Evaluate/Manage OSA

Posted on Oct 11, 2011 in Articles | 2 comments

The Evaluation and Management of Obstructive Sleep Apnea Syndrome

 

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Learning Objectives

After participating in this educational activity, participants should be able to

1. Recognize the risk factors, comorbidities, signs, and symptoms of obstructive sleep apnea (OSA)
2. Order the appropriate test to confirm the diagnosis of OSA
3. Employ a management plan for patients being treated for OSA to increase adherence
4. Address residual symptoms and comorbidities in regular follow-up visits

Introduction

In their day-to-day practice, primary care providers (PCPs) confront a plethora of clinical issues. In turn, they are faced with the challenge to prioritize these issues in order of importance, despite increased limits on their time and resources. Historically, sleep-related concerns such as insomnia, tiredness, and sleepiness have been given a lower priority than other medical conditions such as cardiovascular and metabolic disease; therefore, they have not been adequately addressed. One of the important causes of sleep-related symptoms is obstructive sleep apnea (OSA) syndrome, a condition that is associated with considerable medical and psychiatric comorbidity and even mortality. Although recognition of this disorder has increased during the past few decades, data indicate that most individuals affected remain undiagnosed.[1] The gap in screening, identification, and effective management of this disorder at the primary care level is vast, especially when the following factors are considered:

1. OSA is highly prevalent, affecting 4% of men and 2% of women[2]
2. OSA reduces life expectancy[3,4] and quality of life[5]
3. OSA is a major cause of accidents and work-related impairments[6]
4. Diagnosis of OSA is relatively straightforward and treatment is typically effective, improving outcomes in many measures, including quality of life and life expectancy

At the primary care level, identification of at-risk individuals for this potentially serious condition continues to pose a challenge. Underrecognition of presenting symptoms by PCPs, and by patients, may be one contributing factor for improper identification and management of OSA.

Definition

OSA is characterized by repetitive episodes of complete (apnea) or partial (hypopnea) upper airway obstruction during sleep.[7] Airflow cessations or reductions produce arousals, fragmented sleep, reductions in blood oxyhemoglobin saturation, and fluctuations in blood pressure and heart rate.[8] An apnea is defined as a cessation of airflow lasting 10 seconds or more, and a hypopnea is defined as a drop in respiratory flow by 30% or greater of baseline lasting for a period of 10 seconds or more, associated with a drop in oxyhemoglobin saturation of 4% or greater from the pre-event baseline.[9] The average number of apneas and hypopneas per hour of sleep is the apnea/hypopnea index (AHI). OSA is diagnosed if the AHI is 5 or greater in the presence of symptoms such as sleepiness, fatigue, inattention, or signs of disturbed sleep (restless sleep and respiratory pauses), or if the AHI is greater than 15 in an otherwise asymptomatic patient.

OSA is considered to be mild if AHI is between 5 and 15, moderate if between 16 and 30, and severe if greater than 30.[5] For children, an AHI of 1 or greater is considered to be diagnostic of OSA, yet severity criteria have not been established for this population. AHI is typically calculated for various conditions during sleep, such as REM (rapid eye movement) and non-REM sleep, and in various body positions, such as supine and nonsupine, to provide further insight into management options.

Epidemiology

Estimates suggest that around one in four adults are at high risk of OSA.[10] The prevalence of individuals in the general population who have an AHI of 5 or greater, without consideration of associated symptoms, is approximately one in five, encompassing 24% of men and 9% of women.[2] In contrast, 2% of women and 4% of men have OSA, defined as an AHI greater than five events per hour accompanied by clinical symptoms of the disorder.[1,11] Prevalence of OSA increases with age, with a plateau occurring at age 55 through 65 years; there is a two- to three-fold higher prevalence among individuals 65 years and older compared with those aged 30 through 64 years.[12] Although men are five times more likely to have OSA, the gap significantly narrows after menopause such that, in later years, the rates between men and women become similar. Certain ethnicities, including African Americans and certain Pacific Islanders, have higher rates of OSA; this observation is independent of body weight. The prevalence of OSA in Asians is similar to that in the United States, despite the lower mean body weight for Asians. These observations suggest that race may be an important risk factor, possibly related to differences in craniofacial structure.[13] 

Pathophysiology

Obstruction of the airway during sleep occurs because of anatomical as well as physiological factors. Anatomical factors include large neck size, micrognathia, crowded pharynx, tonsillar/adenoidal hypertrophy, and nasal obstruction, among others. Physiological factors that contribute to upper airway collapsibility are less understood and are thought to be due to impaired pharyngeal muscle dilator sensitivity and diminished neural output to the upper airway muscles during sleep. Apneas occur when the respiratory drive is below the threshold for inspiratory muscle strength needed to maintain upper airway patency during sleep. As apnea progresses, respiratory drive increases until inspiratory threshold is passed and inspiration can then occur.[14] The arousal response plays a critical role in apnea termination.

Although snoring is noted to occur among individuals without OSA, it is common in OSA and its prevalence increases with age. However, patients who snore loudly on a regular basis are seven times more likely than nonsnorers to develop OSA.[8] Snoring usually occurs during inspiration but can also occur during expiration. Habitual snoring is common, occurring in 44% of males and 28% of females aged 30 through 60 in the general population.[2] It is unclear whether snoring alone eventually progresses to OSA, but evidence suggests that it is likely related to weight gain: a one-point gain in body mass index (BMI) during one year corresponds to an increase in five AHI events per hour.[15]

Consequences

The cumulative effect of multiple apnea episodes throughout the night takes its toll on the patient as the months and years progress. Physiological consequences are shown in Figure 1.

Sleep fragmentation, hypoxia, hypercapnia, and acidosis are thought to lead to excessive daytime somnolence (EDS) and cardiovascular and metabolic consequences, all leading to decreased quality of life and life expectancy and increased morbidity. The odds ratio of some of the consequences is shown in Table 1.

Hypertension is likely caused by sustained sympathetic excitation, reduced parasympathetic activity, and release of endothelin.[16] Numerous studies show a strong association between OSA and hypertension[17] (Figure 2). The strong association between OSA and various cardiovascular conditions (Figure 3), such as hypertension, and improvement in some of these conditions following treatment of OSA, suggests that OSA is an important disorder to identify in the evaluation of these conditions.

 

OSA hazards transcend the patient because cognitive impairment associated with the condition can lead to accidents; the prevalence of motor vehicle accidents in OSA patients is considerably higher than in those without OSA (Figure 4).

Psychiatric conditions, especially depression, are common in OSA patients (Figure 5).[18] PCPs should consider the possibility of OSA in patients with depression, especially depression that does not respond to conventional therapies.

Lastly, OSA has been shown to decrease life expectancy. Several reports have shown an increased mortality for patients with sleep apnea. Figure 6 shows the impact on mortality of disease severity from a retrospective study of sleep apnea patients. Patients with an AHI greater than 20 per hour who elected to forgo treatment were found to have reduced survival compared with patients with an AHI less than 20 (Figure 7). This is most likely due to the cardiovascular consequences previously discussed.

 

Presenting Symptoms

Unlike many patients in primary care settings, patients with OSA generally do not present with acute and readily apparent complaints or symptoms, such as chest pain or shortness of breath.[19] In fact, most patients with OSA do not express concerns relative to their condition during routine office visits.[19] Therefore, actively requesting historical information regarding the condition enhances the likelihood of its identification. Patients who do present with specific concerns relative to the disorder most commonly describe snoring, tiredness, lassitude, or lack of energy.[20] “Tiredness” is a term broadly used to describe many clinical states, including depression, anergy, fatigue, and sleepiness, among others. In the case of OSA, the chief concern is excessive sleepiness (ES), defined as an exaggerated tendency to fall asleep at inopportune times. The Epworth Sleepiness Scale (ESS) is a straightforward and practical self-administered inventory that quantifies ES. This 8-point questionnaire assesses the likelihood of dozing off during regular everyday situations (Figure 8).

A score of 10 or more is considered to reflect an abnormally high level of sleepiness; a group of untreated OSA patients scored 16.[20,21]

Other presenting symptoms of OSA include loud habitual snoring, trouble concentrating, mood or behavioral changes, morning headaches, frequent nighttime urination, gastroesophageal reflux, heavy nighttime sweating, and inability to sleep in a supine position.[22]

Risk Factors: Who’s at Risk?

As discussed, symptoms of OSA can be subtle. Therefore, active screening can be helpful for recognizing at-risk patients. Risk factors are noted in Table 2.

Excessive upper body fat distribution (truncal obesity) is one of the major contributing factors in the development of OSA; 70% of OSA patients are obese.[23] The syndrome increases in prevalence with age and is more common in men than women. Several studies demonstrated a higher risk of development of OSA if there is a family history of the disorder, and the risk increased with the number of affected relatives.[24] Alcohol and sedative medication can contribute to the development of OSA through their relaxant effect on the upper airway muscles.[25] A longitudinal epidemiological study showed that smokers are at an increased risk of OSA, with current smokers at greater risk than nonsmokers and heavy smokers at the greatest risk.[26] Interestingly, cessation of smoking has been shown to eliminate the increased risk.[26]

Upper airway anatomy can also affect OSA risk. Physical findings that can assist in diagnosing a crowded upper airway are increased neck circumference and high BMI.[27] One method of assessing upper airway anatomy and risk of OSA is the Mallampati Scale.

On average, the risk of OSA increases more than two-fold for every 1-point increase in the Mallampati Scale: a Mallampati IV patient has an eight-fold risk of OSA.[28] Such a strong association suggests that if a high Mallampati score is noted during a routine examination, inquiring further about snoring and ES symptoms may be warranted. A neck circumference equal to or greater than 17 inches in men and 16 in women is also associated with a greater OSA risk.[12] Although high BMI is associated with OSA, 30% of OSA patients are not obese.

Diagnosis

The diagnostic process is guided by understanding who to screen or refer for polysomnography (PSG). The STOP-BANG inventory is a simple, office-based screening tool that combines symptoms, historical information, and physical examination results to recognize individuals at high risk of OSA.

If a patient is positive for three or more STOP-BANG factors, the probability of OSA is enough to warrant a careful work-up.

During an acute visit to the PCP, if the patient presents with a narrow airway—especially if neck size is large and other risk factors are present—ask the patient about sleepiness and snoring, and build the case for referral for testing. Also, during visits for medical problems such as hypertension and other cardiovascular diseases, diabetes, hyperlipidemia, and depression, the PCP should consider that this patient might be at risk of OSA and ask the patient some OSA screening questions in case of referral for testing. During routine screening, other than information on family history, active problems, and the physical examination, the PCP should ask about sleep symptoms such as snoring, gasping, choking, and daytime sleepiness. Regarding snoring and other nighttime symptoms, it is almost always necessary to question the bed partner because most patients are unaware that they snore.

Polysomnography

When suspicion is sufficiently high to warrant testing, in-laboratory full-night PSG is the current criterion standard and involves the measurement of multiple physiological parameters while the patient sleeps in the sleep laboratory. Measured parameters include EEG (electroencephalogram), respiratory effort, airflow, eye movements, leg movements, EKG (electrocardiogram), and pulse oximetry.[9] Testing is best initiated by most providers through patient referral to a sleep specialist to first confirm the suspicion and arrange testing. For PCPs who feel capable, it is reasonable to order a PSG and proceed according to the interpretation. The American Academy of Sleep Medicine (AASM) has established standards for testing quality. The sleep study is analyzed and results forwarded to the referring provider. When OSA is diagnosed, patients typically discuss results and therapeutic options with the ordering PCP. If the patient chooses continuous positive airway pressure (CPAP) therapy, the patient typically returns for another study during which a mask is chosen and the CPAP device is titrated.

At times a split-night, attended, in-laboratory PSG is performed where the diagnostic portion of the study is completed during the first part of the night and the CPAP device is titrated during the second part of the night. This is useful to expedite OSA diagnosis and prescribe treatment when time is of the essence in patients who are, for example, dangerously sleepy or who have comorbid medical disorders that mandate rapid OSA management.[29] Split-night studies have also been proposed as cost-effective alternatives to full-night PSG,[30] although more recent studies have challenged this notion.[31] Various factors may produce false negative PSG results, including technical failures. These factors are more likely due to disturbed sleep architecture or curtailed sleep time, producing insufficient sleep quantity or quality to make a proper diagnosis. Factors that can contribute to such an outcome include medication effects, performing the PSG at a time not typical of the patient’s sleep hours (eg, in shift workers), high anxiety levels, and difficulty adapting to new surroundings, among others. When the test is inconclusive for these reasons and clinical suspicion of OSA is high, retesting may be considered.[32]

Home sleep testing (HST) has recently emerged as an alternative to PSG, promising greater convenience and lower cost,[33] although the cost-effectiveness, when considering long-term outcomes and other factors, has been recently challenged.[33] Table 3 summarizes the different types of sleep testing.

Type II devices are essentially the same as Type I devices but are performed in the patient’s home without a monitoring technician. Although desirable, they are less convenient. Type III monitoring devices measure four physiological variables, including two respiratory variables, an EKG tracing, and pulse oximetry. Some devices have additional signals that can detect snoring, determine body position, or detect movement. Sleep variables (eg, sleep stages, sleep continuity) cannot be measured by Type III devices.

Type III and IV devices, although more convenient and possibly less expensive, have important limitations. They do not monitor EEG or EOG (electrooculogram), so they cannot distinguish wakefulness from sleep, detect sleep arousals, or distinguish REM sleep from non-REM. False negative rates have been reported as high as 17% even when patients have been selected for high pretest probability for OSA. False positive rates are reported from 2% to 31%.[34] Overnight pulse oximetry alone yields limited results and is not recommended for diagnostic evaluation of suspected OSA.[35]

The AASM has recommended[36] that HST be considered only after a comprehensive sleep evaluation to properly recognize patients with a high probability of OSA. The most suitable patients include those for whom in-laboratory testing is not possible and who have no confounding comorbid medical conditions that degrade accuracy (eg, moderate-to-severe pulmonary and neuromuscular conditions, congestive heart failure, etc). The AASM also recommends the testing facility be accredited and that PCPs interpreting these tests are board certified in sleep medicine. PCPs who order such tests should be prepared to perform proper follow-up care for instituting and monitoring treatment and to discuss other diagnostic and therapeutic possibilities should testing results prove negative for OSA.

Management

Following diagnosis, sleep disorder centers typically begin treatment and send referral letters to the PCP. In most instances, the PCP’s role is to address the patient’s concerns regarding diagnosis and treatment, establish a long-term follow-up plan to ensure adherence and maximal improvement in symptoms such as poor sleep quality and EDS, and monitor emerging difficulties that might jeopardize adherence.[12]

Management of OSA first and foremost begins with educating the patient on the condition. Education is particularly important since treatment may, at times, be psychologically unpalatable to the patient and the treatment benefits may not be readily evident or understood by the patient. Patients should be informed that treatment will likely improve quality of life and life expectancy and positively impact comorbidities. Education should also include risk counseling in which the patient is informed of the perils of cognitive impairment and drowsiness that OSA causes, which increase the chances of motor vehicle crashes, job-related injuries, and impairment of judgment. In some instances, impairment may require the patient to be restricted from driving until an appropriate remedy is reached. Educated patients are more cooperative and, with PCP guidance, may make more informed decisions that will result in more optimal health outcomes.

Lifestyle changes are often encouraged by the sleep clinic; however, PCPs have an opportunity to emphasize these changes more often during regular office visits. Changes include avoiding CNS depressants such as alcohol, which should be reduced and especially restricted before bedtime. Smoking cessation becomes more important, because smoking irritation of the nasopharynx can worsen OSA. Good sleep hygiene measures should be emphasized, the most important of which is spending sufficient time in bed for sleep. Keeping regular sleep hours and ensuring the bedroom is conducive to sleep are also important.

Weight loss is an important long-range goal. Patients who are obese should be informed that obesity strongly correlates with OSA, particularly with heavy upper body mass. Weight loss can be very effective and, in some cases, even curative, but its rate of success is low. Nonetheless, a 10% weight loss is associated with a 26% decrease in AHI. Regarding bariatric surgery for weight loss, OSA is prevalent in at least 45% of these patients, and preoperative BMI correlates with OSA severity.[36] Surgically induced weight loss significantly improves obesity-related OSA and sleep quality parameters. However, although many such morbidly obese patients who undergo bariatric surgery can expect reduction of AHI and CPAP pressure needed to maintain patent airway, most surgical patients with preoperative OSA will continue to need CPAP after surgery.[37] In patients with significant OSA, other treatments should not be delayed until proper weight loss is achieved, since OSA complications may continue during the weight loss period.

PAP devices are the most common mode of treatment for the disorder, introducing room air into the upper airway through a nasal, oral, or oronasal interface. The interface is typically a mask, although a large variety of interface devices are available to enhance comfort and adherence. These achieve airway patency during sleep by producing a pneumatic splint of the upper airway.[38] CPAP is the modality of first choice, although bilevel PAP (BiPAP) may be used for CPAP-intolerant patients through delivery of PAP at different pressures during inspiration and expiration.

PAP devices have come a long way during the last 20 years to address the various needs of the individual. For dry air, most have humidification devices attached, some with sensors that allow adjustments to the degree of humidification. For discomfort of too much pressure when initiated, a ramp-up mechanism allows PAP to start after the patient falls asleep and gradually increase until the set pressure is reached. All have either recording cards that allow for collecting data on use or modems that send use information directly to the medical provider. Various insurance providers currently require this information collection for confirmation of adequate use of CPAP to confirm coverage.[39]

Benefits of CPAP have been studied extensively and underscore the need for this treatment in patients with OSA. CPAP treatment lessens drowsiness, measured both objectively and subjectively.[40] Preliminary data indicate that CPAP treatment may lower cardiovascular risk parameters, including CRP (C-reactive protein), homocysteine, total cholesterol, total cholesterol/HDL ratio, and ApoB/ApoA ratio.[41] Controlled studies indicate that CPAP treatment of OSA lowers blood pressure,[42] and measures of quality of life, cognitive function, and depression have also been shown to improve.[43] Although methodologically rigorous studies have yet to substantiate the outcome, emerging data suggest that long-term PAP therapy may improve life expectancy.[44-46]

Long-term adherence to PAP therapy is a concern because diminished adherence or complete nonadherence results in diminished benefit and recurrence of OSA.[47] Patient reports can vary widely from objectively assessed adherence; in one study, subjectively reported adherence was quite high, around 75%, yet only half of the patients were assessed as adherent when objective, PAP-machine monitoring devices were used. Adherence in this study was defined by use of CPAP for four or more hours per night on at least five nights per week.[48] Adherence can be enhanced with a number of measures, including, as noted, a careful review with the patient of the risks of untreated OSA and the potential benefits of effective management. Regular follow-up by the PCP is important in this regard, as adherence to PAP therapy can deteriorate if the patient is left unattended. The PCP should inquire at every opportunity about PAP use, and PAP adherence reports should be monitored in a manner similar to the systematic inquiry conducted for smoking and other significant lifestyle issues.

A systematic PAP educational program, typically staffed by trained therapists and technicians, is vital in ensuring and enhancing adherence.[49] Methods for enhancing PAP adherence include having the patient choose the appropriate facial appliance, immediate follow-up after instituting treatment,[50] and having the patient voice concerns and remedying them.[51] The patient should be advised to call the sleep clinic OSA technician, or the respiratory therapist who set up the device and mask, in the event of mask leakage, nasal irritation, excessive pressure, or other difficulties. Various measures are available to address concerns, including changing the type of mask to improve comfort and decrease air leakage. Nasal cannula-type facial appliances (“nasal pillows”) may help people who describe the mask as too uncomfortable or claustrophobic. If there is significant oral leakage, application of a chin strap may be useful. Nasal congestion and airway dryness due to leak or high pressures may respond to use of a humidifier. Patients who have problems falling asleep because of high pressures may benefit from use of a ramp feature. For patients with difficulty tolerating CPAP due to claustrophobia or anxiety, desensitization or gradual habituation can sometimes be helpful. This can be performed at home or in the laboratory. If patients complain of difficulty exhaling against a high expiratory pressure, switching from CPAP to BiPAP may improve the patient’s acceptance of therapy.

Oral appliances are another option for OSA treatment[47]; also referred to as mandibular advancement splints (MAS), they are manufactured individually for the patient to keep the jaw slightly open and/or protruding. MAS can be titrated because the advancement required for appropriate benefit ranges from 50% to 90% of the maximum protrusion. This titration process is based on clinical response over a period of weeks and months, followed by PSG (or home testing; see above). Some patients fail treatment regardless of the degree of advancement, but patient acceptance and tolerance are major determinants of the extent and speed of advancement.[52] MAS is appropriate when patients express preference for it over all other obstruction treatments, as well as nonadherence, nonresponsiveness, or refusal of CPAP. They are appropriate for patients with mild-to-moderate OSA only.[53]

Oral appliances should not be considered for patients who require immediate improvement (patients with severe symptomatic OSA, sleepiness while driving, severe hypoxemia, or active cardiovascular comorbidities), because oral appliances require gradual incremental advancement of the mandible. They should also not be used in cases of severe oxyhemoglobin desaturation, because oral appliance therapy may induce suboptimal improvement.[54] Finally, certain conditions such as TMJ (temporomandibular joint) disease, periodontal disease, insufficient dentition to support appliance retention in the mouth, and inadequate range of motion of the jaw warrant alternate treatment. One study found that 34% of patients with OSA may not be suitable candidates for treatment with an oral appliance.[55] Some adverse effects of oral appliances include TMJ discomfort, dental misalignment, and salivation. They should, whenever possible, be applied by dental professionals with training and expertise in this area.[55]

Studies evaluating outcome for MAS have been limited by methodological issues, yet success rates have been reported around 50% for mild-to-moderate OSA.[47] Most clinical trials that have compared oral appliances with CPAP found the latter superior at improving AHI and oxyhemoglobin saturation values but not symptoms (ie, ES), arousal index, or sleep architecture.[56,57]

Surgical options include uvulopalatopharyngoplasty, laser-assisted uvulopalatopharyngoplasty, radiofrequency tissue volume reduction, genioglossal advancement, maxillomandibular advancement, nasal surgery, and tonsillectomy/adenoidectomy. Although initially appealing to patients as a permanent solution, surgery is not the first or best option as success rates vary (40% at best), and surgery has even been shown to worsen OSA in several cases.[58] Reliable methods for predicting preoperative outcome are lacking and there are no long-term outcome data.[59,60]

Positional therapy may be appropriate for individuals with low AHI in the nonsupine position, a finding usually made during routine PSG.[61,62] Positioning typically involves attaching pillows to the patient’s back to maintain a nonsupine position. Studies into these devices are ongoing. If these therapies are used, however, PSG should be performed throughout to document AHI normalization.[63]

Pharmacological agents such as selective serotonin reuptake inhibitors (SSRIs), methylxanthine derivatives, and estrogen were used anecdotally to treat OSA at a time when few other treatments were available, yet there are no methodologically rigorous studies on these agents to substantiate their use. Pharmacological agents may be helpful to manage comorbid conditions which, in turn, may aggravate OSA. For example, treating rhinitis with topical nasal corticosteroids may improve the AHI in patients with OSA and comorbid rhinitis.[64] Supplemental oxygen administration as a primary OSA treatment is not recommended, since this may prolong apneas and potentially worsen nocturnal hypercapnia in patients with comorbid respiratory disease.[64]

Despite appropriate treatment of OSA, some patients continue to experience ES. One study showed that objectively 65% and subjectively 34% of patients adherent to CPAP continued to have ES.[47] Potential causes of persistent ES include inadequate total sleep time, poor sleep hygiene, diminished PAP adherence, poor mask fit, inadequate CPAP pressure, sleep disruption caused by the CPAP device itself, and coexistent illnesses or medications that cause ES. Therefore, whenever the PCP is confronted with persistent ES, a systematic evaluation should be conducted to identify and manage the underlying cause. For example, poor CPAP adherence due to poor mask fit should be addressed by providing mask education and possibly changing the mask type or attachments.

In some cases a specific cause cannot be isolated, and pharmacological therapy with modafinil or its R-isomer, armodafinil, may be considered. These two medications have been shown to reduce ES in randomized trials, yet they do not positively impact the AHI,[65,66] when administered once in the morning at starting doses of 200 mg for modafinil and 150 mg for armodafinil. Both are classified as schedule IV by the Food and Drug Administration and should be used cautiously in patients with a history of arrhythmias or heart disease. Side effects include headache, nausea, dry mouth, anorexia, and diarrhea. Although rare, serious and life-threatening rashes, including Stevens-Johnson syndrome and toxic epidermal necrolysis, have been reported. Most of these latter cases have occurred within the first five weeks of therapy, although rare cases have occurred after long-term use. Even rare cases of multiorgan hypersensitivity reactions associated with modafinil use, and lone cases of angioedema and anaphylactoid reactions to armodafinil, have also been reported. Hypersensitivity reactions typically present with fever and rash associated with organ-system dysfunction. Patients should be advised to discontinue modafinil or armodafinil at the first sign of rash.[67,68]

OSA in Children

Although less common in children than adults, the incidence of OSA is rising due to the dramatic increases of BMI in children.[69] The condition exists in 2% to 5% of children and may be most common in children aged 2 through 6 years but can occur at any age.[70] Untreated, OSA is a factor implicated in a number of conditions, including cardiovascular disease, impaired growth, and learning and behavioral problems, although studies to confirm these associations are clearly needed.[71-73] Early diagnosis and treatment may decrease morbidity; therefore, it is important, as in the case of adult OSA, for PCPs to be alert for the disorder. As with adults, snoring is present in many children with OSA, and parents should be queried about its presence in children who are excessively sleepy during the day, are failing to thrive, have behavior problems, including “laziness” and irritability, or have cardiovascular problems. If there is snoring and the examination reveals a child with a crowded or small pharynx or substantial adenotonsillar hypertrophy, especially in the presence of these comorbidities, the patient should be sent to an appropriate sleep center accredited in diagnosing and treating OSA in children.

Unlike adults, surgery is a first consideration for children in treating OSA.[74] Tonsillectomy and/or adenoidectomy are often curative, but PAP therapy is used in instances when surgery is too risky or not curative and according to patient preference. As with adults, CPAP is useful in decreasing the signs and symptoms of OSA, although its use is riddled with adherence issues.

Conclusion

A common and highly represented condition in primary care populations, OSA is associated with common and serious comorbidities and potential consequences that make it a critical condition to properly diagnose and manage. Since presentation can be subtle and patients are typically unaware of having stopped breathing in their sleep, the PCP should be alert to test for this possibility. When OSA is diagnosed, patient education regarding poor adherence, as well as continuous follow-up, is important for reinforcing adherence.

 

Paul P. Doghramji, MD, FAAFP
Karl Doghramji, MD
Published on October 11, 2011

 

 

 

 

 

 

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