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Attacking childhood anxiety in primary care
Multiple media outlets and numerous children’s professional organizations are discussing the child and adolescent mental health crisis. Finally, society at large seems to be taking notice that our kids are not okay, and that they haven’t been okay for a long time.
Over the past 5-7 years, both in my practice in tertiary children’s hospital emergency departments and in primary care pediatrics, I have seen a disturbing decline in kids’ mental well-being. What can a primary care physician do to make a difference? How do we capitalize on these discussions about mental health and illness now that it is rising to a priority status?
The U.S. Preventive Services Task Force recently drafted a statement of recommendations specifically discussing anxiety in children and adolescents. It shows supporting evidence that there is a moderate benefit to screening children 8-18 years old for anxiety. We know from the 2018-2019 National Survey of Children’s Health that almost 8% of children/adolescents ages 3-17 years old have an anxiety disorder. And among those 13-18 years old, the lifetime prevalence rises to nearly 33%, according to National Institutes of Health statistics.
Childhood anxiety unquestionably increases the chances of persistent anxiety or depression in adulthood. I have followed children who had excessive social anxiety from age 3 or 4 who progressed to generalized anxiety disorder as adolescents, usually when no intervention was done or when the family waited for the child to “outgrow” it. The DSM-5 has six separate categories for anxiety disorders in children and adolescents: generalized anxiety disorder, separation anxiety disorder, specific phobias, social phobia, agoraphobia, and panic disorder. Unfortunately, these illnesses cannot be wished away.
Screening, diagnosis, and follow-up
A few simple screening tools can be used to check for anxiety in children and adolescents. These include SCARED (Screen for Child Anxiety Related Emotional Disorders), GAD-7 (Generalized Anxiety Disorder-7), and/or the PHQ-A (Patient Health Questionnaire for Adolescents). Keep in mind that a screening tool is just that – a screen. Diagnostic confirmation and follow-up are appropriate after a positive screen. I like all of these particular screens as they are easy to administer and can be incorporated into a busy practice without extra training to administer. They are also easy for parents and patients to complete prior to a visit or during a visit.
Ideally, after a positive screen, the next step is to consult a child and adolescent psychiatrist (CAP); however, according to statistics from the American Academy of Child and Adolescent Psychiatry (AACAP), there are only 8,300 CAPs in the United States. The reality is that not a single state in the entire country has a “mostly sufficient supply” of CAP’s (defined as ≥ 47 per 100,000 children). In fact, most have a “severe shortage,” defined as 1-17 per 100,000 children
Adding a child/adolescent therapist is also necessary for patients 8 years old and up, but the harsh truth is that it may take up to several months before the child is seen. If a patient is in a rural or other underserved area, it may be even longer.
So, what does this mean for primary care physicians? When you are faced with a positive screening for childhood anxiety, the next step is “tag, you’re it!” Understandably, this is frightening for many physicians who feel unqualified.
Don’t be afraid! Like the old adage says, a journey of a thousand miles begins with a single step. Starting the conversation with patients and families is foremost. Physicians must be first in line to end the stigma surrounding mental illness, and the easiest way to do that is to start the conversation. Remember that anxiety in kids can present as classic fear or worry, but it also can present as irritability, anger outbursts, and attention issues. There have been so many patients referred to me for “being out of control” or “always angry” or “probable ADHD” who turned out to have significant anxiety.
Part of a routine medical evaluation includes obtaining personal, family, and social history; there should be no difference when considering an anxiety disorder. Obtaining information about family history, personality traits, environmental components, early attachment issues, developmental history, parental style, parental conflict, occupants in the home, any adverse childhood events, and history of child maltreatment is crucial. Assessing other risk factors, including socioeconomic status, race, ethnicity, and gender, is key as well. I have seen families literally breathe a sigh of relief when these questions are asked. Parents feel heard and seen. And, equally significant, so does the child/adolescent.
The ‘Big 4’
An in-depth assessment of patient and family lifestyle factors such as nutrition, sleep, physical activity/exercise, and screen time habits is also basic and essential. This kind of evaluation usually cannot be done in the typical 15-minute visit and often will need to be done over several patient visits. I have had numerous conversations with my patients regarding what I call the “Big 4” – simple but not easy concepts and actions. They include nutrition, sleep, exercise, and screen time. Parents will look at me and say, “I can’t believe I never thought of this!” Some of my favorite moments with patients over the years have involved partnering with the patient and family and encouraging them to do the “simple” but not “easy” things.
Nutrition
Does the child have proper nutrition? That is not meant to be an exercise in labeling foods as “good” or “bad” but meant to confirm whether there is a balance of different foods. It’s also a way of exploring whether there are family meals in the home. Family meals have been shown to have a protective factor for children’s social development and emotional regulation.
Sleep
Review the child’s sleep habits, such as difficulty falling/staying asleep, bedtime routine (soothing, relaxing activities vs. the opposite), nightmares, snoring, nighttime cough, etc. The physical sleeping environment is important as well. Is it quiet? Is it a crowded room?
Exercise
Discuss physical activity with the family. Is there time for the child to play outside without a defined goal? So much of a child’s day is structured, in school or with after-school activities, but can the kid simply be a kid? Does the family take walks together? Is it safe to play outside?
Screen time
Reviewing screen time is important for multiple reasons, especially because the more time spent in front of a TV, computer, or video game, the less time there is to be physically active. Numerous experts, including the American Academy of Pediatrics, recommend limits on screen time for children. For adolescents, there appears to be some evidence that excessive screen time contributes to depression/anxiety.
I am not embarrassed to say that with my own kids I felt so strongly about screen time that we did not own any kind of video games or iPad (that was theirs alone), and they spent the summers until they turned 14 building a two-story bamboo fort in our backyard instead of vegging out in front of the TV or computer. It didn’t hurt them a bit; one is an engineer and the other is in nursing school.
It is easy to see that lifestyle factors can come into play with childhood anxiety and are often ignored in the clinical setting. They do not involve technologically advanced techniques or procedures, which are more likely to be reimbursed. They are straightforward – but not easy – concepts, and require active participation from the patient and family. Some of my most exciting moments with families is when they return for follow up and say, “It worked!”
We need to be as comfortable taking care of a child’s mind and spirit as we are taking care of a child’s physical body. Is this easy in a busy office? No. Is this easy in a 15-minute visit? No. Is this easy with poor reimbursement from insurance companies? No. Is it necessary? Unequivocally YES. Start the conversation.
Tag, you’re it!
Dr. Contrucci is an assistant professor of pediatrics, clinical education department, Philadelphia College of Osteopathic Medicine, Georgia Campus, Suwanee. She disclosed no relevant conflict of interest.
A version of this article first appeared on Medscape.com.
Multiple media outlets and numerous children’s professional organizations are discussing the child and adolescent mental health crisis. Finally, society at large seems to be taking notice that our kids are not okay, and that they haven’t been okay for a long time.
Over the past 5-7 years, both in my practice in tertiary children’s hospital emergency departments and in primary care pediatrics, I have seen a disturbing decline in kids’ mental well-being. What can a primary care physician do to make a difference? How do we capitalize on these discussions about mental health and illness now that it is rising to a priority status?
The U.S. Preventive Services Task Force recently drafted a statement of recommendations specifically discussing anxiety in children and adolescents. It shows supporting evidence that there is a moderate benefit to screening children 8-18 years old for anxiety. We know from the 2018-2019 National Survey of Children’s Health that almost 8% of children/adolescents ages 3-17 years old have an anxiety disorder. And among those 13-18 years old, the lifetime prevalence rises to nearly 33%, according to National Institutes of Health statistics.
Childhood anxiety unquestionably increases the chances of persistent anxiety or depression in adulthood. I have followed children who had excessive social anxiety from age 3 or 4 who progressed to generalized anxiety disorder as adolescents, usually when no intervention was done or when the family waited for the child to “outgrow” it. The DSM-5 has six separate categories for anxiety disorders in children and adolescents: generalized anxiety disorder, separation anxiety disorder, specific phobias, social phobia, agoraphobia, and panic disorder. Unfortunately, these illnesses cannot be wished away.
Screening, diagnosis, and follow-up
A few simple screening tools can be used to check for anxiety in children and adolescents. These include SCARED (Screen for Child Anxiety Related Emotional Disorders), GAD-7 (Generalized Anxiety Disorder-7), and/or the PHQ-A (Patient Health Questionnaire for Adolescents). Keep in mind that a screening tool is just that – a screen. Diagnostic confirmation and follow-up are appropriate after a positive screen. I like all of these particular screens as they are easy to administer and can be incorporated into a busy practice without extra training to administer. They are also easy for parents and patients to complete prior to a visit or during a visit.
Ideally, after a positive screen, the next step is to consult a child and adolescent psychiatrist (CAP); however, according to statistics from the American Academy of Child and Adolescent Psychiatry (AACAP), there are only 8,300 CAPs in the United States. The reality is that not a single state in the entire country has a “mostly sufficient supply” of CAP’s (defined as ≥ 47 per 100,000 children). In fact, most have a “severe shortage,” defined as 1-17 per 100,000 children
Adding a child/adolescent therapist is also necessary for patients 8 years old and up, but the harsh truth is that it may take up to several months before the child is seen. If a patient is in a rural or other underserved area, it may be even longer.
So, what does this mean for primary care physicians? When you are faced with a positive screening for childhood anxiety, the next step is “tag, you’re it!” Understandably, this is frightening for many physicians who feel unqualified.
Don’t be afraid! Like the old adage says, a journey of a thousand miles begins with a single step. Starting the conversation with patients and families is foremost. Physicians must be first in line to end the stigma surrounding mental illness, and the easiest way to do that is to start the conversation. Remember that anxiety in kids can present as classic fear or worry, but it also can present as irritability, anger outbursts, and attention issues. There have been so many patients referred to me for “being out of control” or “always angry” or “probable ADHD” who turned out to have significant anxiety.
Part of a routine medical evaluation includes obtaining personal, family, and social history; there should be no difference when considering an anxiety disorder. Obtaining information about family history, personality traits, environmental components, early attachment issues, developmental history, parental style, parental conflict, occupants in the home, any adverse childhood events, and history of child maltreatment is crucial. Assessing other risk factors, including socioeconomic status, race, ethnicity, and gender, is key as well. I have seen families literally breathe a sigh of relief when these questions are asked. Parents feel heard and seen. And, equally significant, so does the child/adolescent.
The ‘Big 4’
An in-depth assessment of patient and family lifestyle factors such as nutrition, sleep, physical activity/exercise, and screen time habits is also basic and essential. This kind of evaluation usually cannot be done in the typical 15-minute visit and often will need to be done over several patient visits. I have had numerous conversations with my patients regarding what I call the “Big 4” – simple but not easy concepts and actions. They include nutrition, sleep, exercise, and screen time. Parents will look at me and say, “I can’t believe I never thought of this!” Some of my favorite moments with patients over the years have involved partnering with the patient and family and encouraging them to do the “simple” but not “easy” things.
Nutrition
Does the child have proper nutrition? That is not meant to be an exercise in labeling foods as “good” or “bad” but meant to confirm whether there is a balance of different foods. It’s also a way of exploring whether there are family meals in the home. Family meals have been shown to have a protective factor for children’s social development and emotional regulation.
Sleep
Review the child’s sleep habits, such as difficulty falling/staying asleep, bedtime routine (soothing, relaxing activities vs. the opposite), nightmares, snoring, nighttime cough, etc. The physical sleeping environment is important as well. Is it quiet? Is it a crowded room?
Exercise
Discuss physical activity with the family. Is there time for the child to play outside without a defined goal? So much of a child’s day is structured, in school or with after-school activities, but can the kid simply be a kid? Does the family take walks together? Is it safe to play outside?
Screen time
Reviewing screen time is important for multiple reasons, especially because the more time spent in front of a TV, computer, or video game, the less time there is to be physically active. Numerous experts, including the American Academy of Pediatrics, recommend limits on screen time for children. For adolescents, there appears to be some evidence that excessive screen time contributes to depression/anxiety.
I am not embarrassed to say that with my own kids I felt so strongly about screen time that we did not own any kind of video games or iPad (that was theirs alone), and they spent the summers until they turned 14 building a two-story bamboo fort in our backyard instead of vegging out in front of the TV or computer. It didn’t hurt them a bit; one is an engineer and the other is in nursing school.
It is easy to see that lifestyle factors can come into play with childhood anxiety and are often ignored in the clinical setting. They do not involve technologically advanced techniques or procedures, which are more likely to be reimbursed. They are straightforward – but not easy – concepts, and require active participation from the patient and family. Some of my most exciting moments with families is when they return for follow up and say, “It worked!”
We need to be as comfortable taking care of a child’s mind and spirit as we are taking care of a child’s physical body. Is this easy in a busy office? No. Is this easy in a 15-minute visit? No. Is this easy with poor reimbursement from insurance companies? No. Is it necessary? Unequivocally YES. Start the conversation.
Tag, you’re it!
Dr. Contrucci is an assistant professor of pediatrics, clinical education department, Philadelphia College of Osteopathic Medicine, Georgia Campus, Suwanee. She disclosed no relevant conflict of interest.
A version of this article first appeared on Medscape.com.
Multiple media outlets and numerous children’s professional organizations are discussing the child and adolescent mental health crisis. Finally, society at large seems to be taking notice that our kids are not okay, and that they haven’t been okay for a long time.
Over the past 5-7 years, both in my practice in tertiary children’s hospital emergency departments and in primary care pediatrics, I have seen a disturbing decline in kids’ mental well-being. What can a primary care physician do to make a difference? How do we capitalize on these discussions about mental health and illness now that it is rising to a priority status?
The U.S. Preventive Services Task Force recently drafted a statement of recommendations specifically discussing anxiety in children and adolescents. It shows supporting evidence that there is a moderate benefit to screening children 8-18 years old for anxiety. We know from the 2018-2019 National Survey of Children’s Health that almost 8% of children/adolescents ages 3-17 years old have an anxiety disorder. And among those 13-18 years old, the lifetime prevalence rises to nearly 33%, according to National Institutes of Health statistics.
Childhood anxiety unquestionably increases the chances of persistent anxiety or depression in adulthood. I have followed children who had excessive social anxiety from age 3 or 4 who progressed to generalized anxiety disorder as adolescents, usually when no intervention was done or when the family waited for the child to “outgrow” it. The DSM-5 has six separate categories for anxiety disorders in children and adolescents: generalized anxiety disorder, separation anxiety disorder, specific phobias, social phobia, agoraphobia, and panic disorder. Unfortunately, these illnesses cannot be wished away.
Screening, diagnosis, and follow-up
A few simple screening tools can be used to check for anxiety in children and adolescents. These include SCARED (Screen for Child Anxiety Related Emotional Disorders), GAD-7 (Generalized Anxiety Disorder-7), and/or the PHQ-A (Patient Health Questionnaire for Adolescents). Keep in mind that a screening tool is just that – a screen. Diagnostic confirmation and follow-up are appropriate after a positive screen. I like all of these particular screens as they are easy to administer and can be incorporated into a busy practice without extra training to administer. They are also easy for parents and patients to complete prior to a visit or during a visit.
Ideally, after a positive screen, the next step is to consult a child and adolescent psychiatrist (CAP); however, according to statistics from the American Academy of Child and Adolescent Psychiatry (AACAP), there are only 8,300 CAPs in the United States. The reality is that not a single state in the entire country has a “mostly sufficient supply” of CAP’s (defined as ≥ 47 per 100,000 children). In fact, most have a “severe shortage,” defined as 1-17 per 100,000 children
Adding a child/adolescent therapist is also necessary for patients 8 years old and up, but the harsh truth is that it may take up to several months before the child is seen. If a patient is in a rural or other underserved area, it may be even longer.
So, what does this mean for primary care physicians? When you are faced with a positive screening for childhood anxiety, the next step is “tag, you’re it!” Understandably, this is frightening for many physicians who feel unqualified.
Don’t be afraid! Like the old adage says, a journey of a thousand miles begins with a single step. Starting the conversation with patients and families is foremost. Physicians must be first in line to end the stigma surrounding mental illness, and the easiest way to do that is to start the conversation. Remember that anxiety in kids can present as classic fear or worry, but it also can present as irritability, anger outbursts, and attention issues. There have been so many patients referred to me for “being out of control” or “always angry” or “probable ADHD” who turned out to have significant anxiety.
Part of a routine medical evaluation includes obtaining personal, family, and social history; there should be no difference when considering an anxiety disorder. Obtaining information about family history, personality traits, environmental components, early attachment issues, developmental history, parental style, parental conflict, occupants in the home, any adverse childhood events, and history of child maltreatment is crucial. Assessing other risk factors, including socioeconomic status, race, ethnicity, and gender, is key as well. I have seen families literally breathe a sigh of relief when these questions are asked. Parents feel heard and seen. And, equally significant, so does the child/adolescent.
The ‘Big 4’
An in-depth assessment of patient and family lifestyle factors such as nutrition, sleep, physical activity/exercise, and screen time habits is also basic and essential. This kind of evaluation usually cannot be done in the typical 15-minute visit and often will need to be done over several patient visits. I have had numerous conversations with my patients regarding what I call the “Big 4” – simple but not easy concepts and actions. They include nutrition, sleep, exercise, and screen time. Parents will look at me and say, “I can’t believe I never thought of this!” Some of my favorite moments with patients over the years have involved partnering with the patient and family and encouraging them to do the “simple” but not “easy” things.
Nutrition
Does the child have proper nutrition? That is not meant to be an exercise in labeling foods as “good” or “bad” but meant to confirm whether there is a balance of different foods. It’s also a way of exploring whether there are family meals in the home. Family meals have been shown to have a protective factor for children’s social development and emotional regulation.
Sleep
Review the child’s sleep habits, such as difficulty falling/staying asleep, bedtime routine (soothing, relaxing activities vs. the opposite), nightmares, snoring, nighttime cough, etc. The physical sleeping environment is important as well. Is it quiet? Is it a crowded room?
Exercise
Discuss physical activity with the family. Is there time for the child to play outside without a defined goal? So much of a child’s day is structured, in school or with after-school activities, but can the kid simply be a kid? Does the family take walks together? Is it safe to play outside?
Screen time
Reviewing screen time is important for multiple reasons, especially because the more time spent in front of a TV, computer, or video game, the less time there is to be physically active. Numerous experts, including the American Academy of Pediatrics, recommend limits on screen time for children. For adolescents, there appears to be some evidence that excessive screen time contributes to depression/anxiety.
I am not embarrassed to say that with my own kids I felt so strongly about screen time that we did not own any kind of video games or iPad (that was theirs alone), and they spent the summers until they turned 14 building a two-story bamboo fort in our backyard instead of vegging out in front of the TV or computer. It didn’t hurt them a bit; one is an engineer and the other is in nursing school.
It is easy to see that lifestyle factors can come into play with childhood anxiety and are often ignored in the clinical setting. They do not involve technologically advanced techniques or procedures, which are more likely to be reimbursed. They are straightforward – but not easy – concepts, and require active participation from the patient and family. Some of my most exciting moments with families is when they return for follow up and say, “It worked!”
We need to be as comfortable taking care of a child’s mind and spirit as we are taking care of a child’s physical body. Is this easy in a busy office? No. Is this easy in a 15-minute visit? No. Is this easy with poor reimbursement from insurance companies? No. Is it necessary? Unequivocally YES. Start the conversation.
Tag, you’re it!
Dr. Contrucci is an assistant professor of pediatrics, clinical education department, Philadelphia College of Osteopathic Medicine, Georgia Campus, Suwanee. She disclosed no relevant conflict of interest.
A version of this article first appeared on Medscape.com.
To vaccinate 6-month- to 5-year-olds against SARS-CoV-2 or not to vaccinate
A family’s decision to vaccinate their child is best made jointly with a trusted medical provider who knows the child and family. The American Academy of Pediatrics created a toolkit with resources for answering questions about the recently authorized SARS-CoV-2 mRNA vaccines (Pfizer and Moderna) for 6-month- to 5-year-olds with science-backed vaccine facts, including links to other useful AAP information websites, talking points, graphics, and videos.1
SARS-CoV-2 seasonality
SARS-CoV-2 is now endemic, not a once-a-year seasonal virus. Seasons (aka surges) will occur whenever a new variant arises (twice yearly since 2020, Omicron BA.4/BA.5 currently), or when enough vaccine holdouts, newborns, and/or those with waning of prior immunity (vaccine or infection induced) accrue.
Emergency use authorization submission data for mRNA vaccine responses in young children2,3
Moderna in 6-month- through 5-year-olds. Two 25-mcg doses given 4-8 weeks apart produced 37.8% (95% confidence interval, 20.9%-51.1%) protection against symptomatic Omicron SARS-CoV-2 infections through 3 months of follow-up. Immunobridging analysis of antibody responses compared to 18- to 25-year-olds (100-mcg doses) showed the children’s responses were noninferior. Thus, the committee inferred that vaccine effectiveness in children should be similar to that in 18- to 25-year-olds. Fever, irritability, or local reaction/pain occurred in two-thirds after the second dose. Grade 3 reactions were noted in less than 5%.
Pfizer in 6-month- through 4-year-olds. Three 3-mcg doses, two doses 3-8 weeks apart and the third dose at least 8 weeks later (median 16 weeks), produced 80.3% (95% CI, 13.9%-96.7%) protection against symptomatic COVID-19 during the 6 weeks after the third dose. Local and systemic reactions occurred in 63.8%; less than 5% had grade 3 reactions (fever in about 3%, irritability in 1.3%, fatigue in 0.8%) mostly after second dose.
Neither duration of follow-up is very long. The Moderna data tell me that a third primary dose would have been better but restarting the trial to evaluate third doses would have delayed Moderna’s EUA another 4-6 months. The three-dose Pfizer data look better but may not have been as good with another 6 weeks of follow-up.
Additional post-EUA data will be collected. Boosters will be needed when immunity from both vaccines wanes (one estimate is about 6 months after the primary series). The Advisory Committee on Immunization Practices noted in their deliberations that vaccine-induced antibody responses are higher and cross-neutralize variants (even Omicron) better than infection-induced immunity.4
Are there downsides to the vaccines? Naysayers question vaccinating children less than 5 years old with reasons containing enough “truth” that they catch people’s attention, for example, “young children don’t get very sick with COVID-19,” “most have been infected already,” “RNA for the spike protein stays in the body for months,” or “myocarditis.” Naysayers can quote references in reputable journals but seem to spin selected data out of context or quote unconfirmed data from the Vaccine Adverse Event Reporting System.
Reasons to vaccinate
- While children have milder disease than adults, mid-June 2022 surveillance indicated 50 hospitalizations and 1 pediatric death each day from SARS-CoV-2.5
- Vaccinating young children endows a foundation of vaccine-induced SARS-CoV-2 immunity that is superior to infection-induced immunity.4
- Long-term effects of large numbers of SARS-CoV-2 particles that enter every organ of a developing child have not been determined.
- Viral loads are lowered by prior vaccine; fewer viral replications lessen chances for newer variants to arise.
- Transmission is less in breakthrough infections than infections in the unvaccinated.
- Thirty percent of 5- to 11-year-olds hospitalized for SARS-CoV-2 had no underlying conditions;6 hospitalization rates in newborn to 4-year-olds have been the highest in the Omicron surge.7
- No myocarditis or pericarditis episodes have been detected in 6-month- to 11-year-old trials.
- The AAP and ACIP recommend the mRNA vaccines.
My thoughts are that SARS-CoV-2 vaccine is just another “routine” childhood vaccine that prepares children for healthier futures, pandemic or not, and the vaccines are as safe as other routine vaccines.
And like other pediatric vaccines, it should be no surprise that boosters will be needed, even if no newer variants than Omicron BA.4/BA.5 arise. But we know newer variants will arise and, similar to influenza vaccine, new formulations, perhaps with multiple SARS-CoV-2 strain antigens, will be needed every year or so. Everyone will get SARS-CoV-2 multiple times in their lives no matter how careful they are. So isn’t it good medical practice to establish early the best available foundation for maintaining lifelong SARS-CoV-2 immunity?
To me it is like pertussis. Most pertussis-infected children are sick enough to be hospitalized; very few die. They are miserable with illnesses that take weeks to months to subside. The worst disease usually occurs in unvaccinated young children or those with underlying conditions. Reactogenicity was reduced with acellular vaccine but resulted in less immunogenicity, so we give boosters at intervals that best match waning immunity. Circulating strains can be different than the vaccine strain, so protection against infection is 80%. Finally, even the safest vaccine may very rarely have sequelae. That is why The National Vaccine Injury Compensation Program was created. Yet the benefit-to-harm ratio for children and society favors universal pertussis vaccine use. And we vaccinate even those who have had pertussis because even infection-based immunity is incomplete and protection wanes. If arguments similar to those by SARS-CoV-2 vaccine naysayers were applied to acellular pertussis vaccine, it seems they would argue against pertussis vaccine for young children.
Another major issue has been “safety concerns” about the vaccines’ small amount of mRNA for the spike protein encased in microscopic lipid bubbles injected in the arm or leg. This mRNA is picked up by human cells, and in the cytoplasm (not the nucleus where our DNA resides) produces a limited supply of spike protein that is then picked up by antigen-presenting cells for short-lived distribution (days to 2 weeks at most) to regional lymph nodes where immune-memory processes are jump-started. Contrast that to even asymptomatic SARS-CoV-2 infection where multibillions of virus particles are produced for up to 14 days with access to every bodily organ that contains ACE-2 receptors (they all do). Each virus particle hijacks a human cell producing thousands of mRNA for spike protein (and multiple other SARS-CoV-2 proteins), eventually releasing multibillions of lipid fragments from the ruptured cell. Comparing the amount of these components in the mRNA vaccines to those from infection is like comparing a campfire to the many-thousand-acre wildfire. So, if one is worried about the effects of spike protein and lipid fragments, the limited localized amounts in mRNA vaccines should make one much less concerned than the enormous amounts circulating throughout the body as a result of a SARS-CoV-2 infection.
My take is that children 6-months to 5-years-old deserve SARS-CoV-2–induced vaccine protection and we can and should strongly recommend it as medical providers and child advocates.
*Dr. Harrison is professor, University of Missouri Kansas City School of Medicine, department of medicine, infectious diseases section, Kansas City. Email him at [email protected].
References
1. AAP. 2022 Jun 21. As COVID-19 vaccines become available for children ages 6 months to 4 years, AAP urges families to reach out to pediatricians to ask questions and access vaccine. www.aap.org.
2. CDC. Grading of recommendations, assessment, development, and evaluation (GRADE): Moderna COVID-19 vaccine for children aged 6 months–5 years. www.cdc.gov.
3. CDC. ACIP evidence to recommendations for use of Moderna COVID-19 vaccine in children ages 6 months–5 years and Pfizer-BioNTech COVID-19 vaccine in children ages 6 months–4 years under an emergency use authorization. www.cdc.gov.
4. Tang J et al. Nat Commun. 2022;13:2979.
5. Children and COVID-19: State Data Report. 2022 Jun 30. www.aap.org.
6. Shi DS et al. MMWR Morb Mortal Wkly Rep. 2022;71:574-81.
7. Marks KJ et al. MMWR Morb Mortal Wkly Rep. 2022;71:429-36.
Other good resources for families are https://getvaccineanswers.org/ or www.mayoclinic.org/diseases-conditions/coronavirus/in-depth/coronavirus-in-babies-and-children/art-20484405.
*This story was updated on July 19, 2022.
A family’s decision to vaccinate their child is best made jointly with a trusted medical provider who knows the child and family. The American Academy of Pediatrics created a toolkit with resources for answering questions about the recently authorized SARS-CoV-2 mRNA vaccines (Pfizer and Moderna) for 6-month- to 5-year-olds with science-backed vaccine facts, including links to other useful AAP information websites, talking points, graphics, and videos.1
SARS-CoV-2 seasonality
SARS-CoV-2 is now endemic, not a once-a-year seasonal virus. Seasons (aka surges) will occur whenever a new variant arises (twice yearly since 2020, Omicron BA.4/BA.5 currently), or when enough vaccine holdouts, newborns, and/or those with waning of prior immunity (vaccine or infection induced) accrue.
Emergency use authorization submission data for mRNA vaccine responses in young children2,3
Moderna in 6-month- through 5-year-olds. Two 25-mcg doses given 4-8 weeks apart produced 37.8% (95% confidence interval, 20.9%-51.1%) protection against symptomatic Omicron SARS-CoV-2 infections through 3 months of follow-up. Immunobridging analysis of antibody responses compared to 18- to 25-year-olds (100-mcg doses) showed the children’s responses were noninferior. Thus, the committee inferred that vaccine effectiveness in children should be similar to that in 18- to 25-year-olds. Fever, irritability, or local reaction/pain occurred in two-thirds after the second dose. Grade 3 reactions were noted in less than 5%.
Pfizer in 6-month- through 4-year-olds. Three 3-mcg doses, two doses 3-8 weeks apart and the third dose at least 8 weeks later (median 16 weeks), produced 80.3% (95% CI, 13.9%-96.7%) protection against symptomatic COVID-19 during the 6 weeks after the third dose. Local and systemic reactions occurred in 63.8%; less than 5% had grade 3 reactions (fever in about 3%, irritability in 1.3%, fatigue in 0.8%) mostly after second dose.
Neither duration of follow-up is very long. The Moderna data tell me that a third primary dose would have been better but restarting the trial to evaluate third doses would have delayed Moderna’s EUA another 4-6 months. The three-dose Pfizer data look better but may not have been as good with another 6 weeks of follow-up.
Additional post-EUA data will be collected. Boosters will be needed when immunity from both vaccines wanes (one estimate is about 6 months after the primary series). The Advisory Committee on Immunization Practices noted in their deliberations that vaccine-induced antibody responses are higher and cross-neutralize variants (even Omicron) better than infection-induced immunity.4
Are there downsides to the vaccines? Naysayers question vaccinating children less than 5 years old with reasons containing enough “truth” that they catch people’s attention, for example, “young children don’t get very sick with COVID-19,” “most have been infected already,” “RNA for the spike protein stays in the body for months,” or “myocarditis.” Naysayers can quote references in reputable journals but seem to spin selected data out of context or quote unconfirmed data from the Vaccine Adverse Event Reporting System.
Reasons to vaccinate
- While children have milder disease than adults, mid-June 2022 surveillance indicated 50 hospitalizations and 1 pediatric death each day from SARS-CoV-2.5
- Vaccinating young children endows a foundation of vaccine-induced SARS-CoV-2 immunity that is superior to infection-induced immunity.4
- Long-term effects of large numbers of SARS-CoV-2 particles that enter every organ of a developing child have not been determined.
- Viral loads are lowered by prior vaccine; fewer viral replications lessen chances for newer variants to arise.
- Transmission is less in breakthrough infections than infections in the unvaccinated.
- Thirty percent of 5- to 11-year-olds hospitalized for SARS-CoV-2 had no underlying conditions;6 hospitalization rates in newborn to 4-year-olds have been the highest in the Omicron surge.7
- No myocarditis or pericarditis episodes have been detected in 6-month- to 11-year-old trials.
- The AAP and ACIP recommend the mRNA vaccines.
My thoughts are that SARS-CoV-2 vaccine is just another “routine” childhood vaccine that prepares children for healthier futures, pandemic or not, and the vaccines are as safe as other routine vaccines.
And like other pediatric vaccines, it should be no surprise that boosters will be needed, even if no newer variants than Omicron BA.4/BA.5 arise. But we know newer variants will arise and, similar to influenza vaccine, new formulations, perhaps with multiple SARS-CoV-2 strain antigens, will be needed every year or so. Everyone will get SARS-CoV-2 multiple times in their lives no matter how careful they are. So isn’t it good medical practice to establish early the best available foundation for maintaining lifelong SARS-CoV-2 immunity?
To me it is like pertussis. Most pertussis-infected children are sick enough to be hospitalized; very few die. They are miserable with illnesses that take weeks to months to subside. The worst disease usually occurs in unvaccinated young children or those with underlying conditions. Reactogenicity was reduced with acellular vaccine but resulted in less immunogenicity, so we give boosters at intervals that best match waning immunity. Circulating strains can be different than the vaccine strain, so protection against infection is 80%. Finally, even the safest vaccine may very rarely have sequelae. That is why The National Vaccine Injury Compensation Program was created. Yet the benefit-to-harm ratio for children and society favors universal pertussis vaccine use. And we vaccinate even those who have had pertussis because even infection-based immunity is incomplete and protection wanes. If arguments similar to those by SARS-CoV-2 vaccine naysayers were applied to acellular pertussis vaccine, it seems they would argue against pertussis vaccine for young children.
Another major issue has been “safety concerns” about the vaccines’ small amount of mRNA for the spike protein encased in microscopic lipid bubbles injected in the arm or leg. This mRNA is picked up by human cells, and in the cytoplasm (not the nucleus where our DNA resides) produces a limited supply of spike protein that is then picked up by antigen-presenting cells for short-lived distribution (days to 2 weeks at most) to regional lymph nodes where immune-memory processes are jump-started. Contrast that to even asymptomatic SARS-CoV-2 infection where multibillions of virus particles are produced for up to 14 days with access to every bodily organ that contains ACE-2 receptors (they all do). Each virus particle hijacks a human cell producing thousands of mRNA for spike protein (and multiple other SARS-CoV-2 proteins), eventually releasing multibillions of lipid fragments from the ruptured cell. Comparing the amount of these components in the mRNA vaccines to those from infection is like comparing a campfire to the many-thousand-acre wildfire. So, if one is worried about the effects of spike protein and lipid fragments, the limited localized amounts in mRNA vaccines should make one much less concerned than the enormous amounts circulating throughout the body as a result of a SARS-CoV-2 infection.
My take is that children 6-months to 5-years-old deserve SARS-CoV-2–induced vaccine protection and we can and should strongly recommend it as medical providers and child advocates.
*Dr. Harrison is professor, University of Missouri Kansas City School of Medicine, department of medicine, infectious diseases section, Kansas City. Email him at [email protected].
References
1. AAP. 2022 Jun 21. As COVID-19 vaccines become available for children ages 6 months to 4 years, AAP urges families to reach out to pediatricians to ask questions and access vaccine. www.aap.org.
2. CDC. Grading of recommendations, assessment, development, and evaluation (GRADE): Moderna COVID-19 vaccine for children aged 6 months–5 years. www.cdc.gov.
3. CDC. ACIP evidence to recommendations for use of Moderna COVID-19 vaccine in children ages 6 months–5 years and Pfizer-BioNTech COVID-19 vaccine in children ages 6 months–4 years under an emergency use authorization. www.cdc.gov.
4. Tang J et al. Nat Commun. 2022;13:2979.
5. Children and COVID-19: State Data Report. 2022 Jun 30. www.aap.org.
6. Shi DS et al. MMWR Morb Mortal Wkly Rep. 2022;71:574-81.
7. Marks KJ et al. MMWR Morb Mortal Wkly Rep. 2022;71:429-36.
Other good resources for families are https://getvaccineanswers.org/ or www.mayoclinic.org/diseases-conditions/coronavirus/in-depth/coronavirus-in-babies-and-children/art-20484405.
*This story was updated on July 19, 2022.
A family’s decision to vaccinate their child is best made jointly with a trusted medical provider who knows the child and family. The American Academy of Pediatrics created a toolkit with resources for answering questions about the recently authorized SARS-CoV-2 mRNA vaccines (Pfizer and Moderna) for 6-month- to 5-year-olds with science-backed vaccine facts, including links to other useful AAP information websites, talking points, graphics, and videos.1
SARS-CoV-2 seasonality
SARS-CoV-2 is now endemic, not a once-a-year seasonal virus. Seasons (aka surges) will occur whenever a new variant arises (twice yearly since 2020, Omicron BA.4/BA.5 currently), or when enough vaccine holdouts, newborns, and/or those with waning of prior immunity (vaccine or infection induced) accrue.
Emergency use authorization submission data for mRNA vaccine responses in young children2,3
Moderna in 6-month- through 5-year-olds. Two 25-mcg doses given 4-8 weeks apart produced 37.8% (95% confidence interval, 20.9%-51.1%) protection against symptomatic Omicron SARS-CoV-2 infections through 3 months of follow-up. Immunobridging analysis of antibody responses compared to 18- to 25-year-olds (100-mcg doses) showed the children’s responses were noninferior. Thus, the committee inferred that vaccine effectiveness in children should be similar to that in 18- to 25-year-olds. Fever, irritability, or local reaction/pain occurred in two-thirds after the second dose. Grade 3 reactions were noted in less than 5%.
Pfizer in 6-month- through 4-year-olds. Three 3-mcg doses, two doses 3-8 weeks apart and the third dose at least 8 weeks later (median 16 weeks), produced 80.3% (95% CI, 13.9%-96.7%) protection against symptomatic COVID-19 during the 6 weeks after the third dose. Local and systemic reactions occurred in 63.8%; less than 5% had grade 3 reactions (fever in about 3%, irritability in 1.3%, fatigue in 0.8%) mostly after second dose.
Neither duration of follow-up is very long. The Moderna data tell me that a third primary dose would have been better but restarting the trial to evaluate third doses would have delayed Moderna’s EUA another 4-6 months. The three-dose Pfizer data look better but may not have been as good with another 6 weeks of follow-up.
Additional post-EUA data will be collected. Boosters will be needed when immunity from both vaccines wanes (one estimate is about 6 months after the primary series). The Advisory Committee on Immunization Practices noted in their deliberations that vaccine-induced antibody responses are higher and cross-neutralize variants (even Omicron) better than infection-induced immunity.4
Are there downsides to the vaccines? Naysayers question vaccinating children less than 5 years old with reasons containing enough “truth” that they catch people’s attention, for example, “young children don’t get very sick with COVID-19,” “most have been infected already,” “RNA for the spike protein stays in the body for months,” or “myocarditis.” Naysayers can quote references in reputable journals but seem to spin selected data out of context or quote unconfirmed data from the Vaccine Adverse Event Reporting System.
Reasons to vaccinate
- While children have milder disease than adults, mid-June 2022 surveillance indicated 50 hospitalizations and 1 pediatric death each day from SARS-CoV-2.5
- Vaccinating young children endows a foundation of vaccine-induced SARS-CoV-2 immunity that is superior to infection-induced immunity.4
- Long-term effects of large numbers of SARS-CoV-2 particles that enter every organ of a developing child have not been determined.
- Viral loads are lowered by prior vaccine; fewer viral replications lessen chances for newer variants to arise.
- Transmission is less in breakthrough infections than infections in the unvaccinated.
- Thirty percent of 5- to 11-year-olds hospitalized for SARS-CoV-2 had no underlying conditions;6 hospitalization rates in newborn to 4-year-olds have been the highest in the Omicron surge.7
- No myocarditis or pericarditis episodes have been detected in 6-month- to 11-year-old trials.
- The AAP and ACIP recommend the mRNA vaccines.
My thoughts are that SARS-CoV-2 vaccine is just another “routine” childhood vaccine that prepares children for healthier futures, pandemic or not, and the vaccines are as safe as other routine vaccines.
And like other pediatric vaccines, it should be no surprise that boosters will be needed, even if no newer variants than Omicron BA.4/BA.5 arise. But we know newer variants will arise and, similar to influenza vaccine, new formulations, perhaps with multiple SARS-CoV-2 strain antigens, will be needed every year or so. Everyone will get SARS-CoV-2 multiple times in their lives no matter how careful they are. So isn’t it good medical practice to establish early the best available foundation for maintaining lifelong SARS-CoV-2 immunity?
To me it is like pertussis. Most pertussis-infected children are sick enough to be hospitalized; very few die. They are miserable with illnesses that take weeks to months to subside. The worst disease usually occurs in unvaccinated young children or those with underlying conditions. Reactogenicity was reduced with acellular vaccine but resulted in less immunogenicity, so we give boosters at intervals that best match waning immunity. Circulating strains can be different than the vaccine strain, so protection against infection is 80%. Finally, even the safest vaccine may very rarely have sequelae. That is why The National Vaccine Injury Compensation Program was created. Yet the benefit-to-harm ratio for children and society favors universal pertussis vaccine use. And we vaccinate even those who have had pertussis because even infection-based immunity is incomplete and protection wanes. If arguments similar to those by SARS-CoV-2 vaccine naysayers were applied to acellular pertussis vaccine, it seems they would argue against pertussis vaccine for young children.
Another major issue has been “safety concerns” about the vaccines’ small amount of mRNA for the spike protein encased in microscopic lipid bubbles injected in the arm or leg. This mRNA is picked up by human cells, and in the cytoplasm (not the nucleus where our DNA resides) produces a limited supply of spike protein that is then picked up by antigen-presenting cells for short-lived distribution (days to 2 weeks at most) to regional lymph nodes where immune-memory processes are jump-started. Contrast that to even asymptomatic SARS-CoV-2 infection where multibillions of virus particles are produced for up to 14 days with access to every bodily organ that contains ACE-2 receptors (they all do). Each virus particle hijacks a human cell producing thousands of mRNA for spike protein (and multiple other SARS-CoV-2 proteins), eventually releasing multibillions of lipid fragments from the ruptured cell. Comparing the amount of these components in the mRNA vaccines to those from infection is like comparing a campfire to the many-thousand-acre wildfire. So, if one is worried about the effects of spike protein and lipid fragments, the limited localized amounts in mRNA vaccines should make one much less concerned than the enormous amounts circulating throughout the body as a result of a SARS-CoV-2 infection.
My take is that children 6-months to 5-years-old deserve SARS-CoV-2–induced vaccine protection and we can and should strongly recommend it as medical providers and child advocates.
*Dr. Harrison is professor, University of Missouri Kansas City School of Medicine, department of medicine, infectious diseases section, Kansas City. Email him at [email protected].
References
1. AAP. 2022 Jun 21. As COVID-19 vaccines become available for children ages 6 months to 4 years, AAP urges families to reach out to pediatricians to ask questions and access vaccine. www.aap.org.
2. CDC. Grading of recommendations, assessment, development, and evaluation (GRADE): Moderna COVID-19 vaccine for children aged 6 months–5 years. www.cdc.gov.
3. CDC. ACIP evidence to recommendations for use of Moderna COVID-19 vaccine in children ages 6 months–5 years and Pfizer-BioNTech COVID-19 vaccine in children ages 6 months–4 years under an emergency use authorization. www.cdc.gov.
4. Tang J et al. Nat Commun. 2022;13:2979.
5. Children and COVID-19: State Data Report. 2022 Jun 30. www.aap.org.
6. Shi DS et al. MMWR Morb Mortal Wkly Rep. 2022;71:574-81.
7. Marks KJ et al. MMWR Morb Mortal Wkly Rep. 2022;71:429-36.
Other good resources for families are https://getvaccineanswers.org/ or www.mayoclinic.org/diseases-conditions/coronavirus/in-depth/coronavirus-in-babies-and-children/art-20484405.
*This story was updated on July 19, 2022.
Precocious puberty – how early is too soon?
A 6-year-old girl presents with breast development. Her medical history is unremarkable. The parents are of average height, and the mother reports her thelarche was age 11 years. The girl is at the 97th percentile for her height and 90th percentile for her weight. She has Tanner stage 3 breast development and Tanner stage 2 pubic hair development. She has grown slightly more than 3 inches over the past year. How should she be evaluated and managed (N Engl J Med. 2008;358:2366-77)?
The premature onset of puberty, i.e., precocious puberty (PP), can be an emotionally traumatic event for the child and parents. Over the past century, improvements in public health and nutrition, and, more recently, increased obesity, have been associated with earlier puberty and the dominant factor has been attributed to genetics (Curr Opin Endocrinol Diabetes Obes. 2018;25[1]:49-54). This month’s article will focus on understanding what is considered “early” puberty, evaluating for causes, and managing precocious puberty.
More commonly seen in girls than boys, PP is defined as the onset of secondary sexual characteristics before age 7.5 years in Black and Hispanic girls, and prior to 8 years in White girls, which is 2-2.5 standard deviations below the average age of pubertal onset in healthy children (J Pediatr Adolesc Gynecol. 2019;32:455-9). As a comparison, PP is diagnosed with onset before age 9 years in boys. For White compared with Black girls, the average timing of thelarche is age 10 vs. 9.5 years, peak growth velocity is age 11.5, menarche is age 12.5 vs. 12, while completion of puberty is near age 14.5 vs. 13.5, respectively (J Pediatr. 1985;107:317). Fortunately, most girls with PP have common variants rather than serious pathology.
Classification: Central (CPP) vs. peripheral (PPP)
CPP is gonadotropin dependent, meaning the hypothalamic-pituitary-ovarian axis (HPO) is prematurely activated resulting in the normal progression of puberty.
PPP is gonadotropin independent, caused by sex steroid secretion from any source – ovaries, adrenal gland, exogenous or ectopic production, e.g., germ-cell tumor. This results in a disordered progression of pubertal milestones.
Whereas CPP is typically isosexual development, i.e., consistent with the child’s gender, PPP can be isosexual or contrasexual, e.g., virilization of girls. A third classification is “benign or nonprogressive pubertal variants” manifesting as isolated premature thelarche or adrenarche.
Causes (see table)
CPP. Idiopathic causes account for 80%-90% of presentations in girls and 25%-80% in boys. Remarkably, international and domestic adoption, as well as a family history of PP increases the likelihood of CPP in girls. Other etiologies include CNS lesions, e.g., hamartomas, which are the most common cause of PP in young children. MRI with contrast has been the traditional mode of diagnosis for CNS tumors, yet the yield is dubious in girls above age 6. Genetic causes are found in only a small percentage of PP cases. Rarely, CPP can result from gonadotropin-secreting tumors because of elevated luteinizing hormone levels.
PPP. As a result of sex steroid secretion, peripheral causes of PPP include ovarian cysts and ovarian tumors that increase circulating estradiol, such as granulosa cell tumors, which would cause isosexual PPP and Sertoli-Leydig cell tumors that secrete testosterone, which can result in contrasexual PPP. Mild congenital adrenal hyperplasia can result in PPP with virilization (contrasexual) and markedly advanced bone age.
McCune-Albright syndrome is rare and presents with the classic triad of PPP, skin pigmentation called café-au-lait, and fibrous dysplasia of bone. The pathophysiology of McCune-Albright syndrome is autoactivation of the G-protein leading to activation of ovarian tissue that results in formation of large ovarian cysts and extreme elevations in serum estradiol as well as the potential production of other hormones, e.g., thyrotoxicosis, excess growth hormone (acromegaly), and Cushing syndrome.
Premature thelarche. Premature thelarche typically occurs in girls between the ages of 1 and 3 years and is limited to breast enlargement. While no cause has been determined, the plausible explanations include partial activation of the HPO axis, endocrine-disrupting chemicals (EDCs), or a genetic origin. A small percentage of these girls progress to CPP.
EDCs have been considered as potential influencers of early puberty, but no consensus has been established. (Examples of EDCs in the environment include air, soil, or water supply along with food sources, personal care products, and manufactured products that can affect the endocrine system.)
Premature adenarche. Premature adrenarche presents with adult body odor and/or body hair (pubic and/or axillary) in girls who have an elevated body mass index, most commonly at the ages of 6-7 years. The presumed mechanism is normal maturation of the adrenal gland with resultant elevation of circulating androgens. Bone age may be mildly accelerated and DHEAS is prematurely elevated for age. These girls appear to be at increased risk for polycystic ovary syndrome.
Evaluation
The initial step in the evaluation of PP is to determine whether the cause is CPP or PPP; the latter includes distinguishing isosexual from contrasexual development. A thorough history (growth, headaches, behavior or visual change, seizures, abdominal pain), physical exam, including Tanner staging, and bone age is required. However, with isolated premature thelarche or adrenarche, a bone age may not be necessary, as initial close clinical observation for pubertal progression is likely sufficient.
For CPP, the diagnosis is based on serum LH, whether random levels or elevations follow GnRH stimulation. Puberty milestones progress normally although adrenarche is not consistently apparent. For girls younger than age 6, a brain MRI is recommended but not in asymptomatic older girls with CPP. LH and FSH along with estradiol or testosterone, the latter especially in boys, are the first line of serum testing. Serum TSH is recommended for suspicion of primary hypothyroidism. In girls with premature adrenarche, a bone age, testosterone, DHEAS, and 17-OHP to rule out adrenal hyperplasia should be obtained. Pelvic ultrasound may be a useful adjunct to assess uterine volume and/or ovarian cysts/tumors.
Rapidity of onset can also lead the evaluation since a normal growth chart and skeletal maturation suggests a benign pubertal variant whereas a more rapid rate can signal CPP or PPP. Of note, health care providers should ensure prescription, over-the-counter oral or topical sources of hormones, and EDCs are ruled out.
Consequences
An association between childhood sexual abuse and earlier pubertal onset has been cited. These girls may be at increased risk for psychosocial difficulties, menstrual and fertility problems, and even reproductive cancers because of prolonged exposure to sex hormones (J Adolesc Health. 2016;60[1]:65-71).
Treatment
The mainstay of CPP treatment is maximizing adult height, typically through the use of a GnRH agonist for HPO suppression from pituitary downregulation. For girls above age 8 years, attempts at improving adult height have not shown a benefit.
In girls with PPP, treatment is directed at the prevailing pathology. Interestingly, early PPP can activate the HPO axis thereby converting to “secondary” CPP. In PPP, McCune-Albright syndrome treatment targets reducing circulating estrogens through letrozole or tamoxifen as well as addressing other autoactivated hormone production. Ovarian and adrenal tumors, albeit rare, can cause PP; therefore, surgical excision is the goal of treatment.
PP should be approached with equal concerns about the physical and emotional effects while including the family to help them understand the pathophysiology and psychosocial risks.
Dr. Mark P. Trolice is director of The IVF Center in Winter Park, Fla., and professor of obstetrics and gynecology at the University of Central Florida, Orlando.
A 6-year-old girl presents with breast development. Her medical history is unremarkable. The parents are of average height, and the mother reports her thelarche was age 11 years. The girl is at the 97th percentile for her height and 90th percentile for her weight. She has Tanner stage 3 breast development and Tanner stage 2 pubic hair development. She has grown slightly more than 3 inches over the past year. How should she be evaluated and managed (N Engl J Med. 2008;358:2366-77)?
The premature onset of puberty, i.e., precocious puberty (PP), can be an emotionally traumatic event for the child and parents. Over the past century, improvements in public health and nutrition, and, more recently, increased obesity, have been associated with earlier puberty and the dominant factor has been attributed to genetics (Curr Opin Endocrinol Diabetes Obes. 2018;25[1]:49-54). This month’s article will focus on understanding what is considered “early” puberty, evaluating for causes, and managing precocious puberty.
More commonly seen in girls than boys, PP is defined as the onset of secondary sexual characteristics before age 7.5 years in Black and Hispanic girls, and prior to 8 years in White girls, which is 2-2.5 standard deviations below the average age of pubertal onset in healthy children (J Pediatr Adolesc Gynecol. 2019;32:455-9). As a comparison, PP is diagnosed with onset before age 9 years in boys. For White compared with Black girls, the average timing of thelarche is age 10 vs. 9.5 years, peak growth velocity is age 11.5, menarche is age 12.5 vs. 12, while completion of puberty is near age 14.5 vs. 13.5, respectively (J Pediatr. 1985;107:317). Fortunately, most girls with PP have common variants rather than serious pathology.
Classification: Central (CPP) vs. peripheral (PPP)
CPP is gonadotropin dependent, meaning the hypothalamic-pituitary-ovarian axis (HPO) is prematurely activated resulting in the normal progression of puberty.
PPP is gonadotropin independent, caused by sex steroid secretion from any source – ovaries, adrenal gland, exogenous or ectopic production, e.g., germ-cell tumor. This results in a disordered progression of pubertal milestones.
Whereas CPP is typically isosexual development, i.e., consistent with the child’s gender, PPP can be isosexual or contrasexual, e.g., virilization of girls. A third classification is “benign or nonprogressive pubertal variants” manifesting as isolated premature thelarche or adrenarche.
Causes (see table)
CPP. Idiopathic causes account for 80%-90% of presentations in girls and 25%-80% in boys. Remarkably, international and domestic adoption, as well as a family history of PP increases the likelihood of CPP in girls. Other etiologies include CNS lesions, e.g., hamartomas, which are the most common cause of PP in young children. MRI with contrast has been the traditional mode of diagnosis for CNS tumors, yet the yield is dubious in girls above age 6. Genetic causes are found in only a small percentage of PP cases. Rarely, CPP can result from gonadotropin-secreting tumors because of elevated luteinizing hormone levels.
PPP. As a result of sex steroid secretion, peripheral causes of PPP include ovarian cysts and ovarian tumors that increase circulating estradiol, such as granulosa cell tumors, which would cause isosexual PPP and Sertoli-Leydig cell tumors that secrete testosterone, which can result in contrasexual PPP. Mild congenital adrenal hyperplasia can result in PPP with virilization (contrasexual) and markedly advanced bone age.
McCune-Albright syndrome is rare and presents with the classic triad of PPP, skin pigmentation called café-au-lait, and fibrous dysplasia of bone. The pathophysiology of McCune-Albright syndrome is autoactivation of the G-protein leading to activation of ovarian tissue that results in formation of large ovarian cysts and extreme elevations in serum estradiol as well as the potential production of other hormones, e.g., thyrotoxicosis, excess growth hormone (acromegaly), and Cushing syndrome.
Premature thelarche. Premature thelarche typically occurs in girls between the ages of 1 and 3 years and is limited to breast enlargement. While no cause has been determined, the plausible explanations include partial activation of the HPO axis, endocrine-disrupting chemicals (EDCs), or a genetic origin. A small percentage of these girls progress to CPP.
EDCs have been considered as potential influencers of early puberty, but no consensus has been established. (Examples of EDCs in the environment include air, soil, or water supply along with food sources, personal care products, and manufactured products that can affect the endocrine system.)
Premature adenarche. Premature adrenarche presents with adult body odor and/or body hair (pubic and/or axillary) in girls who have an elevated body mass index, most commonly at the ages of 6-7 years. The presumed mechanism is normal maturation of the adrenal gland with resultant elevation of circulating androgens. Bone age may be mildly accelerated and DHEAS is prematurely elevated for age. These girls appear to be at increased risk for polycystic ovary syndrome.
Evaluation
The initial step in the evaluation of PP is to determine whether the cause is CPP or PPP; the latter includes distinguishing isosexual from contrasexual development. A thorough history (growth, headaches, behavior or visual change, seizures, abdominal pain), physical exam, including Tanner staging, and bone age is required. However, with isolated premature thelarche or adrenarche, a bone age may not be necessary, as initial close clinical observation for pubertal progression is likely sufficient.
For CPP, the diagnosis is based on serum LH, whether random levels or elevations follow GnRH stimulation. Puberty milestones progress normally although adrenarche is not consistently apparent. For girls younger than age 6, a brain MRI is recommended but not in asymptomatic older girls with CPP. LH and FSH along with estradiol or testosterone, the latter especially in boys, are the first line of serum testing. Serum TSH is recommended for suspicion of primary hypothyroidism. In girls with premature adrenarche, a bone age, testosterone, DHEAS, and 17-OHP to rule out adrenal hyperplasia should be obtained. Pelvic ultrasound may be a useful adjunct to assess uterine volume and/or ovarian cysts/tumors.
Rapidity of onset can also lead the evaluation since a normal growth chart and skeletal maturation suggests a benign pubertal variant whereas a more rapid rate can signal CPP or PPP. Of note, health care providers should ensure prescription, over-the-counter oral or topical sources of hormones, and EDCs are ruled out.
Consequences
An association between childhood sexual abuse and earlier pubertal onset has been cited. These girls may be at increased risk for psychosocial difficulties, menstrual and fertility problems, and even reproductive cancers because of prolonged exposure to sex hormones (J Adolesc Health. 2016;60[1]:65-71).
Treatment
The mainstay of CPP treatment is maximizing adult height, typically through the use of a GnRH agonist for HPO suppression from pituitary downregulation. For girls above age 8 years, attempts at improving adult height have not shown a benefit.
In girls with PPP, treatment is directed at the prevailing pathology. Interestingly, early PPP can activate the HPO axis thereby converting to “secondary” CPP. In PPP, McCune-Albright syndrome treatment targets reducing circulating estrogens through letrozole or tamoxifen as well as addressing other autoactivated hormone production. Ovarian and adrenal tumors, albeit rare, can cause PP; therefore, surgical excision is the goal of treatment.
PP should be approached with equal concerns about the physical and emotional effects while including the family to help them understand the pathophysiology and psychosocial risks.
Dr. Mark P. Trolice is director of The IVF Center in Winter Park, Fla., and professor of obstetrics and gynecology at the University of Central Florida, Orlando.
A 6-year-old girl presents with breast development. Her medical history is unremarkable. The parents are of average height, and the mother reports her thelarche was age 11 years. The girl is at the 97th percentile for her height and 90th percentile for her weight. She has Tanner stage 3 breast development and Tanner stage 2 pubic hair development. She has grown slightly more than 3 inches over the past year. How should she be evaluated and managed (N Engl J Med. 2008;358:2366-77)?
The premature onset of puberty, i.e., precocious puberty (PP), can be an emotionally traumatic event for the child and parents. Over the past century, improvements in public health and nutrition, and, more recently, increased obesity, have been associated with earlier puberty and the dominant factor has been attributed to genetics (Curr Opin Endocrinol Diabetes Obes. 2018;25[1]:49-54). This month’s article will focus on understanding what is considered “early” puberty, evaluating for causes, and managing precocious puberty.
More commonly seen in girls than boys, PP is defined as the onset of secondary sexual characteristics before age 7.5 years in Black and Hispanic girls, and prior to 8 years in White girls, which is 2-2.5 standard deviations below the average age of pubertal onset in healthy children (J Pediatr Adolesc Gynecol. 2019;32:455-9). As a comparison, PP is diagnosed with onset before age 9 years in boys. For White compared with Black girls, the average timing of thelarche is age 10 vs. 9.5 years, peak growth velocity is age 11.5, menarche is age 12.5 vs. 12, while completion of puberty is near age 14.5 vs. 13.5, respectively (J Pediatr. 1985;107:317). Fortunately, most girls with PP have common variants rather than serious pathology.
Classification: Central (CPP) vs. peripheral (PPP)
CPP is gonadotropin dependent, meaning the hypothalamic-pituitary-ovarian axis (HPO) is prematurely activated resulting in the normal progression of puberty.
PPP is gonadotropin independent, caused by sex steroid secretion from any source – ovaries, adrenal gland, exogenous or ectopic production, e.g., germ-cell tumor. This results in a disordered progression of pubertal milestones.
Whereas CPP is typically isosexual development, i.e., consistent with the child’s gender, PPP can be isosexual or contrasexual, e.g., virilization of girls. A third classification is “benign or nonprogressive pubertal variants” manifesting as isolated premature thelarche or adrenarche.
Causes (see table)
CPP. Idiopathic causes account for 80%-90% of presentations in girls and 25%-80% in boys. Remarkably, international and domestic adoption, as well as a family history of PP increases the likelihood of CPP in girls. Other etiologies include CNS lesions, e.g., hamartomas, which are the most common cause of PP in young children. MRI with contrast has been the traditional mode of diagnosis for CNS tumors, yet the yield is dubious in girls above age 6. Genetic causes are found in only a small percentage of PP cases. Rarely, CPP can result from gonadotropin-secreting tumors because of elevated luteinizing hormone levels.
PPP. As a result of sex steroid secretion, peripheral causes of PPP include ovarian cysts and ovarian tumors that increase circulating estradiol, such as granulosa cell tumors, which would cause isosexual PPP and Sertoli-Leydig cell tumors that secrete testosterone, which can result in contrasexual PPP. Mild congenital adrenal hyperplasia can result in PPP with virilization (contrasexual) and markedly advanced bone age.
McCune-Albright syndrome is rare and presents with the classic triad of PPP, skin pigmentation called café-au-lait, and fibrous dysplasia of bone. The pathophysiology of McCune-Albright syndrome is autoactivation of the G-protein leading to activation of ovarian tissue that results in formation of large ovarian cysts and extreme elevations in serum estradiol as well as the potential production of other hormones, e.g., thyrotoxicosis, excess growth hormone (acromegaly), and Cushing syndrome.
Premature thelarche. Premature thelarche typically occurs in girls between the ages of 1 and 3 years and is limited to breast enlargement. While no cause has been determined, the plausible explanations include partial activation of the HPO axis, endocrine-disrupting chemicals (EDCs), or a genetic origin. A small percentage of these girls progress to CPP.
EDCs have been considered as potential influencers of early puberty, but no consensus has been established. (Examples of EDCs in the environment include air, soil, or water supply along with food sources, personal care products, and manufactured products that can affect the endocrine system.)
Premature adenarche. Premature adrenarche presents with adult body odor and/or body hair (pubic and/or axillary) in girls who have an elevated body mass index, most commonly at the ages of 6-7 years. The presumed mechanism is normal maturation of the adrenal gland with resultant elevation of circulating androgens. Bone age may be mildly accelerated and DHEAS is prematurely elevated for age. These girls appear to be at increased risk for polycystic ovary syndrome.
Evaluation
The initial step in the evaluation of PP is to determine whether the cause is CPP or PPP; the latter includes distinguishing isosexual from contrasexual development. A thorough history (growth, headaches, behavior or visual change, seizures, abdominal pain), physical exam, including Tanner staging, and bone age is required. However, with isolated premature thelarche or adrenarche, a bone age may not be necessary, as initial close clinical observation for pubertal progression is likely sufficient.
For CPP, the diagnosis is based on serum LH, whether random levels or elevations follow GnRH stimulation. Puberty milestones progress normally although adrenarche is not consistently apparent. For girls younger than age 6, a brain MRI is recommended but not in asymptomatic older girls with CPP. LH and FSH along with estradiol or testosterone, the latter especially in boys, are the first line of serum testing. Serum TSH is recommended for suspicion of primary hypothyroidism. In girls with premature adrenarche, a bone age, testosterone, DHEAS, and 17-OHP to rule out adrenal hyperplasia should be obtained. Pelvic ultrasound may be a useful adjunct to assess uterine volume and/or ovarian cysts/tumors.
Rapidity of onset can also lead the evaluation since a normal growth chart and skeletal maturation suggests a benign pubertal variant whereas a more rapid rate can signal CPP or PPP. Of note, health care providers should ensure prescription, over-the-counter oral or topical sources of hormones, and EDCs are ruled out.
Consequences
An association between childhood sexual abuse and earlier pubertal onset has been cited. These girls may be at increased risk for psychosocial difficulties, menstrual and fertility problems, and even reproductive cancers because of prolonged exposure to sex hormones (J Adolesc Health. 2016;60[1]:65-71).
Treatment
The mainstay of CPP treatment is maximizing adult height, typically through the use of a GnRH agonist for HPO suppression from pituitary downregulation. For girls above age 8 years, attempts at improving adult height have not shown a benefit.
In girls with PPP, treatment is directed at the prevailing pathology. Interestingly, early PPP can activate the HPO axis thereby converting to “secondary” CPP. In PPP, McCune-Albright syndrome treatment targets reducing circulating estrogens through letrozole or tamoxifen as well as addressing other autoactivated hormone production. Ovarian and adrenal tumors, albeit rare, can cause PP; therefore, surgical excision is the goal of treatment.
PP should be approached with equal concerns about the physical and emotional effects while including the family to help them understand the pathophysiology and psychosocial risks.
Dr. Mark P. Trolice is director of The IVF Center in Winter Park, Fla., and professor of obstetrics and gynecology at the University of Central Florida, Orlando.
Surgical Specimens and Margins
We have attended grand rounds presentations at which students announce that Mohs micrographic surgery evaluates 100% of the surgical margin, whereas standard excision samples 1% to 2% of the margin; we have even fielded questions from neighbors who have come across this information on the internet.1-5 This statement describes a best-case scenario for Mohs surgery and a worst-case scenario for standard excision. We believe that it is important for clinicians to have a more nuanced understanding of how simple excisions are processed so that they can have pertinent discussions with patients, especially now that there is increasing access to personal health information along with increased agency in patient decision-making.
Margins for Mohs Surgery
Theoretically, Mohs surgery should sample all true surgical margins by complete circumferential, peripheral, and deep-margin assessment. Unfortunately, some sections are not cut full face—sections may not always sample a complete surface—when technicians make an error or lack expertise. Some sections may have small tissue folds or small gaps that prevent complete visualization. We estimate that the Mohs sections we review in consultation that are prepared by private practice Mohs surgeons in our communities visualize approximately 98% of surgical margins on average. Incomplete sections contribute to the rare tumor recurrences after Mohs surgery of approximately 2% to 3%.6
Standard Excision Margins
When we obtained the references cited in articles asserting that
Here is a simple example to show that more margin is accessed in some cases. Consider this hypothetical situation: If a tumor can be readily visualized grossly and housed entirely within an imaginary cuboid (rectangular) prism that is removed in an elliptical specimen with a length of 6 cm, a width of 2 cm, and a height of 1 cm (Figure), then standard sectioning assesses a greater margin.
Bread-loaf sectioning would be expected to examine the complete surface of 2 sides (faces) of the cuboid. Assessing 2 of the 5 clinically relevant sides provides information for approximately 50% of the margins, as sections in the next parallel plane can be expected to be clear after the first clear section is identified. The clinically useful information is not limited to the sum of the widths of sections. Encountering a clear plane typically indicates that there will be no tumor in more distal parallel planes. Warne et al6 developed a formula that can accurately predict the percentage of the margin evaluated by proxy that considers the curvature of the ellipse.
Comparing Standard Excision and Mohs Surgery
Mohs surgery consistently results in the best outcomes, but standard excision is effective, too. Standard excision is relatively simple, requires less equipment, is less time consuming, and can provide good value when resources are finite. Data on recurrence of basal cell carcinoma after simple excision are limited, but the recurrence rate is reported to be approximately 3%.7,8 A meta-analysis found that the recurrence rate of basal cell carcinoma treated with standard excision was 0.4%, 1.6%, 2.6%, and 4% with 5-mm, 4-mm, 3-mm, and 2-mm surgical margins, respectively.9
Mohs surgery is the best, most effective, and most tissue-sparing technique for certain nonmelanoma skin cancers. This observation is reflected in guidelines worldwide.10 The adequacy of standard approaches to margin evaluation depends on the capabilities and focus of the laboratory team. Dermatopathologists often are called to the laboratory to decide which technique will be best for a particular case.11 Technicians are trained to take more sections in areas where abnormalities are seen, and some laboratories take photographs of specimens or provide sketches for correlation. Dermatopathologists also routinely request additional sections in areas where visible tumor extends close to surgical margins on microscopic examination.
It is not simply a matter of knowing how much of the margin is sampled but if the most pertinent areas are adequately sampled. Simple sectioning can work well and be cost effective. Many clinicians are unaware of how tissue processing can vary from laboratory to laboratory. There are no uniformly accepted standards for how tissue should be processed. Assiduous and thoughtful evaluation of specimens can affect results. As with any service, some laboratories provide more detailed and conscientious care while others focus more on immediate costs. Clinicians should understand how their specimens are processed by discussing margin evaluation with their dermatopathologist.
Final Thoughts
Used appropriately, Mohs surgery is an excellent technique that can provide outstanding results. Standard excision also has an important place in the dermatologist’s armamentarium and typically provides information about more than 1% to 2% of the margin. Understanding the techniques used to process specimens is critical to delivering the best possible care.
- Tolkachjov SN, Brodland DG, Coldiron BM, et al. Understanding Mohs micrographic surgery: a review and practical guide for the nondermatologist. Mayo Clin Proc. 2017;92:1261-1271. doi:10.1016/j.mayocp.2017.04.009
- Thomas RM, Amonette RA. Mohs micrographic surgery. Am Fam Physician. 1988;37:135-142.
- Buker JL, Amonette RA. Micrographic surgery. Clin Dermatol. 1992:10:309-315. doi:10.1016/0738-081x(92)90074-9
- Kauvar ANB. Mohs: the gold standard. The Skin Cancer Foundation website. Updated March 9, 2021. Accessed June 15, 2022. https://www.skincancer.org/treatment-resources/mohs-surgery/mohs-the-gold-standard/
- van Delft LCJ, Nelemans PJ, van Loo E, et al. The illusion of conventional histological resection margin control. Br J Dermatol. 2019;180:1240-1241. doi:10.1111/bjd.17510
- Warne MM, Klawonn MM, Brodell RT. Bread loaf sections provide useful information on more than 0.5% of surgical margins [published July 5, 2022]. Br J Dermatol. doi:10.1111/bjd.21740
- Mehrany K, Weenig RH, Pittelkow MR, et al. High recurrence rates of basal cell carcinoma after Mohs surgery in patients with chronic lymphocytic leukemia. Arch Dermatol. 2004;140:985-988. doi:10.1001/archderm.140.8.985
- Smeets NWJ, Krekels GAM, Ostertag JU, et al. Surgical excision vs Mohs’ micrographic surgery for basal-cell carcinoma of the face: randomised controlled trial. Lancet. 2004;364:1766-1772. doi:10.1016/S0140-6736(04)17399-6
- Gulleth Y, Goldberg N, Silverman RP, et al. What is the best surgical margin for a basal cell carcinoma: a meta-analysis of theliterature. Plast Reconstr Surg. 2010;126:1222-1231. doi:10.1097/PRS.0b013e3181ea450d
- Nahhas AF, Scarbrough CA, Trotter S. A review of the global guidelines on surgical margins for nonmelanoma skin cancers. J Clin Aesthet Dermatol. 2017;10:37-46.
- Rapini RP. Comparison of methods for checking surgical margins. J Am Acad Dermatol. 1990; 23:288-294. doi:10.1016/0190-9622(90)70212-z
We have attended grand rounds presentations at which students announce that Mohs micrographic surgery evaluates 100% of the surgical margin, whereas standard excision samples 1% to 2% of the margin; we have even fielded questions from neighbors who have come across this information on the internet.1-5 This statement describes a best-case scenario for Mohs surgery and a worst-case scenario for standard excision. We believe that it is important for clinicians to have a more nuanced understanding of how simple excisions are processed so that they can have pertinent discussions with patients, especially now that there is increasing access to personal health information along with increased agency in patient decision-making.
Margins for Mohs Surgery
Theoretically, Mohs surgery should sample all true surgical margins by complete circumferential, peripheral, and deep-margin assessment. Unfortunately, some sections are not cut full face—sections may not always sample a complete surface—when technicians make an error or lack expertise. Some sections may have small tissue folds or small gaps that prevent complete visualization. We estimate that the Mohs sections we review in consultation that are prepared by private practice Mohs surgeons in our communities visualize approximately 98% of surgical margins on average. Incomplete sections contribute to the rare tumor recurrences after Mohs surgery of approximately 2% to 3%.6
Standard Excision Margins
When we obtained the references cited in articles asserting that
Here is a simple example to show that more margin is accessed in some cases. Consider this hypothetical situation: If a tumor can be readily visualized grossly and housed entirely within an imaginary cuboid (rectangular) prism that is removed in an elliptical specimen with a length of 6 cm, a width of 2 cm, and a height of 1 cm (Figure), then standard sectioning assesses a greater margin.
Bread-loaf sectioning would be expected to examine the complete surface of 2 sides (faces) of the cuboid. Assessing 2 of the 5 clinically relevant sides provides information for approximately 50% of the margins, as sections in the next parallel plane can be expected to be clear after the first clear section is identified. The clinically useful information is not limited to the sum of the widths of sections. Encountering a clear plane typically indicates that there will be no tumor in more distal parallel planes. Warne et al6 developed a formula that can accurately predict the percentage of the margin evaluated by proxy that considers the curvature of the ellipse.
Comparing Standard Excision and Mohs Surgery
Mohs surgery consistently results in the best outcomes, but standard excision is effective, too. Standard excision is relatively simple, requires less equipment, is less time consuming, and can provide good value when resources are finite. Data on recurrence of basal cell carcinoma after simple excision are limited, but the recurrence rate is reported to be approximately 3%.7,8 A meta-analysis found that the recurrence rate of basal cell carcinoma treated with standard excision was 0.4%, 1.6%, 2.6%, and 4% with 5-mm, 4-mm, 3-mm, and 2-mm surgical margins, respectively.9
Mohs surgery is the best, most effective, and most tissue-sparing technique for certain nonmelanoma skin cancers. This observation is reflected in guidelines worldwide.10 The adequacy of standard approaches to margin evaluation depends on the capabilities and focus of the laboratory team. Dermatopathologists often are called to the laboratory to decide which technique will be best for a particular case.11 Technicians are trained to take more sections in areas where abnormalities are seen, and some laboratories take photographs of specimens or provide sketches for correlation. Dermatopathologists also routinely request additional sections in areas where visible tumor extends close to surgical margins on microscopic examination.
It is not simply a matter of knowing how much of the margin is sampled but if the most pertinent areas are adequately sampled. Simple sectioning can work well and be cost effective. Many clinicians are unaware of how tissue processing can vary from laboratory to laboratory. There are no uniformly accepted standards for how tissue should be processed. Assiduous and thoughtful evaluation of specimens can affect results. As with any service, some laboratories provide more detailed and conscientious care while others focus more on immediate costs. Clinicians should understand how their specimens are processed by discussing margin evaluation with their dermatopathologist.
Final Thoughts
Used appropriately, Mohs surgery is an excellent technique that can provide outstanding results. Standard excision also has an important place in the dermatologist’s armamentarium and typically provides information about more than 1% to 2% of the margin. Understanding the techniques used to process specimens is critical to delivering the best possible care.
We have attended grand rounds presentations at which students announce that Mohs micrographic surgery evaluates 100% of the surgical margin, whereas standard excision samples 1% to 2% of the margin; we have even fielded questions from neighbors who have come across this information on the internet.1-5 This statement describes a best-case scenario for Mohs surgery and a worst-case scenario for standard excision. We believe that it is important for clinicians to have a more nuanced understanding of how simple excisions are processed so that they can have pertinent discussions with patients, especially now that there is increasing access to personal health information along with increased agency in patient decision-making.
Margins for Mohs Surgery
Theoretically, Mohs surgery should sample all true surgical margins by complete circumferential, peripheral, and deep-margin assessment. Unfortunately, some sections are not cut full face—sections may not always sample a complete surface—when technicians make an error or lack expertise. Some sections may have small tissue folds or small gaps that prevent complete visualization. We estimate that the Mohs sections we review in consultation that are prepared by private practice Mohs surgeons in our communities visualize approximately 98% of surgical margins on average. Incomplete sections contribute to the rare tumor recurrences after Mohs surgery of approximately 2% to 3%.6
Standard Excision Margins
When we obtained the references cited in articles asserting that
Here is a simple example to show that more margin is accessed in some cases. Consider this hypothetical situation: If a tumor can be readily visualized grossly and housed entirely within an imaginary cuboid (rectangular) prism that is removed in an elliptical specimen with a length of 6 cm, a width of 2 cm, and a height of 1 cm (Figure), then standard sectioning assesses a greater margin.
Bread-loaf sectioning would be expected to examine the complete surface of 2 sides (faces) of the cuboid. Assessing 2 of the 5 clinically relevant sides provides information for approximately 50% of the margins, as sections in the next parallel plane can be expected to be clear after the first clear section is identified. The clinically useful information is not limited to the sum of the widths of sections. Encountering a clear plane typically indicates that there will be no tumor in more distal parallel planes. Warne et al6 developed a formula that can accurately predict the percentage of the margin evaluated by proxy that considers the curvature of the ellipse.
Comparing Standard Excision and Mohs Surgery
Mohs surgery consistently results in the best outcomes, but standard excision is effective, too. Standard excision is relatively simple, requires less equipment, is less time consuming, and can provide good value when resources are finite. Data on recurrence of basal cell carcinoma after simple excision are limited, but the recurrence rate is reported to be approximately 3%.7,8 A meta-analysis found that the recurrence rate of basal cell carcinoma treated with standard excision was 0.4%, 1.6%, 2.6%, and 4% with 5-mm, 4-mm, 3-mm, and 2-mm surgical margins, respectively.9
Mohs surgery is the best, most effective, and most tissue-sparing technique for certain nonmelanoma skin cancers. This observation is reflected in guidelines worldwide.10 The adequacy of standard approaches to margin evaluation depends on the capabilities and focus of the laboratory team. Dermatopathologists often are called to the laboratory to decide which technique will be best for a particular case.11 Technicians are trained to take more sections in areas where abnormalities are seen, and some laboratories take photographs of specimens or provide sketches for correlation. Dermatopathologists also routinely request additional sections in areas where visible tumor extends close to surgical margins on microscopic examination.
It is not simply a matter of knowing how much of the margin is sampled but if the most pertinent areas are adequately sampled. Simple sectioning can work well and be cost effective. Many clinicians are unaware of how tissue processing can vary from laboratory to laboratory. There are no uniformly accepted standards for how tissue should be processed. Assiduous and thoughtful evaluation of specimens can affect results. As with any service, some laboratories provide more detailed and conscientious care while others focus more on immediate costs. Clinicians should understand how their specimens are processed by discussing margin evaluation with their dermatopathologist.
Final Thoughts
Used appropriately, Mohs surgery is an excellent technique that can provide outstanding results. Standard excision also has an important place in the dermatologist’s armamentarium and typically provides information about more than 1% to 2% of the margin. Understanding the techniques used to process specimens is critical to delivering the best possible care.
- Tolkachjov SN, Brodland DG, Coldiron BM, et al. Understanding Mohs micrographic surgery: a review and practical guide for the nondermatologist. Mayo Clin Proc. 2017;92:1261-1271. doi:10.1016/j.mayocp.2017.04.009
- Thomas RM, Amonette RA. Mohs micrographic surgery. Am Fam Physician. 1988;37:135-142.
- Buker JL, Amonette RA. Micrographic surgery. Clin Dermatol. 1992:10:309-315. doi:10.1016/0738-081x(92)90074-9
- Kauvar ANB. Mohs: the gold standard. The Skin Cancer Foundation website. Updated March 9, 2021. Accessed June 15, 2022. https://www.skincancer.org/treatment-resources/mohs-surgery/mohs-the-gold-standard/
- van Delft LCJ, Nelemans PJ, van Loo E, et al. The illusion of conventional histological resection margin control. Br J Dermatol. 2019;180:1240-1241. doi:10.1111/bjd.17510
- Warne MM, Klawonn MM, Brodell RT. Bread loaf sections provide useful information on more than 0.5% of surgical margins [published July 5, 2022]. Br J Dermatol. doi:10.1111/bjd.21740
- Mehrany K, Weenig RH, Pittelkow MR, et al. High recurrence rates of basal cell carcinoma after Mohs surgery in patients with chronic lymphocytic leukemia. Arch Dermatol. 2004;140:985-988. doi:10.1001/archderm.140.8.985
- Smeets NWJ, Krekels GAM, Ostertag JU, et al. Surgical excision vs Mohs’ micrographic surgery for basal-cell carcinoma of the face: randomised controlled trial. Lancet. 2004;364:1766-1772. doi:10.1016/S0140-6736(04)17399-6
- Gulleth Y, Goldberg N, Silverman RP, et al. What is the best surgical margin for a basal cell carcinoma: a meta-analysis of theliterature. Plast Reconstr Surg. 2010;126:1222-1231. doi:10.1097/PRS.0b013e3181ea450d
- Nahhas AF, Scarbrough CA, Trotter S. A review of the global guidelines on surgical margins for nonmelanoma skin cancers. J Clin Aesthet Dermatol. 2017;10:37-46.
- Rapini RP. Comparison of methods for checking surgical margins. J Am Acad Dermatol. 1990; 23:288-294. doi:10.1016/0190-9622(90)70212-z
- Tolkachjov SN, Brodland DG, Coldiron BM, et al. Understanding Mohs micrographic surgery: a review and practical guide for the nondermatologist. Mayo Clin Proc. 2017;92:1261-1271. doi:10.1016/j.mayocp.2017.04.009
- Thomas RM, Amonette RA. Mohs micrographic surgery. Am Fam Physician. 1988;37:135-142.
- Buker JL, Amonette RA. Micrographic surgery. Clin Dermatol. 1992:10:309-315. doi:10.1016/0738-081x(92)90074-9
- Kauvar ANB. Mohs: the gold standard. The Skin Cancer Foundation website. Updated March 9, 2021. Accessed June 15, 2022. https://www.skincancer.org/treatment-resources/mohs-surgery/mohs-the-gold-standard/
- van Delft LCJ, Nelemans PJ, van Loo E, et al. The illusion of conventional histological resection margin control. Br J Dermatol. 2019;180:1240-1241. doi:10.1111/bjd.17510
- Warne MM, Klawonn MM, Brodell RT. Bread loaf sections provide useful information on more than 0.5% of surgical margins [published July 5, 2022]. Br J Dermatol. doi:10.1111/bjd.21740
- Mehrany K, Weenig RH, Pittelkow MR, et al. High recurrence rates of basal cell carcinoma after Mohs surgery in patients with chronic lymphocytic leukemia. Arch Dermatol. 2004;140:985-988. doi:10.1001/archderm.140.8.985
- Smeets NWJ, Krekels GAM, Ostertag JU, et al. Surgical excision vs Mohs’ micrographic surgery for basal-cell carcinoma of the face: randomised controlled trial. Lancet. 2004;364:1766-1772. doi:10.1016/S0140-6736(04)17399-6
- Gulleth Y, Goldberg N, Silverman RP, et al. What is the best surgical margin for a basal cell carcinoma: a meta-analysis of theliterature. Plast Reconstr Surg. 2010;126:1222-1231. doi:10.1097/PRS.0b013e3181ea450d
- Nahhas AF, Scarbrough CA, Trotter S. A review of the global guidelines on surgical margins for nonmelanoma skin cancers. J Clin Aesthet Dermatol. 2017;10:37-46.
- Rapini RP. Comparison of methods for checking surgical margins. J Am Acad Dermatol. 1990; 23:288-294. doi:10.1016/0190-9622(90)70212-z
Practice Points
- Margin analysis in simple excisions can provide useful information by proxy about more than the 1% of the margin often quoted in the literature.
- Simple excisions of uncomplicated keratinocytic carcinomas are associated with high cure rates.
‘Not their fault:’ Obesity warrants long-term management
This transcript has been edited for clarity.
It’s important to remember and to think about the first time when patients with obesity come to see us: What have they faced? What have been their struggles? What shame and blame and bias have they faced?
One of the first things that I do when a patient comes to see me is invite them to share their weight journey with me. I ask them to tell me about their struggles, about what’s worked and what hasn’t worked, what they would like, and what their health goals are.
As they share their stories, I look for the opportunity to share with them that obesity is not their fault, but that it’s biology driving their body to carry extra weight and their body is super smart. Neither their body nor their brain want them to starve.
Our bodies evolved during a time where there was food scarcity and the potential of famine. We have a complex system that was designed to make sure that we always held on to extra weight, specifically extra fat, because that’s how we store energy. In the current obesogenic environment, what happens is our bodies carry extra weight, or specifically, extra fat.
Again, I say to them, this is biology. Your body’s doing exactly what it was designed to do. Your body’s very smart, but now we have to figure out how to help your body want to carry less fat because it is impacting your health. This is not your fault. Having obesity is not your fault any more than having diabetes or hypertension is anyone’s fault. Now it’s time for all of us to use highly effective tools that target the pathophysiology of obesity.
When a patient comes to me for weight management or to help them treat their obesity, I listen to them, and I look for clues as to what might help that specific patient. Every patient deserves to have individualized treatment. One medicine may be right for one person, another medicine may be right for another, and surgery may be right for another patient. I really try to listen and hear what that patient is telling me.
What we as providers really need is tools – different options – to be able to provide for our patients and basically present them with different options, and then guide them toward the best therapy for them. Whether it’s semaglutide or tirzepatide potentially in the future, these types of medications are excellent options for our patients. They’re highly effective tools with safe profiles.
A question that I often get from providers or patients is, “Well, Doctor, I’ve lost the weight now. How long should I take this medicine? Can I stop it now?”
Then, we have a conversation, and we actually usually have this conversation even before we start the medicine. Basically, we talk about the fact that obesity is a chronic disease. There’s no cure for obesity. Because it’s a chronic disease, we need to treat it like we would treat any other chronic disease.
The example that I often use is, if you have a patient who has hypertension and you start them on an antihypertensive medication, what happens? Their blood pressure goes down. It improves. Now, if their blood pressure is improved with a specific antihypertensive, would you stop that medicine? What would happen if you stopped that antihypertensive? Well, their blood pressure would go up, and we wouldn’t be surprised.
In the same way, if you have a patient who has obesity and you start that patient on an antiobesity medication, and their weight decreases, and their body fat mass at that point decreases, what would happen if you stop that medicine? They lost the weight, but you stop the medicine. Well, their weight gain comes back. They regain the weight.
We should not be surprised that weight gain occurs when we stop the treatment. That really underscores the fact that treatment needs to be continued. If a patient is started on an antiobesity medication and they lose weight, that medication needs to be continued to maintain that weight loss.
Basically, we eat food and our body responds by releasing these hormones. The hormones are made in our gut and in our pancreas and these hormones inform our brain. Are we hungry? Are we full? Where are we with our homeostatic set point of fat mass? Based on that, our brain is like the sensor or the thermostat.
Obesity is a chronic, treatable disease. We should treat obesity as we treat any other chronic disease, with effective and safe approaches that target underlying disease mechanisms. These results in the SURMOUNT-1 trial underscore that tirzepatide may be doing just that. Remarkably, 9 in 10 individuals with obesity lost weight while taking tirzepatide. These results are impressive. They’re an important step forward in potentially expanding effective therapeutic options for people with obesity.
Dr. Jastreboff is an associate professor of medicine and pediatrics at Yale University, New Haven, Conn., and director of weight management and obesity prevention at Yale Stress Center. She reported conducting trials with Eli Lilly, Novo Nordisk, and Rhythm Pharmaceuticals; serving on scientific advisory boards for Ely Lilly, Intellihealth, Novo Nordisk, Pfizer, Rhythm Pharmaceuticals, and WW; and consulting for Boehringer Ingelheim and Scholar Rock.
A version of this article first appeared on Medscape.com.
This transcript has been edited for clarity.
It’s important to remember and to think about the first time when patients with obesity come to see us: What have they faced? What have been their struggles? What shame and blame and bias have they faced?
One of the first things that I do when a patient comes to see me is invite them to share their weight journey with me. I ask them to tell me about their struggles, about what’s worked and what hasn’t worked, what they would like, and what their health goals are.
As they share their stories, I look for the opportunity to share with them that obesity is not their fault, but that it’s biology driving their body to carry extra weight and their body is super smart. Neither their body nor their brain want them to starve.
Our bodies evolved during a time where there was food scarcity and the potential of famine. We have a complex system that was designed to make sure that we always held on to extra weight, specifically extra fat, because that’s how we store energy. In the current obesogenic environment, what happens is our bodies carry extra weight, or specifically, extra fat.
Again, I say to them, this is biology. Your body’s doing exactly what it was designed to do. Your body’s very smart, but now we have to figure out how to help your body want to carry less fat because it is impacting your health. This is not your fault. Having obesity is not your fault any more than having diabetes or hypertension is anyone’s fault. Now it’s time for all of us to use highly effective tools that target the pathophysiology of obesity.
When a patient comes to me for weight management or to help them treat their obesity, I listen to them, and I look for clues as to what might help that specific patient. Every patient deserves to have individualized treatment. One medicine may be right for one person, another medicine may be right for another, and surgery may be right for another patient. I really try to listen and hear what that patient is telling me.
What we as providers really need is tools – different options – to be able to provide for our patients and basically present them with different options, and then guide them toward the best therapy for them. Whether it’s semaglutide or tirzepatide potentially in the future, these types of medications are excellent options for our patients. They’re highly effective tools with safe profiles.
A question that I often get from providers or patients is, “Well, Doctor, I’ve lost the weight now. How long should I take this medicine? Can I stop it now?”
Then, we have a conversation, and we actually usually have this conversation even before we start the medicine. Basically, we talk about the fact that obesity is a chronic disease. There’s no cure for obesity. Because it’s a chronic disease, we need to treat it like we would treat any other chronic disease.
The example that I often use is, if you have a patient who has hypertension and you start them on an antihypertensive medication, what happens? Their blood pressure goes down. It improves. Now, if their blood pressure is improved with a specific antihypertensive, would you stop that medicine? What would happen if you stopped that antihypertensive? Well, their blood pressure would go up, and we wouldn’t be surprised.
In the same way, if you have a patient who has obesity and you start that patient on an antiobesity medication, and their weight decreases, and their body fat mass at that point decreases, what would happen if you stop that medicine? They lost the weight, but you stop the medicine. Well, their weight gain comes back. They regain the weight.
We should not be surprised that weight gain occurs when we stop the treatment. That really underscores the fact that treatment needs to be continued. If a patient is started on an antiobesity medication and they lose weight, that medication needs to be continued to maintain that weight loss.
Basically, we eat food and our body responds by releasing these hormones. The hormones are made in our gut and in our pancreas and these hormones inform our brain. Are we hungry? Are we full? Where are we with our homeostatic set point of fat mass? Based on that, our brain is like the sensor or the thermostat.
Obesity is a chronic, treatable disease. We should treat obesity as we treat any other chronic disease, with effective and safe approaches that target underlying disease mechanisms. These results in the SURMOUNT-1 trial underscore that tirzepatide may be doing just that. Remarkably, 9 in 10 individuals with obesity lost weight while taking tirzepatide. These results are impressive. They’re an important step forward in potentially expanding effective therapeutic options for people with obesity.
Dr. Jastreboff is an associate professor of medicine and pediatrics at Yale University, New Haven, Conn., and director of weight management and obesity prevention at Yale Stress Center. She reported conducting trials with Eli Lilly, Novo Nordisk, and Rhythm Pharmaceuticals; serving on scientific advisory boards for Ely Lilly, Intellihealth, Novo Nordisk, Pfizer, Rhythm Pharmaceuticals, and WW; and consulting for Boehringer Ingelheim and Scholar Rock.
A version of this article first appeared on Medscape.com.
This transcript has been edited for clarity.
It’s important to remember and to think about the first time when patients with obesity come to see us: What have they faced? What have been their struggles? What shame and blame and bias have they faced?
One of the first things that I do when a patient comes to see me is invite them to share their weight journey with me. I ask them to tell me about their struggles, about what’s worked and what hasn’t worked, what they would like, and what their health goals are.
As they share their stories, I look for the opportunity to share with them that obesity is not their fault, but that it’s biology driving their body to carry extra weight and their body is super smart. Neither their body nor their brain want them to starve.
Our bodies evolved during a time where there was food scarcity and the potential of famine. We have a complex system that was designed to make sure that we always held on to extra weight, specifically extra fat, because that’s how we store energy. In the current obesogenic environment, what happens is our bodies carry extra weight, or specifically, extra fat.
Again, I say to them, this is biology. Your body’s doing exactly what it was designed to do. Your body’s very smart, but now we have to figure out how to help your body want to carry less fat because it is impacting your health. This is not your fault. Having obesity is not your fault any more than having diabetes or hypertension is anyone’s fault. Now it’s time for all of us to use highly effective tools that target the pathophysiology of obesity.
When a patient comes to me for weight management or to help them treat their obesity, I listen to them, and I look for clues as to what might help that specific patient. Every patient deserves to have individualized treatment. One medicine may be right for one person, another medicine may be right for another, and surgery may be right for another patient. I really try to listen and hear what that patient is telling me.
What we as providers really need is tools – different options – to be able to provide for our patients and basically present them with different options, and then guide them toward the best therapy for them. Whether it’s semaglutide or tirzepatide potentially in the future, these types of medications are excellent options for our patients. They’re highly effective tools with safe profiles.
A question that I often get from providers or patients is, “Well, Doctor, I’ve lost the weight now. How long should I take this medicine? Can I stop it now?”
Then, we have a conversation, and we actually usually have this conversation even before we start the medicine. Basically, we talk about the fact that obesity is a chronic disease. There’s no cure for obesity. Because it’s a chronic disease, we need to treat it like we would treat any other chronic disease.
The example that I often use is, if you have a patient who has hypertension and you start them on an antihypertensive medication, what happens? Their blood pressure goes down. It improves. Now, if their blood pressure is improved with a specific antihypertensive, would you stop that medicine? What would happen if you stopped that antihypertensive? Well, their blood pressure would go up, and we wouldn’t be surprised.
In the same way, if you have a patient who has obesity and you start that patient on an antiobesity medication, and their weight decreases, and their body fat mass at that point decreases, what would happen if you stop that medicine? They lost the weight, but you stop the medicine. Well, their weight gain comes back. They regain the weight.
We should not be surprised that weight gain occurs when we stop the treatment. That really underscores the fact that treatment needs to be continued. If a patient is started on an antiobesity medication and they lose weight, that medication needs to be continued to maintain that weight loss.
Basically, we eat food and our body responds by releasing these hormones. The hormones are made in our gut and in our pancreas and these hormones inform our brain. Are we hungry? Are we full? Where are we with our homeostatic set point of fat mass? Based on that, our brain is like the sensor or the thermostat.
Obesity is a chronic, treatable disease. We should treat obesity as we treat any other chronic disease, with effective and safe approaches that target underlying disease mechanisms. These results in the SURMOUNT-1 trial underscore that tirzepatide may be doing just that. Remarkably, 9 in 10 individuals with obesity lost weight while taking tirzepatide. These results are impressive. They’re an important step forward in potentially expanding effective therapeutic options for people with obesity.
Dr. Jastreboff is an associate professor of medicine and pediatrics at Yale University, New Haven, Conn., and director of weight management and obesity prevention at Yale Stress Center. She reported conducting trials with Eli Lilly, Novo Nordisk, and Rhythm Pharmaceuticals; serving on scientific advisory boards for Ely Lilly, Intellihealth, Novo Nordisk, Pfizer, Rhythm Pharmaceuticals, and WW; and consulting for Boehringer Ingelheim and Scholar Rock.
A version of this article first appeared on Medscape.com.
Bored? Change the world or read a book
A weekend, for most of us in solo practice, doesn’t really signify time off from work. It just means we’re not seeing patients at the office.
There’s always business stuff to do (like payroll and paying bills), legal cases to review, the never-ending forms for a million things, and all the other stuff there never seems to be enough time to do on weekdays.
So this weekend I started attacking the pile after dinner on Friday and found myself done by Saturday afternoon. Which is rare, usually I spend the better part of a weekend at my desk.
And then, unexpectedly faced with an empty desk, I found myself wondering what to do.
Boredom is one of the odder human conditions. Certainly, there are more ways to waste time now than there ever have been. TV, Netflix, phone games, TikTok, books, just to name a few.
But do we always have to be entertained? Many great scientists have said that world-changing ideas have come to them when they weren’t working, such as while showering or riding to work. Leo Szilard was crossing a London street in 1933 when he suddenly saw how a nuclear chain reaction would be self-sustaining once initiated. (Fortunately, he wasn’t hit by a car in the process.)
But I’m not Szilard. So I rationalized a reason not to exercise and sat on the couch with a book.
The remarkable human brain doesn’t shut down easily. With nothing else to do, most other mammals tend to doze off. But not us. It’s always on, trying to think of the next goal, the next move, the next whatever.
Having nothing to do sounds like a great idea, until you have nothing to do. It may be fine for a few days, but after a while you realize there’s only so long you can stare at the waves or mountains before your mind turns back to “what’s next.”
This isn’t a bad thing. Being bored is probably constructive. Without realizing it we use it to form new ideas and start new plans.
Maybe this is why we’re here. The mind that keeps working is a powerful tool, driving us forward in all walks of life. Perhaps it’s this feature that pushed the development of intelligence further and led us to form civilizations.
Perhaps it’s the real reason we keep moving forward.
Dr. Block has a solo neurology practice in Scottsdale, Ariz.
A weekend, for most of us in solo practice, doesn’t really signify time off from work. It just means we’re not seeing patients at the office.
There’s always business stuff to do (like payroll and paying bills), legal cases to review, the never-ending forms for a million things, and all the other stuff there never seems to be enough time to do on weekdays.
So this weekend I started attacking the pile after dinner on Friday and found myself done by Saturday afternoon. Which is rare, usually I spend the better part of a weekend at my desk.
And then, unexpectedly faced with an empty desk, I found myself wondering what to do.
Boredom is one of the odder human conditions. Certainly, there are more ways to waste time now than there ever have been. TV, Netflix, phone games, TikTok, books, just to name a few.
But do we always have to be entertained? Many great scientists have said that world-changing ideas have come to them when they weren’t working, such as while showering or riding to work. Leo Szilard was crossing a London street in 1933 when he suddenly saw how a nuclear chain reaction would be self-sustaining once initiated. (Fortunately, he wasn’t hit by a car in the process.)
But I’m not Szilard. So I rationalized a reason not to exercise and sat on the couch with a book.
The remarkable human brain doesn’t shut down easily. With nothing else to do, most other mammals tend to doze off. But not us. It’s always on, trying to think of the next goal, the next move, the next whatever.
Having nothing to do sounds like a great idea, until you have nothing to do. It may be fine for a few days, but after a while you realize there’s only so long you can stare at the waves or mountains before your mind turns back to “what’s next.”
This isn’t a bad thing. Being bored is probably constructive. Without realizing it we use it to form new ideas and start new plans.
Maybe this is why we’re here. The mind that keeps working is a powerful tool, driving us forward in all walks of life. Perhaps it’s this feature that pushed the development of intelligence further and led us to form civilizations.
Perhaps it’s the real reason we keep moving forward.
Dr. Block has a solo neurology practice in Scottsdale, Ariz.
A weekend, for most of us in solo practice, doesn’t really signify time off from work. It just means we’re not seeing patients at the office.
There’s always business stuff to do (like payroll and paying bills), legal cases to review, the never-ending forms for a million things, and all the other stuff there never seems to be enough time to do on weekdays.
So this weekend I started attacking the pile after dinner on Friday and found myself done by Saturday afternoon. Which is rare, usually I spend the better part of a weekend at my desk.
And then, unexpectedly faced with an empty desk, I found myself wondering what to do.
Boredom is one of the odder human conditions. Certainly, there are more ways to waste time now than there ever have been. TV, Netflix, phone games, TikTok, books, just to name a few.
But do we always have to be entertained? Many great scientists have said that world-changing ideas have come to them when they weren’t working, such as while showering or riding to work. Leo Szilard was crossing a London street in 1933 when he suddenly saw how a nuclear chain reaction would be self-sustaining once initiated. (Fortunately, he wasn’t hit by a car in the process.)
But I’m not Szilard. So I rationalized a reason not to exercise and sat on the couch with a book.
The remarkable human brain doesn’t shut down easily. With nothing else to do, most other mammals tend to doze off. But not us. It’s always on, trying to think of the next goal, the next move, the next whatever.
Having nothing to do sounds like a great idea, until you have nothing to do. It may be fine for a few days, but after a while you realize there’s only so long you can stare at the waves or mountains before your mind turns back to “what’s next.”
This isn’t a bad thing. Being bored is probably constructive. Without realizing it we use it to form new ideas and start new plans.
Maybe this is why we’re here. The mind that keeps working is a powerful tool, driving us forward in all walks of life. Perhaps it’s this feature that pushed the development of intelligence further and led us to form civilizations.
Perhaps it’s the real reason we keep moving forward.
Dr. Block has a solo neurology practice in Scottsdale, Ariz.
Book Review: Quality improvement in mental health care
Sunil Khushalani and Antonio DePaolo,
“Transforming Mental Healthcare: Applying Performance Improvement Methods to Mental Healthcare”
(London: Routledge, Taylor & Francis, 2022)
Since the publication of our book, “Lean Behavioral Health: The Kings County Hospital Story” (Oxford, England: Oxford University Press, 2014) almost a decade ago, “Transforming Mental Healthcare” is the first major book published about the use of a system for quality improvement across the health care continuum. That it has taken this long is probably surprising to those of us who have spent careers on trying to improve what is universally described as a system that is “broken” and in need of a major overhaul.
Every news cycle that reports mass violence typically spends a good bit of time talking about the failures of the mental health care system. One important lesson I learned when taking over the beleaguered Kings County (N.Y.) psychiatry service in 2009 (a department that has made extraordinary improvements over the years and is now exclaimed by the U.S. Department of Justice as “a model program”), is that the employees on the front line are often erroneously blamed for such failures.
The failure is systemic and usually starts at the top of the table of organization, not at the bottom. Dr. Khushalani and Dr. DePaolo have produced an excellent volume that should be purchased by every mental health care CEO and given “with thanks” to the local leaders overseeing the direct care of some of our nation’s most vulnerable patient populations.
The first part of “Transforming Mental Healthcare” provides an excellent overview of the current state of our mental health care system and its too numerous to name problems. This section could be a primer for all our legislators so their eyes can be opened to the failures on the ground that require their help in correcting. Many of the “failures” of our mental health care are societal failures – lack of affordable housing, access to care, reimbursement for care, gun access, etc. – and cannot be “fixed” by providers of care. Such problems are societal problems that call for societal and governmental solutions, and not only at the local level but from coast to coast.
The remainder of this easy to read and follow text provides many rich resources for the deliverers of mental health care. (e.g., plan-do-act, standard work, and A3 thinking).
The closing section focuses on leadership and culture – often overlooked to the detriment of any organization that doesn’t pay close attention to supporting both. Culture is cultivated and nourished by the organization’s leaders. Culture empowers staff to become problem solvers and agents of improvement. Empowered staff support and enrich their culture. Together a workplace that brings out the best of all its people is created, and burnout is held at bay.
“Transforming Mental Healthcare: Applying Performance Improvement Methods to Mental Healthcare” is a welcome and essential addition to the current morass, which is our mental health care delivery system, an oasis in the desert from which perhaps the lotus flower can emerge.
Dr. Merlino is emeritus professor of psychiatry, SUNY Downstate College of Medicine, Rhinebeck, N.Y., and formerly director of psychiatry at Kings County Hospital Center, Brooklyn, NY. He is the coauthor of “Lean Behavioral Health: The Kings County Hospital Story.” .
Sunil Khushalani and Antonio DePaolo,
“Transforming Mental Healthcare: Applying Performance Improvement Methods to Mental Healthcare”
(London: Routledge, Taylor & Francis, 2022)
Since the publication of our book, “Lean Behavioral Health: The Kings County Hospital Story” (Oxford, England: Oxford University Press, 2014) almost a decade ago, “Transforming Mental Healthcare” is the first major book published about the use of a system for quality improvement across the health care continuum. That it has taken this long is probably surprising to those of us who have spent careers on trying to improve what is universally described as a system that is “broken” and in need of a major overhaul.
Every news cycle that reports mass violence typically spends a good bit of time talking about the failures of the mental health care system. One important lesson I learned when taking over the beleaguered Kings County (N.Y.) psychiatry service in 2009 (a department that has made extraordinary improvements over the years and is now exclaimed by the U.S. Department of Justice as “a model program”), is that the employees on the front line are often erroneously blamed for such failures.
The failure is systemic and usually starts at the top of the table of organization, not at the bottom. Dr. Khushalani and Dr. DePaolo have produced an excellent volume that should be purchased by every mental health care CEO and given “with thanks” to the local leaders overseeing the direct care of some of our nation’s most vulnerable patient populations.
The first part of “Transforming Mental Healthcare” provides an excellent overview of the current state of our mental health care system and its too numerous to name problems. This section could be a primer for all our legislators so their eyes can be opened to the failures on the ground that require their help in correcting. Many of the “failures” of our mental health care are societal failures – lack of affordable housing, access to care, reimbursement for care, gun access, etc. – and cannot be “fixed” by providers of care. Such problems are societal problems that call for societal and governmental solutions, and not only at the local level but from coast to coast.
The remainder of this easy to read and follow text provides many rich resources for the deliverers of mental health care. (e.g., plan-do-act, standard work, and A3 thinking).
The closing section focuses on leadership and culture – often overlooked to the detriment of any organization that doesn’t pay close attention to supporting both. Culture is cultivated and nourished by the organization’s leaders. Culture empowers staff to become problem solvers and agents of improvement. Empowered staff support and enrich their culture. Together a workplace that brings out the best of all its people is created, and burnout is held at bay.
“Transforming Mental Healthcare: Applying Performance Improvement Methods to Mental Healthcare” is a welcome and essential addition to the current morass, which is our mental health care delivery system, an oasis in the desert from which perhaps the lotus flower can emerge.
Dr. Merlino is emeritus professor of psychiatry, SUNY Downstate College of Medicine, Rhinebeck, N.Y., and formerly director of psychiatry at Kings County Hospital Center, Brooklyn, NY. He is the coauthor of “Lean Behavioral Health: The Kings County Hospital Story.” .
Sunil Khushalani and Antonio DePaolo,
“Transforming Mental Healthcare: Applying Performance Improvement Methods to Mental Healthcare”
(London: Routledge, Taylor & Francis, 2022)
Since the publication of our book, “Lean Behavioral Health: The Kings County Hospital Story” (Oxford, England: Oxford University Press, 2014) almost a decade ago, “Transforming Mental Healthcare” is the first major book published about the use of a system for quality improvement across the health care continuum. That it has taken this long is probably surprising to those of us who have spent careers on trying to improve what is universally described as a system that is “broken” and in need of a major overhaul.
Every news cycle that reports mass violence typically spends a good bit of time talking about the failures of the mental health care system. One important lesson I learned when taking over the beleaguered Kings County (N.Y.) psychiatry service in 2009 (a department that has made extraordinary improvements over the years and is now exclaimed by the U.S. Department of Justice as “a model program”), is that the employees on the front line are often erroneously blamed for such failures.
The failure is systemic and usually starts at the top of the table of organization, not at the bottom. Dr. Khushalani and Dr. DePaolo have produced an excellent volume that should be purchased by every mental health care CEO and given “with thanks” to the local leaders overseeing the direct care of some of our nation’s most vulnerable patient populations.
The first part of “Transforming Mental Healthcare” provides an excellent overview of the current state of our mental health care system and its too numerous to name problems. This section could be a primer for all our legislators so their eyes can be opened to the failures on the ground that require their help in correcting. Many of the “failures” of our mental health care are societal failures – lack of affordable housing, access to care, reimbursement for care, gun access, etc. – and cannot be “fixed” by providers of care. Such problems are societal problems that call for societal and governmental solutions, and not only at the local level but from coast to coast.
The remainder of this easy to read and follow text provides many rich resources for the deliverers of mental health care. (e.g., plan-do-act, standard work, and A3 thinking).
The closing section focuses on leadership and culture – often overlooked to the detriment of any organization that doesn’t pay close attention to supporting both. Culture is cultivated and nourished by the organization’s leaders. Culture empowers staff to become problem solvers and agents of improvement. Empowered staff support and enrich their culture. Together a workplace that brings out the best of all its people is created, and burnout is held at bay.
“Transforming Mental Healthcare: Applying Performance Improvement Methods to Mental Healthcare” is a welcome and essential addition to the current morass, which is our mental health care delivery system, an oasis in the desert from which perhaps the lotus flower can emerge.
Dr. Merlino is emeritus professor of psychiatry, SUNY Downstate College of Medicine, Rhinebeck, N.Y., and formerly director of psychiatry at Kings County Hospital Center, Brooklyn, NY. He is the coauthor of “Lean Behavioral Health: The Kings County Hospital Story.” .
Adapting to Changes in Acne Management: Take One Step at a Time
After most dermatology residents graduate from their programs, they go out into practice and will often carry with them what they learned from their teachers, especially clinicians. Everyone else in their dermatology residency programs approaches disease management and the use of different therapies in the same way, right?
It does not take very long before these same dermatology residents realize that things are different in real-world clinical practice in many ways. Most clinicians develop a range of fairly predictable patterns in how they approach and treat common skin disorders such as acne, rosacea, psoriasis, atopic dermatitis/eczema, and seborrheic dermatitis. These patterns often include what testing is performed at baseline and at follow-up.
Recently, I have been giving thought to how clinicians—myself included—change their approaches to management of specific skin diseases over time, especially as new information and therapies emerge. Are we fast adopters, or are we slow adopters? How much evidence do we need to see before we consider adjusting our approach? Is the needle moving too fast or not fast enough?
I would like to use an example that relates to acne treatment, especially as this is one of the most common skin disorders encountered in outpatient dermatologic practice. Despite lack of US Food and Drug Administration (FDA) approval for use in acne, oral spironolactone commonly is used in females, especially adults, with acne vulgaris and has a long history as an acceptable approach in dermatology.1 Because spironolactone is a potassium-sparing diuretic, one question that commonly arises is: Do we monitor serum potassium levels at baseline and periodically during treatment with spironolactone? There has never been a definitive consensus on which approach to take. However, there has been evidence to suggest that such monitoring is not necessary in young healthy women due to a negligible risk for clinically relevant hyperkalemia.2,3
In fact, the suggestion that there is a very low risk for clinically significant hyperkalemia in healthy young women treated with spironolactone is accurate based on population-based studies. Nevertheless, the clinician is faced with confirming the patient is in fact healthy rather than assuming this is the case due to her “young” age. In addition, it is important to exclude potential drug-drug interactions that can increase the risk for hyperkalemia when coadministered with spironolactone and also to exclude an unknown underlying decrease in renal function.1 At the end of the day, I support the continued research that is being done to evaluate questions that can challenge the recycled dogma on how we manage patients, and I do not fault those who follow what they believe to be new cogent evidence. However, in the case of oral spironolactone use, I also could never fault a clinician for monitoring renal function and electrolytes including serum potassium levels in a female patient treated for acne, especially with a drug that has the known potential to cause hyperkalemia in certain clinical situations and is not FDA approved for the indication of acne (ie, the guidance that accompanies the level of investigation needed for such FDA approval is missing). The clinical judgment of the clinician who is responsible for the individual patient trumps the results from population-based studies completed thus far. Ultimately, it is the responsibility of that clinician to assure the safety of their patient in a manner that they are comfortable with.
It takes time to make changes in our approaches to patient management, and in the majority of cases, that is rightfully so. There are several potential limitations to how certain data are collected, and a reasonable verification of results over time is what tends to change behavior patterns. Ultimately, the common goal is to do what is in the best interest of our patients. No one can argue successfully against that.
- Kim GK, Del Rosso JQ. Oral spironolactone in post-teenage female patients with acne vulgaris: practical considerations for the clinician based on current data and clinical experience. J Clin Aesthet Dermatol. 2012;5:37-50.
- Plovanich M, Weng QY, Arash Mostaghimi A. Low usefulness of potassium monitoring among healthy young women taking spironolactone for acne. JAMA Dermatol. 2015;151:941-944.
- Barbieri JS, Margolis DJ, Mostaghimi A. Temporal trends and clinician variability in potassium monitoring of healthy young women treated for acne with spironolactone. JAMA Dermatol. 2021;157:296-300.
After most dermatology residents graduate from their programs, they go out into practice and will often carry with them what they learned from their teachers, especially clinicians. Everyone else in their dermatology residency programs approaches disease management and the use of different therapies in the same way, right?
It does not take very long before these same dermatology residents realize that things are different in real-world clinical practice in many ways. Most clinicians develop a range of fairly predictable patterns in how they approach and treat common skin disorders such as acne, rosacea, psoriasis, atopic dermatitis/eczema, and seborrheic dermatitis. These patterns often include what testing is performed at baseline and at follow-up.
Recently, I have been giving thought to how clinicians—myself included—change their approaches to management of specific skin diseases over time, especially as new information and therapies emerge. Are we fast adopters, or are we slow adopters? How much evidence do we need to see before we consider adjusting our approach? Is the needle moving too fast or not fast enough?
I would like to use an example that relates to acne treatment, especially as this is one of the most common skin disorders encountered in outpatient dermatologic practice. Despite lack of US Food and Drug Administration (FDA) approval for use in acne, oral spironolactone commonly is used in females, especially adults, with acne vulgaris and has a long history as an acceptable approach in dermatology.1 Because spironolactone is a potassium-sparing diuretic, one question that commonly arises is: Do we monitor serum potassium levels at baseline and periodically during treatment with spironolactone? There has never been a definitive consensus on which approach to take. However, there has been evidence to suggest that such monitoring is not necessary in young healthy women due to a negligible risk for clinically relevant hyperkalemia.2,3
In fact, the suggestion that there is a very low risk for clinically significant hyperkalemia in healthy young women treated with spironolactone is accurate based on population-based studies. Nevertheless, the clinician is faced with confirming the patient is in fact healthy rather than assuming this is the case due to her “young” age. In addition, it is important to exclude potential drug-drug interactions that can increase the risk for hyperkalemia when coadministered with spironolactone and also to exclude an unknown underlying decrease in renal function.1 At the end of the day, I support the continued research that is being done to evaluate questions that can challenge the recycled dogma on how we manage patients, and I do not fault those who follow what they believe to be new cogent evidence. However, in the case of oral spironolactone use, I also could never fault a clinician for monitoring renal function and electrolytes including serum potassium levels in a female patient treated for acne, especially with a drug that has the known potential to cause hyperkalemia in certain clinical situations and is not FDA approved for the indication of acne (ie, the guidance that accompanies the level of investigation needed for such FDA approval is missing). The clinical judgment of the clinician who is responsible for the individual patient trumps the results from population-based studies completed thus far. Ultimately, it is the responsibility of that clinician to assure the safety of their patient in a manner that they are comfortable with.
It takes time to make changes in our approaches to patient management, and in the majority of cases, that is rightfully so. There are several potential limitations to how certain data are collected, and a reasonable verification of results over time is what tends to change behavior patterns. Ultimately, the common goal is to do what is in the best interest of our patients. No one can argue successfully against that.
After most dermatology residents graduate from their programs, they go out into practice and will often carry with them what they learned from their teachers, especially clinicians. Everyone else in their dermatology residency programs approaches disease management and the use of different therapies in the same way, right?
It does not take very long before these same dermatology residents realize that things are different in real-world clinical practice in many ways. Most clinicians develop a range of fairly predictable patterns in how they approach and treat common skin disorders such as acne, rosacea, psoriasis, atopic dermatitis/eczema, and seborrheic dermatitis. These patterns often include what testing is performed at baseline and at follow-up.
Recently, I have been giving thought to how clinicians—myself included—change their approaches to management of specific skin diseases over time, especially as new information and therapies emerge. Are we fast adopters, or are we slow adopters? How much evidence do we need to see before we consider adjusting our approach? Is the needle moving too fast or not fast enough?
I would like to use an example that relates to acne treatment, especially as this is one of the most common skin disorders encountered in outpatient dermatologic practice. Despite lack of US Food and Drug Administration (FDA) approval for use in acne, oral spironolactone commonly is used in females, especially adults, with acne vulgaris and has a long history as an acceptable approach in dermatology.1 Because spironolactone is a potassium-sparing diuretic, one question that commonly arises is: Do we monitor serum potassium levels at baseline and periodically during treatment with spironolactone? There has never been a definitive consensus on which approach to take. However, there has been evidence to suggest that such monitoring is not necessary in young healthy women due to a negligible risk for clinically relevant hyperkalemia.2,3
In fact, the suggestion that there is a very low risk for clinically significant hyperkalemia in healthy young women treated with spironolactone is accurate based on population-based studies. Nevertheless, the clinician is faced with confirming the patient is in fact healthy rather than assuming this is the case due to her “young” age. In addition, it is important to exclude potential drug-drug interactions that can increase the risk for hyperkalemia when coadministered with spironolactone and also to exclude an unknown underlying decrease in renal function.1 At the end of the day, I support the continued research that is being done to evaluate questions that can challenge the recycled dogma on how we manage patients, and I do not fault those who follow what they believe to be new cogent evidence. However, in the case of oral spironolactone use, I also could never fault a clinician for monitoring renal function and electrolytes including serum potassium levels in a female patient treated for acne, especially with a drug that has the known potential to cause hyperkalemia in certain clinical situations and is not FDA approved for the indication of acne (ie, the guidance that accompanies the level of investigation needed for such FDA approval is missing). The clinical judgment of the clinician who is responsible for the individual patient trumps the results from population-based studies completed thus far. Ultimately, it is the responsibility of that clinician to assure the safety of their patient in a manner that they are comfortable with.
It takes time to make changes in our approaches to patient management, and in the majority of cases, that is rightfully so. There are several potential limitations to how certain data are collected, and a reasonable verification of results over time is what tends to change behavior patterns. Ultimately, the common goal is to do what is in the best interest of our patients. No one can argue successfully against that.
- Kim GK, Del Rosso JQ. Oral spironolactone in post-teenage female patients with acne vulgaris: practical considerations for the clinician based on current data and clinical experience. J Clin Aesthet Dermatol. 2012;5:37-50.
- Plovanich M, Weng QY, Arash Mostaghimi A. Low usefulness of potassium monitoring among healthy young women taking spironolactone for acne. JAMA Dermatol. 2015;151:941-944.
- Barbieri JS, Margolis DJ, Mostaghimi A. Temporal trends and clinician variability in potassium monitoring of healthy young women treated for acne with spironolactone. JAMA Dermatol. 2021;157:296-300.
- Kim GK, Del Rosso JQ. Oral spironolactone in post-teenage female patients with acne vulgaris: practical considerations for the clinician based on current data and clinical experience. J Clin Aesthet Dermatol. 2012;5:37-50.
- Plovanich M, Weng QY, Arash Mostaghimi A. Low usefulness of potassium monitoring among healthy young women taking spironolactone for acne. JAMA Dermatol. 2015;151:941-944.
- Barbieri JS, Margolis DJ, Mostaghimi A. Temporal trends and clinician variability in potassium monitoring of healthy young women treated for acne with spironolactone. JAMA Dermatol. 2021;157:296-300.
What is palliative care and what’s new in practicing this type of medicine?
The World Health Organization defines palliative care as “an approach that improves the quality of life of patients (adults and children) and their families who are facing problems associated with life-threatening illness. It prevents and relieves suffering through the early identification, correct assessment, and treatment of pain and other problems, whether physical, psychosocial or spiritual.”1
The common misperception is that palliative care is only for those at end of life or only in the advanced stages of their illness. However, palliative care is ideally most helpful following individuals from diagnosis through their illness trajectory. Another misperception is that palliative care and hospice are the same thing. Though all hospice is palliative care, all palliative care is not hospice. Both palliative care and hospice provide care for individuals facing a serious illness and focus on the same philosophy of care, but palliative care can be initiated at any stage of illness, even if the goal is to pursue curative and life-prolonging therapies/interventions.
In contrast, hospice is considered for those who are at the end of life and are usually not pursuing life-prolonging therapies or interventions, instead focusing on comfort, symptom management, and optimization of quality of life.
Though there is a growing need for palliative care, there is a shortage of specialist palliative care providers. Much of the palliative care needs can be met by all providers who can offer basic symptom management, identification surrounding goals of care and discussions of advance care planning, and understanding of illness/prognosis and treatment options, which is called primary palliative care.2 In fact, two-thirds of patients with a serious illness other than cancer prefer discussion of end-of-life care or advance care planning with their primary care providers.3
Referral to specialty palliative care should be considered when there are more complexities to symptom/pain management and goals of care/end of life, transition to hospice, or complex communication dynamics.4
Though specialty palliative care was shown to be more comprehensive, both primary palliative care and specialty palliative care have led to improvements in the quality of life in individuals living with serious illness.5 Early integration of palliative care into routine care has been shown to improve symptom burden, mood, quality of life, survival, and health care costs.6
Updates in alternative and complementary therapies to palliative care
There are several alternative and complementary therapies to palliative care, including cannabis and psychedelics. These therapies are becoming or may become a familiar part of medical therapies that are listed in a patient’s history as part of their medical regimen, especially as more states continue to legalize and/or decriminalize the use of these alternative therapies for recreational or medicinal use.
Both cannabis and psychedelics have a longstanding history of therapeutic and holistic use. Cannabis has been used to manage symptoms such as pain since the 16th and 17th century.7 In palliative care, more patients may turn to various forms of cannabis as a source of relief from symptoms and suffering as their focus shifts more to quality of life.
Even with the increasing popularity of the use of cannabis among seriously ill patients, there is still a lack of evidence of the benefits of medical cannabis use in palliative care, and there is a lack of standardization of type of cannabis used and state regulations regarding their use.7
A recent systematic review found that despite the reported positive treatment effects of cannabis in palliative care, the results of the studies were conflicting. This highlights the need for further high-quality research to determine whether cannabis products are an effective treatment in palliative care patients.8
One limitation to note is that the majority of the included studies focused on cannabis use in patients with cancer for cancer-related symptoms. Few studies included patients with other serious conditions.
Psychedelics
There is evidence that psychedelic assisted therapy (PAT) is a safe and effective treatment for individuals with refractory depression, posttraumatic stress disorder, and substance use disorder.9 Plus, there have been ample studies providing support that PAT improves symptoms such as refractory anxiety/depression, demoralization, and existential distress in seriously ill patients, thus improving their quality of life and overall well-being.9
Nine U.S. cities and the State of Oregon have decriminalized or legalized the psychedelic psilocybin, based on the medical benefits patients have experienced evidenced from using it.10
In light of the increasing interest in PAT, Dr. Ira Byock provided the following points on what “all clinicians should know as they enter this uncharted territory”:
- Psychedelics have been around for a long time.
- Psychedelic-assisted therapies’ therapeutic effects are experiential.
- There are a variety of terms for specific categories of psychedelic compounds.
- Some palliative care teams are already caring for patients who undergo psychedelic experiences.
- Use of psychedelics should be well-observed by a skilled clinician with expertise.
I am hoping this provides a general refresher on palliative care and an overview of updates to alternative and complementary therapies for patients living with serious illness.9
Dr. Kang is a geriatrician and palliative care provider at the University of Washington, Seattle in the division of geriatrics and gerontology. She has no conflicts related to the content of this piece.
References
1. World Health Organization. Palliative care. 2020 Aug 5..
2. Weissman DE and Meier DE. Identifying patients in need of a palliative care assessment in the hospital setting a consensus report from the center to advance palliative care. J Palliat Med. 2011;14(1):17-23.
3. Sherry D et al. Is primary care physician involvement associated with earlier advance care planning? A study of patients in an academic primary care setting. J Palliat Med. 2022;25(1):75-80.
4. Quill TE and Abernethy AP. Generalist plus specialist palliative care-creating a more sustainable model. N Engl J Med. 2013;368:1173-75.
5. Ernecoff NC et al. Comparing specialty and primary palliative care interventions: Analysis of a systematic review. J Palliat Med. 2020;23(3):389-96.
6. Temmel JS et al. Early palliative care for patients with metastatic non–small-cell lung cancer. N Engl J Med. 2011;363:733-42.
7. Kogan M and Sexton M. Medical cannabis: A new old tool for palliative care. J Altern Complement Med . 2020 Sep;26(9):776-8.
8. Doppen M et al. Cannabis in palliative care: A systematic review of the current evidence. J Pain Symptom Manage. 2022 Jun 12;S0885-3924(22)00760-6.
9. Byock I. Psychedelics for serious illness: Five things clinicians need to know. The Center to Advance Palliative Care. Psychedelics for Serious Illness, Palliative in Practice, Center to Advance Palliative Care (capc.org). June 13, 2022.
10. Marks M. A strategy for rescheduling psilocybin. Scientific American. Oct. 11, 2021.
The World Health Organization defines palliative care as “an approach that improves the quality of life of patients (adults and children) and their families who are facing problems associated with life-threatening illness. It prevents and relieves suffering through the early identification, correct assessment, and treatment of pain and other problems, whether physical, psychosocial or spiritual.”1
The common misperception is that palliative care is only for those at end of life or only in the advanced stages of their illness. However, palliative care is ideally most helpful following individuals from diagnosis through their illness trajectory. Another misperception is that palliative care and hospice are the same thing. Though all hospice is palliative care, all palliative care is not hospice. Both palliative care and hospice provide care for individuals facing a serious illness and focus on the same philosophy of care, but palliative care can be initiated at any stage of illness, even if the goal is to pursue curative and life-prolonging therapies/interventions.
In contrast, hospice is considered for those who are at the end of life and are usually not pursuing life-prolonging therapies or interventions, instead focusing on comfort, symptom management, and optimization of quality of life.
Though there is a growing need for palliative care, there is a shortage of specialist palliative care providers. Much of the palliative care needs can be met by all providers who can offer basic symptom management, identification surrounding goals of care and discussions of advance care planning, and understanding of illness/prognosis and treatment options, which is called primary palliative care.2 In fact, two-thirds of patients with a serious illness other than cancer prefer discussion of end-of-life care or advance care planning with their primary care providers.3
Referral to specialty palliative care should be considered when there are more complexities to symptom/pain management and goals of care/end of life, transition to hospice, or complex communication dynamics.4
Though specialty palliative care was shown to be more comprehensive, both primary palliative care and specialty palliative care have led to improvements in the quality of life in individuals living with serious illness.5 Early integration of palliative care into routine care has been shown to improve symptom burden, mood, quality of life, survival, and health care costs.6
Updates in alternative and complementary therapies to palliative care
There are several alternative and complementary therapies to palliative care, including cannabis and psychedelics. These therapies are becoming or may become a familiar part of medical therapies that are listed in a patient’s history as part of their medical regimen, especially as more states continue to legalize and/or decriminalize the use of these alternative therapies for recreational or medicinal use.
Both cannabis and psychedelics have a longstanding history of therapeutic and holistic use. Cannabis has been used to manage symptoms such as pain since the 16th and 17th century.7 In palliative care, more patients may turn to various forms of cannabis as a source of relief from symptoms and suffering as their focus shifts more to quality of life.
Even with the increasing popularity of the use of cannabis among seriously ill patients, there is still a lack of evidence of the benefits of medical cannabis use in palliative care, and there is a lack of standardization of type of cannabis used and state regulations regarding their use.7
A recent systematic review found that despite the reported positive treatment effects of cannabis in palliative care, the results of the studies were conflicting. This highlights the need for further high-quality research to determine whether cannabis products are an effective treatment in palliative care patients.8
One limitation to note is that the majority of the included studies focused on cannabis use in patients with cancer for cancer-related symptoms. Few studies included patients with other serious conditions.
Psychedelics
There is evidence that psychedelic assisted therapy (PAT) is a safe and effective treatment for individuals with refractory depression, posttraumatic stress disorder, and substance use disorder.9 Plus, there have been ample studies providing support that PAT improves symptoms such as refractory anxiety/depression, demoralization, and existential distress in seriously ill patients, thus improving their quality of life and overall well-being.9
Nine U.S. cities and the State of Oregon have decriminalized or legalized the psychedelic psilocybin, based on the medical benefits patients have experienced evidenced from using it.10
In light of the increasing interest in PAT, Dr. Ira Byock provided the following points on what “all clinicians should know as they enter this uncharted territory”:
- Psychedelics have been around for a long time.
- Psychedelic-assisted therapies’ therapeutic effects are experiential.
- There are a variety of terms for specific categories of psychedelic compounds.
- Some palliative care teams are already caring for patients who undergo psychedelic experiences.
- Use of psychedelics should be well-observed by a skilled clinician with expertise.
I am hoping this provides a general refresher on palliative care and an overview of updates to alternative and complementary therapies for patients living with serious illness.9
Dr. Kang is a geriatrician and palliative care provider at the University of Washington, Seattle in the division of geriatrics and gerontology. She has no conflicts related to the content of this piece.
References
1. World Health Organization. Palliative care. 2020 Aug 5..
2. Weissman DE and Meier DE. Identifying patients in need of a palliative care assessment in the hospital setting a consensus report from the center to advance palliative care. J Palliat Med. 2011;14(1):17-23.
3. Sherry D et al. Is primary care physician involvement associated with earlier advance care planning? A study of patients in an academic primary care setting. J Palliat Med. 2022;25(1):75-80.
4. Quill TE and Abernethy AP. Generalist plus specialist palliative care-creating a more sustainable model. N Engl J Med. 2013;368:1173-75.
5. Ernecoff NC et al. Comparing specialty and primary palliative care interventions: Analysis of a systematic review. J Palliat Med. 2020;23(3):389-96.
6. Temmel JS et al. Early palliative care for patients with metastatic non–small-cell lung cancer. N Engl J Med. 2011;363:733-42.
7. Kogan M and Sexton M. Medical cannabis: A new old tool for palliative care. J Altern Complement Med . 2020 Sep;26(9):776-8.
8. Doppen M et al. Cannabis in palliative care: A systematic review of the current evidence. J Pain Symptom Manage. 2022 Jun 12;S0885-3924(22)00760-6.
9. Byock I. Psychedelics for serious illness: Five things clinicians need to know. The Center to Advance Palliative Care. Psychedelics for Serious Illness, Palliative in Practice, Center to Advance Palliative Care (capc.org). June 13, 2022.
10. Marks M. A strategy for rescheduling psilocybin. Scientific American. Oct. 11, 2021.
The World Health Organization defines palliative care as “an approach that improves the quality of life of patients (adults and children) and their families who are facing problems associated with life-threatening illness. It prevents and relieves suffering through the early identification, correct assessment, and treatment of pain and other problems, whether physical, psychosocial or spiritual.”1
The common misperception is that palliative care is only for those at end of life or only in the advanced stages of their illness. However, palliative care is ideally most helpful following individuals from diagnosis through their illness trajectory. Another misperception is that palliative care and hospice are the same thing. Though all hospice is palliative care, all palliative care is not hospice. Both palliative care and hospice provide care for individuals facing a serious illness and focus on the same philosophy of care, but palliative care can be initiated at any stage of illness, even if the goal is to pursue curative and life-prolonging therapies/interventions.
In contrast, hospice is considered for those who are at the end of life and are usually not pursuing life-prolonging therapies or interventions, instead focusing on comfort, symptom management, and optimization of quality of life.
Though there is a growing need for palliative care, there is a shortage of specialist palliative care providers. Much of the palliative care needs can be met by all providers who can offer basic symptom management, identification surrounding goals of care and discussions of advance care planning, and understanding of illness/prognosis and treatment options, which is called primary palliative care.2 In fact, two-thirds of patients with a serious illness other than cancer prefer discussion of end-of-life care or advance care planning with their primary care providers.3
Referral to specialty palliative care should be considered when there are more complexities to symptom/pain management and goals of care/end of life, transition to hospice, or complex communication dynamics.4
Though specialty palliative care was shown to be more comprehensive, both primary palliative care and specialty palliative care have led to improvements in the quality of life in individuals living with serious illness.5 Early integration of palliative care into routine care has been shown to improve symptom burden, mood, quality of life, survival, and health care costs.6
Updates in alternative and complementary therapies to palliative care
There are several alternative and complementary therapies to palliative care, including cannabis and psychedelics. These therapies are becoming or may become a familiar part of medical therapies that are listed in a patient’s history as part of their medical regimen, especially as more states continue to legalize and/or decriminalize the use of these alternative therapies for recreational or medicinal use.
Both cannabis and psychedelics have a longstanding history of therapeutic and holistic use. Cannabis has been used to manage symptoms such as pain since the 16th and 17th century.7 In palliative care, more patients may turn to various forms of cannabis as a source of relief from symptoms and suffering as their focus shifts more to quality of life.
Even with the increasing popularity of the use of cannabis among seriously ill patients, there is still a lack of evidence of the benefits of medical cannabis use in palliative care, and there is a lack of standardization of type of cannabis used and state regulations regarding their use.7
A recent systematic review found that despite the reported positive treatment effects of cannabis in palliative care, the results of the studies were conflicting. This highlights the need for further high-quality research to determine whether cannabis products are an effective treatment in palliative care patients.8
One limitation to note is that the majority of the included studies focused on cannabis use in patients with cancer for cancer-related symptoms. Few studies included patients with other serious conditions.
Psychedelics
There is evidence that psychedelic assisted therapy (PAT) is a safe and effective treatment for individuals with refractory depression, posttraumatic stress disorder, and substance use disorder.9 Plus, there have been ample studies providing support that PAT improves symptoms such as refractory anxiety/depression, demoralization, and existential distress in seriously ill patients, thus improving their quality of life and overall well-being.9
Nine U.S. cities and the State of Oregon have decriminalized or legalized the psychedelic psilocybin, based on the medical benefits patients have experienced evidenced from using it.10
In light of the increasing interest in PAT, Dr. Ira Byock provided the following points on what “all clinicians should know as they enter this uncharted territory”:
- Psychedelics have been around for a long time.
- Psychedelic-assisted therapies’ therapeutic effects are experiential.
- There are a variety of terms for specific categories of psychedelic compounds.
- Some palliative care teams are already caring for patients who undergo psychedelic experiences.
- Use of psychedelics should be well-observed by a skilled clinician with expertise.
I am hoping this provides a general refresher on palliative care and an overview of updates to alternative and complementary therapies for patients living with serious illness.9
Dr. Kang is a geriatrician and palliative care provider at the University of Washington, Seattle in the division of geriatrics and gerontology. She has no conflicts related to the content of this piece.
References
1. World Health Organization. Palliative care. 2020 Aug 5..
2. Weissman DE and Meier DE. Identifying patients in need of a palliative care assessment in the hospital setting a consensus report from the center to advance palliative care. J Palliat Med. 2011;14(1):17-23.
3. Sherry D et al. Is primary care physician involvement associated with earlier advance care planning? A study of patients in an academic primary care setting. J Palliat Med. 2022;25(1):75-80.
4. Quill TE and Abernethy AP. Generalist plus specialist palliative care-creating a more sustainable model. N Engl J Med. 2013;368:1173-75.
5. Ernecoff NC et al. Comparing specialty and primary palliative care interventions: Analysis of a systematic review. J Palliat Med. 2020;23(3):389-96.
6. Temmel JS et al. Early palliative care for patients with metastatic non–small-cell lung cancer. N Engl J Med. 2011;363:733-42.
7. Kogan M and Sexton M. Medical cannabis: A new old tool for palliative care. J Altern Complement Med . 2020 Sep;26(9):776-8.
8. Doppen M et al. Cannabis in palliative care: A systematic review of the current evidence. J Pain Symptom Manage. 2022 Jun 12;S0885-3924(22)00760-6.
9. Byock I. Psychedelics for serious illness: Five things clinicians need to know. The Center to Advance Palliative Care. Psychedelics for Serious Illness, Palliative in Practice, Center to Advance Palliative Care (capc.org). June 13, 2022.
10. Marks M. A strategy for rescheduling psilocybin. Scientific American. Oct. 11, 2021.
Caring for the young elite athlete
Concerns about the potential harm resulting from overzealous training regimens and performance schedules for young elite athletes seems to come in cycles much like the Olympics. But, more recently, the media attention has become more intense fueled by the very visible psychological vulnerabilities of some young gymnasts, tennis players, and figure skaters. Accusations of physical and psychological abuse by team physicians and coaches continue to surface with troubling regularity.
A recent article in the Wall St. Journal explores a variety of initiatives aimed at redefining the relationship between youth sports and the physical and mental health of its elite athletes. (Louise Radnofsky, The Wall Street Journal, June 9, 2022).
An example of the new awareness is the recent invitation of Peter Donnelly, PhD, an emeritus professor at the University of Toronto and long-time advocate for regulatory protections for youth athletes, to deliver a paper at a global conference in South Africa devoted to the elimination of child labor. Referring to youth sports, Dr. Donnelly observes “What if McDonalds had the same accident rate? ... There would be huge commissions of inquiry, regulations, and policies.” He suggests that the United Nations Convention on the Rights of the Child might be a mechanism to address the problem.
Writing in the Marquette University Sports Law Review in 2015, Kristin Hoffman, a law student at the time, suggested that the federal Fair Labor Standards Act or state child labor laws could be used to restructure sports like gymnastics or figure skating with tarnished histories. California law prohibits child actors from working more than 5 hours a day on school days and 7 hours on nonschool days but says little about child athletes. On paper, the National Collegiate Athletic Association limits college athletes to 20 hours participation per week but teenagers on club teams are not limited and may sometimes practice 30 hours or more.
Regulation in any form is a tough sell in this country. Coaches, parents, and athletes caught up in the myth that more repetitions and more touches on the ball are always the ticket to success will argue that most elite athletes are self-motivated and don’t view the long hours as a hardship.
Exactly how many are self-driven and how many are being pushed by parents and coaches is unknown. Across the street from us lived a young girl who, despite not having the obvious physical gifts, was clearly committed to excel in sports. She begged her parents to set up lights to allow her to practice well into the evening. She went on to have a good college career as a player and a very successful career as a Division I coach. Now in retirement, she is very open about her mental health history that in large part explains her inner drive and her subsequent troubles.
We need to be realistic in our hope for regulating the current state of youth sports out of its current situation. State laws that put reasonable limits on the hourly commitment to sports much like the California child actor laws feel like a reasonable goal. However, as physicians for these young athletes we must take each child – and we must remind ourselves that they are still children – as an individual.
When faced with patients who are clearly on the elite sport pathway, our goal is to protect their health – both physical and mental. If they are having symptoms of overuse we need to help them find alternative activities that will rest their injuries but still allow them to satisfy their competitive zeal. However, we must be ever alert to the risk that what appears to be unusual self-motivation may be instead a warning that pathologic obsession and compulsion lurk below the surface.
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.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at [email protected].
Concerns about the potential harm resulting from overzealous training regimens and performance schedules for young elite athletes seems to come in cycles much like the Olympics. But, more recently, the media attention has become more intense fueled by the very visible psychological vulnerabilities of some young gymnasts, tennis players, and figure skaters. Accusations of physical and psychological abuse by team physicians and coaches continue to surface with troubling regularity.
A recent article in the Wall St. Journal explores a variety of initiatives aimed at redefining the relationship between youth sports and the physical and mental health of its elite athletes. (Louise Radnofsky, The Wall Street Journal, June 9, 2022).
An example of the new awareness is the recent invitation of Peter Donnelly, PhD, an emeritus professor at the University of Toronto and long-time advocate for regulatory protections for youth athletes, to deliver a paper at a global conference in South Africa devoted to the elimination of child labor. Referring to youth sports, Dr. Donnelly observes “What if McDonalds had the same accident rate? ... There would be huge commissions of inquiry, regulations, and policies.” He suggests that the United Nations Convention on the Rights of the Child might be a mechanism to address the problem.
Writing in the Marquette University Sports Law Review in 2015, Kristin Hoffman, a law student at the time, suggested that the federal Fair Labor Standards Act or state child labor laws could be used to restructure sports like gymnastics or figure skating with tarnished histories. California law prohibits child actors from working more than 5 hours a day on school days and 7 hours on nonschool days but says little about child athletes. On paper, the National Collegiate Athletic Association limits college athletes to 20 hours participation per week but teenagers on club teams are not limited and may sometimes practice 30 hours or more.
Regulation in any form is a tough sell in this country. Coaches, parents, and athletes caught up in the myth that more repetitions and more touches on the ball are always the ticket to success will argue that most elite athletes are self-motivated and don’t view the long hours as a hardship.
Exactly how many are self-driven and how many are being pushed by parents and coaches is unknown. Across the street from us lived a young girl who, despite not having the obvious physical gifts, was clearly committed to excel in sports. She begged her parents to set up lights to allow her to practice well into the evening. She went on to have a good college career as a player and a very successful career as a Division I coach. Now in retirement, she is very open about her mental health history that in large part explains her inner drive and her subsequent troubles.
We need to be realistic in our hope for regulating the current state of youth sports out of its current situation. State laws that put reasonable limits on the hourly commitment to sports much like the California child actor laws feel like a reasonable goal. However, as physicians for these young athletes we must take each child – and we must remind ourselves that they are still children – as an individual.
When faced with patients who are clearly on the elite sport pathway, our goal is to protect their health – both physical and mental. If they are having symptoms of overuse we need to help them find alternative activities that will rest their injuries but still allow them to satisfy their competitive zeal. However, we must be ever alert to the risk that what appears to be unusual self-motivation may be instead a warning that pathologic obsession and compulsion lurk below the surface.
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.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at [email protected].
Concerns about the potential harm resulting from overzealous training regimens and performance schedules for young elite athletes seems to come in cycles much like the Olympics. But, more recently, the media attention has become more intense fueled by the very visible psychological vulnerabilities of some young gymnasts, tennis players, and figure skaters. Accusations of physical and psychological abuse by team physicians and coaches continue to surface with troubling regularity.
A recent article in the Wall St. Journal explores a variety of initiatives aimed at redefining the relationship between youth sports and the physical and mental health of its elite athletes. (Louise Radnofsky, The Wall Street Journal, June 9, 2022).
An example of the new awareness is the recent invitation of Peter Donnelly, PhD, an emeritus professor at the University of Toronto and long-time advocate for regulatory protections for youth athletes, to deliver a paper at a global conference in South Africa devoted to the elimination of child labor. Referring to youth sports, Dr. Donnelly observes “What if McDonalds had the same accident rate? ... There would be huge commissions of inquiry, regulations, and policies.” He suggests that the United Nations Convention on the Rights of the Child might be a mechanism to address the problem.
Writing in the Marquette University Sports Law Review in 2015, Kristin Hoffman, a law student at the time, suggested that the federal Fair Labor Standards Act or state child labor laws could be used to restructure sports like gymnastics or figure skating with tarnished histories. California law prohibits child actors from working more than 5 hours a day on school days and 7 hours on nonschool days but says little about child athletes. On paper, the National Collegiate Athletic Association limits college athletes to 20 hours participation per week but teenagers on club teams are not limited and may sometimes practice 30 hours or more.
Regulation in any form is a tough sell in this country. Coaches, parents, and athletes caught up in the myth that more repetitions and more touches on the ball are always the ticket to success will argue that most elite athletes are self-motivated and don’t view the long hours as a hardship.
Exactly how many are self-driven and how many are being pushed by parents and coaches is unknown. Across the street from us lived a young girl who, despite not having the obvious physical gifts, was clearly committed to excel in sports. She begged her parents to set up lights to allow her to practice well into the evening. She went on to have a good college career as a player and a very successful career as a Division I coach. Now in retirement, she is very open about her mental health history that in large part explains her inner drive and her subsequent troubles.
We need to be realistic in our hope for regulating the current state of youth sports out of its current situation. State laws that put reasonable limits on the hourly commitment to sports much like the California child actor laws feel like a reasonable goal. However, as physicians for these young athletes we must take each child – and we must remind ourselves that they are still children – as an individual.
When faced with patients who are clearly on the elite sport pathway, our goal is to protect their health – both physical and mental. If they are having symptoms of overuse we need to help them find alternative activities that will rest their injuries but still allow them to satisfy their competitive zeal. However, we must be ever alert to the risk that what appears to be unusual self-motivation may be instead a warning that pathologic obsession and compulsion lurk below the surface.
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.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at [email protected].





