“Hemorrhoids” turn out to be cancer

A 49-YEAR-OLD WOMAN, whose husband was on active duty with the US Army, went to an army community hospital in March complaining of hemorrhoids, back pain, and itching, burning, and pain with bowel movements. A guaiac-based fecal occult blood test was positive; no further testing was done to rule out rectal cancer.

The woman was discharged with pain medication but returned the following day, reporting intense anal pain despite taking the medication and bright red blood in her stools. The symptoms were attributed to hemorrhoids, and the patient was given a toilet “donut” and topical medication. Although her records noted a referral to a general surgeon, the referral wasn’t arranged or scheduled.

The patient returned to the hospital in April, May, and June with continuing complaints that included unrelieved constipation. A laxative was prescribed, but no further testing was done, nor was the patient referred to a surgeon.

In August, she went to the emergency department because of rectal bleeding for the previous 2 weeks, abdominal pain, blood in her urine, and difficulty breathing. Once again the symptoms were blamed on hemorrhoids even though the patient questioned the diagnosis.

The patient continued to see various providers at the army community hospital for the rest of the year, during which time she turned 50. None of them recommended a colonoscopy despite standard recommendations to begin colorectal cancer screening at 50 years of age and the woman’s symptoms, which suggested colorectal cancer.

In March of the following year, the patient consulted a bariatric surgeon in private practice, who recommended evaluating the patient’s bloody stools and offered to perform a diagnostic colonoscopy if authorized. The army hospital didn’t immediately authorize the procedure, and it wasn’t performed.

In late September, the patient consulted a surgeon at the hospital, by which time bright red blood was squirting from her anal region and appeared in the toilet water after every bowel movement. She had never undergone a full colon evaluation.

Less than a week after the surgery consult, the patient’s husband was transferred to another military base. Her doctors said that a surgeon at the new base would be told about her medical condition, but that didn’t happen.

Five months later, a surgery consultation at the new military base found a rectal lesion extending 8 cm into the rectum from the anal verge. Pathology confirmed stage IIIC mucinous adenocarcinoma that had spread to the lymph nodes. Two years later, after several surgeries, chemotherapy, and radiation, the patient died at 53 years of age.

PLAINTIFF’S CLAIM If testing to rule out rectal cancer, such as a colonoscopy, had been performed earlier, the cancer would have been diagnosed at a curable stage.

THE DEFENSE No information about the defense is available.

VERDICT $2.15 million Tennessee settlement.

COMMENT Recurrent, unrelenting symptoms should prompt the alert clinician to explore alternative diagnoses.

For want of diagnosis and treatment, kidney function is lost

A FEBRILE ILLNESS prompted a patient to visit his primary care physician. After 3 months of treatment by the primary care doctor, the patient sought a second opinion and treatment from a federally funded community health clinic, where he was treated for 2 more months. During that time, the patient developed signs and symptoms of impaired kidney function, which laboratory results confirmed.

The clinic staff didn’t address the possible loss of kidney function. Three days after his last examination at the clinic, the patient went to a hospital emergency department, where he was promptly diagnosed with subacute bacterial endocarditis. His kidney function could not be restored.

PLAINTIFF’S CLAIM The primary care physician and the staff at the clinic were negligent in failing to diagnose and treat the kidney issues. Also, they didn’t recognize and treat the signs and symptoms of subacute bacterial endocarditis.

THE DEFENSE The primary care physician claimed that the patient’s injuries resulted solely from negligence on the part of the clinic staff. He maintained that the patient’s kidney function was normal when the man left his care. The federal government, on behalf of the clinic staff, claimed that the primary care physician was at least 50% responsible for the patient’s injuries.

VERDICT $1.45 million Texas settlement.

COMMENT Subacute bacterial endocarditis can be a challenging diagnosis because of the subtlety and variety of presentations. Remember the zebras when confronted with unexplained symptoms and signs.

Neuropathy blamed on belated diabetes diagnosis

A PATIENT IN A FAMILY PRACTICE was treated by several of the doctors and a physician assistant in the group over about a decade. After the patient developed neuropathy in his arms and legs, he was diagnosed with type 2 diabetes.

PLAINTIFF’S CLAIM Earlier diagnosis of the diabetes would have prevented development of neuropathy. High blood glucose levels identified on tests weren’t addressed.

THE DEFENSE Only 3 tests had shown excessive levels of glucose; the patient had many comorbidities that required attention. A special diet had been prescribed that would have helped control glucose levels. This was an appropriate initial step to address a diagnosis of type 2 diabetes.

VERDICT $285,000 New York settlement.

COMMENT It’s easy to overlook or postpone treatment of apparently less urgent issues such as glucose intolerance. Clear documentation and explicit discussion with patients might help mitigate the risk of adverse judgments.

Too many narcotic prescriptions

A WOMAN TREATED FOR CHRONIC SINUSITIS by an ear, nose, and throat physician received prescriptions for oxycodone, acetaminophen and oxycodone, and methadone for years to relieve headaches and facial pain. She died at 40 years of age from a methadone overdose. The physician admitted in a deposition that he’d kept on prescribing the medications even after the patient’s health insurer informed him that she was obtaining narcotics from multiple providers.

PLAINTIFF’S CLAIM No information about the plaintiff’s claim is available.

THE DEFENSE No information about the defense is available.

VERDICT $1.05 million New Jersey settlement.

COMMENT Strict tracking and oversight of opioid administration is essential. Clear documentation and regular follow-up remain very important.

Delayed Tx turns skin breakdown into a long-term problem

A NEARLY IMMOBILE WOMAN was discharged from a hospital—where she’d been treated for congestive heart failure, hypertension, diabetes, altered mental status, severe arthritis, and gout—and transported by ambulance to her home. Discharge diagnoses included possible obstructive sleep apnea and hypercapnia. Because the patient needed a great deal of help with activities of daily living, her physician ordered home health services.

Twelve days after discharge, a representative from the home health agency performed an initial assessment in the patient’s home, at which time the patient’s daughter reported that her mother had developed some skin breakdown on her buttocks that required care. The home health nurse allegedly told the daughter that the agency would need an order from her mother’s physician before starting home treatment for the skin breakdown.

The daughter phoned the physician every day for the next few days to get treatment authorization, but the doctor didn’t return her calls. The home health agency didn’t seek authorization from the doctor.

When the home health nurse returned to the patient’s home a week later to begin care, the daughter again mentioned the areas of skin breakdown, which by that time had become pressure sores. The nurse didn’t treat the pressure sores. The home health agency tried to contact the patient’s physician, who didn’t return their calls.

The agency finally received an order to treat the pressure sores 6 days after the home health nurse had begun caring for the patient, by which time the sores were infected and considerably larger. Healing required more than a year of treatment.

PLAINTIFF’S CLAIM As a result of the delay in treating the pressure sores, the patient’s condition was worse that it otherwise would have been.

THE DEFENSE The defendants denied any negligence.

VERDICT Alabama defense verdict.

COMMENT Better communication and coordination of care between home health providers and a patient’s medical home are important to provide optimal care—and avoid lawsuits.

“Hemorrhoids” turn out to be cancer

A 49-YEAR-OLD WOMAN, whose husband was on active duty with the US Army, went to an army community hospital in March complaining of hemorrhoids, back pain, and itching, burning, and pain with bowel movements. A guaiac-based fecal occult blood test was positive; no further testing was done to rule out rectal cancer.

The woman was discharged with pain medication but returned the following day, reporting intense anal pain despite taking the medication and bright red blood in her stools. The symptoms were attributed to hemorrhoids, and the patient was given a toilet “donut” and topical medication. Although her records noted a referral to a general surgeon, the referral wasn’t arranged or scheduled.

The patient returned to the hospital in April, May, and June with continuing complaints that included unrelieved constipation. A laxative was prescribed, but no further testing was done, nor was the patient referred to a surgeon.

In August, she went to the emergency department because of rectal bleeding for the previous 2 weeks, abdominal pain, blood in her urine, and difficulty breathing. Once again the symptoms were blamed on hemorrhoids even though the patient questioned the diagnosis.

The patient continued to see various providers at the army community hospital for the rest of the year, during which time she turned 50. None of them recommended a colonoscopy despite standard recommendations to begin colorectal cancer screening at 50 years of age and the woman’s symptoms, which suggested colorectal cancer.

In March of the following year, the patient consulted a bariatric surgeon in private practice, who recommended evaluating the patient’s bloody stools and offered to perform a diagnostic colonoscopy if authorized. The army hospital didn’t immediately authorize the procedure, and it wasn’t performed.

In late September, the patient consulted a surgeon at the hospital, by which time bright red blood was squirting from her anal region and appeared in the toilet water after every bowel movement. She had never undergone a full colon evaluation.

Less than a week after the surgery consult, the patient’s husband was transferred to another military base. Her doctors said that a surgeon at the new base would be told about her medical condition, but that didn’t happen.

Five months later, a surgery consultation at the new military base found a rectal lesion extending 8 cm into the rectum from the anal verge. Pathology confirmed stage IIIC mucinous adenocarcinoma that had spread to the lymph nodes. Two years later, after several surgeries, chemotherapy, and radiation, the patient died at 53 years of age.

PLAINTIFF’S CLAIM If testing to rule out rectal cancer, such as a colonoscopy, had been performed earlier, the cancer would have been diagnosed at a curable stage.

THE DEFENSE No information about the defense is available.

VERDICT $2.15 million Tennessee settlement.

COMMENT Recurrent, unrelenting symptoms should prompt the alert clinician to explore alternative diagnoses.

For want of diagnosis and treatment, kidney function is lost

A FEBRILE ILLNESS prompted a patient to visit his primary care physician. After 3 months of treatment by the primary care doctor, the patient sought a second opinion and treatment from a federally funded community health clinic, where he was treated for 2 more months. During that time, the patient developed signs and symptoms of impaired kidney function, which laboratory results confirmed.

The clinic staff didn’t address the possible loss of kidney function. Three days after his last examination at the clinic, the patient went to a hospital emergency department, where he was promptly diagnosed with subacute bacterial endocarditis. His kidney function could not be restored.

PLAINTIFF’S CLAIM The primary care physician and the staff at the clinic were negligent in failing to diagnose and treat the kidney issues. Also, they didn’t recognize and treat the signs and symptoms of subacute bacterial endocarditis.

THE DEFENSE The primary care physician claimed that the patient’s injuries resulted solely from negligence on the part of the clinic staff. He maintained that the patient’s kidney function was normal when the man left his care. The federal government, on behalf of the clinic staff, claimed that the primary care physician was at least 50% responsible for the patient’s injuries.

VERDICT $1.45 million Texas settlement.

COMMENT Subacute bacterial endocarditis can be a challenging diagnosis because of the subtlety and variety of presentations. Remember the zebras when confronted with unexplained symptoms and signs.

Neuropathy blamed on belated diabetes diagnosis

A PATIENT IN A FAMILY PRACTICE was treated by several of the doctors and a physician assistant in the group over about a decade. After the patient developed neuropathy in his arms and legs, he was diagnosed with type 2 diabetes.

PLAINTIFF’S CLAIM Earlier diagnosis of the diabetes would have prevented development of neuropathy. High blood glucose levels identified on tests weren’t addressed.

THE DEFENSE Only 3 tests had shown excessive levels of glucose; the patient had many comorbidities that required attention. A special diet had been prescribed that would have helped control glucose levels. This was an appropriate initial step to address a diagnosis of type 2 diabetes.

VERDICT $285,000 New York settlement.

COMMENT It’s easy to overlook or postpone treatment of apparently less urgent issues such as glucose intolerance. Clear documentation and explicit discussion with patients might help mitigate the risk of adverse judgments.

Too many narcotic prescriptions

A WOMAN TREATED FOR CHRONIC SINUSITIS by an ear, nose, and throat physician received prescriptions for oxycodone, acetaminophen and oxycodone, and methadone for years to relieve headaches and facial pain. She died at 40 years of age from a methadone overdose. The physician admitted in a deposition that he’d kept on prescribing the medications even after the patient’s health insurer informed him that she was obtaining narcotics from multiple providers.

PLAINTIFF’S CLAIM No information about the plaintiff’s claim is available.

THE DEFENSE No information about the defense is available.

VERDICT $1.05 million New Jersey settlement.

COMMENT Strict tracking and oversight of opioid administration is essential. Clear documentation and regular follow-up remain very important.

Delayed Tx turns skin breakdown into a long-term problem

A NEARLY IMMOBILE WOMAN was discharged from a hospital—where she’d been treated for congestive heart failure, hypertension, diabetes, altered mental status, severe arthritis, and gout—and transported by ambulance to her home. Discharge diagnoses included possible obstructive sleep apnea and hypercapnia. Because the patient needed a great deal of help with activities of daily living, her physician ordered home health services.

Twelve days after discharge, a representative from the home health agency performed an initial assessment in the patient’s home, at which time the patient’s daughter reported that her mother had developed some skin breakdown on her buttocks that required care. The home health nurse allegedly told the daughter that the agency would need an order from her mother’s physician before starting home treatment for the skin breakdown.

The daughter phoned the physician every day for the next few days to get treatment authorization, but the doctor didn’t return her calls. The home health agency didn’t seek authorization from the doctor.

When the home health nurse returned to the patient’s home a week later to begin care, the daughter again mentioned the areas of skin breakdown, which by that time had become pressure sores. The nurse didn’t treat the pressure sores. The home health agency tried to contact the patient’s physician, who didn’t return their calls.

The agency finally received an order to treat the pressure sores 6 days after the home health nurse had begun caring for the patient, by which time the sores were infected and considerably larger. Healing required more than a year of treatment.

PLAINTIFF’S CLAIM As a result of the delay in treating the pressure sores, the patient’s condition was worse that it otherwise would have been.

THE DEFENSE The defendants denied any negligence.

VERDICT Alabama defense verdict.

COMMENT Better communication and coordination of care between home health providers and a patient’s medical home are important to provide optimal care—and avoid lawsuits.

“Hemorrhoids” turn out to be cancer

A 49-YEAR-OLD WOMAN, whose husband was on active duty with the US Army, went to an army community hospital in March complaining of hemorrhoids, back pain, and itching, burning, and pain with bowel movements. A guaiac-based fecal occult blood test was positive; no further testing was done to rule out rectal cancer.

The woman was discharged with pain medication but returned the following day, reporting intense anal pain despite taking the medication and bright red blood in her stools. The symptoms were attributed to hemorrhoids, and the patient was given a toilet “donut” and topical medication. Although her records noted a referral to a general surgeon, the referral wasn’t arranged or scheduled.

The patient returned to the hospital in April, May, and June with continuing complaints that included unrelieved constipation. A laxative was prescribed, but no further testing was done, nor was the patient referred to a surgeon.

In August, she went to the emergency department because of rectal bleeding for the previous 2 weeks, abdominal pain, blood in her urine, and difficulty breathing. Once again the symptoms were blamed on hemorrhoids even though the patient questioned the diagnosis.

The patient continued to see various providers at the army community hospital for the rest of the year, during which time she turned 50. None of them recommended a colonoscopy despite standard recommendations to begin colorectal cancer screening at 50 years of age and the woman’s symptoms, which suggested colorectal cancer.

In March of the following year, the patient consulted a bariatric surgeon in private practice, who recommended evaluating the patient’s bloody stools and offered to perform a diagnostic colonoscopy if authorized. The army hospital didn’t immediately authorize the procedure, and it wasn’t performed.

In late September, the patient consulted a surgeon at the hospital, by which time bright red blood was squirting from her anal region and appeared in the toilet water after every bowel movement. She had never undergone a full colon evaluation.

Less than a week after the surgery consult, the patient’s husband was transferred to another military base. Her doctors said that a surgeon at the new base would be told about her medical condition, but that didn’t happen.

Five months later, a surgery consultation at the new military base found a rectal lesion extending 8 cm into the rectum from the anal verge. Pathology confirmed stage IIIC mucinous adenocarcinoma that had spread to the lymph nodes. Two years later, after several surgeries, chemotherapy, and radiation, the patient died at 53 years of age.

PLAINTIFF’S CLAIM If testing to rule out rectal cancer, such as a colonoscopy, had been performed earlier, the cancer would have been diagnosed at a curable stage.

THE DEFENSE No information about the defense is available.

VERDICT $2.15 million Tennessee settlement.

COMMENT Recurrent, unrelenting symptoms should prompt the alert clinician to explore alternative diagnoses.

For want of diagnosis and treatment, kidney function is lost

A FEBRILE ILLNESS prompted a patient to visit his primary care physician. After 3 months of treatment by the primary care doctor, the patient sought a second opinion and treatment from a federally funded community health clinic, where he was treated for 2 more months. During that time, the patient developed signs and symptoms of impaired kidney function, which laboratory results confirmed.

The clinic staff didn’t address the possible loss of kidney function. Three days after his last examination at the clinic, the patient went to a hospital emergency department, where he was promptly diagnosed with subacute bacterial endocarditis. His kidney function could not be restored.

PLAINTIFF’S CLAIM The primary care physician and the staff at the clinic were negligent in failing to diagnose and treat the kidney issues. Also, they didn’t recognize and treat the signs and symptoms of subacute bacterial endocarditis.

THE DEFENSE The primary care physician claimed that the patient’s injuries resulted solely from negligence on the part of the clinic staff. He maintained that the patient’s kidney function was normal when the man left his care. The federal government, on behalf of the clinic staff, claimed that the primary care physician was at least 50% responsible for the patient’s injuries.

VERDICT $1.45 million Texas settlement.

COMMENT Subacute bacterial endocarditis can be a challenging diagnosis because of the subtlety and variety of presentations. Remember the zebras when confronted with unexplained symptoms and signs.

Neuropathy blamed on belated diabetes diagnosis

A PATIENT IN A FAMILY PRACTICE was treated by several of the doctors and a physician assistant in the group over about a decade. After the patient developed neuropathy in his arms and legs, he was diagnosed with type 2 diabetes.

PLAINTIFF’S CLAIM Earlier diagnosis of the diabetes would have prevented development of neuropathy. High blood glucose levels identified on tests weren’t addressed.

THE DEFENSE Only 3 tests had shown excessive levels of glucose; the patient had many comorbidities that required attention. A special diet had been prescribed that would have helped control glucose levels. This was an appropriate initial step to address a diagnosis of type 2 diabetes.

VERDICT $285,000 New York settlement.

COMMENT It’s easy to overlook or postpone treatment of apparently less urgent issues such as glucose intolerance. Clear documentation and explicit discussion with patients might help mitigate the risk of adverse judgments.

Too many narcotic prescriptions

A WOMAN TREATED FOR CHRONIC SINUSITIS by an ear, nose, and throat physician received prescriptions for oxycodone, acetaminophen and oxycodone, and methadone for years to relieve headaches and facial pain. She died at 40 years of age from a methadone overdose. The physician admitted in a deposition that he’d kept on prescribing the medications even after the patient’s health insurer informed him that she was obtaining narcotics from multiple providers.

PLAINTIFF’S CLAIM No information about the plaintiff’s claim is available.

THE DEFENSE No information about the defense is available.

VERDICT $1.05 million New Jersey settlement.

COMMENT Strict tracking and oversight of opioid administration is essential. Clear documentation and regular follow-up remain very important.

Delayed Tx turns skin breakdown into a long-term problem

A NEARLY IMMOBILE WOMAN was discharged from a hospital—where she’d been treated for congestive heart failure, hypertension, diabetes, altered mental status, severe arthritis, and gout—and transported by ambulance to her home. Discharge diagnoses included possible obstructive sleep apnea and hypercapnia. Because the patient needed a great deal of help with activities of daily living, her physician ordered home health services.

Twelve days after discharge, a representative from the home health agency performed an initial assessment in the patient’s home, at which time the patient’s daughter reported that her mother had developed some skin breakdown on her buttocks that required care. The home health nurse allegedly told the daughter that the agency would need an order from her mother’s physician before starting home treatment for the skin breakdown.

The daughter phoned the physician every day for the next few days to get treatment authorization, but the doctor didn’t return her calls. The home health agency didn’t seek authorization from the doctor.

When the home health nurse returned to the patient’s home a week later to begin care, the daughter again mentioned the areas of skin breakdown, which by that time had become pressure sores. The nurse didn’t treat the pressure sores. The home health agency tried to contact the patient’s physician, who didn’t return their calls.

The agency finally received an order to treat the pressure sores 6 days after the home health nurse had begun caring for the patient, by which time the sores were infected and considerably larger. Healing required more than a year of treatment.

PLAINTIFF’S CLAIM As a result of the delay in treating the pressure sores, the patient’s condition was worse that it otherwise would have been.

THE DEFENSE The defendants denied any negligence.

VERDICT Alabama defense verdict.

COMMENT Better communication and coordination of care between home health providers and a patient’s medical home are important to provide optimal care—and avoid lawsuits.

Recently, the US Preventive Services Task Force (USPSTF) finalized 7 recommendations on 5 topics and posted draft recommendations on an additional 10 topics. It also implemented new procedures that include posting draft recommendations for public comment (see “A new review process for the USPSTF”). This article reviews the USPSTF activity in 2011, as well as cervical cancer screening recommendations issued earlier this year.

2012 recommendations

Screening for cervical cancer
The USPSTF released its new recommendations on screening for cervical cancer in March (TABLE 1).¹ The final document varied from the 2011 draft recommendations in 2 areas: the roles of human papillomavirus (HPV) testing and sexual history.

1. The draft issued an I statement (insufficient evidence) for the role of HPV testing. Subsequently, based on stakeholder and public comment (as well as a review of 2 large recently published studies), the USPSTF gave an A recommendation to the use of HPV testing in conjunction with cervical cytology as an option for women ages 30 years and older who want to increase the interval between screening to 5 years.^2,3
2. The draft stated that the age at which screening should be initiated depends on a patient’s sexual history. The final recommendations state that screening should not begin until age 21, regardless of sexual history.

TABLE 1

These new recommendations balance the proven benefits of cervical cytology with the harms from overscreening and are now essentially the same as those of other organizations, including the American Cancer Society, the American Society for Colposcopy and Cervical Pathology, and the American Society for Clinical Pathology. They differ in minor ways from those of the American Congress of Obstetricians and Gynecologists, and the American Academy of Family Physicians is assessing whether to endorse them.

Importantly, the new recommendations identify individuals for whom cervical cytology should be avoided—women younger than age 21, most women older than age 65, and those who have had a hysterectomy with removal of the cervix. A decision to stop screening after the 65th birthday depends on whether the patient has had adequate screening yielding normal findings: This is defined by the USPSTF as 3 consecutive negative cytology results (or 2 consecutive negative co-test results with cytology and HIV testing) within 10 years of the proposed time of cessation, with the most recent test having been performed within 5 years. Avoiding cytology testing after hysterectomy is contingent on the procedure having been performed for an indication other than a high-grade precancerous lesion or cervical cancer. In addition, the recommendations advise against HPV testing in women younger than age 30, as it offers little advantage and leads to much overdiagnosis.

Liquid vs conventional cytology. As a minor point, the USPSTF says the evidence clearly shows that liquid cytology offers no advantage over conventional cytology. But it recognizes that the screening method used is often not determined by the physician.

Recommendations finalized in 2011

TABLE 2 summarizes recommendations completed by the USPSTF last year.

Neonatal gonococcal eye infection prevention
The recommendation to use topical medication (erythromycin ointment) to prevent neonatal gonococcal eye infection is an update and reaffirmation of a previous recommendation. Blindness due to this disease has become rare in the United States because of the routine use of a neonatal topical antibiotic, and there is good evidence that it causes no significant harm. Its use continues to be recommended for all newborns.⁴

TABLE 2

Vision screening for children
Vision screening for preschool children can detect visual acuity problems such as amblyopia and refractive errors. A variety of screening tests are available, including visual acuity, stereoacuity, cover-uncover, Hirschberg light reflex, and auto-refractor tests (automated optical instruments that detect refractive errors). The most benefit is obtained by discovering and correcting amblyopia.

There is no evidence that detecting problems before age 3 years leads to better outcomes than detection between 3 and 5 years of age. Testing is more difficult in younger children and can yield inconclusive or false-positive results more frequently. This led the USPSTF to reaffirm vision testing once for children ages 3 to 5 years, and to state that the evidence is insufficient to make a recommendation for younger children.⁵

Screening for osteoporosis
The recommendations indicate that all women ages 65 and older should undergo screening, although the optimal frequency of screening is not known. The clinical discussion accompanying the recommendation indicates there is reason to believe that screening men may reduce morbidity and mortality, but that sufficient evidence for or against this is lacking.⁶

Screening can be done with dual-energy x-ray absorptiometry (DEXA) of the hip and lumbar spine, or quantitative ultrasonography of the calcaneus. DEXA is most commonly used, and is the basis for most treatment recommendations.

The recommendation to screen some women younger than 65 years, based on risk, is somewhat complex. The USPSTF recommends screening younger women if their 10-year risk of fracture is comparable to that of a 65-year-old white woman with no additional risk factors (a risk of 9.3% over 10 years). To calculate that risk, the USPSTF recommends using the FRAX (Fracture Risk Assessment) tool developed by the World Health Organization Collaborating Centre for Metabolic Bone Diseases, Sheffield, United Kingdom, which is available free to clinicians and the public (www.shef.ac.uk/FRAX/).

Screening for testicular cancer
The recommendation against screening for testicular cancer may surprise many physicians, even though it is a reaffirmation of a previous recommendation. Testicular cancer is uncommon (5 cases per 100,000 males per year) and treatment is successful in a large proportion of patients, regardless of the stage at which it is discovered. Patients or their partners discover these tumors in time for a cure and there is no evidence physician exams improve outcomes. Physician discovery of incidental and inconsequential findings such as spermatoceles and varicoceles can lead to unnecessary testing and follow-up.⁷

Screening for bladder cancer
The USPSTF issued an I statement for bladder cancer screening because there is little evidence regarding the diagnostic accuracy of available tests (urinalysis for microscopic hematuria, urine cytology, or tests for urine biomarkers) in detecting bladder cancer in asymptomatic patients. In addition, there is no evidence regarding the potential benefits of detecting asymptomatic bladder cancer.⁸

Current draft recommendations

The USPSTF posts recommendations on its Web site for public comment for 30 days. To see current draft recommendations, go to http://www.uspreventiveservicestaskforce.org/tfcomment.htm.

Recently, the US Preventive Services Task Force (USPSTF) finalized 7 recommendations on 5 topics and posted draft recommendations on an additional 10 topics. It also implemented new procedures that include posting draft recommendations for public comment (see “A new review process for the USPSTF”). This article reviews the USPSTF activity in 2011, as well as cervical cancer screening recommendations issued earlier this year.

2012 recommendations

Screening for cervical cancer
The USPSTF released its new recommendations on screening for cervical cancer in March (TABLE 1).¹ The final document varied from the 2011 draft recommendations in 2 areas: the roles of human papillomavirus (HPV) testing and sexual history.

1. The draft issued an I statement (insufficient evidence) for the role of HPV testing. Subsequently, based on stakeholder and public comment (as well as a review of 2 large recently published studies), the USPSTF gave an A recommendation to the use of HPV testing in conjunction with cervical cytology as an option for women ages 30 years and older who want to increase the interval between screening to 5 years.^2,3
2. The draft stated that the age at which screening should be initiated depends on a patient’s sexual history. The final recommendations state that screening should not begin until age 21, regardless of sexual history.

TABLE 1

These new recommendations balance the proven benefits of cervical cytology with the harms from overscreening and are now essentially the same as those of other organizations, including the American Cancer Society, the American Society for Colposcopy and Cervical Pathology, and the American Society for Clinical Pathology. They differ in minor ways from those of the American Congress of Obstetricians and Gynecologists, and the American Academy of Family Physicians is assessing whether to endorse them.

Importantly, the new recommendations identify individuals for whom cervical cytology should be avoided—women younger than age 21, most women older than age 65, and those who have had a hysterectomy with removal of the cervix. A decision to stop screening after the 65th birthday depends on whether the patient has had adequate screening yielding normal findings: This is defined by the USPSTF as 3 consecutive negative cytology results (or 2 consecutive negative co-test results with cytology and HIV testing) within 10 years of the proposed time of cessation, with the most recent test having been performed within 5 years. Avoiding cytology testing after hysterectomy is contingent on the procedure having been performed for an indication other than a high-grade precancerous lesion or cervical cancer. In addition, the recommendations advise against HPV testing in women younger than age 30, as it offers little advantage and leads to much overdiagnosis.

Liquid vs conventional cytology. As a minor point, the USPSTF says the evidence clearly shows that liquid cytology offers no advantage over conventional cytology. But it recognizes that the screening method used is often not determined by the physician.

Recommendations finalized in 2011

TABLE 2 summarizes recommendations completed by the USPSTF last year.

Neonatal gonococcal eye infection prevention
The recommendation to use topical medication (erythromycin ointment) to prevent neonatal gonococcal eye infection is an update and reaffirmation of a previous recommendation. Blindness due to this disease has become rare in the United States because of the routine use of a neonatal topical antibiotic, and there is good evidence that it causes no significant harm. Its use continues to be recommended for all newborns.⁴

TABLE 2

Vision screening for children
Vision screening for preschool children can detect visual acuity problems such as amblyopia and refractive errors. A variety of screening tests are available, including visual acuity, stereoacuity, cover-uncover, Hirschberg light reflex, and auto-refractor tests (automated optical instruments that detect refractive errors). The most benefit is obtained by discovering and correcting amblyopia.

There is no evidence that detecting problems before age 3 years leads to better outcomes than detection between 3 and 5 years of age. Testing is more difficult in younger children and can yield inconclusive or false-positive results more frequently. This led the USPSTF to reaffirm vision testing once for children ages 3 to 5 years, and to state that the evidence is insufficient to make a recommendation for younger children.⁵

Screening for osteoporosis
The recommendations indicate that all women ages 65 and older should undergo screening, although the optimal frequency of screening is not known. The clinical discussion accompanying the recommendation indicates there is reason to believe that screening men may reduce morbidity and mortality, but that sufficient evidence for or against this is lacking.⁶

Screening can be done with dual-energy x-ray absorptiometry (DEXA) of the hip and lumbar spine, or quantitative ultrasonography of the calcaneus. DEXA is most commonly used, and is the basis for most treatment recommendations.

The recommendation to screen some women younger than 65 years, based on risk, is somewhat complex. The USPSTF recommends screening younger women if their 10-year risk of fracture is comparable to that of a 65-year-old white woman with no additional risk factors (a risk of 9.3% over 10 years). To calculate that risk, the USPSTF recommends using the FRAX (Fracture Risk Assessment) tool developed by the World Health Organization Collaborating Centre for Metabolic Bone Diseases, Sheffield, United Kingdom, which is available free to clinicians and the public (www.shef.ac.uk/FRAX/).

Screening for testicular cancer
The recommendation against screening for testicular cancer may surprise many physicians, even though it is a reaffirmation of a previous recommendation. Testicular cancer is uncommon (5 cases per 100,000 males per year) and treatment is successful in a large proportion of patients, regardless of the stage at which it is discovered. Patients or their partners discover these tumors in time for a cure and there is no evidence physician exams improve outcomes. Physician discovery of incidental and inconsequential findings such as spermatoceles and varicoceles can lead to unnecessary testing and follow-up.⁷

Screening for bladder cancer
The USPSTF issued an I statement for bladder cancer screening because there is little evidence regarding the diagnostic accuracy of available tests (urinalysis for microscopic hematuria, urine cytology, or tests for urine biomarkers) in detecting bladder cancer in asymptomatic patients. In addition, there is no evidence regarding the potential benefits of detecting asymptomatic bladder cancer.⁸

Current draft recommendations

The USPSTF posts recommendations on its Web site for public comment for 30 days. To see current draft recommendations, go to http://www.uspreventiveservicestaskforce.org/tfcomment.htm.

Recently, the US Preventive Services Task Force (USPSTF) finalized 7 recommendations on 5 topics and posted draft recommendations on an additional 10 topics. It also implemented new procedures that include posting draft recommendations for public comment (see “A new review process for the USPSTF”). This article reviews the USPSTF activity in 2011, as well as cervical cancer screening recommendations issued earlier this year.

2012 recommendations

Screening for cervical cancer
The USPSTF released its new recommendations on screening for cervical cancer in March (TABLE 1).¹ The final document varied from the 2011 draft recommendations in 2 areas: the roles of human papillomavirus (HPV) testing and sexual history.

1. The draft issued an I statement (insufficient evidence) for the role of HPV testing. Subsequently, based on stakeholder and public comment (as well as a review of 2 large recently published studies), the USPSTF gave an A recommendation to the use of HPV testing in conjunction with cervical cytology as an option for women ages 30 years and older who want to increase the interval between screening to 5 years.^2,3
2. The draft stated that the age at which screening should be initiated depends on a patient’s sexual history. The final recommendations state that screening should not begin until age 21, regardless of sexual history.

TABLE 1

These new recommendations balance the proven benefits of cervical cytology with the harms from overscreening and are now essentially the same as those of other organizations, including the American Cancer Society, the American Society for Colposcopy and Cervical Pathology, and the American Society for Clinical Pathology. They differ in minor ways from those of the American Congress of Obstetricians and Gynecologists, and the American Academy of Family Physicians is assessing whether to endorse them.

Importantly, the new recommendations identify individuals for whom cervical cytology should be avoided—women younger than age 21, most women older than age 65, and those who have had a hysterectomy with removal of the cervix. A decision to stop screening after the 65th birthday depends on whether the patient has had adequate screening yielding normal findings: This is defined by the USPSTF as 3 consecutive negative cytology results (or 2 consecutive negative co-test results with cytology and HIV testing) within 10 years of the proposed time of cessation, with the most recent test having been performed within 5 years. Avoiding cytology testing after hysterectomy is contingent on the procedure having been performed for an indication other than a high-grade precancerous lesion or cervical cancer. In addition, the recommendations advise against HPV testing in women younger than age 30, as it offers little advantage and leads to much overdiagnosis.

Liquid vs conventional cytology. As a minor point, the USPSTF says the evidence clearly shows that liquid cytology offers no advantage over conventional cytology. But it recognizes that the screening method used is often not determined by the physician.

Recommendations finalized in 2011

TABLE 2 summarizes recommendations completed by the USPSTF last year.

Neonatal gonococcal eye infection prevention
The recommendation to use topical medication (erythromycin ointment) to prevent neonatal gonococcal eye infection is an update and reaffirmation of a previous recommendation. Blindness due to this disease has become rare in the United States because of the routine use of a neonatal topical antibiotic, and there is good evidence that it causes no significant harm. Its use continues to be recommended for all newborns.⁴

TABLE 2

Vision screening for children
Vision screening for preschool children can detect visual acuity problems such as amblyopia and refractive errors. A variety of screening tests are available, including visual acuity, stereoacuity, cover-uncover, Hirschberg light reflex, and auto-refractor tests (automated optical instruments that detect refractive errors). The most benefit is obtained by discovering and correcting amblyopia.

There is no evidence that detecting problems before age 3 years leads to better outcomes than detection between 3 and 5 years of age. Testing is more difficult in younger children and can yield inconclusive or false-positive results more frequently. This led the USPSTF to reaffirm vision testing once for children ages 3 to 5 years, and to state that the evidence is insufficient to make a recommendation for younger children.⁵

Screening for osteoporosis
The recommendations indicate that all women ages 65 and older should undergo screening, although the optimal frequency of screening is not known. The clinical discussion accompanying the recommendation indicates there is reason to believe that screening men may reduce morbidity and mortality, but that sufficient evidence for or against this is lacking.⁶

Screening can be done with dual-energy x-ray absorptiometry (DEXA) of the hip and lumbar spine, or quantitative ultrasonography of the calcaneus. DEXA is most commonly used, and is the basis for most treatment recommendations.

The recommendation to screen some women younger than 65 years, based on risk, is somewhat complex. The USPSTF recommends screening younger women if their 10-year risk of fracture is comparable to that of a 65-year-old white woman with no additional risk factors (a risk of 9.3% over 10 years). To calculate that risk, the USPSTF recommends using the FRAX (Fracture Risk Assessment) tool developed by the World Health Organization Collaborating Centre for Metabolic Bone Diseases, Sheffield, United Kingdom, which is available free to clinicians and the public (www.shef.ac.uk/FRAX/).

Screening for testicular cancer
The recommendation against screening for testicular cancer may surprise many physicians, even though it is a reaffirmation of a previous recommendation. Testicular cancer is uncommon (5 cases per 100,000 males per year) and treatment is successful in a large proportion of patients, regardless of the stage at which it is discovered. Patients or their partners discover these tumors in time for a cure and there is no evidence physician exams improve outcomes. Physician discovery of incidental and inconsequential findings such as spermatoceles and varicoceles can lead to unnecessary testing and follow-up.⁷

Screening for bladder cancer
The USPSTF issued an I statement for bladder cancer screening because there is little evidence regarding the diagnostic accuracy of available tests (urinalysis for microscopic hematuria, urine cytology, or tests for urine biomarkers) in detecting bladder cancer in asymptomatic patients. In addition, there is no evidence regarding the potential benefits of detecting asymptomatic bladder cancer.⁸

Current draft recommendations

The USPSTF posts recommendations on its Web site for public comment for 30 days. To see current draft recommendations, go to http://www.uspreventiveservicestaskforce.org/tfcomment.htm.

Evidence summary

Although PLMD often occurs in association with restless legs syndrome, sleep apnea, narcolepsy, and other sleep disorders, it is itself an intrinsic sleep disorder characterized by stereotyped limb movements and sleep disruption.¹ Most treatment studies of PLMD report both subjective and objective measures of sleep quality. Two commonly used objective measures, obtained by PSG, are the periodic leg movement (PLM) index and the PLM arousal index. The TABLE summarizes the evidence of medication trials.

Clonazepam improves subjective sleep measures, leg movements
Three comparative trials evaluated clonazepam against placebo, temazepam, and cognitive behavioral therapy (CBT).^1-3 In the placebo-controlled and temazepam trials, clonazepam significantly improved subjective sleep parameters and leg movements.^1,2 However, the studies produced conflicting results as to whether clonazepam reduced awakening from limb movements. Both temazepam and clonazepam appeared to be comparably effective; the trial was underpowered to detect a difference between them.

The CBT trial didn’t describe the frequency or duration of CBT clearly.³ It isn’t included in the TABLE.

L-Dopa decreases leg motions, effects on subjective sleep symptoms vary
Two comparison trials evaluated L-dopa (combined with carbidopa). One trial compared L-dopa with propoxyphene and placebo, and the other compared it with pergolide, a bromocriptine agonist available in Canada and Europe.^4,5

In both trials, L-dopa consistently reduced leg motions at night but produced a variable response in subjective sleep symptoms and nocturnal waking. Propoxyphene yielded modest improvements in subjective sleep symptoms and nocturnal waking over placebo. The L-dopa–propoxyphene comparison trial was underpowered to allow a statistical comparison between the 2 medications.

Melatonin and valproate produce opposite effects in small studies
Three very small trials recorded symptoms and PSG findings in patients taking melatonin, apomorphine, or valproate, and compared them with the values observed at baseline.^6-8 Melatonin significantly improved objective measures, but most patients didn’t feel less sleepy. Valproate produced the opposite effect—no clear PSG improvements, but all study patients felt better. Injected apomorphine reduced limb movements but not awakenings.

Estrogen replacement therapy doesn’t help
An RCT of estrogen replacement therapy for PLMD enrolled postmenopausal women, about half of whom were found to have PLMD.⁹ The study found estrogen replacement therapy to be ineffective for treating menopause-associated PLMD.

Recommendations

Practice parameters developed by the American Academy of Sleep Medicine state that clonazepam, pergolide, L-dopa (with a decarboxylase inhibitor), oxycodone, and propoxyphene are all reasonable choices for medical treatment of PLMD.¹⁰ The practice parameters don’t specify a preference for any of these medications.

Evidence summary

Although PLMD often occurs in association with restless legs syndrome, sleep apnea, narcolepsy, and other sleep disorders, it is itself an intrinsic sleep disorder characterized by stereotyped limb movements and sleep disruption.¹ Most treatment studies of PLMD report both subjective and objective measures of sleep quality. Two commonly used objective measures, obtained by PSG, are the periodic leg movement (PLM) index and the PLM arousal index. The TABLE summarizes the evidence of medication trials.

Clonazepam improves subjective sleep measures, leg movements
Three comparative trials evaluated clonazepam against placebo, temazepam, and cognitive behavioral therapy (CBT).^1-3 In the placebo-controlled and temazepam trials, clonazepam significantly improved subjective sleep parameters and leg movements.^1,2 However, the studies produced conflicting results as to whether clonazepam reduced awakening from limb movements. Both temazepam and clonazepam appeared to be comparably effective; the trial was underpowered to detect a difference between them.

The CBT trial didn’t describe the frequency or duration of CBT clearly.³ It isn’t included in the TABLE.

L-Dopa decreases leg motions, effects on subjective sleep symptoms vary
Two comparison trials evaluated L-dopa (combined with carbidopa). One trial compared L-dopa with propoxyphene and placebo, and the other compared it with pergolide, a bromocriptine agonist available in Canada and Europe.^4,5

In both trials, L-dopa consistently reduced leg motions at night but produced a variable response in subjective sleep symptoms and nocturnal waking. Propoxyphene yielded modest improvements in subjective sleep symptoms and nocturnal waking over placebo. The L-dopa–propoxyphene comparison trial was underpowered to allow a statistical comparison between the 2 medications.

Melatonin and valproate produce opposite effects in small studies
Three very small trials recorded symptoms and PSG findings in patients taking melatonin, apomorphine, or valproate, and compared them with the values observed at baseline.^6-8 Melatonin significantly improved objective measures, but most patients didn’t feel less sleepy. Valproate produced the opposite effect—no clear PSG improvements, but all study patients felt better. Injected apomorphine reduced limb movements but not awakenings.

Estrogen replacement therapy doesn’t help
An RCT of estrogen replacement therapy for PLMD enrolled postmenopausal women, about half of whom were found to have PLMD.⁹ The study found estrogen replacement therapy to be ineffective for treating menopause-associated PLMD.

Recommendations

Practice parameters developed by the American Academy of Sleep Medicine state that clonazepam, pergolide, L-dopa (with a decarboxylase inhibitor), oxycodone, and propoxyphene are all reasonable choices for medical treatment of PLMD.¹⁰ The practice parameters don’t specify a preference for any of these medications.

Evidence summary

Although PLMD often occurs in association with restless legs syndrome, sleep apnea, narcolepsy, and other sleep disorders, it is itself an intrinsic sleep disorder characterized by stereotyped limb movements and sleep disruption.¹ Most treatment studies of PLMD report both subjective and objective measures of sleep quality. Two commonly used objective measures, obtained by PSG, are the periodic leg movement (PLM) index and the PLM arousal index. The TABLE summarizes the evidence of medication trials.

Clonazepam improves subjective sleep measures, leg movements
Three comparative trials evaluated clonazepam against placebo, temazepam, and cognitive behavioral therapy (CBT).^1-3 In the placebo-controlled and temazepam trials, clonazepam significantly improved subjective sleep parameters and leg movements.^1,2 However, the studies produced conflicting results as to whether clonazepam reduced awakening from limb movements. Both temazepam and clonazepam appeared to be comparably effective; the trial was underpowered to detect a difference between them.

The CBT trial didn’t describe the frequency or duration of CBT clearly.³ It isn’t included in the TABLE.

L-Dopa decreases leg motions, effects on subjective sleep symptoms vary
Two comparison trials evaluated L-dopa (combined with carbidopa). One trial compared L-dopa with propoxyphene and placebo, and the other compared it with pergolide, a bromocriptine agonist available in Canada and Europe.^4,5

In both trials, L-dopa consistently reduced leg motions at night but produced a variable response in subjective sleep symptoms and nocturnal waking. Propoxyphene yielded modest improvements in subjective sleep symptoms and nocturnal waking over placebo. The L-dopa–propoxyphene comparison trial was underpowered to allow a statistical comparison between the 2 medications.

Melatonin and valproate produce opposite effects in small studies
Three very small trials recorded symptoms and PSG findings in patients taking melatonin, apomorphine, or valproate, and compared them with the values observed at baseline.^6-8 Melatonin significantly improved objective measures, but most patients didn’t feel less sleepy. Valproate produced the opposite effect—no clear PSG improvements, but all study patients felt better. Injected apomorphine reduced limb movements but not awakenings.

Estrogen replacement therapy doesn’t help
An RCT of estrogen replacement therapy for PLMD enrolled postmenopausal women, about half of whom were found to have PLMD.⁹ The study found estrogen replacement therapy to be ineffective for treating menopause-associated PLMD.

Recommendations

Practice parameters developed by the American Academy of Sleep Medicine state that clonazepam, pergolide, L-dopa (with a decarboxylase inhibitor), oxycodone, and propoxyphene are all reasonable choices for medical treatment of PLMD.¹⁰ The practice parameters don’t specify a preference for any of these medications.

Evidence summary

A systematic review from the US Surgeon General’s office of studies addressing the relationship between secondhand smoke exposure and asthma severity in children from 0 to 18 years of age found that children with asthma who were exposed to secondhand smoke had “greater disease severity” than unexposed children.¹ The studies—including 8 prospective and retrospective cohort studies (N=6095), one case-control study (N=149), and 11 uncontrolled case series (N=2932)—were performed in the United States, Canada, the United Kingdom, Sweden, Singapore, South Africa, Kenya, and Nigeria.

Investigators found a significant worsening of asthma caused by secondhand smoke in 6 of 11 clinic-based studies and 2 of 9 population-based studies. Children with asthma who were exposed to secondhand smoke had more doctor visits, more frequent flares, and higher disease severity scores than children who weren’t exposed. Heterogeneity among the studies prevented a meta-analysis of data on severity of asthma.

Where there’s smoke, there are worse health outcomes
Three of 4 subsequent cohort studies found poorer health outcomes among children with asthma who were exposed to smoking than children who weren’t. The first study, of 523 children 4 to 16 years of age with physician-diagnosed asthma, correlated smoke exposure, as indicated by serum cotinine levels, with pulmonary function tests and clinical outcomes.² Children with high serum cotinine levels (>0.63 mg/mL) were more likely to have asthma symptoms monthly or more often, as reported by the family (adjusted odds ratio [OR]=2.7; 95% confidence interval [CI], 1.1-6.5), than children with low cotinine levels (<0.116 ng/mL). High cotinine levels weren’t associated with significant changes in forced expiratory volume in one second, decreased school attendance, or increased physician visits.

Another study of 438 children ages 2 to 12 years with physician-diagnosed asthma and at least one parent who smoked, correlated salivary cotinine levels with the likelihood of contacting a physician for asthma symptoms.³ Children with high salivary cotinine levels (>4.5 ng/mL) had higher asthma-related physician contact rates than children with low cotinine levels (≤2 ng/mL) (incidence rate ratio=1.2; 95% CI, 1.1-1.4).

A third study evaluated asthma treatment response in 167 children from families throughout France who were 6 to 12 years of age and recently diagnosed with mild or moderate persistent asthma.⁴ Investigators performed pulmonary function tests and collected data on symptoms every 4 months for 3 years. Children who lived with someone who smoked were less likely to have controlled asthma symptoms (OR=0.34; 95% CI, 0.13–0.91).

The fourth study, of 126 urban children ages 6 to 12 years with physician-diagnosed asthma and in-home smoke exposure, correlated urinary cotinine levels and rates of clinical illness. It found no significant differences in parent-reported illness between children with higher urinary cotinine levels and children with lower levels.⁵

Recommendations

The National Asthma Education and Prevention Program Expert Panel recommends that physicians ask patients about their smoking status and refer adults who have children with asthma to smoking cessation programs.⁶ The panel further recommends that clinicians advise people with asthma to avoid smoking and limit exposure to environmental tobacco smoke.

Evidence summary

A systematic review from the US Surgeon General’s office of studies addressing the relationship between secondhand smoke exposure and asthma severity in children from 0 to 18 years of age found that children with asthma who were exposed to secondhand smoke had “greater disease severity” than unexposed children.¹ The studies—including 8 prospective and retrospective cohort studies (N=6095), one case-control study (N=149), and 11 uncontrolled case series (N=2932)—were performed in the United States, Canada, the United Kingdom, Sweden, Singapore, South Africa, Kenya, and Nigeria.

Investigators found a significant worsening of asthma caused by secondhand smoke in 6 of 11 clinic-based studies and 2 of 9 population-based studies. Children with asthma who were exposed to secondhand smoke had more doctor visits, more frequent flares, and higher disease severity scores than children who weren’t exposed. Heterogeneity among the studies prevented a meta-analysis of data on severity of asthma.

Where there’s smoke, there are worse health outcomes
Three of 4 subsequent cohort studies found poorer health outcomes among children with asthma who were exposed to smoking than children who weren’t. The first study, of 523 children 4 to 16 years of age with physician-diagnosed asthma, correlated smoke exposure, as indicated by serum cotinine levels, with pulmonary function tests and clinical outcomes.² Children with high serum cotinine levels (>0.63 mg/mL) were more likely to have asthma symptoms monthly or more often, as reported by the family (adjusted odds ratio [OR]=2.7; 95% confidence interval [CI], 1.1-6.5), than children with low cotinine levels (<0.116 ng/mL). High cotinine levels weren’t associated with significant changes in forced expiratory volume in one second, decreased school attendance, or increased physician visits.

Another study of 438 children ages 2 to 12 years with physician-diagnosed asthma and at least one parent who smoked, correlated salivary cotinine levels with the likelihood of contacting a physician for asthma symptoms.³ Children with high salivary cotinine levels (>4.5 ng/mL) had higher asthma-related physician contact rates than children with low cotinine levels (≤2 ng/mL) (incidence rate ratio=1.2; 95% CI, 1.1-1.4).

A third study evaluated asthma treatment response in 167 children from families throughout France who were 6 to 12 years of age and recently diagnosed with mild or moderate persistent asthma.⁴ Investigators performed pulmonary function tests and collected data on symptoms every 4 months for 3 years. Children who lived with someone who smoked were less likely to have controlled asthma symptoms (OR=0.34; 95% CI, 0.13–0.91).

The fourth study, of 126 urban children ages 6 to 12 years with physician-diagnosed asthma and in-home smoke exposure, correlated urinary cotinine levels and rates of clinical illness. It found no significant differences in parent-reported illness between children with higher urinary cotinine levels and children with lower levels.⁵

Recommendations

The National Asthma Education and Prevention Program Expert Panel recommends that physicians ask patients about their smoking status and refer adults who have children with asthma to smoking cessation programs.⁶ The panel further recommends that clinicians advise people with asthma to avoid smoking and limit exposure to environmental tobacco smoke.

Evidence summary

A systematic review from the US Surgeon General’s office of studies addressing the relationship between secondhand smoke exposure and asthma severity in children from 0 to 18 years of age found that children with asthma who were exposed to secondhand smoke had “greater disease severity” than unexposed children.¹ The studies—including 8 prospective and retrospective cohort studies (N=6095), one case-control study (N=149), and 11 uncontrolled case series (N=2932)—were performed in the United States, Canada, the United Kingdom, Sweden, Singapore, South Africa, Kenya, and Nigeria.

Investigators found a significant worsening of asthma caused by secondhand smoke in 6 of 11 clinic-based studies and 2 of 9 population-based studies. Children with asthma who were exposed to secondhand smoke had more doctor visits, more frequent flares, and higher disease severity scores than children who weren’t exposed. Heterogeneity among the studies prevented a meta-analysis of data on severity of asthma.

Where there’s smoke, there are worse health outcomes
Three of 4 subsequent cohort studies found poorer health outcomes among children with asthma who were exposed to smoking than children who weren’t. The first study, of 523 children 4 to 16 years of age with physician-diagnosed asthma, correlated smoke exposure, as indicated by serum cotinine levels, with pulmonary function tests and clinical outcomes.² Children with high serum cotinine levels (>0.63 mg/mL) were more likely to have asthma symptoms monthly or more often, as reported by the family (adjusted odds ratio [OR]=2.7; 95% confidence interval [CI], 1.1-6.5), than children with low cotinine levels (<0.116 ng/mL). High cotinine levels weren’t associated with significant changes in forced expiratory volume in one second, decreased school attendance, or increased physician visits.

Another study of 438 children ages 2 to 12 years with physician-diagnosed asthma and at least one parent who smoked, correlated salivary cotinine levels with the likelihood of contacting a physician for asthma symptoms.³ Children with high salivary cotinine levels (>4.5 ng/mL) had higher asthma-related physician contact rates than children with low cotinine levels (≤2 ng/mL) (incidence rate ratio=1.2; 95% CI, 1.1-1.4).

A third study evaluated asthma treatment response in 167 children from families throughout France who were 6 to 12 years of age and recently diagnosed with mild or moderate persistent asthma.⁴ Investigators performed pulmonary function tests and collected data on symptoms every 4 months for 3 years. Children who lived with someone who smoked were less likely to have controlled asthma symptoms (OR=0.34; 95% CI, 0.13–0.91).

The fourth study, of 126 urban children ages 6 to 12 years with physician-diagnosed asthma and in-home smoke exposure, correlated urinary cotinine levels and rates of clinical illness. It found no significant differences in parent-reported illness between children with higher urinary cotinine levels and children with lower levels.⁵

Recommendations

The National Asthma Education and Prevention Program Expert Panel recommends that physicians ask patients about their smoking status and refer adults who have children with asthma to smoking cessation programs.⁶ The panel further recommends that clinicians advise people with asthma to avoid smoking and limit exposure to environmental tobacco smoke.

Hearing impairment is a widespread problem, affecting approximately 36 million US adults¹ and an increasing number of children.² Yet it often goes undetected. The consequences of untreated or undertreated hearing loss can be severe.

Adverse effects are often age-dependent: In children, hearing loss is associated with a broad range of complications, including delays in language development, decreased reading comprehension, and poor academic performance, as well as social and emotional problems.^2,3 In adults—particularly the elderly—hearing impairment can lead to social isolation, depression, and a diminished quality of life.^4,5

Early detection and treatment can do much to alleviate these adverse effects. But many physicians received little training in the identification and treatment of hearing loss in medical school. What’s more, people with significant hearing loss tend to have fewer interactions with health care providers than their counterparts with no hearing impairment⁶—a finding that some attribute to fear, mistrust, and frustration.⁷

Physician awareness of the problems facing people with hearing loss, the importance of screening, and the need to improve communication with hearing-impaired patients (TABLE 1)⁸ can help change that. The strategies presented here were developed with this in mind.

TABLE 1
How to better communicate with patients who have hearing loss⁸

The scope of hearing loss across the lifespan

Hearing loss affects 1 to 3 in every 1000 newborns.⁹ The prevalence increases to 2% among 5-year-olds, and to 10% to 20% by age 18.^10,11 The risk accelerates in “early older life” (defined as ages 50-69 years), with men affected more often than women.¹² Hearing loss is the fourth most common chronic condition among older adults, and it is estimated that ≥70% of nursing home residents have some degree of impairment.¹³

Hearing loss can be categorized as mild (a loss of 20-40 decibels [dB]), moderate (41-55 dB loss), moderate to severe (56-70 dB loss), severe (71-90 dB loss), or profound (>91 dB loss), but any degree of hearing loss should be considered noteworthy.

In children, the impact of mild impairment is often minimized by both professionals and parents, especially among those whose speech developed normally. Unfortunately, the failure to respond appropriately in such cases often increases the adverse effects of the hearing loss.¹⁴

In adults, even mild to moderate impairment can lead to significant functional impairment and, therefore, a decreased quality of life.⁵ And in elderly patients, any undetected hearing loss can adversely affect their performance on cognitive tests, leading to an incorrect diagnosis of cognitive impairment. Elderly patients often minimize hearing deficits, and many believe—incorrectly—that hearing loss due to aging is not amenable to treatment.¹⁵

Hearing loss in children may be congenital or acquired
In children, hearing loss can be divided into 2 main categories: congenital and acquired. Congenital etiologies include genetic diseases such as Down syndrome, Usher syndrome, and Alport syndrome—thought to account for 50% of pediatric hearing loss—and intrauterine infections. Causes of acquired hearing loss include recurrent otitis media—most common among infants and young children—and environmental noise (TABLE 2).^16-18

TABLE 2
Common causes of hearing loss^16-18

Adolescents and young adults often expose themselves to loud noises from personal electronic devices, and the use of hearing protection in this population is low.¹⁹ The results of one small study suggest that almost a third of adolescents regularly use the highest volume on their iPods or MP3 players, which can cause hearing damage over time.²⁰ Noise levels at which hearing loss occurs can be found at http://www.cdc.gov/niosh/topics/noise/noisemeter.html.²¹ It is important for adolescents as well as adults to be aware of the risk of hearing loss from repeated exposure to loud noise, but evidence suggests that education about this danger is more likely to lead to behavior change in working-age adults than in teens.²²

Screening parameters for infants and children
The US Preventive Services Task Force (USPSTF) recommends universal newborn hearing screening,²³ but this does not always happen. That’s why it’s important to ask all new parents whether their baby underwent hearing screening shortly after birth. If the answer is No (or they’re not sure), you may want to order it at this time.

Infants at increased risk for hearing loss—those who spent >2 days on a neonatal intensive care unit; have a congenital syndrome, family history of hereditary childhood sensorineural hearing loss, or craniofacial abnormalities; or were exposed to certain intrauterine infections—should be screened again at 24 to 30 months of age.²³ Those with positive results on a newborn hearing screen require repeat screening within 3 months.^24,25 If the repeat screen is also positive, a full audiologic evaluation is necessary.

Testing newborns. The most common methods of screening newborns for hearing loss are otoacoustic emissions (OAE) and automated auditory brainstem response (AABR). The average age of detection of congenital hearing loss prior to the availability of these tests was 2 to 3 years. Earlier detection is associated with better developmental outcomes.²⁶

OAE assesses cochlear integrity and measures outer hair cell function. AABR assesses auditory function from the eighth nerve through the auditory brainstem.

Testing toddlers and older children. Any child exhibiting signs of possible hearing loss, such as learning disabilities or speech delay, should be referred for audiometric testing, as should those who have had recurrent otitis media. Tympanograms can be used to diagnose conductive hearing loss, which often results from middle ear effusion. A parent’s expression of concern about a child’s hearing also warrants a referral, as parents can be 12 months ahead of physicians in identifying hearing loss.²⁷

“Play audiometry,” a behavioral test of auditory thresholds in response to speech and frequency-specific stimuli, is commonly used for children between the ages of 2 and 4 years. In this test, the child is instructed to place a block into a box whenever he or she hears a sound.

Children >4 years are typically tested with conventional audiometry, and instructed to raise their hand in response to speech and frequency-specific stimuli. This technique may also be used in adolescents.

Consults, resources required after diagnosis
All children diagnosed with hearing loss after an audiologic evaluation require consultation with specialists in otolaryngology, ophthalmology, and genetics. They should also be offered special educational services, beginning with early intervention and continuing with appropriate monitoring and support throughout the school years. In addition, their parents should be given contact information for hearing loss resources ( TABLE 3). Adolescents and young adults with any degree of hearing loss should also receive counseling about noise exposure.^28,29 We’ll review treatment options for hearing-impaired patients of all ages in a bit.

TABLE 3
Hearing loss resources for parents and patients

In adults, most hearing loss is age-related

Advancing age is the single most important (and nonmodifiable) risk factor for hearing loss among older adults. Physiologic changes, including cerumen buildup, tympanic membrane thickening, degeneration of middle ear auditory structures, and decreased central auditory processing all may contribute to presbycusis—age-related sensorineural hearing impairment.³⁰ High-frequency hearing loss is characteristic of presbycusis, and since consonants are high-frequency sounds, patients with this type of hearing loss often complain that they’re unable to understand speech.

Conductive hearing loss may be caused by cerumen buildup, foreign bodies, otosclerosis, cholesteatoma, or tympanic membrane perforation—all of which may be treatable. Potentially modifiable risk factors for hearing loss include smoking, diabetes, exposure to ototoxic medications, and occupational noise, as well as cerumen buildup.¹⁷

Maintain an index of suspicion
The most important factor in diagnosing hearing loss in older adults is simply remembering to screen. Elderly patients should be evaluated for hearing loss during their initial visit, and once a year thereafter.³¹ But all too often, that doesn’t happen. One study found that only 18% of patients between the ages of 65 and 74 years and 22% of patients ages 75 and older had undergone screening for hearing loss during their most recent physical examination.⁴

But what impact does screening actually have on patients’ quality of life? The evidence is mixed. One study in which asymptomatic individuals >50 years (mean age=61 years) underwent hearing screening found that, although screening increased hearing aid use at one year, it did not lead to an improvement in quality of life.^32,33 Another study with a significantly older population (mean age=72 years) found that screening did positively affect quality of life.¹³

Screening tools—and a question
Several testing techniques have about the same accuracy rates in diagnosing hearing loss in adult patients. These include:

• the whisper test (which should be administered from a distance of 2 feet)
• handheld audiometry testing (with frequencies of 500-4000 Hertz [Hz] at 40 dB, these devices are 94% sensitive and 72% specific for detecting hearing loss)¹⁵
• the 10-question Hearing Handicap Inventory for the Elderly-Screening version (HHIE-S), available at http://www.asha.org/docs/html/GL1997-00199-T19.html.

The HHIE-S takes <5 minutes to administer and can be used in conjunction with audiometry testing for increased accuracy in diagnosing hearing loss. An alternative is to ask just one question:

“Do you have a hearing problem now?” This question alone appears to be as effective as the HHIE-S in identifying older patients with hearing loss,³⁴ and is likely to be the most efficient screening method for busy primary care physicians.

Consultation is needed when hearing loss is suspected
An audiology consultation should be considered when a patient’s caregiver or family member—or the patient himself—expresses concern about hearing loss. A positive result on a hearing screen, as well as clinical expression of hearing loss, also indicates a need for referral.

An otolaryngology consult is required for complicated presentations, including persistent cerumen impaction, foreign bodies, otosclerosis, cholesteatoma, tympanic membrane perforation, and asymmetrical hearing loss, which could be caused by a tumor.

Treating hearing loss in patients of all ages

Cerumen can contribute to hearing loss in children and adults alike, and can often be treated in an outpatient setting. A recent Cochrane review of various means of cerumen removal found the strongest evidence for irrigation, followed by cerumenolytic treatment and manual removal.³⁵ The use of cerumenolytic agents appears to be more effective than no treatment, but there is no evidence favoring one product over another. (To learn more about self-removal, see “Wax removal: Help patients help themselves” (J Fam Pract. 2011;60:671-673).

Hearing aids are first-line treatment
Hearing aids should be considered as first-line treatment for children and adults with hearing loss in which easily treatable etiologies such as cerumen impaction have been excluded. They have been shown to improve the ability to understand speech and environmental sounds, as well as the quality of life, for patients of all ages.³⁶ Even infants can be fitted with hearing aids, which are appropriate for mild, moderate, and severe hearing loss.³⁷ But only about 20% of older patients who could benefit from hearing aids ever buy them—and an estimated 25% to 40% of those who have hearing aids use them only occasionally, stop using them completely, or continue to wear them despite receiving limited benefit.⁴

Cost is one potential barrier to greater use. Hearing aids range in price from about $1000 to $4000 or more for a pair. And, while insurance coverage varies from one health plan to another, hearing aids are not covered by Medicare.

What’s more, elderly patients sometimes have difficulty adjusting to hearing aids (see “Hearing aids don’t work if patients don’t wear them”).³⁸ Cognitive deficits, difficulty manipulating hearing aids, and embarrassment often contribute to suboptimal use of hearing aids.

Is a cochlear implant a viable alternative?
For older adults for whom the cost of hearing aids is prohibitive, a less expensive pocket amplifier with headphones may be a good choice. Middle ear implants, which mechanically vibrate the middle ear structures to produce amplification, are another option for patients with presbycusis.

National Institute for Health and Clinical Excellence (NICE) guidelines recommend consideration of cochlear implantation for children and adults after multidisciplinary team assessment.³⁷ Cochlear implants are indicated for severe to profound hearing loss, and have been shown to improve speech recognition abilities equally in adolescents and older adults.³⁹ And, unlike hearing aids, cochlear implants are covered by most health insurance plans.

CORRESPONDENCE Paul George, MD, Alpert Medical School of Brown University, 222 Richmond Street, Providence, RI 02912; [email protected]

Hearing impairment is a widespread problem, affecting approximately 36 million US adults¹ and an increasing number of children.² Yet it often goes undetected. The consequences of untreated or undertreated hearing loss can be severe.

Adverse effects are often age-dependent: In children, hearing loss is associated with a broad range of complications, including delays in language development, decreased reading comprehension, and poor academic performance, as well as social and emotional problems.^2,3 In adults—particularly the elderly—hearing impairment can lead to social isolation, depression, and a diminished quality of life.^4,5

Early detection and treatment can do much to alleviate these adverse effects. But many physicians received little training in the identification and treatment of hearing loss in medical school. What’s more, people with significant hearing loss tend to have fewer interactions with health care providers than their counterparts with no hearing impairment⁶—a finding that some attribute to fear, mistrust, and frustration.⁷

Physician awareness of the problems facing people with hearing loss, the importance of screening, and the need to improve communication with hearing-impaired patients (TABLE 1)⁸ can help change that. The strategies presented here were developed with this in mind.

TABLE 1
How to better communicate with patients who have hearing loss⁸

The scope of hearing loss across the lifespan

Hearing loss affects 1 to 3 in every 1000 newborns.⁹ The prevalence increases to 2% among 5-year-olds, and to 10% to 20% by age 18.^10,11 The risk accelerates in “early older life” (defined as ages 50-69 years), with men affected more often than women.¹² Hearing loss is the fourth most common chronic condition among older adults, and it is estimated that ≥70% of nursing home residents have some degree of impairment.¹³

Hearing loss can be categorized as mild (a loss of 20-40 decibels [dB]), moderate (41-55 dB loss), moderate to severe (56-70 dB loss), severe (71-90 dB loss), or profound (>91 dB loss), but any degree of hearing loss should be considered noteworthy.

In children, the impact of mild impairment is often minimized by both professionals and parents, especially among those whose speech developed normally. Unfortunately, the failure to respond appropriately in such cases often increases the adverse effects of the hearing loss.¹⁴

In adults, even mild to moderate impairment can lead to significant functional impairment and, therefore, a decreased quality of life.⁵ And in elderly patients, any undetected hearing loss can adversely affect their performance on cognitive tests, leading to an incorrect diagnosis of cognitive impairment. Elderly patients often minimize hearing deficits, and many believe—incorrectly—that hearing loss due to aging is not amenable to treatment.¹⁵

Hearing loss in children may be congenital or acquired
In children, hearing loss can be divided into 2 main categories: congenital and acquired. Congenital etiologies include genetic diseases such as Down syndrome, Usher syndrome, and Alport syndrome—thought to account for 50% of pediatric hearing loss—and intrauterine infections. Causes of acquired hearing loss include recurrent otitis media—most common among infants and young children—and environmental noise (TABLE 2).^16-18

TABLE 2
Common causes of hearing loss^16-18

Adolescents and young adults often expose themselves to loud noises from personal electronic devices, and the use of hearing protection in this population is low.¹⁹ The results of one small study suggest that almost a third of adolescents regularly use the highest volume on their iPods or MP3 players, which can cause hearing damage over time.²⁰ Noise levels at which hearing loss occurs can be found at http://www.cdc.gov/niosh/topics/noise/noisemeter.html.²¹ It is important for adolescents as well as adults to be aware of the risk of hearing loss from repeated exposure to loud noise, but evidence suggests that education about this danger is more likely to lead to behavior change in working-age adults than in teens.²²

Screening parameters for infants and children
The US Preventive Services Task Force (USPSTF) recommends universal newborn hearing screening,²³ but this does not always happen. That’s why it’s important to ask all new parents whether their baby underwent hearing screening shortly after birth. If the answer is No (or they’re not sure), you may want to order it at this time.

Infants at increased risk for hearing loss—those who spent >2 days on a neonatal intensive care unit; have a congenital syndrome, family history of hereditary childhood sensorineural hearing loss, or craniofacial abnormalities; or were exposed to certain intrauterine infections—should be screened again at 24 to 30 months of age.²³ Those with positive results on a newborn hearing screen require repeat screening within 3 months.^24,25 If the repeat screen is also positive, a full audiologic evaluation is necessary.

Testing newborns. The most common methods of screening newborns for hearing loss are otoacoustic emissions (OAE) and automated auditory brainstem response (AABR). The average age of detection of congenital hearing loss prior to the availability of these tests was 2 to 3 years. Earlier detection is associated with better developmental outcomes.²⁶

OAE assesses cochlear integrity and measures outer hair cell function. AABR assesses auditory function from the eighth nerve through the auditory brainstem.

Testing toddlers and older children. Any child exhibiting signs of possible hearing loss, such as learning disabilities or speech delay, should be referred for audiometric testing, as should those who have had recurrent otitis media. Tympanograms can be used to diagnose conductive hearing loss, which often results from middle ear effusion. A parent’s expression of concern about a child’s hearing also warrants a referral, as parents can be 12 months ahead of physicians in identifying hearing loss.²⁷

“Play audiometry,” a behavioral test of auditory thresholds in response to speech and frequency-specific stimuli, is commonly used for children between the ages of 2 and 4 years. In this test, the child is instructed to place a block into a box whenever he or she hears a sound.

Children >4 years are typically tested with conventional audiometry, and instructed to raise their hand in response to speech and frequency-specific stimuli. This technique may also be used in adolescents.

Consults, resources required after diagnosis
All children diagnosed with hearing loss after an audiologic evaluation require consultation with specialists in otolaryngology, ophthalmology, and genetics. They should also be offered special educational services, beginning with early intervention and continuing with appropriate monitoring and support throughout the school years. In addition, their parents should be given contact information for hearing loss resources ( TABLE 3). Adolescents and young adults with any degree of hearing loss should also receive counseling about noise exposure.^28,29 We’ll review treatment options for hearing-impaired patients of all ages in a bit.

TABLE 3
Hearing loss resources for parents and patients

In adults, most hearing loss is age-related

Advancing age is the single most important (and nonmodifiable) risk factor for hearing loss among older adults. Physiologic changes, including cerumen buildup, tympanic membrane thickening, degeneration of middle ear auditory structures, and decreased central auditory processing all may contribute to presbycusis—age-related sensorineural hearing impairment.³⁰ High-frequency hearing loss is characteristic of presbycusis, and since consonants are high-frequency sounds, patients with this type of hearing loss often complain that they’re unable to understand speech.

Conductive hearing loss may be caused by cerumen buildup, foreign bodies, otosclerosis, cholesteatoma, or tympanic membrane perforation—all of which may be treatable. Potentially modifiable risk factors for hearing loss include smoking, diabetes, exposure to ototoxic medications, and occupational noise, as well as cerumen buildup.¹⁷

Maintain an index of suspicion
The most important factor in diagnosing hearing loss in older adults is simply remembering to screen. Elderly patients should be evaluated for hearing loss during their initial visit, and once a year thereafter.³¹ But all too often, that doesn’t happen. One study found that only 18% of patients between the ages of 65 and 74 years and 22% of patients ages 75 and older had undergone screening for hearing loss during their most recent physical examination.⁴

But what impact does screening actually have on patients’ quality of life? The evidence is mixed. One study in which asymptomatic individuals >50 years (mean age=61 years) underwent hearing screening found that, although screening increased hearing aid use at one year, it did not lead to an improvement in quality of life.^32,33 Another study with a significantly older population (mean age=72 years) found that screening did positively affect quality of life.¹³

Screening tools—and a question
Several testing techniques have about the same accuracy rates in diagnosing hearing loss in adult patients. These include:

• the whisper test (which should be administered from a distance of 2 feet)
• handheld audiometry testing (with frequencies of 500-4000 Hertz [Hz] at 40 dB, these devices are 94% sensitive and 72% specific for detecting hearing loss)¹⁵
• the 10-question Hearing Handicap Inventory for the Elderly-Screening version (HHIE-S), available at http://www.asha.org/docs/html/GL1997-00199-T19.html.

The HHIE-S takes <5 minutes to administer and can be used in conjunction with audiometry testing for increased accuracy in diagnosing hearing loss. An alternative is to ask just one question:

“Do you have a hearing problem now?” This question alone appears to be as effective as the HHIE-S in identifying older patients with hearing loss,³⁴ and is likely to be the most efficient screening method for busy primary care physicians.

Consultation is needed when hearing loss is suspected
An audiology consultation should be considered when a patient’s caregiver or family member—or the patient himself—expresses concern about hearing loss. A positive result on a hearing screen, as well as clinical expression of hearing loss, also indicates a need for referral.

An otolaryngology consult is required for complicated presentations, including persistent cerumen impaction, foreign bodies, otosclerosis, cholesteatoma, tympanic membrane perforation, and asymmetrical hearing loss, which could be caused by a tumor.

Treating hearing loss in patients of all ages

Cerumen can contribute to hearing loss in children and adults alike, and can often be treated in an outpatient setting. A recent Cochrane review of various means of cerumen removal found the strongest evidence for irrigation, followed by cerumenolytic treatment and manual removal.³⁵ The use of cerumenolytic agents appears to be more effective than no treatment, but there is no evidence favoring one product over another. (To learn more about self-removal, see “Wax removal: Help patients help themselves” (J Fam Pract. 2011;60:671-673).

Hearing aids are first-line treatment
Hearing aids should be considered as first-line treatment for children and adults with hearing loss in which easily treatable etiologies such as cerumen impaction have been excluded. They have been shown to improve the ability to understand speech and environmental sounds, as well as the quality of life, for patients of all ages.³⁶ Even infants can be fitted with hearing aids, which are appropriate for mild, moderate, and severe hearing loss.³⁷ But only about 20% of older patients who could benefit from hearing aids ever buy them—and an estimated 25% to 40% of those who have hearing aids use them only occasionally, stop using them completely, or continue to wear them despite receiving limited benefit.⁴

Cost is one potential barrier to greater use. Hearing aids range in price from about $1000 to $4000 or more for a pair. And, while insurance coverage varies from one health plan to another, hearing aids are not covered by Medicare.

What’s more, elderly patients sometimes have difficulty adjusting to hearing aids (see “Hearing aids don’t work if patients don’t wear them”).³⁸ Cognitive deficits, difficulty manipulating hearing aids, and embarrassment often contribute to suboptimal use of hearing aids.

Is a cochlear implant a viable alternative?
For older adults for whom the cost of hearing aids is prohibitive, a less expensive pocket amplifier with headphones may be a good choice. Middle ear implants, which mechanically vibrate the middle ear structures to produce amplification, are another option for patients with presbycusis.

National Institute for Health and Clinical Excellence (NICE) guidelines recommend consideration of cochlear implantation for children and adults after multidisciplinary team assessment.³⁷ Cochlear implants are indicated for severe to profound hearing loss, and have been shown to improve speech recognition abilities equally in adolescents and older adults.³⁹ And, unlike hearing aids, cochlear implants are covered by most health insurance plans.

CORRESPONDENCE Paul George, MD, Alpert Medical School of Brown University, 222 Richmond Street, Providence, RI 02912; [email protected]

Hearing impairment is a widespread problem, affecting approximately 36 million US adults¹ and an increasing number of children.² Yet it often goes undetected. The consequences of untreated or undertreated hearing loss can be severe.

Adverse effects are often age-dependent: In children, hearing loss is associated with a broad range of complications, including delays in language development, decreased reading comprehension, and poor academic performance, as well as social and emotional problems.^2,3 In adults—particularly the elderly—hearing impairment can lead to social isolation, depression, and a diminished quality of life.^4,5

Early detection and treatment can do much to alleviate these adverse effects. But many physicians received little training in the identification and treatment of hearing loss in medical school. What’s more, people with significant hearing loss tend to have fewer interactions with health care providers than their counterparts with no hearing impairment⁶—a finding that some attribute to fear, mistrust, and frustration.⁷

Physician awareness of the problems facing people with hearing loss, the importance of screening, and the need to improve communication with hearing-impaired patients (TABLE 1)⁸ can help change that. The strategies presented here were developed with this in mind.

TABLE 1
How to better communicate with patients who have hearing loss⁸

The scope of hearing loss across the lifespan

Hearing loss affects 1 to 3 in every 1000 newborns.⁹ The prevalence increases to 2% among 5-year-olds, and to 10% to 20% by age 18.^10,11 The risk accelerates in “early older life” (defined as ages 50-69 years), with men affected more often than women.¹² Hearing loss is the fourth most common chronic condition among older adults, and it is estimated that ≥70% of nursing home residents have some degree of impairment.¹³

Hearing loss can be categorized as mild (a loss of 20-40 decibels [dB]), moderate (41-55 dB loss), moderate to severe (56-70 dB loss), severe (71-90 dB loss), or profound (>91 dB loss), but any degree of hearing loss should be considered noteworthy.

In children, the impact of mild impairment is often minimized by both professionals and parents, especially among those whose speech developed normally. Unfortunately, the failure to respond appropriately in such cases often increases the adverse effects of the hearing loss.¹⁴

In adults, even mild to moderate impairment can lead to significant functional impairment and, therefore, a decreased quality of life.⁵ And in elderly patients, any undetected hearing loss can adversely affect their performance on cognitive tests, leading to an incorrect diagnosis of cognitive impairment. Elderly patients often minimize hearing deficits, and many believe—incorrectly—that hearing loss due to aging is not amenable to treatment.¹⁵

Hearing loss in children may be congenital or acquired
In children, hearing loss can be divided into 2 main categories: congenital and acquired. Congenital etiologies include genetic diseases such as Down syndrome, Usher syndrome, and Alport syndrome—thought to account for 50% of pediatric hearing loss—and intrauterine infections. Causes of acquired hearing loss include recurrent otitis media—most common among infants and young children—and environmental noise (TABLE 2).^16-18

TABLE 2
Common causes of hearing loss^16-18

Adolescents and young adults often expose themselves to loud noises from personal electronic devices, and the use of hearing protection in this population is low.¹⁹ The results of one small study suggest that almost a third of adolescents regularly use the highest volume on their iPods or MP3 players, which can cause hearing damage over time.²⁰ Noise levels at which hearing loss occurs can be found at http://www.cdc.gov/niosh/topics/noise/noisemeter.html.²¹ It is important for adolescents as well as adults to be aware of the risk of hearing loss from repeated exposure to loud noise, but evidence suggests that education about this danger is more likely to lead to behavior change in working-age adults than in teens.²²

Screening parameters for infants and children
The US Preventive Services Task Force (USPSTF) recommends universal newborn hearing screening,²³ but this does not always happen. That’s why it’s important to ask all new parents whether their baby underwent hearing screening shortly after birth. If the answer is No (or they’re not sure), you may want to order it at this time.

Infants at increased risk for hearing loss—those who spent >2 days on a neonatal intensive care unit; have a congenital syndrome, family history of hereditary childhood sensorineural hearing loss, or craniofacial abnormalities; or were exposed to certain intrauterine infections—should be screened again at 24 to 30 months of age.²³ Those with positive results on a newborn hearing screen require repeat screening within 3 months.^24,25 If the repeat screen is also positive, a full audiologic evaluation is necessary.

Testing newborns. The most common methods of screening newborns for hearing loss are otoacoustic emissions (OAE) and automated auditory brainstem response (AABR). The average age of detection of congenital hearing loss prior to the availability of these tests was 2 to 3 years. Earlier detection is associated with better developmental outcomes.²⁶

OAE assesses cochlear integrity and measures outer hair cell function. AABR assesses auditory function from the eighth nerve through the auditory brainstem.

Testing toddlers and older children. Any child exhibiting signs of possible hearing loss, such as learning disabilities or speech delay, should be referred for audiometric testing, as should those who have had recurrent otitis media. Tympanograms can be used to diagnose conductive hearing loss, which often results from middle ear effusion. A parent’s expression of concern about a child’s hearing also warrants a referral, as parents can be 12 months ahead of physicians in identifying hearing loss.²⁷

“Play audiometry,” a behavioral test of auditory thresholds in response to speech and frequency-specific stimuli, is commonly used for children between the ages of 2 and 4 years. In this test, the child is instructed to place a block into a box whenever he or she hears a sound.

Children >4 years are typically tested with conventional audiometry, and instructed to raise their hand in response to speech and frequency-specific stimuli. This technique may also be used in adolescents.

Consults, resources required after diagnosis
All children diagnosed with hearing loss after an audiologic evaluation require consultation with specialists in otolaryngology, ophthalmology, and genetics. They should also be offered special educational services, beginning with early intervention and continuing with appropriate monitoring and support throughout the school years. In addition, their parents should be given contact information for hearing loss resources ( TABLE 3). Adolescents and young adults with any degree of hearing loss should also receive counseling about noise exposure.^28,29 We’ll review treatment options for hearing-impaired patients of all ages in a bit.

TABLE 3
Hearing loss resources for parents and patients

In adults, most hearing loss is age-related

Advancing age is the single most important (and nonmodifiable) risk factor for hearing loss among older adults. Physiologic changes, including cerumen buildup, tympanic membrane thickening, degeneration of middle ear auditory structures, and decreased central auditory processing all may contribute to presbycusis—age-related sensorineural hearing impairment.³⁰ High-frequency hearing loss is characteristic of presbycusis, and since consonants are high-frequency sounds, patients with this type of hearing loss often complain that they’re unable to understand speech.

Conductive hearing loss may be caused by cerumen buildup, foreign bodies, otosclerosis, cholesteatoma, or tympanic membrane perforation—all of which may be treatable. Potentially modifiable risk factors for hearing loss include smoking, diabetes, exposure to ototoxic medications, and occupational noise, as well as cerumen buildup.¹⁷

Maintain an index of suspicion
The most important factor in diagnosing hearing loss in older adults is simply remembering to screen. Elderly patients should be evaluated for hearing loss during their initial visit, and once a year thereafter.³¹ But all too often, that doesn’t happen. One study found that only 18% of patients between the ages of 65 and 74 years and 22% of patients ages 75 and older had undergone screening for hearing loss during their most recent physical examination.⁴

But what impact does screening actually have on patients’ quality of life? The evidence is mixed. One study in which asymptomatic individuals >50 years (mean age=61 years) underwent hearing screening found that, although screening increased hearing aid use at one year, it did not lead to an improvement in quality of life.^32,33 Another study with a significantly older population (mean age=72 years) found that screening did positively affect quality of life.¹³

Screening tools—and a question
Several testing techniques have about the same accuracy rates in diagnosing hearing loss in adult patients. These include:

• the whisper test (which should be administered from a distance of 2 feet)
• handheld audiometry testing (with frequencies of 500-4000 Hertz [Hz] at 40 dB, these devices are 94% sensitive and 72% specific for detecting hearing loss)¹⁵
• the 10-question Hearing Handicap Inventory for the Elderly-Screening version (HHIE-S), available at http://www.asha.org/docs/html/GL1997-00199-T19.html.

The HHIE-S takes <5 minutes to administer and can be used in conjunction with audiometry testing for increased accuracy in diagnosing hearing loss. An alternative is to ask just one question:

“Do you have a hearing problem now?” This question alone appears to be as effective as the HHIE-S in identifying older patients with hearing loss,³⁴ and is likely to be the most efficient screening method for busy primary care physicians.

Consultation is needed when hearing loss is suspected
An audiology consultation should be considered when a patient’s caregiver or family member—or the patient himself—expresses concern about hearing loss. A positive result on a hearing screen, as well as clinical expression of hearing loss, also indicates a need for referral.

An otolaryngology consult is required for complicated presentations, including persistent cerumen impaction, foreign bodies, otosclerosis, cholesteatoma, tympanic membrane perforation, and asymmetrical hearing loss, which could be caused by a tumor.

Treating hearing loss in patients of all ages

Cerumen can contribute to hearing loss in children and adults alike, and can often be treated in an outpatient setting. A recent Cochrane review of various means of cerumen removal found the strongest evidence for irrigation, followed by cerumenolytic treatment and manual removal.³⁵ The use of cerumenolytic agents appears to be more effective than no treatment, but there is no evidence favoring one product over another. (To learn more about self-removal, see “Wax removal: Help patients help themselves” (J Fam Pract. 2011;60:671-673).

Hearing aids are first-line treatment
Hearing aids should be considered as first-line treatment for children and adults with hearing loss in which easily treatable etiologies such as cerumen impaction have been excluded. They have been shown to improve the ability to understand speech and environmental sounds, as well as the quality of life, for patients of all ages.³⁶ Even infants can be fitted with hearing aids, which are appropriate for mild, moderate, and severe hearing loss.³⁷ But only about 20% of older patients who could benefit from hearing aids ever buy them—and an estimated 25% to 40% of those who have hearing aids use them only occasionally, stop using them completely, or continue to wear them despite receiving limited benefit.⁴

Cost is one potential barrier to greater use. Hearing aids range in price from about $1000 to $4000 or more for a pair. And, while insurance coverage varies from one health plan to another, hearing aids are not covered by Medicare.

What’s more, elderly patients sometimes have difficulty adjusting to hearing aids (see “Hearing aids don’t work if patients don’t wear them”).³⁸ Cognitive deficits, difficulty manipulating hearing aids, and embarrassment often contribute to suboptimal use of hearing aids.

Is a cochlear implant a viable alternative?
For older adults for whom the cost of hearing aids is prohibitive, a less expensive pocket amplifier with headphones may be a good choice. Middle ear implants, which mechanically vibrate the middle ear structures to produce amplification, are another option for patients with presbycusis.

National Institute for Health and Clinical Excellence (NICE) guidelines recommend consideration of cochlear implantation for children and adults after multidisciplinary team assessment.³⁷ Cochlear implants are indicated for severe to profound hearing loss, and have been shown to improve speech recognition abilities equally in adolescents and older adults.³⁹ And, unlike hearing aids, cochlear implants are covered by most health insurance plans.

CORRESPONDENCE Paul George, MD, Alpert Medical School of Brown University, 222 Richmond Street, Providence, RI 02912; [email protected]

I found Dr. Scott Freeman’s article on suicide prevention (“Suicide assessment: Targeting acute risk factors,” Current Psychiatry, January 2012, p. 52-57) to be bold and courageous. Two of the 6 suicide risk factors he described are related to anxiety symptomatology: panic attacks and psychic anxiety. In the case study, Mr. L was prescribed clonazepam, a benzodiazepine, despite his history of comorbid alcohol abuse. Often, patients with substance abuse have related anxiety disorders—including posttraumatic stress disorder—and management with selective serotonin reuptake inhibitors (SSRIs) is not sufficient.

Because clinicians are hesitant to prescribe benzodiazepines to patients with a substance abuse history, patients often are forced to purchase these medications on the street or feel compelled to relapse to substance abuse in a frantic, albeit misguided, effort to contain their crippling symptoms. Even in inpatient drug rehabilitation settings, benzodiazepines often are not an option because they are not allowed. The “safer” SSRIs may be more dangerous when given to substance abusers in whom a comorbid mood disorder often is missed.

Current Psychiatry has never been shy in addressing the truth or uncomfortable issues in our complex field. Do we have the courage to open this up for dialogue and conversation?

Robert Barris, MD
Attending Psychiatrist
Nassau University Medical Center
East Meadow, NY

I found Dr. Scott Freeman’s article on suicide prevention (“Suicide assessment: Targeting acute risk factors,” Current Psychiatry, January 2012, p. 52-57) to be bold and courageous. Two of the 6 suicide risk factors he described are related to anxiety symptomatology: panic attacks and psychic anxiety. In the case study, Mr. L was prescribed clonazepam, a benzodiazepine, despite his history of comorbid alcohol abuse. Often, patients with substance abuse have related anxiety disorders—including posttraumatic stress disorder—and management with selective serotonin reuptake inhibitors (SSRIs) is not sufficient.

Because clinicians are hesitant to prescribe benzodiazepines to patients with a substance abuse history, patients often are forced to purchase these medications on the street or feel compelled to relapse to substance abuse in a frantic, albeit misguided, effort to contain their crippling symptoms. Even in inpatient drug rehabilitation settings, benzodiazepines often are not an option because they are not allowed. The “safer” SSRIs may be more dangerous when given to substance abusers in whom a comorbid mood disorder often is missed.

Current Psychiatry has never been shy in addressing the truth or uncomfortable issues in our complex field. Do we have the courage to open this up for dialogue and conversation?

Robert Barris, MD
Attending Psychiatrist
Nassau University Medical Center
East Meadow, NY

I found Dr. Scott Freeman’s article on suicide prevention (“Suicide assessment: Targeting acute risk factors,” Current Psychiatry, January 2012, p. 52-57) to be bold and courageous. Two of the 6 suicide risk factors he described are related to anxiety symptomatology: panic attacks and psychic anxiety. In the case study, Mr. L was prescribed clonazepam, a benzodiazepine, despite his history of comorbid alcohol abuse. Often, patients with substance abuse have related anxiety disorders—including posttraumatic stress disorder—and management with selective serotonin reuptake inhibitors (SSRIs) is not sufficient.

Because clinicians are hesitant to prescribe benzodiazepines to patients with a substance abuse history, patients often are forced to purchase these medications on the street or feel compelled to relapse to substance abuse in a frantic, albeit misguided, effort to contain their crippling symptoms. Even in inpatient drug rehabilitation settings, benzodiazepines often are not an option because they are not allowed. The “safer” SSRIs may be more dangerous when given to substance abusers in whom a comorbid mood disorder often is missed.

Current Psychiatry has never been shy in addressing the truth or uncomfortable issues in our complex field. Do we have the courage to open this up for dialogue and conversation?

Robert Barris, MD
Attending Psychiatrist
Nassau University Medical Center
East Meadow, NY

I found Dr. Scott Freeman’s article on suicide prevention (“Suicide assessment: Targeting acute risk factors,” Current Psychiatry, January 2012, p. 52-57) to be bold and courageous. Two of the 6 suicide risk factors he described are related to anxiety symptomatology: panic attacks and psychic anxiety. In the case study, Mr. L was prescribed clonazepam, a benzodiazepine, despite his history of comorbid alcohol abuse. Often, patients with substance abuse have related anxiety disorders—including posttraumatic stress disorder—and management with selective serotonin reuptake inhibitors (SSRIs) is not sufficient.

Because clinicians are hesitant to prescribe benzodiazepines to patients with a substance abuse history, patients often are forced to purchase these medications on the street or feel compelled to relapse to substance abuse in a frantic, albeit misguided, effort to contain their crippling symptoms. Even in inpatient drug rehabilitation settings, benzodiazepines often are not an option because they are not allowed. The “safer” SSRIs may be more dangerous when given to substance abusers in whom a comorbid mood disorder often is missed.

Current Psychiatry has never been shy in addressing the truth or uncomfortable issues in our complex field. Do we have the courage to open this up for dialogue and conversation?

Robert Barris, MD
Attending Psychiatrist
Nassau University Medical Center
East Meadow, NY

I found Dr. Scott Freeman’s article on suicide prevention (“Suicide assessment: Targeting acute risk factors,” Current Psychiatry, January 2012, p. 52-57) to be bold and courageous. Two of the 6 suicide risk factors he described are related to anxiety symptomatology: panic attacks and psychic anxiety. In the case study, Mr. L was prescribed clonazepam, a benzodiazepine, despite his history of comorbid alcohol abuse. Often, patients with substance abuse have related anxiety disorders—including posttraumatic stress disorder—and management with selective serotonin reuptake inhibitors (SSRIs) is not sufficient.

Because clinicians are hesitant to prescribe benzodiazepines to patients with a substance abuse history, patients often are forced to purchase these medications on the street or feel compelled to relapse to substance abuse in a frantic, albeit misguided, effort to contain their crippling symptoms. Even in inpatient drug rehabilitation settings, benzodiazepines often are not an option because they are not allowed. The “safer” SSRIs may be more dangerous when given to substance abusers in whom a comorbid mood disorder often is missed.

Current Psychiatry has never been shy in addressing the truth or uncomfortable issues in our complex field. Do we have the courage to open this up for dialogue and conversation?

Robert Barris, MD
Attending Psychiatrist
Nassau University Medical Center
East Meadow, NY

I found Dr. Scott Freeman’s article on suicide prevention (“Suicide assessment: Targeting acute risk factors,” Current Psychiatry, January 2012, p. 52-57) to be bold and courageous. Two of the 6 suicide risk factors he described are related to anxiety symptomatology: panic attacks and psychic anxiety. In the case study, Mr. L was prescribed clonazepam, a benzodiazepine, despite his history of comorbid alcohol abuse. Often, patients with substance abuse have related anxiety disorders—including posttraumatic stress disorder—and management with selective serotonin reuptake inhibitors (SSRIs) is not sufficient.

Because clinicians are hesitant to prescribe benzodiazepines to patients with a substance abuse history, patients often are forced to purchase these medications on the street or feel compelled to relapse to substance abuse in a frantic, albeit misguided, effort to contain their crippling symptoms. Even in inpatient drug rehabilitation settings, benzodiazepines often are not an option because they are not allowed. The “safer” SSRIs may be more dangerous when given to substance abusers in whom a comorbid mood disorder often is missed.

Current Psychiatry has never been shy in addressing the truth or uncomfortable issues in our complex field. Do we have the courage to open this up for dialogue and conversation?

Robert Barris, MD
Attending Psychiatrist
Nassau University Medical Center
East Meadow, NY

Binge eating is consumption of an unusually large amount of food coupled with a feeling of loss of control over eating. Binge eating disorder (BED) is characterized by recurrent episodes of binge eating without inappropriate compensatory behaviors (eg, self-induced vomiting, misuse of laxatives, diuretics, or other agents, excessive exercise).¹ It is the most common eating disorder in the United States, with a lifetime prevalence of approximately 3.5% in women and 2% in men.² The diagnosis falls within the DSM-IV-TR category of eating disorders not otherwise specified,¹ but clinicians often view it as a distinct clinical phenomenon. In DSM-IV-TR, an individual would meet criteria for BED if he or she engages in regular binge eating behavior in the absence of recurrent compensatory behaviors ≥2 days per week over 6 months.¹ Proposed changes for DSM-5 recognize a distinct BED diagnosis, reduce the frequency criterion to once per week and the duration criterion to the past 3 months, and shift the focus from binge days to binge episodes (Table 1).³

Table 1

Proposed DSM-5 criteria for binge eating disorder

BED can occur in individuals of all body mass indices (BMI), but is common among individuals who are overweight or obese as well as those with depression or type 2 diabetes; BED can complicate treatment of these conditions.^2,4,5 Primary treatment goals are:

• abstinence from binge eating
• improved psychological functioning
• appropriate weight regulation in overweight patients.

We report on 3 approaches to BED treatment: medication only, behavioral intervention only, and medication plus behavioral intervention. This article provides insights about emerging changes in diagnostic criteria for BED as well as evidence-informed treatment options and recommendations.

The evidence base

We conducted a review of 23 BED studies: 7 medication only, 5 medication plus behavioral, and 11 behavioral only. We focused on studies conducted since September 2005 that included binge frequency, weight, and depression as primary outcomes (see Berkman et al⁶ for a review of BED treatment studies before 2005). The studies included 2,527 participants (2,216 women and 311 men). Although the sex distribution of BED in the general population tends to slightly favor women,² the proportion of women presenting for treatment generally is considerably higher than that of men. In studies that reported on race and/or ethnicity, 1,639 participants were identified as white, 191 as African American, 25 as Hispanic, 2 as Asian, 1 as Native American, and 25 as “other.” Ages ranged from 18 to 77.

Several medications are effective

In placebo-controlled studies, a high-dose selective serotonin reuptake inhibitor (escitalopram⁷), 2 anticonvulsants (zonisamide⁸ and topiramate⁹), a selective norepinephrine reuptake inhibitor (atomoxetine¹⁰), and an appetite suppressant (sibutramine¹¹) were associated with significant decreases in binge eating frequency, weight, and BMI in overweight/obese patients diagnosed with BED (Table 2). In an open-label trial, memantine—a N-methyl-D-aspartate receptor antagonist often used to treat symptoms of Alzheimer’s disease—was associated with a significant reduction in binge eating but no change in weight.¹² Lamotrigine was not significantly different from placebo in reducing binge eating or weight, but showed promise in reducing metabolic parameters such as glucose and triglyceride levels commonly associated with obesity and type 2 diabetes.¹³ Because BED often is comorbid with obesity and type 2 diabetes, lamotrigine augmentation when treating obese individuals with BED warrants further investigation. As with any pharmacologic agent, carefully consider potential side effects and interactions with other drugs before prescribing medications for BED. Informing patients of potential side effects is crucial for patient safety and accuracy of the data collected in well-controlled treatment studies.

Table 2

Pharmacotherapy for binge eating disorder

CBT vs other behavioral approaches

Cognitive-behavioral therapy (CBT), which focuses on identifying and modifying unhealthy thoughts that maintain disordered eating behaviors, is the most widely studied behavioral intervention for BED. Other studied treatments include interpersonal psychotherapy (IPT), motivational interviewing (MI), and structured behavioral weight loss (BWL) (Table 3).^14-24 IPT is a psychodynamically based, time-limited treatment that focuses on the interpersonal context of the disorder and on building interpersonal skills. MI emphasizes exploring and resolving ambivalence about treatment, and works to facilitate change through motivational processes. BWL is centered on making dietary and physical activity changes to achieve weight loss. Behavioral treatments have been delivered in various formats, such as an individual or group setting, by electronic interface, and via self-help approaches. Most studies compared active treatment to a control group, but some compared active treatments head-to-head.

Table 3

CBT and other behavioral interventions for BED

Studies found that CBT and IPT are effective in reducing the frequency of binge eating, whether measured by the number of binge eating episodes or days a patient reports having engaged in binge eating.^14-23 However, some studies suggested that CBT can help a substantial number of patients achieve abstinence from binge eating.^16,20 Adding MI to a self-help approach may improve binge eating outcomes,²⁴ and binge eating can be successfully reduced using individual, group, and CD-ROM delivery formats.²¹ In direct comparisons, individual CBT outperformed group CBT in helping patients recover from BED (ie, no longer meeting diagnostic criteria),¹⁹ and CBT delivered via guided self-help outperformed BWL in helping patients achieve remission.¹⁸

Psychological features of BED typically include low levels of cognitive restraint and high levels of disinhibition, hunger, and shape and weight concerns. Improvements in these psychological measures were observed with CBT,^15-20,22 IPT,²² and MI.²⁴ In direct comparisons, self-help CBT demonstrated greater reductions in perceived hunger and disinhibition than self-help BWL,¹⁸ and individual CBT outperformed group CBT in reducing shape and weight concerns.¹⁹ Isolated studies reported improvements in depression after self-help CBT¹⁸ and MI,²⁴ and sustained improvements²² after group CBT (6 months) and group IPT (12 months). Additional research is needed to determine whether CBT crafted specifically for BED improves self-rated depression or if enhancements targeting depressive symptoms are required.

The impact of behavioral interventions on weight in overweight patients has been mixed. Although some CBT studies reported a substantial decrease in weight,^17,19 others suggested that weight loss among patients treated with CBT is not superior to those in a wait-list control group¹⁶ or is not significant over the course of treatment.^20,21 The impact of BWL on weight outcomes in BED also has been unimpressive: after 12 weeks, self-help BWL was no better than self-help CBT in reducing BMI¹⁸; after 16 weeks, BWL was better than CBT and IPT in achieving clinically significant (≥5%) weight loss, but this advantage was not sustained at 1- and 2-year follow-up.²³ It is difficult to determine why successfully treated BED patients fail to lose weight because one would expect decreases in binge eating to lead to weight loss. It is possible that calories previously consumed during binge eating episodes are distributed over non-binge meals or that patients label binges and non-binge meals differently as a result of treatment.

Combining treatments

BED patients often are treated with a combination of psychotherapy and pharmacotherapy (Table 4).^25-29 When added to CBT, topiramate was associated with improvements in weight and some psychological outcomes,^25,26 but fluoxetine was not.^27,28 Direct comparisons also showed that CBT, alone or combined with fluoxetine, was better than fluoxetine alone in reducing binge eating.²⁷ When combined with an individualized hypocaloric diet, the anti-obesity medication orlistat reduced weight in obese BED patients but had no appreciable effect on binge eating.²⁹ Collectively, the studies we reviewed suggested that combining medication and CBT may improve binge eating and weight loss outcomes; however, additional trials are necessary to determine more definitively which medications combined with CBT are best at producing sustained weight loss while reducing binge eating frequency.

Table 4

Combining medication with behavioral interventions for BED

Recommendations

Evidence suggests that pharmacotherapy and CBT—alone or in combination—are effective in reducing binge eating, and pharmacotherapy is effective in reducing weight in overweight individuals with BED. More research is needed for IPT and MI. It is unclear which medications provide the greatest benefit in terms of binge eating remission; however, pharmacotherapy has a clear advantage in facilitating short-term weight loss. Also, all BED patients should receive medical management to address possible complications such as hypertension or type 2 diabetes. In addition to reducing binge eating, CBT can improve related psychological comorbidities (eg, eating-related psychopathology and depression) and may have additional benefit when combined with pharmacotherapy.

In light of these findings, we recommend augmenting psychotherapeutic care with pharmacotherapy and medical management to address all relevant psychological and medical domains. Future investigations should address the benefits of coordinated psychological and medical care and evaluate how to maintain treatment gains.

Related Resources

• Binge Eating Disorder Association. www.bedaonline.com.
• Brownley KA, Berkman ND, Sedway JA, et al. Binge eating disorder treatment: a systematic review of randomized controlled trials. Int J Eat Disord. 2007;40(4):337-348.

Drug Brand Names

• Atomoxetine • Strattera
• Escitalopram • Lexapro
• Fluoxetine • Prozac
• Lamotrigine • Lamictal
• Memantine • Namenda
• Orlistat • Alli, Xenical
• Sertraline • Zoloft
• Sibutramine • Meridia
• Topiramate • Topamax, Topiragen
• Zonisamide • Zonegram

Disclosures

Dr. Peat receives a post-doctoral trainee grant from the National Institutes of Health.

Drs. Brownley, Berkman, and Bulik report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Binge eating is consumption of an unusually large amount of food coupled with a feeling of loss of control over eating. Binge eating disorder (BED) is characterized by recurrent episodes of binge eating without inappropriate compensatory behaviors (eg, self-induced vomiting, misuse of laxatives, diuretics, or other agents, excessive exercise).¹ It is the most common eating disorder in the United States, with a lifetime prevalence of approximately 3.5% in women and 2% in men.² The diagnosis falls within the DSM-IV-TR category of eating disorders not otherwise specified,¹ but clinicians often view it as a distinct clinical phenomenon. In DSM-IV-TR, an individual would meet criteria for BED if he or she engages in regular binge eating behavior in the absence of recurrent compensatory behaviors ≥2 days per week over 6 months.¹ Proposed changes for DSM-5 recognize a distinct BED diagnosis, reduce the frequency criterion to once per week and the duration criterion to the past 3 months, and shift the focus from binge days to binge episodes (Table 1).³

Table 1

Proposed DSM-5 criteria for binge eating disorder

BED can occur in individuals of all body mass indices (BMI), but is common among individuals who are overweight or obese as well as those with depression or type 2 diabetes; BED can complicate treatment of these conditions.^2,4,5 Primary treatment goals are:

• abstinence from binge eating
• improved psychological functioning
• appropriate weight regulation in overweight patients.

We report on 3 approaches to BED treatment: medication only, behavioral intervention only, and medication plus behavioral intervention. This article provides insights about emerging changes in diagnostic criteria for BED as well as evidence-informed treatment options and recommendations.

The evidence base

We conducted a review of 23 BED studies: 7 medication only, 5 medication plus behavioral, and 11 behavioral only. We focused on studies conducted since September 2005 that included binge frequency, weight, and depression as primary outcomes (see Berkman et al⁶ for a review of BED treatment studies before 2005). The studies included 2,527 participants (2,216 women and 311 men). Although the sex distribution of BED in the general population tends to slightly favor women,² the proportion of women presenting for treatment generally is considerably higher than that of men. In studies that reported on race and/or ethnicity, 1,639 participants were identified as white, 191 as African American, 25 as Hispanic, 2 as Asian, 1 as Native American, and 25 as “other.” Ages ranged from 18 to 77.

Several medications are effective

In placebo-controlled studies, a high-dose selective serotonin reuptake inhibitor (escitalopram⁷), 2 anticonvulsants (zonisamide⁸ and topiramate⁹), a selective norepinephrine reuptake inhibitor (atomoxetine¹⁰), and an appetite suppressant (sibutramine¹¹) were associated with significant decreases in binge eating frequency, weight, and BMI in overweight/obese patients diagnosed with BED (Table 2). In an open-label trial, memantine—a N-methyl-D-aspartate receptor antagonist often used to treat symptoms of Alzheimer’s disease—was associated with a significant reduction in binge eating but no change in weight.¹² Lamotrigine was not significantly different from placebo in reducing binge eating or weight, but showed promise in reducing metabolic parameters such as glucose and triglyceride levels commonly associated with obesity and type 2 diabetes.¹³ Because BED often is comorbid with obesity and type 2 diabetes, lamotrigine augmentation when treating obese individuals with BED warrants further investigation. As with any pharmacologic agent, carefully consider potential side effects and interactions with other drugs before prescribing medications for BED. Informing patients of potential side effects is crucial for patient safety and accuracy of the data collected in well-controlled treatment studies.

Table 2

Pharmacotherapy for binge eating disorder

CBT vs other behavioral approaches

Cognitive-behavioral therapy (CBT), which focuses on identifying and modifying unhealthy thoughts that maintain disordered eating behaviors, is the most widely studied behavioral intervention for BED. Other studied treatments include interpersonal psychotherapy (IPT), motivational interviewing (MI), and structured behavioral weight loss (BWL) (Table 3).^14-24 IPT is a psychodynamically based, time-limited treatment that focuses on the interpersonal context of the disorder and on building interpersonal skills. MI emphasizes exploring and resolving ambivalence about treatment, and works to facilitate change through motivational processes. BWL is centered on making dietary and physical activity changes to achieve weight loss. Behavioral treatments have been delivered in various formats, such as an individual or group setting, by electronic interface, and via self-help approaches. Most studies compared active treatment to a control group, but some compared active treatments head-to-head.

Table 3

CBT and other behavioral interventions for BED

Studies found that CBT and IPT are effective in reducing the frequency of binge eating, whether measured by the number of binge eating episodes or days a patient reports having engaged in binge eating.^14-23 However, some studies suggested that CBT can help a substantial number of patients achieve abstinence from binge eating.^16,20 Adding MI to a self-help approach may improve binge eating outcomes,²⁴ and binge eating can be successfully reduced using individual, group, and CD-ROM delivery formats.²¹ In direct comparisons, individual CBT outperformed group CBT in helping patients recover from BED (ie, no longer meeting diagnostic criteria),¹⁹ and CBT delivered via guided self-help outperformed BWL in helping patients achieve remission.¹⁸

Psychological features of BED typically include low levels of cognitive restraint and high levels of disinhibition, hunger, and shape and weight concerns. Improvements in these psychological measures were observed with CBT,^15-20,22 IPT,²² and MI.²⁴ In direct comparisons, self-help CBT demonstrated greater reductions in perceived hunger and disinhibition than self-help BWL,¹⁸ and individual CBT outperformed group CBT in reducing shape and weight concerns.¹⁹ Isolated studies reported improvements in depression after self-help CBT¹⁸ and MI,²⁴ and sustained improvements²² after group CBT (6 months) and group IPT (12 months). Additional research is needed to determine whether CBT crafted specifically for BED improves self-rated depression or if enhancements targeting depressive symptoms are required.

The impact of behavioral interventions on weight in overweight patients has been mixed. Although some CBT studies reported a substantial decrease in weight,^17,19 others suggested that weight loss among patients treated with CBT is not superior to those in a wait-list control group¹⁶ or is not significant over the course of treatment.^20,21 The impact of BWL on weight outcomes in BED also has been unimpressive: after 12 weeks, self-help BWL was no better than self-help CBT in reducing BMI¹⁸; after 16 weeks, BWL was better than CBT and IPT in achieving clinically significant (≥5%) weight loss, but this advantage was not sustained at 1- and 2-year follow-up.²³ It is difficult to determine why successfully treated BED patients fail to lose weight because one would expect decreases in binge eating to lead to weight loss. It is possible that calories previously consumed during binge eating episodes are distributed over non-binge meals or that patients label binges and non-binge meals differently as a result of treatment.

Combining treatments

BED patients often are treated with a combination of psychotherapy and pharmacotherapy (Table 4).^25-29 When added to CBT, topiramate was associated with improvements in weight and some psychological outcomes,^25,26 but fluoxetine was not.^27,28 Direct comparisons also showed that CBT, alone or combined with fluoxetine, was better than fluoxetine alone in reducing binge eating.²⁷ When combined with an individualized hypocaloric diet, the anti-obesity medication orlistat reduced weight in obese BED patients but had no appreciable effect on binge eating.²⁹ Collectively, the studies we reviewed suggested that combining medication and CBT may improve binge eating and weight loss outcomes; however, additional trials are necessary to determine more definitively which medications combined with CBT are best at producing sustained weight loss while reducing binge eating frequency.

Table 4

Combining medication with behavioral interventions for BED

Recommendations

Evidence suggests that pharmacotherapy and CBT—alone or in combination—are effective in reducing binge eating, and pharmacotherapy is effective in reducing weight in overweight individuals with BED. More research is needed for IPT and MI. It is unclear which medications provide the greatest benefit in terms of binge eating remission; however, pharmacotherapy has a clear advantage in facilitating short-term weight loss. Also, all BED patients should receive medical management to address possible complications such as hypertension or type 2 diabetes. In addition to reducing binge eating, CBT can improve related psychological comorbidities (eg, eating-related psychopathology and depression) and may have additional benefit when combined with pharmacotherapy.

In light of these findings, we recommend augmenting psychotherapeutic care with pharmacotherapy and medical management to address all relevant psychological and medical domains. Future investigations should address the benefits of coordinated psychological and medical care and evaluate how to maintain treatment gains.

Related Resources

• Binge Eating Disorder Association. www.bedaonline.com.
• Brownley KA, Berkman ND, Sedway JA, et al. Binge eating disorder treatment: a systematic review of randomized controlled trials. Int J Eat Disord. 2007;40(4):337-348.

Drug Brand Names

• Atomoxetine • Strattera
• Escitalopram • Lexapro
• Fluoxetine • Prozac
• Lamotrigine • Lamictal
• Memantine • Namenda
• Orlistat • Alli, Xenical
• Sertraline • Zoloft
• Sibutramine • Meridia
• Topiramate • Topamax, Topiragen
• Zonisamide • Zonegram

Disclosures

Dr. Peat receives a post-doctoral trainee grant from the National Institutes of Health.

Drs. Brownley, Berkman, and Bulik report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Binge eating is consumption of an unusually large amount of food coupled with a feeling of loss of control over eating. Binge eating disorder (BED) is characterized by recurrent episodes of binge eating without inappropriate compensatory behaviors (eg, self-induced vomiting, misuse of laxatives, diuretics, or other agents, excessive exercise).¹ It is the most common eating disorder in the United States, with a lifetime prevalence of approximately 3.5% in women and 2% in men.² The diagnosis falls within the DSM-IV-TR category of eating disorders not otherwise specified,¹ but clinicians often view it as a distinct clinical phenomenon. In DSM-IV-TR, an individual would meet criteria for BED if he or she engages in regular binge eating behavior in the absence of recurrent compensatory behaviors ≥2 days per week over 6 months.¹ Proposed changes for DSM-5 recognize a distinct BED diagnosis, reduce the frequency criterion to once per week and the duration criterion to the past 3 months, and shift the focus from binge days to binge episodes (Table 1).³

Table 1

Proposed DSM-5 criteria for binge eating disorder

BED can occur in individuals of all body mass indices (BMI), but is common among individuals who are overweight or obese as well as those with depression or type 2 diabetes; BED can complicate treatment of these conditions.^2,4,5 Primary treatment goals are:

• abstinence from binge eating
• improved psychological functioning
• appropriate weight regulation in overweight patients.

We report on 3 approaches to BED treatment: medication only, behavioral intervention only, and medication plus behavioral intervention. This article provides insights about emerging changes in diagnostic criteria for BED as well as evidence-informed treatment options and recommendations.

The evidence base

We conducted a review of 23 BED studies: 7 medication only, 5 medication plus behavioral, and 11 behavioral only. We focused on studies conducted since September 2005 that included binge frequency, weight, and depression as primary outcomes (see Berkman et al⁶ for a review of BED treatment studies before 2005). The studies included 2,527 participants (2,216 women and 311 men). Although the sex distribution of BED in the general population tends to slightly favor women,² the proportion of women presenting for treatment generally is considerably higher than that of men. In studies that reported on race and/or ethnicity, 1,639 participants were identified as white, 191 as African American, 25 as Hispanic, 2 as Asian, 1 as Native American, and 25 as “other.” Ages ranged from 18 to 77.

Several medications are effective

In placebo-controlled studies, a high-dose selective serotonin reuptake inhibitor (escitalopram⁷), 2 anticonvulsants (zonisamide⁸ and topiramate⁹), a selective norepinephrine reuptake inhibitor (atomoxetine¹⁰), and an appetite suppressant (sibutramine¹¹) were associated with significant decreases in binge eating frequency, weight, and BMI in overweight/obese patients diagnosed with BED (Table 2). In an open-label trial, memantine—a N-methyl-D-aspartate receptor antagonist often used to treat symptoms of Alzheimer’s disease—was associated with a significant reduction in binge eating but no change in weight.¹² Lamotrigine was not significantly different from placebo in reducing binge eating or weight, but showed promise in reducing metabolic parameters such as glucose and triglyceride levels commonly associated with obesity and type 2 diabetes.¹³ Because BED often is comorbid with obesity and type 2 diabetes, lamotrigine augmentation when treating obese individuals with BED warrants further investigation. As with any pharmacologic agent, carefully consider potential side effects and interactions with other drugs before prescribing medications for BED. Informing patients of potential side effects is crucial for patient safety and accuracy of the data collected in well-controlled treatment studies.

Table 2

Pharmacotherapy for binge eating disorder

CBT vs other behavioral approaches

Cognitive-behavioral therapy (CBT), which focuses on identifying and modifying unhealthy thoughts that maintain disordered eating behaviors, is the most widely studied behavioral intervention for BED. Other studied treatments include interpersonal psychotherapy (IPT), motivational interviewing (MI), and structured behavioral weight loss (BWL) (Table 3).^14-24 IPT is a psychodynamically based, time-limited treatment that focuses on the interpersonal context of the disorder and on building interpersonal skills. MI emphasizes exploring and resolving ambivalence about treatment, and works to facilitate change through motivational processes. BWL is centered on making dietary and physical activity changes to achieve weight loss. Behavioral treatments have been delivered in various formats, such as an individual or group setting, by electronic interface, and via self-help approaches. Most studies compared active treatment to a control group, but some compared active treatments head-to-head.

Table 3

CBT and other behavioral interventions for BED

Studies found that CBT and IPT are effective in reducing the frequency of binge eating, whether measured by the number of binge eating episodes or days a patient reports having engaged in binge eating.^14-23 However, some studies suggested that CBT can help a substantial number of patients achieve abstinence from binge eating.^16,20 Adding MI to a self-help approach may improve binge eating outcomes,²⁴ and binge eating can be successfully reduced using individual, group, and CD-ROM delivery formats.²¹ In direct comparisons, individual CBT outperformed group CBT in helping patients recover from BED (ie, no longer meeting diagnostic criteria),¹⁹ and CBT delivered via guided self-help outperformed BWL in helping patients achieve remission.¹⁸

Psychological features of BED typically include low levels of cognitive restraint and high levels of disinhibition, hunger, and shape and weight concerns. Improvements in these psychological measures were observed with CBT,^15-20,22 IPT,²² and MI.²⁴ In direct comparisons, self-help CBT demonstrated greater reductions in perceived hunger and disinhibition than self-help BWL,¹⁸ and individual CBT outperformed group CBT in reducing shape and weight concerns.¹⁹ Isolated studies reported improvements in depression after self-help CBT¹⁸ and MI,²⁴ and sustained improvements²² after group CBT (6 months) and group IPT (12 months). Additional research is needed to determine whether CBT crafted specifically for BED improves self-rated depression or if enhancements targeting depressive symptoms are required.

The impact of behavioral interventions on weight in overweight patients has been mixed. Although some CBT studies reported a substantial decrease in weight,^17,19 others suggested that weight loss among patients treated with CBT is not superior to those in a wait-list control group¹⁶ or is not significant over the course of treatment.^20,21 The impact of BWL on weight outcomes in BED also has been unimpressive: after 12 weeks, self-help BWL was no better than self-help CBT in reducing BMI¹⁸; after 16 weeks, BWL was better than CBT and IPT in achieving clinically significant (≥5%) weight loss, but this advantage was not sustained at 1- and 2-year follow-up.²³ It is difficult to determine why successfully treated BED patients fail to lose weight because one would expect decreases in binge eating to lead to weight loss. It is possible that calories previously consumed during binge eating episodes are distributed over non-binge meals or that patients label binges and non-binge meals differently as a result of treatment.

Combining treatments

BED patients often are treated with a combination of psychotherapy and pharmacotherapy (Table 4).^25-29 When added to CBT, topiramate was associated with improvements in weight and some psychological outcomes,^25,26 but fluoxetine was not.^27,28 Direct comparisons also showed that CBT, alone or combined with fluoxetine, was better than fluoxetine alone in reducing binge eating.²⁷ When combined with an individualized hypocaloric diet, the anti-obesity medication orlistat reduced weight in obese BED patients but had no appreciable effect on binge eating.²⁹ Collectively, the studies we reviewed suggested that combining medication and CBT may improve binge eating and weight loss outcomes; however, additional trials are necessary to determine more definitively which medications combined with CBT are best at producing sustained weight loss while reducing binge eating frequency.

Table 4

Combining medication with behavioral interventions for BED

Recommendations

Evidence suggests that pharmacotherapy and CBT—alone or in combination—are effective in reducing binge eating, and pharmacotherapy is effective in reducing weight in overweight individuals with BED. More research is needed for IPT and MI. It is unclear which medications provide the greatest benefit in terms of binge eating remission; however, pharmacotherapy has a clear advantage in facilitating short-term weight loss. Also, all BED patients should receive medical management to address possible complications such as hypertension or type 2 diabetes. In addition to reducing binge eating, CBT can improve related psychological comorbidities (eg, eating-related psychopathology and depression) and may have additional benefit when combined with pharmacotherapy.

In light of these findings, we recommend augmenting psychotherapeutic care with pharmacotherapy and medical management to address all relevant psychological and medical domains. Future investigations should address the benefits of coordinated psychological and medical care and evaluate how to maintain treatment gains.

Related Resources

• Binge Eating Disorder Association. www.bedaonline.com.
• Brownley KA, Berkman ND, Sedway JA, et al. Binge eating disorder treatment: a systematic review of randomized controlled trials. Int J Eat Disord. 2007;40(4):337-348.

Drug Brand Names

• Atomoxetine • Strattera
• Escitalopram • Lexapro
• Fluoxetine • Prozac
• Lamotrigine • Lamictal
• Memantine • Namenda
• Orlistat • Alli, Xenical
• Sertraline • Zoloft
• Sibutramine • Meridia
• Topiramate • Topamax, Topiragen
• Zonisamide • Zonegram

Disclosures

Dr. Peat receives a post-doctoral trainee grant from the National Institutes of Health.

Drs. Brownley, Berkman, and Bulik report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.