results in signi-ficant physiologic consequences such as sleep disruption and oxyhemoglobin desaturation. Once thought to be an uncommon disorder, a recent community-based study estimated that 2-4% of randomly chosen middle-aged working adults have this condition.1 Evidence indicates OSA syndrome is associated with an increased rate of automobile and work-related accidents. OSA syndrome has also been associated with an increased prevalence of hypertension, coronary artery disease (CAD), cerebrovascular accidents, and increased mortality.
The purpose of this article is to outline the clinically relevant underlying pathophysiology, presenting symptoms, and signs, diagnosis, and treatment of OSA syndrome. Because OSA is clearly a major public health problem, and because many cases are often unsuspected, it is essential that primary care physicians as well as the public at large become more aware of the clinical presentation of this common disorder.
Pathogenesis2
Narrowing of the human pharynx or upper airway and the resultant elevated upper airway resistance are responsible for all the consequences associated with OSA syndrome. Therefore, individuals with this condition must have some abnormality or abnormalities of the determinants of the caliber of their upper airway. These determinants include the baseline pharyngeal area, which is determined by both craniofacial (bony) and soft tissue structures (i.e., fat around the airway), the collapsibility of the airway, the pressures inside the airway and in the tissues surrounding the pharyngeal wall, the outward pressure exerted by pharyngeal dilating muscles, the shape of the upper airway, and lung volume. Disorders that predispose to the development of OSA do so by influencing one or more of these determinants of upper airway size. Such predisposing conditions include anatomic abnormalities such as retrognathia; obesity; hypothyroidism; acromegaly; neuromuscular disorders; alcohol; sedative-hypnotics; nasal congestion; the supine position; and sleep deprivation. Such predisposing factors should be looked for in all patients suspected of having OSA syndrome.
Physiologic Consequences
The physiologic consequences of OSA syndrome can be divided into two categories—those due to arousal from sleep, and that secondary to oxyhemoglobin desaturation and hypercapnia (see Tables 1 and 2). Daytime sleepiness and visual motor incoordination are the presumed cause of the increased rate of automobile and work-related accidents in patients with OSA compared with the general population.3 Unrecognized sleep apnea occurs in approximately 20-30% of hypertensive patients in the United States.4 OSA syndrome is also associated with increased prevalence of CAD and cerebral vascular accidents as well as excess mortality.5-7 Because current morbidity and mortality data are based on retrospective studies, the true effect of sleep disordered breathing on society remains unknown. A randomized trial is clearly required and, in fact, is presently ongoing.
| Table 1. Consequences of Arousal from Sleep |
| Sleep fragmentation |
| • Excessive daytime sleepiness |
| • Personality changes |
| • Intellectual deterioration |
| • Visual-motor incoordination |
| • Impotence |
| Insomnia |
| Restlessness |
| Choking, gagging, gasping, resuscitative snorting |
Definitions
An apnea is defined as the complete or near complete cessation of airflow that lasts for at least 10 seconds.8 A hypopnea is defined as a 50% or higher decrease in airflow or less than a 50% decrease with either an oxyhemoglobin desaturation of 3% or more or an arousal from sleep lasting at least 10 seconds.8 Both abnormal breathing events are associated with similar sequelae and are treated in the same manner. They often occur together in the same patient.
Apneas and hypopneas are further divided into obstructive, central, and mixed. They are considered obstructive if there is continued or increasing respiratory efforts despite absent or diminished airflow, and central if there is absent respiratory effort. An event is labeled mixed if it begins as a central apnea or hypopnea and is terminated by an obstructive event (see Figure 1).
The upper airway resistance syndrome (UARS) is a newly described syndrome in which upper airway narrowing alone, without an associated apnea, hypopnea, or oxyhemoglobin desaturation, causes arousal from sleep.9 These repetitive episodes of upper airway narrowing and consequent arousals lead to excessive daytime sleepiness (EDS) or tiredness. Since both obstructive hypopneas and increased upper airway resistance alone can have profound physiological consequences, the term OSA is not, strictly speaking, applicable to the entire spectrum of sleep-disordered breathing. It is best reserved for those individuals with the most severe form of the disease. The term obstructive sleep-disordered breathing (OSDB) syndrome better describes the entire spectrum of obstructive breathing abnormalities during sleep. On one end of the continuum of upper airway narrowing and consequent increased upper airway resistance is primary, asymptomatic snoring. This is followed by the UARS, then the obstructive sleep hypopnea syndrome, and finally by the OSA syndrome (see Figure 2).
Indicators of the severity of OSDB syndrome include the apnea index, which is the number of apneas per hour of sleep, the hypopnea index, which is the number of hypopneas per hour of sleep, the respiratory disturbance index (RDI), which is the number of apneas plus hypopneas per hour of sleep and the oxyhemoglobin desaturation index, which is the number of oxyhemoglobin desaturation episodes 3-4% or more per hour.
Diagnosis
The possibility of sleep disordered breathing should be considered in any patient with any of the predisposing factors, signs, or symptoms mentioned above (see Tables 1 and 2). Talking with the bed partner, family members, friends, or fellow employees can be helpful, as they will often notice signs such as apneas or falling asleep unintentionally that the patient may be unaware of or deny. The next step is to estimate a clinical likelihood or pretest probability of sleep disordered breathing based on a focused history and physical examination. This evaluation should include searching for alternative explanations for symptoms such as insufficient sleep or shift work causing EDS (see Table 3). Although commonly reported, the following symptoms of EDS do not distinguish sleep apnea from other nonpulmonary sleep disorders: unrefreshing or nonrestorative sleep, morning headaches, cognitive impairment, depression, nocturnal esophageal reflux, nocturia or enuresis, hearing loss, automatic behavior, sleep drunkenness (disorientation, confusion upon awakening), hypnagogic hallucinations and night sweats.
| Table 2. Consequences of Nocturnal Hypoxia/Hypercapnia |
| • Polycythemia |
| • Pulmonary hypertension |
| • Cor Pulmonale |
| • Chronic hypercapnia |
| • Morning and nocturnal headache |
| • Left-sided congestive heart failure |
| • Cardiac dysrhythmias |
| • Nocturnal angina |
| • Diurnal systemic hypertension |
In any patient presenting with a complaint of daytime sleepiness, the degree of sleepiness should be quantitated. The sleepier the individual, the more likely he has sleep disordered breathing or some other significant disorder, and the more severe the condition, the latter influencing treatment. A reasonable approach is to divide sleepiness into mild, moderate, and severe, based on the frequency of sleep episodes, the degree of impairment of social and occupational function, and in what situations sleep episodes occur. With mild sleepiness, sleep episodes are infrequent, may not occur every day, and occur at times of rest or when little attention is required, such as while watching TV, reading, or traveling as a passenger. Sleepiness is considered severe when it is present daily, and when sleep episodes occur even during activities requiring sustained attention such as eating, conversation, walking, and driving. Moderate sleepiness lies somewhere in between these extremes. It is important to remember that daytime sleepiness is underreported.10,11 Fatigue may be the only symptom. Thus, the absence of sleepiness cannot be used to reliably exclude OSA. In addition, sleep disordered breathing is not the only cause of EDS. (See Table 4.) That is, EDS is not specific for sleep disordered breathing either.
Those physical examination findings that significantly increase the likelihood of sleep disordered breathing are listed in Table 3. Other features that should be searched for include craniofacial and upper airway abnormalities, such as retrognathia, tonsillar hypertrophy (especially in children), and an enlarged soft palate. The size and consistency of the tongue; presence of pharyngeal edema or abnormal reddish coloring of the pharynx; appearance of the soft palate; size, length, and position of the uvula; and evidence of trauma. Nares, including whether they collapse with inspiration, particularly while the patient is supine, should also be noted.
| Table 3. Features most Useful in Determining the Probability of Obstructive Sleep Disordered Breathing |
| • Male sex |
| • Age > 40 |
| • Habitual snoring |
| • Nocturnal gasping, choking, or resuscitative snorting |
| • Witnessed apnea |
| • BMI > 25 kg/m2 or neck circumference ³ 17 inches in males, ³ 16 inches in females |
| • Systemic hypertension |
| Table 4. Differential Diagnosis of Excessive Daytime Sleepiness |
| Insufficient Sleep |
| Central nervous system abnormality |
| • Narcolepsy |
| • Post-traumatic hypersomnia |
| • Recurrent hypersomnia |
| • Drugs |
| • Depression |
| • Idiopathic hypersomnia |
| Circadian rhythm disorder |
| Sleep Fragmentation |
| • Periodic limb movement disorder |
| • Sleep disordered breathing |
| • Medical disorders (i.e., arthritis) |
| • Neurological disorders (i.e., Parkinson's disease) |
Unfortunately, subjective impression alone, based on history and physical examination, lacks both sensitivity (52-78%) as well as specificity (50-79%).12-15 Although plugging clinical variables into regression formulas improves these operating characteristics somewhat (sensitivity [79-92%], specificity [50-51%]), many involve complicated mathematical formulas, which limits their usefulness.13,15,16 Moreover, even if the clinical likelihood is low, the post-test probability for OSA, defined as a respiratory disturbance index (RDI) greater than 10, still varies between 16% and 21%.13,16,17 In addition, patients with symptoms secondary to UARS would have been missed in these studies, decreasing the sensitivity of clinical assessment even further. Whether a post-test probability for OSA of 16-21% is low enough will depend on the threshold at which a physician is willing to accept diagnostic uncertainty. The threshold for pursuing further diagnostic testing should be lower in patients with severe daytime sleepiness, comorbid illnesses such as CAD, a driving accident record, and certain occupations (i.e., school bus driver).
If further diagnostic testing is deemed necessary, options include a formal sleep study or polysomnogram (PSG) and a variety of portable monitoring systems. The gold standard for diagnosing OSA syndrome is a polysomnogram. Variables typically recorded include the following: electroencephalogram (EEG), electrooculogram (EOG), and submental electromyogram (EMG) to stage sleep; airflow and respiratory effort to detect and diagnose hypoventilation or the type of apnea or hypopnea; oxygen saturation; electrocardiogram (ECG); and tibialis anterior EMG to detect periodic leg movements, a cause of excessive daytime sleepiness. To decrease the cost of PSG and facilitate treatment, a split night study can be performed. With a split night study, the initial portion of the evening is spent determining whether sleep disordered breathing is present. If sleep disordered breathing is documented, the remainder of the night is spent finding and titrating the most effective treatment.
Because of the cost and frequent unavailability of PSG, investigators have sought less expensive alternatives to formal sleep studies performed in sleep laboratories. These portable recording devices differ in the number and types of parameters measured, varying from pulse oximetry alone to all those variables measured in the sleep laboratory. Each is associated with its own advantages as well as disadvantages. Advantages of these portable systems include lower cost, greater availability, and ability to perform in the patient’s home. Of those devices that have been studied and the results published in peer reviewed journals, their sensitivities vary from 78% to 100%, and their specificity varies from 67% to 100%, depending on the particular system, the number of variables monitored, and the definition of sleep apnea.18
The major disadvantage of portable systems and pulse oximetry is the possibility of false-negative results. The likelihood of a false-negative study depends on the number of variables monitored and is due to not staging sleep, observing body position, or detecting UARS. In addition, these systems cannot diagnose other etiologies of excessive sleepiness such as periodic leg movements and narcolepsy. Finally, even if these portable systems were 100% specific, a formal PSG is still required if significant sleep disordered breathing is documented. The optimum nasal continuous positive airway pressure (CPAP) must be determined and, at least at the present time, this is done primarily in a sleep laboratory. However, with the advent of self-titrating or Auto-CPAP devices, some of which have the capability to diagnose sleep disordered breathing as well as initiate treatment, this situation may soon change. A recent study comparing the cost-utility of treating OSA syndrome based on polysomnography, home testing, and bedside diagnosis concluded that polysomnography was superior.19
At the present time, the following is the approach I use to determine the presence of OSDB (see Figure 3): 1) Consider the diagnosis of sleep disordered breathing in anyone with any predisposing factor, sign, or symptom consistent with the diagnosis; 2) Estimate a clinical likelihood or pretest probability based on the number and predictive value of the patient’s signs and symptoms and predisposing factors, as well as the presence of alternative explanations (i.e., insufficient sleep or shift work as the cause of their daytime sleepiness); 3) Take into account the potential consequences of missing the diagnosis. That is, have a lower threshold for pursuing the diagnosis in a school bus driver, someone who has already had an auto accident, or someone with underlying CAD. A Multiple Sleep Latency Test (MSLT) consists of a series of four or five opportunities to sleep administered at two-hour intervals using standard procedures. Sleepiness is measured as the speed of falling asleep (sleep latency); the presence of rapid eye movement (REM) sleep is also noted. An average sleep latency for all naps of less than five minutes is considered severely sleepy; 5-8 minutes moderately sleepy; 8-10 minutes mildly sleepy; and 10 minutes or more normal. The appearance of REM sleep in two or more naps is suggestive of narcolepsy. A positive oximetry study is defined as one with a pattern of repetitive, short duration oxyhemoglobin desaturation.20 No absolute (i.e., £ 90%) or relative (i.e., ³ 3-4%) decrease in oxyhemoglobin saturation is used. With this criteria, the negative predictive value of nocturnal pulse oximetry is good (96.9%), but the positive predictive value is not (61.4%). Consequently, every abnormal oximetry requires follow-up. Finally, for any other constellation of signs or symptoms, perform a split night PSG.
Treatment
I use the following definitions of OSDB syndrome: AI > 20 or RDI ³ 30 regardless of symptoms; RDI ³ 5 or number of arousals due to respiratory effort-related arousal > 10 plus some physiologic consequence, such as excessive daytime sleepiness, impaired cognition, mood disorder, insomnia, or documented cardiovascular disease such as hypertension, ischemic heart disease, or stroke.8 Since the optimum therapy for OSDB depends on the severity of disease, the first task is to estimate this severity (see Table 5).
| Table 5. Severity Scale for Sleep Disordered Breathing | |||||
| Severity | Respiratory Disturbance |
Minimum Oxygen |
Cardiac Dysrhythmia |
Excessive Daytime |
|
Index (RDI) |
Saturation |
Sleepiness |
|||
MSLT |
ESS |
||||
(min) |
|||||
| Mild | > 5-20 |
³ 85% |
Tachy-bradycardia |
8-10 |
> 10-12 |
| Moderate | 21-50 |
65-84% |
Severe tachy- |
5-8 |
12-16 |
bradycardia |
|||||
| Severe | > 50 |
< 65% |
Ventricular |
> 16 |
|
tachycardia; |
|||||
sinus arrest |
|||||
or pause |
|||||
> 3 seconds |
|||||
The goals of treatment are the elimination, in all sleep positions and sleep stages, of all evidence of increased upper airway resistance, which includes hypopneas and apneas; an oxyhemoglobin saturation 88-90% or above; no sleep disruption from respiratory effort-related arousals, hypopneas, or apneas; and no snoring. Therapeutic options for sleep disordered breathing can be divided into conservative, medical, and surgical.
Conservative Treatment
Although the importance of avoiding factors that can increase the severity of sleep disordered breathing should be discussed with all patients, if the patient has mild disease and a clear predisposing factor, conservative therapy may be all that is required. Patients should avoid factors that can increase the severity of upper airway resistance such as sleep deprivation, alcohol, and sedative-hypnotic agents. In some individuals, sleep disordered breathing occurs only in the supine position. Training individuals to sleep primarily in the supine position may completely alleviate their sleep disordered breathing, though the long-term effectiveness of this intervention is unclear. One technique is to place one or more tennis balls (or a similar object) in a pocket sewn in the back of a nightshirt or in a sock that is then pinned to the garment. Hopefully in time, the person will be "trained" to sleep in the lateral recumbent position and, therefore, no longer require the tennis ball(s). Some patients may benefit from elevating the head of the bed at a 30-60° angle. The head-up or lateral recumbent position may also benefit the patient who is suboptimally treated on maximally tolerable positive-pressure therapy such as CPAP. If present, treatment of increased nasal resistance with a combination of nasal steroids, decongestants, and/or antihistamines should be undertaken. Likewise, hypothyroidism and acromegaly should be appropriately treated. Since treatment of hypothyroidism without concomitant treatment of OSA may result in more severe oxyhemoglobin desaturation due to increased oxygen consumption, both should be treated concurrently (i.e., with nasal CPAP). Nasal CPAP treatment may be discontinued after treatment of the endocrine abnormality, if a follow-up PSG no longer demonstrates significant sleep disordered breathing. In obese individuals, dietary weight loss can significantly improve OSA.
Medical Treatment
Nasal Continuous Positive Airway Pressure (CPAP).21 For patients with moderate-to-severe disease, conservative treatment alone is rarely adequate, and treatment with nasal CPAP becomes the next therapeutic option. With this device, CPAP is applied to the upper airway with a nasal mask, nasal prongs, or an oronasal mask. Although there are numerous proposed mechanisms, CPAP acts predominantly by providing a "positive pressure or pneumatic splint" to the upper airway, preventing the airway narrowing that occurs when dilator muscle activity decreases at sleep onset (see Figure 4).
If tolerated, nasal CPAP is effective in the majority of cases of OSDB. Thus, the major limiting factor is compliance, with subjective estimates by the patient being much higher than objective measurements. In one study, only 46% of patients complied with treatment.22 Compliance appears more closely linked to relief of daytime symptoms such as decreased alertness than to the severity of the RDI.23 It can be improved with simple interventions such as weekly phone calls and written information about sleep apnea and the importance of regular CPAP use.24
At least part of the reason for the poor compliance with nasal CPAP is side effects, which can be divided into nasopharyngeal (congestion, dry nose/mouth, sinus discomfort, headache, ear discomfort/infection, epistaxis) and pressure-related (chest wall discomfort, ear discomfort, smothering sensation, and barotrauma [pneumothorax, pneumomediastinum, pneumoencephalos] symptoms). Mouth opening, claustrophobia, conjunctivitis, bridge of nose bruise/ulceration, allergic reaction, and the inconvenience of being attached to a machine may also be problematic. Although the precise cause of the nasopharyngeal symptoms is unknown, they likely result from the machine’s cool, dry air injuring the lining epithelium and/or stimulating nerves in the nasopharynx (see Table 6). The function of the ramp option found on most CPAP machines is to allow the CPAP pressure to gradually increase to the prescribed level over a period of 5-45 minutes.
| Table 6. Treatment of Adverse Effects of Nasal CPAP |
| Nasopharyngeal Symptoms |
| Humidification |
| • Nasal salt solution/spray |
| • Add humidifier to machine |
| Nasal steroids |
| Other |
| For nasal congestion: |
| • Infrequent: alpha-adrenergic spray |
| • Frequent: alpha-adrenergic pill |
| • Intractable: oronasal mask |
| For rhinorrhea: |
| • Anticholinergic spray |
| • Nasal Nedocromil |
| • Nasal Cromolyn sodium |
| Pressure-related symptoms |
| Ramp |
| BiPAP |
| Auto-CPAP |
| Relaxation techniques |
| Mouth opening |
| Chin strap |
| Form fitting mouth guard |
| Oronasal mask |
| Claustrophobia |
| Different mask |
| Relaxation techniques |
| Desensitization |
| Conjunctivitis |
| Adjust mask fit |
| Different mask |
| Bridge of nose bruise/ulceration |
| Reinforce area |
| Different mask |
| Allergic reaction |
| Different mask |
Devices that automatically adjust or self titrate the nasal CPAP based on the pressure required to maintain upper airway patency have recently been developed. Some of these "Auto-CPAP" devices are effective in determining the optimal CPAP setting for most OSA patients.25 They allow reduction in the average nasal CPAP required and titration of CPAP without the immediate involvement of a technologist. Treatment with auto-titrating nasal CPAP systems have shown slight increases in adherence when compared to fixed-pressure nasal CPAP.26,27 Additional studies, particularly in the home setting, are needed to determine the optimal role of "autotitrating" CPAP devices in the treatment of OSDB. At the present time, it would be reasonable to use one of these devices in patients having difficulty tolerating "fixed" CPAP due to pressure-related symptoms.
Nasal Bilevel Positive Airway Pressure. Bilevel positive airway pressure systems differ from nasal CPAP in that the former allows the independent adjustment of inspiratory positive airway pressure (IPAP) and expiratory positive airway pressure (EPAP). With nasal CPAP, the IPAP and EPAP must be the same. Depending on the particular machine, bilevel systems also allow the operator to set a back-up respiratory rate, change the IPAP percentage, and adjust the flow sensitivity. Thus, unlike nasal CPAP, bilevel systems permit ventilation of the patient. However, ventilation is typically not required with OSDB, unless hypoventilation coexists.
Since a higher pressure is required to maintain adequate upper airway patency during inspiration than expiration, if a bilevel system is used, the EPAP can usually be decreased. This lower EPAP may diminish problems with exhaling or a "smothering" sensation, the risk of barotrauma (due to a lower mean alveolar pressure), the risk of hypercapnia (since ventilation can be instituted), and significant mask air leakage. However, although patient acceptance may be better with bilevel systems, compliance is similar to that with CPAP.28 BiPAP is the bilevel system manufactured by Respironics, Inc., in Murrysville, PA.
Oral Appliances.29-33 Currently, oral or dental appliances are considered useful for primary snoring but are considered second-line therapy for OSDB. These devices are most effective for patients with mild OSA who do not respond to conservative measures. Since some patients with moderate-to-severe disease may respond as well, I consider an oral appliance in such individuals if they are intolerant of, refuse, or are not candidates for nasal CPAP, a bilevel system, or surgery. Nonobese individuals and those with OSDB predominantly in the supine position are more likely to improve with an oral appliance. Those devices that work appear to do so by increasing the posterior airway space by providing a stable anterior position of the mandible, by advancing the tongue or soft palate, and possibly by changing genioglossus muscle activity. Close cooperation between physician and dentist is necessary to ensure optimal patient selection and follow-up and to avoid potential side effects. Problems include tongue, gum, or temporomandibular joint (TMJ) soreness and orthodontic problems. Compliance ranges from 50% to 100% and, in a recent study, was preferred over nasal CPAP. As for surgical procedures for OSA, it is difficult to predict success, and treatment may improve OSA somewhat, but the patient is still left with significant residual disease. Consequently, a follow-up sleep study is required for moderate-to-severe disease, but not primary snoring or mild OSA.
Medications.34 Overall, medications are not effective in the treatment of OSDB or OHS. With the exception, perhaps, of fluoxetine and tricyclic antidepressants in patients with mild OSDB, oxygen for central apnea and hypoventilation, and anorexiant drugs for weight loss, medications for the treatment of OSDB should be limited to patients who refuse, cannot tolerate, or have contraindications to weight loss, nasal positive airway pressure, oral appliances, and surgery. When used, follow-up PSG in patients who appear to have responded to treatment is mandatory. Fluoxetine and tricyclic antidepressants work by suppressing REM sleep and increasing upper airway dilator muscle tone. These agents may also allow a decrease in high nasal CPAP. The role of anorexiant drugs in the treatment of OSA remains unclear.
Moreover, the association of fenfluramine and phentermine with cardiac valvulopathies and primary pulmonary hypertension has resulted in their being removed from the market.
Surgical Treatment35
The goal of surgery is to improve one or more of the determinants of upper airway caliber.
Nasal Surgery. Nasal surgery alone is rarely curative but is often used in conjunction with other surgical procedures (i.e., as part of Phase 1 surgery for OSA).
Adenotonsillectomy. Although this procedure can be curative in children and adolescents with OSA, it is not usually helpful in adults.36 However, in carefully selected adults, it may be the only treatment required.37
Uvulopalatopharyngoplasty (UPPP).38-41 The most commonly performed surgical procedure for OSDB is UPPP. The procedure involves removal of the tonsils, uvula, redundant soft palate, and pharyngeal folds. The overall success rate is less than 50%. Preoperative imaging studies and testing cannot reliably predict surgical success. This procedure is most likely to be successful if upper airway collapse is limited to the oropharynx, and if the RDI is less than 20-30, that is, with less severe disease. Unfortunately, in 75% of cases, there is more than one site of upper airway obstruction, a fact that is the likely explanation for the poor success rate. Potential complications include nasal reflux and speech problems. Post-operative pain is significant.
Laser-assisted Uvulopalatoplasty (LAUP).38,42-45 LAUP has recently been introduced as an outpatient treatment for snoring and potentially for OSDB. It involves removing part of the uvula and associated soft palate with a CO2 laser in 1-7 sessions. Unlike the surgical UPPP, neither the tonsils nor the lateral pharyngeal tissues are removed or altered. Compared to UPPP, LAUP is less expensive, bloodless, requires less time off from work, does not require general anesthesia and hospitalization, and is not associated with velopharyngeal insufficiency or stenosis. Although less painful than UPPP, 60-75% of patients report severe postoperative pain from one to eight and, up to, 21 days. Snoring is subjectively cured or softer in 76-90% of cases, with best results occurring when a long uvula or a draping soft palate is present. Considering the advantages over UPPP, it may be the most appropriate surgical treatment for snoring. Although not previously recommended for the treatment of OSDB, recent evidence indicates that in carefully selected patients with mild, moderate, or severe disease, LAUP may be considered a surgical option. However, some patients may have worse OSDB postoperatively and LAUP may decrease nasal mask tolerance. Thus, if performed for OSDB, a postoperative PSG to document efficacy is essential. One potential problem with LAUP is that the elimination of snoring removes one of the signs of OSDB and may provide a false sense of security.
Maxillofacial Surgery.42,46,47 Because of the poor and unpredictable results with UPPP, a variety of other procedures have been developed to further increase the size of the upper airway. Such surgeries ideally have both an otorhinolaryngologist and oral surgeon involved. Inferior sagittal mandibular osteotomy plus genioglossal advancement, with or without a hyoid myotomy and suspension, enlarges the retrolingual (behind the tongue) airway. These procedures may be performed in conjunction with a UPPP and nasal surgery. With success being defined as an RDI less than 20 and a 50% or more decrease, there is a 66-67% response rate to this Phase 1 surgery. Complications include need for a root canal, numbness, dysesthesia of the chin for 3-6 months, and facial contour changes.
If the patient has significant craniofacial abnormalities and/or has not responded to "Phase 1" surgery, maxillomandibular osteotomy and advancement is an option. This procedure further advances the tongue and enlarges the retropalatal airway as well. In the right hands, results have been good, with more than a 90% success rate being reported.46 Average hospital stay is two days, the major complications being dysesthesia or paresthesia of the face that lasts six weeks to six months.
Tongue Reduction Surgery. Laser midline glossectomy is also an option for those who fail the above mentioned surgical procedures. However, this procedure is associated with a long difficult recovery, speech problems, and some persistent sensory loss. The substantial associated edema requires placement of a temporary tracheostomy.
Tracheostomy. With the many surgical options and, in particular, the advent of nasal CPAP and BiPAP, tracheostomy is infrequently used as treatment for OSA. This procedure should be required in less than 5% of cases. Nonetheless, there is a small subgroup of patients with severe OSDB who cannot tolerate or do not respond to other therapeutic options. In these individuals, tracheostomy, which completely bypasses the upper airway obstruction, can provide dramatic improvement and can be lifesaving. However, the potential for additional medical as well as psychological morbidity needs to be taken into account.48,49
Radiofrequency Volumetric Tissue Reduction.50 Performed in the office under local anesthesia, radiofrequency volumetric tissue reduction has recently been FDA approved for the treatment of snoring but not OSDB. Its role in the surgical management of OSDB remains to be defined.
Bariatric Surgery.51 For significantly obese individuals with either OSDB, surgical weight loss procedures are another option. Weight-loss surgical procedures that have been studied include gastric bypass, jejuno-ileal bypass, and gastroplasty. Results have been impressive and include a weight change of 31-72.5%, an increase in RDI of 89% to 98%, improved nocturnal oxyhemoglobin saturation, decreased cardiac dysrhythmias, improved subjective daytime somnolence, and improved sleep continuity and architecture (increased total sleep time, % slow wave sleep, % REM sleep). Unfortunately, all studies of the effect of weight loss on sleep disordered breathing thus far are poorly designed, and are little more than a series of case reports. Moreover, good data on the risks and benefits of surgery, the effects of bariatric surgery on waking performance, and long-term follow-up on either the weight loss or improvements in sleep and sleep-disordered breathing are lacking. Clearly more and better-controlled studies are needed.
Summary
OSA syndrome is a common disorder and a clinically significant disease affecting 6% of the middle-aged adult working population. It is associated with significant adverse health effects, can present subtlely, and is frequently overlooked. If undiagnosed, OSA syndrome may be associated with significant morbidity and even mortality. Moreover, it is readily and noninvasively diagnosed, and typically easily treated. Consequently, it would behoove all primary care physicians to at least consider obstructive sleep disordered breathing in any patient who has any predisposing factor, sign, or symptom associated with this disease.
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19. Chervin RD, et al. Cost-utility of three approaches to the diagnosis of sleep apnea: polysomnography, home testing, and empirical therapy. Ann Intern Med 1999;130:496-505.
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Physician CME Questions
30. Of the following statements about obstructive sleep apnea, which is incorrect?
a. Only obese individuals develop obstructive sleep apnea syndrome.
b. Unrecognized sleep apnea occurs in 20-30% of hypertensive patients in the United States
c. Two to four percent of middle-aged adults have obstructive sleep apnea syndrome.
d. Severe obstructive sleep apnea syndrome is associated with increased mortality.
e. Patients with obstructive sleep apnea syndrome may not report excessive daytime sleepiness.
31. Of the following, which is most reliable in establishing or eliminating the diagnosis of obstructive sleep apnea syndrome?
a. History
b. Physical examination
c. Nocturnal oximetry
d. Portable recording device
e. Polysomnogram
32. If tolerated, which of the following is the most effective treatment for most cases of obstructive sleep apnea in adults?
a. Uvulopalatopharyngoplasty (UPPP)
b. Oral appliance
c. Nasal continuous positive airway pressure (CPAP)
d. Oxygen
e. Adenotonsillectomy
33. Which of the following statements about nasal continuous positive airway pressure (CPAP) is incorrect?
a. Nasal CPAP acts predominantly as a "positive pressure splint" to the upper airway.
b. Compliance is not a problem with nasal CPAP.
c. Auto-titrating nasal CPAP machines may allow reduction in the average pressure required to maintain upper airway patency.
d. Nasal congestion and sinus discomfort may result from nasal CPAP use.
e. The inspiratory and expiratory positive airway pressures can not be adjusted independently.
34. Which of the following statements about uvulopalatopharyngoplasty (UPPP) is correct?
a. UPPP is effective treatment for the majority of patients with obstructive sleep apnea.
b. Preoperative imaging studies and testing can reliably predict surgical success.
c. Post-operative pain is significant and potential complications include speech problems.
d. Success rates are similar with mild and severe obstructive sleep apnea.
e. It is the surgical procedure of choice for snoring.
Attention Primary Care Reports Subscribers
Three new recommendations from the Centers for Disease Control and Prevention (CDC) were announced in July 1999, after the July 12, 1999 issue, Immunization Update, was sent to the printer.
1. Use of the rotavirus vaccine has been suspended until November 1999 because of concerns about an apparent increased incidence of intussusception within the first week or two after vaccine administration. The data on this are being analyzed and an updated recommendation will be made in October, prior to the expected seasonal increase in rotavirus infections.
2. In an effort to minimize exposure in young infants to thimersol, a mercury-containing preservative used in vaccines, low-risk infants should not receive their first dose of thimersol-containing hepatitis B vaccine until age 2 to 6 months. Recommendations for infants born to HbsAg-positive women (or women of unknown HbsAg status) remain unchanged from the 1999 Recommended Childhood Immunization Schedule, with immunization recommended at birth. COMVAX is a combination vaccine containing thimersol-free hepatitis B and Hib (PRP-OMP). COMVAX is the only thimersol-free hepatitis B preparation currently available. Recommended dosing schedule for COMVAX is ages 2 months, 4 months and 12 to 15 months.
3. Effective January 1, 2000, an all-inactivated poliovirus (IPV) schedule will be recommended. Oral poliovirus vaccine (OPV) will be acceptable in limited situations for the remainder of the 2000 calendar year, after which it will not be recommended for use.
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