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Family dinners are good medicine
Intuitively, we have come to believe that adding more to each family members’ schedule – a lesson, an activity, more homework time – is more enriching or meaningful than is a family dinner, which appears to have less direct impact. However, there is a growing body of evidence that, when an entire family eats dinner together 5 or more nights weekly, the emotional health and well-being of all family members is improved. Not only is their health improved, as there is a greater likelihood of eating nutritious food, but so are a child’s school performance and emotional well-being.
But less than 60% of children eat five or more meals with their parents each week (National Center on Addiction and Substance Abuse [CASA], 2012). Few people would suggest that encouraging families to eat dinner together is a bad idea, but time is the ultimate scarce resource. Preparing food and eating together takes time, and parents and children have many demands on that time that feel nonnegotiable, such as homework, exercise, team practice, or work obligations. When you meet with your patients and explain the tremendous health benefits of eating dinner together, you help your patients and their parents make informed decisions about how to rebalance time to prioritize family dinners that have real but fewer obvious impacts then do a piano lesson or dance class.
Of course, children who eat regular family dinners eat more fruits and vegetables and fewer fried foods and soft drinks than do their peers who eat dinner with their families less often. They are less likely to become obese in youth and more likely to eat healthily and maintain a healthy weight once they live on their own as adults.
Scientific evidence of the mental health benefits to children of eating meals with their families first emerged in the 1990s when the National Center on Addiction and Substance Abuse at Columbia University, New York, began surveying various family behaviors and correlating them with the risk of adolescent substance use and misuse. They found strong evidence that when families ate dinner together five or more times weekly (we’ll call this “frequent family dinners”), their adolescents were far less likely to initiate alcohol and cigarette use and less likely to regularly abuse alcohol and drugs. Subsequent studies have demonstrated that the protective effect may be greater for girls than boys and may be greater for alcohol, cigarettes, and marijuana than for other drugs. But earlier age of first use of substances substantially raises the risk of later addiction, so the health benefits of any delay in first use are significant.
Since CASA’s first studies in the 1990s, researchers began paying closer attention to family meals and a variety of psychiatric problems in youth. They demonstrated that frequent family dinners lowered the risk of other externalizing behaviors in youth, including risky sexual behaviors, threats of physical harm, aggression, fights leading to injury, and carrying or using a weapon.1,2 Frequent family dinners are associated with lower rates of disordered eating behaviors and disordered body image in adolescent girls.3,4 Multiple studies have found a powerful association between frequent family dinners and lower rates of depressive symptoms and suicide attempts in both male and female adolescents.1 Frequent family dinners even have been shown to mitigate against the risks of multiple poor health and academic outcomes in children with high adverse childhood experience (ACE) scores.5
Beyond protecting against problems, frequent family meals are associated with improved well-being and performance. Studies have demonstrated positive associations between frequent family meals and higher levels of self-esteem, self-efficacy, and well-being in adolescents, both male and female. They have consistently found significant associations between frequent family meals and higher grade point averages, commitment to learning, and rich vocabularies in children and adolescents, even after adjustment for demographic and other familial factors.6 And children are not the only ones who benefit. Frequent family meals even have been shown to be associated with higher self-reported levels of well-being and self-esteem, and lower levels of stress among parents.7,8 While investing the time in preparing meals and eating them together may sound stressful, it’s clear the benefits outweigh the risks for parents as well as for their children.
It is important to set the framework for what really matters in a family dinner so that your patients can enjoy all of these benefits. Parents may assume that the meal must be prepared from scratch with only fresh, local, or organic ingredients. But what matters most is that the food is delicious and nutritious, and that the time spent eating (and preparing it) is fun, and promotes conversation and connection. Homemade food usually is more nutritious and will bring more of the physical health benefits, but many store-bought ingredients or even take-out options can be healthy and can promote time for the family to sit together and connect. If parents enjoy preparing food, then it’s worthwhile! And they should not worry about having every member of the family together at every meal. Even if only one parent and child are present for a dinner, they each will enjoy the benefits.
Parents can use this time to help promote good habits in their children. Talking about why manners matter while practicing them at the table is powerful for young children. Let them know manners are how we show people that we care about them, whether by taking turns talking or chewing with our mouths closed! Older children and adolescents can learn about how effort is an essential ingredient in every important area in life, from school to meals. Tell them that sometimes the work or effort will be uncomfortable, and pitching in to share the effort lightens everyone’s load. When parents ask for help, they show their children how to do the same and that they have confidence in their child’s ability to be helpful.
Parents should share the joy of the effort, too! They can invite their young children to help with the meal preparation in age-appropriate ways: pulling herbs off of their stems, rinsing vegetables, sprinkling spices, or emptying a box of spaghetti into a pot of water. Older children feel honored to be given bigger responsibilities, such as carrying plates to the table or cutting vegetables (with supervision, when appropriate). And adolescents, exploring their interests and enjoying their independence, may enjoy building their own menus for the family, doing the shopping or leading the preparation of a dish or full meal themselves.
While there is a role for supporting good manners and helpful habits, help parents avoid getting into power struggles with their children over what they will eat or how they conduct themselves at the table. There should be reasonable rules and expectations around mealtime, and predictable, reasonable consequences. If children try a food and don’t like it, they can have a bowl of (nutritious) cereal and stay at the table with the family. Phones should not be allowed at the table, and televisions should be off during the meal (although music may enhance the sense of pleasure or celebration). Mealtime should be time for relaxing, listening, and connecting.
Offer some ideas about how to facilitate conversations. Asking about how a child’s day went may spark conversations sometimes, but usually people benefit from specific questions. What made you really laugh today? What did you have for lunch? Whom did you sit next to on the bus? If a parent starts by telling a story about his or her day, even better! This is especially potent if a parent talks about something embarrassing or challenging, or mentions a failure. Young children will have plenty of these stories, and adolescents build resilience by internalizing the idea that setbacks and difficulties are a normal, healthy part of every day. This is a great time to talk about current events, whether in the news, entertainment, or sports. And telling stories about when children were younger, when the parents were children, or even about grandparents or more distant ancestors is a wonderful way to engage children in the greater story of their family narrative, and is always engaging and memorable.
At a deeper level, the family dinner is a time that recognizes each person’s contribution to a discussion, and facilitates a calm discussion of the families’ history and values. There is connection, communication, and building of trust. Families that cannot schedule a minimum number of dinners or that have dinners filled with tension and conflict, are very likely to have children at risk. For those conflicted and often unhappy families, a pediatrician’s early recognition and intervention could make a meaningful difference.
Dr. Swick is physician in chief at Ohana, Center for Child and Adolescent Behavioral Health, Community Hospital of the Monterey (Calif.) Peninsula. Dr. Jellinek is professor emeritus of psychiatry and pediatrics, Harvard Medical School, Boston. Email them at [email protected].
References
1. J Adolesc Health. 2006;39(3):337-45.
2. J Adolesc. 2010;33(1):187-96.
3. J Adolesc Health. 2009;44(5):431-6.
4. Health Psychol. 2008;27(Suppl 2):s109-17.
5. J Adolesc Health. 2009;45(4):389-95.
6. Pediatrics. 2019 Jul 8. doi: 10.1542/peds.2018-945.
7. Arch Pediatr Adolesc Med. 2004;158(8):792-6.
8. Prev Med. 2018;113:7-12.
Intuitively, we have come to believe that adding more to each family members’ schedule – a lesson, an activity, more homework time – is more enriching or meaningful than is a family dinner, which appears to have less direct impact. However, there is a growing body of evidence that, when an entire family eats dinner together 5 or more nights weekly, the emotional health and well-being of all family members is improved. Not only is their health improved, as there is a greater likelihood of eating nutritious food, but so are a child’s school performance and emotional well-being.
But less than 60% of children eat five or more meals with their parents each week (National Center on Addiction and Substance Abuse [CASA], 2012). Few people would suggest that encouraging families to eat dinner together is a bad idea, but time is the ultimate scarce resource. Preparing food and eating together takes time, and parents and children have many demands on that time that feel nonnegotiable, such as homework, exercise, team practice, or work obligations. When you meet with your patients and explain the tremendous health benefits of eating dinner together, you help your patients and their parents make informed decisions about how to rebalance time to prioritize family dinners that have real but fewer obvious impacts then do a piano lesson or dance class.
Of course, children who eat regular family dinners eat more fruits and vegetables and fewer fried foods and soft drinks than do their peers who eat dinner with their families less often. They are less likely to become obese in youth and more likely to eat healthily and maintain a healthy weight once they live on their own as adults.
Scientific evidence of the mental health benefits to children of eating meals with their families first emerged in the 1990s when the National Center on Addiction and Substance Abuse at Columbia University, New York, began surveying various family behaviors and correlating them with the risk of adolescent substance use and misuse. They found strong evidence that when families ate dinner together five or more times weekly (we’ll call this “frequent family dinners”), their adolescents were far less likely to initiate alcohol and cigarette use and less likely to regularly abuse alcohol and drugs. Subsequent studies have demonstrated that the protective effect may be greater for girls than boys and may be greater for alcohol, cigarettes, and marijuana than for other drugs. But earlier age of first use of substances substantially raises the risk of later addiction, so the health benefits of any delay in first use are significant.
Since CASA’s first studies in the 1990s, researchers began paying closer attention to family meals and a variety of psychiatric problems in youth. They demonstrated that frequent family dinners lowered the risk of other externalizing behaviors in youth, including risky sexual behaviors, threats of physical harm, aggression, fights leading to injury, and carrying or using a weapon.1,2 Frequent family dinners are associated with lower rates of disordered eating behaviors and disordered body image in adolescent girls.3,4 Multiple studies have found a powerful association between frequent family dinners and lower rates of depressive symptoms and suicide attempts in both male and female adolescents.1 Frequent family dinners even have been shown to mitigate against the risks of multiple poor health and academic outcomes in children with high adverse childhood experience (ACE) scores.5
Beyond protecting against problems, frequent family meals are associated with improved well-being and performance. Studies have demonstrated positive associations between frequent family meals and higher levels of self-esteem, self-efficacy, and well-being in adolescents, both male and female. They have consistently found significant associations between frequent family meals and higher grade point averages, commitment to learning, and rich vocabularies in children and adolescents, even after adjustment for demographic and other familial factors.6 And children are not the only ones who benefit. Frequent family meals even have been shown to be associated with higher self-reported levels of well-being and self-esteem, and lower levels of stress among parents.7,8 While investing the time in preparing meals and eating them together may sound stressful, it’s clear the benefits outweigh the risks for parents as well as for their children.
It is important to set the framework for what really matters in a family dinner so that your patients can enjoy all of these benefits. Parents may assume that the meal must be prepared from scratch with only fresh, local, or organic ingredients. But what matters most is that the food is delicious and nutritious, and that the time spent eating (and preparing it) is fun, and promotes conversation and connection. Homemade food usually is more nutritious and will bring more of the physical health benefits, but many store-bought ingredients or even take-out options can be healthy and can promote time for the family to sit together and connect. If parents enjoy preparing food, then it’s worthwhile! And they should not worry about having every member of the family together at every meal. Even if only one parent and child are present for a dinner, they each will enjoy the benefits.
Parents can use this time to help promote good habits in their children. Talking about why manners matter while practicing them at the table is powerful for young children. Let them know manners are how we show people that we care about them, whether by taking turns talking or chewing with our mouths closed! Older children and adolescents can learn about how effort is an essential ingredient in every important area in life, from school to meals. Tell them that sometimes the work or effort will be uncomfortable, and pitching in to share the effort lightens everyone’s load. When parents ask for help, they show their children how to do the same and that they have confidence in their child’s ability to be helpful.
Parents should share the joy of the effort, too! They can invite their young children to help with the meal preparation in age-appropriate ways: pulling herbs off of their stems, rinsing vegetables, sprinkling spices, or emptying a box of spaghetti into a pot of water. Older children feel honored to be given bigger responsibilities, such as carrying plates to the table or cutting vegetables (with supervision, when appropriate). And adolescents, exploring their interests and enjoying their independence, may enjoy building their own menus for the family, doing the shopping or leading the preparation of a dish or full meal themselves.
While there is a role for supporting good manners and helpful habits, help parents avoid getting into power struggles with their children over what they will eat or how they conduct themselves at the table. There should be reasonable rules and expectations around mealtime, and predictable, reasonable consequences. If children try a food and don’t like it, they can have a bowl of (nutritious) cereal and stay at the table with the family. Phones should not be allowed at the table, and televisions should be off during the meal (although music may enhance the sense of pleasure or celebration). Mealtime should be time for relaxing, listening, and connecting.
Offer some ideas about how to facilitate conversations. Asking about how a child’s day went may spark conversations sometimes, but usually people benefit from specific questions. What made you really laugh today? What did you have for lunch? Whom did you sit next to on the bus? If a parent starts by telling a story about his or her day, even better! This is especially potent if a parent talks about something embarrassing or challenging, or mentions a failure. Young children will have plenty of these stories, and adolescents build resilience by internalizing the idea that setbacks and difficulties are a normal, healthy part of every day. This is a great time to talk about current events, whether in the news, entertainment, or sports. And telling stories about when children were younger, when the parents were children, or even about grandparents or more distant ancestors is a wonderful way to engage children in the greater story of their family narrative, and is always engaging and memorable.
At a deeper level, the family dinner is a time that recognizes each person’s contribution to a discussion, and facilitates a calm discussion of the families’ history and values. There is connection, communication, and building of trust. Families that cannot schedule a minimum number of dinners or that have dinners filled with tension and conflict, are very likely to have children at risk. For those conflicted and often unhappy families, a pediatrician’s early recognition and intervention could make a meaningful difference.
Dr. Swick is physician in chief at Ohana, Center for Child and Adolescent Behavioral Health, Community Hospital of the Monterey (Calif.) Peninsula. Dr. Jellinek is professor emeritus of psychiatry and pediatrics, Harvard Medical School, Boston. Email them at [email protected].
References
1. J Adolesc Health. 2006;39(3):337-45.
2. J Adolesc. 2010;33(1):187-96.
3. J Adolesc Health. 2009;44(5):431-6.
4. Health Psychol. 2008;27(Suppl 2):s109-17.
5. J Adolesc Health. 2009;45(4):389-95.
6. Pediatrics. 2019 Jul 8. doi: 10.1542/peds.2018-945.
7. Arch Pediatr Adolesc Med. 2004;158(8):792-6.
8. Prev Med. 2018;113:7-12.
Intuitively, we have come to believe that adding more to each family members’ schedule – a lesson, an activity, more homework time – is more enriching or meaningful than is a family dinner, which appears to have less direct impact. However, there is a growing body of evidence that, when an entire family eats dinner together 5 or more nights weekly, the emotional health and well-being of all family members is improved. Not only is their health improved, as there is a greater likelihood of eating nutritious food, but so are a child’s school performance and emotional well-being.
But less than 60% of children eat five or more meals with their parents each week (National Center on Addiction and Substance Abuse [CASA], 2012). Few people would suggest that encouraging families to eat dinner together is a bad idea, but time is the ultimate scarce resource. Preparing food and eating together takes time, and parents and children have many demands on that time that feel nonnegotiable, such as homework, exercise, team practice, or work obligations. When you meet with your patients and explain the tremendous health benefits of eating dinner together, you help your patients and their parents make informed decisions about how to rebalance time to prioritize family dinners that have real but fewer obvious impacts then do a piano lesson or dance class.
Of course, children who eat regular family dinners eat more fruits and vegetables and fewer fried foods and soft drinks than do their peers who eat dinner with their families less often. They are less likely to become obese in youth and more likely to eat healthily and maintain a healthy weight once they live on their own as adults.
Scientific evidence of the mental health benefits to children of eating meals with their families first emerged in the 1990s when the National Center on Addiction and Substance Abuse at Columbia University, New York, began surveying various family behaviors and correlating them with the risk of adolescent substance use and misuse. They found strong evidence that when families ate dinner together five or more times weekly (we’ll call this “frequent family dinners”), their adolescents were far less likely to initiate alcohol and cigarette use and less likely to regularly abuse alcohol and drugs. Subsequent studies have demonstrated that the protective effect may be greater for girls than boys and may be greater for alcohol, cigarettes, and marijuana than for other drugs. But earlier age of first use of substances substantially raises the risk of later addiction, so the health benefits of any delay in first use are significant.
Since CASA’s first studies in the 1990s, researchers began paying closer attention to family meals and a variety of psychiatric problems in youth. They demonstrated that frequent family dinners lowered the risk of other externalizing behaviors in youth, including risky sexual behaviors, threats of physical harm, aggression, fights leading to injury, and carrying or using a weapon.1,2 Frequent family dinners are associated with lower rates of disordered eating behaviors and disordered body image in adolescent girls.3,4 Multiple studies have found a powerful association between frequent family dinners and lower rates of depressive symptoms and suicide attempts in both male and female adolescents.1 Frequent family dinners even have been shown to mitigate against the risks of multiple poor health and academic outcomes in children with high adverse childhood experience (ACE) scores.5
Beyond protecting against problems, frequent family meals are associated with improved well-being and performance. Studies have demonstrated positive associations between frequent family meals and higher levels of self-esteem, self-efficacy, and well-being in adolescents, both male and female. They have consistently found significant associations between frequent family meals and higher grade point averages, commitment to learning, and rich vocabularies in children and adolescents, even after adjustment for demographic and other familial factors.6 And children are not the only ones who benefit. Frequent family meals even have been shown to be associated with higher self-reported levels of well-being and self-esteem, and lower levels of stress among parents.7,8 While investing the time in preparing meals and eating them together may sound stressful, it’s clear the benefits outweigh the risks for parents as well as for their children.
It is important to set the framework for what really matters in a family dinner so that your patients can enjoy all of these benefits. Parents may assume that the meal must be prepared from scratch with only fresh, local, or organic ingredients. But what matters most is that the food is delicious and nutritious, and that the time spent eating (and preparing it) is fun, and promotes conversation and connection. Homemade food usually is more nutritious and will bring more of the physical health benefits, but many store-bought ingredients or even take-out options can be healthy and can promote time for the family to sit together and connect. If parents enjoy preparing food, then it’s worthwhile! And they should not worry about having every member of the family together at every meal. Even if only one parent and child are present for a dinner, they each will enjoy the benefits.
Parents can use this time to help promote good habits in their children. Talking about why manners matter while practicing them at the table is powerful for young children. Let them know manners are how we show people that we care about them, whether by taking turns talking or chewing with our mouths closed! Older children and adolescents can learn about how effort is an essential ingredient in every important area in life, from school to meals. Tell them that sometimes the work or effort will be uncomfortable, and pitching in to share the effort lightens everyone’s load. When parents ask for help, they show their children how to do the same and that they have confidence in their child’s ability to be helpful.
Parents should share the joy of the effort, too! They can invite their young children to help with the meal preparation in age-appropriate ways: pulling herbs off of their stems, rinsing vegetables, sprinkling spices, or emptying a box of spaghetti into a pot of water. Older children feel honored to be given bigger responsibilities, such as carrying plates to the table or cutting vegetables (with supervision, when appropriate). And adolescents, exploring their interests and enjoying their independence, may enjoy building their own menus for the family, doing the shopping or leading the preparation of a dish or full meal themselves.
While there is a role for supporting good manners and helpful habits, help parents avoid getting into power struggles with their children over what they will eat or how they conduct themselves at the table. There should be reasonable rules and expectations around mealtime, and predictable, reasonable consequences. If children try a food and don’t like it, they can have a bowl of (nutritious) cereal and stay at the table with the family. Phones should not be allowed at the table, and televisions should be off during the meal (although music may enhance the sense of pleasure or celebration). Mealtime should be time for relaxing, listening, and connecting.
Offer some ideas about how to facilitate conversations. Asking about how a child’s day went may spark conversations sometimes, but usually people benefit from specific questions. What made you really laugh today? What did you have for lunch? Whom did you sit next to on the bus? If a parent starts by telling a story about his or her day, even better! This is especially potent if a parent talks about something embarrassing or challenging, or mentions a failure. Young children will have plenty of these stories, and adolescents build resilience by internalizing the idea that setbacks and difficulties are a normal, healthy part of every day. This is a great time to talk about current events, whether in the news, entertainment, or sports. And telling stories about when children were younger, when the parents were children, or even about grandparents or more distant ancestors is a wonderful way to engage children in the greater story of their family narrative, and is always engaging and memorable.
At a deeper level, the family dinner is a time that recognizes each person’s contribution to a discussion, and facilitates a calm discussion of the families’ history and values. There is connection, communication, and building of trust. Families that cannot schedule a minimum number of dinners or that have dinners filled with tension and conflict, are very likely to have children at risk. For those conflicted and often unhappy families, a pediatrician’s early recognition and intervention could make a meaningful difference.
Dr. Swick is physician in chief at Ohana, Center for Child and Adolescent Behavioral Health, Community Hospital of the Monterey (Calif.) Peninsula. Dr. Jellinek is professor emeritus of psychiatry and pediatrics, Harvard Medical School, Boston. Email them at [email protected].
References
1. J Adolesc Health. 2006;39(3):337-45.
2. J Adolesc. 2010;33(1):187-96.
3. J Adolesc Health. 2009;44(5):431-6.
4. Health Psychol. 2008;27(Suppl 2):s109-17.
5. J Adolesc Health. 2009;45(4):389-95.
6. Pediatrics. 2019 Jul 8. doi: 10.1542/peds.2018-945.
7. Arch Pediatr Adolesc Med. 2004;158(8):792-6.
8. Prev Med. 2018;113:7-12.
Hiring the right employees
Many of the personnel questions I receive concern the dreaded “marginal employee” – a person who has never done anything truly heinous to merit firing, but neither anything special to merit continued employment. I advise getting rid of such people and then changing the hiring criteria that bring you marginal employees in the first place.
Most bad hires come about because employers do not have a clear vision of the kind of employee they want. Many office manuals do not contain detailed job descriptions. If you don’t know exactly what you are looking for, your entire selection process will be inadequate from initial screening of applicants through assessments of their skills and personalities. Many physicians compound the problem with poor interview techniques and inadequate verification.
. Take a hard look at your job descriptions, and update them if necessary. A good job description lists the major responsibilities of the position, with the relative importance of each duty and the critical knowledge, skills, and education levels necessary for each function. In other words, it describes, accurately and in detail, exactly what you expect from the employee you will hire to perform that job.
Once you have a clear job description in mind (and in print), take all the time you need to find the best possible match for it. This is not a place to cut corners. Screen your candidates carefully and avoid lowering your expectations. This is the point at which it might be tempting to settle for a marginal candidate, just to get the process over with.
It also is tempting to hire the candidate that you have the “best feeling” about, even though he or she is a poor match for the job, and then try to mold the job to that person. Every doctor knows that hunches are no substitute for hard data.
Be alert for red flags in résumés: significant time gaps between jobs; positions at companies that are no longer in business, or are otherwise impossible to verify; job titles that don’t make sense, given the applicant’s qualifications.
Background checks are a dicey subject, but publicly available information can be found, cheaply or free, on multiple websites created for that purpose. Be sure to tell applicants that you will be verifying facts in their résumés; it’s usually wise to get their written consent to do so.
Many employers skip the essential step of verification; many applicants know that. (I once actually overheard a new hire say, “I won’t be here long if they check my references.” And by golly, she was right!) If a reference is reluctant to tell you anything substantive, ask, “Would you hire this person again?” You can interpret a lot from the answer – or lack of one.
Interviews often get short shrift as well. Many doctors tend to do all the talking. The purpose of an interview is to allow you to size up the prospective employee, not to deliver a lecture on the sterling attributes of your office. Important interview topics include educational background, skills, experience, and unrelated job history.
By law, you cannot ask an applicant’s age, date of birth, sex, creed, color, religion, or national origin. Other forbidden subjects include disabilities, marital status, military record, number of children (or who cares for them), addiction history, citizenship, criminal record, psychiatric history, absenteeism, or workers’ compensation.
There are acceptable alternatives to some of those questions, however: You can ask if applicants have ever gone by another name (for your background check), for example. You can ask if they are legally authorized to work in this country, and whether they will be physically able to perform the duties specified in the job description. While past addictions are off limits, you do have a right to know about current addictions to illegal substances.
Once you have hired people whose skills and personalities best fit your needs, train them well, and then give them the opportunity to succeed. “The best executive,” wrote Theodore Roosevelt, “is the one who has sense enough to pick good [people] to do what he [or she] wants done, and self-restraint enough to keep from meddling with them while they do it.”
Dr. Eastern practices dermatology and dermatologic surgery in Belleville, N.J. He is the author of numerous articles and textbook chapters, and is a longtime monthly columnist for Dermatology News. Write to him at [email protected].
Many of the personnel questions I receive concern the dreaded “marginal employee” – a person who has never done anything truly heinous to merit firing, but neither anything special to merit continued employment. I advise getting rid of such people and then changing the hiring criteria that bring you marginal employees in the first place.
Most bad hires come about because employers do not have a clear vision of the kind of employee they want. Many office manuals do not contain detailed job descriptions. If you don’t know exactly what you are looking for, your entire selection process will be inadequate from initial screening of applicants through assessments of their skills and personalities. Many physicians compound the problem with poor interview techniques and inadequate verification.
. Take a hard look at your job descriptions, and update them if necessary. A good job description lists the major responsibilities of the position, with the relative importance of each duty and the critical knowledge, skills, and education levels necessary for each function. In other words, it describes, accurately and in detail, exactly what you expect from the employee you will hire to perform that job.
Once you have a clear job description in mind (and in print), take all the time you need to find the best possible match for it. This is not a place to cut corners. Screen your candidates carefully and avoid lowering your expectations. This is the point at which it might be tempting to settle for a marginal candidate, just to get the process over with.
It also is tempting to hire the candidate that you have the “best feeling” about, even though he or she is a poor match for the job, and then try to mold the job to that person. Every doctor knows that hunches are no substitute for hard data.
Be alert for red flags in résumés: significant time gaps between jobs; positions at companies that are no longer in business, or are otherwise impossible to verify; job titles that don’t make sense, given the applicant’s qualifications.
Background checks are a dicey subject, but publicly available information can be found, cheaply or free, on multiple websites created for that purpose. Be sure to tell applicants that you will be verifying facts in their résumés; it’s usually wise to get their written consent to do so.
Many employers skip the essential step of verification; many applicants know that. (I once actually overheard a new hire say, “I won’t be here long if they check my references.” And by golly, she was right!) If a reference is reluctant to tell you anything substantive, ask, “Would you hire this person again?” You can interpret a lot from the answer – or lack of one.
Interviews often get short shrift as well. Many doctors tend to do all the talking. The purpose of an interview is to allow you to size up the prospective employee, not to deliver a lecture on the sterling attributes of your office. Important interview topics include educational background, skills, experience, and unrelated job history.
By law, you cannot ask an applicant’s age, date of birth, sex, creed, color, religion, or national origin. Other forbidden subjects include disabilities, marital status, military record, number of children (or who cares for them), addiction history, citizenship, criminal record, psychiatric history, absenteeism, or workers’ compensation.
There are acceptable alternatives to some of those questions, however: You can ask if applicants have ever gone by another name (for your background check), for example. You can ask if they are legally authorized to work in this country, and whether they will be physically able to perform the duties specified in the job description. While past addictions are off limits, you do have a right to know about current addictions to illegal substances.
Once you have hired people whose skills and personalities best fit your needs, train them well, and then give them the opportunity to succeed. “The best executive,” wrote Theodore Roosevelt, “is the one who has sense enough to pick good [people] to do what he [or she] wants done, and self-restraint enough to keep from meddling with them while they do it.”
Dr. Eastern practices dermatology and dermatologic surgery in Belleville, N.J. He is the author of numerous articles and textbook chapters, and is a longtime monthly columnist for Dermatology News. Write to him at [email protected].
Many of the personnel questions I receive concern the dreaded “marginal employee” – a person who has never done anything truly heinous to merit firing, but neither anything special to merit continued employment. I advise getting rid of such people and then changing the hiring criteria that bring you marginal employees in the first place.
Most bad hires come about because employers do not have a clear vision of the kind of employee they want. Many office manuals do not contain detailed job descriptions. If you don’t know exactly what you are looking for, your entire selection process will be inadequate from initial screening of applicants through assessments of their skills and personalities. Many physicians compound the problem with poor interview techniques and inadequate verification.
. Take a hard look at your job descriptions, and update them if necessary. A good job description lists the major responsibilities of the position, with the relative importance of each duty and the critical knowledge, skills, and education levels necessary for each function. In other words, it describes, accurately and in detail, exactly what you expect from the employee you will hire to perform that job.
Once you have a clear job description in mind (and in print), take all the time you need to find the best possible match for it. This is not a place to cut corners. Screen your candidates carefully and avoid lowering your expectations. This is the point at which it might be tempting to settle for a marginal candidate, just to get the process over with.
It also is tempting to hire the candidate that you have the “best feeling” about, even though he or she is a poor match for the job, and then try to mold the job to that person. Every doctor knows that hunches are no substitute for hard data.
Be alert for red flags in résumés: significant time gaps between jobs; positions at companies that are no longer in business, or are otherwise impossible to verify; job titles that don’t make sense, given the applicant’s qualifications.
Background checks are a dicey subject, but publicly available information can be found, cheaply or free, on multiple websites created for that purpose. Be sure to tell applicants that you will be verifying facts in their résumés; it’s usually wise to get their written consent to do so.
Many employers skip the essential step of verification; many applicants know that. (I once actually overheard a new hire say, “I won’t be here long if they check my references.” And by golly, she was right!) If a reference is reluctant to tell you anything substantive, ask, “Would you hire this person again?” You can interpret a lot from the answer – or lack of one.
Interviews often get short shrift as well. Many doctors tend to do all the talking. The purpose of an interview is to allow you to size up the prospective employee, not to deliver a lecture on the sterling attributes of your office. Important interview topics include educational background, skills, experience, and unrelated job history.
By law, you cannot ask an applicant’s age, date of birth, sex, creed, color, religion, or national origin. Other forbidden subjects include disabilities, marital status, military record, number of children (or who cares for them), addiction history, citizenship, criminal record, psychiatric history, absenteeism, or workers’ compensation.
There are acceptable alternatives to some of those questions, however: You can ask if applicants have ever gone by another name (for your background check), for example. You can ask if they are legally authorized to work in this country, and whether they will be physically able to perform the duties specified in the job description. While past addictions are off limits, you do have a right to know about current addictions to illegal substances.
Once you have hired people whose skills and personalities best fit your needs, train them well, and then give them the opportunity to succeed. “The best executive,” wrote Theodore Roosevelt, “is the one who has sense enough to pick good [people] to do what he [or she] wants done, and self-restraint enough to keep from meddling with them while they do it.”
Dr. Eastern practices dermatology and dermatologic surgery in Belleville, N.J. He is the author of numerous articles and textbook chapters, and is a longtime monthly columnist for Dermatology News. Write to him at [email protected].
Predicting outcomes in acute leukemia, NSCLC
In this edition of “How I will treat my next patient,” I take a look at recent studies that examined ways to predict important outcomes in two very different settings, acute leukemia and advanced non–small cell lung cancer (NSCLC). They share the virtue of helping cancer specialists to increase their vigilance for clinically relevant complications and situations and to educate patients and families.
VTE risk in acute leukemia
The risk of venous thromboembolism (VTE) in cancer patients depends upon multiple patient-, tumor-, anatomic-, and treatment-related factors. The Khorana score has become an accepted standard for predicting the risks of VTE and assessing the relative value of various anticoagulants in cancer patients. However, the only hematologic malignancy that is specifically listed among the primary cancer sites in the Khorana score is “lymphoma.” VTE can develop during treatment for acute leukemia, especially among patients with acute lymphoblastic leukemia (ALL).
At the 2019 annual congress of the European Hematology Association, Alejandro Lazo-Langer, MD, and his colleagues proposed a scoring system to quantify the risks of VTE based on a retrospective cohort study of more than 500 acute leukemia patients, diagnosed from 2006-2017. They identified 77 patients with a VTE event, with a median time from diagnosis to VTE of 64 days. Among 20 possible predictive factors, 3 emerged in the final multivariate model – platelet count greater than 50,000 (1 point), ALL (2 points), and prior history of VTE (3 points).
Over a period of 12 months, patients with a score of more than 3 points had a cumulative incidence of VTE of 44%, in comparison with 10.5% among patients with lower scores. They were unable to discern whether particular antineoplastic regimens or drugs enhanced the risk.
The authors proposed that, if verified in a validation cohort study, the scoring system could lead to better patient education about signs and symptoms, more intensive surveillance for high-risk patients, and preventive interventions.
What this means in practice
Although a large number of patient records were reviewed for Dr. Lazo-Langer’s study, there were just 74 ALL patients, and it is unclear whether particular treatment regimens or drugs (such as L-asparaginase in ALL) enhance risk. Further study with a validation cohort (as was performed for the Khorana score for patients with other malignancies), is warranted. The study is thought provoking, but for now, in my opinion, standard clinical vigilance, surveillance, and education regarding VTE in leukemia patients remain appropriate.
Steroid impact in NSCLC with ICI therapy
Patients with autoimmune disease and individuals requiring active treatment with steroids (prednisone at 10 mg/day or more or the equivalent) were excluded from clinical trials that led to Food and Drug Administration approval of immune checkpoint inhibitor (ICI) agents. Recently published data indicate that treatment with 10 mg or more of daily prednisone correlates with poor outcome in NSCLC patients receiving ICI therapy (J Clin Oncol. 2018;36:2872-8; J Thoracic Oncol. 2018;13:1771-5). However, at the 2019 annual meeting of the American Society of Clinical Oncology, analyses of the CancerLinQ database showed that, among NSCLC patients, autoimmune disease and treatment for autoimmune disease are surprisingly prevalent. Should oncologists refuse to treat these patients with ICI agents, alone and in combination with chemotherapy or CTLA4 inhibitors?
Biagio Ricciuti, MD, and colleagues published a retrospective, single-institution record review of 650 advanced NSCLC patients who were treated with ICI plus or minus CTLA-4 inhibition on a correlative intramural research study. Patients who received ICI with concurrent cytotoxic chemotherapy were excluded. They gathered clinical-pathologic information about whether patients received concurrent corticosteroids (10 mg/day or more vs. less than 10 mg/day of prednisone or the equivalent) and the reason for steroid use (oncologic vs. cancer-unrelated indications).
Importantly, they gathered information about programmed death-ligand 1 (PD-L1) tumor proportion scores and tumor mutational burden.
Among the 14.3% patients receiving prednisone 10 mg/day or more at the start of ICI therapy, progression-free survival and overall survival were significantly worse – but only among the 66 patients who needed steroids for oncologic reasons (pain, brain metastases, anorexia, cancer-associated dyspnea). Among the 27 patients who received steroids for cancer-unrelated reasons (autoimmune disease, chronic obstructive pulmonary disease, hypersensitivity pneumonitis), progression-free and overall survival were no different than for patients on prednisone 0-9 mg/day. Imbalances in PD-L1 tumor proportion scores among the groups analyzed did not clearly account for the differences in survival.
What this means in practice
The potential for great treatment outcomes with single-agent ICIs in a subset of advanced NSCLC patients, coupled with the lack of an air-tight biomarker for benefit, has changed the timing of discussions between oncologists and patients about stopping antineoplastic treatment. Since we cannot identify the patients for whom ICI use is futile, the default position has been lenient on using these expensive and potentially toxic therapies.
If verified in a multi-institutional setting, with larger numbers of NSCLC patients receiving steroids for cancer-unrelated reasons, the observations of Dr. Ricciuti and colleagues could help clinicians confidently identify the time to focus discussions on supportive care only. In patients with short survival and strong rationale for maximizing supportive care, analyses like this one could help us deliver more appropriate treatment, instead of more treatment, thereby furthering the goals of personalized cancer patient management.
Dr. Lyss has been a community-based medical oncologist and clinical researcher for more than 35 years, practicing in St. Louis. His clinical and research interests are in the prevention, diagnosis, and treatment of breast and lung cancers and in expanding access to clinical trials to medically underserved populations.
In this edition of “How I will treat my next patient,” I take a look at recent studies that examined ways to predict important outcomes in two very different settings, acute leukemia and advanced non–small cell lung cancer (NSCLC). They share the virtue of helping cancer specialists to increase their vigilance for clinically relevant complications and situations and to educate patients and families.
VTE risk in acute leukemia
The risk of venous thromboembolism (VTE) in cancer patients depends upon multiple patient-, tumor-, anatomic-, and treatment-related factors. The Khorana score has become an accepted standard for predicting the risks of VTE and assessing the relative value of various anticoagulants in cancer patients. However, the only hematologic malignancy that is specifically listed among the primary cancer sites in the Khorana score is “lymphoma.” VTE can develop during treatment for acute leukemia, especially among patients with acute lymphoblastic leukemia (ALL).
At the 2019 annual congress of the European Hematology Association, Alejandro Lazo-Langer, MD, and his colleagues proposed a scoring system to quantify the risks of VTE based on a retrospective cohort study of more than 500 acute leukemia patients, diagnosed from 2006-2017. They identified 77 patients with a VTE event, with a median time from diagnosis to VTE of 64 days. Among 20 possible predictive factors, 3 emerged in the final multivariate model – platelet count greater than 50,000 (1 point), ALL (2 points), and prior history of VTE (3 points).
Over a period of 12 months, patients with a score of more than 3 points had a cumulative incidence of VTE of 44%, in comparison with 10.5% among patients with lower scores. They were unable to discern whether particular antineoplastic regimens or drugs enhanced the risk.
The authors proposed that, if verified in a validation cohort study, the scoring system could lead to better patient education about signs and symptoms, more intensive surveillance for high-risk patients, and preventive interventions.
What this means in practice
Although a large number of patient records were reviewed for Dr. Lazo-Langer’s study, there were just 74 ALL patients, and it is unclear whether particular treatment regimens or drugs (such as L-asparaginase in ALL) enhance risk. Further study with a validation cohort (as was performed for the Khorana score for patients with other malignancies), is warranted. The study is thought provoking, but for now, in my opinion, standard clinical vigilance, surveillance, and education regarding VTE in leukemia patients remain appropriate.
Steroid impact in NSCLC with ICI therapy
Patients with autoimmune disease and individuals requiring active treatment with steroids (prednisone at 10 mg/day or more or the equivalent) were excluded from clinical trials that led to Food and Drug Administration approval of immune checkpoint inhibitor (ICI) agents. Recently published data indicate that treatment with 10 mg or more of daily prednisone correlates with poor outcome in NSCLC patients receiving ICI therapy (J Clin Oncol. 2018;36:2872-8; J Thoracic Oncol. 2018;13:1771-5). However, at the 2019 annual meeting of the American Society of Clinical Oncology, analyses of the CancerLinQ database showed that, among NSCLC patients, autoimmune disease and treatment for autoimmune disease are surprisingly prevalent. Should oncologists refuse to treat these patients with ICI agents, alone and in combination with chemotherapy or CTLA4 inhibitors?
Biagio Ricciuti, MD, and colleagues published a retrospective, single-institution record review of 650 advanced NSCLC patients who were treated with ICI plus or minus CTLA-4 inhibition on a correlative intramural research study. Patients who received ICI with concurrent cytotoxic chemotherapy were excluded. They gathered clinical-pathologic information about whether patients received concurrent corticosteroids (10 mg/day or more vs. less than 10 mg/day of prednisone or the equivalent) and the reason for steroid use (oncologic vs. cancer-unrelated indications).
Importantly, they gathered information about programmed death-ligand 1 (PD-L1) tumor proportion scores and tumor mutational burden.
Among the 14.3% patients receiving prednisone 10 mg/day or more at the start of ICI therapy, progression-free survival and overall survival were significantly worse – but only among the 66 patients who needed steroids for oncologic reasons (pain, brain metastases, anorexia, cancer-associated dyspnea). Among the 27 patients who received steroids for cancer-unrelated reasons (autoimmune disease, chronic obstructive pulmonary disease, hypersensitivity pneumonitis), progression-free and overall survival were no different than for patients on prednisone 0-9 mg/day. Imbalances in PD-L1 tumor proportion scores among the groups analyzed did not clearly account for the differences in survival.
What this means in practice
The potential for great treatment outcomes with single-agent ICIs in a subset of advanced NSCLC patients, coupled with the lack of an air-tight biomarker for benefit, has changed the timing of discussions between oncologists and patients about stopping antineoplastic treatment. Since we cannot identify the patients for whom ICI use is futile, the default position has been lenient on using these expensive and potentially toxic therapies.
If verified in a multi-institutional setting, with larger numbers of NSCLC patients receiving steroids for cancer-unrelated reasons, the observations of Dr. Ricciuti and colleagues could help clinicians confidently identify the time to focus discussions on supportive care only. In patients with short survival and strong rationale for maximizing supportive care, analyses like this one could help us deliver more appropriate treatment, instead of more treatment, thereby furthering the goals of personalized cancer patient management.
Dr. Lyss has been a community-based medical oncologist and clinical researcher for more than 35 years, practicing in St. Louis. His clinical and research interests are in the prevention, diagnosis, and treatment of breast and lung cancers and in expanding access to clinical trials to medically underserved populations.
In this edition of “How I will treat my next patient,” I take a look at recent studies that examined ways to predict important outcomes in two very different settings, acute leukemia and advanced non–small cell lung cancer (NSCLC). They share the virtue of helping cancer specialists to increase their vigilance for clinically relevant complications and situations and to educate patients and families.
VTE risk in acute leukemia
The risk of venous thromboembolism (VTE) in cancer patients depends upon multiple patient-, tumor-, anatomic-, and treatment-related factors. The Khorana score has become an accepted standard for predicting the risks of VTE and assessing the relative value of various anticoagulants in cancer patients. However, the only hematologic malignancy that is specifically listed among the primary cancer sites in the Khorana score is “lymphoma.” VTE can develop during treatment for acute leukemia, especially among patients with acute lymphoblastic leukemia (ALL).
At the 2019 annual congress of the European Hematology Association, Alejandro Lazo-Langer, MD, and his colleagues proposed a scoring system to quantify the risks of VTE based on a retrospective cohort study of more than 500 acute leukemia patients, diagnosed from 2006-2017. They identified 77 patients with a VTE event, with a median time from diagnosis to VTE of 64 days. Among 20 possible predictive factors, 3 emerged in the final multivariate model – platelet count greater than 50,000 (1 point), ALL (2 points), and prior history of VTE (3 points).
Over a period of 12 months, patients with a score of more than 3 points had a cumulative incidence of VTE of 44%, in comparison with 10.5% among patients with lower scores. They were unable to discern whether particular antineoplastic regimens or drugs enhanced the risk.
The authors proposed that, if verified in a validation cohort study, the scoring system could lead to better patient education about signs and symptoms, more intensive surveillance for high-risk patients, and preventive interventions.
What this means in practice
Although a large number of patient records were reviewed for Dr. Lazo-Langer’s study, there were just 74 ALL patients, and it is unclear whether particular treatment regimens or drugs (such as L-asparaginase in ALL) enhance risk. Further study with a validation cohort (as was performed for the Khorana score for patients with other malignancies), is warranted. The study is thought provoking, but for now, in my opinion, standard clinical vigilance, surveillance, and education regarding VTE in leukemia patients remain appropriate.
Steroid impact in NSCLC with ICI therapy
Patients with autoimmune disease and individuals requiring active treatment with steroids (prednisone at 10 mg/day or more or the equivalent) were excluded from clinical trials that led to Food and Drug Administration approval of immune checkpoint inhibitor (ICI) agents. Recently published data indicate that treatment with 10 mg or more of daily prednisone correlates with poor outcome in NSCLC patients receiving ICI therapy (J Clin Oncol. 2018;36:2872-8; J Thoracic Oncol. 2018;13:1771-5). However, at the 2019 annual meeting of the American Society of Clinical Oncology, analyses of the CancerLinQ database showed that, among NSCLC patients, autoimmune disease and treatment for autoimmune disease are surprisingly prevalent. Should oncologists refuse to treat these patients with ICI agents, alone and in combination with chemotherapy or CTLA4 inhibitors?
Biagio Ricciuti, MD, and colleagues published a retrospective, single-institution record review of 650 advanced NSCLC patients who were treated with ICI plus or minus CTLA-4 inhibition on a correlative intramural research study. Patients who received ICI with concurrent cytotoxic chemotherapy were excluded. They gathered clinical-pathologic information about whether patients received concurrent corticosteroids (10 mg/day or more vs. less than 10 mg/day of prednisone or the equivalent) and the reason for steroid use (oncologic vs. cancer-unrelated indications).
Importantly, they gathered information about programmed death-ligand 1 (PD-L1) tumor proportion scores and tumor mutational burden.
Among the 14.3% patients receiving prednisone 10 mg/day or more at the start of ICI therapy, progression-free survival and overall survival were significantly worse – but only among the 66 patients who needed steroids for oncologic reasons (pain, brain metastases, anorexia, cancer-associated dyspnea). Among the 27 patients who received steroids for cancer-unrelated reasons (autoimmune disease, chronic obstructive pulmonary disease, hypersensitivity pneumonitis), progression-free and overall survival were no different than for patients on prednisone 0-9 mg/day. Imbalances in PD-L1 tumor proportion scores among the groups analyzed did not clearly account for the differences in survival.
What this means in practice
The potential for great treatment outcomes with single-agent ICIs in a subset of advanced NSCLC patients, coupled with the lack of an air-tight biomarker for benefit, has changed the timing of discussions between oncologists and patients about stopping antineoplastic treatment. Since we cannot identify the patients for whom ICI use is futile, the default position has been lenient on using these expensive and potentially toxic therapies.
If verified in a multi-institutional setting, with larger numbers of NSCLC patients receiving steroids for cancer-unrelated reasons, the observations of Dr. Ricciuti and colleagues could help clinicians confidently identify the time to focus discussions on supportive care only. In patients with short survival and strong rationale for maximizing supportive care, analyses like this one could help us deliver more appropriate treatment, instead of more treatment, thereby furthering the goals of personalized cancer patient management.
Dr. Lyss has been a community-based medical oncologist and clinical researcher for more than 35 years, practicing in St. Louis. His clinical and research interests are in the prevention, diagnosis, and treatment of breast and lung cancers and in expanding access to clinical trials to medically underserved populations.
Y 2 the ED? (Why patients go to the emergency department)
Along with terminal care and inflated drug prices, the excessive number of “inappropriate” ED visits often is cited as a major driver of health care costs in the United States. Why do so many patients choose to go to the ED for complaints that might be better or more economically treated in another setting?
A report by two researchers in the division of emergency medicine at the Boston Children’s Hospital that appeared in the June 2019 Pediatrics suggests that, at least for pediatric patients, “increased insurance coverage neither drove nor counteracted” the recent trends in ED visits. (“Trends in Pediatric Emergency Department Use After the Affordable Care Act,” Pediatrics. 2019 Jun 1. doi: 10.1542/peds.2018-3542).
I guess it’s not surprising – and somewhat comforting – to learn that, when parents believe their child has an emergent condition they give little thought to the cost of care. Is the trend of increasing ED use a result of an evolving definition of an “emergency”? Your grandparents, or certainly your great grandparents, might claim that, when they were young most minor injuries were handled at home, or at least in the neighborhood by someone with first aid experience who wasn’t put off by the sight of blood. However, a trend away from self-reliance in everything from food preparation to auto repair, combined with media overexposure to the serious complications of apparently minor illness and injury, has left most parents feeling fearful and helpless in the face of adversity.
We have to accept as a given that many parents are going to interpret their child’s situation as emergent, even though you and I might not. But what are the factors that prompt a concerned parent to take his child to the ED instead of a physician’s office? It may simply be the path of least resistance. The parent’s past experience may include frustrating and time-consuming attempts to navigate a clunky phone system only to be met by a receptionist or triage nurse who seems more committed to deflecting calls and protecting the physician’s schedule than getting the patient seen.
The call may miraculously get through to someone with a caring voice and the patience to listen, but the parent then learns that the office doesn’t do minor wound care or he is told that the physician almost certainly will want to do an x-ray of any injured extremity and that the ED is a better choice. It doesn’t take very many scenarios like this to prompt a parent to make his first and only call to the ED. To some extent, physician behavior has helped mold parents’ definition of an emergency.
We are encouraged to make our offices a “medical home.” However, it appears the medical home model is one that is built around chronic conditions and behavioral problems and gives little attention to the acute complaints. When you came running into the house with a skinned knee, did your mother tell to you go across the street to the neighbor’s house because blood made her squeamish and she didn’t have any bandages?
There are ways to structure an office and a schedule which are more welcoming to patients with minor emergencies, and I know it is a difficult sell to physicians who are handcuffed by their EHRs and already overwhelmed by patients with time-consuming behavioral complaints. However, if your practice is facing competition from pop-up urgent care centers or if you are increasingly troubled that your patients are receiving fragmented care, it may not be too late to make your practice into a true medical home that welcomes minor emergencies.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Email him at [email protected].
Along with terminal care and inflated drug prices, the excessive number of “inappropriate” ED visits often is cited as a major driver of health care costs in the United States. Why do so many patients choose to go to the ED for complaints that might be better or more economically treated in another setting?
A report by two researchers in the division of emergency medicine at the Boston Children’s Hospital that appeared in the June 2019 Pediatrics suggests that, at least for pediatric patients, “increased insurance coverage neither drove nor counteracted” the recent trends in ED visits. (“Trends in Pediatric Emergency Department Use After the Affordable Care Act,” Pediatrics. 2019 Jun 1. doi: 10.1542/peds.2018-3542).
I guess it’s not surprising – and somewhat comforting – to learn that, when parents believe their child has an emergent condition they give little thought to the cost of care. Is the trend of increasing ED use a result of an evolving definition of an “emergency”? Your grandparents, or certainly your great grandparents, might claim that, when they were young most minor injuries were handled at home, or at least in the neighborhood by someone with first aid experience who wasn’t put off by the sight of blood. However, a trend away from self-reliance in everything from food preparation to auto repair, combined with media overexposure to the serious complications of apparently minor illness and injury, has left most parents feeling fearful and helpless in the face of adversity.
We have to accept as a given that many parents are going to interpret their child’s situation as emergent, even though you and I might not. But what are the factors that prompt a concerned parent to take his child to the ED instead of a physician’s office? It may simply be the path of least resistance. The parent’s past experience may include frustrating and time-consuming attempts to navigate a clunky phone system only to be met by a receptionist or triage nurse who seems more committed to deflecting calls and protecting the physician’s schedule than getting the patient seen.
The call may miraculously get through to someone with a caring voice and the patience to listen, but the parent then learns that the office doesn’t do minor wound care or he is told that the physician almost certainly will want to do an x-ray of any injured extremity and that the ED is a better choice. It doesn’t take very many scenarios like this to prompt a parent to make his first and only call to the ED. To some extent, physician behavior has helped mold parents’ definition of an emergency.
We are encouraged to make our offices a “medical home.” However, it appears the medical home model is one that is built around chronic conditions and behavioral problems and gives little attention to the acute complaints. When you came running into the house with a skinned knee, did your mother tell to you go across the street to the neighbor’s house because blood made her squeamish and she didn’t have any bandages?
There are ways to structure an office and a schedule which are more welcoming to patients with minor emergencies, and I know it is a difficult sell to physicians who are handcuffed by their EHRs and already overwhelmed by patients with time-consuming behavioral complaints. However, if your practice is facing competition from pop-up urgent care centers or if you are increasingly troubled that your patients are receiving fragmented care, it may not be too late to make your practice into a true medical home that welcomes minor emergencies.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Email him at [email protected].
Along with terminal care and inflated drug prices, the excessive number of “inappropriate” ED visits often is cited as a major driver of health care costs in the United States. Why do so many patients choose to go to the ED for complaints that might be better or more economically treated in another setting?
A report by two researchers in the division of emergency medicine at the Boston Children’s Hospital that appeared in the June 2019 Pediatrics suggests that, at least for pediatric patients, “increased insurance coverage neither drove nor counteracted” the recent trends in ED visits. (“Trends in Pediatric Emergency Department Use After the Affordable Care Act,” Pediatrics. 2019 Jun 1. doi: 10.1542/peds.2018-3542).
I guess it’s not surprising – and somewhat comforting – to learn that, when parents believe their child has an emergent condition they give little thought to the cost of care. Is the trend of increasing ED use a result of an evolving definition of an “emergency”? Your grandparents, or certainly your great grandparents, might claim that, when they were young most minor injuries were handled at home, or at least in the neighborhood by someone with first aid experience who wasn’t put off by the sight of blood. However, a trend away from self-reliance in everything from food preparation to auto repair, combined with media overexposure to the serious complications of apparently minor illness and injury, has left most parents feeling fearful and helpless in the face of adversity.
We have to accept as a given that many parents are going to interpret their child’s situation as emergent, even though you and I might not. But what are the factors that prompt a concerned parent to take his child to the ED instead of a physician’s office? It may simply be the path of least resistance. The parent’s past experience may include frustrating and time-consuming attempts to navigate a clunky phone system only to be met by a receptionist or triage nurse who seems more committed to deflecting calls and protecting the physician’s schedule than getting the patient seen.
The call may miraculously get through to someone with a caring voice and the patience to listen, but the parent then learns that the office doesn’t do minor wound care or he is told that the physician almost certainly will want to do an x-ray of any injured extremity and that the ED is a better choice. It doesn’t take very many scenarios like this to prompt a parent to make his first and only call to the ED. To some extent, physician behavior has helped mold parents’ definition of an emergency.
We are encouraged to make our offices a “medical home.” However, it appears the medical home model is one that is built around chronic conditions and behavioral problems and gives little attention to the acute complaints. When you came running into the house with a skinned knee, did your mother tell to you go across the street to the neighbor’s house because blood made her squeamish and she didn’t have any bandages?
There are ways to structure an office and a schedule which are more welcoming to patients with minor emergencies, and I know it is a difficult sell to physicians who are handcuffed by their EHRs and already overwhelmed by patients with time-consuming behavioral complaints. However, if your practice is facing competition from pop-up urgent care centers or if you are increasingly troubled that your patients are receiving fragmented care, it may not be too late to make your practice into a true medical home that welcomes minor emergencies.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Email him at [email protected].
Hyperthyroid? She sure doesn’t look like it
A 50-year-old woman returns for routine follow-up. She has a 15-year history of hypothyroidism, pernicious anemia, and celiac disease. She has had some recent abdominal pain, but no changes in her bowel patterns, and she has not experienced any problems with chest pain, palpitations, or weakness recently. The only medication she is taking is levothyroxine 125 mcg. She has reported no recent weight loss, her blood pressure is 100/60 mm Hg, pulse is 66 beats per minute, temperature is 36.8 degrees Celsius, body mass index is 20, and she does not have a neck goiter. Her cardiac exam was normal and her neurological exam revealed no tremor. Her lab for thyroid-stimulating hormone (TSH) was less than 0.03, and her lab for free thyroxine (FT4) was 2.2, while her TSH level had been 1.4 a year ago. Her levothyroxine dose was decreased to 100 mcg/day, and her repeat lab for TSH, which occurred 12 weeks later, was still less than 0.03. What is the best explanation for why this patient’s labs look like hyperthyroidism, but this patient clinically does not appear to have hyperthyroidism?
A) She was initially given too much levothyroxine; her TSH response is lagging to dose reduction.
B) She has Graves’ disease.
C) She has acute thyroiditis.
D) She is taking extra thyroid hormone.
E) She is taking biotin.
This patient has a history that includes multiple autoimmune diseases including hypothyroidism. It would be extremely unlikely that she would develop Graves' disease or develop acute thyroiditis in the setting of a gland that has been underfunctioning for years. She has no symptoms suggesting that she has hyperthyroidism, which makes taking more thyroid hormone than she is reporting less likely, although this could be possible. The TSH response can lag after dose adjustments of thyroid, but usually a 6-week interval is adequate. This patient’s testing was done 12 weeks after dose reduction making this very unlikely.
The cause for the labs that look like hyperthyroidism in this patient who appears clinically euthyroid is that she is taking biotin. Biotin (vitamin B7) has become a very popular supplement in the past few years for thin hair, brittle nails, and fatigue. The RDA for biotin is 30 mcg. It is widely available in high doses – 5,000-10,000 mcg – which are common doses for supplements.
Biotin has been used extensively as a key component of immunoassays. Streptavidin, a protein produced by the bacteria Streptomyces avidinii, binds biotin with an extremely high affinity, and this binding is utilized in a number of immunoassays, including the assays for thyroid hormone and TSH.1
High serum levels of biotin can make the assays inaccurate, with lower-than-actual TSH and higher-than-actual thyroid hormone levels. Multiple case reports have documented this happening clinically.1-3 I personally saw a case of this recently in my practice. Katzman and colleagues looked at the prevalence of biotin use in outpatients.4 They found that 7.7% were taking supplemental biotin, while 7.4% had levels of biotin in serum samples that were at a level that could interfere with biotin-based serum assays.
Theoretically, biotin can affect multiple other assays that use the streptavidin-biotin assay. The most concerning of these potential problems is with troponin assays. Biotin can falsely lower troponin assays and this can lead to missing the diagnosis of cardiac injury. The Food and Drug Administration released a warning about this and other biotin lab interactions in November 2017.5 Several studies have demonstrated that this effect can occur at serum levels achievable with available over-the-counter doses of biotin.6,7
Not all troponin assays are affected by high serum levels of biotin: The Gen 5 cTnT assay is the only troponin assay affected.7 I could not find any case reports that have been published where biotin had caused a clinical missed diagnosis with troponins.
Pearls
Consider biotin supplement use when you have patients whose labs look like hyperthyroidism, but clinically do not appear to be hyperthyroid.
Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and serves as third-year medical student clerkship director at the University of Washington. Contact Dr. Paauw at [email protected].
References
1. Charles S, Agrawal N, and Blum M. Erroneous thyroid diagnosis due to over-the-counter biotin. Nutrition 2019;57:257-8.
2. Elston MS et al. Factitious Graves’ disease due to a biotin immunoassay interference – a case and review of the literature. J Clin Endocrinol Metab 2016;101:3251-5.
3. Barbesino G. Misdiagnosis of Graves ’disease with apparent severe hyperthyroidism in a patient taking biotin megadoses. Thyroid 2016;26(6):860-3.
4. Katzman et al. Prevalence of biotin supplement usage in outpatients and plasma biotin concentrations in patients presenting to the emergency department. Clin Biochem. 2018 Sep;60:11-16.
5. “The FDA Warns that Biotin May Interfere with Lab Tests: FDA Safety Communication,” Nov. 28, 2017.
6. Trambas et al. Characterization of the scope and magnitude of biotin interference in susceptible Roche Elecsys competitive and sandwich immunoassays. Ann Clin Biochem. 2018 Mar;55(2):205-15.
7. Frame IJ et al. Susceptibility of cardiac troponin assays to biotin interference. Am J Clin Pathol. 2019 Apr 2;151(5):486-93.
A 50-year-old woman returns for routine follow-up. She has a 15-year history of hypothyroidism, pernicious anemia, and celiac disease. She has had some recent abdominal pain, but no changes in her bowel patterns, and she has not experienced any problems with chest pain, palpitations, or weakness recently. The only medication she is taking is levothyroxine 125 mcg. She has reported no recent weight loss, her blood pressure is 100/60 mm Hg, pulse is 66 beats per minute, temperature is 36.8 degrees Celsius, body mass index is 20, and she does not have a neck goiter. Her cardiac exam was normal and her neurological exam revealed no tremor. Her lab for thyroid-stimulating hormone (TSH) was less than 0.03, and her lab for free thyroxine (FT4) was 2.2, while her TSH level had been 1.4 a year ago. Her levothyroxine dose was decreased to 100 mcg/day, and her repeat lab for TSH, which occurred 12 weeks later, was still less than 0.03. What is the best explanation for why this patient’s labs look like hyperthyroidism, but this patient clinically does not appear to have hyperthyroidism?
A) She was initially given too much levothyroxine; her TSH response is lagging to dose reduction.
B) She has Graves’ disease.
C) She has acute thyroiditis.
D) She is taking extra thyroid hormone.
E) She is taking biotin.
This patient has a history that includes multiple autoimmune diseases including hypothyroidism. It would be extremely unlikely that she would develop Graves' disease or develop acute thyroiditis in the setting of a gland that has been underfunctioning for years. She has no symptoms suggesting that she has hyperthyroidism, which makes taking more thyroid hormone than she is reporting less likely, although this could be possible. The TSH response can lag after dose adjustments of thyroid, but usually a 6-week interval is adequate. This patient’s testing was done 12 weeks after dose reduction making this very unlikely.
The cause for the labs that look like hyperthyroidism in this patient who appears clinically euthyroid is that she is taking biotin. Biotin (vitamin B7) has become a very popular supplement in the past few years for thin hair, brittle nails, and fatigue. The RDA for biotin is 30 mcg. It is widely available in high doses – 5,000-10,000 mcg – which are common doses for supplements.
Biotin has been used extensively as a key component of immunoassays. Streptavidin, a protein produced by the bacteria Streptomyces avidinii, binds biotin with an extremely high affinity, and this binding is utilized in a number of immunoassays, including the assays for thyroid hormone and TSH.1
High serum levels of biotin can make the assays inaccurate, with lower-than-actual TSH and higher-than-actual thyroid hormone levels. Multiple case reports have documented this happening clinically.1-3 I personally saw a case of this recently in my practice. Katzman and colleagues looked at the prevalence of biotin use in outpatients.4 They found that 7.7% were taking supplemental biotin, while 7.4% had levels of biotin in serum samples that were at a level that could interfere with biotin-based serum assays.
Theoretically, biotin can affect multiple other assays that use the streptavidin-biotin assay. The most concerning of these potential problems is with troponin assays. Biotin can falsely lower troponin assays and this can lead to missing the diagnosis of cardiac injury. The Food and Drug Administration released a warning about this and other biotin lab interactions in November 2017.5 Several studies have demonstrated that this effect can occur at serum levels achievable with available over-the-counter doses of biotin.6,7
Not all troponin assays are affected by high serum levels of biotin: The Gen 5 cTnT assay is the only troponin assay affected.7 I could not find any case reports that have been published where biotin had caused a clinical missed diagnosis with troponins.
Pearls
Consider biotin supplement use when you have patients whose labs look like hyperthyroidism, but clinically do not appear to be hyperthyroid.
Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and serves as third-year medical student clerkship director at the University of Washington. Contact Dr. Paauw at [email protected].
References
1. Charles S, Agrawal N, and Blum M. Erroneous thyroid diagnosis due to over-the-counter biotin. Nutrition 2019;57:257-8.
2. Elston MS et al. Factitious Graves’ disease due to a biotin immunoassay interference – a case and review of the literature. J Clin Endocrinol Metab 2016;101:3251-5.
3. Barbesino G. Misdiagnosis of Graves ’disease with apparent severe hyperthyroidism in a patient taking biotin megadoses. Thyroid 2016;26(6):860-3.
4. Katzman et al. Prevalence of biotin supplement usage in outpatients and plasma biotin concentrations in patients presenting to the emergency department. Clin Biochem. 2018 Sep;60:11-16.
5. “The FDA Warns that Biotin May Interfere with Lab Tests: FDA Safety Communication,” Nov. 28, 2017.
6. Trambas et al. Characterization of the scope and magnitude of biotin interference in susceptible Roche Elecsys competitive and sandwich immunoassays. Ann Clin Biochem. 2018 Mar;55(2):205-15.
7. Frame IJ et al. Susceptibility of cardiac troponin assays to biotin interference. Am J Clin Pathol. 2019 Apr 2;151(5):486-93.
A 50-year-old woman returns for routine follow-up. She has a 15-year history of hypothyroidism, pernicious anemia, and celiac disease. She has had some recent abdominal pain, but no changes in her bowel patterns, and she has not experienced any problems with chest pain, palpitations, or weakness recently. The only medication she is taking is levothyroxine 125 mcg. She has reported no recent weight loss, her blood pressure is 100/60 mm Hg, pulse is 66 beats per minute, temperature is 36.8 degrees Celsius, body mass index is 20, and she does not have a neck goiter. Her cardiac exam was normal and her neurological exam revealed no tremor. Her lab for thyroid-stimulating hormone (TSH) was less than 0.03, and her lab for free thyroxine (FT4) was 2.2, while her TSH level had been 1.4 a year ago. Her levothyroxine dose was decreased to 100 mcg/day, and her repeat lab for TSH, which occurred 12 weeks later, was still less than 0.03. What is the best explanation for why this patient’s labs look like hyperthyroidism, but this patient clinically does not appear to have hyperthyroidism?
A) She was initially given too much levothyroxine; her TSH response is lagging to dose reduction.
B) She has Graves’ disease.
C) She has acute thyroiditis.
D) She is taking extra thyroid hormone.
E) She is taking biotin.
This patient has a history that includes multiple autoimmune diseases including hypothyroidism. It would be extremely unlikely that she would develop Graves' disease or develop acute thyroiditis in the setting of a gland that has been underfunctioning for years. She has no symptoms suggesting that she has hyperthyroidism, which makes taking more thyroid hormone than she is reporting less likely, although this could be possible. The TSH response can lag after dose adjustments of thyroid, but usually a 6-week interval is adequate. This patient’s testing was done 12 weeks after dose reduction making this very unlikely.
The cause for the labs that look like hyperthyroidism in this patient who appears clinically euthyroid is that she is taking biotin. Biotin (vitamin B7) has become a very popular supplement in the past few years for thin hair, brittle nails, and fatigue. The RDA for biotin is 30 mcg. It is widely available in high doses – 5,000-10,000 mcg – which are common doses for supplements.
Biotin has been used extensively as a key component of immunoassays. Streptavidin, a protein produced by the bacteria Streptomyces avidinii, binds biotin with an extremely high affinity, and this binding is utilized in a number of immunoassays, including the assays for thyroid hormone and TSH.1
High serum levels of biotin can make the assays inaccurate, with lower-than-actual TSH and higher-than-actual thyroid hormone levels. Multiple case reports have documented this happening clinically.1-3 I personally saw a case of this recently in my practice. Katzman and colleagues looked at the prevalence of biotin use in outpatients.4 They found that 7.7% were taking supplemental biotin, while 7.4% had levels of biotin in serum samples that were at a level that could interfere with biotin-based serum assays.
Theoretically, biotin can affect multiple other assays that use the streptavidin-biotin assay. The most concerning of these potential problems is with troponin assays. Biotin can falsely lower troponin assays and this can lead to missing the diagnosis of cardiac injury. The Food and Drug Administration released a warning about this and other biotin lab interactions in November 2017.5 Several studies have demonstrated that this effect can occur at serum levels achievable with available over-the-counter doses of biotin.6,7
Not all troponin assays are affected by high serum levels of biotin: The Gen 5 cTnT assay is the only troponin assay affected.7 I could not find any case reports that have been published where biotin had caused a clinical missed diagnosis with troponins.
Pearls
Consider biotin supplement use when you have patients whose labs look like hyperthyroidism, but clinically do not appear to be hyperthyroid.
Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and serves as third-year medical student clerkship director at the University of Washington. Contact Dr. Paauw at [email protected].
References
1. Charles S, Agrawal N, and Blum M. Erroneous thyroid diagnosis due to over-the-counter biotin. Nutrition 2019;57:257-8.
2. Elston MS et al. Factitious Graves’ disease due to a biotin immunoassay interference – a case and review of the literature. J Clin Endocrinol Metab 2016;101:3251-5.
3. Barbesino G. Misdiagnosis of Graves ’disease with apparent severe hyperthyroidism in a patient taking biotin megadoses. Thyroid 2016;26(6):860-3.
4. Katzman et al. Prevalence of biotin supplement usage in outpatients and plasma biotin concentrations in patients presenting to the emergency department. Clin Biochem. 2018 Sep;60:11-16.
5. “The FDA Warns that Biotin May Interfere with Lab Tests: FDA Safety Communication,” Nov. 28, 2017.
6. Trambas et al. Characterization of the scope and magnitude of biotin interference in susceptible Roche Elecsys competitive and sandwich immunoassays. Ann Clin Biochem. 2018 Mar;55(2):205-15.
7. Frame IJ et al. Susceptibility of cardiac troponin assays to biotin interference. Am J Clin Pathol. 2019 Apr 2;151(5):486-93.
New research in otitis media
New research was presented at the International Society for Otitis Media meeting in June 2019, which I attended. I would like to share a selection of new findings from the many presentations.
Transtympanic antibiotic delivery
Topical therapy has been used to treat only otitis externa and acute otitis media (AOM) with ear discharge. Giving antibiotics through the tympanic membrane could mitigate many of the concerns about antibiotic use driving antibiotic resistance of bacteria among children. Up to now, using antibiotics in the ear canal to treat AOM has not been considered because the tympanic membrane is highly impermeable to the transtympanic diffusion of any drugs. However, in recent years, a number of different drug delivery systems have been developed, and in some cases, animal studies have shown that noninvasive transtympanic delivery is possible so that drugs can reach high concentrations in the middle ear without damage. Nanovesicles and nanoliposomes that contain antibiotics and are small enough to pass through the eardrum have been developed and tested in animal models; these show promise. Ototopical administration of a drug called vinpocetine that was repurposed has been tested in mice and shown to reduce inflammation and mucus production in the middle ear during otitis media.
Biofilms
Antibiotic treatment failure can occur in AOM for several reasons. The treatment of choice, amoxicillin, for example may fail to achieve an adequate concentration because of poor absorption in the gastrointestinal tract or poor penetration into the middle ear. Or, the antibiotic chosen may not be effective because of resistance of the strain causing the infection. Another explanation, especially in recurrent AOM and chronic AOM, could be the presence of biofilms. Biofilms are multicellular bacterial communities incorporated in a polymeric, plasticlike matrix in which pathogens are protected from antibiotic activity. The biofilm provides a physical barrier to antibiotic penetration, and bacteria can persist in the middle ear and periodically cause a new AOM. If AOM persists or becomes a more chronic otitis media with effusion, the “glue ear” causes an environment in the middle ear that is low in oxygen. A low-oxygen environment is favorable to biofilms. Also one might expect that middle ear pus would have a low pH, but actual measurements show the pH is highly alkaline. Species of Haemophilus influenzae have been identified as more virulent when in an alkaline pH or the alkaline pH makes the H. influenzae persist better in the middle ear, perhaps in a biofilm. To eliminate biofilms and improve antibiotic efficacy, a vaccine against a protein expressed by H. influenzae has been developed. Antibodies against this protein have been shown to disrupt and prevent the formation of biofilms in an animal model.
Probiotics
The normal bacteria that live in the nasopharynx of children with recurrent AOM is now known to differ from that of children who experience infrequent AOM or remain AOM-free throughout childhood. The use of oral pre- and probiotics for AOM prophylaxis remains debated because the results of studies are conflicting and frequently show no effect. So the idea of using prebiotics or probiotics to create a favorable “microbiome” of the nose is under investigation. Two species of bacteria that are gathering the most attention are Corynebacterium species (a few types in particular) and a bacteria called Dolosigranulum pigrum. Delivery of the commensal species would be as a nose spray.
Vaccines
The use of pneumococcal conjugate vaccines (PCVs) has reduced the frequency of AOM caused by Streptococcus pneumoniae. PCVs are not as effective against AOM as they are against invasive pneumococcal disease, but they still help a lot. However, because there are now at least 96 different serotypes of the pneumococcus based on different capsular types, we see a pattern of replacement of disease-causing strains by new strains within a few years of introduction of a new formulation. We started with 7 serotypes (Prevnar 7) in year 2000, and it was replaced by the current formulation with 13 serotypes (Prevnar 13) in 2010. Replacements have occurred again so vaccine companies are making new formulations for the future that include more serotypes, up to 20 serotypes. But, technically and feasibility-wise there is a limit to making such vaccines. A vaccine based on killed unencapsulated bacteria has been tested for safety and immunogenicity in young children. There is no test so far for prevention of AOM. Another type of vaccine based on proteins expressed by the pneumococcus that could be vaccine targets was tested in American Navajo children, and it failed to be as efficacious as hoped.
Biomarkers.
Due to recurrent AOM or persistent otitis media with effusion, about 15% of children in the United States receive tympanostomy tubes. Among those who receive tubes, about 20% go on to receive a second set of tubes, often with adenotonsillectomy. To find a biomarker that could identify children likely to require a second set of tubes, the fluid in the middle ear was tested when a first set of tubes were inserted. If bacteria were detected by polymerase chain reaction (PCR) testing or if a profile of specific inflammatory cytokines was measured, those results could be used to predict a high likelihood for a second set of tubes.
Overdiagnosis
Diagnosis of AOM is challenging in young children, in whom it most frequently occurs. The ear canal is typically about 3 mm wide, the child struggles during the examination, and diagnostic skills are not taught in training, resulting in a high overdiagnosis rate. I presented data that suggest too many children who are not truly otitis prone have been classified as otitis prone based on incorrect clinical diagnosis. My colleagues and I found that 30% of children reach the threshold of three episodes of AOM in 6 months or four within a year when diagnosed by community pediatricians, similar to many other studies. Validated otoscopists (trained by experts with diagnosis definitively proven as at least 85% accurate using tympanocentesis) classify 15% of children as otitis prone – half as many. If tympanocentesis is used to prove middle ear fluid has bacterial pathogens (about 95% yield a bacterial otopathogen using culture and PCR), then about 10% of children are classified as otitis prone – one-third as many. This suggests that children clinically diagnosed by community-based pediatricians are overdiagnosed with AOM, perhaps three times more often than true. And that leads to overuse of antibiotics and referrals for tympanostomy tube surgery more often than should occur. So we need to improve diagnostic methods beyond otoscopy. New types of imaging for the eardrum and middle ear using novel technologies are in early clinical trials.
Immunity
The notion that young children get AOM because of Eustachian tube dysfunction in their early years of life (horizontal anatomy) may be true, but there is more to the story. After 10 years of work, the scientists in my research group have shown that children in the first 3 years of life can have an immune system that is suppressed – it is poorly responsive to pathogens and routine pediatric vaccines. Many features resemble a neonatal immune system, beginning life with a suppressed immune system or being in cytokine storm from birth. We introduced the term “prolonged neonatal-like immune profile (PNIP)” to give a general description of the immune responses we have found in otitis-prone children. They outgrow this. So the immune maturation is delayed but not permanent. It is mostly resolved by age 3 years. We found problems in both innate and adaptive immunity. It may be that the main explanation for recurrent AOM in the first years of life is PNIP. Scientists from Australia also reported immunity problems in Aboriginal children and they are very otitis prone, often progressing to chronic suppurative otitis media. Animal model studies of AOM show inadequate innate and adaptive immunity importantly contribute to the infection as well.
Dr. Pichichero is a specialist in pediatric infectious diseases and director of the Research Institute at Rochester (N.Y.) General Hospital. He has no conflicts to declare. Email him at [email protected].
New research was presented at the International Society for Otitis Media meeting in June 2019, which I attended. I would like to share a selection of new findings from the many presentations.
Transtympanic antibiotic delivery
Topical therapy has been used to treat only otitis externa and acute otitis media (AOM) with ear discharge. Giving antibiotics through the tympanic membrane could mitigate many of the concerns about antibiotic use driving antibiotic resistance of bacteria among children. Up to now, using antibiotics in the ear canal to treat AOM has not been considered because the tympanic membrane is highly impermeable to the transtympanic diffusion of any drugs. However, in recent years, a number of different drug delivery systems have been developed, and in some cases, animal studies have shown that noninvasive transtympanic delivery is possible so that drugs can reach high concentrations in the middle ear without damage. Nanovesicles and nanoliposomes that contain antibiotics and are small enough to pass through the eardrum have been developed and tested in animal models; these show promise. Ototopical administration of a drug called vinpocetine that was repurposed has been tested in mice and shown to reduce inflammation and mucus production in the middle ear during otitis media.
Biofilms
Antibiotic treatment failure can occur in AOM for several reasons. The treatment of choice, amoxicillin, for example may fail to achieve an adequate concentration because of poor absorption in the gastrointestinal tract or poor penetration into the middle ear. Or, the antibiotic chosen may not be effective because of resistance of the strain causing the infection. Another explanation, especially in recurrent AOM and chronic AOM, could be the presence of biofilms. Biofilms are multicellular bacterial communities incorporated in a polymeric, plasticlike matrix in which pathogens are protected from antibiotic activity. The biofilm provides a physical barrier to antibiotic penetration, and bacteria can persist in the middle ear and periodically cause a new AOM. If AOM persists or becomes a more chronic otitis media with effusion, the “glue ear” causes an environment in the middle ear that is low in oxygen. A low-oxygen environment is favorable to biofilms. Also one might expect that middle ear pus would have a low pH, but actual measurements show the pH is highly alkaline. Species of Haemophilus influenzae have been identified as more virulent when in an alkaline pH or the alkaline pH makes the H. influenzae persist better in the middle ear, perhaps in a biofilm. To eliminate biofilms and improve antibiotic efficacy, a vaccine against a protein expressed by H. influenzae has been developed. Antibodies against this protein have been shown to disrupt and prevent the formation of biofilms in an animal model.
Probiotics
The normal bacteria that live in the nasopharynx of children with recurrent AOM is now known to differ from that of children who experience infrequent AOM or remain AOM-free throughout childhood. The use of oral pre- and probiotics for AOM prophylaxis remains debated because the results of studies are conflicting and frequently show no effect. So the idea of using prebiotics or probiotics to create a favorable “microbiome” of the nose is under investigation. Two species of bacteria that are gathering the most attention are Corynebacterium species (a few types in particular) and a bacteria called Dolosigranulum pigrum. Delivery of the commensal species would be as a nose spray.
Vaccines
The use of pneumococcal conjugate vaccines (PCVs) has reduced the frequency of AOM caused by Streptococcus pneumoniae. PCVs are not as effective against AOM as they are against invasive pneumococcal disease, but they still help a lot. However, because there are now at least 96 different serotypes of the pneumococcus based on different capsular types, we see a pattern of replacement of disease-causing strains by new strains within a few years of introduction of a new formulation. We started with 7 serotypes (Prevnar 7) in year 2000, and it was replaced by the current formulation with 13 serotypes (Prevnar 13) in 2010. Replacements have occurred again so vaccine companies are making new formulations for the future that include more serotypes, up to 20 serotypes. But, technically and feasibility-wise there is a limit to making such vaccines. A vaccine based on killed unencapsulated bacteria has been tested for safety and immunogenicity in young children. There is no test so far for prevention of AOM. Another type of vaccine based on proteins expressed by the pneumococcus that could be vaccine targets was tested in American Navajo children, and it failed to be as efficacious as hoped.
Biomarkers.
Due to recurrent AOM or persistent otitis media with effusion, about 15% of children in the United States receive tympanostomy tubes. Among those who receive tubes, about 20% go on to receive a second set of tubes, often with adenotonsillectomy. To find a biomarker that could identify children likely to require a second set of tubes, the fluid in the middle ear was tested when a first set of tubes were inserted. If bacteria were detected by polymerase chain reaction (PCR) testing or if a profile of specific inflammatory cytokines was measured, those results could be used to predict a high likelihood for a second set of tubes.
Overdiagnosis
Diagnosis of AOM is challenging in young children, in whom it most frequently occurs. The ear canal is typically about 3 mm wide, the child struggles during the examination, and diagnostic skills are not taught in training, resulting in a high overdiagnosis rate. I presented data that suggest too many children who are not truly otitis prone have been classified as otitis prone based on incorrect clinical diagnosis. My colleagues and I found that 30% of children reach the threshold of three episodes of AOM in 6 months or four within a year when diagnosed by community pediatricians, similar to many other studies. Validated otoscopists (trained by experts with diagnosis definitively proven as at least 85% accurate using tympanocentesis) classify 15% of children as otitis prone – half as many. If tympanocentesis is used to prove middle ear fluid has bacterial pathogens (about 95% yield a bacterial otopathogen using culture and PCR), then about 10% of children are classified as otitis prone – one-third as many. This suggests that children clinically diagnosed by community-based pediatricians are overdiagnosed with AOM, perhaps three times more often than true. And that leads to overuse of antibiotics and referrals for tympanostomy tube surgery more often than should occur. So we need to improve diagnostic methods beyond otoscopy. New types of imaging for the eardrum and middle ear using novel technologies are in early clinical trials.
Immunity
The notion that young children get AOM because of Eustachian tube dysfunction in their early years of life (horizontal anatomy) may be true, but there is more to the story. After 10 years of work, the scientists in my research group have shown that children in the first 3 years of life can have an immune system that is suppressed – it is poorly responsive to pathogens and routine pediatric vaccines. Many features resemble a neonatal immune system, beginning life with a suppressed immune system or being in cytokine storm from birth. We introduced the term “prolonged neonatal-like immune profile (PNIP)” to give a general description of the immune responses we have found in otitis-prone children. They outgrow this. So the immune maturation is delayed but not permanent. It is mostly resolved by age 3 years. We found problems in both innate and adaptive immunity. It may be that the main explanation for recurrent AOM in the first years of life is PNIP. Scientists from Australia also reported immunity problems in Aboriginal children and they are very otitis prone, often progressing to chronic suppurative otitis media. Animal model studies of AOM show inadequate innate and adaptive immunity importantly contribute to the infection as well.
Dr. Pichichero is a specialist in pediatric infectious diseases and director of the Research Institute at Rochester (N.Y.) General Hospital. He has no conflicts to declare. Email him at [email protected].
New research was presented at the International Society for Otitis Media meeting in June 2019, which I attended. I would like to share a selection of new findings from the many presentations.
Transtympanic antibiotic delivery
Topical therapy has been used to treat only otitis externa and acute otitis media (AOM) with ear discharge. Giving antibiotics through the tympanic membrane could mitigate many of the concerns about antibiotic use driving antibiotic resistance of bacteria among children. Up to now, using antibiotics in the ear canal to treat AOM has not been considered because the tympanic membrane is highly impermeable to the transtympanic diffusion of any drugs. However, in recent years, a number of different drug delivery systems have been developed, and in some cases, animal studies have shown that noninvasive transtympanic delivery is possible so that drugs can reach high concentrations in the middle ear without damage. Nanovesicles and nanoliposomes that contain antibiotics and are small enough to pass through the eardrum have been developed and tested in animal models; these show promise. Ototopical administration of a drug called vinpocetine that was repurposed has been tested in mice and shown to reduce inflammation and mucus production in the middle ear during otitis media.
Biofilms
Antibiotic treatment failure can occur in AOM for several reasons. The treatment of choice, amoxicillin, for example may fail to achieve an adequate concentration because of poor absorption in the gastrointestinal tract or poor penetration into the middle ear. Or, the antibiotic chosen may not be effective because of resistance of the strain causing the infection. Another explanation, especially in recurrent AOM and chronic AOM, could be the presence of biofilms. Biofilms are multicellular bacterial communities incorporated in a polymeric, plasticlike matrix in which pathogens are protected from antibiotic activity. The biofilm provides a physical barrier to antibiotic penetration, and bacteria can persist in the middle ear and periodically cause a new AOM. If AOM persists or becomes a more chronic otitis media with effusion, the “glue ear” causes an environment in the middle ear that is low in oxygen. A low-oxygen environment is favorable to biofilms. Also one might expect that middle ear pus would have a low pH, but actual measurements show the pH is highly alkaline. Species of Haemophilus influenzae have been identified as more virulent when in an alkaline pH or the alkaline pH makes the H. influenzae persist better in the middle ear, perhaps in a biofilm. To eliminate biofilms and improve antibiotic efficacy, a vaccine against a protein expressed by H. influenzae has been developed. Antibodies against this protein have been shown to disrupt and prevent the formation of biofilms in an animal model.
Probiotics
The normal bacteria that live in the nasopharynx of children with recurrent AOM is now known to differ from that of children who experience infrequent AOM or remain AOM-free throughout childhood. The use of oral pre- and probiotics for AOM prophylaxis remains debated because the results of studies are conflicting and frequently show no effect. So the idea of using prebiotics or probiotics to create a favorable “microbiome” of the nose is under investigation. Two species of bacteria that are gathering the most attention are Corynebacterium species (a few types in particular) and a bacteria called Dolosigranulum pigrum. Delivery of the commensal species would be as a nose spray.
Vaccines
The use of pneumococcal conjugate vaccines (PCVs) has reduced the frequency of AOM caused by Streptococcus pneumoniae. PCVs are not as effective against AOM as they are against invasive pneumococcal disease, but they still help a lot. However, because there are now at least 96 different serotypes of the pneumococcus based on different capsular types, we see a pattern of replacement of disease-causing strains by new strains within a few years of introduction of a new formulation. We started with 7 serotypes (Prevnar 7) in year 2000, and it was replaced by the current formulation with 13 serotypes (Prevnar 13) in 2010. Replacements have occurred again so vaccine companies are making new formulations for the future that include more serotypes, up to 20 serotypes. But, technically and feasibility-wise there is a limit to making such vaccines. A vaccine based on killed unencapsulated bacteria has been tested for safety and immunogenicity in young children. There is no test so far for prevention of AOM. Another type of vaccine based on proteins expressed by the pneumococcus that could be vaccine targets was tested in American Navajo children, and it failed to be as efficacious as hoped.
Biomarkers.
Due to recurrent AOM or persistent otitis media with effusion, about 15% of children in the United States receive tympanostomy tubes. Among those who receive tubes, about 20% go on to receive a second set of tubes, often with adenotonsillectomy. To find a biomarker that could identify children likely to require a second set of tubes, the fluid in the middle ear was tested when a first set of tubes were inserted. If bacteria were detected by polymerase chain reaction (PCR) testing or if a profile of specific inflammatory cytokines was measured, those results could be used to predict a high likelihood for a second set of tubes.
Overdiagnosis
Diagnosis of AOM is challenging in young children, in whom it most frequently occurs. The ear canal is typically about 3 mm wide, the child struggles during the examination, and diagnostic skills are not taught in training, resulting in a high overdiagnosis rate. I presented data that suggest too many children who are not truly otitis prone have been classified as otitis prone based on incorrect clinical diagnosis. My colleagues and I found that 30% of children reach the threshold of three episodes of AOM in 6 months or four within a year when diagnosed by community pediatricians, similar to many other studies. Validated otoscopists (trained by experts with diagnosis definitively proven as at least 85% accurate using tympanocentesis) classify 15% of children as otitis prone – half as many. If tympanocentesis is used to prove middle ear fluid has bacterial pathogens (about 95% yield a bacterial otopathogen using culture and PCR), then about 10% of children are classified as otitis prone – one-third as many. This suggests that children clinically diagnosed by community-based pediatricians are overdiagnosed with AOM, perhaps three times more often than true. And that leads to overuse of antibiotics and referrals for tympanostomy tube surgery more often than should occur. So we need to improve diagnostic methods beyond otoscopy. New types of imaging for the eardrum and middle ear using novel technologies are in early clinical trials.
Immunity
The notion that young children get AOM because of Eustachian tube dysfunction in their early years of life (horizontal anatomy) may be true, but there is more to the story. After 10 years of work, the scientists in my research group have shown that children in the first 3 years of life can have an immune system that is suppressed – it is poorly responsive to pathogens and routine pediatric vaccines. Many features resemble a neonatal immune system, beginning life with a suppressed immune system or being in cytokine storm from birth. We introduced the term “prolonged neonatal-like immune profile (PNIP)” to give a general description of the immune responses we have found in otitis-prone children. They outgrow this. So the immune maturation is delayed but not permanent. It is mostly resolved by age 3 years. We found problems in both innate and adaptive immunity. It may be that the main explanation for recurrent AOM in the first years of life is PNIP. Scientists from Australia also reported immunity problems in Aboriginal children and they are very otitis prone, often progressing to chronic suppurative otitis media. Animal model studies of AOM show inadequate innate and adaptive immunity importantly contribute to the infection as well.
Dr. Pichichero is a specialist in pediatric infectious diseases and director of the Research Institute at Rochester (N.Y.) General Hospital. He has no conflicts to declare. Email him at [email protected].
Whose needs come first – the patient’s or the trial’s?
Debra Banks (not her real name) had hope. There was a clinical trial open at an academic hospital 200 miles from where she lived. She would commute or find local housing. It would cost her, but this is what her savings were for, she reasoned. What expense could be more important than her life?
Next came the tests. Blood tests, an ultrasound of her heart, breathing tests. She gave vials of blood, lay in scanners, and eagerly jumped through every hoop placed before her. Then came the call from the trial coordinator. Her heart ultrasound showed a mild dysfunction in how it pumped. It excluded her from the trial.
“Not eligible.” The two words that took away everything reverberated in her mind. Her heart had never caused her any problems before. So after the shock wore off, she tried to bargain with the trial coordinator: Had the study drug been shown to cause or worsen heart damage? Could they repeat the ultrasound? Did this blip in her heart function really matter?
When the trial coordinator couldn’t answer all these questions, she encouraged Debra to come into the clinic and talk to the doctors directly. That’s where I met her.
Debra found herself in the middle of a painful crossroads she had no interest being in. What happens when the needs of an individual patient and the needs of medical research are at odds? From Debra’s perspective, she had one goal. She wanted the therapy that would give her the best chance of living.
But the aim of the trial was not to help Debra – not directly, at least. Clinical trials help patient populations. The goal is to add to a body of knowledge: To study new therapies, demonstrate safety and efficacy, and ultimately find better treatments. The bulk of benefit goes to future patients, not individual participants. If an individual participant does benefit, all the better. But this is a bonus, not a requirement.
In order to meet these goals, trials come with inclusion and exclusion criteria. These are often strict. Individuals with certain other medical conditions are frequently excluded, as the person needs to be able to tolerate the toxicities of the drug being tested.
This, of course, is very different from our usual approach to patient care. Outside of trials, the needs of the individual patient are our North Star. Instead of inclusion and exclusion criteria, we have guidelines: general goalposts that hint at the right answer, but are able to be bent based on individual circumstances. It’s something I love about medicine. Part science, part art. Part algorithmic, part creative.
I can give chemotherapy to a patient with a low platelet count, if I think it’s best. I can override an elevated bilirubin. I can simply not check a heart ultrasound in the first place, if I don’t believe it will change my management.
I understand why trial criteria exist. I fully support investing in novel therapies that will help future patients on a large scale. There will invariably be individuals for whom a clinical trial is unsafe or inappropriate for a multitude of reasons, and our job as oncologists is to make that call and convey that news.
Still, that can be hard to square with the human being sitting in front of you. Debra was only in her mid-50s. She was an artist, an educator, a parent. She was a person who was so, so not ready to die. That she would because of a glitch in her heart function – the significance of which nobody knew – was excruciating.
While we can’t enroll every patient in every trial, the least we can do is comb through trial criteria thoughtfully. With the role of clinical investigator comes great responsibility. Are we choosing a cutoff because it makes clinical sense – or because that’s how it was done before? Is there a medical justification behind each and every exclusion criterion? A careless cutoff is not just a line on a protocol. It can be the difference between someone’s last hope – and no more options.
Every time I saw Debra in clinic, she asked about the trial. Then one day she stopped asking. She was distracted by more pressing problems. Her breathing had worsened and her energy levels were so low she could hardly get out of bed. Debra became sicker and sicker until she could no longer request the last hope that might make her better.
A wonderful physician-scientist I worked with once said she split her time between patient care and medical research because they complement each other. Whenever she lost a patient, she turned that pain into motivation to delve deeper into her research. She coped with individual loss by helping to make small, incremental improvements for the needs of many.
I think about this, months later, as I look around the empty exam room where I first met Debra. I imagine a roomful of patients, alive and healthy, for whom the research she was excluded from has benefited.
Dr. Yurkiewicz is a fellow in hematology and oncology at Stanford (Calif.) University. Follow her on Twitter @ilanayurkiewicz.
Debra Banks (not her real name) had hope. There was a clinical trial open at an academic hospital 200 miles from where she lived. She would commute or find local housing. It would cost her, but this is what her savings were for, she reasoned. What expense could be more important than her life?
Next came the tests. Blood tests, an ultrasound of her heart, breathing tests. She gave vials of blood, lay in scanners, and eagerly jumped through every hoop placed before her. Then came the call from the trial coordinator. Her heart ultrasound showed a mild dysfunction in how it pumped. It excluded her from the trial.
“Not eligible.” The two words that took away everything reverberated in her mind. Her heart had never caused her any problems before. So after the shock wore off, she tried to bargain with the trial coordinator: Had the study drug been shown to cause or worsen heart damage? Could they repeat the ultrasound? Did this blip in her heart function really matter?
When the trial coordinator couldn’t answer all these questions, she encouraged Debra to come into the clinic and talk to the doctors directly. That’s where I met her.
Debra found herself in the middle of a painful crossroads she had no interest being in. What happens when the needs of an individual patient and the needs of medical research are at odds? From Debra’s perspective, she had one goal. She wanted the therapy that would give her the best chance of living.
But the aim of the trial was not to help Debra – not directly, at least. Clinical trials help patient populations. The goal is to add to a body of knowledge: To study new therapies, demonstrate safety and efficacy, and ultimately find better treatments. The bulk of benefit goes to future patients, not individual participants. If an individual participant does benefit, all the better. But this is a bonus, not a requirement.
In order to meet these goals, trials come with inclusion and exclusion criteria. These are often strict. Individuals with certain other medical conditions are frequently excluded, as the person needs to be able to tolerate the toxicities of the drug being tested.
This, of course, is very different from our usual approach to patient care. Outside of trials, the needs of the individual patient are our North Star. Instead of inclusion and exclusion criteria, we have guidelines: general goalposts that hint at the right answer, but are able to be bent based on individual circumstances. It’s something I love about medicine. Part science, part art. Part algorithmic, part creative.
I can give chemotherapy to a patient with a low platelet count, if I think it’s best. I can override an elevated bilirubin. I can simply not check a heart ultrasound in the first place, if I don’t believe it will change my management.
I understand why trial criteria exist. I fully support investing in novel therapies that will help future patients on a large scale. There will invariably be individuals for whom a clinical trial is unsafe or inappropriate for a multitude of reasons, and our job as oncologists is to make that call and convey that news.
Still, that can be hard to square with the human being sitting in front of you. Debra was only in her mid-50s. She was an artist, an educator, a parent. She was a person who was so, so not ready to die. That she would because of a glitch in her heart function – the significance of which nobody knew – was excruciating.
While we can’t enroll every patient in every trial, the least we can do is comb through trial criteria thoughtfully. With the role of clinical investigator comes great responsibility. Are we choosing a cutoff because it makes clinical sense – or because that’s how it was done before? Is there a medical justification behind each and every exclusion criterion? A careless cutoff is not just a line on a protocol. It can be the difference between someone’s last hope – and no more options.
Every time I saw Debra in clinic, she asked about the trial. Then one day she stopped asking. She was distracted by more pressing problems. Her breathing had worsened and her energy levels were so low she could hardly get out of bed. Debra became sicker and sicker until she could no longer request the last hope that might make her better.
A wonderful physician-scientist I worked with once said she split her time between patient care and medical research because they complement each other. Whenever she lost a patient, she turned that pain into motivation to delve deeper into her research. She coped with individual loss by helping to make small, incremental improvements for the needs of many.
I think about this, months later, as I look around the empty exam room where I first met Debra. I imagine a roomful of patients, alive and healthy, for whom the research she was excluded from has benefited.
Dr. Yurkiewicz is a fellow in hematology and oncology at Stanford (Calif.) University. Follow her on Twitter @ilanayurkiewicz.
Debra Banks (not her real name) had hope. There was a clinical trial open at an academic hospital 200 miles from where she lived. She would commute or find local housing. It would cost her, but this is what her savings were for, she reasoned. What expense could be more important than her life?
Next came the tests. Blood tests, an ultrasound of her heart, breathing tests. She gave vials of blood, lay in scanners, and eagerly jumped through every hoop placed before her. Then came the call from the trial coordinator. Her heart ultrasound showed a mild dysfunction in how it pumped. It excluded her from the trial.
“Not eligible.” The two words that took away everything reverberated in her mind. Her heart had never caused her any problems before. So after the shock wore off, she tried to bargain with the trial coordinator: Had the study drug been shown to cause or worsen heart damage? Could they repeat the ultrasound? Did this blip in her heart function really matter?
When the trial coordinator couldn’t answer all these questions, she encouraged Debra to come into the clinic and talk to the doctors directly. That’s where I met her.
Debra found herself in the middle of a painful crossroads she had no interest being in. What happens when the needs of an individual patient and the needs of medical research are at odds? From Debra’s perspective, she had one goal. She wanted the therapy that would give her the best chance of living.
But the aim of the trial was not to help Debra – not directly, at least. Clinical trials help patient populations. The goal is to add to a body of knowledge: To study new therapies, demonstrate safety and efficacy, and ultimately find better treatments. The bulk of benefit goes to future patients, not individual participants. If an individual participant does benefit, all the better. But this is a bonus, not a requirement.
In order to meet these goals, trials come with inclusion and exclusion criteria. These are often strict. Individuals with certain other medical conditions are frequently excluded, as the person needs to be able to tolerate the toxicities of the drug being tested.
This, of course, is very different from our usual approach to patient care. Outside of trials, the needs of the individual patient are our North Star. Instead of inclusion and exclusion criteria, we have guidelines: general goalposts that hint at the right answer, but are able to be bent based on individual circumstances. It’s something I love about medicine. Part science, part art. Part algorithmic, part creative.
I can give chemotherapy to a patient with a low platelet count, if I think it’s best. I can override an elevated bilirubin. I can simply not check a heart ultrasound in the first place, if I don’t believe it will change my management.
I understand why trial criteria exist. I fully support investing in novel therapies that will help future patients on a large scale. There will invariably be individuals for whom a clinical trial is unsafe or inappropriate for a multitude of reasons, and our job as oncologists is to make that call and convey that news.
Still, that can be hard to square with the human being sitting in front of you. Debra was only in her mid-50s. She was an artist, an educator, a parent. She was a person who was so, so not ready to die. That she would because of a glitch in her heart function – the significance of which nobody knew – was excruciating.
While we can’t enroll every patient in every trial, the least we can do is comb through trial criteria thoughtfully. With the role of clinical investigator comes great responsibility. Are we choosing a cutoff because it makes clinical sense – or because that’s how it was done before? Is there a medical justification behind each and every exclusion criterion? A careless cutoff is not just a line on a protocol. It can be the difference between someone’s last hope – and no more options.
Every time I saw Debra in clinic, she asked about the trial. Then one day she stopped asking. She was distracted by more pressing problems. Her breathing had worsened and her energy levels were so low she could hardly get out of bed. Debra became sicker and sicker until she could no longer request the last hope that might make her better.
A wonderful physician-scientist I worked with once said she split her time between patient care and medical research because they complement each other. Whenever she lost a patient, she turned that pain into motivation to delve deeper into her research. She coped with individual loss by helping to make small, incremental improvements for the needs of many.
I think about this, months later, as I look around the empty exam room where I first met Debra. I imagine a roomful of patients, alive and healthy, for whom the research she was excluded from has benefited.
Dr. Yurkiewicz is a fellow in hematology and oncology at Stanford (Calif.) University. Follow her on Twitter @ilanayurkiewicz.
Polypharmacy: When might it make sense?
Polypharmacy is often defined as the simultaneous prescription of multiple medications (usually ≥5) to a single patient for a single condition or multiple conditions.1 Patients with psychiatric illnesses may easily be prescribed multiple psychotropic medications regardless of how many other medications they may already take for nonpsychiatric comorbidities. According to 2011-2014 Centers for Disease Control and Prevention data, 11.9% of the US population used ≥5 medications in the past 30 days.2 Risks of polypharmacy include higher rates of adverse effects as well as treatment noncompliance.3
There are, however, many patients for whom a combination of psychotropic agents can be beneficial. It is important to carefully assess your patient’s regimen, and to document the rationale for prescribing multiple medications. Here I describe some factors that can help you to determine whether a multi-medication regimen might be warranted for your patient.
Accepted medication pairings. This describes a medication combination that has been recognized as generally safe and may provide more benefits than either single agent alone. Examples of clinically accepted medication combinations include4,5:
- a selective serotonin reuptake inhibitor (SSRI) or serotonin-norepinephrine reuptake inhibitor (SNRI) plus bupropion
- an SSRI or SNRI plus mirtazapine
- ziprasidone as an adjunct to valproate or lithium for treating bipolar disorder
- aripiprazole as an adjunctive treatment for major depressive disorder (MDD).
Comorbid diagnoses. Each of a patient’s psychiatric comorbidities may require a different medication to address specific symptoms.3 Psychiatric comorbidities that might be appropriate for multiple medications include attention-deficit/hyperactivity disorder and bipolar disorder, MDD and generalized anxiety disorder, and a mood disorder and a substance use disorder.
Treatment resistance. The patient has demonstrated poor or no response to prior trials with simpler medication regimens, and/or there is a history of decompensation or hospitalization when medications were pared down.
Severe acute symptoms. The patient has been experiencing acute symptoms that do not respond to one medication class. For example, a patient with bipolar disorder who has acute mania and psychosis may require significant doses of both a mood stabilizer and an antipsychotic.
Amelioration of adverse effects. One medication may be prescribed to address the adverse effects of other medications. For example, propranolol may be added to address akathisia from aripiprazole or tremors from lithium. In these cases, it is important to determine if the medication that’s causing adverse effects continues to provide benefits, in order to justify continuing it as well as adding a new agent.3
Continue to: After reviewing...
After reviewing your patient’s medication regimen, if one of these scenarios does not clearly exist, consider a “deprescribing” approach—reducing or stopping medications—to address unnecessary and potentially detrimental polypharmacy. For more information on dep
1. Masnoon N, Shakib S, Kalisch-Ellett L, et al. What is polypharmacy? A systematic review of definitions. BMC Geriatr. 2017;17(1):230.
Polypharmacy is often defined as the simultaneous prescription of multiple medications (usually ≥5) to a single patient for a single condition or multiple conditions.1 Patients with psychiatric illnesses may easily be prescribed multiple psychotropic medications regardless of how many other medications they may already take for nonpsychiatric comorbidities. According to 2011-2014 Centers for Disease Control and Prevention data, 11.9% of the US population used ≥5 medications in the past 30 days.2 Risks of polypharmacy include higher rates of adverse effects as well as treatment noncompliance.3
There are, however, many patients for whom a combination of psychotropic agents can be beneficial. It is important to carefully assess your patient’s regimen, and to document the rationale for prescribing multiple medications. Here I describe some factors that can help you to determine whether a multi-medication regimen might be warranted for your patient.
Accepted medication pairings. This describes a medication combination that has been recognized as generally safe and may provide more benefits than either single agent alone. Examples of clinically accepted medication combinations include4,5:
- a selective serotonin reuptake inhibitor (SSRI) or serotonin-norepinephrine reuptake inhibitor (SNRI) plus bupropion
- an SSRI or SNRI plus mirtazapine
- ziprasidone as an adjunct to valproate or lithium for treating bipolar disorder
- aripiprazole as an adjunctive treatment for major depressive disorder (MDD).
Comorbid diagnoses. Each of a patient’s psychiatric comorbidities may require a different medication to address specific symptoms.3 Psychiatric comorbidities that might be appropriate for multiple medications include attention-deficit/hyperactivity disorder and bipolar disorder, MDD and generalized anxiety disorder, and a mood disorder and a substance use disorder.
Treatment resistance. The patient has demonstrated poor or no response to prior trials with simpler medication regimens, and/or there is a history of decompensation or hospitalization when medications were pared down.
Severe acute symptoms. The patient has been experiencing acute symptoms that do not respond to one medication class. For example, a patient with bipolar disorder who has acute mania and psychosis may require significant doses of both a mood stabilizer and an antipsychotic.
Amelioration of adverse effects. One medication may be prescribed to address the adverse effects of other medications. For example, propranolol may be added to address akathisia from aripiprazole or tremors from lithium. In these cases, it is important to determine if the medication that’s causing adverse effects continues to provide benefits, in order to justify continuing it as well as adding a new agent.3
Continue to: After reviewing...
After reviewing your patient’s medication regimen, if one of these scenarios does not clearly exist, consider a “deprescribing” approach—reducing or stopping medications—to address unnecessary and potentially detrimental polypharmacy. For more information on dep
Polypharmacy is often defined as the simultaneous prescription of multiple medications (usually ≥5) to a single patient for a single condition or multiple conditions.1 Patients with psychiatric illnesses may easily be prescribed multiple psychotropic medications regardless of how many other medications they may already take for nonpsychiatric comorbidities. According to 2011-2014 Centers for Disease Control and Prevention data, 11.9% of the US population used ≥5 medications in the past 30 days.2 Risks of polypharmacy include higher rates of adverse effects as well as treatment noncompliance.3
There are, however, many patients for whom a combination of psychotropic agents can be beneficial. It is important to carefully assess your patient’s regimen, and to document the rationale for prescribing multiple medications. Here I describe some factors that can help you to determine whether a multi-medication regimen might be warranted for your patient.
Accepted medication pairings. This describes a medication combination that has been recognized as generally safe and may provide more benefits than either single agent alone. Examples of clinically accepted medication combinations include4,5:
- a selective serotonin reuptake inhibitor (SSRI) or serotonin-norepinephrine reuptake inhibitor (SNRI) plus bupropion
- an SSRI or SNRI plus mirtazapine
- ziprasidone as an adjunct to valproate or lithium for treating bipolar disorder
- aripiprazole as an adjunctive treatment for major depressive disorder (MDD).
Comorbid diagnoses. Each of a patient’s psychiatric comorbidities may require a different medication to address specific symptoms.3 Psychiatric comorbidities that might be appropriate for multiple medications include attention-deficit/hyperactivity disorder and bipolar disorder, MDD and generalized anxiety disorder, and a mood disorder and a substance use disorder.
Treatment resistance. The patient has demonstrated poor or no response to prior trials with simpler medication regimens, and/or there is a history of decompensation or hospitalization when medications were pared down.
Severe acute symptoms. The patient has been experiencing acute symptoms that do not respond to one medication class. For example, a patient with bipolar disorder who has acute mania and psychosis may require significant doses of both a mood stabilizer and an antipsychotic.
Amelioration of adverse effects. One medication may be prescribed to address the adverse effects of other medications. For example, propranolol may be added to address akathisia from aripiprazole or tremors from lithium. In these cases, it is important to determine if the medication that’s causing adverse effects continues to provide benefits, in order to justify continuing it as well as adding a new agent.3
Continue to: After reviewing...
After reviewing your patient’s medication regimen, if one of these scenarios does not clearly exist, consider a “deprescribing” approach—reducing or stopping medications—to address unnecessary and potentially detrimental polypharmacy. For more information on dep
1. Masnoon N, Shakib S, Kalisch-Ellett L, et al. What is polypharmacy? A systematic review of definitions. BMC Geriatr. 2017;17(1):230.
1. Masnoon N, Shakib S, Kalisch-Ellett L, et al. What is polypharmacy? A systematic review of definitions. BMC Geriatr. 2017;17(1):230.
Psychosis as a common thread across psychiatric disorders
Ask a psychiatrist to name a psychotic disorder, and the answer will most likely be “schizophrenia.” But if you closely examine the symptom structure of DSM-5 psychiatric disorders, you will note the presence of psychosis in almost all of them.
Fixed false beliefs and impaired reality testing are core features of psychosis. Those are certainly prominent in severe psychoses such as schizophrenia, schizoaffective disorder, or delusional disorder. But psychosis is actually a continuum of varying severity across most psychiatric disorders, although they carry different diagnostic labels. Irrational false beliefs and impaired functioning due to poor reality testing are embedded among many DSM-5 disorders. Hallucinations are less common; they are perceptual aberrations, not thought abnormalities, although they can trigger delusional explanations as to their causation.
Consider the following:
- Bipolar disorder. A large proportion of patients with bipolar disorder manifest delusions, usually grandiose, but often paranoid or referential.
- Major depressive disorder (MDD). Although regarded as a “pure mood disorder,” the core symptoms of MDD—self-deprecation and sense of worthlessness—as well as the poor reality testing of suicidal thoughts (that death is a better option than living) are psychotic false beliefs.
- Anxiety and panic disorder. The central symptom in anxiety and panic attacks is a belief in impending doom and/or death. The fear in anxiety disorders is actually based on a false belief (eg, if I get on the plane, it will crash, and I will die). Thus, technically an irrational/psychotic thought process underpins the terror and fear of anxiety disorders.
- Borderline personality disorder. Frank psychotic symptoms, such as paranoid beliefs, are known to be a component of borderline personality disorder symptoms. Although these symptoms tend to be brief and episodic, they can have a deleterious effect on the person’s coping and relationships.
- Other personality disorders. While many individuals with narcissistic personality disorder are functional, their exaggerated sense of self-importance, entitlement, and self-aggrandizement certainly qualifies as a fixed false belief. Patients with other personality disorders, such as schizotypal and paranoid, are known to harbor false beliefs or magical thinking.
- Body dysmorphic disorder. False beliefs about one’s appearance (such as blemishes or asymmetry) are at the center of this disorder, and it meets the litmus test of a psychosis.
- Anorexia nervosa. This disorder is well known to be characterized by a fixed false belief that one is “fat,” even when the patient’s body borders on being cachectic in appearance according to objective observers.
- Autism. This spectrum of diseases includes false beliefs that drive the ritualistic or odd behaviors.
- Obsessive-compulsive disorder. Although obsessions are usually ego-dystonic, in severe cases, they become ego-syntonic, similar to delusions. On the other hand, compulsions are often driven by a false belief, such as believing that one’s hands are dirty and must be washed incessantly, or that the locks on the door must be rechecked repeatedly because an intruder may break into the house and harm the inhabitants.
- Neurodegenerative syndromes. Neurodegenerative syndromes are neuropsychiatric disorders that very frequently include psychotic symptoms, such as paranoid delusions, delusions of marital infidelity, Capgras syndrome, or folie à deux. These disorders include Alzheimer’s disease, Parkinson’s disease, Lewy body dementia, frontal temporal dementia, metachromatic leukodystrophy, Huntington’s chorea, temporal lobe epilepsy, stroke, xenomelia, reduplicative phenomena, etc. This reflects the common emergence of faulty thinking with disintegration of neural tissue, both gray and white matter.
Continue to: So it should not be...
So it should not be surprising that antipsychotic medications, especially second-generation agents, have been shown to be helpful as monotherapy or adjunctive therapy in practically all the above psychiatric disorders, whether on-label or off-label.
Finally, it should also be noted that a case has been made for the existence of one dimension in all mental disorders manifesting in multiple psychopathologies.1 It is possible that a continuum of delusional thinking is a common thread across many psychiatric disorders due to this putative shared dimension. The milder form of this dimension may also explain the presence of pre-psychotic thinking in a significant proportion of the general population who do not seek psychiatric help.2 Just think of how many people you befriend, socialize with, and regard as perfectly “normal” endorse wild superstitions and astrological predictions, or believe in various conspiracy theories that have no basis in reality.
To comment on this editorial or other topics of interest: [email protected].
1. Caspi A, Moffitt TE. All for one and one for all: mental disorders in one dimension. Am J Psychiatry. 2018;175(9):831-844.
2. van Os J, Linscott RJ, Myin-Germeys I, et al. A systematic review and meta-analysis of the psychosis continuum: evidence for a psychosis proneness-persistence-impairment model of psychotic disorder. Psychol Med. 2009;39(2):179-195.
Ask a psychiatrist to name a psychotic disorder, and the answer will most likely be “schizophrenia.” But if you closely examine the symptom structure of DSM-5 psychiatric disorders, you will note the presence of psychosis in almost all of them.
Fixed false beliefs and impaired reality testing are core features of psychosis. Those are certainly prominent in severe psychoses such as schizophrenia, schizoaffective disorder, or delusional disorder. But psychosis is actually a continuum of varying severity across most psychiatric disorders, although they carry different diagnostic labels. Irrational false beliefs and impaired functioning due to poor reality testing are embedded among many DSM-5 disorders. Hallucinations are less common; they are perceptual aberrations, not thought abnormalities, although they can trigger delusional explanations as to their causation.
Consider the following:
- Bipolar disorder. A large proportion of patients with bipolar disorder manifest delusions, usually grandiose, but often paranoid or referential.
- Major depressive disorder (MDD). Although regarded as a “pure mood disorder,” the core symptoms of MDD—self-deprecation and sense of worthlessness—as well as the poor reality testing of suicidal thoughts (that death is a better option than living) are psychotic false beliefs.
- Anxiety and panic disorder. The central symptom in anxiety and panic attacks is a belief in impending doom and/or death. The fear in anxiety disorders is actually based on a false belief (eg, if I get on the plane, it will crash, and I will die). Thus, technically an irrational/psychotic thought process underpins the terror and fear of anxiety disorders.
- Borderline personality disorder. Frank psychotic symptoms, such as paranoid beliefs, are known to be a component of borderline personality disorder symptoms. Although these symptoms tend to be brief and episodic, they can have a deleterious effect on the person’s coping and relationships.
- Other personality disorders. While many individuals with narcissistic personality disorder are functional, their exaggerated sense of self-importance, entitlement, and self-aggrandizement certainly qualifies as a fixed false belief. Patients with other personality disorders, such as schizotypal and paranoid, are known to harbor false beliefs or magical thinking.
- Body dysmorphic disorder. False beliefs about one’s appearance (such as blemishes or asymmetry) are at the center of this disorder, and it meets the litmus test of a psychosis.
- Anorexia nervosa. This disorder is well known to be characterized by a fixed false belief that one is “fat,” even when the patient’s body borders on being cachectic in appearance according to objective observers.
- Autism. This spectrum of diseases includes false beliefs that drive the ritualistic or odd behaviors.
- Obsessive-compulsive disorder. Although obsessions are usually ego-dystonic, in severe cases, they become ego-syntonic, similar to delusions. On the other hand, compulsions are often driven by a false belief, such as believing that one’s hands are dirty and must be washed incessantly, or that the locks on the door must be rechecked repeatedly because an intruder may break into the house and harm the inhabitants.
- Neurodegenerative syndromes. Neurodegenerative syndromes are neuropsychiatric disorders that very frequently include psychotic symptoms, such as paranoid delusions, delusions of marital infidelity, Capgras syndrome, or folie à deux. These disorders include Alzheimer’s disease, Parkinson’s disease, Lewy body dementia, frontal temporal dementia, metachromatic leukodystrophy, Huntington’s chorea, temporal lobe epilepsy, stroke, xenomelia, reduplicative phenomena, etc. This reflects the common emergence of faulty thinking with disintegration of neural tissue, both gray and white matter.
Continue to: So it should not be...
So it should not be surprising that antipsychotic medications, especially second-generation agents, have been shown to be helpful as monotherapy or adjunctive therapy in practically all the above psychiatric disorders, whether on-label or off-label.
Finally, it should also be noted that a case has been made for the existence of one dimension in all mental disorders manifesting in multiple psychopathologies.1 It is possible that a continuum of delusional thinking is a common thread across many psychiatric disorders due to this putative shared dimension. The milder form of this dimension may also explain the presence of pre-psychotic thinking in a significant proportion of the general population who do not seek psychiatric help.2 Just think of how many people you befriend, socialize with, and regard as perfectly “normal” endorse wild superstitions and astrological predictions, or believe in various conspiracy theories that have no basis in reality.
To comment on this editorial or other topics of interest: [email protected].
Ask a psychiatrist to name a psychotic disorder, and the answer will most likely be “schizophrenia.” But if you closely examine the symptom structure of DSM-5 psychiatric disorders, you will note the presence of psychosis in almost all of them.
Fixed false beliefs and impaired reality testing are core features of psychosis. Those are certainly prominent in severe psychoses such as schizophrenia, schizoaffective disorder, or delusional disorder. But psychosis is actually a continuum of varying severity across most psychiatric disorders, although they carry different diagnostic labels. Irrational false beliefs and impaired functioning due to poor reality testing are embedded among many DSM-5 disorders. Hallucinations are less common; they are perceptual aberrations, not thought abnormalities, although they can trigger delusional explanations as to their causation.
Consider the following:
- Bipolar disorder. A large proportion of patients with bipolar disorder manifest delusions, usually grandiose, but often paranoid or referential.
- Major depressive disorder (MDD). Although regarded as a “pure mood disorder,” the core symptoms of MDD—self-deprecation and sense of worthlessness—as well as the poor reality testing of suicidal thoughts (that death is a better option than living) are psychotic false beliefs.
- Anxiety and panic disorder. The central symptom in anxiety and panic attacks is a belief in impending doom and/or death. The fear in anxiety disorders is actually based on a false belief (eg, if I get on the plane, it will crash, and I will die). Thus, technically an irrational/psychotic thought process underpins the terror and fear of anxiety disorders.
- Borderline personality disorder. Frank psychotic symptoms, such as paranoid beliefs, are known to be a component of borderline personality disorder symptoms. Although these symptoms tend to be brief and episodic, they can have a deleterious effect on the person’s coping and relationships.
- Other personality disorders. While many individuals with narcissistic personality disorder are functional, their exaggerated sense of self-importance, entitlement, and self-aggrandizement certainly qualifies as a fixed false belief. Patients with other personality disorders, such as schizotypal and paranoid, are known to harbor false beliefs or magical thinking.
- Body dysmorphic disorder. False beliefs about one’s appearance (such as blemishes or asymmetry) are at the center of this disorder, and it meets the litmus test of a psychosis.
- Anorexia nervosa. This disorder is well known to be characterized by a fixed false belief that one is “fat,” even when the patient’s body borders on being cachectic in appearance according to objective observers.
- Autism. This spectrum of diseases includes false beliefs that drive the ritualistic or odd behaviors.
- Obsessive-compulsive disorder. Although obsessions are usually ego-dystonic, in severe cases, they become ego-syntonic, similar to delusions. On the other hand, compulsions are often driven by a false belief, such as believing that one’s hands are dirty and must be washed incessantly, or that the locks on the door must be rechecked repeatedly because an intruder may break into the house and harm the inhabitants.
- Neurodegenerative syndromes. Neurodegenerative syndromes are neuropsychiatric disorders that very frequently include psychotic symptoms, such as paranoid delusions, delusions of marital infidelity, Capgras syndrome, or folie à deux. These disorders include Alzheimer’s disease, Parkinson’s disease, Lewy body dementia, frontal temporal dementia, metachromatic leukodystrophy, Huntington’s chorea, temporal lobe epilepsy, stroke, xenomelia, reduplicative phenomena, etc. This reflects the common emergence of faulty thinking with disintegration of neural tissue, both gray and white matter.
Continue to: So it should not be...
So it should not be surprising that antipsychotic medications, especially second-generation agents, have been shown to be helpful as monotherapy or adjunctive therapy in practically all the above psychiatric disorders, whether on-label or off-label.
Finally, it should also be noted that a case has been made for the existence of one dimension in all mental disorders manifesting in multiple psychopathologies.1 It is possible that a continuum of delusional thinking is a common thread across many psychiatric disorders due to this putative shared dimension. The milder form of this dimension may also explain the presence of pre-psychotic thinking in a significant proportion of the general population who do not seek psychiatric help.2 Just think of how many people you befriend, socialize with, and regard as perfectly “normal” endorse wild superstitions and astrological predictions, or believe in various conspiracy theories that have no basis in reality.
To comment on this editorial or other topics of interest: [email protected].
1. Caspi A, Moffitt TE. All for one and one for all: mental disorders in one dimension. Am J Psychiatry. 2018;175(9):831-844.
2. van Os J, Linscott RJ, Myin-Germeys I, et al. A systematic review and meta-analysis of the psychosis continuum: evidence for a psychosis proneness-persistence-impairment model of psychotic disorder. Psychol Med. 2009;39(2):179-195.
1. Caspi A, Moffitt TE. All for one and one for all: mental disorders in one dimension. Am J Psychiatry. 2018;175(9):831-844.
2. van Os J, Linscott RJ, Myin-Germeys I, et al. A systematic review and meta-analysis of the psychosis continuum: evidence for a psychosis proneness-persistence-impairment model of psychotic disorder. Psychol Med. 2009;39(2):179-195.
Career Choices: Academic psychiatry
Editor’s note: Career Choices features a psychiatry resident/fellow interviewing a psychiatrist about why he or she has chosen a specific career path. The goal is to inform trainees about the various psychiatric career options, and to give them a feel for the pros and cons of the various paths.
In this Career Choices, Saeed Ahmed, MD, Chief Resident at Nassau University Medical Center, East Meadow, New York, talked with Donald W. Black, MD, Professor of Psychiatry, Department of Psychiatry, University of Iowa Roy J. and Lucille A. Carver College of Medicine, Iowa City, Iowa. Dr. Black is also Editor-in-Chief of
Dr. Ahmed: What made you choose the academic track, and how did your training lead you towards this path?
Dr. Black: I had always been interested in the idea of working at a medical school, and enjoyed writing and speaking. I was exposed to clinical research as a resident, and that confirmed my interest in academia, because I could envision combining all my interests, along with patient care. I always thought that patients were a major source of ideas for research and writing.
Dr. Ahmed: What are some of the pros and cons of working in academia?
Dr. Black: The pros include being able to influence future physicians through my teaching and writing; being able to pursue important research; and not being isolated from peers. Other advantages are being largely protected from utilization review; having more free time than peers in the private sector, who have difficulty finding coverage; and having defined benefits and a steady salary. I also share call with many peers.
When it comes to the cons, salaries are lower than in the private sector. The cons also include not being my own boss, and sometimes having to bend to the whims of an institution or supervisor.
Continue to: Dr. Ahmed...
Dr. Ahmed: Are you required to conduct research?
Dr. Black: Yes. This is one of the best aspects of my job: being able to make clinical discoveries that I can disseminate through writing and speaking. Over time, this has become increasingly challenging due to the difficulty of obtaining research funding from foundations or the federal government. This has become highly problematic, particularly for clinical researchers, because the National Institutes of Health has clearly been favoring neuroscience.
Dr. Ahmed: What is your typical day like?
Dr. Black: Because of the many hats I wear (or have worn), each day is different from the other. I combine patient care with research, writing, speaking, teaching, and administration. As a tenure-track faculty member, I am expected to write grants, conduct research, and publish. My clinical-track peers primarily provide patient care and teach students and residents.
Dr. Ahmed: What is unique about working in a training institute vs private practice?
Continue to: Dr. Black...
Dr. Black: As an academic psychiatrist, I feel I have the best of both worlds: patient care combined with opportunities my private practice colleagues do not have. Because I have published widely, and have developed a reputation, I am frequently invited to speak at meetings throughout the United States, and sometimes internationally. Travel is a perk of academia, and as someone who loves travel, that is important.
Dr. Ahmed: Where do you see psychiatry going?
Dr. Black: Psychiatry will always be an important specialty because no one else truly cares about patients with psychiatric illnesses. Mental illness will not go away, and society needs highly trained individuals to provide care. There are many “me too” clinicians who now share in caring for patients with psychiatric illnesses, but psychiatrists will always have the most training, and are in a position to provide supervision to others and to direct mental health care teams.
Dr. Ahmed: What advice do you have for residents contemplating a career in academic psychiatry?
Dr. Black: Because most medical schools now have both tenure and clinical tracks, no one needs to feel left out. Those who are interested in scholarly activities will gravitate to the tenure tract, and all that requires in terms of grants and papers, while those who are primarily interested in patient care and teaching will choose the clinical track.
Editor’s note: Career Choices features a psychiatry resident/fellow interviewing a psychiatrist about why he or she has chosen a specific career path. The goal is to inform trainees about the various psychiatric career options, and to give them a feel for the pros and cons of the various paths.
In this Career Choices, Saeed Ahmed, MD, Chief Resident at Nassau University Medical Center, East Meadow, New York, talked with Donald W. Black, MD, Professor of Psychiatry, Department of Psychiatry, University of Iowa Roy J. and Lucille A. Carver College of Medicine, Iowa City, Iowa. Dr. Black is also Editor-in-Chief of
Dr. Ahmed: What made you choose the academic track, and how did your training lead you towards this path?
Dr. Black: I had always been interested in the idea of working at a medical school, and enjoyed writing and speaking. I was exposed to clinical research as a resident, and that confirmed my interest in academia, because I could envision combining all my interests, along with patient care. I always thought that patients were a major source of ideas for research and writing.
Dr. Ahmed: What are some of the pros and cons of working in academia?
Dr. Black: The pros include being able to influence future physicians through my teaching and writing; being able to pursue important research; and not being isolated from peers. Other advantages are being largely protected from utilization review; having more free time than peers in the private sector, who have difficulty finding coverage; and having defined benefits and a steady salary. I also share call with many peers.
When it comes to the cons, salaries are lower than in the private sector. The cons also include not being my own boss, and sometimes having to bend to the whims of an institution or supervisor.
Continue to: Dr. Ahmed...
Dr. Ahmed: Are you required to conduct research?
Dr. Black: Yes. This is one of the best aspects of my job: being able to make clinical discoveries that I can disseminate through writing and speaking. Over time, this has become increasingly challenging due to the difficulty of obtaining research funding from foundations or the federal government. This has become highly problematic, particularly for clinical researchers, because the National Institutes of Health has clearly been favoring neuroscience.
Dr. Ahmed: What is your typical day like?
Dr. Black: Because of the many hats I wear (or have worn), each day is different from the other. I combine patient care with research, writing, speaking, teaching, and administration. As a tenure-track faculty member, I am expected to write grants, conduct research, and publish. My clinical-track peers primarily provide patient care and teach students and residents.
Dr. Ahmed: What is unique about working in a training institute vs private practice?
Continue to: Dr. Black...
Dr. Black: As an academic psychiatrist, I feel I have the best of both worlds: patient care combined with opportunities my private practice colleagues do not have. Because I have published widely, and have developed a reputation, I am frequently invited to speak at meetings throughout the United States, and sometimes internationally. Travel is a perk of academia, and as someone who loves travel, that is important.
Dr. Ahmed: Where do you see psychiatry going?
Dr. Black: Psychiatry will always be an important specialty because no one else truly cares about patients with psychiatric illnesses. Mental illness will not go away, and society needs highly trained individuals to provide care. There are many “me too” clinicians who now share in caring for patients with psychiatric illnesses, but psychiatrists will always have the most training, and are in a position to provide supervision to others and to direct mental health care teams.
Dr. Ahmed: What advice do you have for residents contemplating a career in academic psychiatry?
Dr. Black: Because most medical schools now have both tenure and clinical tracks, no one needs to feel left out. Those who are interested in scholarly activities will gravitate to the tenure tract, and all that requires in terms of grants and papers, while those who are primarily interested in patient care and teaching will choose the clinical track.
Editor’s note: Career Choices features a psychiatry resident/fellow interviewing a psychiatrist about why he or she has chosen a specific career path. The goal is to inform trainees about the various psychiatric career options, and to give them a feel for the pros and cons of the various paths.
In this Career Choices, Saeed Ahmed, MD, Chief Resident at Nassau University Medical Center, East Meadow, New York, talked with Donald W. Black, MD, Professor of Psychiatry, Department of Psychiatry, University of Iowa Roy J. and Lucille A. Carver College of Medicine, Iowa City, Iowa. Dr. Black is also Editor-in-Chief of
Dr. Ahmed: What made you choose the academic track, and how did your training lead you towards this path?
Dr. Black: I had always been interested in the idea of working at a medical school, and enjoyed writing and speaking. I was exposed to clinical research as a resident, and that confirmed my interest in academia, because I could envision combining all my interests, along with patient care. I always thought that patients were a major source of ideas for research and writing.
Dr. Ahmed: What are some of the pros and cons of working in academia?
Dr. Black: The pros include being able to influence future physicians through my teaching and writing; being able to pursue important research; and not being isolated from peers. Other advantages are being largely protected from utilization review; having more free time than peers in the private sector, who have difficulty finding coverage; and having defined benefits and a steady salary. I also share call with many peers.
When it comes to the cons, salaries are lower than in the private sector. The cons also include not being my own boss, and sometimes having to bend to the whims of an institution or supervisor.
Continue to: Dr. Ahmed...
Dr. Ahmed: Are you required to conduct research?
Dr. Black: Yes. This is one of the best aspects of my job: being able to make clinical discoveries that I can disseminate through writing and speaking. Over time, this has become increasingly challenging due to the difficulty of obtaining research funding from foundations or the federal government. This has become highly problematic, particularly for clinical researchers, because the National Institutes of Health has clearly been favoring neuroscience.
Dr. Ahmed: What is your typical day like?
Dr. Black: Because of the many hats I wear (or have worn), each day is different from the other. I combine patient care with research, writing, speaking, teaching, and administration. As a tenure-track faculty member, I am expected to write grants, conduct research, and publish. My clinical-track peers primarily provide patient care and teach students and residents.
Dr. Ahmed: What is unique about working in a training institute vs private practice?
Continue to: Dr. Black...
Dr. Black: As an academic psychiatrist, I feel I have the best of both worlds: patient care combined with opportunities my private practice colleagues do not have. Because I have published widely, and have developed a reputation, I am frequently invited to speak at meetings throughout the United States, and sometimes internationally. Travel is a perk of academia, and as someone who loves travel, that is important.
Dr. Ahmed: Where do you see psychiatry going?
Dr. Black: Psychiatry will always be an important specialty because no one else truly cares about patients with psychiatric illnesses. Mental illness will not go away, and society needs highly trained individuals to provide care. There are many “me too” clinicians who now share in caring for patients with psychiatric illnesses, but psychiatrists will always have the most training, and are in a position to provide supervision to others and to direct mental health care teams.
Dr. Ahmed: What advice do you have for residents contemplating a career in academic psychiatry?
Dr. Black: Because most medical schools now have both tenure and clinical tracks, no one needs to feel left out. Those who are interested in scholarly activities will gravitate to the tenure tract, and all that requires in terms of grants and papers, while those who are primarily interested in patient care and teaching will choose the clinical track.
