Opinion

 

I’m a little concerned about my grandchildren. I worry that when they are in their twenties, no one will want them as trivia teammates. Or when they are hanging out with other 40-something couples, they will fade into the wallpaper when the conversation turns to, “Remember that episode of Big Bang Theory when ... .”

The 5½-year-old and the 8-year-old have grown up in a household that has never had a TV, and the 10- and 12-year-old are surviving with a cable connection so basic that it barely gets more than a few shopping channels and the local school board meetings.

This situation is not the direct result of the TV environments in which their parents grew up. While we were among the last families in the neighborhood with a color TV, we did watch TV. We did put some limits on TV viewing, and our children were in their late teens before they realized that our TV was capable of receiving cartoons on Saturday mornings. They thought this kind of special connection existed only in motel rooms. Other than putting a few restrictions on TV viewing, we weren’t militant supervisors of our children’s viewing habits.

Our children were just too busy doing things to watch much TV. Now as adults they have been paying attention to what they have heard and read about the potential negative influence that TV may have on their own children, and imposed restrictions far more severe than those under which they were raised. It has been interesting to watch how their children are responding to these TV-deprived environments.

For the most part, there has been no whining or begging to turn on the TV. The younger two have no other option and don’t realize what they are missing. The older two, who watched some Sesame Street as toddlers, have been similarly disinterested, although my 10-year-old grandson enjoys watching some sports when the opportunity arises.

So what do my grandchildren do with the 28 hours each week that their peers are spending in front of a TV (“Television and Children,” University of Michigan Medical School/Michigan Medicine website)? The two older girls are voracious readers. One spends hours drawing, and with her younger sister, always has a craft project or two going. The older two are skillful board and card game players, and they play musical instruments. All four are involved in at least one sport per season, and when asked, they would prefer to be playing something outside. And they go to bed at a healthy hour.

In a recent article in AAP News (“How to provide evidence-based pediatric care for the digital age,” May 2017), Michael O. Rich, MD, a member of the American Academy of Pediatrics Council on Communications and Media, writes, “Our traditional advice to limit screen time and restrict content is no longer relevant and often unheard by families.” I agree that for many years that AAP advice had been too focused on content. However, seeing my grandchildren thrive in an environment of what many might consider an extreme screen time restriction has further reinforced my previous observations that the critical issue with screen time is that it replaces health-promoting active alternatives. Even screen time that requires some interaction relegates the child to the role of a sedentary spectator.

Although Dr. Rich is to be commended for suggesting that we look at evidence-based studies as we decide how to counsel parents about screen time, I am always skeptical about the validity of short-term “evidence.” I fear that some of the evidence-based studies are being used to excuse or rationalize an already unhealthy situation. At some point we need to step back and take the longer look. Would you rather see your grandchildren hunched over a screen or couched in front of a television watching other people doing things, or would you prefer that they be physically active doers and creators themselves?
 

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.”

 

I’m a little concerned about my grandchildren. I worry that when they are in their twenties, no one will want them as trivia teammates. Or when they are hanging out with other 40-something couples, they will fade into the wallpaper when the conversation turns to, “Remember that episode of Big Bang Theory when ... .”

The 5½-year-old and the 8-year-old have grown up in a household that has never had a TV, and the 10- and 12-year-old are surviving with a cable connection so basic that it barely gets more than a few shopping channels and the local school board meetings.

This situation is not the direct result of the TV environments in which their parents grew up. While we were among the last families in the neighborhood with a color TV, we did watch TV. We did put some limits on TV viewing, and our children were in their late teens before they realized that our TV was capable of receiving cartoons on Saturday mornings. They thought this kind of special connection existed only in motel rooms. Other than putting a few restrictions on TV viewing, we weren’t militant supervisors of our children’s viewing habits.

Our children were just too busy doing things to watch much TV. Now as adults they have been paying attention to what they have heard and read about the potential negative influence that TV may have on their own children, and imposed restrictions far more severe than those under which they were raised. It has been interesting to watch how their children are responding to these TV-deprived environments.

For the most part, there has been no whining or begging to turn on the TV. The younger two have no other option and don’t realize what they are missing. The older two, who watched some Sesame Street as toddlers, have been similarly disinterested, although my 10-year-old grandson enjoys watching some sports when the opportunity arises.

So what do my grandchildren do with the 28 hours each week that their peers are spending in front of a TV (“Television and Children,” University of Michigan Medical School/Michigan Medicine website)? The two older girls are voracious readers. One spends hours drawing, and with her younger sister, always has a craft project or two going. The older two are skillful board and card game players, and they play musical instruments. All four are involved in at least one sport per season, and when asked, they would prefer to be playing something outside. And they go to bed at a healthy hour.

In a recent article in AAP News (“How to provide evidence-based pediatric care for the digital age,” May 2017), Michael O. Rich, MD, a member of the American Academy of Pediatrics Council on Communications and Media, writes, “Our traditional advice to limit screen time and restrict content is no longer relevant and often unheard by families.” I agree that for many years that AAP advice had been too focused on content. However, seeing my grandchildren thrive in an environment of what many might consider an extreme screen time restriction has further reinforced my previous observations that the critical issue with screen time is that it replaces health-promoting active alternatives. Even screen time that requires some interaction relegates the child to the role of a sedentary spectator.

Although Dr. Rich is to be commended for suggesting that we look at evidence-based studies as we decide how to counsel parents about screen time, I am always skeptical about the validity of short-term “evidence.” I fear that some of the evidence-based studies are being used to excuse or rationalize an already unhealthy situation. At some point we need to step back and take the longer look. Would you rather see your grandchildren hunched over a screen or couched in front of a television watching other people doing things, or would you prefer that they be physically active doers and creators themselves?
 

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.”

 

I’m a little concerned about my grandchildren. I worry that when they are in their twenties, no one will want them as trivia teammates. Or when they are hanging out with other 40-something couples, they will fade into the wallpaper when the conversation turns to, “Remember that episode of Big Bang Theory when ... .”

The 5½-year-old and the 8-year-old have grown up in a household that has never had a TV, and the 10- and 12-year-old are surviving with a cable connection so basic that it barely gets more than a few shopping channels and the local school board meetings.

This situation is not the direct result of the TV environments in which their parents grew up. While we were among the last families in the neighborhood with a color TV, we did watch TV. We did put some limits on TV viewing, and our children were in their late teens before they realized that our TV was capable of receiving cartoons on Saturday mornings. They thought this kind of special connection existed only in motel rooms. Other than putting a few restrictions on TV viewing, we weren’t militant supervisors of our children’s viewing habits.

Our children were just too busy doing things to watch much TV. Now as adults they have been paying attention to what they have heard and read about the potential negative influence that TV may have on their own children, and imposed restrictions far more severe than those under which they were raised. It has been interesting to watch how their children are responding to these TV-deprived environments.

For the most part, there has been no whining or begging to turn on the TV. The younger two have no other option and don’t realize what they are missing. The older two, who watched some Sesame Street as toddlers, have been similarly disinterested, although my 10-year-old grandson enjoys watching some sports when the opportunity arises.

So what do my grandchildren do with the 28 hours each week that their peers are spending in front of a TV (“Television and Children,” University of Michigan Medical School/Michigan Medicine website)? The two older girls are voracious readers. One spends hours drawing, and with her younger sister, always has a craft project or two going. The older two are skillful board and card game players, and they play musical instruments. All four are involved in at least one sport per season, and when asked, they would prefer to be playing something outside. And they go to bed at a healthy hour.

In a recent article in AAP News (“How to provide evidence-based pediatric care for the digital age,” May 2017), Michael O. Rich, MD, a member of the American Academy of Pediatrics Council on Communications and Media, writes, “Our traditional advice to limit screen time and restrict content is no longer relevant and often unheard by families.” I agree that for many years that AAP advice had been too focused on content. However, seeing my grandchildren thrive in an environment of what many might consider an extreme screen time restriction has further reinforced my previous observations that the critical issue with screen time is that it replaces health-promoting active alternatives. Even screen time that requires some interaction relegates the child to the role of a sedentary spectator.

Although Dr. Rich is to be commended for suggesting that we look at evidence-based studies as we decide how to counsel parents about screen time, I am always skeptical about the validity of short-term “evidence.” I fear that some of the evidence-based studies are being used to excuse or rationalize an already unhealthy situation. At some point we need to step back and take the longer look. Would you rather see your grandchildren hunched over a screen or couched in front of a television watching other people doing things, or would you prefer that they be physically active doers and creators themselves?
 

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.”

 

I have a repertoire of about a dozen soups that I enjoy preparing, but I certainly don’t consider myself a gourmet chef. However, I can legitimately claim to be a master of the microwave. Hand me a potentially edible substance, and I will nuke it to a palatable temperature in one step. This skill comes from 30 years of practice and requires a sixth sense that includes factoring in the object’s water content, shape, and density, and knowing whether I am starting from the frozen state, refrigerator cool, or room temperature.

Sadly, our 30-some-year-old microwave nuked its last leftover in a shower of sparks a few weeks ago, and I have been forced to recalibrate my technique with a new machine. Not to worry, I am just one or two more rewarmed meals away from returning to my old “nukelear” mastery.

I recently learned that Amana introduced the first countertop microwave in 1967, the same year that Pediatric News began publication (Susan Strasser. “What’s in Your Microwave Oven?” The New York Times. April 14, 2017). Over those ensuing 50 years, the microwave has been one of the major forces molding what, when, and how North Americans eat. It has been a tremendous time-saver for those saddled with the task of preparing family meals. The microwave oven also has allowed millions of adults and children without even the most basic kitchen skills or equipment to prepare themselves warm and nutritious meals at any time they choose or when their schedules allow.

Unfortunately, as with any new technology, the ubiquity of countertop microwave ovens has come with some downsides. While they do offer the cooking challenged among us a broad choice of foods we can prepare in minutes or seconds, the choices we make are not always nutritiously sound.

The microwave oven and single-serving prepared frozen meals have been a great boon to people who live alone or live or work on schedules out of sync with their families’ meal schedule. However, there is a point when this technologically-enabled nutritional independence begins to take precedence over communal dining. The family meal slips on to the endangered species list. Although there is some debate about whether family meals are any more valuable as character-building exercises than other shared family experiences, there is no question that children in families who dine together on a regular basis enjoy substantial health benefits, such as less depressive symptoms, more healthy foods, fewer weight problems, and less delinquency.

The forces that have driven the family meal into decline are numerous and powerful. However, we should not underestimate the role that the microwave oven has had in greasing this path toward extinction. Even if the family has one member with the time, skills, and commitment to create nutritious and complete meals, the microwave oven offers even the youngest member an easy way to opt out of sharing it with the rest of his family. A parent who must work late can rewarm his serving at 9:00 p.m. when he or she gets home. The high school thespian can nuke her own prepared frozen dinner at 5 p.m. so she can get to a rehearsal at 6 p.m. And, the 4-year-old picky eater who won’t touch anything green can have his treasured mac ‘n cheese warmed to his taste while everyone else is enjoying fish tacos. And, there you have it. Poof! With the touch of a couple buttons, the opportunity for a family to enjoy a meal together and share their experiences of the day has vanished into thin air along with a valuable lesson in cooperation and compromise.

But, we needn’t worry about those family members who are dining separately getting lonely because more than likely they each have their own electronic companion to keep them company while they eat their microwaved meal.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.”

 

I have a repertoire of about a dozen soups that I enjoy preparing, but I certainly don’t consider myself a gourmet chef. However, I can legitimately claim to be a master of the microwave. Hand me a potentially edible substance, and I will nuke it to a palatable temperature in one step. This skill comes from 30 years of practice and requires a sixth sense that includes factoring in the object’s water content, shape, and density, and knowing whether I am starting from the frozen state, refrigerator cool, or room temperature.

Sadly, our 30-some-year-old microwave nuked its last leftover in a shower of sparks a few weeks ago, and I have been forced to recalibrate my technique with a new machine. Not to worry, I am just one or two more rewarmed meals away from returning to my old “nukelear” mastery.

I recently learned that Amana introduced the first countertop microwave in 1967, the same year that Pediatric News began publication (Susan Strasser. “What’s in Your Microwave Oven?” The New York Times. April 14, 2017). Over those ensuing 50 years, the microwave has been one of the major forces molding what, when, and how North Americans eat. It has been a tremendous time-saver for those saddled with the task of preparing family meals. The microwave oven also has allowed millions of adults and children without even the most basic kitchen skills or equipment to prepare themselves warm and nutritious meals at any time they choose or when their schedules allow.

Unfortunately, as with any new technology, the ubiquity of countertop microwave ovens has come with some downsides. While they do offer the cooking challenged among us a broad choice of foods we can prepare in minutes or seconds, the choices we make are not always nutritiously sound.

The microwave oven and single-serving prepared frozen meals have been a great boon to people who live alone or live or work on schedules out of sync with their families’ meal schedule. However, there is a point when this technologically-enabled nutritional independence begins to take precedence over communal dining. The family meal slips on to the endangered species list. Although there is some debate about whether family meals are any more valuable as character-building exercises than other shared family experiences, there is no question that children in families who dine together on a regular basis enjoy substantial health benefits, such as less depressive symptoms, more healthy foods, fewer weight problems, and less delinquency.

The forces that have driven the family meal into decline are numerous and powerful. However, we should not underestimate the role that the microwave oven has had in greasing this path toward extinction. Even if the family has one member with the time, skills, and commitment to create nutritious and complete meals, the microwave oven offers even the youngest member an easy way to opt out of sharing it with the rest of his family. A parent who must work late can rewarm his serving at 9:00 p.m. when he or she gets home. The high school thespian can nuke her own prepared frozen dinner at 5 p.m. so she can get to a rehearsal at 6 p.m. And, the 4-year-old picky eater who won’t touch anything green can have his treasured mac ‘n cheese warmed to his taste while everyone else is enjoying fish tacos. And, there you have it. Poof! With the touch of a couple buttons, the opportunity for a family to enjoy a meal together and share their experiences of the day has vanished into thin air along with a valuable lesson in cooperation and compromise.

But, we needn’t worry about those family members who are dining separately getting lonely because more than likely they each have their own electronic companion to keep them company while they eat their microwaved meal.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.”

 

I have a repertoire of about a dozen soups that I enjoy preparing, but I certainly don’t consider myself a gourmet chef. However, I can legitimately claim to be a master of the microwave. Hand me a potentially edible substance, and I will nuke it to a palatable temperature in one step. This skill comes from 30 years of practice and requires a sixth sense that includes factoring in the object’s water content, shape, and density, and knowing whether I am starting from the frozen state, refrigerator cool, or room temperature.

Sadly, our 30-some-year-old microwave nuked its last leftover in a shower of sparks a few weeks ago, and I have been forced to recalibrate my technique with a new machine. Not to worry, I am just one or two more rewarmed meals away from returning to my old “nukelear” mastery.

I recently learned that Amana introduced the first countertop microwave in 1967, the same year that Pediatric News began publication (Susan Strasser. “What’s in Your Microwave Oven?” The New York Times. April 14, 2017). Over those ensuing 50 years, the microwave has been one of the major forces molding what, when, and how North Americans eat. It has been a tremendous time-saver for those saddled with the task of preparing family meals. The microwave oven also has allowed millions of adults and children without even the most basic kitchen skills or equipment to prepare themselves warm and nutritious meals at any time they choose or when their schedules allow.

Unfortunately, as with any new technology, the ubiquity of countertop microwave ovens has come with some downsides. While they do offer the cooking challenged among us a broad choice of foods we can prepare in minutes or seconds, the choices we make are not always nutritiously sound.

The microwave oven and single-serving prepared frozen meals have been a great boon to people who live alone or live or work on schedules out of sync with their families’ meal schedule. However, there is a point when this technologically-enabled nutritional independence begins to take precedence over communal dining. The family meal slips on to the endangered species list. Although there is some debate about whether family meals are any more valuable as character-building exercises than other shared family experiences, there is no question that children in families who dine together on a regular basis enjoy substantial health benefits, such as less depressive symptoms, more healthy foods, fewer weight problems, and less delinquency.

The forces that have driven the family meal into decline are numerous and powerful. However, we should not underestimate the role that the microwave oven has had in greasing this path toward extinction. Even if the family has one member with the time, skills, and commitment to create nutritious and complete meals, the microwave oven offers even the youngest member an easy way to opt out of sharing it with the rest of his family. A parent who must work late can rewarm his serving at 9:00 p.m. when he or she gets home. The high school thespian can nuke her own prepared frozen dinner at 5 p.m. so she can get to a rehearsal at 6 p.m. And, the 4-year-old picky eater who won’t touch anything green can have his treasured mac ‘n cheese warmed to his taste while everyone else is enjoying fish tacos. And, there you have it. Poof! With the touch of a couple buttons, the opportunity for a family to enjoy a meal together and share their experiences of the day has vanished into thin air along with a valuable lesson in cooperation and compromise.

But, we needn’t worry about those family members who are dining separately getting lonely because more than likely they each have their own electronic companion to keep them company while they eat their microwaved meal.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.”

 

Robert Lowell knew civic valor. Sixteen times and more he had been down on his knees in madness, he said. Sixteen times and more he had gotten up. He had gone back to his work, entered back into life. He had faced down uncertainty and madness, had created new forms when pushed to stay with the old, had brought back imaginative order from chaos. It was a different kind of courage, this civic courage, and the rules of engagement were unclear. Lowell’s life, as his daughter observed, was a messy one, difficult for him and for those who knew him. But it was lived with iron, and often with grace. He kept always in the front of his mind what he thought he ought to be, even when he couldn’t be it; he believed in what his country could be, even if it wasn’t. He worked hard at his art.

–Kay Redfield Jamison, PhD, in “Robert Lowell, Setting the River on Fire: A Study of Genius, Mania, and Character” (New York: Alfred A. Knopf, 2017).

Kay Jamison starts her newest book by telling the reader, up front, this is not a biography of the great poet, Robert Lowell. It is, instead, a psychological account of his life and of his mind. Her magnificent study is an unconventional way of approaching the life of another human being, taken in the context of both Lowell’s personal struggle with mental illness and as the culmination of generations of genius and mania in a long and complicated family history. There have been many reviews of Jamison’s book, and for the reader who is interested in a more conventional read, I will steer you to Elizabeth Bosworth’s review in The New York Times (“A poet’s pathologies: Inside Robert Lowell’s restless mind,” March 1, 2017) or Helen Vendler’s review in The New York Review of Books (“The two Robert Lowells,” April 20, 2017). Instead, of a review, per se, I’d like to recount what I thought about as I read “Setting The River On Fire.”

Lowell, who lived from 1917 to 1977, was a two-time Pulitzer Prize winner, deemed to be the greatest American poet of his time. He studied the classics and was obsessed with Napoleon as a child, and he drew on the work of other great poets and classicists as influences for his own work. I must confess, I came to this psychological study having never read the work of Robert Lowell. My only familiarity with the poet came directly from the author. I heard Dr. Jamison, a professor of psychiatry at Johns Hopkins University, Baltimore, speak several years ago at the Johns Hopkins Annual Mood Disorders Symposium about her then work-in-progress as she was researching this book. What I heard was intriguing enough that I was eager to read and review a long and solid book about a great poet whose work I had never read.

As I began “Setting The River On Fire,” my first thought was that the writing itself was astounding. Dr. Jamison’s words flow, her metaphors never fall flat or feel artificial, the ride itself is lovely. I looked for a few lines to quote as an example, and I was left at a standstill. One line was more gracious than the next. I finally settled on the quote I used at the beginning of this piece, benignly chosen from page 403 because it encapsulated not just the beautiful writing but a synopsis of who Lowell was and what he had achieved, set in the context of attempted differentiation between the man, the madness, and the interplay of the two.

Dr. Jamison’s research on Lowell’s life is nothing short of astounding and was clearly a labor that took both sustained passion and years of her time. Dr. Jamison quoted the poet at length. She is an expert on his many volumes of poetry and prose, as well as his life and loves – three marriages and many intimate friendships – documented through letters and conversations. In addition, she quoted many other poets as examples of how their work influenced Lowell. Beyond the literature and correspondence, Dr. Jamison interviewed those who knew Lowell well. She unearthed his medical and psychiatric records, and she plotted out the course of his life in an uncanny way, linking so much of his work to the ebbs and flows of his illness. My only “criticism” of the book would be in how extensive it is. She sometimes makes a point by quoting several sources, each of whom drive at the same idea. It makes for very strong rhetoric.

Lowell lived through the heyday of psychoanalysis, a time when psychiatry focused on the idea that mental aberration was a result of unconscious conflicts and issues left unaddressed from childhood. Lowell’s life was certainly ripe for the psychoanalyst, as Dr. Jamison documented his mother’s psychopathology and his father’s passive distance from his own emotions . In fact, Robert Lowell was treated at some of the great institutions steeped in psychoanalytic learning: Payne Whitney Clinic, McLean Hospital, and Massachusetts Mental Health Center (formerly Boston Psychopathic Hospital), where his treatments included electroconvulsive therapy, chlorpromazine, and eventually lithium.

His second wife, Elizabeth Hardwick, had a striking understanding of his illness as a biological disorder beyond his control. Her sympathy for his behavior as a product of illness allowed her to tolerate actions that many people would not, even with our current day emphasis on disease states, including sexual indiscretions. His friends, too, saw the uncharacteristic chaos of his manias as the result of a state of illness, and, as such, as forgivable. These were often not subtle indiscretions: Jamison describes intense delusional states, combative behavior, police with straightjackets, often at very public and professional events worldwide. If psychoanalytic thinking weighed in on an understanding of Lowell’s motivations, Dr. Jamison did not include it in her study of Lowell, and she makes a point at the end of saying that she focused on his illness and did not include the content of psychotherapy notes. Still, I was struck by the understanding of his depressions and manias as a state of illness by lay people in his life and thought that, given the time period, it was noteworthy.

On a similar vein, I wondered if Lowell could live his life now as he lived his life then. A crucial arena for his career was Harvard College, where he returned over and over to teach. Dr. Jamison says that Lowell lectured in an acutely psychotic and disorganized state. She says that, while students clamored to take his classes, so, too, they were afraid of him. I cannot quite imagine that, in our world of “trigger warnings,” microaggressions, and college safe spaces, we might ever allow an openly ill genius to reign in a classroom of students. I am never certain if we are aimed forward or backward in our struggle against stigma, and “Setting The River On Fire” may be one more example in which we have lost ground in a quest for tolerance.

Once again, Dr. Jamison pulled me into her world. “Setting The River On Fire” is no one’s version of a light or happy read, it is a serious study of an intensely brilliant and often desperately ill poet – and it does not disappoint.

 

Dr. Miller, who practices in Baltimore, is coauthor with Annette Hanson, MD, of “Committed: The Battle Over Involuntary Psychiatric Care,” (Baltimore: Johns Hopkins University Press, 2016).

 

Robert Lowell knew civic valor. Sixteen times and more he had been down on his knees in madness, he said. Sixteen times and more he had gotten up. He had gone back to his work, entered back into life. He had faced down uncertainty and madness, had created new forms when pushed to stay with the old, had brought back imaginative order from chaos. It was a different kind of courage, this civic courage, and the rules of engagement were unclear. Lowell’s life, as his daughter observed, was a messy one, difficult for him and for those who knew him. But it was lived with iron, and often with grace. He kept always in the front of his mind what he thought he ought to be, even when he couldn’t be it; he believed in what his country could be, even if it wasn’t. He worked hard at his art.

–Kay Redfield Jamison, PhD, in “Robert Lowell, Setting the River on Fire: A Study of Genius, Mania, and Character” (New York: Alfred A. Knopf, 2017).

Kay Jamison starts her newest book by telling the reader, up front, this is not a biography of the great poet, Robert Lowell. It is, instead, a psychological account of his life and of his mind. Her magnificent study is an unconventional way of approaching the life of another human being, taken in the context of both Lowell’s personal struggle with mental illness and as the culmination of generations of genius and mania in a long and complicated family history. There have been many reviews of Jamison’s book, and for the reader who is interested in a more conventional read, I will steer you to Elizabeth Bosworth’s review in The New York Times (“A poet’s pathologies: Inside Robert Lowell’s restless mind,” March 1, 2017) or Helen Vendler’s review in The New York Review of Books (“The two Robert Lowells,” April 20, 2017). Instead, of a review, per se, I’d like to recount what I thought about as I read “Setting The River On Fire.”

Lowell, who lived from 1917 to 1977, was a two-time Pulitzer Prize winner, deemed to be the greatest American poet of his time. He studied the classics and was obsessed with Napoleon as a child, and he drew on the work of other great poets and classicists as influences for his own work. I must confess, I came to this psychological study having never read the work of Robert Lowell. My only familiarity with the poet came directly from the author. I heard Dr. Jamison, a professor of psychiatry at Johns Hopkins University, Baltimore, speak several years ago at the Johns Hopkins Annual Mood Disorders Symposium about her then work-in-progress as she was researching this book. What I heard was intriguing enough that I was eager to read and review a long and solid book about a great poet whose work I had never read.

As I began “Setting The River On Fire,” my first thought was that the writing itself was astounding. Dr. Jamison’s words flow, her metaphors never fall flat or feel artificial, the ride itself is lovely. I looked for a few lines to quote as an example, and I was left at a standstill. One line was more gracious than the next. I finally settled on the quote I used at the beginning of this piece, benignly chosen from page 403 because it encapsulated not just the beautiful writing but a synopsis of who Lowell was and what he had achieved, set in the context of attempted differentiation between the man, the madness, and the interplay of the two.

Dr. Jamison’s research on Lowell’s life is nothing short of astounding and was clearly a labor that took both sustained passion and years of her time. Dr. Jamison quoted the poet at length. She is an expert on his many volumes of poetry and prose, as well as his life and loves – three marriages and many intimate friendships – documented through letters and conversations. In addition, she quoted many other poets as examples of how their work influenced Lowell. Beyond the literature and correspondence, Dr. Jamison interviewed those who knew Lowell well. She unearthed his medical and psychiatric records, and she plotted out the course of his life in an uncanny way, linking so much of his work to the ebbs and flows of his illness. My only “criticism” of the book would be in how extensive it is. She sometimes makes a point by quoting several sources, each of whom drive at the same idea. It makes for very strong rhetoric.

Lowell lived through the heyday of psychoanalysis, a time when psychiatry focused on the idea that mental aberration was a result of unconscious conflicts and issues left unaddressed from childhood. Lowell’s life was certainly ripe for the psychoanalyst, as Dr. Jamison documented his mother’s psychopathology and his father’s passive distance from his own emotions . In fact, Robert Lowell was treated at some of the great institutions steeped in psychoanalytic learning: Payne Whitney Clinic, McLean Hospital, and Massachusetts Mental Health Center (formerly Boston Psychopathic Hospital), where his treatments included electroconvulsive therapy, chlorpromazine, and eventually lithium.

His second wife, Elizabeth Hardwick, had a striking understanding of his illness as a biological disorder beyond his control. Her sympathy for his behavior as a product of illness allowed her to tolerate actions that many people would not, even with our current day emphasis on disease states, including sexual indiscretions. His friends, too, saw the uncharacteristic chaos of his manias as the result of a state of illness, and, as such, as forgivable. These were often not subtle indiscretions: Jamison describes intense delusional states, combative behavior, police with straightjackets, often at very public and professional events worldwide. If psychoanalytic thinking weighed in on an understanding of Lowell’s motivations, Dr. Jamison did not include it in her study of Lowell, and she makes a point at the end of saying that she focused on his illness and did not include the content of psychotherapy notes. Still, I was struck by the understanding of his depressions and manias as a state of illness by lay people in his life and thought that, given the time period, it was noteworthy.

On a similar vein, I wondered if Lowell could live his life now as he lived his life then. A crucial arena for his career was Harvard College, where he returned over and over to teach. Dr. Jamison says that Lowell lectured in an acutely psychotic and disorganized state. She says that, while students clamored to take his classes, so, too, they were afraid of him. I cannot quite imagine that, in our world of “trigger warnings,” microaggressions, and college safe spaces, we might ever allow an openly ill genius to reign in a classroom of students. I am never certain if we are aimed forward or backward in our struggle against stigma, and “Setting The River On Fire” may be one more example in which we have lost ground in a quest for tolerance.

Once again, Dr. Jamison pulled me into her world. “Setting The River On Fire” is no one’s version of a light or happy read, it is a serious study of an intensely brilliant and often desperately ill poet – and it does not disappoint.

 

Dr. Miller, who practices in Baltimore, is coauthor with Annette Hanson, MD, of “Committed: The Battle Over Involuntary Psychiatric Care,” (Baltimore: Johns Hopkins University Press, 2016).

 

Robert Lowell knew civic valor. Sixteen times and more he had been down on his knees in madness, he said. Sixteen times and more he had gotten up. He had gone back to his work, entered back into life. He had faced down uncertainty and madness, had created new forms when pushed to stay with the old, had brought back imaginative order from chaos. It was a different kind of courage, this civic courage, and the rules of engagement were unclear. Lowell’s life, as his daughter observed, was a messy one, difficult for him and for those who knew him. But it was lived with iron, and often with grace. He kept always in the front of his mind what he thought he ought to be, even when he couldn’t be it; he believed in what his country could be, even if it wasn’t. He worked hard at his art.

–Kay Redfield Jamison, PhD, in “Robert Lowell, Setting the River on Fire: A Study of Genius, Mania, and Character” (New York: Alfred A. Knopf, 2017).

Kay Jamison starts her newest book by telling the reader, up front, this is not a biography of the great poet, Robert Lowell. It is, instead, a psychological account of his life and of his mind. Her magnificent study is an unconventional way of approaching the life of another human being, taken in the context of both Lowell’s personal struggle with mental illness and as the culmination of generations of genius and mania in a long and complicated family history. There have been many reviews of Jamison’s book, and for the reader who is interested in a more conventional read, I will steer you to Elizabeth Bosworth’s review in The New York Times (“A poet’s pathologies: Inside Robert Lowell’s restless mind,” March 1, 2017) or Helen Vendler’s review in The New York Review of Books (“The two Robert Lowells,” April 20, 2017). Instead, of a review, per se, I’d like to recount what I thought about as I read “Setting The River On Fire.”

Lowell, who lived from 1917 to 1977, was a two-time Pulitzer Prize winner, deemed to be the greatest American poet of his time. He studied the classics and was obsessed with Napoleon as a child, and he drew on the work of other great poets and classicists as influences for his own work. I must confess, I came to this psychological study having never read the work of Robert Lowell. My only familiarity with the poet came directly from the author. I heard Dr. Jamison, a professor of psychiatry at Johns Hopkins University, Baltimore, speak several years ago at the Johns Hopkins Annual Mood Disorders Symposium about her then work-in-progress as she was researching this book. What I heard was intriguing enough that I was eager to read and review a long and solid book about a great poet whose work I had never read.

As I began “Setting The River On Fire,” my first thought was that the writing itself was astounding. Dr. Jamison’s words flow, her metaphors never fall flat or feel artificial, the ride itself is lovely. I looked for a few lines to quote as an example, and I was left at a standstill. One line was more gracious than the next. I finally settled on the quote I used at the beginning of this piece, benignly chosen from page 403 because it encapsulated not just the beautiful writing but a synopsis of who Lowell was and what he had achieved, set in the context of attempted differentiation between the man, the madness, and the interplay of the two.

Dr. Jamison’s research on Lowell’s life is nothing short of astounding and was clearly a labor that took both sustained passion and years of her time. Dr. Jamison quoted the poet at length. She is an expert on his many volumes of poetry and prose, as well as his life and loves – three marriages and many intimate friendships – documented through letters and conversations. In addition, she quoted many other poets as examples of how their work influenced Lowell. Beyond the literature and correspondence, Dr. Jamison interviewed those who knew Lowell well. She unearthed his medical and psychiatric records, and she plotted out the course of his life in an uncanny way, linking so much of his work to the ebbs and flows of his illness. My only “criticism” of the book would be in how extensive it is. She sometimes makes a point by quoting several sources, each of whom drive at the same idea. It makes for very strong rhetoric.

Lowell lived through the heyday of psychoanalysis, a time when psychiatry focused on the idea that mental aberration was a result of unconscious conflicts and issues left unaddressed from childhood. Lowell’s life was certainly ripe for the psychoanalyst, as Dr. Jamison documented his mother’s psychopathology and his father’s passive distance from his own emotions . In fact, Robert Lowell was treated at some of the great institutions steeped in psychoanalytic learning: Payne Whitney Clinic, McLean Hospital, and Massachusetts Mental Health Center (formerly Boston Psychopathic Hospital), where his treatments included electroconvulsive therapy, chlorpromazine, and eventually lithium.

His second wife, Elizabeth Hardwick, had a striking understanding of his illness as a biological disorder beyond his control. Her sympathy for his behavior as a product of illness allowed her to tolerate actions that many people would not, even with our current day emphasis on disease states, including sexual indiscretions. His friends, too, saw the uncharacteristic chaos of his manias as the result of a state of illness, and, as such, as forgivable. These were often not subtle indiscretions: Jamison describes intense delusional states, combative behavior, police with straightjackets, often at very public and professional events worldwide. If psychoanalytic thinking weighed in on an understanding of Lowell’s motivations, Dr. Jamison did not include it in her study of Lowell, and she makes a point at the end of saying that she focused on his illness and did not include the content of psychotherapy notes. Still, I was struck by the understanding of his depressions and manias as a state of illness by lay people in his life and thought that, given the time period, it was noteworthy.

On a similar vein, I wondered if Lowell could live his life now as he lived his life then. A crucial arena for his career was Harvard College, where he returned over and over to teach. Dr. Jamison says that Lowell lectured in an acutely psychotic and disorganized state. She says that, while students clamored to take his classes, so, too, they were afraid of him. I cannot quite imagine that, in our world of “trigger warnings,” microaggressions, and college safe spaces, we might ever allow an openly ill genius to reign in a classroom of students. I am never certain if we are aimed forward or backward in our struggle against stigma, and “Setting The River On Fire” may be one more example in which we have lost ground in a quest for tolerance.

Once again, Dr. Jamison pulled me into her world. “Setting The River On Fire” is no one’s version of a light or happy read, it is a serious study of an intensely brilliant and often desperately ill poet – and it does not disappoint.

 

Dr. Miller, who practices in Baltimore, is coauthor with Annette Hanson, MD, of “Committed: The Battle Over Involuntary Psychiatric Care,” (Baltimore: Johns Hopkins University Press, 2016).

 

As chair of the American Academy of Dermatology’s Patient Access and Payer Relations Committee, I traveled around the United States for three years with other well-versed dermatologists and explained the value of dermatology to insurance company medical directors (thanks to James Zalla, Scott Collins, Howard Rogers, Alexa Kimball, Clifford Lober, Sabra Sullivan, Mark Lebwohl, Beth Lertzman, Bruce Brod, Carrie Kovarik, Brent Moody, George Hruza, and Carl Johnson).

We showed them the statistics, clinical guidelines, and clinical photos and explained how cost effective dermatologists are in treating skin disease. We argued against using blunt tools, like average provider expense, as a proxy for quality. I thought it was a pretty compelling story, but the medical directors always asked for a reproducible quality metric. Almost no one in specialty medicine has reproducible quality metrics, and these are very difficult to develop.

Finally, on April 28, in JAMA Dermatology, the American College of Mohs Surgery (ACMS), with its Improving Wisely Study Group partner Johns Hopkins University, published a quality metric using the ratio of Mohs layers, which can be used by physicians, payers, and patients alike (2017 Apr 28. doi: 10.1001/jamadermatol.2017.1450). The effects of this metric on practice behavior can be monitored in real time.

The average number of layers taken for Mohs surgery of head, neck, hands, feet, and genitalia was calculated for all physicians reporting the codes to Medicare from 2012 to 2014. The Accreditation Council for Graduate Medical Education training programs were separately analyzed, since theoretically, they should get referrals of the more complex and difficult cases.

The average proved to be 1.74 stages per case, with a median of 1.69. Of 2,305 physicians billing for Mohs surgery, there were 137 extremely high outliers in at least 1 of 3 years, and 49 persistent high outliers (greater than two standard deviations in all three years), who averaged more than 2.41 layers per case. There were also 92 extremely low outliers (1.28 stages per case, in at least 1 of the 3 years), 20 of whom were persistent in all 3 years. High outliers were more likely to work in a solo practice setting.

The Improving Wisely program is based on the concept that reducing unnecessary variations in care can improve patient safety and quality of care while also reducing costs. It works on the premise that many outliers are unaware they are an outlier, no one wants to be an outlier, and confidential, collegial education and peer mentoring within a medical specialty society can reduce unnecessary variations in care.

Last month, all ACMS members received confidential data reports with their own personal ratio in relation to the entire cohort. Educational and mentoring resources are available for members, and outliers are encouraged to engage with the ACMS to identify opportunities for modifying and improving their practice patterns.

Now, these numbers must not be taken as an indictment of anyone. They are for educational purposes, and the goal is to help identify physicians who are unaware of their deviation and bring these outliers back into the norm. Supporting this premise, solo practitioners were at greatest risk of being outliers, which may be explained by lack of collegial interaction, peer review, and feedback.

In addition, there may be good reasons for being an outlier depending on one’s patient population, and the ACMS is interested in examples. The Mohs College is devoting considerable resources to help outliers. Much of this variation may also result from incorrect coding or processing of specimens. Nonetheless, no patient, payer, or physician wants unnecessary surgery or avoidable charges.

Low outliers are particularly puzzling, since someone would need godlike abilities to almost never have a positive margin in Mohs. I have heard of some practices whose patients all present in the morning, one layer is performed, and the rest of the day is spent processing and interpreting their slides. (Mohs is time consuming.)

I am also aware of some rural providers who travel to distant sites, take a layer, return to the city to process the tissue, and return a few days later to complete the case. This may not indicate bad care, just an unusual practice pattern or adaptation to difficult circumstances. However, it must also be noted that not completing cases on the same day could result in increased payments because of the coding system that reimburses more for first stages than for additional ones.

You must be aware that all these numbers, with a two-year lag, are available to physicians, payers, and patients. If you don’t know your ratio of first to additional Mohs layers, I encourage you to look your numbers up and calculate your ratio (CPT code 17311 plus 17312/code 17311). The easiest website to use is provided by the Wall Street Journal. If you are an outlier, you should ask yourself why, and consider some peer review and other appropriate changes. If your patterns change, they will be noticed quickly, since Johns Hopkins and the Improving Wisely program has leveraged their relationship with the Robert Wood Johnson Foundation to gain more immediate access to current Medicare data.

Everyone is hoping we see normalization of the patterns in layer usage, since this will give great credibility to Mohs surgeons and be better for our patients and the health care system in general. Kudos to the ACMS and the Jama Dermatology paper’s senior author, John Albertini, MD, of Winston-Salem, NC, in particular, for making this benchmark become a reality.
 

 

Dr. Coldiron is in private practice but maintains a clinical assistant professorship at the University of Cincinnati. He cares for patients, teaches medical students and residents, and has several active clinical research projects. Dr. Coldiron is the author of more than 80 scientific letters, papers, and several book chapters, and he speaks frequently on a variety of topics. He is a past president of the American Academy of Dermatology. Write to him at dermnews@frontlinemedcom.com.

 

As chair of the American Academy of Dermatology’s Patient Access and Payer Relations Committee, I traveled around the United States for three years with other well-versed dermatologists and explained the value of dermatology to insurance company medical directors (thanks to James Zalla, Scott Collins, Howard Rogers, Alexa Kimball, Clifford Lober, Sabra Sullivan, Mark Lebwohl, Beth Lertzman, Bruce Brod, Carrie Kovarik, Brent Moody, George Hruza, and Carl Johnson).

We showed them the statistics, clinical guidelines, and clinical photos and explained how cost effective dermatologists are in treating skin disease. We argued against using blunt tools, like average provider expense, as a proxy for quality. I thought it was a pretty compelling story, but the medical directors always asked for a reproducible quality metric. Almost no one in specialty medicine has reproducible quality metrics, and these are very difficult to develop.

Finally, on April 28, in JAMA Dermatology, the American College of Mohs Surgery (ACMS), with its Improving Wisely Study Group partner Johns Hopkins University, published a quality metric using the ratio of Mohs layers, which can be used by physicians, payers, and patients alike (2017 Apr 28. doi: 10.1001/jamadermatol.2017.1450). The effects of this metric on practice behavior can be monitored in real time.

The average number of layers taken for Mohs surgery of head, neck, hands, feet, and genitalia was calculated for all physicians reporting the codes to Medicare from 2012 to 2014. The Accreditation Council for Graduate Medical Education training programs were separately analyzed, since theoretically, they should get referrals of the more complex and difficult cases.

The average proved to be 1.74 stages per case, with a median of 1.69. Of 2,305 physicians billing for Mohs surgery, there were 137 extremely high outliers in at least 1 of 3 years, and 49 persistent high outliers (greater than two standard deviations in all three years), who averaged more than 2.41 layers per case. There were also 92 extremely low outliers (1.28 stages per case, in at least 1 of the 3 years), 20 of whom were persistent in all 3 years. High outliers were more likely to work in a solo practice setting.

The Improving Wisely program is based on the concept that reducing unnecessary variations in care can improve patient safety and quality of care while also reducing costs. It works on the premise that many outliers are unaware they are an outlier, no one wants to be an outlier, and confidential, collegial education and peer mentoring within a medical specialty society can reduce unnecessary variations in care.

Last month, all ACMS members received confidential data reports with their own personal ratio in relation to the entire cohort. Educational and mentoring resources are available for members, and outliers are encouraged to engage with the ACMS to identify opportunities for modifying and improving their practice patterns.

Now, these numbers must not be taken as an indictment of anyone. They are for educational purposes, and the goal is to help identify physicians who are unaware of their deviation and bring these outliers back into the norm. Supporting this premise, solo practitioners were at greatest risk of being outliers, which may be explained by lack of collegial interaction, peer review, and feedback.

In addition, there may be good reasons for being an outlier depending on one’s patient population, and the ACMS is interested in examples. The Mohs College is devoting considerable resources to help outliers. Much of this variation may also result from incorrect coding or processing of specimens. Nonetheless, no patient, payer, or physician wants unnecessary surgery or avoidable charges.

Low outliers are particularly puzzling, since someone would need godlike abilities to almost never have a positive margin in Mohs. I have heard of some practices whose patients all present in the morning, one layer is performed, and the rest of the day is spent processing and interpreting their slides. (Mohs is time consuming.)

I am also aware of some rural providers who travel to distant sites, take a layer, return to the city to process the tissue, and return a few days later to complete the case. This may not indicate bad care, just an unusual practice pattern or adaptation to difficult circumstances. However, it must also be noted that not completing cases on the same day could result in increased payments because of the coding system that reimburses more for first stages than for additional ones.

You must be aware that all these numbers, with a two-year lag, are available to physicians, payers, and patients. If you don’t know your ratio of first to additional Mohs layers, I encourage you to look your numbers up and calculate your ratio (CPT code 17311 plus 17312/code 17311). The easiest website to use is provided by the Wall Street Journal. If you are an outlier, you should ask yourself why, and consider some peer review and other appropriate changes. If your patterns change, they will be noticed quickly, since Johns Hopkins and the Improving Wisely program has leveraged their relationship with the Robert Wood Johnson Foundation to gain more immediate access to current Medicare data.

Everyone is hoping we see normalization of the patterns in layer usage, since this will give great credibility to Mohs surgeons and be better for our patients and the health care system in general. Kudos to the ACMS and the Jama Dermatology paper’s senior author, John Albertini, MD, of Winston-Salem, NC, in particular, for making this benchmark become a reality.
 

 

Dr. Coldiron is in private practice but maintains a clinical assistant professorship at the University of Cincinnati. He cares for patients, teaches medical students and residents, and has several active clinical research projects. Dr. Coldiron is the author of more than 80 scientific letters, papers, and several book chapters, and he speaks frequently on a variety of topics. He is a past president of the American Academy of Dermatology. Write to him at dermnews@frontlinemedcom.com.

 

As chair of the American Academy of Dermatology’s Patient Access and Payer Relations Committee, I traveled around the United States for three years with other well-versed dermatologists and explained the value of dermatology to insurance company medical directors (thanks to James Zalla, Scott Collins, Howard Rogers, Alexa Kimball, Clifford Lober, Sabra Sullivan, Mark Lebwohl, Beth Lertzman, Bruce Brod, Carrie Kovarik, Brent Moody, George Hruza, and Carl Johnson).

We showed them the statistics, clinical guidelines, and clinical photos and explained how cost effective dermatologists are in treating skin disease. We argued against using blunt tools, like average provider expense, as a proxy for quality. I thought it was a pretty compelling story, but the medical directors always asked for a reproducible quality metric. Almost no one in specialty medicine has reproducible quality metrics, and these are very difficult to develop.

Finally, on April 28, in JAMA Dermatology, the American College of Mohs Surgery (ACMS), with its Improving Wisely Study Group partner Johns Hopkins University, published a quality metric using the ratio of Mohs layers, which can be used by physicians, payers, and patients alike (2017 Apr 28. doi: 10.1001/jamadermatol.2017.1450). The effects of this metric on practice behavior can be monitored in real time.

The average number of layers taken for Mohs surgery of head, neck, hands, feet, and genitalia was calculated for all physicians reporting the codes to Medicare from 2012 to 2014. The Accreditation Council for Graduate Medical Education training programs were separately analyzed, since theoretically, they should get referrals of the more complex and difficult cases.

The average proved to be 1.74 stages per case, with a median of 1.69. Of 2,305 physicians billing for Mohs surgery, there were 137 extremely high outliers in at least 1 of 3 years, and 49 persistent high outliers (greater than two standard deviations in all three years), who averaged more than 2.41 layers per case. There were also 92 extremely low outliers (1.28 stages per case, in at least 1 of the 3 years), 20 of whom were persistent in all 3 years. High outliers were more likely to work in a solo practice setting.

The Improving Wisely program is based on the concept that reducing unnecessary variations in care can improve patient safety and quality of care while also reducing costs. It works on the premise that many outliers are unaware they are an outlier, no one wants to be an outlier, and confidential, collegial education and peer mentoring within a medical specialty society can reduce unnecessary variations in care.

Last month, all ACMS members received confidential data reports with their own personal ratio in relation to the entire cohort. Educational and mentoring resources are available for members, and outliers are encouraged to engage with the ACMS to identify opportunities for modifying and improving their practice patterns.

Now, these numbers must not be taken as an indictment of anyone. They are for educational purposes, and the goal is to help identify physicians who are unaware of their deviation and bring these outliers back into the norm. Supporting this premise, solo practitioners were at greatest risk of being outliers, which may be explained by lack of collegial interaction, peer review, and feedback.

In addition, there may be good reasons for being an outlier depending on one’s patient population, and the ACMS is interested in examples. The Mohs College is devoting considerable resources to help outliers. Much of this variation may also result from incorrect coding or processing of specimens. Nonetheless, no patient, payer, or physician wants unnecessary surgery or avoidable charges.

Low outliers are particularly puzzling, since someone would need godlike abilities to almost never have a positive margin in Mohs. I have heard of some practices whose patients all present in the morning, one layer is performed, and the rest of the day is spent processing and interpreting their slides. (Mohs is time consuming.)

I am also aware of some rural providers who travel to distant sites, take a layer, return to the city to process the tissue, and return a few days later to complete the case. This may not indicate bad care, just an unusual practice pattern or adaptation to difficult circumstances. However, it must also be noted that not completing cases on the same day could result in increased payments because of the coding system that reimburses more for first stages than for additional ones.

You must be aware that all these numbers, with a two-year lag, are available to physicians, payers, and patients. If you don’t know your ratio of first to additional Mohs layers, I encourage you to look your numbers up and calculate your ratio (CPT code 17311 plus 17312/code 17311). The easiest website to use is provided by the Wall Street Journal. If you are an outlier, you should ask yourself why, and consider some peer review and other appropriate changes. If your patterns change, they will be noticed quickly, since Johns Hopkins and the Improving Wisely program has leveraged their relationship with the Robert Wood Johnson Foundation to gain more immediate access to current Medicare data.

Everyone is hoping we see normalization of the patterns in layer usage, since this will give great credibility to Mohs surgeons and be better for our patients and the health care system in general. Kudos to the ACMS and the Jama Dermatology paper’s senior author, John Albertini, MD, of Winston-Salem, NC, in particular, for making this benchmark become a reality.
 

 

Dr. Coldiron is in private practice but maintains a clinical assistant professorship at the University of Cincinnati. He cares for patients, teaches medical students and residents, and has several active clinical research projects. Dr. Coldiron is the author of more than 80 scientific letters, papers, and several book chapters, and he speaks frequently on a variety of topics. He is a past president of the American Academy of Dermatology. Write to him at dermnews@frontlinemedcom.com.

 

When we started publishing the EHR Report several years ago, our very first column was a brief overview of a new federal incentive program known as Meaningful Use. At that time, the prospect of receiving thousands of dollars to adopt an electronic health record seemed exciting, and our dream of health care’s digital future appeared to be coming true.

Best of all, we as physicians would be paid to simply embrace it!

Unfortunately, it wasn’t long before that dream (for many at least) devolved into a nightmare. Electronic health records hadn’t been designed to fit into physicians’ long-established work flows, and just weren’t up to the challenge of increasing efficiency. In fact, EHRs quickly became virtual taskmasters, leaving physicians mired in a sea of clicks and slow-moving screens.

Frankly speaking, Meaningful Use hasn’t lived up to its promises. With measures obligating users to fill in a myriad of check-boxes and document often irrelevant information, the program has seemed less like an incentive and more like a penance.

To top it off, the all-or-nothing requirement has meant that – after a year of hard work – providers missing even one goal receive no payments at all, and instead are assessed financial penalties!

All of this has appropriately led physicians to become jaded – not excited – about the digital future.

Thankfully, there is reason for hope: 2017 marks the end of Meaningful Use under Medicare.

What’s new for 2017?

In spite of great initial intentions and several revisions, the EHR Incentive Program has never made the use of electronic records “meaningful,” but it will soon disappear. Along with two other incentive payment programs (the Physician Quality Reporting System and the Value-Based Payment Modifier), it is being consolidated under the Quality Payment Program, established as part of the Medicare Access and CHIP Reauthorization Act of 2015 (MACRA).

MACRA has a much grander scope and sets an even loftier goal: transforming care delivery to achieve better value and ultimately healthier patients.

Now, in case you’re not already confused by the number of programs cited above, there is one more we need to mention to explain the future of EHR incentives: the Merit-based Incentive Payment System, or MIPS, one of two tracks in the Quality Payment Program.

The majority of Medicare providers will choose this track, which focuses on four major components to determine reimbursement incentives: quality, improvement activities, advancing care information, and cost.

Depending on performance in each of these areas, participants will see a variable payment adjustment (upward or downward) in subsequent years (this is a percentage of Medicare payments that increases annually, beginning with a possible +/– 4% in 2019, to a maximum of +/– 9% in 2022).

Providers under MIPS who choose to attest for this year can select from three levels of participation:

1. Test: submission of only a minimal amount of 2017 data (such as one or two measures) to avoid penalty.

2. Partial: submission of 90 days’ worth of data, which may result in a neutral or positive payment adjustment (and may even earn the max adjustment).

3. Full: submission of a full year of data.

Here’s an example of how this will work: A provider who attests in March 2018 for the full 2017 year and does really well could see up to a 4% incentive bonus on Medicare payments in 2019. A provider who chooses not to attest would receive a penalty of 4%.

It’s worth noting here that MIPS expands upon the inclusion criteria set for Meaningful Use under Medicare. Medicare Part B clinicians are eligible to participate if they bill $30,000 in charges and see at least 100 Medicare patients annually. MIPS also broadens the list of eligible provider types. Physicians, nurse practitioners, physician assistants, clinical nurse specialists, and certified registered nurse anesthetists are all able to attest.

Advancing Care Information

Under MIPS, Meaningful Use is replaced by an initiative called Advancing Care Information, or ACI. In this new incarnation, there are fewer required measures, and they are much less onerous than they were under the former program.

Also, there are a number of optional measures. A provider may choose to attest to these nonrequired metrics to improve his or her chances of achieving the maximum incentive, but it isn’t necessary. There are also bonus measures involving public health registry reporting. These are optional but a sure bet to increase incentives. In all, the ACI component composes 25% of a provider’s final MIPS score.

For 2017, participants are able to choose one of two tracks in the ACI program, depending on their EHR’s certification year. (If you are confused by this or don’t know the status of your product, check with your vendor or go to https://chpl.healthit.gov to figure it out).

Providers with technology certified to the 2015 edition (or a combination of technologies from the 2014 and 2015 editions) can fully attest to the ACI objectives and measures or elect to use the transition objectives and measures. Those with 2014 edition software must choose the transition measures.

We will cover the specific measures in a future column, but for now we’ll note that both tracks are very similar and focus on protecting patient data, encouraging patient access to their own records, and sharing information electronically with other providers.

 

Rekindling the dream

We are certain that changing legislation won’t solve all of the problems inherent in current EHR systems, but we are always encouraged by any attempt to reduce the documentation burden on physicians. By eschewing thresholds, eliminating the all-or-nothing requirement, and reducing the number of required measures, the ACI program does seem to shift the focus away from volume and toward value.

That alone has the potential to restore our hope of a brighter future, and make our use of electronic health records significantly more meaningful.
 

Note: To learn more about Quality Payment Program and MIPS, we highly recommend an online resource published by the Centers for Medicare & Medicaid Services that is easy to follow and is full of useful information. It can be found at https://qpp.cms.gov.

Dr. Notte is a family physician and clinical informaticist for Abington (Pa.) Memorial Hospital. He is a partner in EHR Practice Consultants, a firm that aids physicians in adopting electronic health records. Dr. Skolnik is professor of family and community medicine at Sidney Kimmel Medical College, Thomas Jefferson University, Philadelphia, and associate director of the family medicine residency program at Abington (Pa.) Jefferson Health.

 

When we started publishing the EHR Report several years ago, our very first column was a brief overview of a new federal incentive program known as Meaningful Use. At that time, the prospect of receiving thousands of dollars to adopt an electronic health record seemed exciting, and our dream of health care’s digital future appeared to be coming true.

Best of all, we as physicians would be paid to simply embrace it!

Unfortunately, it wasn’t long before that dream (for many at least) devolved into a nightmare. Electronic health records hadn’t been designed to fit into physicians’ long-established work flows, and just weren’t up to the challenge of increasing efficiency. In fact, EHRs quickly became virtual taskmasters, leaving physicians mired in a sea of clicks and slow-moving screens.

Frankly speaking, Meaningful Use hasn’t lived up to its promises. With measures obligating users to fill in a myriad of check-boxes and document often irrelevant information, the program has seemed less like an incentive and more like a penance.

To top it off, the all-or-nothing requirement has meant that – after a year of hard work – providers missing even one goal receive no payments at all, and instead are assessed financial penalties!

All of this has appropriately led physicians to become jaded – not excited – about the digital future.

Thankfully, there is reason for hope: 2017 marks the end of Meaningful Use under Medicare.

What’s new for 2017?

In spite of great initial intentions and several revisions, the EHR Incentive Program has never made the use of electronic records “meaningful,” but it will soon disappear. Along with two other incentive payment programs (the Physician Quality Reporting System and the Value-Based Payment Modifier), it is being consolidated under the Quality Payment Program, established as part of the Medicare Access and CHIP Reauthorization Act of 2015 (MACRA).

MACRA has a much grander scope and sets an even loftier goal: transforming care delivery to achieve better value and ultimately healthier patients.

Now, in case you’re not already confused by the number of programs cited above, there is one more we need to mention to explain the future of EHR incentives: the Merit-based Incentive Payment System, or MIPS, one of two tracks in the Quality Payment Program.

The majority of Medicare providers will choose this track, which focuses on four major components to determine reimbursement incentives: quality, improvement activities, advancing care information, and cost.

Depending on performance in each of these areas, participants will see a variable payment adjustment (upward or downward) in subsequent years (this is a percentage of Medicare payments that increases annually, beginning with a possible +/– 4% in 2019, to a maximum of +/– 9% in 2022).

Providers under MIPS who choose to attest for this year can select from three levels of participation:

1. Test: submission of only a minimal amount of 2017 data (such as one or two measures) to avoid penalty.

2. Partial: submission of 90 days’ worth of data, which may result in a neutral or positive payment adjustment (and may even earn the max adjustment).

3. Full: submission of a full year of data.

Here’s an example of how this will work: A provider who attests in March 2018 for the full 2017 year and does really well could see up to a 4% incentive bonus on Medicare payments in 2019. A provider who chooses not to attest would receive a penalty of 4%.

It’s worth noting here that MIPS expands upon the inclusion criteria set for Meaningful Use under Medicare. Medicare Part B clinicians are eligible to participate if they bill $30,000 in charges and see at least 100 Medicare patients annually. MIPS also broadens the list of eligible provider types. Physicians, nurse practitioners, physician assistants, clinical nurse specialists, and certified registered nurse anesthetists are all able to attest.

Advancing Care Information

Under MIPS, Meaningful Use is replaced by an initiative called Advancing Care Information, or ACI. In this new incarnation, there are fewer required measures, and they are much less onerous than they were under the former program.

Also, there are a number of optional measures. A provider may choose to attest to these nonrequired metrics to improve his or her chances of achieving the maximum incentive, but it isn’t necessary. There are also bonus measures involving public health registry reporting. These are optional but a sure bet to increase incentives. In all, the ACI component composes 25% of a provider’s final MIPS score.

For 2017, participants are able to choose one of two tracks in the ACI program, depending on their EHR’s certification year. (If you are confused by this or don’t know the status of your product, check with your vendor or go to https://chpl.healthit.gov to figure it out).

Providers with technology certified to the 2015 edition (or a combination of technologies from the 2014 and 2015 editions) can fully attest to the ACI objectives and measures or elect to use the transition objectives and measures. Those with 2014 edition software must choose the transition measures.

We will cover the specific measures in a future column, but for now we’ll note that both tracks are very similar and focus on protecting patient data, encouraging patient access to their own records, and sharing information electronically with other providers.

 

Rekindling the dream

We are certain that changing legislation won’t solve all of the problems inherent in current EHR systems, but we are always encouraged by any attempt to reduce the documentation burden on physicians. By eschewing thresholds, eliminating the all-or-nothing requirement, and reducing the number of required measures, the ACI program does seem to shift the focus away from volume and toward value.

That alone has the potential to restore our hope of a brighter future, and make our use of electronic health records significantly more meaningful.
 

Note: To learn more about Quality Payment Program and MIPS, we highly recommend an online resource published by the Centers for Medicare & Medicaid Services that is easy to follow and is full of useful information. It can be found at https://qpp.cms.gov.

Dr. Notte is a family physician and clinical informaticist for Abington (Pa.) Memorial Hospital. He is a partner in EHR Practice Consultants, a firm that aids physicians in adopting electronic health records. Dr. Skolnik is professor of family and community medicine at Sidney Kimmel Medical College, Thomas Jefferson University, Philadelphia, and associate director of the family medicine residency program at Abington (Pa.) Jefferson Health.

 

When we started publishing the EHR Report several years ago, our very first column was a brief overview of a new federal incentive program known as Meaningful Use. At that time, the prospect of receiving thousands of dollars to adopt an electronic health record seemed exciting, and our dream of health care’s digital future appeared to be coming true.

Best of all, we as physicians would be paid to simply embrace it!

Unfortunately, it wasn’t long before that dream (for many at least) devolved into a nightmare. Electronic health records hadn’t been designed to fit into physicians’ long-established work flows, and just weren’t up to the challenge of increasing efficiency. In fact, EHRs quickly became virtual taskmasters, leaving physicians mired in a sea of clicks and slow-moving screens.

Frankly speaking, Meaningful Use hasn’t lived up to its promises. With measures obligating users to fill in a myriad of check-boxes and document often irrelevant information, the program has seemed less like an incentive and more like a penance.

To top it off, the all-or-nothing requirement has meant that – after a year of hard work – providers missing even one goal receive no payments at all, and instead are assessed financial penalties!

All of this has appropriately led physicians to become jaded – not excited – about the digital future.

Thankfully, there is reason for hope: 2017 marks the end of Meaningful Use under Medicare.

What’s new for 2017?

In spite of great initial intentions and several revisions, the EHR Incentive Program has never made the use of electronic records “meaningful,” but it will soon disappear. Along with two other incentive payment programs (the Physician Quality Reporting System and the Value-Based Payment Modifier), it is being consolidated under the Quality Payment Program, established as part of the Medicare Access and CHIP Reauthorization Act of 2015 (MACRA).

MACRA has a much grander scope and sets an even loftier goal: transforming care delivery to achieve better value and ultimately healthier patients.

Now, in case you’re not already confused by the number of programs cited above, there is one more we need to mention to explain the future of EHR incentives: the Merit-based Incentive Payment System, or MIPS, one of two tracks in the Quality Payment Program.

The majority of Medicare providers will choose this track, which focuses on four major components to determine reimbursement incentives: quality, improvement activities, advancing care information, and cost.

Depending on performance in each of these areas, participants will see a variable payment adjustment (upward or downward) in subsequent years (this is a percentage of Medicare payments that increases annually, beginning with a possible +/– 4% in 2019, to a maximum of +/– 9% in 2022).

Providers under MIPS who choose to attest for this year can select from three levels of participation:

1. Test: submission of only a minimal amount of 2017 data (such as one or two measures) to avoid penalty.

2. Partial: submission of 90 days’ worth of data, which may result in a neutral or positive payment adjustment (and may even earn the max adjustment).

3. Full: submission of a full year of data.

Here’s an example of how this will work: A provider who attests in March 2018 for the full 2017 year and does really well could see up to a 4% incentive bonus on Medicare payments in 2019. A provider who chooses not to attest would receive a penalty of 4%.

It’s worth noting here that MIPS expands upon the inclusion criteria set for Meaningful Use under Medicare. Medicare Part B clinicians are eligible to participate if they bill $30,000 in charges and see at least 100 Medicare patients annually. MIPS also broadens the list of eligible provider types. Physicians, nurse practitioners, physician assistants, clinical nurse specialists, and certified registered nurse anesthetists are all able to attest.

Advancing Care Information

Under MIPS, Meaningful Use is replaced by an initiative called Advancing Care Information, or ACI. In this new incarnation, there are fewer required measures, and they are much less onerous than they were under the former program.

Also, there are a number of optional measures. A provider may choose to attest to these nonrequired metrics to improve his or her chances of achieving the maximum incentive, but it isn’t necessary. There are also bonus measures involving public health registry reporting. These are optional but a sure bet to increase incentives. In all, the ACI component composes 25% of a provider’s final MIPS score.

For 2017, participants are able to choose one of two tracks in the ACI program, depending on their EHR’s certification year. (If you are confused by this or don’t know the status of your product, check with your vendor or go to https://chpl.healthit.gov to figure it out).

Providers with technology certified to the 2015 edition (or a combination of technologies from the 2014 and 2015 editions) can fully attest to the ACI objectives and measures or elect to use the transition objectives and measures. Those with 2014 edition software must choose the transition measures.

We will cover the specific measures in a future column, but for now we’ll note that both tracks are very similar and focus on protecting patient data, encouraging patient access to their own records, and sharing information electronically with other providers.

 

Rekindling the dream

We are certain that changing legislation won’t solve all of the problems inherent in current EHR systems, but we are always encouraged by any attempt to reduce the documentation burden on physicians. By eschewing thresholds, eliminating the all-or-nothing requirement, and reducing the number of required measures, the ACI program does seem to shift the focus away from volume and toward value.

That alone has the potential to restore our hope of a brighter future, and make our use of electronic health records significantly more meaningful.
 

Note: To learn more about Quality Payment Program and MIPS, we highly recommend an online resource published by the Centers for Medicare & Medicaid Services that is easy to follow and is full of useful information. It can be found at https://qpp.cms.gov.

Dr. Notte is a family physician and clinical informaticist for Abington (Pa.) Memorial Hospital. He is a partner in EHR Practice Consultants, a firm that aids physicians in adopting electronic health records. Dr. Skolnik is professor of family and community medicine at Sidney Kimmel Medical College, Thomas Jefferson University, Philadelphia, and associate director of the family medicine residency program at Abington (Pa.) Jefferson Health.

 

Chronic pelvic pain continues not only to burden the individual, but society as well.

One in seven women between the ages of 18 and 50 endure chronic pelvic pain; with a lifetime incidence of as high as 33%, according to one Gallup poll. Interstitial cystitis/bladder pain syndrome (IC/BPS) has been estimated to have a prevalence of 850 in 100,000 women and 60 in 100,000 men in self-report studies. The RAND Interstitial Cystitis Epidemiology (RICE) study, a symptoms survey, showed that between 2.7% and 6.5% of women (3.3 to 7.9 million women) in the United States have symptoms consistent with a diagnosis of IC/BPS.

Unfortunately, there is little known about the etiology and pathogenesis of IC/PBS. Moreover, oftentimes, the diagnosis is one of exclusion.

To demystify interstitial cystitis/bladder pain syndrome, I have elicited the assistance of Dr. Kenneth Peters, a urologist on staff at William Beaumont Hospital, Royal Oak, Mich. Dr. Peters is the professor and chairman of urology at Oakland University, William Beaumont School of Medicine, and the chairman of urology at Beaumont Health, Royal Oak, Mich.

In his discussion, Dr. Peters will point out that interstitial cystitis actually consists of two different entities: a classic presentation featuring the pathognomonic Hunner’s lesion on cystoscopy and interstitial cystitis/painful bladder syndrome.

It must be acknowledged that Dr. Peters is a practicing urologist. Therefore, some of his recommendations, such as cauterizing Hunner’s lesions via a resectoscope, are beyond the scope of practicing gynecologists. However, it is important for us to realize what our potential referrals possess in their armamentarium. Moreover, it is obvious there is much that can be learned from this excellent diagnostician who professes the importance of physical examination.
 

Dr. Miller is clinical associate professor at the University of Illinois at Chicago, and past president of the AAGL. He is a reproductive endocrinologist and minimally invasive gynecologic surgeon in metropolitan Chicago; director of minimally invasive gynecologic surgery at Advocate Lutheran General Hospital, Park Ridge, Ill.; and the medical editor of this column. He is an investigator on an interstitial cystitis study sponsored by Allergan.

 

Chronic pelvic pain continues not only to burden the individual, but society as well.

One in seven women between the ages of 18 and 50 endure chronic pelvic pain; with a lifetime incidence of as high as 33%, according to one Gallup poll. Interstitial cystitis/bladder pain syndrome (IC/BPS) has been estimated to have a prevalence of 850 in 100,000 women and 60 in 100,000 men in self-report studies. The RAND Interstitial Cystitis Epidemiology (RICE) study, a symptoms survey, showed that between 2.7% and 6.5% of women (3.3 to 7.9 million women) in the United States have symptoms consistent with a diagnosis of IC/BPS.

Unfortunately, there is little known about the etiology and pathogenesis of IC/PBS. Moreover, oftentimes, the diagnosis is one of exclusion.

To demystify interstitial cystitis/bladder pain syndrome, I have elicited the assistance of Dr. Kenneth Peters, a urologist on staff at William Beaumont Hospital, Royal Oak, Mich. Dr. Peters is the professor and chairman of urology at Oakland University, William Beaumont School of Medicine, and the chairman of urology at Beaumont Health, Royal Oak, Mich.

In his discussion, Dr. Peters will point out that interstitial cystitis actually consists of two different entities: a classic presentation featuring the pathognomonic Hunner’s lesion on cystoscopy and interstitial cystitis/painful bladder syndrome.

It must be acknowledged that Dr. Peters is a practicing urologist. Therefore, some of his recommendations, such as cauterizing Hunner’s lesions via a resectoscope, are beyond the scope of practicing gynecologists. However, it is important for us to realize what our potential referrals possess in their armamentarium. Moreover, it is obvious there is much that can be learned from this excellent diagnostician who professes the importance of physical examination.
 

Dr. Miller is clinical associate professor at the University of Illinois at Chicago, and past president of the AAGL. He is a reproductive endocrinologist and minimally invasive gynecologic surgeon in metropolitan Chicago; director of minimally invasive gynecologic surgery at Advocate Lutheran General Hospital, Park Ridge, Ill.; and the medical editor of this column. He is an investigator on an interstitial cystitis study sponsored by Allergan.

 

Chronic pelvic pain continues not only to burden the individual, but society as well.

One in seven women between the ages of 18 and 50 endure chronic pelvic pain; with a lifetime incidence of as high as 33%, according to one Gallup poll. Interstitial cystitis/bladder pain syndrome (IC/BPS) has been estimated to have a prevalence of 850 in 100,000 women and 60 in 100,000 men in self-report studies. The RAND Interstitial Cystitis Epidemiology (RICE) study, a symptoms survey, showed that between 2.7% and 6.5% of women (3.3 to 7.9 million women) in the United States have symptoms consistent with a diagnosis of IC/BPS.

Unfortunately, there is little known about the etiology and pathogenesis of IC/PBS. Moreover, oftentimes, the diagnosis is one of exclusion.

To demystify interstitial cystitis/bladder pain syndrome, I have elicited the assistance of Dr. Kenneth Peters, a urologist on staff at William Beaumont Hospital, Royal Oak, Mich. Dr. Peters is the professor and chairman of urology at Oakland University, William Beaumont School of Medicine, and the chairman of urology at Beaumont Health, Royal Oak, Mich.

In his discussion, Dr. Peters will point out that interstitial cystitis actually consists of two different entities: a classic presentation featuring the pathognomonic Hunner’s lesion on cystoscopy and interstitial cystitis/painful bladder syndrome.

It must be acknowledged that Dr. Peters is a practicing urologist. Therefore, some of his recommendations, such as cauterizing Hunner’s lesions via a resectoscope, are beyond the scope of practicing gynecologists. However, it is important for us to realize what our potential referrals possess in their armamentarium. Moreover, it is obvious there is much that can be learned from this excellent diagnostician who professes the importance of physical examination.
 

Dr. Miller is clinical associate professor at the University of Illinois at Chicago, and past president of the AAGL. He is a reproductive endocrinologist and minimally invasive gynecologic surgeon in metropolitan Chicago; director of minimally invasive gynecologic surgery at Advocate Lutheran General Hospital, Park Ridge, Ill.; and the medical editor of this column. He is an investigator on an interstitial cystitis study sponsored by Allergan.

 

Interstitial cystitis (IC) is a controversial diagnosis that has become muddied and oversimplified. It was originally described as a distinct ulcer (Hunner’s lesion) seen in the bladder on cystoscopy, the treatment of which often led to symptomatic relief. Hunner’s lesion IC is the “classic” form of IC and should be considered a separate disease; it is not a progression of nonulcerative interstitial cystitis/painful bladder syndrome (IC/BPS).

Only a fraction of patients with the key symptoms of IC/BPS – urinary frequency, urgency, and pelvic pain – have ulcers within the bladder. And many of the patients who are diagnosed with IC/BPS are found not to have bladder pathology as the name implies, but rather pelvic floor dysfunction. That the bladder is often an innocent bystander to a larger process means that, as clinicians, we must be thoughtful and astute about our diagnostic process.

Hunner’s lesions

Patients with Hunner’s lesions have a rapid onset of symptoms, typically are older, and have a visible lesion in their bladder that almost always is on the dome or lateral walls. The lesion is often erythematous with central vascularity and mucosal sloughing.

Courtesy Beaumont Urology

The bladder is a storage organ and urine is toxic. The exposed ulcer results in severe pain with bladder filling and also pain at the end of voiding as the bladder collapses, causing ulcerated tissue to come into contact with other sections of the bladder wall and sending a “jolt” of pain through the pelvis.

If the initial cystoscopy demonstrates inflammatory-appearing lesions or ulcerations suggestive of Hunner’s lesions, I will still do a hydrodistension. By stretching the bladder, the lesions typically expand, crack, and bleed. This helps define the entire diseased area and shows what areas of the bladder need to be cauterized to seal the ulcers and destroy the exposed nerve endings. If this is a new diagnosis, the lesion should be biopsied after the hydrodistension to rule out carcinoma.

Hunner’s lesions can lead to rapid disease progression due to chronic inflammation and subsequent collagen deposition and scarring. Even on initial diagnosis of Hunner’s lesions, a capacity of 350 cc or less (compared with 1,100 cc in a normal bladder) on hydrodistension under anesthesia is not uncommon. This markedly reduced bladder capacity may lead to end-stage bladder impacting the kidneys and requiring a urinary diversion.

Eradicating the ulcers with resection or cautery often results in marked and immediate improvement in bladder pain, albeit not long-lasting. I will typically place a resectoscope and use a roller ball at 25 watts of current. The entire ulcerated areas are cauterized by rapidly rolling the ball over the area of inflammation and avoiding a deep thermal burn. The goal is to seal the ulcer and destroy the exposed nerve endings so that urine can no longer act as an irritant. Recurrence in 6 months to 1 year is common and retreatment is almost always necessary. We have demonstrated, however, that recurrent cautery of ulcers does not lead to smaller anesthetic bladder capacities (Urology. 2015 Jan;85[1]:74-8).

Low-dose cyclosporine can be very effective at reducing Hunner’s lesion recurrence and improving storage symptoms (Exp Ther Med. 2016 Jul;12[1]:445-50). I use 100 mg twice a day for a month and then 1 pill a day thereafter. This is a relatively low dose, but hypertension can be a side effect and blood pressure should be monitored along with routine labs.

The broader picture

Hunner’s lesion IC is pretty straightforward and clearly a bladder disease. However, in recent years the term IC/BPS has been broadly used to describe women who have symptoms of pelvic pain, urinary urgency, and frequency, but no true bladder pathology to explain their symptoms. One problem: There is no definitive diagnostic test or evidence-based diagnostic process for IC/BPS. In fact, the diagnosis section of the American Urological Association guideline on diagnosis and treatment of IC/BPS, last updated in 2015, is almost entirely consensus-based (J Urol. 2015 May;193[5]:1545-53). It largely remains a diagnosis of exclusion.

As the AUA guidelines state, a careful history, physical examination, and laboratory assessment are all important for documenting symptoms and signs and ruling out significant causes of the symptoms. I frequently see patients who have been diagnosed with IC who have frequency and urgency but no pain (in which case overactive bladder should be considered) or who have pelvic pain but no bladder symptoms, again likely not IC. Pain that worsens with bladder filling and improves after bladder emptying is typical of IC/BPS. This finding in the absence of other confusing symptoms supports the diagnosis of IC/BPS.

It has become too easy for the average clinician to apply a label of IC/BPS to a patient complaining of pelvic pain; this often results in the patient undergoing invasive and nonhelpful therapies such as cystoscopy, hydrodistension, urodynamics, bladder instillations, and other bladder-directed therapies.

More than 20 years of research supported by the National Institutes of Health and industry have failed to show that bladder-directed therapy is superior to placebo. This fact suggests that the bladder may be an innocent bystander in a larger pelvic process. As clinicians, we must be willing to look beyond the bladder and examine for pelvic floor issues and other causes of patient’s symptoms and not be too quick to begin bladder-focused treatments.

A number of disease processes – such as recurrent urinary tract infection, urethral diverticulum, endometriosis, and pudendal neuropathy – can mimic the symptoms of IC/BPS. The most common missed diagnosis in the IC patient is pelvic floor dysfunction that results in a hypertonic contracted state of the levator muscles – a chronic spasm, in essence – that in turn leads to decreased muscle function, increased myofascial pain, and myofascial trigger points (Curr Urol Rep. 2006 Nov;7[6]:450-5).

We and others have reported that up to 85% of patients labeled with IC/BPS have been found on examination to have pelvic floor dysfunction or a diffuse pelvic floor hypersensitivity. The pelvic floor is important in maintaining healthy bladder, bowel, and sexual function. If the pelvic floor is in spasm, this can result in urinary frequency, hesitancy, and pelvic pain.

Many of these patients with contracted pelvic floor muscles report pain with sexual intercourse – often so severe as to cause abstention. In fact, when patients answer no to the question of whether they have pain with intercourse, I know it is unlikely that they have significant pelvic floor dysfunction. This is a key question for history taking.

Other key questions concern the impact of stress on symptoms and a history of any type of abuse. In a study we conducted about 10 years ago, we found that among 76 women who were diagnosed with IC and subsequently evaluated in our clinic, almost half (49%) reported abuse (emotional, physical, and/or sexual). The vast majority (85%) had levator pain (J Urol. 2007 Sep;178[3 Pt 1]:891-5).

Other types of stress – from past surgeries to traumatic life events – may similarly serve as triggers or precursors to pelvic floor dysfunction in some women. I often tell patients that people put stress in different areas of their bodies. While some get tension headaches or low-back aches, others get pelvic pain from contracting and guarding the levator muscles.

 

Pelvic floor dysfunction

The most important component of the physical exam in patients with the symptoms of frequency, urgency, and pelvic pain – and the most overlooked – is assessment of the levator muscles for tightness and tenderness. Levator pain and trigger points may be identified during the pelvic exam by pressing laterally on the levator complex in each quadrant of the vagina and at the ischial spines. The tension of the muscles and severity of pain should be assessed, and it is helpful to ask the patient if the pain reproduces her normal pelvic pain symptoms.

Courtesy Beaumont Urology

We’ve found that identifying and treating pelvic floor dysfunction with modalities such as pelvic floor physical therapy with intravaginal myofascial release, intravaginal valium, trigger point injections into the levator complex, pudendal nerve blocks, and neuromodulation can frequently resolve or significantly lessen the patient’s pain and bladder symptoms, suggesting that the diagnosis of IC/BPS was wrong.

Courtesy Beaumont Urology

Pelvic floor physical therapy works to stretch the contracted anterior pelvic muscles by releasing trigger points and connective tissue restrictions, and by decreasing periurethral tension; it also may decrease neurogenic triggers and central nervous system sensitivity. Kegel exercises will worsen pain in these patients and should be avoided.

When pelvic floor dysfunction is identified, such treatment by a therapist knowledgeable in intravaginal myofascial release is a next reasonable step before any medications or invasive testing, such as bladder hydrodistension, are used.

One of the only National Institutes of Health–funded studies to show benefit of a treatment in an IC population, in fact, was a multicenter randomized controlled trial comparing 10 sessions of myofascial pelvic floor physical therapy with “global therapeutic massage.” Myofascial physical therapy led to significant improvement, compared with the generalized spa-like massage (J Urol. 2012 Jun;187[6]:2113-8).

In our practice, we often use intravaginal valium, transvaginal trigger point injections, and pudendal nerve blocks as an adjunct to physical therapy. It is not uncommon for a therapist to report to us that progress in therapy is being stymied by pain in a particular area; in such cases a trigger point injection in the office with local anesthetic and sometimes corticosteroids will help the muscle relax enough and provide enough pain relief so that physical therapy can move forward successfully.

Our patients with IC/BPS symptoms and pelvic floor dysfunction require 1-2 visits weekly for an average of 12 weeks for tightness and tenderness to be significantly minimized or eliminated. Patients are also prescribed home stretching exercises and advised to use internal vaginal dilators. Most patients will report resolution of their pelvic pain, sexual pain, and bladder symptoms – especially with the combination of physical therapy and trigger point injections. In more severe cases, we may use sacral or pudendal neuromodulation to improve the frequency, urgency and pelvic pain.

Turning to the bladder

When urinary symptoms persist after the completion of pelvic floor therapy, or when pelvic floor dysfunction is not identified in the first place, we proceed with bladder-specific therapies. I will often suggest trials of amitriptyline or hydroxyzine, for instance, and/or changes in hydration and caffeine consumption. I am not a fan of pentosan polysulfate sodium (Elmiron) as it is a very expensive medication that has minimal benefit for the majority of patients.

When conservative therapies do not work, I move to cystoscopy with hydrodistension. The procedure can serve several purposes. It can be diagnostic, enabling us to rule out other potential symptom-causing pathologies, and it can be prognostic, helping us to understand when bladder capacity is severely reduced and to plan treatment. In some patients, it can even be therapeutic. Some of my patients have significant relief of symptoms from a hydrodistension of the bladder once or twice a year.

There is no standard method for performing a hydrodistension. I perform a complete cystoscopy to look for tumors, stones, diverticulum or Hunner’s lesions and, if the bladder is normal in appearance, I proceed with a 2-minute hydrodistension at 80-100 cm of water pressure under anesthesia. The bag is raised above the bladder, allowing the bladder to fill with the force of gravity and the pressures to equalize. The urethra must be compressed so that water doesn’t leak around the cystoscope. After 2 minutes of hydrodistension, the bladder is drained, volume is measured, and the procedure is repeated.

After the hydrodistension, the bladder is reinspected to be certain there is no bladder perforation and to evaluate for diffuse glomerulations (petechial hemorrhages) that are suggestive, but not diagnostic, of IC/BPS.

 

A holistic approach

Managing patients with voiding dysfunction and chronic pelvic pain can be a challenge, and a multidisciplinary approach is most effective. At Beaumont, we have a Women’s Urology Center that includes urologists, gynecologists, nurse practitioners, pelvic floor physical therapists, pain psychologists, colorectal specialists, sex therapists, and naturopathic and integrative medicine specialists who perform acupuncture, Reiki therapy, medical massage, and guided imagery.

The goal is to break out of our box of specialties and look at the whole patient – mind, body, and soul – while identifying pain triggers and directing therapy toward these triggers using a multidisciplinary, collaborative approach. For us, this approach has been very effective for managing complex pelvic pain issues (Transl Androl Urol. 2015 Dec;4[6]:611-9).

Ongoing studies

A number of research studies are ongoing to help treat the symptoms of IC/BPS. We currently have a Department of Defense grant to prospectively assess bladder-directed therapy (instillations) compared to pelvic floor physical therapy. Patients diagnosed with IC/BPS are being randomized into these two treatment arms and we hope to get a better understanding of the role of these modalities in managing IC/BPS.

Allergan is completing a phase II placebo-controlled trial using a lidocaine delivery device that is placed in the bladder and continuously releases lidocaine over 14 days. The LiNKA trial is designed to assess the impact of lidocaine on not only improving bladder symptoms, but also eradicating Hunner’s lesions through the anti-inflammatory effect of lidocaine. Early open-label data were very promising. In addition, a new medication for IC/BPS that modulates the SHIP1 pathway is being studied by Aquinox Pharmaceuticals. The agent, AQX-1125, is an activator of SHIP1, which controls the phosphoinositide 3-kinase (PI3K) cellular signaling pathway. If the PI3K pathway is overactive, immune cells can produce an abundance of proinflammatory signaling molecules and migrate to and concentrate in tissues, resulting in excessive or chronic inflammation. Early data in IC/BPS patients were supportive of the compound’s potential for reducing the pain associated with this condition.
 

A note from Charles E. Miller, MD, Master Class Medical Editor:

In a double-blind, placebo-controlled study by J.C. Nickel, et al., pentosan polysulfate sodium was shown to improve pain, urgency, and frequency over the control group (Urology. 2005 Apr;65[4]:654-8). Also, longer duration of treatment with pentosan polysulfate sodium was associated with greater response rates – 50% improved by 26 weeks (J Urol. 2005 Dec;174[6]:2235-8).
 

Dr. Peters is professor and chairman of urology at Oakland University William Beaumont School of Medicine, Royal Oak, Mich. He reported serving as a consultant for Taris, Medtronic, StimGuard, and Amphora Medical.

 

Interstitial cystitis (IC) is a controversial diagnosis that has become muddied and oversimplified. It was originally described as a distinct ulcer (Hunner’s lesion) seen in the bladder on cystoscopy, the treatment of which often led to symptomatic relief. Hunner’s lesion IC is the “classic” form of IC and should be considered a separate disease; it is not a progression of nonulcerative interstitial cystitis/painful bladder syndrome (IC/BPS).

Only a fraction of patients with the key symptoms of IC/BPS – urinary frequency, urgency, and pelvic pain – have ulcers within the bladder. And many of the patients who are diagnosed with IC/BPS are found not to have bladder pathology as the name implies, but rather pelvic floor dysfunction. That the bladder is often an innocent bystander to a larger process means that, as clinicians, we must be thoughtful and astute about our diagnostic process.

Hunner’s lesions

Patients with Hunner’s lesions have a rapid onset of symptoms, typically are older, and have a visible lesion in their bladder that almost always is on the dome or lateral walls. The lesion is often erythematous with central vascularity and mucosal sloughing.

Courtesy Beaumont Urology

The bladder is a storage organ and urine is toxic. The exposed ulcer results in severe pain with bladder filling and also pain at the end of voiding as the bladder collapses, causing ulcerated tissue to come into contact with other sections of the bladder wall and sending a “jolt” of pain through the pelvis.

If the initial cystoscopy demonstrates inflammatory-appearing lesions or ulcerations suggestive of Hunner’s lesions, I will still do a hydrodistension. By stretching the bladder, the lesions typically expand, crack, and bleed. This helps define the entire diseased area and shows what areas of the bladder need to be cauterized to seal the ulcers and destroy the exposed nerve endings. If this is a new diagnosis, the lesion should be biopsied after the hydrodistension to rule out carcinoma.

Hunner’s lesions can lead to rapid disease progression due to chronic inflammation and subsequent collagen deposition and scarring. Even on initial diagnosis of Hunner’s lesions, a capacity of 350 cc or less (compared with 1,100 cc in a normal bladder) on hydrodistension under anesthesia is not uncommon. This markedly reduced bladder capacity may lead to end-stage bladder impacting the kidneys and requiring a urinary diversion.

Eradicating the ulcers with resection or cautery often results in marked and immediate improvement in bladder pain, albeit not long-lasting. I will typically place a resectoscope and use a roller ball at 25 watts of current. The entire ulcerated areas are cauterized by rapidly rolling the ball over the area of inflammation and avoiding a deep thermal burn. The goal is to seal the ulcer and destroy the exposed nerve endings so that urine can no longer act as an irritant. Recurrence in 6 months to 1 year is common and retreatment is almost always necessary. We have demonstrated, however, that recurrent cautery of ulcers does not lead to smaller anesthetic bladder capacities (Urology. 2015 Jan;85[1]:74-8).

Low-dose cyclosporine can be very effective at reducing Hunner’s lesion recurrence and improving storage symptoms (Exp Ther Med. 2016 Jul;12[1]:445-50). I use 100 mg twice a day for a month and then 1 pill a day thereafter. This is a relatively low dose, but hypertension can be a side effect and blood pressure should be monitored along with routine labs.

The broader picture

Hunner’s lesion IC is pretty straightforward and clearly a bladder disease. However, in recent years the term IC/BPS has been broadly used to describe women who have symptoms of pelvic pain, urinary urgency, and frequency, but no true bladder pathology to explain their symptoms. One problem: There is no definitive diagnostic test or evidence-based diagnostic process for IC/BPS. In fact, the diagnosis section of the American Urological Association guideline on diagnosis and treatment of IC/BPS, last updated in 2015, is almost entirely consensus-based (J Urol. 2015 May;193[5]:1545-53). It largely remains a diagnosis of exclusion.

As the AUA guidelines state, a careful history, physical examination, and laboratory assessment are all important for documenting symptoms and signs and ruling out significant causes of the symptoms. I frequently see patients who have been diagnosed with IC who have frequency and urgency but no pain (in which case overactive bladder should be considered) or who have pelvic pain but no bladder symptoms, again likely not IC. Pain that worsens with bladder filling and improves after bladder emptying is typical of IC/BPS. This finding in the absence of other confusing symptoms supports the diagnosis of IC/BPS.

It has become too easy for the average clinician to apply a label of IC/BPS to a patient complaining of pelvic pain; this often results in the patient undergoing invasive and nonhelpful therapies such as cystoscopy, hydrodistension, urodynamics, bladder instillations, and other bladder-directed therapies.

More than 20 years of research supported by the National Institutes of Health and industry have failed to show that bladder-directed therapy is superior to placebo. This fact suggests that the bladder may be an innocent bystander in a larger pelvic process. As clinicians, we must be willing to look beyond the bladder and examine for pelvic floor issues and other causes of patient’s symptoms and not be too quick to begin bladder-focused treatments.

A number of disease processes – such as recurrent urinary tract infection, urethral diverticulum, endometriosis, and pudendal neuropathy – can mimic the symptoms of IC/BPS. The most common missed diagnosis in the IC patient is pelvic floor dysfunction that results in a hypertonic contracted state of the levator muscles – a chronic spasm, in essence – that in turn leads to decreased muscle function, increased myofascial pain, and myofascial trigger points (Curr Urol Rep. 2006 Nov;7[6]:450-5).

We and others have reported that up to 85% of patients labeled with IC/BPS have been found on examination to have pelvic floor dysfunction or a diffuse pelvic floor hypersensitivity. The pelvic floor is important in maintaining healthy bladder, bowel, and sexual function. If the pelvic floor is in spasm, this can result in urinary frequency, hesitancy, and pelvic pain.

Many of these patients with contracted pelvic floor muscles report pain with sexual intercourse – often so severe as to cause abstention. In fact, when patients answer no to the question of whether they have pain with intercourse, I know it is unlikely that they have significant pelvic floor dysfunction. This is a key question for history taking.

Other key questions concern the impact of stress on symptoms and a history of any type of abuse. In a study we conducted about 10 years ago, we found that among 76 women who were diagnosed with IC and subsequently evaluated in our clinic, almost half (49%) reported abuse (emotional, physical, and/or sexual). The vast majority (85%) had levator pain (J Urol. 2007 Sep;178[3 Pt 1]:891-5).

Other types of stress – from past surgeries to traumatic life events – may similarly serve as triggers or precursors to pelvic floor dysfunction in some women. I often tell patients that people put stress in different areas of their bodies. While some get tension headaches or low-back aches, others get pelvic pain from contracting and guarding the levator muscles.

 

Pelvic floor dysfunction

The most important component of the physical exam in patients with the symptoms of frequency, urgency, and pelvic pain – and the most overlooked – is assessment of the levator muscles for tightness and tenderness. Levator pain and trigger points may be identified during the pelvic exam by pressing laterally on the levator complex in each quadrant of the vagina and at the ischial spines. The tension of the muscles and severity of pain should be assessed, and it is helpful to ask the patient if the pain reproduces her normal pelvic pain symptoms.

Courtesy Beaumont Urology

We’ve found that identifying and treating pelvic floor dysfunction with modalities such as pelvic floor physical therapy with intravaginal myofascial release, intravaginal valium, trigger point injections into the levator complex, pudendal nerve blocks, and neuromodulation can frequently resolve or significantly lessen the patient’s pain and bladder symptoms, suggesting that the diagnosis of IC/BPS was wrong.

Courtesy Beaumont Urology

Pelvic floor physical therapy works to stretch the contracted anterior pelvic muscles by releasing trigger points and connective tissue restrictions, and by decreasing periurethral tension; it also may decrease neurogenic triggers and central nervous system sensitivity. Kegel exercises will worsen pain in these patients and should be avoided.

When pelvic floor dysfunction is identified, such treatment by a therapist knowledgeable in intravaginal myofascial release is a next reasonable step before any medications or invasive testing, such as bladder hydrodistension, are used.

One of the only National Institutes of Health–funded studies to show benefit of a treatment in an IC population, in fact, was a multicenter randomized controlled trial comparing 10 sessions of myofascial pelvic floor physical therapy with “global therapeutic massage.” Myofascial physical therapy led to significant improvement, compared with the generalized spa-like massage (J Urol. 2012 Jun;187[6]:2113-8).

In our practice, we often use intravaginal valium, transvaginal trigger point injections, and pudendal nerve blocks as an adjunct to physical therapy. It is not uncommon for a therapist to report to us that progress in therapy is being stymied by pain in a particular area; in such cases a trigger point injection in the office with local anesthetic and sometimes corticosteroids will help the muscle relax enough and provide enough pain relief so that physical therapy can move forward successfully.

Our patients with IC/BPS symptoms and pelvic floor dysfunction require 1-2 visits weekly for an average of 12 weeks for tightness and tenderness to be significantly minimized or eliminated. Patients are also prescribed home stretching exercises and advised to use internal vaginal dilators. Most patients will report resolution of their pelvic pain, sexual pain, and bladder symptoms – especially with the combination of physical therapy and trigger point injections. In more severe cases, we may use sacral or pudendal neuromodulation to improve the frequency, urgency and pelvic pain.

Turning to the bladder

When urinary symptoms persist after the completion of pelvic floor therapy, or when pelvic floor dysfunction is not identified in the first place, we proceed with bladder-specific therapies. I will often suggest trials of amitriptyline or hydroxyzine, for instance, and/or changes in hydration and caffeine consumption. I am not a fan of pentosan polysulfate sodium (Elmiron) as it is a very expensive medication that has minimal benefit for the majority of patients.

When conservative therapies do not work, I move to cystoscopy with hydrodistension. The procedure can serve several purposes. It can be diagnostic, enabling us to rule out other potential symptom-causing pathologies, and it can be prognostic, helping us to understand when bladder capacity is severely reduced and to plan treatment. In some patients, it can even be therapeutic. Some of my patients have significant relief of symptoms from a hydrodistension of the bladder once or twice a year.

There is no standard method for performing a hydrodistension. I perform a complete cystoscopy to look for tumors, stones, diverticulum or Hunner’s lesions and, if the bladder is normal in appearance, I proceed with a 2-minute hydrodistension at 80-100 cm of water pressure under anesthesia. The bag is raised above the bladder, allowing the bladder to fill with the force of gravity and the pressures to equalize. The urethra must be compressed so that water doesn’t leak around the cystoscope. After 2 minutes of hydrodistension, the bladder is drained, volume is measured, and the procedure is repeated.

After the hydrodistension, the bladder is reinspected to be certain there is no bladder perforation and to evaluate for diffuse glomerulations (petechial hemorrhages) that are suggestive, but not diagnostic, of IC/BPS.

 

A holistic approach

Managing patients with voiding dysfunction and chronic pelvic pain can be a challenge, and a multidisciplinary approach is most effective. At Beaumont, we have a Women’s Urology Center that includes urologists, gynecologists, nurse practitioners, pelvic floor physical therapists, pain psychologists, colorectal specialists, sex therapists, and naturopathic and integrative medicine specialists who perform acupuncture, Reiki therapy, medical massage, and guided imagery.

The goal is to break out of our box of specialties and look at the whole patient – mind, body, and soul – while identifying pain triggers and directing therapy toward these triggers using a multidisciplinary, collaborative approach. For us, this approach has been very effective for managing complex pelvic pain issues (Transl Androl Urol. 2015 Dec;4[6]:611-9).

Ongoing studies

A number of research studies are ongoing to help treat the symptoms of IC/BPS. We currently have a Department of Defense grant to prospectively assess bladder-directed therapy (instillations) compared to pelvic floor physical therapy. Patients diagnosed with IC/BPS are being randomized into these two treatment arms and we hope to get a better understanding of the role of these modalities in managing IC/BPS.

Allergan is completing a phase II placebo-controlled trial using a lidocaine delivery device that is placed in the bladder and continuously releases lidocaine over 14 days. The LiNKA trial is designed to assess the impact of lidocaine on not only improving bladder symptoms, but also eradicating Hunner’s lesions through the anti-inflammatory effect of lidocaine. Early open-label data were very promising. In addition, a new medication for IC/BPS that modulates the SHIP1 pathway is being studied by Aquinox Pharmaceuticals. The agent, AQX-1125, is an activator of SHIP1, which controls the phosphoinositide 3-kinase (PI3K) cellular signaling pathway. If the PI3K pathway is overactive, immune cells can produce an abundance of proinflammatory signaling molecules and migrate to and concentrate in tissues, resulting in excessive or chronic inflammation. Early data in IC/BPS patients were supportive of the compound’s potential for reducing the pain associated with this condition.
 

A note from Charles E. Miller, MD, Master Class Medical Editor:

In a double-blind, placebo-controlled study by J.C. Nickel, et al., pentosan polysulfate sodium was shown to improve pain, urgency, and frequency over the control group (Urology. 2005 Apr;65[4]:654-8). Also, longer duration of treatment with pentosan polysulfate sodium was associated with greater response rates – 50% improved by 26 weeks (J Urol. 2005 Dec;174[6]:2235-8).
 

Dr. Peters is professor and chairman of urology at Oakland University William Beaumont School of Medicine, Royal Oak, Mich. He reported serving as a consultant for Taris, Medtronic, StimGuard, and Amphora Medical.

 

Interstitial cystitis (IC) is a controversial diagnosis that has become muddied and oversimplified. It was originally described as a distinct ulcer (Hunner’s lesion) seen in the bladder on cystoscopy, the treatment of which often led to symptomatic relief. Hunner’s lesion IC is the “classic” form of IC and should be considered a separate disease; it is not a progression of nonulcerative interstitial cystitis/painful bladder syndrome (IC/BPS).

Only a fraction of patients with the key symptoms of IC/BPS – urinary frequency, urgency, and pelvic pain – have ulcers within the bladder. And many of the patients who are diagnosed with IC/BPS are found not to have bladder pathology as the name implies, but rather pelvic floor dysfunction. That the bladder is often an innocent bystander to a larger process means that, as clinicians, we must be thoughtful and astute about our diagnostic process.

Hunner’s lesions

Patients with Hunner’s lesions have a rapid onset of symptoms, typically are older, and have a visible lesion in their bladder that almost always is on the dome or lateral walls. The lesion is often erythematous with central vascularity and mucosal sloughing.

Courtesy Beaumont Urology

The bladder is a storage organ and urine is toxic. The exposed ulcer results in severe pain with bladder filling and also pain at the end of voiding as the bladder collapses, causing ulcerated tissue to come into contact with other sections of the bladder wall and sending a “jolt” of pain through the pelvis.

If the initial cystoscopy demonstrates inflammatory-appearing lesions or ulcerations suggestive of Hunner’s lesions, I will still do a hydrodistension. By stretching the bladder, the lesions typically expand, crack, and bleed. This helps define the entire diseased area and shows what areas of the bladder need to be cauterized to seal the ulcers and destroy the exposed nerve endings. If this is a new diagnosis, the lesion should be biopsied after the hydrodistension to rule out carcinoma.

Hunner’s lesions can lead to rapid disease progression due to chronic inflammation and subsequent collagen deposition and scarring. Even on initial diagnosis of Hunner’s lesions, a capacity of 350 cc or less (compared with 1,100 cc in a normal bladder) on hydrodistension under anesthesia is not uncommon. This markedly reduced bladder capacity may lead to end-stage bladder impacting the kidneys and requiring a urinary diversion.

Eradicating the ulcers with resection or cautery often results in marked and immediate improvement in bladder pain, albeit not long-lasting. I will typically place a resectoscope and use a roller ball at 25 watts of current. The entire ulcerated areas are cauterized by rapidly rolling the ball over the area of inflammation and avoiding a deep thermal burn. The goal is to seal the ulcer and destroy the exposed nerve endings so that urine can no longer act as an irritant. Recurrence in 6 months to 1 year is common and retreatment is almost always necessary. We have demonstrated, however, that recurrent cautery of ulcers does not lead to smaller anesthetic bladder capacities (Urology. 2015 Jan;85[1]:74-8).

Low-dose cyclosporine can be very effective at reducing Hunner’s lesion recurrence and improving storage symptoms (Exp Ther Med. 2016 Jul;12[1]:445-50). I use 100 mg twice a day for a month and then 1 pill a day thereafter. This is a relatively low dose, but hypertension can be a side effect and blood pressure should be monitored along with routine labs.

The broader picture

Hunner’s lesion IC is pretty straightforward and clearly a bladder disease. However, in recent years the term IC/BPS has been broadly used to describe women who have symptoms of pelvic pain, urinary urgency, and frequency, but no true bladder pathology to explain their symptoms. One problem: There is no definitive diagnostic test or evidence-based diagnostic process for IC/BPS. In fact, the diagnosis section of the American Urological Association guideline on diagnosis and treatment of IC/BPS, last updated in 2015, is almost entirely consensus-based (J Urol. 2015 May;193[5]:1545-53). It largely remains a diagnosis of exclusion.

As the AUA guidelines state, a careful history, physical examination, and laboratory assessment are all important for documenting symptoms and signs and ruling out significant causes of the symptoms. I frequently see patients who have been diagnosed with IC who have frequency and urgency but no pain (in which case overactive bladder should be considered) or who have pelvic pain but no bladder symptoms, again likely not IC. Pain that worsens with bladder filling and improves after bladder emptying is typical of IC/BPS. This finding in the absence of other confusing symptoms supports the diagnosis of IC/BPS.

It has become too easy for the average clinician to apply a label of IC/BPS to a patient complaining of pelvic pain; this often results in the patient undergoing invasive and nonhelpful therapies such as cystoscopy, hydrodistension, urodynamics, bladder instillations, and other bladder-directed therapies.

More than 20 years of research supported by the National Institutes of Health and industry have failed to show that bladder-directed therapy is superior to placebo. This fact suggests that the bladder may be an innocent bystander in a larger pelvic process. As clinicians, we must be willing to look beyond the bladder and examine for pelvic floor issues and other causes of patient’s symptoms and not be too quick to begin bladder-focused treatments.

A number of disease processes – such as recurrent urinary tract infection, urethral diverticulum, endometriosis, and pudendal neuropathy – can mimic the symptoms of IC/BPS. The most common missed diagnosis in the IC patient is pelvic floor dysfunction that results in a hypertonic contracted state of the levator muscles – a chronic spasm, in essence – that in turn leads to decreased muscle function, increased myofascial pain, and myofascial trigger points (Curr Urol Rep. 2006 Nov;7[6]:450-5).

We and others have reported that up to 85% of patients labeled with IC/BPS have been found on examination to have pelvic floor dysfunction or a diffuse pelvic floor hypersensitivity. The pelvic floor is important in maintaining healthy bladder, bowel, and sexual function. If the pelvic floor is in spasm, this can result in urinary frequency, hesitancy, and pelvic pain.

Many of these patients with contracted pelvic floor muscles report pain with sexual intercourse – often so severe as to cause abstention. In fact, when patients answer no to the question of whether they have pain with intercourse, I know it is unlikely that they have significant pelvic floor dysfunction. This is a key question for history taking.

Other key questions concern the impact of stress on symptoms and a history of any type of abuse. In a study we conducted about 10 years ago, we found that among 76 women who were diagnosed with IC and subsequently evaluated in our clinic, almost half (49%) reported abuse (emotional, physical, and/or sexual). The vast majority (85%) had levator pain (J Urol. 2007 Sep;178[3 Pt 1]:891-5).

Other types of stress – from past surgeries to traumatic life events – may similarly serve as triggers or precursors to pelvic floor dysfunction in some women. I often tell patients that people put stress in different areas of their bodies. While some get tension headaches or low-back aches, others get pelvic pain from contracting and guarding the levator muscles.

 

Pelvic floor dysfunction

The most important component of the physical exam in patients with the symptoms of frequency, urgency, and pelvic pain – and the most overlooked – is assessment of the levator muscles for tightness and tenderness. Levator pain and trigger points may be identified during the pelvic exam by pressing laterally on the levator complex in each quadrant of the vagina and at the ischial spines. The tension of the muscles and severity of pain should be assessed, and it is helpful to ask the patient if the pain reproduces her normal pelvic pain symptoms.

Courtesy Beaumont Urology

We’ve found that identifying and treating pelvic floor dysfunction with modalities such as pelvic floor physical therapy with intravaginal myofascial release, intravaginal valium, trigger point injections into the levator complex, pudendal nerve blocks, and neuromodulation can frequently resolve or significantly lessen the patient’s pain and bladder symptoms, suggesting that the diagnosis of IC/BPS was wrong.

Courtesy Beaumont Urology

Pelvic floor physical therapy works to stretch the contracted anterior pelvic muscles by releasing trigger points and connective tissue restrictions, and by decreasing periurethral tension; it also may decrease neurogenic triggers and central nervous system sensitivity. Kegel exercises will worsen pain in these patients and should be avoided.

When pelvic floor dysfunction is identified, such treatment by a therapist knowledgeable in intravaginal myofascial release is a next reasonable step before any medications or invasive testing, such as bladder hydrodistension, are used.

One of the only National Institutes of Health–funded studies to show benefit of a treatment in an IC population, in fact, was a multicenter randomized controlled trial comparing 10 sessions of myofascial pelvic floor physical therapy with “global therapeutic massage.” Myofascial physical therapy led to significant improvement, compared with the generalized spa-like massage (J Urol. 2012 Jun;187[6]:2113-8).

In our practice, we often use intravaginal valium, transvaginal trigger point injections, and pudendal nerve blocks as an adjunct to physical therapy. It is not uncommon for a therapist to report to us that progress in therapy is being stymied by pain in a particular area; in such cases a trigger point injection in the office with local anesthetic and sometimes corticosteroids will help the muscle relax enough and provide enough pain relief so that physical therapy can move forward successfully.

Our patients with IC/BPS symptoms and pelvic floor dysfunction require 1-2 visits weekly for an average of 12 weeks for tightness and tenderness to be significantly minimized or eliminated. Patients are also prescribed home stretching exercises and advised to use internal vaginal dilators. Most patients will report resolution of their pelvic pain, sexual pain, and bladder symptoms – especially with the combination of physical therapy and trigger point injections. In more severe cases, we may use sacral or pudendal neuromodulation to improve the frequency, urgency and pelvic pain.

Turning to the bladder

When urinary symptoms persist after the completion of pelvic floor therapy, or when pelvic floor dysfunction is not identified in the first place, we proceed with bladder-specific therapies. I will often suggest trials of amitriptyline or hydroxyzine, for instance, and/or changes in hydration and caffeine consumption. I am not a fan of pentosan polysulfate sodium (Elmiron) as it is a very expensive medication that has minimal benefit for the majority of patients.

When conservative therapies do not work, I move to cystoscopy with hydrodistension. The procedure can serve several purposes. It can be diagnostic, enabling us to rule out other potential symptom-causing pathologies, and it can be prognostic, helping us to understand when bladder capacity is severely reduced and to plan treatment. In some patients, it can even be therapeutic. Some of my patients have significant relief of symptoms from a hydrodistension of the bladder once or twice a year.

There is no standard method for performing a hydrodistension. I perform a complete cystoscopy to look for tumors, stones, diverticulum or Hunner’s lesions and, if the bladder is normal in appearance, I proceed with a 2-minute hydrodistension at 80-100 cm of water pressure under anesthesia. The bag is raised above the bladder, allowing the bladder to fill with the force of gravity and the pressures to equalize. The urethra must be compressed so that water doesn’t leak around the cystoscope. After 2 minutes of hydrodistension, the bladder is drained, volume is measured, and the procedure is repeated.

After the hydrodistension, the bladder is reinspected to be certain there is no bladder perforation and to evaluate for diffuse glomerulations (petechial hemorrhages) that are suggestive, but not diagnostic, of IC/BPS.

 

A holistic approach

Managing patients with voiding dysfunction and chronic pelvic pain can be a challenge, and a multidisciplinary approach is most effective. At Beaumont, we have a Women’s Urology Center that includes urologists, gynecologists, nurse practitioners, pelvic floor physical therapists, pain psychologists, colorectal specialists, sex therapists, and naturopathic and integrative medicine specialists who perform acupuncture, Reiki therapy, medical massage, and guided imagery.

The goal is to break out of our box of specialties and look at the whole patient – mind, body, and soul – while identifying pain triggers and directing therapy toward these triggers using a multidisciplinary, collaborative approach. For us, this approach has been very effective for managing complex pelvic pain issues (Transl Androl Urol. 2015 Dec;4[6]:611-9).

Ongoing studies

A number of research studies are ongoing to help treat the symptoms of IC/BPS. We currently have a Department of Defense grant to prospectively assess bladder-directed therapy (instillations) compared to pelvic floor physical therapy. Patients diagnosed with IC/BPS are being randomized into these two treatment arms and we hope to get a better understanding of the role of these modalities in managing IC/BPS.

Allergan is completing a phase II placebo-controlled trial using a lidocaine delivery device that is placed in the bladder and continuously releases lidocaine over 14 days. The LiNKA trial is designed to assess the impact of lidocaine on not only improving bladder symptoms, but also eradicating Hunner’s lesions through the anti-inflammatory effect of lidocaine. Early open-label data were very promising. In addition, a new medication for IC/BPS that modulates the SHIP1 pathway is being studied by Aquinox Pharmaceuticals. The agent, AQX-1125, is an activator of SHIP1, which controls the phosphoinositide 3-kinase (PI3K) cellular signaling pathway. If the PI3K pathway is overactive, immune cells can produce an abundance of proinflammatory signaling molecules and migrate to and concentrate in tissues, resulting in excessive or chronic inflammation. Early data in IC/BPS patients were supportive of the compound’s potential for reducing the pain associated with this condition.
 

A note from Charles E. Miller, MD, Master Class Medical Editor:

In a double-blind, placebo-controlled study by J.C. Nickel, et al., pentosan polysulfate sodium was shown to improve pain, urgency, and frequency over the control group (Urology. 2005 Apr;65[4]:654-8). Also, longer duration of treatment with pentosan polysulfate sodium was associated with greater response rates – 50% improved by 26 weeks (J Urol. 2005 Dec;174[6]:2235-8).
 

Dr. Peters is professor and chairman of urology at Oakland University William Beaumont School of Medicine, Royal Oak, Mich. He reported serving as a consultant for Taris, Medtronic, StimGuard, and Amphora Medical.

 

Corticosteroids such as prednisone are relatively frequently administered in pregnancy for their immunosuppressive and anti-inflammatory effects. Treatment may be initiated on a short-term basis for acute conditions. Alternatively, treatment may be more or less ongoing for severe chronic diseases such as asthma or a variety of other autoimmune conditions when disease symptoms do not remit in pregnancy. However, the safety of corticosteroid use with respect to risk of specific birth defects, preterm delivery, and low birth weight has been the subject of debate over some time.

Concerns about the teratogenicity of corticosteroids were raised as early as the 1950s, based on animal studies suggesting an increased risk for oral clefts. The association between corticosteroids and oral clefts has also been observed in some human epidemiologic studies. However, results of these studies have been inconsistent.

Earlier studies that were incorporated into a meta-analysis published in 2000 suggested a 3.4-times increased odds of cleft lip with or without cleft palate following first trimester corticosteroid use (95% confidence interval, 2.0-5.7).¹ However, a 2014 update from the multisite U.S. National Birth Defects Prevention case-control study (NBDPS) demonstrated that, while data from 1997 to 2002 indicated an elevated risk for oral clefts, more recent data from 2003 to 2009 did not.² The authors speculated that typical doses of corticosteroids or duration of use in pregnancy could have declined over time as more disease modifying alternative treatments have become available for some conditions and that this could have resulted in attenuated risk estimates in recent years.

Similar to the NBDPS findings, in a large Danish cohort study covering 832,636 live births from 1996 to 2008, exposure to any corticosteroids during the first trimester was not associated with an increased risk for cleft lip or cleft palate. Only those exposed to topical corticosteroids had a higher risk of cleft lip with or without cleft palate (odds ratio, 1.45; 95% CI, 1.03-2.05).³ Another, smaller Danish study covered primiparous births from 1999 to 2009 (n = 83,043). The unadjusted odds of oral clefts following exposure to any corticosteroids (inhaled or oral) in the first trimester was null (OR, 0.4; 95% CI, 0.1-2.8).⁴

Inconsistencies across these studies, as speculated by authors of the NBDPS analysis, may result from a lack of information on the dose of drug used by the mother, the indication for its use, or any measure of the severity of the underlying maternal disease for which the corticosteroids were prescribed. It is possible that maternal disease or disease activity in and of itself is a direct cause of oral clefts or that corticosteroids are linked to increased risk for clefts through co-occurring other exposures such as smoking, alcohol, or obesity. However, these questions have yet to be answered.

With respect to other birth outcomes, a few disease-specific studies have examined birth weight or intrauterine growth restriction following corticosteroid use. In general, study findings have been reassuring. Among Danish women with Crohn’s disease, corticosteroids were not associated with reduced birth weight after adjusting for gestational age and disease activity (adjusted risk ratio, 1.1; 95% CI, 0.2-5.7).⁵ In another study of pregnant women with rheumatoid arthritis, birth weight was not associated with prednisone use after adjustment for gestational age at delivery and sex of the newborn.⁶ In a third cohort study of pregnant women with systemic lupus erythematosus, there was no a significant elevation in odds of intrauterine growth restriction following prednisone use.⁷

Several disease-specific studies have also examined corticosteroid use and risk of preterm birth. From the Danish cohort of pregnant women with Crohn’s disease, the researchers reported no association between prednisolone and preterm birth after adjustment for covariates. In contrast, in a separate Danish cohort of pregnant women with irritable bowel disease, there was an increased risk of preterm delivery following systemic corticosteroid use, compared with women without disease (adjusted hazard ratio, 6.3; 95% CI, 3.1-12.7).⁸ However, data were not available to address underlying disease severity as a possible contributing factor. Of note, among women with irritable bowel disease who did not use medication in pregnancy, there was a 50% increase in the risk of preterm birth, compared with women without disease (aHR, 1.5; 95% CI, 1.0-2.4). This suggests that the disease itself contributed to the increased risk of preterm birth.

Currently available data regarding corticosteroid use and adverse birth outcomes are generally reassuring. Recent estimates for oral clefts suggest a low elevation in risk, if any at all. This translates to a very low absolute risk for clefts, which occur in the general population in approximately 1 in 1,000 births. The clinical benefit of adequate treatment in the first trimester for inflammatory or immune-mediated diseases may far outweigh any small and tenuous risks for oral clefts.

With respect to reduced birth weight and preterm delivery, available evidence suggests either no association or that maternal disease and disease severity are driving any increased risks noted for these outcomes. Future studies of pregnancy safety for medications used to treat maternal diseases that themselves are potentially linked to adverse outcomes must incorporate appropriate measures of disease type and disease severity in the study designs.

 

Dr. Chambers is a professor of pediatrics and director of clinical research at Rady Children’s Hospital and associate director of the Clinical and Translational Research Institute at the University of California, San Diego. She is also director of MotherToBaby California, a past president of the Organization of Teratology Information Specialists, and past president of the Teratology Society. She has no relevant financial disclosures. To comment, e-mail her at obnews@frontlinemedcom.com.

References

1. Teratology. 2000 Dec;62(6):385-92.

2. Birth Defects Res A Clin Mol Teratol. 2014 Jun;100(6):499-506.

3. CMAJ. 2011 Apr 19;183(7):796-804.

4. Am J Ther. 2014 Mar-Apr;21(2):73-80.

5. Am J Gastroenterol. 2007 Jul;102(7):1406-13.

6. Arthritis Rheum. 2009 Nov;60(11):3196-206.

7. Lupus. 2010 Dec;19(14):1665-73.

8. PLoS One. 2015 Jun 17;10(6):e0129567.

 

Corticosteroids such as prednisone are relatively frequently administered in pregnancy for their immunosuppressive and anti-inflammatory effects. Treatment may be initiated on a short-term basis for acute conditions. Alternatively, treatment may be more or less ongoing for severe chronic diseases such as asthma or a variety of other autoimmune conditions when disease symptoms do not remit in pregnancy. However, the safety of corticosteroid use with respect to risk of specific birth defects, preterm delivery, and low birth weight has been the subject of debate over some time.

Concerns about the teratogenicity of corticosteroids were raised as early as the 1950s, based on animal studies suggesting an increased risk for oral clefts. The association between corticosteroids and oral clefts has also been observed in some human epidemiologic studies. However, results of these studies have been inconsistent.

Earlier studies that were incorporated into a meta-analysis published in 2000 suggested a 3.4-times increased odds of cleft lip with or without cleft palate following first trimester corticosteroid use (95% confidence interval, 2.0-5.7).¹ However, a 2014 update from the multisite U.S. National Birth Defects Prevention case-control study (NBDPS) demonstrated that, while data from 1997 to 2002 indicated an elevated risk for oral clefts, more recent data from 2003 to 2009 did not.² The authors speculated that typical doses of corticosteroids or duration of use in pregnancy could have declined over time as more disease modifying alternative treatments have become available for some conditions and that this could have resulted in attenuated risk estimates in recent years.

Similar to the NBDPS findings, in a large Danish cohort study covering 832,636 live births from 1996 to 2008, exposure to any corticosteroids during the first trimester was not associated with an increased risk for cleft lip or cleft palate. Only those exposed to topical corticosteroids had a higher risk of cleft lip with or without cleft palate (odds ratio, 1.45; 95% CI, 1.03-2.05).³ Another, smaller Danish study covered primiparous births from 1999 to 2009 (n = 83,043). The unadjusted odds of oral clefts following exposure to any corticosteroids (inhaled or oral) in the first trimester was null (OR, 0.4; 95% CI, 0.1-2.8).⁴

Inconsistencies across these studies, as speculated by authors of the NBDPS analysis, may result from a lack of information on the dose of drug used by the mother, the indication for its use, or any measure of the severity of the underlying maternal disease for which the corticosteroids were prescribed. It is possible that maternal disease or disease activity in and of itself is a direct cause of oral clefts or that corticosteroids are linked to increased risk for clefts through co-occurring other exposures such as smoking, alcohol, or obesity. However, these questions have yet to be answered.

With respect to other birth outcomes, a few disease-specific studies have examined birth weight or intrauterine growth restriction following corticosteroid use. In general, study findings have been reassuring. Among Danish women with Crohn’s disease, corticosteroids were not associated with reduced birth weight after adjusting for gestational age and disease activity (adjusted risk ratio, 1.1; 95% CI, 0.2-5.7).⁵ In another study of pregnant women with rheumatoid arthritis, birth weight was not associated with prednisone use after adjustment for gestational age at delivery and sex of the newborn.⁶ In a third cohort study of pregnant women with systemic lupus erythematosus, there was no a significant elevation in odds of intrauterine growth restriction following prednisone use.⁷

Several disease-specific studies have also examined corticosteroid use and risk of preterm birth. From the Danish cohort of pregnant women with Crohn’s disease, the researchers reported no association between prednisolone and preterm birth after adjustment for covariates. In contrast, in a separate Danish cohort of pregnant women with irritable bowel disease, there was an increased risk of preterm delivery following systemic corticosteroid use, compared with women without disease (adjusted hazard ratio, 6.3; 95% CI, 3.1-12.7).⁸ However, data were not available to address underlying disease severity as a possible contributing factor. Of note, among women with irritable bowel disease who did not use medication in pregnancy, there was a 50% increase in the risk of preterm birth, compared with women without disease (aHR, 1.5; 95% CI, 1.0-2.4). This suggests that the disease itself contributed to the increased risk of preterm birth.

Currently available data regarding corticosteroid use and adverse birth outcomes are generally reassuring. Recent estimates for oral clefts suggest a low elevation in risk, if any at all. This translates to a very low absolute risk for clefts, which occur in the general population in approximately 1 in 1,000 births. The clinical benefit of adequate treatment in the first trimester for inflammatory or immune-mediated diseases may far outweigh any small and tenuous risks for oral clefts.

With respect to reduced birth weight and preterm delivery, available evidence suggests either no association or that maternal disease and disease severity are driving any increased risks noted for these outcomes. Future studies of pregnancy safety for medications used to treat maternal diseases that themselves are potentially linked to adverse outcomes must incorporate appropriate measures of disease type and disease severity in the study designs.

 

Dr. Chambers is a professor of pediatrics and director of clinical research at Rady Children’s Hospital and associate director of the Clinical and Translational Research Institute at the University of California, San Diego. She is also director of MotherToBaby California, a past president of the Organization of Teratology Information Specialists, and past president of the Teratology Society. She has no relevant financial disclosures. To comment, e-mail her at obnews@frontlinemedcom.com.

References

1. Teratology. 2000 Dec;62(6):385-92.

2. Birth Defects Res A Clin Mol Teratol. 2014 Jun;100(6):499-506.

3. CMAJ. 2011 Apr 19;183(7):796-804.

4. Am J Ther. 2014 Mar-Apr;21(2):73-80.

5. Am J Gastroenterol. 2007 Jul;102(7):1406-13.

6. Arthritis Rheum. 2009 Nov;60(11):3196-206.

7. Lupus. 2010 Dec;19(14):1665-73.

8. PLoS One. 2015 Jun 17;10(6):e0129567.

 

Corticosteroids such as prednisone are relatively frequently administered in pregnancy for their immunosuppressive and anti-inflammatory effects. Treatment may be initiated on a short-term basis for acute conditions. Alternatively, treatment may be more or less ongoing for severe chronic diseases such as asthma or a variety of other autoimmune conditions when disease symptoms do not remit in pregnancy. However, the safety of corticosteroid use with respect to risk of specific birth defects, preterm delivery, and low birth weight has been the subject of debate over some time.

Concerns about the teratogenicity of corticosteroids were raised as early as the 1950s, based on animal studies suggesting an increased risk for oral clefts. The association between corticosteroids and oral clefts has also been observed in some human epidemiologic studies. However, results of these studies have been inconsistent.

Earlier studies that were incorporated into a meta-analysis published in 2000 suggested a 3.4-times increased odds of cleft lip with or without cleft palate following first trimester corticosteroid use (95% confidence interval, 2.0-5.7).¹ However, a 2014 update from the multisite U.S. National Birth Defects Prevention case-control study (NBDPS) demonstrated that, while data from 1997 to 2002 indicated an elevated risk for oral clefts, more recent data from 2003 to 2009 did not.² The authors speculated that typical doses of corticosteroids or duration of use in pregnancy could have declined over time as more disease modifying alternative treatments have become available for some conditions and that this could have resulted in attenuated risk estimates in recent years.

Similar to the NBDPS findings, in a large Danish cohort study covering 832,636 live births from 1996 to 2008, exposure to any corticosteroids during the first trimester was not associated with an increased risk for cleft lip or cleft palate. Only those exposed to topical corticosteroids had a higher risk of cleft lip with or without cleft palate (odds ratio, 1.45; 95% CI, 1.03-2.05).³ Another, smaller Danish study covered primiparous births from 1999 to 2009 (n = 83,043). The unadjusted odds of oral clefts following exposure to any corticosteroids (inhaled or oral) in the first trimester was null (OR, 0.4; 95% CI, 0.1-2.8).⁴

Inconsistencies across these studies, as speculated by authors of the NBDPS analysis, may result from a lack of information on the dose of drug used by the mother, the indication for its use, or any measure of the severity of the underlying maternal disease for which the corticosteroids were prescribed. It is possible that maternal disease or disease activity in and of itself is a direct cause of oral clefts or that corticosteroids are linked to increased risk for clefts through co-occurring other exposures such as smoking, alcohol, or obesity. However, these questions have yet to be answered.

With respect to other birth outcomes, a few disease-specific studies have examined birth weight or intrauterine growth restriction following corticosteroid use. In general, study findings have been reassuring. Among Danish women with Crohn’s disease, corticosteroids were not associated with reduced birth weight after adjusting for gestational age and disease activity (adjusted risk ratio, 1.1; 95% CI, 0.2-5.7).⁵ In another study of pregnant women with rheumatoid arthritis, birth weight was not associated with prednisone use after adjustment for gestational age at delivery and sex of the newborn.⁶ In a third cohort study of pregnant women with systemic lupus erythematosus, there was no a significant elevation in odds of intrauterine growth restriction following prednisone use.⁷

Several disease-specific studies have also examined corticosteroid use and risk of preterm birth. From the Danish cohort of pregnant women with Crohn’s disease, the researchers reported no association between prednisolone and preterm birth after adjustment for covariates. In contrast, in a separate Danish cohort of pregnant women with irritable bowel disease, there was an increased risk of preterm delivery following systemic corticosteroid use, compared with women without disease (adjusted hazard ratio, 6.3; 95% CI, 3.1-12.7).⁸ However, data were not available to address underlying disease severity as a possible contributing factor. Of note, among women with irritable bowel disease who did not use medication in pregnancy, there was a 50% increase in the risk of preterm birth, compared with women without disease (aHR, 1.5; 95% CI, 1.0-2.4). This suggests that the disease itself contributed to the increased risk of preterm birth.

Currently available data regarding corticosteroid use and adverse birth outcomes are generally reassuring. Recent estimates for oral clefts suggest a low elevation in risk, if any at all. This translates to a very low absolute risk for clefts, which occur in the general population in approximately 1 in 1,000 births. The clinical benefit of adequate treatment in the first trimester for inflammatory or immune-mediated diseases may far outweigh any small and tenuous risks for oral clefts.

With respect to reduced birth weight and preterm delivery, available evidence suggests either no association or that maternal disease and disease severity are driving any increased risks noted for these outcomes. Future studies of pregnancy safety for medications used to treat maternal diseases that themselves are potentially linked to adverse outcomes must incorporate appropriate measures of disease type and disease severity in the study designs.

 

Dr. Chambers is a professor of pediatrics and director of clinical research at Rady Children’s Hospital and associate director of the Clinical and Translational Research Institute at the University of California, San Diego. She is also director of MotherToBaby California, a past president of the Organization of Teratology Information Specialists, and past president of the Teratology Society. She has no relevant financial disclosures. To comment, e-mail her at obnews@frontlinemedcom.com.

References

1. Teratology. 2000 Dec;62(6):385-92.

2. Birth Defects Res A Clin Mol Teratol. 2014 Jun;100(6):499-506.

3. CMAJ. 2011 Apr 19;183(7):796-804.

4. Am J Ther. 2014 Mar-Apr;21(2):73-80.

5. Am J Gastroenterol. 2007 Jul;102(7):1406-13.

6. Arthritis Rheum. 2009 Nov;60(11):3196-206.

7. Lupus. 2010 Dec;19(14):1665-73.

8. PLoS One. 2015 Jun 17;10(6):e0129567.

 

Gynecologic cancers contribute to approximately 15% of cancer survivorship care for women. Many patients share surveillance visits between their gynecologic oncologist and their ob.gyn. or primary care physician to capitalize on preexisting relationships and ensure the provision of comprehensive wellness care. Providing high quality surveillance care is challenging because it requires vigilance in the detection of recurrence but also avoidance of unnecessary, costly, and inaccurate testing.

The oncologic benefits for various surveillance guidelines are not well established by prospective studies. However, in updated surveillance recommendations, the Society of Gynecologic Oncology (SGO) takes available data, costs, and benefits into consideration.¹ The guidelines, authored by Ritu Salani, MD, provide an excellent resource for understanding appropriate testing and evaluation during surveillance care.

As with screening, the goal of surveillance is to detect recurrence and, thereby, extend survival or palliate symptoms.

The cornerstone of a surveillance visit is a thorough symptom assessment. Positive reporting of symptoms remains the most sensitive method for detecting recurrences; therefore, patients should be educated and quizzed on common recurrence symptoms. For example, endometrial cancer most commonly recurs in the vagina with symptoms of vaginal bleeding or discharge. Lower extremity swelling can signify pelvic sidewall recurrences and abdominal bloating or pain can signify peritoneal recurrence of ovarian or endometrial cancer.

All women who are undergoing surveillance for gynecologic cancers should receive physical examinations that include a pelvic exam with a speculum and bimanual exam with rectovaginal exam. Many locoregional recurrences are salvageable for most gynecologic cancers, which is not true for most distant recurrences, emphasizing the importance of pelvic examinations.

In addition to surveillance of recurrence, these visits should focus on risk modification – tobacco, obesity, bone demineralization – as well as preventive health strategies, such as vaccinations, nongynecologic cancer screenings, and cardiovascular disease intervention. Clinicians should also ask about sequelae to cancer therapy, such as neuropathy, lymphedema, sexual dysfunction, depression, and fatigue.

Dr. Rossi

Endometrial cancer

Endometrial cancer recurs most commonly among women with a history of advanced stage cancer or early stage disease with high/intermediate risk factors, but all survivors should be evaluated regularly for recurrence. The vagina is the most common site for recurrence. Fortunately, many vaginal recurrences can be cured with salvage therapies.

Women with the lowest risk for recurrence (stage IA, grades 1 and 2 disease) who did not originally qualify for adjuvant therapy can be followed every 6 months for 2 years and then annually.

Vaginal cytology is no longer recommended for the routine surveillance of endometrial cancer because of its poor sensitivity in detecting recurrence and low positive predictive value (particularly after vaginal radiation).² Any suspicious lesions identified on speculum examination should be biopsied, rather than sampled with cytologic smear. Routine imaging (with CT or PET/CT) and cancer antigen (CA) 125 tumor marker assessment is not supported unless the initial stage was advanced. These tests should be reserved for confirmation of concerning symptoms or examination findings.

This group of patients has particular survivorship needs with respect to obesity interventions. Obesity is associated with poor prognosis from endometrial cancer, and patients should be counseled about this and offered strategies for weight loss and lifestyle modification. Lynch syndrome testing and colon cancer screening are also an important consideration in this population.
 

Ovarian cancer

Ovarian cancer recurrence rates are high, and, while salvage therapies are rarely curative, enduring responses may be achieved in some patients, making surveillance visits critical. The SGO recommends surveillance visits every 3 months in the first 2 years, every 4 months in year 3, and then every 6 months for an additional 2 years. At these visits, patients should be queried about symptoms with particular emphasis on peritoneal signs (bloating, distension, gastrointestinal disturbance, and abdominal pain) as most recurrences will be within the peritoneal cavity.

CA 125 tumor marker elevation during the surveillance phase may signal recurrence prior to the development of symptoms but initiating chemotherapy early because of elevations in CA 125 does not improve survival.³ However, in the platinum-sensitive population with a longer disease-free interval, earlier detection of recurrence by CA 125 may identify patients in whom complete secondary cytoreduction is more attainable and is associated with improved survival.⁴ Therefore, the SGO suggests that CA 125 assessment is optional. The benefits and limitations of earlier detection of recurrence should be discussed with each patient. This recommendation differs for survivors of nonepithelial ovarian cancers (such as germ-cell or sex-cord stromal), in which case the measurement of the appropriate tumor markers (such as alpha-fetoprotein, human chorionic gonadotropin, and inhibin) should be performed routinely as part of surveillance evaluation.

Evidence does not support routine imaging (such as CT or PET). It should be reserved as a confirmatory measure for patients with concerning symptoms, examination findings, or elevations in tumor markers. When ovarian cancer has been treated with fertility-preserving surgery in women of younger reproductive ages, pelvic ultrasounds may be used as part of their surveillance care to monitor retained ovaries and pelvic structures.

BRCA-gene testing should be offered to all women with epithelial ovarian, fallopian tube, and primary peritoneal cancer as it impacts future cancer risk, as well as chemotherapy selection.⁵
 

 

Cervical cancer

In the first 2 years after completing primary treatment for cervical cancer, those at high risk for recurrence (including those who were recommended to adjuvant therapy) should be evaluated every 3 months for 2 years, followed by visits at 6-month intervals for an additional 3 years. Low-risk patients can be followed every 6 months for 2 years, followed by annual visits thereafter.

Pap testing should be performed annually, rather than at each surveillance visit. It should not to detect recurrence – for which it has poor sensitivity and specificity – but rather to detect new HPV-related dysplasia.⁶

Many patients with cervical cancer have a tobacco use history, placing them at risk for other cancers. Educate patients about the risk and provide cessation assistance.
 

Vulvar cancer

Prognosis for early stage vulvar cancer is very good; however, local recurrences are common (as much as 40%) in the 10 years following diagnosis.⁷ It is important to thoroughly inspect the vulva, vagina, and cervix at each surveillance visit. In high-risk patients, examinations should take place every 3 months for the first 2 years after completing primary treatment and every 6 months until 5 years post treatment. Low-risk patients can be followed every 6 months for 2 years and annually thereafter.

Identification and early treatment of dysplasia is important. Careful attention should also be made to palpation of the inguinal nodal regions. One in 10 women will have a late recurrence (greater than 5 years), so vulvar inspections should continue at least annually for the remainder of a woman’s life.
 

Dr. Rossi is an assistant professor in the division of gynecologic oncology at the University of North Carolina at Chapel Hill. She reported having no relevant financial disclosures.

References

1. Gynecol Oncol. 2017 Mar 31. doi: 10.1016/j.ygno.2017.03.022.

2. Obstet Gynecol. 2013 Jan;121(1):129-35.

3. Lancet. 2010 Oct 2;376(9747):1155-63.

4. Gynecol Oncol. 2009 Jan;112(1):265-74.

5. Gynecol Oncol. 2015 Jan;136(1):3-7.

6. Obstet Gynecol. 2011 Sep;118(3):548-53.

7. Gynecol Oncol. 2016 Jan;140(1):8-14.

 

Gynecologic cancers contribute to approximately 15% of cancer survivorship care for women. Many patients share surveillance visits between their gynecologic oncologist and their ob.gyn. or primary care physician to capitalize on preexisting relationships and ensure the provision of comprehensive wellness care. Providing high quality surveillance care is challenging because it requires vigilance in the detection of recurrence but also avoidance of unnecessary, costly, and inaccurate testing.

The oncologic benefits for various surveillance guidelines are not well established by prospective studies. However, in updated surveillance recommendations, the Society of Gynecologic Oncology (SGO) takes available data, costs, and benefits into consideration.¹ The guidelines, authored by Ritu Salani, MD, provide an excellent resource for understanding appropriate testing and evaluation during surveillance care.

As with screening, the goal of surveillance is to detect recurrence and, thereby, extend survival or palliate symptoms.

The cornerstone of a surveillance visit is a thorough symptom assessment. Positive reporting of symptoms remains the most sensitive method for detecting recurrences; therefore, patients should be educated and quizzed on common recurrence symptoms. For example, endometrial cancer most commonly recurs in the vagina with symptoms of vaginal bleeding or discharge. Lower extremity swelling can signify pelvic sidewall recurrences and abdominal bloating or pain can signify peritoneal recurrence of ovarian or endometrial cancer.

All women who are undergoing surveillance for gynecologic cancers should receive physical examinations that include a pelvic exam with a speculum and bimanual exam with rectovaginal exam. Many locoregional recurrences are salvageable for most gynecologic cancers, which is not true for most distant recurrences, emphasizing the importance of pelvic examinations.

In addition to surveillance of recurrence, these visits should focus on risk modification – tobacco, obesity, bone demineralization – as well as preventive health strategies, such as vaccinations, nongynecologic cancer screenings, and cardiovascular disease intervention. Clinicians should also ask about sequelae to cancer therapy, such as neuropathy, lymphedema, sexual dysfunction, depression, and fatigue.

Dr. Rossi

Endometrial cancer

Endometrial cancer recurs most commonly among women with a history of advanced stage cancer or early stage disease with high/intermediate risk factors, but all survivors should be evaluated regularly for recurrence. The vagina is the most common site for recurrence. Fortunately, many vaginal recurrences can be cured with salvage therapies.

Women with the lowest risk for recurrence (stage IA, grades 1 and 2 disease) who did not originally qualify for adjuvant therapy can be followed every 6 months for 2 years and then annually.

Vaginal cytology is no longer recommended for the routine surveillance of endometrial cancer because of its poor sensitivity in detecting recurrence and low positive predictive value (particularly after vaginal radiation).² Any suspicious lesions identified on speculum examination should be biopsied, rather than sampled with cytologic smear. Routine imaging (with CT or PET/CT) and cancer antigen (CA) 125 tumor marker assessment is not supported unless the initial stage was advanced. These tests should be reserved for confirmation of concerning symptoms or examination findings.

This group of patients has particular survivorship needs with respect to obesity interventions. Obesity is associated with poor prognosis from endometrial cancer, and patients should be counseled about this and offered strategies for weight loss and lifestyle modification. Lynch syndrome testing and colon cancer screening are also an important consideration in this population.
 

Ovarian cancer

Ovarian cancer recurrence rates are high, and, while salvage therapies are rarely curative, enduring responses may be achieved in some patients, making surveillance visits critical. The SGO recommends surveillance visits every 3 months in the first 2 years, every 4 months in year 3, and then every 6 months for an additional 2 years. At these visits, patients should be queried about symptoms with particular emphasis on peritoneal signs (bloating, distension, gastrointestinal disturbance, and abdominal pain) as most recurrences will be within the peritoneal cavity.

CA 125 tumor marker elevation during the surveillance phase may signal recurrence prior to the development of symptoms but initiating chemotherapy early because of elevations in CA 125 does not improve survival.³ However, in the platinum-sensitive population with a longer disease-free interval, earlier detection of recurrence by CA 125 may identify patients in whom complete secondary cytoreduction is more attainable and is associated with improved survival.⁴ Therefore, the SGO suggests that CA 125 assessment is optional. The benefits and limitations of earlier detection of recurrence should be discussed with each patient. This recommendation differs for survivors of nonepithelial ovarian cancers (such as germ-cell or sex-cord stromal), in which case the measurement of the appropriate tumor markers (such as alpha-fetoprotein, human chorionic gonadotropin, and inhibin) should be performed routinely as part of surveillance evaluation.

Evidence does not support routine imaging (such as CT or PET). It should be reserved as a confirmatory measure for patients with concerning symptoms, examination findings, or elevations in tumor markers. When ovarian cancer has been treated with fertility-preserving surgery in women of younger reproductive ages, pelvic ultrasounds may be used as part of their surveillance care to monitor retained ovaries and pelvic structures.

BRCA-gene testing should be offered to all women with epithelial ovarian, fallopian tube, and primary peritoneal cancer as it impacts future cancer risk, as well as chemotherapy selection.⁵
 

 

Cervical cancer

In the first 2 years after completing primary treatment for cervical cancer, those at high risk for recurrence (including those who were recommended to adjuvant therapy) should be evaluated every 3 months for 2 years, followed by visits at 6-month intervals for an additional 3 years. Low-risk patients can be followed every 6 months for 2 years, followed by annual visits thereafter.

Pap testing should be performed annually, rather than at each surveillance visit. It should not to detect recurrence – for which it has poor sensitivity and specificity – but rather to detect new HPV-related dysplasia.⁶

Many patients with cervical cancer have a tobacco use history, placing them at risk for other cancers. Educate patients about the risk and provide cessation assistance.
 

Vulvar cancer

Prognosis for early stage vulvar cancer is very good; however, local recurrences are common (as much as 40%) in the 10 years following diagnosis.⁷ It is important to thoroughly inspect the vulva, vagina, and cervix at each surveillance visit. In high-risk patients, examinations should take place every 3 months for the first 2 years after completing primary treatment and every 6 months until 5 years post treatment. Low-risk patients can be followed every 6 months for 2 years and annually thereafter.

Identification and early treatment of dysplasia is important. Careful attention should also be made to palpation of the inguinal nodal regions. One in 10 women will have a late recurrence (greater than 5 years), so vulvar inspections should continue at least annually for the remainder of a woman’s life.
 

Dr. Rossi is an assistant professor in the division of gynecologic oncology at the University of North Carolina at Chapel Hill. She reported having no relevant financial disclosures.

References

1. Gynecol Oncol. 2017 Mar 31. doi: 10.1016/j.ygno.2017.03.022.

2. Obstet Gynecol. 2013 Jan;121(1):129-35.

3. Lancet. 2010 Oct 2;376(9747):1155-63.

4. Gynecol Oncol. 2009 Jan;112(1):265-74.

5. Gynecol Oncol. 2015 Jan;136(1):3-7.

6. Obstet Gynecol. 2011 Sep;118(3):548-53.

7. Gynecol Oncol. 2016 Jan;140(1):8-14.

 

Gynecologic cancers contribute to approximately 15% of cancer survivorship care for women. Many patients share surveillance visits between their gynecologic oncologist and their ob.gyn. or primary care physician to capitalize on preexisting relationships and ensure the provision of comprehensive wellness care. Providing high quality surveillance care is challenging because it requires vigilance in the detection of recurrence but also avoidance of unnecessary, costly, and inaccurate testing.

The oncologic benefits for various surveillance guidelines are not well established by prospective studies. However, in updated surveillance recommendations, the Society of Gynecologic Oncology (SGO) takes available data, costs, and benefits into consideration.¹ The guidelines, authored by Ritu Salani, MD, provide an excellent resource for understanding appropriate testing and evaluation during surveillance care.

As with screening, the goal of surveillance is to detect recurrence and, thereby, extend survival or palliate symptoms.

The cornerstone of a surveillance visit is a thorough symptom assessment. Positive reporting of symptoms remains the most sensitive method for detecting recurrences; therefore, patients should be educated and quizzed on common recurrence symptoms. For example, endometrial cancer most commonly recurs in the vagina with symptoms of vaginal bleeding or discharge. Lower extremity swelling can signify pelvic sidewall recurrences and abdominal bloating or pain can signify peritoneal recurrence of ovarian or endometrial cancer.

All women who are undergoing surveillance for gynecologic cancers should receive physical examinations that include a pelvic exam with a speculum and bimanual exam with rectovaginal exam. Many locoregional recurrences are salvageable for most gynecologic cancers, which is not true for most distant recurrences, emphasizing the importance of pelvic examinations.

In addition to surveillance of recurrence, these visits should focus on risk modification – tobacco, obesity, bone demineralization – as well as preventive health strategies, such as vaccinations, nongynecologic cancer screenings, and cardiovascular disease intervention. Clinicians should also ask about sequelae to cancer therapy, such as neuropathy, lymphedema, sexual dysfunction, depression, and fatigue.

Dr. Rossi

Endometrial cancer

Endometrial cancer recurs most commonly among women with a history of advanced stage cancer or early stage disease with high/intermediate risk factors, but all survivors should be evaluated regularly for recurrence. The vagina is the most common site for recurrence. Fortunately, many vaginal recurrences can be cured with salvage therapies.

Women with the lowest risk for recurrence (stage IA, grades 1 and 2 disease) who did not originally qualify for adjuvant therapy can be followed every 6 months for 2 years and then annually.

Vaginal cytology is no longer recommended for the routine surveillance of endometrial cancer because of its poor sensitivity in detecting recurrence and low positive predictive value (particularly after vaginal radiation).² Any suspicious lesions identified on speculum examination should be biopsied, rather than sampled with cytologic smear. Routine imaging (with CT or PET/CT) and cancer antigen (CA) 125 tumor marker assessment is not supported unless the initial stage was advanced. These tests should be reserved for confirmation of concerning symptoms or examination findings.

This group of patients has particular survivorship needs with respect to obesity interventions. Obesity is associated with poor prognosis from endometrial cancer, and patients should be counseled about this and offered strategies for weight loss and lifestyle modification. Lynch syndrome testing and colon cancer screening are also an important consideration in this population.
 

Ovarian cancer

Ovarian cancer recurrence rates are high, and, while salvage therapies are rarely curative, enduring responses may be achieved in some patients, making surveillance visits critical. The SGO recommends surveillance visits every 3 months in the first 2 years, every 4 months in year 3, and then every 6 months for an additional 2 years. At these visits, patients should be queried about symptoms with particular emphasis on peritoneal signs (bloating, distension, gastrointestinal disturbance, and abdominal pain) as most recurrences will be within the peritoneal cavity.

CA 125 tumor marker elevation during the surveillance phase may signal recurrence prior to the development of symptoms but initiating chemotherapy early because of elevations in CA 125 does not improve survival.³ However, in the platinum-sensitive population with a longer disease-free interval, earlier detection of recurrence by CA 125 may identify patients in whom complete secondary cytoreduction is more attainable and is associated with improved survival.⁴ Therefore, the SGO suggests that CA 125 assessment is optional. The benefits and limitations of earlier detection of recurrence should be discussed with each patient. This recommendation differs for survivors of nonepithelial ovarian cancers (such as germ-cell or sex-cord stromal), in which case the measurement of the appropriate tumor markers (such as alpha-fetoprotein, human chorionic gonadotropin, and inhibin) should be performed routinely as part of surveillance evaluation.

Evidence does not support routine imaging (such as CT or PET). It should be reserved as a confirmatory measure for patients with concerning symptoms, examination findings, or elevations in tumor markers. When ovarian cancer has been treated with fertility-preserving surgery in women of younger reproductive ages, pelvic ultrasounds may be used as part of their surveillance care to monitor retained ovaries and pelvic structures.

BRCA-gene testing should be offered to all women with epithelial ovarian, fallopian tube, and primary peritoneal cancer as it impacts future cancer risk, as well as chemotherapy selection.⁵
 

 

Cervical cancer

In the first 2 years after completing primary treatment for cervical cancer, those at high risk for recurrence (including those who were recommended to adjuvant therapy) should be evaluated every 3 months for 2 years, followed by visits at 6-month intervals for an additional 3 years. Low-risk patients can be followed every 6 months for 2 years, followed by annual visits thereafter.

Pap testing should be performed annually, rather than at each surveillance visit. It should not to detect recurrence – for which it has poor sensitivity and specificity – but rather to detect new HPV-related dysplasia.⁶

Many patients with cervical cancer have a tobacco use history, placing them at risk for other cancers. Educate patients about the risk and provide cessation assistance.
 

Vulvar cancer

Prognosis for early stage vulvar cancer is very good; however, local recurrences are common (as much as 40%) in the 10 years following diagnosis.⁷ It is important to thoroughly inspect the vulva, vagina, and cervix at each surveillance visit. In high-risk patients, examinations should take place every 3 months for the first 2 years after completing primary treatment and every 6 months until 5 years post treatment. Low-risk patients can be followed every 6 months for 2 years and annually thereafter.

Identification and early treatment of dysplasia is important. Careful attention should also be made to palpation of the inguinal nodal regions. One in 10 women will have a late recurrence (greater than 5 years), so vulvar inspections should continue at least annually for the remainder of a woman’s life.
 

Dr. Rossi is an assistant professor in the division of gynecologic oncology at the University of North Carolina at Chapel Hill. She reported having no relevant financial disclosures.

References

1. Gynecol Oncol. 2017 Mar 31. doi: 10.1016/j.ygno.2017.03.022.

2. Obstet Gynecol. 2013 Jan;121(1):129-35.

3. Lancet. 2010 Oct 2;376(9747):1155-63.

4. Gynecol Oncol. 2009 Jan;112(1):265-74.

5. Gynecol Oncol. 2015 Jan;136(1):3-7.

6. Obstet Gynecol. 2011 Sep;118(3):548-53.

7. Gynecol Oncol. 2016 Jan;140(1):8-14.

 

Editor’s Note: This is the fourth installment of a six-part series that will review key concepts and articles that ob.gyns. can use to prepare for the American Board of Obstetrics and Gynecology Maintenance of Certification examination. The series is adapted from Ob/Gyn Board Master (obgynboardmaster.com), an online board review course created by Erudyte Inc. The series will cover issues in reproductive endocrinology and infertility, maternal-fetal medicine, gynecologic oncology, and female pelvic medicine, as well as general test-taking and study tips.

The American College of Obstetricians and Gynecologists’ “Practice Bulletins” are important practice management guidelines for ob.gyn. clinicians. The Practice Bulletins are rich sources of material often tested on board exams. In February 2016, ACOG issued a revised Practice Bulletin (#161) on external cephalic version outlining clinical considerations and recommendations and providing an algorithm for patient management.¹ We recommend you read this bulletin and review this topic carefully.

Let’s begin with a possible medical board question: According to the Practice Bulletin, which of the following is TRUE about external cephalic version (ECV)?

A. Success rate is lower in women with a previous cesarean delivery.

B. Placental location affects the success rate.

C. External cephalic version should be stopped after 15 minutes.

D. Women at 37 weeks’ gestation are preferred candidates.

E. Tocolysis decreases success rate.

The correct answer is D.

Women at 37 weeks’ gestation are the preferred candidates for an ECV because spontaneous version would likely have already occurred by this time and the risk of spontaneous reversion is lower. Answers A-C and E are incorrect statements.

Key points

Women at 37 weeks’ gestation are the preferred candidates for an ECV.

The overall pooled success rate for ECV is 58% with a 6% pooled complication rate.

The use of parenteral tocolysis has been associated with increased success rates of ECV, though there are not enough data to make a recommendation regarding use of regional anesthesia with the procedure.

Literature summary

ECV is a procedure designed to turn a fetus into vertex presentation by applying external pressure to a woman’s abdomen. Women at 37 weeks’ gestation are the preferred candidates. At this gestational age, spontaneous version is most likely to have occurred, and there is decreased risk of spontaneous reversion after the ECV. All patients who are near term and found to have a fetus in a nonvertex presentation should be offered an ECV as long as there are no contraindications to the procedure. ECV is not appropriate for women who have a contraindication to a vaginal delivery.

There are limited studies of ECV in women who undergo the procedure in early labor and in those who have had a previous uterine surgery. ECV success rates are not affected by a previous cesarean delivery, though the risks of uterine rupture are not clear. The procedure should be attempted only in settings where cesarean delivery services are immediately available.

The success rates of ECV have been reported to be anywhere from 16% to 100%, with an overall pooled success of 58% with a 6% pooled complication rate. Some studies have documented higher success rates with higher parity and a transverse or oblique fetal lie. However, placental location, maternal weight, and amniotic fluid volume have not been consistently found to be predictive of ECV success. The use of parenteral tocolysis has been associated with increased success rates of ECV, though there are not enough data to make a recommendation regarding use of regional anesthesia with the procedure.

ECV should be stopped in the face of a prolonged or significant fetal bradycardia or if the patient is experiencing intolerable levels of discomfort. However, there are no guidelines to recommend the total time limit of the procedure. After the ECV, there should be fetal heart rate monitoring for at least 30 minutes and anti-D immune globulin should be administered to those women who are Rh-negative if delivery is not anticipated in the next 72 hours.
 

Dr. Siddighi is editor-in-chief of the Ob/Gyn Board Master and director of female pelvic medicine and reconstructive surgery and director of grand rounds at Loma Linda University Health in California. Ob.Gyn. News and Ob/Gyn Board Master are owned by the same parent company, Frontline Medical Communications.

Reference

1. Obstet Gynecol. 2016 Feb;127(2):e54-61.

 

Editor’s Note: This is the fourth installment of a six-part series that will review key concepts and articles that ob.gyns. can use to prepare for the American Board of Obstetrics and Gynecology Maintenance of Certification examination. The series is adapted from Ob/Gyn Board Master (obgynboardmaster.com), an online board review course created by Erudyte Inc. The series will cover issues in reproductive endocrinology and infertility, maternal-fetal medicine, gynecologic oncology, and female pelvic medicine, as well as general test-taking and study tips.

The American College of Obstetricians and Gynecologists’ “Practice Bulletins” are important practice management guidelines for ob.gyn. clinicians. The Practice Bulletins are rich sources of material often tested on board exams. In February 2016, ACOG issued a revised Practice Bulletin (#161) on external cephalic version outlining clinical considerations and recommendations and providing an algorithm for patient management.¹ We recommend you read this bulletin and review this topic carefully.

Let’s begin with a possible medical board question: According to the Practice Bulletin, which of the following is TRUE about external cephalic version (ECV)?

A. Success rate is lower in women with a previous cesarean delivery.

B. Placental location affects the success rate.

C. External cephalic version should be stopped after 15 minutes.

D. Women at 37 weeks’ gestation are preferred candidates.

E. Tocolysis decreases success rate.

The correct answer is D.

Women at 37 weeks’ gestation are the preferred candidates for an ECV because spontaneous version would likely have already occurred by this time and the risk of spontaneous reversion is lower. Answers A-C and E are incorrect statements.

Key points

Women at 37 weeks’ gestation are the preferred candidates for an ECV.

The overall pooled success rate for ECV is 58% with a 6% pooled complication rate.

The use of parenteral tocolysis has been associated with increased success rates of ECV, though there are not enough data to make a recommendation regarding use of regional anesthesia with the procedure.

Literature summary

ECV is a procedure designed to turn a fetus into vertex presentation by applying external pressure to a woman’s abdomen. Women at 37 weeks’ gestation are the preferred candidates. At this gestational age, spontaneous version is most likely to have occurred, and there is decreased risk of spontaneous reversion after the ECV. All patients who are near term and found to have a fetus in a nonvertex presentation should be offered an ECV as long as there are no contraindications to the procedure. ECV is not appropriate for women who have a contraindication to a vaginal delivery.

There are limited studies of ECV in women who undergo the procedure in early labor and in those who have had a previous uterine surgery. ECV success rates are not affected by a previous cesarean delivery, though the risks of uterine rupture are not clear. The procedure should be attempted only in settings where cesarean delivery services are immediately available.

The success rates of ECV have been reported to be anywhere from 16% to 100%, with an overall pooled success of 58% with a 6% pooled complication rate. Some studies have documented higher success rates with higher parity and a transverse or oblique fetal lie. However, placental location, maternal weight, and amniotic fluid volume have not been consistently found to be predictive of ECV success. The use of parenteral tocolysis has been associated with increased success rates of ECV, though there are not enough data to make a recommendation regarding use of regional anesthesia with the procedure.

ECV should be stopped in the face of a prolonged or significant fetal bradycardia or if the patient is experiencing intolerable levels of discomfort. However, there are no guidelines to recommend the total time limit of the procedure. After the ECV, there should be fetal heart rate monitoring for at least 30 minutes and anti-D immune globulin should be administered to those women who are Rh-negative if delivery is not anticipated in the next 72 hours.
 

Dr. Siddighi is editor-in-chief of the Ob/Gyn Board Master and director of female pelvic medicine and reconstructive surgery and director of grand rounds at Loma Linda University Health in California. Ob.Gyn. News and Ob/Gyn Board Master are owned by the same parent company, Frontline Medical Communications.

Reference

1. Obstet Gynecol. 2016 Feb;127(2):e54-61.

 

Editor’s Note: This is the fourth installment of a six-part series that will review key concepts and articles that ob.gyns. can use to prepare for the American Board of Obstetrics and Gynecology Maintenance of Certification examination. The series is adapted from Ob/Gyn Board Master (obgynboardmaster.com), an online board review course created by Erudyte Inc. The series will cover issues in reproductive endocrinology and infertility, maternal-fetal medicine, gynecologic oncology, and female pelvic medicine, as well as general test-taking and study tips.

The American College of Obstetricians and Gynecologists’ “Practice Bulletins” are important practice management guidelines for ob.gyn. clinicians. The Practice Bulletins are rich sources of material often tested on board exams. In February 2016, ACOG issued a revised Practice Bulletin (#161) on external cephalic version outlining clinical considerations and recommendations and providing an algorithm for patient management.¹ We recommend you read this bulletin and review this topic carefully.

Let’s begin with a possible medical board question: According to the Practice Bulletin, which of the following is TRUE about external cephalic version (ECV)?

A. Success rate is lower in women with a previous cesarean delivery.

B. Placental location affects the success rate.

C. External cephalic version should be stopped after 15 minutes.

D. Women at 37 weeks’ gestation are preferred candidates.

E. Tocolysis decreases success rate.

The correct answer is D.

Women at 37 weeks’ gestation are the preferred candidates for an ECV because spontaneous version would likely have already occurred by this time and the risk of spontaneous reversion is lower. Answers A-C and E are incorrect statements.

Key points

Women at 37 weeks’ gestation are the preferred candidates for an ECV.

The overall pooled success rate for ECV is 58% with a 6% pooled complication rate.

The use of parenteral tocolysis has been associated with increased success rates of ECV, though there are not enough data to make a recommendation regarding use of regional anesthesia with the procedure.

Literature summary

ECV is a procedure designed to turn a fetus into vertex presentation by applying external pressure to a woman’s abdomen. Women at 37 weeks’ gestation are the preferred candidates. At this gestational age, spontaneous version is most likely to have occurred, and there is decreased risk of spontaneous reversion after the ECV. All patients who are near term and found to have a fetus in a nonvertex presentation should be offered an ECV as long as there are no contraindications to the procedure. ECV is not appropriate for women who have a contraindication to a vaginal delivery.

There are limited studies of ECV in women who undergo the procedure in early labor and in those who have had a previous uterine surgery. ECV success rates are not affected by a previous cesarean delivery, though the risks of uterine rupture are not clear. The procedure should be attempted only in settings where cesarean delivery services are immediately available.

The success rates of ECV have been reported to be anywhere from 16% to 100%, with an overall pooled success of 58% with a 6% pooled complication rate. Some studies have documented higher success rates with higher parity and a transverse or oblique fetal lie. However, placental location, maternal weight, and amniotic fluid volume have not been consistently found to be predictive of ECV success. The use of parenteral tocolysis has been associated with increased success rates of ECV, though there are not enough data to make a recommendation regarding use of regional anesthesia with the procedure.

ECV should be stopped in the face of a prolonged or significant fetal bradycardia or if the patient is experiencing intolerable levels of discomfort. However, there are no guidelines to recommend the total time limit of the procedure. After the ECV, there should be fetal heart rate monitoring for at least 30 minutes and anti-D immune globulin should be administered to those women who are Rh-negative if delivery is not anticipated in the next 72 hours.
 

Dr. Siddighi is editor-in-chief of the Ob/Gyn Board Master and director of female pelvic medicine and reconstructive surgery and director of grand rounds at Loma Linda University Health in California. Ob.Gyn. News and Ob/Gyn Board Master are owned by the same parent company, Frontline Medical Communications.

Reference

1. Obstet Gynecol. 2016 Feb;127(2):e54-61.