Why it's important to open the sexual health dialogue

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In this 5-minute audiocast, Dr. Krychman offers key takeaways from his seminar, "Sexuality in the Elder Woman," at the 62nd Annual Clinical Meeting of the American College of Obstetricians and Gynecologists.

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In this 5-minute audiocast, Dr. Krychman offers key takeaways from his seminar, "Sexuality in the Elder Woman," at the 62nd Annual Clinical Meeting of the American College of Obstetricians and Gynecologists.

In this 5-minute audiocast, Dr. Krychman offers key takeaways from his seminar, "Sexuality in the Elder Woman," at the 62nd Annual Clinical Meeting of the American College of Obstetricians and Gynecologists.

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Should the adnexae be removed during hysterectomy for benign disease to reduce the risk of ovarian cancer?

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Should the adnexae be removed during hysterectomy for benign disease to reduce the risk of ovarian cancer?

The decision-making surrounding gynecologic surgery for benign disease is increasingly complex. Patients and their physicians must balance the potential benefits of salpingo-oophorectomy against possible adverse consequence as they consider various health goals, including longevity, cancer risk, and quality of life.

Chan and colleagues add important data to our understanding of this equation. Analyzing a large cohort of patients from Kaiser Permanente Northern California who underwent hysterectomy for benign disease, they found that removal of the fallopian tubes and ovaries significantly reduced the risk of developing ovarian cancer. The incidence of ovarian cancer per 100,000 person-years was 26.2 for women undergoing hysterectomy alone (95% confidence interval [CI], 15.5–37.0), 17.5 for hysterectomy with unilateral salpingo-oophorectomy (95% CI, 0–39.1), and 1.7 for hysterectomy with bilateral salpingo-oophorectomy (95% CI, 0.4–3.0).

The hazard ratio (HR) for ovarian cancer was 0.58 for women undergoing unilateral salpingo-oophorectomy (95% CI, 0.18–1.90) and 0.12 for women undergoing bilateral salpingo-oophorectomy (95% CI, 0.05–0.28), compared with women undergoing hysterectomy alone.

Notable strengths of the analysis include the large size of the study population and the duration of patient follow-up (18 years). The authors acknowledge several limitations of the study, including the lack of data on BRCA mutation status and family history of cancer, as well as several other demographic data points possibly relevant to a risk of developing adnexal or peritoneal malignancy.

Related article: What is the gynecologist’s role in the care of BRCA previvors? Robert L. Barbieri, MD (Editorial, September 2013)

Keep these findings in context
As the authors discuss, this report should be considered in the context of other work suggesting that the lower mortality rate associated with ovarian conservation at the time of hysterectomy for benign disease arises mostly from a protective effect against cardiovascular disease (CVD)—perhaps from subclinical hormone production following menopause. Given that CVD remains the leading cause of death among American women, an individualized assessment of risk is necessary when planning the extent of surgery in this circumstance.

Related article: Oophorectomy or salpingectomy—which makes more sense? William H. Parker, MD (March 2014)

It also is interesting to consider the authors’ finding of a notable but statistically insignificant decrease in the risk of ovarian cancer associated with removal of only one tube and ovary. However, recognizing the possible limitations of their demographic information on this point, they suggest that this may be an area for further investigation, which would necessarily include characterization of the trends in the laterality of adnexal cancers. The preservation of hormonal function makes this an interesting option to consider.

We also need to further investigate the role of bilateral salpingectomy at the time of hysterectomy, with ovarian conservation, as an alternate therapeutic option, based upon evidence that extrauterine serous carcinoma may to a significant degree arise from the tubal epithelium rather than the ovarian cortex.

WHAT THIS EVIDENCE MEANS FOR PRACTICE
Removal of the adnexae significantly reduces the risk of ovarian cancer among the cohort of women undergoing hysterectomy for benign disease. However, the decision of whether or not to remove the adnexae when planning surgery should take into account other factors that may affect the risk of adnexal malignancy, including family history and BRCA mutation status, as well as other patient comorbidities.
Andrew W. Menzin, MD

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Andrew W. Menzin, MD, is Vice Chairman for Academic Affairs and ObGyn Residency Program Director at North Shore University Hospital and LIJ Medical Center in Manhasset, New York. He serves as the Associate Chief of Gynecologic Oncology for the North Shore LIJ Health System and is Professor of Obstetrics and Gynecology at the Hofstra North Shore LIJ School of Medicine.

The author reports no financial relationships relevant to this article.

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The decision-making surrounding gynecologic surgery for benign disease is increasingly complex. Patients and their physicians must balance the potential benefits of salpingo-oophorectomy against possible adverse consequence as they consider various health goals, including longevity, cancer risk, and quality of life.

Chan and colleagues add important data to our understanding of this equation. Analyzing a large cohort of patients from Kaiser Permanente Northern California who underwent hysterectomy for benign disease, they found that removal of the fallopian tubes and ovaries significantly reduced the risk of developing ovarian cancer. The incidence of ovarian cancer per 100,000 person-years was 26.2 for women undergoing hysterectomy alone (95% confidence interval [CI], 15.5–37.0), 17.5 for hysterectomy with unilateral salpingo-oophorectomy (95% CI, 0–39.1), and 1.7 for hysterectomy with bilateral salpingo-oophorectomy (95% CI, 0.4–3.0).

The hazard ratio (HR) for ovarian cancer was 0.58 for women undergoing unilateral salpingo-oophorectomy (95% CI, 0.18–1.90) and 0.12 for women undergoing bilateral salpingo-oophorectomy (95% CI, 0.05–0.28), compared with women undergoing hysterectomy alone.

Notable strengths of the analysis include the large size of the study population and the duration of patient follow-up (18 years). The authors acknowledge several limitations of the study, including the lack of data on BRCA mutation status and family history of cancer, as well as several other demographic data points possibly relevant to a risk of developing adnexal or peritoneal malignancy.

Related article: What is the gynecologist’s role in the care of BRCA previvors? Robert L. Barbieri, MD (Editorial, September 2013)

Keep these findings in context
As the authors discuss, this report should be considered in the context of other work suggesting that the lower mortality rate associated with ovarian conservation at the time of hysterectomy for benign disease arises mostly from a protective effect against cardiovascular disease (CVD)—perhaps from subclinical hormone production following menopause. Given that CVD remains the leading cause of death among American women, an individualized assessment of risk is necessary when planning the extent of surgery in this circumstance.

Related article: Oophorectomy or salpingectomy—which makes more sense? William H. Parker, MD (March 2014)

It also is interesting to consider the authors’ finding of a notable but statistically insignificant decrease in the risk of ovarian cancer associated with removal of only one tube and ovary. However, recognizing the possible limitations of their demographic information on this point, they suggest that this may be an area for further investigation, which would necessarily include characterization of the trends in the laterality of adnexal cancers. The preservation of hormonal function makes this an interesting option to consider.

We also need to further investigate the role of bilateral salpingectomy at the time of hysterectomy, with ovarian conservation, as an alternate therapeutic option, based upon evidence that extrauterine serous carcinoma may to a significant degree arise from the tubal epithelium rather than the ovarian cortex.

WHAT THIS EVIDENCE MEANS FOR PRACTICE
Removal of the adnexae significantly reduces the risk of ovarian cancer among the cohort of women undergoing hysterectomy for benign disease. However, the decision of whether or not to remove the adnexae when planning surgery should take into account other factors that may affect the risk of adnexal malignancy, including family history and BRCA mutation status, as well as other patient comorbidities.
Andrew W. Menzin, MD

Tell us what you think!
Drop us a line and let us know what you think about this or other current articles, which topics you'd like to see covered in future issues, and what challenges you face in daily practice. Tell us what you think by emailing us at: [email protected] Please include your name, city and state.
Stay in touch! Your feedback is important to us!

The decision-making surrounding gynecologic surgery for benign disease is increasingly complex. Patients and their physicians must balance the potential benefits of salpingo-oophorectomy against possible adverse consequence as they consider various health goals, including longevity, cancer risk, and quality of life.

Chan and colleagues add important data to our understanding of this equation. Analyzing a large cohort of patients from Kaiser Permanente Northern California who underwent hysterectomy for benign disease, they found that removal of the fallopian tubes and ovaries significantly reduced the risk of developing ovarian cancer. The incidence of ovarian cancer per 100,000 person-years was 26.2 for women undergoing hysterectomy alone (95% confidence interval [CI], 15.5–37.0), 17.5 for hysterectomy with unilateral salpingo-oophorectomy (95% CI, 0–39.1), and 1.7 for hysterectomy with bilateral salpingo-oophorectomy (95% CI, 0.4–3.0).

The hazard ratio (HR) for ovarian cancer was 0.58 for women undergoing unilateral salpingo-oophorectomy (95% CI, 0.18–1.90) and 0.12 for women undergoing bilateral salpingo-oophorectomy (95% CI, 0.05–0.28), compared with women undergoing hysterectomy alone.

Notable strengths of the analysis include the large size of the study population and the duration of patient follow-up (18 years). The authors acknowledge several limitations of the study, including the lack of data on BRCA mutation status and family history of cancer, as well as several other demographic data points possibly relevant to a risk of developing adnexal or peritoneal malignancy.

Related article: What is the gynecologist’s role in the care of BRCA previvors? Robert L. Barbieri, MD (Editorial, September 2013)

Keep these findings in context
As the authors discuss, this report should be considered in the context of other work suggesting that the lower mortality rate associated with ovarian conservation at the time of hysterectomy for benign disease arises mostly from a protective effect against cardiovascular disease (CVD)—perhaps from subclinical hormone production following menopause. Given that CVD remains the leading cause of death among American women, an individualized assessment of risk is necessary when planning the extent of surgery in this circumstance.

Related article: Oophorectomy or salpingectomy—which makes more sense? William H. Parker, MD (March 2014)

It also is interesting to consider the authors’ finding of a notable but statistically insignificant decrease in the risk of ovarian cancer associated with removal of only one tube and ovary. However, recognizing the possible limitations of their demographic information on this point, they suggest that this may be an area for further investigation, which would necessarily include characterization of the trends in the laterality of adnexal cancers. The preservation of hormonal function makes this an interesting option to consider.

We also need to further investigate the role of bilateral salpingectomy at the time of hysterectomy, with ovarian conservation, as an alternate therapeutic option, based upon evidence that extrauterine serous carcinoma may to a significant degree arise from the tubal epithelium rather than the ovarian cortex.

WHAT THIS EVIDENCE MEANS FOR PRACTICE
Removal of the adnexae significantly reduces the risk of ovarian cancer among the cohort of women undergoing hysterectomy for benign disease. However, the decision of whether or not to remove the adnexae when planning surgery should take into account other factors that may affect the risk of adnexal malignancy, including family history and BRCA mutation status, as well as other patient comorbidities.
Andrew W. Menzin, MD

Tell us what you think!
Drop us a line and let us know what you think about this or other current articles, which topics you'd like to see covered in future issues, and what challenges you face in daily practice. Tell us what you think by emailing us at: [email protected] Please include your name, city and state.
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Problem Solving In Multi-Site Hospital Medicine Groups

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Dr. Nelson

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Serving as the lead physician for a hospital medicine group (HMG) makes for challenging work. And the challenges and complexity only increase for anyone who serves as the physician leader for multiple practice sites in the same hospital system. In my November 2013 column on multi-site HMG leaders, I listed a few of the tricky issues they face and will mention a few more here.

Large-Small Friction

Unfortunately, tension between hospitalists at the big hospital and doctors at the small, “feeder” hospitals seems pretty common, and I think it’s due largely to high stress and a wide variation in workload, neither of which are in our direct control. At facilities where there is significant tension, I’m impressed by how vigorously the hospitalists at both the small and large hospitals argue that their own site faces the most stress and challenges. (This is a little like the endless debate about who works harder, those who work with residents and those who don’t.)

The hospitalists at the small site point out that they work with little or no subspecialty help and might even have to take night call from home while working during the day. Those at the big hospital say they are the ones with the very large scope of clinical practice and that, rather than making their life easier, the presence of lots of subspecialists makes for additional work coordinating care and communicating with all parties.

Where it exists, this tension is most evident during a transfer from one of the small hospitals to the large one. After all, one of the reasons to form a system of hospitals is so that nearly all patient needs can be met at one of the facilities in the system. Yet, for many reasons, the hospitalists at the large hospital are—sometimes—not as receptive to transfers as might be ideal. They might be short staffed or facing a high census or an unusually high number of admissions from their own ED. Or, perhaps, they’re concerned that the subspecialty services for which the patient is being transferred (e.g. to be scoped by a GI doctor) won’t be as helpful or prompt as needed. Or maybe they’ve felt “burned” by their colleagues at the small hospital for past transfers that didn’t seem necessary.

Where it exists, this tension is most evident during a transfer from one of the small hospitals to the large one. After all, one of the reasons to form a system of hospitals is so that nearly all patient needs can be met at one of the facilities in the system. Yet, for many reasons, the hospitalists at the large hospital are—sometimes—not as receptive to transfers as might be ideal.

The result can be that the doctors at the smaller hospital complain that the “mother ship” hospitalists often are unfriendly and unreceptive to transfer requests. Although there may not be a definitive “cure” for this issue, there are several ways to help address the problem.

  • In my last column, I mentioned the value of one or more in-person meetings between those who tend to be on the sending and receiving end of transfers, to establish some criteria regarding transfers that are appropriate and review the process of requesting a transfer and making the associated arrangements. In most cases there will be value in the parties meeting routinely—perhaps two to four times annually—to review how the system is working and address any difficulties.
  • Periodic social meetings among the hospitalists at each site will help to form relationships that can make it less likely that any conversation about transfers will go in an unhelpful direction. Things can be very different when the people on each end of the phone call know each other personally.
  • Record the phone calls between those seeking and accepting/declining each transfer. Scott Rissmiller, MD, the lead hospitalist for the 17 practice sites in Carolinas Healthcare, has said that having underperforming doctors listen to recordings of their phone calls about transfers has, in most cases he’s been involved with, proven to be a very effective way to encourage improvement.
 

 

Shared Staffing

The small hospitals in many systems sometimes struggle to find a way to provide economical night coverage. Hospitals below a certain size find it very difficult to justify a separate, in-house night provider. Some hospital systems have had success sharing night staffing, with the large hospital’s night hospitalist, nurse practitioner, or physician assistant providing telephone coverage for “cross cover” issues that arise after hours.

For example, when a nurse at the small hospital needs to contact a night hospitalist, staff will page the provider at the big hospital, and, in many cases, the issue can be managed effectively by phone. This works best when both hospitals are on the same electronic medical record, so that the responding provider can look through the record as needed.

The hospitalist at the small hospital typically stays on back-up call and is contacted if bedside attention is required.

Or, if the large and small hospitals are a short drive apart, the night hospitalist at the large facility might make the short drive to the small hospital when needed. In the case of emergencies (i.e., a code blue), the in-house night ED physician is relied on as the first responder.


Dr. Nelson has been a practicing hospitalist since 1988. He is co-founder and past president of SHM, and principal in Nelson Flores Hospital Medicine Consultants. He is co-director for SHM’s “Best Practices in Managing a Hospital Medicine Program” course. Write to him at [email protected].

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Dr. Nelson

Dr. Nelson

Serving as the lead physician for a hospital medicine group (HMG) makes for challenging work. And the challenges and complexity only increase for anyone who serves as the physician leader for multiple practice sites in the same hospital system. In my November 2013 column on multi-site HMG leaders, I listed a few of the tricky issues they face and will mention a few more here.

Large-Small Friction

Unfortunately, tension between hospitalists at the big hospital and doctors at the small, “feeder” hospitals seems pretty common, and I think it’s due largely to high stress and a wide variation in workload, neither of which are in our direct control. At facilities where there is significant tension, I’m impressed by how vigorously the hospitalists at both the small and large hospitals argue that their own site faces the most stress and challenges. (This is a little like the endless debate about who works harder, those who work with residents and those who don’t.)

The hospitalists at the small site point out that they work with little or no subspecialty help and might even have to take night call from home while working during the day. Those at the big hospital say they are the ones with the very large scope of clinical practice and that, rather than making their life easier, the presence of lots of subspecialists makes for additional work coordinating care and communicating with all parties.

Where it exists, this tension is most evident during a transfer from one of the small hospitals to the large one. After all, one of the reasons to form a system of hospitals is so that nearly all patient needs can be met at one of the facilities in the system. Yet, for many reasons, the hospitalists at the large hospital are—sometimes—not as receptive to transfers as might be ideal. They might be short staffed or facing a high census or an unusually high number of admissions from their own ED. Or, perhaps, they’re concerned that the subspecialty services for which the patient is being transferred (e.g. to be scoped by a GI doctor) won’t be as helpful or prompt as needed. Or maybe they’ve felt “burned” by their colleagues at the small hospital for past transfers that didn’t seem necessary.

Where it exists, this tension is most evident during a transfer from one of the small hospitals to the large one. After all, one of the reasons to form a system of hospitals is so that nearly all patient needs can be met at one of the facilities in the system. Yet, for many reasons, the hospitalists at the large hospital are—sometimes—not as receptive to transfers as might be ideal.

The result can be that the doctors at the smaller hospital complain that the “mother ship” hospitalists often are unfriendly and unreceptive to transfer requests. Although there may not be a definitive “cure” for this issue, there are several ways to help address the problem.

  • In my last column, I mentioned the value of one or more in-person meetings between those who tend to be on the sending and receiving end of transfers, to establish some criteria regarding transfers that are appropriate and review the process of requesting a transfer and making the associated arrangements. In most cases there will be value in the parties meeting routinely—perhaps two to four times annually—to review how the system is working and address any difficulties.
  • Periodic social meetings among the hospitalists at each site will help to form relationships that can make it less likely that any conversation about transfers will go in an unhelpful direction. Things can be very different when the people on each end of the phone call know each other personally.
  • Record the phone calls between those seeking and accepting/declining each transfer. Scott Rissmiller, MD, the lead hospitalist for the 17 practice sites in Carolinas Healthcare, has said that having underperforming doctors listen to recordings of their phone calls about transfers has, in most cases he’s been involved with, proven to be a very effective way to encourage improvement.
 

 

Shared Staffing

The small hospitals in many systems sometimes struggle to find a way to provide economical night coverage. Hospitals below a certain size find it very difficult to justify a separate, in-house night provider. Some hospital systems have had success sharing night staffing, with the large hospital’s night hospitalist, nurse practitioner, or physician assistant providing telephone coverage for “cross cover” issues that arise after hours.

For example, when a nurse at the small hospital needs to contact a night hospitalist, staff will page the provider at the big hospital, and, in many cases, the issue can be managed effectively by phone. This works best when both hospitals are on the same electronic medical record, so that the responding provider can look through the record as needed.

The hospitalist at the small hospital typically stays on back-up call and is contacted if bedside attention is required.

Or, if the large and small hospitals are a short drive apart, the night hospitalist at the large facility might make the short drive to the small hospital when needed. In the case of emergencies (i.e., a code blue), the in-house night ED physician is relied on as the first responder.


Dr. Nelson has been a practicing hospitalist since 1988. He is co-founder and past president of SHM, and principal in Nelson Flores Hospital Medicine Consultants. He is co-director for SHM’s “Best Practices in Managing a Hospital Medicine Program” course. Write to him at [email protected].

Dr. Nelson

Dr. Nelson

Serving as the lead physician for a hospital medicine group (HMG) makes for challenging work. And the challenges and complexity only increase for anyone who serves as the physician leader for multiple practice sites in the same hospital system. In my November 2013 column on multi-site HMG leaders, I listed a few of the tricky issues they face and will mention a few more here.

Large-Small Friction

Unfortunately, tension between hospitalists at the big hospital and doctors at the small, “feeder” hospitals seems pretty common, and I think it’s due largely to high stress and a wide variation in workload, neither of which are in our direct control. At facilities where there is significant tension, I’m impressed by how vigorously the hospitalists at both the small and large hospitals argue that their own site faces the most stress and challenges. (This is a little like the endless debate about who works harder, those who work with residents and those who don’t.)

The hospitalists at the small site point out that they work with little or no subspecialty help and might even have to take night call from home while working during the day. Those at the big hospital say they are the ones with the very large scope of clinical practice and that, rather than making their life easier, the presence of lots of subspecialists makes for additional work coordinating care and communicating with all parties.

Where it exists, this tension is most evident during a transfer from one of the small hospitals to the large one. After all, one of the reasons to form a system of hospitals is so that nearly all patient needs can be met at one of the facilities in the system. Yet, for many reasons, the hospitalists at the large hospital are—sometimes—not as receptive to transfers as might be ideal. They might be short staffed or facing a high census or an unusually high number of admissions from their own ED. Or, perhaps, they’re concerned that the subspecialty services for which the patient is being transferred (e.g. to be scoped by a GI doctor) won’t be as helpful or prompt as needed. Or maybe they’ve felt “burned” by their colleagues at the small hospital for past transfers that didn’t seem necessary.

Where it exists, this tension is most evident during a transfer from one of the small hospitals to the large one. After all, one of the reasons to form a system of hospitals is so that nearly all patient needs can be met at one of the facilities in the system. Yet, for many reasons, the hospitalists at the large hospital are—sometimes—not as receptive to transfers as might be ideal.

The result can be that the doctors at the smaller hospital complain that the “mother ship” hospitalists often are unfriendly and unreceptive to transfer requests. Although there may not be a definitive “cure” for this issue, there are several ways to help address the problem.

  • In my last column, I mentioned the value of one or more in-person meetings between those who tend to be on the sending and receiving end of transfers, to establish some criteria regarding transfers that are appropriate and review the process of requesting a transfer and making the associated arrangements. In most cases there will be value in the parties meeting routinely—perhaps two to four times annually—to review how the system is working and address any difficulties.
  • Periodic social meetings among the hospitalists at each site will help to form relationships that can make it less likely that any conversation about transfers will go in an unhelpful direction. Things can be very different when the people on each end of the phone call know each other personally.
  • Record the phone calls between those seeking and accepting/declining each transfer. Scott Rissmiller, MD, the lead hospitalist for the 17 practice sites in Carolinas Healthcare, has said that having underperforming doctors listen to recordings of their phone calls about transfers has, in most cases he’s been involved with, proven to be a very effective way to encourage improvement.
 

 

Shared Staffing

The small hospitals in many systems sometimes struggle to find a way to provide economical night coverage. Hospitals below a certain size find it very difficult to justify a separate, in-house night provider. Some hospital systems have had success sharing night staffing, with the large hospital’s night hospitalist, nurse practitioner, or physician assistant providing telephone coverage for “cross cover” issues that arise after hours.

For example, when a nurse at the small hospital needs to contact a night hospitalist, staff will page the provider at the big hospital, and, in many cases, the issue can be managed effectively by phone. This works best when both hospitals are on the same electronic medical record, so that the responding provider can look through the record as needed.

The hospitalist at the small hospital typically stays on back-up call and is contacted if bedside attention is required.

Or, if the large and small hospitals are a short drive apart, the night hospitalist at the large facility might make the short drive to the small hospital when needed. In the case of emergencies (i.e., a code blue), the in-house night ED physician is relied on as the first responder.


Dr. Nelson has been a practicing hospitalist since 1988. He is co-founder and past president of SHM, and principal in Nelson Flores Hospital Medicine Consultants. He is co-director for SHM’s “Best Practices in Managing a Hospital Medicine Program” course. Write to him at [email protected].

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Does maternal obesity increase the risk of preterm delivery?

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The developed world is in the midst of an unprecedented increase in human body mass. This increase can be attributed to widespread access to large amounts of inexpensive calories—particularly carbohydrates—and diminishing physical exertion. We have “evolved” from creatures struggling to get enough food to survive to vertebrates drowning in an ocean of calories and ease.

Although obesity clearly lies on the causal pathway for diseases such as diabetes and endometrial cancer, it also is associated with many other unhealthy behaviors and exposures. For example, obese women tend to earn less money, achieve less in school, smoke, and live farther away from markets and playgrounds—and the list of confounders goes on and on. We can measure height and weight with ease and precision, but we can’t assess and quantify most of these other confounders.

Related Article: Should you start prescribing lorcaserin or orlistat to your overweight or obese patients? Robert L. Barbieri, MD (Editorial, October 2013)

Cnattingius and colleagues give us another “obesity is bad” paper, this time with the outcome of preterm delivery. They found not only an association between obesity and preterm delivery but also a “mass response effect”—that is, the association increased along with maternal BMI.

The magnitude of the associations was small (odds ratios <3.0 for preterm delivery among overweight and obese women, compared with women of normal weight), and despite valiant efforts by the investigators to control for confounding, the imprecision I mentioned above limits their findings.

I declared a personal moratorium on reading “obesity is bad” papers a few years back. Even if obesity is a real risk factor for poor perinatal outcomes and not a proxy for residual confounding, we still have no idea, short of invasive surgery, how to modify that risk. Real progress will require effective lifestyle intervention—and we know so little about how to get people to lead healthy lives. It is difficult enough to modify our own behavior (recall your New Year’s resolutions), even harder to motivate our patients to lose weight and exercise.

What this evidence means for practice
Obesity is at best a weak risk factor for preterm delivery. Unless you are more successful than I have been at getting women to modify their diet and exercise, I would not make heavy mothers feel any worse.
John M. Thorp Jr., MD

TELL US WHAT YOU THINK!
Share your thoughts on this article or on any topic relevant to ObGyns and women’s health practitioners. Tell us which topics you’d like to see covered in future issues, and what challenges you face in daily practice. We will consider publishing your letter and in a future issue.
Send your letter to: [email protected] Please include the city and state in which you practice.
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The author reports no financial relationships relevant to this article.

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The author reports no financial relationships relevant to this article.

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John M. Thorp Jr., MD, is Hugh McAllister Distinguished Professor of Obstetrics and Gynecology; Division Director, Women’s Primary Healthcare; and Vice Chair of Research, Department of Obstetrics and Gynecology, at the University of North Carolina School of Medicine in Chapel Hill, North Carolina. He also is Professor of Maternal and Child Health at the University of North Carolina School of Public Health.

The author reports no financial relationships relevant to this article.

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The developed world is in the midst of an unprecedented increase in human body mass. This increase can be attributed to widespread access to large amounts of inexpensive calories—particularly carbohydrates—and diminishing physical exertion. We have “evolved” from creatures struggling to get enough food to survive to vertebrates drowning in an ocean of calories and ease.

Although obesity clearly lies on the causal pathway for diseases such as diabetes and endometrial cancer, it also is associated with many other unhealthy behaviors and exposures. For example, obese women tend to earn less money, achieve less in school, smoke, and live farther away from markets and playgrounds—and the list of confounders goes on and on. We can measure height and weight with ease and precision, but we can’t assess and quantify most of these other confounders.

Related Article: Should you start prescribing lorcaserin or orlistat to your overweight or obese patients? Robert L. Barbieri, MD (Editorial, October 2013)

Cnattingius and colleagues give us another “obesity is bad” paper, this time with the outcome of preterm delivery. They found not only an association between obesity and preterm delivery but also a “mass response effect”—that is, the association increased along with maternal BMI.

The magnitude of the associations was small (odds ratios <3.0 for preterm delivery among overweight and obese women, compared with women of normal weight), and despite valiant efforts by the investigators to control for confounding, the imprecision I mentioned above limits their findings.

I declared a personal moratorium on reading “obesity is bad” papers a few years back. Even if obesity is a real risk factor for poor perinatal outcomes and not a proxy for residual confounding, we still have no idea, short of invasive surgery, how to modify that risk. Real progress will require effective lifestyle intervention—and we know so little about how to get people to lead healthy lives. It is difficult enough to modify our own behavior (recall your New Year’s resolutions), even harder to motivate our patients to lose weight and exercise.

What this evidence means for practice
Obesity is at best a weak risk factor for preterm delivery. Unless you are more successful than I have been at getting women to modify their diet and exercise, I would not make heavy mothers feel any worse.
John M. Thorp Jr., MD

TELL US WHAT YOU THINK!
Share your thoughts on this article or on any topic relevant to ObGyns and women’s health practitioners. Tell us which topics you’d like to see covered in future issues, and what challenges you face in daily practice. We will consider publishing your letter and in a future issue.
Send your letter to: [email protected] Please include the city and state in which you practice.
Stay in touch! Your feedback is important to us!

The developed world is in the midst of an unprecedented increase in human body mass. This increase can be attributed to widespread access to large amounts of inexpensive calories—particularly carbohydrates—and diminishing physical exertion. We have “evolved” from creatures struggling to get enough food to survive to vertebrates drowning in an ocean of calories and ease.

Although obesity clearly lies on the causal pathway for diseases such as diabetes and endometrial cancer, it also is associated with many other unhealthy behaviors and exposures. For example, obese women tend to earn less money, achieve less in school, smoke, and live farther away from markets and playgrounds—and the list of confounders goes on and on. We can measure height and weight with ease and precision, but we can’t assess and quantify most of these other confounders.

Related Article: Should you start prescribing lorcaserin or orlistat to your overweight or obese patients? Robert L. Barbieri, MD (Editorial, October 2013)

Cnattingius and colleagues give us another “obesity is bad” paper, this time with the outcome of preterm delivery. They found not only an association between obesity and preterm delivery but also a “mass response effect”—that is, the association increased along with maternal BMI.

The magnitude of the associations was small (odds ratios <3.0 for preterm delivery among overweight and obese women, compared with women of normal weight), and despite valiant efforts by the investigators to control for confounding, the imprecision I mentioned above limits their findings.

I declared a personal moratorium on reading “obesity is bad” papers a few years back. Even if obesity is a real risk factor for poor perinatal outcomes and not a proxy for residual confounding, we still have no idea, short of invasive surgery, how to modify that risk. Real progress will require effective lifestyle intervention—and we know so little about how to get people to lead healthy lives. It is difficult enough to modify our own behavior (recall your New Year’s resolutions), even harder to motivate our patients to lose weight and exercise.

What this evidence means for practice
Obesity is at best a weak risk factor for preterm delivery. Unless you are more successful than I have been at getting women to modify their diet and exercise, I would not make heavy mothers feel any worse.
John M. Thorp Jr., MD

TELL US WHAT YOU THINK!
Share your thoughts on this article or on any topic relevant to ObGyns and women’s health practitioners. Tell us which topics you’d like to see covered in future issues, and what challenges you face in daily practice. We will consider publishing your letter and in a future issue.
Send your letter to: [email protected] Please include the city and state in which you practice.
Stay in touch! Your feedback is important to us!

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In the latest report from the WHI, the data contradict the conclusions

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In the latest report from the WHI, the data contradict the conclusions

In October 2013, the Women’s Health Initiative (WHI) investigators published a comprehensive overview of findings from their two hormone therapy (HT) trials, including extended follow-up representing 13 years of cumulative data.1 When I analyzed this latest WHI report, I initially focused almost exclusively on the data presented in figures and tables within the article itself, as well as on supplemental data presented on the Internet.2 Only then did I read the discussion comments by its authors. I would recommend this approach to anyone who has not yet reviewed this publication.

Overall, the WHI investigators maintain a negative stance toward the preventive and therapeutic benefits of menopausal HT. In my opinion, they also under-emphasize the importance of time since menopause in patient selection. These are the same WHI investigators who initially published un-adjudicated data3 and who delayed reporting age-stratified data.4 They also erroneously concluded that HT might increase the risk of ovarian cancer, even though their own data showed otherwise.5,6

The tables and figures contain the most important data point from this extended WHI follow-up: a reduction in all-cause mortality among women who initiated HT within 10 years of menopause, whether they used estrogen-alone (hysterectomized women) or estrogen-progestin therapy (women with an intact uterus), compared with women in the placebo group.1

Related Article: When should a menopausal woman discontinue hormone therapy? Andrew M. Kaunitz, MD (Cases in Menopause, February 2014)

DO THE RISKS OF HT REALLY OUTWEIGH THE BENEFITS?
The dramatic benefits of estrogen-alone HT, in particular, recently were highlighted by Sarrel and colleagues in an analysis that suggests that as many as 90,000 deaths may have occurred after publication of the initial WHI findings, when estrogen therapy was widely withheld.7 The study by Sarrel and colleagues also was highlighted in a recent issue of this journal.8

However, based on a “global index,” which has not been validated, the WHI investigators concluded that the risks of estrogen-progestin therapy outweigh the benefits regardless of age. Yet, the global index does not include all key concerns, omitting several quality-of-life concerns, including sleep disturbance, work productivity, and sexual function, as well as type 2 diabetes mellitus, osteoarthritis, and nonosteoporotic musculoskeletal problems. Nor does the global index provide individual weights.

Although the WHI data show reductions in the incidence of some serious chronic diseases, such as osteoporotic fracture and cardiovascular disease (in women within 10 years of menopause), Manson and colleagues make the blanket statement that HT should not be used for disease prevention, although they admit that it may be a “reasonable option for the management of moderate to severe menopausal symptoms among generally healthy women during early menopause.”1

Related Article: Update on Osteoporosis Steven R. Goldstein, MD (December 2013)

For some time, Wulf H. Utian, MD, PhD, a founder of both the International Menopause Society and the North American Menopause Society, has been calling for an independent commission to reevaluate all of the major WHI reports “to determine whether the data justified the conclusions drawn.”9 I support his call and suggest that this latest WHI publication be included in that reevaluation. The fact that total mortality is reduced among women using HT—according to the WHI’s own data—is not only impressive, it argues for, not against, the use of HT for chronic disease reduction.

KEEP YOUR EYE ON THE DATA
I have no doubt that medical history books will note the destructive effects of misinterpretation of WHI data. Until then, it is up to all practitioners and educators to counsel our patients and our trainees about menopause and menopausal HT and to look beyond the textual conclusions of WHI reports to assess the data themselves.

Other important research, such as the Study of Women’s Health Across the Nation (SWAN), shows that untreated menopausal women fall off the work productivity ladder.10 This is important because economic stability is a critical component of health and wellness. I have heard many women remark that someone will have to “pry” their hormones out of their “cold, dead hands”—meaning that they intend to take HT even if it shortens their lifespan—which is ironic, given that HT is likely to extend their lifespan!

Coronary heart disease (CHD) is the major killer of American women, and the long-term WHI data actually suggest that HT can prevent it, provided it is initiated within 10 years of menopause. In a two-part article, Hodis and Mack shrewdly compare the risks associated with HT with those associated with other commonly used medications in women’s health.11,12 They note that evidence-based data from randomized, clinical trials are very reassuring, as HT-associated risks are rare (less than 1 event per 1,000 women treated)—and even rarer when HT is initiated within 10 years of menopause. HT reduces CHD and total mortality, whereas aspirin and statins (as primary preventives) do not.11,12

 

 

Related Article: Update: Menopause Andrew M. Kaunitz, MD (May 2010)

THE BOTTOM LINE
We need to look at the totality of the data on menopausal HT, evaluate our patients individually, treat those who are truly hormonally deficient and suffering, and counsel them that many of the harms linked to HT have been exaggerated.

The pendulum is finally swinging back toward a more balanced assessment of the benefits and risks of HT, indicating that it may be appropriate for primary prevention of cardiovascular disease, osteoporosis, and type 2 diabetes—and thus can potentially expand the lifespan. It’s up to us to communicate this fact to our patients.

TELL US WHAT YOU THINK!
Share your thoughts on this article or on any topic relevant to ObGyns and women’s health practitioners. Tell us which topics you’d like to see covered in future issues, and what challenges you face in daily practice.
We will consider publishing your letter and in a future issue.
Send your letter to: [email protected]
Please include the city and state in which you practice.
Stay in touch! Your feedback is important to us!

References

  1. Manson JE, Chlebowski RT, Stefanick ML, et al. Menopausal hormone therapy and health outcomes during the intervention and extended poststopping phases of the Women’s Health Initiative randomized trials. JAMA. 2013;310(13):1353–1368.
  2. Supplemental content published online by the Journal of the American Medical Association. http://jama.jamanetwork.com/article
    .aspx?articleid=1745676. Accessed January 27, 2014 [subscription required]. 
  3. Rossouw JE, Anderson GL, Prentice RL, et al; Writing Group for the Women’s Health Initiative Investigators. Risks and benefits of estrogen plus progestin in healthy postmenopausal women. JAMA. 2002;288(3):321–333.
  4. Rossouw JE, Prentice RL, Manson JE, et al. Postmenopausal hormone therapy and risk of cardiovascular disease by age and years since menopause. JAMA. 2007;297(13):1465–1477.
  5. Utian WH. Hormone therapy and risk of gynecologic cancers [letter]. JAMA. 2004;291(1):42.
  6. Anderson GL, Judd HL, Kaunitz AM, et al. Hormone therapy and risk of gynecologic cancers—reply [letter]. JAMA. 2004;291(1):42.
  7. Sarrel PM, Njike VY, Vinante V, Katz DL. The mortality toll of estrogen avoidance: an analysis of excess deaths among hysterectomized women aged 50 to 59. Am J Pub Health. 2013;103(9):1583–1588.
  8. Kaunitz AM. In young hysterectomized women, does unopposed estrogen therapy increase overall survival? OBG Manag. 2013;25(10):55–56.
  9. Utian WH. A decade post WHI, menopausal hormone therapy comes full circule—need for independent commission. Climacteric. 2012;15(4):320–325.
  10. Tseng LA, El Khoudary SR, Young EA, et al. The association of menopausal status with physical function: The Study of Women’s Health Across the Nation. Menopause. 2012;19(11):1186–1192.
  11. Hodis HN, Mack WJ. The timing hypothesis and hormone replacement therapy: a paradigm shift in the primary prevention of coronary heart disease in women. Part 1: Comparison of therapeutic efficacy. J Am Geriatric Soc. 2013;61(6):1005–1010.
  12. Hodis HN, Mack WJ. The timing hypothesis and hormone replacement therapy: a paradigm shift in the primary prevention of coronary heart disease in women. Part 2: Comparative risks. J Am Geriatric Soc. 2013;61(6):1011–1018.
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Dr. Thacker reports that she has served as a speaker for Amgen, Novartis, Novo Nordisk, and Shionogi; is a consultant for Myriad, Noven, and Pfizer; and is Executive Director of the National Speaking of Women’s Health Foundation.

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Dr. Thacker reports that she has served as a speaker for Amgen, Novartis, Novo Nordisk, and Shionogi; is a consultant for Myriad, Noven, and Pfizer; and is Executive Director of the National Speaking of Women’s Health Foundation.

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Holly Thacker, MD, is Director of the Center for Specialized Women’s Health at the Cleveland Clinic in Cleveland, Ohio, and Professor of Obstetrics and Gynecology and Women’s Health at the Cleveland Clinic Lerner College of Medicine of Case Western Reserve University. She is the author of The Cleveland Clinic Guide to Menopause (2009) and Women’s Health: Your Body, Your Hormones, Your Choices (2007).

Dr. Thacker reports that she has served as a speaker for Amgen, Novartis, Novo Nordisk, and Shionogi; is a consultant for Myriad, Noven, and Pfizer; and is Executive Director of the National Speaking of Women’s Health Foundation.

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In October 2013, the Women’s Health Initiative (WHI) investigators published a comprehensive overview of findings from their two hormone therapy (HT) trials, including extended follow-up representing 13 years of cumulative data.1 When I analyzed this latest WHI report, I initially focused almost exclusively on the data presented in figures and tables within the article itself, as well as on supplemental data presented on the Internet.2 Only then did I read the discussion comments by its authors. I would recommend this approach to anyone who has not yet reviewed this publication.

Overall, the WHI investigators maintain a negative stance toward the preventive and therapeutic benefits of menopausal HT. In my opinion, they also under-emphasize the importance of time since menopause in patient selection. These are the same WHI investigators who initially published un-adjudicated data3 and who delayed reporting age-stratified data.4 They also erroneously concluded that HT might increase the risk of ovarian cancer, even though their own data showed otherwise.5,6

The tables and figures contain the most important data point from this extended WHI follow-up: a reduction in all-cause mortality among women who initiated HT within 10 years of menopause, whether they used estrogen-alone (hysterectomized women) or estrogen-progestin therapy (women with an intact uterus), compared with women in the placebo group.1

Related Article: When should a menopausal woman discontinue hormone therapy? Andrew M. Kaunitz, MD (Cases in Menopause, February 2014)

DO THE RISKS OF HT REALLY OUTWEIGH THE BENEFITS?
The dramatic benefits of estrogen-alone HT, in particular, recently were highlighted by Sarrel and colleagues in an analysis that suggests that as many as 90,000 deaths may have occurred after publication of the initial WHI findings, when estrogen therapy was widely withheld.7 The study by Sarrel and colleagues also was highlighted in a recent issue of this journal.8

However, based on a “global index,” which has not been validated, the WHI investigators concluded that the risks of estrogen-progestin therapy outweigh the benefits regardless of age. Yet, the global index does not include all key concerns, omitting several quality-of-life concerns, including sleep disturbance, work productivity, and sexual function, as well as type 2 diabetes mellitus, osteoarthritis, and nonosteoporotic musculoskeletal problems. Nor does the global index provide individual weights.

Although the WHI data show reductions in the incidence of some serious chronic diseases, such as osteoporotic fracture and cardiovascular disease (in women within 10 years of menopause), Manson and colleagues make the blanket statement that HT should not be used for disease prevention, although they admit that it may be a “reasonable option for the management of moderate to severe menopausal symptoms among generally healthy women during early menopause.”1

Related Article: Update on Osteoporosis Steven R. Goldstein, MD (December 2013)

For some time, Wulf H. Utian, MD, PhD, a founder of both the International Menopause Society and the North American Menopause Society, has been calling for an independent commission to reevaluate all of the major WHI reports “to determine whether the data justified the conclusions drawn.”9 I support his call and suggest that this latest WHI publication be included in that reevaluation. The fact that total mortality is reduced among women using HT—according to the WHI’s own data—is not only impressive, it argues for, not against, the use of HT for chronic disease reduction.

KEEP YOUR EYE ON THE DATA
I have no doubt that medical history books will note the destructive effects of misinterpretation of WHI data. Until then, it is up to all practitioners and educators to counsel our patients and our trainees about menopause and menopausal HT and to look beyond the textual conclusions of WHI reports to assess the data themselves.

Other important research, such as the Study of Women’s Health Across the Nation (SWAN), shows that untreated menopausal women fall off the work productivity ladder.10 This is important because economic stability is a critical component of health and wellness. I have heard many women remark that someone will have to “pry” their hormones out of their “cold, dead hands”—meaning that they intend to take HT even if it shortens their lifespan—which is ironic, given that HT is likely to extend their lifespan!

Coronary heart disease (CHD) is the major killer of American women, and the long-term WHI data actually suggest that HT can prevent it, provided it is initiated within 10 years of menopause. In a two-part article, Hodis and Mack shrewdly compare the risks associated with HT with those associated with other commonly used medications in women’s health.11,12 They note that evidence-based data from randomized, clinical trials are very reassuring, as HT-associated risks are rare (less than 1 event per 1,000 women treated)—and even rarer when HT is initiated within 10 years of menopause. HT reduces CHD and total mortality, whereas aspirin and statins (as primary preventives) do not.11,12

 

 

Related Article: Update: Menopause Andrew M. Kaunitz, MD (May 2010)

THE BOTTOM LINE
We need to look at the totality of the data on menopausal HT, evaluate our patients individually, treat those who are truly hormonally deficient and suffering, and counsel them that many of the harms linked to HT have been exaggerated.

The pendulum is finally swinging back toward a more balanced assessment of the benefits and risks of HT, indicating that it may be appropriate for primary prevention of cardiovascular disease, osteoporosis, and type 2 diabetes—and thus can potentially expand the lifespan. It’s up to us to communicate this fact to our patients.

TELL US WHAT YOU THINK!
Share your thoughts on this article or on any topic relevant to ObGyns and women’s health practitioners. Tell us which topics you’d like to see covered in future issues, and what challenges you face in daily practice.
We will consider publishing your letter and in a future issue.
Send your letter to: [email protected]
Please include the city and state in which you practice.
Stay in touch! Your feedback is important to us!

In October 2013, the Women’s Health Initiative (WHI) investigators published a comprehensive overview of findings from their two hormone therapy (HT) trials, including extended follow-up representing 13 years of cumulative data.1 When I analyzed this latest WHI report, I initially focused almost exclusively on the data presented in figures and tables within the article itself, as well as on supplemental data presented on the Internet.2 Only then did I read the discussion comments by its authors. I would recommend this approach to anyone who has not yet reviewed this publication.

Overall, the WHI investigators maintain a negative stance toward the preventive and therapeutic benefits of menopausal HT. In my opinion, they also under-emphasize the importance of time since menopause in patient selection. These are the same WHI investigators who initially published un-adjudicated data3 and who delayed reporting age-stratified data.4 They also erroneously concluded that HT might increase the risk of ovarian cancer, even though their own data showed otherwise.5,6

The tables and figures contain the most important data point from this extended WHI follow-up: a reduction in all-cause mortality among women who initiated HT within 10 years of menopause, whether they used estrogen-alone (hysterectomized women) or estrogen-progestin therapy (women with an intact uterus), compared with women in the placebo group.1

Related Article: When should a menopausal woman discontinue hormone therapy? Andrew M. Kaunitz, MD (Cases in Menopause, February 2014)

DO THE RISKS OF HT REALLY OUTWEIGH THE BENEFITS?
The dramatic benefits of estrogen-alone HT, in particular, recently were highlighted by Sarrel and colleagues in an analysis that suggests that as many as 90,000 deaths may have occurred after publication of the initial WHI findings, when estrogen therapy was widely withheld.7 The study by Sarrel and colleagues also was highlighted in a recent issue of this journal.8

However, based on a “global index,” which has not been validated, the WHI investigators concluded that the risks of estrogen-progestin therapy outweigh the benefits regardless of age. Yet, the global index does not include all key concerns, omitting several quality-of-life concerns, including sleep disturbance, work productivity, and sexual function, as well as type 2 diabetes mellitus, osteoarthritis, and nonosteoporotic musculoskeletal problems. Nor does the global index provide individual weights.

Although the WHI data show reductions in the incidence of some serious chronic diseases, such as osteoporotic fracture and cardiovascular disease (in women within 10 years of menopause), Manson and colleagues make the blanket statement that HT should not be used for disease prevention, although they admit that it may be a “reasonable option for the management of moderate to severe menopausal symptoms among generally healthy women during early menopause.”1

Related Article: Update on Osteoporosis Steven R. Goldstein, MD (December 2013)

For some time, Wulf H. Utian, MD, PhD, a founder of both the International Menopause Society and the North American Menopause Society, has been calling for an independent commission to reevaluate all of the major WHI reports “to determine whether the data justified the conclusions drawn.”9 I support his call and suggest that this latest WHI publication be included in that reevaluation. The fact that total mortality is reduced among women using HT—according to the WHI’s own data—is not only impressive, it argues for, not against, the use of HT for chronic disease reduction.

KEEP YOUR EYE ON THE DATA
I have no doubt that medical history books will note the destructive effects of misinterpretation of WHI data. Until then, it is up to all practitioners and educators to counsel our patients and our trainees about menopause and menopausal HT and to look beyond the textual conclusions of WHI reports to assess the data themselves.

Other important research, such as the Study of Women’s Health Across the Nation (SWAN), shows that untreated menopausal women fall off the work productivity ladder.10 This is important because economic stability is a critical component of health and wellness. I have heard many women remark that someone will have to “pry” their hormones out of their “cold, dead hands”—meaning that they intend to take HT even if it shortens their lifespan—which is ironic, given that HT is likely to extend their lifespan!

Coronary heart disease (CHD) is the major killer of American women, and the long-term WHI data actually suggest that HT can prevent it, provided it is initiated within 10 years of menopause. In a two-part article, Hodis and Mack shrewdly compare the risks associated with HT with those associated with other commonly used medications in women’s health.11,12 They note that evidence-based data from randomized, clinical trials are very reassuring, as HT-associated risks are rare (less than 1 event per 1,000 women treated)—and even rarer when HT is initiated within 10 years of menopause. HT reduces CHD and total mortality, whereas aspirin and statins (as primary preventives) do not.11,12

 

 

Related Article: Update: Menopause Andrew M. Kaunitz, MD (May 2010)

THE BOTTOM LINE
We need to look at the totality of the data on menopausal HT, evaluate our patients individually, treat those who are truly hormonally deficient and suffering, and counsel them that many of the harms linked to HT have been exaggerated.

The pendulum is finally swinging back toward a more balanced assessment of the benefits and risks of HT, indicating that it may be appropriate for primary prevention of cardiovascular disease, osteoporosis, and type 2 diabetes—and thus can potentially expand the lifespan. It’s up to us to communicate this fact to our patients.

TELL US WHAT YOU THINK!
Share your thoughts on this article or on any topic relevant to ObGyns and women’s health practitioners. Tell us which topics you’d like to see covered in future issues, and what challenges you face in daily practice.
We will consider publishing your letter and in a future issue.
Send your letter to: [email protected]
Please include the city and state in which you practice.
Stay in touch! Your feedback is important to us!

References

  1. Manson JE, Chlebowski RT, Stefanick ML, et al. Menopausal hormone therapy and health outcomes during the intervention and extended poststopping phases of the Women’s Health Initiative randomized trials. JAMA. 2013;310(13):1353–1368.
  2. Supplemental content published online by the Journal of the American Medical Association. http://jama.jamanetwork.com/article
    .aspx?articleid=1745676. Accessed January 27, 2014 [subscription required]. 
  3. Rossouw JE, Anderson GL, Prentice RL, et al; Writing Group for the Women’s Health Initiative Investigators. Risks and benefits of estrogen plus progestin in healthy postmenopausal women. JAMA. 2002;288(3):321–333.
  4. Rossouw JE, Prentice RL, Manson JE, et al. Postmenopausal hormone therapy and risk of cardiovascular disease by age and years since menopause. JAMA. 2007;297(13):1465–1477.
  5. Utian WH. Hormone therapy and risk of gynecologic cancers [letter]. JAMA. 2004;291(1):42.
  6. Anderson GL, Judd HL, Kaunitz AM, et al. Hormone therapy and risk of gynecologic cancers—reply [letter]. JAMA. 2004;291(1):42.
  7. Sarrel PM, Njike VY, Vinante V, Katz DL. The mortality toll of estrogen avoidance: an analysis of excess deaths among hysterectomized women aged 50 to 59. Am J Pub Health. 2013;103(9):1583–1588.
  8. Kaunitz AM. In young hysterectomized women, does unopposed estrogen therapy increase overall survival? OBG Manag. 2013;25(10):55–56.
  9. Utian WH. A decade post WHI, menopausal hormone therapy comes full circule—need for independent commission. Climacteric. 2012;15(4):320–325.
  10. Tseng LA, El Khoudary SR, Young EA, et al. The association of menopausal status with physical function: The Study of Women’s Health Across the Nation. Menopause. 2012;19(11):1186–1192.
  11. Hodis HN, Mack WJ. The timing hypothesis and hormone replacement therapy: a paradigm shift in the primary prevention of coronary heart disease in women. Part 1: Comparison of therapeutic efficacy. J Am Geriatric Soc. 2013;61(6):1005–1010.
  12. Hodis HN, Mack WJ. The timing hypothesis and hormone replacement therapy: a paradigm shift in the primary prevention of coronary heart disease in women. Part 2: Comparative risks. J Am Geriatric Soc. 2013;61(6):1011–1018.
References

  1. Manson JE, Chlebowski RT, Stefanick ML, et al. Menopausal hormone therapy and health outcomes during the intervention and extended poststopping phases of the Women’s Health Initiative randomized trials. JAMA. 2013;310(13):1353–1368.
  2. Supplemental content published online by the Journal of the American Medical Association. http://jama.jamanetwork.com/article
    .aspx?articleid=1745676. Accessed January 27, 2014 [subscription required]. 
  3. Rossouw JE, Anderson GL, Prentice RL, et al; Writing Group for the Women’s Health Initiative Investigators. Risks and benefits of estrogen plus progestin in healthy postmenopausal women. JAMA. 2002;288(3):321–333.
  4. Rossouw JE, Prentice RL, Manson JE, et al. Postmenopausal hormone therapy and risk of cardiovascular disease by age and years since menopause. JAMA. 2007;297(13):1465–1477.
  5. Utian WH. Hormone therapy and risk of gynecologic cancers [letter]. JAMA. 2004;291(1):42.
  6. Anderson GL, Judd HL, Kaunitz AM, et al. Hormone therapy and risk of gynecologic cancers—reply [letter]. JAMA. 2004;291(1):42.
  7. Sarrel PM, Njike VY, Vinante V, Katz DL. The mortality toll of estrogen avoidance: an analysis of excess deaths among hysterectomized women aged 50 to 59. Am J Pub Health. 2013;103(9):1583–1588.
  8. Kaunitz AM. In young hysterectomized women, does unopposed estrogen therapy increase overall survival? OBG Manag. 2013;25(10):55–56.
  9. Utian WH. A decade post WHI, menopausal hormone therapy comes full circule—need for independent commission. Climacteric. 2012;15(4):320–325.
  10. Tseng LA, El Khoudary SR, Young EA, et al. The association of menopausal status with physical function: The Study of Women’s Health Across the Nation. Menopause. 2012;19(11):1186–1192.
  11. Hodis HN, Mack WJ. The timing hypothesis and hormone replacement therapy: a paradigm shift in the primary prevention of coronary heart disease in women. Part 1: Comparison of therapeutic efficacy. J Am Geriatric Soc. 2013;61(6):1005–1010.
  12. Hodis HN, Mack WJ. The timing hypothesis and hormone replacement therapy: a paradigm shift in the primary prevention of coronary heart disease in women. Part 2: Comparative risks. J Am Geriatric Soc. 2013;61(6):1011–1018.
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Does vaginal prolapse repair using synthetic mesh confer long-term benefit over native-tissue colpopexy?

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This is the third report from Gutman and colleagues on the outcomes of a double-blind, multicenter, randomized, controlled trial of vaginal prolapse repair using synthetic mesh versus native-tissue colpopexy in women with significant vaginal prolapse.

The trial involved 33 women who underwent mesh repair and 32 who underwent repair without mesh. (The mesh-free repair consisted primarily of uterosacral suspension and concurrent colporrhaphy.) It was halted when it reached a predetermined threshold for discontinuation, which was a mesh erosion rate of 15% or more.

Investigators found no difference in long-term cure rates between the mesh and no-mesh groups, regardless of the definition of cure (ie, anatomic, symptomatic, or combined). Nor was there a difference in the overall recurrence rate.

Summary of earlier reports
Three-month outcomes.
The first report from this trial described 3-month objective treatment outcomes, with success described as prolapse no greater than stage 1.1 It found a high erosion rate (15.6%) for vaginal mesh, with no differences between groups in overall subjective or objective cure rates, with an overall recurrence rate of 59.4% (19 cases) in the mesh group versus 70.4% (24 cases) in the no-mesh group (P = .28), with recurrence defined as prolapse beyond stage 1 in any compartment. Investigators also observed potential benefit in the mesh group in the anterior vaginal wall at point Ba at a median of 9.7 months after surgery.

Related Article: Stop using synthetic mesh for routine repair of pelvic organ prolapse Cheryl B. Iglesia, MD (Stop/Start, April 2013)

One-year outcomes. The second report described 1-year objective and functional outcomes in all participants of the trial.2 It found comparable objective and subjective cure rates between groups but a higher reoperation rate for mesh repairs. Prolapse recurred in the anterior department in 46.9% of women in the mesh group versus 60.6% in the no-mesh group (P = .40).

Subjective quality-of-life assessments continued to reflect significant improvement in symptoms from baseline. Vaginal bulging was relieved in 96.2% of women in the mesh group, compared with 90.9% in the no-mesh group (P = .62).

More women in the mesh group required reoperation for recurrent prolapse or mesh exposure (5 in the mesh group vs 0 in the no-mesh group; P = .017).

Strengths and limitations of the trial
Gutman and colleagues are to be congratulated for continuing to monitor longer-term outcomes of vaginal prolapse repairs augmented with synthetic mesh, as data are sorely needed on both early complications and those more remote from surgery. However, it is regrettable that continued attrition in this trial led to minimal power to compare outcomes between groups.

Cure rates were assessed three ways: anatomically, by virtue of symptoms, and by a combination of the two measures. Participants had documentation of at least 2-year anatomic outcomes and 3-year subjective outcomes using validated measures. 

Forty-one (63%) of the original 65 women in the trial had anatomic outcomes (20 in the mesh group vs 21 in the no-mesh group), and 51 (78%) of the original 65 women had evaluable subjective outcomes (25 in the mesh group vs 26 in the no-mesh group).

Women who underwent reoperation for recurrent prolapse were removed from any outcomes analysis and considered to have failed composite outcomes measures (anatomic and subjective assessment and whether reoperation or a pessary was required for recurrent prolapse).

The length of follow-up was similar between groups (median, 3 years; interquartile range, 2.97–3.15), and both groups demonstrated significant anatomic and subjective improvement from baseline.

No difference was observed between groups in the original primary anatomic outcome, which was a POP-Q stage no greater than 1 (45% in the mesh group vs 43% in the no-mesh group; P >.99). Nor was there a difference between groups in any other anatomic outcome, including POP-Q point Ba (median, –1.5 for mesh [range, –2.5, 1.0] vs –0.5 [range, –3.0, 4.0] for the no-mesh group; P = .21) and bulge symptoms (92% for the mesh group vs 81% for the no-mesh group; relative risk, 1.4; 95% confidence interval, 0.91–1.42).

Despite small numbers and markedly reduced comparative validity (readily acknowledged by the investigators), these longer-term outcomes were assessed by examiners blinded to treatment and using validated objective and subjective outcome measures.

The only other randomized trial of mesh versus native-tissue repair with 3-year outcomes had a much larger sample size and follow-up but addressed only anterior-compartment prolapse.3

What this evidence means for practice
The 3-year data presented by Gutman and colleagues should be viewed with caution, owing to the trial’s reduced sample size and power. However, they may be useful in designing future trials.
In the meantime, given the limited longer-term outcomes data available at present, I would recommend continued individualized use of mesh versus native-tissue repair in women presenting with prolapse, including educating patients about the risks and benefits of both approaches. It also is important that outcomes be followed in all of our patients in a robust, unbiased fashion. The new American Urogynecologic Society Pelvic Floor Disorders Registry provides the opportunity for this.
Holly E. Richter, PhD, MD

 

 

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References

  1. Iglesia CB, Sokol AI, Sokol ER, et al. Vaginal mesh for prolapse: A randomized controlled trial. Obstet Gynecol. 2010;116(2 Pt 1):293–303.
  2. Sokol AI, Iglesia CB, Kudish BI, et al. One-year objective and functional outcomes of a randomized clinical trial of vaginal mesh for prolapse. Am J Obstet Gynecol. 2012;206(1):86.e1–e9.
  3. Nieminen K, Hiltunen R, Takala T, et al. Outcomes after anterior vaginal wall repair with mesh: A randomized, controlled trial with a 3-year follow-up. Am J Obstet Gynecol. 2010;203(3):235.e1–e8.
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This is the third report from Gutman and colleagues on the outcomes of a double-blind, multicenter, randomized, controlled trial of vaginal prolapse repair using synthetic mesh versus native-tissue colpopexy in women with significant vaginal prolapse.

The trial involved 33 women who underwent mesh repair and 32 who underwent repair without mesh. (The mesh-free repair consisted primarily of uterosacral suspension and concurrent colporrhaphy.) It was halted when it reached a predetermined threshold for discontinuation, which was a mesh erosion rate of 15% or more.

Investigators found no difference in long-term cure rates between the mesh and no-mesh groups, regardless of the definition of cure (ie, anatomic, symptomatic, or combined). Nor was there a difference in the overall recurrence rate.

Summary of earlier reports
Three-month outcomes.
The first report from this trial described 3-month objective treatment outcomes, with success described as prolapse no greater than stage 1.1 It found a high erosion rate (15.6%) for vaginal mesh, with no differences between groups in overall subjective or objective cure rates, with an overall recurrence rate of 59.4% (19 cases) in the mesh group versus 70.4% (24 cases) in the no-mesh group (P = .28), with recurrence defined as prolapse beyond stage 1 in any compartment. Investigators also observed potential benefit in the mesh group in the anterior vaginal wall at point Ba at a median of 9.7 months after surgery.

Related Article: Stop using synthetic mesh for routine repair of pelvic organ prolapse Cheryl B. Iglesia, MD (Stop/Start, April 2013)

One-year outcomes. The second report described 1-year objective and functional outcomes in all participants of the trial.2 It found comparable objective and subjective cure rates between groups but a higher reoperation rate for mesh repairs. Prolapse recurred in the anterior department in 46.9% of women in the mesh group versus 60.6% in the no-mesh group (P = .40).

Subjective quality-of-life assessments continued to reflect significant improvement in symptoms from baseline. Vaginal bulging was relieved in 96.2% of women in the mesh group, compared with 90.9% in the no-mesh group (P = .62).

More women in the mesh group required reoperation for recurrent prolapse or mesh exposure (5 in the mesh group vs 0 in the no-mesh group; P = .017).

Strengths and limitations of the trial
Gutman and colleagues are to be congratulated for continuing to monitor longer-term outcomes of vaginal prolapse repairs augmented with synthetic mesh, as data are sorely needed on both early complications and those more remote from surgery. However, it is regrettable that continued attrition in this trial led to minimal power to compare outcomes between groups.

Cure rates were assessed three ways: anatomically, by virtue of symptoms, and by a combination of the two measures. Participants had documentation of at least 2-year anatomic outcomes and 3-year subjective outcomes using validated measures. 

Forty-one (63%) of the original 65 women in the trial had anatomic outcomes (20 in the mesh group vs 21 in the no-mesh group), and 51 (78%) of the original 65 women had evaluable subjective outcomes (25 in the mesh group vs 26 in the no-mesh group).

Women who underwent reoperation for recurrent prolapse were removed from any outcomes analysis and considered to have failed composite outcomes measures (anatomic and subjective assessment and whether reoperation or a pessary was required for recurrent prolapse).

The length of follow-up was similar between groups (median, 3 years; interquartile range, 2.97–3.15), and both groups demonstrated significant anatomic and subjective improvement from baseline.

No difference was observed between groups in the original primary anatomic outcome, which was a POP-Q stage no greater than 1 (45% in the mesh group vs 43% in the no-mesh group; P >.99). Nor was there a difference between groups in any other anatomic outcome, including POP-Q point Ba (median, –1.5 for mesh [range, –2.5, 1.0] vs –0.5 [range, –3.0, 4.0] for the no-mesh group; P = .21) and bulge symptoms (92% for the mesh group vs 81% for the no-mesh group; relative risk, 1.4; 95% confidence interval, 0.91–1.42).

Despite small numbers and markedly reduced comparative validity (readily acknowledged by the investigators), these longer-term outcomes were assessed by examiners blinded to treatment and using validated objective and subjective outcome measures.

The only other randomized trial of mesh versus native-tissue repair with 3-year outcomes had a much larger sample size and follow-up but addressed only anterior-compartment prolapse.3

What this evidence means for practice
The 3-year data presented by Gutman and colleagues should be viewed with caution, owing to the trial’s reduced sample size and power. However, they may be useful in designing future trials.
In the meantime, given the limited longer-term outcomes data available at present, I would recommend continued individualized use of mesh versus native-tissue repair in women presenting with prolapse, including educating patients about the risks and benefits of both approaches. It also is important that outcomes be followed in all of our patients in a robust, unbiased fashion. The new American Urogynecologic Society Pelvic Floor Disorders Registry provides the opportunity for this.
Holly E. Richter, PhD, MD

 

 

WE WANT TO HEAR FROM YOU!
Drop us a line and let us know what you think about current articles, which topics you'd like to see covered in future issues, and what challenges you face in daily practice. Tell us what you think by emailing us at: [email protected]


This is the third report from Gutman and colleagues on the outcomes of a double-blind, multicenter, randomized, controlled trial of vaginal prolapse repair using synthetic mesh versus native-tissue colpopexy in women with significant vaginal prolapse.

The trial involved 33 women who underwent mesh repair and 32 who underwent repair without mesh. (The mesh-free repair consisted primarily of uterosacral suspension and concurrent colporrhaphy.) It was halted when it reached a predetermined threshold for discontinuation, which was a mesh erosion rate of 15% or more.

Investigators found no difference in long-term cure rates between the mesh and no-mesh groups, regardless of the definition of cure (ie, anatomic, symptomatic, or combined). Nor was there a difference in the overall recurrence rate.

Summary of earlier reports
Three-month outcomes.
The first report from this trial described 3-month objective treatment outcomes, with success described as prolapse no greater than stage 1.1 It found a high erosion rate (15.6%) for vaginal mesh, with no differences between groups in overall subjective or objective cure rates, with an overall recurrence rate of 59.4% (19 cases) in the mesh group versus 70.4% (24 cases) in the no-mesh group (P = .28), with recurrence defined as prolapse beyond stage 1 in any compartment. Investigators also observed potential benefit in the mesh group in the anterior vaginal wall at point Ba at a median of 9.7 months after surgery.

Related Article: Stop using synthetic mesh for routine repair of pelvic organ prolapse Cheryl B. Iglesia, MD (Stop/Start, April 2013)

One-year outcomes. The second report described 1-year objective and functional outcomes in all participants of the trial.2 It found comparable objective and subjective cure rates between groups but a higher reoperation rate for mesh repairs. Prolapse recurred in the anterior department in 46.9% of women in the mesh group versus 60.6% in the no-mesh group (P = .40).

Subjective quality-of-life assessments continued to reflect significant improvement in symptoms from baseline. Vaginal bulging was relieved in 96.2% of women in the mesh group, compared with 90.9% in the no-mesh group (P = .62).

More women in the mesh group required reoperation for recurrent prolapse or mesh exposure (5 in the mesh group vs 0 in the no-mesh group; P = .017).

Strengths and limitations of the trial
Gutman and colleagues are to be congratulated for continuing to monitor longer-term outcomes of vaginal prolapse repairs augmented with synthetic mesh, as data are sorely needed on both early complications and those more remote from surgery. However, it is regrettable that continued attrition in this trial led to minimal power to compare outcomes between groups.

Cure rates were assessed three ways: anatomically, by virtue of symptoms, and by a combination of the two measures. Participants had documentation of at least 2-year anatomic outcomes and 3-year subjective outcomes using validated measures. 

Forty-one (63%) of the original 65 women in the trial had anatomic outcomes (20 in the mesh group vs 21 in the no-mesh group), and 51 (78%) of the original 65 women had evaluable subjective outcomes (25 in the mesh group vs 26 in the no-mesh group).

Women who underwent reoperation for recurrent prolapse were removed from any outcomes analysis and considered to have failed composite outcomes measures (anatomic and subjective assessment and whether reoperation or a pessary was required for recurrent prolapse).

The length of follow-up was similar between groups (median, 3 years; interquartile range, 2.97–3.15), and both groups demonstrated significant anatomic and subjective improvement from baseline.

No difference was observed between groups in the original primary anatomic outcome, which was a POP-Q stage no greater than 1 (45% in the mesh group vs 43% in the no-mesh group; P >.99). Nor was there a difference between groups in any other anatomic outcome, including POP-Q point Ba (median, –1.5 for mesh [range, –2.5, 1.0] vs –0.5 [range, –3.0, 4.0] for the no-mesh group; P = .21) and bulge symptoms (92% for the mesh group vs 81% for the no-mesh group; relative risk, 1.4; 95% confidence interval, 0.91–1.42).

Despite small numbers and markedly reduced comparative validity (readily acknowledged by the investigators), these longer-term outcomes were assessed by examiners blinded to treatment and using validated objective and subjective outcome measures.

The only other randomized trial of mesh versus native-tissue repair with 3-year outcomes had a much larger sample size and follow-up but addressed only anterior-compartment prolapse.3

What this evidence means for practice
The 3-year data presented by Gutman and colleagues should be viewed with caution, owing to the trial’s reduced sample size and power. However, they may be useful in designing future trials.
In the meantime, given the limited longer-term outcomes data available at present, I would recommend continued individualized use of mesh versus native-tissue repair in women presenting with prolapse, including educating patients about the risks and benefits of both approaches. It also is important that outcomes be followed in all of our patients in a robust, unbiased fashion. The new American Urogynecologic Society Pelvic Floor Disorders Registry provides the opportunity for this.
Holly E. Richter, PhD, MD

 

 

WE WANT TO HEAR FROM YOU!
Drop us a line and let us know what you think about current articles, which topics you'd like to see covered in future issues, and what challenges you face in daily practice. Tell us what you think by emailing us at: [email protected]

References

  1. Iglesia CB, Sokol AI, Sokol ER, et al. Vaginal mesh for prolapse: A randomized controlled trial. Obstet Gynecol. 2010;116(2 Pt 1):293–303.
  2. Sokol AI, Iglesia CB, Kudish BI, et al. One-year objective and functional outcomes of a randomized clinical trial of vaginal mesh for prolapse. Am J Obstet Gynecol. 2012;206(1):86.e1–e9.
  3. Nieminen K, Hiltunen R, Takala T, et al. Outcomes after anterior vaginal wall repair with mesh: A randomized, controlled trial with a 3-year follow-up. Am J Obstet Gynecol. 2010;203(3):235.e1–e8.
References

  1. Iglesia CB, Sokol AI, Sokol ER, et al. Vaginal mesh for prolapse: A randomized controlled trial. Obstet Gynecol. 2010;116(2 Pt 1):293–303.
  2. Sokol AI, Iglesia CB, Kudish BI, et al. One-year objective and functional outcomes of a randomized clinical trial of vaginal mesh for prolapse. Am J Obstet Gynecol. 2012;206(1):86.e1–e9.
  3. Nieminen K, Hiltunen R, Takala T, et al. Outcomes after anterior vaginal wall repair with mesh: A randomized, controlled trial with a 3-year follow-up. Am J Obstet Gynecol. 2010;203(3):235.e1–e8.
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What's the appropriate lens to use in rigid cystoscopy to evaluate the bladder?

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Dr. Gebhart says an angled lens is critical to viewing the bladder, but which angle is ideal?

When Dr. Gebhart surveyed attendees of the Pelvic Anatomy and Gynecology Symposium in Las Vegas, Nevada, in December 2013, as to which lens angle was the best option, the majority chose the 30-degree lens. Listen to why Dr. Gebhart recommends the 70-degree lens.

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Dr. Gebhart says an angled lens is critical to viewing the bladder, but which angle is ideal?

When Dr. Gebhart surveyed attendees of the Pelvic Anatomy and Gynecology Symposium in Las Vegas, Nevada, in December 2013, as to which lens angle was the best option, the majority chose the 30-degree lens. Listen to why Dr. Gebhart recommends the 70-degree lens.

Dr. Gebhart says an angled lens is critical to viewing the bladder, but which angle is ideal?

When Dr. Gebhart surveyed attendees of the Pelvic Anatomy and Gynecology Symposium in Las Vegas, Nevada, in December 2013, as to which lens angle was the best option, the majority chose the 30-degree lens. Listen to why Dr. Gebhart recommends the 70-degree lens.

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Electronic Health Records Can Complicate Who Does What in a Hospital

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Dr. Nelson

Dr. Nelson

The accumulated wisdom, research data, and opinions regarding the use of electronic health records (EHRs) are vast. A quick Internet search turns up many informative articles on their positive and negative effects. But I haven’t found many that explicitly review the unanticipated effects EHRs have on who does what in the hospital.

For example, when reports such as admission and discharge notes are done via recorded dictation and transcription, the author would typically dictate where copies of the report should be sent (“copy to Dr. Matheny”) and rely on others to ensure it reached its intended destination. In many hospitals, such reports are now typed directly into the EHR, often using speech recognition software, and it is up to the author to click several buttons to ensure that it is routed to the intended recipients. So now a clerical function, sending reports, is handled by providers. This can be a good thing—reduced clerical staffing costs, faster transmission of reports—but often means that there is no documentation within the report itself of whom it was sent to (i.e., no list of “cc’s”). It also means that when the recipient isn’t easy to find, the report author is likely to give up, and the report may never be sent.

Any hospitalist using an EHR could easily list dozens of similar unanticipated effects, both good and bad. The magnitude and risk of these are difficult to quantify.

Altered Referral Patterns, Division of Labor

A hospitalist-specific side effect of EHR adoption is that they tend to cause many other doctors to resist serving as attending physician, instead asking hospitalists to replace them in that role. Even without EHRs, shifting attending responsibility to hospitalists has been a trend at nearly every hospital for years, but it can be accelerated dramatically at the time of a “go live.” So, in addition to the stress of adapting to the new EHR, hospitalists typically face higher than usual patient volumes resulting from increased referrals from other doctors.

If you’re a hospitalist facing an upcoming “go live,” it would be worth talking to other doctors in multiple specialties regarding your capacity to handle additional work. Keep in mind the possibility of higher than typical winter 2014 patient volumes that could result from patients who are newly insured through health exchanges.

So, in addition to the stress of adapting to the new EHR, hospitalists typically face higher than usual patient volumes resulting from increased referrals from other doctors.

Many factors, in addition to EHRs, are moving physicians away from a willingness to serve as attending, including the complexity of managing inpatient vs. observation status, keeping up with ever-changing documentation, pay-for-performance initiatives, the stress of ED call, and so on. As I’ve written before (see my January 2011 column, “Health IT Hurdles,”), I think effective management of hospital systems is becoming as complicated as safely piloting a jumbo jet. It will be increasingly difficult for doctors in any specialty to stay proficient at “piloting” a hospital unless they do it all or most of the time. And, staying proficient at multiple hospitals simultaneously may not be feasible at some point. We’ll see.

When Do Things Get Done?

A friend of mine, Dr. John Maa, is a general surgeon who was instrumental in establishing one of the first general surgery hospitalist practices. He tells a very personal and tragic story of his mother’s death, which, he has come to believe, might have been made more likely because of the unintended effect of an EHR.

 

 

She was a healthy 69-year-old who developed new onset atrial fibrillation and went to “one of the most highly regarded academic medical centers on the West Coast,” albeit not a facility where John was practicing. She was admitted with orders for anticoagulation but spent her first night on a stretcher in the ED because no inpatient bed was available. She went to a hospital room the next day, but her late arrival there delayed the planned transesophageal echo and cardioversion by another day.

Tragically, before the cardioversion could be done, she had a very large embolic stroke that led to brain herniation. A short time later, John and his father made the wrenching decision to discontinue mechanical ventilation. She died 112 hours after walking into the hospital.

What John later learned is that the admission orders written while she was in the ED were put into “sign and hold” status in the hospital’s EHR. Her caregivers had not anticipated a significant delay in moving her to an inpatient bed, and for the 18 or so hours she spent boarding in the ED, her admission orders were not acted on, and anticoagulation was delayed many hours. She might have had the same outcome even if anticoagulation had been started promptly, but it would have been much less likely.

John believes that the “sign and hold” status of the admission orders was a major contributor to the treatment delay. It increased the risk that the ED caregivers never acted on those orders, and may not have even seen them, since the EHR essentially holds them for presentation to the receiving inpatient unit.

John only recognized this vulnerability three years after his mother’s passing, when he underwent the physician training for the same EHR system. The course teachers agreed that this problem could arise if a patient was boarded in the ED for a prolonged period but felt that the responsibility rested with hospital administrators to minimize overcrowding in the ED. John also raised the issue with hospital leadership, who shared his concern but believed that a software remedy should be the solution. Ultimately, the answer may come from medical hospitalists, who recognize that every day and night, patients across America are at risk for a repeat of the incident John’s family suffered nearly five years ago.

In a very well written and moving essay, John describes his mother’s care.1 Though he doesn’t specifically mention the likely contribution of the “sign and hold” orders, it is one more example of EHR-related confusion that can arise around who does what and when they should do it. Clearly, the same sort of confusion exists in a non-EHR hospital, but it is the EHR-related change in the previous way of doing things that likely increases risk.

It can be very difficult—even impossible—to see all of these issues in advance. Even when acknowledged, the challenges can be difficult to address. But the first step is to recognize a problem, or potential problem, and think carefully about how it should be addressed.


Dr. Nelson has been a practicing hospitalist since 1988. He is co-founder and past president of SHM, and principal in Nelson Flores Hospital Medicine Consultants. He is co-director for SHM’s “Best Practices in Managing a Hospital Medicine Program” course. Write to him at [email protected].

Reference

  1. Maa J. The waits that matter. N Engl J Med. 2011;364(24):2279-2281.

Issue
The Hospitalist - 2014(01)
Publications
Sections

Dr. Nelson

Dr. Nelson

The accumulated wisdom, research data, and opinions regarding the use of electronic health records (EHRs) are vast. A quick Internet search turns up many informative articles on their positive and negative effects. But I haven’t found many that explicitly review the unanticipated effects EHRs have on who does what in the hospital.

For example, when reports such as admission and discharge notes are done via recorded dictation and transcription, the author would typically dictate where copies of the report should be sent (“copy to Dr. Matheny”) and rely on others to ensure it reached its intended destination. In many hospitals, such reports are now typed directly into the EHR, often using speech recognition software, and it is up to the author to click several buttons to ensure that it is routed to the intended recipients. So now a clerical function, sending reports, is handled by providers. This can be a good thing—reduced clerical staffing costs, faster transmission of reports—but often means that there is no documentation within the report itself of whom it was sent to (i.e., no list of “cc’s”). It also means that when the recipient isn’t easy to find, the report author is likely to give up, and the report may never be sent.

Any hospitalist using an EHR could easily list dozens of similar unanticipated effects, both good and bad. The magnitude and risk of these are difficult to quantify.

Altered Referral Patterns, Division of Labor

A hospitalist-specific side effect of EHR adoption is that they tend to cause many other doctors to resist serving as attending physician, instead asking hospitalists to replace them in that role. Even without EHRs, shifting attending responsibility to hospitalists has been a trend at nearly every hospital for years, but it can be accelerated dramatically at the time of a “go live.” So, in addition to the stress of adapting to the new EHR, hospitalists typically face higher than usual patient volumes resulting from increased referrals from other doctors.

If you’re a hospitalist facing an upcoming “go live,” it would be worth talking to other doctors in multiple specialties regarding your capacity to handle additional work. Keep in mind the possibility of higher than typical winter 2014 patient volumes that could result from patients who are newly insured through health exchanges.

So, in addition to the stress of adapting to the new EHR, hospitalists typically face higher than usual patient volumes resulting from increased referrals from other doctors.

Many factors, in addition to EHRs, are moving physicians away from a willingness to serve as attending, including the complexity of managing inpatient vs. observation status, keeping up with ever-changing documentation, pay-for-performance initiatives, the stress of ED call, and so on. As I’ve written before (see my January 2011 column, “Health IT Hurdles,”), I think effective management of hospital systems is becoming as complicated as safely piloting a jumbo jet. It will be increasingly difficult for doctors in any specialty to stay proficient at “piloting” a hospital unless they do it all or most of the time. And, staying proficient at multiple hospitals simultaneously may not be feasible at some point. We’ll see.

When Do Things Get Done?

A friend of mine, Dr. John Maa, is a general surgeon who was instrumental in establishing one of the first general surgery hospitalist practices. He tells a very personal and tragic story of his mother’s death, which, he has come to believe, might have been made more likely because of the unintended effect of an EHR.

 

 

She was a healthy 69-year-old who developed new onset atrial fibrillation and went to “one of the most highly regarded academic medical centers on the West Coast,” albeit not a facility where John was practicing. She was admitted with orders for anticoagulation but spent her first night on a stretcher in the ED because no inpatient bed was available. She went to a hospital room the next day, but her late arrival there delayed the planned transesophageal echo and cardioversion by another day.

Tragically, before the cardioversion could be done, she had a very large embolic stroke that led to brain herniation. A short time later, John and his father made the wrenching decision to discontinue mechanical ventilation. She died 112 hours after walking into the hospital.

What John later learned is that the admission orders written while she was in the ED were put into “sign and hold” status in the hospital’s EHR. Her caregivers had not anticipated a significant delay in moving her to an inpatient bed, and for the 18 or so hours she spent boarding in the ED, her admission orders were not acted on, and anticoagulation was delayed many hours. She might have had the same outcome even if anticoagulation had been started promptly, but it would have been much less likely.

John believes that the “sign and hold” status of the admission orders was a major contributor to the treatment delay. It increased the risk that the ED caregivers never acted on those orders, and may not have even seen them, since the EHR essentially holds them for presentation to the receiving inpatient unit.

John only recognized this vulnerability three years after his mother’s passing, when he underwent the physician training for the same EHR system. The course teachers agreed that this problem could arise if a patient was boarded in the ED for a prolonged period but felt that the responsibility rested with hospital administrators to minimize overcrowding in the ED. John also raised the issue with hospital leadership, who shared his concern but believed that a software remedy should be the solution. Ultimately, the answer may come from medical hospitalists, who recognize that every day and night, patients across America are at risk for a repeat of the incident John’s family suffered nearly five years ago.

In a very well written and moving essay, John describes his mother’s care.1 Though he doesn’t specifically mention the likely contribution of the “sign and hold” orders, it is one more example of EHR-related confusion that can arise around who does what and when they should do it. Clearly, the same sort of confusion exists in a non-EHR hospital, but it is the EHR-related change in the previous way of doing things that likely increases risk.

It can be very difficult—even impossible—to see all of these issues in advance. Even when acknowledged, the challenges can be difficult to address. But the first step is to recognize a problem, or potential problem, and think carefully about how it should be addressed.


Dr. Nelson has been a practicing hospitalist since 1988. He is co-founder and past president of SHM, and principal in Nelson Flores Hospital Medicine Consultants. He is co-director for SHM’s “Best Practices in Managing a Hospital Medicine Program” course. Write to him at [email protected].

Reference

  1. Maa J. The waits that matter. N Engl J Med. 2011;364(24):2279-2281.

Dr. Nelson

Dr. Nelson

The accumulated wisdom, research data, and opinions regarding the use of electronic health records (EHRs) are vast. A quick Internet search turns up many informative articles on their positive and negative effects. But I haven’t found many that explicitly review the unanticipated effects EHRs have on who does what in the hospital.

For example, when reports such as admission and discharge notes are done via recorded dictation and transcription, the author would typically dictate where copies of the report should be sent (“copy to Dr. Matheny”) and rely on others to ensure it reached its intended destination. In many hospitals, such reports are now typed directly into the EHR, often using speech recognition software, and it is up to the author to click several buttons to ensure that it is routed to the intended recipients. So now a clerical function, sending reports, is handled by providers. This can be a good thing—reduced clerical staffing costs, faster transmission of reports—but often means that there is no documentation within the report itself of whom it was sent to (i.e., no list of “cc’s”). It also means that when the recipient isn’t easy to find, the report author is likely to give up, and the report may never be sent.

Any hospitalist using an EHR could easily list dozens of similar unanticipated effects, both good and bad. The magnitude and risk of these are difficult to quantify.

Altered Referral Patterns, Division of Labor

A hospitalist-specific side effect of EHR adoption is that they tend to cause many other doctors to resist serving as attending physician, instead asking hospitalists to replace them in that role. Even without EHRs, shifting attending responsibility to hospitalists has been a trend at nearly every hospital for years, but it can be accelerated dramatically at the time of a “go live.” So, in addition to the stress of adapting to the new EHR, hospitalists typically face higher than usual patient volumes resulting from increased referrals from other doctors.

If you’re a hospitalist facing an upcoming “go live,” it would be worth talking to other doctors in multiple specialties regarding your capacity to handle additional work. Keep in mind the possibility of higher than typical winter 2014 patient volumes that could result from patients who are newly insured through health exchanges.

So, in addition to the stress of adapting to the new EHR, hospitalists typically face higher than usual patient volumes resulting from increased referrals from other doctors.

Many factors, in addition to EHRs, are moving physicians away from a willingness to serve as attending, including the complexity of managing inpatient vs. observation status, keeping up with ever-changing documentation, pay-for-performance initiatives, the stress of ED call, and so on. As I’ve written before (see my January 2011 column, “Health IT Hurdles,”), I think effective management of hospital systems is becoming as complicated as safely piloting a jumbo jet. It will be increasingly difficult for doctors in any specialty to stay proficient at “piloting” a hospital unless they do it all or most of the time. And, staying proficient at multiple hospitals simultaneously may not be feasible at some point. We’ll see.

When Do Things Get Done?

A friend of mine, Dr. John Maa, is a general surgeon who was instrumental in establishing one of the first general surgery hospitalist practices. He tells a very personal and tragic story of his mother’s death, which, he has come to believe, might have been made more likely because of the unintended effect of an EHR.

 

 

She was a healthy 69-year-old who developed new onset atrial fibrillation and went to “one of the most highly regarded academic medical centers on the West Coast,” albeit not a facility where John was practicing. She was admitted with orders for anticoagulation but spent her first night on a stretcher in the ED because no inpatient bed was available. She went to a hospital room the next day, but her late arrival there delayed the planned transesophageal echo and cardioversion by another day.

Tragically, before the cardioversion could be done, she had a very large embolic stroke that led to brain herniation. A short time later, John and his father made the wrenching decision to discontinue mechanical ventilation. She died 112 hours after walking into the hospital.

What John later learned is that the admission orders written while she was in the ED were put into “sign and hold” status in the hospital’s EHR. Her caregivers had not anticipated a significant delay in moving her to an inpatient bed, and for the 18 or so hours she spent boarding in the ED, her admission orders were not acted on, and anticoagulation was delayed many hours. She might have had the same outcome even if anticoagulation had been started promptly, but it would have been much less likely.

John believes that the “sign and hold” status of the admission orders was a major contributor to the treatment delay. It increased the risk that the ED caregivers never acted on those orders, and may not have even seen them, since the EHR essentially holds them for presentation to the receiving inpatient unit.

John only recognized this vulnerability three years after his mother’s passing, when he underwent the physician training for the same EHR system. The course teachers agreed that this problem could arise if a patient was boarded in the ED for a prolonged period but felt that the responsibility rested with hospital administrators to minimize overcrowding in the ED. John also raised the issue with hospital leadership, who shared his concern but believed that a software remedy should be the solution. Ultimately, the answer may come from medical hospitalists, who recognize that every day and night, patients across America are at risk for a repeat of the incident John’s family suffered nearly five years ago.

In a very well written and moving essay, John describes his mother’s care.1 Though he doesn’t specifically mention the likely contribution of the “sign and hold” orders, it is one more example of EHR-related confusion that can arise around who does what and when they should do it. Clearly, the same sort of confusion exists in a non-EHR hospital, but it is the EHR-related change in the previous way of doing things that likely increases risk.

It can be very difficult—even impossible—to see all of these issues in advance. Even when acknowledged, the challenges can be difficult to address. But the first step is to recognize a problem, or potential problem, and think carefully about how it should be addressed.


Dr. Nelson has been a practicing hospitalist since 1988. He is co-founder and past president of SHM, and principal in Nelson Flores Hospital Medicine Consultants. He is co-director for SHM’s “Best Practices in Managing a Hospital Medicine Program” course. Write to him at [email protected].

Reference

  1. Maa J. The waits that matter. N Engl J Med. 2011;364(24):2279-2281.

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Performance Evaluation Program for Individual Physicians Directional at Best

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Dr. Whitcomb

Dr. Whitcomb
Figure 1. Resource utilization, OPPE report 2013

Dr. Whitcomb
Figure 2. 30-day readmissions, OPPE report 2013

Dr. Whitcomb
Figure 3. Mortality observed vs. expected, OPPE report 2013 (0.01=1%)

What makes a great doctor? Heck if I know. Maybe it’s like pornography. A great physician, well, “You know one when you see one.” That approach worked from the time of Hippocrates until the recent past, when the Centers for Medicare & Medicaid Services (CMS), the Joint Commission, and others embarked on programs to measure and report physician quality. Of course, bodies like the American Board of Internal Medicine have been certifying physicians for a long time.

Ongoing Professional Practice Evaluation (OPPE) is one such measurement program, now over four years old, with standards put forth by the Joint Commission in an effort to monitor individual physician—and non-physician provider—performance across a number of domains. The program requires accredited hospitals to monitor and report performance to the physician/provider at least every 11 months, and to use such information in the credentialing process.

This year, I received two OPPE reports, causing me to reflect on how helpful these reports are in judging and improving the quality of my practice. Before I discuss some of the “grades” I received, let me start with my conclusion: Physician quality measurement is in its infancy, and the measures are at best “directional” for most physicians, including hospitalists. Some measurement is better than none at all, however, and selected measures, such as surgical site infection and other measures of harm, may be grounds for closer monitoring, or even corrective action, of a physician’s practice. Unfortunately, my stance that OPPE quality measures are “directional” might not help a physician whose privileges are on the line.

Attribution

For hospitalists, the first concern in measuring and reporting quality is, “How can I attribute quality to an individual hospitalist, when several different hospitalists see the patient?” My perspective is that unless a quality measure can be attributed to an individual hospitalist (e.g. discharge medication reconciliation), it should be attributed at the group level.

However, the OPPE program is specifically intended to address the individual physician/provider for purposes of credentialing, and group attribution is a non-starter. In my performance examples below, I believe that attributing outcomes like mortality, readmissions, or resource utilization to individual hospitalists does not make sense—and is probably unfair.

Resource Utilization

The report lists my performance (Practitioner) compared to an Internal Comparison Group for a specified time period (see Figure 1). The comparison group is described as “practitioners in your specialty...from within your health system.” My data were generated based on only 45 cases (I see patients only part time), while the comparison group was based on 4,530 cases. What I take home from this is that, for cost/resource, I look favorable in “supplies” and “pharmacy”; for most of the others, I’m expensive in comparison.

Will this change my practice? Maybe I will think twice about incurring laboratory or pharmacy costs, but I can’t say I am going to fundamentally rethink how or what I order. And I take all these data with a grain of salt, because I share responsibility for patients with several other hospitalists.

Readmissions

My 30-day readmissions performance (see Figure 2) is weak compared to the Internal Comp Group, which I defined above, and the Peer group, which in my report is defined as derived from practitioners at facilities with 501 beds or more (my facility has 700-plus beds). I accept the “directional” nature of the data, meaning that it provides a general idea but not a precise measurement, and vow to reflect on the processes underlying my approach to hospital discharge (teach back, medication reconciliation, PCP communication, and so on).

 

 

Mortality

For this category (see Figure 3), I’m looking better. The blue bar is “observed,” while the red bar is “expected.” Although my patients are sicker (higher “expected” mortality), my “observed” mortality is lower than the comparison group. I’m not sure why my observed mortality is lower, but I’m convinced that part of the reason for a higher expected mortality is that my documentation is better than the comparison group.

Will OPPE Change My Practice?

There are other data in my report, including process (core) measures, length of stay, hospital-acquired conditions, and patient flow measures. The OPPE report is but one of a growing number of physician report cards: The Massachusetts Board of Medicine, Physician Compare (CMS), and Health Grades are just a few of the organizations that have public websites reporting my performance. Perhaps at this stage, the primary impact of these reports is through the oft-invoked “Hawthorne Effect,” where subjects modify behavior simply because they are being observed, as opposed to any particular piece of feedback.

My sense is that hospitalists are particularly open to the type of feedback offered in OPPE and similar reports, as long as the data are credible, even if reflecting group level performance. The 2012 SHM State of Hospital Medicine survey shows that the percent of hospitalist compensation based on performance (other than production/billings) increased to 7% from 4% in 2011. It seems that performance measurement with consequences, be it for credentialing or compensation, is here to stay.


Dr. Whitcombis Chief Medical Officer of Remedy Partners. He is co-founder and past president of SHM. Email him at [email protected].

Issue
The Hospitalist - 2014(01)
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Dr. Whitcomb

Dr. Whitcomb
Figure 1. Resource utilization, OPPE report 2013

Dr. Whitcomb
Figure 2. 30-day readmissions, OPPE report 2013

Dr. Whitcomb
Figure 3. Mortality observed vs. expected, OPPE report 2013 (0.01=1%)

What makes a great doctor? Heck if I know. Maybe it’s like pornography. A great physician, well, “You know one when you see one.” That approach worked from the time of Hippocrates until the recent past, when the Centers for Medicare & Medicaid Services (CMS), the Joint Commission, and others embarked on programs to measure and report physician quality. Of course, bodies like the American Board of Internal Medicine have been certifying physicians for a long time.

Ongoing Professional Practice Evaluation (OPPE) is one such measurement program, now over four years old, with standards put forth by the Joint Commission in an effort to monitor individual physician—and non-physician provider—performance across a number of domains. The program requires accredited hospitals to monitor and report performance to the physician/provider at least every 11 months, and to use such information in the credentialing process.

This year, I received two OPPE reports, causing me to reflect on how helpful these reports are in judging and improving the quality of my practice. Before I discuss some of the “grades” I received, let me start with my conclusion: Physician quality measurement is in its infancy, and the measures are at best “directional” for most physicians, including hospitalists. Some measurement is better than none at all, however, and selected measures, such as surgical site infection and other measures of harm, may be grounds for closer monitoring, or even corrective action, of a physician’s practice. Unfortunately, my stance that OPPE quality measures are “directional” might not help a physician whose privileges are on the line.

Attribution

For hospitalists, the first concern in measuring and reporting quality is, “How can I attribute quality to an individual hospitalist, when several different hospitalists see the patient?” My perspective is that unless a quality measure can be attributed to an individual hospitalist (e.g. discharge medication reconciliation), it should be attributed at the group level.

However, the OPPE program is specifically intended to address the individual physician/provider for purposes of credentialing, and group attribution is a non-starter. In my performance examples below, I believe that attributing outcomes like mortality, readmissions, or resource utilization to individual hospitalists does not make sense—and is probably unfair.

Resource Utilization

The report lists my performance (Practitioner) compared to an Internal Comparison Group for a specified time period (see Figure 1). The comparison group is described as “practitioners in your specialty...from within your health system.” My data were generated based on only 45 cases (I see patients only part time), while the comparison group was based on 4,530 cases. What I take home from this is that, for cost/resource, I look favorable in “supplies” and “pharmacy”; for most of the others, I’m expensive in comparison.

Will this change my practice? Maybe I will think twice about incurring laboratory or pharmacy costs, but I can’t say I am going to fundamentally rethink how or what I order. And I take all these data with a grain of salt, because I share responsibility for patients with several other hospitalists.

Readmissions

My 30-day readmissions performance (see Figure 2) is weak compared to the Internal Comp Group, which I defined above, and the Peer group, which in my report is defined as derived from practitioners at facilities with 501 beds or more (my facility has 700-plus beds). I accept the “directional” nature of the data, meaning that it provides a general idea but not a precise measurement, and vow to reflect on the processes underlying my approach to hospital discharge (teach back, medication reconciliation, PCP communication, and so on).

 

 

Mortality

For this category (see Figure 3), I’m looking better. The blue bar is “observed,” while the red bar is “expected.” Although my patients are sicker (higher “expected” mortality), my “observed” mortality is lower than the comparison group. I’m not sure why my observed mortality is lower, but I’m convinced that part of the reason for a higher expected mortality is that my documentation is better than the comparison group.

Will OPPE Change My Practice?

There are other data in my report, including process (core) measures, length of stay, hospital-acquired conditions, and patient flow measures. The OPPE report is but one of a growing number of physician report cards: The Massachusetts Board of Medicine, Physician Compare (CMS), and Health Grades are just a few of the organizations that have public websites reporting my performance. Perhaps at this stage, the primary impact of these reports is through the oft-invoked “Hawthorne Effect,” where subjects modify behavior simply because they are being observed, as opposed to any particular piece of feedback.

My sense is that hospitalists are particularly open to the type of feedback offered in OPPE and similar reports, as long as the data are credible, even if reflecting group level performance. The 2012 SHM State of Hospital Medicine survey shows that the percent of hospitalist compensation based on performance (other than production/billings) increased to 7% from 4% in 2011. It seems that performance measurement with consequences, be it for credentialing or compensation, is here to stay.


Dr. Whitcombis Chief Medical Officer of Remedy Partners. He is co-founder and past president of SHM. Email him at [email protected].

Dr. Whitcomb

Dr. Whitcomb
Figure 1. Resource utilization, OPPE report 2013

Dr. Whitcomb
Figure 2. 30-day readmissions, OPPE report 2013

Dr. Whitcomb
Figure 3. Mortality observed vs. expected, OPPE report 2013 (0.01=1%)

What makes a great doctor? Heck if I know. Maybe it’s like pornography. A great physician, well, “You know one when you see one.” That approach worked from the time of Hippocrates until the recent past, when the Centers for Medicare & Medicaid Services (CMS), the Joint Commission, and others embarked on programs to measure and report physician quality. Of course, bodies like the American Board of Internal Medicine have been certifying physicians for a long time.

Ongoing Professional Practice Evaluation (OPPE) is one such measurement program, now over four years old, with standards put forth by the Joint Commission in an effort to monitor individual physician—and non-physician provider—performance across a number of domains. The program requires accredited hospitals to monitor and report performance to the physician/provider at least every 11 months, and to use such information in the credentialing process.

This year, I received two OPPE reports, causing me to reflect on how helpful these reports are in judging and improving the quality of my practice. Before I discuss some of the “grades” I received, let me start with my conclusion: Physician quality measurement is in its infancy, and the measures are at best “directional” for most physicians, including hospitalists. Some measurement is better than none at all, however, and selected measures, such as surgical site infection and other measures of harm, may be grounds for closer monitoring, or even corrective action, of a physician’s practice. Unfortunately, my stance that OPPE quality measures are “directional” might not help a physician whose privileges are on the line.

Attribution

For hospitalists, the first concern in measuring and reporting quality is, “How can I attribute quality to an individual hospitalist, when several different hospitalists see the patient?” My perspective is that unless a quality measure can be attributed to an individual hospitalist (e.g. discharge medication reconciliation), it should be attributed at the group level.

However, the OPPE program is specifically intended to address the individual physician/provider for purposes of credentialing, and group attribution is a non-starter. In my performance examples below, I believe that attributing outcomes like mortality, readmissions, or resource utilization to individual hospitalists does not make sense—and is probably unfair.

Resource Utilization

The report lists my performance (Practitioner) compared to an Internal Comparison Group for a specified time period (see Figure 1). The comparison group is described as “practitioners in your specialty...from within your health system.” My data were generated based on only 45 cases (I see patients only part time), while the comparison group was based on 4,530 cases. What I take home from this is that, for cost/resource, I look favorable in “supplies” and “pharmacy”; for most of the others, I’m expensive in comparison.

Will this change my practice? Maybe I will think twice about incurring laboratory or pharmacy costs, but I can’t say I am going to fundamentally rethink how or what I order. And I take all these data with a grain of salt, because I share responsibility for patients with several other hospitalists.

Readmissions

My 30-day readmissions performance (see Figure 2) is weak compared to the Internal Comp Group, which I defined above, and the Peer group, which in my report is defined as derived from practitioners at facilities with 501 beds or more (my facility has 700-plus beds). I accept the “directional” nature of the data, meaning that it provides a general idea but not a precise measurement, and vow to reflect on the processes underlying my approach to hospital discharge (teach back, medication reconciliation, PCP communication, and so on).

 

 

Mortality

For this category (see Figure 3), I’m looking better. The blue bar is “observed,” while the red bar is “expected.” Although my patients are sicker (higher “expected” mortality), my “observed” mortality is lower than the comparison group. I’m not sure why my observed mortality is lower, but I’m convinced that part of the reason for a higher expected mortality is that my documentation is better than the comparison group.

Will OPPE Change My Practice?

There are other data in my report, including process (core) measures, length of stay, hospital-acquired conditions, and patient flow measures. The OPPE report is but one of a growing number of physician report cards: The Massachusetts Board of Medicine, Physician Compare (CMS), and Health Grades are just a few of the organizations that have public websites reporting my performance. Perhaps at this stage, the primary impact of these reports is through the oft-invoked “Hawthorne Effect,” where subjects modify behavior simply because they are being observed, as opposed to any particular piece of feedback.

My sense is that hospitalists are particularly open to the type of feedback offered in OPPE and similar reports, as long as the data are credible, even if reflecting group level performance. The 2012 SHM State of Hospital Medicine survey shows that the percent of hospitalist compensation based on performance (other than production/billings) increased to 7% from 4% in 2011. It seems that performance measurement with consequences, be it for credentialing or compensation, is here to stay.


Dr. Whitcombis Chief Medical Officer of Remedy Partners. He is co-founder and past president of SHM. Email him at [email protected].

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Is one oral estrogen formulation safer than another for menopausal women?

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Is one oral estrogen formulation safer than another for menopausal women?

Although numerous investigators, including the Women’s Health Initiative (WHI) team, have compared cardiovascular risks in women using menopausal hormone therapy (HT) versus nonusers, few researchers have addressed the comparative safety of different oral estrogen formulations.

Related Article: Update on Menopause (Andrew M. Kaunitz, MD, June 2013)

In this case-control study, Smith and colleagues compared the safety of oral estradiol and CEE in menopausal members of a large US Health Maintenance Organization who were using these oral estrogens between 2003 and 2009.

Details of the study
Cases were women diagnosed with deep venous thrombosis, including pulmonary embolism; myocardial infarction; or ischemic stroke. Women in the control group had no history of cardiovascular events. The endogenous thrombin potential-based normalized activated protein C sensitivity ratio (nAPCsr), which has been shown to predict venous thromboembolism (VTE) in the setting of estrogen therapy, was measured in the control group.

Between 2003 and 2009, incident VTE, MI, and stroke were diagnosed in 68, 67, and 49 cases, respectively, and 201 controls were identified. Cases were more likely than controls to have cardiovascular risk factors.

More than 90% of participants were white, with a mean age ranging from 63.2 to 67.6 years.

Among women in the control group, those using oral estradiol had slightly more cardiovascular risk factors than those using CEE, although age, body mass index, and the recency of HT initiation were similar among women using the two oral estrogens.

Although the ORs for VTE and MI were elevated among CEE users, the risk for ischemic stroke was similar for estradiol and CEE users. Women using CEE had higher nAPCsrs (P <.001), however, suggesting a greater tendency to clot.

WHAT THIS EVIDENCE MEANS FOR PRACTICE
Although the risk of VTE appears to be higher among users of oral estrogen than among those using a transdermal formulation,1 many menopausal women prefer oral estrogen for its convenience and because patch adherence can sometimes be an issue.
Oral estradiol and oral CEE appear to be equally effective in relieving menopausal symptoms. However, there is a significant cost differential: A 1-month supply of 1-mg estradiol tablets costs $4 at some chain pharmacies, whereas 0.625-mg tablets of CEE cost $84.92 (according to goodrx.com). Therefore, for menopausal women who elect to use an oral estrogen formulation, estradiol appears to be a wise choice for both safety and  economy.
Andrew M. Kaunitz, MD

WE WANT TO HEAR FROM YOU. Tell us what you think.

References

Reference

  1. Postmenopausal estrogen therapy: route of administration and risk of venous thromboembolism. Committee Opinion #556. American College of Obstetricians and Gynecologists. Obstet Gynecol. 2013;121(4):887–890.
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Andrew M. Kaunitz, MD, Professor and Associate Chairman, Department of Obstetrics and Gynecology, University of Florida College of Medicine–Jacksonville. Dr. Kaunitz serves on the OBG Management Board of Editors.

The author reports that he receives grant or research support from Agile, Bayer, Noven, and Teva, and is a consultant to Actavis, Bayer, and Teva.

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Andrew M. Kaunitz,oral estrogen,menopausal women,conjugated equine estrogens,CEE,estradiol,myocardial infarction,MI,Women’s Health Initiative,WHI,hormone therapy,HT,deep venous thrombosis,DVT,pulmonary embolism,PE,ischemic stroke,normalized activated protein C sensitivity ratio,nAPCsr,postmenopause,Examining the Evidence
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Andrew M. Kaunitz, MD, Professor and Associate Chairman, Department of Obstetrics and Gynecology, University of Florida College of Medicine–Jacksonville. Dr. Kaunitz serves on the OBG Management Board of Editors.

The author reports that he receives grant or research support from Agile, Bayer, Noven, and Teva, and is a consultant to Actavis, Bayer, and Teva.

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EXPERT COMMENTARY

Andrew M. Kaunitz, MD, Professor and Associate Chairman, Department of Obstetrics and Gynecology, University of Florida College of Medicine–Jacksonville. Dr. Kaunitz serves on the OBG Management Board of Editors.

The author reports that he receives grant or research support from Agile, Bayer, Noven, and Teva, and is a consultant to Actavis, Bayer, and Teva.

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Related Articles

Although numerous investigators, including the Women’s Health Initiative (WHI) team, have compared cardiovascular risks in women using menopausal hormone therapy (HT) versus nonusers, few researchers have addressed the comparative safety of different oral estrogen formulations.

Related Article: Update on Menopause (Andrew M. Kaunitz, MD, June 2013)

In this case-control study, Smith and colleagues compared the safety of oral estradiol and CEE in menopausal members of a large US Health Maintenance Organization who were using these oral estrogens between 2003 and 2009.

Details of the study
Cases were women diagnosed with deep venous thrombosis, including pulmonary embolism; myocardial infarction; or ischemic stroke. Women in the control group had no history of cardiovascular events. The endogenous thrombin potential-based normalized activated protein C sensitivity ratio (nAPCsr), which has been shown to predict venous thromboembolism (VTE) in the setting of estrogen therapy, was measured in the control group.

Between 2003 and 2009, incident VTE, MI, and stroke were diagnosed in 68, 67, and 49 cases, respectively, and 201 controls were identified. Cases were more likely than controls to have cardiovascular risk factors.

More than 90% of participants were white, with a mean age ranging from 63.2 to 67.6 years.

Among women in the control group, those using oral estradiol had slightly more cardiovascular risk factors than those using CEE, although age, body mass index, and the recency of HT initiation were similar among women using the two oral estrogens.

Although the ORs for VTE and MI were elevated among CEE users, the risk for ischemic stroke was similar for estradiol and CEE users. Women using CEE had higher nAPCsrs (P <.001), however, suggesting a greater tendency to clot.

WHAT THIS EVIDENCE MEANS FOR PRACTICE
Although the risk of VTE appears to be higher among users of oral estrogen than among those using a transdermal formulation,1 many menopausal women prefer oral estrogen for its convenience and because patch adherence can sometimes be an issue.
Oral estradiol and oral CEE appear to be equally effective in relieving menopausal symptoms. However, there is a significant cost differential: A 1-month supply of 1-mg estradiol tablets costs $4 at some chain pharmacies, whereas 0.625-mg tablets of CEE cost $84.92 (according to goodrx.com). Therefore, for menopausal women who elect to use an oral estrogen formulation, estradiol appears to be a wise choice for both safety and  economy.
Andrew M. Kaunitz, MD

WE WANT TO HEAR FROM YOU. Tell us what you think.

Although numerous investigators, including the Women’s Health Initiative (WHI) team, have compared cardiovascular risks in women using menopausal hormone therapy (HT) versus nonusers, few researchers have addressed the comparative safety of different oral estrogen formulations.

Related Article: Update on Menopause (Andrew M. Kaunitz, MD, June 2013)

In this case-control study, Smith and colleagues compared the safety of oral estradiol and CEE in menopausal members of a large US Health Maintenance Organization who were using these oral estrogens between 2003 and 2009.

Details of the study
Cases were women diagnosed with deep venous thrombosis, including pulmonary embolism; myocardial infarction; or ischemic stroke. Women in the control group had no history of cardiovascular events. The endogenous thrombin potential-based normalized activated protein C sensitivity ratio (nAPCsr), which has been shown to predict venous thromboembolism (VTE) in the setting of estrogen therapy, was measured in the control group.

Between 2003 and 2009, incident VTE, MI, and stroke were diagnosed in 68, 67, and 49 cases, respectively, and 201 controls were identified. Cases were more likely than controls to have cardiovascular risk factors.

More than 90% of participants were white, with a mean age ranging from 63.2 to 67.6 years.

Among women in the control group, those using oral estradiol had slightly more cardiovascular risk factors than those using CEE, although age, body mass index, and the recency of HT initiation were similar among women using the two oral estrogens.

Although the ORs for VTE and MI were elevated among CEE users, the risk for ischemic stroke was similar for estradiol and CEE users. Women using CEE had higher nAPCsrs (P <.001), however, suggesting a greater tendency to clot.

WHAT THIS EVIDENCE MEANS FOR PRACTICE
Although the risk of VTE appears to be higher among users of oral estrogen than among those using a transdermal formulation,1 many menopausal women prefer oral estrogen for its convenience and because patch adherence can sometimes be an issue.
Oral estradiol and oral CEE appear to be equally effective in relieving menopausal symptoms. However, there is a significant cost differential: A 1-month supply of 1-mg estradiol tablets costs $4 at some chain pharmacies, whereas 0.625-mg tablets of CEE cost $84.92 (according to goodrx.com). Therefore, for menopausal women who elect to use an oral estrogen formulation, estradiol appears to be a wise choice for both safety and  economy.
Andrew M. Kaunitz, MD

WE WANT TO HEAR FROM YOU. Tell us what you think.

References

Reference

  1. Postmenopausal estrogen therapy: route of administration and risk of venous thromboembolism. Committee Opinion #556. American College of Obstetricians and Gynecologists. Obstet Gynecol. 2013;121(4):887–890.
References

Reference

  1. Postmenopausal estrogen therapy: route of administration and risk of venous thromboembolism. Committee Opinion #556. American College of Obstetricians and Gynecologists. Obstet Gynecol. 2013;121(4):887–890.
Issue
OBG Management - 26(1)
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OBG Management - 26(1)
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50-51
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50-51
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Is one oral estrogen formulation safer than another for menopausal women?
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Is one oral estrogen formulation safer than another for menopausal women?
Legacy Keywords
Andrew M. Kaunitz,oral estrogen,menopausal women,conjugated equine estrogens,CEE,estradiol,myocardial infarction,MI,Women’s Health Initiative,WHI,hormone therapy,HT,deep venous thrombosis,DVT,pulmonary embolism,PE,ischemic stroke,normalized activated protein C sensitivity ratio,nAPCsr,postmenopause,Examining the Evidence
Legacy Keywords
Andrew M. Kaunitz,oral estrogen,menopausal women,conjugated equine estrogens,CEE,estradiol,myocardial infarction,MI,Women’s Health Initiative,WHI,hormone therapy,HT,deep venous thrombosis,DVT,pulmonary embolism,PE,ischemic stroke,normalized activated protein C sensitivity ratio,nAPCsr,postmenopause,Examining the Evidence
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