Gregory Rutecki, MD

In Reply: The questions posed by Dr. Rose reflect critical issues primary care physicians encounter when prescribing medications for patients who are taking serotonergic agents. “Switching strategies” have been described for starting or discontinuing serotonergic antidepressants.¹ Options range from conservative exchanges requiring 5 half-lives between discontinuation of 1 antidepressant and initiation of another vs a direct cross-taper exchange. Decisions regarding specific patients should take into account previous adverse effects from serotonergic medications and half-lives of discontinued antidepressants. To our knowledge, switching strategies have not been validated and are based on expert opinion. Scenarios are complicated further if patients have already been prescribed 2 or more antidepressants and 1 medication is exchanged or dose-adjusted while another is added. With this degree of complexity, we recommend referral to a psychiatrist.

Dr. Rose’s questions on prescribing nonpsychiatric serotonergic drugs concurrently with antidepressants broaches a topic with even less evidence. Some data exist about nonpsychiatric serotonergic drugs given in combination with triptans. Soldin et al² reviewed the US Food and Drug Administration’s Adverse Event Reporting System and discovered 38 cases of serotonin syndrome in patients using triptans. Eleven of these patients were using triptans without concomitant antidepressants. Though definitive evidence is lacking for safe prescribing practice with triptans, the authors noted that most cases of triptan-induced serotonin toxicity occur within hours of triptan ingestion.²

The evidence on the risk of serotonin syndrome with other medications is limited to case reports. In regard to linezolid, a review suggested that when linezolid was administered to a patient on long-term citalopram, a prolonged serotonin syndrome was precipitated, which is not an issue with other antidepressants.³ The World Health Organization has issued warnings for serotonin toxicity with ondansetron and other 5-HT3 receptor antagonists based on case reports.^4,5 No data are available for the appropriate prescribing of 5-HT3 antagonists with antidepressants. A review of cases suggests a link between fluconazole and severe serotonin toxicity in patients taking citalopram; however, no prescribing guidelines have been established for fluconazole either.⁶

Dr. Rose asks important clinical questions, but evidence-based answers are not available.  We can only recommend that patients be advised to report symptoms immediately after starting any medication associated with serotonin syndrome. For patients on multiple antidepressants, psychiatric assistance is advised. An observational cohort study of patients using antidepressants while exposed to other suspect drugs may better delineate effects of several pharmaceuticals on the serotonergic axis. Only then may safe prescribing practices be validated with evidence.

In Reply: The questions posed by Dr. Rose reflect critical issues primary care physicians encounter when prescribing medications for patients who are taking serotonergic agents. “Switching strategies” have been described for starting or discontinuing serotonergic antidepressants.¹ Options range from conservative exchanges requiring 5 half-lives between discontinuation of 1 antidepressant and initiation of another vs a direct cross-taper exchange. Decisions regarding specific patients should take into account previous adverse effects from serotonergic medications and half-lives of discontinued antidepressants. To our knowledge, switching strategies have not been validated and are based on expert opinion. Scenarios are complicated further if patients have already been prescribed 2 or more antidepressants and 1 medication is exchanged or dose-adjusted while another is added. With this degree of complexity, we recommend referral to a psychiatrist.

Dr. Rose’s questions on prescribing nonpsychiatric serotonergic drugs concurrently with antidepressants broaches a topic with even less evidence. Some data exist about nonpsychiatric serotonergic drugs given in combination with triptans. Soldin et al² reviewed the US Food and Drug Administration’s Adverse Event Reporting System and discovered 38 cases of serotonin syndrome in patients using triptans. Eleven of these patients were using triptans without concomitant antidepressants. Though definitive evidence is lacking for safe prescribing practice with triptans, the authors noted that most cases of triptan-induced serotonin toxicity occur within hours of triptan ingestion.²

The evidence on the risk of serotonin syndrome with other medications is limited to case reports. In regard to linezolid, a review suggested that when linezolid was administered to a patient on long-term citalopram, a prolonged serotonin syndrome was precipitated, which is not an issue with other antidepressants.³ The World Health Organization has issued warnings for serotonin toxicity with ondansetron and other 5-HT3 receptor antagonists based on case reports.^4,5 No data are available for the appropriate prescribing of 5-HT3 antagonists with antidepressants. A review of cases suggests a link between fluconazole and severe serotonin toxicity in patients taking citalopram; however, no prescribing guidelines have been established for fluconazole either.⁶

Dr. Rose asks important clinical questions, but evidence-based answers are not available.  We can only recommend that patients be advised to report symptoms immediately after starting any medication associated with serotonin syndrome. For patients on multiple antidepressants, psychiatric assistance is advised. An observational cohort study of patients using antidepressants while exposed to other suspect drugs may better delineate effects of several pharmaceuticals on the serotonergic axis. Only then may safe prescribing practices be validated with evidence.

In Reply: The questions posed by Dr. Rose reflect critical issues primary care physicians encounter when prescribing medications for patients who are taking serotonergic agents. “Switching strategies” have been described for starting or discontinuing serotonergic antidepressants.¹ Options range from conservative exchanges requiring 5 half-lives between discontinuation of 1 antidepressant and initiation of another vs a direct cross-taper exchange. Decisions regarding specific patients should take into account previous adverse effects from serotonergic medications and half-lives of discontinued antidepressants. To our knowledge, switching strategies have not been validated and are based on expert opinion. Scenarios are complicated further if patients have already been prescribed 2 or more antidepressants and 1 medication is exchanged or dose-adjusted while another is added. With this degree of complexity, we recommend referral to a psychiatrist.

Dr. Rose’s questions on prescribing nonpsychiatric serotonergic drugs concurrently with antidepressants broaches a topic with even less evidence. Some data exist about nonpsychiatric serotonergic drugs given in combination with triptans. Soldin et al² reviewed the US Food and Drug Administration’s Adverse Event Reporting System and discovered 38 cases of serotonin syndrome in patients using triptans. Eleven of these patients were using triptans without concomitant antidepressants. Though definitive evidence is lacking for safe prescribing practice with triptans, the authors noted that most cases of triptan-induced serotonin toxicity occur within hours of triptan ingestion.²

The evidence on the risk of serotonin syndrome with other medications is limited to case reports. In regard to linezolid, a review suggested that when linezolid was administered to a patient on long-term citalopram, a prolonged serotonin syndrome was precipitated, which is not an issue with other antidepressants.³ The World Health Organization has issued warnings for serotonin toxicity with ondansetron and other 5-HT3 receptor antagonists based on case reports.^4,5 No data are available for the appropriate prescribing of 5-HT3 antagonists with antidepressants. A review of cases suggests a link between fluconazole and severe serotonin toxicity in patients taking citalopram; however, no prescribing guidelines have been established for fluconazole either.⁶

Dr. Rose asks important clinical questions, but evidence-based answers are not available.  We can only recommend that patients be advised to report symptoms immediately after starting any medication associated with serotonin syndrome. For patients on multiple antidepressants, psychiatric assistance is advised. An observational cohort study of patients using antidepressants while exposed to other suspect drugs may better delineate effects of several pharmaceuticals on the serotonergic axis. Only then may safe prescribing practices be validated with evidence.

In Reply: We thank Dr. Keller for his thorough reading of our article.¹

Regarding the predictive value of neck circumference for obstructive sleep apnea, (OSA), neck circumference is one of many tools to screen for OSA. If neck circumference greater than 38 cm is applied without other predictors (such as the presence of snoring, daytime sleepiness, or elevated body mass index), it provides only a 58% sensitivity and 79% specificity.² It is less an issue of inches vs collar size vs centimeters than of combining circumference with other parameters (as in the STOP-BANG questionnaire) before proceeding with a sleep study. The senior author of our article (G.R.) uses 38 cm.

With respect to home vs sleep lab monitoring, the question was beyond the scope of the paper and outside our expertise, as we are both general internists. The home venue recommendations in this instance were taken directly from the American Academy of Sleep Medicine.³ We would rely on consultation with a sleep specialist before ordering home monitoring to determine the potential success of non-CPAP interventions for OSA.

As for Parkinson disease as an exception to OSA and hypertension, we wrote in the paper, “Untreated OSA is associated with a number of conditions.”¹ Yes, resistant hypertension is prominent in today’s epidemic of obesity, diabetes, and OSA, but not everyone with coronary artery disease, atrial fibrillation, or heart failure—as in persons with Parkinson disease—has hypertension. The associated conditions in our paper are more typical of a general medical practice, but we agree that Parkinson disease is associated with OSA. Patients with hypertension and OSA are more prevalent because the clinical risk factors for OSA and hypertension are common to both conditions.⁴

In adults, apnea is considered present when the airflow drops by 90% or more from the pre-event baseline. Hypopnea in adults is present when the airflow drops by 30% or more of the pre-event baseline for 10 or more seconds in association with either 3% or greater arterial oxygen desaturation or an electroencephalographic arousal.⁵ Studies have shown that episodes of hypopnea with 2% oxygen desaturation are associated with an increased prevalence of metabolic impairment.⁶ A higher degree of desaturation, ie, more than 4%, was associated with increased prevalence of self-reported cardiovascular disease.⁷ But the significance of episodes of hypopnea without arterial desaturation is not well known to us and was beyond the scope of our article.

Our article was primarily focused on screening for OSA in ambulatory clinical practice and was not intended as a comprehensive review of screening in different settings of patient care. As to the importance of recognizing OSA in patients undergoing elective surgery under general anesthesia, we agree that screening is important to reduce the risk of postoperative adverse respiratory events in patients with a high pretest probability of OSA. In a recent study by Seet et al,⁸ patients with high STOP-BANG questionnaire scores (≥ 3) had higher rates of intraoperative and early postoperative adverse events than those with low scores (< 3). The risk of adverse events correlated with higher scores, and  patients with a STOP-BANG score of 5 or more had a five times greater risk of unexpected intraoperative and early postoperative adverse events, whereas those with a STOP-BANG score of 3 or more had a one in four chance of an adverse event. We recommend polysomnography for patients with a STOP-BANG score of 5 or more before elective surgery.

In Reply: We thank Dr. Keller for his thorough reading of our article.¹

Regarding the predictive value of neck circumference for obstructive sleep apnea, (OSA), neck circumference is one of many tools to screen for OSA. If neck circumference greater than 38 cm is applied without other predictors (such as the presence of snoring, daytime sleepiness, or elevated body mass index), it provides only a 58% sensitivity and 79% specificity.² It is less an issue of inches vs collar size vs centimeters than of combining circumference with other parameters (as in the STOP-BANG questionnaire) before proceeding with a sleep study. The senior author of our article (G.R.) uses 38 cm.

With respect to home vs sleep lab monitoring, the question was beyond the scope of the paper and outside our expertise, as we are both general internists. The home venue recommendations in this instance were taken directly from the American Academy of Sleep Medicine.³ We would rely on consultation with a sleep specialist before ordering home monitoring to determine the potential success of non-CPAP interventions for OSA.

As for Parkinson disease as an exception to OSA and hypertension, we wrote in the paper, “Untreated OSA is associated with a number of conditions.”¹ Yes, resistant hypertension is prominent in today’s epidemic of obesity, diabetes, and OSA, but not everyone with coronary artery disease, atrial fibrillation, or heart failure—as in persons with Parkinson disease—has hypertension. The associated conditions in our paper are more typical of a general medical practice, but we agree that Parkinson disease is associated with OSA. Patients with hypertension and OSA are more prevalent because the clinical risk factors for OSA and hypertension are common to both conditions.⁴

In adults, apnea is considered present when the airflow drops by 90% or more from the pre-event baseline. Hypopnea in adults is present when the airflow drops by 30% or more of the pre-event baseline for 10 or more seconds in association with either 3% or greater arterial oxygen desaturation or an electroencephalographic arousal.⁵ Studies have shown that episodes of hypopnea with 2% oxygen desaturation are associated with an increased prevalence of metabolic impairment.⁶ A higher degree of desaturation, ie, more than 4%, was associated with increased prevalence of self-reported cardiovascular disease.⁷ But the significance of episodes of hypopnea without arterial desaturation is not well known to us and was beyond the scope of our article.

Our article was primarily focused on screening for OSA in ambulatory clinical practice and was not intended as a comprehensive review of screening in different settings of patient care. As to the importance of recognizing OSA in patients undergoing elective surgery under general anesthesia, we agree that screening is important to reduce the risk of postoperative adverse respiratory events in patients with a high pretest probability of OSA. In a recent study by Seet et al,⁸ patients with high STOP-BANG questionnaire scores (≥ 3) had higher rates of intraoperative and early postoperative adverse events than those with low scores (< 3). The risk of adverse events correlated with higher scores, and  patients with a STOP-BANG score of 5 or more had a five times greater risk of unexpected intraoperative and early postoperative adverse events, whereas those with a STOP-BANG score of 3 or more had a one in four chance of an adverse event. We recommend polysomnography for patients with a STOP-BANG score of 5 or more before elective surgery.

In Reply: We thank Dr. Keller for his thorough reading of our article.¹

Regarding the predictive value of neck circumference for obstructive sleep apnea, (OSA), neck circumference is one of many tools to screen for OSA. If neck circumference greater than 38 cm is applied without other predictors (such as the presence of snoring, daytime sleepiness, or elevated body mass index), it provides only a 58% sensitivity and 79% specificity.² It is less an issue of inches vs collar size vs centimeters than of combining circumference with other parameters (as in the STOP-BANG questionnaire) before proceeding with a sleep study. The senior author of our article (G.R.) uses 38 cm.

With respect to home vs sleep lab monitoring, the question was beyond the scope of the paper and outside our expertise, as we are both general internists. The home venue recommendations in this instance were taken directly from the American Academy of Sleep Medicine.³ We would rely on consultation with a sleep specialist before ordering home monitoring to determine the potential success of non-CPAP interventions for OSA.

As for Parkinson disease as an exception to OSA and hypertension, we wrote in the paper, “Untreated OSA is associated with a number of conditions.”¹ Yes, resistant hypertension is prominent in today’s epidemic of obesity, diabetes, and OSA, but not everyone with coronary artery disease, atrial fibrillation, or heart failure—as in persons with Parkinson disease—has hypertension. The associated conditions in our paper are more typical of a general medical practice, but we agree that Parkinson disease is associated with OSA. Patients with hypertension and OSA are more prevalent because the clinical risk factors for OSA and hypertension are common to both conditions.⁴

In adults, apnea is considered present when the airflow drops by 90% or more from the pre-event baseline. Hypopnea in adults is present when the airflow drops by 30% or more of the pre-event baseline for 10 or more seconds in association with either 3% or greater arterial oxygen desaturation or an electroencephalographic arousal.⁵ Studies have shown that episodes of hypopnea with 2% oxygen desaturation are associated with an increased prevalence of metabolic impairment.⁶ A higher degree of desaturation, ie, more than 4%, was associated with increased prevalence of self-reported cardiovascular disease.⁷ But the significance of episodes of hypopnea without arterial desaturation is not well known to us and was beyond the scope of our article.

Our article was primarily focused on screening for OSA in ambulatory clinical practice and was not intended as a comprehensive review of screening in different settings of patient care. As to the importance of recognizing OSA in patients undergoing elective surgery under general anesthesia, we agree that screening is important to reduce the risk of postoperative adverse respiratory events in patients with a high pretest probability of OSA. In a recent study by Seet et al,⁸ patients with high STOP-BANG questionnaire scores (≥ 3) had higher rates of intraoperative and early postoperative adverse events than those with low scores (< 3). The risk of adverse events correlated with higher scores, and  patients with a STOP-BANG score of 5 or more had a five times greater risk of unexpected intraoperative and early postoperative adverse events, whereas those with a STOP-BANG score of 3 or more had a one in four chance of an adverse event. We recommend polysomnography for patients with a STOP-BANG score of 5 or more before elective surgery.

Patients who have risk factors for obstructive sleep apnea (OSA) or who report symptoms of OSA should be screened for it, first with a complete sleep history and standardized questionnaire, and then by objective testing if indicated. The gold standard test for OSA is polysomnography performed overnight in a sleep laboratory. Home testing is an option in certain instances.

Common risk factors include obesity, resistant hypertension, retrognathia, large neck circumference (> 17 inches in men, > 16 inches in women), and history of stroke, atrial fibrillation, nocturnal arrhythmias, heart failure, and pulmonary hypertension. Screening is also recommended for any patient who is found on physical examination to have upper-airway narrowing or who reports symptoms such as loud snoring, observed episodes of apnea, gasping or choking at night, unrefreshing sleep, morning headaches, unexplained fatigue, and excessive tiredness during the day.

The American Academy of Sleep Medicine suggests three opportunities to screen for OSA¹:

• At routine health maintenance visits
• If the patient reports clinical symptoms of OSA
• If the patient has risk factors.

A DISMAL STATISTIC

The prevalence of OSA in the United States is high, estimated to be 2% in women and 4% in men in the middle-aged work force,² and even more in blacks, Asians, and older adults.³ Yet only 10% of people with OSA are diagnosed⁴—a dismal statistic considering the association of OSA with resistant hypertension⁵ and with a greater risk of stroke,⁶ cardiovascular disease, and death.⁷

CONSEQUENCES OF UNTREATED OSA

Untreated OSA is associated with a number of conditions⁷:

• Hypertension. OSA is one of the most common conditions associated with resistant hypertension. Patients with severe OSA and resistant hypertension who comply with continuous positive airway pressure (CPAP) treatment have significant reductions in blood pressure.
• Coronary artery disease. OSA is twice as common in people with coronary artery disease as in those with no coronary artery disease. In patients with coronary artery disease and OSA, CPAP may reduce the rate of nonfatal and fatal cardiovascular events.
• Heart failure. OSA is common in patients with systolic dysfunction (11% to 37%). OSA also has been detected in more than 50% of patients with heart failure with preserved systolic function. CPAP treatment can improve ejection fraction in patients with systolic dysfunction.
• Arrythmias. Atrial fibrillation, nonsustained ventricular tachycardia, and complex ventricular ectopy have been reported to be significantly more common in people with OSA.⁸ If the underlying cardiac conduction system is normal and there is no significant thyroid dysfunction, bradyarrhythmias and heart block may be treated effectively with CPAP.⁷ Treatment of OSA may decrease the incidence and severity of ventricular arrhythmias.⁷
• Sudden cardiac death. OSA was independently associated with sudden cardiac death in a longitudinal study.⁹
• Stroke. The Sleep Heart Health Study⁶ showed that OSA is 30% more common in patients who developed ischemic stroke. Long-term CPAP treatment in moderate to severe OSA and ischemic stroke is associated with a reduction in the mortality rate.¹⁰
• Diabetes. The Sleep Heart Health Study showed that OSA is independently associated with glucose intolerance and insulin resistance and may lead to type 2 diabetes mellitus.¹¹

A QUESTIONNAIRE HELPS IDENTIFY WHO NEEDS TESTING

manne_obstructivesleepapneatesting_t1.gif

If you suspect OSA, consider administering a sleep disorder questionnaire such as the Berlin,¹² the Epworth Sleepiness Scale, or the STOP-Bang questionnaire (Table 1). The STOP-Bang questionnaire is an easy-to-use tool that expands on the STOP questionnaire (snoring, tiredness, observed apnea, high blood pressure) with the addition of body mass index, age, neck size, and gender. The Berlin questionnaire has been validated in the primary care setting.¹² The STOP-Bang questionnaire has been validated in preoperative settings¹³ but not in the primary care setting (although it has been commonly used in primary care).

WHICH TEST TO ORDER?

If the score on the questionnaire indicates a moderate or high risk of OSA, the patient should undergo objective testing with polysomnography or, in certain instances, home testing.¹ Polysomnography is the gold standard. Home testing costs less and is easier to arrange, but the American Academy of Sleep Medicine recommends it as an alternative to polysomnography, in conjunction with a comprehensive sleep evaluation, only in the following situations¹⁴:

• If the patient has a high pretest probability of moderate to severe OSA
• If immobility or critical illness makes polysomnography unfeasible
• If direct monitoring of the response to non-CPAP treatments for sleep apnea is needed.

Home testing for OSA should not be used in the following situations:

• If the patient has significant morbidity such as moderate to severe pulmonary disease, neuromuscular disease, or congestive heart failure
• In evaluating a patient suspected of having comorbid sleep disorders such as central sleep apnea, periodic limb movement disorder, insomnia, parasomnias, circadian rhythm disorder, or narcolepsy
• In screening of asymptomatic patients.

Home testing has important drawbacks. It may underestimate the severity of sleep apnea. The rate of false-negative results may be as high as 17%. If the home test was thought to be technically inadequate or the results were inconsistent with those that were expected—ie, if the patient has a high pretest probability of OSA based on risk factors or symptoms but negative results on home testing—then the patient should undergo polysomnography.¹⁴

DIAGNOSIS

The diagnosis of OSA is confirmed if the number of apnea events per hour (ie, the apnea-hypopnea index) on polysomnography or home testing is more than 15, regardless of symptoms, or more than 5 in a patient who reports OSA symptoms. An apnea-hypopnea index of 5 to 14 indicates mild OSA, 15 to 30 indicates moderate OSA, and greater than 30 indicates severe OSA.

BENEFITS OF TREATMENT

Treatment of OSA with CPAP reduces the 10-year risk of fatal and nonfatal motor vehicle accidents by 52%, the 10-year expected number of myocardial infarctions by 49%, and the 10-year risk of stroke by 31%.⁷ It has also been found to be cost-effective, for men and women of all ages with moderate to severe OSA.¹⁵

Patients who have risk factors for obstructive sleep apnea (OSA) or who report symptoms of OSA should be screened for it, first with a complete sleep history and standardized questionnaire, and then by objective testing if indicated. The gold standard test for OSA is polysomnography performed overnight in a sleep laboratory. Home testing is an option in certain instances.

Common risk factors include obesity, resistant hypertension, retrognathia, large neck circumference (> 17 inches in men, > 16 inches in women), and history of stroke, atrial fibrillation, nocturnal arrhythmias, heart failure, and pulmonary hypertension. Screening is also recommended for any patient who is found on physical examination to have upper-airway narrowing or who reports symptoms such as loud snoring, observed episodes of apnea, gasping or choking at night, unrefreshing sleep, morning headaches, unexplained fatigue, and excessive tiredness during the day.

The American Academy of Sleep Medicine suggests three opportunities to screen for OSA¹:

• At routine health maintenance visits
• If the patient reports clinical symptoms of OSA
• If the patient has risk factors.

A DISMAL STATISTIC

The prevalence of OSA in the United States is high, estimated to be 2% in women and 4% in men in the middle-aged work force,² and even more in blacks, Asians, and older adults.³ Yet only 10% of people with OSA are diagnosed⁴—a dismal statistic considering the association of OSA with resistant hypertension⁵ and with a greater risk of stroke,⁶ cardiovascular disease, and death.⁷

CONSEQUENCES OF UNTREATED OSA

Untreated OSA is associated with a number of conditions⁷:

• Hypertension. OSA is one of the most common conditions associated with resistant hypertension. Patients with severe OSA and resistant hypertension who comply with continuous positive airway pressure (CPAP) treatment have significant reductions in blood pressure.
• Coronary artery disease. OSA is twice as common in people with coronary artery disease as in those with no coronary artery disease. In patients with coronary artery disease and OSA, CPAP may reduce the rate of nonfatal and fatal cardiovascular events.
• Heart failure. OSA is common in patients with systolic dysfunction (11% to 37%). OSA also has been detected in more than 50% of patients with heart failure with preserved systolic function. CPAP treatment can improve ejection fraction in patients with systolic dysfunction.
• Arrythmias. Atrial fibrillation, nonsustained ventricular tachycardia, and complex ventricular ectopy have been reported to be significantly more common in people with OSA.⁸ If the underlying cardiac conduction system is normal and there is no significant thyroid dysfunction, bradyarrhythmias and heart block may be treated effectively with CPAP.⁷ Treatment of OSA may decrease the incidence and severity of ventricular arrhythmias.⁷
• Sudden cardiac death. OSA was independently associated with sudden cardiac death in a longitudinal study.⁹
• Stroke. The Sleep Heart Health Study⁶ showed that OSA is 30% more common in patients who developed ischemic stroke. Long-term CPAP treatment in moderate to severe OSA and ischemic stroke is associated with a reduction in the mortality rate.¹⁰
• Diabetes. The Sleep Heart Health Study showed that OSA is independently associated with glucose intolerance and insulin resistance and may lead to type 2 diabetes mellitus.¹¹

A QUESTIONNAIRE HELPS IDENTIFY WHO NEEDS TESTING

manne_obstructivesleepapneatesting_t1.gif

If you suspect OSA, consider administering a sleep disorder questionnaire such as the Berlin,¹² the Epworth Sleepiness Scale, or the STOP-Bang questionnaire (Table 1). The STOP-Bang questionnaire is an easy-to-use tool that expands on the STOP questionnaire (snoring, tiredness, observed apnea, high blood pressure) with the addition of body mass index, age, neck size, and gender. The Berlin questionnaire has been validated in the primary care setting.¹² The STOP-Bang questionnaire has been validated in preoperative settings¹³ but not in the primary care setting (although it has been commonly used in primary care).

WHICH TEST TO ORDER?

If the score on the questionnaire indicates a moderate or high risk of OSA, the patient should undergo objective testing with polysomnography or, in certain instances, home testing.¹ Polysomnography is the gold standard. Home testing costs less and is easier to arrange, but the American Academy of Sleep Medicine recommends it as an alternative to polysomnography, in conjunction with a comprehensive sleep evaluation, only in the following situations¹⁴:

• If the patient has a high pretest probability of moderate to severe OSA
• If immobility or critical illness makes polysomnography unfeasible
• If direct monitoring of the response to non-CPAP treatments for sleep apnea is needed.

Home testing for OSA should not be used in the following situations:

• If the patient has significant morbidity such as moderate to severe pulmonary disease, neuromuscular disease, or congestive heart failure
• In evaluating a patient suspected of having comorbid sleep disorders such as central sleep apnea, periodic limb movement disorder, insomnia, parasomnias, circadian rhythm disorder, or narcolepsy
• In screening of asymptomatic patients.

Home testing has important drawbacks. It may underestimate the severity of sleep apnea. The rate of false-negative results may be as high as 17%. If the home test was thought to be technically inadequate or the results were inconsistent with those that were expected—ie, if the patient has a high pretest probability of OSA based on risk factors or symptoms but negative results on home testing—then the patient should undergo polysomnography.¹⁴

DIAGNOSIS

The diagnosis of OSA is confirmed if the number of apnea events per hour (ie, the apnea-hypopnea index) on polysomnography or home testing is more than 15, regardless of symptoms, or more than 5 in a patient who reports OSA symptoms. An apnea-hypopnea index of 5 to 14 indicates mild OSA, 15 to 30 indicates moderate OSA, and greater than 30 indicates severe OSA.

BENEFITS OF TREATMENT

Treatment of OSA with CPAP reduces the 10-year risk of fatal and nonfatal motor vehicle accidents by 52%, the 10-year expected number of myocardial infarctions by 49%, and the 10-year risk of stroke by 31%.⁷ It has also been found to be cost-effective, for men and women of all ages with moderate to severe OSA.¹⁵

Patients who have risk factors for obstructive sleep apnea (OSA) or who report symptoms of OSA should be screened for it, first with a complete sleep history and standardized questionnaire, and then by objective testing if indicated. The gold standard test for OSA is polysomnography performed overnight in a sleep laboratory. Home testing is an option in certain instances.

Common risk factors include obesity, resistant hypertension, retrognathia, large neck circumference (> 17 inches in men, > 16 inches in women), and history of stroke, atrial fibrillation, nocturnal arrhythmias, heart failure, and pulmonary hypertension. Screening is also recommended for any patient who is found on physical examination to have upper-airway narrowing or who reports symptoms such as loud snoring, observed episodes of apnea, gasping or choking at night, unrefreshing sleep, morning headaches, unexplained fatigue, and excessive tiredness during the day.

The American Academy of Sleep Medicine suggests three opportunities to screen for OSA¹:

• At routine health maintenance visits
• If the patient reports clinical symptoms of OSA
• If the patient has risk factors.

A DISMAL STATISTIC

The prevalence of OSA in the United States is high, estimated to be 2% in women and 4% in men in the middle-aged work force,² and even more in blacks, Asians, and older adults.³ Yet only 10% of people with OSA are diagnosed⁴—a dismal statistic considering the association of OSA with resistant hypertension⁵ and with a greater risk of stroke,⁶ cardiovascular disease, and death.⁷

CONSEQUENCES OF UNTREATED OSA

Untreated OSA is associated with a number of conditions⁷:

• Hypertension. OSA is one of the most common conditions associated with resistant hypertension. Patients with severe OSA and resistant hypertension who comply with continuous positive airway pressure (CPAP) treatment have significant reductions in blood pressure.
• Coronary artery disease. OSA is twice as common in people with coronary artery disease as in those with no coronary artery disease. In patients with coronary artery disease and OSA, CPAP may reduce the rate of nonfatal and fatal cardiovascular events.
• Heart failure. OSA is common in patients with systolic dysfunction (11% to 37%). OSA also has been detected in more than 50% of patients with heart failure with preserved systolic function. CPAP treatment can improve ejection fraction in patients with systolic dysfunction.
• Arrythmias. Atrial fibrillation, nonsustained ventricular tachycardia, and complex ventricular ectopy have been reported to be significantly more common in people with OSA.⁸ If the underlying cardiac conduction system is normal and there is no significant thyroid dysfunction, bradyarrhythmias and heart block may be treated effectively with CPAP.⁷ Treatment of OSA may decrease the incidence and severity of ventricular arrhythmias.⁷
• Sudden cardiac death. OSA was independently associated with sudden cardiac death in a longitudinal study.⁹
• Stroke. The Sleep Heart Health Study⁶ showed that OSA is 30% more common in patients who developed ischemic stroke. Long-term CPAP treatment in moderate to severe OSA and ischemic stroke is associated with a reduction in the mortality rate.¹⁰
• Diabetes. The Sleep Heart Health Study showed that OSA is independently associated with glucose intolerance and insulin resistance and may lead to type 2 diabetes mellitus.¹¹

A QUESTIONNAIRE HELPS IDENTIFY WHO NEEDS TESTING

manne_obstructivesleepapneatesting_t1.gif

If you suspect OSA, consider administering a sleep disorder questionnaire such as the Berlin,¹² the Epworth Sleepiness Scale, or the STOP-Bang questionnaire (Table 1). The STOP-Bang questionnaire is an easy-to-use tool that expands on the STOP questionnaire (snoring, tiredness, observed apnea, high blood pressure) with the addition of body mass index, age, neck size, and gender. The Berlin questionnaire has been validated in the primary care setting.¹² The STOP-Bang questionnaire has been validated in preoperative settings¹³ but not in the primary care setting (although it has been commonly used in primary care).

WHICH TEST TO ORDER?

If the score on the questionnaire indicates a moderate or high risk of OSA, the patient should undergo objective testing with polysomnography or, in certain instances, home testing.¹ Polysomnography is the gold standard. Home testing costs less and is easier to arrange, but the American Academy of Sleep Medicine recommends it as an alternative to polysomnography, in conjunction with a comprehensive sleep evaluation, only in the following situations¹⁴:

• If the patient has a high pretest probability of moderate to severe OSA
• If immobility or critical illness makes polysomnography unfeasible
• If direct monitoring of the response to non-CPAP treatments for sleep apnea is needed.

Home testing for OSA should not be used in the following situations:

• If the patient has significant morbidity such as moderate to severe pulmonary disease, neuromuscular disease, or congestive heart failure
• In evaluating a patient suspected of having comorbid sleep disorders such as central sleep apnea, periodic limb movement disorder, insomnia, parasomnias, circadian rhythm disorder, or narcolepsy
• In screening of asymptomatic patients.

Home testing has important drawbacks. It may underestimate the severity of sleep apnea. The rate of false-negative results may be as high as 17%. If the home test was thought to be technically inadequate or the results were inconsistent with those that were expected—ie, if the patient has a high pretest probability of OSA based on risk factors or symptoms but negative results on home testing—then the patient should undergo polysomnography.¹⁴

DIAGNOSIS

The diagnosis of OSA is confirmed if the number of apnea events per hour (ie, the apnea-hypopnea index) on polysomnography or home testing is more than 15, regardless of symptoms, or more than 5 in a patient who reports OSA symptoms. An apnea-hypopnea index of 5 to 14 indicates mild OSA, 15 to 30 indicates moderate OSA, and greater than 30 indicates severe OSA.

BENEFITS OF TREATMENT

Treatment of OSA with CPAP reduces the 10-year risk of fatal and nonfatal motor vehicle accidents by 52%, the 10-year expected number of myocardial infarctions by 49%, and the 10-year risk of stroke by 31%.⁷ It has also been found to be cost-effective, for men and women of all ages with moderate to severe OSA.¹⁵