User login
Is metformin more effective than glyburide for treating gestational diabetes?
Traditionally, insulin has been prescribed to treat gestational diabetes when medical nutrition therapy fails to achieve the desired level of glucose control, but insulin must be administered by injection and carries the inherent risk of hypoglycemia if caloric intake is not appropriately matched. The oral agent glyburide, a sulfonylurea, also carries a risk of hypoglycemia. Another oral drug, metformin, a biguanide, carries no risk of hypoglycemia. It would be highly desirable if oral antidiabetic agents could be used in pregnancy.
Randomized trials of glyburide and metformin have demonstrated efficacy similar to that of insulin, although some treated patients needed additional insulin when predetermined maximal doses did not control the glucose level.3,4
In this latest trial, the two oral agents produced similar glucose levels among gravidas in whom either drug was effective. However, the failure rate of metformin (35%) was significantly higher than that of glyburide (16%). In this study, the likelihood of failure was similar to that described in the MiG trial for metformin (46%) and in a large case series for glyburide (16%).5
Do oral agents cross the placenta?
An important consideration in regard to these oral agents is safety. Although an in vitro study of isolated perfused placental cotyledons showed little transplacental passage of glyburide,6 and the original randomized trial of glyburide3 found that the drug could not be identified in cord blood of exposed newborns, a recent publication from the National Institute of Child Health and Human Development Obstetric-Fetal Pharmacology Research Unit Network demonstrated that the average fetal glyburide level was 70% of the maternal level.7 Metformin also crosses the placenta and is concentrated in the fetal compartment, with the fetal level approximately double that of the maternal circulation.8
In published reports to date, no significant increase in adverse outcomes has been reported with metformin or glyburide. A number of questions remain unanswered, however.
For example, the role of in utero programming on the development of problems such as insulin resistance syndrome in later life has drawn a great deal of attention. Just as exposure to hyperglycemia in utero has been shown to predispose to the development of glucose intolerance9 in adulthood, might exposure to an insulin sensitizer such as metformin, or an insulin secretagogue such as glyburide, have long-lasting effects on offspring? Studies of animal models are needed, as well as long-term follow-up of exposed humans, to establish the safety of these agents in gestational diabetes.
The temptation is great to use an oral agent instead of insulin to manage gestational diabetes. I urge caution about this strategy, however, until more is known about the potential fetal effects of those oral agents.
Insulin does not cross the placenta to a significant extent, and its use in pregnancy has withstood the test of time. The high likelihood that supplemental insulin will be needed when metformin is used, and the concentration of metformin in the fetal compartment make it a somewhat less attractive treatment option. And the recent evidence of transplacental passage of glyburide is disappointing.
I no longer prescribe glyburide routinely to treat gestational diabetes. When using it does appear appropriate—such as in a patient who refuses insulin despite a high glucose level—I make certain to document that she has been counseled about the unknown potential long-term effects on offspring. I also explain that no harmful effects have yet been found.—DONALD R. COUSTAN, MD
1. Getahun D, Nath C, Ananth CV, et al. Gestational diabetes in the United States: temporal trends 1989 through 2004. Am J Obstet Gynecol. 2008;198(5):525.e1-5.
2. International Association of Diabetes and Pregnancy Study Groups Consensus Panel. International Association of Diabetes and Pregnancy Study Groups recommendations on the diagnosis and classification of hyperglycemia during pregnancy. Diabetes Care. 2010;33 [in press].
3. Langer O, Conway DL, Berkus MD, Xenakis EM, Gonzales O. A comparison of glyburide and insulin in women with gestational diabetes mellitus. N Engl J Med. 2000;343(16):1134-1138.
4. Rowan JA, Hague WM, Gao W, Battin MR, Moore MP. For the MiG Trial Investigators. Metformin versus insulin for the treatment of gestational diabetes. N Engl J Med. 2008;358(19):2003-2015.
5. Conway DL, Gonzales O, Skiver D. Use of glyburide for the treatment of gestational diabetes: the San Antonio experience. J Matern Fetal Neonatal Med. 2004;15(1):51-55.
6. Elliott BD, Langer O, Schenker S, Johnson RF. Insignificant transfer of glyburide occurs across the human placenta. Am J Obstet Gynecol. 1991;165(4):807-812.
7. Hebert MF, Ma X, Naraharisetti SB, et al. For the Obstetric-Fetal Pharmacology Research Unit Network. Are we optimizing gestational diabetes treatment with glyburide? The pharmacologic basis for better clinical practice. Clin Pharmacol Ther. 2009;85(6):607-614.
8. Vanky E, Zahlsen K, Spigset O, Carlsen SM. Placental passage of metformin in women with polycystic ovary syndrome. Fertil Steril. 2005;83(5):1575-1578.
9. Pettitt DJ, Bennett PH, Saad MF, et al. Abnormal glucose tolerance during pregnancy in Pima Indian women. Long-term effects on off spring. Diabetes. 1991;40(suppl 2):126-130.
Traditionally, insulin has been prescribed to treat gestational diabetes when medical nutrition therapy fails to achieve the desired level of glucose control, but insulin must be administered by injection and carries the inherent risk of hypoglycemia if caloric intake is not appropriately matched. The oral agent glyburide, a sulfonylurea, also carries a risk of hypoglycemia. Another oral drug, metformin, a biguanide, carries no risk of hypoglycemia. It would be highly desirable if oral antidiabetic agents could be used in pregnancy.
Randomized trials of glyburide and metformin have demonstrated efficacy similar to that of insulin, although some treated patients needed additional insulin when predetermined maximal doses did not control the glucose level.3,4
In this latest trial, the two oral agents produced similar glucose levels among gravidas in whom either drug was effective. However, the failure rate of metformin (35%) was significantly higher than that of glyburide (16%). In this study, the likelihood of failure was similar to that described in the MiG trial for metformin (46%) and in a large case series for glyburide (16%).5
Do oral agents cross the placenta?
An important consideration in regard to these oral agents is safety. Although an in vitro study of isolated perfused placental cotyledons showed little transplacental passage of glyburide,6 and the original randomized trial of glyburide3 found that the drug could not be identified in cord blood of exposed newborns, a recent publication from the National Institute of Child Health and Human Development Obstetric-Fetal Pharmacology Research Unit Network demonstrated that the average fetal glyburide level was 70% of the maternal level.7 Metformin also crosses the placenta and is concentrated in the fetal compartment, with the fetal level approximately double that of the maternal circulation.8
In published reports to date, no significant increase in adverse outcomes has been reported with metformin or glyburide. A number of questions remain unanswered, however.
For example, the role of in utero programming on the development of problems such as insulin resistance syndrome in later life has drawn a great deal of attention. Just as exposure to hyperglycemia in utero has been shown to predispose to the development of glucose intolerance9 in adulthood, might exposure to an insulin sensitizer such as metformin, or an insulin secretagogue such as glyburide, have long-lasting effects on offspring? Studies of animal models are needed, as well as long-term follow-up of exposed humans, to establish the safety of these agents in gestational diabetes.
The temptation is great to use an oral agent instead of insulin to manage gestational diabetes. I urge caution about this strategy, however, until more is known about the potential fetal effects of those oral agents.
Insulin does not cross the placenta to a significant extent, and its use in pregnancy has withstood the test of time. The high likelihood that supplemental insulin will be needed when metformin is used, and the concentration of metformin in the fetal compartment make it a somewhat less attractive treatment option. And the recent evidence of transplacental passage of glyburide is disappointing.
I no longer prescribe glyburide routinely to treat gestational diabetes. When using it does appear appropriate—such as in a patient who refuses insulin despite a high glucose level—I make certain to document that she has been counseled about the unknown potential long-term effects on offspring. I also explain that no harmful effects have yet been found.—DONALD R. COUSTAN, MD
Traditionally, insulin has been prescribed to treat gestational diabetes when medical nutrition therapy fails to achieve the desired level of glucose control, but insulin must be administered by injection and carries the inherent risk of hypoglycemia if caloric intake is not appropriately matched. The oral agent glyburide, a sulfonylurea, also carries a risk of hypoglycemia. Another oral drug, metformin, a biguanide, carries no risk of hypoglycemia. It would be highly desirable if oral antidiabetic agents could be used in pregnancy.
Randomized trials of glyburide and metformin have demonstrated efficacy similar to that of insulin, although some treated patients needed additional insulin when predetermined maximal doses did not control the glucose level.3,4
In this latest trial, the two oral agents produced similar glucose levels among gravidas in whom either drug was effective. However, the failure rate of metformin (35%) was significantly higher than that of glyburide (16%). In this study, the likelihood of failure was similar to that described in the MiG trial for metformin (46%) and in a large case series for glyburide (16%).5
Do oral agents cross the placenta?
An important consideration in regard to these oral agents is safety. Although an in vitro study of isolated perfused placental cotyledons showed little transplacental passage of glyburide,6 and the original randomized trial of glyburide3 found that the drug could not be identified in cord blood of exposed newborns, a recent publication from the National Institute of Child Health and Human Development Obstetric-Fetal Pharmacology Research Unit Network demonstrated that the average fetal glyburide level was 70% of the maternal level.7 Metformin also crosses the placenta and is concentrated in the fetal compartment, with the fetal level approximately double that of the maternal circulation.8
In published reports to date, no significant increase in adverse outcomes has been reported with metformin or glyburide. A number of questions remain unanswered, however.
For example, the role of in utero programming on the development of problems such as insulin resistance syndrome in later life has drawn a great deal of attention. Just as exposure to hyperglycemia in utero has been shown to predispose to the development of glucose intolerance9 in adulthood, might exposure to an insulin sensitizer such as metformin, or an insulin secretagogue such as glyburide, have long-lasting effects on offspring? Studies of animal models are needed, as well as long-term follow-up of exposed humans, to establish the safety of these agents in gestational diabetes.
The temptation is great to use an oral agent instead of insulin to manage gestational diabetes. I urge caution about this strategy, however, until more is known about the potential fetal effects of those oral agents.
Insulin does not cross the placenta to a significant extent, and its use in pregnancy has withstood the test of time. The high likelihood that supplemental insulin will be needed when metformin is used, and the concentration of metformin in the fetal compartment make it a somewhat less attractive treatment option. And the recent evidence of transplacental passage of glyburide is disappointing.
I no longer prescribe glyburide routinely to treat gestational diabetes. When using it does appear appropriate—such as in a patient who refuses insulin despite a high glucose level—I make certain to document that she has been counseled about the unknown potential long-term effects on offspring. I also explain that no harmful effects have yet been found.—DONALD R. COUSTAN, MD
1. Getahun D, Nath C, Ananth CV, et al. Gestational diabetes in the United States: temporal trends 1989 through 2004. Am J Obstet Gynecol. 2008;198(5):525.e1-5.
2. International Association of Diabetes and Pregnancy Study Groups Consensus Panel. International Association of Diabetes and Pregnancy Study Groups recommendations on the diagnosis and classification of hyperglycemia during pregnancy. Diabetes Care. 2010;33 [in press].
3. Langer O, Conway DL, Berkus MD, Xenakis EM, Gonzales O. A comparison of glyburide and insulin in women with gestational diabetes mellitus. N Engl J Med. 2000;343(16):1134-1138.
4. Rowan JA, Hague WM, Gao W, Battin MR, Moore MP. For the MiG Trial Investigators. Metformin versus insulin for the treatment of gestational diabetes. N Engl J Med. 2008;358(19):2003-2015.
5. Conway DL, Gonzales O, Skiver D. Use of glyburide for the treatment of gestational diabetes: the San Antonio experience. J Matern Fetal Neonatal Med. 2004;15(1):51-55.
6. Elliott BD, Langer O, Schenker S, Johnson RF. Insignificant transfer of glyburide occurs across the human placenta. Am J Obstet Gynecol. 1991;165(4):807-812.
7. Hebert MF, Ma X, Naraharisetti SB, et al. For the Obstetric-Fetal Pharmacology Research Unit Network. Are we optimizing gestational diabetes treatment with glyburide? The pharmacologic basis for better clinical practice. Clin Pharmacol Ther. 2009;85(6):607-614.
8. Vanky E, Zahlsen K, Spigset O, Carlsen SM. Placental passage of metformin in women with polycystic ovary syndrome. Fertil Steril. 2005;83(5):1575-1578.
9. Pettitt DJ, Bennett PH, Saad MF, et al. Abnormal glucose tolerance during pregnancy in Pima Indian women. Long-term effects on off spring. Diabetes. 1991;40(suppl 2):126-130.
1. Getahun D, Nath C, Ananth CV, et al. Gestational diabetes in the United States: temporal trends 1989 through 2004. Am J Obstet Gynecol. 2008;198(5):525.e1-5.
2. International Association of Diabetes and Pregnancy Study Groups Consensus Panel. International Association of Diabetes and Pregnancy Study Groups recommendations on the diagnosis and classification of hyperglycemia during pregnancy. Diabetes Care. 2010;33 [in press].
3. Langer O, Conway DL, Berkus MD, Xenakis EM, Gonzales O. A comparison of glyburide and insulin in women with gestational diabetes mellitus. N Engl J Med. 2000;343(16):1134-1138.
4. Rowan JA, Hague WM, Gao W, Battin MR, Moore MP. For the MiG Trial Investigators. Metformin versus insulin for the treatment of gestational diabetes. N Engl J Med. 2008;358(19):2003-2015.
5. Conway DL, Gonzales O, Skiver D. Use of glyburide for the treatment of gestational diabetes: the San Antonio experience. J Matern Fetal Neonatal Med. 2004;15(1):51-55.
6. Elliott BD, Langer O, Schenker S, Johnson RF. Insignificant transfer of glyburide occurs across the human placenta. Am J Obstet Gynecol. 1991;165(4):807-812.
7. Hebert MF, Ma X, Naraharisetti SB, et al. For the Obstetric-Fetal Pharmacology Research Unit Network. Are we optimizing gestational diabetes treatment with glyburide? The pharmacologic basis for better clinical practice. Clin Pharmacol Ther. 2009;85(6):607-614.
8. Vanky E, Zahlsen K, Spigset O, Carlsen SM. Placental passage of metformin in women with polycystic ovary syndrome. Fertil Steril. 2005;83(5):1575-1578.
9. Pettitt DJ, Bennett PH, Saad MF, et al. Abnormal glucose tolerance during pregnancy in Pima Indian women. Long-term effects on off spring. Diabetes. 1991;40(suppl 2):126-130.
Patient Distribution
Editor’s note: This is the first of a three-part series.
My experience is that some, maybe even most, hospitalists tend to assume there is a standard or “right” way to organize things like work schedules, compensation, or even the assignment of patients among the group’s providers. Some will say things like “SHM says the best hospitalist schedule is …” or “The best way to compensate hospitalists is …”
But there really isn’t a “best” way to manage any particular attribute of a practice. Don’t make the mistake of assuming your method is best, or that it’s the way “everybody else does it.” Although scheduling and compensation are marquee issues for hospitalists, approaches to distributing new patients is much less visible. Many groups tend to assume their method is the only reasonable approach. The best approach, however, varies from one practice to the next. You should be open to hearing approaches to scheduling that are different from your own.
Assign Patients by “Load Leveling”
I’ve come across a lot—and I mean a lot—of different approaches to distributing new patients in HM groups around the country, but it seems pretty clear that the most common method is to undertake “load leveling” on a daily or ongoing basis.
For example, groups that have a separate night shift (the night doctor performs no daytime work the day before or the day after a night shift) typically distribute the night’s new patients with the intent of having each daytime doctor start with the same number of patients. The group might more heavily weight some patients, such as those in the ICU (e.g., each ICU patient counts as 1.5 or two non-ICU patients), but most groups don’t. Over the course of the day shift, new referrals will be distributed evenly among the doctors one at a time, sort of like dealing a deck of cards.
This approach aims to avoid significant imbalances in patient loads and has the potential cultural benefit of everyone sharing equally in busy and slow days. Groups that use it tend to see it as the best option because it is the fairest way to divide up the workload.
Practices that use load-leveling almost always use a schedule built on shifts of a predetermined and fixed duration. For example, say the day shift always works from 7 a.m. to 7 p.m. This schedule usually has the majority of compensation paid via a fixed annual salary or fixed shift rate. One potential problem with this approach is that the doctor who is efficient and discharges a lot of patients today is “rewarded” with more new patients tomorrow. Hospitalists who are allergic to work might have an incentive to have a patient wait until tomorrow to discharge to avoid having to assume the care of yet another patient tomorrow morning. Hospital executives who are focused on length-of-stay management might be concerned if they knew this was a potential issue. Of course, the reverse is true as well. In a practice that doesn’t aggressively undertake load-leveling, a less-than-admirable hospitalist could push patients to discharge earlier than optimal just to have one less patient the next day.
Another cost of this approach is that the distribution of patients can be time-consuming each morning. It also offers the opportunity for some in the group to decide they’re treated unfairly. For instance, you might hear the occasional “just last Tuesday, I started with 16 patients, compared with 15 for everyone else. Now you want me to do it again? You’re being unfair to me; it’s someone else’s turn to take the extra patient.”
Assignment by Location
Groups that use “unit-based” hospitalists distribute patients according to the unit the patient is admitted to—and the hospitalist covering that unit. The pros and cons of unit-based hospitalists are many (see “A Unit-Based Approach,” September 2007), but there is an obvious tension between keeping patient loads even among hospitalists and ensuring that all of a hospitalist’s patients are on “their” unit. Practicality usually requires a compromise between pure unit-based assignment and load-leveling.
Uneven Assignments
Some groups assign patients according to a predetermined algorithm and employ load-leveling only when patient loads become extremely unbalanced. For example, Dr. Jones gets all the new referrals today, and Dr. James gets them tomorrow. The idea is that patient loads end up close to even over time, even if they’re unbalanced on any given day.
A system like this allows everyone, including the hospitalists themselves, ED staff, etc., to know who will take the next patient. It decreases the need to communicate the “who’s next” information time after time during the course of the day. In small- to medium-sized practices, it could mean no one needs to function as the triage doctor (i.e., the person who inefficiently answers the service calls, scribbles down clinical information, then calls the hospitalist who is due to take the next patient and relays all the pertinent patient info). This system allows the
hospitalists to know which days will be harder (e.g., taking on the care of new patients) and which days will be easier (e.g., rounding but not assuming care of new patients). Allowing uneven loads also eliminates the need to spend energy working to even the loads and risking that some in the group feel as if they aren’t being treated fairly.
Uncommon yet Intriguing Approaches
Pair referring primary-care physicians (PCPs) with specific hospitalists. I’ve encountered two groups that had hospitalists always admit patients from the same PCPs. In other words, hospitalist Dr. Hancock always serves as attending for patients referred by the same nine PCPs, and hospitalist Dr. Franklin always attends to patients from a different set of PCPs. It seems to me that there could be tremendous benefit in working closely with the same PCPs, most notably getting to know the PCPs’ office staff. But this system raises the risk of creating out-of-balance patient loads, among other problems. It is really attractive to me, but most groups will decide its costs outweigh its benefits.
Hospitalist and patient stay connected during admission. I’m not aware of any group that uses this method (let me know if you do!), but there could be benefits to having each patient see the same hospitalist during each hospital stay. Of course, that is assuming the hospitalist is on duty. Hospitalist and patient could be paired upon the patient’s first admission. The hospitalist could form an excellent relationship with the patient and family; the time spent by the hospitalist getting to know patients on admission would be reduced, and I suspect there might be some benefit in the quality of care.
This method, however, likely results in the most uneven patient loads, and load-leveling would be difficult, if not impossible. Even if hospitalist and patient did form a tight bond, there is a high probability that the hospitalist would be off for the duration of the patient’s next admission. So despite what I suspect are tremendous benefits, this approach may not be feasible for any group.
In next month’s column, I will discuss issues related to the way patients are distributed. TH
Dr. Nelson has been a practicing hospitalist since 1988 and is co-founder and past president of SHM. He is a principal in Nelson Flores Hospital Medicine Consultants, a national hospitalist practice management consulting firm (www.nelsonflores.com). He is co-director and faculty for SHM’s “Best Practices in Managing a Hospital Medicine Program” course. This column represents his views and is not intended to reflect an official position of SHM.
Editor’s note: This is the first of a three-part series.
My experience is that some, maybe even most, hospitalists tend to assume there is a standard or “right” way to organize things like work schedules, compensation, or even the assignment of patients among the group’s providers. Some will say things like “SHM says the best hospitalist schedule is …” or “The best way to compensate hospitalists is …”
But there really isn’t a “best” way to manage any particular attribute of a practice. Don’t make the mistake of assuming your method is best, or that it’s the way “everybody else does it.” Although scheduling and compensation are marquee issues for hospitalists, approaches to distributing new patients is much less visible. Many groups tend to assume their method is the only reasonable approach. The best approach, however, varies from one practice to the next. You should be open to hearing approaches to scheduling that are different from your own.
Assign Patients by “Load Leveling”
I’ve come across a lot—and I mean a lot—of different approaches to distributing new patients in HM groups around the country, but it seems pretty clear that the most common method is to undertake “load leveling” on a daily or ongoing basis.
For example, groups that have a separate night shift (the night doctor performs no daytime work the day before or the day after a night shift) typically distribute the night’s new patients with the intent of having each daytime doctor start with the same number of patients. The group might more heavily weight some patients, such as those in the ICU (e.g., each ICU patient counts as 1.5 or two non-ICU patients), but most groups don’t. Over the course of the day shift, new referrals will be distributed evenly among the doctors one at a time, sort of like dealing a deck of cards.
This approach aims to avoid significant imbalances in patient loads and has the potential cultural benefit of everyone sharing equally in busy and slow days. Groups that use it tend to see it as the best option because it is the fairest way to divide up the workload.
Practices that use load-leveling almost always use a schedule built on shifts of a predetermined and fixed duration. For example, say the day shift always works from 7 a.m. to 7 p.m. This schedule usually has the majority of compensation paid via a fixed annual salary or fixed shift rate. One potential problem with this approach is that the doctor who is efficient and discharges a lot of patients today is “rewarded” with more new patients tomorrow. Hospitalists who are allergic to work might have an incentive to have a patient wait until tomorrow to discharge to avoid having to assume the care of yet another patient tomorrow morning. Hospital executives who are focused on length-of-stay management might be concerned if they knew this was a potential issue. Of course, the reverse is true as well. In a practice that doesn’t aggressively undertake load-leveling, a less-than-admirable hospitalist could push patients to discharge earlier than optimal just to have one less patient the next day.
Another cost of this approach is that the distribution of patients can be time-consuming each morning. It also offers the opportunity for some in the group to decide they’re treated unfairly. For instance, you might hear the occasional “just last Tuesday, I started with 16 patients, compared with 15 for everyone else. Now you want me to do it again? You’re being unfair to me; it’s someone else’s turn to take the extra patient.”
Assignment by Location
Groups that use “unit-based” hospitalists distribute patients according to the unit the patient is admitted to—and the hospitalist covering that unit. The pros and cons of unit-based hospitalists are many (see “A Unit-Based Approach,” September 2007), but there is an obvious tension between keeping patient loads even among hospitalists and ensuring that all of a hospitalist’s patients are on “their” unit. Practicality usually requires a compromise between pure unit-based assignment and load-leveling.
Uneven Assignments
Some groups assign patients according to a predetermined algorithm and employ load-leveling only when patient loads become extremely unbalanced. For example, Dr. Jones gets all the new referrals today, and Dr. James gets them tomorrow. The idea is that patient loads end up close to even over time, even if they’re unbalanced on any given day.
A system like this allows everyone, including the hospitalists themselves, ED staff, etc., to know who will take the next patient. It decreases the need to communicate the “who’s next” information time after time during the course of the day. In small- to medium-sized practices, it could mean no one needs to function as the triage doctor (i.e., the person who inefficiently answers the service calls, scribbles down clinical information, then calls the hospitalist who is due to take the next patient and relays all the pertinent patient info). This system allows the
hospitalists to know which days will be harder (e.g., taking on the care of new patients) and which days will be easier (e.g., rounding but not assuming care of new patients). Allowing uneven loads also eliminates the need to spend energy working to even the loads and risking that some in the group feel as if they aren’t being treated fairly.
Uncommon yet Intriguing Approaches
Pair referring primary-care physicians (PCPs) with specific hospitalists. I’ve encountered two groups that had hospitalists always admit patients from the same PCPs. In other words, hospitalist Dr. Hancock always serves as attending for patients referred by the same nine PCPs, and hospitalist Dr. Franklin always attends to patients from a different set of PCPs. It seems to me that there could be tremendous benefit in working closely with the same PCPs, most notably getting to know the PCPs’ office staff. But this system raises the risk of creating out-of-balance patient loads, among other problems. It is really attractive to me, but most groups will decide its costs outweigh its benefits.
Hospitalist and patient stay connected during admission. I’m not aware of any group that uses this method (let me know if you do!), but there could be benefits to having each patient see the same hospitalist during each hospital stay. Of course, that is assuming the hospitalist is on duty. Hospitalist and patient could be paired upon the patient’s first admission. The hospitalist could form an excellent relationship with the patient and family; the time spent by the hospitalist getting to know patients on admission would be reduced, and I suspect there might be some benefit in the quality of care.
This method, however, likely results in the most uneven patient loads, and load-leveling would be difficult, if not impossible. Even if hospitalist and patient did form a tight bond, there is a high probability that the hospitalist would be off for the duration of the patient’s next admission. So despite what I suspect are tremendous benefits, this approach may not be feasible for any group.
In next month’s column, I will discuss issues related to the way patients are distributed. TH
Dr. Nelson has been a practicing hospitalist since 1988 and is co-founder and past president of SHM. He is a principal in Nelson Flores Hospital Medicine Consultants, a national hospitalist practice management consulting firm (www.nelsonflores.com). He is co-director and faculty for SHM’s “Best Practices in Managing a Hospital Medicine Program” course. This column represents his views and is not intended to reflect an official position of SHM.
Editor’s note: This is the first of a three-part series.
My experience is that some, maybe even most, hospitalists tend to assume there is a standard or “right” way to organize things like work schedules, compensation, or even the assignment of patients among the group’s providers. Some will say things like “SHM says the best hospitalist schedule is …” or “The best way to compensate hospitalists is …”
But there really isn’t a “best” way to manage any particular attribute of a practice. Don’t make the mistake of assuming your method is best, or that it’s the way “everybody else does it.” Although scheduling and compensation are marquee issues for hospitalists, approaches to distributing new patients is much less visible. Many groups tend to assume their method is the only reasonable approach. The best approach, however, varies from one practice to the next. You should be open to hearing approaches to scheduling that are different from your own.
Assign Patients by “Load Leveling”
I’ve come across a lot—and I mean a lot—of different approaches to distributing new patients in HM groups around the country, but it seems pretty clear that the most common method is to undertake “load leveling” on a daily or ongoing basis.
For example, groups that have a separate night shift (the night doctor performs no daytime work the day before or the day after a night shift) typically distribute the night’s new patients with the intent of having each daytime doctor start with the same number of patients. The group might more heavily weight some patients, such as those in the ICU (e.g., each ICU patient counts as 1.5 or two non-ICU patients), but most groups don’t. Over the course of the day shift, new referrals will be distributed evenly among the doctors one at a time, sort of like dealing a deck of cards.
This approach aims to avoid significant imbalances in patient loads and has the potential cultural benefit of everyone sharing equally in busy and slow days. Groups that use it tend to see it as the best option because it is the fairest way to divide up the workload.
Practices that use load-leveling almost always use a schedule built on shifts of a predetermined and fixed duration. For example, say the day shift always works from 7 a.m. to 7 p.m. This schedule usually has the majority of compensation paid via a fixed annual salary or fixed shift rate. One potential problem with this approach is that the doctor who is efficient and discharges a lot of patients today is “rewarded” with more new patients tomorrow. Hospitalists who are allergic to work might have an incentive to have a patient wait until tomorrow to discharge to avoid having to assume the care of yet another patient tomorrow morning. Hospital executives who are focused on length-of-stay management might be concerned if they knew this was a potential issue. Of course, the reverse is true as well. In a practice that doesn’t aggressively undertake load-leveling, a less-than-admirable hospitalist could push patients to discharge earlier than optimal just to have one less patient the next day.
Another cost of this approach is that the distribution of patients can be time-consuming each morning. It also offers the opportunity for some in the group to decide they’re treated unfairly. For instance, you might hear the occasional “just last Tuesday, I started with 16 patients, compared with 15 for everyone else. Now you want me to do it again? You’re being unfair to me; it’s someone else’s turn to take the extra patient.”
Assignment by Location
Groups that use “unit-based” hospitalists distribute patients according to the unit the patient is admitted to—and the hospitalist covering that unit. The pros and cons of unit-based hospitalists are many (see “A Unit-Based Approach,” September 2007), but there is an obvious tension between keeping patient loads even among hospitalists and ensuring that all of a hospitalist’s patients are on “their” unit. Practicality usually requires a compromise between pure unit-based assignment and load-leveling.
Uneven Assignments
Some groups assign patients according to a predetermined algorithm and employ load-leveling only when patient loads become extremely unbalanced. For example, Dr. Jones gets all the new referrals today, and Dr. James gets them tomorrow. The idea is that patient loads end up close to even over time, even if they’re unbalanced on any given day.
A system like this allows everyone, including the hospitalists themselves, ED staff, etc., to know who will take the next patient. It decreases the need to communicate the “who’s next” information time after time during the course of the day. In small- to medium-sized practices, it could mean no one needs to function as the triage doctor (i.e., the person who inefficiently answers the service calls, scribbles down clinical information, then calls the hospitalist who is due to take the next patient and relays all the pertinent patient info). This system allows the
hospitalists to know which days will be harder (e.g., taking on the care of new patients) and which days will be easier (e.g., rounding but not assuming care of new patients). Allowing uneven loads also eliminates the need to spend energy working to even the loads and risking that some in the group feel as if they aren’t being treated fairly.
Uncommon yet Intriguing Approaches
Pair referring primary-care physicians (PCPs) with specific hospitalists. I’ve encountered two groups that had hospitalists always admit patients from the same PCPs. In other words, hospitalist Dr. Hancock always serves as attending for patients referred by the same nine PCPs, and hospitalist Dr. Franklin always attends to patients from a different set of PCPs. It seems to me that there could be tremendous benefit in working closely with the same PCPs, most notably getting to know the PCPs’ office staff. But this system raises the risk of creating out-of-balance patient loads, among other problems. It is really attractive to me, but most groups will decide its costs outweigh its benefits.
Hospitalist and patient stay connected during admission. I’m not aware of any group that uses this method (let me know if you do!), but there could be benefits to having each patient see the same hospitalist during each hospital stay. Of course, that is assuming the hospitalist is on duty. Hospitalist and patient could be paired upon the patient’s first admission. The hospitalist could form an excellent relationship with the patient and family; the time spent by the hospitalist getting to know patients on admission would be reduced, and I suspect there might be some benefit in the quality of care.
This method, however, likely results in the most uneven patient loads, and load-leveling would be difficult, if not impossible. Even if hospitalist and patient did form a tight bond, there is a high probability that the hospitalist would be off for the duration of the patient’s next admission. So despite what I suspect are tremendous benefits, this approach may not be feasible for any group.
In next month’s column, I will discuss issues related to the way patients are distributed. TH
Dr. Nelson has been a practicing hospitalist since 1988 and is co-founder and past president of SHM. He is a principal in Nelson Flores Hospital Medicine Consultants, a national hospitalist practice management consulting firm (www.nelsonflores.com). He is co-director and faculty for SHM’s “Best Practices in Managing a Hospital Medicine Program” course. This column represents his views and is not intended to reflect an official position of SHM.
Is new-onset breast tenderness after the start of hormone therapy a sign of elevated cancer risk?
Breast tenderness is a common side effect of postmenopausal hormone therapy (HT); generally, it is dose-dependent. In this study by Crandall and colleagues, investigators assessed self-reported breast tenderness at the beginning of the WHI and after 12 months of HT, exploring any association between that tenderness and the risk of breast cancer. Here is what they found:
- Among women who reported no breast tenderness at study entry, the incidence of breast tenderness after 12 months was three times higher in those assigned to HT than in those assigned to placebo (36.1% vs 11.8%; P <.001).
- Women who reported the onset of breast tenderness after starting HT were older and more likely to be black or Hispanic than were women who did not.
- More than 75% of women who reported new breast tenderness (most often rated as mild) had been assigned to HT.
- Women taking HT who reported new breast tenderness had a risk of breast cancer 48% higher than those who did not report this complaint (P=.02).
- New-onset breast tenderness in women assigned to the placebo group was not associated with an elevated risk of breast cancer.
Does breast tenderness reflect an increase in cell proliferation?
Earlier studies have linked breast tenderness in women taking CEE plus MPA to high mammographic density, an independent risk factor for breast cancer. They have also established a link between estrogen-progestin therapy and breast cell proliferation. Therefore, as Crandall and colleagues observe, “breast discomfort may be a clinical manifestation of increased proliferation that is manifest radiographically as increased breast density.”
Keep in mind that the original WHI estrogen-progestin trial demonstrated that CEE plus MPA is associated with eight additional cases of breast cancer per 10,000 woman-years—a modest increase in risk. Although the study by Crandall and colleagues suggests that new-onset breast tenderness further increases the risk of breast cancer among users of estrogen-progestin therapy, the absolute magnitude of this increased risk is modest.
New-onset breast tenderness has a sensitivity and specificity similar to those of the Gail model for predicting the risk of invasive breast cancer. In this study, based on a mean follow-up of 5.6 years, the sensitivity and specificity of new-onset breast tenderness were 41% and 64%, respectively, and the positive predictive value was 2.7%. In comparison, using a threshold risk of breast cancer of 1.67% over 5 years, the Gail model has sensitivity, specificity, and a positive predictive value of 44%, 66%, and 6.6%, respectively.
Counsel women who are considering or continuing estrogen-progestin hormone therapy (HT) about its risks (including a modestly increased risk of breast cancer) and benefits. Also counsel them that breast tenderness commonly occurs after initiation of HT.
During follow-up visits, any woman reporting breast tenderness should be advised that this side effect suggests that her risk of breast cancer may be higher than that of women who use HT but do not experience breast tenderness. This information may factor into decisions about HT continuation and dosage, as well as strategies for breast-cancer surveillance.—ANDREW M. KAUNITZ, MD
Breast tenderness is a common side effect of postmenopausal hormone therapy (HT); generally, it is dose-dependent. In this study by Crandall and colleagues, investigators assessed self-reported breast tenderness at the beginning of the WHI and after 12 months of HT, exploring any association between that tenderness and the risk of breast cancer. Here is what they found:
- Among women who reported no breast tenderness at study entry, the incidence of breast tenderness after 12 months was three times higher in those assigned to HT than in those assigned to placebo (36.1% vs 11.8%; P <.001).
- Women who reported the onset of breast tenderness after starting HT were older and more likely to be black or Hispanic than were women who did not.
- More than 75% of women who reported new breast tenderness (most often rated as mild) had been assigned to HT.
- Women taking HT who reported new breast tenderness had a risk of breast cancer 48% higher than those who did not report this complaint (P=.02).
- New-onset breast tenderness in women assigned to the placebo group was not associated with an elevated risk of breast cancer.
Does breast tenderness reflect an increase in cell proliferation?
Earlier studies have linked breast tenderness in women taking CEE plus MPA to high mammographic density, an independent risk factor for breast cancer. They have also established a link between estrogen-progestin therapy and breast cell proliferation. Therefore, as Crandall and colleagues observe, “breast discomfort may be a clinical manifestation of increased proliferation that is manifest radiographically as increased breast density.”
Keep in mind that the original WHI estrogen-progestin trial demonstrated that CEE plus MPA is associated with eight additional cases of breast cancer per 10,000 woman-years—a modest increase in risk. Although the study by Crandall and colleagues suggests that new-onset breast tenderness further increases the risk of breast cancer among users of estrogen-progestin therapy, the absolute magnitude of this increased risk is modest.
New-onset breast tenderness has a sensitivity and specificity similar to those of the Gail model for predicting the risk of invasive breast cancer. In this study, based on a mean follow-up of 5.6 years, the sensitivity and specificity of new-onset breast tenderness were 41% and 64%, respectively, and the positive predictive value was 2.7%. In comparison, using a threshold risk of breast cancer of 1.67% over 5 years, the Gail model has sensitivity, specificity, and a positive predictive value of 44%, 66%, and 6.6%, respectively.
Counsel women who are considering or continuing estrogen-progestin hormone therapy (HT) about its risks (including a modestly increased risk of breast cancer) and benefits. Also counsel them that breast tenderness commonly occurs after initiation of HT.
During follow-up visits, any woman reporting breast tenderness should be advised that this side effect suggests that her risk of breast cancer may be higher than that of women who use HT but do not experience breast tenderness. This information may factor into decisions about HT continuation and dosage, as well as strategies for breast-cancer surveillance.—ANDREW M. KAUNITZ, MD
Breast tenderness is a common side effect of postmenopausal hormone therapy (HT); generally, it is dose-dependent. In this study by Crandall and colleagues, investigators assessed self-reported breast tenderness at the beginning of the WHI and after 12 months of HT, exploring any association between that tenderness and the risk of breast cancer. Here is what they found:
- Among women who reported no breast tenderness at study entry, the incidence of breast tenderness after 12 months was three times higher in those assigned to HT than in those assigned to placebo (36.1% vs 11.8%; P <.001).
- Women who reported the onset of breast tenderness after starting HT were older and more likely to be black or Hispanic than were women who did not.
- More than 75% of women who reported new breast tenderness (most often rated as mild) had been assigned to HT.
- Women taking HT who reported new breast tenderness had a risk of breast cancer 48% higher than those who did not report this complaint (P=.02).
- New-onset breast tenderness in women assigned to the placebo group was not associated with an elevated risk of breast cancer.
Does breast tenderness reflect an increase in cell proliferation?
Earlier studies have linked breast tenderness in women taking CEE plus MPA to high mammographic density, an independent risk factor for breast cancer. They have also established a link between estrogen-progestin therapy and breast cell proliferation. Therefore, as Crandall and colleagues observe, “breast discomfort may be a clinical manifestation of increased proliferation that is manifest radiographically as increased breast density.”
Keep in mind that the original WHI estrogen-progestin trial demonstrated that CEE plus MPA is associated with eight additional cases of breast cancer per 10,000 woman-years—a modest increase in risk. Although the study by Crandall and colleagues suggests that new-onset breast tenderness further increases the risk of breast cancer among users of estrogen-progestin therapy, the absolute magnitude of this increased risk is modest.
New-onset breast tenderness has a sensitivity and specificity similar to those of the Gail model for predicting the risk of invasive breast cancer. In this study, based on a mean follow-up of 5.6 years, the sensitivity and specificity of new-onset breast tenderness were 41% and 64%, respectively, and the positive predictive value was 2.7%. In comparison, using a threshold risk of breast cancer of 1.67% over 5 years, the Gail model has sensitivity, specificity, and a positive predictive value of 44%, 66%, and 6.6%, respectively.
Counsel women who are considering or continuing estrogen-progestin hormone therapy (HT) about its risks (including a modestly increased risk of breast cancer) and benefits. Also counsel them that breast tenderness commonly occurs after initiation of HT.
During follow-up visits, any woman reporting breast tenderness should be advised that this side effect suggests that her risk of breast cancer may be higher than that of women who use HT but do not experience breast tenderness. This information may factor into decisions about HT continuation and dosage, as well as strategies for breast-cancer surveillance.—ANDREW M. KAUNITZ, MD
Necessary Evil: Change
The amount and complexity of medical knowledge we need to keep up with is changing and growing at a remarkable rate. I was trained in an era in which it was taken as a given that congestive heart failure patients should not receive beta-blockers; now it is a big mistake if we don’t prescribe them in most cases. But even before starting medical school, most of us realize that things will change a lot, and many of us see that as a good thing. It keeps our work interesting. Just recently, our hospital had a guest speaker who talked about potential medical applications of nanotechnology. It was way over my head, but it sounded pretty cool.
While I was prepared for ongoing changes in medical knowledge, I failed to anticipate how quickly the business of medicine would change during my career. I think the need to keep up with ever-increasing financial and regulatory issues siphons a lot of time and energy that could be used to keep up with the medical knowledge base. I wasn’t prepared for this when I started my career.
Because it is the start of a new year, I thought I would highlight one issue related to CPT coding: Medicare stopped recognizing consult codes as of Jan. 1 (see “Consultation Elimination,” p. 31).
What It Means for Hospitalists
The good news is that we can just use initial hospital visit codes, inpatient or observation, for all new visits. For example, it won’t matter anymore whether I’m admitting and serving as attending for a patient, or whether a surgeon admitted the patient and asked me to consult for preoperative medical evaluation (“clearance”). I should use the same CPT code in either situation, simply appending a modifier if I’m the admitting physician. And for billing purposes, we won’t have to worry about documenting which doctor requested that we see the patient, though it is a good idea to document it as part of the clinical record anyway.
But it gets a little more complicated. The codes aren’t going away or being removed from the CPT “bible” published by the American Medical Association (AMA). Instead, Medicare simply won’t recognize them anymore. Other payors probably will follow suit within a few months, but that isn’t certain. So it is possible that when asked by a surgeon to provide a preoperative evaluation, you will need to bill an initial hospital (or office or nursing facility) care visit if the patient is on Medicare but bill a consult code if the patient has other insurance. You should check with your billers to ensure you’re doing this correctly.
Medicare-paid consults are at a slightly higher rate than the equivalent service billed as initial hospital care (e.g., when the hospitalist is attending). So a higher reimbursing code has been replaced with one that pays a little less. For example, a 99253 consultation code requires a detailed history, detailed examination, and medical decision-making of low complexity; last year, 99253 was reimbursed by Medicare at an average rate of $114.69. The equivalent admission code for a detailed history, detailed examination, and low-complexity medical decision-making is a 99221 code, for which Medicare pays about $99.90. This represents a difference of about 14%.
However, the net financial impact of this change probably will be positive for most HM groups because you probably bill very few initial consult codes, and instead were stuck billing a follow-up visit code when seeing co-management “consults” (i.e., a patient admitted by a surgeon who asks you to follow and manage diabetes and other medical issues). Now, at least in the case of Medicare, it is appropriate for us to bill an initial hospital visit code, which provides significantly higher reimbursement than follow-up codes.
In addition, there is a modest (about 0.3%) proposed increase in work relative value units attached to the initial hospital visit codes, which will benefit us not only when we’re consulting, but also when we admit and serve as a patient’s attending.
Some specialists may be less interested in consulting on our patients because the initial visit codes will reimburse a little less than similar consultation codes. I don’t anticipate this will be a significant problem for most of us, particularly since many specialists bill the highest level of consultation code (99255), which pays about the same as the equivalent admission code (99223).
Although I think elimination of the use of consultation codes seems like a reasonable step toward simplifying how hospitalists bill for our services, keeping up with these frequent coding changes requires a high level of diligence on our part, and on the part of our administrative and clerical staffs. And it consumes time and resources that I—and my team—could better spend keeping up with changes in clinical practice.
Perhaps when all the dust settles around the healthcare reform debate, we will begin to move toward new, more creative payment models that will allow us to focus on what we do best. TH
Dr. Nelson has been a practicing hospitalist since 1988 and is cofounder and past president of SHM. He is a principal in Nelson Flores Hospital Medicine Consultants, a national hospitalist practice management consulting firm (www.nelsonflores.com). He is also course co-director and faculty for SHM’s “Best Practices in Managing a Hospital Medicine Program” course. This column represents his views and is not intended to reflect an official position of SHM.
The amount and complexity of medical knowledge we need to keep up with is changing and growing at a remarkable rate. I was trained in an era in which it was taken as a given that congestive heart failure patients should not receive beta-blockers; now it is a big mistake if we don’t prescribe them in most cases. But even before starting medical school, most of us realize that things will change a lot, and many of us see that as a good thing. It keeps our work interesting. Just recently, our hospital had a guest speaker who talked about potential medical applications of nanotechnology. It was way over my head, but it sounded pretty cool.
While I was prepared for ongoing changes in medical knowledge, I failed to anticipate how quickly the business of medicine would change during my career. I think the need to keep up with ever-increasing financial and regulatory issues siphons a lot of time and energy that could be used to keep up with the medical knowledge base. I wasn’t prepared for this when I started my career.
Because it is the start of a new year, I thought I would highlight one issue related to CPT coding: Medicare stopped recognizing consult codes as of Jan. 1 (see “Consultation Elimination,” p. 31).
What It Means for Hospitalists
The good news is that we can just use initial hospital visit codes, inpatient or observation, for all new visits. For example, it won’t matter anymore whether I’m admitting and serving as attending for a patient, or whether a surgeon admitted the patient and asked me to consult for preoperative medical evaluation (“clearance”). I should use the same CPT code in either situation, simply appending a modifier if I’m the admitting physician. And for billing purposes, we won’t have to worry about documenting which doctor requested that we see the patient, though it is a good idea to document it as part of the clinical record anyway.
But it gets a little more complicated. The codes aren’t going away or being removed from the CPT “bible” published by the American Medical Association (AMA). Instead, Medicare simply won’t recognize them anymore. Other payors probably will follow suit within a few months, but that isn’t certain. So it is possible that when asked by a surgeon to provide a preoperative evaluation, you will need to bill an initial hospital (or office or nursing facility) care visit if the patient is on Medicare but bill a consult code if the patient has other insurance. You should check with your billers to ensure you’re doing this correctly.
Medicare-paid consults are at a slightly higher rate than the equivalent service billed as initial hospital care (e.g., when the hospitalist is attending). So a higher reimbursing code has been replaced with one that pays a little less. For example, a 99253 consultation code requires a detailed history, detailed examination, and medical decision-making of low complexity; last year, 99253 was reimbursed by Medicare at an average rate of $114.69. The equivalent admission code for a detailed history, detailed examination, and low-complexity medical decision-making is a 99221 code, for which Medicare pays about $99.90. This represents a difference of about 14%.
However, the net financial impact of this change probably will be positive for most HM groups because you probably bill very few initial consult codes, and instead were stuck billing a follow-up visit code when seeing co-management “consults” (i.e., a patient admitted by a surgeon who asks you to follow and manage diabetes and other medical issues). Now, at least in the case of Medicare, it is appropriate for us to bill an initial hospital visit code, which provides significantly higher reimbursement than follow-up codes.
In addition, there is a modest (about 0.3%) proposed increase in work relative value units attached to the initial hospital visit codes, which will benefit us not only when we’re consulting, but also when we admit and serve as a patient’s attending.
Some specialists may be less interested in consulting on our patients because the initial visit codes will reimburse a little less than similar consultation codes. I don’t anticipate this will be a significant problem for most of us, particularly since many specialists bill the highest level of consultation code (99255), which pays about the same as the equivalent admission code (99223).
Although I think elimination of the use of consultation codes seems like a reasonable step toward simplifying how hospitalists bill for our services, keeping up with these frequent coding changes requires a high level of diligence on our part, and on the part of our administrative and clerical staffs. And it consumes time and resources that I—and my team—could better spend keeping up with changes in clinical practice.
Perhaps when all the dust settles around the healthcare reform debate, we will begin to move toward new, more creative payment models that will allow us to focus on what we do best. TH
Dr. Nelson has been a practicing hospitalist since 1988 and is cofounder and past president of SHM. He is a principal in Nelson Flores Hospital Medicine Consultants, a national hospitalist practice management consulting firm (www.nelsonflores.com). He is also course co-director and faculty for SHM’s “Best Practices in Managing a Hospital Medicine Program” course. This column represents his views and is not intended to reflect an official position of SHM.
The amount and complexity of medical knowledge we need to keep up with is changing and growing at a remarkable rate. I was trained in an era in which it was taken as a given that congestive heart failure patients should not receive beta-blockers; now it is a big mistake if we don’t prescribe them in most cases. But even before starting medical school, most of us realize that things will change a lot, and many of us see that as a good thing. It keeps our work interesting. Just recently, our hospital had a guest speaker who talked about potential medical applications of nanotechnology. It was way over my head, but it sounded pretty cool.
While I was prepared for ongoing changes in medical knowledge, I failed to anticipate how quickly the business of medicine would change during my career. I think the need to keep up with ever-increasing financial and regulatory issues siphons a lot of time and energy that could be used to keep up with the medical knowledge base. I wasn’t prepared for this when I started my career.
Because it is the start of a new year, I thought I would highlight one issue related to CPT coding: Medicare stopped recognizing consult codes as of Jan. 1 (see “Consultation Elimination,” p. 31).
What It Means for Hospitalists
The good news is that we can just use initial hospital visit codes, inpatient or observation, for all new visits. For example, it won’t matter anymore whether I’m admitting and serving as attending for a patient, or whether a surgeon admitted the patient and asked me to consult for preoperative medical evaluation (“clearance”). I should use the same CPT code in either situation, simply appending a modifier if I’m the admitting physician. And for billing purposes, we won’t have to worry about documenting which doctor requested that we see the patient, though it is a good idea to document it as part of the clinical record anyway.
But it gets a little more complicated. The codes aren’t going away or being removed from the CPT “bible” published by the American Medical Association (AMA). Instead, Medicare simply won’t recognize them anymore. Other payors probably will follow suit within a few months, but that isn’t certain. So it is possible that when asked by a surgeon to provide a preoperative evaluation, you will need to bill an initial hospital (or office or nursing facility) care visit if the patient is on Medicare but bill a consult code if the patient has other insurance. You should check with your billers to ensure you’re doing this correctly.
Medicare-paid consults are at a slightly higher rate than the equivalent service billed as initial hospital care (e.g., when the hospitalist is attending). So a higher reimbursing code has been replaced with one that pays a little less. For example, a 99253 consultation code requires a detailed history, detailed examination, and medical decision-making of low complexity; last year, 99253 was reimbursed by Medicare at an average rate of $114.69. The equivalent admission code for a detailed history, detailed examination, and low-complexity medical decision-making is a 99221 code, for which Medicare pays about $99.90. This represents a difference of about 14%.
However, the net financial impact of this change probably will be positive for most HM groups because you probably bill very few initial consult codes, and instead were stuck billing a follow-up visit code when seeing co-management “consults” (i.e., a patient admitted by a surgeon who asks you to follow and manage diabetes and other medical issues). Now, at least in the case of Medicare, it is appropriate for us to bill an initial hospital visit code, which provides significantly higher reimbursement than follow-up codes.
In addition, there is a modest (about 0.3%) proposed increase in work relative value units attached to the initial hospital visit codes, which will benefit us not only when we’re consulting, but also when we admit and serve as a patient’s attending.
Some specialists may be less interested in consulting on our patients because the initial visit codes will reimburse a little less than similar consultation codes. I don’t anticipate this will be a significant problem for most of us, particularly since many specialists bill the highest level of consultation code (99255), which pays about the same as the equivalent admission code (99223).
Although I think elimination of the use of consultation codes seems like a reasonable step toward simplifying how hospitalists bill for our services, keeping up with these frequent coding changes requires a high level of diligence on our part, and on the part of our administrative and clerical staffs. And it consumes time and resources that I—and my team—could better spend keeping up with changes in clinical practice.
Perhaps when all the dust settles around the healthcare reform debate, we will begin to move toward new, more creative payment models that will allow us to focus on what we do best. TH
Dr. Nelson has been a practicing hospitalist since 1988 and is cofounder and past president of SHM. He is a principal in Nelson Flores Hospital Medicine Consultants, a national hospitalist practice management consulting firm (www.nelsonflores.com). He is also course co-director and faculty for SHM’s “Best Practices in Managing a Hospital Medicine Program” course. This column represents his views and is not intended to reflect an official position of SHM.
Does treatment of mild gestational diabetes improve pregnancy outcome?
Whether testing for GDM is justified has been a source of contention for more than 20 years. The identification of people who are afflicted with any disease is most useful when treatment is known to produce a benefit. Until recently, evidence that treatment of GDM provides maternal, fetal, or neonatal benefit has been observational. This lack of definitive data has been particularly striking in cases involving glucose intolerance not severe enough to require initial treatment with anything more than diet.
Two blinded, randomized, controlled trials published within the past 5 years—one from Australia (the Australian Carbohydrate Intolerance Study in Pregnant Women [ACHOIS study]1 ) and the other from the Maternal–Fetal Medicine Units (MFMU) Network (cited above)—provide evidence that treatment of less severe GDM does reduce the incidence of adverse maternal and perinatal outcomes.
Details of the trials
Both studies randomized women who had mild GDM to a treatment group and a group that received only routine prenatal care. Treatment consisted of changes in diet, with the addition of insulin if certain maternal glycemic thresholds were met during the course of pregnancy.
Although sample size and results of the 50-g 1-hour glucose screening test and fasting glucose tolerance test were similar in both studies, comparison between the trials is difficult because of differences in:
- maternal prepregnancy body mass indices
- selection of candidates for glucose tolerance testing
- glucose loads during the glucose tolerance test (75 and 100 g in the ACHOIS and MFMU studies, respectively)
- glycemic thresholds and number of exceeded thresholds needed to define GDM
- percentage of patients requiring insulin in addition to diet treatment (20% and 8% in the ACHOIS and MFMU studies, respectively).
Absent from both studies is reporting of daily blood glucose values, which would have facilitated analysis of the nature of the relationship between maternal glucose concentrations and clinical outcomes.
Nonetheless, after adjusting for confounders, both studies found a reduction in the rate of macrosomia, preeclampsia, and maternal weight gain among women in the study group, compared with the control group.
In these studies, positive outcomes were achieved for most subjects using a simple and inexpensive intervention: diet change. Because the majority of large babies are born to women who are overweight and obese and who do not have GDM, it seems reasonable to speculate that the application of diet change and weight monitoring to this growing subset of the obstetric population may achieve positive short- and long-term outcomes for both mother and baby. Confirmation of this speculation awaits the execution of well-designed, adequately powered randomized trials. Until then, it seems reasonable for you to advocate weight loss and balanced nutrition for your patients who are planning to conceive or who are already pregnant, with an eye toward reduced rates of macrosomia, shoulder dystocia, cesarean delivery, and hypertensive disorders.—DAVID A. SACKS, MD
Reference
1. Crowther CA, Hiller JE, Moss JR, McPhee AJ, Jeffries WS, Robinson JS. Effect of treatment of gestational diabetes mellitus on pregnancy outcomes. N Engl J Med. 2005;352:2477-2486.
Whether testing for GDM is justified has been a source of contention for more than 20 years. The identification of people who are afflicted with any disease is most useful when treatment is known to produce a benefit. Until recently, evidence that treatment of GDM provides maternal, fetal, or neonatal benefit has been observational. This lack of definitive data has been particularly striking in cases involving glucose intolerance not severe enough to require initial treatment with anything more than diet.
Two blinded, randomized, controlled trials published within the past 5 years—one from Australia (the Australian Carbohydrate Intolerance Study in Pregnant Women [ACHOIS study]1 ) and the other from the Maternal–Fetal Medicine Units (MFMU) Network (cited above)—provide evidence that treatment of less severe GDM does reduce the incidence of adverse maternal and perinatal outcomes.
Details of the trials
Both studies randomized women who had mild GDM to a treatment group and a group that received only routine prenatal care. Treatment consisted of changes in diet, with the addition of insulin if certain maternal glycemic thresholds were met during the course of pregnancy.
Although sample size and results of the 50-g 1-hour glucose screening test and fasting glucose tolerance test were similar in both studies, comparison between the trials is difficult because of differences in:
- maternal prepregnancy body mass indices
- selection of candidates for glucose tolerance testing
- glucose loads during the glucose tolerance test (75 and 100 g in the ACHOIS and MFMU studies, respectively)
- glycemic thresholds and number of exceeded thresholds needed to define GDM
- percentage of patients requiring insulin in addition to diet treatment (20% and 8% in the ACHOIS and MFMU studies, respectively).
Absent from both studies is reporting of daily blood glucose values, which would have facilitated analysis of the nature of the relationship between maternal glucose concentrations and clinical outcomes.
Nonetheless, after adjusting for confounders, both studies found a reduction in the rate of macrosomia, preeclampsia, and maternal weight gain among women in the study group, compared with the control group.
In these studies, positive outcomes were achieved for most subjects using a simple and inexpensive intervention: diet change. Because the majority of large babies are born to women who are overweight and obese and who do not have GDM, it seems reasonable to speculate that the application of diet change and weight monitoring to this growing subset of the obstetric population may achieve positive short- and long-term outcomes for both mother and baby. Confirmation of this speculation awaits the execution of well-designed, adequately powered randomized trials. Until then, it seems reasonable for you to advocate weight loss and balanced nutrition for your patients who are planning to conceive or who are already pregnant, with an eye toward reduced rates of macrosomia, shoulder dystocia, cesarean delivery, and hypertensive disorders.—DAVID A. SACKS, MD
Whether testing for GDM is justified has been a source of contention for more than 20 years. The identification of people who are afflicted with any disease is most useful when treatment is known to produce a benefit. Until recently, evidence that treatment of GDM provides maternal, fetal, or neonatal benefit has been observational. This lack of definitive data has been particularly striking in cases involving glucose intolerance not severe enough to require initial treatment with anything more than diet.
Two blinded, randomized, controlled trials published within the past 5 years—one from Australia (the Australian Carbohydrate Intolerance Study in Pregnant Women [ACHOIS study]1 ) and the other from the Maternal–Fetal Medicine Units (MFMU) Network (cited above)—provide evidence that treatment of less severe GDM does reduce the incidence of adverse maternal and perinatal outcomes.
Details of the trials
Both studies randomized women who had mild GDM to a treatment group and a group that received only routine prenatal care. Treatment consisted of changes in diet, with the addition of insulin if certain maternal glycemic thresholds were met during the course of pregnancy.
Although sample size and results of the 50-g 1-hour glucose screening test and fasting glucose tolerance test were similar in both studies, comparison between the trials is difficult because of differences in:
- maternal prepregnancy body mass indices
- selection of candidates for glucose tolerance testing
- glucose loads during the glucose tolerance test (75 and 100 g in the ACHOIS and MFMU studies, respectively)
- glycemic thresholds and number of exceeded thresholds needed to define GDM
- percentage of patients requiring insulin in addition to diet treatment (20% and 8% in the ACHOIS and MFMU studies, respectively).
Absent from both studies is reporting of daily blood glucose values, which would have facilitated analysis of the nature of the relationship between maternal glucose concentrations and clinical outcomes.
Nonetheless, after adjusting for confounders, both studies found a reduction in the rate of macrosomia, preeclampsia, and maternal weight gain among women in the study group, compared with the control group.
In these studies, positive outcomes were achieved for most subjects using a simple and inexpensive intervention: diet change. Because the majority of large babies are born to women who are overweight and obese and who do not have GDM, it seems reasonable to speculate that the application of diet change and weight monitoring to this growing subset of the obstetric population may achieve positive short- and long-term outcomes for both mother and baby. Confirmation of this speculation awaits the execution of well-designed, adequately powered randomized trials. Until then, it seems reasonable for you to advocate weight loss and balanced nutrition for your patients who are planning to conceive or who are already pregnant, with an eye toward reduced rates of macrosomia, shoulder dystocia, cesarean delivery, and hypertensive disorders.—DAVID A. SACKS, MD
Reference
1. Crowther CA, Hiller JE, Moss JR, McPhee AJ, Jeffries WS, Robinson JS. Effect of treatment of gestational diabetes mellitus on pregnancy outcomes. N Engl J Med. 2005;352:2477-2486.
Reference
1. Crowther CA, Hiller JE, Moss JR, McPhee AJ, Jeffries WS, Robinson JS. Effect of treatment of gestational diabetes mellitus on pregnancy outcomes. N Engl J Med. 2005;352:2477-2486.
Does the clinical breast exam boost the sensitivity of mammography?
Historically, physicians relied on CBE to identify masses. With the advent of mammography, however, and increasing evidence of its efficacy in detecting malignancy, mammography became the new norm for screening, and remains the gold standard for detection of breast cancer. It is clear that mammography can detect some types of lesions long before they can be palpated on clinical exam.
Mammography isn’t perfect
The sensitivity of mammography to detect breast cancer ranges from 68% to 88%, depending on the patient’s menopausal status, breast density, and other characteristics. Certain types of breast cancer, such as invasive lobular carcinoma, are more difficult to detect with mammography. Many major medical organizations, including ACOG and the American Cancer Society, continue to recommend CBE as a component of the screening process. Most ObGyns value their role in screening women for cancer and generally believe that CBE is an important element of well-woman care. In addition, as Barton and colleagues point out, some women are more accepting of CBE than of mammography.2
CBE took 8 to 10 minutes
The Chiarelli study is a large, well-designed study that included women 50 to 69 years old who participated in breast-screening programs in Ontario. Women were screened by mammography alone or mammography combined with CBE. Examinations were standardized and performed by well-trained and certified nurses, and the CBE took an average of 8 to 10 minutes.
Surveys of American women suggest that most of them would accept the possibility of undergoing biopsy for a negative finding for the sake of improving detection of breast cancer. The study by Chiarelli and colleagues supports the current practice of ObGyns and other primary care providers who perform CBE as a component of screening, and is congruent with our patients’ wish to optimize the sensitivity of screening.
To be effective, however, the quality of our exams must be consistent with those described in the study. In a published review, CBE in the community setting did not yield the same sensitivity reported in randomized trials.3 We must remain cognizant of the goals of CBE and educate our patients about the benefits, limitations, and risks of screening.
After counseling the patient about the possibility of false-positive findings, perform clinical breast examination as part of breast cancer screening (i.e., including mammography). Barton and colleagues suggest that CBE include at least 3 minutes of palpation per breast using specific techniques, including the following:
- Begin palpation in the axilla and continue in a straight line down the midaxillary line to the bra line. Move the fingers medially and continue palpation up the chest in a straight line to the clavicle. Move the fingers medially again and palpate back down to the bra line, continuing in this fashion until the entire breast has been covered, with overlapping rows.
- Hold the middle three fingers together and slightly flex the metacarpal-phalangeal joint. Use the pads—not the fingertips—to examine the surface of the breast, and palpate each area by moving the fingers in a small circle, as though tracing the outline of a dime. Make three circles at each spot using light, medium, and then deep pressure to ensure that all levels of tissue are palpated.
- Palpate the supraclavicular and axillary regions as well as the breast to detect any adenopathy.
- Palpate the nipple in the same manner as the rest of the breast.2
—JENNIFER GRIFFIN, MD, MARK PEARLMAN, MD
1. American Cancer Society. Breast Cancer Facts & Figures 2009–2010. Atlanta: ACS; 2009.
2. Barton MB, Harris R, Fletcher SW. The rational clinical examination. Does this patient have breast cancer? The screening clinical breast examination: should it be done? How? JAMA. 1999;282:1270-1280.
3. Elmore JG, Armstrong K, Lehman CD, Fletcher SW. Screening for breast cancer. JAMA. 2005;293:1245-1256.
Historically, physicians relied on CBE to identify masses. With the advent of mammography, however, and increasing evidence of its efficacy in detecting malignancy, mammography became the new norm for screening, and remains the gold standard for detection of breast cancer. It is clear that mammography can detect some types of lesions long before they can be palpated on clinical exam.
Mammography isn’t perfect
The sensitivity of mammography to detect breast cancer ranges from 68% to 88%, depending on the patient’s menopausal status, breast density, and other characteristics. Certain types of breast cancer, such as invasive lobular carcinoma, are more difficult to detect with mammography. Many major medical organizations, including ACOG and the American Cancer Society, continue to recommend CBE as a component of the screening process. Most ObGyns value their role in screening women for cancer and generally believe that CBE is an important element of well-woman care. In addition, as Barton and colleagues point out, some women are more accepting of CBE than of mammography.2
CBE took 8 to 10 minutes
The Chiarelli study is a large, well-designed study that included women 50 to 69 years old who participated in breast-screening programs in Ontario. Women were screened by mammography alone or mammography combined with CBE. Examinations were standardized and performed by well-trained and certified nurses, and the CBE took an average of 8 to 10 minutes.
Surveys of American women suggest that most of them would accept the possibility of undergoing biopsy for a negative finding for the sake of improving detection of breast cancer. The study by Chiarelli and colleagues supports the current practice of ObGyns and other primary care providers who perform CBE as a component of screening, and is congruent with our patients’ wish to optimize the sensitivity of screening.
To be effective, however, the quality of our exams must be consistent with those described in the study. In a published review, CBE in the community setting did not yield the same sensitivity reported in randomized trials.3 We must remain cognizant of the goals of CBE and educate our patients about the benefits, limitations, and risks of screening.
After counseling the patient about the possibility of false-positive findings, perform clinical breast examination as part of breast cancer screening (i.e., including mammography). Barton and colleagues suggest that CBE include at least 3 minutes of palpation per breast using specific techniques, including the following:
- Begin palpation in the axilla and continue in a straight line down the midaxillary line to the bra line. Move the fingers medially and continue palpation up the chest in a straight line to the clavicle. Move the fingers medially again and palpate back down to the bra line, continuing in this fashion until the entire breast has been covered, with overlapping rows.
- Hold the middle three fingers together and slightly flex the metacarpal-phalangeal joint. Use the pads—not the fingertips—to examine the surface of the breast, and palpate each area by moving the fingers in a small circle, as though tracing the outline of a dime. Make three circles at each spot using light, medium, and then deep pressure to ensure that all levels of tissue are palpated.
- Palpate the supraclavicular and axillary regions as well as the breast to detect any adenopathy.
- Palpate the nipple in the same manner as the rest of the breast.2
—JENNIFER GRIFFIN, MD, MARK PEARLMAN, MD
Historically, physicians relied on CBE to identify masses. With the advent of mammography, however, and increasing evidence of its efficacy in detecting malignancy, mammography became the new norm for screening, and remains the gold standard for detection of breast cancer. It is clear that mammography can detect some types of lesions long before they can be palpated on clinical exam.
Mammography isn’t perfect
The sensitivity of mammography to detect breast cancer ranges from 68% to 88%, depending on the patient’s menopausal status, breast density, and other characteristics. Certain types of breast cancer, such as invasive lobular carcinoma, are more difficult to detect with mammography. Many major medical organizations, including ACOG and the American Cancer Society, continue to recommend CBE as a component of the screening process. Most ObGyns value their role in screening women for cancer and generally believe that CBE is an important element of well-woman care. In addition, as Barton and colleagues point out, some women are more accepting of CBE than of mammography.2
CBE took 8 to 10 minutes
The Chiarelli study is a large, well-designed study that included women 50 to 69 years old who participated in breast-screening programs in Ontario. Women were screened by mammography alone or mammography combined with CBE. Examinations were standardized and performed by well-trained and certified nurses, and the CBE took an average of 8 to 10 minutes.
Surveys of American women suggest that most of them would accept the possibility of undergoing biopsy for a negative finding for the sake of improving detection of breast cancer. The study by Chiarelli and colleagues supports the current practice of ObGyns and other primary care providers who perform CBE as a component of screening, and is congruent with our patients’ wish to optimize the sensitivity of screening.
To be effective, however, the quality of our exams must be consistent with those described in the study. In a published review, CBE in the community setting did not yield the same sensitivity reported in randomized trials.3 We must remain cognizant of the goals of CBE and educate our patients about the benefits, limitations, and risks of screening.
After counseling the patient about the possibility of false-positive findings, perform clinical breast examination as part of breast cancer screening (i.e., including mammography). Barton and colleagues suggest that CBE include at least 3 minutes of palpation per breast using specific techniques, including the following:
- Begin palpation in the axilla and continue in a straight line down the midaxillary line to the bra line. Move the fingers medially and continue palpation up the chest in a straight line to the clavicle. Move the fingers medially again and palpate back down to the bra line, continuing in this fashion until the entire breast has been covered, with overlapping rows.
- Hold the middle three fingers together and slightly flex the metacarpal-phalangeal joint. Use the pads—not the fingertips—to examine the surface of the breast, and palpate each area by moving the fingers in a small circle, as though tracing the outline of a dime. Make three circles at each spot using light, medium, and then deep pressure to ensure that all levels of tissue are palpated.
- Palpate the supraclavicular and axillary regions as well as the breast to detect any adenopathy.
- Palpate the nipple in the same manner as the rest of the breast.2
—JENNIFER GRIFFIN, MD, MARK PEARLMAN, MD
1. American Cancer Society. Breast Cancer Facts & Figures 2009–2010. Atlanta: ACS; 2009.
2. Barton MB, Harris R, Fletcher SW. The rational clinical examination. Does this patient have breast cancer? The screening clinical breast examination: should it be done? How? JAMA. 1999;282:1270-1280.
3. Elmore JG, Armstrong K, Lehman CD, Fletcher SW. Screening for breast cancer. JAMA. 2005;293:1245-1256.
1. American Cancer Society. Breast Cancer Facts & Figures 2009–2010. Atlanta: ACS; 2009.
2. Barton MB, Harris R, Fletcher SW. The rational clinical examination. Does this patient have breast cancer? The screening clinical breast examination: should it be done? How? JAMA. 1999;282:1270-1280.
3. Elmore JG, Armstrong K, Lehman CD, Fletcher SW. Screening for breast cancer. JAMA. 2005;293:1245-1256.
Are a short cervix and a history of preterm birth absolute indications for cervical cerclage?
- 1) a history of second-trimester loss involving painless cervical dilatation in the absence of infection, bleeding, amniorrhexis, and fetal demise
- 2) asymptomatic cervical changes in the current pregnancy.
Although our understanding of cervical insufficiency has undergone many revisions and reinterpretations in the intervening years, we still lack an accepted diagnostic test or proven criteria for diagnosis. Cerclage is placed in 1% of all pregnancies in the United States, but there is no consensus on indications, and the effectiveness is still a matter of debate.1 Cerclage placement based on ultrasonographic (US) measurement of cervical length has been proposed as the solution to this clinical quagmire, in the wake of evidence suggesting that cervical length may act as a surrogate for cervical competence.
A patient-level meta-analysis of four randomized trials of cervical cerclage, published in 2005, reconfirmed the original indication for cerclage. In women who had a cervical length below 25 mm, cerclage reduced the rate of preterm birth at less than 35 weeks’ gestation only if they had a history of preterm birth.2 This finding prompted the question: Would such women represent a truly homogeneous population in terms of therapeutic response to cerclage?
The Owen trial attempts to answer this specific question.
Details of the trial
Women who had a cervix shorter than 25 mm and a history of preterm birth and who were pregnant with a singleton gestation were eligible. Candidates for elective cerclage based on history, or for emergency cerclage based on cervical dilatation of at least 2 cm with visible membranes, were excluded from the study—possibly reducing the generalizability of the findings.
For the remaining 302 participants, cerclage appeared to have an overall benefit when survival analysis took the duration of gestation into consideration. But only women who had a cervical length below 15 mm had a significant reduction in the primary outcome (preterm birth at less than 35 weeks’ gestation) with cerclage. These results are somewhat reminiscent of the findings of a randomized comparison of cerclage and 17α-hydroxyprogesterone caproate in women who had a short cervix (measured by US), in which cerclage proved to be superior only when cervical length was less than 15 mm.3
Why the 15-mm cutoff isn’t definitive
Despite these findings, the 15-mm measurement cannot be assumed to be completely prescriptive because it was selected somewhat arbitrarily. Furthermore, it may be inadvisable to wait for cervical length to decrease below 15 mm. In pregnancies in which cervical length is below 5 mm, there is a significantly higher expression of intra-amniotic inflammation than in those in which cervical length is 6 to 25 mm, according to another recent study.4 Women who have a very short cervix may be far along the inflammatory cascade and may have already entered the irreversible phase of parturition, reducing the efficacy and even the advisability of cerclage. A positive fetal fibronectin test (as a marker of inflammation and choriodecidual disruption) and an increased level of interleukin-8 in cervical mucus reportedly identified a subgroup of women with a short cervix who would not benefit from cerclage—and who might even be harmed by it.5,6
Because preterm birth is such a complex disorder, it is unlikely that one intervention will be effective in all women—even within a certain stratum of cervical length. Rather, it may be necessary to identify subsets of pregnant women amenable to targeted or tailored intervention.
Ultrasonographic surveillance of cervical length can provide you with useful information when a woman who has a history of spontaneous preterm birth at less than 34 weeks’ gestation is pregnant with a singleton gestation. Serial sonographic surveillance of cervical length may be conducted every 1 to 2 weeks, between 16 and 24 weeks’ gestation. This approach may help identify the candidate likely to benefit from cerclage and may prevent unnecessary surgical intervention in another. Do not place cerclage “just in case”; it may benefit some gravidas but harm others.
Emerging evidence appears to show that only women who have historical risk factors plus a short cervix (—ALEX C. VIDAEFF, MD, MPH
1. Berghella V, Seibel-Seamon J. Contemporary use of cervical cerclage. Clin Obstet Gynecol. 2007;50:468-477.
2. Berghella V, Odibo AO, To MS, Rust OA, Athuisius SM. Cerclage for short cervix on ultrasonography: meta-analysis of trials using individual patient-level data. Obstet Gynecol. 2005;106:181-189.
3. Keeler SM, Kiefer D, Rochon M, Quinones JN, Novetsky AP, Rust O. A randomized trial of cerclage vs 17 alpha-hydroxyprogesterone caproate for treatment of short cervix. J Perinat Med. 2009;37:473-479.
4. Kiefer DG, Keeler SM, Rust OA, Wayock CP, Vintzileos AM, Hanna N. Is midtrimester short cervix a sign of intraamniotic inflammation? Am J Obstet Gynecol. 2009;200:374.e1-374.e5.
5. Keeler SM, Roman AS, Coletta JM, Kiefer DG, Feuerman M, Rust OA. Fetal fibronectin testing in patients with short cervix in the midtrimester: can it identify optimal candidates for ultrasound-indicated cerclage? Am J Obstet Gynecol. 2009;200:158.e1-158.e6.
6. Sakai M, Shiozaki A, Tabata M, et al. Evaluation of effectiveness of prophylactic cerclage of a short cervix according to interleukin-8 in cervical mucus. Am J Obstet Gynecol. 2006;194:14-19.
- 1) a history of second-trimester loss involving painless cervical dilatation in the absence of infection, bleeding, amniorrhexis, and fetal demise
- 2) asymptomatic cervical changes in the current pregnancy.
Although our understanding of cervical insufficiency has undergone many revisions and reinterpretations in the intervening years, we still lack an accepted diagnostic test or proven criteria for diagnosis. Cerclage is placed in 1% of all pregnancies in the United States, but there is no consensus on indications, and the effectiveness is still a matter of debate.1 Cerclage placement based on ultrasonographic (US) measurement of cervical length has been proposed as the solution to this clinical quagmire, in the wake of evidence suggesting that cervical length may act as a surrogate for cervical competence.
A patient-level meta-analysis of four randomized trials of cervical cerclage, published in 2005, reconfirmed the original indication for cerclage. In women who had a cervical length below 25 mm, cerclage reduced the rate of preterm birth at less than 35 weeks’ gestation only if they had a history of preterm birth.2 This finding prompted the question: Would such women represent a truly homogeneous population in terms of therapeutic response to cerclage?
The Owen trial attempts to answer this specific question.
Details of the trial
Women who had a cervix shorter than 25 mm and a history of preterm birth and who were pregnant with a singleton gestation were eligible. Candidates for elective cerclage based on history, or for emergency cerclage based on cervical dilatation of at least 2 cm with visible membranes, were excluded from the study—possibly reducing the generalizability of the findings.
For the remaining 302 participants, cerclage appeared to have an overall benefit when survival analysis took the duration of gestation into consideration. But only women who had a cervical length below 15 mm had a significant reduction in the primary outcome (preterm birth at less than 35 weeks’ gestation) with cerclage. These results are somewhat reminiscent of the findings of a randomized comparison of cerclage and 17α-hydroxyprogesterone caproate in women who had a short cervix (measured by US), in which cerclage proved to be superior only when cervical length was less than 15 mm.3
Why the 15-mm cutoff isn’t definitive
Despite these findings, the 15-mm measurement cannot be assumed to be completely prescriptive because it was selected somewhat arbitrarily. Furthermore, it may be inadvisable to wait for cervical length to decrease below 15 mm. In pregnancies in which cervical length is below 5 mm, there is a significantly higher expression of intra-amniotic inflammation than in those in which cervical length is 6 to 25 mm, according to another recent study.4 Women who have a very short cervix may be far along the inflammatory cascade and may have already entered the irreversible phase of parturition, reducing the efficacy and even the advisability of cerclage. A positive fetal fibronectin test (as a marker of inflammation and choriodecidual disruption) and an increased level of interleukin-8 in cervical mucus reportedly identified a subgroup of women with a short cervix who would not benefit from cerclage—and who might even be harmed by it.5,6
Because preterm birth is such a complex disorder, it is unlikely that one intervention will be effective in all women—even within a certain stratum of cervical length. Rather, it may be necessary to identify subsets of pregnant women amenable to targeted or tailored intervention.
Ultrasonographic surveillance of cervical length can provide you with useful information when a woman who has a history of spontaneous preterm birth at less than 34 weeks’ gestation is pregnant with a singleton gestation. Serial sonographic surveillance of cervical length may be conducted every 1 to 2 weeks, between 16 and 24 weeks’ gestation. This approach may help identify the candidate likely to benefit from cerclage and may prevent unnecessary surgical intervention in another. Do not place cerclage “just in case”; it may benefit some gravidas but harm others.
Emerging evidence appears to show that only women who have historical risk factors plus a short cervix (—ALEX C. VIDAEFF, MD, MPH
- 1) a history of second-trimester loss involving painless cervical dilatation in the absence of infection, bleeding, amniorrhexis, and fetal demise
- 2) asymptomatic cervical changes in the current pregnancy.
Although our understanding of cervical insufficiency has undergone many revisions and reinterpretations in the intervening years, we still lack an accepted diagnostic test or proven criteria for diagnosis. Cerclage is placed in 1% of all pregnancies in the United States, but there is no consensus on indications, and the effectiveness is still a matter of debate.1 Cerclage placement based on ultrasonographic (US) measurement of cervical length has been proposed as the solution to this clinical quagmire, in the wake of evidence suggesting that cervical length may act as a surrogate for cervical competence.
A patient-level meta-analysis of four randomized trials of cervical cerclage, published in 2005, reconfirmed the original indication for cerclage. In women who had a cervical length below 25 mm, cerclage reduced the rate of preterm birth at less than 35 weeks’ gestation only if they had a history of preterm birth.2 This finding prompted the question: Would such women represent a truly homogeneous population in terms of therapeutic response to cerclage?
The Owen trial attempts to answer this specific question.
Details of the trial
Women who had a cervix shorter than 25 mm and a history of preterm birth and who were pregnant with a singleton gestation were eligible. Candidates for elective cerclage based on history, or for emergency cerclage based on cervical dilatation of at least 2 cm with visible membranes, were excluded from the study—possibly reducing the generalizability of the findings.
For the remaining 302 participants, cerclage appeared to have an overall benefit when survival analysis took the duration of gestation into consideration. But only women who had a cervical length below 15 mm had a significant reduction in the primary outcome (preterm birth at less than 35 weeks’ gestation) with cerclage. These results are somewhat reminiscent of the findings of a randomized comparison of cerclage and 17α-hydroxyprogesterone caproate in women who had a short cervix (measured by US), in which cerclage proved to be superior only when cervical length was less than 15 mm.3
Why the 15-mm cutoff isn’t definitive
Despite these findings, the 15-mm measurement cannot be assumed to be completely prescriptive because it was selected somewhat arbitrarily. Furthermore, it may be inadvisable to wait for cervical length to decrease below 15 mm. In pregnancies in which cervical length is below 5 mm, there is a significantly higher expression of intra-amniotic inflammation than in those in which cervical length is 6 to 25 mm, according to another recent study.4 Women who have a very short cervix may be far along the inflammatory cascade and may have already entered the irreversible phase of parturition, reducing the efficacy and even the advisability of cerclage. A positive fetal fibronectin test (as a marker of inflammation and choriodecidual disruption) and an increased level of interleukin-8 in cervical mucus reportedly identified a subgroup of women with a short cervix who would not benefit from cerclage—and who might even be harmed by it.5,6
Because preterm birth is such a complex disorder, it is unlikely that one intervention will be effective in all women—even within a certain stratum of cervical length. Rather, it may be necessary to identify subsets of pregnant women amenable to targeted or tailored intervention.
Ultrasonographic surveillance of cervical length can provide you with useful information when a woman who has a history of spontaneous preterm birth at less than 34 weeks’ gestation is pregnant with a singleton gestation. Serial sonographic surveillance of cervical length may be conducted every 1 to 2 weeks, between 16 and 24 weeks’ gestation. This approach may help identify the candidate likely to benefit from cerclage and may prevent unnecessary surgical intervention in another. Do not place cerclage “just in case”; it may benefit some gravidas but harm others.
Emerging evidence appears to show that only women who have historical risk factors plus a short cervix (—ALEX C. VIDAEFF, MD, MPH
1. Berghella V, Seibel-Seamon J. Contemporary use of cervical cerclage. Clin Obstet Gynecol. 2007;50:468-477.
2. Berghella V, Odibo AO, To MS, Rust OA, Athuisius SM. Cerclage for short cervix on ultrasonography: meta-analysis of trials using individual patient-level data. Obstet Gynecol. 2005;106:181-189.
3. Keeler SM, Kiefer D, Rochon M, Quinones JN, Novetsky AP, Rust O. A randomized trial of cerclage vs 17 alpha-hydroxyprogesterone caproate for treatment of short cervix. J Perinat Med. 2009;37:473-479.
4. Kiefer DG, Keeler SM, Rust OA, Wayock CP, Vintzileos AM, Hanna N. Is midtrimester short cervix a sign of intraamniotic inflammation? Am J Obstet Gynecol. 2009;200:374.e1-374.e5.
5. Keeler SM, Roman AS, Coletta JM, Kiefer DG, Feuerman M, Rust OA. Fetal fibronectin testing in patients with short cervix in the midtrimester: can it identify optimal candidates for ultrasound-indicated cerclage? Am J Obstet Gynecol. 2009;200:158.e1-158.e6.
6. Sakai M, Shiozaki A, Tabata M, et al. Evaluation of effectiveness of prophylactic cerclage of a short cervix according to interleukin-8 in cervical mucus. Am J Obstet Gynecol. 2006;194:14-19.
1. Berghella V, Seibel-Seamon J. Contemporary use of cervical cerclage. Clin Obstet Gynecol. 2007;50:468-477.
2. Berghella V, Odibo AO, To MS, Rust OA, Athuisius SM. Cerclage for short cervix on ultrasonography: meta-analysis of trials using individual patient-level data. Obstet Gynecol. 2005;106:181-189.
3. Keeler SM, Kiefer D, Rochon M, Quinones JN, Novetsky AP, Rust O. A randomized trial of cerclage vs 17 alpha-hydroxyprogesterone caproate for treatment of short cervix. J Perinat Med. 2009;37:473-479.
4. Kiefer DG, Keeler SM, Rust OA, Wayock CP, Vintzileos AM, Hanna N. Is midtrimester short cervix a sign of intraamniotic inflammation? Am J Obstet Gynecol. 2009;200:374.e1-374.e5.
5. Keeler SM, Roman AS, Coletta JM, Kiefer DG, Feuerman M, Rust OA. Fetal fibronectin testing in patients with short cervix in the midtrimester: can it identify optimal candidates for ultrasound-indicated cerclage? Am J Obstet Gynecol. 2009;200:158.e1-158.e6.
6. Sakai M, Shiozaki A, Tabata M, et al. Evaluation of effectiveness of prophylactic cerclage of a short cervix according to interleukin-8 in cervical mucus. Am J Obstet Gynecol. 2006;194:14-19.
Does benefit always outweigh risk when a SERM is used to prevent primary breast cancer?
In the United States, tamoxifen is usually prescribed as adjuvant endocrine therapy after treatment of estrogen-receptor–positive breast cancer in both premenopausal and post-menopausal women. Raloxifene is most often prescribed for the prevention and treatment of osteoporosis in postmenopausal women. Use of these agents as chemoprophylaxis in women who have no history of breast cancer is less common, largely because of the risks and side effects of these drugs.
The increase in venous thromboembolism is of particular concern for women who have an elevated risk of this outcome, including overweight women and those of advanced age. The elevated risk of malignant and benign gynecologic disease associated with tamoxifen is of concern in all women who have an intact uterus.
Details of the review
Nelson and colleagues performed a systematic review, funded by the Agency for Health-care Research and Quality, that involved the aggregation of findings from seven placebo-controlled trials and one head-to-head, randomized, clinical trial involving women who had no history of preinvasive or invasive breast cancer. In the process, they focused on harms as well as benefits associated with use of these chemoprophylactic agents.
Tamoxifen and raloxifene reduced the risk of invasive breast cancer by 7 to 10 cases in every 1,000 women annually. These agents reduced the risk of estrogen-receptor–positive malignancy, but not estrogen-receptor–negative tumors, noninvasive cancer, or breast cancer–related mortality.
Tamoxifen and raloxifene were similarly effective in premenopausal and postmenopausal populations; both drugs also reduced the rate of osteoporotic fracture.
Most of the participants in the prevention trials were white and relatively healthy. Therefore, the relevance of these findings to women of other racial and ethnic groups and to women who have chronic disease or other morbidity is uncertain.
Aromatase inhibitors are being assessed for chemoprophylaxis, so we should have information on their risk-benefit ratio in the near future.
Clinicians who care for women at high risk of primary breast cancer should thoroughly counsel each candidate for chemoprophylaxis about the potential benefits and risks of these agents in her particular circumstances. It may be that the risks outweigh the benefits in some women—such as those who already have an elevated risk of venous thromboembolism.
In addition, because most of the participants in the studies included in this review were healthy and white, we cannot be certain how generalizable these findings are to other subpopulations.—ANDREW M. KAUNITZ, MD
In the United States, tamoxifen is usually prescribed as adjuvant endocrine therapy after treatment of estrogen-receptor–positive breast cancer in both premenopausal and post-menopausal women. Raloxifene is most often prescribed for the prevention and treatment of osteoporosis in postmenopausal women. Use of these agents as chemoprophylaxis in women who have no history of breast cancer is less common, largely because of the risks and side effects of these drugs.
The increase in venous thromboembolism is of particular concern for women who have an elevated risk of this outcome, including overweight women and those of advanced age. The elevated risk of malignant and benign gynecologic disease associated with tamoxifen is of concern in all women who have an intact uterus.
Details of the review
Nelson and colleagues performed a systematic review, funded by the Agency for Health-care Research and Quality, that involved the aggregation of findings from seven placebo-controlled trials and one head-to-head, randomized, clinical trial involving women who had no history of preinvasive or invasive breast cancer. In the process, they focused on harms as well as benefits associated with use of these chemoprophylactic agents.
Tamoxifen and raloxifene reduced the risk of invasive breast cancer by 7 to 10 cases in every 1,000 women annually. These agents reduced the risk of estrogen-receptor–positive malignancy, but not estrogen-receptor–negative tumors, noninvasive cancer, or breast cancer–related mortality.
Tamoxifen and raloxifene were similarly effective in premenopausal and postmenopausal populations; both drugs also reduced the rate of osteoporotic fracture.
Most of the participants in the prevention trials were white and relatively healthy. Therefore, the relevance of these findings to women of other racial and ethnic groups and to women who have chronic disease or other morbidity is uncertain.
Aromatase inhibitors are being assessed for chemoprophylaxis, so we should have information on their risk-benefit ratio in the near future.
Clinicians who care for women at high risk of primary breast cancer should thoroughly counsel each candidate for chemoprophylaxis about the potential benefits and risks of these agents in her particular circumstances. It may be that the risks outweigh the benefits in some women—such as those who already have an elevated risk of venous thromboembolism.
In addition, because most of the participants in the studies included in this review were healthy and white, we cannot be certain how generalizable these findings are to other subpopulations.—ANDREW M. KAUNITZ, MD
In the United States, tamoxifen is usually prescribed as adjuvant endocrine therapy after treatment of estrogen-receptor–positive breast cancer in both premenopausal and post-menopausal women. Raloxifene is most often prescribed for the prevention and treatment of osteoporosis in postmenopausal women. Use of these agents as chemoprophylaxis in women who have no history of breast cancer is less common, largely because of the risks and side effects of these drugs.
The increase in venous thromboembolism is of particular concern for women who have an elevated risk of this outcome, including overweight women and those of advanced age. The elevated risk of malignant and benign gynecologic disease associated with tamoxifen is of concern in all women who have an intact uterus.
Details of the review
Nelson and colleagues performed a systematic review, funded by the Agency for Health-care Research and Quality, that involved the aggregation of findings from seven placebo-controlled trials and one head-to-head, randomized, clinical trial involving women who had no history of preinvasive or invasive breast cancer. In the process, they focused on harms as well as benefits associated with use of these chemoprophylactic agents.
Tamoxifen and raloxifene reduced the risk of invasive breast cancer by 7 to 10 cases in every 1,000 women annually. These agents reduced the risk of estrogen-receptor–positive malignancy, but not estrogen-receptor–negative tumors, noninvasive cancer, or breast cancer–related mortality.
Tamoxifen and raloxifene were similarly effective in premenopausal and postmenopausal populations; both drugs also reduced the rate of osteoporotic fracture.
Most of the participants in the prevention trials were white and relatively healthy. Therefore, the relevance of these findings to women of other racial and ethnic groups and to women who have chronic disease or other morbidity is uncertain.
Aromatase inhibitors are being assessed for chemoprophylaxis, so we should have information on their risk-benefit ratio in the near future.
Clinicians who care for women at high risk of primary breast cancer should thoroughly counsel each candidate for chemoprophylaxis about the potential benefits and risks of these agents in her particular circumstances. It may be that the risks outweigh the benefits in some women—such as those who already have an elevated risk of venous thromboembolism.
In addition, because most of the participants in the studies included in this review were healthy and white, we cannot be certain how generalizable these findings are to other subpopulations.—ANDREW M. KAUNITZ, MD
Why we must make a stronger commitment to lesbian family health
The author reports no financial relationships relevant to this article.
CASE 1: Refusal to treat—is it legal?
Two lesbians in South Carolina, together for 7 years, seek insemination services from their HMO gynecology service. The doctors at that service decline to inseminate them—saying that they do not offer this service to lesbians because they believe that only heterosexual, married women should have children—and refer them to another physician outside the HMO. The couple pays $8,000 out of pocket to conceive their son. Because it is legal to discriminate against homosexuals in South Carolina, the doctors cannot be sued, and ACOG cannot discipline the doctors.
Currently, 25% to 45% of clinics in the United States report that they refuse to inseminate lesbians.1,2 What can we do to end such discrimination?
“Physicians and other health care professionals have the duty to refer patients in a timely manner to other providers if they do not feel that they can in conscience provide the standard reproductive services that their patients request.” So says Committee Opinion #385 of the American College of Obstetricians and Gynecologists (ACOG).3 This formal opinion implies that a physician who objects to same-sex couples may refer a lesbian patient to another physician for insemination, thereby communicating his or her discrimination to the patient.
In addition, ACOG’s Committee on Underserved Women released Committee Opinion #428, endorsing “equitable treatment for lesbians and their families, not only for direct health care needs but also for indirect health care issues; this should include the same legal protections afforded married couples.”4 The opinion does not endorse access to civil marriage, per se.
And although ACOG includes a nondiscrimination clause in its Code of Professional Ethics stating that the “principle of justice requires strict avoidance of discrimination on the basis of race, color, religion, national origin, or any other basis that would constitute illegal discrimination,” sexual orientation and gender identity are not specified.
To remain consistent with its mission of “advancing women’s health,” ACOG must include sexual orientation and gender identity in its nondiscrimination statement and endorse access for same-sex couples to civil marriage—not just “equitable treatment.”
In 44 states, laws mandating so-called equitable treatment deny the families of lesbian couples the legal and financial protections of civil marriage that are deemed essential to the health of families headed by heterosexual couples.
In 30 states, ACOG’s nondiscrimination policy, as written, could be interpreted to permit gynecologists to discriminate on the basis of sexual orientation in their practices.
The American Society for Reproductive Medicine issued a statement affirming that there is no justification for denying same-sex couples assisted reproductive technologies.5
Both the American Academy of Pediatrics (AAP) and the American Psychiatric Association (APA) prohibit discrimination on the basis of sexual orientation and endorse civil marriage for same-sex couples in richly evidence-based policy statements. Both organizations affirm that:
- homosexuality is natural, immutable, and noncontagious
- the children of homosexual parents develop with outcomes equal to those of heterosexual parents
- the families of same-sex couples need the same protections that their heterosexual counterparts enjoy.
The American Medical Association (AMA) issued policy statements prohibiting discrimination based on sexual orientation and gender identity because of documented health disparities that arise from discrimination.
In this article, I present evidence to support these positions; provide examples of how the current ACOG statement contributes to disparities; and challenge ACOG to clarify the wording of its opinions.
There is no scientific rationale for any discrimination against same-sex families. There is abundant scientific evidence that these families are harmed by discriminatory laws and treatment.
Civil unions, domestic partnerships do not equal civil marriage
ACOG Committee Opinion #428 makes it clear that “equitable treatment” does not affect religious rules about marriage ceremonies: Marriage licenses must be solemnized either in a religious ceremony performed by a clergy member, or in a civil ceremony performed by a judge, justice of the peace, or elected official.4 The Committee Opinion recognizes that domestic partnerships and civil unions do not provide the same rights as a state civil marriage license, and notes that neither is portable to all other states or recognized by the United States government.4
The opinion further acknowledges that marriage has a uniquely universal dignity and recognition in our society and grants the couple access to more than 1,000 federal rights deemed important for the health of its partners and their families.4
ACOG Committee Opinion #385 concedes that to refer a homosexual patient seeking insemination or surrogacy services does indeed communicate the physician’s discriminatory attitude to the patient and may cause harm.3 The AMA prohibits such discrimination by requiring that physicians only offer those services that they can provide to all patients without discrimination. This would allow a physician to refuse to do any procedure that is deemed unconscionable—but any service provided to some must be provided to all.
How the first trimester may influence sexual orientation
Fetal brain circuitry is permanently organized during the first trimester of pregnancy under the influence of various hormones and hormonelike substances, conferring an innate sexual orientation and gender identity, which children gradually come to recognize.6 Any subtle or not-so-subtle exposure to androgenic substances during early gestation of a 46 XX fetus can influence neural patterns in the phenotypic female child. These patterns may manifest as more aggressive play activity and masculinized somatic skeletal structure, neural structure, behavioral and biophysiologic skills, or gynephilic sexual orientation, and possibly confer a male gender identity.7-11
Congenital adrenal hyperplasia (CAH) demonstrates the biological effects of prenatal hormones on sexual orientation and gender identity. CAH is a condition in which an enzyme (21-hydroxylase) in the cortisone synthesis pathway is missing or dysfunctional, resulting in buildup of precursor androgens in the fetal blood. Female infants with CAH can be born with virilization of their external genitals or ambiguous genitalia.
Since 1968, 13 published studies have revealed that 20% to 50% of females who have CAH will identify as lesbian or bisexual in adulthood.10 A smaller percentage will come to recognize a male gender identity, particularly when their CAH is the more severe salt-wasting type.11
Homosexual orientation is also more frequent among women who had prenatal exposure to the complex steroid diethylstilbestrol,12 and among those who have polycystic ovarian syndrome (PCOS).13 Further evidence of the influence of prenatal androgen exposure on female sexual orientation is seen among females who gestated with a fraternal male co-twin.14 These girls are reported to have more aggressive play patterns during childhood and are more likely to identify as lesbian later in life.
Female-to-male transgender individuals have been shown to have higher adult androgen levels, a higher incidence of PCOS, and a greater likelihood of a history of CAH.15,16
It is unclear whether all homosexual females or female-to-male transsexuals were influenced by some form of first-trimester androgen excess. There are many endogenous and exogenous sources of androgen-like substances. They include maternal adrenal steroids arising from a high level of stress, anabolic steroids ingested from poultry or beef, and subclinical variations of fetal 21-hydroxylase concentration or efficiency, for example.
Homosexuality is not a disorder
The APA backs evidence that homosexuality cannot be spread by exposure or influence, nor can it be “repaired” or eradicated by disciplinary treatment. In fact, published evidence shows that the mental health and development of children are significantly harmed by parental, familial, and school peer rejection, whereas developmental parameters are much improved by their parents’ celebration of the youth’s diversity and the school’s enforcement of its diversity policy.17 Still, recognition of one’s sexual orientation can be difficult because of legal and social proscriptions against homosexuality.
Although most homosexuals have experienced some form of discriminatory treatment in their lives—be it verbal or physical abuse, or different treatment at their school or job or by existing federal and state laws—most still report a full and rewarding life.18 Experiences of discrimination, however, are potent psychic stressors for which many seek counseling and support, and which may undermine mental and physical health.19,20 Such discrimination may lie at the root of the documented higher rates of obesity, smoking, and alcoholism among lesbians compared with heterosexual women reported in the Women’s Health Initiative and the Nurses Health Study.21,22
Most young people, including those who will realize that they are gay, are raised with a strong appreciation for family and cultural traditions and an anticipation of adulthood with a career and marriage.23 Although marriage systems may differ, marriage across world cultures is a publicly acknowledged, highly respected, singular union, designed to create kinship obligations and sharing of resources between two adults and protect any children that they may produce.
Like heterosexual women, many lesbians desire to create families secured by civil marriage laws. These families need and deserve the same protections established by law to support and protect families headed by heterosexual couples. The marriage license is a state-regulated contract between two individuals. Each couple must then separately have the license solemnized, either by a designated state official (civil marriage) or by a clergy member (religious marriage).
All of the states with laws that permit civil marriage for same-sex couples have explicitly endorsed a religious right for clergy to refuse to certify same-sex couples’ licenses according to their beliefs.
Married parents provide a greater sense of security
In comparison with mere cohabitation, marriage confers more health benefits to the couple and has been correlated with a lower rate of cardiac disease24 and cancer risk factors,25 and with greater longevity.26 Marriage also provides greater security to any children in the family unit.27 When federal and state laws treat homosexual families differently than heterosexuals, this discrimination conveys a lower societal respect to all members of the family, but especially to the children.28 When children eventually learn that their parents—unlike other children’s parents—are not allowed to marry, they may lose some faith in their parents and be subject to bullying.29
The AAP reported significant, reliable evidence that lesbian and gay parents are as fit, effective, and successful as heterosexual parents.28 The organization also confirmed research showing that children of same-sex couples are as emotionally healthy and socially well-adjusted and at least as educationally and socially successful as children raised by heterosexual parents.28
The APA issued a pamphlet that states:
- Both heterosexual behavior and homosexual behavior are normal aspects of human sexuality. Both have been documented in many different cultures and historical eras. Despite the persistence of stereotypes that portray lesbian, gay, and bisexual people as disturbed, several decades of research and clinical experience have led all mainstream medical and mental health organizations in this country to conclude that these orientations represent normal forms of human experience.30
Case studies in discrimination
In 44 states, “equitable treatment” for same-sex couples, reflected in local law, entails denial of civil marriage and the family protections it confers. In nine states, equitable treatment means prohibition of adoption by same-sex couples. In 30 states, equitable treatment includes discrimination in housing or jobs based on sexual orientation and gender identity.
Consider the following vignettes, all possible (as is Case 1) under current laws in the geographic areas specified:
CASE 2
A Massachusetts lesbian married to a same-sex spouse who bore the couple’s children is offered a job promotion managing the Arkansas branch of her company. She has to decline the promotion because her company cannot continue her family’s medical insurance in Arkansas. Nor would she have legal custody of her children in that state or be able to adopt them there.
CASE 3
A married lesbian is hit by a car while crossing the street at a medical conference in Dallas. The funeral home refuses to release her body to her spouse for burial near their home in Connecticut. The decedent’s brother is called because he is the closest legal relative under Texas law, but since he never approved of his sister’s lesbian sexual orientation, he has her body transported to his family’s plot in Virginia.
CASE 4
A physician who is a lesbian is recruited to a state university in Michigan in 2003. She moves there with her domestic partner and their two adopted children, one of whom has cerebral palsy, and is promoted to the rank of associate professor in 2007. The next year, the Michigan Supreme Court interprets a 2004 constitutional amendment to mean that state institutions are prohibited from providing domestic partner benefits to same-sex couples. This leaves her stay-at-home spouse and their children without health insurance.
In each case, “equitable treatment” that is legal nevertheless injures the stability, integrity, and health of families, and ACOG’s Code of Professional Ethics fails to serve its mission of promoting women’s and family health.
AAP, APA endorse civil marriage
After reviewing 25 scientific articles on families parented by same-sex couples and the development of children in those families, the AAP concluded in 2006 that:
- These data have demonstrated no risk to children as a result of growing up in a family with one or more gay parents. Conscientious and nurturing adults, whether they are men or women, heterosexual or homosexual, can be excellent parents. The rights, benefits, and protections of civil marriage can further strengthen these families.28
The APA in 2004 endorsed civil marriage.31 For its part, the AMA has taken historic social and political stands endorsing nondiscrimination in school education programs for youth, in youth scouting organizations, in medical education, and in insurance coverage. The AMA also issued support of legislation to allow adoption by same-sex partners and co-parents. The AMA seeks to reduce the health disparities suffered because of unequal treatment of minor children and same-sex parents by supporting equality in laws affecting the health care of members of same-sex partner households and their dependent children.32 The AMA also issued a nondiscrimination clause that states:
- The AMA reaffirms its longstanding policy that there is no basis for the denial to any human being of equal rights, privileges, and responsibilities commensurate with his or her individual capabilities and ethical character because of an individual’s sex, sexual orientation, gender, gender identity, or transgender status, race, religion, disability, ethnic origin, national origin, or age [emphasis mine].32
Just as ACOG expects to be consulted for testimony in any legislation or court proceeding about gynecologic and obstetric issues, the expertise of the APA and AAP in the areas of child and family mental health are indisputable.
We should take a principled stand on this matter
The AMA Principles of Medical Ethics stipulate that “a physician shall recognize a responsibility to participate in activities contributing to the improvement of the community and the betterment of public health.” Our scientific ACOG community possesses access to knowledge that the lay community does not have. We have a responsibility to reflect the evidence in our ACOG policies and share the information in our communities for the health and well-being of our patients.
When society is broadly misinformed about issues related to homosexuality and frequently votes in ways that harm lesbians and their families, ACOG—whose mission is “advancing women’s health”—should take an unequivocally principled stand, as the AAP and the APA have already done.
The endorsement of civil marriage per se and inclusion of sexual orientation and gender identity in the nondiscrimination clause in no way oppose any of ACOG’s values but, rather, reflect and support ACOG’s mission for America’s women.
In the past, ACOG did not at first endorse “equitable treatment” for women who had unintended pregnancy. ACOG took the highly controversial but principled stand of endorsing women’s self-determination or “choice” to continue or abort an early gestation. ACOG endorsed what scientific evidence had proved to be healthiest for the woman and her family, and should do so now again.
ACOG could accomplish its mission for women’s health more fully if it would reconvene the Committees on Ethics and on Underserved Women and ask the committees to unambiguously prohibit all discrimination based on sexual orientation and gender identity, and endorse equal access to civil marriage across the country for the health of lesbian couples and parents. ACOG also should revise the Code of Professional Ethics to include sexual orientation and gender identity in the nondiscrimination clause.
1. Stern JE, Cramer CP, Garrod A, Green RM. Access to services at assisted reproductive technology clinics: a survey of policies and practices. Am J Obstet Gynecol. 2001;184:591-597.
2. Kingsberg SA, Applegarth LD, Janata JW. Embryo donation programs and policies in North America: survey results and implications for health and mental health professionals. Fertil Steril. 2000;73:215-220.
3. American College of Obstetricians and Gynecologists. ACOG Committee Opinion. No. 385. November 2007. The limits of conscientious refusal in reproductive medicine. Obstet Gynecol. 2007;110:1203-1208.
4. American College of Obstetricians and Gynecologists ACOG Committee Opinion. No. 428. February 2009. Legal status: health impact for lesbian couples. Obstet Gynecol. 2009;113(2 Pt 1):469-472.
5. Ethics Committee of the American Society for Reproductive Medicine. Access to fertility treatment by gays, lesbians, and unmarried persons. Fertil Steril. 2009;92:1190-1193.
6. Rahman Q. The neurodevelopment of human sexual orientation. Neurosci Biobehav Rev. 2005;29:1057-1066.
7. Pasterski V, Hindmarsh P, Geffner M, Brook C, Brain C, Hines M. Increased aggression and activity level in 3- to 11-year-old girls with congenital adrenal hyperplasia (CAH). Horm Behav. 2007;52:368-374.
8. Savic I, Lindstrom P. PET and MRI show differences in cerebral asymmetry and functional connectivity between homo- and heterosexual subjects. PNAS. 2008;105:9403-9408.
9. Rahman Q, Koerting J. Sexual orientation-related differences in allocentric spatial memory tasks. Hippocampus. 2008;18:55-63.
10. Meyer-Bahlburg HF, Dolezal C, Baker SW, New MI. Sexual orientation in women with classical or non-classical congenital adrenal hyperplasia as a function of degree of prenatal androgen excess. Arch Sex Behav. 2008;37:85-99.
11. Meyer-Bahlburg HF, Dolezal C, Baker SW, Ehrhardt AA, New MI. Gender development in women with congenital adrenal hyperplasia as a function of disorder severity. Arch Sex Behav. 2006;35:667-684.
12. Ehrhardt AA, Meyer-Bahlburg HF, Rosen LR, et al. Sexual orientation after prenatal exposure to exogenous estrogen. Arch Sex Behav. 1985;14:57-77.
13. Agrawal R, Sharma S, Bekir J, et al. Prevalence of polycystic ovaries and polycystic ovary syndrome in lesbian women compared with heterosexual women. Fertil Steril. 2004;82:1352-1357.
14. Bailey JM, Pillard RC, Neale MC, Agyei Y. Heritable factors influence sexual orientation in women. Arch Gen Psychiatry. 1993;50:217-223.
15. Baba T, Endo T, Honnma H, et al. Association between polycystic ovary syndrome and female-to-male transsexuality. Hum Reprod. 2007;22:1011-1016.
16. Bosinski HA, Peter M, Bonatz G, et al. A higher rate of hyperandrogenic disorders in female-to-male transsexuals. Psychoneuroendocrinology. 1997;22:361-380.
17. Ryan C, Huebner D, Diaz RM, Sanchez J. Family rejection as a predictor of negative health outcomes in white and Latino lesbian, gay, and bisexual young adults. Pediatrics. 2009;123:346-352.
18. Henry J. Kaiser Family Foundation. A Report on the Experiences of Lesbians, Gays and Bisexuals in America and the Public’s Views on Issues and Policies Related to Sexual Orientation. Menlo Park, Calif: Henry J. Kaiser Family Foundation; 2001.
19. Mays VM, Cochran SD. Mental health correlates of perceived discrimination among lesbian, gay, and bisexual adults in the United States. Am J Public Health. 2001;91:1869-1876.
20. Mays VM, Cochran SD, Barnes NW. Race, race-based discrimination, and health outcomes among African Americans. Annu Rev Psychol. 2007;58:201-225.
21. Valanis BG, Bowen DJ, Bassford T, Whitlock E, Charney P, Carter RA. Sexual orientation and health: comparisons in the Women’s Health Initiative sample. Arch Fam Med. 2000;9:843-853.
22. Case P, Austin SB, Hunter DJ, et al. Sexual orientation, health risk factors, and physical functioning in the Nurses’ Health Study II. J Womens Health. 2004;13:1033-1047.
23. Meezan W, Rauch J. Gay marriage, same-sex parenting, and America’s children. Future Child. 2005;15:97-115.
24. Eaker ED, Sullivan LM, Kelly-Hayes M, D’Agostino RB, Sr, Benjamin EJ. Marital status, marital strain, and risk of coronary heart disease or total mortality: the Framingham Offspring Study. Psychosom Med. 2007;69:509-513.
25. Shenson D, Adams M, Bolen J. Delivery of preventive services to adults aged 50–64: monitoring performance using a composite measure, 1997-2004. J Gen Intern Med. 2008;23:733-740.
26. Kaplan RM, Kronick RG. Marital status and longevity in the United States population. J Epidemiol Community Health. 2006;60:760-765.
27. Aronson SR, Huston AC. The mother-infant relationship in single, cohabiting, and married families: a case for marriage? J Fam Psychol. 2004;18:5-18.
28. Pawelski JG, Perrin EC, Foy JM, et al. The effects of marriage, civil union, and domestic partnership laws on the health and well-being of children. Pediatrics. 2006;118:349-364.
29. Gartrell N, Banks A, Hamilton J, Reed N, Bishop H, Rodas C. The National Lesbian Family Study: 2. Interviews with mothers of toddlers. Am J Orthopsychiatry. 1999;69:362-369.
30. American Psychological Association. Answers to your questions for a better understanding of sexual orientation and homosexuality. Available at: http://www.apa.org/topics/sorientation.html. Accessed Oct. 13, 2009.
31. American Psychiatric Association. Same sex marriage resource document. Resource documents approved by the Board of Trustees, American Psychiatric Association. November 2004. Available at: http://archive.psych.org/edu/other_res/lib_archives/archives/200417.pdf. Accessed Oct. 13, 2009.
32. American Medical Association. GLBT policy compendium. 2005. Available at: http://www.ama-assn.org/ama1/pub/upload/mm/42/glbt_policy0905.pdf. Accessed Oct. 13, 2009.
The author reports no financial relationships relevant to this article.
CASE 1: Refusal to treat—is it legal?
Two lesbians in South Carolina, together for 7 years, seek insemination services from their HMO gynecology service. The doctors at that service decline to inseminate them—saying that they do not offer this service to lesbians because they believe that only heterosexual, married women should have children—and refer them to another physician outside the HMO. The couple pays $8,000 out of pocket to conceive their son. Because it is legal to discriminate against homosexuals in South Carolina, the doctors cannot be sued, and ACOG cannot discipline the doctors.
Currently, 25% to 45% of clinics in the United States report that they refuse to inseminate lesbians.1,2 What can we do to end such discrimination?
“Physicians and other health care professionals have the duty to refer patients in a timely manner to other providers if they do not feel that they can in conscience provide the standard reproductive services that their patients request.” So says Committee Opinion #385 of the American College of Obstetricians and Gynecologists (ACOG).3 This formal opinion implies that a physician who objects to same-sex couples may refer a lesbian patient to another physician for insemination, thereby communicating his or her discrimination to the patient.
In addition, ACOG’s Committee on Underserved Women released Committee Opinion #428, endorsing “equitable treatment for lesbians and their families, not only for direct health care needs but also for indirect health care issues; this should include the same legal protections afforded married couples.”4 The opinion does not endorse access to civil marriage, per se.
And although ACOG includes a nondiscrimination clause in its Code of Professional Ethics stating that the “principle of justice requires strict avoidance of discrimination on the basis of race, color, religion, national origin, or any other basis that would constitute illegal discrimination,” sexual orientation and gender identity are not specified.
To remain consistent with its mission of “advancing women’s health,” ACOG must include sexual orientation and gender identity in its nondiscrimination statement and endorse access for same-sex couples to civil marriage—not just “equitable treatment.”
In 44 states, laws mandating so-called equitable treatment deny the families of lesbian couples the legal and financial protections of civil marriage that are deemed essential to the health of families headed by heterosexual couples.
In 30 states, ACOG’s nondiscrimination policy, as written, could be interpreted to permit gynecologists to discriminate on the basis of sexual orientation in their practices.
The American Society for Reproductive Medicine issued a statement affirming that there is no justification for denying same-sex couples assisted reproductive technologies.5
Both the American Academy of Pediatrics (AAP) and the American Psychiatric Association (APA) prohibit discrimination on the basis of sexual orientation and endorse civil marriage for same-sex couples in richly evidence-based policy statements. Both organizations affirm that:
- homosexuality is natural, immutable, and noncontagious
- the children of homosexual parents develop with outcomes equal to those of heterosexual parents
- the families of same-sex couples need the same protections that their heterosexual counterparts enjoy.
The American Medical Association (AMA) issued policy statements prohibiting discrimination based on sexual orientation and gender identity because of documented health disparities that arise from discrimination.
In this article, I present evidence to support these positions; provide examples of how the current ACOG statement contributes to disparities; and challenge ACOG to clarify the wording of its opinions.
There is no scientific rationale for any discrimination against same-sex families. There is abundant scientific evidence that these families are harmed by discriminatory laws and treatment.
Civil unions, domestic partnerships do not equal civil marriage
ACOG Committee Opinion #428 makes it clear that “equitable treatment” does not affect religious rules about marriage ceremonies: Marriage licenses must be solemnized either in a religious ceremony performed by a clergy member, or in a civil ceremony performed by a judge, justice of the peace, or elected official.4 The Committee Opinion recognizes that domestic partnerships and civil unions do not provide the same rights as a state civil marriage license, and notes that neither is portable to all other states or recognized by the United States government.4
The opinion further acknowledges that marriage has a uniquely universal dignity and recognition in our society and grants the couple access to more than 1,000 federal rights deemed important for the health of its partners and their families.4
ACOG Committee Opinion #385 concedes that to refer a homosexual patient seeking insemination or surrogacy services does indeed communicate the physician’s discriminatory attitude to the patient and may cause harm.3 The AMA prohibits such discrimination by requiring that physicians only offer those services that they can provide to all patients without discrimination. This would allow a physician to refuse to do any procedure that is deemed unconscionable—but any service provided to some must be provided to all.
How the first trimester may influence sexual orientation
Fetal brain circuitry is permanently organized during the first trimester of pregnancy under the influence of various hormones and hormonelike substances, conferring an innate sexual orientation and gender identity, which children gradually come to recognize.6 Any subtle or not-so-subtle exposure to androgenic substances during early gestation of a 46 XX fetus can influence neural patterns in the phenotypic female child. These patterns may manifest as more aggressive play activity and masculinized somatic skeletal structure, neural structure, behavioral and biophysiologic skills, or gynephilic sexual orientation, and possibly confer a male gender identity.7-11
Congenital adrenal hyperplasia (CAH) demonstrates the biological effects of prenatal hormones on sexual orientation and gender identity. CAH is a condition in which an enzyme (21-hydroxylase) in the cortisone synthesis pathway is missing or dysfunctional, resulting in buildup of precursor androgens in the fetal blood. Female infants with CAH can be born with virilization of their external genitals or ambiguous genitalia.
Since 1968, 13 published studies have revealed that 20% to 50% of females who have CAH will identify as lesbian or bisexual in adulthood.10 A smaller percentage will come to recognize a male gender identity, particularly when their CAH is the more severe salt-wasting type.11
Homosexual orientation is also more frequent among women who had prenatal exposure to the complex steroid diethylstilbestrol,12 and among those who have polycystic ovarian syndrome (PCOS).13 Further evidence of the influence of prenatal androgen exposure on female sexual orientation is seen among females who gestated with a fraternal male co-twin.14 These girls are reported to have more aggressive play patterns during childhood and are more likely to identify as lesbian later in life.
Female-to-male transgender individuals have been shown to have higher adult androgen levels, a higher incidence of PCOS, and a greater likelihood of a history of CAH.15,16
It is unclear whether all homosexual females or female-to-male transsexuals were influenced by some form of first-trimester androgen excess. There are many endogenous and exogenous sources of androgen-like substances. They include maternal adrenal steroids arising from a high level of stress, anabolic steroids ingested from poultry or beef, and subclinical variations of fetal 21-hydroxylase concentration or efficiency, for example.
Homosexuality is not a disorder
The APA backs evidence that homosexuality cannot be spread by exposure or influence, nor can it be “repaired” or eradicated by disciplinary treatment. In fact, published evidence shows that the mental health and development of children are significantly harmed by parental, familial, and school peer rejection, whereas developmental parameters are much improved by their parents’ celebration of the youth’s diversity and the school’s enforcement of its diversity policy.17 Still, recognition of one’s sexual orientation can be difficult because of legal and social proscriptions against homosexuality.
Although most homosexuals have experienced some form of discriminatory treatment in their lives—be it verbal or physical abuse, or different treatment at their school or job or by existing federal and state laws—most still report a full and rewarding life.18 Experiences of discrimination, however, are potent psychic stressors for which many seek counseling and support, and which may undermine mental and physical health.19,20 Such discrimination may lie at the root of the documented higher rates of obesity, smoking, and alcoholism among lesbians compared with heterosexual women reported in the Women’s Health Initiative and the Nurses Health Study.21,22
Most young people, including those who will realize that they are gay, are raised with a strong appreciation for family and cultural traditions and an anticipation of adulthood with a career and marriage.23 Although marriage systems may differ, marriage across world cultures is a publicly acknowledged, highly respected, singular union, designed to create kinship obligations and sharing of resources between two adults and protect any children that they may produce.
Like heterosexual women, many lesbians desire to create families secured by civil marriage laws. These families need and deserve the same protections established by law to support and protect families headed by heterosexual couples. The marriage license is a state-regulated contract between two individuals. Each couple must then separately have the license solemnized, either by a designated state official (civil marriage) or by a clergy member (religious marriage).
All of the states with laws that permit civil marriage for same-sex couples have explicitly endorsed a religious right for clergy to refuse to certify same-sex couples’ licenses according to their beliefs.
Married parents provide a greater sense of security
In comparison with mere cohabitation, marriage confers more health benefits to the couple and has been correlated with a lower rate of cardiac disease24 and cancer risk factors,25 and with greater longevity.26 Marriage also provides greater security to any children in the family unit.27 When federal and state laws treat homosexual families differently than heterosexuals, this discrimination conveys a lower societal respect to all members of the family, but especially to the children.28 When children eventually learn that their parents—unlike other children’s parents—are not allowed to marry, they may lose some faith in their parents and be subject to bullying.29
The AAP reported significant, reliable evidence that lesbian and gay parents are as fit, effective, and successful as heterosexual parents.28 The organization also confirmed research showing that children of same-sex couples are as emotionally healthy and socially well-adjusted and at least as educationally and socially successful as children raised by heterosexual parents.28
The APA issued a pamphlet that states:
- Both heterosexual behavior and homosexual behavior are normal aspects of human sexuality. Both have been documented in many different cultures and historical eras. Despite the persistence of stereotypes that portray lesbian, gay, and bisexual people as disturbed, several decades of research and clinical experience have led all mainstream medical and mental health organizations in this country to conclude that these orientations represent normal forms of human experience.30
Case studies in discrimination
In 44 states, “equitable treatment” for same-sex couples, reflected in local law, entails denial of civil marriage and the family protections it confers. In nine states, equitable treatment means prohibition of adoption by same-sex couples. In 30 states, equitable treatment includes discrimination in housing or jobs based on sexual orientation and gender identity.
Consider the following vignettes, all possible (as is Case 1) under current laws in the geographic areas specified:
CASE 2
A Massachusetts lesbian married to a same-sex spouse who bore the couple’s children is offered a job promotion managing the Arkansas branch of her company. She has to decline the promotion because her company cannot continue her family’s medical insurance in Arkansas. Nor would she have legal custody of her children in that state or be able to adopt them there.
CASE 3
A married lesbian is hit by a car while crossing the street at a medical conference in Dallas. The funeral home refuses to release her body to her spouse for burial near their home in Connecticut. The decedent’s brother is called because he is the closest legal relative under Texas law, but since he never approved of his sister’s lesbian sexual orientation, he has her body transported to his family’s plot in Virginia.
CASE 4
A physician who is a lesbian is recruited to a state university in Michigan in 2003. She moves there with her domestic partner and their two adopted children, one of whom has cerebral palsy, and is promoted to the rank of associate professor in 2007. The next year, the Michigan Supreme Court interprets a 2004 constitutional amendment to mean that state institutions are prohibited from providing domestic partner benefits to same-sex couples. This leaves her stay-at-home spouse and their children without health insurance.
In each case, “equitable treatment” that is legal nevertheless injures the stability, integrity, and health of families, and ACOG’s Code of Professional Ethics fails to serve its mission of promoting women’s and family health.
AAP, APA endorse civil marriage
After reviewing 25 scientific articles on families parented by same-sex couples and the development of children in those families, the AAP concluded in 2006 that:
- These data have demonstrated no risk to children as a result of growing up in a family with one or more gay parents. Conscientious and nurturing adults, whether they are men or women, heterosexual or homosexual, can be excellent parents. The rights, benefits, and protections of civil marriage can further strengthen these families.28
The APA in 2004 endorsed civil marriage.31 For its part, the AMA has taken historic social and political stands endorsing nondiscrimination in school education programs for youth, in youth scouting organizations, in medical education, and in insurance coverage. The AMA also issued support of legislation to allow adoption by same-sex partners and co-parents. The AMA seeks to reduce the health disparities suffered because of unequal treatment of minor children and same-sex parents by supporting equality in laws affecting the health care of members of same-sex partner households and their dependent children.32 The AMA also issued a nondiscrimination clause that states:
- The AMA reaffirms its longstanding policy that there is no basis for the denial to any human being of equal rights, privileges, and responsibilities commensurate with his or her individual capabilities and ethical character because of an individual’s sex, sexual orientation, gender, gender identity, or transgender status, race, religion, disability, ethnic origin, national origin, or age [emphasis mine].32
Just as ACOG expects to be consulted for testimony in any legislation or court proceeding about gynecologic and obstetric issues, the expertise of the APA and AAP in the areas of child and family mental health are indisputable.
We should take a principled stand on this matter
The AMA Principles of Medical Ethics stipulate that “a physician shall recognize a responsibility to participate in activities contributing to the improvement of the community and the betterment of public health.” Our scientific ACOG community possesses access to knowledge that the lay community does not have. We have a responsibility to reflect the evidence in our ACOG policies and share the information in our communities for the health and well-being of our patients.
When society is broadly misinformed about issues related to homosexuality and frequently votes in ways that harm lesbians and their families, ACOG—whose mission is “advancing women’s health”—should take an unequivocally principled stand, as the AAP and the APA have already done.
The endorsement of civil marriage per se and inclusion of sexual orientation and gender identity in the nondiscrimination clause in no way oppose any of ACOG’s values but, rather, reflect and support ACOG’s mission for America’s women.
In the past, ACOG did not at first endorse “equitable treatment” for women who had unintended pregnancy. ACOG took the highly controversial but principled stand of endorsing women’s self-determination or “choice” to continue or abort an early gestation. ACOG endorsed what scientific evidence had proved to be healthiest for the woman and her family, and should do so now again.
ACOG could accomplish its mission for women’s health more fully if it would reconvene the Committees on Ethics and on Underserved Women and ask the committees to unambiguously prohibit all discrimination based on sexual orientation and gender identity, and endorse equal access to civil marriage across the country for the health of lesbian couples and parents. ACOG also should revise the Code of Professional Ethics to include sexual orientation and gender identity in the nondiscrimination clause.
The author reports no financial relationships relevant to this article.
CASE 1: Refusal to treat—is it legal?
Two lesbians in South Carolina, together for 7 years, seek insemination services from their HMO gynecology service. The doctors at that service decline to inseminate them—saying that they do not offer this service to lesbians because they believe that only heterosexual, married women should have children—and refer them to another physician outside the HMO. The couple pays $8,000 out of pocket to conceive their son. Because it is legal to discriminate against homosexuals in South Carolina, the doctors cannot be sued, and ACOG cannot discipline the doctors.
Currently, 25% to 45% of clinics in the United States report that they refuse to inseminate lesbians.1,2 What can we do to end such discrimination?
“Physicians and other health care professionals have the duty to refer patients in a timely manner to other providers if they do not feel that they can in conscience provide the standard reproductive services that their patients request.” So says Committee Opinion #385 of the American College of Obstetricians and Gynecologists (ACOG).3 This formal opinion implies that a physician who objects to same-sex couples may refer a lesbian patient to another physician for insemination, thereby communicating his or her discrimination to the patient.
In addition, ACOG’s Committee on Underserved Women released Committee Opinion #428, endorsing “equitable treatment for lesbians and their families, not only for direct health care needs but also for indirect health care issues; this should include the same legal protections afforded married couples.”4 The opinion does not endorse access to civil marriage, per se.
And although ACOG includes a nondiscrimination clause in its Code of Professional Ethics stating that the “principle of justice requires strict avoidance of discrimination on the basis of race, color, religion, national origin, or any other basis that would constitute illegal discrimination,” sexual orientation and gender identity are not specified.
To remain consistent with its mission of “advancing women’s health,” ACOG must include sexual orientation and gender identity in its nondiscrimination statement and endorse access for same-sex couples to civil marriage—not just “equitable treatment.”
In 44 states, laws mandating so-called equitable treatment deny the families of lesbian couples the legal and financial protections of civil marriage that are deemed essential to the health of families headed by heterosexual couples.
In 30 states, ACOG’s nondiscrimination policy, as written, could be interpreted to permit gynecologists to discriminate on the basis of sexual orientation in their practices.
The American Society for Reproductive Medicine issued a statement affirming that there is no justification for denying same-sex couples assisted reproductive technologies.5
Both the American Academy of Pediatrics (AAP) and the American Psychiatric Association (APA) prohibit discrimination on the basis of sexual orientation and endorse civil marriage for same-sex couples in richly evidence-based policy statements. Both organizations affirm that:
- homosexuality is natural, immutable, and noncontagious
- the children of homosexual parents develop with outcomes equal to those of heterosexual parents
- the families of same-sex couples need the same protections that their heterosexual counterparts enjoy.
The American Medical Association (AMA) issued policy statements prohibiting discrimination based on sexual orientation and gender identity because of documented health disparities that arise from discrimination.
In this article, I present evidence to support these positions; provide examples of how the current ACOG statement contributes to disparities; and challenge ACOG to clarify the wording of its opinions.
There is no scientific rationale for any discrimination against same-sex families. There is abundant scientific evidence that these families are harmed by discriminatory laws and treatment.
Civil unions, domestic partnerships do not equal civil marriage
ACOG Committee Opinion #428 makes it clear that “equitable treatment” does not affect religious rules about marriage ceremonies: Marriage licenses must be solemnized either in a religious ceremony performed by a clergy member, or in a civil ceremony performed by a judge, justice of the peace, or elected official.4 The Committee Opinion recognizes that domestic partnerships and civil unions do not provide the same rights as a state civil marriage license, and notes that neither is portable to all other states or recognized by the United States government.4
The opinion further acknowledges that marriage has a uniquely universal dignity and recognition in our society and grants the couple access to more than 1,000 federal rights deemed important for the health of its partners and their families.4
ACOG Committee Opinion #385 concedes that to refer a homosexual patient seeking insemination or surrogacy services does indeed communicate the physician’s discriminatory attitude to the patient and may cause harm.3 The AMA prohibits such discrimination by requiring that physicians only offer those services that they can provide to all patients without discrimination. This would allow a physician to refuse to do any procedure that is deemed unconscionable—but any service provided to some must be provided to all.
How the first trimester may influence sexual orientation
Fetal brain circuitry is permanently organized during the first trimester of pregnancy under the influence of various hormones and hormonelike substances, conferring an innate sexual orientation and gender identity, which children gradually come to recognize.6 Any subtle or not-so-subtle exposure to androgenic substances during early gestation of a 46 XX fetus can influence neural patterns in the phenotypic female child. These patterns may manifest as more aggressive play activity and masculinized somatic skeletal structure, neural structure, behavioral and biophysiologic skills, or gynephilic sexual orientation, and possibly confer a male gender identity.7-11
Congenital adrenal hyperplasia (CAH) demonstrates the biological effects of prenatal hormones on sexual orientation and gender identity. CAH is a condition in which an enzyme (21-hydroxylase) in the cortisone synthesis pathway is missing or dysfunctional, resulting in buildup of precursor androgens in the fetal blood. Female infants with CAH can be born with virilization of their external genitals or ambiguous genitalia.
Since 1968, 13 published studies have revealed that 20% to 50% of females who have CAH will identify as lesbian or bisexual in adulthood.10 A smaller percentage will come to recognize a male gender identity, particularly when their CAH is the more severe salt-wasting type.11
Homosexual orientation is also more frequent among women who had prenatal exposure to the complex steroid diethylstilbestrol,12 and among those who have polycystic ovarian syndrome (PCOS).13 Further evidence of the influence of prenatal androgen exposure on female sexual orientation is seen among females who gestated with a fraternal male co-twin.14 These girls are reported to have more aggressive play patterns during childhood and are more likely to identify as lesbian later in life.
Female-to-male transgender individuals have been shown to have higher adult androgen levels, a higher incidence of PCOS, and a greater likelihood of a history of CAH.15,16
It is unclear whether all homosexual females or female-to-male transsexuals were influenced by some form of first-trimester androgen excess. There are many endogenous and exogenous sources of androgen-like substances. They include maternal adrenal steroids arising from a high level of stress, anabolic steroids ingested from poultry or beef, and subclinical variations of fetal 21-hydroxylase concentration or efficiency, for example.
Homosexuality is not a disorder
The APA backs evidence that homosexuality cannot be spread by exposure or influence, nor can it be “repaired” or eradicated by disciplinary treatment. In fact, published evidence shows that the mental health and development of children are significantly harmed by parental, familial, and school peer rejection, whereas developmental parameters are much improved by their parents’ celebration of the youth’s diversity and the school’s enforcement of its diversity policy.17 Still, recognition of one’s sexual orientation can be difficult because of legal and social proscriptions against homosexuality.
Although most homosexuals have experienced some form of discriminatory treatment in their lives—be it verbal or physical abuse, or different treatment at their school or job or by existing federal and state laws—most still report a full and rewarding life.18 Experiences of discrimination, however, are potent psychic stressors for which many seek counseling and support, and which may undermine mental and physical health.19,20 Such discrimination may lie at the root of the documented higher rates of obesity, smoking, and alcoholism among lesbians compared with heterosexual women reported in the Women’s Health Initiative and the Nurses Health Study.21,22
Most young people, including those who will realize that they are gay, are raised with a strong appreciation for family and cultural traditions and an anticipation of adulthood with a career and marriage.23 Although marriage systems may differ, marriage across world cultures is a publicly acknowledged, highly respected, singular union, designed to create kinship obligations and sharing of resources between two adults and protect any children that they may produce.
Like heterosexual women, many lesbians desire to create families secured by civil marriage laws. These families need and deserve the same protections established by law to support and protect families headed by heterosexual couples. The marriage license is a state-regulated contract between two individuals. Each couple must then separately have the license solemnized, either by a designated state official (civil marriage) or by a clergy member (religious marriage).
All of the states with laws that permit civil marriage for same-sex couples have explicitly endorsed a religious right for clergy to refuse to certify same-sex couples’ licenses according to their beliefs.
Married parents provide a greater sense of security
In comparison with mere cohabitation, marriage confers more health benefits to the couple and has been correlated with a lower rate of cardiac disease24 and cancer risk factors,25 and with greater longevity.26 Marriage also provides greater security to any children in the family unit.27 When federal and state laws treat homosexual families differently than heterosexuals, this discrimination conveys a lower societal respect to all members of the family, but especially to the children.28 When children eventually learn that their parents—unlike other children’s parents—are not allowed to marry, they may lose some faith in their parents and be subject to bullying.29
The AAP reported significant, reliable evidence that lesbian and gay parents are as fit, effective, and successful as heterosexual parents.28 The organization also confirmed research showing that children of same-sex couples are as emotionally healthy and socially well-adjusted and at least as educationally and socially successful as children raised by heterosexual parents.28
The APA issued a pamphlet that states:
- Both heterosexual behavior and homosexual behavior are normal aspects of human sexuality. Both have been documented in many different cultures and historical eras. Despite the persistence of stereotypes that portray lesbian, gay, and bisexual people as disturbed, several decades of research and clinical experience have led all mainstream medical and mental health organizations in this country to conclude that these orientations represent normal forms of human experience.30
Case studies in discrimination
In 44 states, “equitable treatment” for same-sex couples, reflected in local law, entails denial of civil marriage and the family protections it confers. In nine states, equitable treatment means prohibition of adoption by same-sex couples. In 30 states, equitable treatment includes discrimination in housing or jobs based on sexual orientation and gender identity.
Consider the following vignettes, all possible (as is Case 1) under current laws in the geographic areas specified:
CASE 2
A Massachusetts lesbian married to a same-sex spouse who bore the couple’s children is offered a job promotion managing the Arkansas branch of her company. She has to decline the promotion because her company cannot continue her family’s medical insurance in Arkansas. Nor would she have legal custody of her children in that state or be able to adopt them there.
CASE 3
A married lesbian is hit by a car while crossing the street at a medical conference in Dallas. The funeral home refuses to release her body to her spouse for burial near their home in Connecticut. The decedent’s brother is called because he is the closest legal relative under Texas law, but since he never approved of his sister’s lesbian sexual orientation, he has her body transported to his family’s plot in Virginia.
CASE 4
A physician who is a lesbian is recruited to a state university in Michigan in 2003. She moves there with her domestic partner and their two adopted children, one of whom has cerebral palsy, and is promoted to the rank of associate professor in 2007. The next year, the Michigan Supreme Court interprets a 2004 constitutional amendment to mean that state institutions are prohibited from providing domestic partner benefits to same-sex couples. This leaves her stay-at-home spouse and their children without health insurance.
In each case, “equitable treatment” that is legal nevertheless injures the stability, integrity, and health of families, and ACOG’s Code of Professional Ethics fails to serve its mission of promoting women’s and family health.
AAP, APA endorse civil marriage
After reviewing 25 scientific articles on families parented by same-sex couples and the development of children in those families, the AAP concluded in 2006 that:
- These data have demonstrated no risk to children as a result of growing up in a family with one or more gay parents. Conscientious and nurturing adults, whether they are men or women, heterosexual or homosexual, can be excellent parents. The rights, benefits, and protections of civil marriage can further strengthen these families.28
The APA in 2004 endorsed civil marriage.31 For its part, the AMA has taken historic social and political stands endorsing nondiscrimination in school education programs for youth, in youth scouting organizations, in medical education, and in insurance coverage. The AMA also issued support of legislation to allow adoption by same-sex partners and co-parents. The AMA seeks to reduce the health disparities suffered because of unequal treatment of minor children and same-sex parents by supporting equality in laws affecting the health care of members of same-sex partner households and their dependent children.32 The AMA also issued a nondiscrimination clause that states:
- The AMA reaffirms its longstanding policy that there is no basis for the denial to any human being of equal rights, privileges, and responsibilities commensurate with his or her individual capabilities and ethical character because of an individual’s sex, sexual orientation, gender, gender identity, or transgender status, race, religion, disability, ethnic origin, national origin, or age [emphasis mine].32
Just as ACOG expects to be consulted for testimony in any legislation or court proceeding about gynecologic and obstetric issues, the expertise of the APA and AAP in the areas of child and family mental health are indisputable.
We should take a principled stand on this matter
The AMA Principles of Medical Ethics stipulate that “a physician shall recognize a responsibility to participate in activities contributing to the improvement of the community and the betterment of public health.” Our scientific ACOG community possesses access to knowledge that the lay community does not have. We have a responsibility to reflect the evidence in our ACOG policies and share the information in our communities for the health and well-being of our patients.
When society is broadly misinformed about issues related to homosexuality and frequently votes in ways that harm lesbians and their families, ACOG—whose mission is “advancing women’s health”—should take an unequivocally principled stand, as the AAP and the APA have already done.
The endorsement of civil marriage per se and inclusion of sexual orientation and gender identity in the nondiscrimination clause in no way oppose any of ACOG’s values but, rather, reflect and support ACOG’s mission for America’s women.
In the past, ACOG did not at first endorse “equitable treatment” for women who had unintended pregnancy. ACOG took the highly controversial but principled stand of endorsing women’s self-determination or “choice” to continue or abort an early gestation. ACOG endorsed what scientific evidence had proved to be healthiest for the woman and her family, and should do so now again.
ACOG could accomplish its mission for women’s health more fully if it would reconvene the Committees on Ethics and on Underserved Women and ask the committees to unambiguously prohibit all discrimination based on sexual orientation and gender identity, and endorse equal access to civil marriage across the country for the health of lesbian couples and parents. ACOG also should revise the Code of Professional Ethics to include sexual orientation and gender identity in the nondiscrimination clause.
1. Stern JE, Cramer CP, Garrod A, Green RM. Access to services at assisted reproductive technology clinics: a survey of policies and practices. Am J Obstet Gynecol. 2001;184:591-597.
2. Kingsberg SA, Applegarth LD, Janata JW. Embryo donation programs and policies in North America: survey results and implications for health and mental health professionals. Fertil Steril. 2000;73:215-220.
3. American College of Obstetricians and Gynecologists. ACOG Committee Opinion. No. 385. November 2007. The limits of conscientious refusal in reproductive medicine. Obstet Gynecol. 2007;110:1203-1208.
4. American College of Obstetricians and Gynecologists ACOG Committee Opinion. No. 428. February 2009. Legal status: health impact for lesbian couples. Obstet Gynecol. 2009;113(2 Pt 1):469-472.
5. Ethics Committee of the American Society for Reproductive Medicine. Access to fertility treatment by gays, lesbians, and unmarried persons. Fertil Steril. 2009;92:1190-1193.
6. Rahman Q. The neurodevelopment of human sexual orientation. Neurosci Biobehav Rev. 2005;29:1057-1066.
7. Pasterski V, Hindmarsh P, Geffner M, Brook C, Brain C, Hines M. Increased aggression and activity level in 3- to 11-year-old girls with congenital adrenal hyperplasia (CAH). Horm Behav. 2007;52:368-374.
8. Savic I, Lindstrom P. PET and MRI show differences in cerebral asymmetry and functional connectivity between homo- and heterosexual subjects. PNAS. 2008;105:9403-9408.
9. Rahman Q, Koerting J. Sexual orientation-related differences in allocentric spatial memory tasks. Hippocampus. 2008;18:55-63.
10. Meyer-Bahlburg HF, Dolezal C, Baker SW, New MI. Sexual orientation in women with classical or non-classical congenital adrenal hyperplasia as a function of degree of prenatal androgen excess. Arch Sex Behav. 2008;37:85-99.
11. Meyer-Bahlburg HF, Dolezal C, Baker SW, Ehrhardt AA, New MI. Gender development in women with congenital adrenal hyperplasia as a function of disorder severity. Arch Sex Behav. 2006;35:667-684.
12. Ehrhardt AA, Meyer-Bahlburg HF, Rosen LR, et al. Sexual orientation after prenatal exposure to exogenous estrogen. Arch Sex Behav. 1985;14:57-77.
13. Agrawal R, Sharma S, Bekir J, et al. Prevalence of polycystic ovaries and polycystic ovary syndrome in lesbian women compared with heterosexual women. Fertil Steril. 2004;82:1352-1357.
14. Bailey JM, Pillard RC, Neale MC, Agyei Y. Heritable factors influence sexual orientation in women. Arch Gen Psychiatry. 1993;50:217-223.
15. Baba T, Endo T, Honnma H, et al. Association between polycystic ovary syndrome and female-to-male transsexuality. Hum Reprod. 2007;22:1011-1016.
16. Bosinski HA, Peter M, Bonatz G, et al. A higher rate of hyperandrogenic disorders in female-to-male transsexuals. Psychoneuroendocrinology. 1997;22:361-380.
17. Ryan C, Huebner D, Diaz RM, Sanchez J. Family rejection as a predictor of negative health outcomes in white and Latino lesbian, gay, and bisexual young adults. Pediatrics. 2009;123:346-352.
18. Henry J. Kaiser Family Foundation. A Report on the Experiences of Lesbians, Gays and Bisexuals in America and the Public’s Views on Issues and Policies Related to Sexual Orientation. Menlo Park, Calif: Henry J. Kaiser Family Foundation; 2001.
19. Mays VM, Cochran SD. Mental health correlates of perceived discrimination among lesbian, gay, and bisexual adults in the United States. Am J Public Health. 2001;91:1869-1876.
20. Mays VM, Cochran SD, Barnes NW. Race, race-based discrimination, and health outcomes among African Americans. Annu Rev Psychol. 2007;58:201-225.
21. Valanis BG, Bowen DJ, Bassford T, Whitlock E, Charney P, Carter RA. Sexual orientation and health: comparisons in the Women’s Health Initiative sample. Arch Fam Med. 2000;9:843-853.
22. Case P, Austin SB, Hunter DJ, et al. Sexual orientation, health risk factors, and physical functioning in the Nurses’ Health Study II. J Womens Health. 2004;13:1033-1047.
23. Meezan W, Rauch J. Gay marriage, same-sex parenting, and America’s children. Future Child. 2005;15:97-115.
24. Eaker ED, Sullivan LM, Kelly-Hayes M, D’Agostino RB, Sr, Benjamin EJ. Marital status, marital strain, and risk of coronary heart disease or total mortality: the Framingham Offspring Study. Psychosom Med. 2007;69:509-513.
25. Shenson D, Adams M, Bolen J. Delivery of preventive services to adults aged 50–64: monitoring performance using a composite measure, 1997-2004. J Gen Intern Med. 2008;23:733-740.
26. Kaplan RM, Kronick RG. Marital status and longevity in the United States population. J Epidemiol Community Health. 2006;60:760-765.
27. Aronson SR, Huston AC. The mother-infant relationship in single, cohabiting, and married families: a case for marriage? J Fam Psychol. 2004;18:5-18.
28. Pawelski JG, Perrin EC, Foy JM, et al. The effects of marriage, civil union, and domestic partnership laws on the health and well-being of children. Pediatrics. 2006;118:349-364.
29. Gartrell N, Banks A, Hamilton J, Reed N, Bishop H, Rodas C. The National Lesbian Family Study: 2. Interviews with mothers of toddlers. Am J Orthopsychiatry. 1999;69:362-369.
30. American Psychological Association. Answers to your questions for a better understanding of sexual orientation and homosexuality. Available at: http://www.apa.org/topics/sorientation.html. Accessed Oct. 13, 2009.
31. American Psychiatric Association. Same sex marriage resource document. Resource documents approved by the Board of Trustees, American Psychiatric Association. November 2004. Available at: http://archive.psych.org/edu/other_res/lib_archives/archives/200417.pdf. Accessed Oct. 13, 2009.
32. American Medical Association. GLBT policy compendium. 2005. Available at: http://www.ama-assn.org/ama1/pub/upload/mm/42/glbt_policy0905.pdf. Accessed Oct. 13, 2009.
1. Stern JE, Cramer CP, Garrod A, Green RM. Access to services at assisted reproductive technology clinics: a survey of policies and practices. Am J Obstet Gynecol. 2001;184:591-597.
2. Kingsberg SA, Applegarth LD, Janata JW. Embryo donation programs and policies in North America: survey results and implications for health and mental health professionals. Fertil Steril. 2000;73:215-220.
3. American College of Obstetricians and Gynecologists. ACOG Committee Opinion. No. 385. November 2007. The limits of conscientious refusal in reproductive medicine. Obstet Gynecol. 2007;110:1203-1208.
4. American College of Obstetricians and Gynecologists ACOG Committee Opinion. No. 428. February 2009. Legal status: health impact for lesbian couples. Obstet Gynecol. 2009;113(2 Pt 1):469-472.
5. Ethics Committee of the American Society for Reproductive Medicine. Access to fertility treatment by gays, lesbians, and unmarried persons. Fertil Steril. 2009;92:1190-1193.
6. Rahman Q. The neurodevelopment of human sexual orientation. Neurosci Biobehav Rev. 2005;29:1057-1066.
7. Pasterski V, Hindmarsh P, Geffner M, Brook C, Brain C, Hines M. Increased aggression and activity level in 3- to 11-year-old girls with congenital adrenal hyperplasia (CAH). Horm Behav. 2007;52:368-374.
8. Savic I, Lindstrom P. PET and MRI show differences in cerebral asymmetry and functional connectivity between homo- and heterosexual subjects. PNAS. 2008;105:9403-9408.
9. Rahman Q, Koerting J. Sexual orientation-related differences in allocentric spatial memory tasks. Hippocampus. 2008;18:55-63.
10. Meyer-Bahlburg HF, Dolezal C, Baker SW, New MI. Sexual orientation in women with classical or non-classical congenital adrenal hyperplasia as a function of degree of prenatal androgen excess. Arch Sex Behav. 2008;37:85-99.
11. Meyer-Bahlburg HF, Dolezal C, Baker SW, Ehrhardt AA, New MI. Gender development in women with congenital adrenal hyperplasia as a function of disorder severity. Arch Sex Behav. 2006;35:667-684.
12. Ehrhardt AA, Meyer-Bahlburg HF, Rosen LR, et al. Sexual orientation after prenatal exposure to exogenous estrogen. Arch Sex Behav. 1985;14:57-77.
13. Agrawal R, Sharma S, Bekir J, et al. Prevalence of polycystic ovaries and polycystic ovary syndrome in lesbian women compared with heterosexual women. Fertil Steril. 2004;82:1352-1357.
14. Bailey JM, Pillard RC, Neale MC, Agyei Y. Heritable factors influence sexual orientation in women. Arch Gen Psychiatry. 1993;50:217-223.
15. Baba T, Endo T, Honnma H, et al. Association between polycystic ovary syndrome and female-to-male transsexuality. Hum Reprod. 2007;22:1011-1016.
16. Bosinski HA, Peter M, Bonatz G, et al. A higher rate of hyperandrogenic disorders in female-to-male transsexuals. Psychoneuroendocrinology. 1997;22:361-380.
17. Ryan C, Huebner D, Diaz RM, Sanchez J. Family rejection as a predictor of negative health outcomes in white and Latino lesbian, gay, and bisexual young adults. Pediatrics. 2009;123:346-352.
18. Henry J. Kaiser Family Foundation. A Report on the Experiences of Lesbians, Gays and Bisexuals in America and the Public’s Views on Issues and Policies Related to Sexual Orientation. Menlo Park, Calif: Henry J. Kaiser Family Foundation; 2001.
19. Mays VM, Cochran SD. Mental health correlates of perceived discrimination among lesbian, gay, and bisexual adults in the United States. Am J Public Health. 2001;91:1869-1876.
20. Mays VM, Cochran SD, Barnes NW. Race, race-based discrimination, and health outcomes among African Americans. Annu Rev Psychol. 2007;58:201-225.
21. Valanis BG, Bowen DJ, Bassford T, Whitlock E, Charney P, Carter RA. Sexual orientation and health: comparisons in the Women’s Health Initiative sample. Arch Fam Med. 2000;9:843-853.
22. Case P, Austin SB, Hunter DJ, et al. Sexual orientation, health risk factors, and physical functioning in the Nurses’ Health Study II. J Womens Health. 2004;13:1033-1047.
23. Meezan W, Rauch J. Gay marriage, same-sex parenting, and America’s children. Future Child. 2005;15:97-115.
24. Eaker ED, Sullivan LM, Kelly-Hayes M, D’Agostino RB, Sr, Benjamin EJ. Marital status, marital strain, and risk of coronary heart disease or total mortality: the Framingham Offspring Study. Psychosom Med. 2007;69:509-513.
25. Shenson D, Adams M, Bolen J. Delivery of preventive services to adults aged 50–64: monitoring performance using a composite measure, 1997-2004. J Gen Intern Med. 2008;23:733-740.
26. Kaplan RM, Kronick RG. Marital status and longevity in the United States population. J Epidemiol Community Health. 2006;60:760-765.
27. Aronson SR, Huston AC. The mother-infant relationship in single, cohabiting, and married families: a case for marriage? J Fam Psychol. 2004;18:5-18.
28. Pawelski JG, Perrin EC, Foy JM, et al. The effects of marriage, civil union, and domestic partnership laws on the health and well-being of children. Pediatrics. 2006;118:349-364.
29. Gartrell N, Banks A, Hamilton J, Reed N, Bishop H, Rodas C. The National Lesbian Family Study: 2. Interviews with mothers of toddlers. Am J Orthopsychiatry. 1999;69:362-369.
30. American Psychological Association. Answers to your questions for a better understanding of sexual orientation and homosexuality. Available at: http://www.apa.org/topics/sorientation.html. Accessed Oct. 13, 2009.
31. American Psychiatric Association. Same sex marriage resource document. Resource documents approved by the Board of Trustees, American Psychiatric Association. November 2004. Available at: http://archive.psych.org/edu/other_res/lib_archives/archives/200417.pdf. Accessed Oct. 13, 2009.
32. American Medical Association. GLBT policy compendium. 2005. Available at: http://www.ama-assn.org/ama1/pub/upload/mm/42/glbt_policy0905.pdf. Accessed Oct. 13, 2009.
Does antenatal magnesium sulfate lower the risk of cerebral palsy in infants born before 34 weeks?
Preterm birth is among the most significant risk factors for CP. Although they constitute fewer than 3% of births in the United States, infants born before 34 weeks’ gestation account for nearly one of every four new cases of CP.3
To date, few, if any, obstetric interventions have proved to be effective for preventing or reducing the likelihood or consequences of CP. During the 1990s, several observational studies found an association between treatment with magnesium sulfate during pregnancy and a reduction in the risk of CP among infants born preterm or at low birth weight. However, other observational series failed to confirm this association. As a result, considerable controversy clouded this issue.
Since that time, several randomized, controlled trials have explored the association. The overarching purpose of this meta-analysis by Conde-Agudelo and Romero is to assess the impact of magnesium sulfate for neuroprotection against CP among infants born before 34 weeks’ gestation.
Reasons this meta-analysis is credible
Conde-Agudelo and Romero conducted this review in concordance with a prospectively prepared protocol and followed Quality of Reporting of Meta-analyses (QUOROM) guidelines. Their search strategy and literature review were comprehensive and included all relevant studies in this arena. In addition, they utilized rigorous inclusion criteria and assessed heterogeneity in the various study designs and populations.
Besides including pooled relative risks in the results of the meta-analysis, they also calculated the number needed to treat (NNT), a measure of utility that is important to the clinician and clinical research. In this analysis, the number of women who were at risk of preterm delivery before 34 weeks’ gestation who needed to be treated with magnesium sulfate rather than placebo to prevent one case of CP was 52 (95% confidence interval, 31–154).
Last, the authors provided a measure of the impact of the use of magnesium sulfate on the public health and economic sectors, placing the problem and intervention in a broader, highly relevant context.
No revelations about magnesium in multiple versus singleton gestations
The trials included in this meta-analysis had limitations, of course. As a result, Conde-Agudelo and Romero were unable to estimate the direction and magnitude of the effect of magnesium sulfate on the risk of CP among multiple versus singleton gestations. Nor were they able to comment on the relative influence of the various dosing and treatment protocols employed in the primary trials. Therefore, this analysis cannot be used to advocate a specific dosage or protocol.
This important analysis suggests that antenatal magnesium sulfate for neuroprotection reduces the frequency of cerebral palsy among infants born before 34 weeks’ gestation. The authors recommend magnesium sulfate for this application in patients who are at high risk of delivering before 34 weeks, such as women who have premature rupture of membranes, active labor, or planned delivery within 24 hours.
Although the authors were unable to identify an optimal dosing strategy, they recommended that loading and maintenance dosages of magnesium sulfate and the duration of treatment not exceed 6 g, 1 to 2 g/hour, and 24 hours, respectively.
The findings of this excellent meta-analysis certainly justify continuing research.—HYAGRIV N. SIMHAN, MD, MSCR
1. Vohr BR, Msall ME, Wilson D, Wright LL, McDonald S, Poole WK. Spectrum of gross motor function in extremely low birth weight children with cerebral palsy at 18 months of age. Pediatrics. 2005;116:123-129.
2. Prevalence and characteristics of children with cerebral palsy in Europe. Dev Med Child Neurol. 2002;44:633-640.
3. Yeargin-Allsopp M, Van Naarden Braun K, Doernberg NS, et al. Prevalence of cerebral palsy in 8-year-old children in three areas of the United States in 2002: a multisite collaboration. Pediatrics. 2008;121:547-554.
Preterm birth is among the most significant risk factors for CP. Although they constitute fewer than 3% of births in the United States, infants born before 34 weeks’ gestation account for nearly one of every four new cases of CP.3
To date, few, if any, obstetric interventions have proved to be effective for preventing or reducing the likelihood or consequences of CP. During the 1990s, several observational studies found an association between treatment with magnesium sulfate during pregnancy and a reduction in the risk of CP among infants born preterm or at low birth weight. However, other observational series failed to confirm this association. As a result, considerable controversy clouded this issue.
Since that time, several randomized, controlled trials have explored the association. The overarching purpose of this meta-analysis by Conde-Agudelo and Romero is to assess the impact of magnesium sulfate for neuroprotection against CP among infants born before 34 weeks’ gestation.
Reasons this meta-analysis is credible
Conde-Agudelo and Romero conducted this review in concordance with a prospectively prepared protocol and followed Quality of Reporting of Meta-analyses (QUOROM) guidelines. Their search strategy and literature review were comprehensive and included all relevant studies in this arena. In addition, they utilized rigorous inclusion criteria and assessed heterogeneity in the various study designs and populations.
Besides including pooled relative risks in the results of the meta-analysis, they also calculated the number needed to treat (NNT), a measure of utility that is important to the clinician and clinical research. In this analysis, the number of women who were at risk of preterm delivery before 34 weeks’ gestation who needed to be treated with magnesium sulfate rather than placebo to prevent one case of CP was 52 (95% confidence interval, 31–154).
Last, the authors provided a measure of the impact of the use of magnesium sulfate on the public health and economic sectors, placing the problem and intervention in a broader, highly relevant context.
No revelations about magnesium in multiple versus singleton gestations
The trials included in this meta-analysis had limitations, of course. As a result, Conde-Agudelo and Romero were unable to estimate the direction and magnitude of the effect of magnesium sulfate on the risk of CP among multiple versus singleton gestations. Nor were they able to comment on the relative influence of the various dosing and treatment protocols employed in the primary trials. Therefore, this analysis cannot be used to advocate a specific dosage or protocol.
This important analysis suggests that antenatal magnesium sulfate for neuroprotection reduces the frequency of cerebral palsy among infants born before 34 weeks’ gestation. The authors recommend magnesium sulfate for this application in patients who are at high risk of delivering before 34 weeks, such as women who have premature rupture of membranes, active labor, or planned delivery within 24 hours.
Although the authors were unable to identify an optimal dosing strategy, they recommended that loading and maintenance dosages of magnesium sulfate and the duration of treatment not exceed 6 g, 1 to 2 g/hour, and 24 hours, respectively.
The findings of this excellent meta-analysis certainly justify continuing research.—HYAGRIV N. SIMHAN, MD, MSCR
Preterm birth is among the most significant risk factors for CP. Although they constitute fewer than 3% of births in the United States, infants born before 34 weeks’ gestation account for nearly one of every four new cases of CP.3
To date, few, if any, obstetric interventions have proved to be effective for preventing or reducing the likelihood or consequences of CP. During the 1990s, several observational studies found an association between treatment with magnesium sulfate during pregnancy and a reduction in the risk of CP among infants born preterm or at low birth weight. However, other observational series failed to confirm this association. As a result, considerable controversy clouded this issue.
Since that time, several randomized, controlled trials have explored the association. The overarching purpose of this meta-analysis by Conde-Agudelo and Romero is to assess the impact of magnesium sulfate for neuroprotection against CP among infants born before 34 weeks’ gestation.
Reasons this meta-analysis is credible
Conde-Agudelo and Romero conducted this review in concordance with a prospectively prepared protocol and followed Quality of Reporting of Meta-analyses (QUOROM) guidelines. Their search strategy and literature review were comprehensive and included all relevant studies in this arena. In addition, they utilized rigorous inclusion criteria and assessed heterogeneity in the various study designs and populations.
Besides including pooled relative risks in the results of the meta-analysis, they also calculated the number needed to treat (NNT), a measure of utility that is important to the clinician and clinical research. In this analysis, the number of women who were at risk of preterm delivery before 34 weeks’ gestation who needed to be treated with magnesium sulfate rather than placebo to prevent one case of CP was 52 (95% confidence interval, 31–154).
Last, the authors provided a measure of the impact of the use of magnesium sulfate on the public health and economic sectors, placing the problem and intervention in a broader, highly relevant context.
No revelations about magnesium in multiple versus singleton gestations
The trials included in this meta-analysis had limitations, of course. As a result, Conde-Agudelo and Romero were unable to estimate the direction and magnitude of the effect of magnesium sulfate on the risk of CP among multiple versus singleton gestations. Nor were they able to comment on the relative influence of the various dosing and treatment protocols employed in the primary trials. Therefore, this analysis cannot be used to advocate a specific dosage or protocol.
This important analysis suggests that antenatal magnesium sulfate for neuroprotection reduces the frequency of cerebral palsy among infants born before 34 weeks’ gestation. The authors recommend magnesium sulfate for this application in patients who are at high risk of delivering before 34 weeks, such as women who have premature rupture of membranes, active labor, or planned delivery within 24 hours.
Although the authors were unable to identify an optimal dosing strategy, they recommended that loading and maintenance dosages of magnesium sulfate and the duration of treatment not exceed 6 g, 1 to 2 g/hour, and 24 hours, respectively.
The findings of this excellent meta-analysis certainly justify continuing research.—HYAGRIV N. SIMHAN, MD, MSCR
1. Vohr BR, Msall ME, Wilson D, Wright LL, McDonald S, Poole WK. Spectrum of gross motor function in extremely low birth weight children with cerebral palsy at 18 months of age. Pediatrics. 2005;116:123-129.
2. Prevalence and characteristics of children with cerebral palsy in Europe. Dev Med Child Neurol. 2002;44:633-640.
3. Yeargin-Allsopp M, Van Naarden Braun K, Doernberg NS, et al. Prevalence of cerebral palsy in 8-year-old children in three areas of the United States in 2002: a multisite collaboration. Pediatrics. 2008;121:547-554.
1. Vohr BR, Msall ME, Wilson D, Wright LL, McDonald S, Poole WK. Spectrum of gross motor function in extremely low birth weight children with cerebral palsy at 18 months of age. Pediatrics. 2005;116:123-129.
2. Prevalence and characteristics of children with cerebral palsy in Europe. Dev Med Child Neurol. 2002;44:633-640.
3. Yeargin-Allsopp M, Van Naarden Braun K, Doernberg NS, et al. Prevalence of cerebral palsy in 8-year-old children in three areas of the United States in 2002: a multisite collaboration. Pediatrics. 2008;121:547-554.