Commentary

‘Enough!’ We need to take back our profession

Every day, I am grateful that I became a physician and a psychiatrist. Every minute that I spend with patients is an honor and a privilege. I have never forgotten that. But it is heartbreaking to see my precious profession being destroyed by bureaucrats.

An example: I am concerned about the effect that passage of the Medicare Access and CHIP Reauthorization Act of 2015 (MACRA) will have on physicians. I read articles telling us how we should handle this new plan for reimbursement, but I also read that 86% of physicians are not in favor of MACRA. How did we get stuck with it?

Another example of why it has become virtually impossible to do our job: I spend a fair amount of time obtaining prior authorization for generic medications that are available at big-box stores for $10 or $15; often, these authorizations need approval by the medical director. I have been beaten down enough over the years to learn that I should no longer prescribe brand-name medications—only generic medications (which still require authorization!), even when my patient has been taking the medication for 10 or 15 years. The last time I sought authorization to prescribe a medication, the reviewer asked me why I had not tried 3 different generics over the past year. I had to remind her that I had an active prior authorization in place from the year before, and so why would I do what she was proposing?

Physicians are some of the most highly trained professionals. It takes 7 to 15 years to be able to be somewhat proficient at the job, then another 30 or 40 years of practice to become really good at it. But we’ve become technicians at the mercy of business executives: We go to our office and spend our time checking off boxes, trying to figure out proper coding and the proper diagnosis, so that we can get an appropriate amount of money for the service we’re providing. How has it come to this? Why can’t we take back our profession?

Another problem is that physicians are being paid for their performance and the outcomes they produce. But people are not refrigerators: We can do everything right and the patient still dies. I have a number of patients who have no insight into their psychiatric illness; no matter what I say, or do, or how much time I spend with them, they are nonadherent. How is this my fault?

Physicians are not given the opportunity to think for themselves, or to prescribe treatments that they see fit and document in ways that they were trained. Where is the American Medical Association, the Connecticut State Medical Society, the Hartford County Medical Association, and all the other associations that supposedly represent us? How have they allowed this to happen?

In the future, health care will be provided by physician assistants and nurse practitioners; physicians will provide background supervision, or perform surgery, but the patient will never meet them. I respect NPs and PAs, but they do not have the rigorous training that physicians have. But they’re less expensive—and isn’t that what it’s all about?

If we are not going to speak up, or if we are not going to elect officials to truly represent us and advocate for us, then we have nobody to blame but ourselves.

Carole Black Cohen, MD

Private psychiatric practice

Farmington, Connecticut

In Dr. Nasrallah’s August essay (From the Editor, Current Psychiatry. "Unresolved questions about the specialty lurk in the cortex of psychiatrists," p. 10,11,19,19A), he asks, as he often does, provocative, unanswered questions. There are probably many more questions to include in his list, but I’ll just add 1—the one that I think is the biggest problem in our field: Why is the burnout rate of physicians steadily climbing, to the extent that it exceeds the epidemic rate of 50%? Although you would think that we, as psychiatrists, should be expert at understanding and addressing this problem, our own burnout rate is >40%. Moreover, why haven’t we developed programs to prevent and reduce burnout, when other specialties, such as urology and emergency medicine, have done so?

H. Steven Moffic, MD

Retired Tenured Professor of Psychiatry
Medical College of Wisconsin
Milwaukee, Wisconsin

Dr. Nasrallah responds

Dr. Moffic is spot-on about the escalating rate of burnout among physicians, including psychiatrists. The reason I did not include burnout in the list of questions is because I intended to pose questions related to external forces that interfere with patient care. Burnout is a vicious internal typhoon of emotional turmoil that might be related to multiple idiosyncratic personal variables and only partially to frustrations in clinical practice.

Burnout is, one might say, a subcortical event (generated in the amygdala?)—not a cortical process like the “why” questions that beg for answers. Admittedly, however, the cumulative burden of practice frustrations—especially the inability to erase the personal, social, financial, and vocational stigmata that plague our patients’ lives—can, eventually, take a toll on our morale and quality of life.

Fortunately, we psychiatrists generally are a resilient breed. We can manage personal stress using techniques that we employ in our practices. That might be why burnout is lower in psychiatry than it is in other medical specialties.

Henry A. Nasrallah, MD

Professor and Chair
Department of Psychiatry
Saint Louis University School of Medicine
St. Louis, Missouri

‘Enough!’ We need to take back our profession

Every day, I am grateful that I became a physician and a psychiatrist. Every minute that I spend with patients is an honor and a privilege. I have never forgotten that. But it is heartbreaking to see my precious profession being destroyed by bureaucrats.

An example: I am concerned about the effect that passage of the Medicare Access and CHIP Reauthorization Act of 2015 (MACRA) will have on physicians. I read articles telling us how we should handle this new plan for reimbursement, but I also read that 86% of physicians are not in favor of MACRA. How did we get stuck with it?

Another example of why it has become virtually impossible to do our job: I spend a fair amount of time obtaining prior authorization for generic medications that are available at big-box stores for $10 or $15; often, these authorizations need approval by the medical director. I have been beaten down enough over the years to learn that I should no longer prescribe brand-name medications—only generic medications (which still require authorization!), even when my patient has been taking the medication for 10 or 15 years. The last time I sought authorization to prescribe a medication, the reviewer asked me why I had not tried 3 different generics over the past year. I had to remind her that I had an active prior authorization in place from the year before, and so why would I do what she was proposing?

Physicians are some of the most highly trained professionals. It takes 7 to 15 years to be able to be somewhat proficient at the job, then another 30 or 40 years of practice to become really good at it. But we’ve become technicians at the mercy of business executives: We go to our office and spend our time checking off boxes, trying to figure out proper coding and the proper diagnosis, so that we can get an appropriate amount of money for the service we’re providing. How has it come to this? Why can’t we take back our profession?

Another problem is that physicians are being paid for their performance and the outcomes they produce. But people are not refrigerators: We can do everything right and the patient still dies. I have a number of patients who have no insight into their psychiatric illness; no matter what I say, or do, or how much time I spend with them, they are nonadherent. How is this my fault?

Physicians are not given the opportunity to think for themselves, or to prescribe treatments that they see fit and document in ways that they were trained. Where is the American Medical Association, the Connecticut State Medical Society, the Hartford County Medical Association, and all the other associations that supposedly represent us? How have they allowed this to happen?

In the future, health care will be provided by physician assistants and nurse practitioners; physicians will provide background supervision, or perform surgery, but the patient will never meet them. I respect NPs and PAs, but they do not have the rigorous training that physicians have. But they’re less expensive—and isn’t that what it’s all about?

If we are not going to speak up, or if we are not going to elect officials to truly represent us and advocate for us, then we have nobody to blame but ourselves.

Carole Black Cohen, MD

Private psychiatric practice

Farmington, Connecticut

In Dr. Nasrallah’s August essay (From the Editor, Current Psychiatry. "Unresolved questions about the specialty lurk in the cortex of psychiatrists," p. 10,11,19,19A), he asks, as he often does, provocative, unanswered questions. There are probably many more questions to include in his list, but I’ll just add 1—the one that I think is the biggest problem in our field: Why is the burnout rate of physicians steadily climbing, to the extent that it exceeds the epidemic rate of 50%? Although you would think that we, as psychiatrists, should be expert at understanding and addressing this problem, our own burnout rate is >40%. Moreover, why haven’t we developed programs to prevent and reduce burnout, when other specialties, such as urology and emergency medicine, have done so?

H. Steven Moffic, MD

Retired Tenured Professor of Psychiatry
Medical College of Wisconsin
Milwaukee, Wisconsin

Dr. Nasrallah responds

Dr. Moffic is spot-on about the escalating rate of burnout among physicians, including psychiatrists. The reason I did not include burnout in the list of questions is because I intended to pose questions related to external forces that interfere with patient care. Burnout is a vicious internal typhoon of emotional turmoil that might be related to multiple idiosyncratic personal variables and only partially to frustrations in clinical practice.

Burnout is, one might say, a subcortical event (generated in the amygdala?)—not a cortical process like the “why” questions that beg for answers. Admittedly, however, the cumulative burden of practice frustrations—especially the inability to erase the personal, social, financial, and vocational stigmata that plague our patients’ lives—can, eventually, take a toll on our morale and quality of life.

Fortunately, we psychiatrists generally are a resilient breed. We can manage personal stress using techniques that we employ in our practices. That might be why burnout is lower in psychiatry than it is in other medical specialties.

Henry A. Nasrallah, MD

Professor and Chair
Department of Psychiatry
Saint Louis University School of Medicine
St. Louis, Missouri

‘Enough!’ We need to take back our profession

Every day, I am grateful that I became a physician and a psychiatrist. Every minute that I spend with patients is an honor and a privilege. I have never forgotten that. But it is heartbreaking to see my precious profession being destroyed by bureaucrats.

An example: I am concerned about the effect that passage of the Medicare Access and CHIP Reauthorization Act of 2015 (MACRA) will have on physicians. I read articles telling us how we should handle this new plan for reimbursement, but I also read that 86% of physicians are not in favor of MACRA. How did we get stuck with it?

Another example of why it has become virtually impossible to do our job: I spend a fair amount of time obtaining prior authorization for generic medications that are available at big-box stores for $10 or $15; often, these authorizations need approval by the medical director. I have been beaten down enough over the years to learn that I should no longer prescribe brand-name medications—only generic medications (which still require authorization!), even when my patient has been taking the medication for 10 or 15 years. The last time I sought authorization to prescribe a medication, the reviewer asked me why I had not tried 3 different generics over the past year. I had to remind her that I had an active prior authorization in place from the year before, and so why would I do what she was proposing?

Physicians are some of the most highly trained professionals. It takes 7 to 15 years to be able to be somewhat proficient at the job, then another 30 or 40 years of practice to become really good at it. But we’ve become technicians at the mercy of business executives: We go to our office and spend our time checking off boxes, trying to figure out proper coding and the proper diagnosis, so that we can get an appropriate amount of money for the service we’re providing. How has it come to this? Why can’t we take back our profession?

Another problem is that physicians are being paid for their performance and the outcomes they produce. But people are not refrigerators: We can do everything right and the patient still dies. I have a number of patients who have no insight into their psychiatric illness; no matter what I say, or do, or how much time I spend with them, they are nonadherent. How is this my fault?

Physicians are not given the opportunity to think for themselves, or to prescribe treatments that they see fit and document in ways that they were trained. Where is the American Medical Association, the Connecticut State Medical Society, the Hartford County Medical Association, and all the other associations that supposedly represent us? How have they allowed this to happen?

In the future, health care will be provided by physician assistants and nurse practitioners; physicians will provide background supervision, or perform surgery, but the patient will never meet them. I respect NPs and PAs, but they do not have the rigorous training that physicians have. But they’re less expensive—and isn’t that what it’s all about?

If we are not going to speak up, or if we are not going to elect officials to truly represent us and advocate for us, then we have nobody to blame but ourselves.

Carole Black Cohen, MD

Private psychiatric practice

Farmington, Connecticut

In Dr. Nasrallah’s August essay (From the Editor, Current Psychiatry. "Unresolved questions about the specialty lurk in the cortex of psychiatrists," p. 10,11,19,19A), he asks, as he often does, provocative, unanswered questions. There are probably many more questions to include in his list, but I’ll just add 1—the one that I think is the biggest problem in our field: Why is the burnout rate of physicians steadily climbing, to the extent that it exceeds the epidemic rate of 50%? Although you would think that we, as psychiatrists, should be expert at understanding and addressing this problem, our own burnout rate is >40%. Moreover, why haven’t we developed programs to prevent and reduce burnout, when other specialties, such as urology and emergency medicine, have done so?

H. Steven Moffic, MD

Retired Tenured Professor of Psychiatry
Medical College of Wisconsin
Milwaukee, Wisconsin

Dr. Nasrallah responds

Dr. Moffic is spot-on about the escalating rate of burnout among physicians, including psychiatrists. The reason I did not include burnout in the list of questions is because I intended to pose questions related to external forces that interfere with patient care. Burnout is a vicious internal typhoon of emotional turmoil that might be related to multiple idiosyncratic personal variables and only partially to frustrations in clinical practice.

Burnout is, one might say, a subcortical event (generated in the amygdala?)—not a cortical process like the “why” questions that beg for answers. Admittedly, however, the cumulative burden of practice frustrations—especially the inability to erase the personal, social, financial, and vocational stigmata that plague our patients’ lives—can, eventually, take a toll on our morale and quality of life.

Fortunately, we psychiatrists generally are a resilient breed. We can manage personal stress using techniques that we employ in our practices. That might be why burnout is lower in psychiatry than it is in other medical specialties.

Henry A. Nasrallah, MD

Professor and Chair
Department of Psychiatry
Saint Louis University School of Medicine
St. Louis, Missouri

VAPING DANGERS: CLEARING THE AIR

The liquid base of an e-cigarette contains either vegetable glycerin (VG) or propylene glycol, or more commonly, a proprietary combination of both. Each of these ingredients has varying effects on the body.

However, the first paragraph of Randy D. Danielsen’s editorial alluded to what I consider a bigger concern regarding the future medical complications of vaping. The description of a “… huge puff of cherry-scented smoke …” indicates that vapes are not puffed on the way cigarettes are.

Cigarette smoking is similar to drinking through a straw—the smoke is first captured in the mouth, then cooled and inhaled. In contrast, vaping involves inhaling smoke directly into the lungs. This action, along with the thick VG base, produces a high volume of smoke. Vape shops even sponsor contests to see who can produce the largest cloud of smoke.

Therefore, my concern regarding vaping is not limited to the toxicity of the ingredients; it extends to how the toxicants are delivered to the poor, unsuspecting alveoli.

Gary Dula, FNP-C
Houston, TX

Continue for Millenials: Not All Sitting at the Kids' Table >>

MILLENIALS: NOT ALL SITTING AT THE KIDS' TABLES

I received my master’s degree in 2015 and am nearing completion of a year-long FNP fellowship program. I was an Army nurse for four years and a float nurse at various hospitals for five. I am a “millennial”—and, according to the published letters about precepting, am hated by older nurses because of it. Considering I have practiced with many hard-working people my age who would lay down their lives for this country, I find this unprecedented.

I work hard, but the school I attended for my FNP did not prepare me well; it was difficult to get people to teach and precept me during school. This led me to apply for my current fellowship.

Throughout my nine-year nursing career, I have precepted many nurses, including those with associate degrees. I will continue to mentor and precept as an APRN. I take issue with the portrayal of millennials as lazy and unable to work hard. Why? Because we will not work for free, would like to collaboratively learn, and need help to develop our skills?

One day, you will grow old and need someone to take care of you. Why on earth would you berate the people who will be doing just that? Complaining about this generation is not going to change the fact that they are here and present in the workforce. We need more providers, and chastising the younger generation is not going to solve that problem.

Stephanie Butler-Cleland, FNP-BC
Colorado Springs, CO

Continue for The Pros of Precepting >>

THE PROS OF PRECEPTING

I am an urgent care NP in urban communities on the West Coast of Florida. I had taken a break from precepting as a result of negative experiences, but I recently resumed to precept my first NP student in years.

Prior to accepting the student I precepted, I received requests from two other students. One asked if I could change my schedule to be closer to where she lived. The other clearly didn’t want to commit to the drive or the hours I was available, and asked if I would work more weekends to accommodate her schedule. Needless to say, I refused both students.

Instead, I precepted a smart 28-year-old student from my alma mater, one of the Florida state universities. She was attentive, prepared, and eager. I was very, very impressed with her. She had been a nurse for four years and was a second-semester student. It was a pleasure to have her; I like being questioned and challenged. It was fun to see her enjoying my job, and it reminded me of why I love what I do.

Anne Conklin, MS, ARNP-C
Bradenton, FL

Continue for A Scheming Industry >>

A SCHEMING INDUSTRY

Intelligent health care policy has been frustrated by the enormous amount of money brought to bear on Congress by the insurance and pharmaceutical industries. Each dollar paid to an insurance company is used to construct buildings, hire workers, create a sales staff, and ultimately pay their shareholders a profit.

Since the insurance industry obtained an antitrust exemption in the 1940s, they are essentially immune from prosecution for price collusion. Until recently, it was difficult to know how much of the money paid was returned in the form of medical benefits. In order to keep profits rising, they must enroll more people. Promising coverage while impeding medical workups and care, making great profits, and needing more and more enrollees fits the definition of a Ponzi scheme.

Several years ago in California, the state insurance commission (under threat of decertification) got an industry representative to admit that the maximum percentage of dollars used for services was 70%. In other words, for each dollar spent, a patient would be lucky to get 70 cents worth of services.

All of us who practice know how the companies do this: We request a needed diagnostic test or treatment and are denied. I have interrupted my schedule on many days to call for a “peer to peer” review—only once was I denied. This is a roadblock that many busy practitioners will not challenge. Since insurance companies market how great their coverage is, patients often get angry at the provider.

The repeated argument is that the market forces will lower medical costs. This fallacy is easily debunked by noting the ever-escalating costs and comparing health care costs as a percent of gross domestic product (GDP) in our country versus others. France, for example, expends 12% of GDP on health and ranks first in health care outcomes by world standards. In the US, we are approaching 20% of GDP.

Since insurance adds nothing to care and increases costs dramatically (every provider has to have billers for the various insurance companies, since each has its own requirements), a single-payer system is the only system that will lower costs. Those who benefit from the current system declare that we can’t have “socialized medicine.” To which I would respond, fine; we’ll continue to pay 30% to 50% more so that insurance companies can have their profits at our expense.

Nelson Herilhy, PA-C, MHS
Concord, CA

VAPING DANGERS: CLEARING THE AIR

The liquid base of an e-cigarette contains either vegetable glycerin (VG) or propylene glycol, or more commonly, a proprietary combination of both. Each of these ingredients has varying effects on the body.

However, the first paragraph of Randy D. Danielsen’s editorial alluded to what I consider a bigger concern regarding the future medical complications of vaping. The description of a “… huge puff of cherry-scented smoke …” indicates that vapes are not puffed on the way cigarettes are.

Cigarette smoking is similar to drinking through a straw—the smoke is first captured in the mouth, then cooled and inhaled. In contrast, vaping involves inhaling smoke directly into the lungs. This action, along with the thick VG base, produces a high volume of smoke. Vape shops even sponsor contests to see who can produce the largest cloud of smoke.

Therefore, my concern regarding vaping is not limited to the toxicity of the ingredients; it extends to how the toxicants are delivered to the poor, unsuspecting alveoli.

Gary Dula, FNP-C
Houston, TX

Continue for Millenials: Not All Sitting at the Kids' Table >>

MILLENIALS: NOT ALL SITTING AT THE KIDS' TABLES

I received my master’s degree in 2015 and am nearing completion of a year-long FNP fellowship program. I was an Army nurse for four years and a float nurse at various hospitals for five. I am a “millennial”—and, according to the published letters about precepting, am hated by older nurses because of it. Considering I have practiced with many hard-working people my age who would lay down their lives for this country, I find this unprecedented.

I work hard, but the school I attended for my FNP did not prepare me well; it was difficult to get people to teach and precept me during school. This led me to apply for my current fellowship.

Throughout my nine-year nursing career, I have precepted many nurses, including those with associate degrees. I will continue to mentor and precept as an APRN. I take issue with the portrayal of millennials as lazy and unable to work hard. Why? Because we will not work for free, would like to collaboratively learn, and need help to develop our skills?

One day, you will grow old and need someone to take care of you. Why on earth would you berate the people who will be doing just that? Complaining about this generation is not going to change the fact that they are here and present in the workforce. We need more providers, and chastising the younger generation is not going to solve that problem.

Stephanie Butler-Cleland, FNP-BC
Colorado Springs, CO

Continue for The Pros of Precepting >>

THE PROS OF PRECEPTING

I am an urgent care NP in urban communities on the West Coast of Florida. I had taken a break from precepting as a result of negative experiences, but I recently resumed to precept my first NP student in years.

Prior to accepting the student I precepted, I received requests from two other students. One asked if I could change my schedule to be closer to where she lived. The other clearly didn’t want to commit to the drive or the hours I was available, and asked if I would work more weekends to accommodate her schedule. Needless to say, I refused both students.

Instead, I precepted a smart 28-year-old student from my alma mater, one of the Florida state universities. She was attentive, prepared, and eager. I was very, very impressed with her. She had been a nurse for four years and was a second-semester student. It was a pleasure to have her; I like being questioned and challenged. It was fun to see her enjoying my job, and it reminded me of why I love what I do.

Anne Conklin, MS, ARNP-C
Bradenton, FL

Continue for A Scheming Industry >>

A SCHEMING INDUSTRY

Intelligent health care policy has been frustrated by the enormous amount of money brought to bear on Congress by the insurance and pharmaceutical industries. Each dollar paid to an insurance company is used to construct buildings, hire workers, create a sales staff, and ultimately pay their shareholders a profit.

Since the insurance industry obtained an antitrust exemption in the 1940s, they are essentially immune from prosecution for price collusion. Until recently, it was difficult to know how much of the money paid was returned in the form of medical benefits. In order to keep profits rising, they must enroll more people. Promising coverage while impeding medical workups and care, making great profits, and needing more and more enrollees fits the definition of a Ponzi scheme.

Several years ago in California, the state insurance commission (under threat of decertification) got an industry representative to admit that the maximum percentage of dollars used for services was 70%. In other words, for each dollar spent, a patient would be lucky to get 70 cents worth of services.

All of us who practice know how the companies do this: We request a needed diagnostic test or treatment and are denied. I have interrupted my schedule on many days to call for a “peer to peer” review—only once was I denied. This is a roadblock that many busy practitioners will not challenge. Since insurance companies market how great their coverage is, patients often get angry at the provider.

The repeated argument is that the market forces will lower medical costs. This fallacy is easily debunked by noting the ever-escalating costs and comparing health care costs as a percent of gross domestic product (GDP) in our country versus others. France, for example, expends 12% of GDP on health and ranks first in health care outcomes by world standards. In the US, we are approaching 20% of GDP.

Since insurance adds nothing to care and increases costs dramatically (every provider has to have billers for the various insurance companies, since each has its own requirements), a single-payer system is the only system that will lower costs. Those who benefit from the current system declare that we can’t have “socialized medicine.” To which I would respond, fine; we’ll continue to pay 30% to 50% more so that insurance companies can have their profits at our expense.

Nelson Herilhy, PA-C, MHS
Concord, CA

VAPING DANGERS: CLEARING THE AIR

The liquid base of an e-cigarette contains either vegetable glycerin (VG) or propylene glycol, or more commonly, a proprietary combination of both. Each of these ingredients has varying effects on the body.

However, the first paragraph of Randy D. Danielsen’s editorial alluded to what I consider a bigger concern regarding the future medical complications of vaping. The description of a “… huge puff of cherry-scented smoke …” indicates that vapes are not puffed on the way cigarettes are.

Cigarette smoking is similar to drinking through a straw—the smoke is first captured in the mouth, then cooled and inhaled. In contrast, vaping involves inhaling smoke directly into the lungs. This action, along with the thick VG base, produces a high volume of smoke. Vape shops even sponsor contests to see who can produce the largest cloud of smoke.

Therefore, my concern regarding vaping is not limited to the toxicity of the ingredients; it extends to how the toxicants are delivered to the poor, unsuspecting alveoli.

Gary Dula, FNP-C
Houston, TX

Continue for Millenials: Not All Sitting at the Kids' Table >>

MILLENIALS: NOT ALL SITTING AT THE KIDS' TABLES

I received my master’s degree in 2015 and am nearing completion of a year-long FNP fellowship program. I was an Army nurse for four years and a float nurse at various hospitals for five. I am a “millennial”—and, according to the published letters about precepting, am hated by older nurses because of it. Considering I have practiced with many hard-working people my age who would lay down their lives for this country, I find this unprecedented.

I work hard, but the school I attended for my FNP did not prepare me well; it was difficult to get people to teach and precept me during school. This led me to apply for my current fellowship.

Throughout my nine-year nursing career, I have precepted many nurses, including those with associate degrees. I will continue to mentor and precept as an APRN. I take issue with the portrayal of millennials as lazy and unable to work hard. Why? Because we will not work for free, would like to collaboratively learn, and need help to develop our skills?

One day, you will grow old and need someone to take care of you. Why on earth would you berate the people who will be doing just that? Complaining about this generation is not going to change the fact that they are here and present in the workforce. We need more providers, and chastising the younger generation is not going to solve that problem.

Stephanie Butler-Cleland, FNP-BC
Colorado Springs, CO

Continue for The Pros of Precepting >>

THE PROS OF PRECEPTING

I am an urgent care NP in urban communities on the West Coast of Florida. I had taken a break from precepting as a result of negative experiences, but I recently resumed to precept my first NP student in years.

Prior to accepting the student I precepted, I received requests from two other students. One asked if I could change my schedule to be closer to where she lived. The other clearly didn’t want to commit to the drive or the hours I was available, and asked if I would work more weekends to accommodate her schedule. Needless to say, I refused both students.

Instead, I precepted a smart 28-year-old student from my alma mater, one of the Florida state universities. She was attentive, prepared, and eager. I was very, very impressed with her. She had been a nurse for four years and was a second-semester student. It was a pleasure to have her; I like being questioned and challenged. It was fun to see her enjoying my job, and it reminded me of why I love what I do.

Anne Conklin, MS, ARNP-C
Bradenton, FL

Continue for A Scheming Industry >>

A SCHEMING INDUSTRY

Intelligent health care policy has been frustrated by the enormous amount of money brought to bear on Congress by the insurance and pharmaceutical industries. Each dollar paid to an insurance company is used to construct buildings, hire workers, create a sales staff, and ultimately pay their shareholders a profit.

Since the insurance industry obtained an antitrust exemption in the 1940s, they are essentially immune from prosecution for price collusion. Until recently, it was difficult to know how much of the money paid was returned in the form of medical benefits. In order to keep profits rising, they must enroll more people. Promising coverage while impeding medical workups and care, making great profits, and needing more and more enrollees fits the definition of a Ponzi scheme.

Several years ago in California, the state insurance commission (under threat of decertification) got an industry representative to admit that the maximum percentage of dollars used for services was 70%. In other words, for each dollar spent, a patient would be lucky to get 70 cents worth of services.

All of us who practice know how the companies do this: We request a needed diagnostic test or treatment and are denied. I have interrupted my schedule on many days to call for a “peer to peer” review—only once was I denied. This is a roadblock that many busy practitioners will not challenge. Since insurance companies market how great their coverage is, patients often get angry at the provider.

The repeated argument is that the market forces will lower medical costs. This fallacy is easily debunked by noting the ever-escalating costs and comparing health care costs as a percent of gross domestic product (GDP) in our country versus others. France, for example, expends 12% of GDP on health and ranks first in health care outcomes by world standards. In the US, we are approaching 20% of GDP.

Since insurance adds nothing to care and increases costs dramatically (every provider has to have billers for the various insurance companies, since each has its own requirements), a single-payer system is the only system that will lower costs. Those who benefit from the current system declare that we can’t have “socialized medicine.” To which I would respond, fine; we’ll continue to pay 30% to 50% more so that insurance companies can have their profits at our expense.

Nelson Herilhy, PA-C, MHS
Concord, CA

On May 25, 2016, the Department of Veterans Affairs (VA) published a proposed rule change in the Federal Register under the simple heading “Advanced Practice Registered Nurses.” From such modest beginnings stemmed a potential game-changer for advanced practice clinicians in this country: In summary, the VA proposed to “amend its medical regulations to permit full practice authority of all VA advanced practice registered nurses (APRNs) when they are acting within the scope of their VA employment.”¹

The impetus for the VA’s proposal is that 505,000 veterans wait 30 days to access care within the VA system—and 300,000 wait between 31 and 60 days for health services.² Granting plenary practice to VA APRNs would enable them to respond to this backlog of patients, since veterans would have direct access to APRNs who practice within the VA system, regardless of their state of licensure.

More than 4,800 NPs work within the VA; they provide clinical assessments, order appropriate tests and medications, and develop patient-centered care plans.^2,3 Research has documented that outcomes for patients whose care is managed by NPs are equal to or better than outcomes for similar patients who are managed by physicians.⁴ As Major General Vincent Boles of the US Army (retired) stated, “Veterans rely on VA health care to take care of them, and the VA’s nurse practitioners are qualified to provide our veterans with the care they need and deserve.”⁴

Allowing veterans access to high-quality care is a 21st century solution that is “zero risk, zero cost, zero delay,” according to Dr. Cindy Cooke, President of the American Association of Nurse Practitioners (AANP).⁴ And it is not just the AANP that supports this rule change. Ninety-one percent of US households that are home to a veteran, and 88% of Americans overall, express support for the VA proposal. In a Mellman Group survey of more than 1,000 adults, strong support was noted across party lines (91% of Republicans; 90% of Democrats)—a rarity in our current political climate.⁴

Support for full practice authority for NPs at the VA has come from more than 60 organizations, including the Military Officers’ Association of America, the Air Force Sergeants Association, AARP (with 3.7 million veteran households in its membership), and 80 bipartisan members of Congress.⁵ At the AANP annual conference in San Antonio, Dr. Cooke was joined by leaders from the local American Legion and retired military officers who announced their support for this “change in practice.”³

However, among the more than 162,000 comments received by the VA during the public comment period, there were dissenting opinions. On July 13, 2016, Dr. Robert Wergin, Chair of the Board of the American Academy of Family Physicians (AAFP), sent a letter to Dr. David Shulkin, the Undersecretary of Health in the VA, stating that there were “significant concerns” about the rule change. His main point was that granting full practice authority to NPs would “alter the consistent standards of care for veterans over nonveterans in the states; further fragment the health care system; and dismantle physician-led team-based health care models.” He also stated that “the AAFP strongly opposes the unprecedented proposal to dismiss state practice authority regarding the authority of NPs.”⁶

Unprecedented? I don’t think so. I practiced as a family NP in the Navy for more than 20 years. I had my own patient panel, cared for active duty members and their families, and evaluated outcomes the same way my physician ­colleagues did. We practiced collaboratively and respectfully. We discussed patient plan issues, provided peer review on one another’s charts, and accepted new patients into our panels. It was a true collaborative practice.

Military nurses only need to be licensed in one state. The guidelines for NP practice were not based on the rules of the state in which we were licensed but were established by our professional practice association—just as the guidelines for physician practice were not based on the rules extant in their licensing state. I practiced successfully in many states and overseas, although I was licensed in a state that did not recognize plenary practice at the time.

The VA is attempting to respond to veterans’ need for access to care by adopting a model similar to what the military employs. It’s not a matter of superseding state regulations; it’s a matter of recognizing the education and training of health care professionals who can improve patient outcomes.

The opportunity to respond to the proposed amendment has now closed. Through its grassroots Veterans Deserve Care campaign, the AANP and its partners and supporters—clinicians, veterans, families, and others—submitted nearly 60,000 comments.² Now we wait for the VA to review the abundance of feedback and issue their final decision.

I am hopeful that the VA will acknowledge the overwhelming evidence that our veterans deserve access to care led by highly qualified professionals. The old system isn’t working. Einstein said that the definition of insanity was to do the same thing over and over and expect a different outcome; maintaining a faulty system fits that description. NPs have a well-tested, evidence-based, high-quality education that encourages their ability to lead health care teams, perform collaboratively, and improve outcomes for those who have served our country.

Caring for active duty military and veterans is in the DNA of nurses. Florence Nightingale spent much of her post-Crimea life using evidence-based proposals and political influence to improve the health care of the soldiers and veterans of the British Empire. In Notes on Nursing, she spurred nurses to political action: “Let whoever [sic] is in charge keep this simple question in her [sic] head (not how can I always do this right thing myself, but) how can I provide for this right thing to be always done?”⁷ This advice should be taken to heart by all health care professionals: We can honor our veterans by advocating for and providing the health care access they need.

To share your thoughts, please contact us at [email protected]

On May 25, 2016, the Department of Veterans Affairs (VA) published a proposed rule change in the Federal Register under the simple heading “Advanced Practice Registered Nurses.” From such modest beginnings stemmed a potential game-changer for advanced practice clinicians in this country: In summary, the VA proposed to “amend its medical regulations to permit full practice authority of all VA advanced practice registered nurses (APRNs) when they are acting within the scope of their VA employment.”¹

The impetus for the VA’s proposal is that 505,000 veterans wait 30 days to access care within the VA system—and 300,000 wait between 31 and 60 days for health services.² Granting plenary practice to VA APRNs would enable them to respond to this backlog of patients, since veterans would have direct access to APRNs who practice within the VA system, regardless of their state of licensure.

More than 4,800 NPs work within the VA; they provide clinical assessments, order appropriate tests and medications, and develop patient-centered care plans.^2,3 Research has documented that outcomes for patients whose care is managed by NPs are equal to or better than outcomes for similar patients who are managed by physicians.⁴ As Major General Vincent Boles of the US Army (retired) stated, “Veterans rely on VA health care to take care of them, and the VA’s nurse practitioners are qualified to provide our veterans with the care they need and deserve.”⁴

Allowing veterans access to high-quality care is a 21st century solution that is “zero risk, zero cost, zero delay,” according to Dr. Cindy Cooke, President of the American Association of Nurse Practitioners (AANP).⁴ And it is not just the AANP that supports this rule change. Ninety-one percent of US households that are home to a veteran, and 88% of Americans overall, express support for the VA proposal. In a Mellman Group survey of more than 1,000 adults, strong support was noted across party lines (91% of Republicans; 90% of Democrats)—a rarity in our current political climate.⁴

Support for full practice authority for NPs at the VA has come from more than 60 organizations, including the Military Officers’ Association of America, the Air Force Sergeants Association, AARP (with 3.7 million veteran households in its membership), and 80 bipartisan members of Congress.⁵ At the AANP annual conference in San Antonio, Dr. Cooke was joined by leaders from the local American Legion and retired military officers who announced their support for this “change in practice.”³

However, among the more than 162,000 comments received by the VA during the public comment period, there were dissenting opinions. On July 13, 2016, Dr. Robert Wergin, Chair of the Board of the American Academy of Family Physicians (AAFP), sent a letter to Dr. David Shulkin, the Undersecretary of Health in the VA, stating that there were “significant concerns” about the rule change. His main point was that granting full practice authority to NPs would “alter the consistent standards of care for veterans over nonveterans in the states; further fragment the health care system; and dismantle physician-led team-based health care models.” He also stated that “the AAFP strongly opposes the unprecedented proposal to dismiss state practice authority regarding the authority of NPs.”⁶

Unprecedented? I don’t think so. I practiced as a family NP in the Navy for more than 20 years. I had my own patient panel, cared for active duty members and their families, and evaluated outcomes the same way my physician ­colleagues did. We practiced collaboratively and respectfully. We discussed patient plan issues, provided peer review on one another’s charts, and accepted new patients into our panels. It was a true collaborative practice.

Military nurses only need to be licensed in one state. The guidelines for NP practice were not based on the rules of the state in which we were licensed but were established by our professional practice association—just as the guidelines for physician practice were not based on the rules extant in their licensing state. I practiced successfully in many states and overseas, although I was licensed in a state that did not recognize plenary practice at the time.

The VA is attempting to respond to veterans’ need for access to care by adopting a model similar to what the military employs. It’s not a matter of superseding state regulations; it’s a matter of recognizing the education and training of health care professionals who can improve patient outcomes.

The opportunity to respond to the proposed amendment has now closed. Through its grassroots Veterans Deserve Care campaign, the AANP and its partners and supporters—clinicians, veterans, families, and others—submitted nearly 60,000 comments.² Now we wait for the VA to review the abundance of feedback and issue their final decision.

I am hopeful that the VA will acknowledge the overwhelming evidence that our veterans deserve access to care led by highly qualified professionals. The old system isn’t working. Einstein said that the definition of insanity was to do the same thing over and over and expect a different outcome; maintaining a faulty system fits that description. NPs have a well-tested, evidence-based, high-quality education that encourages their ability to lead health care teams, perform collaboratively, and improve outcomes for those who have served our country.

Caring for active duty military and veterans is in the DNA of nurses. Florence Nightingale spent much of her post-Crimea life using evidence-based proposals and political influence to improve the health care of the soldiers and veterans of the British Empire. In Notes on Nursing, she spurred nurses to political action: “Let whoever [sic] is in charge keep this simple question in her [sic] head (not how can I always do this right thing myself, but) how can I provide for this right thing to be always done?”⁷ This advice should be taken to heart by all health care professionals: We can honor our veterans by advocating for and providing the health care access they need.

To share your thoughts, please contact us at [email protected]

On May 25, 2016, the Department of Veterans Affairs (VA) published a proposed rule change in the Federal Register under the simple heading “Advanced Practice Registered Nurses.” From such modest beginnings stemmed a potential game-changer for advanced practice clinicians in this country: In summary, the VA proposed to “amend its medical regulations to permit full practice authority of all VA advanced practice registered nurses (APRNs) when they are acting within the scope of their VA employment.”¹

The impetus for the VA’s proposal is that 505,000 veterans wait 30 days to access care within the VA system—and 300,000 wait between 31 and 60 days for health services.² Granting plenary practice to VA APRNs would enable them to respond to this backlog of patients, since veterans would have direct access to APRNs who practice within the VA system, regardless of their state of licensure.

More than 4,800 NPs work within the VA; they provide clinical assessments, order appropriate tests and medications, and develop patient-centered care plans.^2,3 Research has documented that outcomes for patients whose care is managed by NPs are equal to or better than outcomes for similar patients who are managed by physicians.⁴ As Major General Vincent Boles of the US Army (retired) stated, “Veterans rely on VA health care to take care of them, and the VA’s nurse practitioners are qualified to provide our veterans with the care they need and deserve.”⁴

Allowing veterans access to high-quality care is a 21st century solution that is “zero risk, zero cost, zero delay,” according to Dr. Cindy Cooke, President of the American Association of Nurse Practitioners (AANP).⁴ And it is not just the AANP that supports this rule change. Ninety-one percent of US households that are home to a veteran, and 88% of Americans overall, express support for the VA proposal. In a Mellman Group survey of more than 1,000 adults, strong support was noted across party lines (91% of Republicans; 90% of Democrats)—a rarity in our current political climate.⁴

Support for full practice authority for NPs at the VA has come from more than 60 organizations, including the Military Officers’ Association of America, the Air Force Sergeants Association, AARP (with 3.7 million veteran households in its membership), and 80 bipartisan members of Congress.⁵ At the AANP annual conference in San Antonio, Dr. Cooke was joined by leaders from the local American Legion and retired military officers who announced their support for this “change in practice.”³

However, among the more than 162,000 comments received by the VA during the public comment period, there were dissenting opinions. On July 13, 2016, Dr. Robert Wergin, Chair of the Board of the American Academy of Family Physicians (AAFP), sent a letter to Dr. David Shulkin, the Undersecretary of Health in the VA, stating that there were “significant concerns” about the rule change. His main point was that granting full practice authority to NPs would “alter the consistent standards of care for veterans over nonveterans in the states; further fragment the health care system; and dismantle physician-led team-based health care models.” He also stated that “the AAFP strongly opposes the unprecedented proposal to dismiss state practice authority regarding the authority of NPs.”⁶

Unprecedented? I don’t think so. I practiced as a family NP in the Navy for more than 20 years. I had my own patient panel, cared for active duty members and their families, and evaluated outcomes the same way my physician ­colleagues did. We practiced collaboratively and respectfully. We discussed patient plan issues, provided peer review on one another’s charts, and accepted new patients into our panels. It was a true collaborative practice.

Military nurses only need to be licensed in one state. The guidelines for NP practice were not based on the rules of the state in which we were licensed but were established by our professional practice association—just as the guidelines for physician practice were not based on the rules extant in their licensing state. I practiced successfully in many states and overseas, although I was licensed in a state that did not recognize plenary practice at the time.

The VA is attempting to respond to veterans’ need for access to care by adopting a model similar to what the military employs. It’s not a matter of superseding state regulations; it’s a matter of recognizing the education and training of health care professionals who can improve patient outcomes.

The opportunity to respond to the proposed amendment has now closed. Through its grassroots Veterans Deserve Care campaign, the AANP and its partners and supporters—clinicians, veterans, families, and others—submitted nearly 60,000 comments.² Now we wait for the VA to review the abundance of feedback and issue their final decision.

I am hopeful that the VA will acknowledge the overwhelming evidence that our veterans deserve access to care led by highly qualified professionals. The old system isn’t working. Einstein said that the definition of insanity was to do the same thing over and over and expect a different outcome; maintaining a faulty system fits that description. NPs have a well-tested, evidence-based, high-quality education that encourages their ability to lead health care teams, perform collaboratively, and improve outcomes for those who have served our country.

Caring for active duty military and veterans is in the DNA of nurses. Florence Nightingale spent much of her post-Crimea life using evidence-based proposals and political influence to improve the health care of the soldiers and veterans of the British Empire. In Notes on Nursing, she spurred nurses to political action: “Let whoever [sic] is in charge keep this simple question in her [sic] head (not how can I always do this right thing myself, but) how can I provide for this right thing to be always done?”⁷ This advice should be taken to heart by all health care professionals: We can honor our veterans by advocating for and providing the health care access they need.

To share your thoughts, please contact us at [email protected]

Origin of pain: Brain vs body. Recent research provides strong evidence that in some cases of intractable chronic pain, the origin of the pain signal is in the brain—rather than the body. In this issue of JFP, Davis and Vanderah discuss this type of pain as “a third kind” that needs to be treated in a manner that completely differs from that for peripherally generated pain. They refer to the traditional kinds of pain as either nociceptive (resulting from tissue damage or insult), or neuropathic (due to dysfunctional stimulation of peripheral nerves). The neurophysiology of the third kind of pain, which I will call “centrally generated pain,” is not fully understood, but neuroimaging and other sophisticated methods are identifying areas of the brain that become activated by psychological trauma, leading to significant painful suffering in the absence of tissue damage, or that is far out of proportion to physical insult.

The bad news for primary care physicians is that this third kind of pain is difficult, if not impossible, to treat with our traditional armamentarium of pain medications and physical modalities. In fact, these patients are often at risk for addiction, as doses of ineffective narcotics are escalated.

Recent research provides strong evidence that in some cases of intractable chronic pain, the origin of the pain signal is in the brain—rather than the body.

The good news is that clinical researchers have begun to identify ways to effectively treat centrally generated pain. For example, Schubiner et al used a novel psychological approach that involved helping patients "learn that their pain is influenced primarily by central nervous system psychological processes, and to enhance awareness and expression of emotions related to psychological trauma or conflict."¹ Thirty percent of the 72 participants in the preliminary, uncontrolled trial experienced a 70% reduction in pain. Dr. Schubiner’s research is ongoing and supported by funding from the National Institutes of Health.

Proper diagnosis is paramount. Of course, proper diagnosis is paramount because an individual may suffer from more than one of the 3 kinds of pain and require different approaches for each. Thorough evaluation at a multidisciplinary pain clinic is a good place to start. Once the diagnoses are sorted out, it will then be possible to treat each component of pain appropriately.

Dr. Schubiner’s methods and other new and developing treatment approaches to chronic pain will help us better relieve patients’ suffering, reduce narcotic overuse, and relieve our own anxiety about caring for these challenging patients.

1. Burger AJ, Lumley MA, Carty JN, et al. The effects of a novel psychological attribution and emotional awareness and expression therapy for chronic musculoskeletal pain: a preliminary, uncontrolled trial. J Psychosom Res. 2016;81:1-8.

Origin of pain: Brain vs body. Recent research provides strong evidence that in some cases of intractable chronic pain, the origin of the pain signal is in the brain—rather than the body. In this issue of JFP, Davis and Vanderah discuss this type of pain as “a third kind” that needs to be treated in a manner that completely differs from that for peripherally generated pain. They refer to the traditional kinds of pain as either nociceptive (resulting from tissue damage or insult), or neuropathic (due to dysfunctional stimulation of peripheral nerves). The neurophysiology of the third kind of pain, which I will call “centrally generated pain,” is not fully understood, but neuroimaging and other sophisticated methods are identifying areas of the brain that become activated by psychological trauma, leading to significant painful suffering in the absence of tissue damage, or that is far out of proportion to physical insult.

The bad news for primary care physicians is that this third kind of pain is difficult, if not impossible, to treat with our traditional armamentarium of pain medications and physical modalities. In fact, these patients are often at risk for addiction, as doses of ineffective narcotics are escalated.

Recent research provides strong evidence that in some cases of intractable chronic pain, the origin of the pain signal is in the brain—rather than the body.

The good news is that clinical researchers have begun to identify ways to effectively treat centrally generated pain. For example, Schubiner et al used a novel psychological approach that involved helping patients "learn that their pain is influenced primarily by central nervous system psychological processes, and to enhance awareness and expression of emotions related to psychological trauma or conflict."¹ Thirty percent of the 72 participants in the preliminary, uncontrolled trial experienced a 70% reduction in pain. Dr. Schubiner’s research is ongoing and supported by funding from the National Institutes of Health.

Proper diagnosis is paramount. Of course, proper diagnosis is paramount because an individual may suffer from more than one of the 3 kinds of pain and require different approaches for each. Thorough evaluation at a multidisciplinary pain clinic is a good place to start. Once the diagnoses are sorted out, it will then be possible to treat each component of pain appropriately.

Dr. Schubiner’s methods and other new and developing treatment approaches to chronic pain will help us better relieve patients’ suffering, reduce narcotic overuse, and relieve our own anxiety about caring for these challenging patients.

1. Burger AJ, Lumley MA, Carty JN, et al. The effects of a novel psychological attribution and emotional awareness and expression therapy for chronic musculoskeletal pain: a preliminary, uncontrolled trial. J Psychosom Res. 2016;81:1-8.

Origin of pain: Brain vs body. Recent research provides strong evidence that in some cases of intractable chronic pain, the origin of the pain signal is in the brain—rather than the body. In this issue of JFP, Davis and Vanderah discuss this type of pain as “a third kind” that needs to be treated in a manner that completely differs from that for peripherally generated pain. They refer to the traditional kinds of pain as either nociceptive (resulting from tissue damage or insult), or neuropathic (due to dysfunctional stimulation of peripheral nerves). The neurophysiology of the third kind of pain, which I will call “centrally generated pain,” is not fully understood, but neuroimaging and other sophisticated methods are identifying areas of the brain that become activated by psychological trauma, leading to significant painful suffering in the absence of tissue damage, or that is far out of proportion to physical insult.

The bad news for primary care physicians is that this third kind of pain is difficult, if not impossible, to treat with our traditional armamentarium of pain medications and physical modalities. In fact, these patients are often at risk for addiction, as doses of ineffective narcotics are escalated.

Recent research provides strong evidence that in some cases of intractable chronic pain, the origin of the pain signal is in the brain—rather than the body.

The good news is that clinical researchers have begun to identify ways to effectively treat centrally generated pain. For example, Schubiner et al used a novel psychological approach that involved helping patients "learn that their pain is influenced primarily by central nervous system psychological processes, and to enhance awareness and expression of emotions related to psychological trauma or conflict."¹ Thirty percent of the 72 participants in the preliminary, uncontrolled trial experienced a 70% reduction in pain. Dr. Schubiner’s research is ongoing and supported by funding from the National Institutes of Health.

Proper diagnosis is paramount. Of course, proper diagnosis is paramount because an individual may suffer from more than one of the 3 kinds of pain and require different approaches for each. Thorough evaluation at a multidisciplinary pain clinic is a good place to start. Once the diagnoses are sorted out, it will then be possible to treat each component of pain appropriately.

Dr. Schubiner’s methods and other new and developing treatment approaches to chronic pain will help us better relieve patients’ suffering, reduce narcotic overuse, and relieve our own anxiety about caring for these challenging patients.

1. Burger AJ, Lumley MA, Carty JN, et al. The effects of a novel psychological attribution and emotional awareness and expression therapy for chronic musculoskeletal pain: a preliminary, uncontrolled trial. J Psychosom Res. 2016;81:1-8.

Atopic dermatitis (AD) is the most common inflammatory skin disease in both adults and children.¹ Unfortunately, the current treatment armamentarium is largely confined to topical calcineurin inhibitors, topical and systemic steroids, phototherapy, cyclosporine (not approved by the US Food and Drug Administration for AD), and other oral immunosuppressants.² The availability of partially helpful and highly toxic treatments creates a huge unmet need for more effective and safer treatments, particularly for patients with moderate to severe AD who often require systemic approaches.

Recent extensive translational (bench top to bedside and back) investigations in skin of AD patients has shown that skin phenotype is characterized by increased T-cell infiltration and related inflammatory cytokines as well as epidermal abnormalities (eg, hyperplasia, aberrant differentiation).³ Clinical improvement of AD has been demonstrated with broad T-cell targeted therapeutics, such as cyclosporine and narrowband UVB, coupled with decreases of T-cell infiltrates and inflammatory gene products as well as improvement of the pathologic epidermal phenotype.^4,5

In the past, AD was conceptualized as a T helper cell T_H2 (acute disease)/T_H1 (chronic disease) bipolar cytokine disorder.⁶ Acute lesions are characterized by high T_H2, T_H22, and some T_H17 signals, with intensification of these axes and T_H1 augmentation orchestrating the chronic phenotype.⁷ The identification of the inflammatory pathways underlying AD has led to the development and testing of more than 10 broad or targeted therapeutics (Table).⁸ Phase 1 and phase 2 studies of dupilumab (targeting IL-4Rα) have shown not only tremendous AD improvement (~70%) but also tissue reversal of the immune and barrier abnormalities, including inflammatory cytokines and epidermal hyperplasia.^9-11 As a result, other T_H2 axis inhibitors (anti–IL-13/tralokinumab, anti–IL-31RA/CIM 331) are now in clinical trials. The identification of IL-22 in AD lesions has prompted trials with an anti–IL-22 (ILV 094) and an IL-12/IL-23p40 (ustekinumab) inhibitor.¹² For psoriasis, ustekinumab showed 75% improvement in approximately 70% of patients,¹³ but for AD, despite clear clinical and molecular effects, differences compared to placebo were not statistically significant,¹² probably due to underdosing of the drug in an excessively immune-activated disease¹⁴ as well as allowing topical steroids in patients, which may minimize the differences in treatment effect between drug and placebo.

The developments seen in AD are now moving into other inflammatory skin diseases, particularly alopecia areata (AA), a T-cell–mediated disease that shares phenotypic similarities with AD and often is associated with it.¹⁵ There is a paucity of effective, remission-sustaining treatments of AA, particularly for patients with severe disease who rarely experience spontaneous hair regrowth and who have a limited response to topical interventions.^16,17 Our clinical experience showed that successfully treating patients with concurrent AD and AA has led to hair regrowth. Inspired by these clinical observations and by results obtained in AD,^9-12 studying AA skin showed an upregulation of not only the traditionally suspected culprit T_H1 but also T_H2 and T_H9 axes, IL-23 cytokines, and phosphodiesterase 4.¹⁸ Subsequently, a pilot study of 3 patients with extensive AA treated with ustekinumab showed that all 3 patients not only experienced hair regrowth but also had a reduction in inflammatory markers in scalp lesions.¹⁹ Although these results are promising, AA is an immunologically complex disease and it is yet to be determined if therapeutically targeting 1 (eg, IL-4) rather than a wide array of cytokines can reverse disease phenotype. There are ongoing clinical trials directed at different pathogenic targets (eg, Jak inhibitors, IL-13 antagonist, IL-17 antagonist, phosphodiesterase 4 antagonist); some showed some efficacy in small studies.^20,21

The finding of a commonly upregulated T_H2 pathway in both AD and AA will pave the way for studies with T_H2 antagonists in AA patients. Future targeted therapeutic studies will shed light on the pathogenic pathways of this devastating skin disease and answer the extensive unmet therapeutic need it presents.

Atopic dermatitis (AD) is the most common inflammatory skin disease in both adults and children.¹ Unfortunately, the current treatment armamentarium is largely confined to topical calcineurin inhibitors, topical and systemic steroids, phototherapy, cyclosporine (not approved by the US Food and Drug Administration for AD), and other oral immunosuppressants.² The availability of partially helpful and highly toxic treatments creates a huge unmet need for more effective and safer treatments, particularly for patients with moderate to severe AD who often require systemic approaches.

Recent extensive translational (bench top to bedside and back) investigations in skin of AD patients has shown that skin phenotype is characterized by increased T-cell infiltration and related inflammatory cytokines as well as epidermal abnormalities (eg, hyperplasia, aberrant differentiation).³ Clinical improvement of AD has been demonstrated with broad T-cell targeted therapeutics, such as cyclosporine and narrowband UVB, coupled with decreases of T-cell infiltrates and inflammatory gene products as well as improvement of the pathologic epidermal phenotype.^4,5

In the past, AD was conceptualized as a T helper cell T_H2 (acute disease)/T_H1 (chronic disease) bipolar cytokine disorder.⁶ Acute lesions are characterized by high T_H2, T_H22, and some T_H17 signals, with intensification of these axes and T_H1 augmentation orchestrating the chronic phenotype.⁷ The identification of the inflammatory pathways underlying AD has led to the development and testing of more than 10 broad or targeted therapeutics (Table).⁸ Phase 1 and phase 2 studies of dupilumab (targeting IL-4Rα) have shown not only tremendous AD improvement (~70%) but also tissue reversal of the immune and barrier abnormalities, including inflammatory cytokines and epidermal hyperplasia.^9-11 As a result, other T_H2 axis inhibitors (anti–IL-13/tralokinumab, anti–IL-31RA/CIM 331) are now in clinical trials. The identification of IL-22 in AD lesions has prompted trials with an anti–IL-22 (ILV 094) and an IL-12/IL-23p40 (ustekinumab) inhibitor.¹² For psoriasis, ustekinumab showed 75% improvement in approximately 70% of patients,¹³ but for AD, despite clear clinical and molecular effects, differences compared to placebo were not statistically significant,¹² probably due to underdosing of the drug in an excessively immune-activated disease¹⁴ as well as allowing topical steroids in patients, which may minimize the differences in treatment effect between drug and placebo.

The developments seen in AD are now moving into other inflammatory skin diseases, particularly alopecia areata (AA), a T-cell–mediated disease that shares phenotypic similarities with AD and often is associated with it.¹⁵ There is a paucity of effective, remission-sustaining treatments of AA, particularly for patients with severe disease who rarely experience spontaneous hair regrowth and who have a limited response to topical interventions.^16,17 Our clinical experience showed that successfully treating patients with concurrent AD and AA has led to hair regrowth. Inspired by these clinical observations and by results obtained in AD,^9-12 studying AA skin showed an upregulation of not only the traditionally suspected culprit T_H1 but also T_H2 and T_H9 axes, IL-23 cytokines, and phosphodiesterase 4.¹⁸ Subsequently, a pilot study of 3 patients with extensive AA treated with ustekinumab showed that all 3 patients not only experienced hair regrowth but also had a reduction in inflammatory markers in scalp lesions.¹⁹ Although these results are promising, AA is an immunologically complex disease and it is yet to be determined if therapeutically targeting 1 (eg, IL-4) rather than a wide array of cytokines can reverse disease phenotype. There are ongoing clinical trials directed at different pathogenic targets (eg, Jak inhibitors, IL-13 antagonist, IL-17 antagonist, phosphodiesterase 4 antagonist); some showed some efficacy in small studies.^20,21

The finding of a commonly upregulated T_H2 pathway in both AD and AA will pave the way for studies with T_H2 antagonists in AA patients. Future targeted therapeutic studies will shed light on the pathogenic pathways of this devastating skin disease and answer the extensive unmet therapeutic need it presents.

Atopic dermatitis (AD) is the most common inflammatory skin disease in both adults and children.¹ Unfortunately, the current treatment armamentarium is largely confined to topical calcineurin inhibitors, topical and systemic steroids, phototherapy, cyclosporine (not approved by the US Food and Drug Administration for AD), and other oral immunosuppressants.² The availability of partially helpful and highly toxic treatments creates a huge unmet need for more effective and safer treatments, particularly for patients with moderate to severe AD who often require systemic approaches.

Recent extensive translational (bench top to bedside and back) investigations in skin of AD patients has shown that skin phenotype is characterized by increased T-cell infiltration and related inflammatory cytokines as well as epidermal abnormalities (eg, hyperplasia, aberrant differentiation).³ Clinical improvement of AD has been demonstrated with broad T-cell targeted therapeutics, such as cyclosporine and narrowband UVB, coupled with decreases of T-cell infiltrates and inflammatory gene products as well as improvement of the pathologic epidermal phenotype.^4,5

In the past, AD was conceptualized as a T helper cell T_H2 (acute disease)/T_H1 (chronic disease) bipolar cytokine disorder.⁶ Acute lesions are characterized by high T_H2, T_H22, and some T_H17 signals, with intensification of these axes and T_H1 augmentation orchestrating the chronic phenotype.⁷ The identification of the inflammatory pathways underlying AD has led to the development and testing of more than 10 broad or targeted therapeutics (Table).⁸ Phase 1 and phase 2 studies of dupilumab (targeting IL-4Rα) have shown not only tremendous AD improvement (~70%) but also tissue reversal of the immune and barrier abnormalities, including inflammatory cytokines and epidermal hyperplasia.^9-11 As a result, other T_H2 axis inhibitors (anti–IL-13/tralokinumab, anti–IL-31RA/CIM 331) are now in clinical trials. The identification of IL-22 in AD lesions has prompted trials with an anti–IL-22 (ILV 094) and an IL-12/IL-23p40 (ustekinumab) inhibitor.¹² For psoriasis, ustekinumab showed 75% improvement in approximately 70% of patients,¹³ but for AD, despite clear clinical and molecular effects, differences compared to placebo were not statistically significant,¹² probably due to underdosing of the drug in an excessively immune-activated disease¹⁴ as well as allowing topical steroids in patients, which may minimize the differences in treatment effect between drug and placebo.

The developments seen in AD are now moving into other inflammatory skin diseases, particularly alopecia areata (AA), a T-cell–mediated disease that shares phenotypic similarities with AD and often is associated with it.¹⁵ There is a paucity of effective, remission-sustaining treatments of AA, particularly for patients with severe disease who rarely experience spontaneous hair regrowth and who have a limited response to topical interventions.^16,17 Our clinical experience showed that successfully treating patients with concurrent AD and AA has led to hair regrowth. Inspired by these clinical observations and by results obtained in AD,^9-12 studying AA skin showed an upregulation of not only the traditionally suspected culprit T_H1 but also T_H2 and T_H9 axes, IL-23 cytokines, and phosphodiesterase 4.¹⁸ Subsequently, a pilot study of 3 patients with extensive AA treated with ustekinumab showed that all 3 patients not only experienced hair regrowth but also had a reduction in inflammatory markers in scalp lesions.¹⁹ Although these results are promising, AA is an immunologically complex disease and it is yet to be determined if therapeutically targeting 1 (eg, IL-4) rather than a wide array of cytokines can reverse disease phenotype. There are ongoing clinical trials directed at different pathogenic targets (eg, Jak inhibitors, IL-13 antagonist, IL-17 antagonist, phosphodiesterase 4 antagonist); some showed some efficacy in small studies.^20,21

The finding of a commonly upregulated T_H2 pathway in both AD and AA will pave the way for studies with T_H2 antagonists in AA patients. Future targeted therapeutic studies will shed light on the pathogenic pathways of this devastating skin disease and answer the extensive unmet therapeutic need it presents.

In an increasingly sleepless society inundated with caffeine drinks and social media, it is not surprising that 15%-30% of teens present with complaints of fatigue.¹ As fatigue can be a symptom of many disorders, a careful work-up is important.

Fewer than 8 hours’ sleep, large intake of caffeine, and several hours on social media each day are linked with fatigue. Poor eating habits are more likely than not; nearly 21% of teens are overweight.² Video games have also contributed to symptoms of fatigue by encouraging a sedentary life style.

The work-up for teens with fatigue requires a detailed history of present symptoms and a careful review of systems, which should specifically address weight gain or loss, menstrual change, palpitations, and respiratory changes. It is important to screen for signs of stress and depression.

The physical exam should identify systems that need further work-up, and a standard serum screen would include a complete blood cell count (CBC), complete metabolic panel (CMP), and a thyroid panel.

As many experienced physicians can attest, more often than not, this work-up results in normal findings. Suggesting that the basis for fatigue may be a psychiatric cause is usually not well received.

Another consideration is a diagnosis of chronic fatigue syndrome (CFS), a well-documented disorder with defined diagnostic criteria since 1994. Although CFS is more common in adults, research now reveals an annual incidence of 0.5% and a prevalence of 0.19%-1.29% in teens.³ The characteristics are severe and disabling new-onset fatigue lasting greater than 6 months and four of the following symptoms: impaired memory, sore throat, tender cervical and axillary lymph nodes, muscle pain, headaches, unrefreshing sleep, generalized malaise. Orthostatic intolerance has also been identified as a symptom.⁴

The cause of CFS is unknown, although its onset usually follows an illness.¹ The diagnosis is challenging, as there is no definitive test. If the criteria are met, however, a diagnosis of CFS should be given. This allows the patient to feel validated and can foster a better physician-patient relationship.

Treatment for CFS is symptomatic. The first step is good “sleep hygiene.” Reducing or eliminating caffeine and promoting exercise and a healthy diet all contribute to better sleep. Also, the blue light emitted by electronic devices suppresses melatonin and makes it more difficult to fall asleep.⁵

Resuming normal activity and improving school attendance is the goal achieved through graded exercises, behavioral therapy, and management of pain with acetaminophen and NSAIDs. Tricyclic antidepressants have been studied in CFS but their effectiveness has not been proven.¹ Significant improvements are seen in 50% of teens who are appropriately diagnosed and adhere to treatments.¹

CFS is a debilitating disorder that can be frustrating to treat. Acknowledging CFS as a legitimate syndrome can aid in treatment by fostering a good physician-patient relationship.

References

1. Findlay, SM. “The Tired Teen: A Review of the Assessment and Management of the Adolescent with Sleepiness and Fatigue” Paediatr Child Health. 2008 Jan;13(1):37-42. Print.

2. Prevalence of Childhood Obesity in the United States, 2011-2012, CDC.

3. Nijhof SL, et al. “Adolescent Chronic Fatigue Syndrome: Prevalence, Incidence, and Morbidity” Pediatrics. 2011 May;127(5):e1169-e1175.

4. Orthostatic intolerance in adolescent chronic fatigue syndrome. Stewart JM, et al. Pediatrics. 1999 Jan;103(1):116-21.

5. “The impact of light from computer monitors on melatonin levels in college students” Figueiro MG, et al. Neuro Endocrinol Lett. 2011;32(2):158-163.

In an increasingly sleepless society inundated with caffeine drinks and social media, it is not surprising that 15%-30% of teens present with complaints of fatigue.¹ As fatigue can be a symptom of many disorders, a careful work-up is important.

Fewer than 8 hours’ sleep, large intake of caffeine, and several hours on social media each day are linked with fatigue. Poor eating habits are more likely than not; nearly 21% of teens are overweight.² Video games have also contributed to symptoms of fatigue by encouraging a sedentary life style.

The work-up for teens with fatigue requires a detailed history of present symptoms and a careful review of systems, which should specifically address weight gain or loss, menstrual change, palpitations, and respiratory changes. It is important to screen for signs of stress and depression.

The physical exam should identify systems that need further work-up, and a standard serum screen would include a complete blood cell count (CBC), complete metabolic panel (CMP), and a thyroid panel.

As many experienced physicians can attest, more often than not, this work-up results in normal findings. Suggesting that the basis for fatigue may be a psychiatric cause is usually not well received.

Another consideration is a diagnosis of chronic fatigue syndrome (CFS), a well-documented disorder with defined diagnostic criteria since 1994. Although CFS is more common in adults, research now reveals an annual incidence of 0.5% and a prevalence of 0.19%-1.29% in teens.³ The characteristics are severe and disabling new-onset fatigue lasting greater than 6 months and four of the following symptoms: impaired memory, sore throat, tender cervical and axillary lymph nodes, muscle pain, headaches, unrefreshing sleep, generalized malaise. Orthostatic intolerance has also been identified as a symptom.⁴

The cause of CFS is unknown, although its onset usually follows an illness.¹ The diagnosis is challenging, as there is no definitive test. If the criteria are met, however, a diagnosis of CFS should be given. This allows the patient to feel validated and can foster a better physician-patient relationship.

Treatment for CFS is symptomatic. The first step is good “sleep hygiene.” Reducing or eliminating caffeine and promoting exercise and a healthy diet all contribute to better sleep. Also, the blue light emitted by electronic devices suppresses melatonin and makes it more difficult to fall asleep.⁵

Resuming normal activity and improving school attendance is the goal achieved through graded exercises, behavioral therapy, and management of pain with acetaminophen and NSAIDs. Tricyclic antidepressants have been studied in CFS but their effectiveness has not been proven.¹ Significant improvements are seen in 50% of teens who are appropriately diagnosed and adhere to treatments.¹

CFS is a debilitating disorder that can be frustrating to treat. Acknowledging CFS as a legitimate syndrome can aid in treatment by fostering a good physician-patient relationship.

References

1. Findlay, SM. “The Tired Teen: A Review of the Assessment and Management of the Adolescent with Sleepiness and Fatigue” Paediatr Child Health. 2008 Jan;13(1):37-42. Print.

2. Prevalence of Childhood Obesity in the United States, 2011-2012, CDC.

3. Nijhof SL, et al. “Adolescent Chronic Fatigue Syndrome: Prevalence, Incidence, and Morbidity” Pediatrics. 2011 May;127(5):e1169-e1175.

4. Orthostatic intolerance in adolescent chronic fatigue syndrome. Stewart JM, et al. Pediatrics. 1999 Jan;103(1):116-21.

5. “The impact of light from computer monitors on melatonin levels in college students” Figueiro MG, et al. Neuro Endocrinol Lett. 2011;32(2):158-163.

In an increasingly sleepless society inundated with caffeine drinks and social media, it is not surprising that 15%-30% of teens present with complaints of fatigue.¹ As fatigue can be a symptom of many disorders, a careful work-up is important.

Fewer than 8 hours’ sleep, large intake of caffeine, and several hours on social media each day are linked with fatigue. Poor eating habits are more likely than not; nearly 21% of teens are overweight.² Video games have also contributed to symptoms of fatigue by encouraging a sedentary life style.

The work-up for teens with fatigue requires a detailed history of present symptoms and a careful review of systems, which should specifically address weight gain or loss, menstrual change, palpitations, and respiratory changes. It is important to screen for signs of stress and depression.

The physical exam should identify systems that need further work-up, and a standard serum screen would include a complete blood cell count (CBC), complete metabolic panel (CMP), and a thyroid panel.

As many experienced physicians can attest, more often than not, this work-up results in normal findings. Suggesting that the basis for fatigue may be a psychiatric cause is usually not well received.

Another consideration is a diagnosis of chronic fatigue syndrome (CFS), a well-documented disorder with defined diagnostic criteria since 1994. Although CFS is more common in adults, research now reveals an annual incidence of 0.5% and a prevalence of 0.19%-1.29% in teens.³ The characteristics are severe and disabling new-onset fatigue lasting greater than 6 months and four of the following symptoms: impaired memory, sore throat, tender cervical and axillary lymph nodes, muscle pain, headaches, unrefreshing sleep, generalized malaise. Orthostatic intolerance has also been identified as a symptom.⁴

The cause of CFS is unknown, although its onset usually follows an illness.¹ The diagnosis is challenging, as there is no definitive test. If the criteria are met, however, a diagnosis of CFS should be given. This allows the patient to feel validated and can foster a better physician-patient relationship.

Treatment for CFS is symptomatic. The first step is good “sleep hygiene.” Reducing or eliminating caffeine and promoting exercise and a healthy diet all contribute to better sleep. Also, the blue light emitted by electronic devices suppresses melatonin and makes it more difficult to fall asleep.⁵

Resuming normal activity and improving school attendance is the goal achieved through graded exercises, behavioral therapy, and management of pain with acetaminophen and NSAIDs. Tricyclic antidepressants have been studied in CFS but their effectiveness has not been proven.¹ Significant improvements are seen in 50% of teens who are appropriately diagnosed and adhere to treatments.¹

CFS is a debilitating disorder that can be frustrating to treat. Acknowledging CFS as a legitimate syndrome can aid in treatment by fostering a good physician-patient relationship.

References

1. Findlay, SM. “The Tired Teen: A Review of the Assessment and Management of the Adolescent with Sleepiness and Fatigue” Paediatr Child Health. 2008 Jan;13(1):37-42. Print.

2. Prevalence of Childhood Obesity in the United States, 2011-2012, CDC.

3. Nijhof SL, et al. “Adolescent Chronic Fatigue Syndrome: Prevalence, Incidence, and Morbidity” Pediatrics. 2011 May;127(5):e1169-e1175.

4. Orthostatic intolerance in adolescent chronic fatigue syndrome. Stewart JM, et al. Pediatrics. 1999 Jan;103(1):116-21.

5. “The impact of light from computer monitors on melatonin levels in college students” Figueiro MG, et al. Neuro Endocrinol Lett. 2011;32(2):158-163.

“STOP USING RECTAL MISOPROSTOL FOR THE TREATMENT OF POSTPARTUM HEMORRHAGE CAUSED BY UTERINE ATONY”Robert L. Barbieri, MD (Editorial; July 2016)

The BEPCOP strategy for uterine atony

I appreciated Dr. Barbieri’s editorial about oxytocics for postpartum uterine atony and have personally noted the poor effectiveness of rectal misoprostol. I was reminded of his previous editorial that recommended administering intravenous (IV) oxytocin to postcesarean delivery patients for about 6 to 8 hours to reduce the risk of postoperative hemorrhage.

At my current hospital we usually use postpartum oxytocin, 30 units in 500 mL of 5% dextrose in water (D5W) for vaginal deliveries, and that infusion typically is administered for only 1 to 2 hours. Cesarean delivery patients receive oxytocin, 20 units in 1,000 mL of Ringer’s lactate, over the first 1 to 2 hours postoperatively. As an OB hospitalist I have been summoned occasionally to the bedside of patients who have uterine atony and hemorrhage, which usually occurs several hours after their oxytocin infusion has finished.

With this in mind I developed a proactive protocol that I call BEPCOP, an acronym for “Barnes’ Excellent Post Cesarean Oxytocin Protocol.” This involves simply running a 500-mL bag of oxytocin (30 units in 500 mL of D5W) at a constant rate of 50 mL/hour, which provides 50 mU/min oxytocin over the first 10 hours postdelivery.

I recommend BEPCOP for every cesarean delivery patient, as well as for any vaginally delivered patients who are at increased risk for atony, such as those with prolonged labor, large babies, polyhydramnios, multifetal gestation, chorioamnio‑nitis, and history of hemorrhage after a previous delivery, and for patients who are Jehovah’s Witnesses. It is important to reduce the rate of the mainline IV bag while the oxytocin is infusing to reduce the risk of fluid overload.

Since starting this routine I have seen a noticeable decrease in postpartum and postcesarean uterine atony.

E. Darryl Barnes, MD
Mechanicsville, Virginia
 

Nondissolving misoprostol is ineffective

There is something about misoprostol that is not mentioned in Dr. Barbieri’s editorial. There are 2 types of misoprostol: the proprietary formulation (Cytotec, Pfizer) and the generic form (probably the one used in most hospitals, and possibly also the one used in the randomized studies alluded to).

The generic form, manufactured overseas, is literally insoluble. In my experience, these undissolved tabletsare expelled intact from the rectum5 hours after insertion and they therefore do nothing. The proprietary brand of misoprostol dissolves instantly in the rectum, and the results are dramatic to say the least.

Helio Zapata, MD
Skokie, Illinois

Bundles of care protocols useful in critical events

We often assume the etiology of the postpartum hemorrhage (PPH) is purely and exclusively uterine atony. A frequent clinical scenario is as follows: A hospital birth is conducted by a trained attendant, in a US learning hospital, on a parturient assessed as being at low risk; the single circulating nurse is busy at the keyboard complying with the data entry requirements; the just-delivered patient is enjoying skin-to-skin contact as recommended; and the new father is obtaining all the appropriate pictorial material when a massive vaginal bleed ensues, diagnosed as due to uterine atony. There is little time to remember the results of the randomized controlled trials condemning the use of misoprostol, or the effectiveness of the individual components of the AMTSL (active management of the third stage of labor). The IV oxytocin at the prescribed dose is running wide open, extra personnel are summoned to help, the first doses of methylergonovine are given, and the misoprostol tablets are stored in the nearby drawer as prescribed by the institution’s protocol.

Currently, a multi-state, multi-institutional initiative spearheaded by the American College of Obstetricians and Gynecologists and known as AIM (Alliance for Innovation in Maternity Care) supports the use of “bundles of care” to standardize obstetric care as recommended by the Joint Commission and the Society for Maternal-Fetal Medicine. One of the “bundles” addresses PPH. It is understood that each institution may adjust the steps in accord with its individual capabilities. Included in the algorithm is the use of rectal misoprostol 800 to 1,000 μg.¹⁻⁵

The International Federation of Gynecology and Obstetrics, in referencing the Blum trial,⁶ states that the results indicated misoprostol was noninferior to oxytocin at controlling bleeding (90% vs 89%) and preventing additional blood loss (31% vs 34%).⁷ Misoprostol’s contraindications and side effects are recognized by all investigators. In the field of obstetrics, changes are slow in permeating into daily practice.⁸ Dr. Barbieri’s recommendation, originating from an influential academic institution, opens the door to continue the dialog on a critical clinical event.

Federico G. Mariona, MD
Dearborn, Michigan

References

1. Shields LE, Wiesner S, Fulton J, Pelletreau B. Comprehensive maternal hemorrhage protocols reduce the use of blood products and improve patient safety. Am J Obstet Gynecol. 2015;212(3):272–280.
2. Obstetric hemorrhage checklist. Beaumont Health, Michigan. October 2015.
3. California Maternal Quality Care Collaborative, California Department of Public Health. OB hemorrhage toolkit, Version 2.0. https://www.cmqcc.org/resources-tool-kits/toolkits/ob-hemorrhage-toolkit. Published March 24, 2015. Accessed August 24, 2015.
4. Main EK, Goffman D, Scavone BM, et al; National Partnership for Maternal Safety Council on Patient Safety in Women’s Health Care. Consensus bundle on obstetric hemorrhage. Obstet Gynecol. 2015;126(1):155–162.
5. American College of Obstetricians and Gynecologists. ACOG Practice Bulletin No. 76: postpartum hemorrhage. Obstet Gynecol. 2006;108(4):1039–1047.
6. Blum J, Winikoff B, Raghavan S, et al. Treatment of post-partum haemorrhage with sublingual misoprostol versus oxytocin in women receiving prophylactic oxytocin: a double blind randomised, non-inferiority trial. Lancet. 2010;375(9710):217–223.
7. International Federation of Gynecology and Obstetrics. Treatment of post-partum haemorrhage with misoprostol. FIGO guideline, annotated version. http://www.figo.org/sites/default/files/uploads/project-publications/Miso/PPH%20treatment/Annotated%20versions/Treatment%20of%20PPH%20with%20Misoprostol_Annotated_2012_English.pdf. Published May 2012. Accessed August 24, 2015.
8. Mariona FG, Roura LC. The role of placental alpha macroglobulin-1 amnisure in determining the status of the fetal membranes; its associations with preterm birth. Traditions, traditions. J Matern Fetal Neonatal Med. 2016;29(6):1016–1020.

Rectal misoprostol has merit

It is well established in medicine that IV medications have a rapid onset of action. Therefore, IV uterotonics would be the first choice to control PPH. Most likely they will control the majority of uterine atony.

However, the causes of uterine atony are numerous, and they most commonly include prolonged labor and/or infection. Like any fatigued muscle, there is rebound relaxation. Intravenous uterotonics have a very short half-life and have a maximum total dose. Repeating oxytocin 40 U in a 1,000-mL infusion over 15 minutes carries the risk of water intoxication due to the antidiuretic effect.

Misoprostol 800 to 1,000 mg when used rectally will have a longer effect—up to 4 hours—and fewer side effects. It should be used in combination with other parenteral uterotonics to act in synergistic way. This way the more serious cases of PPH can be reduced or even prevented.

Raymond Michael, MD
Marshall, Minnesota

Dr. Barbieri responds

I deeply appreciate the perspectives provided by Drs. Barnes, Zapata, Mariona, and Michael. The obstetricians and gynecologists who read OBG Management have vast clinical experience, expertise, and exceptional insights. By sharing our knowledge with each other we best advance the care provided to women and their families.

As a hospitalist, Dr. Barnes is privileged to care for women at the highest-risk time of their pregnancy. I think his BEPCOP proactive protocol to reduce the rate of PPH is superb and urge him to publish his experience. I appreciate Dr. Zapata’s insight that misoprostol tablets from different manufacturers have markedly different rates of dissolution. I agree with him that I have seen entire, undissolved misoprostol tablets expelled from the rectum many hours after they were administered for the treatment of PPH. If the tablet does not dissolve, it certainly cannot work. Dr. Mariona’s guidance to adhere to protocol bundles and continuously improve and update the bundles is absolutely critical to advancing health care for pregnant women. Dr. Michael rightly points out that one advantage of misoprostol is that it has a longer half-life than many parenteral uterotonics. However, in my practice I prefer Dr. Barnes’ BEPCOP protocol involving the multi-hour administration of oxytocin to prevent and treat a PPH.

“STOP USING RECTAL MISOPROSTOL FOR THE TREATMENT OF POSTPARTUM HEMORRHAGE CAUSED BY UTERINE ATONY”Robert L. Barbieri, MD (Editorial; July 2016)

The BEPCOP strategy for uterine atony

I appreciated Dr. Barbieri’s editorial about oxytocics for postpartum uterine atony and have personally noted the poor effectiveness of rectal misoprostol. I was reminded of his previous editorial that recommended administering intravenous (IV) oxytocin to postcesarean delivery patients for about 6 to 8 hours to reduce the risk of postoperative hemorrhage.

At my current hospital we usually use postpartum oxytocin, 30 units in 500 mL of 5% dextrose in water (D5W) for vaginal deliveries, and that infusion typically is administered for only 1 to 2 hours. Cesarean delivery patients receive oxytocin, 20 units in 1,000 mL of Ringer’s lactate, over the first 1 to 2 hours postoperatively. As an OB hospitalist I have been summoned occasionally to the bedside of patients who have uterine atony and hemorrhage, which usually occurs several hours after their oxytocin infusion has finished.

With this in mind I developed a proactive protocol that I call BEPCOP, an acronym for “Barnes’ Excellent Post Cesarean Oxytocin Protocol.” This involves simply running a 500-mL bag of oxytocin (30 units in 500 mL of D5W) at a constant rate of 50 mL/hour, which provides 50 mU/min oxytocin over the first 10 hours postdelivery.

I recommend BEPCOP for every cesarean delivery patient, as well as for any vaginally delivered patients who are at increased risk for atony, such as those with prolonged labor, large babies, polyhydramnios, multifetal gestation, chorioamnio‑nitis, and history of hemorrhage after a previous delivery, and for patients who are Jehovah’s Witnesses. It is important to reduce the rate of the mainline IV bag while the oxytocin is infusing to reduce the risk of fluid overload.

Since starting this routine I have seen a noticeable decrease in postpartum and postcesarean uterine atony.

E. Darryl Barnes, MD
Mechanicsville, Virginia
 

Nondissolving misoprostol is ineffective

There is something about misoprostol that is not mentioned in Dr. Barbieri’s editorial. There are 2 types of misoprostol: the proprietary formulation (Cytotec, Pfizer) and the generic form (probably the one used in most hospitals, and possibly also the one used in the randomized studies alluded to).

The generic form, manufactured overseas, is literally insoluble. In my experience, these undissolved tabletsare expelled intact from the rectum5 hours after insertion and they therefore do nothing. The proprietary brand of misoprostol dissolves instantly in the rectum, and the results are dramatic to say the least.

Helio Zapata, MD
Skokie, Illinois

Bundles of care protocols useful in critical events

We often assume the etiology of the postpartum hemorrhage (PPH) is purely and exclusively uterine atony. A frequent clinical scenario is as follows: A hospital birth is conducted by a trained attendant, in a US learning hospital, on a parturient assessed as being at low risk; the single circulating nurse is busy at the keyboard complying with the data entry requirements; the just-delivered patient is enjoying skin-to-skin contact as recommended; and the new father is obtaining all the appropriate pictorial material when a massive vaginal bleed ensues, diagnosed as due to uterine atony. There is little time to remember the results of the randomized controlled trials condemning the use of misoprostol, or the effectiveness of the individual components of the AMTSL (active management of the third stage of labor). The IV oxytocin at the prescribed dose is running wide open, extra personnel are summoned to help, the first doses of methylergonovine are given, and the misoprostol tablets are stored in the nearby drawer as prescribed by the institution’s protocol.

Currently, a multi-state, multi-institutional initiative spearheaded by the American College of Obstetricians and Gynecologists and known as AIM (Alliance for Innovation in Maternity Care) supports the use of “bundles of care” to standardize obstetric care as recommended by the Joint Commission and the Society for Maternal-Fetal Medicine. One of the “bundles” addresses PPH. It is understood that each institution may adjust the steps in accord with its individual capabilities. Included in the algorithm is the use of rectal misoprostol 800 to 1,000 μg.¹⁻⁵

The International Federation of Gynecology and Obstetrics, in referencing the Blum trial,⁶ states that the results indicated misoprostol was noninferior to oxytocin at controlling bleeding (90% vs 89%) and preventing additional blood loss (31% vs 34%).⁷ Misoprostol’s contraindications and side effects are recognized by all investigators. In the field of obstetrics, changes are slow in permeating into daily practice.⁸ Dr. Barbieri’s recommendation, originating from an influential academic institution, opens the door to continue the dialog on a critical clinical event.

Federico G. Mariona, MD
Dearborn, Michigan

References

1. Shields LE, Wiesner S, Fulton J, Pelletreau B. Comprehensive maternal hemorrhage protocols reduce the use of blood products and improve patient safety. Am J Obstet Gynecol. 2015;212(3):272–280.
2. Obstetric hemorrhage checklist. Beaumont Health, Michigan. October 2015.
3. California Maternal Quality Care Collaborative, California Department of Public Health. OB hemorrhage toolkit, Version 2.0. https://www.cmqcc.org/resources-tool-kits/toolkits/ob-hemorrhage-toolkit. Published March 24, 2015. Accessed August 24, 2015.
4. Main EK, Goffman D, Scavone BM, et al; National Partnership for Maternal Safety Council on Patient Safety in Women’s Health Care. Consensus bundle on obstetric hemorrhage. Obstet Gynecol. 2015;126(1):155–162.
5. American College of Obstetricians and Gynecologists. ACOG Practice Bulletin No. 76: postpartum hemorrhage. Obstet Gynecol. 2006;108(4):1039–1047.
6. Blum J, Winikoff B, Raghavan S, et al. Treatment of post-partum haemorrhage with sublingual misoprostol versus oxytocin in women receiving prophylactic oxytocin: a double blind randomised, non-inferiority trial. Lancet. 2010;375(9710):217–223.
7. International Federation of Gynecology and Obstetrics. Treatment of post-partum haemorrhage with misoprostol. FIGO guideline, annotated version. http://www.figo.org/sites/default/files/uploads/project-publications/Miso/PPH%20treatment/Annotated%20versions/Treatment%20of%20PPH%20with%20Misoprostol_Annotated_2012_English.pdf. Published May 2012. Accessed August 24, 2015.
8. Mariona FG, Roura LC. The role of placental alpha macroglobulin-1 amnisure in determining the status of the fetal membranes; its associations with preterm birth. Traditions, traditions. J Matern Fetal Neonatal Med. 2016;29(6):1016–1020.

Rectal misoprostol has merit

It is well established in medicine that IV medications have a rapid onset of action. Therefore, IV uterotonics would be the first choice to control PPH. Most likely they will control the majority of uterine atony.

However, the causes of uterine atony are numerous, and they most commonly include prolonged labor and/or infection. Like any fatigued muscle, there is rebound relaxation. Intravenous uterotonics have a very short half-life and have a maximum total dose. Repeating oxytocin 40 U in a 1,000-mL infusion over 15 minutes carries the risk of water intoxication due to the antidiuretic effect.

Misoprostol 800 to 1,000 mg when used rectally will have a longer effect—up to 4 hours—and fewer side effects. It should be used in combination with other parenteral uterotonics to act in synergistic way. This way the more serious cases of PPH can be reduced or even prevented.

Raymond Michael, MD
Marshall, Minnesota

Dr. Barbieri responds

I deeply appreciate the perspectives provided by Drs. Barnes, Zapata, Mariona, and Michael. The obstetricians and gynecologists who read OBG Management have vast clinical experience, expertise, and exceptional insights. By sharing our knowledge with each other we best advance the care provided to women and their families.

As a hospitalist, Dr. Barnes is privileged to care for women at the highest-risk time of their pregnancy. I think his BEPCOP proactive protocol to reduce the rate of PPH is superb and urge him to publish his experience. I appreciate Dr. Zapata’s insight that misoprostol tablets from different manufacturers have markedly different rates of dissolution. I agree with him that I have seen entire, undissolved misoprostol tablets expelled from the rectum many hours after they were administered for the treatment of PPH. If the tablet does not dissolve, it certainly cannot work. Dr. Mariona’s guidance to adhere to protocol bundles and continuously improve and update the bundles is absolutely critical to advancing health care for pregnant women. Dr. Michael rightly points out that one advantage of misoprostol is that it has a longer half-life than many parenteral uterotonics. However, in my practice I prefer Dr. Barnes’ BEPCOP protocol involving the multi-hour administration of oxytocin to prevent and treat a PPH.

“STOP USING RECTAL MISOPROSTOL FOR THE TREATMENT OF POSTPARTUM HEMORRHAGE CAUSED BY UTERINE ATONY”Robert L. Barbieri, MD (Editorial; July 2016)

The BEPCOP strategy for uterine atony

I appreciated Dr. Barbieri’s editorial about oxytocics for postpartum uterine atony and have personally noted the poor effectiveness of rectal misoprostol. I was reminded of his previous editorial that recommended administering intravenous (IV) oxytocin to postcesarean delivery patients for about 6 to 8 hours to reduce the risk of postoperative hemorrhage.

At my current hospital we usually use postpartum oxytocin, 30 units in 500 mL of 5% dextrose in water (D5W) for vaginal deliveries, and that infusion typically is administered for only 1 to 2 hours. Cesarean delivery patients receive oxytocin, 20 units in 1,000 mL of Ringer’s lactate, over the first 1 to 2 hours postoperatively. As an OB hospitalist I have been summoned occasionally to the bedside of patients who have uterine atony and hemorrhage, which usually occurs several hours after their oxytocin infusion has finished.

With this in mind I developed a proactive protocol that I call BEPCOP, an acronym for “Barnes’ Excellent Post Cesarean Oxytocin Protocol.” This involves simply running a 500-mL bag of oxytocin (30 units in 500 mL of D5W) at a constant rate of 50 mL/hour, which provides 50 mU/min oxytocin over the first 10 hours postdelivery.

I recommend BEPCOP for every cesarean delivery patient, as well as for any vaginally delivered patients who are at increased risk for atony, such as those with prolonged labor, large babies, polyhydramnios, multifetal gestation, chorioamnio‑nitis, and history of hemorrhage after a previous delivery, and for patients who are Jehovah’s Witnesses. It is important to reduce the rate of the mainline IV bag while the oxytocin is infusing to reduce the risk of fluid overload.

Since starting this routine I have seen a noticeable decrease in postpartum and postcesarean uterine atony.

E. Darryl Barnes, MD
Mechanicsville, Virginia
 

Nondissolving misoprostol is ineffective

There is something about misoprostol that is not mentioned in Dr. Barbieri’s editorial. There are 2 types of misoprostol: the proprietary formulation (Cytotec, Pfizer) and the generic form (probably the one used in most hospitals, and possibly also the one used in the randomized studies alluded to).

The generic form, manufactured overseas, is literally insoluble. In my experience, these undissolved tabletsare expelled intact from the rectum5 hours after insertion and they therefore do nothing. The proprietary brand of misoprostol dissolves instantly in the rectum, and the results are dramatic to say the least.

Helio Zapata, MD
Skokie, Illinois

Bundles of care protocols useful in critical events

We often assume the etiology of the postpartum hemorrhage (PPH) is purely and exclusively uterine atony. A frequent clinical scenario is as follows: A hospital birth is conducted by a trained attendant, in a US learning hospital, on a parturient assessed as being at low risk; the single circulating nurse is busy at the keyboard complying with the data entry requirements; the just-delivered patient is enjoying skin-to-skin contact as recommended; and the new father is obtaining all the appropriate pictorial material when a massive vaginal bleed ensues, diagnosed as due to uterine atony. There is little time to remember the results of the randomized controlled trials condemning the use of misoprostol, or the effectiveness of the individual components of the AMTSL (active management of the third stage of labor). The IV oxytocin at the prescribed dose is running wide open, extra personnel are summoned to help, the first doses of methylergonovine are given, and the misoprostol tablets are stored in the nearby drawer as prescribed by the institution’s protocol.

Currently, a multi-state, multi-institutional initiative spearheaded by the American College of Obstetricians and Gynecologists and known as AIM (Alliance for Innovation in Maternity Care) supports the use of “bundles of care” to standardize obstetric care as recommended by the Joint Commission and the Society for Maternal-Fetal Medicine. One of the “bundles” addresses PPH. It is understood that each institution may adjust the steps in accord with its individual capabilities. Included in the algorithm is the use of rectal misoprostol 800 to 1,000 μg.¹⁻⁵

The International Federation of Gynecology and Obstetrics, in referencing the Blum trial,⁶ states that the results indicated misoprostol was noninferior to oxytocin at controlling bleeding (90% vs 89%) and preventing additional blood loss (31% vs 34%).⁷ Misoprostol’s contraindications and side effects are recognized by all investigators. In the field of obstetrics, changes are slow in permeating into daily practice.⁸ Dr. Barbieri’s recommendation, originating from an influential academic institution, opens the door to continue the dialog on a critical clinical event.

Federico G. Mariona, MD
Dearborn, Michigan

References

1. Shields LE, Wiesner S, Fulton J, Pelletreau B. Comprehensive maternal hemorrhage protocols reduce the use of blood products and improve patient safety. Am J Obstet Gynecol. 2015;212(3):272–280.
2. Obstetric hemorrhage checklist. Beaumont Health, Michigan. October 2015.
3. California Maternal Quality Care Collaborative, California Department of Public Health. OB hemorrhage toolkit, Version 2.0. https://www.cmqcc.org/resources-tool-kits/toolkits/ob-hemorrhage-toolkit. Published March 24, 2015. Accessed August 24, 2015.
4. Main EK, Goffman D, Scavone BM, et al; National Partnership for Maternal Safety Council on Patient Safety in Women’s Health Care. Consensus bundle on obstetric hemorrhage. Obstet Gynecol. 2015;126(1):155–162.
5. American College of Obstetricians and Gynecologists. ACOG Practice Bulletin No. 76: postpartum hemorrhage. Obstet Gynecol. 2006;108(4):1039–1047.
6. Blum J, Winikoff B, Raghavan S, et al. Treatment of post-partum haemorrhage with sublingual misoprostol versus oxytocin in women receiving prophylactic oxytocin: a double blind randomised, non-inferiority trial. Lancet. 2010;375(9710):217–223.
7. International Federation of Gynecology and Obstetrics. Treatment of post-partum haemorrhage with misoprostol. FIGO guideline, annotated version. http://www.figo.org/sites/default/files/uploads/project-publications/Miso/PPH%20treatment/Annotated%20versions/Treatment%20of%20PPH%20with%20Misoprostol_Annotated_2012_English.pdf. Published May 2012. Accessed August 24, 2015.
8. Mariona FG, Roura LC. The role of placental alpha macroglobulin-1 amnisure in determining the status of the fetal membranes; its associations with preterm birth. Traditions, traditions. J Matern Fetal Neonatal Med. 2016;29(6):1016–1020.

Rectal misoprostol has merit

It is well established in medicine that IV medications have a rapid onset of action. Therefore, IV uterotonics would be the first choice to control PPH. Most likely they will control the majority of uterine atony.

However, the causes of uterine atony are numerous, and they most commonly include prolonged labor and/or infection. Like any fatigued muscle, there is rebound relaxation. Intravenous uterotonics have a very short half-life and have a maximum total dose. Repeating oxytocin 40 U in a 1,000-mL infusion over 15 minutes carries the risk of water intoxication due to the antidiuretic effect.

Misoprostol 800 to 1,000 mg when used rectally will have a longer effect—up to 4 hours—and fewer side effects. It should be used in combination with other parenteral uterotonics to act in synergistic way. This way the more serious cases of PPH can be reduced or even prevented.

Raymond Michael, MD
Marshall, Minnesota

Dr. Barbieri responds

I deeply appreciate the perspectives provided by Drs. Barnes, Zapata, Mariona, and Michael. The obstetricians and gynecologists who read OBG Management have vast clinical experience, expertise, and exceptional insights. By sharing our knowledge with each other we best advance the care provided to women and their families.

As a hospitalist, Dr. Barnes is privileged to care for women at the highest-risk time of their pregnancy. I think his BEPCOP proactive protocol to reduce the rate of PPH is superb and urge him to publish his experience. I appreciate Dr. Zapata’s insight that misoprostol tablets from different manufacturers have markedly different rates of dissolution. I agree with him that I have seen entire, undissolved misoprostol tablets expelled from the rectum many hours after they were administered for the treatment of PPH. If the tablet does not dissolve, it certainly cannot work. Dr. Mariona’s guidance to adhere to protocol bundles and continuously improve and update the bundles is absolutely critical to advancing health care for pregnant women. Dr. Michael rightly points out that one advantage of misoprostol is that it has a longer half-life than many parenteral uterotonics. However, in my practice I prefer Dr. Barnes’ BEPCOP protocol involving the multi-hour administration of oxytocin to prevent and treat a PPH.

Walking around the Cardiac Intensive Care Unit (CICU) with one of my heart failure colleagues, I was struck by the relative absence of patients with acute myocardial infarctions. Over the past 50 years, they have been replaced by patients with advanced heart failure, many of whom had been implanted with left ventricular assist devices or connected to a variety of extracorporeal support devices.

Although some of the patients were new New York Heart Association class IV patients, many had been treated for years with beta-blockers and renal ACE inhibitors or aldosterone antagonists. Their disease had now recurred and progressed despite what I had presumed to be curative drug therapy. They were experiencing the relentless progression of heart failure despite treatment that was developed almost 20 years ago and which has not advanced much since then. Many cardiologists of my generation presumed that heart failure was no longer a problem even though we knew that annual mortality rates of heart failure remained in the 10% range and that its incidence was increasing.

It has become clear to many of us that there has been little advance in the treatment of heart failure since the introduction of those 20th century drugs, notwithstanding the importance of the development of end stage cardiac support devices.

It seems our success in treating patients with ischemic heart disease had only delayed the expression and progression of cardiac dysfunction. Even with our success in treating patients with nonischemic heart failure, whatever that is, after reaching a brief plateau with drug therapy, they often experienced recurrence. It is true that many patients had improved as a result of drug therapy and that progression had been arrested and in some patients heart failure had actually been reversed. But many, like the patients I saw in our CICU, had progressed to advanced heart failure with little to be offered other than end-stage device therapy or heart transplantation. Both of these outcomes, although lifesaving, represent therapeutic failures.

It is time that we refocus our efforts on the treatment and eradication of heart failure. Although a number of contemporary treatment strategies have been developed, for the most part they have only resulted in modest additive benefit. We need to reconsider the protection of the heart during and after an ischemic event and prevent the insidious progression of ischemia in those patients with chronic coronary heart disease. In addition we need to direct our research to understand the pathophysiology of the “heart” in heart failure and to unlock the mysticism associated with the many etiologies of idiopathic nonischemic heart failure. Our knowledge in this disease or diseases is embarrassingly poor.

It is time to move on from the 20th century drug foundation of therapy based on neurohumoral control, to a 21st century understanding of the cellular and molecular targets affecting cardiac function. Recent investigations of collagen synthesis and degradation, cardiac energetics, and mitochondrial function have provided provocative information but represent only forays into the vast unknown mechanism of heart failure. The solution to worldwide heart failure is not in device therapy for everyone but in a deeper understanding of the mechanisms of heart failure and its application to therapy.

Dr. Goldstein, medical editor of Cardiology News, is professor of medicine at Wayne State University and division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit. He is on data safety monitoring committees for the National Institutes of Health and several pharmaceutical companies.

Walking around the Cardiac Intensive Care Unit (CICU) with one of my heart failure colleagues, I was struck by the relative absence of patients with acute myocardial infarctions. Over the past 50 years, they have been replaced by patients with advanced heart failure, many of whom had been implanted with left ventricular assist devices or connected to a variety of extracorporeal support devices.

Although some of the patients were new New York Heart Association class IV patients, many had been treated for years with beta-blockers and renal ACE inhibitors or aldosterone antagonists. Their disease had now recurred and progressed despite what I had presumed to be curative drug therapy. They were experiencing the relentless progression of heart failure despite treatment that was developed almost 20 years ago and which has not advanced much since then. Many cardiologists of my generation presumed that heart failure was no longer a problem even though we knew that annual mortality rates of heart failure remained in the 10% range and that its incidence was increasing.

It has become clear to many of us that there has been little advance in the treatment of heart failure since the introduction of those 20th century drugs, notwithstanding the importance of the development of end stage cardiac support devices.

It seems our success in treating patients with ischemic heart disease had only delayed the expression and progression of cardiac dysfunction. Even with our success in treating patients with nonischemic heart failure, whatever that is, after reaching a brief plateau with drug therapy, they often experienced recurrence. It is true that many patients had improved as a result of drug therapy and that progression had been arrested and in some patients heart failure had actually been reversed. But many, like the patients I saw in our CICU, had progressed to advanced heart failure with little to be offered other than end-stage device therapy or heart transplantation. Both of these outcomes, although lifesaving, represent therapeutic failures.

It is time that we refocus our efforts on the treatment and eradication of heart failure. Although a number of contemporary treatment strategies have been developed, for the most part they have only resulted in modest additive benefit. We need to reconsider the protection of the heart during and after an ischemic event and prevent the insidious progression of ischemia in those patients with chronic coronary heart disease. In addition we need to direct our research to understand the pathophysiology of the “heart” in heart failure and to unlock the mysticism associated with the many etiologies of idiopathic nonischemic heart failure. Our knowledge in this disease or diseases is embarrassingly poor.

It is time to move on from the 20th century drug foundation of therapy based on neurohumoral control, to a 21st century understanding of the cellular and molecular targets affecting cardiac function. Recent investigations of collagen synthesis and degradation, cardiac energetics, and mitochondrial function have provided provocative information but represent only forays into the vast unknown mechanism of heart failure. The solution to worldwide heart failure is not in device therapy for everyone but in a deeper understanding of the mechanisms of heart failure and its application to therapy.

Dr. Goldstein, medical editor of Cardiology News, is professor of medicine at Wayne State University and division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit. He is on data safety monitoring committees for the National Institutes of Health and several pharmaceutical companies.

Walking around the Cardiac Intensive Care Unit (CICU) with one of my heart failure colleagues, I was struck by the relative absence of patients with acute myocardial infarctions. Over the past 50 years, they have been replaced by patients with advanced heart failure, many of whom had been implanted with left ventricular assist devices or connected to a variety of extracorporeal support devices.

Although some of the patients were new New York Heart Association class IV patients, many had been treated for years with beta-blockers and renal ACE inhibitors or aldosterone antagonists. Their disease had now recurred and progressed despite what I had presumed to be curative drug therapy. They were experiencing the relentless progression of heart failure despite treatment that was developed almost 20 years ago and which has not advanced much since then. Many cardiologists of my generation presumed that heart failure was no longer a problem even though we knew that annual mortality rates of heart failure remained in the 10% range and that its incidence was increasing.

It has become clear to many of us that there has been little advance in the treatment of heart failure since the introduction of those 20th century drugs, notwithstanding the importance of the development of end stage cardiac support devices.

It seems our success in treating patients with ischemic heart disease had only delayed the expression and progression of cardiac dysfunction. Even with our success in treating patients with nonischemic heart failure, whatever that is, after reaching a brief plateau with drug therapy, they often experienced recurrence. It is true that many patients had improved as a result of drug therapy and that progression had been arrested and in some patients heart failure had actually been reversed. But many, like the patients I saw in our CICU, had progressed to advanced heart failure with little to be offered other than end-stage device therapy or heart transplantation. Both of these outcomes, although lifesaving, represent therapeutic failures.

It is time that we refocus our efforts on the treatment and eradication of heart failure. Although a number of contemporary treatment strategies have been developed, for the most part they have only resulted in modest additive benefit. We need to reconsider the protection of the heart during and after an ischemic event and prevent the insidious progression of ischemia in those patients with chronic coronary heart disease. In addition we need to direct our research to understand the pathophysiology of the “heart” in heart failure and to unlock the mysticism associated with the many etiologies of idiopathic nonischemic heart failure. Our knowledge in this disease or diseases is embarrassingly poor.

It is time to move on from the 20th century drug foundation of therapy based on neurohumoral control, to a 21st century understanding of the cellular and molecular targets affecting cardiac function. Recent investigations of collagen synthesis and degradation, cardiac energetics, and mitochondrial function have provided provocative information but represent only forays into the vast unknown mechanism of heart failure. The solution to worldwide heart failure is not in device therapy for everyone but in a deeper understanding of the mechanisms of heart failure and its application to therapy.

Dr. Goldstein, medical editor of Cardiology News, is professor of medicine at Wayne State University and division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit. He is on data safety monitoring committees for the National Institutes of Health and several pharmaceutical companies.

I refuse to do retreads.

This has nothing to do with my car. If a retread tire gives me the same performance and safety at a lower price, I’m all for it.

Sometimes patients fire me. This is often acrimonious, with them sending me a letter complaining about my competence, bedside manner, personal appearance, staff, office decor, phone system ... whatever. For some reason they weren’t happy with me and instead of just sending a release of records, they decided to let me know in no uncertain terms that they aren’t coming back. We all get these notes.

When I was younger this would really upset me. I took a lot of things personally when I first started out. Now, after almost 20 years on the neurology front lines, it’s just another day. I learned a long time ago that you can’t please everyone or be the doctor they all love. So I fax their chart to wherever they want and move on.

Surprisingly, a few times a year patients will try to come back. Maybe they didn’t like the new doc, or are sorry about their outburst, or can’t find someone else nearby who takes their insurance. So they call and try to make a follow-up. Not surprisingly, they never mention their previous letter. When it’s brought up, they typically claim we misinterpreted it, that they didn’t mean it, or that they’ve decided to forgive me.

This is what I call a retread. A patient who wants to come back after leaving under unpleasant circumstances. I don’t allow it.

To me the doctor-patient relationship is based on trust and objectivity. Once a patient sends an acrimonious letter, it’s very difficult to return to an impartial condition. The fact that they did it once means they may do it again, or think they can get their way with threatening or insulting behavior. These are not things that are good for the connection between us.

So I turn them away. Some just hang up. Others yell, and a few threaten me with legal action. But I don’t back down. Do you want to care for someone who’s done the same to you?

This is a high-stress field. I don’t need the additional distraction of dealing with a toxic medical relationship. If you don’t like me, I have no issue with that. Not everyone does. But once you’ve made that decision, you’re stuck with it.

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

I refuse to do retreads.

This has nothing to do with my car. If a retread tire gives me the same performance and safety at a lower price, I’m all for it.

Sometimes patients fire me. This is often acrimonious, with them sending me a letter complaining about my competence, bedside manner, personal appearance, staff, office decor, phone system ... whatever. For some reason they weren’t happy with me and instead of just sending a release of records, they decided to let me know in no uncertain terms that they aren’t coming back. We all get these notes.

When I was younger this would really upset me. I took a lot of things personally when I first started out. Now, after almost 20 years on the neurology front lines, it’s just another day. I learned a long time ago that you can’t please everyone or be the doctor they all love. So I fax their chart to wherever they want and move on.

Surprisingly, a few times a year patients will try to come back. Maybe they didn’t like the new doc, or are sorry about their outburst, or can’t find someone else nearby who takes their insurance. So they call and try to make a follow-up. Not surprisingly, they never mention their previous letter. When it’s brought up, they typically claim we misinterpreted it, that they didn’t mean it, or that they’ve decided to forgive me.

This is what I call a retread. A patient who wants to come back after leaving under unpleasant circumstances. I don’t allow it.

To me the doctor-patient relationship is based on trust and objectivity. Once a patient sends an acrimonious letter, it’s very difficult to return to an impartial condition. The fact that they did it once means they may do it again, or think they can get their way with threatening or insulting behavior. These are not things that are good for the connection between us.

So I turn them away. Some just hang up. Others yell, and a few threaten me with legal action. But I don’t back down. Do you want to care for someone who’s done the same to you?

This is a high-stress field. I don’t need the additional distraction of dealing with a toxic medical relationship. If you don’t like me, I have no issue with that. Not everyone does. But once you’ve made that decision, you’re stuck with it.

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

I refuse to do retreads.

This has nothing to do with my car. If a retread tire gives me the same performance and safety at a lower price, I’m all for it.

Sometimes patients fire me. This is often acrimonious, with them sending me a letter complaining about my competence, bedside manner, personal appearance, staff, office decor, phone system ... whatever. For some reason they weren’t happy with me and instead of just sending a release of records, they decided to let me know in no uncertain terms that they aren’t coming back. We all get these notes.

When I was younger this would really upset me. I took a lot of things personally when I first started out. Now, after almost 20 years on the neurology front lines, it’s just another day. I learned a long time ago that you can’t please everyone or be the doctor they all love. So I fax their chart to wherever they want and move on.

Surprisingly, a few times a year patients will try to come back. Maybe they didn’t like the new doc, or are sorry about their outburst, or can’t find someone else nearby who takes their insurance. So they call and try to make a follow-up. Not surprisingly, they never mention their previous letter. When it’s brought up, they typically claim we misinterpreted it, that they didn’t mean it, or that they’ve decided to forgive me.

This is what I call a retread. A patient who wants to come back after leaving under unpleasant circumstances. I don’t allow it.

To me the doctor-patient relationship is based on trust and objectivity. Once a patient sends an acrimonious letter, it’s very difficult to return to an impartial condition. The fact that they did it once means they may do it again, or think they can get their way with threatening or insulting behavior. These are not things that are good for the connection between us.

So I turn them away. Some just hang up. Others yell, and a few threaten me with legal action. But I don’t back down. Do you want to care for someone who’s done the same to you?

This is a high-stress field. I don’t need the additional distraction of dealing with a toxic medical relationship. If you don’t like me, I have no issue with that. Not everyone does. But once you’ve made that decision, you’re stuck with it.

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

Two children presented with influenza, and both recovered without the need for hospitalization. This scenario would fail to pique the interest of any pediatrician in January. But what about when it happens in July?

In early August, public health authorities in Ohio announced that two children had tested positive for the variant swine influenza virus H3N2v. Both children had direct contact with pigs at the Clark County Fair in late July. Along with a handful of cases diagnosed in Michigan, these represent the first H₃N_2v cases in the United States in 2016.

Influenza viruses that normally circulate in swine are designated as “variant” when they infect humans. According to the Centers for Disease Control and Prevention (CDC), human infections with H₁N_1v, H₁N_2v, and H₃N_2v have been identified in the United States. Influenza A H3N2v viruses carrying the matrix gene from the 2009 H₁N₁ pandemic virus were first detected in pigs in 2010, and in people in the summer of 2011. Since that time, 357 human cases have been reported from 14 states, with nearly 75% occurring in Indiana and Ohio. Most infections occurred after prolonged exposure to pigs at agricultural fairs.

Fortunately, most H₃N_2v infections have been mild: Since July 2012, only 21 individuals have required hospitalization and a single case resulted in death. Notably, though, many of the hospitalizations involved children.

On Aug. 15, the Centers for Disease Control and Prevention released Interim Guidance for Clinicians on Human Infections with Variant Influenza Viruses.

Because variant virus infection is indistinguishable from seasonal influenza or any other virus that cause influenzalike illness (think fever, cough, sore throat), physicians and other frontline providers need to maintain an index of suspicion. The key is eliciting a history of swine exposure in the week before illness onset. Practically, this means asking about direct contact with pigs, indirect contact with pigs, or close contact with an ill person who has had contact with pigs. Kudos to the astute clinicians in Ohio who thought to send the appropriate influenza testing in July.

When variant influenza virus is suspected, a nasopharyngeal swab or aspirate should be obtained for testing at a state public health lab or the CDC. Rapid antigen tests for influenza may be falsely negative in the setting of H₃N_2v infection, just as they may be with seasonal influenza infection. Molecular tests such as reverse transcription polymerase chain reaction (RT-PCR) are likely more sensitive, but cannot distinguish variant influenza A viruses from seasonal influenza A viruses.

The Kentucky State Fair opened on Aug. 18, making the CDC guidance especially timely for health care providers in my area. I called a friend who is a pediatric emergency medicine physician to ask if she and her colleagues were routinely screening patients for encounters of the porcine kind.

“For example, are you asking, ‘Have you been showing, raising or feeding swine? Have you been to the pig barn at the fair?’ ”

When my friend quit laughing, I confessed to her that I had not been doing that routinely either. The exposure history is often the most interesting part of the infectious disease evaluation and in the last month, I’ve asked about exposure to sheep (a risk factor for Q fever), exposure to chickens (a risk factor for Salmonella infections), and exposure to beaver dams (a risk factor for blastomycosis). But I’ve not asked about exposure to pigs.

“The emergency medicine approach is to avoid a lot of viral diagnostic testing unless it is going to impact management,” she said. “Tell me how this changes management of my patient.”

From the patient perspective, making a presumptive diagnosis of H₃N_2v infection would open the door to empiric treatment with antivirals, at least for individuals who are hospitalized, have severe or progressive disease, or who at high risk for complications of influenza. Neuraminidase inhibitors, including oral oseltamivir, inhaled zanamivir, and intravenous peramivir, can be used for treatment of H₃N_2v infections.

From a societal perspective, making the diagnosis gives public health experts the opportunity to investigate and potentially prevent further infections by isolating sick pigs. Human to human transmission of H₃N_2v is rare, but has occasionally occurred in households and in one instance, a child care setting. Careful surveillance of each swine flu case in a human is important to exclude the possibility that the virus has developed the ability to spread efficiently from person to person, creating the risk for an epidemic.

Seasonal influenza vaccine does not prevent infection with variant viruses, so avoidance is key. Those at high risk for complications from influenza infection, including children younger than 5 years of age and those with asthma, diabetes, heart disease, immunocompromised conditions, and neurologic or neurodevelopmental disorders, are urged to avoid pigs and swine barns when visiting fairs where the animals are present. Everyone else needs to follow common sense measures to prevent the spread of infection.

• Don’t take food or drink into pig areas; don’t eat, drink or put anything in your mouth in pig areas.

• Don’t take toys, pacifiers, cups, baby bottles, strollers, or similar items into pig areas.

• Wash your hands often with soap and running water before and after exposure to pigs. If soap and water are not available, use an alcohol-based hand rub.

• Avoid close contact with pigs that look or act ill.

• Take protective measures if you must come in contact with pigs that are known or suspected to be sick. This includes wearing personal protective equipment like protective clothing, gloves, and masks that cover your mouth and nose when contact is required.

• To further reduce the risk of infection, minimize contact with pigs in the pig barn and arenas.

It shouldn’t be surprising that flu viruses spread from pigs to people in the same way that regular seasonal influenza spread from person to person. An infected pig coughs or sneezes influenza-containing droplets, and these droplets are inhaled or swallowed by a susceptible human. That makes avoiding contact with pigs that look or act ill especially important. For the record, a pig with flu might have fever, depression, cough, nasal or eye discharge, eye redness, or a poor appetite.

On the bright side, you can’t get H₃N_2v or any other variant virus from eating properly prepared pork meat. Fairgoers can feel free to indulge in a deep-fried pork chop or one of this year’s featured food items: a basket of French fries topped with smoked pork, cheddar cheese sauce, red onions, jalapeño peppers and barbecue sauce.

Or maybe not. The CDC has a web page devoted to food safety at fairs and festivals. It notes that cases of foodborne illness increase during summer months, and usual safety controls “like monitoring of food temperatures, refrigeration, workers trained in food safety and washing facilities, may not be available when cooking and dining at fairs and festivals.”

The public is urged to seek out “healthy options” from fair vendors first. If healthy options aren’t available, we’re advised to consider bringing food from home to save money and calories.

Sigh. I remember when summer used to be more fun.

Dr. Bryant is a pediatrician specializing in infectious diseases at the University of Louisville, Ky. and Kosair Children’s Hospital, also in Louisville.

Two children presented with influenza, and both recovered without the need for hospitalization. This scenario would fail to pique the interest of any pediatrician in January. But what about when it happens in July?

In early August, public health authorities in Ohio announced that two children had tested positive for the variant swine influenza virus H3N2v. Both children had direct contact with pigs at the Clark County Fair in late July. Along with a handful of cases diagnosed in Michigan, these represent the first H₃N_2v cases in the United States in 2016.

Influenza viruses that normally circulate in swine are designated as “variant” when they infect humans. According to the Centers for Disease Control and Prevention (CDC), human infections with H₁N_1v, H₁N_2v, and H₃N_2v have been identified in the United States. Influenza A H3N2v viruses carrying the matrix gene from the 2009 H₁N₁ pandemic virus were first detected in pigs in 2010, and in people in the summer of 2011. Since that time, 357 human cases have been reported from 14 states, with nearly 75% occurring in Indiana and Ohio. Most infections occurred after prolonged exposure to pigs at agricultural fairs.

Fortunately, most H₃N_2v infections have been mild: Since July 2012, only 21 individuals have required hospitalization and a single case resulted in death. Notably, though, many of the hospitalizations involved children.

On Aug. 15, the Centers for Disease Control and Prevention released Interim Guidance for Clinicians on Human Infections with Variant Influenza Viruses.

Because variant virus infection is indistinguishable from seasonal influenza or any other virus that cause influenzalike illness (think fever, cough, sore throat), physicians and other frontline providers need to maintain an index of suspicion. The key is eliciting a history of swine exposure in the week before illness onset. Practically, this means asking about direct contact with pigs, indirect contact with pigs, or close contact with an ill person who has had contact with pigs. Kudos to the astute clinicians in Ohio who thought to send the appropriate influenza testing in July.

When variant influenza virus is suspected, a nasopharyngeal swab or aspirate should be obtained for testing at a state public health lab or the CDC. Rapid antigen tests for influenza may be falsely negative in the setting of H₃N_2v infection, just as they may be with seasonal influenza infection. Molecular tests such as reverse transcription polymerase chain reaction (RT-PCR) are likely more sensitive, but cannot distinguish variant influenza A viruses from seasonal influenza A viruses.

The Kentucky State Fair opened on Aug. 18, making the CDC guidance especially timely for health care providers in my area. I called a friend who is a pediatric emergency medicine physician to ask if she and her colleagues were routinely screening patients for encounters of the porcine kind.

“For example, are you asking, ‘Have you been showing, raising or feeding swine? Have you been to the pig barn at the fair?’ ”

When my friend quit laughing, I confessed to her that I had not been doing that routinely either. The exposure history is often the most interesting part of the infectious disease evaluation and in the last month, I’ve asked about exposure to sheep (a risk factor for Q fever), exposure to chickens (a risk factor for Salmonella infections), and exposure to beaver dams (a risk factor for blastomycosis). But I’ve not asked about exposure to pigs.

“The emergency medicine approach is to avoid a lot of viral diagnostic testing unless it is going to impact management,” she said. “Tell me how this changes management of my patient.”

From the patient perspective, making a presumptive diagnosis of H₃N_2v infection would open the door to empiric treatment with antivirals, at least for individuals who are hospitalized, have severe or progressive disease, or who at high risk for complications of influenza. Neuraminidase inhibitors, including oral oseltamivir, inhaled zanamivir, and intravenous peramivir, can be used for treatment of H₃N_2v infections.

From a societal perspective, making the diagnosis gives public health experts the opportunity to investigate and potentially prevent further infections by isolating sick pigs. Human to human transmission of H₃N_2v is rare, but has occasionally occurred in households and in one instance, a child care setting. Careful surveillance of each swine flu case in a human is important to exclude the possibility that the virus has developed the ability to spread efficiently from person to person, creating the risk for an epidemic.

Seasonal influenza vaccine does not prevent infection with variant viruses, so avoidance is key. Those at high risk for complications from influenza infection, including children younger than 5 years of age and those with asthma, diabetes, heart disease, immunocompromised conditions, and neurologic or neurodevelopmental disorders, are urged to avoid pigs and swine barns when visiting fairs where the animals are present. Everyone else needs to follow common sense measures to prevent the spread of infection.

• Don’t take food or drink into pig areas; don’t eat, drink or put anything in your mouth in pig areas.

• Don’t take toys, pacifiers, cups, baby bottles, strollers, or similar items into pig areas.

• Wash your hands often with soap and running water before and after exposure to pigs. If soap and water are not available, use an alcohol-based hand rub.

• Avoid close contact with pigs that look or act ill.

• Take protective measures if you must come in contact with pigs that are known or suspected to be sick. This includes wearing personal protective equipment like protective clothing, gloves, and masks that cover your mouth and nose when contact is required.

• To further reduce the risk of infection, minimize contact with pigs in the pig barn and arenas.

It shouldn’t be surprising that flu viruses spread from pigs to people in the same way that regular seasonal influenza spread from person to person. An infected pig coughs or sneezes influenza-containing droplets, and these droplets are inhaled or swallowed by a susceptible human. That makes avoiding contact with pigs that look or act ill especially important. For the record, a pig with flu might have fever, depression, cough, nasal or eye discharge, eye redness, or a poor appetite.

On the bright side, you can’t get H₃N_2v or any other variant virus from eating properly prepared pork meat. Fairgoers can feel free to indulge in a deep-fried pork chop or one of this year’s featured food items: a basket of French fries topped with smoked pork, cheddar cheese sauce, red onions, jalapeño peppers and barbecue sauce.

Or maybe not. The CDC has a web page devoted to food safety at fairs and festivals. It notes that cases of foodborne illness increase during summer months, and usual safety controls “like monitoring of food temperatures, refrigeration, workers trained in food safety and washing facilities, may not be available when cooking and dining at fairs and festivals.”

The public is urged to seek out “healthy options” from fair vendors first. If healthy options aren’t available, we’re advised to consider bringing food from home to save money and calories.

Sigh. I remember when summer used to be more fun.

Dr. Bryant is a pediatrician specializing in infectious diseases at the University of Louisville, Ky. and Kosair Children’s Hospital, also in Louisville.

Two children presented with influenza, and both recovered without the need for hospitalization. This scenario would fail to pique the interest of any pediatrician in January. But what about when it happens in July?

In early August, public health authorities in Ohio announced that two children had tested positive for the variant swine influenza virus H3N2v. Both children had direct contact with pigs at the Clark County Fair in late July. Along with a handful of cases diagnosed in Michigan, these represent the first H₃N_2v cases in the United States in 2016.

Influenza viruses that normally circulate in swine are designated as “variant” when they infect humans. According to the Centers for Disease Control and Prevention (CDC), human infections with H₁N_1v, H₁N_2v, and H₃N_2v have been identified in the United States. Influenza A H3N2v viruses carrying the matrix gene from the 2009 H₁N₁ pandemic virus were first detected in pigs in 2010, and in people in the summer of 2011. Since that time, 357 human cases have been reported from 14 states, with nearly 75% occurring in Indiana and Ohio. Most infections occurred after prolonged exposure to pigs at agricultural fairs.

Fortunately, most H₃N_2v infections have been mild: Since July 2012, only 21 individuals have required hospitalization and a single case resulted in death. Notably, though, many of the hospitalizations involved children.

On Aug. 15, the Centers for Disease Control and Prevention released Interim Guidance for Clinicians on Human Infections with Variant Influenza Viruses.

Because variant virus infection is indistinguishable from seasonal influenza or any other virus that cause influenzalike illness (think fever, cough, sore throat), physicians and other frontline providers need to maintain an index of suspicion. The key is eliciting a history of swine exposure in the week before illness onset. Practically, this means asking about direct contact with pigs, indirect contact with pigs, or close contact with an ill person who has had contact with pigs. Kudos to the astute clinicians in Ohio who thought to send the appropriate influenza testing in July.

When variant influenza virus is suspected, a nasopharyngeal swab or aspirate should be obtained for testing at a state public health lab or the CDC. Rapid antigen tests for influenza may be falsely negative in the setting of H₃N_2v infection, just as they may be with seasonal influenza infection. Molecular tests such as reverse transcription polymerase chain reaction (RT-PCR) are likely more sensitive, but cannot distinguish variant influenza A viruses from seasonal influenza A viruses.

The Kentucky State Fair opened on Aug. 18, making the CDC guidance especially timely for health care providers in my area. I called a friend who is a pediatric emergency medicine physician to ask if she and her colleagues were routinely screening patients for encounters of the porcine kind.

“For example, are you asking, ‘Have you been showing, raising or feeding swine? Have you been to the pig barn at the fair?’ ”

When my friend quit laughing, I confessed to her that I had not been doing that routinely either. The exposure history is often the most interesting part of the infectious disease evaluation and in the last month, I’ve asked about exposure to sheep (a risk factor for Q fever), exposure to chickens (a risk factor for Salmonella infections), and exposure to beaver dams (a risk factor for blastomycosis). But I’ve not asked about exposure to pigs.

“The emergency medicine approach is to avoid a lot of viral diagnostic testing unless it is going to impact management,” she said. “Tell me how this changes management of my patient.”

From the patient perspective, making a presumptive diagnosis of H₃N_2v infection would open the door to empiric treatment with antivirals, at least for individuals who are hospitalized, have severe or progressive disease, or who at high risk for complications of influenza. Neuraminidase inhibitors, including oral oseltamivir, inhaled zanamivir, and intravenous peramivir, can be used for treatment of H₃N_2v infections.

From a societal perspective, making the diagnosis gives public health experts the opportunity to investigate and potentially prevent further infections by isolating sick pigs. Human to human transmission of H₃N_2v is rare, but has occasionally occurred in households and in one instance, a child care setting. Careful surveillance of each swine flu case in a human is important to exclude the possibility that the virus has developed the ability to spread efficiently from person to person, creating the risk for an epidemic.

Seasonal influenza vaccine does not prevent infection with variant viruses, so avoidance is key. Those at high risk for complications from influenza infection, including children younger than 5 years of age and those with asthma, diabetes, heart disease, immunocompromised conditions, and neurologic or neurodevelopmental disorders, are urged to avoid pigs and swine barns when visiting fairs where the animals are present. Everyone else needs to follow common sense measures to prevent the spread of infection.

• Don’t take food or drink into pig areas; don’t eat, drink or put anything in your mouth in pig areas.

• Don’t take toys, pacifiers, cups, baby bottles, strollers, or similar items into pig areas.

• Wash your hands often with soap and running water before and after exposure to pigs. If soap and water are not available, use an alcohol-based hand rub.

• Avoid close contact with pigs that look or act ill.

• Take protective measures if you must come in contact with pigs that are known or suspected to be sick. This includes wearing personal protective equipment like protective clothing, gloves, and masks that cover your mouth and nose when contact is required.

• To further reduce the risk of infection, minimize contact with pigs in the pig barn and arenas.

It shouldn’t be surprising that flu viruses spread from pigs to people in the same way that regular seasonal influenza spread from person to person. An infected pig coughs or sneezes influenza-containing droplets, and these droplets are inhaled or swallowed by a susceptible human. That makes avoiding contact with pigs that look or act ill especially important. For the record, a pig with flu might have fever, depression, cough, nasal or eye discharge, eye redness, or a poor appetite.

On the bright side, you can’t get H₃N_2v or any other variant virus from eating properly prepared pork meat. Fairgoers can feel free to indulge in a deep-fried pork chop or one of this year’s featured food items: a basket of French fries topped with smoked pork, cheddar cheese sauce, red onions, jalapeño peppers and barbecue sauce.

Or maybe not. The CDC has a web page devoted to food safety at fairs and festivals. It notes that cases of foodborne illness increase during summer months, and usual safety controls “like monitoring of food temperatures, refrigeration, workers trained in food safety and washing facilities, may not be available when cooking and dining at fairs and festivals.”

The public is urged to seek out “healthy options” from fair vendors first. If healthy options aren’t available, we’re advised to consider bringing food from home to save money and calories.

Sigh. I remember when summer used to be more fun.

Dr. Bryant is a pediatrician specializing in infectious diseases at the University of Louisville, Ky. and Kosair Children’s Hospital, also in Louisville.