Commentary

Do health effects of menopausal estrogen therapy differ between women with bilateral oophorectomy versus those with conserved ovaries? To answer this question a group of investigators performed a subanalysis of the Women’s Health Initiative (WHI) Estrogen-Alone Trial,¹ which included 40 clinical centers across the United States. They examined estrogen therapy outcomes by bilateral salpingo-oophorectomy (BSO) status, with additional stratification by 10-year age groups in 9,939 women aged 50 to 79 years with prior hysterectomy and known oophorectomy status. In the WHI trial, women were randomly assigned to conjugated equine estrogens (CEE) 0.625 mg/d or placebo for a median of 7.2 years. Investigators assessed the incidence of coronary heart disease and invasive breast cancer (the trial’s 2 primary end points), all-cause mortality, and a “global index”—these end points plus stroke, pulmonary embolism, colorectal cancer, and hip fracture—during the intervention phase and 18-year cumulative follow-up.

OBG Management caught up with lead author JoAnn E. Manson, MD, DrPH, NCMP, to discuss the study’s results.
 

OBG Management: How many women undergo BSO with their hysterectomy?

Dr. JoAnn E. Manson, MD, DrPH, NCMP: Of the 425,000 women who undergo hysterectomy in the United States for benign reasons each year,^2,3 about 40% of them undergo BSO—so between 150,000 and 200,000 women per year undergo BSO with their hysterectomy.^4,5
 

OBG Management: Although BSO is performed with hysterectomy to minimize patients’ future ovarian cancer risk, does BSO have health risks of its own, and how has estrogen been shown to affect these risks?

Dr. Manson: First, yes, BSO has been associated with health risks, especially when it is performed at a young age, such as before age 45. It has been linked to an increased risk of heart disease, osteoporosis, cognitive decline, and all-cause mortality. According to observational studies, estrogen therapy appears to offset many of these risks, particularly those related to heart disease and osteoporosis (the evidence is less clear on cognitive deficits).⁵
 

OBG Management: What did you find in your trial when you randomly assigned women in the age groups of 50 to 79 who underwent hysterectomy with and without BSO to estrogen therapy or placebo?

Dr. Manson: The WHI is the first study to be conducted in a randomized trial setting to analyze the health risks and benefits of estrogen therapy according to whether or not women had their ovaries removed. What we found was that the woman’s age had a strong influence on the effects of estrogen therapy among women who had BSO but only a negligible effect among women who had conserved ovaries. Overall, across the full age range, the effects of estrogen therapy did not differ substantially between women who had a BSO and those who had their ovaries conserved.

However, there were major differences by age group among the women who had BSO. A significant 32% reduction in all-cause mortality emerged during the 18-year follow-up period among the younger women (below age 60) who had BSO when they received estrogen therapy as compared with placebo. By contrast, the women who had conserved ovaries did not have this significant reduction in all-cause mortality, or in most of the other outcomes on estrogen compared with placebo. Overall, the effects of estrogen therapy tended to be relatively neutral in the women with conserved ovaries.

Now, the reduction in all-cause mortality with estrogen therapy was particularly pronounced among women who had BSO before age 45. They had a 40% statistically significant reduction in all-cause mortality with estrogen therapy compared with placebo. Also, among the women with BSO, there was a strong association between the timing of estrogen initiation and the magnitude of reduction in mortality. Women who started the estrogen therapy within 10 years of having the BSO had a 34% significant reduction in all-cause mortality, and those who started estrogen more than 20 years after having their ovaries removed had no reduction in mortality.
 

Continue to: OBG Management: Do your data give support to the timing hypothesis?

OBG Management: Do your data give support to the timing hypothesis?

Dr. Manson: Yes, our findings do support a timing hypothesis that was particularly pronounced for women who underwent BSO. It was the women who had early surgical menopause (before age 45) and those who started the estrogen therapy within 10 years of having their ovaries removed who had the greatest reduction in all-cause mortality and the most favorable benefit-risk profile from hormone therapy. So, the results do lend support to the timing hypothesis.

By contrast, women who had BSO at hysterectomy and began hormone therapy at age 70 or older had net adverse effects from hormone therapy. They posted a 40% increase in the global index—which is a summary measure of adverse effects on cardiovascular disease, cancer, and other major health outcomes. So, the women with BSO who were randomized in the trial at age 70 and older, had unfavorable results from estrogen therapy and an increase in the global index, in contrast to the women who were below age 60 or within 10 years of menopause.
 

OBG Management: Given your study findings, in which women would you recommend estrogen therapy? And are there groups of women in which you would advise avoiding estrogen therapy?

Dr. Manson: Current guidelines^6,7 recommend estrogen therapy for women who have early menopause, particularly an early surgical menopause and BSO prior to the average age at natural menopause. Unless the woman has contraindications to estrogen therapy, the recommendations are to treat with estrogen until the average age of menopause—until about age 50 to 51.

Our study findings provide reassurance that, if a woman continues to have indications for estrogen (vasomotor symptoms, or other indications for estrogen therapy), there is relative safety of continuing estrogen-alone therapy through her 50s, until age 60. For example, a woman who, after the average age of menopause continues to have vasomotor symptoms, or if she has bone health problems, our study would suggest that estrogen therapy would continue to have a favorable benefit-risk profile until at least the age of 60. Decisions would have to be individualized, especially after age 60, with shared decision-making particularly important for those decisions. (Some women, depending on their risk profile, may continue to be candidates for estrogen therapy past age 60.)

So, this study provides reassurance regarding use of estrogen therapy for women in their 50s if they have had BSO. Actually, the women who had conserved ovaries also had relative safety with estrogen therapy until age 60. They just didn’t show the significant benefits for all-cause mortality. Overall, their pattern of health-related benefits and risks was neutral. Thus, if vasomotor symptom management, quality of life benefits, or bone health effects are sought, taking hormone therapy is a quite reasonable choice for these women.

By contrast, women who have had a BSO and are age 70 or older should really avoid initiating estrogen therapy because it would follow a prolonged period of estrogen deficiency, or very low estrogen levels, and these women appeared to have a net adverse effect from initiating hormone therapy (with increases in the global index found).

Continue to: OBG Management: Did taking estrogen therapy prior to trial enrollment make a difference when it came to study outcomes?

OBG Management: Did taking estrogen therapy prior to trial enrollment make a difference when it came to study outcomes?

Dr. Manson: We found minimal if any effect in our analyses. In fact, even the women who did not have prior (pre-randomization) use of estrogen therapy tended to do well on estrogen-alone therapy if they were younger than age 60. This was particularly true for the women who had BSO. Even if they had not used estrogen previously, and they were many years past the BSO, they still did well on estrogen therapy if they were below age 60.

Do health effects of menopausal estrogen therapy differ between women with bilateral oophorectomy versus those with conserved ovaries? To answer this question a group of investigators performed a subanalysis of the Women’s Health Initiative (WHI) Estrogen-Alone Trial,¹ which included 40 clinical centers across the United States. They examined estrogen therapy outcomes by bilateral salpingo-oophorectomy (BSO) status, with additional stratification by 10-year age groups in 9,939 women aged 50 to 79 years with prior hysterectomy and known oophorectomy status. In the WHI trial, women were randomly assigned to conjugated equine estrogens (CEE) 0.625 mg/d or placebo for a median of 7.2 years. Investigators assessed the incidence of coronary heart disease and invasive breast cancer (the trial’s 2 primary end points), all-cause mortality, and a “global index”—these end points plus stroke, pulmonary embolism, colorectal cancer, and hip fracture—during the intervention phase and 18-year cumulative follow-up.

OBG Management caught up with lead author JoAnn E. Manson, MD, DrPH, NCMP, to discuss the study’s results.
 

OBG Management: How many women undergo BSO with their hysterectomy?

Dr. JoAnn E. Manson, MD, DrPH, NCMP: Of the 425,000 women who undergo hysterectomy in the United States for benign reasons each year,^2,3 about 40% of them undergo BSO—so between 150,000 and 200,000 women per year undergo BSO with their hysterectomy.^4,5
 

OBG Management: Although BSO is performed with hysterectomy to minimize patients’ future ovarian cancer risk, does BSO have health risks of its own, and how has estrogen been shown to affect these risks?

Dr. Manson: First, yes, BSO has been associated with health risks, especially when it is performed at a young age, such as before age 45. It has been linked to an increased risk of heart disease, osteoporosis, cognitive decline, and all-cause mortality. According to observational studies, estrogen therapy appears to offset many of these risks, particularly those related to heart disease and osteoporosis (the evidence is less clear on cognitive deficits).⁵
 

OBG Management: What did you find in your trial when you randomly assigned women in the age groups of 50 to 79 who underwent hysterectomy with and without BSO to estrogen therapy or placebo?

Dr. Manson: The WHI is the first study to be conducted in a randomized trial setting to analyze the health risks and benefits of estrogen therapy according to whether or not women had their ovaries removed. What we found was that the woman’s age had a strong influence on the effects of estrogen therapy among women who had BSO but only a negligible effect among women who had conserved ovaries. Overall, across the full age range, the effects of estrogen therapy did not differ substantially between women who had a BSO and those who had their ovaries conserved.

However, there were major differences by age group among the women who had BSO. A significant 32% reduction in all-cause mortality emerged during the 18-year follow-up period among the younger women (below age 60) who had BSO when they received estrogen therapy as compared with placebo. By contrast, the women who had conserved ovaries did not have this significant reduction in all-cause mortality, or in most of the other outcomes on estrogen compared with placebo. Overall, the effects of estrogen therapy tended to be relatively neutral in the women with conserved ovaries.

Now, the reduction in all-cause mortality with estrogen therapy was particularly pronounced among women who had BSO before age 45. They had a 40% statistically significant reduction in all-cause mortality with estrogen therapy compared with placebo. Also, among the women with BSO, there was a strong association between the timing of estrogen initiation and the magnitude of reduction in mortality. Women who started the estrogen therapy within 10 years of having the BSO had a 34% significant reduction in all-cause mortality, and those who started estrogen more than 20 years after having their ovaries removed had no reduction in mortality.
 

Continue to: OBG Management: Do your data give support to the timing hypothesis?

OBG Management: Do your data give support to the timing hypothesis?

Dr. Manson: Yes, our findings do support a timing hypothesis that was particularly pronounced for women who underwent BSO. It was the women who had early surgical menopause (before age 45) and those who started the estrogen therapy within 10 years of having their ovaries removed who had the greatest reduction in all-cause mortality and the most favorable benefit-risk profile from hormone therapy. So, the results do lend support to the timing hypothesis.

By contrast, women who had BSO at hysterectomy and began hormone therapy at age 70 or older had net adverse effects from hormone therapy. They posted a 40% increase in the global index—which is a summary measure of adverse effects on cardiovascular disease, cancer, and other major health outcomes. So, the women with BSO who were randomized in the trial at age 70 and older, had unfavorable results from estrogen therapy and an increase in the global index, in contrast to the women who were below age 60 or within 10 years of menopause.
 

OBG Management: Given your study findings, in which women would you recommend estrogen therapy? And are there groups of women in which you would advise avoiding estrogen therapy?

Dr. Manson: Current guidelines^6,7 recommend estrogen therapy for women who have early menopause, particularly an early surgical menopause and BSO prior to the average age at natural menopause. Unless the woman has contraindications to estrogen therapy, the recommendations are to treat with estrogen until the average age of menopause—until about age 50 to 51.

Our study findings provide reassurance that, if a woman continues to have indications for estrogen (vasomotor symptoms, or other indications for estrogen therapy), there is relative safety of continuing estrogen-alone therapy through her 50s, until age 60. For example, a woman who, after the average age of menopause continues to have vasomotor symptoms, or if she has bone health problems, our study would suggest that estrogen therapy would continue to have a favorable benefit-risk profile until at least the age of 60. Decisions would have to be individualized, especially after age 60, with shared decision-making particularly important for those decisions. (Some women, depending on their risk profile, may continue to be candidates for estrogen therapy past age 60.)

So, this study provides reassurance regarding use of estrogen therapy for women in their 50s if they have had BSO. Actually, the women who had conserved ovaries also had relative safety with estrogen therapy until age 60. They just didn’t show the significant benefits for all-cause mortality. Overall, their pattern of health-related benefits and risks was neutral. Thus, if vasomotor symptom management, quality of life benefits, or bone health effects are sought, taking hormone therapy is a quite reasonable choice for these women.

By contrast, women who have had a BSO and are age 70 or older should really avoid initiating estrogen therapy because it would follow a prolonged period of estrogen deficiency, or very low estrogen levels, and these women appeared to have a net adverse effect from initiating hormone therapy (with increases in the global index found).

Continue to: OBG Management: Did taking estrogen therapy prior to trial enrollment make a difference when it came to study outcomes?

OBG Management: Did taking estrogen therapy prior to trial enrollment make a difference when it came to study outcomes?

Dr. Manson: We found minimal if any effect in our analyses. In fact, even the women who did not have prior (pre-randomization) use of estrogen therapy tended to do well on estrogen-alone therapy if they were younger than age 60. This was particularly true for the women who had BSO. Even if they had not used estrogen previously, and they were many years past the BSO, they still did well on estrogen therapy if they were below age 60.

Do health effects of menopausal estrogen therapy differ between women with bilateral oophorectomy versus those with conserved ovaries? To answer this question a group of investigators performed a subanalysis of the Women’s Health Initiative (WHI) Estrogen-Alone Trial,¹ which included 40 clinical centers across the United States. They examined estrogen therapy outcomes by bilateral salpingo-oophorectomy (BSO) status, with additional stratification by 10-year age groups in 9,939 women aged 50 to 79 years with prior hysterectomy and known oophorectomy status. In the WHI trial, women were randomly assigned to conjugated equine estrogens (CEE) 0.625 mg/d or placebo for a median of 7.2 years. Investigators assessed the incidence of coronary heart disease and invasive breast cancer (the trial’s 2 primary end points), all-cause mortality, and a “global index”—these end points plus stroke, pulmonary embolism, colorectal cancer, and hip fracture—during the intervention phase and 18-year cumulative follow-up.

OBG Management caught up with lead author JoAnn E. Manson, MD, DrPH, NCMP, to discuss the study’s results.
 

OBG Management: How many women undergo BSO with their hysterectomy?

Dr. JoAnn E. Manson, MD, DrPH, NCMP: Of the 425,000 women who undergo hysterectomy in the United States for benign reasons each year,^2,3 about 40% of them undergo BSO—so between 150,000 and 200,000 women per year undergo BSO with their hysterectomy.^4,5
 

OBG Management: Although BSO is performed with hysterectomy to minimize patients’ future ovarian cancer risk, does BSO have health risks of its own, and how has estrogen been shown to affect these risks?

Dr. Manson: First, yes, BSO has been associated with health risks, especially when it is performed at a young age, such as before age 45. It has been linked to an increased risk of heart disease, osteoporosis, cognitive decline, and all-cause mortality. According to observational studies, estrogen therapy appears to offset many of these risks, particularly those related to heart disease and osteoporosis (the evidence is less clear on cognitive deficits).⁵
 

OBG Management: What did you find in your trial when you randomly assigned women in the age groups of 50 to 79 who underwent hysterectomy with and without BSO to estrogen therapy or placebo?

Dr. Manson: The WHI is the first study to be conducted in a randomized trial setting to analyze the health risks and benefits of estrogen therapy according to whether or not women had their ovaries removed. What we found was that the woman’s age had a strong influence on the effects of estrogen therapy among women who had BSO but only a negligible effect among women who had conserved ovaries. Overall, across the full age range, the effects of estrogen therapy did not differ substantially between women who had a BSO and those who had their ovaries conserved.

However, there were major differences by age group among the women who had BSO. A significant 32% reduction in all-cause mortality emerged during the 18-year follow-up period among the younger women (below age 60) who had BSO when they received estrogen therapy as compared with placebo. By contrast, the women who had conserved ovaries did not have this significant reduction in all-cause mortality, or in most of the other outcomes on estrogen compared with placebo. Overall, the effects of estrogen therapy tended to be relatively neutral in the women with conserved ovaries.

Now, the reduction in all-cause mortality with estrogen therapy was particularly pronounced among women who had BSO before age 45. They had a 40% statistically significant reduction in all-cause mortality with estrogen therapy compared with placebo. Also, among the women with BSO, there was a strong association between the timing of estrogen initiation and the magnitude of reduction in mortality. Women who started the estrogen therapy within 10 years of having the BSO had a 34% significant reduction in all-cause mortality, and those who started estrogen more than 20 years after having their ovaries removed had no reduction in mortality.
 

Continue to: OBG Management: Do your data give support to the timing hypothesis?

OBG Management: Do your data give support to the timing hypothesis?

Dr. Manson: Yes, our findings do support a timing hypothesis that was particularly pronounced for women who underwent BSO. It was the women who had early surgical menopause (before age 45) and those who started the estrogen therapy within 10 years of having their ovaries removed who had the greatest reduction in all-cause mortality and the most favorable benefit-risk profile from hormone therapy. So, the results do lend support to the timing hypothesis.

By contrast, women who had BSO at hysterectomy and began hormone therapy at age 70 or older had net adverse effects from hormone therapy. They posted a 40% increase in the global index—which is a summary measure of adverse effects on cardiovascular disease, cancer, and other major health outcomes. So, the women with BSO who were randomized in the trial at age 70 and older, had unfavorable results from estrogen therapy and an increase in the global index, in contrast to the women who were below age 60 or within 10 years of menopause.
 

OBG Management: Given your study findings, in which women would you recommend estrogen therapy? And are there groups of women in which you would advise avoiding estrogen therapy?

Dr. Manson: Current guidelines^6,7 recommend estrogen therapy for women who have early menopause, particularly an early surgical menopause and BSO prior to the average age at natural menopause. Unless the woman has contraindications to estrogen therapy, the recommendations are to treat with estrogen until the average age of menopause—until about age 50 to 51.

Our study findings provide reassurance that, if a woman continues to have indications for estrogen (vasomotor symptoms, or other indications for estrogen therapy), there is relative safety of continuing estrogen-alone therapy through her 50s, until age 60. For example, a woman who, after the average age of menopause continues to have vasomotor symptoms, or if she has bone health problems, our study would suggest that estrogen therapy would continue to have a favorable benefit-risk profile until at least the age of 60. Decisions would have to be individualized, especially after age 60, with shared decision-making particularly important for those decisions. (Some women, depending on their risk profile, may continue to be candidates for estrogen therapy past age 60.)

So, this study provides reassurance regarding use of estrogen therapy for women in their 50s if they have had BSO. Actually, the women who had conserved ovaries also had relative safety with estrogen therapy until age 60. They just didn’t show the significant benefits for all-cause mortality. Overall, their pattern of health-related benefits and risks was neutral. Thus, if vasomotor symptom management, quality of life benefits, or bone health effects are sought, taking hormone therapy is a quite reasonable choice for these women.

By contrast, women who have had a BSO and are age 70 or older should really avoid initiating estrogen therapy because it would follow a prolonged period of estrogen deficiency, or very low estrogen levels, and these women appeared to have a net adverse effect from initiating hormone therapy (with increases in the global index found).

Continue to: OBG Management: Did taking estrogen therapy prior to trial enrollment make a difference when it came to study outcomes?

OBG Management: Did taking estrogen therapy prior to trial enrollment make a difference when it came to study outcomes?

Dr. Manson: We found minimal if any effect in our analyses. In fact, even the women who did not have prior (pre-randomization) use of estrogen therapy tended to do well on estrogen-alone therapy if they were younger than age 60. This was particularly true for the women who had BSO. Even if they had not used estrogen previously, and they were many years past the BSO, they still did well on estrogen therapy if they were below age 60.

To the Editor:

We read with great interest the recent Cutis article by Golda et al,¹ “Intraoperative Electrosurgical Smoke During Outpatient Surgery: A Survey of Dermatologic Surgeon and Staff Preferences.” We applaud the growing interest in the topic of dermatologist safety, as there are currently no established guidelines for precautions while performing surgical procedures. In 2018 we conducted a comprehensive review² to characterize the specific risks, hazard reduction strategies available, and current use of surgical smoke safety techniques during surgery among dermatologists, and ultimately recommend guidance based on the current available evidence. To conduct this review, we collected data from 45 manuscripts in the dermatology, surgery, infectious disease, obstetrics, and cancer biology literature. Herein, we summarize key findings.²

Dermatologic surgeons, residents, staff, and patients are exposed to many infectious, inhalational, chemical, and mutagenic hazards when performing procedures that liberate smoke and plume. These risks are commonplace; however, they are particularly notable during ablative laser and laser hair removal procedures, which produce a heavy plume (averaging >100,000 particles/cm³). Brief periods of heavy plume exposure also are commonplace during electrosurgery.

Infectious particles in surgical plume have been extensively studied, and viral transmission has been demonstrated in animal studies. Human papillomavirus transmission appears to be the most prevalent risk. Surgical smoke has been shown to cause acute and chronic inhalational injury in rat and sheep studies.^3-6

Additionally, chemicals with carcinogenic potential are present in surgical smoke and have been described.^7,8 Chemicals in the greatest quantity include hydrocarbons, nitriles, fatty acids, and phenols. Although there have been no human studies on smoke carcinogenesis to date, surgical smoke has been shown to have carcinogenic properties in vitro.

Given these risks—both evidence based and theoretical—we believe that diligent hazard reduction strategies should be employed whenever possible. Surgical masks and high-efficiency particulate air respirators, such as N95 respirator masks, have been well studied and do provide smoke protection. High-efficiency particulate air masks can be worn when possible, especially during procedures that produce heavy plume, though surgical masks are capable of filtering most of the noxious chemicals in surgical smoke. It should be noted that proper fit with minimal air leak is the most important aspect of overall performance.

Smoke evacuators provide another level of protection. The physician should consider the evacuator’s filtration efficiency, capture velocity, and suction strength when evaluating overall performance. Furthermore, the smoke collection tip should be within 2 in of the surgical field to maximize efficacy. Maintenance for smoke evacuation systems should include regular (as defined by manufacturer instructions) flushing of the smoke evacuator lines.

Despite the risks of surgical smoke and the available options of minimizing these risks, the hazards of surgical smoke and the importance of protection are likely underemphasized. Many dermatologic surgeons do not use surgical masks or smoke evacuators in routine practice, according to several survey studies.^9-11

It is important for the dermatologic community to consider effective ways of spreading awareness. We propose that surgical smoke safety be taught early in residency training. Additionally, smoke safety can be implemented into certification examinations. Access to masks and smoke evacuation devices are an important part of dermatology training. Accreditation Council for Graduate Medical Education funds should be appropriated to provide for such resources.

Finally, and perhaps most importantly, continued awareness should be established in the dermatology community via standardized guidelines and periodic updates in the dermatology literature and lectures at local and national conferences. Not until these strategies are implemented will surgical smoke protection be viewed as a necessary and important component of routine practice when performing dermatologic surgical procedures.

To the Editor:

We read with great interest the recent Cutis article by Golda et al,¹ “Intraoperative Electrosurgical Smoke During Outpatient Surgery: A Survey of Dermatologic Surgeon and Staff Preferences.” We applaud the growing interest in the topic of dermatologist safety, as there are currently no established guidelines for precautions while performing surgical procedures. In 2018 we conducted a comprehensive review² to characterize the specific risks, hazard reduction strategies available, and current use of surgical smoke safety techniques during surgery among dermatologists, and ultimately recommend guidance based on the current available evidence. To conduct this review, we collected data from 45 manuscripts in the dermatology, surgery, infectious disease, obstetrics, and cancer biology literature. Herein, we summarize key findings.²

Dermatologic surgeons, residents, staff, and patients are exposed to many infectious, inhalational, chemical, and mutagenic hazards when performing procedures that liberate smoke and plume. These risks are commonplace; however, they are particularly notable during ablative laser and laser hair removal procedures, which produce a heavy plume (averaging >100,000 particles/cm³). Brief periods of heavy plume exposure also are commonplace during electrosurgery.

Infectious particles in surgical plume have been extensively studied, and viral transmission has been demonstrated in animal studies. Human papillomavirus transmission appears to be the most prevalent risk. Surgical smoke has been shown to cause acute and chronic inhalational injury in rat and sheep studies.^3-6

Additionally, chemicals with carcinogenic potential are present in surgical smoke and have been described.^7,8 Chemicals in the greatest quantity include hydrocarbons, nitriles, fatty acids, and phenols. Although there have been no human studies on smoke carcinogenesis to date, surgical smoke has been shown to have carcinogenic properties in vitro.

Given these risks—both evidence based and theoretical—we believe that diligent hazard reduction strategies should be employed whenever possible. Surgical masks and high-efficiency particulate air respirators, such as N95 respirator masks, have been well studied and do provide smoke protection. High-efficiency particulate air masks can be worn when possible, especially during procedures that produce heavy plume, though surgical masks are capable of filtering most of the noxious chemicals in surgical smoke. It should be noted that proper fit with minimal air leak is the most important aspect of overall performance.

Smoke evacuators provide another level of protection. The physician should consider the evacuator’s filtration efficiency, capture velocity, and suction strength when evaluating overall performance. Furthermore, the smoke collection tip should be within 2 in of the surgical field to maximize efficacy. Maintenance for smoke evacuation systems should include regular (as defined by manufacturer instructions) flushing of the smoke evacuator lines.

Despite the risks of surgical smoke and the available options of minimizing these risks, the hazards of surgical smoke and the importance of protection are likely underemphasized. Many dermatologic surgeons do not use surgical masks or smoke evacuators in routine practice, according to several survey studies.^9-11

It is important for the dermatologic community to consider effective ways of spreading awareness. We propose that surgical smoke safety be taught early in residency training. Additionally, smoke safety can be implemented into certification examinations. Access to masks and smoke evacuation devices are an important part of dermatology training. Accreditation Council for Graduate Medical Education funds should be appropriated to provide for such resources.

Finally, and perhaps most importantly, continued awareness should be established in the dermatology community via standardized guidelines and periodic updates in the dermatology literature and lectures at local and national conferences. Not until these strategies are implemented will surgical smoke protection be viewed as a necessary and important component of routine practice when performing dermatologic surgical procedures.

To the Editor:

We read with great interest the recent Cutis article by Golda et al,¹ “Intraoperative Electrosurgical Smoke During Outpatient Surgery: A Survey of Dermatologic Surgeon and Staff Preferences.” We applaud the growing interest in the topic of dermatologist safety, as there are currently no established guidelines for precautions while performing surgical procedures. In 2018 we conducted a comprehensive review² to characterize the specific risks, hazard reduction strategies available, and current use of surgical smoke safety techniques during surgery among dermatologists, and ultimately recommend guidance based on the current available evidence. To conduct this review, we collected data from 45 manuscripts in the dermatology, surgery, infectious disease, obstetrics, and cancer biology literature. Herein, we summarize key findings.²

Dermatologic surgeons, residents, staff, and patients are exposed to many infectious, inhalational, chemical, and mutagenic hazards when performing procedures that liberate smoke and plume. These risks are commonplace; however, they are particularly notable during ablative laser and laser hair removal procedures, which produce a heavy plume (averaging >100,000 particles/cm³). Brief periods of heavy plume exposure also are commonplace during electrosurgery.

Infectious particles in surgical plume have been extensively studied, and viral transmission has been demonstrated in animal studies. Human papillomavirus transmission appears to be the most prevalent risk. Surgical smoke has been shown to cause acute and chronic inhalational injury in rat and sheep studies.^3-6

Additionally, chemicals with carcinogenic potential are present in surgical smoke and have been described.^7,8 Chemicals in the greatest quantity include hydrocarbons, nitriles, fatty acids, and phenols. Although there have been no human studies on smoke carcinogenesis to date, surgical smoke has been shown to have carcinogenic properties in vitro.

Given these risks—both evidence based and theoretical—we believe that diligent hazard reduction strategies should be employed whenever possible. Surgical masks and high-efficiency particulate air respirators, such as N95 respirator masks, have been well studied and do provide smoke protection. High-efficiency particulate air masks can be worn when possible, especially during procedures that produce heavy plume, though surgical masks are capable of filtering most of the noxious chemicals in surgical smoke. It should be noted that proper fit with minimal air leak is the most important aspect of overall performance.

Smoke evacuators provide another level of protection. The physician should consider the evacuator’s filtration efficiency, capture velocity, and suction strength when evaluating overall performance. Furthermore, the smoke collection tip should be within 2 in of the surgical field to maximize efficacy. Maintenance for smoke evacuation systems should include regular (as defined by manufacturer instructions) flushing of the smoke evacuator lines.

Despite the risks of surgical smoke and the available options of minimizing these risks, the hazards of surgical smoke and the importance of protection are likely underemphasized. Many dermatologic surgeons do not use surgical masks or smoke evacuators in routine practice, according to several survey studies.^9-11

It is important for the dermatologic community to consider effective ways of spreading awareness. We propose that surgical smoke safety be taught early in residency training. Additionally, smoke safety can be implemented into certification examinations. Access to masks and smoke evacuation devices are an important part of dermatology training. Accreditation Council for Graduate Medical Education funds should be appropriated to provide for such resources.

Finally, and perhaps most importantly, continued awareness should be established in the dermatology community via standardized guidelines and periodic updates in the dermatology literature and lectures at local and national conferences. Not until these strategies are implemented will surgical smoke protection be viewed as a necessary and important component of routine practice when performing dermatologic surgical procedures.

While the incidence of most cancers is falling, endometrial cancer rates continue to rise, in large part because of increasing life expectancy and obesity rates. However, what is even more alarming is the observation that there is a clear disparity in outcomes between black and white women with this disease. But there are things that all health care providers, including nononcologists, can do to help to overcome this disparity.

Black women are nearly twice as likely as non-Hispanic white women to die from the endometrial cancer. The 5-year survival for stage III and IV cancer is 43% for non-Hispanic white women, yet only 25% for black women.¹ For a long time, this survival disparity was assumed to be a function of the more aggressive cancer histologies, such as serous, which are more commonly seen in black women. These high-grade cancers are more likely to present in advanced stages and with poorer responses to treatments; however, the predisposition to aggressive cancers tells only part of the story of racial disparities in endometrial cancer and their presentation at later stages. Indeed, fueling the problem are the findings that black women report symptoms less, experience more delays in diagnosis or more frequent deviations from guideline-directed diagnostics, undergo more morbid surgical approaches, receive less surgical staging, are enrolled less in clinical trials, have lower socioeconomic status and lower rates of health insurance, and receive less differential administration of adjuvant therapies, as well as have a background of higher all-cause mortality and comorbidities. While this array of contributing factors may seem overwhelming, it also can be considered a guide for health care providers because most of these factors, unlike histologic cell type, are modifiable, and it is important that we all consider what role we can play in dismantling them.

Black women are less likely to receive guideline-recommended care upon presentation. Research by Kemi M. Doll, MD, from the University of Washington, Seattle, demonstrated that, among women with endometrial cancers, black women were less likely to have documented histories of postmenopausal bleeding within 2 years of the diagnosis, presumably because of factors related to underreporting and inadequate ascertainment by medical professionals of whether or not they had experienced postmenopausal bleeding.² Additionally, when postmenopausal bleeding was reported by these women, they were less likely to receive the appropriate diagnostic work-up as described by American College of Obstetricians and Gynecologists guidelines, and their bleeding was more likely to be ascribed to nonmalignant pathologies. Her work raises the important question about how black women view the health care profession and their willingness to engage early in good faith that their concerns will be met. These concerns are understandable given the documented different responsiveness of providers to black patients’ symptoms such as pain.³

Once diagnosed with endometrial cancer, black women are less likely to receive comprehensive surgical staging and less likely to have their surgery performed by a minimally invasive route, both of which are considered the standard of care.^1,4 Lower rates of minimally invasive surgery expose black women to increased morbidity and are deleterious to quality of life, return to work, and functionality. If surgical staging is omitted, which is more common for these women, clinicians are less able to appropriately prescribe adjuvant therapies which might prevent lethal recurrences from unrecognized advanced cancer or they may overtreat early-stage cancers with adjuvant therapy to make up for gaps in staging information.^1,5 However, adjuvant therapy is not a benign intervention, and itself is associated with morbidity.

As mentioned earlier, black women are at a higher risk for developing more aggressive cancer subtypes, and this phenomenon may appear unmodifiable. However, important research is looking at the concept of epigenetics and how modifiable environmental factors may contribute to the development of more aggressive types of cancer through gene expression. Additionally, differences in the gene mutations and gene expression of cancers more frequently acquired by black women may negatively influence how these cancers respond to conventional therapies. In the GOG210 study, which evaluated the outcomes of women with comprehensively staged endometrial cancer, black women demonstrated worse survival from cancer, even though they were more likely to receive chemotherapy.⁵ One explanation for this finding is that these women’s cancers were less responsive to conventional chemotherapy agents.

This raises a critical issue of disparity in clinical trial inclusion. Black women are underrepresented in clinical trials in the United States. There is a dark history in medical research and minority populations, particularly African American populations, which continues to be remembered and felt. However, not all of this underrepresentation may be from unwillingness to participate: For black women, issues of lack of access to or being considered for clinical trials is also a factor. But without adequate representation in trials of novel agents, we will not know whether they are effective for all populations, and indeed it would appear that we should not assume they are equally effective based on the results to date.

So how can we all individually help to overcome these disparities in endometrial cancer outcomes? To begin with, it is important to acknowledge that black women commonly report negative experiences with reproductive health care. From early in their lives, we must sensitively engage all of our patients and ensure they all feel heard and valued. They should know that their symptoms, including pain or bleeding, are taken and treated seriously. If we can do better with this throughout a woman’s earlier reproductive health care experiences, perhaps later in her life, when she experiences postmenopausal bleeding, she will feel comfortable raising this issue with her health care provider who in turn must take this symptom seriously and expeditiously engage all of the appropriate diagnostic resources. Health care delivery is about more than simply offering the best treatment. We also are responsible for education and shared decision making to ensure that we can deliver the best treatment.

We also can support organizations such as ECANA (Endometrial Cancer Action Network for African Americans) which serves to inform black women in their communities about the threat that endometrial cancer plays and empowers them through education about its symptoms and the need to seek care.

Systematically we must ensure black women have access to the same standards in surgical and nonsurgical management of these cancers. This includes referral of all women with cancer, including minorities, to high-volume centers with oncology specialists and explaining to those who may be reluctant to travel that this is associated with improved outcomes in the short and long term. We also must actively consider our black patients for clinical trials, sensitively educate them about their benefits, and overcome barriers to access. One simple way to do this is to explain that the treatments that we have developed for endometrial cancer have mostly been tested on white women, which may explain in part why they do not work so well for nonwhite women.

The racial disparity in endometrial cancer outcomes cannot entirely be attributed to the passive phenomenon of patient and tumor genetics, particularly with consideration that race is a social construct rather than a biological phenomenon. We can all make a difference through advocacy, access, education, and heightened awareness to combat this inequity and overcome these disparate outcomes.
 

Dr. Rossi is assistant professor in the division of gynecologic oncology at the University of North Carolina at Chapel Hill. She said she had no relevant financial disclosures. Email her at obnews@mdedge.com.

References

1. Gynecol Oncol. 2016 Oct;143(1):98-104.

2. Am J Obstet Gynecol. 2018 Dec;219(6):593.e1-14.

3. J Clin Oncol. 2012 Jun 1;30(16):1980-8.

4. Obstet Gynecol. 2016 Sep;128(3):526-34.

5. Am J Obstet Gynecol. 2018 Nov;219(5):459.e1-11.

While the incidence of most cancers is falling, endometrial cancer rates continue to rise, in large part because of increasing life expectancy and obesity rates. However, what is even more alarming is the observation that there is a clear disparity in outcomes between black and white women with this disease. But there are things that all health care providers, including nononcologists, can do to help to overcome this disparity.

Black women are nearly twice as likely as non-Hispanic white women to die from the endometrial cancer. The 5-year survival for stage III and IV cancer is 43% for non-Hispanic white women, yet only 25% for black women.¹ For a long time, this survival disparity was assumed to be a function of the more aggressive cancer histologies, such as serous, which are more commonly seen in black women. These high-grade cancers are more likely to present in advanced stages and with poorer responses to treatments; however, the predisposition to aggressive cancers tells only part of the story of racial disparities in endometrial cancer and their presentation at later stages. Indeed, fueling the problem are the findings that black women report symptoms less, experience more delays in diagnosis or more frequent deviations from guideline-directed diagnostics, undergo more morbid surgical approaches, receive less surgical staging, are enrolled less in clinical trials, have lower socioeconomic status and lower rates of health insurance, and receive less differential administration of adjuvant therapies, as well as have a background of higher all-cause mortality and comorbidities. While this array of contributing factors may seem overwhelming, it also can be considered a guide for health care providers because most of these factors, unlike histologic cell type, are modifiable, and it is important that we all consider what role we can play in dismantling them.

Black women are less likely to receive guideline-recommended care upon presentation. Research by Kemi M. Doll, MD, from the University of Washington, Seattle, demonstrated that, among women with endometrial cancers, black women were less likely to have documented histories of postmenopausal bleeding within 2 years of the diagnosis, presumably because of factors related to underreporting and inadequate ascertainment by medical professionals of whether or not they had experienced postmenopausal bleeding.² Additionally, when postmenopausal bleeding was reported by these women, they were less likely to receive the appropriate diagnostic work-up as described by American College of Obstetricians and Gynecologists guidelines, and their bleeding was more likely to be ascribed to nonmalignant pathologies. Her work raises the important question about how black women view the health care profession and their willingness to engage early in good faith that their concerns will be met. These concerns are understandable given the documented different responsiveness of providers to black patients’ symptoms such as pain.³

Once diagnosed with endometrial cancer, black women are less likely to receive comprehensive surgical staging and less likely to have their surgery performed by a minimally invasive route, both of which are considered the standard of care.^1,4 Lower rates of minimally invasive surgery expose black women to increased morbidity and are deleterious to quality of life, return to work, and functionality. If surgical staging is omitted, which is more common for these women, clinicians are less able to appropriately prescribe adjuvant therapies which might prevent lethal recurrences from unrecognized advanced cancer or they may overtreat early-stage cancers with adjuvant therapy to make up for gaps in staging information.^1,5 However, adjuvant therapy is not a benign intervention, and itself is associated with morbidity.

As mentioned earlier, black women are at a higher risk for developing more aggressive cancer subtypes, and this phenomenon may appear unmodifiable. However, important research is looking at the concept of epigenetics and how modifiable environmental factors may contribute to the development of more aggressive types of cancer through gene expression. Additionally, differences in the gene mutations and gene expression of cancers more frequently acquired by black women may negatively influence how these cancers respond to conventional therapies. In the GOG210 study, which evaluated the outcomes of women with comprehensively staged endometrial cancer, black women demonstrated worse survival from cancer, even though they were more likely to receive chemotherapy.⁵ One explanation for this finding is that these women’s cancers were less responsive to conventional chemotherapy agents.

This raises a critical issue of disparity in clinical trial inclusion. Black women are underrepresented in clinical trials in the United States. There is a dark history in medical research and minority populations, particularly African American populations, which continues to be remembered and felt. However, not all of this underrepresentation may be from unwillingness to participate: For black women, issues of lack of access to or being considered for clinical trials is also a factor. But without adequate representation in trials of novel agents, we will not know whether they are effective for all populations, and indeed it would appear that we should not assume they are equally effective based on the results to date.

So how can we all individually help to overcome these disparities in endometrial cancer outcomes? To begin with, it is important to acknowledge that black women commonly report negative experiences with reproductive health care. From early in their lives, we must sensitively engage all of our patients and ensure they all feel heard and valued. They should know that their symptoms, including pain or bleeding, are taken and treated seriously. If we can do better with this throughout a woman’s earlier reproductive health care experiences, perhaps later in her life, when she experiences postmenopausal bleeding, she will feel comfortable raising this issue with her health care provider who in turn must take this symptom seriously and expeditiously engage all of the appropriate diagnostic resources. Health care delivery is about more than simply offering the best treatment. We also are responsible for education and shared decision making to ensure that we can deliver the best treatment.

We also can support organizations such as ECANA (Endometrial Cancer Action Network for African Americans) which serves to inform black women in their communities about the threat that endometrial cancer plays and empowers them through education about its symptoms and the need to seek care.

Systematically we must ensure black women have access to the same standards in surgical and nonsurgical management of these cancers. This includes referral of all women with cancer, including minorities, to high-volume centers with oncology specialists and explaining to those who may be reluctant to travel that this is associated with improved outcomes in the short and long term. We also must actively consider our black patients for clinical trials, sensitively educate them about their benefits, and overcome barriers to access. One simple way to do this is to explain that the treatments that we have developed for endometrial cancer have mostly been tested on white women, which may explain in part why they do not work so well for nonwhite women.

The racial disparity in endometrial cancer outcomes cannot entirely be attributed to the passive phenomenon of patient and tumor genetics, particularly with consideration that race is a social construct rather than a biological phenomenon. We can all make a difference through advocacy, access, education, and heightened awareness to combat this inequity and overcome these disparate outcomes.
 

Dr. Rossi is assistant professor in the division of gynecologic oncology at the University of North Carolina at Chapel Hill. She said she had no relevant financial disclosures. Email her at obnews@mdedge.com.

References

1. Gynecol Oncol. 2016 Oct;143(1):98-104.

2. Am J Obstet Gynecol. 2018 Dec;219(6):593.e1-14.

3. J Clin Oncol. 2012 Jun 1;30(16):1980-8.

4. Obstet Gynecol. 2016 Sep;128(3):526-34.

5. Am J Obstet Gynecol. 2018 Nov;219(5):459.e1-11.

While the incidence of most cancers is falling, endometrial cancer rates continue to rise, in large part because of increasing life expectancy and obesity rates. However, what is even more alarming is the observation that there is a clear disparity in outcomes between black and white women with this disease. But there are things that all health care providers, including nononcologists, can do to help to overcome this disparity.

Black women are nearly twice as likely as non-Hispanic white women to die from the endometrial cancer. The 5-year survival for stage III and IV cancer is 43% for non-Hispanic white women, yet only 25% for black women.¹ For a long time, this survival disparity was assumed to be a function of the more aggressive cancer histologies, such as serous, which are more commonly seen in black women. These high-grade cancers are more likely to present in advanced stages and with poorer responses to treatments; however, the predisposition to aggressive cancers tells only part of the story of racial disparities in endometrial cancer and their presentation at later stages. Indeed, fueling the problem are the findings that black women report symptoms less, experience more delays in diagnosis or more frequent deviations from guideline-directed diagnostics, undergo more morbid surgical approaches, receive less surgical staging, are enrolled less in clinical trials, have lower socioeconomic status and lower rates of health insurance, and receive less differential administration of adjuvant therapies, as well as have a background of higher all-cause mortality and comorbidities. While this array of contributing factors may seem overwhelming, it also can be considered a guide for health care providers because most of these factors, unlike histologic cell type, are modifiable, and it is important that we all consider what role we can play in dismantling them.

Black women are less likely to receive guideline-recommended care upon presentation. Research by Kemi M. Doll, MD, from the University of Washington, Seattle, demonstrated that, among women with endometrial cancers, black women were less likely to have documented histories of postmenopausal bleeding within 2 years of the diagnosis, presumably because of factors related to underreporting and inadequate ascertainment by medical professionals of whether or not they had experienced postmenopausal bleeding.² Additionally, when postmenopausal bleeding was reported by these women, they were less likely to receive the appropriate diagnostic work-up as described by American College of Obstetricians and Gynecologists guidelines, and their bleeding was more likely to be ascribed to nonmalignant pathologies. Her work raises the important question about how black women view the health care profession and their willingness to engage early in good faith that their concerns will be met. These concerns are understandable given the documented different responsiveness of providers to black patients’ symptoms such as pain.³

Once diagnosed with endometrial cancer, black women are less likely to receive comprehensive surgical staging and less likely to have their surgery performed by a minimally invasive route, both of which are considered the standard of care.^1,4 Lower rates of minimally invasive surgery expose black women to increased morbidity and are deleterious to quality of life, return to work, and functionality. If surgical staging is omitted, which is more common for these women, clinicians are less able to appropriately prescribe adjuvant therapies which might prevent lethal recurrences from unrecognized advanced cancer or they may overtreat early-stage cancers with adjuvant therapy to make up for gaps in staging information.^1,5 However, adjuvant therapy is not a benign intervention, and itself is associated with morbidity.

As mentioned earlier, black women are at a higher risk for developing more aggressive cancer subtypes, and this phenomenon may appear unmodifiable. However, important research is looking at the concept of epigenetics and how modifiable environmental factors may contribute to the development of more aggressive types of cancer through gene expression. Additionally, differences in the gene mutations and gene expression of cancers more frequently acquired by black women may negatively influence how these cancers respond to conventional therapies. In the GOG210 study, which evaluated the outcomes of women with comprehensively staged endometrial cancer, black women demonstrated worse survival from cancer, even though they were more likely to receive chemotherapy.⁵ One explanation for this finding is that these women’s cancers were less responsive to conventional chemotherapy agents.

This raises a critical issue of disparity in clinical trial inclusion. Black women are underrepresented in clinical trials in the United States. There is a dark history in medical research and minority populations, particularly African American populations, which continues to be remembered and felt. However, not all of this underrepresentation may be from unwillingness to participate: For black women, issues of lack of access to or being considered for clinical trials is also a factor. But without adequate representation in trials of novel agents, we will not know whether they are effective for all populations, and indeed it would appear that we should not assume they are equally effective based on the results to date.

So how can we all individually help to overcome these disparities in endometrial cancer outcomes? To begin with, it is important to acknowledge that black women commonly report negative experiences with reproductive health care. From early in their lives, we must sensitively engage all of our patients and ensure they all feel heard and valued. They should know that their symptoms, including pain or bleeding, are taken and treated seriously. If we can do better with this throughout a woman’s earlier reproductive health care experiences, perhaps later in her life, when she experiences postmenopausal bleeding, she will feel comfortable raising this issue with her health care provider who in turn must take this symptom seriously and expeditiously engage all of the appropriate diagnostic resources. Health care delivery is about more than simply offering the best treatment. We also are responsible for education and shared decision making to ensure that we can deliver the best treatment.

We also can support organizations such as ECANA (Endometrial Cancer Action Network for African Americans) which serves to inform black women in their communities about the threat that endometrial cancer plays and empowers them through education about its symptoms and the need to seek care.

Systematically we must ensure black women have access to the same standards in surgical and nonsurgical management of these cancers. This includes referral of all women with cancer, including minorities, to high-volume centers with oncology specialists and explaining to those who may be reluctant to travel that this is associated with improved outcomes in the short and long term. We also must actively consider our black patients for clinical trials, sensitively educate them about their benefits, and overcome barriers to access. One simple way to do this is to explain that the treatments that we have developed for endometrial cancer have mostly been tested on white women, which may explain in part why they do not work so well for nonwhite women.

The racial disparity in endometrial cancer outcomes cannot entirely be attributed to the passive phenomenon of patient and tumor genetics, particularly with consideration that race is a social construct rather than a biological phenomenon. We can all make a difference through advocacy, access, education, and heightened awareness to combat this inequity and overcome these disparate outcomes.
 

Dr. Rossi is assistant professor in the division of gynecologic oncology at the University of North Carolina at Chapel Hill. She said she had no relevant financial disclosures. Email her at obnews@mdedge.com.

References

1. Gynecol Oncol. 2016 Oct;143(1):98-104.

2. Am J Obstet Gynecol. 2018 Dec;219(6):593.e1-14.

3. J Clin Oncol. 2012 Jun 1;30(16):1980-8.

4. Obstet Gynecol. 2016 Sep;128(3):526-34.

5. Am J Obstet Gynecol. 2018 Nov;219(5):459.e1-11.

Despite guidelines recommending low-dose oral glucocorticoids over high-dose intravenous (IV) glucocorticoids for inpatient management of acute exacerbations of chronic obstructive pulmonary disease (COPD), we have observed that most patients still receive high-dose IV therapy before being transitioned to low-dose oral therapy at discharge. Clinical inertia undoubtedly plays a significant role in the slow adoption of new recommendations, but in this era of evidence-based practice, the unfortunate lack of data supporting low over high steroid doses for acute exacerbations of COPD also contributes to hesitancy of physicians.

A SIGNIFICANT AND GROWING BURDEN

COPD is one of the most common pulmonary conditions managed by hospitalists today, and by the year 2030, it is predicted to become the third leading cause of death worldwide.¹

COPD is also a significant economic burden, costing $50 billion to manage in the United States, most of that from the cost of lengthy hospital stays.² COPD patients have 1 to 2 exacerbations per year.³ Bacterial and viral infections are responsible for most exacerbations, and 15% to 20% are from air pollution and other environmental causes of airway inflammation.³

CHALLENGES TO CHANGING PRACTICE

Glucocorticoids are the gold standard for treatment of acute exacerbations of COPD. It is well-documented that compared with placebo, glucocorticoids reduce mortality risk, length of hospital stay, and exacerbation recurrence after 1 month.⁴ And while high-dose IV steroid therapy has been the standard approach, oral administration has been found to be noninferior to IV administration with regard to treatment and length of hospital stay.⁵

While adverse effects are more common at higher doses, the optimal dose and duration of systemic glucocorticoid therapy for acute exacerbations of COPD are still largely at the discretion of the physician. The 2019 report of the Global Initiative for Chronic Obstructive Lung Disease (GOLD) recommends low doses (40 mg) for no more than 5 to 7 days for exacerbations, based on reports that showed no worse outcomes with low-dose oral than with high-dose IV therapy.^6,7 (In the 2010 study by Lindenauer et al,⁷ 92% of nearly 80,000 patients received high-dose IV steroids, reflecting standard practice at that time.) However, the GOLD guidelines do not address mortality rates, length of stay, or readmission rates for either approach, as they are devised to direct treatment in patients with stable mild to advanced COPD, not exacerbations.

 

 

THE EVIDENCE FOR LOW-DOSE STEROIDS

Mortality rates

Aksoy et al⁸ established that, compared with placebo, low-dose steroids improved mortality rates in a subset of patients with acute exacerbations, specifically those with eosinophilic exacerbations. This study followed the 2013 Reduction in the Use of Corticosteroids in Exacerbated COPD (REDUCE) trial, which showed mortality rates were not lower with 14 days of low-dose prednisone treatment than with 5 days.9

Length of hospital stay

With regard to length of hospital stay, in 2011 Wang et al¹⁰ found no statistically significant difference between high- and low-dose steroid treatment.However, the REDUCE trial found that low-dose steroids shortened the median length of stay by 1 day compared with placebo.⁹

Hospital readmission rates

The REDUCE trial found no statistically significant difference in readmission rates when comparing 5 days of low-dose treatment vs 14 days.⁹ However, Aksoy et al⁸ found that readmission rates were significantly lower with low-dose treatment than with placebo.No study has yet examined readmission rates with high-dose vs low-dose steroid treatment.

What does the evidence tell us?

Low-dose oral glucocorticoid treatment shows definitive benefits in terms of lower mortality rates, shorter hospital length of stay, and lower readmission rates vs placebo in the treatment of acute exacerbations of COPD. Furthermore, a 14-day course is no better than 5 days in terms of mortality rates. And low-dose glucocorticoid treatment shows reduced mortality rates in addition to similar hospital length of stay when compared to high-dose glucocorticoid treatment.

Together, these findings lend credibility to the current GOLD recommendations. However, we have observed that in sharp contrast to the leading clinical guidelines, most patients hospitalized for acute exacerbations of COPD are still treated initially with high-dose IV corticosteroids. Why?

Obstacles that perpetuate the use of high-dose over low-dose treatment include lack of knowledge of glucocorticoid pharmacokinetics among clinicians, use of outdated order sets, and the reflex notion that more of a drug is more efficacious in its desired effect. In addition, administrative obstacles include using high-dose IV steroids to justify an inpatient stay or continued hospitalization.

COUNTERING THE OBSTACLES: THE HOSPITALIST’S ROLE

To counter these obstacles, we propose standardization of inpatient treatment of acute exacerbations of COPD to include initial low-dose steroid treatment in accordance with the most recent GOLD guidelines.⁶ This would benefit the patient by reducing undesirable effects of high-dose steroids, and at the same time reduce the economic burden of managing COPD exacerbations. Considering the large number of hospitalizations for COPD exacerbation each year, hospitalists can play a large role in this effort by routinely incorporating the low-dose steroid recommendation into their clinical practice.

Despite guidelines recommending low-dose oral glucocorticoids over high-dose intravenous (IV) glucocorticoids for inpatient management of acute exacerbations of chronic obstructive pulmonary disease (COPD), we have observed that most patients still receive high-dose IV therapy before being transitioned to low-dose oral therapy at discharge. Clinical inertia undoubtedly plays a significant role in the slow adoption of new recommendations, but in this era of evidence-based practice, the unfortunate lack of data supporting low over high steroid doses for acute exacerbations of COPD also contributes to hesitancy of physicians.

A SIGNIFICANT AND GROWING BURDEN

COPD is one of the most common pulmonary conditions managed by hospitalists today, and by the year 2030, it is predicted to become the third leading cause of death worldwide.¹

COPD is also a significant economic burden, costing $50 billion to manage in the United States, most of that from the cost of lengthy hospital stays.² COPD patients have 1 to 2 exacerbations per year.³ Bacterial and viral infections are responsible for most exacerbations, and 15% to 20% are from air pollution and other environmental causes of airway inflammation.³

CHALLENGES TO CHANGING PRACTICE

Glucocorticoids are the gold standard for treatment of acute exacerbations of COPD. It is well-documented that compared with placebo, glucocorticoids reduce mortality risk, length of hospital stay, and exacerbation recurrence after 1 month.⁴ And while high-dose IV steroid therapy has been the standard approach, oral administration has been found to be noninferior to IV administration with regard to treatment and length of hospital stay.⁵

While adverse effects are more common at higher doses, the optimal dose and duration of systemic glucocorticoid therapy for acute exacerbations of COPD are still largely at the discretion of the physician. The 2019 report of the Global Initiative for Chronic Obstructive Lung Disease (GOLD) recommends low doses (40 mg) for no more than 5 to 7 days for exacerbations, based on reports that showed no worse outcomes with low-dose oral than with high-dose IV therapy.^6,7 (In the 2010 study by Lindenauer et al,⁷ 92% of nearly 80,000 patients received high-dose IV steroids, reflecting standard practice at that time.) However, the GOLD guidelines do not address mortality rates, length of stay, or readmission rates for either approach, as they are devised to direct treatment in patients with stable mild to advanced COPD, not exacerbations.

 

 

THE EVIDENCE FOR LOW-DOSE STEROIDS

Mortality rates

Aksoy et al⁸ established that, compared with placebo, low-dose steroids improved mortality rates in a subset of patients with acute exacerbations, specifically those with eosinophilic exacerbations. This study followed the 2013 Reduction in the Use of Corticosteroids in Exacerbated COPD (REDUCE) trial, which showed mortality rates were not lower with 14 days of low-dose prednisone treatment than with 5 days.9

Length of hospital stay

With regard to length of hospital stay, in 2011 Wang et al¹⁰ found no statistically significant difference between high- and low-dose steroid treatment.However, the REDUCE trial found that low-dose steroids shortened the median length of stay by 1 day compared with placebo.⁹

Hospital readmission rates

The REDUCE trial found no statistically significant difference in readmission rates when comparing 5 days of low-dose treatment vs 14 days.⁹ However, Aksoy et al⁸ found that readmission rates were significantly lower with low-dose treatment than with placebo.No study has yet examined readmission rates with high-dose vs low-dose steroid treatment.

What does the evidence tell us?

Low-dose oral glucocorticoid treatment shows definitive benefits in terms of lower mortality rates, shorter hospital length of stay, and lower readmission rates vs placebo in the treatment of acute exacerbations of COPD. Furthermore, a 14-day course is no better than 5 days in terms of mortality rates. And low-dose glucocorticoid treatment shows reduced mortality rates in addition to similar hospital length of stay when compared to high-dose glucocorticoid treatment.

Together, these findings lend credibility to the current GOLD recommendations. However, we have observed that in sharp contrast to the leading clinical guidelines, most patients hospitalized for acute exacerbations of COPD are still treated initially with high-dose IV corticosteroids. Why?

Obstacles that perpetuate the use of high-dose over low-dose treatment include lack of knowledge of glucocorticoid pharmacokinetics among clinicians, use of outdated order sets, and the reflex notion that more of a drug is more efficacious in its desired effect. In addition, administrative obstacles include using high-dose IV steroids to justify an inpatient stay or continued hospitalization.

COUNTERING THE OBSTACLES: THE HOSPITALIST’S ROLE

To counter these obstacles, we propose standardization of inpatient treatment of acute exacerbations of COPD to include initial low-dose steroid treatment in accordance with the most recent GOLD guidelines.⁶ This would benefit the patient by reducing undesirable effects of high-dose steroids, and at the same time reduce the economic burden of managing COPD exacerbations. Considering the large number of hospitalizations for COPD exacerbation each year, hospitalists can play a large role in this effort by routinely incorporating the low-dose steroid recommendation into their clinical practice.

Despite guidelines recommending low-dose oral glucocorticoids over high-dose intravenous (IV) glucocorticoids for inpatient management of acute exacerbations of chronic obstructive pulmonary disease (COPD), we have observed that most patients still receive high-dose IV therapy before being transitioned to low-dose oral therapy at discharge. Clinical inertia undoubtedly plays a significant role in the slow adoption of new recommendations, but in this era of evidence-based practice, the unfortunate lack of data supporting low over high steroid doses for acute exacerbations of COPD also contributes to hesitancy of physicians.

A SIGNIFICANT AND GROWING BURDEN

COPD is one of the most common pulmonary conditions managed by hospitalists today, and by the year 2030, it is predicted to become the third leading cause of death worldwide.¹

COPD is also a significant economic burden, costing $50 billion to manage in the United States, most of that from the cost of lengthy hospital stays.² COPD patients have 1 to 2 exacerbations per year.³ Bacterial and viral infections are responsible for most exacerbations, and 15% to 20% are from air pollution and other environmental causes of airway inflammation.³

CHALLENGES TO CHANGING PRACTICE

Glucocorticoids are the gold standard for treatment of acute exacerbations of COPD. It is well-documented that compared with placebo, glucocorticoids reduce mortality risk, length of hospital stay, and exacerbation recurrence after 1 month.⁴ And while high-dose IV steroid therapy has been the standard approach, oral administration has been found to be noninferior to IV administration with regard to treatment and length of hospital stay.⁵

While adverse effects are more common at higher doses, the optimal dose and duration of systemic glucocorticoid therapy for acute exacerbations of COPD are still largely at the discretion of the physician. The 2019 report of the Global Initiative for Chronic Obstructive Lung Disease (GOLD) recommends low doses (40 mg) for no more than 5 to 7 days for exacerbations, based on reports that showed no worse outcomes with low-dose oral than with high-dose IV therapy.^6,7 (In the 2010 study by Lindenauer et al,⁷ 92% of nearly 80,000 patients received high-dose IV steroids, reflecting standard practice at that time.) However, the GOLD guidelines do not address mortality rates, length of stay, or readmission rates for either approach, as they are devised to direct treatment in patients with stable mild to advanced COPD, not exacerbations.

 

 

THE EVIDENCE FOR LOW-DOSE STEROIDS

Mortality rates

Aksoy et al⁸ established that, compared with placebo, low-dose steroids improved mortality rates in a subset of patients with acute exacerbations, specifically those with eosinophilic exacerbations. This study followed the 2013 Reduction in the Use of Corticosteroids in Exacerbated COPD (REDUCE) trial, which showed mortality rates were not lower with 14 days of low-dose prednisone treatment than with 5 days.9

Length of hospital stay

With regard to length of hospital stay, in 2011 Wang et al¹⁰ found no statistically significant difference between high- and low-dose steroid treatment.However, the REDUCE trial found that low-dose steroids shortened the median length of stay by 1 day compared with placebo.⁹

Hospital readmission rates

The REDUCE trial found no statistically significant difference in readmission rates when comparing 5 days of low-dose treatment vs 14 days.⁹ However, Aksoy et al⁸ found that readmission rates were significantly lower with low-dose treatment than with placebo.No study has yet examined readmission rates with high-dose vs low-dose steroid treatment.

What does the evidence tell us?

Low-dose oral glucocorticoid treatment shows definitive benefits in terms of lower mortality rates, shorter hospital length of stay, and lower readmission rates vs placebo in the treatment of acute exacerbations of COPD. Furthermore, a 14-day course is no better than 5 days in terms of mortality rates. And low-dose glucocorticoid treatment shows reduced mortality rates in addition to similar hospital length of stay when compared to high-dose glucocorticoid treatment.

Together, these findings lend credibility to the current GOLD recommendations. However, we have observed that in sharp contrast to the leading clinical guidelines, most patients hospitalized for acute exacerbations of COPD are still treated initially with high-dose IV corticosteroids. Why?

Obstacles that perpetuate the use of high-dose over low-dose treatment include lack of knowledge of glucocorticoid pharmacokinetics among clinicians, use of outdated order sets, and the reflex notion that more of a drug is more efficacious in its desired effect. In addition, administrative obstacles include using high-dose IV steroids to justify an inpatient stay or continued hospitalization.

COUNTERING THE OBSTACLES: THE HOSPITALIST’S ROLE

To counter these obstacles, we propose standardization of inpatient treatment of acute exacerbations of COPD to include initial low-dose steroid treatment in accordance with the most recent GOLD guidelines.⁶ This would benefit the patient by reducing undesirable effects of high-dose steroids, and at the same time reduce the economic burden of managing COPD exacerbations. Considering the large number of hospitalizations for COPD exacerbation each year, hospitalists can play a large role in this effort by routinely incorporating the low-dose steroid recommendation into their clinical practice.

One of our lead articles stems from the annual Partners in Value meeting, which was developed by the AGA in partnership with the Digestive Health Physicians Association (Chicago, Oct. 4, 2019). This is an annual meeting about innovations and “what’s next” for GI practices. Anton Decker, MD, an expert in the business of GI and Chair of the Practice Management and Economics Committee, discussed “digital disruption.”

When we discuss digital innovations in health care, most think of telehealth, social media, self-care apps, and remote patient monitoring. As a health system executive, my viewpoint about digital technology has been expanded by other critical needs. At the University of Michigan, we are space constrained (land locked without sufficient parking) and are living with shrinking clinical margins. We see digital technology as a solution to both. As we consolidate our call centers from 27 sites to 1, we plan for 30% of our staff to work from home. Setting up a home work station costs $3,000, compared with office space costs (about $5,000/year). A new clinical site might cost $20 million to build, but that is a fraction of the true life-cycle cost of the building. We have a widely distributed patient base (imagine traveling from Michigan’s Upper Penisula to Ann Arbor for a 20-minute clinic visit).

Many people appreciate “seeing” their doctor from the comfort of their living room. We plan to convert at least 15% of patient visits to telehealth over the next few years although reimbursement rules are still limiting. This year, more than 80% of postsurgical visits (90-day bundled payment) were conducted virtually – mostly by NPs or PAs. Our GI psychologist converted 1,500 patient visit hours to virtual visits last year. In 2019, we completed over 4,000 evisits (management of simple conditions initiated by a patient – essential during flu season) and an increasing number of econsults (primary consultations to specialists). Project ECHO (N Engl J Med. 2011;364:2199) remains the star example of how digital health can improve access, especially for underserved communities.

Virtual care, telehealth, remote patient monitoring, telecommuting and other digital innovations are becoming standards for health systems. Now is the time to think of “face-to-face” visits as option B.
 

John I. Allen, MD, MBD, AGAF
Editor in Chief

One of our lead articles stems from the annual Partners in Value meeting, which was developed by the AGA in partnership with the Digestive Health Physicians Association (Chicago, Oct. 4, 2019). This is an annual meeting about innovations and “what’s next” for GI practices. Anton Decker, MD, an expert in the business of GI and Chair of the Practice Management and Economics Committee, discussed “digital disruption.”

When we discuss digital innovations in health care, most think of telehealth, social media, self-care apps, and remote patient monitoring. As a health system executive, my viewpoint about digital technology has been expanded by other critical needs. At the University of Michigan, we are space constrained (land locked without sufficient parking) and are living with shrinking clinical margins. We see digital technology as a solution to both. As we consolidate our call centers from 27 sites to 1, we plan for 30% of our staff to work from home. Setting up a home work station costs $3,000, compared with office space costs (about $5,000/year). A new clinical site might cost $20 million to build, but that is a fraction of the true life-cycle cost of the building. We have a widely distributed patient base (imagine traveling from Michigan’s Upper Penisula to Ann Arbor for a 20-minute clinic visit).

Many people appreciate “seeing” their doctor from the comfort of their living room. We plan to convert at least 15% of patient visits to telehealth over the next few years although reimbursement rules are still limiting. This year, more than 80% of postsurgical visits (90-day bundled payment) were conducted virtually – mostly by NPs or PAs. Our GI psychologist converted 1,500 patient visit hours to virtual visits last year. In 2019, we completed over 4,000 evisits (management of simple conditions initiated by a patient – essential during flu season) and an increasing number of econsults (primary consultations to specialists). Project ECHO (N Engl J Med. 2011;364:2199) remains the star example of how digital health can improve access, especially for underserved communities.

Virtual care, telehealth, remote patient monitoring, telecommuting and other digital innovations are becoming standards for health systems. Now is the time to think of “face-to-face” visits as option B.
 

John I. Allen, MD, MBD, AGAF
Editor in Chief

One of our lead articles stems from the annual Partners in Value meeting, which was developed by the AGA in partnership with the Digestive Health Physicians Association (Chicago, Oct. 4, 2019). This is an annual meeting about innovations and “what’s next” for GI practices. Anton Decker, MD, an expert in the business of GI and Chair of the Practice Management and Economics Committee, discussed “digital disruption.”

When we discuss digital innovations in health care, most think of telehealth, social media, self-care apps, and remote patient monitoring. As a health system executive, my viewpoint about digital technology has been expanded by other critical needs. At the University of Michigan, we are space constrained (land locked without sufficient parking) and are living with shrinking clinical margins. We see digital technology as a solution to both. As we consolidate our call centers from 27 sites to 1, we plan for 30% of our staff to work from home. Setting up a home work station costs $3,000, compared with office space costs (about $5,000/year). A new clinical site might cost $20 million to build, but that is a fraction of the true life-cycle cost of the building. We have a widely distributed patient base (imagine traveling from Michigan’s Upper Penisula to Ann Arbor for a 20-minute clinic visit).

Many people appreciate “seeing” their doctor from the comfort of their living room. We plan to convert at least 15% of patient visits to telehealth over the next few years although reimbursement rules are still limiting. This year, more than 80% of postsurgical visits (90-day bundled payment) were conducted virtually – mostly by NPs or PAs. Our GI psychologist converted 1,500 patient visit hours to virtual visits last year. In 2019, we completed over 4,000 evisits (management of simple conditions initiated by a patient – essential during flu season) and an increasing number of econsults (primary consultations to specialists). Project ECHO (N Engl J Med. 2011;364:2199) remains the star example of how digital health can improve access, especially for underserved communities.

Virtual care, telehealth, remote patient monitoring, telecommuting and other digital innovations are becoming standards for health systems. Now is the time to think of “face-to-face” visits as option B.
 

John I. Allen, MD, MBD, AGAF
Editor in Chief

Recent advances in neuroscience and genetics are providing a new view of brain function in health and disease.¹ As discussed in Drs. Hripsime Kalanderian and Henry Nasrallah’s article “Artificial intelligence in psychiatry” (Evidence-Based Reviews, Current Psychiatry. August 2019, p. 33-38), machine learning technologies are capable of analyzing vast amounts of personal and biologic data for diagnosing and treating mental disorders.

In a 2016 article, Dr. Arshya Vahabzadeh² wrote, “In the near term, humans will continue to make the majority of psychiatric diagnoses and provide treatment.” He predicted that data science—specifically machine learning—will help revolutionize how we diagnose, treat, and monitor depression. He foresees a future where AI machines or learning machines will more accurately diagnose and treat depression.

These predictions remind us of the promises made with the introduction of psychoactive drugs to the practice of psychiatry. In the 1970s, the increased emphasis on neurotransmitters led to new biologic models of mental illness and the expansion of the Diagnostic and Statistical Manual of Mental Disorders. The increased use of psychoactive medications relegated the practice of psychotherapy to other mental health professionals. Psychiatry became a “drug-intensive” specialty, and psychiatrists saw themselves as psychopharmacologists.³ During this time, psychiatry became progressively dominated by the pharmaceutical industry. The deregulation of the markets and the for-profit ideology of the pharmaceutical industry resulted in an economically and mutually beneficial alliance between pharmaceutical companies, academic faculty, and individual psychiatrists.

Using the same for-profit ideology and ethics of the pharmaceutical industry, technology-based corporations are making massive investments in the application of these technologies in neuroscience research and clinical practice. The “promise” that AI will diagnose and treat depression more accurately than clinicians will again radically change the psychiatrist’s role. Most of a psychiatrist’s clinical work eventually will be replicated by machine learning and technicians. The human-to-human encounter that is at core of the profession will be replaced by the machine-to-human encounter.⁴

From the social economic perspective, the American health care system is designed to increase profit and maximize the earnings of the industries.⁵ Unless social policy changes, expensive new technologies will increase the cost and limit accessibility to health care, benefiting the few at the expense of the majority of people. These technologies will produce a robust return on investment, but the wealth they create will benefit fewer and fewer people.

Several writers have called attention to the social, economic, and ethical consequences of these advances and recommended that the academics and technologists who support AI and machine learning in medicine must “receive sufficient training in ethics” and gain exposure to social and economic issues.⁶ Darcy et al⁷ warns of the risks of introducing these advanced technologies in medicine: “As machine learning enters the state-of-the-art clinical practice, medicine thus has the immense obligation to ensure that this technology is harnessed for societal and individual good, fulfilling the ethical basis of the profession.… Ethical design thinking is essential at every stage of development and application of machine learning in advancing health. Toward this aim, physicians with integrity and sophistication should partner closely with computer and data scientists to reimagine clinical medicine and to anticipate its ethical implications. It is important to systematically validate data from mobile health and consumer-facing technologies, particularly for cases in which dynamic intervention is provided.”

Marco T. Carpio, MD
Psychiatrist, Private Practice
Lynbrook, New York

Disclosure: The author reports no financial relationships with any companies whose products are mentioned in this article, or with manufacturers of competing products.

Recent advances in neuroscience and genetics are providing a new view of brain function in health and disease.¹ As discussed in Drs. Hripsime Kalanderian and Henry Nasrallah’s article “Artificial intelligence in psychiatry” (Evidence-Based Reviews, Current Psychiatry. August 2019, p. 33-38), machine learning technologies are capable of analyzing vast amounts of personal and biologic data for diagnosing and treating mental disorders.

In a 2016 article, Dr. Arshya Vahabzadeh² wrote, “In the near term, humans will continue to make the majority of psychiatric diagnoses and provide treatment.” He predicted that data science—specifically machine learning—will help revolutionize how we diagnose, treat, and monitor depression. He foresees a future where AI machines or learning machines will more accurately diagnose and treat depression.

These predictions remind us of the promises made with the introduction of psychoactive drugs to the practice of psychiatry. In the 1970s, the increased emphasis on neurotransmitters led to new biologic models of mental illness and the expansion of the Diagnostic and Statistical Manual of Mental Disorders. The increased use of psychoactive medications relegated the practice of psychotherapy to other mental health professionals. Psychiatry became a “drug-intensive” specialty, and psychiatrists saw themselves as psychopharmacologists.³ During this time, psychiatry became progressively dominated by the pharmaceutical industry. The deregulation of the markets and the for-profit ideology of the pharmaceutical industry resulted in an economically and mutually beneficial alliance between pharmaceutical companies, academic faculty, and individual psychiatrists.

Using the same for-profit ideology and ethics of the pharmaceutical industry, technology-based corporations are making massive investments in the application of these technologies in neuroscience research and clinical practice. The “promise” that AI will diagnose and treat depression more accurately than clinicians will again radically change the psychiatrist’s role. Most of a psychiatrist’s clinical work eventually will be replicated by machine learning and technicians. The human-to-human encounter that is at core of the profession will be replaced by the machine-to-human encounter.⁴

From the social economic perspective, the American health care system is designed to increase profit and maximize the earnings of the industries.⁵ Unless social policy changes, expensive new technologies will increase the cost and limit accessibility to health care, benefiting the few at the expense of the majority of people. These technologies will produce a robust return on investment, but the wealth they create will benefit fewer and fewer people.

Several writers have called attention to the social, economic, and ethical consequences of these advances and recommended that the academics and technologists who support AI and machine learning in medicine must “receive sufficient training in ethics” and gain exposure to social and economic issues.⁶ Darcy et al⁷ warns of the risks of introducing these advanced technologies in medicine: “As machine learning enters the state-of-the-art clinical practice, medicine thus has the immense obligation to ensure that this technology is harnessed for societal and individual good, fulfilling the ethical basis of the profession.… Ethical design thinking is essential at every stage of development and application of machine learning in advancing health. Toward this aim, physicians with integrity and sophistication should partner closely with computer and data scientists to reimagine clinical medicine and to anticipate its ethical implications. It is important to systematically validate data from mobile health and consumer-facing technologies, particularly for cases in which dynamic intervention is provided.”

Marco T. Carpio, MD
Psychiatrist, Private Practice
Lynbrook, New York

Disclosure: The author reports no financial relationships with any companies whose products are mentioned in this article, or with manufacturers of competing products.

Recent advances in neuroscience and genetics are providing a new view of brain function in health and disease.¹ As discussed in Drs. Hripsime Kalanderian and Henry Nasrallah’s article “Artificial intelligence in psychiatry” (Evidence-Based Reviews, Current Psychiatry. August 2019, p. 33-38), machine learning technologies are capable of analyzing vast amounts of personal and biologic data for diagnosing and treating mental disorders.

In a 2016 article, Dr. Arshya Vahabzadeh² wrote, “In the near term, humans will continue to make the majority of psychiatric diagnoses and provide treatment.” He predicted that data science—specifically machine learning—will help revolutionize how we diagnose, treat, and monitor depression. He foresees a future where AI machines or learning machines will more accurately diagnose and treat depression.

These predictions remind us of the promises made with the introduction of psychoactive drugs to the practice of psychiatry. In the 1970s, the increased emphasis on neurotransmitters led to new biologic models of mental illness and the expansion of the Diagnostic and Statistical Manual of Mental Disorders. The increased use of psychoactive medications relegated the practice of psychotherapy to other mental health professionals. Psychiatry became a “drug-intensive” specialty, and psychiatrists saw themselves as psychopharmacologists.³ During this time, psychiatry became progressively dominated by the pharmaceutical industry. The deregulation of the markets and the for-profit ideology of the pharmaceutical industry resulted in an economically and mutually beneficial alliance between pharmaceutical companies, academic faculty, and individual psychiatrists.

Using the same for-profit ideology and ethics of the pharmaceutical industry, technology-based corporations are making massive investments in the application of these technologies in neuroscience research and clinical practice. The “promise” that AI will diagnose and treat depression more accurately than clinicians will again radically change the psychiatrist’s role. Most of a psychiatrist’s clinical work eventually will be replicated by machine learning and technicians. The human-to-human encounter that is at core of the profession will be replaced by the machine-to-human encounter.⁴

From the social economic perspective, the American health care system is designed to increase profit and maximize the earnings of the industries.⁵ Unless social policy changes, expensive new technologies will increase the cost and limit accessibility to health care, benefiting the few at the expense of the majority of people. These technologies will produce a robust return on investment, but the wealth they create will benefit fewer and fewer people.

Several writers have called attention to the social, economic, and ethical consequences of these advances and recommended that the academics and technologists who support AI and machine learning in medicine must “receive sufficient training in ethics” and gain exposure to social and economic issues.⁶ Darcy et al⁷ warns of the risks of introducing these advanced technologies in medicine: “As machine learning enters the state-of-the-art clinical practice, medicine thus has the immense obligation to ensure that this technology is harnessed for societal and individual good, fulfilling the ethical basis of the profession.… Ethical design thinking is essential at every stage of development and application of machine learning in advancing health. Toward this aim, physicians with integrity and sophistication should partner closely with computer and data scientists to reimagine clinical medicine and to anticipate its ethical implications. It is important to systematically validate data from mobile health and consumer-facing technologies, particularly for cases in which dynamic intervention is provided.”

Marco T. Carpio, MD
Psychiatrist, Private Practice
Lynbrook, New York

Disclosure: The author reports no financial relationships with any companies whose products are mentioned in this article, or with manufacturers of competing products.

The quarterly report of the State Medical Board can be a sobering read. In addition to the usual updates about new regulations or requirements for licensed physicians, there is always the disciplinary actions “blacklist” of dozens of medical practitioners in all specialties whose licenses were revoked or suspended due to a shocking array of serious violations.

Those infractions range from Medicare billing fraud to prescribing narcotics to fictitious patients to engaging in sex with a patient to walking into the operating room drunk. It is truly disheartening to see dozens of physicians destroy their careers by committing a panoply of odious, repugnant, or illegal actions.

The term “anathema” comes to mind when I read about those miscreants. This Greek term is occasionally used in scholarly or religious publications, but rarely in everyday conversations or articles. Anathema refers to something detested, shunned, or denounced. When used by the clergy, it connotes something to condemn, such as a sinful or evil act.

Like all other medical specialists, we psychiatrists have a noble mission of treating and relieving the suffering of those afflicted with brain disorders that manifest as mood, thought, perceptual, behavioral, or cognitive abnormalities. Our main goal is to restore health, wellness, and quality of life to the millions of individuals who buckle under the weight of genetic redispersion, adverse environmental events, or both. So psychiatrists do a lot of “good,” which benefits all those who live with mental illness. However, psychiatric practice may have some pitfalls that occasionally lead to anathemas, no matter how diligently a practitioner tries to avoid them. The code of psychiatric ethics is a shield that can preempt anathemas from contaminating clinical practice, but human error will occur when the ethical compass fails.

Here are some examples of anathemas that may rear their ugly heads if a practitioner is not constantly on the alert. It is likely you, the readers of Current Psychiatry, may think of additional anathemas not listed below. If so, I encourage you to send them to me at henry.nasrallah@currentpsychiatry.com in the form of a brief Letter to the Editor, which may be considered for publication.

• Sexual contact with a patient. This major anathema must not occur under any circumstance. It will have grave professional consequences for the practitioner and serious emotional repercussions for the patient.
• Breach of confidentiality. This is a sacred rule in psychiatric practice that must not be broken under any circumstance. Breaching confidentiality will rupture the therapeutic bond and trust that a patient has with a psychiatrist (or psychiatric nurse practitioner).
• Causing physical or emotional harm. This anathema can have serious legal implications in addition to being an unacceptable professional violation.
• Failure to assess patients for suicidal or homicidal risk. The life of the patient, and others, may be at stake if this critical component is missing in the evaluation of psychiatric patients, even if they appear “stable.”
• Irrational and hazardous polypharmacy. This type of harm must never occur during medical management of psychiatric patients, and may have legal consequences.
• Not seeking collateral information. This may seem like a “minor” anathema, but it can have major repercussions if a gap of clinically important data about the patient leads to erroneous diagnosis or inappropriate treatment. Regrettably, informants are sometimes unavailable.
• Assessing patients from the neck up only. Psychiatrists are, first and foremost, physicians who must evaluate the entire medical status of the patient, not just his/her mind. There are numerous bidirectional effects between the body and the brain that can influence diagnosis, holistic treatment, medical outcomes, and prognosis.
• Treating patients with medication only, without any concomitant psychotherapy. Such a suboptimal practice is an anathema that is not excusable due to a “lack of time.” Every psychiatric patient deserves a biopsychosocial treatment approach.
• Not inquiring about adherence at every visit. It is impossible to assess the effectiveness of treatment if adherence is partial or poor. Patients must be constantly reminded that while their psychiatrists are committed to their care, full adherence is a vital responsibility for them to fulfill to ensure optimal outcome.
• Ignoring the patient’s cues, both verbal and nonverbal. Being rushed by a large workload, a full schedule, or the demands of electronic medical records that distract a psychiatrist from fully attending to what the patient’s words, facial expressions, or body language convey can lead to a failure to meet the patient’s needs. Even worse, it may lead to missing a serious message a patient is consciously or unconsciously trying to relay.
• Lowering expectations. Nothing is more devastating for patients than to feel that the psychiatrist does not believe he/she will ever achieve wellness, or that they are beyond help and will never improve, recover, or overcome disabling psychiatric illness. This will generate profound hopelessness in vulnerable patients, who crave having a normal life free from illness or disability.
• Using the same medication for all patients. This is an anathema because one size does not fit all, and patients deserve to have their psychiatrists customize their pharmacotherapy to match their medical status and tolerability. For example, the 11 FDA-approved second-generation antipsychotics are not all the same, and a psychiatrist must select the member of that class that is most likely to be a good match for each patient based on that patient’s medical history and the safety/tolerability profile of each antipsychotic.
• Not continuously upgrading one’s practice to incorporate new evidence-based findings of more effective therapeutic strategies. It is an anathema to continue practicing what was learned in residency 25 to 30 years ago when there’s new knowledge and many advances permeating psychiatric practice today.
• Using alcohol or recreational drugs during a shift in the clinic or the hospital. No explanation is needed for this anathema!
• Prescribing for patients without a full evaluation. That’s poor clinical practice, and also is illegal.
• Billing for patients who were never examined. That’s fraudulent, and stupid!

In an editorial I wrote last year intended for graduates of psychiatry residency training programs about the “DNA of psychiatric practice,” I described what comprises good psychiatric practice.¹ Anathemas can be regarded as “mutations” within the DNA of psychiatric practice. It is always my hope that none of the freshly minted psychiatrists going into practice will ever commit an anathema, and end up on the “list of shame” in their State Medical Board’s quarterly report….

The quarterly report of the State Medical Board can be a sobering read. In addition to the usual updates about new regulations or requirements for licensed physicians, there is always the disciplinary actions “blacklist” of dozens of medical practitioners in all specialties whose licenses were revoked or suspended due to a shocking array of serious violations.

Those infractions range from Medicare billing fraud to prescribing narcotics to fictitious patients to engaging in sex with a patient to walking into the operating room drunk. It is truly disheartening to see dozens of physicians destroy their careers by committing a panoply of odious, repugnant, or illegal actions.

The term “anathema” comes to mind when I read about those miscreants. This Greek term is occasionally used in scholarly or religious publications, but rarely in everyday conversations or articles. Anathema refers to something detested, shunned, or denounced. When used by the clergy, it connotes something to condemn, such as a sinful or evil act.

Like all other medical specialists, we psychiatrists have a noble mission of treating and relieving the suffering of those afflicted with brain disorders that manifest as mood, thought, perceptual, behavioral, or cognitive abnormalities. Our main goal is to restore health, wellness, and quality of life to the millions of individuals who buckle under the weight of genetic redispersion, adverse environmental events, or both. So psychiatrists do a lot of “good,” which benefits all those who live with mental illness. However, psychiatric practice may have some pitfalls that occasionally lead to anathemas, no matter how diligently a practitioner tries to avoid them. The code of psychiatric ethics is a shield that can preempt anathemas from contaminating clinical practice, but human error will occur when the ethical compass fails.

Here are some examples of anathemas that may rear their ugly heads if a practitioner is not constantly on the alert. It is likely you, the readers of Current Psychiatry, may think of additional anathemas not listed below. If so, I encourage you to send them to me at henry.nasrallah@currentpsychiatry.com in the form of a brief Letter to the Editor, which may be considered for publication.

• Sexual contact with a patient. This major anathema must not occur under any circumstance. It will have grave professional consequences for the practitioner and serious emotional repercussions for the patient.
• Breach of confidentiality. This is a sacred rule in psychiatric practice that must not be broken under any circumstance. Breaching confidentiality will rupture the therapeutic bond and trust that a patient has with a psychiatrist (or psychiatric nurse practitioner).
• Causing physical or emotional harm. This anathema can have serious legal implications in addition to being an unacceptable professional violation.
• Failure to assess patients for suicidal or homicidal risk. The life of the patient, and others, may be at stake if this critical component is missing in the evaluation of psychiatric patients, even if they appear “stable.”
• Irrational and hazardous polypharmacy. This type of harm must never occur during medical management of psychiatric patients, and may have legal consequences.
• Not seeking collateral information. This may seem like a “minor” anathema, but it can have major repercussions if a gap of clinically important data about the patient leads to erroneous diagnosis or inappropriate treatment. Regrettably, informants are sometimes unavailable.
• Assessing patients from the neck up only. Psychiatrists are, first and foremost, physicians who must evaluate the entire medical status of the patient, not just his/her mind. There are numerous bidirectional effects between the body and the brain that can influence diagnosis, holistic treatment, medical outcomes, and prognosis.
• Treating patients with medication only, without any concomitant psychotherapy. Such a suboptimal practice is an anathema that is not excusable due to a “lack of time.” Every psychiatric patient deserves a biopsychosocial treatment approach.
• Not inquiring about adherence at every visit. It is impossible to assess the effectiveness of treatment if adherence is partial or poor. Patients must be constantly reminded that while their psychiatrists are committed to their care, full adherence is a vital responsibility for them to fulfill to ensure optimal outcome.
• Ignoring the patient’s cues, both verbal and nonverbal. Being rushed by a large workload, a full schedule, or the demands of electronic medical records that distract a psychiatrist from fully attending to what the patient’s words, facial expressions, or body language convey can lead to a failure to meet the patient’s needs. Even worse, it may lead to missing a serious message a patient is consciously or unconsciously trying to relay.
• Lowering expectations. Nothing is more devastating for patients than to feel that the psychiatrist does not believe he/she will ever achieve wellness, or that they are beyond help and will never improve, recover, or overcome disabling psychiatric illness. This will generate profound hopelessness in vulnerable patients, who crave having a normal life free from illness or disability.
• Using the same medication for all patients. This is an anathema because one size does not fit all, and patients deserve to have their psychiatrists customize their pharmacotherapy to match their medical status and tolerability. For example, the 11 FDA-approved second-generation antipsychotics are not all the same, and a psychiatrist must select the member of that class that is most likely to be a good match for each patient based on that patient’s medical history and the safety/tolerability profile of each antipsychotic.
• Not continuously upgrading one’s practice to incorporate new evidence-based findings of more effective therapeutic strategies. It is an anathema to continue practicing what was learned in residency 25 to 30 years ago when there’s new knowledge and many advances permeating psychiatric practice today.
• Using alcohol or recreational drugs during a shift in the clinic or the hospital. No explanation is needed for this anathema!
• Prescribing for patients without a full evaluation. That’s poor clinical practice, and also is illegal.
• Billing for patients who were never examined. That’s fraudulent, and stupid!

In an editorial I wrote last year intended for graduates of psychiatry residency training programs about the “DNA of psychiatric practice,” I described what comprises good psychiatric practice.¹ Anathemas can be regarded as “mutations” within the DNA of psychiatric practice. It is always my hope that none of the freshly minted psychiatrists going into practice will ever commit an anathema, and end up on the “list of shame” in their State Medical Board’s quarterly report….

The quarterly report of the State Medical Board can be a sobering read. In addition to the usual updates about new regulations or requirements for licensed physicians, there is always the disciplinary actions “blacklist” of dozens of medical practitioners in all specialties whose licenses were revoked or suspended due to a shocking array of serious violations.

Those infractions range from Medicare billing fraud to prescribing narcotics to fictitious patients to engaging in sex with a patient to walking into the operating room drunk. It is truly disheartening to see dozens of physicians destroy their careers by committing a panoply of odious, repugnant, or illegal actions.

The term “anathema” comes to mind when I read about those miscreants. This Greek term is occasionally used in scholarly or religious publications, but rarely in everyday conversations or articles. Anathema refers to something detested, shunned, or denounced. When used by the clergy, it connotes something to condemn, such as a sinful or evil act.

Like all other medical specialists, we psychiatrists have a noble mission of treating and relieving the suffering of those afflicted with brain disorders that manifest as mood, thought, perceptual, behavioral, or cognitive abnormalities. Our main goal is to restore health, wellness, and quality of life to the millions of individuals who buckle under the weight of genetic redispersion, adverse environmental events, or both. So psychiatrists do a lot of “good,” which benefits all those who live with mental illness. However, psychiatric practice may have some pitfalls that occasionally lead to anathemas, no matter how diligently a practitioner tries to avoid them. The code of psychiatric ethics is a shield that can preempt anathemas from contaminating clinical practice, but human error will occur when the ethical compass fails.

Here are some examples of anathemas that may rear their ugly heads if a practitioner is not constantly on the alert. It is likely you, the readers of Current Psychiatry, may think of additional anathemas not listed below. If so, I encourage you to send them to me at henry.nasrallah@currentpsychiatry.com in the form of a brief Letter to the Editor, which may be considered for publication.

• Sexual contact with a patient. This major anathema must not occur under any circumstance. It will have grave professional consequences for the practitioner and serious emotional repercussions for the patient.
• Breach of confidentiality. This is a sacred rule in psychiatric practice that must not be broken under any circumstance. Breaching confidentiality will rupture the therapeutic bond and trust that a patient has with a psychiatrist (or psychiatric nurse practitioner).
• Causing physical or emotional harm. This anathema can have serious legal implications in addition to being an unacceptable professional violation.
• Failure to assess patients for suicidal or homicidal risk. The life of the patient, and others, may be at stake if this critical component is missing in the evaluation of psychiatric patients, even if they appear “stable.”
• Irrational and hazardous polypharmacy. This type of harm must never occur during medical management of psychiatric patients, and may have legal consequences.
• Not seeking collateral information. This may seem like a “minor” anathema, but it can have major repercussions if a gap of clinically important data about the patient leads to erroneous diagnosis or inappropriate treatment. Regrettably, informants are sometimes unavailable.
• Assessing patients from the neck up only. Psychiatrists are, first and foremost, physicians who must evaluate the entire medical status of the patient, not just his/her mind. There are numerous bidirectional effects between the body and the brain that can influence diagnosis, holistic treatment, medical outcomes, and prognosis.
• Treating patients with medication only, without any concomitant psychotherapy. Such a suboptimal practice is an anathema that is not excusable due to a “lack of time.” Every psychiatric patient deserves a biopsychosocial treatment approach.
• Not inquiring about adherence at every visit. It is impossible to assess the effectiveness of treatment if adherence is partial or poor. Patients must be constantly reminded that while their psychiatrists are committed to their care, full adherence is a vital responsibility for them to fulfill to ensure optimal outcome.
• Ignoring the patient’s cues, both verbal and nonverbal. Being rushed by a large workload, a full schedule, or the demands of electronic medical records that distract a psychiatrist from fully attending to what the patient’s words, facial expressions, or body language convey can lead to a failure to meet the patient’s needs. Even worse, it may lead to missing a serious message a patient is consciously or unconsciously trying to relay.
• Lowering expectations. Nothing is more devastating for patients than to feel that the psychiatrist does not believe he/she will ever achieve wellness, or that they are beyond help and will never improve, recover, or overcome disabling psychiatric illness. This will generate profound hopelessness in vulnerable patients, who crave having a normal life free from illness or disability.
• Using the same medication for all patients. This is an anathema because one size does not fit all, and patients deserve to have their psychiatrists customize their pharmacotherapy to match their medical status and tolerability. For example, the 11 FDA-approved second-generation antipsychotics are not all the same, and a psychiatrist must select the member of that class that is most likely to be a good match for each patient based on that patient’s medical history and the safety/tolerability profile of each antipsychotic.
• Not continuously upgrading one’s practice to incorporate new evidence-based findings of more effective therapeutic strategies. It is an anathema to continue practicing what was learned in residency 25 to 30 years ago when there’s new knowledge and many advances permeating psychiatric practice today.
• Using alcohol or recreational drugs during a shift in the clinic or the hospital. No explanation is needed for this anathema!
• Prescribing for patients without a full evaluation. That’s poor clinical practice, and also is illegal.
• Billing for patients who were never examined. That’s fraudulent, and stupid!

In an editorial I wrote last year intended for graduates of psychiatry residency training programs about the “DNA of psychiatric practice,” I described what comprises good psychiatric practice.¹ Anathemas can be regarded as “mutations” within the DNA of psychiatric practice. It is always my hope that none of the freshly minted psychiatrists going into practice will ever commit an anathema, and end up on the “list of shame” in their State Medical Board’s quarterly report….

In our experience, most psychiatrists are uncomfortable with prescribing a medication when they feel that doing so would be outside their scope of practice. But there are many situations when prescribing a nonpsychotropic medication would be the correct choice. In this article, we discuss the scope of psychiatric practice, and present 4 case studies that illustrate situations in which psychiatrists should feel comfortable prescribing nonpsychotropic medications.

Defining the scope of practice

What is the scope of a psychiatrist’s practice? Scope of practice usually describes activities that a health care practitioner is allowed to undertake as defined by the terms of his/her license. A license to practice medicine does not include any stipulation restricting practice to a specific medical specialty. However, a local entity may delineate scope of practice within its organization. For instance, local practice standards held by the Detroit Wayne Mental Health Authority (DWMHA) state “Psychiatrists…shall not exceed their scope of practice as per DWMHA credentialing and privileging. For example, a Psychiatrist…who [has] not been appropriately privileged to deliver services to children shall not treat children, excepting crisis situations.”¹

Like physicians in other specialties, psychiatrists are not limited to prescribing only a subset of medications commonly associated with their specialty. But for many psychiatrists, prescribing nonpsychotropic medications is complicated by individual and local factors. On one hand, some psychiatrists do not feel it is their role to prescribe nonpsychotropic medications,² or even some psychotropic medications that may be more complex to prescribe, such as lithium, clozapine, or monoamine oxidase inhibitors.^3-5 However, many feel comfortable prescribing complex combinations of psychotropic medications, or prescribing in a way that does not necessarily make sense (eg, prescribing benztropine as prophylaxis for dystonia when starting an antipsychotic).

Reviewing an average day at one urban psychiatric clinic, these questions seem to come up in half of the patient population, especially in patients with chronic mental illness, multiple medical comorbidities, and limited access to health care. When a young patient walks in without an appointment with an acute dystonic reaction secondary to the initiation of antipsychotics a couple of days ago, there is no hesitation to swiftly and appropriately prescribe an IM anticholinergic medication. But why are psychiatrists often hesitant to prescribe nonpsychotropic medications to treat other adverse effects of medications? Lack of knowledge? Lack of training?

Psychiatrists who practice in hospital systems often have immediate access to consultants, and this availability may encourage them to defer to the consultant for treatment of certain adverse effects. We have seen psychiatrists consult Neurology regarding the prescription of donepezil for mild neurocognitive disorder due to Alzheimer’s disease, or Endocrinology regarding prescription of levothyroxine for lithium-induced hypothyroidism.

However, there are numerous scenarios in which psychiatrists should feel comfortable prescribing nonpsychotropic medications or managing medication adverse effects, regardless of whether they consider it to be within or outside their scope of practice. The following case examples illustrate several such situations.

CASE 1

Ms. W, age 30, has been diagnosed with schizophrenia. She requests a refill of quetiapine, 800 mg/d. This medication has been clearly beneficial in alleviating her psychotic symptoms. However, since her last visit 3 months ago, her face appears more round, and she has gained 9 kg. Further evaluation indicates that she has developed metabolic syndrome and pre-diabetes.

Continue to: Metabolic adverse effects

Metabolic adverse effects, such as metabolic syndrome, diabetic ketoacidosis, and cardiovascular disease, are well-known risks of prescribing second-generation antipsychotics.⁶ In such situations, psychiatrists often advise patients to modify their diet, increase physical activity, and follow up with their primary care physician to determine if other medications are needed. However, getting a patient with a serious mental illness to exercise and modify her/his diet is difficult, and many of these patients do not have a primary care physician.

For patients such as Ms. W, a psychiatrist should consider prescribing metformin. Wu et al⁷ found that in addition to lifestyle modifications, metformin had the greatest effect on antipsychotic-induced weight gain. In this study, metformin alone had more impact on reversing weight gain and increasing insulin sensitivity than lifestyle modifications alone.⁷ This is crucial because these patients are especially vulnerable to cardiac disease.⁸ Metformin is well tolerated and has a low risk of causing hypoglycemia. Concerns regarding lactic acidosis have abated to the extent that the estimated glomerular filtration rate (eGFR) limits for using metformin have been lowered significantly. After reviewing the contraindications, the only knowledge needed to prescribe metformin is the patient’s kidney function and a brief understanding of the titration needed to minimize gastrointestinal adverse effects.⁹ Thus, prescribing metformin would be a fairly logical and easy first step for managing metabolic syndrome, especially in a patient whose motivation for increasing physical activity and modifying his/her diet is doubtful.

CASE 2

Mr. B, age 45, has major depressive disorder that has been well-controlled on paroxetine, 40 mg/d, for the past 2 years. He has no history of physical illness. On his most recent visit, he appears uncomfortable and nervous. After a long discussion, he discloses that his sex life isn’t what it used to be since starting paroxetine. He is bothered by erectile problems and asks whether he can “get some Viagra.”

Sexual adverse effects, such as erectile dysfunction, are frequently associated with the use of selective serotonin reuptake inhibitors.¹⁰ Although managing these adverse effects requires careful evaluation, in most cases, psychiatrists should be able to treat them.¹⁰ The logical choice in this case would be to prescribe one of the 4 FDA-approved phosphodiesterase-5 inhibitors (sildenafil [Viagra], tadalafil [Cialis], vardenafil [Levitra], and avanafil [Stendra]. However, Balon et al¹¹ found that few psychiatrists prescribe phosphodiesterase-5 inhibitors, although they believed that they should be prescribing to treat their patients’ sexual dysfunction. Managing these adverse effects is important not only for the patient’s quality of life and relationship with his/her partner, but also for the therapeutic alliance. In a systematic review of 23 trials, Taylor et al¹² examined >1,800 patients who were prescribed a medication to address sexual dysfunction secondary to antidepressants. They found that for men, adding a phosphodiesterase-5 inhibitor was appropriate and effective, and for women, adding bupropion at high doses should be considered.¹² Like many other adverse effects, sexual adverse effects surely play a role in medication compliance. Dording et al¹³ found that the addition of sildenafil, 50 to 100 mg as needed, resulted in increased treatment satisfaction and overall contentment in 102 patients who complained of sexual dysfunction in the follow-up phase of the Sequenced Treatment Alternatives to Relieve Depression (STAR*D) antidepressant trials. In most cases, with proper psychoeducation, prescription of phosphodiesterase-5 inhibitors is fairly straightforward.

CASE 3

Ms. G, age 22, was recently discharged from an inpatient psychiatric unit after an episode of mania. She was prescribed carbamazepine, 600 mg/d, and ziprasidone, 40 mg twice a day, and appears to be doing well on this regimen. When asked about what led to her admission, she recalls having an elevated mood, increased energy, hypersexuality, impulsivity, and poor judgment. She reveals that she had several sexual partners during her manic episode, and worries that if such behavior occurs again, she may get pregnant. Yet Ms. G was not prescribed birth control upon discharge.

Continue to: Contraception

Contraception. We believe that psychiatrists have an obligation to protect patients from consequences of mental illness. Much the same way that psychiatrists hope to prevent suicide in a patient who has depression, patients should be protected from risks encountered in the manic phase of bipolar disorder. Another reason to prescribe contraceptives in such patients is the teratogenic effects of mood stabilizers. Pagano et al¹⁴ reviewed 6 studies that examined common forms of hormonal birth control to determine their safety in patients with depression or bipolar disorder. They found that overall, use of hormonal contraception was not associated with a worse clinical course of disease.

Many available forms of birth control are available. When prescribing in an outpatient setting, a daily oral medication or a monthly depot injection are convenient options.

CASE 4

Mr. P, age 65, has bipolar I disorder and is stable on risperidone long-acting injection, 37.7 mg bimonthly, and lithium, 1,200 mg/d. He reports that he is doing well but has noticed a recent decrease in energy and weight gain without any change in mood. Laboratory testing conducted prior to this visit revealed a thyroid-stimulating hormone (TSH) level of 4 mU/L (normal range: 0.4 to 4.0 mU/L). Six months ago, Mr. P’s TSH level was 2.8 mU/L. The resident supervisor suggests discussing the case with an endocrinologist.

Thyroid function. The impact of lithium on the thyroid gland is well established; however, psychiatrists’ response to such changes are not.¹⁵ Gitlin¹⁶ reviewed the many adverse effects of lithium and presented various management strategies to address findings such as Mr. P’s. Two important points are that lithium should not be discontinued in light of hypothyroidism, and synthetic thyroxine (levothyroxine) can be initiated and titrated to return TSH levels to a normal range.¹⁶ Levothyroxine can be started at low doses (eg, 25 to 50 mcg/d) and increased every 6 weeks until a normal TSH level is achieved.¹⁷ Managing lithium-induced clinical or subclinical hypothyroidism can prevent further pathology and possible relapse to depression.

Incorporating integrated care

In all these cases, the prescription of a medication with which some psychiatrists are not comfortable prescribing would have been the logical, easiest, and preferable choice. Of course, when initiating any medication, boxed warnings, contraindications, and drug–drug interactions should be reviewed. Initial dosages and titration schedules can be found in every medication’s FDA-approved prescribing information document (package insert), as well as in numerous reference books and articles.

Continue to: We acknowledge...

We acknowledge that prescribing a nonpsychotropic medication is not always a psychiatrist’s best choice, and that in patients with multiple medical comorbidities and drug–drug interactions that are not clearly defined, referring to or consulting a specialist is appropriate. We in no way support reckless prescribing, but instead present an opportunity to expand the perception of what should be considered within a psychiatrist’s scope of practice, and call for further education of psychiatrists so that they are more comfortable managing these adverse effects and/or prescribing at least some nonpsychotropic medications. For example, metabolic syndrome, uncomplicated hypertension, and hypothyroidism (not necessarily lithium-induced) could be managed by psychiatrists practicing integrated care (Table).

We exhort integrated medical care during this time of a physician shortage; however, we do not practice this way. Interestingly, physicians in primary care, such as those in family medicine or obstetrics and gynecology, frequently attempt to treat patients with psychiatric conditions in an attempt to provide integrated care. Numerous articles have discussed these efforts.^18-20 However, this type of integrated care seems less frequent in psychiatry, even though the practice of modern psychiatry in the United States shows substantial overlap with the practice of physicians in primary care specialties.²¹ There are few articles or practical guidelines for psychiatrists who wish to treat patients’ physical illnesses, particularly patients with severe mental illness (see Related Resources, page 56). If we practice in an integrated manner to treat one of the simple conditions we described above, we can eliminate the need for a patient to visit a second physician, pay another co-pay, pay another bus fare, and take another day off work. This can be particularly helpful for patients who at times have to decide between paying for groceries or for medications. Having one clinician manage a patient’s medications also can decrease the risk of polypharmacy.

In addition to the case scenarios described in this article, there are more clinical situations and nonpsychotropic medications that psychiatrists could manage. Considering them outside the scope of psychiatric practice and being uncomfortable or ambivalent about them is not an excuse. We hope that psychiatrists can increase their expertise in this area, and can start to practice as the primary care physicians they claim they are, and should be.

Bottom Line

Many psychiatrists are uncomfortable prescribing nonpsychotropic medications, but there are numerous clinical scenarios in which the practice would make sense. This could include cases of metabolic syndrome, sexual dysfunction secondary to antidepressant use, or other adverse effects of commonly prescribed psychotropic medications.

Related Resources

• McCarron RM, Xiong GL, Keenan CR, et al. Preventive medical care in psychiatry. A practical guide for clinicians. Arlington, VA: American Psychiatric Association Publishing; 2015.
• McCarron RM, Xiong GL, Keenan CR, et al. Study guide to preventive medical care in psychiatry. Arlington, VA: American Psychiatric Association Publishing; 2017.
• Goldberg JF, Ernst CL. Managing the side effects of psychotropic medications. Washington, DC: American Psychiatric Association Publishing; 2019.

Drug Brand Names

Avanafil • Stendra
Benztropine • Cogentin
Bupropion • Wellbutrin, Zyban
Carbamazepine • Carbatrol, Tegretol
Clozapine • Clozaril
Donepezil • Aricept
Levothyroxine • Levoxyl, Synthroid
Lithium • Eskalith, Lithobid
Metformin • Fortamet, Glucophage
Paroxetine • Paxil
Quetiapine • Seroquel
Risperidone long-acting injection • Risperdal Consta
Sildenafil • Viagra
Tadalafil • Cialis
Vardenafil • Levitra
Ziprasidone • Geodon

In our experience, most psychiatrists are uncomfortable with prescribing a medication when they feel that doing so would be outside their scope of practice. But there are many situations when prescribing a nonpsychotropic medication would be the correct choice. In this article, we discuss the scope of psychiatric practice, and present 4 case studies that illustrate situations in which psychiatrists should feel comfortable prescribing nonpsychotropic medications.

Defining the scope of practice

What is the scope of a psychiatrist’s practice? Scope of practice usually describes activities that a health care practitioner is allowed to undertake as defined by the terms of his/her license. A license to practice medicine does not include any stipulation restricting practice to a specific medical specialty. However, a local entity may delineate scope of practice within its organization. For instance, local practice standards held by the Detroit Wayne Mental Health Authority (DWMHA) state “Psychiatrists…shall not exceed their scope of practice as per DWMHA credentialing and privileging. For example, a Psychiatrist…who [has] not been appropriately privileged to deliver services to children shall not treat children, excepting crisis situations.”¹

Like physicians in other specialties, psychiatrists are not limited to prescribing only a subset of medications commonly associated with their specialty. But for many psychiatrists, prescribing nonpsychotropic medications is complicated by individual and local factors. On one hand, some psychiatrists do not feel it is their role to prescribe nonpsychotropic medications,² or even some psychotropic medications that may be more complex to prescribe, such as lithium, clozapine, or monoamine oxidase inhibitors.^3-5 However, many feel comfortable prescribing complex combinations of psychotropic medications, or prescribing in a way that does not necessarily make sense (eg, prescribing benztropine as prophylaxis for dystonia when starting an antipsychotic).

Reviewing an average day at one urban psychiatric clinic, these questions seem to come up in half of the patient population, especially in patients with chronic mental illness, multiple medical comorbidities, and limited access to health care. When a young patient walks in without an appointment with an acute dystonic reaction secondary to the initiation of antipsychotics a couple of days ago, there is no hesitation to swiftly and appropriately prescribe an IM anticholinergic medication. But why are psychiatrists often hesitant to prescribe nonpsychotropic medications to treat other adverse effects of medications? Lack of knowledge? Lack of training?

Psychiatrists who practice in hospital systems often have immediate access to consultants, and this availability may encourage them to defer to the consultant for treatment of certain adverse effects. We have seen psychiatrists consult Neurology regarding the prescription of donepezil for mild neurocognitive disorder due to Alzheimer’s disease, or Endocrinology regarding prescription of levothyroxine for lithium-induced hypothyroidism.

However, there are numerous scenarios in which psychiatrists should feel comfortable prescribing nonpsychotropic medications or managing medication adverse effects, regardless of whether they consider it to be within or outside their scope of practice. The following case examples illustrate several such situations.

CASE 1

Ms. W, age 30, has been diagnosed with schizophrenia. She requests a refill of quetiapine, 800 mg/d. This medication has been clearly beneficial in alleviating her psychotic symptoms. However, since her last visit 3 months ago, her face appears more round, and she has gained 9 kg. Further evaluation indicates that she has developed metabolic syndrome and pre-diabetes.

Continue to: Metabolic adverse effects

Metabolic adverse effects, such as metabolic syndrome, diabetic ketoacidosis, and cardiovascular disease, are well-known risks of prescribing second-generation antipsychotics.⁶ In such situations, psychiatrists often advise patients to modify their diet, increase physical activity, and follow up with their primary care physician to determine if other medications are needed. However, getting a patient with a serious mental illness to exercise and modify her/his diet is difficult, and many of these patients do not have a primary care physician.

For patients such as Ms. W, a psychiatrist should consider prescribing metformin. Wu et al⁷ found that in addition to lifestyle modifications, metformin had the greatest effect on antipsychotic-induced weight gain. In this study, metformin alone had more impact on reversing weight gain and increasing insulin sensitivity than lifestyle modifications alone.⁷ This is crucial because these patients are especially vulnerable to cardiac disease.⁸ Metformin is well tolerated and has a low risk of causing hypoglycemia. Concerns regarding lactic acidosis have abated to the extent that the estimated glomerular filtration rate (eGFR) limits for using metformin have been lowered significantly. After reviewing the contraindications, the only knowledge needed to prescribe metformin is the patient’s kidney function and a brief understanding of the titration needed to minimize gastrointestinal adverse effects.⁹ Thus, prescribing metformin would be a fairly logical and easy first step for managing metabolic syndrome, especially in a patient whose motivation for increasing physical activity and modifying his/her diet is doubtful.

CASE 2

Mr. B, age 45, has major depressive disorder that has been well-controlled on paroxetine, 40 mg/d, for the past 2 years. He has no history of physical illness. On his most recent visit, he appears uncomfortable and nervous. After a long discussion, he discloses that his sex life isn’t what it used to be since starting paroxetine. He is bothered by erectile problems and asks whether he can “get some Viagra.”

Sexual adverse effects, such as erectile dysfunction, are frequently associated with the use of selective serotonin reuptake inhibitors.¹⁰ Although managing these adverse effects requires careful evaluation, in most cases, psychiatrists should be able to treat them.¹⁰ The logical choice in this case would be to prescribe one of the 4 FDA-approved phosphodiesterase-5 inhibitors (sildenafil [Viagra], tadalafil [Cialis], vardenafil [Levitra], and avanafil [Stendra]. However, Balon et al¹¹ found that few psychiatrists prescribe phosphodiesterase-5 inhibitors, although they believed that they should be prescribing to treat their patients’ sexual dysfunction. Managing these adverse effects is important not only for the patient’s quality of life and relationship with his/her partner, but also for the therapeutic alliance. In a systematic review of 23 trials, Taylor et al¹² examined >1,800 patients who were prescribed a medication to address sexual dysfunction secondary to antidepressants. They found that for men, adding a phosphodiesterase-5 inhibitor was appropriate and effective, and for women, adding bupropion at high doses should be considered.¹² Like many other adverse effects, sexual adverse effects surely play a role in medication compliance. Dording et al¹³ found that the addition of sildenafil, 50 to 100 mg as needed, resulted in increased treatment satisfaction and overall contentment in 102 patients who complained of sexual dysfunction in the follow-up phase of the Sequenced Treatment Alternatives to Relieve Depression (STAR*D) antidepressant trials. In most cases, with proper psychoeducation, prescription of phosphodiesterase-5 inhibitors is fairly straightforward.

CASE 3

Ms. G, age 22, was recently discharged from an inpatient psychiatric unit after an episode of mania. She was prescribed carbamazepine, 600 mg/d, and ziprasidone, 40 mg twice a day, and appears to be doing well on this regimen. When asked about what led to her admission, she recalls having an elevated mood, increased energy, hypersexuality, impulsivity, and poor judgment. She reveals that she had several sexual partners during her manic episode, and worries that if such behavior occurs again, she may get pregnant. Yet Ms. G was not prescribed birth control upon discharge.

Continue to: Contraception

Contraception. We believe that psychiatrists have an obligation to protect patients from consequences of mental illness. Much the same way that psychiatrists hope to prevent suicide in a patient who has depression, patients should be protected from risks encountered in the manic phase of bipolar disorder. Another reason to prescribe contraceptives in such patients is the teratogenic effects of mood stabilizers. Pagano et al¹⁴ reviewed 6 studies that examined common forms of hormonal birth control to determine their safety in patients with depression or bipolar disorder. They found that overall, use of hormonal contraception was not associated with a worse clinical course of disease.

Many available forms of birth control are available. When prescribing in an outpatient setting, a daily oral medication or a monthly depot injection are convenient options.

CASE 4

Mr. P, age 65, has bipolar I disorder and is stable on risperidone long-acting injection, 37.7 mg bimonthly, and lithium, 1,200 mg/d. He reports that he is doing well but has noticed a recent decrease in energy and weight gain without any change in mood. Laboratory testing conducted prior to this visit revealed a thyroid-stimulating hormone (TSH) level of 4 mU/L (normal range: 0.4 to 4.0 mU/L). Six months ago, Mr. P’s TSH level was 2.8 mU/L. The resident supervisor suggests discussing the case with an endocrinologist.

Thyroid function. The impact of lithium on the thyroid gland is well established; however, psychiatrists’ response to such changes are not.¹⁵ Gitlin¹⁶ reviewed the many adverse effects of lithium and presented various management strategies to address findings such as Mr. P’s. Two important points are that lithium should not be discontinued in light of hypothyroidism, and synthetic thyroxine (levothyroxine) can be initiated and titrated to return TSH levels to a normal range.¹⁶ Levothyroxine can be started at low doses (eg, 25 to 50 mcg/d) and increased every 6 weeks until a normal TSH level is achieved.¹⁷ Managing lithium-induced clinical or subclinical hypothyroidism can prevent further pathology and possible relapse to depression.

Incorporating integrated care

In all these cases, the prescription of a medication with which some psychiatrists are not comfortable prescribing would have been the logical, easiest, and preferable choice. Of course, when initiating any medication, boxed warnings, contraindications, and drug–drug interactions should be reviewed. Initial dosages and titration schedules can be found in every medication’s FDA-approved prescribing information document (package insert), as well as in numerous reference books and articles.

Continue to: We acknowledge...

We acknowledge that prescribing a nonpsychotropic medication is not always a psychiatrist’s best choice, and that in patients with multiple medical comorbidities and drug–drug interactions that are not clearly defined, referring to or consulting a specialist is appropriate. We in no way support reckless prescribing, but instead present an opportunity to expand the perception of what should be considered within a psychiatrist’s scope of practice, and call for further education of psychiatrists so that they are more comfortable managing these adverse effects and/or prescribing at least some nonpsychotropic medications. For example, metabolic syndrome, uncomplicated hypertension, and hypothyroidism (not necessarily lithium-induced) could be managed by psychiatrists practicing integrated care (Table).

We exhort integrated medical care during this time of a physician shortage; however, we do not practice this way. Interestingly, physicians in primary care, such as those in family medicine or obstetrics and gynecology, frequently attempt to treat patients with psychiatric conditions in an attempt to provide integrated care. Numerous articles have discussed these efforts.^18-20 However, this type of integrated care seems less frequent in psychiatry, even though the practice of modern psychiatry in the United States shows substantial overlap with the practice of physicians in primary care specialties.²¹ There are few articles or practical guidelines for psychiatrists who wish to treat patients’ physical illnesses, particularly patients with severe mental illness (see Related Resources, page 56). If we practice in an integrated manner to treat one of the simple conditions we described above, we can eliminate the need for a patient to visit a second physician, pay another co-pay, pay another bus fare, and take another day off work. This can be particularly helpful for patients who at times have to decide between paying for groceries or for medications. Having one clinician manage a patient’s medications also can decrease the risk of polypharmacy.

In addition to the case scenarios described in this article, there are more clinical situations and nonpsychotropic medications that psychiatrists could manage. Considering them outside the scope of psychiatric practice and being uncomfortable or ambivalent about them is not an excuse. We hope that psychiatrists can increase their expertise in this area, and can start to practice as the primary care physicians they claim they are, and should be.

Bottom Line

Many psychiatrists are uncomfortable prescribing nonpsychotropic medications, but there are numerous clinical scenarios in which the practice would make sense. This could include cases of metabolic syndrome, sexual dysfunction secondary to antidepressant use, or other adverse effects of commonly prescribed psychotropic medications.

Related Resources

• McCarron RM, Xiong GL, Keenan CR, et al. Preventive medical care in psychiatry. A practical guide for clinicians. Arlington, VA: American Psychiatric Association Publishing; 2015.
• McCarron RM, Xiong GL, Keenan CR, et al. Study guide to preventive medical care in psychiatry. Arlington, VA: American Psychiatric Association Publishing; 2017.
• Goldberg JF, Ernst CL. Managing the side effects of psychotropic medications. Washington, DC: American Psychiatric Association Publishing; 2019.

Drug Brand Names

Avanafil • Stendra
Benztropine • Cogentin
Bupropion • Wellbutrin, Zyban
Carbamazepine • Carbatrol, Tegretol
Clozapine • Clozaril
Donepezil • Aricept
Levothyroxine • Levoxyl, Synthroid
Lithium • Eskalith, Lithobid
Metformin • Fortamet, Glucophage
Paroxetine • Paxil
Quetiapine • Seroquel
Risperidone long-acting injection • Risperdal Consta
Sildenafil • Viagra
Tadalafil • Cialis
Vardenafil • Levitra
Ziprasidone • Geodon

In our experience, most psychiatrists are uncomfortable with prescribing a medication when they feel that doing so would be outside their scope of practice. But there are many situations when prescribing a nonpsychotropic medication would be the correct choice. In this article, we discuss the scope of psychiatric practice, and present 4 case studies that illustrate situations in which psychiatrists should feel comfortable prescribing nonpsychotropic medications.

Defining the scope of practice

What is the scope of a psychiatrist’s practice? Scope of practice usually describes activities that a health care practitioner is allowed to undertake as defined by the terms of his/her license. A license to practice medicine does not include any stipulation restricting practice to a specific medical specialty. However, a local entity may delineate scope of practice within its organization. For instance, local practice standards held by the Detroit Wayne Mental Health Authority (DWMHA) state “Psychiatrists…shall not exceed their scope of practice as per DWMHA credentialing and privileging. For example, a Psychiatrist…who [has] not been appropriately privileged to deliver services to children shall not treat children, excepting crisis situations.”¹

Like physicians in other specialties, psychiatrists are not limited to prescribing only a subset of medications commonly associated with their specialty. But for many psychiatrists, prescribing nonpsychotropic medications is complicated by individual and local factors. On one hand, some psychiatrists do not feel it is their role to prescribe nonpsychotropic medications,² or even some psychotropic medications that may be more complex to prescribe, such as lithium, clozapine, or monoamine oxidase inhibitors.^3-5 However, many feel comfortable prescribing complex combinations of psychotropic medications, or prescribing in a way that does not necessarily make sense (eg, prescribing benztropine as prophylaxis for dystonia when starting an antipsychotic).

Reviewing an average day at one urban psychiatric clinic, these questions seem to come up in half of the patient population, especially in patients with chronic mental illness, multiple medical comorbidities, and limited access to health care. When a young patient walks in without an appointment with an acute dystonic reaction secondary to the initiation of antipsychotics a couple of days ago, there is no hesitation to swiftly and appropriately prescribe an IM anticholinergic medication. But why are psychiatrists often hesitant to prescribe nonpsychotropic medications to treat other adverse effects of medications? Lack of knowledge? Lack of training?

Psychiatrists who practice in hospital systems often have immediate access to consultants, and this availability may encourage them to defer to the consultant for treatment of certain adverse effects. We have seen psychiatrists consult Neurology regarding the prescription of donepezil for mild neurocognitive disorder due to Alzheimer’s disease, or Endocrinology regarding prescription of levothyroxine for lithium-induced hypothyroidism.

However, there are numerous scenarios in which psychiatrists should feel comfortable prescribing nonpsychotropic medications or managing medication adverse effects, regardless of whether they consider it to be within or outside their scope of practice. The following case examples illustrate several such situations.

CASE 1

Ms. W, age 30, has been diagnosed with schizophrenia. She requests a refill of quetiapine, 800 mg/d. This medication has been clearly beneficial in alleviating her psychotic symptoms. However, since her last visit 3 months ago, her face appears more round, and she has gained 9 kg. Further evaluation indicates that she has developed metabolic syndrome and pre-diabetes.

Continue to: Metabolic adverse effects

Metabolic adverse effects, such as metabolic syndrome, diabetic ketoacidosis, and cardiovascular disease, are well-known risks of prescribing second-generation antipsychotics.⁶ In such situations, psychiatrists often advise patients to modify their diet, increase physical activity, and follow up with their primary care physician to determine if other medications are needed. However, getting a patient with a serious mental illness to exercise and modify her/his diet is difficult, and many of these patients do not have a primary care physician.

For patients such as Ms. W, a psychiatrist should consider prescribing metformin. Wu et al⁷ found that in addition to lifestyle modifications, metformin had the greatest effect on antipsychotic-induced weight gain. In this study, metformin alone had more impact on reversing weight gain and increasing insulin sensitivity than lifestyle modifications alone.⁷ This is crucial because these patients are especially vulnerable to cardiac disease.⁸ Metformin is well tolerated and has a low risk of causing hypoglycemia. Concerns regarding lactic acidosis have abated to the extent that the estimated glomerular filtration rate (eGFR) limits for using metformin have been lowered significantly. After reviewing the contraindications, the only knowledge needed to prescribe metformin is the patient’s kidney function and a brief understanding of the titration needed to minimize gastrointestinal adverse effects.⁹ Thus, prescribing metformin would be a fairly logical and easy first step for managing metabolic syndrome, especially in a patient whose motivation for increasing physical activity and modifying his/her diet is doubtful.

CASE 2

Mr. B, age 45, has major depressive disorder that has been well-controlled on paroxetine, 40 mg/d, for the past 2 years. He has no history of physical illness. On his most recent visit, he appears uncomfortable and nervous. After a long discussion, he discloses that his sex life isn’t what it used to be since starting paroxetine. He is bothered by erectile problems and asks whether he can “get some Viagra.”

Sexual adverse effects, such as erectile dysfunction, are frequently associated with the use of selective serotonin reuptake inhibitors.¹⁰ Although managing these adverse effects requires careful evaluation, in most cases, psychiatrists should be able to treat them.¹⁰ The logical choice in this case would be to prescribe one of the 4 FDA-approved phosphodiesterase-5 inhibitors (sildenafil [Viagra], tadalafil [Cialis], vardenafil [Levitra], and avanafil [Stendra]. However, Balon et al¹¹ found that few psychiatrists prescribe phosphodiesterase-5 inhibitors, although they believed that they should be prescribing to treat their patients’ sexual dysfunction. Managing these adverse effects is important not only for the patient’s quality of life and relationship with his/her partner, but also for the therapeutic alliance. In a systematic review of 23 trials, Taylor et al¹² examined >1,800 patients who were prescribed a medication to address sexual dysfunction secondary to antidepressants. They found that for men, adding a phosphodiesterase-5 inhibitor was appropriate and effective, and for women, adding bupropion at high doses should be considered.¹² Like many other adverse effects, sexual adverse effects surely play a role in medication compliance. Dording et al¹³ found that the addition of sildenafil, 50 to 100 mg as needed, resulted in increased treatment satisfaction and overall contentment in 102 patients who complained of sexual dysfunction in the follow-up phase of the Sequenced Treatment Alternatives to Relieve Depression (STAR*D) antidepressant trials. In most cases, with proper psychoeducation, prescription of phosphodiesterase-5 inhibitors is fairly straightforward.

CASE 3

Ms. G, age 22, was recently discharged from an inpatient psychiatric unit after an episode of mania. She was prescribed carbamazepine, 600 mg/d, and ziprasidone, 40 mg twice a day, and appears to be doing well on this regimen. When asked about what led to her admission, she recalls having an elevated mood, increased energy, hypersexuality, impulsivity, and poor judgment. She reveals that she had several sexual partners during her manic episode, and worries that if such behavior occurs again, she may get pregnant. Yet Ms. G was not prescribed birth control upon discharge.

Continue to: Contraception

Contraception. We believe that psychiatrists have an obligation to protect patients from consequences of mental illness. Much the same way that psychiatrists hope to prevent suicide in a patient who has depression, patients should be protected from risks encountered in the manic phase of bipolar disorder. Another reason to prescribe contraceptives in such patients is the teratogenic effects of mood stabilizers. Pagano et al¹⁴ reviewed 6 studies that examined common forms of hormonal birth control to determine their safety in patients with depression or bipolar disorder. They found that overall, use of hormonal contraception was not associated with a worse clinical course of disease.

Many available forms of birth control are available. When prescribing in an outpatient setting, a daily oral medication or a monthly depot injection are convenient options.

CASE 4

Mr. P, age 65, has bipolar I disorder and is stable on risperidone long-acting injection, 37.7 mg bimonthly, and lithium, 1,200 mg/d. He reports that he is doing well but has noticed a recent decrease in energy and weight gain without any change in mood. Laboratory testing conducted prior to this visit revealed a thyroid-stimulating hormone (TSH) level of 4 mU/L (normal range: 0.4 to 4.0 mU/L). Six months ago, Mr. P’s TSH level was 2.8 mU/L. The resident supervisor suggests discussing the case with an endocrinologist.

Thyroid function. The impact of lithium on the thyroid gland is well established; however, psychiatrists’ response to such changes are not.¹⁵ Gitlin¹⁶ reviewed the many adverse effects of lithium and presented various management strategies to address findings such as Mr. P’s. Two important points are that lithium should not be discontinued in light of hypothyroidism, and synthetic thyroxine (levothyroxine) can be initiated and titrated to return TSH levels to a normal range.¹⁶ Levothyroxine can be started at low doses (eg, 25 to 50 mcg/d) and increased every 6 weeks until a normal TSH level is achieved.¹⁷ Managing lithium-induced clinical or subclinical hypothyroidism can prevent further pathology and possible relapse to depression.

Incorporating integrated care

In all these cases, the prescription of a medication with which some psychiatrists are not comfortable prescribing would have been the logical, easiest, and preferable choice. Of course, when initiating any medication, boxed warnings, contraindications, and drug–drug interactions should be reviewed. Initial dosages and titration schedules can be found in every medication’s FDA-approved prescribing information document (package insert), as well as in numerous reference books and articles.

Continue to: We acknowledge...

We acknowledge that prescribing a nonpsychotropic medication is not always a psychiatrist’s best choice, and that in patients with multiple medical comorbidities and drug–drug interactions that are not clearly defined, referring to or consulting a specialist is appropriate. We in no way support reckless prescribing, but instead present an opportunity to expand the perception of what should be considered within a psychiatrist’s scope of practice, and call for further education of psychiatrists so that they are more comfortable managing these adverse effects and/or prescribing at least some nonpsychotropic medications. For example, metabolic syndrome, uncomplicated hypertension, and hypothyroidism (not necessarily lithium-induced) could be managed by psychiatrists practicing integrated care (Table).

We exhort integrated medical care during this time of a physician shortage; however, we do not practice this way. Interestingly, physicians in primary care, such as those in family medicine or obstetrics and gynecology, frequently attempt to treat patients with psychiatric conditions in an attempt to provide integrated care. Numerous articles have discussed these efforts.^18-20 However, this type of integrated care seems less frequent in psychiatry, even though the practice of modern psychiatry in the United States shows substantial overlap with the practice of physicians in primary care specialties.²¹ There are few articles or practical guidelines for psychiatrists who wish to treat patients’ physical illnesses, particularly patients with severe mental illness (see Related Resources, page 56). If we practice in an integrated manner to treat one of the simple conditions we described above, we can eliminate the need for a patient to visit a second physician, pay another co-pay, pay another bus fare, and take another day off work. This can be particularly helpful for patients who at times have to decide between paying for groceries or for medications. Having one clinician manage a patient’s medications also can decrease the risk of polypharmacy.

In addition to the case scenarios described in this article, there are more clinical situations and nonpsychotropic medications that psychiatrists could manage. Considering them outside the scope of psychiatric practice and being uncomfortable or ambivalent about them is not an excuse. We hope that psychiatrists can increase their expertise in this area, and can start to practice as the primary care physicians they claim they are, and should be.

Bottom Line

Many psychiatrists are uncomfortable prescribing nonpsychotropic medications, but there are numerous clinical scenarios in which the practice would make sense. This could include cases of metabolic syndrome, sexual dysfunction secondary to antidepressant use, or other adverse effects of commonly prescribed psychotropic medications.

Related Resources

• McCarron RM, Xiong GL, Keenan CR, et al. Preventive medical care in psychiatry. A practical guide for clinicians. Arlington, VA: American Psychiatric Association Publishing; 2015.
• McCarron RM, Xiong GL, Keenan CR, et al. Study guide to preventive medical care in psychiatry. Arlington, VA: American Psychiatric Association Publishing; 2017.
• Goldberg JF, Ernst CL. Managing the side effects of psychotropic medications. Washington, DC: American Psychiatric Association Publishing; 2019.

Drug Brand Names

Avanafil • Stendra
Benztropine • Cogentin
Bupropion • Wellbutrin, Zyban
Carbamazepine • Carbatrol, Tegretol
Clozapine • Clozaril
Donepezil • Aricept
Levothyroxine • Levoxyl, Synthroid
Lithium • Eskalith, Lithobid
Metformin • Fortamet, Glucophage
Paroxetine • Paxil
Quetiapine • Seroquel
Risperidone long-acting injection • Risperdal Consta
Sildenafil • Viagra
Tadalafil • Cialis
Vardenafil • Levitra
Ziprasidone • Geodon

The rapid development and identification of novel drugs has translated into innovative therapies in hematology and oncology. The aim of this piece is to present newly approved drugs and expanded indications to serve as a reference guide for practicing clinicians.

This article reviews therapies that were newly approved so far in 2019, as well as those previously approved whose indications were expanded this past year. The list highlights the most clinically important approvals, as well as adverse events that are unique or especially severe.
 

New approvals

Fedratinib (Inrebic)

Class: JAK2 and FLT3 selective kinase inhibitor.

Disease: Intermediate or high-risk primary or secondary (postpolycythemia vera or postessential thrombocythemia) myelofibrosis.

Dose: 400 mg orally once daily, with or without food.

Adverse events (AEs): Black box warning: Fatal encephalopathy, including Wernicke’s (thiamine level monitoring suggested).

Trials: In JAKARTA (NCT01437787), 37% of patients achieved a 35% or greater reduction in spleen volume and 40% received a 50% or greater reduction in myelofibrosis-related symptoms. In Jakarta-2, there was a 55% spleen response in patients resistant or intolerant to ruxolitinib.

Entrectinib (Rozlytrek)

Class: Tropomyosin receptor tyrosine kinase inhibitor.

Disease: Solid tumors that have a neurotrophic tyrosine receptor kinase (NTRK) gene fusion and for ROS-1 positive non–small cell lung cancer (NSCLC).

Dose: 600 mg orally once daily.

AEs: Heart failure, QT prolongation, skeletal fractures, hepatotoxicity, central nervous system effects, and hyperuricemia.

Trial: ALKA, STARTRK-1 (NCT02097810) and STARTRK-2 (NCT02568267): Overall response rate of 57% for NTRK positive patients; response rate of 77% in ROS-1 positive NSCLC.

Pexidartinib (Turalio)

Class: Small molecule tyrosine kinase inhibitor targeting CSF1R.

Disease: Symptomatic tenosynovial giant cell tumor.

Dose: 400 mg orally twice daily without food.

AEs: Black box warning on hepatotoxicity.

Trial: ENLIVEN (NCT02371369): Overall response rate of 38% at 25 weeks, with a 15% complete response rate and a 23% partial response rate.

Darolutamide (Nubeqa)

Class: Androgen receptor inhibitor.

Disease: Nonmetastatic castration-resistant prostate cancer.

Dose: 600 mg orally twice daily with food with concomitant androgen deprivation therapy.

AEs: Fatigue, extremity pain, and rash.

Trial: ARAMIS (NCT02200614): Median metastasis free survival was 40.4 months for patients with darolutamide, compared with 18.4 months for controls.

Selinexor (Xpovio)

Class: Reversible inhibitor of nuclear export of tumor suppressor proteins, growth regulators, and mRNAs of oncogenic proteins.

Disease: Relapsed or refractory multiple myeloma. Indicated for patients who have received at least four prior therapies, including at least two immunomodulatory agents and an anti-CD38 monoclonal antibody.

Dose: 80 mg orally in combination with oral dexamethasone on days 1 and 3 of each week.

AEs: Thrombocytopenia, fatigue, pancytopenia, and hyponatremia.

Trial: STORM (NCT02336815): Overall response rate 25.3% with a median time to first response of 4 weeks and 3.8-month median duration of response.

Polatuzumab vedotin-piiq (Polivy)

Class: CD79b-directed antibody-drug conjugate.

Disease: Relapsed or refractory diffuse large B-cell lymphoma. Indicated for patients who have had at least two prior therapies.

Dose: 1.8 mg/kg intravenous infusion every 21 days for six cycles in combination with bendamustine and a rituximab product.

AEs: Pancytopenia, peripheral neuropathy.

Trial: GO29365 (NCT02257567): Complete response rate was 40% for polatuzumab vedotin-piiq plus bendamustine/rituximab, compared with 18% with bendamustine/rituximab alone.*

Caplacizumab-yhdp (Cablivi)

Class: Monoclonal antibody fragment directed against von Willebrand factor.

Disease: Thrombotic thrombocytopenic purpura.

Dose: 11 mg IV initially, then daily subcutaneously; in combination with plasma exchange and immunosuppressive therapy.

AEs: Epistaxis, headache, and gingival bleeding.

Trial: Hercules trial (NCT02553317): More rapid normalization of platelets, lower incidence of composite TTP-related death, and lower rate of recurrence when added to plasma exchange and steroids.
 

Alpelisib (Piqray)

Class: Phosphatidylinositol-3-kinase (PI3K) inhibitor.

Disease: Hormone receptor positive HER2-negative PIK3CA-mutated, advanced or metastatic breast cancer.

Dose: 300 mg orally once daily with food with concomitant fulvestrant.

AEs: Hyperglycemia, pancytopenia.

Trial: SOLAR-1 (NCT02437318): 11-month progression-free survival among patients treated with alpelisib and fulvestrant, compared with 5.7 months in fulvestrant alone control arm; overall response rate of 36% versus 16%, respectively.

Erdafitinib (Balversa)

Class: Fibroblast growth factor receptor kinase inhibitor.

Disease: Locally advanced or metastatic urothelial carcinoma with FGFR3 or FGFR2 mutations.

Dose: 8 mg orally once daily, with or without food.

AEs: Ocular disorders including retinopathy or retinal detachment.

Trial: BLC2001 (NCT02365597): Objective response rate of 32.2%, with a complete response in 2.3% of patients and partial response in 29.9% of patients.

Biosimilar approvals

Trastuzumab and hyaluronidase-oysk (Herceptin Hylecta)

Biosimilar to: Trastuzumab.

Indication: HER2-overexpressing breast cancer.
 

Dr. Bryer is a resident in the department of internal medicine at the University of Pennsylvania, Philadelphia. Dr. Mintzer is chief of hematology-oncology at Pennsylvania Hospital and professor of medicine at the University of Pennsylvania. Dr. Henry is a hematologist-oncologist at Pennsylvania Hospital and professor of medicine at the University of Pennsylvania.

*Correction, 11/7/2019: An earlier version of this article misstated the drug combination in the GO29365 trial. 

The rapid development and identification of novel drugs has translated into innovative therapies in hematology and oncology. The aim of this piece is to present newly approved drugs and expanded indications to serve as a reference guide for practicing clinicians.

This article reviews therapies that were newly approved so far in 2019, as well as those previously approved whose indications were expanded this past year. The list highlights the most clinically important approvals, as well as adverse events that are unique or especially severe.
 

New approvals

Fedratinib (Inrebic)

Class: JAK2 and FLT3 selective kinase inhibitor.

Disease: Intermediate or high-risk primary or secondary (postpolycythemia vera or postessential thrombocythemia) myelofibrosis.

Dose: 400 mg orally once daily, with or without food.

Adverse events (AEs): Black box warning: Fatal encephalopathy, including Wernicke’s (thiamine level monitoring suggested).

Trials: In JAKARTA (NCT01437787), 37% of patients achieved a 35% or greater reduction in spleen volume and 40% received a 50% or greater reduction in myelofibrosis-related symptoms. In Jakarta-2, there was a 55% spleen response in patients resistant or intolerant to ruxolitinib.

Entrectinib (Rozlytrek)

Class: Tropomyosin receptor tyrosine kinase inhibitor.

Disease: Solid tumors that have a neurotrophic tyrosine receptor kinase (NTRK) gene fusion and for ROS-1 positive non–small cell lung cancer (NSCLC).

Dose: 600 mg orally once daily.

AEs: Heart failure, QT prolongation, skeletal fractures, hepatotoxicity, central nervous system effects, and hyperuricemia.

Trial: ALKA, STARTRK-1 (NCT02097810) and STARTRK-2 (NCT02568267): Overall response rate of 57% for NTRK positive patients; response rate of 77% in ROS-1 positive NSCLC.

Pexidartinib (Turalio)

Class: Small molecule tyrosine kinase inhibitor targeting CSF1R.

Disease: Symptomatic tenosynovial giant cell tumor.

Dose: 400 mg orally twice daily without food.

AEs: Black box warning on hepatotoxicity.

Trial: ENLIVEN (NCT02371369): Overall response rate of 38% at 25 weeks, with a 15% complete response rate and a 23% partial response rate.

Darolutamide (Nubeqa)

Class: Androgen receptor inhibitor.

Disease: Nonmetastatic castration-resistant prostate cancer.

Dose: 600 mg orally twice daily with food with concomitant androgen deprivation therapy.

AEs: Fatigue, extremity pain, and rash.

Trial: ARAMIS (NCT02200614): Median metastasis free survival was 40.4 months for patients with darolutamide, compared with 18.4 months for controls.

Selinexor (Xpovio)

Class: Reversible inhibitor of nuclear export of tumor suppressor proteins, growth regulators, and mRNAs of oncogenic proteins.

Disease: Relapsed or refractory multiple myeloma. Indicated for patients who have received at least four prior therapies, including at least two immunomodulatory agents and an anti-CD38 monoclonal antibody.

Dose: 80 mg orally in combination with oral dexamethasone on days 1 and 3 of each week.

AEs: Thrombocytopenia, fatigue, pancytopenia, and hyponatremia.

Trial: STORM (NCT02336815): Overall response rate 25.3% with a median time to first response of 4 weeks and 3.8-month median duration of response.

Polatuzumab vedotin-piiq (Polivy)

Class: CD79b-directed antibody-drug conjugate.

Disease: Relapsed or refractory diffuse large B-cell lymphoma. Indicated for patients who have had at least two prior therapies.

Dose: 1.8 mg/kg intravenous infusion every 21 days for six cycles in combination with bendamustine and a rituximab product.

AEs: Pancytopenia, peripheral neuropathy.

Trial: GO29365 (NCT02257567): Complete response rate was 40% for polatuzumab vedotin-piiq plus bendamustine/rituximab, compared with 18% with bendamustine/rituximab alone.*

Caplacizumab-yhdp (Cablivi)

Class: Monoclonal antibody fragment directed against von Willebrand factor.

Disease: Thrombotic thrombocytopenic purpura.

Dose: 11 mg IV initially, then daily subcutaneously; in combination with plasma exchange and immunosuppressive therapy.

AEs: Epistaxis, headache, and gingival bleeding.

Trial: Hercules trial (NCT02553317): More rapid normalization of platelets, lower incidence of composite TTP-related death, and lower rate of recurrence when added to plasma exchange and steroids.
 

Alpelisib (Piqray)

Class: Phosphatidylinositol-3-kinase (PI3K) inhibitor.

Disease: Hormone receptor positive HER2-negative PIK3CA-mutated, advanced or metastatic breast cancer.

Dose: 300 mg orally once daily with food with concomitant fulvestrant.

AEs: Hyperglycemia, pancytopenia.

Trial: SOLAR-1 (NCT02437318): 11-month progression-free survival among patients treated with alpelisib and fulvestrant, compared with 5.7 months in fulvestrant alone control arm; overall response rate of 36% versus 16%, respectively.

Erdafitinib (Balversa)

Class: Fibroblast growth factor receptor kinase inhibitor.

Disease: Locally advanced or metastatic urothelial carcinoma with FGFR3 or FGFR2 mutations.

Dose: 8 mg orally once daily, with or without food.

AEs: Ocular disorders including retinopathy or retinal detachment.

Trial: BLC2001 (NCT02365597): Objective response rate of 32.2%, with a complete response in 2.3% of patients and partial response in 29.9% of patients.

Biosimilar approvals

Trastuzumab and hyaluronidase-oysk (Herceptin Hylecta)

Biosimilar to: Trastuzumab.

Indication: HER2-overexpressing breast cancer.
 

Dr. Bryer is a resident in the department of internal medicine at the University of Pennsylvania, Philadelphia. Dr. Mintzer is chief of hematology-oncology at Pennsylvania Hospital and professor of medicine at the University of Pennsylvania. Dr. Henry is a hematologist-oncologist at Pennsylvania Hospital and professor of medicine at the University of Pennsylvania.

*Correction, 11/7/2019: An earlier version of this article misstated the drug combination in the GO29365 trial. 

The rapid development and identification of novel drugs has translated into innovative therapies in hematology and oncology. The aim of this piece is to present newly approved drugs and expanded indications to serve as a reference guide for practicing clinicians.

This article reviews therapies that were newly approved so far in 2019, as well as those previously approved whose indications were expanded this past year. The list highlights the most clinically important approvals, as well as adverse events that are unique or especially severe.
 

New approvals

Fedratinib (Inrebic)

Class: JAK2 and FLT3 selective kinase inhibitor.

Disease: Intermediate or high-risk primary or secondary (postpolycythemia vera or postessential thrombocythemia) myelofibrosis.

Dose: 400 mg orally once daily, with or without food.

Adverse events (AEs): Black box warning: Fatal encephalopathy, including Wernicke’s (thiamine level monitoring suggested).

Trials: In JAKARTA (NCT01437787), 37% of patients achieved a 35% or greater reduction in spleen volume and 40% received a 50% or greater reduction in myelofibrosis-related symptoms. In Jakarta-2, there was a 55% spleen response in patients resistant or intolerant to ruxolitinib.

Entrectinib (Rozlytrek)

Class: Tropomyosin receptor tyrosine kinase inhibitor.

Disease: Solid tumors that have a neurotrophic tyrosine receptor kinase (NTRK) gene fusion and for ROS-1 positive non–small cell lung cancer (NSCLC).

Dose: 600 mg orally once daily.

AEs: Heart failure, QT prolongation, skeletal fractures, hepatotoxicity, central nervous system effects, and hyperuricemia.

Trial: ALKA, STARTRK-1 (NCT02097810) and STARTRK-2 (NCT02568267): Overall response rate of 57% for NTRK positive patients; response rate of 77% in ROS-1 positive NSCLC.

Pexidartinib (Turalio)

Class: Small molecule tyrosine kinase inhibitor targeting CSF1R.

Disease: Symptomatic tenosynovial giant cell tumor.

Dose: 400 mg orally twice daily without food.

AEs: Black box warning on hepatotoxicity.

Trial: ENLIVEN (NCT02371369): Overall response rate of 38% at 25 weeks, with a 15% complete response rate and a 23% partial response rate.

Darolutamide (Nubeqa)

Class: Androgen receptor inhibitor.

Disease: Nonmetastatic castration-resistant prostate cancer.

Dose: 600 mg orally twice daily with food with concomitant androgen deprivation therapy.

AEs: Fatigue, extremity pain, and rash.

Trial: ARAMIS (NCT02200614): Median metastasis free survival was 40.4 months for patients with darolutamide, compared with 18.4 months for controls.

Selinexor (Xpovio)

Class: Reversible inhibitor of nuclear export of tumor suppressor proteins, growth regulators, and mRNAs of oncogenic proteins.

Disease: Relapsed or refractory multiple myeloma. Indicated for patients who have received at least four prior therapies, including at least two immunomodulatory agents and an anti-CD38 monoclonal antibody.

Dose: 80 mg orally in combination with oral dexamethasone on days 1 and 3 of each week.

AEs: Thrombocytopenia, fatigue, pancytopenia, and hyponatremia.

Trial: STORM (NCT02336815): Overall response rate 25.3% with a median time to first response of 4 weeks and 3.8-month median duration of response.

Polatuzumab vedotin-piiq (Polivy)

Class: CD79b-directed antibody-drug conjugate.

Disease: Relapsed or refractory diffuse large B-cell lymphoma. Indicated for patients who have had at least two prior therapies.

Dose: 1.8 mg/kg intravenous infusion every 21 days for six cycles in combination with bendamustine and a rituximab product.

AEs: Pancytopenia, peripheral neuropathy.

Trial: GO29365 (NCT02257567): Complete response rate was 40% for polatuzumab vedotin-piiq plus bendamustine/rituximab, compared with 18% with bendamustine/rituximab alone.*

Caplacizumab-yhdp (Cablivi)

Class: Monoclonal antibody fragment directed against von Willebrand factor.

Disease: Thrombotic thrombocytopenic purpura.

Dose: 11 mg IV initially, then daily subcutaneously; in combination with plasma exchange and immunosuppressive therapy.

AEs: Epistaxis, headache, and gingival bleeding.

Trial: Hercules trial (NCT02553317): More rapid normalization of platelets, lower incidence of composite TTP-related death, and lower rate of recurrence when added to plasma exchange and steroids.
 

Alpelisib (Piqray)

Class: Phosphatidylinositol-3-kinase (PI3K) inhibitor.

Disease: Hormone receptor positive HER2-negative PIK3CA-mutated, advanced or metastatic breast cancer.

Dose: 300 mg orally once daily with food with concomitant fulvestrant.

AEs: Hyperglycemia, pancytopenia.

Trial: SOLAR-1 (NCT02437318): 11-month progression-free survival among patients treated with alpelisib and fulvestrant, compared with 5.7 months in fulvestrant alone control arm; overall response rate of 36% versus 16%, respectively.

Erdafitinib (Balversa)

Class: Fibroblast growth factor receptor kinase inhibitor.

Disease: Locally advanced or metastatic urothelial carcinoma with FGFR3 or FGFR2 mutations.

Dose: 8 mg orally once daily, with or without food.

AEs: Ocular disorders including retinopathy or retinal detachment.

Trial: BLC2001 (NCT02365597): Objective response rate of 32.2%, with a complete response in 2.3% of patients and partial response in 29.9% of patients.

Biosimilar approvals

Trastuzumab and hyaluronidase-oysk (Herceptin Hylecta)

Biosimilar to: Trastuzumab.

Indication: HER2-overexpressing breast cancer.
 

Dr. Bryer is a resident in the department of internal medicine at the University of Pennsylvania, Philadelphia. Dr. Mintzer is chief of hematology-oncology at Pennsylvania Hospital and professor of medicine at the University of Pennsylvania. Dr. Henry is a hematologist-oncologist at Pennsylvania Hospital and professor of medicine at the University of Pennsylvania.

*Correction, 11/7/2019: An earlier version of this article misstated the drug combination in the GO29365 trial.