Clinical Review

In the 18 months since the Patient Protection and Affordable Care Act—otherwise known as ACA, or health-care reform—was signed into law by President Barack Obama, the outlook for private practice, in any specialty, has dimmed. As a recent report on the ramifications of the ACA put it:

The imperative to care for more patients, to provide higher perceived quality, at less cost, with increased reporting and tracking demands, in an environment of high potential liability and problematic reimbursement, will put additional stress on physicians, particularly those in private practice.¹

To explore the impact of these stresses on ObGyns specifically, the editors of OBG Management invited Lucia DiVenere, Senior Director of Government Affairs for the American Congress of Obstetricians and Gynecologists (ACOG), to talk about the outlook for private practice in the coming years. In the exchange, Ms. DiVenere discusses the short- and long-term effects of the ACA, the ways in which ObGyn practice is (or is not) evolving, the challenge of making the switch to electronic health records (EHRs), the reasons ACOG opposed the ACA, and other issues related to the current practice environment. In addition, two ObGyns in private practice describe the many challenges they face (see “The view from private practice,” pages 44 and 52).

What nonlegislative forces have affected private practice?

OBG Management: A recent report on the ramifications of the ACA argues that formal reform was inevitable. It also asserts that private practice was subject to many negative pressures long before health-care reform was passed.¹ Do you agree?

Ms. DiVenere: Our nation’s health-care system is always evolving, and over the past decade, we’ve seen a clear trend toward system integration—that is, larger, physician-led group practices and hospital employment of physicians.

Looking at physicians as a whole, the percentage who practice solo or in two-physician practices fell from 40.7% in 1996–97 to 32.5% by 2004–05, according to a 2007 survey.² And the American Medical Association (AMA) reported that the percentage of physicians “with an ownership stake in their practice declined from 61.6% to 54.4% as more physicians opted for employment. Both the trends away from solo and two-physician practices and toward employment were more pronounced for specialists and older physicians.”²

OBG Management: What has the trend been for ObGyns, specifically?

Ms. DiVenere: The ObGyn specialty employs the group practice model—health care delivered by three or more physicians—more frequently than other specialties do, largely because of the support it provides for 24–7 OB call schedules.

As for private practice, ObGyns have been moving away from it for 10 years or longer. Data from a 1991 ACOG survey shows that 77% of respondents were in private practice; by 2003, that percentage had fallen to 70%.³ In 2003, ObGyns in private practice tended to be older (median age: 47 years) than their salaried colleagues (median: 42 years) and were more likely to be male (87% vs 77%).³ The demographic change toward women ObGyns may add to this trend line.

OBG Management: What economic forces have shaped practice paradigms in ObGyn?

Ms. DiVenere: Median expenses for private practices have been steadily rising in relation to revenues—from 52% in 1990 to 71% in 2002—making it difficult for practices to remain solvent.⁴ In addition, a 2011 survey from Medscape reveals that ObGyns in solo practice earn $15,000 to $25,000 less annually than their employed colleagues.⁵

ObGyns who have made the switch from private to hospital practice, or who have become ObGyn hospitalists, often point to the difficulties of maintaining a solvent private practice, especially given the push toward electronic health records (EHRs) and increasing regulatory and administrative burdens. These and other issues contribute to rising practice costs and increasing demands on an ObGyn’s time and attention.

What are the short-term effects of formal reform?

OBG Management: What effect has health-care reform had so far?

Ms. DiVenere: In 2010, twice as many physician practices were bought by hospitals and health systems as in 2009. We can’t conclude that the 2010 law is responsible for these changes, but we know that the architects of health reform were aware of this trend, believed it was beneficial, and looked for ways to encourage it, including through development of accountable care organizations (ACOs), which give hospitals a new and potentially lucrative reason to purchase private practices.

OBG Management: What exactly is an ACO?

Ms. DiVenere: An ACO consists of aligned providers—most likely, large multispecialty groups, often affiliated with the same hospital—who agree to manage patients for a set fee, sharing the risk and potential profit. ACOs are required to have shared governance, which gives them the authority to impose standards for practice, reporting, and compensation—including rewards and penalties—across a group of physicians.

Each ACO must sign a 3-year contract with the US Department of Health and Human Services (HHS) and include a sufficient number of primary care professionals to care for at least 5,000 beneficiaries. ACOs will be evaluated by quality-performance measures to be determined by the Secretary of HHS.

What aspects of ACA will have the biggest impact?

OBG Management: What provision of the new law will have the most direct impact on ObGyns in private practice?

Ms. DiVenere: All ObGyns may benefit from the guarantee of insurance coverage for our patients for maternity and preventive care. And all ObGyns should join ACOG’s fight to repeal the Independent Payment Advisory Board, which may hold enormous power to cut physician reimbursement.

Here’s the quote all ObGyns—especially those in private practice—should read, from an article written by President Obama’s health-reform deputies:

To realize the full benefits of the Affordable Care Act, physicians will need to embrace rather than resist change. The economic forces put in motion by the Act are likely to lead to vertical organization of providers and accelerate physician employment by hospitals and aggregation into larger physician groups. The most successful physicians will be those who most effectively collaborate with other providers to improve outcomes, care productivity, and patient experience.⁶

OBG Management: Do these health-reform deputies offer any concrete vision of how this change will be achieved?

Ms. DiVenere: They detail what physicians need to do, and how they should change the way they practice, under the Act. For example, to meet the increasing demand for health care, they recommend that practices:

• “Redesign care to include a team of nonphysician providers, such as nurse practitioners, physician assistants, care coordinators, and dieticians”
• “Develop approaches to engage and monitor patients outside of the office.”⁶

And to meet the requirements for payment reform, information transparency, and quality, they suggest that practices:

• “Focus care around exceptional patient experience and shared clinical outcome goals”
• “Engage in shared decision-making discussions regarding treatment goals and approaches”
• “Proactively manage preventive care”
• “Establish teams to take part in bundled payments and incentive programs”
• “Expand use of electronic health records”
• “Collaborate with hospitals to dramatically reduce readmissions and hospital-acquired infections”
• “Incorporate patient-centered outcomes research to tailor care.”⁶

To capture value, the authors recommend that practices “redesign medical office processes to capture savings from administrative simplification.”⁶

OBG Management: Do they propose any method for implementing these changes?

Ms. DiVenere: The White House is hoping that ACOs can lead. Medicare ACOs will attempt to accomplish these changes by managing hospital and physician services, prompting physicians and hospitals to change how they are both clinically organized and paid for services—this change, in particular, is considered by some to be essential to improving the quality and efficiency of health care.

The new Centers for Medicaid and Medicare Services (CMS) Innovation Center, created by the ACA, is given broad authority to test, evaluate, and adopt systems that foster patient-centered care, improve quality, and contain the costs of Medicare, Medicaid, and the Children’s Health Insurance Program (CHIP). The law specifically guides the Innovation Center to look for ways to encourage physicians to transition from fee-for-service to salary-based payment.

We can safely assume that the experts behind these provisions believe that large, hospital-centered systems or large, physician-led groups can better serve the needs of patients and our health-care system in general than can small private practices. Today, 24% of ObGyns run solo practices, and 27% are in single-specialty practices. Health-care reform can mean big changes for them.

Is the EHR a realistic goal for private practices?

OBG Management: How does the push for EHRs affect physicians in private practice?

Ms. DiVenere: Very profoundly. From the point of view of an ObGyn in private practice, EHRs offer a number of benefits. They can:

• help make sense of our increasingly fragmented health-care system
• improve patient safety
• increase efficiency
• reduce paperwork.

In addition, insurers may save by reducing unnecessary tests, and patients can certainly benefit from better coordination and documentation of care. These advantages don’t necessarily translate into savings or revenue for physician practices, however. Many ObGyns—especially those in solo or small practices—don’t feel confident making such a large capital investment. In fact, only about one third of ObGyn practices have an EHR.

OBG Management: Is it primarily cost that deters ObGyns from adopting EHRs?

Ms. DiVenere: That, and the fact that EHR systems are not yet fully interoperable across small practices, insurers, and government agencies. The initial cost of purchasing an EHR system for a small practice is about $50,000 per physician, and there are ongoing costs in staff training and hardware and software updates. A steep learning curve means fewer patients can be seen in an hour. It can take a practice months—even years—for physicians to return to their previous level of productivity. That’s a lot to ask a busy practicing physician to take on.

OBG Management: Is there any way around the push for EHRs?

Ms. DiVenere: Congress wants to move us to full adoption of health information technology (HIT). Under health-care reform, beginning in 2013, all health insurance plans must comply with a uniform standard for electronic transactions, including eligibility verification and health claim status.

In 2014, uniform standards must:

• allow automatic reconciliation of electronic funds transfers and HIPAA payment and remittance
• use standardized and consistent methods of health plan enrollment and editing of claims
• use unique health plan identifiers to simplify and improve routing of health-care transactions
• use standardized claims attachments
• improve practice data collection and evaluation.

Uniformity and standardization can help address one of the major roadblocks to physician adoption of HIT. Still, it’s little wonder that median expenses for private practices have been steadily rising in relation to revenues.

Is there a physician shortage in ObGyn?

OBG Management: There has been a lot of attention focused on the shortage of physicians in this country. How severe is the shortage likely to be in the specialty of ObGyn?

Ms. DiVenere: William F. Rayburn, MD, MBA, from the University of New Mexico Health Sciences Center and School of Medicine in Albuquerque, has provided ACOG with important work on this topic. Dr. Rayburn is Randolph V. Seligman Professor and Chair in the Department of Obstetrics and Gynecology at that institution. His report⁷ shows that the gap between the supply of ObGyns and the demand for women’s health care is widening.

Data from this report point to a shortage of 9,000 to 14,000 ObGyns in 20 years. After 2030, the ObGyn shortage may be even more pronounced, as the population of women is projected to increase 36% by 2050, while the number of ObGyns remains constant.

OBG Management: Would the incorporation of more midlevel providers—that is, nurse midwives, physician assistants, and others—ease some of the strains on the ObGyn workforce in general and on private practice specifically?

Ms. DiVenere: That’s very possible and is one of the reasons ACOG encourages greater use of collaborative care. It’s certainly true that the ObGyn specialty is historically comfortable with collaboration.

In 2008, the average ObGyn practice employed 2.6 nonphysician clinicians, certified nurse midwives (CNMs), physician assistants, or nurse practitioners. ACOG strongly supports collaborative practice between ObGyns and qualified midwives (CNMs, certified midwives) and other nonphysician clinicians.

In a recent issue of Obstetrics & Gynecology, ACOG’s Immediate Past President Richard N. Waldman, MD, and Holly Powell Kennedy, CNM, PhD, president of the American College of Nurse Midwives, wrote about the importance of collaborative practice, which can “increase efficiency, improve clinical outcomes, and enhance provider satisfaction.”⁸ The September 2011 issue of Obstetrics & Gynecology highlights four real-life stories of successful collaborative practice.

Because of our commitment to the benefits of collaborative practice, ACOG supported a provision in the ACA that increases payment for CNMs. Beginning this year, the Medicare program will reimburse CNMs at 100% of the physician payment rate for the same services. Before this law, CNMs were paid at 65% of a physician’s rate for the same services. ACOG’s leadership believes that better reimbursement for CNMs will help ObGyn practices and improve care.

Although ACOG supported that provision in the law, we did not support passage of the ACA. ACOG’s Executive Board carefully considered all elements of the bill and decided that, although it included many provisions that are helpful to our patients, it also included many harmful provisions for our members. We felt that the promise of the women’s health provisions could be realized only if the legislation worked for practicing physicians, too.

Why wasn’t the SGR formula abolished?

OBG Management: What is the effect, for physicians in general and ObGyns in private practice specifically, of the failure to fix the sustainable growth rate (SGR) formula and implement liability reform in the ACA?

Ms. DiVenere: The fact that we have no fix for SGR and no medical liability reform is a disgrace. And the absence of solutions to these two issues is one of the main reasons ACOG decided not to support passage of the ACA. Our Executive Board was very clear in telling Congress that we can’t build a reformed health-care system on broken payment and liability systems—it just won’t work.

ObGyns themselves are the first to point out this fact. ObGyns listed medical liability (65.3%) and financial viability of their practice (44.3%) as their top two professional concerns in a 2008 ACOG survey.⁹

For all ObGyns, these two continuing problems make practice more difficult every day—problems felt most acutely by ObGyns in private practice. Employed physicians often come under a hospital’s or health system’s liability policy and often don’t pay their own premiums. Employed physicians usually are on salary, sheltering them from the vagaries of Congressional action, or inaction, on looming double-digit Medicare physician payment cuts under the SGR.

Some legislators, and some ObGyns, think Medicare doesn’t apply to us. But today, 92% of ObGyns participate in the Medicare program and 63% accept all Medicare patients. This fact reflects ObGyn training and commitment to serve as lifelong principal-care physicians for women, including women who have disabilities. Fifty-six percent of all Medicare beneficiaries are women. With the Baby Boomer generation transitioning to Medicare, and with shortages in primary care physicians, it is likely that ObGyns will become more involved in delivering health care for this population.

Medicare physician payments matter to ObGyns beyond the Medicare program, too, as Tricare and private payers often follow Medicare payment and coverage policies. As a specialty, we have much at stake in ensuring a stable Medicare system for years to come, starting with an improved physician payment system. [Editor’s note: See Dr. Robert L. Barbieri’s editorial on the subject.]

OBG Management: What is ACOG doing to improve this system?

Ms. DiVenere: ACOG is urging the US Congress to ensure that a better system adheres to the following priniciples:

• Medicare payments should fairly and accurately reflect the cost of care. In the final 2011 Medicare physician fee schedule, CMS is proposing to reduce the physician work value for ObGyn care to women by 11% below what is paid to other physicians for similar men’s services—exactly the opposite of what should be done to encourage good care coordination, and in direct contradiction to recommendations by the Resource-Based Relative Value Scale Update Committee (RUC). Medicare payments to obstetricians are already well below the cost of maternity care; no further cuts should be allowed for this care.
• A new payment system should be as simple, coordinated, and transparent as possible and recognize that there is no one-size-fits-all model. A new Medicare system should coordinate closely with other governmental and nongovernmental programs to ensure that information technology is interoperable, that quality measurement relies on high-quality, risk-adjusted data, and to guard against new and special systems that apply to only one program or may only be workable for one type of specialty or only certain types of diseases and conditions. ObGyns often see relatively few Medicare patients, and unique Medicare requirements can pose significant administrative challenges and inefficiencies to ObGyn participation.
• Congress should encourage, and remove barriers to, ObGyn and physician development of ACOs, medical homes for women, and other innovative models. Proposed rules on the Medicare Shared Savings Program allowing for expedited antitrust review should be extended to ACOs and other physician-led models of care that do not participate in the Medicare Shared Savings Program. These models should also recognize the dual role ObGyns may play, as both primary and specialty care providers.
• Congress should repeal the Independent Medicare Payment Advisory Board. Leaving Medicare payment decisions in the hands of an unelected, unaccountable body with minimal congressional oversight is bad for all physicians and for our patients.

The outlook for private practice, in any specialty, has dimmed. Says ACOG’s Lucia DiVenere: “Median expenses for private practices have been steadily rising in relationship to revenues—from 52% in 1990 to 71% in 2002—making it difficult for practices to remain solvent.”

Is private practice doomed?

OBG Management: In your opinion, over the long term, is health reform a positive or a negative for ObGyns in private practice?

Ms. DiVenere: On balance, I believe that the health reform law is a positive for our patients, and that fact may lead to an eventual positive for its Fellows, ACOG hopes. What it may mean for ObGyns in private practice, though, is more troubling.

The law has many intended purposes: 1) cover the uninsured, 2) tilt our health-care system toward primary care and use of nonphysician providers, and 3) push practices toward integration with hospitals and health systems and other paths to physician employment. Support for continuation or growth in any type of physician private practice is hard to find in the ACA.

OBG Management: What changes are in the pipeline?

Ms. DiVenere: Under the ACA, by 2013, the Secretary of HHS, with input from stakeholders, will set up a Physician Compare Web site, modeled after the program that exists for hospitals, using data from the Physician Quality Reporting Initiative (PQRI). Data on this site would be made public on January 1, 2013, comparing physicians in terms of quality of care and patient experience.

By law, these data are intended to be statistically valid and risk-adjusted; each physician must have time to review his or her information before it becomes publicly available; data must ensure appropriate attribution of care when multiple providers are involved; and the Secretary of HHS must give physicians timely performance feedback.

Data elements—to the extent that scientifically sound measures exist—will include:

• quality, patient satisfaction, and health outcomes information on Medicare physicians
• physician care coordination and risk-adjusted resource use
• safety, effectiveness, and timeliness of care.

Physicians who successfully interact with this program will likely be those who have a robust EHR system.

If this and other elements of the Affordable Care Act become real, however, we’ll likely see a fundamental shift in the kinds of settings in which ObGyns and other physicians opt to practice.

We want to hear from you! Tell us what you think.

In the 18 months since the Patient Protection and Affordable Care Act—otherwise known as ACA, or health-care reform—was signed into law by President Barack Obama, the outlook for private practice, in any specialty, has dimmed. As a recent report on the ramifications of the ACA put it:

The imperative to care for more patients, to provide higher perceived quality, at less cost, with increased reporting and tracking demands, in an environment of high potential liability and problematic reimbursement, will put additional stress on physicians, particularly those in private practice.¹

To explore the impact of these stresses on ObGyns specifically, the editors of OBG Management invited Lucia DiVenere, Senior Director of Government Affairs for the American Congress of Obstetricians and Gynecologists (ACOG), to talk about the outlook for private practice in the coming years. In the exchange, Ms. DiVenere discusses the short- and long-term effects of the ACA, the ways in which ObGyn practice is (or is not) evolving, the challenge of making the switch to electronic health records (EHRs), the reasons ACOG opposed the ACA, and other issues related to the current practice environment. In addition, two ObGyns in private practice describe the many challenges they face (see “The view from private practice,” pages 44 and 52).

What nonlegislative forces have affected private practice?

OBG Management: A recent report on the ramifications of the ACA argues that formal reform was inevitable. It also asserts that private practice was subject to many negative pressures long before health-care reform was passed.¹ Do you agree?

Ms. DiVenere: Our nation’s health-care system is always evolving, and over the past decade, we’ve seen a clear trend toward system integration—that is, larger, physician-led group practices and hospital employment of physicians.

Looking at physicians as a whole, the percentage who practice solo or in two-physician practices fell from 40.7% in 1996–97 to 32.5% by 2004–05, according to a 2007 survey.² And the American Medical Association (AMA) reported that the percentage of physicians “with an ownership stake in their practice declined from 61.6% to 54.4% as more physicians opted for employment. Both the trends away from solo and two-physician practices and toward employment were more pronounced for specialists and older physicians.”²

OBG Management: What has the trend been for ObGyns, specifically?

Ms. DiVenere: The ObGyn specialty employs the group practice model—health care delivered by three or more physicians—more frequently than other specialties do, largely because of the support it provides for 24–7 OB call schedules.

As for private practice, ObGyns have been moving away from it for 10 years or longer. Data from a 1991 ACOG survey shows that 77% of respondents were in private practice; by 2003, that percentage had fallen to 70%.³ In 2003, ObGyns in private practice tended to be older (median age: 47 years) than their salaried colleagues (median: 42 years) and were more likely to be male (87% vs 77%).³ The demographic change toward women ObGyns may add to this trend line.

OBG Management: What economic forces have shaped practice paradigms in ObGyn?

Ms. DiVenere: Median expenses for private practices have been steadily rising in relation to revenues—from 52% in 1990 to 71% in 2002—making it difficult for practices to remain solvent.⁴ In addition, a 2011 survey from Medscape reveals that ObGyns in solo practice earn $15,000 to $25,000 less annually than their employed colleagues.⁵

ObGyns who have made the switch from private to hospital practice, or who have become ObGyn hospitalists, often point to the difficulties of maintaining a solvent private practice, especially given the push toward electronic health records (EHRs) and increasing regulatory and administrative burdens. These and other issues contribute to rising practice costs and increasing demands on an ObGyn’s time and attention.

What are the short-term effects of formal reform?

OBG Management: What effect has health-care reform had so far?

Ms. DiVenere: In 2010, twice as many physician practices were bought by hospitals and health systems as in 2009. We can’t conclude that the 2010 law is responsible for these changes, but we know that the architects of health reform were aware of this trend, believed it was beneficial, and looked for ways to encourage it, including through development of accountable care organizations (ACOs), which give hospitals a new and potentially lucrative reason to purchase private practices.

OBG Management: What exactly is an ACO?

Ms. DiVenere: An ACO consists of aligned providers—most likely, large multispecialty groups, often affiliated with the same hospital—who agree to manage patients for a set fee, sharing the risk and potential profit. ACOs are required to have shared governance, which gives them the authority to impose standards for practice, reporting, and compensation—including rewards and penalties—across a group of physicians.

Each ACO must sign a 3-year contract with the US Department of Health and Human Services (HHS) and include a sufficient number of primary care professionals to care for at least 5,000 beneficiaries. ACOs will be evaluated by quality-performance measures to be determined by the Secretary of HHS.

What aspects of ACA will have the biggest impact?

OBG Management: What provision of the new law will have the most direct impact on ObGyns in private practice?

Ms. DiVenere: All ObGyns may benefit from the guarantee of insurance coverage for our patients for maternity and preventive care. And all ObGyns should join ACOG’s fight to repeal the Independent Payment Advisory Board, which may hold enormous power to cut physician reimbursement.

Here’s the quote all ObGyns—especially those in private practice—should read, from an article written by President Obama’s health-reform deputies:

To realize the full benefits of the Affordable Care Act, physicians will need to embrace rather than resist change. The economic forces put in motion by the Act are likely to lead to vertical organization of providers and accelerate physician employment by hospitals and aggregation into larger physician groups. The most successful physicians will be those who most effectively collaborate with other providers to improve outcomes, care productivity, and patient experience.⁶

OBG Management: Do these health-reform deputies offer any concrete vision of how this change will be achieved?

Ms. DiVenere: They detail what physicians need to do, and how they should change the way they practice, under the Act. For example, to meet the increasing demand for health care, they recommend that practices:

• “Redesign care to include a team of nonphysician providers, such as nurse practitioners, physician assistants, care coordinators, and dieticians”
• “Develop approaches to engage and monitor patients outside of the office.”⁶

And to meet the requirements for payment reform, information transparency, and quality, they suggest that practices:

• “Focus care around exceptional patient experience and shared clinical outcome goals”
• “Engage in shared decision-making discussions regarding treatment goals and approaches”
• “Proactively manage preventive care”
• “Establish teams to take part in bundled payments and incentive programs”
• “Expand use of electronic health records”
• “Collaborate with hospitals to dramatically reduce readmissions and hospital-acquired infections”
• “Incorporate patient-centered outcomes research to tailor care.”⁶

To capture value, the authors recommend that practices “redesign medical office processes to capture savings from administrative simplification.”⁶

OBG Management: Do they propose any method for implementing these changes?

Ms. DiVenere: The White House is hoping that ACOs can lead. Medicare ACOs will attempt to accomplish these changes by managing hospital and physician services, prompting physicians and hospitals to change how they are both clinically organized and paid for services—this change, in particular, is considered by some to be essential to improving the quality and efficiency of health care.

The new Centers for Medicaid and Medicare Services (CMS) Innovation Center, created by the ACA, is given broad authority to test, evaluate, and adopt systems that foster patient-centered care, improve quality, and contain the costs of Medicare, Medicaid, and the Children’s Health Insurance Program (CHIP). The law specifically guides the Innovation Center to look for ways to encourage physicians to transition from fee-for-service to salary-based payment.

We can safely assume that the experts behind these provisions believe that large, hospital-centered systems or large, physician-led groups can better serve the needs of patients and our health-care system in general than can small private practices. Today, 24% of ObGyns run solo practices, and 27% are in single-specialty practices. Health-care reform can mean big changes for them.

Is the EHR a realistic goal for private practices?

OBG Management: How does the push for EHRs affect physicians in private practice?

Ms. DiVenere: Very profoundly. From the point of view of an ObGyn in private practice, EHRs offer a number of benefits. They can:

• help make sense of our increasingly fragmented health-care system
• improve patient safety
• increase efficiency
• reduce paperwork.

In addition, insurers may save by reducing unnecessary tests, and patients can certainly benefit from better coordination and documentation of care. These advantages don’t necessarily translate into savings or revenue for physician practices, however. Many ObGyns—especially those in solo or small practices—don’t feel confident making such a large capital investment. In fact, only about one third of ObGyn practices have an EHR.

OBG Management: Is it primarily cost that deters ObGyns from adopting EHRs?

Ms. DiVenere: That, and the fact that EHR systems are not yet fully interoperable across small practices, insurers, and government agencies. The initial cost of purchasing an EHR system for a small practice is about $50,000 per physician, and there are ongoing costs in staff training and hardware and software updates. A steep learning curve means fewer patients can be seen in an hour. It can take a practice months—even years—for physicians to return to their previous level of productivity. That’s a lot to ask a busy practicing physician to take on.

OBG Management: Is there any way around the push for EHRs?

Ms. DiVenere: Congress wants to move us to full adoption of health information technology (HIT). Under health-care reform, beginning in 2013, all health insurance plans must comply with a uniform standard for electronic transactions, including eligibility verification and health claim status.

In 2014, uniform standards must:

• allow automatic reconciliation of electronic funds transfers and HIPAA payment and remittance
• use standardized and consistent methods of health plan enrollment and editing of claims
• use unique health plan identifiers to simplify and improve routing of health-care transactions
• use standardized claims attachments
• improve practice data collection and evaluation.

Uniformity and standardization can help address one of the major roadblocks to physician adoption of HIT. Still, it’s little wonder that median expenses for private practices have been steadily rising in relation to revenues.

Is there a physician shortage in ObGyn?

OBG Management: There has been a lot of attention focused on the shortage of physicians in this country. How severe is the shortage likely to be in the specialty of ObGyn?

Ms. DiVenere: William F. Rayburn, MD, MBA, from the University of New Mexico Health Sciences Center and School of Medicine in Albuquerque, has provided ACOG with important work on this topic. Dr. Rayburn is Randolph V. Seligman Professor and Chair in the Department of Obstetrics and Gynecology at that institution. His report⁷ shows that the gap between the supply of ObGyns and the demand for women’s health care is widening.

Data from this report point to a shortage of 9,000 to 14,000 ObGyns in 20 years. After 2030, the ObGyn shortage may be even more pronounced, as the population of women is projected to increase 36% by 2050, while the number of ObGyns remains constant.

OBG Management: Would the incorporation of more midlevel providers—that is, nurse midwives, physician assistants, and others—ease some of the strains on the ObGyn workforce in general and on private practice specifically?

Ms. DiVenere: That’s very possible and is one of the reasons ACOG encourages greater use of collaborative care. It’s certainly true that the ObGyn specialty is historically comfortable with collaboration.

In 2008, the average ObGyn practice employed 2.6 nonphysician clinicians, certified nurse midwives (CNMs), physician assistants, or nurse practitioners. ACOG strongly supports collaborative practice between ObGyns and qualified midwives (CNMs, certified midwives) and other nonphysician clinicians.

In a recent issue of Obstetrics & Gynecology, ACOG’s Immediate Past President Richard N. Waldman, MD, and Holly Powell Kennedy, CNM, PhD, president of the American College of Nurse Midwives, wrote about the importance of collaborative practice, which can “increase efficiency, improve clinical outcomes, and enhance provider satisfaction.”⁸ The September 2011 issue of Obstetrics & Gynecology highlights four real-life stories of successful collaborative practice.

Because of our commitment to the benefits of collaborative practice, ACOG supported a provision in the ACA that increases payment for CNMs. Beginning this year, the Medicare program will reimburse CNMs at 100% of the physician payment rate for the same services. Before this law, CNMs were paid at 65% of a physician’s rate for the same services. ACOG’s leadership believes that better reimbursement for CNMs will help ObGyn practices and improve care.

Although ACOG supported that provision in the law, we did not support passage of the ACA. ACOG’s Executive Board carefully considered all elements of the bill and decided that, although it included many provisions that are helpful to our patients, it also included many harmful provisions for our members. We felt that the promise of the women’s health provisions could be realized only if the legislation worked for practicing physicians, too.

Why wasn’t the SGR formula abolished?

OBG Management: What is the effect, for physicians in general and ObGyns in private practice specifically, of the failure to fix the sustainable growth rate (SGR) formula and implement liability reform in the ACA?

Ms. DiVenere: The fact that we have no fix for SGR and no medical liability reform is a disgrace. And the absence of solutions to these two issues is one of the main reasons ACOG decided not to support passage of the ACA. Our Executive Board was very clear in telling Congress that we can’t build a reformed health-care system on broken payment and liability systems—it just won’t work.

ObGyns themselves are the first to point out this fact. ObGyns listed medical liability (65.3%) and financial viability of their practice (44.3%) as their top two professional concerns in a 2008 ACOG survey.⁹

For all ObGyns, these two continuing problems make practice more difficult every day—problems felt most acutely by ObGyns in private practice. Employed physicians often come under a hospital’s or health system’s liability policy and often don’t pay their own premiums. Employed physicians usually are on salary, sheltering them from the vagaries of Congressional action, or inaction, on looming double-digit Medicare physician payment cuts under the SGR.

Some legislators, and some ObGyns, think Medicare doesn’t apply to us. But today, 92% of ObGyns participate in the Medicare program and 63% accept all Medicare patients. This fact reflects ObGyn training and commitment to serve as lifelong principal-care physicians for women, including women who have disabilities. Fifty-six percent of all Medicare beneficiaries are women. With the Baby Boomer generation transitioning to Medicare, and with shortages in primary care physicians, it is likely that ObGyns will become more involved in delivering health care for this population.

Medicare physician payments matter to ObGyns beyond the Medicare program, too, as Tricare and private payers often follow Medicare payment and coverage policies. As a specialty, we have much at stake in ensuring a stable Medicare system for years to come, starting with an improved physician payment system. [Editor’s note: See Dr. Robert L. Barbieri’s editorial on the subject.]

OBG Management: What is ACOG doing to improve this system?

Ms. DiVenere: ACOG is urging the US Congress to ensure that a better system adheres to the following priniciples:

• Medicare payments should fairly and accurately reflect the cost of care. In the final 2011 Medicare physician fee schedule, CMS is proposing to reduce the physician work value for ObGyn care to women by 11% below what is paid to other physicians for similar men’s services—exactly the opposite of what should be done to encourage good care coordination, and in direct contradiction to recommendations by the Resource-Based Relative Value Scale Update Committee (RUC). Medicare payments to obstetricians are already well below the cost of maternity care; no further cuts should be allowed for this care.
• A new payment system should be as simple, coordinated, and transparent as possible and recognize that there is no one-size-fits-all model. A new Medicare system should coordinate closely with other governmental and nongovernmental programs to ensure that information technology is interoperable, that quality measurement relies on high-quality, risk-adjusted data, and to guard against new and special systems that apply to only one program or may only be workable for one type of specialty or only certain types of diseases and conditions. ObGyns often see relatively few Medicare patients, and unique Medicare requirements can pose significant administrative challenges and inefficiencies to ObGyn participation.
• Congress should encourage, and remove barriers to, ObGyn and physician development of ACOs, medical homes for women, and other innovative models. Proposed rules on the Medicare Shared Savings Program allowing for expedited antitrust review should be extended to ACOs and other physician-led models of care that do not participate in the Medicare Shared Savings Program. These models should also recognize the dual role ObGyns may play, as both primary and specialty care providers.
• Congress should repeal the Independent Medicare Payment Advisory Board. Leaving Medicare payment decisions in the hands of an unelected, unaccountable body with minimal congressional oversight is bad for all physicians and for our patients.

The outlook for private practice, in any specialty, has dimmed. Says ACOG’s Lucia DiVenere: “Median expenses for private practices have been steadily rising in relationship to revenues—from 52% in 1990 to 71% in 2002—making it difficult for practices to remain solvent.”

Is private practice doomed?

OBG Management: In your opinion, over the long term, is health reform a positive or a negative for ObGyns in private practice?

Ms. DiVenere: On balance, I believe that the health reform law is a positive for our patients, and that fact may lead to an eventual positive for its Fellows, ACOG hopes. What it may mean for ObGyns in private practice, though, is more troubling.

The law has many intended purposes: 1) cover the uninsured, 2) tilt our health-care system toward primary care and use of nonphysician providers, and 3) push practices toward integration with hospitals and health systems and other paths to physician employment. Support for continuation or growth in any type of physician private practice is hard to find in the ACA.

OBG Management: What changes are in the pipeline?

Ms. DiVenere: Under the ACA, by 2013, the Secretary of HHS, with input from stakeholders, will set up a Physician Compare Web site, modeled after the program that exists for hospitals, using data from the Physician Quality Reporting Initiative (PQRI). Data on this site would be made public on January 1, 2013, comparing physicians in terms of quality of care and patient experience.

By law, these data are intended to be statistically valid and risk-adjusted; each physician must have time to review his or her information before it becomes publicly available; data must ensure appropriate attribution of care when multiple providers are involved; and the Secretary of HHS must give physicians timely performance feedback.

Data elements—to the extent that scientifically sound measures exist—will include:

• quality, patient satisfaction, and health outcomes information on Medicare physicians
• physician care coordination and risk-adjusted resource use
• safety, effectiveness, and timeliness of care.

Physicians who successfully interact with this program will likely be those who have a robust EHR system.

If this and other elements of the Affordable Care Act become real, however, we’ll likely see a fundamental shift in the kinds of settings in which ObGyns and other physicians opt to practice.

We want to hear from you! Tell us what you think.

In the 18 months since the Patient Protection and Affordable Care Act—otherwise known as ACA, or health-care reform—was signed into law by President Barack Obama, the outlook for private practice, in any specialty, has dimmed. As a recent report on the ramifications of the ACA put it:

The imperative to care for more patients, to provide higher perceived quality, at less cost, with increased reporting and tracking demands, in an environment of high potential liability and problematic reimbursement, will put additional stress on physicians, particularly those in private practice.¹

To explore the impact of these stresses on ObGyns specifically, the editors of OBG Management invited Lucia DiVenere, Senior Director of Government Affairs for the American Congress of Obstetricians and Gynecologists (ACOG), to talk about the outlook for private practice in the coming years. In the exchange, Ms. DiVenere discusses the short- and long-term effects of the ACA, the ways in which ObGyn practice is (or is not) evolving, the challenge of making the switch to electronic health records (EHRs), the reasons ACOG opposed the ACA, and other issues related to the current practice environment. In addition, two ObGyns in private practice describe the many challenges they face (see “The view from private practice,” pages 44 and 52).

What nonlegislative forces have affected private practice?

OBG Management: A recent report on the ramifications of the ACA argues that formal reform was inevitable. It also asserts that private practice was subject to many negative pressures long before health-care reform was passed.¹ Do you agree?

Ms. DiVenere: Our nation’s health-care system is always evolving, and over the past decade, we’ve seen a clear trend toward system integration—that is, larger, physician-led group practices and hospital employment of physicians.

Looking at physicians as a whole, the percentage who practice solo or in two-physician practices fell from 40.7% in 1996–97 to 32.5% by 2004–05, according to a 2007 survey.² And the American Medical Association (AMA) reported that the percentage of physicians “with an ownership stake in their practice declined from 61.6% to 54.4% as more physicians opted for employment. Both the trends away from solo and two-physician practices and toward employment were more pronounced for specialists and older physicians.”²

OBG Management: What has the trend been for ObGyns, specifically?

Ms. DiVenere: The ObGyn specialty employs the group practice model—health care delivered by three or more physicians—more frequently than other specialties do, largely because of the support it provides for 24–7 OB call schedules.

As for private practice, ObGyns have been moving away from it for 10 years or longer. Data from a 1991 ACOG survey shows that 77% of respondents were in private practice; by 2003, that percentage had fallen to 70%.³ In 2003, ObGyns in private practice tended to be older (median age: 47 years) than their salaried colleagues (median: 42 years) and were more likely to be male (87% vs 77%).³ The demographic change toward women ObGyns may add to this trend line.

OBG Management: What economic forces have shaped practice paradigms in ObGyn?

Ms. DiVenere: Median expenses for private practices have been steadily rising in relation to revenues—from 52% in 1990 to 71% in 2002—making it difficult for practices to remain solvent.⁴ In addition, a 2011 survey from Medscape reveals that ObGyns in solo practice earn $15,000 to $25,000 less annually than their employed colleagues.⁵

ObGyns who have made the switch from private to hospital practice, or who have become ObGyn hospitalists, often point to the difficulties of maintaining a solvent private practice, especially given the push toward electronic health records (EHRs) and increasing regulatory and administrative burdens. These and other issues contribute to rising practice costs and increasing demands on an ObGyn’s time and attention.

What are the short-term effects of formal reform?

OBG Management: What effect has health-care reform had so far?

Ms. DiVenere: In 2010, twice as many physician practices were bought by hospitals and health systems as in 2009. We can’t conclude that the 2010 law is responsible for these changes, but we know that the architects of health reform were aware of this trend, believed it was beneficial, and looked for ways to encourage it, including through development of accountable care organizations (ACOs), which give hospitals a new and potentially lucrative reason to purchase private practices.

OBG Management: What exactly is an ACO?

Ms. DiVenere: An ACO consists of aligned providers—most likely, large multispecialty groups, often affiliated with the same hospital—who agree to manage patients for a set fee, sharing the risk and potential profit. ACOs are required to have shared governance, which gives them the authority to impose standards for practice, reporting, and compensation—including rewards and penalties—across a group of physicians.

Each ACO must sign a 3-year contract with the US Department of Health and Human Services (HHS) and include a sufficient number of primary care professionals to care for at least 5,000 beneficiaries. ACOs will be evaluated by quality-performance measures to be determined by the Secretary of HHS.

What aspects of ACA will have the biggest impact?

OBG Management: What provision of the new law will have the most direct impact on ObGyns in private practice?

Ms. DiVenere: All ObGyns may benefit from the guarantee of insurance coverage for our patients for maternity and preventive care. And all ObGyns should join ACOG’s fight to repeal the Independent Payment Advisory Board, which may hold enormous power to cut physician reimbursement.

Here’s the quote all ObGyns—especially those in private practice—should read, from an article written by President Obama’s health-reform deputies:

To realize the full benefits of the Affordable Care Act, physicians will need to embrace rather than resist change. The economic forces put in motion by the Act are likely to lead to vertical organization of providers and accelerate physician employment by hospitals and aggregation into larger physician groups. The most successful physicians will be those who most effectively collaborate with other providers to improve outcomes, care productivity, and patient experience.⁶

OBG Management: Do these health-reform deputies offer any concrete vision of how this change will be achieved?

Ms. DiVenere: They detail what physicians need to do, and how they should change the way they practice, under the Act. For example, to meet the increasing demand for health care, they recommend that practices:

• “Redesign care to include a team of nonphysician providers, such as nurse practitioners, physician assistants, care coordinators, and dieticians”
• “Develop approaches to engage and monitor patients outside of the office.”⁶

And to meet the requirements for payment reform, information transparency, and quality, they suggest that practices:

• “Focus care around exceptional patient experience and shared clinical outcome goals”
• “Engage in shared decision-making discussions regarding treatment goals and approaches”
• “Proactively manage preventive care”
• “Establish teams to take part in bundled payments and incentive programs”
• “Expand use of electronic health records”
• “Collaborate with hospitals to dramatically reduce readmissions and hospital-acquired infections”
• “Incorporate patient-centered outcomes research to tailor care.”⁶

To capture value, the authors recommend that practices “redesign medical office processes to capture savings from administrative simplification.”⁶

OBG Management: Do they propose any method for implementing these changes?

Ms. DiVenere: The White House is hoping that ACOs can lead. Medicare ACOs will attempt to accomplish these changes by managing hospital and physician services, prompting physicians and hospitals to change how they are both clinically organized and paid for services—this change, in particular, is considered by some to be essential to improving the quality and efficiency of health care.

The new Centers for Medicaid and Medicare Services (CMS) Innovation Center, created by the ACA, is given broad authority to test, evaluate, and adopt systems that foster patient-centered care, improve quality, and contain the costs of Medicare, Medicaid, and the Children’s Health Insurance Program (CHIP). The law specifically guides the Innovation Center to look for ways to encourage physicians to transition from fee-for-service to salary-based payment.

We can safely assume that the experts behind these provisions believe that large, hospital-centered systems or large, physician-led groups can better serve the needs of patients and our health-care system in general than can small private practices. Today, 24% of ObGyns run solo practices, and 27% are in single-specialty practices. Health-care reform can mean big changes for them.

Is the EHR a realistic goal for private practices?

OBG Management: How does the push for EHRs affect physicians in private practice?

Ms. DiVenere: Very profoundly. From the point of view of an ObGyn in private practice, EHRs offer a number of benefits. They can:

• help make sense of our increasingly fragmented health-care system
• improve patient safety
• increase efficiency
• reduce paperwork.

In addition, insurers may save by reducing unnecessary tests, and patients can certainly benefit from better coordination and documentation of care. These advantages don’t necessarily translate into savings or revenue for physician practices, however. Many ObGyns—especially those in solo or small practices—don’t feel confident making such a large capital investment. In fact, only about one third of ObGyn practices have an EHR.

OBG Management: Is it primarily cost that deters ObGyns from adopting EHRs?

Ms. DiVenere: That, and the fact that EHR systems are not yet fully interoperable across small practices, insurers, and government agencies. The initial cost of purchasing an EHR system for a small practice is about $50,000 per physician, and there are ongoing costs in staff training and hardware and software updates. A steep learning curve means fewer patients can be seen in an hour. It can take a practice months—even years—for physicians to return to their previous level of productivity. That’s a lot to ask a busy practicing physician to take on.

OBG Management: Is there any way around the push for EHRs?

Ms. DiVenere: Congress wants to move us to full adoption of health information technology (HIT). Under health-care reform, beginning in 2013, all health insurance plans must comply with a uniform standard for electronic transactions, including eligibility verification and health claim status.

In 2014, uniform standards must:

• allow automatic reconciliation of electronic funds transfers and HIPAA payment and remittance
• use standardized and consistent methods of health plan enrollment and editing of claims
• use unique health plan identifiers to simplify and improve routing of health-care transactions
• use standardized claims attachments
• improve practice data collection and evaluation.

Uniformity and standardization can help address one of the major roadblocks to physician adoption of HIT. Still, it’s little wonder that median expenses for private practices have been steadily rising in relation to revenues.

Is there a physician shortage in ObGyn?

OBG Management: There has been a lot of attention focused on the shortage of physicians in this country. How severe is the shortage likely to be in the specialty of ObGyn?

Ms. DiVenere: William F. Rayburn, MD, MBA, from the University of New Mexico Health Sciences Center and School of Medicine in Albuquerque, has provided ACOG with important work on this topic. Dr. Rayburn is Randolph V. Seligman Professor and Chair in the Department of Obstetrics and Gynecology at that institution. His report⁷ shows that the gap between the supply of ObGyns and the demand for women’s health care is widening.

Data from this report point to a shortage of 9,000 to 14,000 ObGyns in 20 years. After 2030, the ObGyn shortage may be even more pronounced, as the population of women is projected to increase 36% by 2050, while the number of ObGyns remains constant.

OBG Management: Would the incorporation of more midlevel providers—that is, nurse midwives, physician assistants, and others—ease some of the strains on the ObGyn workforce in general and on private practice specifically?

Ms. DiVenere: That’s very possible and is one of the reasons ACOG encourages greater use of collaborative care. It’s certainly true that the ObGyn specialty is historically comfortable with collaboration.

In 2008, the average ObGyn practice employed 2.6 nonphysician clinicians, certified nurse midwives (CNMs), physician assistants, or nurse practitioners. ACOG strongly supports collaborative practice between ObGyns and qualified midwives (CNMs, certified midwives) and other nonphysician clinicians.

In a recent issue of Obstetrics & Gynecology, ACOG’s Immediate Past President Richard N. Waldman, MD, and Holly Powell Kennedy, CNM, PhD, president of the American College of Nurse Midwives, wrote about the importance of collaborative practice, which can “increase efficiency, improve clinical outcomes, and enhance provider satisfaction.”⁸ The September 2011 issue of Obstetrics & Gynecology highlights four real-life stories of successful collaborative practice.

Because of our commitment to the benefits of collaborative practice, ACOG supported a provision in the ACA that increases payment for CNMs. Beginning this year, the Medicare program will reimburse CNMs at 100% of the physician payment rate for the same services. Before this law, CNMs were paid at 65% of a physician’s rate for the same services. ACOG’s leadership believes that better reimbursement for CNMs will help ObGyn practices and improve care.

Although ACOG supported that provision in the law, we did not support passage of the ACA. ACOG’s Executive Board carefully considered all elements of the bill and decided that, although it included many provisions that are helpful to our patients, it also included many harmful provisions for our members. We felt that the promise of the women’s health provisions could be realized only if the legislation worked for practicing physicians, too.

Why wasn’t the SGR formula abolished?

OBG Management: What is the effect, for physicians in general and ObGyns in private practice specifically, of the failure to fix the sustainable growth rate (SGR) formula and implement liability reform in the ACA?

Ms. DiVenere: The fact that we have no fix for SGR and no medical liability reform is a disgrace. And the absence of solutions to these two issues is one of the main reasons ACOG decided not to support passage of the ACA. Our Executive Board was very clear in telling Congress that we can’t build a reformed health-care system on broken payment and liability systems—it just won’t work.

ObGyns themselves are the first to point out this fact. ObGyns listed medical liability (65.3%) and financial viability of their practice (44.3%) as their top two professional concerns in a 2008 ACOG survey.⁹

For all ObGyns, these two continuing problems make practice more difficult every day—problems felt most acutely by ObGyns in private practice. Employed physicians often come under a hospital’s or health system’s liability policy and often don’t pay their own premiums. Employed physicians usually are on salary, sheltering them from the vagaries of Congressional action, or inaction, on looming double-digit Medicare physician payment cuts under the SGR.

Some legislators, and some ObGyns, think Medicare doesn’t apply to us. But today, 92% of ObGyns participate in the Medicare program and 63% accept all Medicare patients. This fact reflects ObGyn training and commitment to serve as lifelong principal-care physicians for women, including women who have disabilities. Fifty-six percent of all Medicare beneficiaries are women. With the Baby Boomer generation transitioning to Medicare, and with shortages in primary care physicians, it is likely that ObGyns will become more involved in delivering health care for this population.

Medicare physician payments matter to ObGyns beyond the Medicare program, too, as Tricare and private payers often follow Medicare payment and coverage policies. As a specialty, we have much at stake in ensuring a stable Medicare system for years to come, starting with an improved physician payment system. [Editor’s note: See Dr. Robert L. Barbieri’s editorial on the subject.]

OBG Management: What is ACOG doing to improve this system?

Ms. DiVenere: ACOG is urging the US Congress to ensure that a better system adheres to the following priniciples:

• Medicare payments should fairly and accurately reflect the cost of care. In the final 2011 Medicare physician fee schedule, CMS is proposing to reduce the physician work value for ObGyn care to women by 11% below what is paid to other physicians for similar men’s services—exactly the opposite of what should be done to encourage good care coordination, and in direct contradiction to recommendations by the Resource-Based Relative Value Scale Update Committee (RUC). Medicare payments to obstetricians are already well below the cost of maternity care; no further cuts should be allowed for this care.
• A new payment system should be as simple, coordinated, and transparent as possible and recognize that there is no one-size-fits-all model. A new Medicare system should coordinate closely with other governmental and nongovernmental programs to ensure that information technology is interoperable, that quality measurement relies on high-quality, risk-adjusted data, and to guard against new and special systems that apply to only one program or may only be workable for one type of specialty or only certain types of diseases and conditions. ObGyns often see relatively few Medicare patients, and unique Medicare requirements can pose significant administrative challenges and inefficiencies to ObGyn participation.
• Congress should encourage, and remove barriers to, ObGyn and physician development of ACOs, medical homes for women, and other innovative models. Proposed rules on the Medicare Shared Savings Program allowing for expedited antitrust review should be extended to ACOs and other physician-led models of care that do not participate in the Medicare Shared Savings Program. These models should also recognize the dual role ObGyns may play, as both primary and specialty care providers.
• Congress should repeal the Independent Medicare Payment Advisory Board. Leaving Medicare payment decisions in the hands of an unelected, unaccountable body with minimal congressional oversight is bad for all physicians and for our patients.

The outlook for private practice, in any specialty, has dimmed. Says ACOG’s Lucia DiVenere: “Median expenses for private practices have been steadily rising in relationship to revenues—from 52% in 1990 to 71% in 2002—making it difficult for practices to remain solvent.”

Is private practice doomed?

OBG Management: In your opinion, over the long term, is health reform a positive or a negative for ObGyns in private practice?

Ms. DiVenere: On balance, I believe that the health reform law is a positive for our patients, and that fact may lead to an eventual positive for its Fellows, ACOG hopes. What it may mean for ObGyns in private practice, though, is more troubling.

The law has many intended purposes: 1) cover the uninsured, 2) tilt our health-care system toward primary care and use of nonphysician providers, and 3) push practices toward integration with hospitals and health systems and other paths to physician employment. Support for continuation or growth in any type of physician private practice is hard to find in the ACA.

OBG Management: What changes are in the pipeline?

Ms. DiVenere: Under the ACA, by 2013, the Secretary of HHS, with input from stakeholders, will set up a Physician Compare Web site, modeled after the program that exists for hospitals, using data from the Physician Quality Reporting Initiative (PQRI). Data on this site would be made public on January 1, 2013, comparing physicians in terms of quality of care and patient experience.

By law, these data are intended to be statistically valid and risk-adjusted; each physician must have time to review his or her information before it becomes publicly available; data must ensure appropriate attribution of care when multiple providers are involved; and the Secretary of HHS must give physicians timely performance feedback.

Data elements—to the extent that scientifically sound measures exist—will include:

• quality, patient satisfaction, and health outcomes information on Medicare physicians
• physician care coordination and risk-adjusted resource use
• safety, effectiveness, and timeliness of care.

Physicians who successfully interact with this program will likely be those who have a robust EHR system.

If this and other elements of the Affordable Care Act become real, however, we’ll likely see a fundamental shift in the kinds of settings in which ObGyns and other physicians opt to practice.

We want to hear from you! Tell us what you think.

Erectile dysfunction (ED) is defined as the recurrent inability, of three months’ duration or longer, to attain or maintain an erection sufficient for satisfactory sexual performance.^1,2 It is classified as either psychogenic or organic; organic ED will be addressed here. Up to 80% of cases of organic ED can be further categorized into vascular, neurogenic, anatomic, or hormonal subtypes,^2,3 with many affected patients vulnerable to potentially serious comorbidities and risk factors.

In the early 1990s, the NIH reported that nearly 30 million US men were affected by ED.² However, increased public awareness of the condition, beginning with the availability of effective oral medications in the late 1990s, may have led to increased numbers of reported cases—and of men seeking treatment.

COMMON CONDITION, COMMONLY UNTREATED

According to results from the 2001-2002 National Health and Nutrition Examination Survey,^4,5 ED affects about 8% of US men: 4% of those in their 50s, 17% of those in their 60s, 47% of men older than 65, and 78% of men 75 or older. More than 27,000 men from Europe and North and South America (ages 20 to 75) were interviewed for the 2004 Men’s Attitudes to Life Events and Sexuality (MALES) study; findings included an overall prevalence for ED of 16%, and 22% among men from the United States.⁶ See information regarding self-reported ED prevalence in Table 1.⁷

An important finding from the MALES study was that only 58% of respondents with self-reported ED had sought medical treatment for the condition.⁶ Some men may be reluctant to broach the subject with a health care provider because they consider ED a purely sexual problem—whereas the etiology is most commonly vascular.⁸ Thus, it is important for health care providers to include the sexual history as a routine component in the wellness exam for all patients, and to be aware of the potential presentation in patients with organic ED, appropriate work-up, and physical examination.

Additionally, ED can be a wake-up call for men at risk for cardiovascular disease (CVD); ED occurs at a mean time of five years before a cardiovascular event.⁹ Therefore, in addition to counseling patients with ED regarding treatment and prevention strategies, clinicians should be prepared to identify and address the risk factors and medical comorbidities associated with ED.

The Mechanisms of Erection

When sexual stimulation occurs, parasympathetic activity increases production of the nucleotide cyclic guanosine monophosphate (cGMP), resulting in relaxation of cavernosal smooth muscle and an influx of blood into the penis. This filling action produces expansion of the sinusoidal spaces in the penis, compressing venous channels and thereby preventing outflow of blood to allow maintenance of a rigid erection.^10,11

Nitric oxide is needed for vasodilation of the corpora cavernosa. Inhibition of the enzyme phosphodiesterase type 5 (PDE-5) allows increased production and accumulation of penile cGMP. This results in relaxation of the smooth-muscle cells and improved erectile function.^1,10,11

PRESENTATION, HISTORY, AND TYPES OF ORGANIC ED

In the primary care setting, the opportunity to assess for and address erectile function generally presents itself at the patient’s annual wellness visit—but could easily go unmentioned if the health care provider does not initiate the discussion. Direct questioning during the review of systems may ease any anxiety for the patient and open up a dialogue regarding other problems or medical conditions. (See box, “How and What To Ask,”¹²)

Providers can also assess the patient’s risk factors for ED and its associated comorbid conditions (see Table 2^1,13,14). The patient’s medical history may hold important clues to a diagnosis of organic ED.

Because certain vasculopathies, including diabetes, are known to accelerate the process of endothelial dysfunction, inquiries should be made into the sexual history of men with these disorders, regardless of age.¹⁰ Marked hyperlipidemia, uncontrolled hypertension, atherosclerosis, and other manifestations of CVD can impair erectile as well as endothelial function, leading to vascular ED.

The potential for atherosclerosis in the penile arteries (which are significantly narrower than the carotid, coronary, or femoral arteries) should prompt the primary care provider to evaluate the patient’s risk for vascular disease and its sequelae in the heart as well.⁸ (Of note, in one study of metabolic syndrome and ED, ED was found to be a predictor for impaired elasticity in the large arteries, independent of cardiovascular risk factors.¹⁵) In addition to damaging the small blood vessels and the endothelium, diabetes and other components of the metabolic syndrome contribute to ED by affecting cavernous nerve terminals and smooth muscle.^1,14

Lifestyle factors, such as overconsumption of alcohol, smoking, recreational drug use, obesity, and inactivity can contribute to decreased libido and ED.¹⁴ Cigarette smoking can cause vasoconstriction and penile venous leak, resulting in poor erectile quality or even loss of erection. While small amounts of alcohol can improve libido and erection due to its anti-anxiety and vasodilatory effects, “more is not better” in this case, as higher doses result in sedation and decreased libido. Chronic alcoholism results in hypogonadism and polyneuropathy.¹⁶

Neurogenic ED can result from abnormalities at the level of the brain, the spinal cord, or the pelvis. Previous pelvic surgery, such as prostatectomy or colectomy, can disrupt the cavernous or pudendal nerves. Spinal cord injury, Parkinson’s disease, multiple sclerosis, diabetes with peripheral neuropathy, or a history of trauma can all result in neurogenic ED.¹⁶

Additionally, there is evidence of perineal compression from frequent bicycle riding leading to vascular, endothelial, and neurogenic dysfunction in men, with increased incidence of ED.¹⁷

Age alone is a risk factor for ED,^7,18 as sexual function declines even in healthy men as they age. Penile sensitivity decreases, and there is increased latency between sexual stimulation and resulting erection, as well as between ejaculations. Ejaculations are less forceful, with less ejaculatory volume.¹⁶ Other factors that may affect the degree of ED include a history of stroke or pelvic surgery, especially in high-risk cardiac patients.¹⁹

Though not the focus of this article, the potential for psychogenic ED should be mentioned, as it warrants screening with a complete psychosocial history to rule out this etiology. The interview should allow time for the patient to discuss current or past relationship difficulties, marital conflict, life stressors, depression, and anxiety. Whatever the etiology of ED, the primary care provider should always elicit a sexual history, including number of sexual partners, current relationship status (ie, committed or casual), and incidence of ED with specific partners.²⁰ The effects of ED on these relationships should be discussed.

A medication history is important for the ED workup. Antidepressants, especially the SSRIs, and certain hypertensives can affect the libido, arousal, and orgasm.²¹ See Table 3^1,13,22 for commonly used agents that can affect erectile function and sexual satisfaction.

Previous Medical History

The patient should be asked whether he has had any previous testing or treatment for ED. Was any therapy used effective? Did he experience any adverse effects during treatment? If treatment results were unsatisfactory, he should be questioned to ensure that he was using treatment correctly. Commonly, patients do not understand that sexual stimulation is necessary to achieve an erection when they are being treated with an oral PDE-5 inhibitor.²³

PHYSICAL EXAMINATION

The clinician who performs the physical examination should take into account the psychogenic, neurogenic, and vasculogenic causes of ED. The genitourinary examination alone is not sufficient; abdominal, vascular, and neurologic exams must be included. The patient should be assessed for body habitus, secondary sex characteristics (including ruling out gynecomastia), and lower extremity pulses.²²

The genitourinary exam should include testicular, rectal, and penile examination to rule out physical abnormalities. Small testicles (< 5 mL) or testicular atrophy on palpation should lead the examiner to consider testosterone testing^24,25 (see “Diagnostic Testing,” below). A digital rectal examination may reveal an enlarged prostate (this finding, in the presence of lower urinary tract symptoms, has been associated with ED²⁶). Palpation of the penis for plaques and questioning about pain with erection or deviation of the erect penis can lead to a diagnosis of Peyronie’s disease²⁷; if this is the case, the patient can be referred to urology for treatment.

The vascular system should be assessed by listening for abdominal or femoral bruits and the lower extremities checked for appropriate hair growth, skin color, and distal pulses. The examiner should note any scars indicating a history of bypass surgery, which may have been overlooked during the surgical history.

DIAGNOSTIC TESTING

A fasting glucose level and a lipid profile should be routinely obtained because of the links between ED and diabetes and CVD.^28,29 A chemistry panel and complete blood count, if one has not been performed recently, can be used to assess the patient’s general health, with a thyroid-stimulating hormone (TSH) level tested in men who report fatigue or weakness.

Men who are older than 50 should be considered for prostate-specific antigen (PSA) testing. Testosterone levels (free and total) are generally reserved for patients with small or atrophic testicles²⁵ or for those who report decreased libido with fatigue or other symptoms of hypogonadism, including depression and decreased muscle strength, muscle mass, or vitality.^22,24,25,30 If testosterone levels are ordered, the patient should be counseled to have samples drawn in the early morning to avoid the influence of daily hormonal fluctuations. In patients found to have low testosterone levels (ie, < 300 ng/dL,¹³ occurring in 12.5% to 35% of men with ED²⁴), prolactin testing may be considered next; in patients with ED, hypoprolactinemia is associated with dyslipidemia, metabolic syndrome, and other risk factors for cardiovascular events.^29,31,32

Imaging Studies

A number of imaging studies, once frequently used in evaluation for ED, are considered outdated and are no longer performed. However, Doppler blood flow analysis or ultrasonographic penile blood flow studies can be useful for identifying and evaluating the specific causes of vasculogenic ED, including arterial insufficiency and veno-occlusive disease.^33,34 Other conditions associated with ED, such as Peyronie’s disease and priapism, can also be identified through these modalities.³³

TREATMENT

The PDE-5 Inhibitors

While historically not the first treatment available for ED, medical therapy is certainly the most popular option for men with ED. The oral PDE-5 inhibitors first became available in the 1990s. All three such agents currently available in the US—silden­afil, tadalafil, and vardenafil—have been demonstrated effective in improving and maintaining erections,^35-38 but their pharmacokinetics differ,³⁹ and few head-to-head studies have been conducted that demonstrate greater efficacy of one agent over another.^39,40 It has been suggested that patients try all three medications to determine preference and satisfaction.³⁹

Qaseem et al²⁴ report that PDE-5 inhibitors demonstrated clinical benefit regardless of baseline severity of dysfunction or ED cause, including diabetes and depression. These medications require sexual stimulation to be effective and typically are effective about one hour after dosing.²³ Tadalafil is remarkable for the length of its half-life, which makes it appropriate at 2.5- or 5.0-mg doses for once-daily dosing⁴¹; it is also noted for a relatively low incidence of associated flushing,⁴² but back pain is more common among tadalafil users than among men using sildenafil or vardenafil.^11,39,43

In addition to back pain and myalgia, the most common adverse effects associated with PDE-5 inhibitor use are dyspepsia, flushing, headache, and nasal congestion.⁴² Because absorption of sildenafil is reduced by food intake, and vardenafil⁴⁴ to a lesser extent, these agents are best avoided in close proximity to meals. Absorption of tadalafil is not affected by food.⁴⁵ Higher doses of sildenafil and vardenafil were associated with greater benefit in treating ED.^24,46

Note: All three PDE-5 inhibitors are contraindicated in men taking long-acting nitrates or nitroglycerin.²⁴ Their effectiveness may be potentiated by use of erythromycin, ketoconazole, and HIV protease inhibitors.³⁹ Information about dosing options and adverse effects can be found in Table 4¹¹.

Testosterone

Hypogonadism, though found in only 5% of men with ED,⁴⁷ may be an indication for testosterone replacement therapy, and testosterone use has been found to improve libido in men with sexual dysfunction.⁴⁸ However, the authors of the American College of Physicians clinical practice guidelines²⁴ found insufficient evidence that testosterone replacement improved erections or quality of sexual intercourse. There was also insufficient evidence that testosterone plus sildenafil was more effective than sildenafil alone.^24,49,50

Additional Pharmacologic Considerations

A careful review of the medication history for the patient with ED may lead the astute clinician to consider whether a change in current prescriptions might improve the man’s sexual function. Among the commonly used agents listed in Table 3, those with the greatest apparent impact on erections are thiazide diuretics and β-blockers, SSRIs, and tricyclic antidepressants.^1,4

For a man who is interested in preserving potency, the clinician should select medications with the least effect on erectile function—for instance, an ACE inhibitor¹ rather than a thiazide or β-blocker for the patient with hypertension. In the patient affected by depression, a trial of bupropion, substituted for or added to his current antidepressant, may be helpful.⁵¹ Medical therapies for hyperglycemia, hyperlipidemia, and hypertension should be considered if warranted, as should cardiovascular screening with exercise stress testing. (See box, “ED, CAD, and PDE-5 Inhibitors”⁵²)

Alternative and Nonpharmacologic Options

A number of herbal products have been touted to improve sexual function. The FDA⁵³ has issued press releases warning consumers about these and other alternatives to prescription medications. According to the FDA, many “sexual enhancement” products have been found to contain active ingredients resembling those found in one or more PDE-5 inhibitors. These products are in violation of federal law, and consumers are advised to avoid supplements that claim to produce effects similar to those of prescription drugs.⁵³

By contrast, one potentially beneficial supplement currently under study is L-citrulline. As the body converts oral L-citrulline to L-arginine, vasodilation and endothelial function improve, often leading to resolution of mild ED. In a small, single-blind placebo-controlled study, patients who took L-citrulline (1.5 g/d in divided doses) reported improvement in hardness scale grading and increased satisfaction regarding sexual function. No adverse effects were reported, making L-citrulline a possible option for patients who hesitate to use a PDE-5 inhibitor.⁵⁴

For patients with lack of response or contraindications to accepted medical therapy, other options include alprostadil intraurethral suppositories, penile prosthetic implants, vacuum erection devices, vascular surgery, yohimbine and other herbal therapies, and trazodone.^1,14,55-59 These methods may require detailed counseling. Primary care providers who are unfamiliar with these modalities or reluctant to introduce them may wish to refer patients to urology.

PATIENT EDUCATION

Aggressive reduction in cardiovascular risks with smoking cessation, weight loss, and physical activity should be encouraged. In a study of obese men with ED (but without diabetes, hypertension, or hyperlipidemia), Esposito et al⁶⁰ found that reducing caloric intake and increasing physical activity was associated with improved sexual function in about one-third of the subjects. Bicycle riders can decrease risks of perineal compression with newer seat designs.¹⁷

Smoking cessation alone has been shown to improve erectile function at one-year follow-up in at least 25% of men who stopped smoking, compared with none of the men who continued to smoke.⁶¹ Patients can help preserve endothelial function with efforts to maintain normal blood pressure and glycemic control.

Researchers are currently looking at occupational exposures as a cause of ED. Exposure to plastics containing bisphenol-A, for example, has been linked to decreased libido.⁶²

CONCLUSION

In addition to addressing erectile dysfunction as a sexual problem, the health care provider should recognize its association with CVD, diabetes, depression, and other serious illnesses. However, it is also important to open a dialogue about sexual function to encourage the patient to discuss the problem of ED. Timely diagnosis and treatment of these conditions may be of even greater benefit to the patient than the effective therapies available for ED itself.  

REFERENCES

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2. NIH Consensus Conference. Impotence: NIH Consensus Development Panel on Impotence. JAMA. 1993;270(1):83-90.

3. Hafez ES, Hafez SD. Erectile dysfunction: anatomical parameters, etiology, diagnosis, and therapy. Arch Androl. 2005;51(1):15-31.

4. Francis ME, Kusek JW, Nyberg LM, Eggers PW. The contribution of common medical conditions and drug exposures to erectile dysfunction in adult males. J Urol. 2007;178(2):591-596.

5. Saigal CS, Wessells H, Pace J, et al. Predictors and prevalence of erectile dysfunction in a racially diverse population. Arch Intern Med. 2006;166 (2):207-212.

6. Rosen RC, Fisher WA, Eardley I, et al. The multinational Men’s Attitudes to Life Events and Sexuality (MALES) study. I. Prevalence of erectile dysfunction and related health concerns in the general population. Curr Med Res Opin. 2004;20 (5):607-617.

7. Lindau ST, Schumm LP, Laumann EO, et al. A study of sexuality and health among older adults in the United States. N Engl J Med. 2007;357(8): 762-774.

8. Batty GD, Li Q, Czernichow S, et al. Erectile dysfunction and later cardiovascular disease in men with type 2 diabetes: prospective cohort study based on the ADVANCE (Action in Diabetes and Vascular Disease: Preterax and Diamicron Modified-Release Controlled Evaluation) trial. J Am Coll Cardiol. 2010;56(23): 1908-1913.

9. Hodges LD, Kirby M, Solanki J, et al. The temporal relationship between erectile dysfunction and cardiovascular disease. Int J Clin Pract. 2007; 61(12):2019-2025.

10. Miner MM, Kuritzky L. Erectile dysfunction: a sentinel marker for cardiovascular disease in primary care. Cleve Clin J Med. 2007;74 suppl 3: S30-S37.

11. McCullough AR. An update on the PDE-5 inhibitors (PDE-5i). J Androl. 2003;24(6 suppl): S52-S58.

12. Rosen RC, Cappelleri JC, Smith MD, et al. Development and evaluation of an abridged, 5-item version of the International Index of Erectile Function (IIEF-5) as a diagnostic tool for erectile dysfunction. Int J Impot Res. 1999;11(6):
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13. Heidelbaugh JJ. Management of erectile dysfunction. Am Fam Physician. 2010;81(3):305-312.

14. Montague DK, Jarow JP, Broderick GA, et al; Erectile Dysfunction Guideline Update Panel. AUA guideline on the management of erectile dysfunction: an update (2006). American Urological Association Education and Research, Inc. www.auanet.org/content/guidelines-and-quality- care/clinical-guidelines.cfm?sub=ed. Accessed August 8, 2011.

15. Pohjantahti-Maaroos H, Palomäki A. Comparison of metabolic syndrome subjects with and without erectile dysfunction: levels of circulating oxidised LDL and arterial elasticity. Int J Clin Pract. 2011;65(3):274-280.

16. Lue TF. Male sexual dysfunction. In: Tanagho EA, McAninch JW, eds. Smith’s General Urology. 16th ed. San Francisco, CA: McGraw-Hill; 2004: 592-596.

17. Sommer F, Goldstein I, Korda JB. Bicycle riding and erectile dysfunction: a review. J Sex Med. 2010;7(7):2346-2358.

18. Feldman HA, Johannes CB, Derby CA, et al. Erectile dysfunction and coronary risk factors: prospective results from the Massachusetts male aging study. Prev Med. 2000;30(4):328-338.

19. Böhm M, Baumhäkel M, Probstfield JL, et al. Sexual function, satisfaction, and association of erectile dysfunction with cardiovascular disease and risk factors in cardiovascular high-risk patients: substudy of the ONgoing Telmisartan Alone and in Combination with Ramipril Global Endpoint Trial/Telmisartan Randomized AssessmeNT Study in ACE-INtolerant Subjects with Cardiovascular Disease (ONTARGET/TRANSCEND). Am Heart J. 2007;154(1):94-101.

20. Athanasiadis L, Papaharitou S, Salpiggidis G, et al. Educating physicians to treat erectile dysfunction patients: development and evaluation of a course on communication and management strategies. J Sex Med. 2006;3(1):47-55.

21. Kennedy SH, Rizvi S. Sexual dysfunction, depression, and the impact of antidepressants.
J Clin Psychopharmacol. 2009;29(2):157-164.

22. Diaz VA Jr, Close JD. Male sexual dysfunction. Prim Care. 2010;37(3):473-489, vii-viii.

23. Carson CC, Lue TF. Phosphodiesterase type 5 inhibitors for erectile dysfunction. BJU Int. 2005; 96(3):257-280.

24. Qaseem A, Snow V, Denberg TD, et al. Hormonal testing and pharmacologic treatment of erectile dysfunction: a clinical practice guideline from the American College of Physicians. Ann Intern Med. 2009;151(9):630-649.

25. Dandona P, Rosenberg MT. A practical guide to male hypogonadism in the primary care setting. Int J Clin Pract. 2010;64(6):682-696.

26. Paick SH, Meehan A, Lee M, et al. The relationship among lower urinary tract symptoms, prostate specific antigen and erectile dysfunction in men with benign prostatic hyperplasia: results from the Proscar Long-Term Efficacy and Safety Study. J Urol. 2005;173(3):903-907.

27. Smith JF, Walsh TJ, Lue TF. Peyronie’s disease: a critical appraisal of current diagnosis and treatment. Int J Impot Res. 2008;20(5):445-459.

28. Gazzaruso C, Coppola A, Giustina A. Erectile dysfunction and coronary artery disease in patients with diabetes. Curr Diabetes Rev. 2011; 7(2):143-147.

29. Vlachopoulos C, Ioakeimidis N, Terentes-Printzios D, Stefanidis C. The triad: erectile dysfunction—endothelial dysfunction—cardiovascular disease. Curr Pharm Des. 2008;14(35): 3700-3704.

30. Makhlouf AA, Mohamed MA, Seftel AD, Niedergerger C. Hypogonadism is associated with overt depression symptoms in men with erectile dysfunction. Int J Impot Res. 2008;20(2): 157-161.

31. Corona G, Rastrelli G, Boddi V, et al. Prolactin levels independently predict major cardiovascular events in patients with erectile dysfunction. Int J Androl. 2011;34(3):217-224.

32. Vlachopoulos C, Rokkas K, Ioakeimidis N, Stefanadis C. Inflammation, metabolic syndrome, erectile dysfunction, and coronary artery disease: common links. Eur Urol. 2007;52(6):1590-1600.

33. LeRoy TJ, Broderick GA. Doppler blood flow analysis of erectile function: who, when, and how. Urol Clin North Am. 2011;38(2):147-154.

34. Aversa A, Sarteschi LM. J Sex Med. The role of penile color-duplex ultrasound for the evaluation of erectile dysfunction. J Sex Med. 2007;4(5): 1437-1447.

35. Fink HA, MacDonald R, Rutks IR, et al. Sildenafil for male erectile dysfunction: a systematic review and meta-analysis. Arch Intern Med. 2002; 16(12):1349-1360.

36. Perimenis P, Roumeguere T, Heidler H, et al. Evaluation of patient expectations and treatment satisfaction after 1-year tadalafil therapy for erectile dysfunction: the DETECT study. J Sex Med. 2009;6(1):257-267.

37. Goldstein I, Kim E, Steers WD, et al. Efficacy and safety of tadalafil in men with erectile dysfunction with a high prevalence of comorbid conditions: results from MOMENTUS: multiple observations in men with erectile dysfunction in National Tadalafil Study in the US. J Sex Med. 2007;4(1):166-175.

38. Van Ahlen H, Zumbé J, Stauch K, Hanisch JU. The Real-Life Safety and Efficacy of vardenafil (REALISE) study: results in men from Europe and overseas with erectile dysfunction and cardiovascular or metabolic conditions. J Sex Med. 2010; 7(9):3161-3169.

39. Raheem AA, Kell P. Patient preference and satisfaction in erectile dysfunction therapy: a comparison of the three phosphodiesterase-5 inhibitors sildenafil, vardenafil and tadalafil. Patient Prefer Adherence. 2009;3:99-104.

40. Jannini EA, Isidori AM, Gravina GL, et al. The ENDOTRIAL study: a spontaneous, open-label, randomized, multicenter, crossover study on the efficacy of sildenafil, tadalafil, and vardenafil in the treatment of erectile dysfunction. J Sex Med. 2009;6(9):2547-2560.

41. Washington SL 3rd, Shindel AW. A once-daily dose of tadalafil for erectile dysfunction: compliance and efficacy. Drug Des Devel Ther. 2010 Sep 7;4:159-171.

42. Brock G, Glina S, Moncada I, et al. Likelihood of tadalafil-associated adverse events in integrated multiclinical trial database: classification tree analysis in men with erectile dysfunction. Urology. 2009;73(4):756-761.

43. Montorsi F, Avera A, Mocada I, et al. A randomized, double-blind, placebo-controlled, parallel study to assess the efficacy and safety of once-a-day tadalafil in men with erectile dysfunction who are naïve to PDE5 inhibitors. J Sex Med. 2011 Jun 27 [Epub ahead of print].

44. Rajagopalan P, Mazzu A, Xia C, et al. Effect of high-fat breakfast and moderate-fat evening meal on the pharmacokinetics of vardenafil, an oral phosphodiesterase-5 inhibitor for the treatment of erectile dysfunction. J Clin Pharmacol. 2003;43 (3):260-267.

45. Eardley I, Donatucci C, Corbin J, et al. Pharmacotherapy for erectile dysfunction. J Sex Med. 2010;7(1 pt 2):524-540.

46. Loran OB, Ströberg P, Lee SW, et al. Sildenafil citrate 100 mg starting dose in men with erectile dysfunction in an international, double-blind, placebo-controlled study: effect on the sexual experience and reducing feelings of anxiety about the next intercourse attempt. J Sex Med. 2009; 6(10):2826-2835.

47. Mihkail N. Does testosterone have a role in erectile function? Am J Med. 2006;119(5):373-382.

48. Boloña ER, Uraga MV, Haddad RM, et al. Testosterone use in men with sexual dysfunction: a systematic review and meta-analysis of randomized placebo-controlled trials. Mayo Clin Proc. 2007;82(1):20-28.

49. Shabsigh R, Kaufman JM, Steidle C, Padma-Nathan H. Randomized study of testosterone gel as adjunctive therapy to sildenafil in hypogonadal men with erectile dysfunction who do not respond to sildenafil alone. J Urol. 2004;172(2): 658-663.

50. Aversa A, Isidori AM, Spera G, et al. Androgens improve cavernous vasodilation and response to sildenafil in patients with erectile dysfunction. Clin Endocrinol (Oxf). 2003;58(5):632-638.

51. Safarinejad MR. The effects of the adjunctive bupropion on male sexual dysfunction induced by a selective serotonin reuptake inhibitor: a double-blind placebo-controlled and randomized study. BJU Int. 2010;106(6):840-847.

52. Gazzaruso C, Solerte SB, Pujia A, et al. Erectile dysfunction as a predictor of cardiovascular events and death in diabetic patients with angiographically proven asymptomatic coronary artery disease: a potential protective role for statins and 5-phosphodiesterase inhibitors. J Am Coll Cardiol. 2008;51(21):2040-2044.

53. FDA. Tainted sexual enhancement products. www.fda.gov/Drugs/ResourcesForYou/Consumers/BuyingUsing MedicineSafely/MedicationHealthFraud/ucm234539.htm. Accessed August 8, 2011.

54. Cormio L, De Siati M, Lorusso F, et al. Oral L-citrulline supplementation improves erection hardness in men with mild erectile dysfunction. Urology. 2011;77(1):119-122.

55. Padma-Nathan H, Hellstrom WJ, Kaiser FE, et al. Treatment of men with erectile dysfunction with transurethral alprostadil: Medicated Urethral System for Erection (MUSE) Study Group. N Engl J Med. 1997;33(1)6:1-17.

56. Wolter CE, Hellstrom JG. The hydrophilic-coated penile prosthesis: 1-year experience. J Sex Med. 2004:1(2):221-224.

57. Yuan J, Hoang AN, Romero CA, et al. Vacuum therapy in erectile dysfunction: science and clinical evidence. Int J Impot Res. 2010;22(4):211-219.

58. Lebret T, Hervé JM, Gorny P, et al. Efficacy and safety of a novel combination of L-arginine glutamate and yohimbine hydrochloride: a new oral therapy for erectile dysfunction. Eur Urol. 2002; 41(6):608-613.

59. Fink HA, MacDonald R, Rutks IR, Wilt TJ. Trazodone for erectile dysfunction: a systematic review and meta-analysis. BJU Int. 2003;92(4): 441-446.

60. Esposito K, Giugliano F, Di Palo C, et al. Effect of lifestyle changes on erectile dysfunction in obese men: a randomized controlled trial. JAMA. 2004;291(24):2978-2984.

61. Pourmand G, Alidaee M, Rasuli S, et al. Do cigarette smokers with erectile dysfunction benefit from stopping? A prospective study. BJU Int. 2004;94(9):1310-1313.

62. Li D, Zhou Z, Qing D, et al. Occupational exposure to bisphenol-A (BPA) and the risk of self-reported male sexual dysfunction. Hum Reprod. 2010;25(2):519-527.

Erectile dysfunction (ED) is defined as the recurrent inability, of three months’ duration or longer, to attain or maintain an erection sufficient for satisfactory sexual performance.^1,2 It is classified as either psychogenic or organic; organic ED will be addressed here. Up to 80% of cases of organic ED can be further categorized into vascular, neurogenic, anatomic, or hormonal subtypes,^2,3 with many affected patients vulnerable to potentially serious comorbidities and risk factors.

In the early 1990s, the NIH reported that nearly 30 million US men were affected by ED.² However, increased public awareness of the condition, beginning with the availability of effective oral medications in the late 1990s, may have led to increased numbers of reported cases—and of men seeking treatment.

COMMON CONDITION, COMMONLY UNTREATED

According to results from the 2001-2002 National Health and Nutrition Examination Survey,^4,5 ED affects about 8% of US men: 4% of those in their 50s, 17% of those in their 60s, 47% of men older than 65, and 78% of men 75 or older. More than 27,000 men from Europe and North and South America (ages 20 to 75) were interviewed for the 2004 Men’s Attitudes to Life Events and Sexuality (MALES) study; findings included an overall prevalence for ED of 16%, and 22% among men from the United States.⁶ See information regarding self-reported ED prevalence in Table 1.⁷

An important finding from the MALES study was that only 58% of respondents with self-reported ED had sought medical treatment for the condition.⁶ Some men may be reluctant to broach the subject with a health care provider because they consider ED a purely sexual problem—whereas the etiology is most commonly vascular.⁸ Thus, it is important for health care providers to include the sexual history as a routine component in the wellness exam for all patients, and to be aware of the potential presentation in patients with organic ED, appropriate work-up, and physical examination.

Additionally, ED can be a wake-up call for men at risk for cardiovascular disease (CVD); ED occurs at a mean time of five years before a cardiovascular event.⁹ Therefore, in addition to counseling patients with ED regarding treatment and prevention strategies, clinicians should be prepared to identify and address the risk factors and medical comorbidities associated with ED.

The Mechanisms of Erection

When sexual stimulation occurs, parasympathetic activity increases production of the nucleotide cyclic guanosine monophosphate (cGMP), resulting in relaxation of cavernosal smooth muscle and an influx of blood into the penis. This filling action produces expansion of the sinusoidal spaces in the penis, compressing venous channels and thereby preventing outflow of blood to allow maintenance of a rigid erection.^10,11

Nitric oxide is needed for vasodilation of the corpora cavernosa. Inhibition of the enzyme phosphodiesterase type 5 (PDE-5) allows increased production and accumulation of penile cGMP. This results in relaxation of the smooth-muscle cells and improved erectile function.^1,10,11

PRESENTATION, HISTORY, AND TYPES OF ORGANIC ED

In the primary care setting, the opportunity to assess for and address erectile function generally presents itself at the patient’s annual wellness visit—but could easily go unmentioned if the health care provider does not initiate the discussion. Direct questioning during the review of systems may ease any anxiety for the patient and open up a dialogue regarding other problems or medical conditions. (See box, “How and What To Ask,”¹²)

Providers can also assess the patient’s risk factors for ED and its associated comorbid conditions (see Table 2^1,13,14). The patient’s medical history may hold important clues to a diagnosis of organic ED.

Because certain vasculopathies, including diabetes, are known to accelerate the process of endothelial dysfunction, inquiries should be made into the sexual history of men with these disorders, regardless of age.¹⁰ Marked hyperlipidemia, uncontrolled hypertension, atherosclerosis, and other manifestations of CVD can impair erectile as well as endothelial function, leading to vascular ED.

The potential for atherosclerosis in the penile arteries (which are significantly narrower than the carotid, coronary, or femoral arteries) should prompt the primary care provider to evaluate the patient’s risk for vascular disease and its sequelae in the heart as well.⁸ (Of note, in one study of metabolic syndrome and ED, ED was found to be a predictor for impaired elasticity in the large arteries, independent of cardiovascular risk factors.¹⁵) In addition to damaging the small blood vessels and the endothelium, diabetes and other components of the metabolic syndrome contribute to ED by affecting cavernous nerve terminals and smooth muscle.^1,14

Lifestyle factors, such as overconsumption of alcohol, smoking, recreational drug use, obesity, and inactivity can contribute to decreased libido and ED.¹⁴ Cigarette smoking can cause vasoconstriction and penile venous leak, resulting in poor erectile quality or even loss of erection. While small amounts of alcohol can improve libido and erection due to its anti-anxiety and vasodilatory effects, “more is not better” in this case, as higher doses result in sedation and decreased libido. Chronic alcoholism results in hypogonadism and polyneuropathy.¹⁶

Neurogenic ED can result from abnormalities at the level of the brain, the spinal cord, or the pelvis. Previous pelvic surgery, such as prostatectomy or colectomy, can disrupt the cavernous or pudendal nerves. Spinal cord injury, Parkinson’s disease, multiple sclerosis, diabetes with peripheral neuropathy, or a history of trauma can all result in neurogenic ED.¹⁶

Additionally, there is evidence of perineal compression from frequent bicycle riding leading to vascular, endothelial, and neurogenic dysfunction in men, with increased incidence of ED.¹⁷

Age alone is a risk factor for ED,^7,18 as sexual function declines even in healthy men as they age. Penile sensitivity decreases, and there is increased latency between sexual stimulation and resulting erection, as well as between ejaculations. Ejaculations are less forceful, with less ejaculatory volume.¹⁶ Other factors that may affect the degree of ED include a history of stroke or pelvic surgery, especially in high-risk cardiac patients.¹⁹

Though not the focus of this article, the potential for psychogenic ED should be mentioned, as it warrants screening with a complete psychosocial history to rule out this etiology. The interview should allow time for the patient to discuss current or past relationship difficulties, marital conflict, life stressors, depression, and anxiety. Whatever the etiology of ED, the primary care provider should always elicit a sexual history, including number of sexual partners, current relationship status (ie, committed or casual), and incidence of ED with specific partners.²⁰ The effects of ED on these relationships should be discussed.

A medication history is important for the ED workup. Antidepressants, especially the SSRIs, and certain hypertensives can affect the libido, arousal, and orgasm.²¹ See Table 3^1,13,22 for commonly used agents that can affect erectile function and sexual satisfaction.

Previous Medical History

The patient should be asked whether he has had any previous testing or treatment for ED. Was any therapy used effective? Did he experience any adverse effects during treatment? If treatment results were unsatisfactory, he should be questioned to ensure that he was using treatment correctly. Commonly, patients do not understand that sexual stimulation is necessary to achieve an erection when they are being treated with an oral PDE-5 inhibitor.²³

PHYSICAL EXAMINATION

The clinician who performs the physical examination should take into account the psychogenic, neurogenic, and vasculogenic causes of ED. The genitourinary examination alone is not sufficient; abdominal, vascular, and neurologic exams must be included. The patient should be assessed for body habitus, secondary sex characteristics (including ruling out gynecomastia), and lower extremity pulses.²²

The genitourinary exam should include testicular, rectal, and penile examination to rule out physical abnormalities. Small testicles (< 5 mL) or testicular atrophy on palpation should lead the examiner to consider testosterone testing^24,25 (see “Diagnostic Testing,” below). A digital rectal examination may reveal an enlarged prostate (this finding, in the presence of lower urinary tract symptoms, has been associated with ED²⁶). Palpation of the penis for plaques and questioning about pain with erection or deviation of the erect penis can lead to a diagnosis of Peyronie’s disease²⁷; if this is the case, the patient can be referred to urology for treatment.

The vascular system should be assessed by listening for abdominal or femoral bruits and the lower extremities checked for appropriate hair growth, skin color, and distal pulses. The examiner should note any scars indicating a history of bypass surgery, which may have been overlooked during the surgical history.

DIAGNOSTIC TESTING

A fasting glucose level and a lipid profile should be routinely obtained because of the links between ED and diabetes and CVD.^28,29 A chemistry panel and complete blood count, if one has not been performed recently, can be used to assess the patient’s general health, with a thyroid-stimulating hormone (TSH) level tested in men who report fatigue or weakness.

Men who are older than 50 should be considered for prostate-specific antigen (PSA) testing. Testosterone levels (free and total) are generally reserved for patients with small or atrophic testicles²⁵ or for those who report decreased libido with fatigue or other symptoms of hypogonadism, including depression and decreased muscle strength, muscle mass, or vitality.^22,24,25,30 If testosterone levels are ordered, the patient should be counseled to have samples drawn in the early morning to avoid the influence of daily hormonal fluctuations. In patients found to have low testosterone levels (ie, < 300 ng/dL,¹³ occurring in 12.5% to 35% of men with ED²⁴), prolactin testing may be considered next; in patients with ED, hypoprolactinemia is associated with dyslipidemia, metabolic syndrome, and other risk factors for cardiovascular events.^29,31,32

Imaging Studies

A number of imaging studies, once frequently used in evaluation for ED, are considered outdated and are no longer performed. However, Doppler blood flow analysis or ultrasonographic penile blood flow studies can be useful for identifying and evaluating the specific causes of vasculogenic ED, including arterial insufficiency and veno-occlusive disease.^33,34 Other conditions associated with ED, such as Peyronie’s disease and priapism, can also be identified through these modalities.³³

TREATMENT

The PDE-5 Inhibitors

While historically not the first treatment available for ED, medical therapy is certainly the most popular option for men with ED. The oral PDE-5 inhibitors first became available in the 1990s. All three such agents currently available in the US—silden­afil, tadalafil, and vardenafil—have been demonstrated effective in improving and maintaining erections,^35-38 but their pharmacokinetics differ,³⁹ and few head-to-head studies have been conducted that demonstrate greater efficacy of one agent over another.^39,40 It has been suggested that patients try all three medications to determine preference and satisfaction.³⁹

Qaseem et al²⁴ report that PDE-5 inhibitors demonstrated clinical benefit regardless of baseline severity of dysfunction or ED cause, including diabetes and depression. These medications require sexual stimulation to be effective and typically are effective about one hour after dosing.²³ Tadalafil is remarkable for the length of its half-life, which makes it appropriate at 2.5- or 5.0-mg doses for once-daily dosing⁴¹; it is also noted for a relatively low incidence of associated flushing,⁴² but back pain is more common among tadalafil users than among men using sildenafil or vardenafil.^11,39,43

In addition to back pain and myalgia, the most common adverse effects associated with PDE-5 inhibitor use are dyspepsia, flushing, headache, and nasal congestion.⁴² Because absorption of sildenafil is reduced by food intake, and vardenafil⁴⁴ to a lesser extent, these agents are best avoided in close proximity to meals. Absorption of tadalafil is not affected by food.⁴⁵ Higher doses of sildenafil and vardenafil were associated with greater benefit in treating ED.^24,46

Note: All three PDE-5 inhibitors are contraindicated in men taking long-acting nitrates or nitroglycerin.²⁴ Their effectiveness may be potentiated by use of erythromycin, ketoconazole, and HIV protease inhibitors.³⁹ Information about dosing options and adverse effects can be found in Table 4¹¹.

Testosterone

Hypogonadism, though found in only 5% of men with ED,⁴⁷ may be an indication for testosterone replacement therapy, and testosterone use has been found to improve libido in men with sexual dysfunction.⁴⁸ However, the authors of the American College of Physicians clinical practice guidelines²⁴ found insufficient evidence that testosterone replacement improved erections or quality of sexual intercourse. There was also insufficient evidence that testosterone plus sildenafil was more effective than sildenafil alone.^24,49,50

Additional Pharmacologic Considerations

A careful review of the medication history for the patient with ED may lead the astute clinician to consider whether a change in current prescriptions might improve the man’s sexual function. Among the commonly used agents listed in Table 3, those with the greatest apparent impact on erections are thiazide diuretics and β-blockers, SSRIs, and tricyclic antidepressants.^1,4

For a man who is interested in preserving potency, the clinician should select medications with the least effect on erectile function—for instance, an ACE inhibitor¹ rather than a thiazide or β-blocker for the patient with hypertension. In the patient affected by depression, a trial of bupropion, substituted for or added to his current antidepressant, may be helpful.⁵¹ Medical therapies for hyperglycemia, hyperlipidemia, and hypertension should be considered if warranted, as should cardiovascular screening with exercise stress testing. (See box, “ED, CAD, and PDE-5 Inhibitors”⁵²)

Alternative and Nonpharmacologic Options

A number of herbal products have been touted to improve sexual function. The FDA⁵³ has issued press releases warning consumers about these and other alternatives to prescription medications. According to the FDA, many “sexual enhancement” products have been found to contain active ingredients resembling those found in one or more PDE-5 inhibitors. These products are in violation of federal law, and consumers are advised to avoid supplements that claim to produce effects similar to those of prescription drugs.⁵³

By contrast, one potentially beneficial supplement currently under study is L-citrulline. As the body converts oral L-citrulline to L-arginine, vasodilation and endothelial function improve, often leading to resolution of mild ED. In a small, single-blind placebo-controlled study, patients who took L-citrulline (1.5 g/d in divided doses) reported improvement in hardness scale grading and increased satisfaction regarding sexual function. No adverse effects were reported, making L-citrulline a possible option for patients who hesitate to use a PDE-5 inhibitor.⁵⁴

For patients with lack of response or contraindications to accepted medical therapy, other options include alprostadil intraurethral suppositories, penile prosthetic implants, vacuum erection devices, vascular surgery, yohimbine and other herbal therapies, and trazodone.^1,14,55-59 These methods may require detailed counseling. Primary care providers who are unfamiliar with these modalities or reluctant to introduce them may wish to refer patients to urology.

PATIENT EDUCATION

Aggressive reduction in cardiovascular risks with smoking cessation, weight loss, and physical activity should be encouraged. In a study of obese men with ED (but without diabetes, hypertension, or hyperlipidemia), Esposito et al⁶⁰ found that reducing caloric intake and increasing physical activity was associated with improved sexual function in about one-third of the subjects. Bicycle riders can decrease risks of perineal compression with newer seat designs.¹⁷

Smoking cessation alone has been shown to improve erectile function at one-year follow-up in at least 25% of men who stopped smoking, compared with none of the men who continued to smoke.⁶¹ Patients can help preserve endothelial function with efforts to maintain normal blood pressure and glycemic control.

Researchers are currently looking at occupational exposures as a cause of ED. Exposure to plastics containing bisphenol-A, for example, has been linked to decreased libido.⁶²

CONCLUSION

In addition to addressing erectile dysfunction as a sexual problem, the health care provider should recognize its association with CVD, diabetes, depression, and other serious illnesses. However, it is also important to open a dialogue about sexual function to encourage the patient to discuss the problem of ED. Timely diagnosis and treatment of these conditions may be of even greater benefit to the patient than the effective therapies available for ED itself.  

REFERENCES

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2. NIH Consensus Conference. Impotence: NIH Consensus Development Panel on Impotence. JAMA. 1993;270(1):83-90.

3. Hafez ES, Hafez SD. Erectile dysfunction: anatomical parameters, etiology, diagnosis, and therapy. Arch Androl. 2005;51(1):15-31.

4. Francis ME, Kusek JW, Nyberg LM, Eggers PW. The contribution of common medical conditions and drug exposures to erectile dysfunction in adult males. J Urol. 2007;178(2):591-596.

5. Saigal CS, Wessells H, Pace J, et al. Predictors and prevalence of erectile dysfunction in a racially diverse population. Arch Intern Med. 2006;166 (2):207-212.

6. Rosen RC, Fisher WA, Eardley I, et al. The multinational Men’s Attitudes to Life Events and Sexuality (MALES) study. I. Prevalence of erectile dysfunction and related health concerns in the general population. Curr Med Res Opin. 2004;20 (5):607-617.

7. Lindau ST, Schumm LP, Laumann EO, et al. A study of sexuality and health among older adults in the United States. N Engl J Med. 2007;357(8): 762-774.

8. Batty GD, Li Q, Czernichow S, et al. Erectile dysfunction and later cardiovascular disease in men with type 2 diabetes: prospective cohort study based on the ADVANCE (Action in Diabetes and Vascular Disease: Preterax and Diamicron Modified-Release Controlled Evaluation) trial. J Am Coll Cardiol. 2010;56(23): 1908-1913.

9. Hodges LD, Kirby M, Solanki J, et al. The temporal relationship between erectile dysfunction and cardiovascular disease. Int J Clin Pract. 2007; 61(12):2019-2025.

10. Miner MM, Kuritzky L. Erectile dysfunction: a sentinel marker for cardiovascular disease in primary care. Cleve Clin J Med. 2007;74 suppl 3: S30-S37.

11. McCullough AR. An update on the PDE-5 inhibitors (PDE-5i). J Androl. 2003;24(6 suppl): S52-S58.

12. Rosen RC, Cappelleri JC, Smith MD, et al. Development and evaluation of an abridged, 5-item version of the International Index of Erectile Function (IIEF-5) as a diagnostic tool for erectile dysfunction. Int J Impot Res. 1999;11(6):
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13. Heidelbaugh JJ. Management of erectile dysfunction. Am Fam Physician. 2010;81(3):305-312.

14. Montague DK, Jarow JP, Broderick GA, et al; Erectile Dysfunction Guideline Update Panel. AUA guideline on the management of erectile dysfunction: an update (2006). American Urological Association Education and Research, Inc. www.auanet.org/content/guidelines-and-quality- care/clinical-guidelines.cfm?sub=ed. Accessed August 8, 2011.

15. Pohjantahti-Maaroos H, Palomäki A. Comparison of metabolic syndrome subjects with and without erectile dysfunction: levels of circulating oxidised LDL and arterial elasticity. Int J Clin Pract. 2011;65(3):274-280.

16. Lue TF. Male sexual dysfunction. In: Tanagho EA, McAninch JW, eds. Smith’s General Urology. 16th ed. San Francisco, CA: McGraw-Hill; 2004: 592-596.

17. Sommer F, Goldstein I, Korda JB. Bicycle riding and erectile dysfunction: a review. J Sex Med. 2010;7(7):2346-2358.

18. Feldman HA, Johannes CB, Derby CA, et al. Erectile dysfunction and coronary risk factors: prospective results from the Massachusetts male aging study. Prev Med. 2000;30(4):328-338.

19. Böhm M, Baumhäkel M, Probstfield JL, et al. Sexual function, satisfaction, and association of erectile dysfunction with cardiovascular disease and risk factors in cardiovascular high-risk patients: substudy of the ONgoing Telmisartan Alone and in Combination with Ramipril Global Endpoint Trial/Telmisartan Randomized AssessmeNT Study in ACE-INtolerant Subjects with Cardiovascular Disease (ONTARGET/TRANSCEND). Am Heart J. 2007;154(1):94-101.

20. Athanasiadis L, Papaharitou S, Salpiggidis G, et al. Educating physicians to treat erectile dysfunction patients: development and evaluation of a course on communication and management strategies. J Sex Med. 2006;3(1):47-55.

21. Kennedy SH, Rizvi S. Sexual dysfunction, depression, and the impact of antidepressants.
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22. Diaz VA Jr, Close JD. Male sexual dysfunction. Prim Care. 2010;37(3):473-489, vii-viii.

23. Carson CC, Lue TF. Phosphodiesterase type 5 inhibitors for erectile dysfunction. BJU Int. 2005; 96(3):257-280.

24. Qaseem A, Snow V, Denberg TD, et al. Hormonal testing and pharmacologic treatment of erectile dysfunction: a clinical practice guideline from the American College of Physicians. Ann Intern Med. 2009;151(9):630-649.

25. Dandona P, Rosenberg MT. A practical guide to male hypogonadism in the primary care setting. Int J Clin Pract. 2010;64(6):682-696.

26. Paick SH, Meehan A, Lee M, et al. The relationship among lower urinary tract symptoms, prostate specific antigen and erectile dysfunction in men with benign prostatic hyperplasia: results from the Proscar Long-Term Efficacy and Safety Study. J Urol. 2005;173(3):903-907.

27. Smith JF, Walsh TJ, Lue TF. Peyronie’s disease: a critical appraisal of current diagnosis and treatment. Int J Impot Res. 2008;20(5):445-459.

28. Gazzaruso C, Coppola A, Giustina A. Erectile dysfunction and coronary artery disease in patients with diabetes. Curr Diabetes Rev. 2011; 7(2):143-147.

29. Vlachopoulos C, Ioakeimidis N, Terentes-Printzios D, Stefanidis C. The triad: erectile dysfunction—endothelial dysfunction—cardiovascular disease. Curr Pharm Des. 2008;14(35): 3700-3704.

30. Makhlouf AA, Mohamed MA, Seftel AD, Niedergerger C. Hypogonadism is associated with overt depression symptoms in men with erectile dysfunction. Int J Impot Res. 2008;20(2): 157-161.

31. Corona G, Rastrelli G, Boddi V, et al. Prolactin levels independently predict major cardiovascular events in patients with erectile dysfunction. Int J Androl. 2011;34(3):217-224.

32. Vlachopoulos C, Rokkas K, Ioakeimidis N, Stefanadis C. Inflammation, metabolic syndrome, erectile dysfunction, and coronary artery disease: common links. Eur Urol. 2007;52(6):1590-1600.

33. LeRoy TJ, Broderick GA. Doppler blood flow analysis of erectile function: who, when, and how. Urol Clin North Am. 2011;38(2):147-154.

34. Aversa A, Sarteschi LM. J Sex Med. The role of penile color-duplex ultrasound for the evaluation of erectile dysfunction. J Sex Med. 2007;4(5): 1437-1447.

35. Fink HA, MacDonald R, Rutks IR, et al. Sildenafil for male erectile dysfunction: a systematic review and meta-analysis. Arch Intern Med. 2002; 16(12):1349-1360.

36. Perimenis P, Roumeguere T, Heidler H, et al. Evaluation of patient expectations and treatment satisfaction after 1-year tadalafil therapy for erectile dysfunction: the DETECT study. J Sex Med. 2009;6(1):257-267.

37. Goldstein I, Kim E, Steers WD, et al. Efficacy and safety of tadalafil in men with erectile dysfunction with a high prevalence of comorbid conditions: results from MOMENTUS: multiple observations in men with erectile dysfunction in National Tadalafil Study in the US. J Sex Med. 2007;4(1):166-175.

38. Van Ahlen H, Zumbé J, Stauch K, Hanisch JU. The Real-Life Safety and Efficacy of vardenafil (REALISE) study: results in men from Europe and overseas with erectile dysfunction and cardiovascular or metabolic conditions. J Sex Med. 2010; 7(9):3161-3169.

39. Raheem AA, Kell P. Patient preference and satisfaction in erectile dysfunction therapy: a comparison of the three phosphodiesterase-5 inhibitors sildenafil, vardenafil and tadalafil. Patient Prefer Adherence. 2009;3:99-104.

40. Jannini EA, Isidori AM, Gravina GL, et al. The ENDOTRIAL study: a spontaneous, open-label, randomized, multicenter, crossover study on the efficacy of sildenafil, tadalafil, and vardenafil in the treatment of erectile dysfunction. J Sex Med. 2009;6(9):2547-2560.

41. Washington SL 3rd, Shindel AW. A once-daily dose of tadalafil for erectile dysfunction: compliance and efficacy. Drug Des Devel Ther. 2010 Sep 7;4:159-171.

42. Brock G, Glina S, Moncada I, et al. Likelihood of tadalafil-associated adverse events in integrated multiclinical trial database: classification tree analysis in men with erectile dysfunction. Urology. 2009;73(4):756-761.

43. Montorsi F, Avera A, Mocada I, et al. A randomized, double-blind, placebo-controlled, parallel study to assess the efficacy and safety of once-a-day tadalafil in men with erectile dysfunction who are naïve to PDE5 inhibitors. J Sex Med. 2011 Jun 27 [Epub ahead of print].

44. Rajagopalan P, Mazzu A, Xia C, et al. Effect of high-fat breakfast and moderate-fat evening meal on the pharmacokinetics of vardenafil, an oral phosphodiesterase-5 inhibitor for the treatment of erectile dysfunction. J Clin Pharmacol. 2003;43 (3):260-267.

45. Eardley I, Donatucci C, Corbin J, et al. Pharmacotherapy for erectile dysfunction. J Sex Med. 2010;7(1 pt 2):524-540.

46. Loran OB, Ströberg P, Lee SW, et al. Sildenafil citrate 100 mg starting dose in men with erectile dysfunction in an international, double-blind, placebo-controlled study: effect on the sexual experience and reducing feelings of anxiety about the next intercourse attempt. J Sex Med. 2009; 6(10):2826-2835.

47. Mihkail N. Does testosterone have a role in erectile function? Am J Med. 2006;119(5):373-382.

48. Boloña ER, Uraga MV, Haddad RM, et al. Testosterone use in men with sexual dysfunction: a systematic review and meta-analysis of randomized placebo-controlled trials. Mayo Clin Proc. 2007;82(1):20-28.

49. Shabsigh R, Kaufman JM, Steidle C, Padma-Nathan H. Randomized study of testosterone gel as adjunctive therapy to sildenafil in hypogonadal men with erectile dysfunction who do not respond to sildenafil alone. J Urol. 2004;172(2): 658-663.

50. Aversa A, Isidori AM, Spera G, et al. Androgens improve cavernous vasodilation and response to sildenafil in patients with erectile dysfunction. Clin Endocrinol (Oxf). 2003;58(5):632-638.

51. Safarinejad MR. The effects of the adjunctive bupropion on male sexual dysfunction induced by a selective serotonin reuptake inhibitor: a double-blind placebo-controlled and randomized study. BJU Int. 2010;106(6):840-847.

52. Gazzaruso C, Solerte SB, Pujia A, et al. Erectile dysfunction as a predictor of cardiovascular events and death in diabetic patients with angiographically proven asymptomatic coronary artery disease: a potential protective role for statins and 5-phosphodiesterase inhibitors. J Am Coll Cardiol. 2008;51(21):2040-2044.

53. FDA. Tainted sexual enhancement products. www.fda.gov/Drugs/ResourcesForYou/Consumers/BuyingUsing MedicineSafely/MedicationHealthFraud/ucm234539.htm. Accessed August 8, 2011.

54. Cormio L, De Siati M, Lorusso F, et al. Oral L-citrulline supplementation improves erection hardness in men with mild erectile dysfunction. Urology. 2011;77(1):119-122.

55. Padma-Nathan H, Hellstrom WJ, Kaiser FE, et al. Treatment of men with erectile dysfunction with transurethral alprostadil: Medicated Urethral System for Erection (MUSE) Study Group. N Engl J Med. 1997;33(1)6:1-17.

56. Wolter CE, Hellstrom JG. The hydrophilic-coated penile prosthesis: 1-year experience. J Sex Med. 2004:1(2):221-224.

57. Yuan J, Hoang AN, Romero CA, et al. Vacuum therapy in erectile dysfunction: science and clinical evidence. Int J Impot Res. 2010;22(4):211-219.

58. Lebret T, Hervé JM, Gorny P, et al. Efficacy and safety of a novel combination of L-arginine glutamate and yohimbine hydrochloride: a new oral therapy for erectile dysfunction. Eur Urol. 2002; 41(6):608-613.

59. Fink HA, MacDonald R, Rutks IR, Wilt TJ. Trazodone for erectile dysfunction: a systematic review and meta-analysis. BJU Int. 2003;92(4): 441-446.

60. Esposito K, Giugliano F, Di Palo C, et al. Effect of lifestyle changes on erectile dysfunction in obese men: a randomized controlled trial. JAMA. 2004;291(24):2978-2984.

61. Pourmand G, Alidaee M, Rasuli S, et al. Do cigarette smokers with erectile dysfunction benefit from stopping? A prospective study. BJU Int. 2004;94(9):1310-1313.

62. Li D, Zhou Z, Qing D, et al. Occupational exposure to bisphenol-A (BPA) and the risk of self-reported male sexual dysfunction. Hum Reprod. 2010;25(2):519-527.

Erectile dysfunction (ED) is defined as the recurrent inability, of three months’ duration or longer, to attain or maintain an erection sufficient for satisfactory sexual performance.^1,2 It is classified as either psychogenic or organic; organic ED will be addressed here. Up to 80% of cases of organic ED can be further categorized into vascular, neurogenic, anatomic, or hormonal subtypes,^2,3 with many affected patients vulnerable to potentially serious comorbidities and risk factors.

In the early 1990s, the NIH reported that nearly 30 million US men were affected by ED.² However, increased public awareness of the condition, beginning with the availability of effective oral medications in the late 1990s, may have led to increased numbers of reported cases—and of men seeking treatment.

COMMON CONDITION, COMMONLY UNTREATED

According to results from the 2001-2002 National Health and Nutrition Examination Survey,^4,5 ED affects about 8% of US men: 4% of those in their 50s, 17% of those in their 60s, 47% of men older than 65, and 78% of men 75 or older. More than 27,000 men from Europe and North and South America (ages 20 to 75) were interviewed for the 2004 Men’s Attitudes to Life Events and Sexuality (MALES) study; findings included an overall prevalence for ED of 16%, and 22% among men from the United States.⁶ See information regarding self-reported ED prevalence in Table 1.⁷

An important finding from the MALES study was that only 58% of respondents with self-reported ED had sought medical treatment for the condition.⁶ Some men may be reluctant to broach the subject with a health care provider because they consider ED a purely sexual problem—whereas the etiology is most commonly vascular.⁸ Thus, it is important for health care providers to include the sexual history as a routine component in the wellness exam for all patients, and to be aware of the potential presentation in patients with organic ED, appropriate work-up, and physical examination.

Additionally, ED can be a wake-up call for men at risk for cardiovascular disease (CVD); ED occurs at a mean time of five years before a cardiovascular event.⁹ Therefore, in addition to counseling patients with ED regarding treatment and prevention strategies, clinicians should be prepared to identify and address the risk factors and medical comorbidities associated with ED.

The Mechanisms of Erection

When sexual stimulation occurs, parasympathetic activity increases production of the nucleotide cyclic guanosine monophosphate (cGMP), resulting in relaxation of cavernosal smooth muscle and an influx of blood into the penis. This filling action produces expansion of the sinusoidal spaces in the penis, compressing venous channels and thereby preventing outflow of blood to allow maintenance of a rigid erection.^10,11

Nitric oxide is needed for vasodilation of the corpora cavernosa. Inhibition of the enzyme phosphodiesterase type 5 (PDE-5) allows increased production and accumulation of penile cGMP. This results in relaxation of the smooth-muscle cells and improved erectile function.^1,10,11

PRESENTATION, HISTORY, AND TYPES OF ORGANIC ED

In the primary care setting, the opportunity to assess for and address erectile function generally presents itself at the patient’s annual wellness visit—but could easily go unmentioned if the health care provider does not initiate the discussion. Direct questioning during the review of systems may ease any anxiety for the patient and open up a dialogue regarding other problems or medical conditions. (See box, “How and What To Ask,”¹²)

Providers can also assess the patient’s risk factors for ED and its associated comorbid conditions (see Table 2^1,13,14). The patient’s medical history may hold important clues to a diagnosis of organic ED.

Because certain vasculopathies, including diabetes, are known to accelerate the process of endothelial dysfunction, inquiries should be made into the sexual history of men with these disorders, regardless of age.¹⁰ Marked hyperlipidemia, uncontrolled hypertension, atherosclerosis, and other manifestations of CVD can impair erectile as well as endothelial function, leading to vascular ED.

The potential for atherosclerosis in the penile arteries (which are significantly narrower than the carotid, coronary, or femoral arteries) should prompt the primary care provider to evaluate the patient’s risk for vascular disease and its sequelae in the heart as well.⁸ (Of note, in one study of metabolic syndrome and ED, ED was found to be a predictor for impaired elasticity in the large arteries, independent of cardiovascular risk factors.¹⁵) In addition to damaging the small blood vessels and the endothelium, diabetes and other components of the metabolic syndrome contribute to ED by affecting cavernous nerve terminals and smooth muscle.^1,14

Lifestyle factors, such as overconsumption of alcohol, smoking, recreational drug use, obesity, and inactivity can contribute to decreased libido and ED.¹⁴ Cigarette smoking can cause vasoconstriction and penile venous leak, resulting in poor erectile quality or even loss of erection. While small amounts of alcohol can improve libido and erection due to its anti-anxiety and vasodilatory effects, “more is not better” in this case, as higher doses result in sedation and decreased libido. Chronic alcoholism results in hypogonadism and polyneuropathy.¹⁶

Neurogenic ED can result from abnormalities at the level of the brain, the spinal cord, or the pelvis. Previous pelvic surgery, such as prostatectomy or colectomy, can disrupt the cavernous or pudendal nerves. Spinal cord injury, Parkinson’s disease, multiple sclerosis, diabetes with peripheral neuropathy, or a history of trauma can all result in neurogenic ED.¹⁶

Additionally, there is evidence of perineal compression from frequent bicycle riding leading to vascular, endothelial, and neurogenic dysfunction in men, with increased incidence of ED.¹⁷

Age alone is a risk factor for ED,^7,18 as sexual function declines even in healthy men as they age. Penile sensitivity decreases, and there is increased latency between sexual stimulation and resulting erection, as well as between ejaculations. Ejaculations are less forceful, with less ejaculatory volume.¹⁶ Other factors that may affect the degree of ED include a history of stroke or pelvic surgery, especially in high-risk cardiac patients.¹⁹

Though not the focus of this article, the potential for psychogenic ED should be mentioned, as it warrants screening with a complete psychosocial history to rule out this etiology. The interview should allow time for the patient to discuss current or past relationship difficulties, marital conflict, life stressors, depression, and anxiety. Whatever the etiology of ED, the primary care provider should always elicit a sexual history, including number of sexual partners, current relationship status (ie, committed or casual), and incidence of ED with specific partners.²⁰ The effects of ED on these relationships should be discussed.

A medication history is important for the ED workup. Antidepressants, especially the SSRIs, and certain hypertensives can affect the libido, arousal, and orgasm.²¹ See Table 3^1,13,22 for commonly used agents that can affect erectile function and sexual satisfaction.

Previous Medical History

The patient should be asked whether he has had any previous testing or treatment for ED. Was any therapy used effective? Did he experience any adverse effects during treatment? If treatment results were unsatisfactory, he should be questioned to ensure that he was using treatment correctly. Commonly, patients do not understand that sexual stimulation is necessary to achieve an erection when they are being treated with an oral PDE-5 inhibitor.²³

PHYSICAL EXAMINATION

The clinician who performs the physical examination should take into account the psychogenic, neurogenic, and vasculogenic causes of ED. The genitourinary examination alone is not sufficient; abdominal, vascular, and neurologic exams must be included. The patient should be assessed for body habitus, secondary sex characteristics (including ruling out gynecomastia), and lower extremity pulses.²²

The genitourinary exam should include testicular, rectal, and penile examination to rule out physical abnormalities. Small testicles (< 5 mL) or testicular atrophy on palpation should lead the examiner to consider testosterone testing^24,25 (see “Diagnostic Testing,” below). A digital rectal examination may reveal an enlarged prostate (this finding, in the presence of lower urinary tract symptoms, has been associated with ED²⁶). Palpation of the penis for plaques and questioning about pain with erection or deviation of the erect penis can lead to a diagnosis of Peyronie’s disease²⁷; if this is the case, the patient can be referred to urology for treatment.

The vascular system should be assessed by listening for abdominal or femoral bruits and the lower extremities checked for appropriate hair growth, skin color, and distal pulses. The examiner should note any scars indicating a history of bypass surgery, which may have been overlooked during the surgical history.

DIAGNOSTIC TESTING

A fasting glucose level and a lipid profile should be routinely obtained because of the links between ED and diabetes and CVD.^28,29 A chemistry panel and complete blood count, if one has not been performed recently, can be used to assess the patient’s general health, with a thyroid-stimulating hormone (TSH) level tested in men who report fatigue or weakness.

Men who are older than 50 should be considered for prostate-specific antigen (PSA) testing. Testosterone levels (free and total) are generally reserved for patients with small or atrophic testicles²⁵ or for those who report decreased libido with fatigue or other symptoms of hypogonadism, including depression and decreased muscle strength, muscle mass, or vitality.^22,24,25,30 If testosterone levels are ordered, the patient should be counseled to have samples drawn in the early morning to avoid the influence of daily hormonal fluctuations. In patients found to have low testosterone levels (ie, < 300 ng/dL,¹³ occurring in 12.5% to 35% of men with ED²⁴), prolactin testing may be considered next; in patients with ED, hypoprolactinemia is associated with dyslipidemia, metabolic syndrome, and other risk factors for cardiovascular events.^29,31,32

Imaging Studies

A number of imaging studies, once frequently used in evaluation for ED, are considered outdated and are no longer performed. However, Doppler blood flow analysis or ultrasonographic penile blood flow studies can be useful for identifying and evaluating the specific causes of vasculogenic ED, including arterial insufficiency and veno-occlusive disease.^33,34 Other conditions associated with ED, such as Peyronie’s disease and priapism, can also be identified through these modalities.³³

TREATMENT

The PDE-5 Inhibitors

While historically not the first treatment available for ED, medical therapy is certainly the most popular option for men with ED. The oral PDE-5 inhibitors first became available in the 1990s. All three such agents currently available in the US—silden­afil, tadalafil, and vardenafil—have been demonstrated effective in improving and maintaining erections,^35-38 but their pharmacokinetics differ,³⁹ and few head-to-head studies have been conducted that demonstrate greater efficacy of one agent over another.^39,40 It has been suggested that patients try all three medications to determine preference and satisfaction.³⁹

Qaseem et al²⁴ report that PDE-5 inhibitors demonstrated clinical benefit regardless of baseline severity of dysfunction or ED cause, including diabetes and depression. These medications require sexual stimulation to be effective and typically are effective about one hour after dosing.²³ Tadalafil is remarkable for the length of its half-life, which makes it appropriate at 2.5- or 5.0-mg doses for once-daily dosing⁴¹; it is also noted for a relatively low incidence of associated flushing,⁴² but back pain is more common among tadalafil users than among men using sildenafil or vardenafil.^11,39,43

In addition to back pain and myalgia, the most common adverse effects associated with PDE-5 inhibitor use are dyspepsia, flushing, headache, and nasal congestion.⁴² Because absorption of sildenafil is reduced by food intake, and vardenafil⁴⁴ to a lesser extent, these agents are best avoided in close proximity to meals. Absorption of tadalafil is not affected by food.⁴⁵ Higher doses of sildenafil and vardenafil were associated with greater benefit in treating ED.^24,46

Note: All three PDE-5 inhibitors are contraindicated in men taking long-acting nitrates or nitroglycerin.²⁴ Their effectiveness may be potentiated by use of erythromycin, ketoconazole, and HIV protease inhibitors.³⁹ Information about dosing options and adverse effects can be found in Table 4¹¹.

Testosterone

Hypogonadism, though found in only 5% of men with ED,⁴⁷ may be an indication for testosterone replacement therapy, and testosterone use has been found to improve libido in men with sexual dysfunction.⁴⁸ However, the authors of the American College of Physicians clinical practice guidelines²⁴ found insufficient evidence that testosterone replacement improved erections or quality of sexual intercourse. There was also insufficient evidence that testosterone plus sildenafil was more effective than sildenafil alone.^24,49,50

Additional Pharmacologic Considerations

A careful review of the medication history for the patient with ED may lead the astute clinician to consider whether a change in current prescriptions might improve the man’s sexual function. Among the commonly used agents listed in Table 3, those with the greatest apparent impact on erections are thiazide diuretics and β-blockers, SSRIs, and tricyclic antidepressants.^1,4

For a man who is interested in preserving potency, the clinician should select medications with the least effect on erectile function—for instance, an ACE inhibitor¹ rather than a thiazide or β-blocker for the patient with hypertension. In the patient affected by depression, a trial of bupropion, substituted for or added to his current antidepressant, may be helpful.⁵¹ Medical therapies for hyperglycemia, hyperlipidemia, and hypertension should be considered if warranted, as should cardiovascular screening with exercise stress testing. (See box, “ED, CAD, and PDE-5 Inhibitors”⁵²)

Alternative and Nonpharmacologic Options

A number of herbal products have been touted to improve sexual function. The FDA⁵³ has issued press releases warning consumers about these and other alternatives to prescription medications. According to the FDA, many “sexual enhancement” products have been found to contain active ingredients resembling those found in one or more PDE-5 inhibitors. These products are in violation of federal law, and consumers are advised to avoid supplements that claim to produce effects similar to those of prescription drugs.⁵³

By contrast, one potentially beneficial supplement currently under study is L-citrulline. As the body converts oral L-citrulline to L-arginine, vasodilation and endothelial function improve, often leading to resolution of mild ED. In a small, single-blind placebo-controlled study, patients who took L-citrulline (1.5 g/d in divided doses) reported improvement in hardness scale grading and increased satisfaction regarding sexual function. No adverse effects were reported, making L-citrulline a possible option for patients who hesitate to use a PDE-5 inhibitor.⁵⁴

For patients with lack of response or contraindications to accepted medical therapy, other options include alprostadil intraurethral suppositories, penile prosthetic implants, vacuum erection devices, vascular surgery, yohimbine and other herbal therapies, and trazodone.^1,14,55-59 These methods may require detailed counseling. Primary care providers who are unfamiliar with these modalities or reluctant to introduce them may wish to refer patients to urology.

PATIENT EDUCATION

Aggressive reduction in cardiovascular risks with smoking cessation, weight loss, and physical activity should be encouraged. In a study of obese men with ED (but without diabetes, hypertension, or hyperlipidemia), Esposito et al⁶⁰ found that reducing caloric intake and increasing physical activity was associated with improved sexual function in about one-third of the subjects. Bicycle riders can decrease risks of perineal compression with newer seat designs.¹⁷

Smoking cessation alone has been shown to improve erectile function at one-year follow-up in at least 25% of men who stopped smoking, compared with none of the men who continued to smoke.⁶¹ Patients can help preserve endothelial function with efforts to maintain normal blood pressure and glycemic control.

Researchers are currently looking at occupational exposures as a cause of ED. Exposure to plastics containing bisphenol-A, for example, has been linked to decreased libido.⁶²

CONCLUSION

In addition to addressing erectile dysfunction as a sexual problem, the health care provider should recognize its association with CVD, diabetes, depression, and other serious illnesses. However, it is also important to open a dialogue about sexual function to encourage the patient to discuss the problem of ED. Timely diagnosis and treatment of these conditions may be of even greater benefit to the patient than the effective therapies available for ED itself.  

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36. Perimenis P, Roumeguere T, Heidler H, et al. Evaluation of patient expectations and treatment satisfaction after 1-year tadalafil therapy for erectile dysfunction: the DETECT study. J Sex Med. 2009;6(1):257-267.

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46. Loran OB, Ströberg P, Lee SW, et al. Sildenafil citrate 100 mg starting dose in men with erectile dysfunction in an international, double-blind, placebo-controlled study: effect on the sexual experience and reducing feelings of anxiety about the next intercourse attempt. J Sex Med. 2009; 6(10):2826-2835.

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Sexual dysfunction is common among women in the United States. One recent study put the prevalence of distressing sexual dysfunction at 22.2%.¹ When cancer enters the picture, that percentage rises—dramatically. A 2010 survey from the Lance Armstrong Foundation found that 46% of people affected by cancer report problems with sex after treatment.²

In this article, I highlight three recent studies that explore the sexual effects of cancer and its treatment:

• a prospective cohort study showing that a majority of women treated for breast cancer experience sexual dysfunction afterward
• two longitudinal studies of women affected by gynecologic cancer, which show significant disruption of sexual function in the short and long term.

I also present the experiences of two cancer survivors who volunteered to relate their stories so that you might develop a better understanding of some of the challenges they face about their sexual function.

Sexual function deteriorates in many women after they are treated for breast Ca

Panjari M, Bell RJ, Davis SR. Sexual function after breast cancer. J Sex Med. 2011;8(1):294–302.

According to this prospective cohort study from Australia, a majority of women report significant sexual dysfunction after treatment for breast cancer—even when their sexual function was good, and satisfying, at the time of diagnosis (TABLE).

The Health and Wellbeing after Breast Cancer Study enrolled 1,684 Australian women within 12 months of their first diagnosis of invasive breast cancer. Each woman completed a questionnaire at the time of enrollment, and will complete annual follow-up questionnaires for 5 years to assess the impact of invasive breast cancer on physical, psychological, and socioeconomic wellbeing. Embedded within the 12-month questionnaire was the validated Menopause-Specific Quality of Life Questionnaire (MENQOL), which was used in this study to explore the sexual consequences of the diagnosis and treatment of invasive breast cancer.

Of the initial cohort, 1,011 women completed the 12-month questionnaire. These were women younger than 70 years who had a sexual partner and no evidence of active breast cancer. The authors describe the women in this cohort as representative of all women in Victoria, Australia, who have a new diagnosis of invasive breast cancer, in regard to both age (mean, 59 ± 11 years) and the stage of tumor (stage I, 48%; stage II–IV, 52%) at diagnosis.

Of this group, 70% were treated with lumpectomy and radiation therapy, and 30% were treated with mastectomy (2.6% with bilateral mastectomy). Of the women who underwent mastectomy, 9.6% had reconstructive surgery during the first year after diagnosis.

Forty-nine percent of women were treated with tamoxifen, and 28.2% were treated with an aromatase inhibitor.

After breast Ca, women experience low desire and less frequent sexual activity – as well as distress over both outcomes

More than two thirds of women reported sexual dysfunction 12 months after treatment

At baseline, 83% of women described their prediagnosis sexual function as good and satisfying. Twelve months later, 70% reported significant sexual dysfunction, and 77% reported vasomotor symptoms.

Women who reported new-onset sexual dysfunction were more likely to:

• have become menopausal since diagnosis
• experience hot flashes or night sweats
• be treated with an aromatase inhibitor.

There was no association between sexual dysfunction and stage of disease at diagnosis; type of surgery (lumpectomy or mastectomy); breast reconstruction; lymphedema; or axillary dissection.

Vasomotor symptoms in women taking endocrine therapy were associated with sexual dysfunction

Further analysis demonstrated that, among women who experienced vasomotor symptoms, those taking an aromatase inhibitor were more than three times as likely to report sexual dysfunction (odds ratio [OR], 3.49; 95% confidence interval [CI], 1.72–7.09), compared with women who were not on endocrine therapy—and those taking tamoxifen were almost twice as likely to report sexual dysfunction (OR, 1.73; 95% CI, 1.04–2.89). Chemotherapy was not independently related to sexual dysfunction.

In summary: 70% of women who were free of breast cancer 1 year after enrollment reported bothersome sexual consequences of their disease and its treatment; 77% reported vasomotor symptoms. Women who were rendered menopausal and those who experienced vasomotor symptoms while taking an aromatase inhibitor were at high risk of sexual dysfunction.

Two survivors report frustration—and resignation—when they sought help for sexual complaints

Katie* and Julie* tell typical stories of deep dissatisfaction with the health system after their cancer treatment

Katie: “I wasn’t prepared”

When my doctor told me I had locally advanced breast cancer 3 years ago, when I was 50, I wasn’t that surprised by the cancer diagnosis (I have a strong family history of breast cancer)—only by the fact that the tumor had developed so fast since my previous mammogram 15 months earlier. As treatment, I underwent neoadjuvant chemotherapy and bilateral mastectomy (I had the unaffected breast removed as a preventive measure). I also had breast reconstruction and started taking an aromatase inhibitor.

At the time of my diagnosis, I lost all desire for sexual intimacy—no big surprise there. But even after my treatment was over, my desire did not return. Part of the problem was the fact that chemotherapy rendered me menopausal, and the aromatase inhibitor I was taking compounded the menopausal experience. Quite suddenly, I was experiencing hot flashes, vaginal dryness and itching, pain during intercourse, severe bone and joint aches, weight gain (particularly around my abdomen), and general lethargy.

No one in my family had ever mentioned these effects of cancer. And none of my doctors prepared me, either. In fact, when I raised the subject, they seemed genuinely surprised! They offered no remedy other than a recommendation to apply a “moisturizer”—but they gave no details about what kind or how to use it. My oncologist did say that local estrogen would help relieve the pain of intercourse—but then she recommended strongly against it because my cancer was hormone-receptor positive.

My plastic surgeon did a much better job of explaining the effects and outcome of reconstruction than any of my other physicians, including my ObGyn, did of preparing me for menopause and sexual dysfunction.

All of my physicians strike me as caring, sensitive people, but their underlying attitude, as I perceive it, is that I should be grateful to be alive. In their view, it seems, enjoyment of sex is icing on the cake and, quite frankly, I am plenty lucky to have the cake. My oncologist even told me to let her know if I started “feeling better and having fewer hot flashes” so that she could perform ovarian ablation (and start the whole cycle over again). I was struck by how matter of factly she gave this advice, as though quality of life counts for nothing.

Three years into my postcancer life, I can say I have “adjusted” to my problems rather than overcome them. I am still taking an aromatase inhibitor. Sex is still slightly painful; I still struggle with vaginal dryness; and I sometimes feel like an old woman because of my bone and joint stiffness and pain. I did find out about an over-the-counter vaginal suppository, made with vitamin E and coconut oils, from another breast cancer survivor. And I switched from one aromatase inhibitor to another in an attempt to alleviate my achy joints. It helped.

I am grateful for my life—very much so—and for the expertise of my physicians, who helped to save it. But I wish they had prepared me better for the aftermath of cancer treatment. And I wish there were more remedies for women like me, who cannot take hormones.

Julie: “I’m on my own”

It was more than a surprise when my new doctor told me I had cancer. Until then, I had avoided doctors. That attitude can mean a premature death sentence when it comes to cervical cancer. It was a pretty awful realization that I could have avoided the drastic measures it took to save my life if I had just gotten annual Pap smears and exams. I was 39 at the time of diagnosis.

But after all the surgery and chemo and radiation were finished, the message I received was essentially: “OK, you’re good, for now. Just come back every few months for a check-up.”

What about the aftermath of all that treatment? What about the other aspects of the experience? I found that my doctors had very little to offer outside of surgery and drugs and the quick advice to get counseling or some other support services.

“I’m on my own” is what I’ve been telling concerned folks who ask how I’m doing. I am truly grateful for the skill, medicine, and machinery that made the killing of an invasive tumor possible. But I’m on my own when it comes to finding or inventing ways to cope with the new challenges of a pelvic area damaged by radiation and detoxing from the heavy metal—platinum—that was an ingredient in the chemo I received.

My partner and I have had to be persistently creative, careful, delicate, uncritical, and extremely patient with each other to bring about the return of a “normal” sex life. We have been successful, for the most part, but there is also a slightly new definition of what “normal” is for us. Our latest triumph is that we no longer have to use copious amounts of lubricant to engage in intercourse. Sex is no longer painful, as the vaginal tissues have been slowly, patiently engaged on a regularly scheduled basis. Can you imagine sex on a schedule? Neither could I, but that is what we found worked from as early as 1 week postradiation. As it turns out, this was good advice—really, the only advice I got when it came to the practicalities of restoring function, but it required a fair amount of tweaking and personalization as well.

Another big change in perception that I had to accept as part of my new norm is learning to talk about my most personal areas in a matter of fact way.

The cancer conveyor-belt approach to treatment is a very streamlined, well-run system. I’ve been impressed with the expertise, efficiency, and demeanor of all the professionals I have encountered. Everyone—even receptionists—has been helpful and empathetic, especially my own ObGyn, who has hugged me and cried with me and offered to put herself on the line for me and speak out to the media when I had no health insurance. But for most patients post-treatment, we figuratively walk off a cliff and find ourselves in new territory without any network or structure like we experienced during the “war” on our cancer. This new territory is a place of possibility within the health-care field—one I hope is developing now.

Dr. Barbara S. Levy asks: How do we respond? We physicians are so focused on treating or curing disease that we often lose sight of the woman who has the disease.

Katie’s case is much too common. Women are often reluctant to address their sexuality with us—especially when we have been dismissive. We must recognize this important aspect of quality of life and relationships and be prepared to raise the issue with our patients before they begin therapy.

Educating ourselves and then our patients about strategies to reduce the impact of treatment and menopause on sexual function is the first step. Acknowledging and validating their concerns and being able to offer practical steps to preserve healthy sexual function is something, I think, that all ObGyns should be able to do. Strategies to maintain vulvovaginal elasticity include avoidance of soaps and drying chemicals, daily perineal and vaginal stretching—either manually, with a dilator, or via frequent sexual intercourse. And topical lubricants and moisturizing agents should be recommended to maintain vaginal pH and reduce the dryness, itching, and overall dysesthesia.

As the studies highlighted in this Update on Sexual Dysfunction demonstrate, the sexual consequences of radical hysterectomy are significant. Julie also became menopausal as a result of treatment—yet no one prepared her for the symptoms she would experience, and no member of her treatment team helped her understand the likely impact of therapy. Radiation oncologists do address the need for vaginal dilators or daily intercourse to maintain depth and caliber of the vagina during and after therapy, but they are less likely to prepare a patient for menopausal symptoms.

If our patients are to have an optimal experience, we need to provide coordinated, cross-disciplinary care that includes management not only of immediate side effects of treatment but also psychosocial and long-term hormonal and sexual sequelae of therapy. Julie charted her own course with the help of a very dedicated and sensitive partner to successfully overcome the negative effects of radiation, chemotherapy, surgery, and menopause on her sexuality.

Gynecologic cancer disrupts sexual function, over the short term and the long term

Jensen PT, Groenvold M, Klee MC, Thranov I, Petersen MA, Machin D. Early-stage cervical carcinoma, radical hysterectomy, and sexual function: a longitudinal study. Cancer. 2004;100(1):97–106.

Vaz AF, Pinto-Neto AM, Conde DM, et al. Quality of life and menopausal and sexual symptoms in gynecologic cancer survivors: a cohort study. Menopause. 2011;18(6):662–669.

These two studies explored sexual function after treatment for gynecologic cancer. The investigators found significant disruption of function.

Jensen et al: Radical hysterectomy for cervical Ca damages sexual function significantly

This was a prospective cohort study of 173 women who had early-stage cervical carcinoma and who underwent radical hysterectomy with pelvic lymphadenectomy (all of them node-negative). A validated questionnaire was administered six times, from 5 weeks to 24 months after surgery. An age-matched group of women without cancer was used for comparison. At the 12-month follow-up, patients were asked to report their sexual function at baseline and compare it to their current status. Overall, the women had a higher level of dissatisfaction with their sexual experiences 12 months after surgery than at baseline.

Details of the study

Women in the Jensen study were 23 to 75 years old (median age, 42.7 years), and 93% were sexually active at the time of diagnosis, reporting an average of one to two sexual activities in a week. Forty-six women (25%) were postmenopausal at diagnosis, compared with 34% of the control group. Only 8% of patients were using HT at study entry, compared with 25% of women in the control group. By 12 months after surgery, however, 25% of gynecologic cancer patients were taking systemic HT.

Findings included low libido and other ills

Severe lack of lubrication and low or no sexual desire were reported by cancer patients throughout the first 2 years after surgery. Patients also reported severe problems achieving orgasm as long as 6 months after surgery, as well as reduced vaginal size; both problems rendered their sexual experiences unsatisfactory. Nevertheless, 40% of patients reported at least some sexual activity by 5 weeks after surgery. By 6 months after surgery, there were almost as many sexually active women among the patient group as there were in the control group. However, at 18 months after treatment, patients reported less interest in intimacy—among both themselves and their partners—than among women in the control group. Overall, women treated for cervical cancer had a higher level of dissatisfaction with their sexual experiences 12 months after surgery than they did before diagnosis.

Although 91% of women who were sexually active before surgery resumed intercourse within 12 months, the frequency of sexual activity declined from one to two times per week to three to four times per month. Major long-term changes occurred in regard to libido (interest in sexual relations), arousal (vaginal lubrication), and vaginal size. Although dyspareunia was a significant problem 5 weeks to 3 months after surgery, it resolved within 1 to 2 years.

Jensen and colleagues concluded that radical hysterectomy for treatment of early-stage cervical cancer has significant negative effects on sexual function in the short and long term. They postulated a neurogenic basis for the sexual complaints and discussed both histologic and clinical studies to support this hypothesis.

They also emphasized the need to discuss the risks and management of sexual dysfunction with patients before and after surgery. Better management of the psychosocial consequences of a cancer diagnosis and the physical effects of radical hysterectomy may help avoid the negative experiences that were reported in this study.

Vaz et al: Rate of dyspareunia was high among women treated for endometrial or cervical Ca

Investigators followed 107 women from initial consultation for radiation therapy through 3 years post-treatment. Although a significant percentage (50%) of the cohort was lost to follow-up—many due to death or tumor recurrence—50% of those who remained reported dyspareunia 3 years after radiotherapy.

Women in this study were 21 to 75 years old (median age, 60 years) and had cervical or endometrial carcinoma. Eighty-nine women (83%) received external pelvic radiation as well as brachytherapy. Before beginning radiation therapy, 37.4% of the cohort underwent surgery for treatment of their cancer. Sixty-four percent of the cohort had stage III or IV disease.

At enrollment, 50% of women reported having a life partner, 82% were postmenopausal, and 11.2% were taking HT. However, only 21.5% of women reported sexual activity. The authors opine that this low rate of sexual activity may have been due to recent surgery, bleeding, or pain related to cancer.

All women were offered “standard” interventions for their dyspareunia, including the use of vaginal dilators twice daily for 2 years, as well as the use of vaginal lubricants. Patients who experienced menopausal symptoms—hot flashes, decreased libido, dyspareunia—were referred to a menopause outpatient clinic.

Before treatment, 20% of women reported dyspareunia. Three years later, 44% of patients reported sexual activity, but 50% had dyspareunia. Twenty-one percent reported lower sexual interest relative to baseline, 8% reported vaginal dryness, and 21% reported vasomotor symptoms. Although there was a trend toward increasing sexual activity with decreasing vaginal dryness, the rise in dyspareunia from 20% to 50% over 3 years is troubling.

We want to hear from you! Tell us what you think.

Sexual dysfunction is common among women in the United States. One recent study put the prevalence of distressing sexual dysfunction at 22.2%.¹ When cancer enters the picture, that percentage rises—dramatically. A 2010 survey from the Lance Armstrong Foundation found that 46% of people affected by cancer report problems with sex after treatment.²

In this article, I highlight three recent studies that explore the sexual effects of cancer and its treatment:

• a prospective cohort study showing that a majority of women treated for breast cancer experience sexual dysfunction afterward
• two longitudinal studies of women affected by gynecologic cancer, which show significant disruption of sexual function in the short and long term.

I also present the experiences of two cancer survivors who volunteered to relate their stories so that you might develop a better understanding of some of the challenges they face about their sexual function.

Sexual function deteriorates in many women after they are treated for breast Ca

Panjari M, Bell RJ, Davis SR. Sexual function after breast cancer. J Sex Med. 2011;8(1):294–302.

According to this prospective cohort study from Australia, a majority of women report significant sexual dysfunction after treatment for breast cancer—even when their sexual function was good, and satisfying, at the time of diagnosis (TABLE).

The Health and Wellbeing after Breast Cancer Study enrolled 1,684 Australian women within 12 months of their first diagnosis of invasive breast cancer. Each woman completed a questionnaire at the time of enrollment, and will complete annual follow-up questionnaires for 5 years to assess the impact of invasive breast cancer on physical, psychological, and socioeconomic wellbeing. Embedded within the 12-month questionnaire was the validated Menopause-Specific Quality of Life Questionnaire (MENQOL), which was used in this study to explore the sexual consequences of the diagnosis and treatment of invasive breast cancer.

Of the initial cohort, 1,011 women completed the 12-month questionnaire. These were women younger than 70 years who had a sexual partner and no evidence of active breast cancer. The authors describe the women in this cohort as representative of all women in Victoria, Australia, who have a new diagnosis of invasive breast cancer, in regard to both age (mean, 59 ± 11 years) and the stage of tumor (stage I, 48%; stage II–IV, 52%) at diagnosis.

Of this group, 70% were treated with lumpectomy and radiation therapy, and 30% were treated with mastectomy (2.6% with bilateral mastectomy). Of the women who underwent mastectomy, 9.6% had reconstructive surgery during the first year after diagnosis.

Forty-nine percent of women were treated with tamoxifen, and 28.2% were treated with an aromatase inhibitor.

After breast Ca, women experience low desire and less frequent sexual activity – as well as distress over both outcomes

More than two thirds of women reported sexual dysfunction 12 months after treatment

At baseline, 83% of women described their prediagnosis sexual function as good and satisfying. Twelve months later, 70% reported significant sexual dysfunction, and 77% reported vasomotor symptoms.

Women who reported new-onset sexual dysfunction were more likely to:

• have become menopausal since diagnosis
• experience hot flashes or night sweats
• be treated with an aromatase inhibitor.

There was no association between sexual dysfunction and stage of disease at diagnosis; type of surgery (lumpectomy or mastectomy); breast reconstruction; lymphedema; or axillary dissection.

Vasomotor symptoms in women taking endocrine therapy were associated with sexual dysfunction

Further analysis demonstrated that, among women who experienced vasomotor symptoms, those taking an aromatase inhibitor were more than three times as likely to report sexual dysfunction (odds ratio [OR], 3.49; 95% confidence interval [CI], 1.72–7.09), compared with women who were not on endocrine therapy—and those taking tamoxifen were almost twice as likely to report sexual dysfunction (OR, 1.73; 95% CI, 1.04–2.89). Chemotherapy was not independently related to sexual dysfunction.

In summary: 70% of women who were free of breast cancer 1 year after enrollment reported bothersome sexual consequences of their disease and its treatment; 77% reported vasomotor symptoms. Women who were rendered menopausal and those who experienced vasomotor symptoms while taking an aromatase inhibitor were at high risk of sexual dysfunction.

Two survivors report frustration—and resignation—when they sought help for sexual complaints

Katie* and Julie* tell typical stories of deep dissatisfaction with the health system after their cancer treatment

Katie: “I wasn’t prepared”

When my doctor told me I had locally advanced breast cancer 3 years ago, when I was 50, I wasn’t that surprised by the cancer diagnosis (I have a strong family history of breast cancer)—only by the fact that the tumor had developed so fast since my previous mammogram 15 months earlier. As treatment, I underwent neoadjuvant chemotherapy and bilateral mastectomy (I had the unaffected breast removed as a preventive measure). I also had breast reconstruction and started taking an aromatase inhibitor.

At the time of my diagnosis, I lost all desire for sexual intimacy—no big surprise there. But even after my treatment was over, my desire did not return. Part of the problem was the fact that chemotherapy rendered me menopausal, and the aromatase inhibitor I was taking compounded the menopausal experience. Quite suddenly, I was experiencing hot flashes, vaginal dryness and itching, pain during intercourse, severe bone and joint aches, weight gain (particularly around my abdomen), and general lethargy.

No one in my family had ever mentioned these effects of cancer. And none of my doctors prepared me, either. In fact, when I raised the subject, they seemed genuinely surprised! They offered no remedy other than a recommendation to apply a “moisturizer”—but they gave no details about what kind or how to use it. My oncologist did say that local estrogen would help relieve the pain of intercourse—but then she recommended strongly against it because my cancer was hormone-receptor positive.

My plastic surgeon did a much better job of explaining the effects and outcome of reconstruction than any of my other physicians, including my ObGyn, did of preparing me for menopause and sexual dysfunction.

All of my physicians strike me as caring, sensitive people, but their underlying attitude, as I perceive it, is that I should be grateful to be alive. In their view, it seems, enjoyment of sex is icing on the cake and, quite frankly, I am plenty lucky to have the cake. My oncologist even told me to let her know if I started “feeling better and having fewer hot flashes” so that she could perform ovarian ablation (and start the whole cycle over again). I was struck by how matter of factly she gave this advice, as though quality of life counts for nothing.

Three years into my postcancer life, I can say I have “adjusted” to my problems rather than overcome them. I am still taking an aromatase inhibitor. Sex is still slightly painful; I still struggle with vaginal dryness; and I sometimes feel like an old woman because of my bone and joint stiffness and pain. I did find out about an over-the-counter vaginal suppository, made with vitamin E and coconut oils, from another breast cancer survivor. And I switched from one aromatase inhibitor to another in an attempt to alleviate my achy joints. It helped.

I am grateful for my life—very much so—and for the expertise of my physicians, who helped to save it. But I wish they had prepared me better for the aftermath of cancer treatment. And I wish there were more remedies for women like me, who cannot take hormones.

Julie: “I’m on my own”

It was more than a surprise when my new doctor told me I had cancer. Until then, I had avoided doctors. That attitude can mean a premature death sentence when it comes to cervical cancer. It was a pretty awful realization that I could have avoided the drastic measures it took to save my life if I had just gotten annual Pap smears and exams. I was 39 at the time of diagnosis.

But after all the surgery and chemo and radiation were finished, the message I received was essentially: “OK, you’re good, for now. Just come back every few months for a check-up.”

What about the aftermath of all that treatment? What about the other aspects of the experience? I found that my doctors had very little to offer outside of surgery and drugs and the quick advice to get counseling or some other support services.

“I’m on my own” is what I’ve been telling concerned folks who ask how I’m doing. I am truly grateful for the skill, medicine, and machinery that made the killing of an invasive tumor possible. But I’m on my own when it comes to finding or inventing ways to cope with the new challenges of a pelvic area damaged by radiation and detoxing from the heavy metal—platinum—that was an ingredient in the chemo I received.

My partner and I have had to be persistently creative, careful, delicate, uncritical, and extremely patient with each other to bring about the return of a “normal” sex life. We have been successful, for the most part, but there is also a slightly new definition of what “normal” is for us. Our latest triumph is that we no longer have to use copious amounts of lubricant to engage in intercourse. Sex is no longer painful, as the vaginal tissues have been slowly, patiently engaged on a regularly scheduled basis. Can you imagine sex on a schedule? Neither could I, but that is what we found worked from as early as 1 week postradiation. As it turns out, this was good advice—really, the only advice I got when it came to the practicalities of restoring function, but it required a fair amount of tweaking and personalization as well.

Another big change in perception that I had to accept as part of my new norm is learning to talk about my most personal areas in a matter of fact way.

The cancer conveyor-belt approach to treatment is a very streamlined, well-run system. I’ve been impressed with the expertise, efficiency, and demeanor of all the professionals I have encountered. Everyone—even receptionists—has been helpful and empathetic, especially my own ObGyn, who has hugged me and cried with me and offered to put herself on the line for me and speak out to the media when I had no health insurance. But for most patients post-treatment, we figuratively walk off a cliff and find ourselves in new territory without any network or structure like we experienced during the “war” on our cancer. This new territory is a place of possibility within the health-care field—one I hope is developing now.

Dr. Barbara S. Levy asks: How do we respond? We physicians are so focused on treating or curing disease that we often lose sight of the woman who has the disease.

Katie’s case is much too common. Women are often reluctant to address their sexuality with us—especially when we have been dismissive. We must recognize this important aspect of quality of life and relationships and be prepared to raise the issue with our patients before they begin therapy.

Educating ourselves and then our patients about strategies to reduce the impact of treatment and menopause on sexual function is the first step. Acknowledging and validating their concerns and being able to offer practical steps to preserve healthy sexual function is something, I think, that all ObGyns should be able to do. Strategies to maintain vulvovaginal elasticity include avoidance of soaps and drying chemicals, daily perineal and vaginal stretching—either manually, with a dilator, or via frequent sexual intercourse. And topical lubricants and moisturizing agents should be recommended to maintain vaginal pH and reduce the dryness, itching, and overall dysesthesia.

As the studies highlighted in this Update on Sexual Dysfunction demonstrate, the sexual consequences of radical hysterectomy are significant. Julie also became menopausal as a result of treatment—yet no one prepared her for the symptoms she would experience, and no member of her treatment team helped her understand the likely impact of therapy. Radiation oncologists do address the need for vaginal dilators or daily intercourse to maintain depth and caliber of the vagina during and after therapy, but they are less likely to prepare a patient for menopausal symptoms.

If our patients are to have an optimal experience, we need to provide coordinated, cross-disciplinary care that includes management not only of immediate side effects of treatment but also psychosocial and long-term hormonal and sexual sequelae of therapy. Julie charted her own course with the help of a very dedicated and sensitive partner to successfully overcome the negative effects of radiation, chemotherapy, surgery, and menopause on her sexuality.

Gynecologic cancer disrupts sexual function, over the short term and the long term

Jensen PT, Groenvold M, Klee MC, Thranov I, Petersen MA, Machin D. Early-stage cervical carcinoma, radical hysterectomy, and sexual function: a longitudinal study. Cancer. 2004;100(1):97–106.

Vaz AF, Pinto-Neto AM, Conde DM, et al. Quality of life and menopausal and sexual symptoms in gynecologic cancer survivors: a cohort study. Menopause. 2011;18(6):662–669.

These two studies explored sexual function after treatment for gynecologic cancer. The investigators found significant disruption of function.

Jensen et al: Radical hysterectomy for cervical Ca damages sexual function significantly

This was a prospective cohort study of 173 women who had early-stage cervical carcinoma and who underwent radical hysterectomy with pelvic lymphadenectomy (all of them node-negative). A validated questionnaire was administered six times, from 5 weeks to 24 months after surgery. An age-matched group of women without cancer was used for comparison. At the 12-month follow-up, patients were asked to report their sexual function at baseline and compare it to their current status. Overall, the women had a higher level of dissatisfaction with their sexual experiences 12 months after surgery than at baseline.

Details of the study

Women in the Jensen study were 23 to 75 years old (median age, 42.7 years), and 93% were sexually active at the time of diagnosis, reporting an average of one to two sexual activities in a week. Forty-six women (25%) were postmenopausal at diagnosis, compared with 34% of the control group. Only 8% of patients were using HT at study entry, compared with 25% of women in the control group. By 12 months after surgery, however, 25% of gynecologic cancer patients were taking systemic HT.

Findings included low libido and other ills

Severe lack of lubrication and low or no sexual desire were reported by cancer patients throughout the first 2 years after surgery. Patients also reported severe problems achieving orgasm as long as 6 months after surgery, as well as reduced vaginal size; both problems rendered their sexual experiences unsatisfactory. Nevertheless, 40% of patients reported at least some sexual activity by 5 weeks after surgery. By 6 months after surgery, there were almost as many sexually active women among the patient group as there were in the control group. However, at 18 months after treatment, patients reported less interest in intimacy—among both themselves and their partners—than among women in the control group. Overall, women treated for cervical cancer had a higher level of dissatisfaction with their sexual experiences 12 months after surgery than they did before diagnosis.

Although 91% of women who were sexually active before surgery resumed intercourse within 12 months, the frequency of sexual activity declined from one to two times per week to three to four times per month. Major long-term changes occurred in regard to libido (interest in sexual relations), arousal (vaginal lubrication), and vaginal size. Although dyspareunia was a significant problem 5 weeks to 3 months after surgery, it resolved within 1 to 2 years.

Jensen and colleagues concluded that radical hysterectomy for treatment of early-stage cervical cancer has significant negative effects on sexual function in the short and long term. They postulated a neurogenic basis for the sexual complaints and discussed both histologic and clinical studies to support this hypothesis.

They also emphasized the need to discuss the risks and management of sexual dysfunction with patients before and after surgery. Better management of the psychosocial consequences of a cancer diagnosis and the physical effects of radical hysterectomy may help avoid the negative experiences that were reported in this study.

Vaz et al: Rate of dyspareunia was high among women treated for endometrial or cervical Ca

Investigators followed 107 women from initial consultation for radiation therapy through 3 years post-treatment. Although a significant percentage (50%) of the cohort was lost to follow-up—many due to death or tumor recurrence—50% of those who remained reported dyspareunia 3 years after radiotherapy.

Women in this study were 21 to 75 years old (median age, 60 years) and had cervical or endometrial carcinoma. Eighty-nine women (83%) received external pelvic radiation as well as brachytherapy. Before beginning radiation therapy, 37.4% of the cohort underwent surgery for treatment of their cancer. Sixty-four percent of the cohort had stage III or IV disease.

At enrollment, 50% of women reported having a life partner, 82% were postmenopausal, and 11.2% were taking HT. However, only 21.5% of women reported sexual activity. The authors opine that this low rate of sexual activity may have been due to recent surgery, bleeding, or pain related to cancer.

All women were offered “standard” interventions for their dyspareunia, including the use of vaginal dilators twice daily for 2 years, as well as the use of vaginal lubricants. Patients who experienced menopausal symptoms—hot flashes, decreased libido, dyspareunia—were referred to a menopause outpatient clinic.

Before treatment, 20% of women reported dyspareunia. Three years later, 44% of patients reported sexual activity, but 50% had dyspareunia. Twenty-one percent reported lower sexual interest relative to baseline, 8% reported vaginal dryness, and 21% reported vasomotor symptoms. Although there was a trend toward increasing sexual activity with decreasing vaginal dryness, the rise in dyspareunia from 20% to 50% over 3 years is troubling.

We want to hear from you! Tell us what you think.

Sexual dysfunction is common among women in the United States. One recent study put the prevalence of distressing sexual dysfunction at 22.2%.¹ When cancer enters the picture, that percentage rises—dramatically. A 2010 survey from the Lance Armstrong Foundation found that 46% of people affected by cancer report problems with sex after treatment.²

In this article, I highlight three recent studies that explore the sexual effects of cancer and its treatment:

• a prospective cohort study showing that a majority of women treated for breast cancer experience sexual dysfunction afterward
• two longitudinal studies of women affected by gynecologic cancer, which show significant disruption of sexual function in the short and long term.

I also present the experiences of two cancer survivors who volunteered to relate their stories so that you might develop a better understanding of some of the challenges they face about their sexual function.

Sexual function deteriorates in many women after they are treated for breast Ca

Panjari M, Bell RJ, Davis SR. Sexual function after breast cancer. J Sex Med. 2011;8(1):294–302.

According to this prospective cohort study from Australia, a majority of women report significant sexual dysfunction after treatment for breast cancer—even when their sexual function was good, and satisfying, at the time of diagnosis (TABLE).

The Health and Wellbeing after Breast Cancer Study enrolled 1,684 Australian women within 12 months of their first diagnosis of invasive breast cancer. Each woman completed a questionnaire at the time of enrollment, and will complete annual follow-up questionnaires for 5 years to assess the impact of invasive breast cancer on physical, psychological, and socioeconomic wellbeing. Embedded within the 12-month questionnaire was the validated Menopause-Specific Quality of Life Questionnaire (MENQOL), which was used in this study to explore the sexual consequences of the diagnosis and treatment of invasive breast cancer.

Of the initial cohort, 1,011 women completed the 12-month questionnaire. These were women younger than 70 years who had a sexual partner and no evidence of active breast cancer. The authors describe the women in this cohort as representative of all women in Victoria, Australia, who have a new diagnosis of invasive breast cancer, in regard to both age (mean, 59 ± 11 years) and the stage of tumor (stage I, 48%; stage II–IV, 52%) at diagnosis.

Of this group, 70% were treated with lumpectomy and radiation therapy, and 30% were treated with mastectomy (2.6% with bilateral mastectomy). Of the women who underwent mastectomy, 9.6% had reconstructive surgery during the first year after diagnosis.

Forty-nine percent of women were treated with tamoxifen, and 28.2% were treated with an aromatase inhibitor.

After breast Ca, women experience low desire and less frequent sexual activity – as well as distress over both outcomes

More than two thirds of women reported sexual dysfunction 12 months after treatment

At baseline, 83% of women described their prediagnosis sexual function as good and satisfying. Twelve months later, 70% reported significant sexual dysfunction, and 77% reported vasomotor symptoms.

Women who reported new-onset sexual dysfunction were more likely to:

• have become menopausal since diagnosis
• experience hot flashes or night sweats
• be treated with an aromatase inhibitor.

There was no association between sexual dysfunction and stage of disease at diagnosis; type of surgery (lumpectomy or mastectomy); breast reconstruction; lymphedema; or axillary dissection.

Vasomotor symptoms in women taking endocrine therapy were associated with sexual dysfunction

Further analysis demonstrated that, among women who experienced vasomotor symptoms, those taking an aromatase inhibitor were more than three times as likely to report sexual dysfunction (odds ratio [OR], 3.49; 95% confidence interval [CI], 1.72–7.09), compared with women who were not on endocrine therapy—and those taking tamoxifen were almost twice as likely to report sexual dysfunction (OR, 1.73; 95% CI, 1.04–2.89). Chemotherapy was not independently related to sexual dysfunction.

In summary: 70% of women who were free of breast cancer 1 year after enrollment reported bothersome sexual consequences of their disease and its treatment; 77% reported vasomotor symptoms. Women who were rendered menopausal and those who experienced vasomotor symptoms while taking an aromatase inhibitor were at high risk of sexual dysfunction.

Two survivors report frustration—and resignation—when they sought help for sexual complaints

Katie* and Julie* tell typical stories of deep dissatisfaction with the health system after their cancer treatment

Katie: “I wasn’t prepared”

When my doctor told me I had locally advanced breast cancer 3 years ago, when I was 50, I wasn’t that surprised by the cancer diagnosis (I have a strong family history of breast cancer)—only by the fact that the tumor had developed so fast since my previous mammogram 15 months earlier. As treatment, I underwent neoadjuvant chemotherapy and bilateral mastectomy (I had the unaffected breast removed as a preventive measure). I also had breast reconstruction and started taking an aromatase inhibitor.

At the time of my diagnosis, I lost all desire for sexual intimacy—no big surprise there. But even after my treatment was over, my desire did not return. Part of the problem was the fact that chemotherapy rendered me menopausal, and the aromatase inhibitor I was taking compounded the menopausal experience. Quite suddenly, I was experiencing hot flashes, vaginal dryness and itching, pain during intercourse, severe bone and joint aches, weight gain (particularly around my abdomen), and general lethargy.

No one in my family had ever mentioned these effects of cancer. And none of my doctors prepared me, either. In fact, when I raised the subject, they seemed genuinely surprised! They offered no remedy other than a recommendation to apply a “moisturizer”—but they gave no details about what kind or how to use it. My oncologist did say that local estrogen would help relieve the pain of intercourse—but then she recommended strongly against it because my cancer was hormone-receptor positive.

My plastic surgeon did a much better job of explaining the effects and outcome of reconstruction than any of my other physicians, including my ObGyn, did of preparing me for menopause and sexual dysfunction.

All of my physicians strike me as caring, sensitive people, but their underlying attitude, as I perceive it, is that I should be grateful to be alive. In their view, it seems, enjoyment of sex is icing on the cake and, quite frankly, I am plenty lucky to have the cake. My oncologist even told me to let her know if I started “feeling better and having fewer hot flashes” so that she could perform ovarian ablation (and start the whole cycle over again). I was struck by how matter of factly she gave this advice, as though quality of life counts for nothing.

Three years into my postcancer life, I can say I have “adjusted” to my problems rather than overcome them. I am still taking an aromatase inhibitor. Sex is still slightly painful; I still struggle with vaginal dryness; and I sometimes feel like an old woman because of my bone and joint stiffness and pain. I did find out about an over-the-counter vaginal suppository, made with vitamin E and coconut oils, from another breast cancer survivor. And I switched from one aromatase inhibitor to another in an attempt to alleviate my achy joints. It helped.

I am grateful for my life—very much so—and for the expertise of my physicians, who helped to save it. But I wish they had prepared me better for the aftermath of cancer treatment. And I wish there were more remedies for women like me, who cannot take hormones.

Julie: “I’m on my own”

It was more than a surprise when my new doctor told me I had cancer. Until then, I had avoided doctors. That attitude can mean a premature death sentence when it comes to cervical cancer. It was a pretty awful realization that I could have avoided the drastic measures it took to save my life if I had just gotten annual Pap smears and exams. I was 39 at the time of diagnosis.

But after all the surgery and chemo and radiation were finished, the message I received was essentially: “OK, you’re good, for now. Just come back every few months for a check-up.”

What about the aftermath of all that treatment? What about the other aspects of the experience? I found that my doctors had very little to offer outside of surgery and drugs and the quick advice to get counseling or some other support services.

“I’m on my own” is what I’ve been telling concerned folks who ask how I’m doing. I am truly grateful for the skill, medicine, and machinery that made the killing of an invasive tumor possible. But I’m on my own when it comes to finding or inventing ways to cope with the new challenges of a pelvic area damaged by radiation and detoxing from the heavy metal—platinum—that was an ingredient in the chemo I received.

My partner and I have had to be persistently creative, careful, delicate, uncritical, and extremely patient with each other to bring about the return of a “normal” sex life. We have been successful, for the most part, but there is also a slightly new definition of what “normal” is for us. Our latest triumph is that we no longer have to use copious amounts of lubricant to engage in intercourse. Sex is no longer painful, as the vaginal tissues have been slowly, patiently engaged on a regularly scheduled basis. Can you imagine sex on a schedule? Neither could I, but that is what we found worked from as early as 1 week postradiation. As it turns out, this was good advice—really, the only advice I got when it came to the practicalities of restoring function, but it required a fair amount of tweaking and personalization as well.

Another big change in perception that I had to accept as part of my new norm is learning to talk about my most personal areas in a matter of fact way.

The cancer conveyor-belt approach to treatment is a very streamlined, well-run system. I’ve been impressed with the expertise, efficiency, and demeanor of all the professionals I have encountered. Everyone—even receptionists—has been helpful and empathetic, especially my own ObGyn, who has hugged me and cried with me and offered to put herself on the line for me and speak out to the media when I had no health insurance. But for most patients post-treatment, we figuratively walk off a cliff and find ourselves in new territory without any network or structure like we experienced during the “war” on our cancer. This new territory is a place of possibility within the health-care field—one I hope is developing now.

Dr. Barbara S. Levy asks: How do we respond? We physicians are so focused on treating or curing disease that we often lose sight of the woman who has the disease.

Katie’s case is much too common. Women are often reluctant to address their sexuality with us—especially when we have been dismissive. We must recognize this important aspect of quality of life and relationships and be prepared to raise the issue with our patients before they begin therapy.

Educating ourselves and then our patients about strategies to reduce the impact of treatment and menopause on sexual function is the first step. Acknowledging and validating their concerns and being able to offer practical steps to preserve healthy sexual function is something, I think, that all ObGyns should be able to do. Strategies to maintain vulvovaginal elasticity include avoidance of soaps and drying chemicals, daily perineal and vaginal stretching—either manually, with a dilator, or via frequent sexual intercourse. And topical lubricants and moisturizing agents should be recommended to maintain vaginal pH and reduce the dryness, itching, and overall dysesthesia.

As the studies highlighted in this Update on Sexual Dysfunction demonstrate, the sexual consequences of radical hysterectomy are significant. Julie also became menopausal as a result of treatment—yet no one prepared her for the symptoms she would experience, and no member of her treatment team helped her understand the likely impact of therapy. Radiation oncologists do address the need for vaginal dilators or daily intercourse to maintain depth and caliber of the vagina during and after therapy, but they are less likely to prepare a patient for menopausal symptoms.

If our patients are to have an optimal experience, we need to provide coordinated, cross-disciplinary care that includes management not only of immediate side effects of treatment but also psychosocial and long-term hormonal and sexual sequelae of therapy. Julie charted her own course with the help of a very dedicated and sensitive partner to successfully overcome the negative effects of radiation, chemotherapy, surgery, and menopause on her sexuality.

Gynecologic cancer disrupts sexual function, over the short term and the long term

Jensen PT, Groenvold M, Klee MC, Thranov I, Petersen MA, Machin D. Early-stage cervical carcinoma, radical hysterectomy, and sexual function: a longitudinal study. Cancer. 2004;100(1):97–106.

Vaz AF, Pinto-Neto AM, Conde DM, et al. Quality of life and menopausal and sexual symptoms in gynecologic cancer survivors: a cohort study. Menopause. 2011;18(6):662–669.

These two studies explored sexual function after treatment for gynecologic cancer. The investigators found significant disruption of function.

Jensen et al: Radical hysterectomy for cervical Ca damages sexual function significantly

This was a prospective cohort study of 173 women who had early-stage cervical carcinoma and who underwent radical hysterectomy with pelvic lymphadenectomy (all of them node-negative). A validated questionnaire was administered six times, from 5 weeks to 24 months after surgery. An age-matched group of women without cancer was used for comparison. At the 12-month follow-up, patients were asked to report their sexual function at baseline and compare it to their current status. Overall, the women had a higher level of dissatisfaction with their sexual experiences 12 months after surgery than at baseline.

Details of the study

Women in the Jensen study were 23 to 75 years old (median age, 42.7 years), and 93% were sexually active at the time of diagnosis, reporting an average of one to two sexual activities in a week. Forty-six women (25%) were postmenopausal at diagnosis, compared with 34% of the control group. Only 8% of patients were using HT at study entry, compared with 25% of women in the control group. By 12 months after surgery, however, 25% of gynecologic cancer patients were taking systemic HT.

Findings included low libido and other ills

Severe lack of lubrication and low or no sexual desire were reported by cancer patients throughout the first 2 years after surgery. Patients also reported severe problems achieving orgasm as long as 6 months after surgery, as well as reduced vaginal size; both problems rendered their sexual experiences unsatisfactory. Nevertheless, 40% of patients reported at least some sexual activity by 5 weeks after surgery. By 6 months after surgery, there were almost as many sexually active women among the patient group as there were in the control group. However, at 18 months after treatment, patients reported less interest in intimacy—among both themselves and their partners—than among women in the control group. Overall, women treated for cervical cancer had a higher level of dissatisfaction with their sexual experiences 12 months after surgery than they did before diagnosis.

Although 91% of women who were sexually active before surgery resumed intercourse within 12 months, the frequency of sexual activity declined from one to two times per week to three to four times per month. Major long-term changes occurred in regard to libido (interest in sexual relations), arousal (vaginal lubrication), and vaginal size. Although dyspareunia was a significant problem 5 weeks to 3 months after surgery, it resolved within 1 to 2 years.

Jensen and colleagues concluded that radical hysterectomy for treatment of early-stage cervical cancer has significant negative effects on sexual function in the short and long term. They postulated a neurogenic basis for the sexual complaints and discussed both histologic and clinical studies to support this hypothesis.

They also emphasized the need to discuss the risks and management of sexual dysfunction with patients before and after surgery. Better management of the psychosocial consequences of a cancer diagnosis and the physical effects of radical hysterectomy may help avoid the negative experiences that were reported in this study.

Vaz et al: Rate of dyspareunia was high among women treated for endometrial or cervical Ca

Investigators followed 107 women from initial consultation for radiation therapy through 3 years post-treatment. Although a significant percentage (50%) of the cohort was lost to follow-up—many due to death or tumor recurrence—50% of those who remained reported dyspareunia 3 years after radiotherapy.

Women in this study were 21 to 75 years old (median age, 60 years) and had cervical or endometrial carcinoma. Eighty-nine women (83%) received external pelvic radiation as well as brachytherapy. Before beginning radiation therapy, 37.4% of the cohort underwent surgery for treatment of their cancer. Sixty-four percent of the cohort had stage III or IV disease.

At enrollment, 50% of women reported having a life partner, 82% were postmenopausal, and 11.2% were taking HT. However, only 21.5% of women reported sexual activity. The authors opine that this low rate of sexual activity may have been due to recent surgery, bleeding, or pain related to cancer.

All women were offered “standard” interventions for their dyspareunia, including the use of vaginal dilators twice daily for 2 years, as well as the use of vaginal lubricants. Patients who experienced menopausal symptoms—hot flashes, decreased libido, dyspareunia—were referred to a menopause outpatient clinic.

Before treatment, 20% of women reported dyspareunia. Three years later, 44% of patients reported sexual activity, but 50% had dyspareunia. Twenty-one percent reported lower sexual interest relative to baseline, 8% reported vaginal dryness, and 21% reported vasomotor symptoms. Although there was a trend toward increasing sexual activity with decreasing vaginal dryness, the rise in dyspareunia from 20% to 50% over 3 years is troubling.

We want to hear from you! Tell us what you think.