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Hospitalist burnout
Some things I’ve been thinking about:
- Physician well-being, morale, and burnout seem to be getting more attention in both the medical and the lay press.
- Leaders from 10 prestigious health systems and the CEO of the American Medical Association wrote a March 2017 post in the Health Affairs Blog titled “Physician Burnout is a Public Health Crisis: A Message To Our Fellow Health Care CEOs.”
- I’m now regularly hearing and reading mention of the “Quadruple Aim.” The “Triple Aim,” first described in 2008, is the pursuit of excellence in 1) patient experience – both quality of care and patient satisfaction; 2) population health; and 3) cost reduction. The November/December 2014 Annals of Family Medicine included an article recommending “that the Triple Aim be expanded to a Quadruple Aim by adding the goal of improving the work life of health care providers, including clinicians and staff.”1
- The CEO at a community hospital near me chose to make addressing physician burnout one of his top priorities and tied success in the effort to his own compensation bonus.
- In the course of my consulting work with hospitalist groups across the country, I’ve noticed a meaningful increase in the number of our colleagues who seem deeply unhappy with their work and/or burned out. The “Hospitalist Morale Index” may be a worthwhile way for a group to conduct an assessment.2
- I’m concerned that many other hospital care givers, including RNs, social workers, and others, are experiencing levels of distress and/or burnout that might be similar to that of physicians. From where I sit, they seem to be getting less attention, and I can’t tell if that is just because I’m not as immersed in their world or if it reflects reality. It’s pretty disappointing if it’s the latter.
For the most part, I think the causes of hospitalist distress and burnout are very similar to that of doctors in other specialties, and interventions to address the problem can be similar across specialties. Yet, each specialty probably differs in ways that are important to keep in mind.
Hospitalists also bear a huge burden related to observation status. Doctors in most other specialties rarely face complex decisions regarding whether observation is the right choice and are not so often the target of patient/family frustration and anger related to it.
Those seeking to address hospitalist burnout and well-being specifically should keep in mind these uniquely hospitalist issues. I think of them as a chronic disease to manage and mitigate, since “curing” them (making them go away entirely) is probably impossible for the foreseeable future.
What to do?
An Internet search on physician burnout, or other terms related to well-being, will yield more articles with advice to address the problem than you’ll ever have time to read. Trying to read all of them would likely lead to burnout! I think interventions can be divided into two broad categories: organizational efforts and personal efforts.
Like the 10 CEOs mentioned above, health care leaders should acknowledge physician distress and burnout as a meaningful issue that can impede organizational performance and that investments to address it can have a meaningful return on investment. The Health Affairs Blog post listed 11 things the CEOs committed to doing. It’s a list anyone working on this issue should review.
Doctors at The Mayo Clinic have published a great deal of research on physician burnout. In the March 7, 2017, JAMA, (summarized in a YouTube video) they describe several worthwhile organizational changes, as well as some personal strategies.3 They wrote about their experiences with interventions such as a deliberate curriculum to train doctors in self-care (self-reflection, mindfulness, etc.) in a series of one-hour lectures over several months.4 In November 2016, they published a meta-analysis of interventions to address burnout.5
In total, all of the worthwhile recommendations to address burnout leave me feeling like they’re a lot of work, and any individual intervention may not be as helpful as hoped, so that the best way to approach this is with a collection of interventions. In many ways, it is similar to the problem of readmissions: There is a lot of research out there, it’s hard to prove that any single intervention really works, and success lies in implementing a broad set of interventions. And success doesn’t equate to eliminating readmissions, only reducing them.
Coda: Is a sabbatical uniquely valuable for hospitalists?
I think a sabbatical might be a good idea for hospitalists. It also seems practical for other doctors, such as radiologists, anesthesiologists, and ED doctors, who don’t have 1:1 continuity relationships with patients. However, it is problematic for primary care doctors and specialists who need to maintain continuity relationships with patients and referring doctors that could be disrupted by a lengthy absence.
I’m not sure a sabbatical would reduce burnout much on its own, but, if properly structured, it seems very likely to reduce staffing turnover, and the sabbatical could be spent in ways that help rejuvenate interest and satisfaction in our work rather than simply taking a long vacation to travel and play golf, etc. It should probably be at least 3 months and better if it lasts a year. A common arrangement is that a doctor becomes eligible for the sabbatical after 10 years and is paid half of her usual compensation while away. I’d like to see more hospitalist groups do this.
Dr. Nelson has had a career in clinical practice as a hospitalist starting in 1988. He is cofounder and past president of SHM and principal in Nelson Flores Hospital Medicine Consultants. He is codirector for SHM’s practice management courses. Write to john.nelson@nelsonflores.com.
References
1. Bodenheimer, T and Sninsky, C. From Triple to Quadruple Aim: Care of the Patient Requires Care of the Provider. Ann Fam Med. Nov/Dec 2014.
2. Chandra, S et al. Introducing the Hospitalist Morale Index: A New Tool That May Be Relevant for Improving Provider Retention. JHM. June 2016.
3. Shanafelt, T, Dyrbye, L, West, C. Addressing Physician Burnout: The Way Forward. JAMA. March 7, 2017.
4. West, C et al. Intervention to Promote Physician Well-being, Job Satisfaction, and Professionalism: A Randomized Clinical Trial. JAMA Intern Med. 2014;174(4):527-33.
5. West, C et al. Interventions to prevent and reduce physician burnout: A systematic review and meta-analysis. The Lancet. Nov 5, 2016.
Some things I’ve been thinking about:
- Physician well-being, morale, and burnout seem to be getting more attention in both the medical and the lay press.
- Leaders from 10 prestigious health systems and the CEO of the American Medical Association wrote a March 2017 post in the Health Affairs Blog titled “Physician Burnout is a Public Health Crisis: A Message To Our Fellow Health Care CEOs.”
- I’m now regularly hearing and reading mention of the “Quadruple Aim.” The “Triple Aim,” first described in 2008, is the pursuit of excellence in 1) patient experience – both quality of care and patient satisfaction; 2) population health; and 3) cost reduction. The November/December 2014 Annals of Family Medicine included an article recommending “that the Triple Aim be expanded to a Quadruple Aim by adding the goal of improving the work life of health care providers, including clinicians and staff.”1
- The CEO at a community hospital near me chose to make addressing physician burnout one of his top priorities and tied success in the effort to his own compensation bonus.
- In the course of my consulting work with hospitalist groups across the country, I’ve noticed a meaningful increase in the number of our colleagues who seem deeply unhappy with their work and/or burned out. The “Hospitalist Morale Index” may be a worthwhile way for a group to conduct an assessment.2
- I’m concerned that many other hospital care givers, including RNs, social workers, and others, are experiencing levels of distress and/or burnout that might be similar to that of physicians. From where I sit, they seem to be getting less attention, and I can’t tell if that is just because I’m not as immersed in their world or if it reflects reality. It’s pretty disappointing if it’s the latter.
For the most part, I think the causes of hospitalist distress and burnout are very similar to that of doctors in other specialties, and interventions to address the problem can be similar across specialties. Yet, each specialty probably differs in ways that are important to keep in mind.
Hospitalists also bear a huge burden related to observation status. Doctors in most other specialties rarely face complex decisions regarding whether observation is the right choice and are not so often the target of patient/family frustration and anger related to it.
Those seeking to address hospitalist burnout and well-being specifically should keep in mind these uniquely hospitalist issues. I think of them as a chronic disease to manage and mitigate, since “curing” them (making them go away entirely) is probably impossible for the foreseeable future.
What to do?
An Internet search on physician burnout, or other terms related to well-being, will yield more articles with advice to address the problem than you’ll ever have time to read. Trying to read all of them would likely lead to burnout! I think interventions can be divided into two broad categories: organizational efforts and personal efforts.
Like the 10 CEOs mentioned above, health care leaders should acknowledge physician distress and burnout as a meaningful issue that can impede organizational performance and that investments to address it can have a meaningful return on investment. The Health Affairs Blog post listed 11 things the CEOs committed to doing. It’s a list anyone working on this issue should review.
Doctors at The Mayo Clinic have published a great deal of research on physician burnout. In the March 7, 2017, JAMA, (summarized in a YouTube video) they describe several worthwhile organizational changes, as well as some personal strategies.3 They wrote about their experiences with interventions such as a deliberate curriculum to train doctors in self-care (self-reflection, mindfulness, etc.) in a series of one-hour lectures over several months.4 In November 2016, they published a meta-analysis of interventions to address burnout.5
In total, all of the worthwhile recommendations to address burnout leave me feeling like they’re a lot of work, and any individual intervention may not be as helpful as hoped, so that the best way to approach this is with a collection of interventions. In many ways, it is similar to the problem of readmissions: There is a lot of research out there, it’s hard to prove that any single intervention really works, and success lies in implementing a broad set of interventions. And success doesn’t equate to eliminating readmissions, only reducing them.
Coda: Is a sabbatical uniquely valuable for hospitalists?
I think a sabbatical might be a good idea for hospitalists. It also seems practical for other doctors, such as radiologists, anesthesiologists, and ED doctors, who don’t have 1:1 continuity relationships with patients. However, it is problematic for primary care doctors and specialists who need to maintain continuity relationships with patients and referring doctors that could be disrupted by a lengthy absence.
I’m not sure a sabbatical would reduce burnout much on its own, but, if properly structured, it seems very likely to reduce staffing turnover, and the sabbatical could be spent in ways that help rejuvenate interest and satisfaction in our work rather than simply taking a long vacation to travel and play golf, etc. It should probably be at least 3 months and better if it lasts a year. A common arrangement is that a doctor becomes eligible for the sabbatical after 10 years and is paid half of her usual compensation while away. I’d like to see more hospitalist groups do this.
Dr. Nelson has had a career in clinical practice as a hospitalist starting in 1988. He is cofounder and past president of SHM and principal in Nelson Flores Hospital Medicine Consultants. He is codirector for SHM’s practice management courses. Write to john.nelson@nelsonflores.com.
References
1. Bodenheimer, T and Sninsky, C. From Triple to Quadruple Aim: Care of the Patient Requires Care of the Provider. Ann Fam Med. Nov/Dec 2014.
2. Chandra, S et al. Introducing the Hospitalist Morale Index: A New Tool That May Be Relevant for Improving Provider Retention. JHM. June 2016.
3. Shanafelt, T, Dyrbye, L, West, C. Addressing Physician Burnout: The Way Forward. JAMA. March 7, 2017.
4. West, C et al. Intervention to Promote Physician Well-being, Job Satisfaction, and Professionalism: A Randomized Clinical Trial. JAMA Intern Med. 2014;174(4):527-33.
5. West, C et al. Interventions to prevent and reduce physician burnout: A systematic review and meta-analysis. The Lancet. Nov 5, 2016.
Some things I’ve been thinking about:
- Physician well-being, morale, and burnout seem to be getting more attention in both the medical and the lay press.
- Leaders from 10 prestigious health systems and the CEO of the American Medical Association wrote a March 2017 post in the Health Affairs Blog titled “Physician Burnout is a Public Health Crisis: A Message To Our Fellow Health Care CEOs.”
- I’m now regularly hearing and reading mention of the “Quadruple Aim.” The “Triple Aim,” first described in 2008, is the pursuit of excellence in 1) patient experience – both quality of care and patient satisfaction; 2) population health; and 3) cost reduction. The November/December 2014 Annals of Family Medicine included an article recommending “that the Triple Aim be expanded to a Quadruple Aim by adding the goal of improving the work life of health care providers, including clinicians and staff.”1
- The CEO at a community hospital near me chose to make addressing physician burnout one of his top priorities and tied success in the effort to his own compensation bonus.
- In the course of my consulting work with hospitalist groups across the country, I’ve noticed a meaningful increase in the number of our colleagues who seem deeply unhappy with their work and/or burned out. The “Hospitalist Morale Index” may be a worthwhile way for a group to conduct an assessment.2
- I’m concerned that many other hospital care givers, including RNs, social workers, and others, are experiencing levels of distress and/or burnout that might be similar to that of physicians. From where I sit, they seem to be getting less attention, and I can’t tell if that is just because I’m not as immersed in their world or if it reflects reality. It’s pretty disappointing if it’s the latter.
For the most part, I think the causes of hospitalist distress and burnout are very similar to that of doctors in other specialties, and interventions to address the problem can be similar across specialties. Yet, each specialty probably differs in ways that are important to keep in mind.
Hospitalists also bear a huge burden related to observation status. Doctors in most other specialties rarely face complex decisions regarding whether observation is the right choice and are not so often the target of patient/family frustration and anger related to it.
Those seeking to address hospitalist burnout and well-being specifically should keep in mind these uniquely hospitalist issues. I think of them as a chronic disease to manage and mitigate, since “curing” them (making them go away entirely) is probably impossible for the foreseeable future.
What to do?
An Internet search on physician burnout, or other terms related to well-being, will yield more articles with advice to address the problem than you’ll ever have time to read. Trying to read all of them would likely lead to burnout! I think interventions can be divided into two broad categories: organizational efforts and personal efforts.
Like the 10 CEOs mentioned above, health care leaders should acknowledge physician distress and burnout as a meaningful issue that can impede organizational performance and that investments to address it can have a meaningful return on investment. The Health Affairs Blog post listed 11 things the CEOs committed to doing. It’s a list anyone working on this issue should review.
Doctors at The Mayo Clinic have published a great deal of research on physician burnout. In the March 7, 2017, JAMA, (summarized in a YouTube video) they describe several worthwhile organizational changes, as well as some personal strategies.3 They wrote about their experiences with interventions such as a deliberate curriculum to train doctors in self-care (self-reflection, mindfulness, etc.) in a series of one-hour lectures over several months.4 In November 2016, they published a meta-analysis of interventions to address burnout.5
In total, all of the worthwhile recommendations to address burnout leave me feeling like they’re a lot of work, and any individual intervention may not be as helpful as hoped, so that the best way to approach this is with a collection of interventions. In many ways, it is similar to the problem of readmissions: There is a lot of research out there, it’s hard to prove that any single intervention really works, and success lies in implementing a broad set of interventions. And success doesn’t equate to eliminating readmissions, only reducing them.
Coda: Is a sabbatical uniquely valuable for hospitalists?
I think a sabbatical might be a good idea for hospitalists. It also seems practical for other doctors, such as radiologists, anesthesiologists, and ED doctors, who don’t have 1:1 continuity relationships with patients. However, it is problematic for primary care doctors and specialists who need to maintain continuity relationships with patients and referring doctors that could be disrupted by a lengthy absence.
I’m not sure a sabbatical would reduce burnout much on its own, but, if properly structured, it seems very likely to reduce staffing turnover, and the sabbatical could be spent in ways that help rejuvenate interest and satisfaction in our work rather than simply taking a long vacation to travel and play golf, etc. It should probably be at least 3 months and better if it lasts a year. A common arrangement is that a doctor becomes eligible for the sabbatical after 10 years and is paid half of her usual compensation while away. I’d like to see more hospitalist groups do this.
Dr. Nelson has had a career in clinical practice as a hospitalist starting in 1988. He is cofounder and past president of SHM and principal in Nelson Flores Hospital Medicine Consultants. He is codirector for SHM’s practice management courses. Write to john.nelson@nelsonflores.com.
References
1. Bodenheimer, T and Sninsky, C. From Triple to Quadruple Aim: Care of the Patient Requires Care of the Provider. Ann Fam Med. Nov/Dec 2014.
2. Chandra, S et al. Introducing the Hospitalist Morale Index: A New Tool That May Be Relevant for Improving Provider Retention. JHM. June 2016.
3. Shanafelt, T, Dyrbye, L, West, C. Addressing Physician Burnout: The Way Forward. JAMA. March 7, 2017.
4. West, C et al. Intervention to Promote Physician Well-being, Job Satisfaction, and Professionalism: A Randomized Clinical Trial. JAMA Intern Med. 2014;174(4):527-33.
5. West, C et al. Interventions to prevent and reduce physician burnout: A systematic review and meta-analysis. The Lancet. Nov 5, 2016.
Coaching ‘No’
In a recent column entitled “To the limit,” I tried to make the case that the negative consequences of permissive parenting are numerous enough to warrant the attention of primary care pediatricians and family physicians. The evidence linking atypical sensory adaptation, behavior difficulties, sleep deprivation, and obesity to a permissive parenting style is just beginning to appear in the literature, but the numbers are in sync with the anecdotal observations of many experienced pediatricians like me. In that previous column,
First, let me make it clear that I don’t consider parenting style to be a topic that needs to occur on the checklist of every patient at every health maintenance visit. You already are overburdened with the demands of experts who have lobbied to have their favorite hot button issues included in your 15 minutes of face-to-face time with your young patients.
We also must accept our limited role as advisors. There are many ways to skin a cat and to raise a child. Homogeneity is not our goal. We must respect the cultural and philosophical differences that exist in our society. However, in my opinion, the unhealthy consequences of permissive parenting deserve a sensitive attempt at education and some gentle anticipatory guidance ... hopefully without an aroma of condescension.
The opportunities for our input begin in the first few months of life when parents are faced with the difficult questions of whether it is safe and appropriate to allow their infant to cry himself to sleep and whether a mom must allow her infant to use her breast as a pacifier. With the transition to solid food comes the challenge of how to manage the inevitable rejection of new tastes, colors, and textures. Of course, most parents find these issues challenging, but to what degree a parent can internalize your reassurance and advice is a good reflection on where he or she sits on the permissive to authoritarian spectrum of parenting.
With an infant’s rapidly advancing motor skills comes the question of when, where, and how to create boundaries to keep the child safe ... and to protect the environment from the surprisingly destructive power of an inquisitive toddler. Here the permissive parent will be continually challenged when he or she finds that simply saying “No” or “Don’t” doesn’t always work ... to some extent because, up to this point, the child has never encountered a situation in which s/he hasn’t gotten what s/he wants.
This is not an issue in which we should allow ourselves to get bogged down in circuitous philosophical arguments. We must keep our advice practical and focused on issues of safety and health. I have found that a significant number of permissive parents can learn the difficult skill of saying “No” to their children. It takes time, but it is time well spent.
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.” Email him at pdnews@frontlinemedcom.com.
In a recent column entitled “To the limit,” I tried to make the case that the negative consequences of permissive parenting are numerous enough to warrant the attention of primary care pediatricians and family physicians. The evidence linking atypical sensory adaptation, behavior difficulties, sleep deprivation, and obesity to a permissive parenting style is just beginning to appear in the literature, but the numbers are in sync with the anecdotal observations of many experienced pediatricians like me. In that previous column,
First, let me make it clear that I don’t consider parenting style to be a topic that needs to occur on the checklist of every patient at every health maintenance visit. You already are overburdened with the demands of experts who have lobbied to have their favorite hot button issues included in your 15 minutes of face-to-face time with your young patients.
We also must accept our limited role as advisors. There are many ways to skin a cat and to raise a child. Homogeneity is not our goal. We must respect the cultural and philosophical differences that exist in our society. However, in my opinion, the unhealthy consequences of permissive parenting deserve a sensitive attempt at education and some gentle anticipatory guidance ... hopefully without an aroma of condescension.
The opportunities for our input begin in the first few months of life when parents are faced with the difficult questions of whether it is safe and appropriate to allow their infant to cry himself to sleep and whether a mom must allow her infant to use her breast as a pacifier. With the transition to solid food comes the challenge of how to manage the inevitable rejection of new tastes, colors, and textures. Of course, most parents find these issues challenging, but to what degree a parent can internalize your reassurance and advice is a good reflection on where he or she sits on the permissive to authoritarian spectrum of parenting.
With an infant’s rapidly advancing motor skills comes the question of when, where, and how to create boundaries to keep the child safe ... and to protect the environment from the surprisingly destructive power of an inquisitive toddler. Here the permissive parent will be continually challenged when he or she finds that simply saying “No” or “Don’t” doesn’t always work ... to some extent because, up to this point, the child has never encountered a situation in which s/he hasn’t gotten what s/he wants.
This is not an issue in which we should allow ourselves to get bogged down in circuitous philosophical arguments. We must keep our advice practical and focused on issues of safety and health. I have found that a significant number of permissive parents can learn the difficult skill of saying “No” to their children. It takes time, but it is time well spent.
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.” Email him at pdnews@frontlinemedcom.com.
In a recent column entitled “To the limit,” I tried to make the case that the negative consequences of permissive parenting are numerous enough to warrant the attention of primary care pediatricians and family physicians. The evidence linking atypical sensory adaptation, behavior difficulties, sleep deprivation, and obesity to a permissive parenting style is just beginning to appear in the literature, but the numbers are in sync with the anecdotal observations of many experienced pediatricians like me. In that previous column,
First, let me make it clear that I don’t consider parenting style to be a topic that needs to occur on the checklist of every patient at every health maintenance visit. You already are overburdened with the demands of experts who have lobbied to have their favorite hot button issues included in your 15 minutes of face-to-face time with your young patients.
We also must accept our limited role as advisors. There are many ways to skin a cat and to raise a child. Homogeneity is not our goal. We must respect the cultural and philosophical differences that exist in our society. However, in my opinion, the unhealthy consequences of permissive parenting deserve a sensitive attempt at education and some gentle anticipatory guidance ... hopefully without an aroma of condescension.
The opportunities for our input begin in the first few months of life when parents are faced with the difficult questions of whether it is safe and appropriate to allow their infant to cry himself to sleep and whether a mom must allow her infant to use her breast as a pacifier. With the transition to solid food comes the challenge of how to manage the inevitable rejection of new tastes, colors, and textures. Of course, most parents find these issues challenging, but to what degree a parent can internalize your reassurance and advice is a good reflection on where he or she sits on the permissive to authoritarian spectrum of parenting.
With an infant’s rapidly advancing motor skills comes the question of when, where, and how to create boundaries to keep the child safe ... and to protect the environment from the surprisingly destructive power of an inquisitive toddler. Here the permissive parent will be continually challenged when he or she finds that simply saying “No” or “Don’t” doesn’t always work ... to some extent because, up to this point, the child has never encountered a situation in which s/he hasn’t gotten what s/he wants.
This is not an issue in which we should allow ourselves to get bogged down in circuitous philosophical arguments. We must keep our advice practical and focused on issues of safety and health. I have found that a significant number of permissive parents can learn the difficult skill of saying “No” to their children. It takes time, but it is time well spent.
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.” Email him at pdnews@frontlinemedcom.com.
To the limit
Do you believe that children whose parents can make and enforce rules are more likely to thrive than those children whose parents are hesitant to set limits? If you don’t see limit setting as a critical function of parenting, you and I are not only marching to different drummers, we aren’t even in the same parade.
You may be tempted to write me off as just another old school ranter because I believe that limit setting is one of the cornerstones of parenting. But, let’s look at some of the evidence. There are several studies demonstrating that children whose parents set bedtimes get more sleep. One recent survey also found that teenagers who got more sleep as a result of enforced bedtimes functioned better in school (Sleep. 2011 Jun 1;34[6]:797-800).
An important question is whether permissive parenting is a problem that warrants our concern as pediatricians. We always are on alert for the red flags of abusive parenting, and, obviously, failure to intervene in cases of abuse can be disastrous. However, if we can believe the results from the studies that have already been completed, it seems pretty clear that permissive parenting can spawn behavioral problems, sleep problems, and the myriad of downstream effects that can result from sleep deprivation. And I haven’t even touched on the possible relationship between permissive parenting and the obesity epidemic.
If we still consider ourselves the preventive medicine specialists, shouldn’t pediatricians and family medicine physicians be more invested in minimizing the unhealthy consequences of permissive parenting? If we can agree on a firm “Yes!” the next question is, When and how should we address the issue?
A more nuanced discussion can be the germ of a future Letters from Maine, but the short answer is that we need to sound as nonjudgmental as possible as we present our case for limit setting. We need to start early before the die is cast, and we should be better about publicizing our supporting evidence. Setting a bedtime can begin in the first 6 months of life. Helping parents learn to say, “No, we aren’t going to feed you only what you like to eat!” can start as an infant makes what can be an unsettling transition to solid food.
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.”
Do you believe that children whose parents can make and enforce rules are more likely to thrive than those children whose parents are hesitant to set limits? If you don’t see limit setting as a critical function of parenting, you and I are not only marching to different drummers, we aren’t even in the same parade.
You may be tempted to write me off as just another old school ranter because I believe that limit setting is one of the cornerstones of parenting. But, let’s look at some of the evidence. There are several studies demonstrating that children whose parents set bedtimes get more sleep. One recent survey also found that teenagers who got more sleep as a result of enforced bedtimes functioned better in school (Sleep. 2011 Jun 1;34[6]:797-800).
An important question is whether permissive parenting is a problem that warrants our concern as pediatricians. We always are on alert for the red flags of abusive parenting, and, obviously, failure to intervene in cases of abuse can be disastrous. However, if we can believe the results from the studies that have already been completed, it seems pretty clear that permissive parenting can spawn behavioral problems, sleep problems, and the myriad of downstream effects that can result from sleep deprivation. And I haven’t even touched on the possible relationship between permissive parenting and the obesity epidemic.
If we still consider ourselves the preventive medicine specialists, shouldn’t pediatricians and family medicine physicians be more invested in minimizing the unhealthy consequences of permissive parenting? If we can agree on a firm “Yes!” the next question is, When and how should we address the issue?
A more nuanced discussion can be the germ of a future Letters from Maine, but the short answer is that we need to sound as nonjudgmental as possible as we present our case for limit setting. We need to start early before the die is cast, and we should be better about publicizing our supporting evidence. Setting a bedtime can begin in the first 6 months of life. Helping parents learn to say, “No, we aren’t going to feed you only what you like to eat!” can start as an infant makes what can be an unsettling transition to solid food.
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.”
Do you believe that children whose parents can make and enforce rules are more likely to thrive than those children whose parents are hesitant to set limits? If you don’t see limit setting as a critical function of parenting, you and I are not only marching to different drummers, we aren’t even in the same parade.
You may be tempted to write me off as just another old school ranter because I believe that limit setting is one of the cornerstones of parenting. But, let’s look at some of the evidence. There are several studies demonstrating that children whose parents set bedtimes get more sleep. One recent survey also found that teenagers who got more sleep as a result of enforced bedtimes functioned better in school (Sleep. 2011 Jun 1;34[6]:797-800).
An important question is whether permissive parenting is a problem that warrants our concern as pediatricians. We always are on alert for the red flags of abusive parenting, and, obviously, failure to intervene in cases of abuse can be disastrous. However, if we can believe the results from the studies that have already been completed, it seems pretty clear that permissive parenting can spawn behavioral problems, sleep problems, and the myriad of downstream effects that can result from sleep deprivation. And I haven’t even touched on the possible relationship between permissive parenting and the obesity epidemic.
If we still consider ourselves the preventive medicine specialists, shouldn’t pediatricians and family medicine physicians be more invested in minimizing the unhealthy consequences of permissive parenting? If we can agree on a firm “Yes!” the next question is, When and how should we address the issue?
A more nuanced discussion can be the germ of a future Letters from Maine, but the short answer is that we need to sound as nonjudgmental as possible as we present our case for limit setting. We need to start early before the die is cast, and we should be better about publicizing our supporting evidence. Setting a bedtime can begin in the first 6 months of life. Helping parents learn to say, “No, we aren’t going to feed you only what you like to eat!” can start as an infant makes what can be an unsettling transition to solid food.
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.”
Treatment of low bone density or osteoporosis to prevent fractures in men and women
Osteoporosis is defined by a clinically diagnosed fragility fracture or a bone mineral density (BMD) of at least 2.5 SD below the mean for young female adults, usually measured by dual-energy x-ray absorptiometry. Risk factors include age, female sex, post-menopause, hypogonadism or premature ovarian failure, history of cigarette smoking or alcohol consumption (3 or more drinks daily), rheumatoid arthritis, or medications including glucocorticoids, anticoagulants, anticonvulsants, and aromatase inhibitors.
This guideline update focuses on treatment with bisphosphonates (alendronate, risedronate, ibandronate, zoledronic acid) and denosumab. Denosumab, a human monoclonal antibody against RANK-ligand, approved by the Food and Drug Administration for treatment of osteoporosis, has been added to the list of allowed medications since publication of the 2008 guideline. Several therapies have been excluded from the update, including calcitonin, which is no longer widely used for osteoporosis treatment, and etidronate and pamidronate, neither of which are FDA-approved for the prevention of fractures or treatment of osteoporosis. It should be noted that the evidence continues to be insufficient regarding the effectiveness of therapies to prevent fractures or to treat osteoporosis in men.
Bisphosphonates are associated with mild upper GI symptoms, atypical subtrochanteric fracture, and rare osteonecrosis of the jaw. There is no significant association between bisphosphonate use and total cardiovascular adverse events. Evidence is insufficient to associate bisphosphonates with increased cancer risk. Zoledronic acid is associated with atrial fibrillation, arthritis/arthralgias, headaches, hypocalcemia, influenza-like symptoms, and an increased incidence of uveitis/episcleritis. Denosumab is associated with mild upper GI symptoms, rash/eczema, and cellulitis.
While in the past additional medications were recommended for osteoporosis, the current guidelines recommend against using raloxifene, ibandronate, teriparatide, menopausal estrogen therapy, or menopausal estrogen plus progesterone therapy for first-line pharmacologic treatment.
The overall effect of calcium, vitamin D, or exercise alone on fracture risk is uncertain. Calcium and vitamin D may be added to treatment regimens, as a majority of trials with bisphosphonate therapy added this supplementation. Dosages should be considered because excessive dosing has been associated with hypercalcemia. Although previous data suggested an association between calcium supplementation and increased risk for myocardial infarction, moderate-quality evidence shows no association, though there is a risk of kidney stones.
Recommendation: Women who have osteoporosis and receive pharmacologic treatment should be treated for 5 years (weak recommendation; low-quality evidence). The evidence to determine the length of treatment is not strong, so recommendation is an extrapolation from existing evidence. High-risk patients may benefit from more than 5 years of treatment. Data suggests that patients treated with alendronate who had preexisting fractures or those with a BMD of –2.5 or less after 5 years of initial therapy may benefit from continued treatment, because these patients experienced a decreased incidence of new clinical vertebral fractures.
Recommendation: Pharmacologic treatment with bisphosphonates to reduce the risk for vertebral fracture can be offered to men who have clinically recognized osteoporosis (weak recommendation, low-quality evidence). No evidence suggests that outcomes associated with pharmacologic treatment would differ between men and women if based on similar BMDs.
Recommendation: Bone density monitoring is not recommended during the 5-year pharmacologic treatment period for osteoporosis in women (weak recommendation, low-quality evidence). Data showed that most women with normal dual-energy x-ray absorptiometry scores did not progress to osteoporosis within 15 years. Data also does not support monitoring BMD during the initial 5 years of treatment in patients taking pharmacologic agents to treat osteoporosis. Several studies showed that women treated with antiresorptive treatment benefited from reduced fractures with treatment even if BMD did not increase.
Only 10% of women with normal or mild osteopenia develop osteoporosis within 15 years; 10% of women with moderate osteopenia develop osteoporosis within 5 years, and 10% of women with advanced osteopenia develop osteoporosis within 1 year.
Recommendation: The decision about whether to treat osteopenic women older then 65 years of age who are at a high risk for fracture should be based on a discussion of with the patient about their risk of fracture and the risk and benefits of treatment. Clinicians can use their judgment regarding the qualitative risk for fracture, or a validated tool such as the FRAX tool that gives 10-year risk of any major osteoporotic fracture and of hip fracture. The FRAX site recommends consideration of treatment for individuals with low bone mass (T-score between –1.0 and –2.5 at the femoral neck or spine) and a 10-year probability of a hip fracture of at least 3% or a 10-year probability of a major osteoporosis-related fracture greater than 20%.
Bottom line:
Clinicians should offer pharmacologic treatment with alendronate, risedronate, zoledronic acid, or denosumab to reduce the risk of hip and vertebral fractures in women who have known osteoporosis diagnosed as a T score less than –2.5 or those with a fragility fracture. Pharmacologic therapy should be used for 5 years; however, high risk patients may benefit from longer treatment. There is no benefit to bone density monitoring during the 5-year pharmacologic treatment period. In addition, bisphosphonates should be considered in men who have clinically recognized osteoporosis.
Reference:
Qaseem, A, Forciea, MA, McLean RM, Denberg TD. Treatment of Low Bone Density or Osteoporosis to Prevent Fractures in Men and Women: A Clinical Practice Guideline Update From the American College of Physicians. Ann Int Med. 2017;166(11):818-39.
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. Dr. Meizinger is a second year resident in the Family Medicine Residency Program at Abington Jefferson Health.
Osteoporosis is defined by a clinically diagnosed fragility fracture or a bone mineral density (BMD) of at least 2.5 SD below the mean for young female adults, usually measured by dual-energy x-ray absorptiometry. Risk factors include age, female sex, post-menopause, hypogonadism or premature ovarian failure, history of cigarette smoking or alcohol consumption (3 or more drinks daily), rheumatoid arthritis, or medications including glucocorticoids, anticoagulants, anticonvulsants, and aromatase inhibitors.
This guideline update focuses on treatment with bisphosphonates (alendronate, risedronate, ibandronate, zoledronic acid) and denosumab. Denosumab, a human monoclonal antibody against RANK-ligand, approved by the Food and Drug Administration for treatment of osteoporosis, has been added to the list of allowed medications since publication of the 2008 guideline. Several therapies have been excluded from the update, including calcitonin, which is no longer widely used for osteoporosis treatment, and etidronate and pamidronate, neither of which are FDA-approved for the prevention of fractures or treatment of osteoporosis. It should be noted that the evidence continues to be insufficient regarding the effectiveness of therapies to prevent fractures or to treat osteoporosis in men.
Bisphosphonates are associated with mild upper GI symptoms, atypical subtrochanteric fracture, and rare osteonecrosis of the jaw. There is no significant association between bisphosphonate use and total cardiovascular adverse events. Evidence is insufficient to associate bisphosphonates with increased cancer risk. Zoledronic acid is associated with atrial fibrillation, arthritis/arthralgias, headaches, hypocalcemia, influenza-like symptoms, and an increased incidence of uveitis/episcleritis. Denosumab is associated with mild upper GI symptoms, rash/eczema, and cellulitis.
While in the past additional medications were recommended for osteoporosis, the current guidelines recommend against using raloxifene, ibandronate, teriparatide, menopausal estrogen therapy, or menopausal estrogen plus progesterone therapy for first-line pharmacologic treatment.
The overall effect of calcium, vitamin D, or exercise alone on fracture risk is uncertain. Calcium and vitamin D may be added to treatment regimens, as a majority of trials with bisphosphonate therapy added this supplementation. Dosages should be considered because excessive dosing has been associated with hypercalcemia. Although previous data suggested an association between calcium supplementation and increased risk for myocardial infarction, moderate-quality evidence shows no association, though there is a risk of kidney stones.
Recommendation: Women who have osteoporosis and receive pharmacologic treatment should be treated for 5 years (weak recommendation; low-quality evidence). The evidence to determine the length of treatment is not strong, so recommendation is an extrapolation from existing evidence. High-risk patients may benefit from more than 5 years of treatment. Data suggests that patients treated with alendronate who had preexisting fractures or those with a BMD of –2.5 or less after 5 years of initial therapy may benefit from continued treatment, because these patients experienced a decreased incidence of new clinical vertebral fractures.
Recommendation: Pharmacologic treatment with bisphosphonates to reduce the risk for vertebral fracture can be offered to men who have clinically recognized osteoporosis (weak recommendation, low-quality evidence). No evidence suggests that outcomes associated with pharmacologic treatment would differ between men and women if based on similar BMDs.
Recommendation: Bone density monitoring is not recommended during the 5-year pharmacologic treatment period for osteoporosis in women (weak recommendation, low-quality evidence). Data showed that most women with normal dual-energy x-ray absorptiometry scores did not progress to osteoporosis within 15 years. Data also does not support monitoring BMD during the initial 5 years of treatment in patients taking pharmacologic agents to treat osteoporosis. Several studies showed that women treated with antiresorptive treatment benefited from reduced fractures with treatment even if BMD did not increase.
Only 10% of women with normal or mild osteopenia develop osteoporosis within 15 years; 10% of women with moderate osteopenia develop osteoporosis within 5 years, and 10% of women with advanced osteopenia develop osteoporosis within 1 year.
Recommendation: The decision about whether to treat osteopenic women older then 65 years of age who are at a high risk for fracture should be based on a discussion of with the patient about their risk of fracture and the risk and benefits of treatment. Clinicians can use their judgment regarding the qualitative risk for fracture, or a validated tool such as the FRAX tool that gives 10-year risk of any major osteoporotic fracture and of hip fracture. The FRAX site recommends consideration of treatment for individuals with low bone mass (T-score between –1.0 and –2.5 at the femoral neck or spine) and a 10-year probability of a hip fracture of at least 3% or a 10-year probability of a major osteoporosis-related fracture greater than 20%.
Bottom line:
Clinicians should offer pharmacologic treatment with alendronate, risedronate, zoledronic acid, or denosumab to reduce the risk of hip and vertebral fractures in women who have known osteoporosis diagnosed as a T score less than –2.5 or those with a fragility fracture. Pharmacologic therapy should be used for 5 years; however, high risk patients may benefit from longer treatment. There is no benefit to bone density monitoring during the 5-year pharmacologic treatment period. In addition, bisphosphonates should be considered in men who have clinically recognized osteoporosis.
Reference:
Qaseem, A, Forciea, MA, McLean RM, Denberg TD. Treatment of Low Bone Density or Osteoporosis to Prevent Fractures in Men and Women: A Clinical Practice Guideline Update From the American College of Physicians. Ann Int Med. 2017;166(11):818-39.
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. Dr. Meizinger is a second year resident in the Family Medicine Residency Program at Abington Jefferson Health.
Osteoporosis is defined by a clinically diagnosed fragility fracture or a bone mineral density (BMD) of at least 2.5 SD below the mean for young female adults, usually measured by dual-energy x-ray absorptiometry. Risk factors include age, female sex, post-menopause, hypogonadism or premature ovarian failure, history of cigarette smoking or alcohol consumption (3 or more drinks daily), rheumatoid arthritis, or medications including glucocorticoids, anticoagulants, anticonvulsants, and aromatase inhibitors.
This guideline update focuses on treatment with bisphosphonates (alendronate, risedronate, ibandronate, zoledronic acid) and denosumab. Denosumab, a human monoclonal antibody against RANK-ligand, approved by the Food and Drug Administration for treatment of osteoporosis, has been added to the list of allowed medications since publication of the 2008 guideline. Several therapies have been excluded from the update, including calcitonin, which is no longer widely used for osteoporosis treatment, and etidronate and pamidronate, neither of which are FDA-approved for the prevention of fractures or treatment of osteoporosis. It should be noted that the evidence continues to be insufficient regarding the effectiveness of therapies to prevent fractures or to treat osteoporosis in men.
Bisphosphonates are associated with mild upper GI symptoms, atypical subtrochanteric fracture, and rare osteonecrosis of the jaw. There is no significant association between bisphosphonate use and total cardiovascular adverse events. Evidence is insufficient to associate bisphosphonates with increased cancer risk. Zoledronic acid is associated with atrial fibrillation, arthritis/arthralgias, headaches, hypocalcemia, influenza-like symptoms, and an increased incidence of uveitis/episcleritis. Denosumab is associated with mild upper GI symptoms, rash/eczema, and cellulitis.
While in the past additional medications were recommended for osteoporosis, the current guidelines recommend against using raloxifene, ibandronate, teriparatide, menopausal estrogen therapy, or menopausal estrogen plus progesterone therapy for first-line pharmacologic treatment.
The overall effect of calcium, vitamin D, or exercise alone on fracture risk is uncertain. Calcium and vitamin D may be added to treatment regimens, as a majority of trials with bisphosphonate therapy added this supplementation. Dosages should be considered because excessive dosing has been associated with hypercalcemia. Although previous data suggested an association between calcium supplementation and increased risk for myocardial infarction, moderate-quality evidence shows no association, though there is a risk of kidney stones.
Recommendation: Women who have osteoporosis and receive pharmacologic treatment should be treated for 5 years (weak recommendation; low-quality evidence). The evidence to determine the length of treatment is not strong, so recommendation is an extrapolation from existing evidence. High-risk patients may benefit from more than 5 years of treatment. Data suggests that patients treated with alendronate who had preexisting fractures or those with a BMD of –2.5 or less after 5 years of initial therapy may benefit from continued treatment, because these patients experienced a decreased incidence of new clinical vertebral fractures.
Recommendation: Pharmacologic treatment with bisphosphonates to reduce the risk for vertebral fracture can be offered to men who have clinically recognized osteoporosis (weak recommendation, low-quality evidence). No evidence suggests that outcomes associated with pharmacologic treatment would differ between men and women if based on similar BMDs.
Recommendation: Bone density monitoring is not recommended during the 5-year pharmacologic treatment period for osteoporosis in women (weak recommendation, low-quality evidence). Data showed that most women with normal dual-energy x-ray absorptiometry scores did not progress to osteoporosis within 15 years. Data also does not support monitoring BMD during the initial 5 years of treatment in patients taking pharmacologic agents to treat osteoporosis. Several studies showed that women treated with antiresorptive treatment benefited from reduced fractures with treatment even if BMD did not increase.
Only 10% of women with normal or mild osteopenia develop osteoporosis within 15 years; 10% of women with moderate osteopenia develop osteoporosis within 5 years, and 10% of women with advanced osteopenia develop osteoporosis within 1 year.
Recommendation: The decision about whether to treat osteopenic women older then 65 years of age who are at a high risk for fracture should be based on a discussion of with the patient about their risk of fracture and the risk and benefits of treatment. Clinicians can use their judgment regarding the qualitative risk for fracture, or a validated tool such as the FRAX tool that gives 10-year risk of any major osteoporotic fracture and of hip fracture. The FRAX site recommends consideration of treatment for individuals with low bone mass (T-score between –1.0 and –2.5 at the femoral neck or spine) and a 10-year probability of a hip fracture of at least 3% or a 10-year probability of a major osteoporosis-related fracture greater than 20%.
Bottom line:
Clinicians should offer pharmacologic treatment with alendronate, risedronate, zoledronic acid, or denosumab to reduce the risk of hip and vertebral fractures in women who have known osteoporosis diagnosed as a T score less than –2.5 or those with a fragility fracture. Pharmacologic therapy should be used for 5 years; however, high risk patients may benefit from longer treatment. There is no benefit to bone density monitoring during the 5-year pharmacologic treatment period. In addition, bisphosphonates should be considered in men who have clinically recognized osteoporosis.
Reference:
Qaseem, A, Forciea, MA, McLean RM, Denberg TD. Treatment of Low Bone Density or Osteoporosis to Prevent Fractures in Men and Women: A Clinical Practice Guideline Update From the American College of Physicians. Ann Int Med. 2017;166(11):818-39.
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. Dr. Meizinger is a second year resident in the Family Medicine Residency Program at Abington Jefferson Health.
Tips and advice for Essure removal
Essure tubal microinserts were not designed to be removed. However, a small minority of women are requesting removal because of regret, complications, or the development of pelvic pain and other symptoms that may or may not be caused by the device.
Minimally invasive gynecologic surgeons have developed a variety of removal procedures and techniques for these women. There is general agreement that hysteroscopic removal is feasible only in the first 3 months following insertion of the device. After that, laparoscopic removal has become the norm. Small published reports and case series have documented the use of laparoscopic bilateral salpingectomy (BS) with and without hysterectomy, laparoscopic BS with cornuectomy, and laparoscopic salpingostomy, often followed by salpingectomy. There is not yet enough data to demonstrate that one method is superior to another, and we each have our own preferred approaches for preoperative imaging and removal.
Here is some of our advice on working with patients to assess the need for, and possible outcomes of, removal, as well as how to approach the surgery.
Counseling, assessment, and consent
Dr. Cohen: We have to be frank with our patients that symptoms may or may not improve following Essure removal. In a recently published case series of 52 women who underwent Essure removal at our institution, three-quarters of the patients reported near or total improvement in the quality of life. However, a relatively high number – roughly 30% – reported some ongoing symptoms (J Minim Invasive Gynecol. 2017 Jun 6. doi: 10:1016/j.jmig.2017.05.015).
The most common indication for Essure removal in this series was pelvic pain (96%), followed by abnormal uterine bleeding (35%) and patient-reported allergic reaction (21%). The indications were not mutually exclusive.
Importantly, could endometriosis or another underlying condition have developed since placement or worsened over time? Or, could her pelvic pain be worsened because of the cessation of hormonal contraception that coincided with Essure placement, rather than the device itself? For some women, Essure removal alone will not cure their symptoms.
In our cohort of 52 women, interestingly, 44% of those with pelvic pain had one or more concomitant or alternate causes of pain, including endometriosis, adenomyosis, and adhesions.
Dr. Levie: We can’t assume that Essure coils are at fault when patients present with pain and other symptoms, nor can we minimize complaints and concerns. We have to explore them.
It’s important that we inform women that pain may not be related to Essure microinserts. However, if, after thorough evaluation, the patient believes that the coils are the etiology of her pain and I cannot find another reason – or if she has regrets or is concerned about potential problems in the future – I am happy to remove them.
Dr. Yunker: In our case series of 29 women who underwent removal for the primary indication of pelvic pain, 88.5% reported significant relief at their postoperative visit (Contraception. 2016 Aug;94[2]:190-2). This, and other unpublished data, show that patients with gynecologic complaints specifically are the most likely to have resolution of symptoms, compared with those with more systemic or nongynecologic complaints.
Some patients have systemic symptoms that they feel are related and new since the device was placed. My counseling in these cases is that, while I do not have any physiologic evidence that the Essure coil is causing their symptoms, I’m hopeful that symptoms will improve with removal. If they do not, these patients must follow up with their primary care doctor for further work-up.
Device structure and use of imaging
Essure is a 4-cm long device (0.8 mm in diameter) with two parts: an inner coil made of stainless steel and PET fibers, the latter of which induces the fibrosis responsible for tubal occlusion, and an outer coil made of nitinol, a nickel titanium alloy.
Dr. Cohen: While the exact mechanism is unclear, it’s possible that the PET fibers may be drivers of the systemic inflammatory-type symptoms that some women report. Nickel allergies are also possible albeit uncommon. They appear to manifest as rash, urticaria, and other symptoms characteristic of contact allergic reactions.
The brittle nature of the outer coil makes a grasp-and-pull approach disadvantageous, unless you’re removing coils early on hysteroscopically. In general, one must avoid fracturing the outer coil, or parts of the device will be left behind. Pulling too hard may also cause the outer coil to unravel and expand to be quite long, which further increases the risk of fracture.
Hysterosalpingogram (HSG) and ultrasound are typically first-line options for looking at coil position. A diagnostic hysteroscopy may also help identify coils, and intraoperative fluoroscopy may be useful for either the hysteroscopic or laparoscopic approach, if there’s any question about portions of the device not being recovered.
Dr. Levie: Ultrasound is often sufficient for operative planning, but, if it does not detect devices in the cornual region, then further imaging may be warranted.
It’s important to be aware that some devices that appear to have correct placement on ultrasound or HSG may actually be partially tracking subserosally. In these cases, the distal portion of the device may have tracked through the mucosal layer and along the muscularis but below the serosa in the fallopian tube, causing pain. Imaging won’t be helpful in making this diagnosis. It will be identified laparoscopically.
Dr. Yunker: When patients have completed the 3-month HSG (to confirm occlusion of the Fallopian tubes post placement), I will review the images myself rather than relying on the report. Without an HSG – and, in many cases, even when I have it in hand – I will order a plain film x-ray of the abdomen and pelvis to look for coils. In almost all cases, I also order an ultrasound, which is helpful in assessing for ovarian and uterine conditions.
I’ve found plain film imaging to be valuable for identifying additional or misplaced Essure inserts. I have found up to four in one tube. In interpreting x-rays, one must appreciate that the outer coil is not radio-opaque (other than the tiny marker at the end) and will not show up. Occasionally we’ll add hysteroscopy to see how much of a coil is trailing into the uterus, but the ultrasound and x-ray are usually enough.
Some patients ask about postremoval imaging. I do not routinely do this, but I’m not opposed to it.
Surgical techniques
Dr. Cohen: I advise dissecting around each coil without cutting the outer portion and removing the coil intact, resecting all the way down to the interstitial portion of the tube, then proceeding with bilateral salpingectomy to ensure contraception.
If the patient’s symptoms are systemic and possibly reflective of PET fiber reactions, a wedge resection of the cornua may provide more peace of mind that PET fibers will not be left in situ. This procedure can be approached similarly to myomectomy, with the use of hemostatic agents such as misoprostol or vasopressin and suture closure in multiple layers.
If there are multiple coils present in the cavity, one option, to avoid having to pull them all out from the abdominal side, is to transect and remove the intracavity portion of the device hysteroscopically then dissect and remove the tubal/interstitial potion laparoscopically. As a general rule, I send all the removed tissue to pathology.
Dr. Levie: In general, I do a linear salpingostomy after using a uterine manipulator and a grasper to first identify the site of the distal portion of the device. One can usually feel where the tubes bend onto the device.
A bit proximal to where I visually and mentally mark the distal end of the device, I make a 2-3 cm incision over the device. With a fine-tip grasper, I can usually release the distal portion of the inner coil. Using two graspers over the inner and outer coils together and a hand-over-hand motion, I pull without excess traction in the access of the tubes, and the proximal portion will usually follow and deliver fairly simply. If the proximal portion breaks, I advise looking for it hysteroscopically and delivering it through the uterus.
Some surgeons have recommended hysteroscopy at the beginning of the procedure with cutting (using scissors) at the proximal end of the outer coil to avoid its getting caught in the cornua.
Most patients continue to want permanent sterilization, so we proceed with salpingectomy. Sometimes, given underlying pathologies, we’ll decide on laparoscopic or vaginal hysterectomy as well or bilateral salpingectomy without doing the salpingostomy. When hysterectomy is part of the surgery, we don’t need to worry at all about broken devices.
When the device is removed separately from the fallopian tube, one should inspect it afterward to ensure that all four markers of the device – the markers that are recommended by the manufacturer for radiologic confirmation of proper placement – have been delivered.
Dr. Yunker: When everything looks normal on the ultrasound – and when the coils on either HSG and/or plain film x-ray appear to be in the appropriate position in the tubes – then removal of the coils and tubes only is an option.
The closer the coil is to the fimbriae, the easier it is to come straight across the tube as you would in a regular salpingectomy without concern of breaking or cutting the coil. However, the closer the coil is the uterine side, the deeper you’ll need to dissect into the cornual region of the uterus. A cornual wedge resection may be necessary in order to remove the coil intact.
Our procedure has evolved over the years and we have moved away from salpingectomy as a means to dissect out the coils. With the theoretical risk of retained coil fragments and PET fibers, we prefer to remove the coils and tubes en bloc.
Dr. Cohen is director of research and the fellowship program director of minimally invasive gynecologic surgery at Brigham and Women’s Hospital, Boston. She reported that she has no financial disclosures. Dr. Levie is professor and associate chairman of the department of obstetrics and gynecology and women’s health and director of the minimally invasive surgery fellowship at Montefiore Medical Center, New York. Dr. Levie reported that he is an investigator in two studies involving Essure and sat on the Essure medical advisory board for Bayer but did not receive personal renumeration. Dr. Yunker is an assistant professor of obstetrics and gynecology at Vanderbilt University, Nashville. She reported that she is a consultant for Olympus.
Essure tubal microinserts were not designed to be removed. However, a small minority of women are requesting removal because of regret, complications, or the development of pelvic pain and other symptoms that may or may not be caused by the device.
Minimally invasive gynecologic surgeons have developed a variety of removal procedures and techniques for these women. There is general agreement that hysteroscopic removal is feasible only in the first 3 months following insertion of the device. After that, laparoscopic removal has become the norm. Small published reports and case series have documented the use of laparoscopic bilateral salpingectomy (BS) with and without hysterectomy, laparoscopic BS with cornuectomy, and laparoscopic salpingostomy, often followed by salpingectomy. There is not yet enough data to demonstrate that one method is superior to another, and we each have our own preferred approaches for preoperative imaging and removal.
Here is some of our advice on working with patients to assess the need for, and possible outcomes of, removal, as well as how to approach the surgery.
Counseling, assessment, and consent
Dr. Cohen: We have to be frank with our patients that symptoms may or may not improve following Essure removal. In a recently published case series of 52 women who underwent Essure removal at our institution, three-quarters of the patients reported near or total improvement in the quality of life. However, a relatively high number – roughly 30% – reported some ongoing symptoms (J Minim Invasive Gynecol. 2017 Jun 6. doi: 10:1016/j.jmig.2017.05.015).
The most common indication for Essure removal in this series was pelvic pain (96%), followed by abnormal uterine bleeding (35%) and patient-reported allergic reaction (21%). The indications were not mutually exclusive.
Importantly, could endometriosis or another underlying condition have developed since placement or worsened over time? Or, could her pelvic pain be worsened because of the cessation of hormonal contraception that coincided with Essure placement, rather than the device itself? For some women, Essure removal alone will not cure their symptoms.
In our cohort of 52 women, interestingly, 44% of those with pelvic pain had one or more concomitant or alternate causes of pain, including endometriosis, adenomyosis, and adhesions.
Dr. Levie: We can’t assume that Essure coils are at fault when patients present with pain and other symptoms, nor can we minimize complaints and concerns. We have to explore them.
It’s important that we inform women that pain may not be related to Essure microinserts. However, if, after thorough evaluation, the patient believes that the coils are the etiology of her pain and I cannot find another reason – or if she has regrets or is concerned about potential problems in the future – I am happy to remove them.
Dr. Yunker: In our case series of 29 women who underwent removal for the primary indication of pelvic pain, 88.5% reported significant relief at their postoperative visit (Contraception. 2016 Aug;94[2]:190-2). This, and other unpublished data, show that patients with gynecologic complaints specifically are the most likely to have resolution of symptoms, compared with those with more systemic or nongynecologic complaints.
Some patients have systemic symptoms that they feel are related and new since the device was placed. My counseling in these cases is that, while I do not have any physiologic evidence that the Essure coil is causing their symptoms, I’m hopeful that symptoms will improve with removal. If they do not, these patients must follow up with their primary care doctor for further work-up.
Device structure and use of imaging
Essure is a 4-cm long device (0.8 mm in diameter) with two parts: an inner coil made of stainless steel and PET fibers, the latter of which induces the fibrosis responsible for tubal occlusion, and an outer coil made of nitinol, a nickel titanium alloy.
Dr. Cohen: While the exact mechanism is unclear, it’s possible that the PET fibers may be drivers of the systemic inflammatory-type symptoms that some women report. Nickel allergies are also possible albeit uncommon. They appear to manifest as rash, urticaria, and other symptoms characteristic of contact allergic reactions.
The brittle nature of the outer coil makes a grasp-and-pull approach disadvantageous, unless you’re removing coils early on hysteroscopically. In general, one must avoid fracturing the outer coil, or parts of the device will be left behind. Pulling too hard may also cause the outer coil to unravel and expand to be quite long, which further increases the risk of fracture.
Hysterosalpingogram (HSG) and ultrasound are typically first-line options for looking at coil position. A diagnostic hysteroscopy may also help identify coils, and intraoperative fluoroscopy may be useful for either the hysteroscopic or laparoscopic approach, if there’s any question about portions of the device not being recovered.
Dr. Levie: Ultrasound is often sufficient for operative planning, but, if it does not detect devices in the cornual region, then further imaging may be warranted.
It’s important to be aware that some devices that appear to have correct placement on ultrasound or HSG may actually be partially tracking subserosally. In these cases, the distal portion of the device may have tracked through the mucosal layer and along the muscularis but below the serosa in the fallopian tube, causing pain. Imaging won’t be helpful in making this diagnosis. It will be identified laparoscopically.
Dr. Yunker: When patients have completed the 3-month HSG (to confirm occlusion of the Fallopian tubes post placement), I will review the images myself rather than relying on the report. Without an HSG – and, in many cases, even when I have it in hand – I will order a plain film x-ray of the abdomen and pelvis to look for coils. In almost all cases, I also order an ultrasound, which is helpful in assessing for ovarian and uterine conditions.
I’ve found plain film imaging to be valuable for identifying additional or misplaced Essure inserts. I have found up to four in one tube. In interpreting x-rays, one must appreciate that the outer coil is not radio-opaque (other than the tiny marker at the end) and will not show up. Occasionally we’ll add hysteroscopy to see how much of a coil is trailing into the uterus, but the ultrasound and x-ray are usually enough.
Some patients ask about postremoval imaging. I do not routinely do this, but I’m not opposed to it.
Surgical techniques
Dr. Cohen: I advise dissecting around each coil without cutting the outer portion and removing the coil intact, resecting all the way down to the interstitial portion of the tube, then proceeding with bilateral salpingectomy to ensure contraception.
If the patient’s symptoms are systemic and possibly reflective of PET fiber reactions, a wedge resection of the cornua may provide more peace of mind that PET fibers will not be left in situ. This procedure can be approached similarly to myomectomy, with the use of hemostatic agents such as misoprostol or vasopressin and suture closure in multiple layers.
If there are multiple coils present in the cavity, one option, to avoid having to pull them all out from the abdominal side, is to transect and remove the intracavity portion of the device hysteroscopically then dissect and remove the tubal/interstitial potion laparoscopically. As a general rule, I send all the removed tissue to pathology.
Dr. Levie: In general, I do a linear salpingostomy after using a uterine manipulator and a grasper to first identify the site of the distal portion of the device. One can usually feel where the tubes bend onto the device.
A bit proximal to where I visually and mentally mark the distal end of the device, I make a 2-3 cm incision over the device. With a fine-tip grasper, I can usually release the distal portion of the inner coil. Using two graspers over the inner and outer coils together and a hand-over-hand motion, I pull without excess traction in the access of the tubes, and the proximal portion will usually follow and deliver fairly simply. If the proximal portion breaks, I advise looking for it hysteroscopically and delivering it through the uterus.
Some surgeons have recommended hysteroscopy at the beginning of the procedure with cutting (using scissors) at the proximal end of the outer coil to avoid its getting caught in the cornua.
Most patients continue to want permanent sterilization, so we proceed with salpingectomy. Sometimes, given underlying pathologies, we’ll decide on laparoscopic or vaginal hysterectomy as well or bilateral salpingectomy without doing the salpingostomy. When hysterectomy is part of the surgery, we don’t need to worry at all about broken devices.
When the device is removed separately from the fallopian tube, one should inspect it afterward to ensure that all four markers of the device – the markers that are recommended by the manufacturer for radiologic confirmation of proper placement – have been delivered.
Dr. Yunker: When everything looks normal on the ultrasound – and when the coils on either HSG and/or plain film x-ray appear to be in the appropriate position in the tubes – then removal of the coils and tubes only is an option.
The closer the coil is to the fimbriae, the easier it is to come straight across the tube as you would in a regular salpingectomy without concern of breaking or cutting the coil. However, the closer the coil is the uterine side, the deeper you’ll need to dissect into the cornual region of the uterus. A cornual wedge resection may be necessary in order to remove the coil intact.
Our procedure has evolved over the years and we have moved away from salpingectomy as a means to dissect out the coils. With the theoretical risk of retained coil fragments and PET fibers, we prefer to remove the coils and tubes en bloc.
Dr. Cohen is director of research and the fellowship program director of minimally invasive gynecologic surgery at Brigham and Women’s Hospital, Boston. She reported that she has no financial disclosures. Dr. Levie is professor and associate chairman of the department of obstetrics and gynecology and women’s health and director of the minimally invasive surgery fellowship at Montefiore Medical Center, New York. Dr. Levie reported that he is an investigator in two studies involving Essure and sat on the Essure medical advisory board for Bayer but did not receive personal renumeration. Dr. Yunker is an assistant professor of obstetrics and gynecology at Vanderbilt University, Nashville. She reported that she is a consultant for Olympus.
Essure tubal microinserts were not designed to be removed. However, a small minority of women are requesting removal because of regret, complications, or the development of pelvic pain and other symptoms that may or may not be caused by the device.
Minimally invasive gynecologic surgeons have developed a variety of removal procedures and techniques for these women. There is general agreement that hysteroscopic removal is feasible only in the first 3 months following insertion of the device. After that, laparoscopic removal has become the norm. Small published reports and case series have documented the use of laparoscopic bilateral salpingectomy (BS) with and without hysterectomy, laparoscopic BS with cornuectomy, and laparoscopic salpingostomy, often followed by salpingectomy. There is not yet enough data to demonstrate that one method is superior to another, and we each have our own preferred approaches for preoperative imaging and removal.
Here is some of our advice on working with patients to assess the need for, and possible outcomes of, removal, as well as how to approach the surgery.
Counseling, assessment, and consent
Dr. Cohen: We have to be frank with our patients that symptoms may or may not improve following Essure removal. In a recently published case series of 52 women who underwent Essure removal at our institution, three-quarters of the patients reported near or total improvement in the quality of life. However, a relatively high number – roughly 30% – reported some ongoing symptoms (J Minim Invasive Gynecol. 2017 Jun 6. doi: 10:1016/j.jmig.2017.05.015).
The most common indication for Essure removal in this series was pelvic pain (96%), followed by abnormal uterine bleeding (35%) and patient-reported allergic reaction (21%). The indications were not mutually exclusive.
Importantly, could endometriosis or another underlying condition have developed since placement or worsened over time? Or, could her pelvic pain be worsened because of the cessation of hormonal contraception that coincided with Essure placement, rather than the device itself? For some women, Essure removal alone will not cure their symptoms.
In our cohort of 52 women, interestingly, 44% of those with pelvic pain had one or more concomitant or alternate causes of pain, including endometriosis, adenomyosis, and adhesions.
Dr. Levie: We can’t assume that Essure coils are at fault when patients present with pain and other symptoms, nor can we minimize complaints and concerns. We have to explore them.
It’s important that we inform women that pain may not be related to Essure microinserts. However, if, after thorough evaluation, the patient believes that the coils are the etiology of her pain and I cannot find another reason – or if she has regrets or is concerned about potential problems in the future – I am happy to remove them.
Dr. Yunker: In our case series of 29 women who underwent removal for the primary indication of pelvic pain, 88.5% reported significant relief at their postoperative visit (Contraception. 2016 Aug;94[2]:190-2). This, and other unpublished data, show that patients with gynecologic complaints specifically are the most likely to have resolution of symptoms, compared with those with more systemic or nongynecologic complaints.
Some patients have systemic symptoms that they feel are related and new since the device was placed. My counseling in these cases is that, while I do not have any physiologic evidence that the Essure coil is causing their symptoms, I’m hopeful that symptoms will improve with removal. If they do not, these patients must follow up with their primary care doctor for further work-up.
Device structure and use of imaging
Essure is a 4-cm long device (0.8 mm in diameter) with two parts: an inner coil made of stainless steel and PET fibers, the latter of which induces the fibrosis responsible for tubal occlusion, and an outer coil made of nitinol, a nickel titanium alloy.
Dr. Cohen: While the exact mechanism is unclear, it’s possible that the PET fibers may be drivers of the systemic inflammatory-type symptoms that some women report. Nickel allergies are also possible albeit uncommon. They appear to manifest as rash, urticaria, and other symptoms characteristic of contact allergic reactions.
The brittle nature of the outer coil makes a grasp-and-pull approach disadvantageous, unless you’re removing coils early on hysteroscopically. In general, one must avoid fracturing the outer coil, or parts of the device will be left behind. Pulling too hard may also cause the outer coil to unravel and expand to be quite long, which further increases the risk of fracture.
Hysterosalpingogram (HSG) and ultrasound are typically first-line options for looking at coil position. A diagnostic hysteroscopy may also help identify coils, and intraoperative fluoroscopy may be useful for either the hysteroscopic or laparoscopic approach, if there’s any question about portions of the device not being recovered.
Dr. Levie: Ultrasound is often sufficient for operative planning, but, if it does not detect devices in the cornual region, then further imaging may be warranted.
It’s important to be aware that some devices that appear to have correct placement on ultrasound or HSG may actually be partially tracking subserosally. In these cases, the distal portion of the device may have tracked through the mucosal layer and along the muscularis but below the serosa in the fallopian tube, causing pain. Imaging won’t be helpful in making this diagnosis. It will be identified laparoscopically.
Dr. Yunker: When patients have completed the 3-month HSG (to confirm occlusion of the Fallopian tubes post placement), I will review the images myself rather than relying on the report. Without an HSG – and, in many cases, even when I have it in hand – I will order a plain film x-ray of the abdomen and pelvis to look for coils. In almost all cases, I also order an ultrasound, which is helpful in assessing for ovarian and uterine conditions.
I’ve found plain film imaging to be valuable for identifying additional or misplaced Essure inserts. I have found up to four in one tube. In interpreting x-rays, one must appreciate that the outer coil is not radio-opaque (other than the tiny marker at the end) and will not show up. Occasionally we’ll add hysteroscopy to see how much of a coil is trailing into the uterus, but the ultrasound and x-ray are usually enough.
Some patients ask about postremoval imaging. I do not routinely do this, but I’m not opposed to it.
Surgical techniques
Dr. Cohen: I advise dissecting around each coil without cutting the outer portion and removing the coil intact, resecting all the way down to the interstitial portion of the tube, then proceeding with bilateral salpingectomy to ensure contraception.
If the patient’s symptoms are systemic and possibly reflective of PET fiber reactions, a wedge resection of the cornua may provide more peace of mind that PET fibers will not be left in situ. This procedure can be approached similarly to myomectomy, with the use of hemostatic agents such as misoprostol or vasopressin and suture closure in multiple layers.
If there are multiple coils present in the cavity, one option, to avoid having to pull them all out from the abdominal side, is to transect and remove the intracavity portion of the device hysteroscopically then dissect and remove the tubal/interstitial potion laparoscopically. As a general rule, I send all the removed tissue to pathology.
Dr. Levie: In general, I do a linear salpingostomy after using a uterine manipulator and a grasper to first identify the site of the distal portion of the device. One can usually feel where the tubes bend onto the device.
A bit proximal to where I visually and mentally mark the distal end of the device, I make a 2-3 cm incision over the device. With a fine-tip grasper, I can usually release the distal portion of the inner coil. Using two graspers over the inner and outer coils together and a hand-over-hand motion, I pull without excess traction in the access of the tubes, and the proximal portion will usually follow and deliver fairly simply. If the proximal portion breaks, I advise looking for it hysteroscopically and delivering it through the uterus.
Some surgeons have recommended hysteroscopy at the beginning of the procedure with cutting (using scissors) at the proximal end of the outer coil to avoid its getting caught in the cornua.
Most patients continue to want permanent sterilization, so we proceed with salpingectomy. Sometimes, given underlying pathologies, we’ll decide on laparoscopic or vaginal hysterectomy as well or bilateral salpingectomy without doing the salpingostomy. When hysterectomy is part of the surgery, we don’t need to worry at all about broken devices.
When the device is removed separately from the fallopian tube, one should inspect it afterward to ensure that all four markers of the device – the markers that are recommended by the manufacturer for radiologic confirmation of proper placement – have been delivered.
Dr. Yunker: When everything looks normal on the ultrasound – and when the coils on either HSG and/or plain film x-ray appear to be in the appropriate position in the tubes – then removal of the coils and tubes only is an option.
The closer the coil is to the fimbriae, the easier it is to come straight across the tube as you would in a regular salpingectomy without concern of breaking or cutting the coil. However, the closer the coil is the uterine side, the deeper you’ll need to dissect into the cornual region of the uterus. A cornual wedge resection may be necessary in order to remove the coil intact.
Our procedure has evolved over the years and we have moved away from salpingectomy as a means to dissect out the coils. With the theoretical risk of retained coil fragments and PET fibers, we prefer to remove the coils and tubes en bloc.
Dr. Cohen is director of research and the fellowship program director of minimally invasive gynecologic surgery at Brigham and Women’s Hospital, Boston. She reported that she has no financial disclosures. Dr. Levie is professor and associate chairman of the department of obstetrics and gynecology and women’s health and director of the minimally invasive surgery fellowship at Montefiore Medical Center, New York. Dr. Levie reported that he is an investigator in two studies involving Essure and sat on the Essure medical advisory board for Bayer but did not receive personal renumeration. Dr. Yunker is an assistant professor of obstetrics and gynecology at Vanderbilt University, Nashville. She reported that she is a consultant for Olympus.
So you want your Essure device removed ...
Despite recent negative lay press and a boxed safety warning from the Food and Drug Administration, Essure tubal microinserts continue to be a popular method of permanent contraception. It is imperative for patients to understand that this method of contraception cannot be reversed, and thereafter, the only method to achieve pregnancy would be via in vitro fertilization. Furthermore, preoperatively, patients must be counseled that placement of the Essure tubal microinserts may be associated with pelvic pain, abnormal bleeding, and even allergic reaction.
Even with our best effort to properly inform our patients as to the risks and benefits of permanent sterilization via Essure tubal microinserts, secondary to undesired side effects, patients desire their removal. This can be a challenging endeavor for the practitioner, especially if the women is not interested in hysterectomy.
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 reported having no financial disclosures related to this column.
Despite recent negative lay press and a boxed safety warning from the Food and Drug Administration, Essure tubal microinserts continue to be a popular method of permanent contraception. It is imperative for patients to understand that this method of contraception cannot be reversed, and thereafter, the only method to achieve pregnancy would be via in vitro fertilization. Furthermore, preoperatively, patients must be counseled that placement of the Essure tubal microinserts may be associated with pelvic pain, abnormal bleeding, and even allergic reaction.
Even with our best effort to properly inform our patients as to the risks and benefits of permanent sterilization via Essure tubal microinserts, secondary to undesired side effects, patients desire their removal. This can be a challenging endeavor for the practitioner, especially if the women is not interested in hysterectomy.
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 reported having no financial disclosures related to this column.
Despite recent negative lay press and a boxed safety warning from the Food and Drug Administration, Essure tubal microinserts continue to be a popular method of permanent contraception. It is imperative for patients to understand that this method of contraception cannot be reversed, and thereafter, the only method to achieve pregnancy would be via in vitro fertilization. Furthermore, preoperatively, patients must be counseled that placement of the Essure tubal microinserts may be associated with pelvic pain, abnormal bleeding, and even allergic reaction.
Even with our best effort to properly inform our patients as to the risks and benefits of permanent sterilization via Essure tubal microinserts, secondary to undesired side effects, patients desire their removal. This can be a challenging endeavor for the practitioner, especially if the women is not interested in hysterectomy.
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 reported having no financial disclosures related to this column.
Evolving practice in perinatal psychopharmacology: Lessons learned
Over the last 2 decades, there has been a growing interest in establishing a rich evidence base for treatment of psychiatric illness in pregnancy and the postpartum period. It seems as if a week does not go by when we don’t find multiple publications in the scientific literature describing a new finding or confirmation or inconsistency with existing data – whether it is a small prospective cohort study or an elegant analysis of a large administrative database. The goals of these reports center on refining our knowledge of safe treatments for perinatal psychiatric disorders.
Despite these strides, my colleagues and I frequently see a divergence between recommendations in the literature and what is done clinically by those who treat women around reproductive associated psychiatric disturbance – premenstrual dysphoric disorder or psychiatric disorder during pregnancy and the postpartum period. In some cases, scientific evidence has not filtered into day to day practice and some physicians continue to follow practices that, while outdated, make intuitive sense. In other clinical situations, limited evidence is being applied too broadly or data are too sparse to clearly inform practice. Regardless of the reason, we frequently see patients in clinical situations in which we are forced to rethink the clinical rationale for advice they have received or the clinical path taken.
Here is a sample of the clinical scenarios in which we have seen inconsistencies between current practice and the best evidence in perinatal psychiatry or situations in which data are too sparse to inform the clearest clinical path.
1. Discontinuation of antidepressants proximate to conception
Despite multiple studies supporting the high risk for relapse of major depression in women on maintenance antidepressant therapy with a history of recurrent depressive illness, it is still quite common for clinicians to routinely advise women to stop antidepressants while planning a pregnancy or after documentation of a pregnancy, regardless of the severity of the underlying illness. This runs counter to data showing high rates of relapse in women who stop antidepressants proximate to conception, the safety of antidepressants in pregnancy, and the harm to the mother and fetus when depression during pregnancy is untreated.
2. Use of a lower dose of antidepressants during pregnancy
It makes intuitive sense to use the smallest dose of medicine like antidepressant during pregnancy. However, multiple studies show that, at least in nonpregnant patients, the dose that gets patients well is typically the dose that keeps them well. One of the quickest paths to relapse in depression is a reduction in the antidepressant dose after someone has gotten well. This is even more relevant in pregnant patients because pregnancy itself dilutes the plasma level of the antidepressant given the rapidly expanding plasma volume seen in pregnancy. One can debate whether clinicians should empirically increase the dose of antidepressant during pregnancy to sustain plasma level of medication, but lowering the dose of this medication proximate or during pregnancy makes little sense.
3. A switch to sertraline in pregnancy/post partum
Another scenario that my colleagues and I often see is a pregnant patient whose depression was previously well controlled with a particular antidepressant, but whose physician, once she decides to conceive or becomes pregnant, switched her to sertraline.
The idea, which has been around for a long time, is that sertraline is the safest antidepressant for pregnant women because it has robust reproductive safety data and has particularly modest amounts of medication (if detected at all) in the plasma of infants of mothers who breastfeed while using the medicine. While we certainly have more safety data on SSRIs that were manufactured earlier, as compared with antidepressants that became available later, we have now accumulated data that fails to demonstrate a clear signal for teratogenicity across many antidepressants manufactured over the last 2 decades. Identifying an antidepressant for a given patient to which she will respond can be a challenging course for the patient. Achieving euthymia and subsequently switching to sertraline or another medication may only put her at risk for recurrence of depression and its attendant morbidity.
4. A change to a Category B label drug
This is another example of switching a patient to a potentially less effective drug in a somewhat misguided effort at finding a treatment that is safer in pregnancy. While the Food and Drug Administration’s drug category label system was a step forward, or at least a well intentioned effort to give women and their clinicians clearer insight into the reproductive safety of a medication, ultimately, the incomplete nature of the information caused the agency to transition to a new system (see the Pregnancy Labeling and Lactation Rule). Switching a woman to a category B medicine with sparse reproductive safety data instead of a category C medicine, which may not be unsafe but has raised some concerns in animal models, is not a better choice. The new labeling system is a step forward.
5. Discontinuation of lithium during pregnancy
Like discontinuation of antidepressants, the discontinuation of lithium during attempts to conceive in a woman whose illness has been well controlled, is associated with a high risk of relapse. In earlier work, it was sometimes recommended that discontinuation of lithium be considered after a long period of wellness. We have learned over time that this can be a risky move. Even women with a remote history of bipolar disorder appear to be at high risk of relapse when a mood stabilizer is stopped. Exquisite response to medicine does not imply less severe illness. Women who have bipolar disorder who have sustained euthymia on lithium should consider maintaining the safest possible regimen before, during, and after pregnancy despite the known small teratogenic risk associated with fetal exposure to this agent.
6. Try supplements or alternative therapies
Out of a desire to avoid any medication with incomplete reproductive safety data, some women and clinicians make the intuitive leap that “alternative treatments” can mitigate relapse in pregnancy, and they stop pharmacological treatments and switch to supplements or alternative therapies, including acupuncture, massage, or light therapy. Unfortunately, data supporting this clinical maneuver are sparse. Frequently, we see women with past histories of severe depression who have stopped antidepressants and who have started supplements as a substitute and who then relapse. Then, they try to restore euthymia with antidepressants and psychotherapy, and the road to restoration of well-being can be long.
Data on efficacy of alternative therapies continues to evolve and is an exciting and important area of research. However, where these treatments are best employed in the algorithm for treating depression in pregnancy, or at other times, has yet to be adequately defined.
7. Stop breastfeeding or defer antidepressant treatment
Many women continue to be counseled to either stop breastfeeding while using antidepressants or to defer treatment with antidepressants if they wish to breastfeed. Not uncommonly, we see women who are suffering from postpartum depression and who are engaged in psychotherapy but who have deferred treatment with antidepressants despite residual depressive symptoms that impair functioning. Clinicians should keep in mind that data supporting evidence of toxicity in newborns of women using antidepressants while breastfeeding are extremely sparse. Unfortunately, some women with postpartum depression are deferring treatment because they were counseled that it is not compatible with their desire to breastfeed.
8. Use of non-benzodiazepine sedative-hypnotics
Insomnia is a common problem in pregnancy, especially when coupled with comorbid anxiety, and, increasingly, it is being treated with non-benzodiazepine sedative-hypnotics. Clinicians should keep in mind that a known small risk may be better than an unknown risk. If a pregnant woman has severe insomnia, she may benefit from a low dose of a benzodiazepine, such as lorazepam or clonazepam, as opposed to a medication such as zolpidem for which reproductive safety data are particularly limited.
9. Pumping and dumping breast milk
Many women are advised to set an alarm to “pump and dump” their breast milk to minimize their baby’s exposure to antidepressants during breastfeeding. Early literature to pump and dump breast milk at peak antidepressant concentration was of great analytic and theoretical interest but has scant clinical application. As an author of many of those early publications, I can say that we never intended for women to sacrifice precious sleep to dump breast milk with the idea that limiting exposure to trace amounts of antidepressants would have beneficial effects over the long term.
10. Failure to bring up contraception use
We continue to see a 50% unplanned pregnancy rate across sociodemographic groups in the United States. This is a critical statistic because it may affect how treatment is managed. Bringing up the topic of reliable contraception prior to pregnancy allows for planned pregnancy and affords us the time to discuss treatment options and the ability to plot a more thoughtful and safe clinical course. However, often, contraception is not discussed.
One of our goals as clinicians is to, first, do no harm and that continues to be a challenge because the data in perinatal psychiatry is still inconsistent in some areas and there are evidence gaps in others. Nevertheless, our task is to take the best available data along with the patient’s wishes and knowledge of her past clinical history and to then translate that into the best care for the individual.
Dr. Cohen is the director of the Ammon-Pinizzotto Center for Women’s Mental Health at Massachusetts General Hospital in Boston, which provides information resources and conducts clinical care and research in reproductive mental health. He has been a consultant to manufacturers of psychiatric medications.
Over the last 2 decades, there has been a growing interest in establishing a rich evidence base for treatment of psychiatric illness in pregnancy and the postpartum period. It seems as if a week does not go by when we don’t find multiple publications in the scientific literature describing a new finding or confirmation or inconsistency with existing data – whether it is a small prospective cohort study or an elegant analysis of a large administrative database. The goals of these reports center on refining our knowledge of safe treatments for perinatal psychiatric disorders.
Despite these strides, my colleagues and I frequently see a divergence between recommendations in the literature and what is done clinically by those who treat women around reproductive associated psychiatric disturbance – premenstrual dysphoric disorder or psychiatric disorder during pregnancy and the postpartum period. In some cases, scientific evidence has not filtered into day to day practice and some physicians continue to follow practices that, while outdated, make intuitive sense. In other clinical situations, limited evidence is being applied too broadly or data are too sparse to clearly inform practice. Regardless of the reason, we frequently see patients in clinical situations in which we are forced to rethink the clinical rationale for advice they have received or the clinical path taken.
Here is a sample of the clinical scenarios in which we have seen inconsistencies between current practice and the best evidence in perinatal psychiatry or situations in which data are too sparse to inform the clearest clinical path.
1. Discontinuation of antidepressants proximate to conception
Despite multiple studies supporting the high risk for relapse of major depression in women on maintenance antidepressant therapy with a history of recurrent depressive illness, it is still quite common for clinicians to routinely advise women to stop antidepressants while planning a pregnancy or after documentation of a pregnancy, regardless of the severity of the underlying illness. This runs counter to data showing high rates of relapse in women who stop antidepressants proximate to conception, the safety of antidepressants in pregnancy, and the harm to the mother and fetus when depression during pregnancy is untreated.
2. Use of a lower dose of antidepressants during pregnancy
It makes intuitive sense to use the smallest dose of medicine like antidepressant during pregnancy. However, multiple studies show that, at least in nonpregnant patients, the dose that gets patients well is typically the dose that keeps them well. One of the quickest paths to relapse in depression is a reduction in the antidepressant dose after someone has gotten well. This is even more relevant in pregnant patients because pregnancy itself dilutes the plasma level of the antidepressant given the rapidly expanding plasma volume seen in pregnancy. One can debate whether clinicians should empirically increase the dose of antidepressant during pregnancy to sustain plasma level of medication, but lowering the dose of this medication proximate or during pregnancy makes little sense.
3. A switch to sertraline in pregnancy/post partum
Another scenario that my colleagues and I often see is a pregnant patient whose depression was previously well controlled with a particular antidepressant, but whose physician, once she decides to conceive or becomes pregnant, switched her to sertraline.
The idea, which has been around for a long time, is that sertraline is the safest antidepressant for pregnant women because it has robust reproductive safety data and has particularly modest amounts of medication (if detected at all) in the plasma of infants of mothers who breastfeed while using the medicine. While we certainly have more safety data on SSRIs that were manufactured earlier, as compared with antidepressants that became available later, we have now accumulated data that fails to demonstrate a clear signal for teratogenicity across many antidepressants manufactured over the last 2 decades. Identifying an antidepressant for a given patient to which she will respond can be a challenging course for the patient. Achieving euthymia and subsequently switching to sertraline or another medication may only put her at risk for recurrence of depression and its attendant morbidity.
4. A change to a Category B label drug
This is another example of switching a patient to a potentially less effective drug in a somewhat misguided effort at finding a treatment that is safer in pregnancy. While the Food and Drug Administration’s drug category label system was a step forward, or at least a well intentioned effort to give women and their clinicians clearer insight into the reproductive safety of a medication, ultimately, the incomplete nature of the information caused the agency to transition to a new system (see the Pregnancy Labeling and Lactation Rule). Switching a woman to a category B medicine with sparse reproductive safety data instead of a category C medicine, which may not be unsafe but has raised some concerns in animal models, is not a better choice. The new labeling system is a step forward.
5. Discontinuation of lithium during pregnancy
Like discontinuation of antidepressants, the discontinuation of lithium during attempts to conceive in a woman whose illness has been well controlled, is associated with a high risk of relapse. In earlier work, it was sometimes recommended that discontinuation of lithium be considered after a long period of wellness. We have learned over time that this can be a risky move. Even women with a remote history of bipolar disorder appear to be at high risk of relapse when a mood stabilizer is stopped. Exquisite response to medicine does not imply less severe illness. Women who have bipolar disorder who have sustained euthymia on lithium should consider maintaining the safest possible regimen before, during, and after pregnancy despite the known small teratogenic risk associated with fetal exposure to this agent.
6. Try supplements or alternative therapies
Out of a desire to avoid any medication with incomplete reproductive safety data, some women and clinicians make the intuitive leap that “alternative treatments” can mitigate relapse in pregnancy, and they stop pharmacological treatments and switch to supplements or alternative therapies, including acupuncture, massage, or light therapy. Unfortunately, data supporting this clinical maneuver are sparse. Frequently, we see women with past histories of severe depression who have stopped antidepressants and who have started supplements as a substitute and who then relapse. Then, they try to restore euthymia with antidepressants and psychotherapy, and the road to restoration of well-being can be long.
Data on efficacy of alternative therapies continues to evolve and is an exciting and important area of research. However, where these treatments are best employed in the algorithm for treating depression in pregnancy, or at other times, has yet to be adequately defined.
7. Stop breastfeeding or defer antidepressant treatment
Many women continue to be counseled to either stop breastfeeding while using antidepressants or to defer treatment with antidepressants if they wish to breastfeed. Not uncommonly, we see women who are suffering from postpartum depression and who are engaged in psychotherapy but who have deferred treatment with antidepressants despite residual depressive symptoms that impair functioning. Clinicians should keep in mind that data supporting evidence of toxicity in newborns of women using antidepressants while breastfeeding are extremely sparse. Unfortunately, some women with postpartum depression are deferring treatment because they were counseled that it is not compatible with their desire to breastfeed.
8. Use of non-benzodiazepine sedative-hypnotics
Insomnia is a common problem in pregnancy, especially when coupled with comorbid anxiety, and, increasingly, it is being treated with non-benzodiazepine sedative-hypnotics. Clinicians should keep in mind that a known small risk may be better than an unknown risk. If a pregnant woman has severe insomnia, she may benefit from a low dose of a benzodiazepine, such as lorazepam or clonazepam, as opposed to a medication such as zolpidem for which reproductive safety data are particularly limited.
9. Pumping and dumping breast milk
Many women are advised to set an alarm to “pump and dump” their breast milk to minimize their baby’s exposure to antidepressants during breastfeeding. Early literature to pump and dump breast milk at peak antidepressant concentration was of great analytic and theoretical interest but has scant clinical application. As an author of many of those early publications, I can say that we never intended for women to sacrifice precious sleep to dump breast milk with the idea that limiting exposure to trace amounts of antidepressants would have beneficial effects over the long term.
10. Failure to bring up contraception use
We continue to see a 50% unplanned pregnancy rate across sociodemographic groups in the United States. This is a critical statistic because it may affect how treatment is managed. Bringing up the topic of reliable contraception prior to pregnancy allows for planned pregnancy and affords us the time to discuss treatment options and the ability to plot a more thoughtful and safe clinical course. However, often, contraception is not discussed.
One of our goals as clinicians is to, first, do no harm and that continues to be a challenge because the data in perinatal psychiatry is still inconsistent in some areas and there are evidence gaps in others. Nevertheless, our task is to take the best available data along with the patient’s wishes and knowledge of her past clinical history and to then translate that into the best care for the individual.
Dr. Cohen is the director of the Ammon-Pinizzotto Center for Women’s Mental Health at Massachusetts General Hospital in Boston, which provides information resources and conducts clinical care and research in reproductive mental health. He has been a consultant to manufacturers of psychiatric medications.
Over the last 2 decades, there has been a growing interest in establishing a rich evidence base for treatment of psychiatric illness in pregnancy and the postpartum period. It seems as if a week does not go by when we don’t find multiple publications in the scientific literature describing a new finding or confirmation or inconsistency with existing data – whether it is a small prospective cohort study or an elegant analysis of a large administrative database. The goals of these reports center on refining our knowledge of safe treatments for perinatal psychiatric disorders.
Despite these strides, my colleagues and I frequently see a divergence between recommendations in the literature and what is done clinically by those who treat women around reproductive associated psychiatric disturbance – premenstrual dysphoric disorder or psychiatric disorder during pregnancy and the postpartum period. In some cases, scientific evidence has not filtered into day to day practice and some physicians continue to follow practices that, while outdated, make intuitive sense. In other clinical situations, limited evidence is being applied too broadly or data are too sparse to clearly inform practice. Regardless of the reason, we frequently see patients in clinical situations in which we are forced to rethink the clinical rationale for advice they have received or the clinical path taken.
Here is a sample of the clinical scenarios in which we have seen inconsistencies between current practice and the best evidence in perinatal psychiatry or situations in which data are too sparse to inform the clearest clinical path.
1. Discontinuation of antidepressants proximate to conception
Despite multiple studies supporting the high risk for relapse of major depression in women on maintenance antidepressant therapy with a history of recurrent depressive illness, it is still quite common for clinicians to routinely advise women to stop antidepressants while planning a pregnancy or after documentation of a pregnancy, regardless of the severity of the underlying illness. This runs counter to data showing high rates of relapse in women who stop antidepressants proximate to conception, the safety of antidepressants in pregnancy, and the harm to the mother and fetus when depression during pregnancy is untreated.
2. Use of a lower dose of antidepressants during pregnancy
It makes intuitive sense to use the smallest dose of medicine like antidepressant during pregnancy. However, multiple studies show that, at least in nonpregnant patients, the dose that gets patients well is typically the dose that keeps them well. One of the quickest paths to relapse in depression is a reduction in the antidepressant dose after someone has gotten well. This is even more relevant in pregnant patients because pregnancy itself dilutes the plasma level of the antidepressant given the rapidly expanding plasma volume seen in pregnancy. One can debate whether clinicians should empirically increase the dose of antidepressant during pregnancy to sustain plasma level of medication, but lowering the dose of this medication proximate or during pregnancy makes little sense.
3. A switch to sertraline in pregnancy/post partum
Another scenario that my colleagues and I often see is a pregnant patient whose depression was previously well controlled with a particular antidepressant, but whose physician, once she decides to conceive or becomes pregnant, switched her to sertraline.
The idea, which has been around for a long time, is that sertraline is the safest antidepressant for pregnant women because it has robust reproductive safety data and has particularly modest amounts of medication (if detected at all) in the plasma of infants of mothers who breastfeed while using the medicine. While we certainly have more safety data on SSRIs that were manufactured earlier, as compared with antidepressants that became available later, we have now accumulated data that fails to demonstrate a clear signal for teratogenicity across many antidepressants manufactured over the last 2 decades. Identifying an antidepressant for a given patient to which she will respond can be a challenging course for the patient. Achieving euthymia and subsequently switching to sertraline or another medication may only put her at risk for recurrence of depression and its attendant morbidity.
4. A change to a Category B label drug
This is another example of switching a patient to a potentially less effective drug in a somewhat misguided effort at finding a treatment that is safer in pregnancy. While the Food and Drug Administration’s drug category label system was a step forward, or at least a well intentioned effort to give women and their clinicians clearer insight into the reproductive safety of a medication, ultimately, the incomplete nature of the information caused the agency to transition to a new system (see the Pregnancy Labeling and Lactation Rule). Switching a woman to a category B medicine with sparse reproductive safety data instead of a category C medicine, which may not be unsafe but has raised some concerns in animal models, is not a better choice. The new labeling system is a step forward.
5. Discontinuation of lithium during pregnancy
Like discontinuation of antidepressants, the discontinuation of lithium during attempts to conceive in a woman whose illness has been well controlled, is associated with a high risk of relapse. In earlier work, it was sometimes recommended that discontinuation of lithium be considered after a long period of wellness. We have learned over time that this can be a risky move. Even women with a remote history of bipolar disorder appear to be at high risk of relapse when a mood stabilizer is stopped. Exquisite response to medicine does not imply less severe illness. Women who have bipolar disorder who have sustained euthymia on lithium should consider maintaining the safest possible regimen before, during, and after pregnancy despite the known small teratogenic risk associated with fetal exposure to this agent.
6. Try supplements or alternative therapies
Out of a desire to avoid any medication with incomplete reproductive safety data, some women and clinicians make the intuitive leap that “alternative treatments” can mitigate relapse in pregnancy, and they stop pharmacological treatments and switch to supplements or alternative therapies, including acupuncture, massage, or light therapy. Unfortunately, data supporting this clinical maneuver are sparse. Frequently, we see women with past histories of severe depression who have stopped antidepressants and who have started supplements as a substitute and who then relapse. Then, they try to restore euthymia with antidepressants and psychotherapy, and the road to restoration of well-being can be long.
Data on efficacy of alternative therapies continues to evolve and is an exciting and important area of research. However, where these treatments are best employed in the algorithm for treating depression in pregnancy, or at other times, has yet to be adequately defined.
7. Stop breastfeeding or defer antidepressant treatment
Many women continue to be counseled to either stop breastfeeding while using antidepressants or to defer treatment with antidepressants if they wish to breastfeed. Not uncommonly, we see women who are suffering from postpartum depression and who are engaged in psychotherapy but who have deferred treatment with antidepressants despite residual depressive symptoms that impair functioning. Clinicians should keep in mind that data supporting evidence of toxicity in newborns of women using antidepressants while breastfeeding are extremely sparse. Unfortunately, some women with postpartum depression are deferring treatment because they were counseled that it is not compatible with their desire to breastfeed.
8. Use of non-benzodiazepine sedative-hypnotics
Insomnia is a common problem in pregnancy, especially when coupled with comorbid anxiety, and, increasingly, it is being treated with non-benzodiazepine sedative-hypnotics. Clinicians should keep in mind that a known small risk may be better than an unknown risk. If a pregnant woman has severe insomnia, she may benefit from a low dose of a benzodiazepine, such as lorazepam or clonazepam, as opposed to a medication such as zolpidem for which reproductive safety data are particularly limited.
9. Pumping and dumping breast milk
Many women are advised to set an alarm to “pump and dump” their breast milk to minimize their baby’s exposure to antidepressants during breastfeeding. Early literature to pump and dump breast milk at peak antidepressant concentration was of great analytic and theoretical interest but has scant clinical application. As an author of many of those early publications, I can say that we never intended for women to sacrifice precious sleep to dump breast milk with the idea that limiting exposure to trace amounts of antidepressants would have beneficial effects over the long term.
10. Failure to bring up contraception use
We continue to see a 50% unplanned pregnancy rate across sociodemographic groups in the United States. This is a critical statistic because it may affect how treatment is managed. Bringing up the topic of reliable contraception prior to pregnancy allows for planned pregnancy and affords us the time to discuss treatment options and the ability to plot a more thoughtful and safe clinical course. However, often, contraception is not discussed.
One of our goals as clinicians is to, first, do no harm and that continues to be a challenge because the data in perinatal psychiatry is still inconsistent in some areas and there are evidence gaps in others. Nevertheless, our task is to take the best available data along with the patient’s wishes and knowledge of her past clinical history and to then translate that into the best care for the individual.
Dr. Cohen is the director of the Ammon-Pinizzotto Center for Women’s Mental Health at Massachusetts General Hospital in Boston, which provides information resources and conducts clinical care and research in reproductive mental health. He has been a consultant to manufacturers of psychiatric medications.
Understanding the human papillomavirus
Human papillomavirus (HPV) is the most prevalent sexually transmitted disease globally. It is causally related to the development of several malignancies, including cervical, anal, and oropharyngeal ones, because of its integration and dysregulation of the genome of infected cells. Fortunately, vaccination is available to prevent development of HPV-related diseases. Understanding this virus, its carcinogenic role, and the importance of prevention through vaccination are critically important for ob.gyns. This column reviews the fundamentals of HPV biology, epidemiology, and carcinogenesis.
Viral anatomy
HPV are members of the A genus of the family Papovaviridae. They contain between 7,800 and 7,900 base pairs. They are nonenveloped, double-stranded DNA viruses with a circular structure. The viral DNA is contained within an icosahedral capsid that measures 45 nm-55 nm. The HPV genome has three critical regions: the long control region, otherwise known as the upstream regulatory region; the early region; and the late region.1
Capsid proteins are similar between groups. Therefore, HPV are categorized into “types” and “subtypes” based on the extent of DNA similarity. There are more than 100 types of HPV in humans.2 The type of HPV is determined by the gene sequences of E6/E7 and L1 and must show more than 10% difference between types. The gene sequences between different subtypes differ by 2%-5%.
Epidemiology of HPV infection
HPV are widely distributed among mammalian species but are species specific. Their tissue affinity varies by type. HPV types 1, 2, and 4 cause common or plantar warts. HPV types 6 and 11 cause condyloma acuminata (genital warts) and low grade dysplasia. HPV types 16 and 18 – in addition to 31 and 52 – are of particular interest to oncologists because they are associated with lower genital tract high grade dysplasia and invasive carcinoma. Infection with HPV 16 is present in about half of invasive cervical cancers, with HPV type 18 present in 20% of cervical cancers. Adenocarcinomas of the cervix are more commonly associated with HPV 18. Anal cancer and oropharyngeal cancer are more commonly associated with HPV 16.3
HPV infections are acquired through cutaneous touching (including hand to genital) and HPV positivity is most commonly present within the first 10 years after sexual debut.4 However, most individuals who acquire HPV do so as a transient infection, which is cleared without sequelae. Those who fail to rapidly clear HPV infection, and in whom it becomes chronic, face an increasing risk of development of dysplasia and invasive carcinoma. The incidence of HPV infection increases again at menopause, but, for these older women, the new finding of HPV detection may be related to reactivation of an earlier infection rather than exclusively new exposure to the virus.5
Diagnosis and testing
HPV infection can be detected through DNA testing, RNA testing, and cellular markers.6
HPV DNA testing was the original form of testing offered. It improved the sensitivity over cytology alone in the detection of precursors to malignancy but had relatively poor specificity, resulting in a high false positive rate and unnecessary referral to colposcopy. The various tests approved by the Food and Drug Administration – Hybrid Capture 2 (HC2), Cervista, and Cobas 4800 – differ in the number and nature of HPV types that they detect.
HPV RNA testing has developed and involves measuring the expression of E6 and E7 RNA. This testing is FDA approved and has the potential to improve upon the specificity of DNA testing procedures by decreasing false positives.
Measurement of cellular markers is currently considered experimental/exploratory and is not yet FDA approved for diagnostic purposes in screening or confirmation of HPV infection or coexisting dysplasia. It involves measuring the downstream cellular targets (such as p16) of E6 or E7 activity.
The mechanism of carcinogenesis
The early region of the HPV genome is downstream from the upstream regulatory region. It codes for proteins involved in viral infection and replication. The two most important genes in the early region are E6 and E7. When integrated into the human genome of the lower genital tract cell, the viral genes E6 and E7 negatively interfere with cell cycle control and mechanisms to halt dysregulation.7
E6 and E7 are considered oncogenes because they cause loss of function of the critical tumor suppressor proteins p53 and the retinoblastoma protein. The p53 protein is typically responsible for controlling cell cycling through the G0/G1 to S phases. It involves stalling cellular mitosis in order to facilitate DNA repair mechanisms in the case of damaged cells, thereby preventing replication of DNA aberrations. The retinoblastoma protein also functions to inhibit cells that have acquired DNA damage from cycling and induces apoptosis in DNA damaged cells. When protein products of E6 and E7 negatively interact with these two tumor suppressor proteins they overcome the cell’s safeguard arrest response.
In the presence of other carcinogens, such as products of tobacco exposure, the increased DNA damage sustained by the genital tract cell is allowed to go relatively unchecked by the HPV coinfection, which has disabled tumor suppressor function. This facilitates immortality of the damaged cell, amplification of additional DNA mutations, and unchecked cellular growth and dysplastic transformation. E6 and E7 are strongly expressed in invasive genital tract lesions to support its important role in carcinogenesis.
HIV coinfection is another factor that promotes carcinogenesis following HPV infection because it inhibits clearance of the virus through T-cell mediated immunosuppression and directly enhances expression of E6 and E7 proteins in the HIV and HPV coinfected cell.8 For these reasons, HIV-positive women are less likely to clear HPV infection and more likely to develop high grade dysplasia or invasive carcinomas.
Prevention and vaccination
HPV vaccinations utilize virus-like particles (VLPs). These VLPs are capsid particles generated from the L1 region of the HPV DNA. The capsid proteins coded for by L1 are highly immunogenic. VLPs are recombinant proteins created in benign biologic systems (such as yeast) and contain no inner DNA core (effectively empty viral capsids) and therefore are not infectious. The L1 gene is incorporated into a plasmid, which is inserted into the nucleus of a eukaryotic cell. Transcription and translation of the L1 gene takes place, creating capsid proteins that self-assemble into VLPs. These VLPs are retrieved and inoculated into candidate patients to illicit an immune response.
Quadrivalent, nine-valent, and bivalent vaccines are available worldwide. However, only the nine-valent vaccine – protective against types 6, 11, 16, 18, 31, 33, 45, 52, and 58 – is available in the United States. This theoretically provides more comprehensive coverage against cervical cancer–causing HPV types, as 70% of cervical cancer is attributable to HPV 16 and 18, but an additional 20% is attributable to HPV 31, 33, 45, 52, and 58. This vaccine also provides protection against the HPV strains that cause genital warts and low-grade dysplastic changes.9
HPV, in most instances, is a transient virus with no sequelae. However, if not cleared from the cells of the lower genital tract, anus, or oropharynx it can result in the breakdown of cellular correction strategies and culminate in invasive carcinoma. Fortunately, highly effective and safe vaccinations are available and should be broadly prescribed.
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. Cancer Epidemiol Biomarkers Prev. 1995 Jun;4(4):415-28.
2. Gynecol Oncol. 2011 Apr;121(1):32-42.
3. Cancer Epidemiol Biomarkers Prev. 2008 Jul;17(7):1611-22.
4. JAMA. 2007 Feb 28;297(8):813-9.
5. J Infect Dis. 2013; 207(2): 272-80.
6. J Natl Cancer Inst. 2011 Mar 2;103(5):368-83.
7. J Natl Cancer Inst. 2000 May 3;92(9):690-8.
8. Lancet. 2002 Jan 12;359(9301):108-13.
9. Obstet Gynecol 2017;129:e173–8.
Human papillomavirus (HPV) is the most prevalent sexually transmitted disease globally. It is causally related to the development of several malignancies, including cervical, anal, and oropharyngeal ones, because of its integration and dysregulation of the genome of infected cells. Fortunately, vaccination is available to prevent development of HPV-related diseases. Understanding this virus, its carcinogenic role, and the importance of prevention through vaccination are critically important for ob.gyns. This column reviews the fundamentals of HPV biology, epidemiology, and carcinogenesis.
Viral anatomy
HPV are members of the A genus of the family Papovaviridae. They contain between 7,800 and 7,900 base pairs. They are nonenveloped, double-stranded DNA viruses with a circular structure. The viral DNA is contained within an icosahedral capsid that measures 45 nm-55 nm. The HPV genome has three critical regions: the long control region, otherwise known as the upstream regulatory region; the early region; and the late region.1
Capsid proteins are similar between groups. Therefore, HPV are categorized into “types” and “subtypes” based on the extent of DNA similarity. There are more than 100 types of HPV in humans.2 The type of HPV is determined by the gene sequences of E6/E7 and L1 and must show more than 10% difference between types. The gene sequences between different subtypes differ by 2%-5%.
Epidemiology of HPV infection
HPV are widely distributed among mammalian species but are species specific. Their tissue affinity varies by type. HPV types 1, 2, and 4 cause common or plantar warts. HPV types 6 and 11 cause condyloma acuminata (genital warts) and low grade dysplasia. HPV types 16 and 18 – in addition to 31 and 52 – are of particular interest to oncologists because they are associated with lower genital tract high grade dysplasia and invasive carcinoma. Infection with HPV 16 is present in about half of invasive cervical cancers, with HPV type 18 present in 20% of cervical cancers. Adenocarcinomas of the cervix are more commonly associated with HPV 18. Anal cancer and oropharyngeal cancer are more commonly associated with HPV 16.3
HPV infections are acquired through cutaneous touching (including hand to genital) and HPV positivity is most commonly present within the first 10 years after sexual debut.4 However, most individuals who acquire HPV do so as a transient infection, which is cleared without sequelae. Those who fail to rapidly clear HPV infection, and in whom it becomes chronic, face an increasing risk of development of dysplasia and invasive carcinoma. The incidence of HPV infection increases again at menopause, but, for these older women, the new finding of HPV detection may be related to reactivation of an earlier infection rather than exclusively new exposure to the virus.5
Diagnosis and testing
HPV infection can be detected through DNA testing, RNA testing, and cellular markers.6
HPV DNA testing was the original form of testing offered. It improved the sensitivity over cytology alone in the detection of precursors to malignancy but had relatively poor specificity, resulting in a high false positive rate and unnecessary referral to colposcopy. The various tests approved by the Food and Drug Administration – Hybrid Capture 2 (HC2), Cervista, and Cobas 4800 – differ in the number and nature of HPV types that they detect.
HPV RNA testing has developed and involves measuring the expression of E6 and E7 RNA. This testing is FDA approved and has the potential to improve upon the specificity of DNA testing procedures by decreasing false positives.
Measurement of cellular markers is currently considered experimental/exploratory and is not yet FDA approved for diagnostic purposes in screening or confirmation of HPV infection or coexisting dysplasia. It involves measuring the downstream cellular targets (such as p16) of E6 or E7 activity.
The mechanism of carcinogenesis
The early region of the HPV genome is downstream from the upstream regulatory region. It codes for proteins involved in viral infection and replication. The two most important genes in the early region are E6 and E7. When integrated into the human genome of the lower genital tract cell, the viral genes E6 and E7 negatively interfere with cell cycle control and mechanisms to halt dysregulation.7
E6 and E7 are considered oncogenes because they cause loss of function of the critical tumor suppressor proteins p53 and the retinoblastoma protein. The p53 protein is typically responsible for controlling cell cycling through the G0/G1 to S phases. It involves stalling cellular mitosis in order to facilitate DNA repair mechanisms in the case of damaged cells, thereby preventing replication of DNA aberrations. The retinoblastoma protein also functions to inhibit cells that have acquired DNA damage from cycling and induces apoptosis in DNA damaged cells. When protein products of E6 and E7 negatively interact with these two tumor suppressor proteins they overcome the cell’s safeguard arrest response.
In the presence of other carcinogens, such as products of tobacco exposure, the increased DNA damage sustained by the genital tract cell is allowed to go relatively unchecked by the HPV coinfection, which has disabled tumor suppressor function. This facilitates immortality of the damaged cell, amplification of additional DNA mutations, and unchecked cellular growth and dysplastic transformation. E6 and E7 are strongly expressed in invasive genital tract lesions to support its important role in carcinogenesis.
HIV coinfection is another factor that promotes carcinogenesis following HPV infection because it inhibits clearance of the virus through T-cell mediated immunosuppression and directly enhances expression of E6 and E7 proteins in the HIV and HPV coinfected cell.8 For these reasons, HIV-positive women are less likely to clear HPV infection and more likely to develop high grade dysplasia or invasive carcinomas.
Prevention and vaccination
HPV vaccinations utilize virus-like particles (VLPs). These VLPs are capsid particles generated from the L1 region of the HPV DNA. The capsid proteins coded for by L1 are highly immunogenic. VLPs are recombinant proteins created in benign biologic systems (such as yeast) and contain no inner DNA core (effectively empty viral capsids) and therefore are not infectious. The L1 gene is incorporated into a plasmid, which is inserted into the nucleus of a eukaryotic cell. Transcription and translation of the L1 gene takes place, creating capsid proteins that self-assemble into VLPs. These VLPs are retrieved and inoculated into candidate patients to illicit an immune response.
Quadrivalent, nine-valent, and bivalent vaccines are available worldwide. However, only the nine-valent vaccine – protective against types 6, 11, 16, 18, 31, 33, 45, 52, and 58 – is available in the United States. This theoretically provides more comprehensive coverage against cervical cancer–causing HPV types, as 70% of cervical cancer is attributable to HPV 16 and 18, but an additional 20% is attributable to HPV 31, 33, 45, 52, and 58. This vaccine also provides protection against the HPV strains that cause genital warts and low-grade dysplastic changes.9
HPV, in most instances, is a transient virus with no sequelae. However, if not cleared from the cells of the lower genital tract, anus, or oropharynx it can result in the breakdown of cellular correction strategies and culminate in invasive carcinoma. Fortunately, highly effective and safe vaccinations are available and should be broadly prescribed.
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. Cancer Epidemiol Biomarkers Prev. 1995 Jun;4(4):415-28.
2. Gynecol Oncol. 2011 Apr;121(1):32-42.
3. Cancer Epidemiol Biomarkers Prev. 2008 Jul;17(7):1611-22.
4. JAMA. 2007 Feb 28;297(8):813-9.
5. J Infect Dis. 2013; 207(2): 272-80.
6. J Natl Cancer Inst. 2011 Mar 2;103(5):368-83.
7. J Natl Cancer Inst. 2000 May 3;92(9):690-8.
8. Lancet. 2002 Jan 12;359(9301):108-13.
9. Obstet Gynecol 2017;129:e173–8.
Human papillomavirus (HPV) is the most prevalent sexually transmitted disease globally. It is causally related to the development of several malignancies, including cervical, anal, and oropharyngeal ones, because of its integration and dysregulation of the genome of infected cells. Fortunately, vaccination is available to prevent development of HPV-related diseases. Understanding this virus, its carcinogenic role, and the importance of prevention through vaccination are critically important for ob.gyns. This column reviews the fundamentals of HPV biology, epidemiology, and carcinogenesis.
Viral anatomy
HPV are members of the A genus of the family Papovaviridae. They contain between 7,800 and 7,900 base pairs. They are nonenveloped, double-stranded DNA viruses with a circular structure. The viral DNA is contained within an icosahedral capsid that measures 45 nm-55 nm. The HPV genome has three critical regions: the long control region, otherwise known as the upstream regulatory region; the early region; and the late region.1
Capsid proteins are similar between groups. Therefore, HPV are categorized into “types” and “subtypes” based on the extent of DNA similarity. There are more than 100 types of HPV in humans.2 The type of HPV is determined by the gene sequences of E6/E7 and L1 and must show more than 10% difference between types. The gene sequences between different subtypes differ by 2%-5%.
Epidemiology of HPV infection
HPV are widely distributed among mammalian species but are species specific. Their tissue affinity varies by type. HPV types 1, 2, and 4 cause common or plantar warts. HPV types 6 and 11 cause condyloma acuminata (genital warts) and low grade dysplasia. HPV types 16 and 18 – in addition to 31 and 52 – are of particular interest to oncologists because they are associated with lower genital tract high grade dysplasia and invasive carcinoma. Infection with HPV 16 is present in about half of invasive cervical cancers, with HPV type 18 present in 20% of cervical cancers. Adenocarcinomas of the cervix are more commonly associated with HPV 18. Anal cancer and oropharyngeal cancer are more commonly associated with HPV 16.3
HPV infections are acquired through cutaneous touching (including hand to genital) and HPV positivity is most commonly present within the first 10 years after sexual debut.4 However, most individuals who acquire HPV do so as a transient infection, which is cleared without sequelae. Those who fail to rapidly clear HPV infection, and in whom it becomes chronic, face an increasing risk of development of dysplasia and invasive carcinoma. The incidence of HPV infection increases again at menopause, but, for these older women, the new finding of HPV detection may be related to reactivation of an earlier infection rather than exclusively new exposure to the virus.5
Diagnosis and testing
HPV infection can be detected through DNA testing, RNA testing, and cellular markers.6
HPV DNA testing was the original form of testing offered. It improved the sensitivity over cytology alone in the detection of precursors to malignancy but had relatively poor specificity, resulting in a high false positive rate and unnecessary referral to colposcopy. The various tests approved by the Food and Drug Administration – Hybrid Capture 2 (HC2), Cervista, and Cobas 4800 – differ in the number and nature of HPV types that they detect.
HPV RNA testing has developed and involves measuring the expression of E6 and E7 RNA. This testing is FDA approved and has the potential to improve upon the specificity of DNA testing procedures by decreasing false positives.
Measurement of cellular markers is currently considered experimental/exploratory and is not yet FDA approved for diagnostic purposes in screening or confirmation of HPV infection or coexisting dysplasia. It involves measuring the downstream cellular targets (such as p16) of E6 or E7 activity.
The mechanism of carcinogenesis
The early region of the HPV genome is downstream from the upstream regulatory region. It codes for proteins involved in viral infection and replication. The two most important genes in the early region are E6 and E7. When integrated into the human genome of the lower genital tract cell, the viral genes E6 and E7 negatively interfere with cell cycle control and mechanisms to halt dysregulation.7
E6 and E7 are considered oncogenes because they cause loss of function of the critical tumor suppressor proteins p53 and the retinoblastoma protein. The p53 protein is typically responsible for controlling cell cycling through the G0/G1 to S phases. It involves stalling cellular mitosis in order to facilitate DNA repair mechanisms in the case of damaged cells, thereby preventing replication of DNA aberrations. The retinoblastoma protein also functions to inhibit cells that have acquired DNA damage from cycling and induces apoptosis in DNA damaged cells. When protein products of E6 and E7 negatively interact with these two tumor suppressor proteins they overcome the cell’s safeguard arrest response.
In the presence of other carcinogens, such as products of tobacco exposure, the increased DNA damage sustained by the genital tract cell is allowed to go relatively unchecked by the HPV coinfection, which has disabled tumor suppressor function. This facilitates immortality of the damaged cell, amplification of additional DNA mutations, and unchecked cellular growth and dysplastic transformation. E6 and E7 are strongly expressed in invasive genital tract lesions to support its important role in carcinogenesis.
HIV coinfection is another factor that promotes carcinogenesis following HPV infection because it inhibits clearance of the virus through T-cell mediated immunosuppression and directly enhances expression of E6 and E7 proteins in the HIV and HPV coinfected cell.8 For these reasons, HIV-positive women are less likely to clear HPV infection and more likely to develop high grade dysplasia or invasive carcinomas.
Prevention and vaccination
HPV vaccinations utilize virus-like particles (VLPs). These VLPs are capsid particles generated from the L1 region of the HPV DNA. The capsid proteins coded for by L1 are highly immunogenic. VLPs are recombinant proteins created in benign biologic systems (such as yeast) and contain no inner DNA core (effectively empty viral capsids) and therefore are not infectious. The L1 gene is incorporated into a plasmid, which is inserted into the nucleus of a eukaryotic cell. Transcription and translation of the L1 gene takes place, creating capsid proteins that self-assemble into VLPs. These VLPs are retrieved and inoculated into candidate patients to illicit an immune response.
Quadrivalent, nine-valent, and bivalent vaccines are available worldwide. However, only the nine-valent vaccine – protective against types 6, 11, 16, 18, 31, 33, 45, 52, and 58 – is available in the United States. This theoretically provides more comprehensive coverage against cervical cancer–causing HPV types, as 70% of cervical cancer is attributable to HPV 16 and 18, but an additional 20% is attributable to HPV 31, 33, 45, 52, and 58. This vaccine also provides protection against the HPV strains that cause genital warts and low-grade dysplastic changes.9
HPV, in most instances, is a transient virus with no sequelae. However, if not cleared from the cells of the lower genital tract, anus, or oropharynx it can result in the breakdown of cellular correction strategies and culminate in invasive carcinoma. Fortunately, highly effective and safe vaccinations are available and should be broadly prescribed.
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. Cancer Epidemiol Biomarkers Prev. 1995 Jun;4(4):415-28.
2. Gynecol Oncol. 2011 Apr;121(1):32-42.
3. Cancer Epidemiol Biomarkers Prev. 2008 Jul;17(7):1611-22.
4. JAMA. 2007 Feb 28;297(8):813-9.
5. J Infect Dis. 2013; 207(2): 272-80.
6. J Natl Cancer Inst. 2011 Mar 2;103(5):368-83.
7. J Natl Cancer Inst. 2000 May 3;92(9):690-8.
8. Lancet. 2002 Jan 12;359(9301):108-13.
9. Obstet Gynecol 2017;129:e173–8.
Not so fast
If you are a busy primary care physician, wouldn’t you like to get some quick confirmation that your patient with a fever and runny nose has a viral upper respiratory infection? If there were a test or a simple physical finding that could give you the answer while the patient was still in the office, you could dispense a quick dose of reassurance and send him or her on their way. It would probably help you inch a bit closer to relieving the congestion in your waiting room.
I am sure most of you realize that relying on the patient’s temperature or the color of his or her nasal mucus is not going to give you that reliable and swift answer you would like. There have been rapid diagnostic tests for influenza on the market for several years, but I have not been aware of a similar test for rhinovirus. But I recently came across a study that offers some hope that such a test might become a reality in the future (EBioMedicine. 2017 Mar;17:172-81). In the study, researchers at Duke University and elsewhere identified a group of proteins in mucus that can confirm – with 86% accuracy – that the patient is infected with a cold or flu virus. They anticipate that this discovery could be adapted into a rapid test that could be performed in the doctor’s office.
However, I am sure that most of you would do a careful exam and spend a few minutes on a slightly more detailed discussion of what worrisome symptoms the parents should be watching for. But let’s be honest. Isn’t it likely that knowing that the patient has a rhinovirus infection might derail your diagnostic process short of a full consideration? Isn’t it tempting to say to yourself, “He only has a viral URI, and I even know the name of the virus. My job is done.”
Although the odds are that the virus is causing all your patient’s symptoms, there is always the chance that he or she is harboring a bacterial coinfection. Or, that what appears to be “only” a virus is actually an early step in the deadly spiral of the first episode of diabetic ketoacidosis.
This quandary is another example of the paradox in which more information can make your job as a diagnostician more difficult. Does your patient’s positive rapid strep test mean that strep is the primary cause of your patient’s fever and sore throat? Couldn’t he or she just be a carrier? Should a positive test that confirms your clinical impression put an end to your evaluation of the patient?
You could answer that you don’t have the time to go looking for zebra stripes hidden on the underbelly of every equine that gallops into your exam room. Of course you don’t. But, you are obligated to keep your mind open to the possibility that a lab test promising to make your job easy may not be telling you the whole story.
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.” Email him at pdnews@frontlinemedcom.com.
If you are a busy primary care physician, wouldn’t you like to get some quick confirmation that your patient with a fever and runny nose has a viral upper respiratory infection? If there were a test or a simple physical finding that could give you the answer while the patient was still in the office, you could dispense a quick dose of reassurance and send him or her on their way. It would probably help you inch a bit closer to relieving the congestion in your waiting room.
I am sure most of you realize that relying on the patient’s temperature or the color of his or her nasal mucus is not going to give you that reliable and swift answer you would like. There have been rapid diagnostic tests for influenza on the market for several years, but I have not been aware of a similar test for rhinovirus. But I recently came across a study that offers some hope that such a test might become a reality in the future (EBioMedicine. 2017 Mar;17:172-81). In the study, researchers at Duke University and elsewhere identified a group of proteins in mucus that can confirm – with 86% accuracy – that the patient is infected with a cold or flu virus. They anticipate that this discovery could be adapted into a rapid test that could be performed in the doctor’s office.
However, I am sure that most of you would do a careful exam and spend a few minutes on a slightly more detailed discussion of what worrisome symptoms the parents should be watching for. But let’s be honest. Isn’t it likely that knowing that the patient has a rhinovirus infection might derail your diagnostic process short of a full consideration? Isn’t it tempting to say to yourself, “He only has a viral URI, and I even know the name of the virus. My job is done.”
Although the odds are that the virus is causing all your patient’s symptoms, there is always the chance that he or she is harboring a bacterial coinfection. Or, that what appears to be “only” a virus is actually an early step in the deadly spiral of the first episode of diabetic ketoacidosis.
This quandary is another example of the paradox in which more information can make your job as a diagnostician more difficult. Does your patient’s positive rapid strep test mean that strep is the primary cause of your patient’s fever and sore throat? Couldn’t he or she just be a carrier? Should a positive test that confirms your clinical impression put an end to your evaluation of the patient?
You could answer that you don’t have the time to go looking for zebra stripes hidden on the underbelly of every equine that gallops into your exam room. Of course you don’t. But, you are obligated to keep your mind open to the possibility that a lab test promising to make your job easy may not be telling you the whole story.
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.” Email him at pdnews@frontlinemedcom.com.
If you are a busy primary care physician, wouldn’t you like to get some quick confirmation that your patient with a fever and runny nose has a viral upper respiratory infection? If there were a test or a simple physical finding that could give you the answer while the patient was still in the office, you could dispense a quick dose of reassurance and send him or her on their way. It would probably help you inch a bit closer to relieving the congestion in your waiting room.
I am sure most of you realize that relying on the patient’s temperature or the color of his or her nasal mucus is not going to give you that reliable and swift answer you would like. There have been rapid diagnostic tests for influenza on the market for several years, but I have not been aware of a similar test for rhinovirus. But I recently came across a study that offers some hope that such a test might become a reality in the future (EBioMedicine. 2017 Mar;17:172-81). In the study, researchers at Duke University and elsewhere identified a group of proteins in mucus that can confirm – with 86% accuracy – that the patient is infected with a cold or flu virus. They anticipate that this discovery could be adapted into a rapid test that could be performed in the doctor’s office.
However, I am sure that most of you would do a careful exam and spend a few minutes on a slightly more detailed discussion of what worrisome symptoms the parents should be watching for. But let’s be honest. Isn’t it likely that knowing that the patient has a rhinovirus infection might derail your diagnostic process short of a full consideration? Isn’t it tempting to say to yourself, “He only has a viral URI, and I even know the name of the virus. My job is done.”
Although the odds are that the virus is causing all your patient’s symptoms, there is always the chance that he or she is harboring a bacterial coinfection. Or, that what appears to be “only” a virus is actually an early step in the deadly spiral of the first episode of diabetic ketoacidosis.
This quandary is another example of the paradox in which more information can make your job as a diagnostician more difficult. Does your patient’s positive rapid strep test mean that strep is the primary cause of your patient’s fever and sore throat? Couldn’t he or she just be a carrier? Should a positive test that confirms your clinical impression put an end to your evaluation of the patient?
You could answer that you don’t have the time to go looking for zebra stripes hidden on the underbelly of every equine that gallops into your exam room. Of course you don’t. But, you are obligated to keep your mind open to the possibility that a lab test promising to make your job easy may not be telling you the whole story.
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.” Email him at pdnews@frontlinemedcom.com.
Pre- and postprocedure skin care guide for your surgical patients
Whether patients are having a biopsy, surgical excision, or Mohs surgery, the outcome will be improved when the proper skin care is used before and after the procedure. This is a guide that you can use to educate your patients about pre- and postprocedure skin care needs.
Presurgery skin care and supplements
The goal is to speed healing and minimize infection, scarring, and hyperpigmentation. For 2 weeks prior to surgery, recommend products that have been shown to speed wound healing by increasing keratinization and/or collagen production. Ingredients that should be used prior to wounding include retinoids such as tretinoin and retinol. Several studies have convincingly shown that pretreatment with tretinoin speeds wound healing.1,2,3 Kligman and associates evaluated healing after punch biopsy and found the wounds on arms pretreated with tretinoin cream 0.05% to 0.1% were significantly smaller – by 35% to 37% – on days 1 and 4, and were 47% to 50% smaller on days 6, 8, and 11, compared with the untreated arms.4 Most studies suggest a 2- to 4-week tretinoin pretreatment regimen5 because peak epidermal hypertrophy occurs after 7 days of tretinoin application and normalizes after 14 days of continued treatment.6 This approach allows the skin to recover from any retinoid dermatitis prior to surgery. Adapalene should be started 5-6 weeks prior to procedures because it has a longer half-life and requires an earlier initiation period.7
Although wound healing studies have not been conducted in this area, pretreating skin with topical ascorbic acid8 and hydroxyacids9 might help speed wound healing by increasing collagen synthesis.
Ingredients and activities to avoid presurgery
Patients should avoid using ingredients that could promote skin tumor growth. Although there are no studies evaluating the effects of growth factors on promoting the growth of skin cancer, caution is prudent. To reduce bruising, patients should avoid aspirin, ibuprofen, naproxen, St. John’s Wort, vitamin E, omega-3 fatty acids supplements, flax seed oil, ginseng, salmon, and alcohol. Most physicians agree that these should be avoided for 10 days prior to the procedure. Smoking should be avoided 4 weeks prior to the procedure.
Postsurgery skin care and supplements
Oral vitamin C and zinc supplements have been shown to speed wound healing in rats when taken immediately after a procedure.10 Oral Arnica tablets and tinctures are often used prior to and after surgery to reduce bruising and inflammation. There is much anecdotal support for the use of Arnica, but clinical trial evidence substantiating its efficacy to prevent bruising and reduce swelling is scant.
A protein important in wound repair, defensin, is available in a topical formulation. Defensin14 has been shown to activate the leucine-rich repeat-containing G-protein–coupled receptors 5 and 6 (also known as LGR5 and LGR6) stem cells. It speeds wound healing by increasing LGR stem cell migration into wound beds. Wounds should be covered to provide protection from sun exposure until reepithelialization occurs. Which occlusive ointments and wound repair products to use are beyond the scope of this article. Once epithelized, zinc oxide sunscreens can be used. These have been shown to be safe with minimal penetration into the skin.15
Ingredients to avoid post surgery
Topical retinoids should not be used post skin cancer surgery until epithelialization is complete. A study by Hung et al.16 in a porcine model used 0.05% tretinoin cream daily for 10 days prior to partial-thickness skin wounding demonstrated that use of tretinoin 10 days prior to wounding sped reepithelialization while use after the procedure slowed wound healing.
Acidic products will sting wounded skin. For this reason, benzoic acid, hydroxy acids, and ascorbic acid should be avoided until the skin has completely reepithelialized. Products with preservatives and fragrance should be avoided if possible.
Vitamin E derived from oral supplement capsules slowed healing after skin cancer surgery and had a high rate of contact dermatitis.17 Chemical sunscreens are more likely to cause an allergic contact dermatitis and should be avoided for 4 weeks after skin surgery. Organic products with essential oils and botanical ingredients may present a higher risk of contact dermatitis due to allergen exposure.
Conclusion
To ensure the best outcome from surgical treatments, patient education is a must! The more that patients know and understand about the ways in which they can prepare for their procedure and treat their skin after the procedure, the better the outcomes will be. Providers should give this type of information in an easy-to-follow printed instruction sheet because studies show that patients cannot remember most of the oral instructions offered by practitioners.
Encourage your patients to ask questions during their consultation and procedure and to get in touch with your office should they have any concerns when they leave. These steps help improve patient compliance and satisfaction, which will help you maintain a trusting relationship with established patients and attract new ones through word-of-mouth referrals.
Please email me at DrB@skintypesolutions.com if you have any other pre- and postprocedure skin care advice.
Dr. Leslie S. Baumann is a private practice dermatologist, researcher, author, and entrepreneur who practices in Miami. She founded the Cosmetic Dermatology Center at the University of Miami in 1997. Dr. Baumann wrote two textbooks: “Cosmetic Dermatology: Principles and Practice” (New York: McGraw-Hill, 2002), and “Cosmeceuticals and Cosmetic Ingredients,” (New York: McGraw-Hill, 2014), and a New York Times Best Sellers book for consumers, “The Skin Type Solution” (New York: Bantam Dell, 2006). Dr. Baumann has received funding for advisory boards and/or clinical research trials from Allergan, Evolus, Galderma, and Revance. She is the founder and CEO of Skin Type Solutions Franchise Systems LLC.
References
1. Aesthetic Plast Surg. 1995 May-Jun;19(3):243-6.
2. Plast Reconstr Surg. 2011 Mar;127(3):1343-5.
3. J Am Acad Dermatol. 1998 Aug;39(2 Pt 3):S79-81.
4. Br J Dermatol. 1995 Jan;132(1):46-53.
5. J Am Acad Dermatol. 2004 Dec;51(6):940-6.
6. J Korean Med Sci. 1996 Aug;11(4):335-41.
7. Eur J Dermatol. 2002 Mar-Apr;12(2):145-8.
8. Proc Natl Acad Sci U S A. 1981 May;78(5):2879-82.
9. Exp Dermatol. 2003;12 Suppl 2:57-63.
10. Surg Today. 2004;34(9):747-51.
11. Ophthal Plast Reconstr Surg. 2017 Jan/Feb;33(1):47-52.
12. Wound Repair Regen. 1998 Mar-Apr;6(2):167-77.
13. Dermatol Surg. 1998 Jun;24(6):661-4.
14. Plast Reconstr Surg. 2013 Nov;132(5):1159-71.
15. ACS Nano. 2016 Feb 23;10(2):1810-9.
16. Arch Dermatol. 1989 Jan;125(1):65-9.
17. Dermatol Surg. 1999 Apr;25(4):311-5.
Retinoids should be used 2-3 times prior to procedures to speed healing.
Retinoids should not be used after the procedure until reepithelization has occurred.
Vitamin C and zinc supplements taken post procedure might speed wound healing.
Retinoids should be used 2-3 times prior to procedures to speed healing.
Retinoids should not be used after the procedure until reepithelization has occurred.
Vitamin C and zinc supplements taken post procedure might speed wound healing.
Retinoids should be used 2-3 times prior to procedures to speed healing.
Retinoids should not be used after the procedure until reepithelization has occurred.
Vitamin C and zinc supplements taken post procedure might speed wound healing.
Whether patients are having a biopsy, surgical excision, or Mohs surgery, the outcome will be improved when the proper skin care is used before and after the procedure. This is a guide that you can use to educate your patients about pre- and postprocedure skin care needs.
Presurgery skin care and supplements
The goal is to speed healing and minimize infection, scarring, and hyperpigmentation. For 2 weeks prior to surgery, recommend products that have been shown to speed wound healing by increasing keratinization and/or collagen production. Ingredients that should be used prior to wounding include retinoids such as tretinoin and retinol. Several studies have convincingly shown that pretreatment with tretinoin speeds wound healing.1,2,3 Kligman and associates evaluated healing after punch biopsy and found the wounds on arms pretreated with tretinoin cream 0.05% to 0.1% were significantly smaller – by 35% to 37% – on days 1 and 4, and were 47% to 50% smaller on days 6, 8, and 11, compared with the untreated arms.4 Most studies suggest a 2- to 4-week tretinoin pretreatment regimen5 because peak epidermal hypertrophy occurs after 7 days of tretinoin application and normalizes after 14 days of continued treatment.6 This approach allows the skin to recover from any retinoid dermatitis prior to surgery. Adapalene should be started 5-6 weeks prior to procedures because it has a longer half-life and requires an earlier initiation period.7
Although wound healing studies have not been conducted in this area, pretreating skin with topical ascorbic acid8 and hydroxyacids9 might help speed wound healing by increasing collagen synthesis.
Ingredients and activities to avoid presurgery
Patients should avoid using ingredients that could promote skin tumor growth. Although there are no studies evaluating the effects of growth factors on promoting the growth of skin cancer, caution is prudent. To reduce bruising, patients should avoid aspirin, ibuprofen, naproxen, St. John’s Wort, vitamin E, omega-3 fatty acids supplements, flax seed oil, ginseng, salmon, and alcohol. Most physicians agree that these should be avoided for 10 days prior to the procedure. Smoking should be avoided 4 weeks prior to the procedure.
Postsurgery skin care and supplements
Oral vitamin C and zinc supplements have been shown to speed wound healing in rats when taken immediately after a procedure.10 Oral Arnica tablets and tinctures are often used prior to and after surgery to reduce bruising and inflammation. There is much anecdotal support for the use of Arnica, but clinical trial evidence substantiating its efficacy to prevent bruising and reduce swelling is scant.
A protein important in wound repair, defensin, is available in a topical formulation. Defensin14 has been shown to activate the leucine-rich repeat-containing G-protein–coupled receptors 5 and 6 (also known as LGR5 and LGR6) stem cells. It speeds wound healing by increasing LGR stem cell migration into wound beds. Wounds should be covered to provide protection from sun exposure until reepithelialization occurs. Which occlusive ointments and wound repair products to use are beyond the scope of this article. Once epithelized, zinc oxide sunscreens can be used. These have been shown to be safe with minimal penetration into the skin.15
Ingredients to avoid post surgery
Topical retinoids should not be used post skin cancer surgery until epithelialization is complete. A study by Hung et al.16 in a porcine model used 0.05% tretinoin cream daily for 10 days prior to partial-thickness skin wounding demonstrated that use of tretinoin 10 days prior to wounding sped reepithelialization while use after the procedure slowed wound healing.
Acidic products will sting wounded skin. For this reason, benzoic acid, hydroxy acids, and ascorbic acid should be avoided until the skin has completely reepithelialized. Products with preservatives and fragrance should be avoided if possible.
Vitamin E derived from oral supplement capsules slowed healing after skin cancer surgery and had a high rate of contact dermatitis.17 Chemical sunscreens are more likely to cause an allergic contact dermatitis and should be avoided for 4 weeks after skin surgery. Organic products with essential oils and botanical ingredients may present a higher risk of contact dermatitis due to allergen exposure.
Conclusion
To ensure the best outcome from surgical treatments, patient education is a must! The more that patients know and understand about the ways in which they can prepare for their procedure and treat their skin after the procedure, the better the outcomes will be. Providers should give this type of information in an easy-to-follow printed instruction sheet because studies show that patients cannot remember most of the oral instructions offered by practitioners.
Encourage your patients to ask questions during their consultation and procedure and to get in touch with your office should they have any concerns when they leave. These steps help improve patient compliance and satisfaction, which will help you maintain a trusting relationship with established patients and attract new ones through word-of-mouth referrals.
Please email me at DrB@skintypesolutions.com if you have any other pre- and postprocedure skin care advice.
Dr. Leslie S. Baumann is a private practice dermatologist, researcher, author, and entrepreneur who practices in Miami. She founded the Cosmetic Dermatology Center at the University of Miami in 1997. Dr. Baumann wrote two textbooks: “Cosmetic Dermatology: Principles and Practice” (New York: McGraw-Hill, 2002), and “Cosmeceuticals and Cosmetic Ingredients,” (New York: McGraw-Hill, 2014), and a New York Times Best Sellers book for consumers, “The Skin Type Solution” (New York: Bantam Dell, 2006). Dr. Baumann has received funding for advisory boards and/or clinical research trials from Allergan, Evolus, Galderma, and Revance. She is the founder and CEO of Skin Type Solutions Franchise Systems LLC.
References
1. Aesthetic Plast Surg. 1995 May-Jun;19(3):243-6.
2. Plast Reconstr Surg. 2011 Mar;127(3):1343-5.
3. J Am Acad Dermatol. 1998 Aug;39(2 Pt 3):S79-81.
4. Br J Dermatol. 1995 Jan;132(1):46-53.
5. J Am Acad Dermatol. 2004 Dec;51(6):940-6.
6. J Korean Med Sci. 1996 Aug;11(4):335-41.
7. Eur J Dermatol. 2002 Mar-Apr;12(2):145-8.
8. Proc Natl Acad Sci U S A. 1981 May;78(5):2879-82.
9. Exp Dermatol. 2003;12 Suppl 2:57-63.
10. Surg Today. 2004;34(9):747-51.
11. Ophthal Plast Reconstr Surg. 2017 Jan/Feb;33(1):47-52.
12. Wound Repair Regen. 1998 Mar-Apr;6(2):167-77.
13. Dermatol Surg. 1998 Jun;24(6):661-4.
14. Plast Reconstr Surg. 2013 Nov;132(5):1159-71.
15. ACS Nano. 2016 Feb 23;10(2):1810-9.
16. Arch Dermatol. 1989 Jan;125(1):65-9.
17. Dermatol Surg. 1999 Apr;25(4):311-5.
Whether patients are having a biopsy, surgical excision, or Mohs surgery, the outcome will be improved when the proper skin care is used before and after the procedure. This is a guide that you can use to educate your patients about pre- and postprocedure skin care needs.
Presurgery skin care and supplements
The goal is to speed healing and minimize infection, scarring, and hyperpigmentation. For 2 weeks prior to surgery, recommend products that have been shown to speed wound healing by increasing keratinization and/or collagen production. Ingredients that should be used prior to wounding include retinoids such as tretinoin and retinol. Several studies have convincingly shown that pretreatment with tretinoin speeds wound healing.1,2,3 Kligman and associates evaluated healing after punch biopsy and found the wounds on arms pretreated with tretinoin cream 0.05% to 0.1% were significantly smaller – by 35% to 37% – on days 1 and 4, and were 47% to 50% smaller on days 6, 8, and 11, compared with the untreated arms.4 Most studies suggest a 2- to 4-week tretinoin pretreatment regimen5 because peak epidermal hypertrophy occurs after 7 days of tretinoin application and normalizes after 14 days of continued treatment.6 This approach allows the skin to recover from any retinoid dermatitis prior to surgery. Adapalene should be started 5-6 weeks prior to procedures because it has a longer half-life and requires an earlier initiation period.7
Although wound healing studies have not been conducted in this area, pretreating skin with topical ascorbic acid8 and hydroxyacids9 might help speed wound healing by increasing collagen synthesis.
Ingredients and activities to avoid presurgery
Patients should avoid using ingredients that could promote skin tumor growth. Although there are no studies evaluating the effects of growth factors on promoting the growth of skin cancer, caution is prudent. To reduce bruising, patients should avoid aspirin, ibuprofen, naproxen, St. John’s Wort, vitamin E, omega-3 fatty acids supplements, flax seed oil, ginseng, salmon, and alcohol. Most physicians agree that these should be avoided for 10 days prior to the procedure. Smoking should be avoided 4 weeks prior to the procedure.
Postsurgery skin care and supplements
Oral vitamin C and zinc supplements have been shown to speed wound healing in rats when taken immediately after a procedure.10 Oral Arnica tablets and tinctures are often used prior to and after surgery to reduce bruising and inflammation. There is much anecdotal support for the use of Arnica, but clinical trial evidence substantiating its efficacy to prevent bruising and reduce swelling is scant.
A protein important in wound repair, defensin, is available in a topical formulation. Defensin14 has been shown to activate the leucine-rich repeat-containing G-protein–coupled receptors 5 and 6 (also known as LGR5 and LGR6) stem cells. It speeds wound healing by increasing LGR stem cell migration into wound beds. Wounds should be covered to provide protection from sun exposure until reepithelialization occurs. Which occlusive ointments and wound repair products to use are beyond the scope of this article. Once epithelized, zinc oxide sunscreens can be used. These have been shown to be safe with minimal penetration into the skin.15
Ingredients to avoid post surgery
Topical retinoids should not be used post skin cancer surgery until epithelialization is complete. A study by Hung et al.16 in a porcine model used 0.05% tretinoin cream daily for 10 days prior to partial-thickness skin wounding demonstrated that use of tretinoin 10 days prior to wounding sped reepithelialization while use after the procedure slowed wound healing.
Acidic products will sting wounded skin. For this reason, benzoic acid, hydroxy acids, and ascorbic acid should be avoided until the skin has completely reepithelialized. Products with preservatives and fragrance should be avoided if possible.
Vitamin E derived from oral supplement capsules slowed healing after skin cancer surgery and had a high rate of contact dermatitis.17 Chemical sunscreens are more likely to cause an allergic contact dermatitis and should be avoided for 4 weeks after skin surgery. Organic products with essential oils and botanical ingredients may present a higher risk of contact dermatitis due to allergen exposure.
Conclusion
To ensure the best outcome from surgical treatments, patient education is a must! The more that patients know and understand about the ways in which they can prepare for their procedure and treat their skin after the procedure, the better the outcomes will be. Providers should give this type of information in an easy-to-follow printed instruction sheet because studies show that patients cannot remember most of the oral instructions offered by practitioners.
Encourage your patients to ask questions during their consultation and procedure and to get in touch with your office should they have any concerns when they leave. These steps help improve patient compliance and satisfaction, which will help you maintain a trusting relationship with established patients and attract new ones through word-of-mouth referrals.
Please email me at DrB@skintypesolutions.com if you have any other pre- and postprocedure skin care advice.
Dr. Leslie S. Baumann is a private practice dermatologist, researcher, author, and entrepreneur who practices in Miami. She founded the Cosmetic Dermatology Center at the University of Miami in 1997. Dr. Baumann wrote two textbooks: “Cosmetic Dermatology: Principles and Practice” (New York: McGraw-Hill, 2002), and “Cosmeceuticals and Cosmetic Ingredients,” (New York: McGraw-Hill, 2014), and a New York Times Best Sellers book for consumers, “The Skin Type Solution” (New York: Bantam Dell, 2006). Dr. Baumann has received funding for advisory boards and/or clinical research trials from Allergan, Evolus, Galderma, and Revance. She is the founder and CEO of Skin Type Solutions Franchise Systems LLC.
References
1. Aesthetic Plast Surg. 1995 May-Jun;19(3):243-6.
2. Plast Reconstr Surg. 2011 Mar;127(3):1343-5.
3. J Am Acad Dermatol. 1998 Aug;39(2 Pt 3):S79-81.
4. Br J Dermatol. 1995 Jan;132(1):46-53.
5. J Am Acad Dermatol. 2004 Dec;51(6):940-6.
6. J Korean Med Sci. 1996 Aug;11(4):335-41.
7. Eur J Dermatol. 2002 Mar-Apr;12(2):145-8.
8. Proc Natl Acad Sci U S A. 1981 May;78(5):2879-82.
9. Exp Dermatol. 2003;12 Suppl 2:57-63.
10. Surg Today. 2004;34(9):747-51.
11. Ophthal Plast Reconstr Surg. 2017 Jan/Feb;33(1):47-52.
12. Wound Repair Regen. 1998 Mar-Apr;6(2):167-77.
13. Dermatol Surg. 1998 Jun;24(6):661-4.
14. Plast Reconstr Surg. 2013 Nov;132(5):1159-71.
15. ACS Nano. 2016 Feb 23;10(2):1810-9.
16. Arch Dermatol. 1989 Jan;125(1):65-9.
17. Dermatol Surg. 1999 Apr;25(4):311-5.
