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New FASD diagnosis guidelines: Comprehensive or overly broad?
One of the most challenging elements in making a diagnosis of fetal alcohol spectrum disorders is obtaining a thorough history of the mother’s drinking during pregnancy. This is something that ob.gyns. have struggled with for many years, and while there are ways to improve the collection of this information, it’s often an uncomfortable conversation that yields unreliable answers.
In August, a group of experts on fetal alcohol spectrum disorders (FASD), organized by the National Institute on Alcohol Abuse and Alcoholism, proposed new clinical guidelines for diagnosing these disorders, the first update since 2005 (Pediatrics. 2016;138[2]:e20154256). The update creates a more inclusive definition of FASD and puts a greater emphasis on the sometimes subtle physical and behavioral changes that occur in children.
Growth restriction
The updated diagnosis begins with the acknowledgment of maternal drinking during pregnancy and growth restriction in the infant, which the new guidelines set at the 10th percentile. That’s an important change because it significantly increases sensitivity, expanding the number of infants who could be diagnosed by raising the growth restriction threshold from the third percentile. Clinicians must take into account other factors, such as the size of the natural parents and whether growth restriction could be caused by other conditions.
Facial changes
A key component on the FASD diagnosis is the assessment of facial changes. The three typical facial changes that have been used to make this diagnosis since the 1970s include short palpebral fissures, a shallow or lack of philtrum, and a thin vermilion border of the upper lip. Previously, if all three of these facial features were present, a history of maternal drinking was not needed in the diagnosis of fetal alcohol syndrome. If two of the three features were present, it was considered partial fetal alcohol syndrome. Now, if maternal drinking has been determined, it’s not necessary to have all three facial features to make a diagnosis of fetal alcohol syndrome.
For the first time, the guidelines describe other facial changes common in FASD that can be used to diagnose partial fetal alcohol syndrome, including a flat nasal bridge, epicanthal folds, and other signs. Again, the guidelines increase sensitivity and make it likely that more cases will be picked up through these criteria.
Neurobehavioral changes
The most devastating part of FASD are the complex neurobehavioral changes, resulting from damage to the fetal brain. Under the updated guidelines, the authors relaxed the criteria so that children can be diagnosed if they have domains of either intellectual impairment or behavioral changes that are 1.5 standard deviations below the age-adjusted mean, rather than the previous 2 standard deviations.
The challenge with making this change is that unlike with the facial changes, there’s a lack of specificity in assessing intellectual impairment and behavioral changes. In addition, these issues often emerge with other conditions unrelated to fetal exposure to alcohol.
Sensitivity vs. specificity
Statistically, the authors of the updated guidelines have moved to increase sensitivity, reaching more children who need interventions for the devastating manifestations of FASD. But the price of this expansion of the diagnostic criteria is a decrease in specificity. The authors seek to combat this potential lack of specificity by emphasizing that an FASD diagnosis should be made not by a single clinician but by a multidisciplinary team that includes physicians, a psychologist, social worker, and speech and language specialists.
While a specialized team will certainly help to make a better diagnosis, the literature shows very large variability in obtaining FASD diagnosis by using different guidelines. A May 2016 paper in Alcoholism: Clinical & Experimental Research found wide diagnostic variation of between roughly 5% (using guidelines from the Centers for Disease Control and Prevention) and 60% (using 2006 guidelines from Hoyme et al.) in the same group of alcohol- and drug-exposed children, when five different guidelines were used (doi: 10.1111/acer.13032). This type of variation would not be acceptable in other conditions, such as autism or attention-deficit/hyperactivity disorder, and it highlights a serious unresolved gap in advancing FASD.
Ob.gyn. role
The role for the ob.gyn. is a complicated one, both in terms of diagnosis and prevention of FASD. Quite often the mother is abusing both alcohol and drugs and the infant may be at risk for neonatal abstinence syndrome in addition to FASD. And because alcohol abuse is often chronic, this is an issue that could affect future children.
While there are still many unanswered questions on the genetics of FASD, we do know that it’s not an equal opportunity condition. Mothers who have had a child with the syndrome have a higher likelihood of its occurring with a second child, compared with mothers who drink heavily but did not have a previous child with FASD.
For now, it’s imperative that ob.gyns. continue to ask about drinking in a nonjudgmental way and that they ask this question of all their patients, not just ones they consider to be in high risk populations.
Dr. Koren is professor of physiology/pharmacology at Western University in Ontario. He is the founder of the Motherisk Program. He reported having no relevant financial disclosures. Email him at [email protected].
One of the most challenging elements in making a diagnosis of fetal alcohol spectrum disorders is obtaining a thorough history of the mother’s drinking during pregnancy. This is something that ob.gyns. have struggled with for many years, and while there are ways to improve the collection of this information, it’s often an uncomfortable conversation that yields unreliable answers.
In August, a group of experts on fetal alcohol spectrum disorders (FASD), organized by the National Institute on Alcohol Abuse and Alcoholism, proposed new clinical guidelines for diagnosing these disorders, the first update since 2005 (Pediatrics. 2016;138[2]:e20154256). The update creates a more inclusive definition of FASD and puts a greater emphasis on the sometimes subtle physical and behavioral changes that occur in children.
Growth restriction
The updated diagnosis begins with the acknowledgment of maternal drinking during pregnancy and growth restriction in the infant, which the new guidelines set at the 10th percentile. That’s an important change because it significantly increases sensitivity, expanding the number of infants who could be diagnosed by raising the growth restriction threshold from the third percentile. Clinicians must take into account other factors, such as the size of the natural parents and whether growth restriction could be caused by other conditions.
Facial changes
A key component on the FASD diagnosis is the assessment of facial changes. The three typical facial changes that have been used to make this diagnosis since the 1970s include short palpebral fissures, a shallow or lack of philtrum, and a thin vermilion border of the upper lip. Previously, if all three of these facial features were present, a history of maternal drinking was not needed in the diagnosis of fetal alcohol syndrome. If two of the three features were present, it was considered partial fetal alcohol syndrome. Now, if maternal drinking has been determined, it’s not necessary to have all three facial features to make a diagnosis of fetal alcohol syndrome.
For the first time, the guidelines describe other facial changes common in FASD that can be used to diagnose partial fetal alcohol syndrome, including a flat nasal bridge, epicanthal folds, and other signs. Again, the guidelines increase sensitivity and make it likely that more cases will be picked up through these criteria.
Neurobehavioral changes
The most devastating part of FASD are the complex neurobehavioral changes, resulting from damage to the fetal brain. Under the updated guidelines, the authors relaxed the criteria so that children can be diagnosed if they have domains of either intellectual impairment or behavioral changes that are 1.5 standard deviations below the age-adjusted mean, rather than the previous 2 standard deviations.
The challenge with making this change is that unlike with the facial changes, there’s a lack of specificity in assessing intellectual impairment and behavioral changes. In addition, these issues often emerge with other conditions unrelated to fetal exposure to alcohol.
Sensitivity vs. specificity
Statistically, the authors of the updated guidelines have moved to increase sensitivity, reaching more children who need interventions for the devastating manifestations of FASD. But the price of this expansion of the diagnostic criteria is a decrease in specificity. The authors seek to combat this potential lack of specificity by emphasizing that an FASD diagnosis should be made not by a single clinician but by a multidisciplinary team that includes physicians, a psychologist, social worker, and speech and language specialists.
While a specialized team will certainly help to make a better diagnosis, the literature shows very large variability in obtaining FASD diagnosis by using different guidelines. A May 2016 paper in Alcoholism: Clinical & Experimental Research found wide diagnostic variation of between roughly 5% (using guidelines from the Centers for Disease Control and Prevention) and 60% (using 2006 guidelines from Hoyme et al.) in the same group of alcohol- and drug-exposed children, when five different guidelines were used (doi: 10.1111/acer.13032). This type of variation would not be acceptable in other conditions, such as autism or attention-deficit/hyperactivity disorder, and it highlights a serious unresolved gap in advancing FASD.
Ob.gyn. role
The role for the ob.gyn. is a complicated one, both in terms of diagnosis and prevention of FASD. Quite often the mother is abusing both alcohol and drugs and the infant may be at risk for neonatal abstinence syndrome in addition to FASD. And because alcohol abuse is often chronic, this is an issue that could affect future children.
While there are still many unanswered questions on the genetics of FASD, we do know that it’s not an equal opportunity condition. Mothers who have had a child with the syndrome have a higher likelihood of its occurring with a second child, compared with mothers who drink heavily but did not have a previous child with FASD.
For now, it’s imperative that ob.gyns. continue to ask about drinking in a nonjudgmental way and that they ask this question of all their patients, not just ones they consider to be in high risk populations.
Dr. Koren is professor of physiology/pharmacology at Western University in Ontario. He is the founder of the Motherisk Program. He reported having no relevant financial disclosures. Email him at [email protected].
One of the most challenging elements in making a diagnosis of fetal alcohol spectrum disorders is obtaining a thorough history of the mother’s drinking during pregnancy. This is something that ob.gyns. have struggled with for many years, and while there are ways to improve the collection of this information, it’s often an uncomfortable conversation that yields unreliable answers.
In August, a group of experts on fetal alcohol spectrum disorders (FASD), organized by the National Institute on Alcohol Abuse and Alcoholism, proposed new clinical guidelines for diagnosing these disorders, the first update since 2005 (Pediatrics. 2016;138[2]:e20154256). The update creates a more inclusive definition of FASD and puts a greater emphasis on the sometimes subtle physical and behavioral changes that occur in children.
Growth restriction
The updated diagnosis begins with the acknowledgment of maternal drinking during pregnancy and growth restriction in the infant, which the new guidelines set at the 10th percentile. That’s an important change because it significantly increases sensitivity, expanding the number of infants who could be diagnosed by raising the growth restriction threshold from the third percentile. Clinicians must take into account other factors, such as the size of the natural parents and whether growth restriction could be caused by other conditions.
Facial changes
A key component on the FASD diagnosis is the assessment of facial changes. The three typical facial changes that have been used to make this diagnosis since the 1970s include short palpebral fissures, a shallow or lack of philtrum, and a thin vermilion border of the upper lip. Previously, if all three of these facial features were present, a history of maternal drinking was not needed in the diagnosis of fetal alcohol syndrome. If two of the three features were present, it was considered partial fetal alcohol syndrome. Now, if maternal drinking has been determined, it’s not necessary to have all three facial features to make a diagnosis of fetal alcohol syndrome.
For the first time, the guidelines describe other facial changes common in FASD that can be used to diagnose partial fetal alcohol syndrome, including a flat nasal bridge, epicanthal folds, and other signs. Again, the guidelines increase sensitivity and make it likely that more cases will be picked up through these criteria.
Neurobehavioral changes
The most devastating part of FASD are the complex neurobehavioral changes, resulting from damage to the fetal brain. Under the updated guidelines, the authors relaxed the criteria so that children can be diagnosed if they have domains of either intellectual impairment or behavioral changes that are 1.5 standard deviations below the age-adjusted mean, rather than the previous 2 standard deviations.
The challenge with making this change is that unlike with the facial changes, there’s a lack of specificity in assessing intellectual impairment and behavioral changes. In addition, these issues often emerge with other conditions unrelated to fetal exposure to alcohol.
Sensitivity vs. specificity
Statistically, the authors of the updated guidelines have moved to increase sensitivity, reaching more children who need interventions for the devastating manifestations of FASD. But the price of this expansion of the diagnostic criteria is a decrease in specificity. The authors seek to combat this potential lack of specificity by emphasizing that an FASD diagnosis should be made not by a single clinician but by a multidisciplinary team that includes physicians, a psychologist, social worker, and speech and language specialists.
While a specialized team will certainly help to make a better diagnosis, the literature shows very large variability in obtaining FASD diagnosis by using different guidelines. A May 2016 paper in Alcoholism: Clinical & Experimental Research found wide diagnostic variation of between roughly 5% (using guidelines from the Centers for Disease Control and Prevention) and 60% (using 2006 guidelines from Hoyme et al.) in the same group of alcohol- and drug-exposed children, when five different guidelines were used (doi: 10.1111/acer.13032). This type of variation would not be acceptable in other conditions, such as autism or attention-deficit/hyperactivity disorder, and it highlights a serious unresolved gap in advancing FASD.
Ob.gyn. role
The role for the ob.gyn. is a complicated one, both in terms of diagnosis and prevention of FASD. Quite often the mother is abusing both alcohol and drugs and the infant may be at risk for neonatal abstinence syndrome in addition to FASD. And because alcohol abuse is often chronic, this is an issue that could affect future children.
While there are still many unanswered questions on the genetics of FASD, we do know that it’s not an equal opportunity condition. Mothers who have had a child with the syndrome have a higher likelihood of its occurring with a second child, compared with mothers who drink heavily but did not have a previous child with FASD.
For now, it’s imperative that ob.gyns. continue to ask about drinking in a nonjudgmental way and that they ask this question of all their patients, not just ones they consider to be in high risk populations.
Dr. Koren is professor of physiology/pharmacology at Western University in Ontario. He is the founder of the Motherisk Program. He reported having no relevant financial disclosures. Email him at [email protected].
The importance of studying the placenta
It makes logical, intellectual sense that the placenta, an organ that is so integrally involved in pregnancy, will be of such great importance to the well-being, sustenance, and growth and development of the fetus. After all, the placental compartment and fetal compartment have the same origin early in embryogenesis, and the placenta is the sole source of nutrients and oxygen for the fetus.
However, the placenta has been extraordinarily poorly understood. Much of medicine has regarded the placenta like the appendix – an organ that may be easily discarded. We know too little about its functions and its biology. We do not even know whether there is a minimum amount of placenta that’s necessary for fetal health.
Over the years, the National Institutes of Health (NIH) has placed an emphasis on certain key areas of study through efforts such as the Human Genome Project, the BRAIN Initiative, and the Cancer Moonshot. Such efforts involve sustained, fundamental research and usually lead to significant findings and subsequent application of the findings.
It is exciting to know that the NIH has launched its Human Placenta Project in an effort to better understand the biology of the placenta and to elucidate its functions. The technology that is employed will play an adjunctive role.
Fortunately, over the years various investigators have studied the placenta using ultrasound, color Doppler technology, and other techniques, and have reported important findings. The work of pathologist Carolyn M. Salafia, MD, and others has called attention to the importance of the shape and vasculature of the placenta, as well as blood flow.
To bring us up to date, as the NIH’s Human Placenta Project proceeds, I have asked Dr. Salafia to provide us with a review discussion of our current knowledge and its implications. Dr. Salafia specializes in reproductive and developmental pathology and reviews thousands of placentas each year through her work with various hospitals and as head of the Placental Modulation Laboratory at the Institute for Basic Research in Developmental Disabilities in Staten Island, N.Y.
Dr. Reece, who specializes in maternal-fetal medicine, is vice president for medical affairs at the University of Maryland, Baltimore, as well as the John Z. and Akiko K. Bowers Distinguished Professor and dean of the school of medicine. Dr. Reece said he had no relevant financial disclosures. He is the medical editor of this column. Contact him at [email protected].
It makes logical, intellectual sense that the placenta, an organ that is so integrally involved in pregnancy, will be of such great importance to the well-being, sustenance, and growth and development of the fetus. After all, the placental compartment and fetal compartment have the same origin early in embryogenesis, and the placenta is the sole source of nutrients and oxygen for the fetus.
However, the placenta has been extraordinarily poorly understood. Much of medicine has regarded the placenta like the appendix – an organ that may be easily discarded. We know too little about its functions and its biology. We do not even know whether there is a minimum amount of placenta that’s necessary for fetal health.
Over the years, the National Institutes of Health (NIH) has placed an emphasis on certain key areas of study through efforts such as the Human Genome Project, the BRAIN Initiative, and the Cancer Moonshot. Such efforts involve sustained, fundamental research and usually lead to significant findings and subsequent application of the findings.
It is exciting to know that the NIH has launched its Human Placenta Project in an effort to better understand the biology of the placenta and to elucidate its functions. The technology that is employed will play an adjunctive role.
Fortunately, over the years various investigators have studied the placenta using ultrasound, color Doppler technology, and other techniques, and have reported important findings. The work of pathologist Carolyn M. Salafia, MD, and others has called attention to the importance of the shape and vasculature of the placenta, as well as blood flow.
To bring us up to date, as the NIH’s Human Placenta Project proceeds, I have asked Dr. Salafia to provide us with a review discussion of our current knowledge and its implications. Dr. Salafia specializes in reproductive and developmental pathology and reviews thousands of placentas each year through her work with various hospitals and as head of the Placental Modulation Laboratory at the Institute for Basic Research in Developmental Disabilities in Staten Island, N.Y.
Dr. Reece, who specializes in maternal-fetal medicine, is vice president for medical affairs at the University of Maryland, Baltimore, as well as the John Z. and Akiko K. Bowers Distinguished Professor and dean of the school of medicine. Dr. Reece said he had no relevant financial disclosures. He is the medical editor of this column. Contact him at [email protected].
It makes logical, intellectual sense that the placenta, an organ that is so integrally involved in pregnancy, will be of such great importance to the well-being, sustenance, and growth and development of the fetus. After all, the placental compartment and fetal compartment have the same origin early in embryogenesis, and the placenta is the sole source of nutrients and oxygen for the fetus.
However, the placenta has been extraordinarily poorly understood. Much of medicine has regarded the placenta like the appendix – an organ that may be easily discarded. We know too little about its functions and its biology. We do not even know whether there is a minimum amount of placenta that’s necessary for fetal health.
Over the years, the National Institutes of Health (NIH) has placed an emphasis on certain key areas of study through efforts such as the Human Genome Project, the BRAIN Initiative, and the Cancer Moonshot. Such efforts involve sustained, fundamental research and usually lead to significant findings and subsequent application of the findings.
It is exciting to know that the NIH has launched its Human Placenta Project in an effort to better understand the biology of the placenta and to elucidate its functions. The technology that is employed will play an adjunctive role.
Fortunately, over the years various investigators have studied the placenta using ultrasound, color Doppler technology, and other techniques, and have reported important findings. The work of pathologist Carolyn M. Salafia, MD, and others has called attention to the importance of the shape and vasculature of the placenta, as well as blood flow.
To bring us up to date, as the NIH’s Human Placenta Project proceeds, I have asked Dr. Salafia to provide us with a review discussion of our current knowledge and its implications. Dr. Salafia specializes in reproductive and developmental pathology and reviews thousands of placentas each year through her work with various hospitals and as head of the Placental Modulation Laboratory at the Institute for Basic Research in Developmental Disabilities in Staten Island, N.Y.
Dr. Reece, who specializes in maternal-fetal medicine, is vice president for medical affairs at the University of Maryland, Baltimore, as well as the John Z. and Akiko K. Bowers Distinguished Professor and dean of the school of medicine. Dr. Reece said he had no relevant financial disclosures. He is the medical editor of this column. Contact him at [email protected].
The Power of Two: Revisiting PA Autonomy
PA autonomy is a hot topic lately—not just within the profession but also in the public press. Earlier this year, Forbes touted efforts to loosen “barriers” to PA practice.1 The American Academy of Physician Assistants has identified 10 federal regulations that impose “unnecessary barriers” to medical care provided by PAs; these include cumbersome countersignatures, unnecessary supervision, and ordering restrictions on everything from home care to diabetic shoes.2 Lifting these barriers makes sense amid a shortage of physicians and an influx of newly insured patients (for more on this topic, see here). But as we acquire greater autonomy, we must not lose sight of the relationship that our profession was founded on—and that makes it unique.
Many PAs aspire to be truly independent practitioners, and some already are (eg, in remote and rural areas). Those of us who practice more closely with physicians may be more apt to appreciate the PA-physician partnership. In my 12 years as a PA, I have partnered with more than 50 physicians in cardiology, internal medicine, gastroenterology, and surgical oncology. I have also had the opportunity to witness the dynamic of other PA-physician relationships. As with all relationships, there is a wide range in synergy, productivity, and trust. Some ill-fated relationships are toxic and nonproductive; those merit a swift exit. At the other end of the spectrum are star-crossed partnerships that radiate competence, creativity, and confidence. In between these two extremes are the majority of PA-physician duos, working it out day to day in a kaleidoscopic health care world. It is clear that the physicians and PAs who not only work hard individually, but also work well within their relationship, benefit the most—and so do their patients.
We surgical PAs have a privileged bond that forms at the operating table. It is not only essential, but empowering, to know what each surgeon is thinking about his or her patient as the case unfolds. In medicine, collaboration may not be as intimate as it is in surgery. Still, there is no substitute for knowing our physicians well. Are our treatment goals in sync with theirs? Are we saying the same things to our patients? When we differ (as we often do), how do we achieve respectful and creative dissention? Can we each do our own thing and still be a credible and productive team?
What exactly is PA autonomy? Our scope of practice is delegated by a supervising physician and is limited to the services for which the physician can provide adequate supervision. The terms of supervision vary by state and by practice. In some states, a PA can have multiple “substitute” supervisors, as long as someone keeps a current list. The primary physician supervisor may or may not be the one the PA works with most closely. Some supervisory relationships are merely paper ones, a de rigueur document for the licensing file. Whatever form it takes, supervision has legal and clinical implications that should be implicit to both parties.
If supervision changes drastically, and PA autonomy becomes a reality, the name of our profession would have to change. Physician associate has been proposed. But until we eliminate the word physician, we are still partners with the very profession from which we intend to secede. Certainly, we need to abolish the possessive physician’s (a semantic that rankles universally). Let us get rid of that annoying (and misleading) apostrophe once and for all.
Many of us chose to become PAs to be extenders, rather than bearing ultimate responsibility. That is not to say that we are not willing to make decisions, take risks, or accept liability—that comes with the license and the territory. But in choosing to assist, we have deliberately chosen a dependent role. While physician assistant indeed implies a subordinate relationship, it is not necessarily a subservient one. There is plenty of room for both shared and separate decision-making, for specifically delegated or situational authority. The PA-physician relationship is built on mutual trust that is earned and reinforced on a daily basis. Decisional confidence and technical competence—not wimpy dependence—is the product of a dynamic PA-physician relationship.
As the health care market changes, we can and should afford ourselves every professional opportunity to work as salaried providers or to sign on as single contractors. There are many alternative PA-physician relationships, both legally and financially. If we so desire, we should pursue advanced degrees and specialty certifications and be compensated accordingly. However, multi-tasseled resumes should remain optional. They are costly and not within the reach of everyone, nor do they necessarily make a better PA.
In this new age of autonomy for advanced practice providers, some will say that only a dinosaur could have made these comments. If that is true, thank you for allowing me to wag my tail. The fact remains that PAs offer something unique. In an era of serious physician shortages, we offer patients the opportunity to have both a relationship with their internist, surgeon, or specialist and access to our own capable care and treatment. This is the “package deal” that, sadly, is in danger of becoming overlooked—if not extinct.
1. Japsen B. States remove barriers to physician assistants . Forbes. March 6, 2016. www.forbes.com/sites/brucejapsen/2016/03/06/states-remove-barriers-to-physician-assistants. Accessed September 13, 2016.
2. American Academy of Physician Assistants. Top ten federal laws & regulations imposing unnecessary barriers to medical care provided by PAs. www.aapa.org/workarea/downloadasset.aspx?id=6442450999. Accessed September 13, 2016.
Carol Mackenzie Jackson is a PA in Surgical Services at Cancer Treatment Centers of America® in Philadelphia.
Carol Mackenzie Jackson is a PA in Surgical Services at Cancer Treatment Centers of America® in Philadelphia.
Carol Mackenzie Jackson is a PA in Surgical Services at Cancer Treatment Centers of America® in Philadelphia.
PA autonomy is a hot topic lately—not just within the profession but also in the public press. Earlier this year, Forbes touted efforts to loosen “barriers” to PA practice.1 The American Academy of Physician Assistants has identified 10 federal regulations that impose “unnecessary barriers” to medical care provided by PAs; these include cumbersome countersignatures, unnecessary supervision, and ordering restrictions on everything from home care to diabetic shoes.2 Lifting these barriers makes sense amid a shortage of physicians and an influx of newly insured patients (for more on this topic, see here). But as we acquire greater autonomy, we must not lose sight of the relationship that our profession was founded on—and that makes it unique.
Many PAs aspire to be truly independent practitioners, and some already are (eg, in remote and rural areas). Those of us who practice more closely with physicians may be more apt to appreciate the PA-physician partnership. In my 12 years as a PA, I have partnered with more than 50 physicians in cardiology, internal medicine, gastroenterology, and surgical oncology. I have also had the opportunity to witness the dynamic of other PA-physician relationships. As with all relationships, there is a wide range in synergy, productivity, and trust. Some ill-fated relationships are toxic and nonproductive; those merit a swift exit. At the other end of the spectrum are star-crossed partnerships that radiate competence, creativity, and confidence. In between these two extremes are the majority of PA-physician duos, working it out day to day in a kaleidoscopic health care world. It is clear that the physicians and PAs who not only work hard individually, but also work well within their relationship, benefit the most—and so do their patients.
We surgical PAs have a privileged bond that forms at the operating table. It is not only essential, but empowering, to know what each surgeon is thinking about his or her patient as the case unfolds. In medicine, collaboration may not be as intimate as it is in surgery. Still, there is no substitute for knowing our physicians well. Are our treatment goals in sync with theirs? Are we saying the same things to our patients? When we differ (as we often do), how do we achieve respectful and creative dissention? Can we each do our own thing and still be a credible and productive team?
What exactly is PA autonomy? Our scope of practice is delegated by a supervising physician and is limited to the services for which the physician can provide adequate supervision. The terms of supervision vary by state and by practice. In some states, a PA can have multiple “substitute” supervisors, as long as someone keeps a current list. The primary physician supervisor may or may not be the one the PA works with most closely. Some supervisory relationships are merely paper ones, a de rigueur document for the licensing file. Whatever form it takes, supervision has legal and clinical implications that should be implicit to both parties.
If supervision changes drastically, and PA autonomy becomes a reality, the name of our profession would have to change. Physician associate has been proposed. But until we eliminate the word physician, we are still partners with the very profession from which we intend to secede. Certainly, we need to abolish the possessive physician’s (a semantic that rankles universally). Let us get rid of that annoying (and misleading) apostrophe once and for all.
Many of us chose to become PAs to be extenders, rather than bearing ultimate responsibility. That is not to say that we are not willing to make decisions, take risks, or accept liability—that comes with the license and the territory. But in choosing to assist, we have deliberately chosen a dependent role. While physician assistant indeed implies a subordinate relationship, it is not necessarily a subservient one. There is plenty of room for both shared and separate decision-making, for specifically delegated or situational authority. The PA-physician relationship is built on mutual trust that is earned and reinforced on a daily basis. Decisional confidence and technical competence—not wimpy dependence—is the product of a dynamic PA-physician relationship.
As the health care market changes, we can and should afford ourselves every professional opportunity to work as salaried providers or to sign on as single contractors. There are many alternative PA-physician relationships, both legally and financially. If we so desire, we should pursue advanced degrees and specialty certifications and be compensated accordingly. However, multi-tasseled resumes should remain optional. They are costly and not within the reach of everyone, nor do they necessarily make a better PA.
In this new age of autonomy for advanced practice providers, some will say that only a dinosaur could have made these comments. If that is true, thank you for allowing me to wag my tail. The fact remains that PAs offer something unique. In an era of serious physician shortages, we offer patients the opportunity to have both a relationship with their internist, surgeon, or specialist and access to our own capable care and treatment. This is the “package deal” that, sadly, is in danger of becoming overlooked—if not extinct.
PA autonomy is a hot topic lately—not just within the profession but also in the public press. Earlier this year, Forbes touted efforts to loosen “barriers” to PA practice.1 The American Academy of Physician Assistants has identified 10 federal regulations that impose “unnecessary barriers” to medical care provided by PAs; these include cumbersome countersignatures, unnecessary supervision, and ordering restrictions on everything from home care to diabetic shoes.2 Lifting these barriers makes sense amid a shortage of physicians and an influx of newly insured patients (for more on this topic, see here). But as we acquire greater autonomy, we must not lose sight of the relationship that our profession was founded on—and that makes it unique.
Many PAs aspire to be truly independent practitioners, and some already are (eg, in remote and rural areas). Those of us who practice more closely with physicians may be more apt to appreciate the PA-physician partnership. In my 12 years as a PA, I have partnered with more than 50 physicians in cardiology, internal medicine, gastroenterology, and surgical oncology. I have also had the opportunity to witness the dynamic of other PA-physician relationships. As with all relationships, there is a wide range in synergy, productivity, and trust. Some ill-fated relationships are toxic and nonproductive; those merit a swift exit. At the other end of the spectrum are star-crossed partnerships that radiate competence, creativity, and confidence. In between these two extremes are the majority of PA-physician duos, working it out day to day in a kaleidoscopic health care world. It is clear that the physicians and PAs who not only work hard individually, but also work well within their relationship, benefit the most—and so do their patients.
We surgical PAs have a privileged bond that forms at the operating table. It is not only essential, but empowering, to know what each surgeon is thinking about his or her patient as the case unfolds. In medicine, collaboration may not be as intimate as it is in surgery. Still, there is no substitute for knowing our physicians well. Are our treatment goals in sync with theirs? Are we saying the same things to our patients? When we differ (as we often do), how do we achieve respectful and creative dissention? Can we each do our own thing and still be a credible and productive team?
What exactly is PA autonomy? Our scope of practice is delegated by a supervising physician and is limited to the services for which the physician can provide adequate supervision. The terms of supervision vary by state and by practice. In some states, a PA can have multiple “substitute” supervisors, as long as someone keeps a current list. The primary physician supervisor may or may not be the one the PA works with most closely. Some supervisory relationships are merely paper ones, a de rigueur document for the licensing file. Whatever form it takes, supervision has legal and clinical implications that should be implicit to both parties.
If supervision changes drastically, and PA autonomy becomes a reality, the name of our profession would have to change. Physician associate has been proposed. But until we eliminate the word physician, we are still partners with the very profession from which we intend to secede. Certainly, we need to abolish the possessive physician’s (a semantic that rankles universally). Let us get rid of that annoying (and misleading) apostrophe once and for all.
Many of us chose to become PAs to be extenders, rather than bearing ultimate responsibility. That is not to say that we are not willing to make decisions, take risks, or accept liability—that comes with the license and the territory. But in choosing to assist, we have deliberately chosen a dependent role. While physician assistant indeed implies a subordinate relationship, it is not necessarily a subservient one. There is plenty of room for both shared and separate decision-making, for specifically delegated or situational authority. The PA-physician relationship is built on mutual trust that is earned and reinforced on a daily basis. Decisional confidence and technical competence—not wimpy dependence—is the product of a dynamic PA-physician relationship.
As the health care market changes, we can and should afford ourselves every professional opportunity to work as salaried providers or to sign on as single contractors. There are many alternative PA-physician relationships, both legally and financially. If we so desire, we should pursue advanced degrees and specialty certifications and be compensated accordingly. However, multi-tasseled resumes should remain optional. They are costly and not within the reach of everyone, nor do they necessarily make a better PA.
In this new age of autonomy for advanced practice providers, some will say that only a dinosaur could have made these comments. If that is true, thank you for allowing me to wag my tail. The fact remains that PAs offer something unique. In an era of serious physician shortages, we offer patients the opportunity to have both a relationship with their internist, surgeon, or specialist and access to our own capable care and treatment. This is the “package deal” that, sadly, is in danger of becoming overlooked—if not extinct.
1. Japsen B. States remove barriers to physician assistants . Forbes. March 6, 2016. www.forbes.com/sites/brucejapsen/2016/03/06/states-remove-barriers-to-physician-assistants. Accessed September 13, 2016.
2. American Academy of Physician Assistants. Top ten federal laws & regulations imposing unnecessary barriers to medical care provided by PAs. www.aapa.org/workarea/downloadasset.aspx?id=6442450999. Accessed September 13, 2016.
1. Japsen B. States remove barriers to physician assistants . Forbes. March 6, 2016. www.forbes.com/sites/brucejapsen/2016/03/06/states-remove-barriers-to-physician-assistants. Accessed September 13, 2016.
2. American Academy of Physician Assistants. Top ten federal laws & regulations imposing unnecessary barriers to medical care provided by PAs. www.aapa.org/workarea/downloadasset.aspx?id=6442450999. Accessed September 13, 2016.
Why placental shape and vasculature matter
The intrauterine environment significantly influences not only fetal and infant health, but adult health risks as well. Yet current efforts in obstetrics to assess the environment and optimize fetal and long-term outcomes are based on diagnostics that focus on and measure fetal signs and symptoms. By and large, the current approach overlooks the placenta – the organ that serves as the principal regulator of fetal growth and health. If the fetus appears free of risk or complications, we assume the placenta must be “okay.”
Yet this isn’t always the case. By assuming the placenta is healthy and not observing and measuring its condition, we are too often too late to effectively alter fetal- and longer-term outcomes once fetal signs and symptoms appear.
Research in recent decades, and particularly in the past 10 years, has demonstrated that placental shape matters, that it’s linked to function, and that quantifying abnormalities in shape and growth can be a meaningful clinical tool for detecting and preventing disease early in pregnancy.
We now know, specifically, that abnormal shapes reflect alterations in placental vascular architecture that lead to reduced placental efficiency. We also now understand that placental weight or size may serve as a proxy for fetoplacental metabolism.
We have more research to do to further develop models, to collect more data, and to more fully understand the placental pathology that precedes detectable fetal and/or maternal disease. We also need to know whether the early detection of placental disease has sufficient positive predictive value to allow for safe and effective intervention.1
The National Institutes of Health is investing more than $40 million in its Human Placenta Project, which aims to develop new technologies to help researchers monitor the placenta in real time. Yet it is possible that the use of ultrasound and Doppler – technologies that we employ routinely and know are safe – may go a long way toward deepening our knowledge that will, in turn, hone our ability to identify early risks.
When I speak to fellow pathologists, my message is, “Let’s stop wasting data.” For ob.gyns., my message is twofold: First, appreciate the potential to predict and alter downstream fetal and/or maternal risks by observing and measuring the placenta. Second, be aware of the value of early in vivo placental images, as well as photographs, and more precise measures of delivered placentas.
Why shape matters
The “average” or “typical” placental shape is round or oval with a centrally inserted umbilical cord. In practice, we see a variety of surface shapes and cord insertion sites, with common variations such as bi- or multi-lobate shapes, or otherwise irregular shapes and cord insertions that are eccentric, marginal, or velamentous. Interestingly, many irregularly shaped placentas display symmetry and have regular, defined geometrical patterns, like snowflakes.2
We have long understood that the microscopic growth of the human placenta involves repeated vascular branching analogous to the roots of a tree. This vascular development, or “placental arborization,” reflects the health of the maternal environment and impacts fetal health.
It is only in recent years, however, that we’ve gained a much better understanding of the relationship of the vascular structure and the shape of the placenta, and an understanding of how early changes in the branching structure of the placenta’s vascular tree drive variation in mature placental shape.
By applying a well-accepted mathematical model for generating highly branched fractals (a model for random growth known in the mathematical physics world as diffusion limited aggregation, or DLA), we have reliably reproduced the variability in placental shapes and related these shapes to the structure of the underlying vascular tree.
When the model is run with unperturbed, random values of a branching growth parameter, we get round-oval fractal shapes. But when the growth parameter is perturbed at a single point in time – when a one-time, early change is introduced – arborization is negatively affected and we get irregular shapes.
The model’s output has explained and verified a clinically observed association between non-round, non-oval placental shapes and smaller newborn birth weight for given placental weight.
This association was evident in an analysis of data collected as part of the National Collaborative Perinatal Project (1959-1974), which included placental measures such as weight, shape, size, and thickness for more than 24,000 women. It also was apparent in an analysis of data and images collected as part of the Pregnancy, Infection, and Nutrition (PIN) Study, conducted in North Carolina.
One take-away from both of these studies has been that increased variability of placental shape is associated with lower placental functional efficiency. Moreover, in the University of North Carolina cohort, the impact of placental vascular pathology (either maternal uteroplacental or fetoplacental) on placental efficiency and function was shown to be dependent on shape. Only in the case of irregularly shaped chorionic plates did each of the two pathologies have a significant association with placental inefficiency.3
The realization that placental size (weight/mass/volume) may serve as a proxy for the fetoplacental basal metabolic rate came after it was shown that Kleiber’s law, which states that basal metabolic rate (BMR) is proportional to the body mass to the 3/4 power, can be applied to the newborn’s birth weight by substituting placental weight for BMR.
This fetal-placental version (placenta weight = .75 birth weight) of Kleiber’s law was validated through an analysis of the sets of placental measures and birth weights stored in the Collaborative Perinatal Project. It has implications for our ability to use ultrasound and Doppler measures to predict risk and to understand pathologic pregnancies, such as those complicated by diabetes or fetal growth restriction.
Research also has shed light on the timing of shape variants. We now know that abnormalities of placental surface shape result mainly from early influences – perturbations of placental growth that occur no later than mid-gestation – rather than from trophotropism (the placenta “grows where it can and does not grow where it can’t”) and passive uterine remodeling later in pregnancy, as has traditionally been believed.4
With respect to the umbilical cord, the location of cord insertion is independent of eventual disk shape, but is to a large degree determined by the end of the first trimester. In addition, cord insertion does influence and is correlated with chorionic vascular density and with disk thickness. Greater eccentricity of cord insertion appears to be linked to increased placental disk thickness, each of which is independently associated with reduced placental functional efficiency.5,6
We have worked with placentas from newborns in families with an older child diagnosed with autism and have found significant differences between these placentas and the placentas of low-risk newborns. In particular, we have measured a reduction in the number or chorionic surface vessel branch points of more than 40%.
Current implications
Irregularities in placental surface shape, disk thickness, and various descriptors of placental size may all be determined from ultrasound and Doppler imaging. We can also assess cord insertion and chorionic surface vessel distribution, track patterns and rates of placental growth, and use various placental measures to understand placental efficiency and to improve the specificity of placental histopathologic diagnoses.
At this point, our use of in vivo imaging of the placenta has mainly involved grayscale ultrasound, but with color or power Doppler and improved surface network tracing protocols, we could save the red and blue areas we visualize as a “shape” and assess the density of surface vessel branching, for instance, and the degree of uniformity in vessel distribution.
We currently have quantitative markers of placental shape and mathematical models to help us identify at-risk pregnancies. What we need are more data from early ultrasounds (from all pregnancies and not only complicated ones) and more comprehensive and precise models of placental growth and function. This will enable us to better identify preclinical fetoplacental pathophysiology and predict downstream risks.
In the meantime, the delivered placenta can be a valuable source of information – an extra dimension for looking back in time. With a paradigm shift toward more thorough pathologic analysis, the delivered placenta can provide unique insights into how placental growth evolved during the pregnancy.
Do not throw away the placenta, and do not just weigh it. Take a photograph, because even with a photograph we can assess vascular density, disk thickness, and other placental characteristics.
In the case of pregnancy complications or suboptimal outcomes, the knowledge we can gain from the delivered placenta can help the physician and patient to understand recurrence risks and to better target evaluation, monitoring, and management in the next pregnancy.
References
1. Am J Perinatol. 2016 Aug 4. doi: 10.1055/s-0036-1586508.
2. Placenta. 2008 Sep;29(9):790-7.
3. Placenta. 2010 Nov;31(11):958-62.
4. Placenta. 2012 Mar;33(3):164-70.
5. J Dev Orig Health Dis. 2011 Aug;2(4):205-11.
6. Placenta. 2009 Dec;30(12):1058-64.
Dr. Salafia leads the Placental Modulation Laboratory at New York State’s Institute for Basic Research in Developmental Disabilities, Staten Island, N.Y. She reported that she has no relevant financial disclosures.
The intrauterine environment significantly influences not only fetal and infant health, but adult health risks as well. Yet current efforts in obstetrics to assess the environment and optimize fetal and long-term outcomes are based on diagnostics that focus on and measure fetal signs and symptoms. By and large, the current approach overlooks the placenta – the organ that serves as the principal regulator of fetal growth and health. If the fetus appears free of risk or complications, we assume the placenta must be “okay.”
Yet this isn’t always the case. By assuming the placenta is healthy and not observing and measuring its condition, we are too often too late to effectively alter fetal- and longer-term outcomes once fetal signs and symptoms appear.
Research in recent decades, and particularly in the past 10 years, has demonstrated that placental shape matters, that it’s linked to function, and that quantifying abnormalities in shape and growth can be a meaningful clinical tool for detecting and preventing disease early in pregnancy.
We now know, specifically, that abnormal shapes reflect alterations in placental vascular architecture that lead to reduced placental efficiency. We also now understand that placental weight or size may serve as a proxy for fetoplacental metabolism.
We have more research to do to further develop models, to collect more data, and to more fully understand the placental pathology that precedes detectable fetal and/or maternal disease. We also need to know whether the early detection of placental disease has sufficient positive predictive value to allow for safe and effective intervention.1
The National Institutes of Health is investing more than $40 million in its Human Placenta Project, which aims to develop new technologies to help researchers monitor the placenta in real time. Yet it is possible that the use of ultrasound and Doppler – technologies that we employ routinely and know are safe – may go a long way toward deepening our knowledge that will, in turn, hone our ability to identify early risks.
When I speak to fellow pathologists, my message is, “Let’s stop wasting data.” For ob.gyns., my message is twofold: First, appreciate the potential to predict and alter downstream fetal and/or maternal risks by observing and measuring the placenta. Second, be aware of the value of early in vivo placental images, as well as photographs, and more precise measures of delivered placentas.
Why shape matters
The “average” or “typical” placental shape is round or oval with a centrally inserted umbilical cord. In practice, we see a variety of surface shapes and cord insertion sites, with common variations such as bi- or multi-lobate shapes, or otherwise irregular shapes and cord insertions that are eccentric, marginal, or velamentous. Interestingly, many irregularly shaped placentas display symmetry and have regular, defined geometrical patterns, like snowflakes.2
We have long understood that the microscopic growth of the human placenta involves repeated vascular branching analogous to the roots of a tree. This vascular development, or “placental arborization,” reflects the health of the maternal environment and impacts fetal health.
It is only in recent years, however, that we’ve gained a much better understanding of the relationship of the vascular structure and the shape of the placenta, and an understanding of how early changes in the branching structure of the placenta’s vascular tree drive variation in mature placental shape.
By applying a well-accepted mathematical model for generating highly branched fractals (a model for random growth known in the mathematical physics world as diffusion limited aggregation, or DLA), we have reliably reproduced the variability in placental shapes and related these shapes to the structure of the underlying vascular tree.
When the model is run with unperturbed, random values of a branching growth parameter, we get round-oval fractal shapes. But when the growth parameter is perturbed at a single point in time – when a one-time, early change is introduced – arborization is negatively affected and we get irregular shapes.
The model’s output has explained and verified a clinically observed association between non-round, non-oval placental shapes and smaller newborn birth weight for given placental weight.
This association was evident in an analysis of data collected as part of the National Collaborative Perinatal Project (1959-1974), which included placental measures such as weight, shape, size, and thickness for more than 24,000 women. It also was apparent in an analysis of data and images collected as part of the Pregnancy, Infection, and Nutrition (PIN) Study, conducted in North Carolina.
One take-away from both of these studies has been that increased variability of placental shape is associated with lower placental functional efficiency. Moreover, in the University of North Carolina cohort, the impact of placental vascular pathology (either maternal uteroplacental or fetoplacental) on placental efficiency and function was shown to be dependent on shape. Only in the case of irregularly shaped chorionic plates did each of the two pathologies have a significant association with placental inefficiency.3
The realization that placental size (weight/mass/volume) may serve as a proxy for the fetoplacental basal metabolic rate came after it was shown that Kleiber’s law, which states that basal metabolic rate (BMR) is proportional to the body mass to the 3/4 power, can be applied to the newborn’s birth weight by substituting placental weight for BMR.
This fetal-placental version (placenta weight = .75 birth weight) of Kleiber’s law was validated through an analysis of the sets of placental measures and birth weights stored in the Collaborative Perinatal Project. It has implications for our ability to use ultrasound and Doppler measures to predict risk and to understand pathologic pregnancies, such as those complicated by diabetes or fetal growth restriction.
Research also has shed light on the timing of shape variants. We now know that abnormalities of placental surface shape result mainly from early influences – perturbations of placental growth that occur no later than mid-gestation – rather than from trophotropism (the placenta “grows where it can and does not grow where it can’t”) and passive uterine remodeling later in pregnancy, as has traditionally been believed.4
With respect to the umbilical cord, the location of cord insertion is independent of eventual disk shape, but is to a large degree determined by the end of the first trimester. In addition, cord insertion does influence and is correlated with chorionic vascular density and with disk thickness. Greater eccentricity of cord insertion appears to be linked to increased placental disk thickness, each of which is independently associated with reduced placental functional efficiency.5,6
We have worked with placentas from newborns in families with an older child diagnosed with autism and have found significant differences between these placentas and the placentas of low-risk newborns. In particular, we have measured a reduction in the number or chorionic surface vessel branch points of more than 40%.
Current implications
Irregularities in placental surface shape, disk thickness, and various descriptors of placental size may all be determined from ultrasound and Doppler imaging. We can also assess cord insertion and chorionic surface vessel distribution, track patterns and rates of placental growth, and use various placental measures to understand placental efficiency and to improve the specificity of placental histopathologic diagnoses.
At this point, our use of in vivo imaging of the placenta has mainly involved grayscale ultrasound, but with color or power Doppler and improved surface network tracing protocols, we could save the red and blue areas we visualize as a “shape” and assess the density of surface vessel branching, for instance, and the degree of uniformity in vessel distribution.
We currently have quantitative markers of placental shape and mathematical models to help us identify at-risk pregnancies. What we need are more data from early ultrasounds (from all pregnancies and not only complicated ones) and more comprehensive and precise models of placental growth and function. This will enable us to better identify preclinical fetoplacental pathophysiology and predict downstream risks.
In the meantime, the delivered placenta can be a valuable source of information – an extra dimension for looking back in time. With a paradigm shift toward more thorough pathologic analysis, the delivered placenta can provide unique insights into how placental growth evolved during the pregnancy.
Do not throw away the placenta, and do not just weigh it. Take a photograph, because even with a photograph we can assess vascular density, disk thickness, and other placental characteristics.
In the case of pregnancy complications or suboptimal outcomes, the knowledge we can gain from the delivered placenta can help the physician and patient to understand recurrence risks and to better target evaluation, monitoring, and management in the next pregnancy.
References
1. Am J Perinatol. 2016 Aug 4. doi: 10.1055/s-0036-1586508.
2. Placenta. 2008 Sep;29(9):790-7.
3. Placenta. 2010 Nov;31(11):958-62.
4. Placenta. 2012 Mar;33(3):164-70.
5. J Dev Orig Health Dis. 2011 Aug;2(4):205-11.
6. Placenta. 2009 Dec;30(12):1058-64.
Dr. Salafia leads the Placental Modulation Laboratory at New York State’s Institute for Basic Research in Developmental Disabilities, Staten Island, N.Y. She reported that she has no relevant financial disclosures.
The intrauterine environment significantly influences not only fetal and infant health, but adult health risks as well. Yet current efforts in obstetrics to assess the environment and optimize fetal and long-term outcomes are based on diagnostics that focus on and measure fetal signs and symptoms. By and large, the current approach overlooks the placenta – the organ that serves as the principal regulator of fetal growth and health. If the fetus appears free of risk or complications, we assume the placenta must be “okay.”
Yet this isn’t always the case. By assuming the placenta is healthy and not observing and measuring its condition, we are too often too late to effectively alter fetal- and longer-term outcomes once fetal signs and symptoms appear.
Research in recent decades, and particularly in the past 10 years, has demonstrated that placental shape matters, that it’s linked to function, and that quantifying abnormalities in shape and growth can be a meaningful clinical tool for detecting and preventing disease early in pregnancy.
We now know, specifically, that abnormal shapes reflect alterations in placental vascular architecture that lead to reduced placental efficiency. We also now understand that placental weight or size may serve as a proxy for fetoplacental metabolism.
We have more research to do to further develop models, to collect more data, and to more fully understand the placental pathology that precedes detectable fetal and/or maternal disease. We also need to know whether the early detection of placental disease has sufficient positive predictive value to allow for safe and effective intervention.1
The National Institutes of Health is investing more than $40 million in its Human Placenta Project, which aims to develop new technologies to help researchers monitor the placenta in real time. Yet it is possible that the use of ultrasound and Doppler – technologies that we employ routinely and know are safe – may go a long way toward deepening our knowledge that will, in turn, hone our ability to identify early risks.
When I speak to fellow pathologists, my message is, “Let’s stop wasting data.” For ob.gyns., my message is twofold: First, appreciate the potential to predict and alter downstream fetal and/or maternal risks by observing and measuring the placenta. Second, be aware of the value of early in vivo placental images, as well as photographs, and more precise measures of delivered placentas.
Why shape matters
The “average” or “typical” placental shape is round or oval with a centrally inserted umbilical cord. In practice, we see a variety of surface shapes and cord insertion sites, with common variations such as bi- or multi-lobate shapes, or otherwise irregular shapes and cord insertions that are eccentric, marginal, or velamentous. Interestingly, many irregularly shaped placentas display symmetry and have regular, defined geometrical patterns, like snowflakes.2
We have long understood that the microscopic growth of the human placenta involves repeated vascular branching analogous to the roots of a tree. This vascular development, or “placental arborization,” reflects the health of the maternal environment and impacts fetal health.
It is only in recent years, however, that we’ve gained a much better understanding of the relationship of the vascular structure and the shape of the placenta, and an understanding of how early changes in the branching structure of the placenta’s vascular tree drive variation in mature placental shape.
By applying a well-accepted mathematical model for generating highly branched fractals (a model for random growth known in the mathematical physics world as diffusion limited aggregation, or DLA), we have reliably reproduced the variability in placental shapes and related these shapes to the structure of the underlying vascular tree.
When the model is run with unperturbed, random values of a branching growth parameter, we get round-oval fractal shapes. But when the growth parameter is perturbed at a single point in time – when a one-time, early change is introduced – arborization is negatively affected and we get irregular shapes.
The model’s output has explained and verified a clinically observed association between non-round, non-oval placental shapes and smaller newborn birth weight for given placental weight.
This association was evident in an analysis of data collected as part of the National Collaborative Perinatal Project (1959-1974), which included placental measures such as weight, shape, size, and thickness for more than 24,000 women. It also was apparent in an analysis of data and images collected as part of the Pregnancy, Infection, and Nutrition (PIN) Study, conducted in North Carolina.
One take-away from both of these studies has been that increased variability of placental shape is associated with lower placental functional efficiency. Moreover, in the University of North Carolina cohort, the impact of placental vascular pathology (either maternal uteroplacental or fetoplacental) on placental efficiency and function was shown to be dependent on shape. Only in the case of irregularly shaped chorionic plates did each of the two pathologies have a significant association with placental inefficiency.3
The realization that placental size (weight/mass/volume) may serve as a proxy for the fetoplacental basal metabolic rate came after it was shown that Kleiber’s law, which states that basal metabolic rate (BMR) is proportional to the body mass to the 3/4 power, can be applied to the newborn’s birth weight by substituting placental weight for BMR.
This fetal-placental version (placenta weight = .75 birth weight) of Kleiber’s law was validated through an analysis of the sets of placental measures and birth weights stored in the Collaborative Perinatal Project. It has implications for our ability to use ultrasound and Doppler measures to predict risk and to understand pathologic pregnancies, such as those complicated by diabetes or fetal growth restriction.
Research also has shed light on the timing of shape variants. We now know that abnormalities of placental surface shape result mainly from early influences – perturbations of placental growth that occur no later than mid-gestation – rather than from trophotropism (the placenta “grows where it can and does not grow where it can’t”) and passive uterine remodeling later in pregnancy, as has traditionally been believed.4
With respect to the umbilical cord, the location of cord insertion is independent of eventual disk shape, but is to a large degree determined by the end of the first trimester. In addition, cord insertion does influence and is correlated with chorionic vascular density and with disk thickness. Greater eccentricity of cord insertion appears to be linked to increased placental disk thickness, each of which is independently associated with reduced placental functional efficiency.5,6
We have worked with placentas from newborns in families with an older child diagnosed with autism and have found significant differences between these placentas and the placentas of low-risk newborns. In particular, we have measured a reduction in the number or chorionic surface vessel branch points of more than 40%.
Current implications
Irregularities in placental surface shape, disk thickness, and various descriptors of placental size may all be determined from ultrasound and Doppler imaging. We can also assess cord insertion and chorionic surface vessel distribution, track patterns and rates of placental growth, and use various placental measures to understand placental efficiency and to improve the specificity of placental histopathologic diagnoses.
At this point, our use of in vivo imaging of the placenta has mainly involved grayscale ultrasound, but with color or power Doppler and improved surface network tracing protocols, we could save the red and blue areas we visualize as a “shape” and assess the density of surface vessel branching, for instance, and the degree of uniformity in vessel distribution.
We currently have quantitative markers of placental shape and mathematical models to help us identify at-risk pregnancies. What we need are more data from early ultrasounds (from all pregnancies and not only complicated ones) and more comprehensive and precise models of placental growth and function. This will enable us to better identify preclinical fetoplacental pathophysiology and predict downstream risks.
In the meantime, the delivered placenta can be a valuable source of information – an extra dimension for looking back in time. With a paradigm shift toward more thorough pathologic analysis, the delivered placenta can provide unique insights into how placental growth evolved during the pregnancy.
Do not throw away the placenta, and do not just weigh it. Take a photograph, because even with a photograph we can assess vascular density, disk thickness, and other placental characteristics.
In the case of pregnancy complications or suboptimal outcomes, the knowledge we can gain from the delivered placenta can help the physician and patient to understand recurrence risks and to better target evaluation, monitoring, and management in the next pregnancy.
References
1. Am J Perinatol. 2016 Aug 4. doi: 10.1055/s-0036-1586508.
2. Placenta. 2008 Sep;29(9):790-7.
3. Placenta. 2010 Nov;31(11):958-62.
4. Placenta. 2012 Mar;33(3):164-70.
5. J Dev Orig Health Dis. 2011 Aug;2(4):205-11.
6. Placenta. 2009 Dec;30(12):1058-64.
Dr. Salafia leads the Placental Modulation Laboratory at New York State’s Institute for Basic Research in Developmental Disabilities, Staten Island, N.Y. She reported that she has no relevant financial disclosures.
Hunting for ‘Woozles’ in the Hundred Acre Wood of ADHD
One fine winter’s day when Piglet was brushing away the snow
in front of his house he happened to look up, and there was
Winnie-the-Pooh. Pooh was walking round and round in a circle,
thinking of something else…
So begins the 1926 Winnie-the-Pooh story.1 In this chapter, the well-meaning yellow bear, Winnie-the-Pooh, has found strange tracks in the snow, which he believes belong to a “Woozle.” Pooh follows the tracks, not realizing that he’s walking in a circle. As such, he begins to notice that the tracks have multiplied, which he interprets as evidence of several Woozles.
This “Woozle Effect” has been well described in research settings and is believed to have resulted in conclusions that are not supported by or are inconsistent with the original data, which are then propagated through successive citations, resulting in a scientific “urban legend.”2
Throughout my training from medical school, through fellowship, and during my tenure as a faculty member, I have found myself, at times, searching for Woozles and often have joined my colleagues on these hunts. Herein, I would like to share with you 3 Woozles that have resulted in current false dogmas related to attention-deficit/hyperactivity disorder (ADHD) and stimulant psychopharmacology.
Stimulants worsen anxiety
FDA-required labeling for stimulants includes strong language noting that these drugs are “contraindicated in marked anxiety, tension, and agitation, since the drug may aggravate these symptoms.”3 However, data from randomized controlled trials and meta-analyses consistently have failed to demonstrate this effect. Moreover, sequenced treatment trials involving adolescents with anxiety disorders and co-occurring ADHD suggest that stimulants actually could reduce anxiety symptoms.
A recent meta-analysis4 that evaluated nearly 2 dozen studies involving approximately 3,000 pediatric patients with ADHD reported that stimulant treatment was associated with a decreased relative risk of anxiety (relative risk: 0.86). The study also observed a dose-response relationship between stimulant dosage and anxiety (Figure, page 6).4 Although the authors note that it is possible that some individuals might experience increased anxiety with stimulants, many patients could show improvement in anxiety symptoms when treated with stimulants, and the authors also advise us, as clinicians, to “consider re-challenging children with ADHD who report … anxiety with psychostimulants, as these symptoms are much more likely to be coincidental rather than caused by psychostimulants.”4
More evidence of a lack of stimulant-induced anxiety comes from a large randomized controlled trial of pediatric patients (age 6 to 17) who met DSM-IV criteria for ADHD and a co-occurring anxiety disorder who were treated with methylphenidate (open-label) and then randomized to fluvoxamine or placebo for treatment of anxiety symptoms.5 However, in this trial >80% of the 32 medication-naïve youth improved after stimulant treatment to the point that they no longer had anxiety symptoms severe enough to be eligible for randomization to adjunctive fluvoxamine or placebo.
Stimulants are contraindicated in patients with tic disorders
The package inserts for most stimulant medications warn clinicians that stimulants are “contraindicated in patients with motor tics or with a family history or diagnosis of Tourette’s syndrome.” This is particularly concerning, especially because of the medicolegal implications of the term “contraindicated” and given that as many as 1 in 5 pediatric patients with ADHD have a tic disorder.6 Therefore, labels that list motor tics as a contraindication to stimulant use potentially eliminate the choice of stimulant pharmacotherapy—the most effective treatment for ADHD—for a large number of patients.
When hunting for the Woozle that linked stimulants and tics and led to this language in the package insert, it is worthwhile to review a recent meta-analysis of 22 studies (involving nearly 2,400 youths with ADHD) that suggested new-onset tics or worsening of tics to be present in 5.7% of patients receiving stimulants and in 6.5% of patients receiving placebo. In addition, in this meta-analysis the class of stimulant, dosage, treatment duration, or patient age did not seem to be associated with onset or worsening of tics.7
Polypharmacy represents a therapeutic failure and is not evidence-based
Although treatment guidelines generally have discouraged combination therapy for treating ADHD, there are—on the basis of efficacy—insufficient data to support this prohibition. Moreover, over the last decade, several studies have suggested benefits for combining ADHD medications that have complimentary mechanisms. In this regard, 2 extended-release formulations of α2 agonists have received FDA approval for as adjunctive treatments in pediatric patients with ADHD (extended-release guanfacine and extended-release clonidine). However, despite these FDA indications as adjunctive treatments, many clinicians remain concerned about combination therapy.
Several months ago, a large, 8-week, National Institutes of Health–sponsored trial shed more light on the use of α2agonist + stimulant combinations. Patients age 7 to 17 (N = 179) were randomized to (1) guanfacine + d-methylphenidate, (2) guanfacine monotherapy, or (3) d-methylphenidate monotherapy.8 In addition to clinical outcomes, the authors evaluated the effects of the medication on background cortical activity. Of interest, monotherapies differed between one another and the combination treatment in their effects on cortical activity. Guanfacine decreased alpha band power and methylphenidate administration was associated with an increase in frontal/central beta power, while combination treatment dampened theta band power and was associated with specific, focal increases in beta power.8 These results, although preliminary, suggest not only that medication results in changes in cortical activity that correlate with symptomatic improvement, but that combination treatment may be associated with a distinct cortical activity pattern that is more than the summation of the effects of the monotherapies. Moreover, these data raise the possibility that this synergistic effect on cortical activity may subtend—or at least—relate to the synergistic clinical effects of the 2 medications.
‘Think it over, think it under’
Having discussed several important Woozles that have inhabited the Hundred Acre Wood of ADHD for decades, it is important to remember there are countless Woozles in the larger “Thousand Acre Wood” of psychiatry and medicine. As we evaluate evidence for our interventions, whether psychopharmacologic or psychotherapeutic, we will do w
1. Milne AA. Winnie-the-Pooh. London, United Kingdom: Methuen & Co. Ltd.; 1926.
2. Strauss MA. Processes Explaining the concealment and distortion of evidence on gender symmetry in partner violence. Eur J Crim Pol Res. 1980;74:227-232.
3. Ritalin LA [package insert]. East Hanover, NJ: Novartis; 2015.
4. Coughlin CG, Cohen SC, Mulqueen JM, et al. Meta-analysis: reduced risk of anxiety with psychostimulant treatment in children with attention-deficit/hyperactivity disorder. J Child Adolesc Psychopharmacol. 2015;25(8):611-617.
5. Abikoff H, McGough J, Vitiello B, et al; RUPP ADHD/Anxiety Study Group. Sequential pharmacotherapy for children with comorbid attention-deficit/hyperactivity and anxiety disorders. J Am Acad Child Adolesc Psychiatry. 2005;44(5):418-427.
6. Bloch MH, Panza KE, Landeros-Weisenberger A, et al. Meta-analysis: treatment of attention-deficit/hyperactivity disorder in children with comorbid tic disorders. J Am Acad Child Adolesc Psychiatry. 2009;48(9):884-893.
7. Cohen SC, Mulqueen JM, Ferracioli-Oda E, et al. Meta-analysis: risk of tics associated with psychostimulant use in randomized, placebo-controlled trials. J Am Acad Child Adolesc Psychiatry. 2015;54(9):728-736.
8. Loo SK, Bilder RM, Cho AL, et al. Effects of d-methylphenidate, guanfacine, and their combination on electroencephalogram resting state spectral power in attention-deficit/hyperactivity disorder. J Am Acad Child Adolesc Psychiatry. 2016;55(8):674-682.e1.
One fine winter’s day when Piglet was brushing away the snow
in front of his house he happened to look up, and there was
Winnie-the-Pooh. Pooh was walking round and round in a circle,
thinking of something else…
So begins the 1926 Winnie-the-Pooh story.1 In this chapter, the well-meaning yellow bear, Winnie-the-Pooh, has found strange tracks in the snow, which he believes belong to a “Woozle.” Pooh follows the tracks, not realizing that he’s walking in a circle. As such, he begins to notice that the tracks have multiplied, which he interprets as evidence of several Woozles.
This “Woozle Effect” has been well described in research settings and is believed to have resulted in conclusions that are not supported by or are inconsistent with the original data, which are then propagated through successive citations, resulting in a scientific “urban legend.”2
Throughout my training from medical school, through fellowship, and during my tenure as a faculty member, I have found myself, at times, searching for Woozles and often have joined my colleagues on these hunts. Herein, I would like to share with you 3 Woozles that have resulted in current false dogmas related to attention-deficit/hyperactivity disorder (ADHD) and stimulant psychopharmacology.
Stimulants worsen anxiety
FDA-required labeling for stimulants includes strong language noting that these drugs are “contraindicated in marked anxiety, tension, and agitation, since the drug may aggravate these symptoms.”3 However, data from randomized controlled trials and meta-analyses consistently have failed to demonstrate this effect. Moreover, sequenced treatment trials involving adolescents with anxiety disorders and co-occurring ADHD suggest that stimulants actually could reduce anxiety symptoms.
A recent meta-analysis4 that evaluated nearly 2 dozen studies involving approximately 3,000 pediatric patients with ADHD reported that stimulant treatment was associated with a decreased relative risk of anxiety (relative risk: 0.86). The study also observed a dose-response relationship between stimulant dosage and anxiety (Figure, page 6).4 Although the authors note that it is possible that some individuals might experience increased anxiety with stimulants, many patients could show improvement in anxiety symptoms when treated with stimulants, and the authors also advise us, as clinicians, to “consider re-challenging children with ADHD who report … anxiety with psychostimulants, as these symptoms are much more likely to be coincidental rather than caused by psychostimulants.”4
More evidence of a lack of stimulant-induced anxiety comes from a large randomized controlled trial of pediatric patients (age 6 to 17) who met DSM-IV criteria for ADHD and a co-occurring anxiety disorder who were treated with methylphenidate (open-label) and then randomized to fluvoxamine or placebo for treatment of anxiety symptoms.5 However, in this trial >80% of the 32 medication-naïve youth improved after stimulant treatment to the point that they no longer had anxiety symptoms severe enough to be eligible for randomization to adjunctive fluvoxamine or placebo.
Stimulants are contraindicated in patients with tic disorders
The package inserts for most stimulant medications warn clinicians that stimulants are “contraindicated in patients with motor tics or with a family history or diagnosis of Tourette’s syndrome.” This is particularly concerning, especially because of the medicolegal implications of the term “contraindicated” and given that as many as 1 in 5 pediatric patients with ADHD have a tic disorder.6 Therefore, labels that list motor tics as a contraindication to stimulant use potentially eliminate the choice of stimulant pharmacotherapy—the most effective treatment for ADHD—for a large number of patients.
When hunting for the Woozle that linked stimulants and tics and led to this language in the package insert, it is worthwhile to review a recent meta-analysis of 22 studies (involving nearly 2,400 youths with ADHD) that suggested new-onset tics or worsening of tics to be present in 5.7% of patients receiving stimulants and in 6.5% of patients receiving placebo. In addition, in this meta-analysis the class of stimulant, dosage, treatment duration, or patient age did not seem to be associated with onset or worsening of tics.7
Polypharmacy represents a therapeutic failure and is not evidence-based
Although treatment guidelines generally have discouraged combination therapy for treating ADHD, there are—on the basis of efficacy—insufficient data to support this prohibition. Moreover, over the last decade, several studies have suggested benefits for combining ADHD medications that have complimentary mechanisms. In this regard, 2 extended-release formulations of α2 agonists have received FDA approval for as adjunctive treatments in pediatric patients with ADHD (extended-release guanfacine and extended-release clonidine). However, despite these FDA indications as adjunctive treatments, many clinicians remain concerned about combination therapy.
Several months ago, a large, 8-week, National Institutes of Health–sponsored trial shed more light on the use of α2agonist + stimulant combinations. Patients age 7 to 17 (N = 179) were randomized to (1) guanfacine + d-methylphenidate, (2) guanfacine monotherapy, or (3) d-methylphenidate monotherapy.8 In addition to clinical outcomes, the authors evaluated the effects of the medication on background cortical activity. Of interest, monotherapies differed between one another and the combination treatment in their effects on cortical activity. Guanfacine decreased alpha band power and methylphenidate administration was associated with an increase in frontal/central beta power, while combination treatment dampened theta band power and was associated with specific, focal increases in beta power.8 These results, although preliminary, suggest not only that medication results in changes in cortical activity that correlate with symptomatic improvement, but that combination treatment may be associated with a distinct cortical activity pattern that is more than the summation of the effects of the monotherapies. Moreover, these data raise the possibility that this synergistic effect on cortical activity may subtend—or at least—relate to the synergistic clinical effects of the 2 medications.
‘Think it over, think it under’
Having discussed several important Woozles that have inhabited the Hundred Acre Wood of ADHD for decades, it is important to remember there are countless Woozles in the larger “Thousand Acre Wood” of psychiatry and medicine. As we evaluate evidence for our interventions, whether psychopharmacologic or psychotherapeutic, we will do w
One fine winter’s day when Piglet was brushing away the snow
in front of his house he happened to look up, and there was
Winnie-the-Pooh. Pooh was walking round and round in a circle,
thinking of something else…
So begins the 1926 Winnie-the-Pooh story.1 In this chapter, the well-meaning yellow bear, Winnie-the-Pooh, has found strange tracks in the snow, which he believes belong to a “Woozle.” Pooh follows the tracks, not realizing that he’s walking in a circle. As such, he begins to notice that the tracks have multiplied, which he interprets as evidence of several Woozles.
This “Woozle Effect” has been well described in research settings and is believed to have resulted in conclusions that are not supported by or are inconsistent with the original data, which are then propagated through successive citations, resulting in a scientific “urban legend.”2
Throughout my training from medical school, through fellowship, and during my tenure as a faculty member, I have found myself, at times, searching for Woozles and often have joined my colleagues on these hunts. Herein, I would like to share with you 3 Woozles that have resulted in current false dogmas related to attention-deficit/hyperactivity disorder (ADHD) and stimulant psychopharmacology.
Stimulants worsen anxiety
FDA-required labeling for stimulants includes strong language noting that these drugs are “contraindicated in marked anxiety, tension, and agitation, since the drug may aggravate these symptoms.”3 However, data from randomized controlled trials and meta-analyses consistently have failed to demonstrate this effect. Moreover, sequenced treatment trials involving adolescents with anxiety disorders and co-occurring ADHD suggest that stimulants actually could reduce anxiety symptoms.
A recent meta-analysis4 that evaluated nearly 2 dozen studies involving approximately 3,000 pediatric patients with ADHD reported that stimulant treatment was associated with a decreased relative risk of anxiety (relative risk: 0.86). The study also observed a dose-response relationship between stimulant dosage and anxiety (Figure, page 6).4 Although the authors note that it is possible that some individuals might experience increased anxiety with stimulants, many patients could show improvement in anxiety symptoms when treated with stimulants, and the authors also advise us, as clinicians, to “consider re-challenging children with ADHD who report … anxiety with psychostimulants, as these symptoms are much more likely to be coincidental rather than caused by psychostimulants.”4
More evidence of a lack of stimulant-induced anxiety comes from a large randomized controlled trial of pediatric patients (age 6 to 17) who met DSM-IV criteria for ADHD and a co-occurring anxiety disorder who were treated with methylphenidate (open-label) and then randomized to fluvoxamine or placebo for treatment of anxiety symptoms.5 However, in this trial >80% of the 32 medication-naïve youth improved after stimulant treatment to the point that they no longer had anxiety symptoms severe enough to be eligible for randomization to adjunctive fluvoxamine or placebo.
Stimulants are contraindicated in patients with tic disorders
The package inserts for most stimulant medications warn clinicians that stimulants are “contraindicated in patients with motor tics or with a family history or diagnosis of Tourette’s syndrome.” This is particularly concerning, especially because of the medicolegal implications of the term “contraindicated” and given that as many as 1 in 5 pediatric patients with ADHD have a tic disorder.6 Therefore, labels that list motor tics as a contraindication to stimulant use potentially eliminate the choice of stimulant pharmacotherapy—the most effective treatment for ADHD—for a large number of patients.
When hunting for the Woozle that linked stimulants and tics and led to this language in the package insert, it is worthwhile to review a recent meta-analysis of 22 studies (involving nearly 2,400 youths with ADHD) that suggested new-onset tics or worsening of tics to be present in 5.7% of patients receiving stimulants and in 6.5% of patients receiving placebo. In addition, in this meta-analysis the class of stimulant, dosage, treatment duration, or patient age did not seem to be associated with onset or worsening of tics.7
Polypharmacy represents a therapeutic failure and is not evidence-based
Although treatment guidelines generally have discouraged combination therapy for treating ADHD, there are—on the basis of efficacy—insufficient data to support this prohibition. Moreover, over the last decade, several studies have suggested benefits for combining ADHD medications that have complimentary mechanisms. In this regard, 2 extended-release formulations of α2 agonists have received FDA approval for as adjunctive treatments in pediatric patients with ADHD (extended-release guanfacine and extended-release clonidine). However, despite these FDA indications as adjunctive treatments, many clinicians remain concerned about combination therapy.
Several months ago, a large, 8-week, National Institutes of Health–sponsored trial shed more light on the use of α2agonist + stimulant combinations. Patients age 7 to 17 (N = 179) were randomized to (1) guanfacine + d-methylphenidate, (2) guanfacine monotherapy, or (3) d-methylphenidate monotherapy.8 In addition to clinical outcomes, the authors evaluated the effects of the medication on background cortical activity. Of interest, monotherapies differed between one another and the combination treatment in their effects on cortical activity. Guanfacine decreased alpha band power and methylphenidate administration was associated with an increase in frontal/central beta power, while combination treatment dampened theta band power and was associated with specific, focal increases in beta power.8 These results, although preliminary, suggest not only that medication results in changes in cortical activity that correlate with symptomatic improvement, but that combination treatment may be associated with a distinct cortical activity pattern that is more than the summation of the effects of the monotherapies. Moreover, these data raise the possibility that this synergistic effect on cortical activity may subtend—or at least—relate to the synergistic clinical effects of the 2 medications.
‘Think it over, think it under’
Having discussed several important Woozles that have inhabited the Hundred Acre Wood of ADHD for decades, it is important to remember there are countless Woozles in the larger “Thousand Acre Wood” of psychiatry and medicine. As we evaluate evidence for our interventions, whether psychopharmacologic or psychotherapeutic, we will do w
1. Milne AA. Winnie-the-Pooh. London, United Kingdom: Methuen & Co. Ltd.; 1926.
2. Strauss MA. Processes Explaining the concealment and distortion of evidence on gender symmetry in partner violence. Eur J Crim Pol Res. 1980;74:227-232.
3. Ritalin LA [package insert]. East Hanover, NJ: Novartis; 2015.
4. Coughlin CG, Cohen SC, Mulqueen JM, et al. Meta-analysis: reduced risk of anxiety with psychostimulant treatment in children with attention-deficit/hyperactivity disorder. J Child Adolesc Psychopharmacol. 2015;25(8):611-617.
5. Abikoff H, McGough J, Vitiello B, et al; RUPP ADHD/Anxiety Study Group. Sequential pharmacotherapy for children with comorbid attention-deficit/hyperactivity and anxiety disorders. J Am Acad Child Adolesc Psychiatry. 2005;44(5):418-427.
6. Bloch MH, Panza KE, Landeros-Weisenberger A, et al. Meta-analysis: treatment of attention-deficit/hyperactivity disorder in children with comorbid tic disorders. J Am Acad Child Adolesc Psychiatry. 2009;48(9):884-893.
7. Cohen SC, Mulqueen JM, Ferracioli-Oda E, et al. Meta-analysis: risk of tics associated with psychostimulant use in randomized, placebo-controlled trials. J Am Acad Child Adolesc Psychiatry. 2015;54(9):728-736.
8. Loo SK, Bilder RM, Cho AL, et al. Effects of d-methylphenidate, guanfacine, and their combination on electroencephalogram resting state spectral power in attention-deficit/hyperactivity disorder. J Am Acad Child Adolesc Psychiatry. 2016;55(8):674-682.e1.
1. Milne AA. Winnie-the-Pooh. London, United Kingdom: Methuen & Co. Ltd.; 1926.
2. Strauss MA. Processes Explaining the concealment and distortion of evidence on gender symmetry in partner violence. Eur J Crim Pol Res. 1980;74:227-232.
3. Ritalin LA [package insert]. East Hanover, NJ: Novartis; 2015.
4. Coughlin CG, Cohen SC, Mulqueen JM, et al. Meta-analysis: reduced risk of anxiety with psychostimulant treatment in children with attention-deficit/hyperactivity disorder. J Child Adolesc Psychopharmacol. 2015;25(8):611-617.
5. Abikoff H, McGough J, Vitiello B, et al; RUPP ADHD/Anxiety Study Group. Sequential pharmacotherapy for children with comorbid attention-deficit/hyperactivity and anxiety disorders. J Am Acad Child Adolesc Psychiatry. 2005;44(5):418-427.
6. Bloch MH, Panza KE, Landeros-Weisenberger A, et al. Meta-analysis: treatment of attention-deficit/hyperactivity disorder in children with comorbid tic disorders. J Am Acad Child Adolesc Psychiatry. 2009;48(9):884-893.
7. Cohen SC, Mulqueen JM, Ferracioli-Oda E, et al. Meta-analysis: risk of tics associated with psychostimulant use in randomized, placebo-controlled trials. J Am Acad Child Adolesc Psychiatry. 2015;54(9):728-736.
8. Loo SK, Bilder RM, Cho AL, et al. Effects of d-methylphenidate, guanfacine, and their combination on electroencephalogram resting state spectral power in attention-deficit/hyperactivity disorder. J Am Acad Child Adolesc Psychiatry. 2016;55(8):674-682.e1.
A tool to help limit patients’ sodium intake
The average American consumes about 3400 mg/d of sodium, which is more than double the 1500 mg recommended by the American Heart Association.1 Excess sodium added to foods during commercial processing and preparation represents the main source of sodium intake in American diets.2 Nevertheless, adding salt at the table is still very common, and people who add salt at the table have 1.5 g higher salt intakes than those who do not add salt.3 And as we know, high sodium intake has been associated with elevated blood pressure and an increased rate of cardiovascular disease.4
I have designed a self-produced “Salt Awareness—Limit Today” (SALT) label (FIGURE). This label is attached to the cap of a salt shaker in such a way that less salt flows through the openings of the cap. Moreover, the label serves as a reminder to limit salt intake in general. The feedback I have received from my patients has been extremely positive; they report increased awareness and decreased sodium intake. I mention it here so that others may benefit.
Zvi Weizman, MD
Beer-Sheva, Israel
1. Cobb LK, Anderson CA, Elliott P, et al; American Heart Association Council on Lifestyle and Metabolic Health. Methodological issues in cohort studies that relate sodium intake to cardiovascular disease outcomes: a science advisory from the American Heart Association. Circulation. 2014;129:1173-1186.
2. Jackson SL, King SM, Zhao L, et al. Prevalence of excess sodium intake in the United States - NHANES, 2009-2012. MMWR Morb Mortal Wkly Rep. 2016;64:1393-1397.
3. Webster J, Su’a SA, Ieremia M, et al. Salt intakes, knowledge, and behavior in Samoa: Monitoring salt-consumption patterns through the World Health Organization’s surveillance of noncommunicable disease risk factors (STEPS). J Clin Hypertens (Greenwich). 2016.
4. Mozaffarian D, Fahimi S, Singh GM, et al; Global Burden of Diseases Nutrition and Chronic Diseases Expert Group. Global sodium consumption and death from cardiovascular causes. N Engl J Med. 2014;371:624-634.
The average American consumes about 3400 mg/d of sodium, which is more than double the 1500 mg recommended by the American Heart Association.1 Excess sodium added to foods during commercial processing and preparation represents the main source of sodium intake in American diets.2 Nevertheless, adding salt at the table is still very common, and people who add salt at the table have 1.5 g higher salt intakes than those who do not add salt.3 And as we know, high sodium intake has been associated with elevated blood pressure and an increased rate of cardiovascular disease.4
I have designed a self-produced “Salt Awareness—Limit Today” (SALT) label (FIGURE). This label is attached to the cap of a salt shaker in such a way that less salt flows through the openings of the cap. Moreover, the label serves as a reminder to limit salt intake in general. The feedback I have received from my patients has been extremely positive; they report increased awareness and decreased sodium intake. I mention it here so that others may benefit.
Zvi Weizman, MD
Beer-Sheva, Israel
The average American consumes about 3400 mg/d of sodium, which is more than double the 1500 mg recommended by the American Heart Association.1 Excess sodium added to foods during commercial processing and preparation represents the main source of sodium intake in American diets.2 Nevertheless, adding salt at the table is still very common, and people who add salt at the table have 1.5 g higher salt intakes than those who do not add salt.3 And as we know, high sodium intake has been associated with elevated blood pressure and an increased rate of cardiovascular disease.4
I have designed a self-produced “Salt Awareness—Limit Today” (SALT) label (FIGURE). This label is attached to the cap of a salt shaker in such a way that less salt flows through the openings of the cap. Moreover, the label serves as a reminder to limit salt intake in general. The feedback I have received from my patients has been extremely positive; they report increased awareness and decreased sodium intake. I mention it here so that others may benefit.
Zvi Weizman, MD
Beer-Sheva, Israel
1. Cobb LK, Anderson CA, Elliott P, et al; American Heart Association Council on Lifestyle and Metabolic Health. Methodological issues in cohort studies that relate sodium intake to cardiovascular disease outcomes: a science advisory from the American Heart Association. Circulation. 2014;129:1173-1186.
2. Jackson SL, King SM, Zhao L, et al. Prevalence of excess sodium intake in the United States - NHANES, 2009-2012. MMWR Morb Mortal Wkly Rep. 2016;64:1393-1397.
3. Webster J, Su’a SA, Ieremia M, et al. Salt intakes, knowledge, and behavior in Samoa: Monitoring salt-consumption patterns through the World Health Organization’s surveillance of noncommunicable disease risk factors (STEPS). J Clin Hypertens (Greenwich). 2016.
4. Mozaffarian D, Fahimi S, Singh GM, et al; Global Burden of Diseases Nutrition and Chronic Diseases Expert Group. Global sodium consumption and death from cardiovascular causes. N Engl J Med. 2014;371:624-634.
1. Cobb LK, Anderson CA, Elliott P, et al; American Heart Association Council on Lifestyle and Metabolic Health. Methodological issues in cohort studies that relate sodium intake to cardiovascular disease outcomes: a science advisory from the American Heart Association. Circulation. 2014;129:1173-1186.
2. Jackson SL, King SM, Zhao L, et al. Prevalence of excess sodium intake in the United States - NHANES, 2009-2012. MMWR Morb Mortal Wkly Rep. 2016;64:1393-1397.
3. Webster J, Su’a SA, Ieremia M, et al. Salt intakes, knowledge, and behavior in Samoa: Monitoring salt-consumption patterns through the World Health Organization’s surveillance of noncommunicable disease risk factors (STEPS). J Clin Hypertens (Greenwich). 2016.
4. Mozaffarian D, Fahimi S, Singh GM, et al; Global Burden of Diseases Nutrition and Chronic Diseases Expert Group. Global sodium consumption and death from cardiovascular causes. N Engl J Med. 2014;371:624-634.
Point-of-care ultrasound: It’s no replacement for the stethoscope
In his August editorial, Dr. Hickner noted that an article in the issue prompted him to “wonder whether ultrasound might become the stethoscope of the future” (J Fam Pract. 2016;65:516). To that I say that we need to avoid conflating the stethoscope with point-of-care ultrasound (POCUS).
It is well documented that auscultation skills rapidly deteriorate (specifically in the cardiology realm) in clinical practice.1 This may occur because many physicians already think ultrasound can replace actually listening to their patients’ hearts. The motto has become, “I’ll just order an echo.”
POCUS is an imaging modality. Period. It can be used to auscultate, but Doppler ultrasound is not as precise as the stethoscope when used by a practiced listener for identifying the source and subtle characteristics of murmurs.2 The stethoscope remains an outstanding, inexpensive, and convenient screening tool and its use needs to be emphasized.
I strongly believe in training all medical students in POCUS—but as a complementary and adjunctive tool—not as something to replace a perfectly functional piece of equipment used around the world to provide good care.
Todd Fredricks, DO
Athens, Ohio
1. Vukanovic-Criley JM, Hovanesyan A, Criley SR, et al. Confidential testing of cardiac examination competency in cardiology and noncardiology faculty and trainees: a multicenter study. Clin Cardiol. 2010;33:738-745.
2. Tavel ME. Cardiac auscultation. A glorious past—but does it have a future? Circulation. 1996;93:1250-1253.
In his August editorial, Dr. Hickner noted that an article in the issue prompted him to “wonder whether ultrasound might become the stethoscope of the future” (J Fam Pract. 2016;65:516). To that I say that we need to avoid conflating the stethoscope with point-of-care ultrasound (POCUS).
It is well documented that auscultation skills rapidly deteriorate (specifically in the cardiology realm) in clinical practice.1 This may occur because many physicians already think ultrasound can replace actually listening to their patients’ hearts. The motto has become, “I’ll just order an echo.”
POCUS is an imaging modality. Period. It can be used to auscultate, but Doppler ultrasound is not as precise as the stethoscope when used by a practiced listener for identifying the source and subtle characteristics of murmurs.2 The stethoscope remains an outstanding, inexpensive, and convenient screening tool and its use needs to be emphasized.
I strongly believe in training all medical students in POCUS—but as a complementary and adjunctive tool—not as something to replace a perfectly functional piece of equipment used around the world to provide good care.
Todd Fredricks, DO
Athens, Ohio
In his August editorial, Dr. Hickner noted that an article in the issue prompted him to “wonder whether ultrasound might become the stethoscope of the future” (J Fam Pract. 2016;65:516). To that I say that we need to avoid conflating the stethoscope with point-of-care ultrasound (POCUS).
It is well documented that auscultation skills rapidly deteriorate (specifically in the cardiology realm) in clinical practice.1 This may occur because many physicians already think ultrasound can replace actually listening to their patients’ hearts. The motto has become, “I’ll just order an echo.”
POCUS is an imaging modality. Period. It can be used to auscultate, but Doppler ultrasound is not as precise as the stethoscope when used by a practiced listener for identifying the source and subtle characteristics of murmurs.2 The stethoscope remains an outstanding, inexpensive, and convenient screening tool and its use needs to be emphasized.
I strongly believe in training all medical students in POCUS—but as a complementary and adjunctive tool—not as something to replace a perfectly functional piece of equipment used around the world to provide good care.
Todd Fredricks, DO
Athens, Ohio
1. Vukanovic-Criley JM, Hovanesyan A, Criley SR, et al. Confidential testing of cardiac examination competency in cardiology and noncardiology faculty and trainees: a multicenter study. Clin Cardiol. 2010;33:738-745.
2. Tavel ME. Cardiac auscultation. A glorious past—but does it have a future? Circulation. 1996;93:1250-1253.
1. Vukanovic-Criley JM, Hovanesyan A, Criley SR, et al. Confidential testing of cardiac examination competency in cardiology and noncardiology faculty and trainees: a multicenter study. Clin Cardiol. 2010;33:738-745.
2. Tavel ME. Cardiac auscultation. A glorious past—but does it have a future? Circulation. 1996;93:1250-1253.
Rethinking A1C targets for patients with mental illness?
The article, “Diabetes update: Your guide to the latest ADA standards,” by Shubrook, et al (J Fam Pract. 2016;65:310-318) is a precise review of current recommendations for diabetes. We would like to draw attention, however, to comorbid diabetes and mental illness.
Diabetes and serious mental illness often coincide, making the treatment of both conditions difficult and leading to higher rates of complications.1
The American Diabetes Association (ADA)’s “Standards of Medical Care in Diabetes” recognizes that hemoglobin A1C targets for patients should be individualized.2 We consider it important to discus
For example, a more lenient A1C goal may be appropriate when:
- the assessment of the patient shows that he or she is struggling with active symptoms of mental illness
- new medications with undesirable metabolic effects are prescribed or titrated
- social support is poor
- patients have limited confidence in their ability to accomplish tasks and goals
- patients have cognitive limitations
- patients abuse substances.
We suggest that when factors are favorable (eg, younger patient, well-controlled serious mental illness, adequate support, good cognitive skills, no hazardous use of substances, good level of confidence in the ability to control diabetes), the A1C target can be set lower. When the factors are less favorable (eg, older patient, poorly controlled mental illness, abusing substances, cognitive impairment), the target should be set higher and incrementally reduced as care engagement, circumstances, and symptom control improve.
There is a need for further research to investigate the factors that can impact diabetes self-management in patients with comorbid mental illness.
Corinna Falck-Ytter, MD
Stephanie W. Kanuch, MEd
Richard McCormick, PhD
Michael Purdum, PhD
Neal V. Dawson, MD
Shari D. Bolen, MD, MPH
Martha Sajatovic, MD
Cleveland, Ohio
1. Ducat L, Philipson LH, Anderson BJ. The mental health comorbidities of diabetes. JAMA. 2014;312:691-692.
2. American Diabetes Association. Standards of Medical Care in Diabetes—2016. Diabetes Care. 2016;39(Suppl 1). Available at: http://care.diabetesjournals.org/content/diacare/suppl/2015/12/21/39.Supplement_1.DC2/2016-Standards-of-Care.pdf. Accessed May 18, 2016.
The article, “Diabetes update: Your guide to the latest ADA standards,” by Shubrook, et al (J Fam Pract. 2016;65:310-318) is a precise review of current recommendations for diabetes. We would like to draw attention, however, to comorbid diabetes and mental illness.
Diabetes and serious mental illness often coincide, making the treatment of both conditions difficult and leading to higher rates of complications.1
The American Diabetes Association (ADA)’s “Standards of Medical Care in Diabetes” recognizes that hemoglobin A1C targets for patients should be individualized.2 We consider it important to discus
For example, a more lenient A1C goal may be appropriate when:
- the assessment of the patient shows that he or she is struggling with active symptoms of mental illness
- new medications with undesirable metabolic effects are prescribed or titrated
- social support is poor
- patients have limited confidence in their ability to accomplish tasks and goals
- patients have cognitive limitations
- patients abuse substances.
We suggest that when factors are favorable (eg, younger patient, well-controlled serious mental illness, adequate support, good cognitive skills, no hazardous use of substances, good level of confidence in the ability to control diabetes), the A1C target can be set lower. When the factors are less favorable (eg, older patient, poorly controlled mental illness, abusing substances, cognitive impairment), the target should be set higher and incrementally reduced as care engagement, circumstances, and symptom control improve.
There is a need for further research to investigate the factors that can impact diabetes self-management in patients with comorbid mental illness.
Corinna Falck-Ytter, MD
Stephanie W. Kanuch, MEd
Richard McCormick, PhD
Michael Purdum, PhD
Neal V. Dawson, MD
Shari D. Bolen, MD, MPH
Martha Sajatovic, MD
Cleveland, Ohio
The article, “Diabetes update: Your guide to the latest ADA standards,” by Shubrook, et al (J Fam Pract. 2016;65:310-318) is a precise review of current recommendations for diabetes. We would like to draw attention, however, to comorbid diabetes and mental illness.
Diabetes and serious mental illness often coincide, making the treatment of both conditions difficult and leading to higher rates of complications.1
The American Diabetes Association (ADA)’s “Standards of Medical Care in Diabetes” recognizes that hemoglobin A1C targets for patients should be individualized.2 We consider it important to discus
For example, a more lenient A1C goal may be appropriate when:
- the assessment of the patient shows that he or she is struggling with active symptoms of mental illness
- new medications with undesirable metabolic effects are prescribed or titrated
- social support is poor
- patients have limited confidence in their ability to accomplish tasks and goals
- patients have cognitive limitations
- patients abuse substances.
We suggest that when factors are favorable (eg, younger patient, well-controlled serious mental illness, adequate support, good cognitive skills, no hazardous use of substances, good level of confidence in the ability to control diabetes), the A1C target can be set lower. When the factors are less favorable (eg, older patient, poorly controlled mental illness, abusing substances, cognitive impairment), the target should be set higher and incrementally reduced as care engagement, circumstances, and symptom control improve.
There is a need for further research to investigate the factors that can impact diabetes self-management in patients with comorbid mental illness.
Corinna Falck-Ytter, MD
Stephanie W. Kanuch, MEd
Richard McCormick, PhD
Michael Purdum, PhD
Neal V. Dawson, MD
Shari D. Bolen, MD, MPH
Martha Sajatovic, MD
Cleveland, Ohio
1. Ducat L, Philipson LH, Anderson BJ. The mental health comorbidities of diabetes. JAMA. 2014;312:691-692.
2. American Diabetes Association. Standards of Medical Care in Diabetes—2016. Diabetes Care. 2016;39(Suppl 1). Available at: http://care.diabetesjournals.org/content/diacare/suppl/2015/12/21/39.Supplement_1.DC2/2016-Standards-of-Care.pdf. Accessed May 18, 2016.
1. Ducat L, Philipson LH, Anderson BJ. The mental health comorbidities of diabetes. JAMA. 2014;312:691-692.
2. American Diabetes Association. Standards of Medical Care in Diabetes—2016. Diabetes Care. 2016;39(Suppl 1). Available at: http://care.diabetesjournals.org/content/diacare/suppl/2015/12/21/39.Supplement_1.DC2/2016-Standards-of-Care.pdf. Accessed May 18, 2016.
Who’s On First: A Look at Workforce Projections
Predicting the future, particularly in the ever-changing realm of health care, is always a gamble. The variables with the potential to impact health care—among them, unpredictable political agendas, unforeseen economic upheaval, and technological issues—make it difficult to identify one “expected” outcome. However, one forecasted trend will certainly make a difference: the quantity of well-educated health care practitioners.
This factor will be one of the most important determinants of our ability to deliver quality, accessible health care in a diverse society with increasingly complex medical needs. Some may say that this is an irrational fear—the US health care system is remarkably adaptable, and as far as we can tell, no serious problems have arisen due to a shortage of providers. So are we overreacting, or is there a viable reason for concern?
While more and more Americans are covered by health insurance thanks to the Affordable Care Act, fewer physicians are entering primary care. The Association of American Medical Colleges (AAMC) has projected a shortage of between 46,000 and 90,000 physicians by 2025. AAMC forecasts a shortage of 12,500 to 31,100 primary care physicians and 21,200 to 63,700 non–primary care physicians; much of the latter deficit will be in the surgical specialties.1 The report emphasizes the need for immediate action because it takes almost a decade to educate a physician for entry into the workforce.
On the surface, these numbers are quite staggering. They may even elicit a sense of doom about access to quality (or even simply adequate) health care in the next decade. To put these projections in context, here are some key statistics
- About 915,000 physicians actively practice in the US.2
- Each year, about 20,000 medical school students graduate and enter postgraduate education.3
- Thirty percent of physicians are older than 60.2
- In 2015, there were 100,000 practicing PAs, with an average age of 38.4
- As of 2016, there are 222,000 practicing NPs, with an average age of 49.5
The US population is projected to increase from 310 million in 2015 to 335 million in 2025.6 There are approximately 45 million Americans older than 65, a number that is projected to increase to almost 70 million by 2025.7,8
This inverse relationship—more potential patients and fewer people to care for them—suggests perilous changes for our health care system. Some anticipated changes—longer wait times for care, increased costs, and more opportunities for error—are real and have already been quantified in reports.9 But with the year 2025 less than a decade away, where is our sense of urgency? Even if we implement changes immediately, they are unlikely to offset the consequences of the workforce shortage. Yet to do nothing will lead to a rapid decline in quality of life for many Americans.
In theory, there are two ways to address this pending “crisis.” We can decrease demand and/or increase supply. In the next few decades, achieving the former will be difficult, because of the unavoidable toll of an aging population. Public health and preventive services may have some impact and deserve increased attention. New and improved modes of treatment offer the potential to ameliorate the impact of chronic diseases such as diabetes and cardiovascular disease. This method, while a noble goal, is also less predictable and harder to “plan” for.
The most direct approach (but certainly not the only one) is to increase the supply of health care providers—specifically, NPs and PAs—in order to meet the rising demand. The professions have long been touted as a solution to problems of access to care in both rural and urban areas. About 83% of NPs are certified in primary care; we cannot ignore the fact that only 24% of PAs practice in primary care while the rest have chosen specialties. But (another plus) patients tend to be as satisfied with care provided by NPs and PAs as by physicians.10,11
Increasing the supply of NPs and PAs requires educating more individuals to enter the professions. Education programs need to do a critical analysis of their curricula to ensure that what happens in the classroom matches real-world needs. If graduates enter the workforce unprepared for the demands of the job, no progress will be made. (For a vigorous discussion on the current state of professional education, please visit www.mdedge.com/clinicianreviews/commentary).
One significant limitation to the growth of the PA supply is the accreditation process, which now takes almost three years from the start of the process until the initial approval of a class (and five years until the first class graduates). This process adds time and expense to the creation of new education programs, many of which await approval and lack the resources to bring the program to maturity. While no one would argue the value of the ARC-PA accreditation, the process should be critically examined to identify any areas that can be streamlined without decreasing the quality of the product.
Which brings us to perhaps the most important aspect of this discussion: What actions need to be taken to mitigate the possible damage of a physician shortage? Here are some recommendations for a variety of stakeholders:
Educators should enhance their competency-based curriculum to enable NPs and PAs to move through their programs at a faster stride (again, without sacrificing valuable learning time) and get into practice sooner.
Accreditors should review current standards and remove barriers to allow education programs to create innovative curricula that help NPs and PAs gain the knowledge (and experience) they need to move into practice.
Regulators should ensure that NPs and PAs are able to practice to the fullest extent of their license and scope of practice (ie, full practice authority, scope of practice determined at the practice level). Barriers should be removed to allow these clinicians to function in rural and underserved regions of the country (eg, adaptable collaboration requirements).10 (For a different perspective on PA autonomy, see here.)
Policymakers should rally around the removal of barriers to postgraduate residencies, which would sustain and possibly increase the physician supply. Reimbursement, particularly in Medicare, should be re-evaluated to assure that all providers are reimbursed for same services. Lack of parity in reimbursement infers a difference in quality that is just not the case.
Practicing NPs and PAs should step up to the plate and volunteer as preceptors to give NP and PA students the opportunity to learn from the best and most experienced.
Physicians should seek out alternatives to retirement from medicine (ie working part-time, becoming an educator). Expanding the period of clinical practice may forestall, or even prevent, some of the shortage—at least, in the short-term.
There are those who say that a provider shortage does not exist and that those crying out about it have a vested interest in expanding medical school output. Others acknowledge the shortage but worry that increasing the supply of NPs and PAs will ultimately “devalue” individual providers (ie, drive down salaries). One thing, however, is certain: As Danish physicist Niels Bohr said, “Prediction is very difficult, especially if it’s about the future.”
What are your thoughts and ideas about the health care workforce and the increasing demand for care? Please share them with us by writing to [email protected].
1. Association of American Medical Colleges. The complexities of physician supply and demand: projections from 2013 to 2025. Washington, DC: HIS, Inc; 2015. www.aamc.org/download/426242/data/ihsreportdownload.pdf. Accessed September 8, 2016.
2. Young A, Chaudhry HJ, Pei X, et al. A census of actively licensed physicians in the United States, 2014. J Med Regulation. 2014;96(4): 10-20.
3. Association of American Medical Colleges. Table B-2.2: total graduates by US medical school and sex, 2010-2011 through 2014-2015. www.aamc.org/download/321532/data/factstableb2-2.pdf. Accessed September 8, 2016.
4. National Commission on Certification of Physician Assistants. 2015 statistical profile of certified physician assistants. www.nccpa.net/Uploads/docs/2015StatisticalProfileofCertifiedPhysicianAssistants.pdf. Accessed September 8, 2016.
5. American Association of Nurse Practitioners. NP fact sheet. www.aanp.org/all-about-nps/np-fact-sheet. Accessed September 8, 2016.
6. US Department of Commerce. Population projections of the United States by age, sex, race, and hispanic origin: 1995 to 2050. www.census.gov/prod/1/pop/p25-1130.pdf. Accessed September 8, 2016.
7. Mather M, Jacobsen LA, Pollard KP. Aging in the United States. Popul Bull. 2015;70:1-23.
8. Ortman JM, Velkoff VA, Hogan HH. An aging nation: the older population in the United States. US Census Bureau. 2014;P25-1140.
9. Institute of Medicine. Crossing the Quality Chasm: A New Health System for the 21st Century. www.nap.edu/books/0309072808/html. Accessed September 8, 2016.
10. Garment V. Nurse practitioners and physician assistants: why you should hire one (or the other). The Profitable Practice blog. 2013. http://profitable-practice.softwareadvice.com/nurse-practitioners-and-physician-assistants-why-you-should-hire-one-or-the-other-0513. Accessed September 8, 2016.
11. American Academy of Physician Assistants. Six key elements. www.aapa.org/six-key-elements. Accessed September 8, 2016.
Randy D. Danielsen, PhD, PA, DFAAPA
O.T. Wendel, PhD
Randy D. Danielsen, PhD, PA, DFAAPA
O.T. Wendel, PhD
Randy D. Danielsen, PhD, PA, DFAAPA
O.T. Wendel, PhD
Predicting the future, particularly in the ever-changing realm of health care, is always a gamble. The variables with the potential to impact health care—among them, unpredictable political agendas, unforeseen economic upheaval, and technological issues—make it difficult to identify one “expected” outcome. However, one forecasted trend will certainly make a difference: the quantity of well-educated health care practitioners.
This factor will be one of the most important determinants of our ability to deliver quality, accessible health care in a diverse society with increasingly complex medical needs. Some may say that this is an irrational fear—the US health care system is remarkably adaptable, and as far as we can tell, no serious problems have arisen due to a shortage of providers. So are we overreacting, or is there a viable reason for concern?
While more and more Americans are covered by health insurance thanks to the Affordable Care Act, fewer physicians are entering primary care. The Association of American Medical Colleges (AAMC) has projected a shortage of between 46,000 and 90,000 physicians by 2025. AAMC forecasts a shortage of 12,500 to 31,100 primary care physicians and 21,200 to 63,700 non–primary care physicians; much of the latter deficit will be in the surgical specialties.1 The report emphasizes the need for immediate action because it takes almost a decade to educate a physician for entry into the workforce.
On the surface, these numbers are quite staggering. They may even elicit a sense of doom about access to quality (or even simply adequate) health care in the next decade. To put these projections in context, here are some key statistics
- About 915,000 physicians actively practice in the US.2
- Each year, about 20,000 medical school students graduate and enter postgraduate education.3
- Thirty percent of physicians are older than 60.2
- In 2015, there were 100,000 practicing PAs, with an average age of 38.4
- As of 2016, there are 222,000 practicing NPs, with an average age of 49.5
The US population is projected to increase from 310 million in 2015 to 335 million in 2025.6 There are approximately 45 million Americans older than 65, a number that is projected to increase to almost 70 million by 2025.7,8
This inverse relationship—more potential patients and fewer people to care for them—suggests perilous changes for our health care system. Some anticipated changes—longer wait times for care, increased costs, and more opportunities for error—are real and have already been quantified in reports.9 But with the year 2025 less than a decade away, where is our sense of urgency? Even if we implement changes immediately, they are unlikely to offset the consequences of the workforce shortage. Yet to do nothing will lead to a rapid decline in quality of life for many Americans.
In theory, there are two ways to address this pending “crisis.” We can decrease demand and/or increase supply. In the next few decades, achieving the former will be difficult, because of the unavoidable toll of an aging population. Public health and preventive services may have some impact and deserve increased attention. New and improved modes of treatment offer the potential to ameliorate the impact of chronic diseases such as diabetes and cardiovascular disease. This method, while a noble goal, is also less predictable and harder to “plan” for.
The most direct approach (but certainly not the only one) is to increase the supply of health care providers—specifically, NPs and PAs—in order to meet the rising demand. The professions have long been touted as a solution to problems of access to care in both rural and urban areas. About 83% of NPs are certified in primary care; we cannot ignore the fact that only 24% of PAs practice in primary care while the rest have chosen specialties. But (another plus) patients tend to be as satisfied with care provided by NPs and PAs as by physicians.10,11
Increasing the supply of NPs and PAs requires educating more individuals to enter the professions. Education programs need to do a critical analysis of their curricula to ensure that what happens in the classroom matches real-world needs. If graduates enter the workforce unprepared for the demands of the job, no progress will be made. (For a vigorous discussion on the current state of professional education, please visit www.mdedge.com/clinicianreviews/commentary).
One significant limitation to the growth of the PA supply is the accreditation process, which now takes almost three years from the start of the process until the initial approval of a class (and five years until the first class graduates). This process adds time and expense to the creation of new education programs, many of which await approval and lack the resources to bring the program to maturity. While no one would argue the value of the ARC-PA accreditation, the process should be critically examined to identify any areas that can be streamlined without decreasing the quality of the product.
Which brings us to perhaps the most important aspect of this discussion: What actions need to be taken to mitigate the possible damage of a physician shortage? Here are some recommendations for a variety of stakeholders:
Educators should enhance their competency-based curriculum to enable NPs and PAs to move through their programs at a faster stride (again, without sacrificing valuable learning time) and get into practice sooner.
Accreditors should review current standards and remove barriers to allow education programs to create innovative curricula that help NPs and PAs gain the knowledge (and experience) they need to move into practice.
Regulators should ensure that NPs and PAs are able to practice to the fullest extent of their license and scope of practice (ie, full practice authority, scope of practice determined at the practice level). Barriers should be removed to allow these clinicians to function in rural and underserved regions of the country (eg, adaptable collaboration requirements).10 (For a different perspective on PA autonomy, see here.)
Policymakers should rally around the removal of barriers to postgraduate residencies, which would sustain and possibly increase the physician supply. Reimbursement, particularly in Medicare, should be re-evaluated to assure that all providers are reimbursed for same services. Lack of parity in reimbursement infers a difference in quality that is just not the case.
Practicing NPs and PAs should step up to the plate and volunteer as preceptors to give NP and PA students the opportunity to learn from the best and most experienced.
Physicians should seek out alternatives to retirement from medicine (ie working part-time, becoming an educator). Expanding the period of clinical practice may forestall, or even prevent, some of the shortage—at least, in the short-term.
There are those who say that a provider shortage does not exist and that those crying out about it have a vested interest in expanding medical school output. Others acknowledge the shortage but worry that increasing the supply of NPs and PAs will ultimately “devalue” individual providers (ie, drive down salaries). One thing, however, is certain: As Danish physicist Niels Bohr said, “Prediction is very difficult, especially if it’s about the future.”
What are your thoughts and ideas about the health care workforce and the increasing demand for care? Please share them with us by writing to [email protected].
Predicting the future, particularly in the ever-changing realm of health care, is always a gamble. The variables with the potential to impact health care—among them, unpredictable political agendas, unforeseen economic upheaval, and technological issues—make it difficult to identify one “expected” outcome. However, one forecasted trend will certainly make a difference: the quantity of well-educated health care practitioners.
This factor will be one of the most important determinants of our ability to deliver quality, accessible health care in a diverse society with increasingly complex medical needs. Some may say that this is an irrational fear—the US health care system is remarkably adaptable, and as far as we can tell, no serious problems have arisen due to a shortage of providers. So are we overreacting, or is there a viable reason for concern?
While more and more Americans are covered by health insurance thanks to the Affordable Care Act, fewer physicians are entering primary care. The Association of American Medical Colleges (AAMC) has projected a shortage of between 46,000 and 90,000 physicians by 2025. AAMC forecasts a shortage of 12,500 to 31,100 primary care physicians and 21,200 to 63,700 non–primary care physicians; much of the latter deficit will be in the surgical specialties.1 The report emphasizes the need for immediate action because it takes almost a decade to educate a physician for entry into the workforce.
On the surface, these numbers are quite staggering. They may even elicit a sense of doom about access to quality (or even simply adequate) health care in the next decade. To put these projections in context, here are some key statistics
- About 915,000 physicians actively practice in the US.2
- Each year, about 20,000 medical school students graduate and enter postgraduate education.3
- Thirty percent of physicians are older than 60.2
- In 2015, there were 100,000 practicing PAs, with an average age of 38.4
- As of 2016, there are 222,000 practicing NPs, with an average age of 49.5
The US population is projected to increase from 310 million in 2015 to 335 million in 2025.6 There are approximately 45 million Americans older than 65, a number that is projected to increase to almost 70 million by 2025.7,8
This inverse relationship—more potential patients and fewer people to care for them—suggests perilous changes for our health care system. Some anticipated changes—longer wait times for care, increased costs, and more opportunities for error—are real and have already been quantified in reports.9 But with the year 2025 less than a decade away, where is our sense of urgency? Even if we implement changes immediately, they are unlikely to offset the consequences of the workforce shortage. Yet to do nothing will lead to a rapid decline in quality of life for many Americans.
In theory, there are two ways to address this pending “crisis.” We can decrease demand and/or increase supply. In the next few decades, achieving the former will be difficult, because of the unavoidable toll of an aging population. Public health and preventive services may have some impact and deserve increased attention. New and improved modes of treatment offer the potential to ameliorate the impact of chronic diseases such as diabetes and cardiovascular disease. This method, while a noble goal, is also less predictable and harder to “plan” for.
The most direct approach (but certainly not the only one) is to increase the supply of health care providers—specifically, NPs and PAs—in order to meet the rising demand. The professions have long been touted as a solution to problems of access to care in both rural and urban areas. About 83% of NPs are certified in primary care; we cannot ignore the fact that only 24% of PAs practice in primary care while the rest have chosen specialties. But (another plus) patients tend to be as satisfied with care provided by NPs and PAs as by physicians.10,11
Increasing the supply of NPs and PAs requires educating more individuals to enter the professions. Education programs need to do a critical analysis of their curricula to ensure that what happens in the classroom matches real-world needs. If graduates enter the workforce unprepared for the demands of the job, no progress will be made. (For a vigorous discussion on the current state of professional education, please visit www.mdedge.com/clinicianreviews/commentary).
One significant limitation to the growth of the PA supply is the accreditation process, which now takes almost three years from the start of the process until the initial approval of a class (and five years until the first class graduates). This process adds time and expense to the creation of new education programs, many of which await approval and lack the resources to bring the program to maturity. While no one would argue the value of the ARC-PA accreditation, the process should be critically examined to identify any areas that can be streamlined without decreasing the quality of the product.
Which brings us to perhaps the most important aspect of this discussion: What actions need to be taken to mitigate the possible damage of a physician shortage? Here are some recommendations for a variety of stakeholders:
Educators should enhance their competency-based curriculum to enable NPs and PAs to move through their programs at a faster stride (again, without sacrificing valuable learning time) and get into practice sooner.
Accreditors should review current standards and remove barriers to allow education programs to create innovative curricula that help NPs and PAs gain the knowledge (and experience) they need to move into practice.
Regulators should ensure that NPs and PAs are able to practice to the fullest extent of their license and scope of practice (ie, full practice authority, scope of practice determined at the practice level). Barriers should be removed to allow these clinicians to function in rural and underserved regions of the country (eg, adaptable collaboration requirements).10 (For a different perspective on PA autonomy, see here.)
Policymakers should rally around the removal of barriers to postgraduate residencies, which would sustain and possibly increase the physician supply. Reimbursement, particularly in Medicare, should be re-evaluated to assure that all providers are reimbursed for same services. Lack of parity in reimbursement infers a difference in quality that is just not the case.
Practicing NPs and PAs should step up to the plate and volunteer as preceptors to give NP and PA students the opportunity to learn from the best and most experienced.
Physicians should seek out alternatives to retirement from medicine (ie working part-time, becoming an educator). Expanding the period of clinical practice may forestall, or even prevent, some of the shortage—at least, in the short-term.
There are those who say that a provider shortage does not exist and that those crying out about it have a vested interest in expanding medical school output. Others acknowledge the shortage but worry that increasing the supply of NPs and PAs will ultimately “devalue” individual providers (ie, drive down salaries). One thing, however, is certain: As Danish physicist Niels Bohr said, “Prediction is very difficult, especially if it’s about the future.”
What are your thoughts and ideas about the health care workforce and the increasing demand for care? Please share them with us by writing to [email protected].
1. Association of American Medical Colleges. The complexities of physician supply and demand: projections from 2013 to 2025. Washington, DC: HIS, Inc; 2015. www.aamc.org/download/426242/data/ihsreportdownload.pdf. Accessed September 8, 2016.
2. Young A, Chaudhry HJ, Pei X, et al. A census of actively licensed physicians in the United States, 2014. J Med Regulation. 2014;96(4): 10-20.
3. Association of American Medical Colleges. Table B-2.2: total graduates by US medical school and sex, 2010-2011 through 2014-2015. www.aamc.org/download/321532/data/factstableb2-2.pdf. Accessed September 8, 2016.
4. National Commission on Certification of Physician Assistants. 2015 statistical profile of certified physician assistants. www.nccpa.net/Uploads/docs/2015StatisticalProfileofCertifiedPhysicianAssistants.pdf. Accessed September 8, 2016.
5. American Association of Nurse Practitioners. NP fact sheet. www.aanp.org/all-about-nps/np-fact-sheet. Accessed September 8, 2016.
6. US Department of Commerce. Population projections of the United States by age, sex, race, and hispanic origin: 1995 to 2050. www.census.gov/prod/1/pop/p25-1130.pdf. Accessed September 8, 2016.
7. Mather M, Jacobsen LA, Pollard KP. Aging in the United States. Popul Bull. 2015;70:1-23.
8. Ortman JM, Velkoff VA, Hogan HH. An aging nation: the older population in the United States. US Census Bureau. 2014;P25-1140.
9. Institute of Medicine. Crossing the Quality Chasm: A New Health System for the 21st Century. www.nap.edu/books/0309072808/html. Accessed September 8, 2016.
10. Garment V. Nurse practitioners and physician assistants: why you should hire one (or the other). The Profitable Practice blog. 2013. http://profitable-practice.softwareadvice.com/nurse-practitioners-and-physician-assistants-why-you-should-hire-one-or-the-other-0513. Accessed September 8, 2016.
11. American Academy of Physician Assistants. Six key elements. www.aapa.org/six-key-elements. Accessed September 8, 2016.
1. Association of American Medical Colleges. The complexities of physician supply and demand: projections from 2013 to 2025. Washington, DC: HIS, Inc; 2015. www.aamc.org/download/426242/data/ihsreportdownload.pdf. Accessed September 8, 2016.
2. Young A, Chaudhry HJ, Pei X, et al. A census of actively licensed physicians in the United States, 2014. J Med Regulation. 2014;96(4): 10-20.
3. Association of American Medical Colleges. Table B-2.2: total graduates by US medical school and sex, 2010-2011 through 2014-2015. www.aamc.org/download/321532/data/factstableb2-2.pdf. Accessed September 8, 2016.
4. National Commission on Certification of Physician Assistants. 2015 statistical profile of certified physician assistants. www.nccpa.net/Uploads/docs/2015StatisticalProfileofCertifiedPhysicianAssistants.pdf. Accessed September 8, 2016.
5. American Association of Nurse Practitioners. NP fact sheet. www.aanp.org/all-about-nps/np-fact-sheet. Accessed September 8, 2016.
6. US Department of Commerce. Population projections of the United States by age, sex, race, and hispanic origin: 1995 to 2050. www.census.gov/prod/1/pop/p25-1130.pdf. Accessed September 8, 2016.
7. Mather M, Jacobsen LA, Pollard KP. Aging in the United States. Popul Bull. 2015;70:1-23.
8. Ortman JM, Velkoff VA, Hogan HH. An aging nation: the older population in the United States. US Census Bureau. 2014;P25-1140.
9. Institute of Medicine. Crossing the Quality Chasm: A New Health System for the 21st Century. www.nap.edu/books/0309072808/html. Accessed September 8, 2016.
10. Garment V. Nurse practitioners and physician assistants: why you should hire one (or the other). The Profitable Practice blog. 2013. http://profitable-practice.softwareadvice.com/nurse-practitioners-and-physician-assistants-why-you-should-hire-one-or-the-other-0513. Accessed September 8, 2016.
11. American Academy of Physician Assistants. Six key elements. www.aapa.org/six-key-elements. Accessed September 8, 2016.
Count on this no matter who wins the election
Health care has not been at the top of the agenda in this presidential campaign, but it remains a highly contentious political issue. Because the Affordable Care Act (aka Obamacare) was all about expanding health care coverage and not much about cost containment, it is not surprising that health care insurance costs continue to escalate.
The Accountable Care Organization demonstrations around the country have shown that some, but not all, health care organizations are able to bend the steep cost incline downward using incentives, bundled payments, excellent primary care access, and care coordination. But we are once again seeing large increases in insurance premiums, and no one is happy about that.
Practical solutions are scarce. Good solutions for controlling rising health care costs are difficult to come by in the United States. There are a variety of suggestions and approaches favored by one party or the other that will be decided through political and administrative channels. The Medicare Access and CHIP Reauthorization Act of 2015 (MACRA), the Merit-based Incentive Payment System (MIPS), and alternative payment models (APMs) are the federal government’s new programs that have been set out to encourage quality, while controlling costs in outpatient settings.1 These programs have bipartisan support and are not going away.
In addition, each state is reorganizing Medicaid in an attempt to improve quality and reduce costs. Usually these cost control/quality improvement programs are foisted on us by federal or state governments (which pay for about 64% of health care costs in the United States), by insurers, or both. Fortunately, the American Academy of Family Physicians has been putting the interests of family physicians in front of legislators and policy makers to try to ease the pain as much as possible.
What can YOU do? If you have the time and the stomach for it, join forces with AAFP to become involved in the politics of health care reform and speak up for family medicine and primary care. In your own office or clinic, put the “Choosing Wisely” campaign2 (from the American Board of Internal Medicine) into practice: Focus on reducing unnecessary tests and treatments.
In the end, no matter which party occupies the White House for the next 4 years, health care payment reform is inevitable. Both parties agree that the steep rise in health care costs is unsustainable. So take your pick of presidential candidates, but don’t expect that choice to make a lot of difference in your practice “hassle factor”—or paycheck.
1. Centers for Medicaid and Medicare Services. MACRA: MIPS and APMs. Available at: https://www.cms.gov/Medicare/Quality-Initiatives-Patient-Assessment-Instruments/Value-Based-Programs/MACRA-MIPS-and-APMs/MACRA-MIPS-and-APMs.html. Accessed September 9, 2016.
2. The American Board of Internal Medicine. Choosing Wisely. Available at: www.choosingwisely.org. Accessed September 12, 2016.
John Hickner, MD, MSc
Editor-in-Chief
John Hickner, MD, MSc
Editor-in-Chief
John Hickner, MD, MSc
Editor-in-Chief
Health care has not been at the top of the agenda in this presidential campaign, but it remains a highly contentious political issue. Because the Affordable Care Act (aka Obamacare) was all about expanding health care coverage and not much about cost containment, it is not surprising that health care insurance costs continue to escalate.
The Accountable Care Organization demonstrations around the country have shown that some, but not all, health care organizations are able to bend the steep cost incline downward using incentives, bundled payments, excellent primary care access, and care coordination. But we are once again seeing large increases in insurance premiums, and no one is happy about that.
Practical solutions are scarce. Good solutions for controlling rising health care costs are difficult to come by in the United States. There are a variety of suggestions and approaches favored by one party or the other that will be decided through political and administrative channels. The Medicare Access and CHIP Reauthorization Act of 2015 (MACRA), the Merit-based Incentive Payment System (MIPS), and alternative payment models (APMs) are the federal government’s new programs that have been set out to encourage quality, while controlling costs in outpatient settings.1 These programs have bipartisan support and are not going away.
In addition, each state is reorganizing Medicaid in an attempt to improve quality and reduce costs. Usually these cost control/quality improvement programs are foisted on us by federal or state governments (which pay for about 64% of health care costs in the United States), by insurers, or both. Fortunately, the American Academy of Family Physicians has been putting the interests of family physicians in front of legislators and policy makers to try to ease the pain as much as possible.
What can YOU do? If you have the time and the stomach for it, join forces with AAFP to become involved in the politics of health care reform and speak up for family medicine and primary care. In your own office or clinic, put the “Choosing Wisely” campaign2 (from the American Board of Internal Medicine) into practice: Focus on reducing unnecessary tests and treatments.
In the end, no matter which party occupies the White House for the next 4 years, health care payment reform is inevitable. Both parties agree that the steep rise in health care costs is unsustainable. So take your pick of presidential candidates, but don’t expect that choice to make a lot of difference in your practice “hassle factor”—or paycheck.
Health care has not been at the top of the agenda in this presidential campaign, but it remains a highly contentious political issue. Because the Affordable Care Act (aka Obamacare) was all about expanding health care coverage and not much about cost containment, it is not surprising that health care insurance costs continue to escalate.
The Accountable Care Organization demonstrations around the country have shown that some, but not all, health care organizations are able to bend the steep cost incline downward using incentives, bundled payments, excellent primary care access, and care coordination. But we are once again seeing large increases in insurance premiums, and no one is happy about that.
Practical solutions are scarce. Good solutions for controlling rising health care costs are difficult to come by in the United States. There are a variety of suggestions and approaches favored by one party or the other that will be decided through political and administrative channels. The Medicare Access and CHIP Reauthorization Act of 2015 (MACRA), the Merit-based Incentive Payment System (MIPS), and alternative payment models (APMs) are the federal government’s new programs that have been set out to encourage quality, while controlling costs in outpatient settings.1 These programs have bipartisan support and are not going away.
In addition, each state is reorganizing Medicaid in an attempt to improve quality and reduce costs. Usually these cost control/quality improvement programs are foisted on us by federal or state governments (which pay for about 64% of health care costs in the United States), by insurers, or both. Fortunately, the American Academy of Family Physicians has been putting the interests of family physicians in front of legislators and policy makers to try to ease the pain as much as possible.
What can YOU do? If you have the time and the stomach for it, join forces with AAFP to become involved in the politics of health care reform and speak up for family medicine and primary care. In your own office or clinic, put the “Choosing Wisely” campaign2 (from the American Board of Internal Medicine) into practice: Focus on reducing unnecessary tests and treatments.
In the end, no matter which party occupies the White House for the next 4 years, health care payment reform is inevitable. Both parties agree that the steep rise in health care costs is unsustainable. So take your pick of presidential candidates, but don’t expect that choice to make a lot of difference in your practice “hassle factor”—or paycheck.
1. Centers for Medicaid and Medicare Services. MACRA: MIPS and APMs. Available at: https://www.cms.gov/Medicare/Quality-Initiatives-Patient-Assessment-Instruments/Value-Based-Programs/MACRA-MIPS-and-APMs/MACRA-MIPS-and-APMs.html. Accessed September 9, 2016.
2. The American Board of Internal Medicine. Choosing Wisely. Available at: www.choosingwisely.org. Accessed September 12, 2016.
1. Centers for Medicaid and Medicare Services. MACRA: MIPS and APMs. Available at: https://www.cms.gov/Medicare/Quality-Initiatives-Patient-Assessment-Instruments/Value-Based-Programs/MACRA-MIPS-and-APMs/MACRA-MIPS-and-APMs.html. Accessed September 9, 2016.
2. The American Board of Internal Medicine. Choosing Wisely. Available at: www.choosingwisely.org. Accessed September 12, 2016.