Commentary

Recent columns on closing, selling, or merging a practice have sparked numerous questions about proper practice valuation.

Too often, physicians are not receiving a fair return on the equity they have worked so hard to build over several decades, either because they have waited too long and must accept what is offered, or because they simply take the buyer’s word for their practice’s value. Don’t put yourself in either of those positions, and don’t entertain any offers until you obtain an objective appraisal from a neutral party.

Of course, a medical practice is trickier to value than an ordinary business, and usually requires the services of an experienced professional appraiser. Entire books have been written about the process, so I can’t hope to cover it completely in 750 words; but three basic yardsticks are essential for determining the equity, or book value, of a practice:

• Tangible assets. Equipment, cash, accounts receivable, and other property owned by the practice.
• Liabilities. Accounts payable, outstanding loans, and anything else owed to others.
• Intangible assets. Sometimes called “good will” – the reputation of the physicians, the location and name recognition of the practice, the loyalty and volume of patients, and other, well, intangibles.

Valuing tangible assets is comparatively straightforward, but there are several ways to do it, and when reviewing a practice appraisal you should ask which of them was used. Depreciated value is the book value of equipment and supplies as determined by their purchase price, less the amount their value has decreased since purchase. Remaining useful life value estimates how long the equipment can be expected to last. Market (or replacement) value is the amount it would cost on the open market to replace all equipment and supplies.

Intangible assets are more difficult to value. Many components are analyzed, including location, interior and exterior decor, accessibility to patients, age and functional status of equipment, systems in place to promote efficiency, reasons why patients come back (if in fact they do), and the overall reputation of the practice in the community. Other important factors include the “payer mix” (what percentage pays cash, how many third-party contracts are in place and how well they pay, etcetera), the extent and strength of the referral base, and the presence of supplemental income streams, such as clinical research.

It is also important to determine to what extent intangible assets are transferable. For example, unique skills with a laser, neurotoxins, or filler substances, or extraordinary personal charisma, may increase your practice’s value to you, but they are worthless to the next owner, and he or she will be unwilling to pay for them unless your services become part of the deal.

Once again there are many ways to estimate intangible asset value, and once again you should ask which were used. Cash flow analysis works on the assumption that cash flow is a measure of intangible value. Capitalization of earnings puts a value, or capitalization, on the practice’s income streams using a variety of assumptions. Guideline comparison uses various databases to compare your practice with other, similar ones that have changed hands in the past.

Two newer techniques that some consider a better estimate of intangible assets are the replacement method, which estimates the costs of starting the practice over again in the current market; and the excess earnings method, which measures how far above average your practice’s earnings (and thus its overall value) are.

Asset-based valuation is the most popular, but by no means the only method available. Income-based valuation looks at the source and strength of a practice’s income stream as a creator of value, as well as whether or not its income stream under a different owner would mirror its present one. This in turn becomes the basis for an understanding of the fair market value of both tangible and intangible assets. Market valuation combines the asset-based and income-based approaches, along with an analysis of sales and mergers of comparable practices in the community, to determine the value of a practice in its local market.

Whatever methods are used, it is important that the appraisal be done by an experienced and independent financial consultant, that all techniques used in the valuation be divulged and explained, and that documentation is supplied to support the conclusions reached. This is especially important if the appraisal will be relied upon in the sale or merger of the practice.

Dr. Eastern practices dermatology and dermatologic surgery in Belleville, N.J. He is the author of numerous articles and textbook chapters, and is a longtime monthly columnist for Dermatology News. Write to him at dermnews@mdedge.com.

Recent columns on closing, selling, or merging a practice have sparked numerous questions about proper practice valuation.

Too often, physicians are not receiving a fair return on the equity they have worked so hard to build over several decades, either because they have waited too long and must accept what is offered, or because they simply take the buyer’s word for their practice’s value. Don’t put yourself in either of those positions, and don’t entertain any offers until you obtain an objective appraisal from a neutral party.

Of course, a medical practice is trickier to value than an ordinary business, and usually requires the services of an experienced professional appraiser. Entire books have been written about the process, so I can’t hope to cover it completely in 750 words; but three basic yardsticks are essential for determining the equity, or book value, of a practice:

• Tangible assets. Equipment, cash, accounts receivable, and other property owned by the practice.
• Liabilities. Accounts payable, outstanding loans, and anything else owed to others.
• Intangible assets. Sometimes called “good will” – the reputation of the physicians, the location and name recognition of the practice, the loyalty and volume of patients, and other, well, intangibles.

Valuing tangible assets is comparatively straightforward, but there are several ways to do it, and when reviewing a practice appraisal you should ask which of them was used. Depreciated value is the book value of equipment and supplies as determined by their purchase price, less the amount their value has decreased since purchase. Remaining useful life value estimates how long the equipment can be expected to last. Market (or replacement) value is the amount it would cost on the open market to replace all equipment and supplies.

Intangible assets are more difficult to value. Many components are analyzed, including location, interior and exterior decor, accessibility to patients, age and functional status of equipment, systems in place to promote efficiency, reasons why patients come back (if in fact they do), and the overall reputation of the practice in the community. Other important factors include the “payer mix” (what percentage pays cash, how many third-party contracts are in place and how well they pay, etcetera), the extent and strength of the referral base, and the presence of supplemental income streams, such as clinical research.

It is also important to determine to what extent intangible assets are transferable. For example, unique skills with a laser, neurotoxins, or filler substances, or extraordinary personal charisma, may increase your practice’s value to you, but they are worthless to the next owner, and he or she will be unwilling to pay for them unless your services become part of the deal.

Once again there are many ways to estimate intangible asset value, and once again you should ask which were used. Cash flow analysis works on the assumption that cash flow is a measure of intangible value. Capitalization of earnings puts a value, or capitalization, on the practice’s income streams using a variety of assumptions. Guideline comparison uses various databases to compare your practice with other, similar ones that have changed hands in the past.

Two newer techniques that some consider a better estimate of intangible assets are the replacement method, which estimates the costs of starting the practice over again in the current market; and the excess earnings method, which measures how far above average your practice’s earnings (and thus its overall value) are.

Asset-based valuation is the most popular, but by no means the only method available. Income-based valuation looks at the source and strength of a practice’s income stream as a creator of value, as well as whether or not its income stream under a different owner would mirror its present one. This in turn becomes the basis for an understanding of the fair market value of both tangible and intangible assets. Market valuation combines the asset-based and income-based approaches, along with an analysis of sales and mergers of comparable practices in the community, to determine the value of a practice in its local market.

Whatever methods are used, it is important that the appraisal be done by an experienced and independent financial consultant, that all techniques used in the valuation be divulged and explained, and that documentation is supplied to support the conclusions reached. This is especially important if the appraisal will be relied upon in the sale or merger of the practice.

Dr. Eastern practices dermatology and dermatologic surgery in Belleville, N.J. He is the author of numerous articles and textbook chapters, and is a longtime monthly columnist for Dermatology News. Write to him at dermnews@mdedge.com.

Recent columns on closing, selling, or merging a practice have sparked numerous questions about proper practice valuation.

Too often, physicians are not receiving a fair return on the equity they have worked so hard to build over several decades, either because they have waited too long and must accept what is offered, or because they simply take the buyer’s word for their practice’s value. Don’t put yourself in either of those positions, and don’t entertain any offers until you obtain an objective appraisal from a neutral party.

Of course, a medical practice is trickier to value than an ordinary business, and usually requires the services of an experienced professional appraiser. Entire books have been written about the process, so I can’t hope to cover it completely in 750 words; but three basic yardsticks are essential for determining the equity, or book value, of a practice:

• Tangible assets. Equipment, cash, accounts receivable, and other property owned by the practice.
• Liabilities. Accounts payable, outstanding loans, and anything else owed to others.
• Intangible assets. Sometimes called “good will” – the reputation of the physicians, the location and name recognition of the practice, the loyalty and volume of patients, and other, well, intangibles.

Valuing tangible assets is comparatively straightforward, but there are several ways to do it, and when reviewing a practice appraisal you should ask which of them was used. Depreciated value is the book value of equipment and supplies as determined by their purchase price, less the amount their value has decreased since purchase. Remaining useful life value estimates how long the equipment can be expected to last. Market (or replacement) value is the amount it would cost on the open market to replace all equipment and supplies.

Intangible assets are more difficult to value. Many components are analyzed, including location, interior and exterior decor, accessibility to patients, age and functional status of equipment, systems in place to promote efficiency, reasons why patients come back (if in fact they do), and the overall reputation of the practice in the community. Other important factors include the “payer mix” (what percentage pays cash, how many third-party contracts are in place and how well they pay, etcetera), the extent and strength of the referral base, and the presence of supplemental income streams, such as clinical research.

It is also important to determine to what extent intangible assets are transferable. For example, unique skills with a laser, neurotoxins, or filler substances, or extraordinary personal charisma, may increase your practice’s value to you, but they are worthless to the next owner, and he or she will be unwilling to pay for them unless your services become part of the deal.

Once again there are many ways to estimate intangible asset value, and once again you should ask which were used. Cash flow analysis works on the assumption that cash flow is a measure of intangible value. Capitalization of earnings puts a value, or capitalization, on the practice’s income streams using a variety of assumptions. Guideline comparison uses various databases to compare your practice with other, similar ones that have changed hands in the past.

Two newer techniques that some consider a better estimate of intangible assets are the replacement method, which estimates the costs of starting the practice over again in the current market; and the excess earnings method, which measures how far above average your practice’s earnings (and thus its overall value) are.

Asset-based valuation is the most popular, but by no means the only method available. Income-based valuation looks at the source and strength of a practice’s income stream as a creator of value, as well as whether or not its income stream under a different owner would mirror its present one. This in turn becomes the basis for an understanding of the fair market value of both tangible and intangible assets. Market valuation combines the asset-based and income-based approaches, along with an analysis of sales and mergers of comparable practices in the community, to determine the value of a practice in its local market.

Whatever methods are used, it is important that the appraisal be done by an experienced and independent financial consultant, that all techniques used in the valuation be divulged and explained, and that documentation is supplied to support the conclusions reached. This is especially important if the appraisal will be relied upon in the sale or merger of the practice.

Dr. Eastern practices dermatology and dermatologic surgery in Belleville, N.J. He is the author of numerous articles and textbook chapters, and is a longtime monthly columnist for Dermatology News. Write to him at dermnews@mdedge.com.

Motionless, every Olympic skater starts off perfectly. Once the music starts, it’s up to them whether they will continue on perfectly or not. In this way, you’re just like an Olympic skater. Each day, a skating program. The music starts the moment your foot touches the floor in the morning. It’s up to you if the rest of the day will continue on flawlessly or not. To this point, I’ve yet to have a perfect day.

If I’m honest, my “perfect day” streak typically ends once I’ve made coffee. By then, I’ll have spilled a few grains of grounds or clinked mugs together when taking one from the cupboard. (D’oh!) Hardly ever can I make it to backing out of the driveway, let alone through a patient encounter. I’ve had a few procedures that when complete I’ve thought, “well, that looks great.” I can remember encounters that went brilliantly despite a high technical difficulty. I’ve also tagged a 7-iron shot 160 downwind yards to within inches of the cup. But I’ve hardly ever done anything in my life perfectly.

What does it mean to be perfect? Well, there have been 23 perfect baseball games. In 1972, the Miami Dolphins had the only perfect NFL season, 14-0 (although my 2007 Patriots went 18-0 before losing to the – ugh – Giants). Every year, several hundred students score a perfect 1600 on the SAT. In an underground vault somewhere in France is a perfect sphere, a perfectly spherical 1-kg mass of pure silicon. There are at least 51 perfect numbers. And model Bella Hadid’s exactly 1.62-ratioed face is said to be perfectly beautiful. But yet, U.S. skater Nathan Chen’s seemingly flawless 113.97-point short program in Beijing, still imperfect.

Attempting a perfect day or perfect surgery or a perfect pour over coffee is a fun game, but perfectionism has an insidious side. Having perfectionistic concerns significantly increases the risk for burnout, depression, and eating disorders. Some of us feel this way every day: We must do it exactly right, every time. Even an insignificant imperfection or error feels like failure. A 3.90 GPA is a fail. 515 on the MCAT, not nearly good enough. For them, the burden of perfection is crushing. It is hard for some to recognize that even if your performance could not be improved, the outcome can still be flawed. A chip in the ice, a patient showing up late, an interviewer with an agenda, a missed referee call can all flub up an otherwise flawless day. It isn’t necessary to abandon hope, all ye who live in the real world. Although achieving perfection is usually impossible, reward comes from the pursuit of perfection, not from holding it. It is called perfectionistic striving and in contrast to perfectionistic concerns, it is associated with resilience and positive mood. To do so you must combine giving your all with acceptance of whatever the outcome.

Keith Jarrett is one of the greatest jazz pianists of all time. He is a true perfectionist, precise in his standards and exacting in expectations. In 1975 in Cologne, Germany, he agreed to play at the behest of a teenage girl who arranged to have him perform at the opera house. Except, there was a miscommunication and only a small, broken rehearsal piano was available. As the story goes, she approached him as he waited to be taken back to his hotel, the concert was canceled and she somehow convinced him to play on the nearly unplayable instrument. The result is the Köln Concert, one of the greatest jazz performances in history. It was perfectly imperfect.

Yes, even the 1-kg sphere has femtogram quantities of other elements mixed in – the universal standard for perfect is itself, imperfect. It doesn’t matter. It’s the pursuit of such that makes life worthwhile. There’s always tomorrow. Have your coffee grinders ready.

Dr. Benabio is director of Healthcare Transformation and chief of dermatology at Kaiser Permanente San Diego. The opinions expressed in this column are his own and do not represent those of Kaiser Permanente. Dr. Benabio is @Dermdoc on Twitter. Write to him at dermnews@mdedge.com

Motionless, every Olympic skater starts off perfectly. Once the music starts, it’s up to them whether they will continue on perfectly or not. In this way, you’re just like an Olympic skater. Each day, a skating program. The music starts the moment your foot touches the floor in the morning. It’s up to you if the rest of the day will continue on flawlessly or not. To this point, I’ve yet to have a perfect day.

If I’m honest, my “perfect day” streak typically ends once I’ve made coffee. By then, I’ll have spilled a few grains of grounds or clinked mugs together when taking one from the cupboard. (D’oh!) Hardly ever can I make it to backing out of the driveway, let alone through a patient encounter. I’ve had a few procedures that when complete I’ve thought, “well, that looks great.” I can remember encounters that went brilliantly despite a high technical difficulty. I’ve also tagged a 7-iron shot 160 downwind yards to within inches of the cup. But I’ve hardly ever done anything in my life perfectly.

What does it mean to be perfect? Well, there have been 23 perfect baseball games. In 1972, the Miami Dolphins had the only perfect NFL season, 14-0 (although my 2007 Patriots went 18-0 before losing to the – ugh – Giants). Every year, several hundred students score a perfect 1600 on the SAT. In an underground vault somewhere in France is a perfect sphere, a perfectly spherical 1-kg mass of pure silicon. There are at least 51 perfect numbers. And model Bella Hadid’s exactly 1.62-ratioed face is said to be perfectly beautiful. But yet, U.S. skater Nathan Chen’s seemingly flawless 113.97-point short program in Beijing, still imperfect.

Attempting a perfect day or perfect surgery or a perfect pour over coffee is a fun game, but perfectionism has an insidious side. Having perfectionistic concerns significantly increases the risk for burnout, depression, and eating disorders. Some of us feel this way every day: We must do it exactly right, every time. Even an insignificant imperfection or error feels like failure. A 3.90 GPA is a fail. 515 on the MCAT, not nearly good enough. For them, the burden of perfection is crushing. It is hard for some to recognize that even if your performance could not be improved, the outcome can still be flawed. A chip in the ice, a patient showing up late, an interviewer with an agenda, a missed referee call can all flub up an otherwise flawless day. It isn’t necessary to abandon hope, all ye who live in the real world. Although achieving perfection is usually impossible, reward comes from the pursuit of perfection, not from holding it. It is called perfectionistic striving and in contrast to perfectionistic concerns, it is associated with resilience and positive mood. To do so you must combine giving your all with acceptance of whatever the outcome.

Keith Jarrett is one of the greatest jazz pianists of all time. He is a true perfectionist, precise in his standards and exacting in expectations. In 1975 in Cologne, Germany, he agreed to play at the behest of a teenage girl who arranged to have him perform at the opera house. Except, there was a miscommunication and only a small, broken rehearsal piano was available. As the story goes, she approached him as he waited to be taken back to his hotel, the concert was canceled and she somehow convinced him to play on the nearly unplayable instrument. The result is the Köln Concert, one of the greatest jazz performances in history. It was perfectly imperfect.

Yes, even the 1-kg sphere has femtogram quantities of other elements mixed in – the universal standard for perfect is itself, imperfect. It doesn’t matter. It’s the pursuit of such that makes life worthwhile. There’s always tomorrow. Have your coffee grinders ready.

Dr. Benabio is director of Healthcare Transformation and chief of dermatology at Kaiser Permanente San Diego. The opinions expressed in this column are his own and do not represent those of Kaiser Permanente. Dr. Benabio is @Dermdoc on Twitter. Write to him at dermnews@mdedge.com

Motionless, every Olympic skater starts off perfectly. Once the music starts, it’s up to them whether they will continue on perfectly or not. In this way, you’re just like an Olympic skater. Each day, a skating program. The music starts the moment your foot touches the floor in the morning. It’s up to you if the rest of the day will continue on flawlessly or not. To this point, I’ve yet to have a perfect day.

If I’m honest, my “perfect day” streak typically ends once I’ve made coffee. By then, I’ll have spilled a few grains of grounds or clinked mugs together when taking one from the cupboard. (D’oh!) Hardly ever can I make it to backing out of the driveway, let alone through a patient encounter. I’ve had a few procedures that when complete I’ve thought, “well, that looks great.” I can remember encounters that went brilliantly despite a high technical difficulty. I’ve also tagged a 7-iron shot 160 downwind yards to within inches of the cup. But I’ve hardly ever done anything in my life perfectly.

What does it mean to be perfect? Well, there have been 23 perfect baseball games. In 1972, the Miami Dolphins had the only perfect NFL season, 14-0 (although my 2007 Patriots went 18-0 before losing to the – ugh – Giants). Every year, several hundred students score a perfect 1600 on the SAT. In an underground vault somewhere in France is a perfect sphere, a perfectly spherical 1-kg mass of pure silicon. There are at least 51 perfect numbers. And model Bella Hadid’s exactly 1.62-ratioed face is said to be perfectly beautiful. But yet, U.S. skater Nathan Chen’s seemingly flawless 113.97-point short program in Beijing, still imperfect.

Attempting a perfect day or perfect surgery or a perfect pour over coffee is a fun game, but perfectionism has an insidious side. Having perfectionistic concerns significantly increases the risk for burnout, depression, and eating disorders. Some of us feel this way every day: We must do it exactly right, every time. Even an insignificant imperfection or error feels like failure. A 3.90 GPA is a fail. 515 on the MCAT, not nearly good enough. For them, the burden of perfection is crushing. It is hard for some to recognize that even if your performance could not be improved, the outcome can still be flawed. A chip in the ice, a patient showing up late, an interviewer with an agenda, a missed referee call can all flub up an otherwise flawless day. It isn’t necessary to abandon hope, all ye who live in the real world. Although achieving perfection is usually impossible, reward comes from the pursuit of perfection, not from holding it. It is called perfectionistic striving and in contrast to perfectionistic concerns, it is associated with resilience and positive mood. To do so you must combine giving your all with acceptance of whatever the outcome.

Keith Jarrett is one of the greatest jazz pianists of all time. He is a true perfectionist, precise in his standards and exacting in expectations. In 1975 in Cologne, Germany, he agreed to play at the behest of a teenage girl who arranged to have him perform at the opera house. Except, there was a miscommunication and only a small, broken rehearsal piano was available. As the story goes, she approached him as he waited to be taken back to his hotel, the concert was canceled and she somehow convinced him to play on the nearly unplayable instrument. The result is the Köln Concert, one of the greatest jazz performances in history. It was perfectly imperfect.

Yes, even the 1-kg sphere has femtogram quantities of other elements mixed in – the universal standard for perfect is itself, imperfect. It doesn’t matter. It’s the pursuit of such that makes life worthwhile. There’s always tomorrow. Have your coffee grinders ready.

Dr. Benabio is director of Healthcare Transformation and chief of dermatology at Kaiser Permanente San Diego. The opinions expressed in this column are his own and do not represent those of Kaiser Permanente. Dr. Benabio is @Dermdoc on Twitter. Write to him at dermnews@mdedge.com

It is a tough time to be a doctor. With the stresses of the pandemic, the continued unfettered rise of insurance company BS, and so many medical groups being bought up that we often don’t even know who makes the decisions, the patient can sometimes be hidden in the equation.

What are ways that we can connect well with our patients so that both the patient and the physician are lifted up by the relationship?

Be curious

When physicians are curious about why patients have symptoms, how those symptoms will affect their lives, and how worried the patient is about them, patients feel cared about.

Ascertaining how concerned patients are about their symptoms will help you make decisions on whether symptoms you are not concerned about actually need to be treated.
 

Limit use of EHRs when possible

Use of the electronic health record during visits is essential, but focusing on it too much can put a barrier between the physician and the patient.

Marmor and colleagues found there is an inverse relationship between time spent on the EHR by a patient’s physician and the patient’s satisfaction.¹

Eye contact with the patient is important, especially when patients are sharing concerns they are scared about and upsetting experiences. There can be awkward pauses when looking things up on the EHR. Fill those pauses by explaining to the patient what you are doing, or chatting with the patient.
 

Consider teaching medical students

When a medical student works with you, it doubles the time the patient gets with a concerned listener. Students also can do a great job with timely follow-up and checking in with worried patients.

By having the student present in the clinic room, with the patient present, the patient can really feel heard. The student shares all the details the patient shared, and now their physician is hearing an organized, thoughtful report of the patients concerns.

In fact, I was involved in a study that showed that patients preferred in room presentations, and that they were more satisfied when students presented in the room.²
 

Use healing words

Some words carry loaded emotions. The word chronic, for example, has negative connotations, whereas the term persisting does not.

I will often ask patients how long they have been suffering from a symptom to imply my concern for what they are going through. The term “chief complaint” is outdated, and upsets patients when they see it in their medical record.

As a patient of mine once said to me: “I never complained about that problem, I just brought it to your attention.” No one wants to be seen as a complainer. Substituting the word concern for complaint works well.
 

Explain as you examine

People love to hear the term normal. When you are examining a patient, let them know when findings are normal.

I also find it helpful to explain to patients why I am doing certain physical exam maneuvers. This helps them assess how thorough we are in our thought process.

When patients feel their physicians are thorough, they have more confidence in them.
 

In summary

• Be curious.
• Do not overly focus on the EHR.
• Consider teaching a medical student.
• Be careful of word choice.
• “Overexplain” the physical exam.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and serves as 3rd-year medical student clerkship director at the University of Washington. He is a member of the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact him at imnews@mdedge.com.

References

1. Marmor RA et al. Appl Clin Inform. 2018 Jan;9(1):11-4.

2. Rogers HD et al. Acad Med. 2003 Sep;78(9):945-9.

It is a tough time to be a doctor. With the stresses of the pandemic, the continued unfettered rise of insurance company BS, and so many medical groups being bought up that we often don’t even know who makes the decisions, the patient can sometimes be hidden in the equation.

What are ways that we can connect well with our patients so that both the patient and the physician are lifted up by the relationship?

Be curious

When physicians are curious about why patients have symptoms, how those symptoms will affect their lives, and how worried the patient is about them, patients feel cared about.

Ascertaining how concerned patients are about their symptoms will help you make decisions on whether symptoms you are not concerned about actually need to be treated.
 

Limit use of EHRs when possible

Use of the electronic health record during visits is essential, but focusing on it too much can put a barrier between the physician and the patient.

Marmor and colleagues found there is an inverse relationship between time spent on the EHR by a patient’s physician and the patient’s satisfaction.¹

Eye contact with the patient is important, especially when patients are sharing concerns they are scared about and upsetting experiences. There can be awkward pauses when looking things up on the EHR. Fill those pauses by explaining to the patient what you are doing, or chatting with the patient.
 

Consider teaching medical students

When a medical student works with you, it doubles the time the patient gets with a concerned listener. Students also can do a great job with timely follow-up and checking in with worried patients.

By having the student present in the clinic room, with the patient present, the patient can really feel heard. The student shares all the details the patient shared, and now their physician is hearing an organized, thoughtful report of the patients concerns.

In fact, I was involved in a study that showed that patients preferred in room presentations, and that they were more satisfied when students presented in the room.²
 

Use healing words

Some words carry loaded emotions. The word chronic, for example, has negative connotations, whereas the term persisting does not.

I will often ask patients how long they have been suffering from a symptom to imply my concern for what they are going through. The term “chief complaint” is outdated, and upsets patients when they see it in their medical record.

As a patient of mine once said to me: “I never complained about that problem, I just brought it to your attention.” No one wants to be seen as a complainer. Substituting the word concern for complaint works well.
 

Explain as you examine

People love to hear the term normal. When you are examining a patient, let them know when findings are normal.

I also find it helpful to explain to patients why I am doing certain physical exam maneuvers. This helps them assess how thorough we are in our thought process.

When patients feel their physicians are thorough, they have more confidence in them.
 

In summary

• Be curious.
• Do not overly focus on the EHR.
• Consider teaching a medical student.
• Be careful of word choice.
• “Overexplain” the physical exam.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and serves as 3rd-year medical student clerkship director at the University of Washington. He is a member of the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact him at imnews@mdedge.com.

References

1. Marmor RA et al. Appl Clin Inform. 2018 Jan;9(1):11-4.

2. Rogers HD et al. Acad Med. 2003 Sep;78(9):945-9.

It is a tough time to be a doctor. With the stresses of the pandemic, the continued unfettered rise of insurance company BS, and so many medical groups being bought up that we often don’t even know who makes the decisions, the patient can sometimes be hidden in the equation.

What are ways that we can connect well with our patients so that both the patient and the physician are lifted up by the relationship?

Be curious

When physicians are curious about why patients have symptoms, how those symptoms will affect their lives, and how worried the patient is about them, patients feel cared about.

Ascertaining how concerned patients are about their symptoms will help you make decisions on whether symptoms you are not concerned about actually need to be treated.
 

Limit use of EHRs when possible

Use of the electronic health record during visits is essential, but focusing on it too much can put a barrier between the physician and the patient.

Marmor and colleagues found there is an inverse relationship between time spent on the EHR by a patient’s physician and the patient’s satisfaction.¹

Eye contact with the patient is important, especially when patients are sharing concerns they are scared about and upsetting experiences. There can be awkward pauses when looking things up on the EHR. Fill those pauses by explaining to the patient what you are doing, or chatting with the patient.
 

Consider teaching medical students

When a medical student works with you, it doubles the time the patient gets with a concerned listener. Students also can do a great job with timely follow-up and checking in with worried patients.

By having the student present in the clinic room, with the patient present, the patient can really feel heard. The student shares all the details the patient shared, and now their physician is hearing an organized, thoughtful report of the patients concerns.

In fact, I was involved in a study that showed that patients preferred in room presentations, and that they were more satisfied when students presented in the room.²
 

Use healing words

Some words carry loaded emotions. The word chronic, for example, has negative connotations, whereas the term persisting does not.

I will often ask patients how long they have been suffering from a symptom to imply my concern for what they are going through. The term “chief complaint” is outdated, and upsets patients when they see it in their medical record.

As a patient of mine once said to me: “I never complained about that problem, I just brought it to your attention.” No one wants to be seen as a complainer. Substituting the word concern for complaint works well.
 

Explain as you examine

People love to hear the term normal. When you are examining a patient, let them know when findings are normal.

I also find it helpful to explain to patients why I am doing certain physical exam maneuvers. This helps them assess how thorough we are in our thought process.

When patients feel their physicians are thorough, they have more confidence in them.
 

In summary

• Be curious.
• Do not overly focus on the EHR.
• Consider teaching a medical student.
• Be careful of word choice.
• “Overexplain” the physical exam.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and serves as 3rd-year medical student clerkship director at the University of Washington. He is a member of the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact him at imnews@mdedge.com.

References

1. Marmor RA et al. Appl Clin Inform. 2018 Jan;9(1):11-4.

2. Rogers HD et al. Acad Med. 2003 Sep;78(9):945-9.

Acute hemorrhagic edema of infancy (AHEI) is a leukocytoclastic vasculitis that typically affects children between 4 months and 2 years of age.¹ Etiology is unknown but the majority of cases are preceded by infections, vaccinations, or certain medications.²

AHEI is a self-limited disease that runs a benign course with spontaneous resolution within days to 3 weeks.³ Classic presentation involves acute onset of fever, purpura, ecchymosis, and inflammatory edema. Edema is often the first sign, and may involve the face, ears, scrotum, or extremities. Hemorrhagic lesions may vary in size but often coalesce and present in a distinctive “cockade” or rosette pattern with scalloped borders. Systemic manifestations are rare, but renal and joint involvement may occur.⁴ Despite the dramatic and sometimes extensive appearance of the dermatologic manifestations, patients with AHEI are usually not in significant distress.

Courtesy Dr. David Schairer

Diagnosis is clinical, but skin biopsy may show leukocytoclastic vasculitis of the superficial small vessels with infiltrations of neutrophils, extravasation of red blood cells, and fibrinoid necrosis.⁵ In most cases, immunofluorescence is negative for perivascular IgA deposition. Treatment is symptomatic as the disease resolves spontaneously. Recurrence is uncommon but may occur, and usually occurs early.

 

What is on the differential?

Kawasaki disease. Similar to AHEI, patients with Kawasaki disease also may present with facial and extremity edema. However, patients with Kawasaki disease appear sicker, have associated lymphadenopathy, conjunctivitis, and fever longer than 5 days. The lack of elevated inflammatory markers, acute-onset, classic dermatologic lesions, and nontoxic appearance in our patient rule out Kawasaki disease and make AHEI more likely.

IgA vasculitis/Henoch-Schönlein purpura. The distinction between AHEI and Henoch-Schönlein purpura is among the most challenging. AHEI commonly afflicts younger children ranging from 4 months to 2 years, whereas Henoch-Schönlein purpura occurs in older children from 3 to 6 years of age. Visceral involvement is rare in AHEI, but frequently presents in Henoch-Schönlein purpura with gastrointestinal and renal complications. Although our patient had both mild renal involvement and a distribution primarily on the buttocks and lower limbs, similar to the classic distribution of Henoch-Schönlein purpura, the younger age and lack of gastrointestinal and arthritic manifestations make AHEI more likely.

Gianotti-Crosti syndrome. Gianotti-Crosti syndrome, also known as papulovesicular acrodermatitis of childhood, mainly affects children between the ages of 6 months and 12 years. Like AHEI, Gianotti-Crosti is a self-limiting condition likely triggered by viral infection or immunization. However, Gianotti-Crosti is characterized by a papular rash that may last for several weeks. Neither AHEI nor Gianotti-Crosti are pruritic, but patients with Gianotti-Crosti tend to have either inguinal or axillary lymphadenopathy. Our patient’s large, coalescing dusky red patches and edematous plaques without lymphadenopathy are more consistent with AHEI.

Courtesy Dr. David Schairer

Erythema multiforme. Erythema multiforme is an acute, immune-mediated condition characterized by distinctive target-like lesions on the skin often accompanied by erosions or bullae. Unlike AHEI, erythema multiforme can involve the oral, genital, and/or ocular mucosae. Erythema multiforme is rare before the age of 4 years. Although the targetoid or annular purpuric configuration of erythema multiforme may present similarly to AHEI in some cases, the young age of our patient and the lack of mucosal involvement make AHEI more likely.

Dr. Matiz is a pediatric dermatologist at Southern California Permanente Medical Group, San Diego. Ms. Kleinman is a pediatric dermatology research associate at the University of California, San Diego, and Rady Children’s Hospital, San Diego. Neither Dr. Matiz nor Ms. Kleinman has any relevant financial disclosures.

References

1. Savino F et al. Pediatr Dermatol. 2013;30(6):e149-e152.

2. Carboni E et al. F1000Res. 2019;8:1771. 2019 Oct 17.

3. Fiore E et al. J Am Acad Dermatol. 2008;59(4):684-95.

4. Watanabe T and Sato Y. Pediatr Nephrol. 2007;22(11):1979-81.

5. Cunha DF et al. Autops Case Rep. 2015;5(3):37-41.

Acute hemorrhagic edema of infancy (AHEI) is a leukocytoclastic vasculitis that typically affects children between 4 months and 2 years of age.¹ Etiology is unknown but the majority of cases are preceded by infections, vaccinations, or certain medications.²

AHEI is a self-limited disease that runs a benign course with spontaneous resolution within days to 3 weeks.³ Classic presentation involves acute onset of fever, purpura, ecchymosis, and inflammatory edema. Edema is often the first sign, and may involve the face, ears, scrotum, or extremities. Hemorrhagic lesions may vary in size but often coalesce and present in a distinctive “cockade” or rosette pattern with scalloped borders. Systemic manifestations are rare, but renal and joint involvement may occur.⁴ Despite the dramatic and sometimes extensive appearance of the dermatologic manifestations, patients with AHEI are usually not in significant distress.

Courtesy Dr. David Schairer

Diagnosis is clinical, but skin biopsy may show leukocytoclastic vasculitis of the superficial small vessels with infiltrations of neutrophils, extravasation of red blood cells, and fibrinoid necrosis.⁵ In most cases, immunofluorescence is negative for perivascular IgA deposition. Treatment is symptomatic as the disease resolves spontaneously. Recurrence is uncommon but may occur, and usually occurs early.

 

What is on the differential?

Kawasaki disease. Similar to AHEI, patients with Kawasaki disease also may present with facial and extremity edema. However, patients with Kawasaki disease appear sicker, have associated lymphadenopathy, conjunctivitis, and fever longer than 5 days. The lack of elevated inflammatory markers, acute-onset, classic dermatologic lesions, and nontoxic appearance in our patient rule out Kawasaki disease and make AHEI more likely.

IgA vasculitis/Henoch-Schönlein purpura. The distinction between AHEI and Henoch-Schönlein purpura is among the most challenging. AHEI commonly afflicts younger children ranging from 4 months to 2 years, whereas Henoch-Schönlein purpura occurs in older children from 3 to 6 years of age. Visceral involvement is rare in AHEI, but frequently presents in Henoch-Schönlein purpura with gastrointestinal and renal complications. Although our patient had both mild renal involvement and a distribution primarily on the buttocks and lower limbs, similar to the classic distribution of Henoch-Schönlein purpura, the younger age and lack of gastrointestinal and arthritic manifestations make AHEI more likely.

Gianotti-Crosti syndrome. Gianotti-Crosti syndrome, also known as papulovesicular acrodermatitis of childhood, mainly affects children between the ages of 6 months and 12 years. Like AHEI, Gianotti-Crosti is a self-limiting condition likely triggered by viral infection or immunization. However, Gianotti-Crosti is characterized by a papular rash that may last for several weeks. Neither AHEI nor Gianotti-Crosti are pruritic, but patients with Gianotti-Crosti tend to have either inguinal or axillary lymphadenopathy. Our patient’s large, coalescing dusky red patches and edematous plaques without lymphadenopathy are more consistent with AHEI.

Courtesy Dr. David Schairer

Erythema multiforme. Erythema multiforme is an acute, immune-mediated condition characterized by distinctive target-like lesions on the skin often accompanied by erosions or bullae. Unlike AHEI, erythema multiforme can involve the oral, genital, and/or ocular mucosae. Erythema multiforme is rare before the age of 4 years. Although the targetoid or annular purpuric configuration of erythema multiforme may present similarly to AHEI in some cases, the young age of our patient and the lack of mucosal involvement make AHEI more likely.

Dr. Matiz is a pediatric dermatologist at Southern California Permanente Medical Group, San Diego. Ms. Kleinman is a pediatric dermatology research associate at the University of California, San Diego, and Rady Children’s Hospital, San Diego. Neither Dr. Matiz nor Ms. Kleinman has any relevant financial disclosures.

References

1. Savino F et al. Pediatr Dermatol. 2013;30(6):e149-e152.

2. Carboni E et al. F1000Res. 2019;8:1771. 2019 Oct 17.

3. Fiore E et al. J Am Acad Dermatol. 2008;59(4):684-95.

4. Watanabe T and Sato Y. Pediatr Nephrol. 2007;22(11):1979-81.

5. Cunha DF et al. Autops Case Rep. 2015;5(3):37-41.

Acute hemorrhagic edema of infancy (AHEI) is a leukocytoclastic vasculitis that typically affects children between 4 months and 2 years of age.¹ Etiology is unknown but the majority of cases are preceded by infections, vaccinations, or certain medications.²

AHEI is a self-limited disease that runs a benign course with spontaneous resolution within days to 3 weeks.³ Classic presentation involves acute onset of fever, purpura, ecchymosis, and inflammatory edema. Edema is often the first sign, and may involve the face, ears, scrotum, or extremities. Hemorrhagic lesions may vary in size but often coalesce and present in a distinctive “cockade” or rosette pattern with scalloped borders. Systemic manifestations are rare, but renal and joint involvement may occur.⁴ Despite the dramatic and sometimes extensive appearance of the dermatologic manifestations, patients with AHEI are usually not in significant distress.

Courtesy Dr. David Schairer

Diagnosis is clinical, but skin biopsy may show leukocytoclastic vasculitis of the superficial small vessels with infiltrations of neutrophils, extravasation of red blood cells, and fibrinoid necrosis.⁵ In most cases, immunofluorescence is negative for perivascular IgA deposition. Treatment is symptomatic as the disease resolves spontaneously. Recurrence is uncommon but may occur, and usually occurs early.

 

What is on the differential?

Kawasaki disease. Similar to AHEI, patients with Kawasaki disease also may present with facial and extremity edema. However, patients with Kawasaki disease appear sicker, have associated lymphadenopathy, conjunctivitis, and fever longer than 5 days. The lack of elevated inflammatory markers, acute-onset, classic dermatologic lesions, and nontoxic appearance in our patient rule out Kawasaki disease and make AHEI more likely.

IgA vasculitis/Henoch-Schönlein purpura. The distinction between AHEI and Henoch-Schönlein purpura is among the most challenging. AHEI commonly afflicts younger children ranging from 4 months to 2 years, whereas Henoch-Schönlein purpura occurs in older children from 3 to 6 years of age. Visceral involvement is rare in AHEI, but frequently presents in Henoch-Schönlein purpura with gastrointestinal and renal complications. Although our patient had both mild renal involvement and a distribution primarily on the buttocks and lower limbs, similar to the classic distribution of Henoch-Schönlein purpura, the younger age and lack of gastrointestinal and arthritic manifestations make AHEI more likely.

Gianotti-Crosti syndrome. Gianotti-Crosti syndrome, also known as papulovesicular acrodermatitis of childhood, mainly affects children between the ages of 6 months and 12 years. Like AHEI, Gianotti-Crosti is a self-limiting condition likely triggered by viral infection or immunization. However, Gianotti-Crosti is characterized by a papular rash that may last for several weeks. Neither AHEI nor Gianotti-Crosti are pruritic, but patients with Gianotti-Crosti tend to have either inguinal or axillary lymphadenopathy. Our patient’s large, coalescing dusky red patches and edematous plaques without lymphadenopathy are more consistent with AHEI.

Courtesy Dr. David Schairer

Erythema multiforme. Erythema multiforme is an acute, immune-mediated condition characterized by distinctive target-like lesions on the skin often accompanied by erosions or bullae. Unlike AHEI, erythema multiforme can involve the oral, genital, and/or ocular mucosae. Erythema multiforme is rare before the age of 4 years. Although the targetoid or annular purpuric configuration of erythema multiforme may present similarly to AHEI in some cases, the young age of our patient and the lack of mucosal involvement make AHEI more likely.

Dr. Matiz is a pediatric dermatologist at Southern California Permanente Medical Group, San Diego. Ms. Kleinman is a pediatric dermatology research associate at the University of California, San Diego, and Rady Children’s Hospital, San Diego. Neither Dr. Matiz nor Ms. Kleinman has any relevant financial disclosures.

References

1. Savino F et al. Pediatr Dermatol. 2013;30(6):e149-e152.

2. Carboni E et al. F1000Res. 2019;8:1771. 2019 Oct 17.

3. Fiore E et al. J Am Acad Dermatol. 2008;59(4):684-95.

4. Watanabe T and Sato Y. Pediatr Nephrol. 2007;22(11):1979-81.

5. Cunha DF et al. Autops Case Rep. 2015;5(3):37-41.

Erythema multiforme (EM) is a hypersensitivity reaction commonly caused by herpes simplex virus (HSV) infection. Less frequently observable infectious agents associated with EM are Mycoplasma pneumoniae, Histoplasma capsulatum, and parapoxvirus (orf). Rarely, EM is triggered by drug eruption or systemic disease. Individuals of all age groups and races can be affected by EM. However, it is predominantly observed in young adult patients (20-40 years of age), and there is a male predominance.

Patients typically present with the abrupt onset of symmetrical red papules that evolve into typical and atypical targetoid lesions. Lesions evolve in 48-72 hours, favoring acrofacial sites that then spread down towards the trunk. Systemic symptoms such as fever and arthralgia may accompany the skin lesions.^1-3

Erythema multiforme is recognized in two forms: EM minor and EM major. Both forms share the same characteristic of target lesions. However, the presence of mucosal involvement distinguishes the two. Mucosal involvement is absent or mild in EM minor, while mucosal involvement in EM major is often severe.^2,3 Painful bullous lesions are commonly present in the mouth, genital, and ocular mucous membranes. Severe symptoms can often result in difficulty eating and drinking.

Diagnosis is largely clinical. Further histologic study may accompany diagnoses to exclude differential diagnosis. In EM, direct immunofluorescence (DIF) is negative. Histopathology reveals apoptosis of individual keratinocytes.^1,2

Therapeutic treatment for painful bullous lesions in the mouth involve antiseptic rinses and anesthetic solutions. Preventive treatment for patients with HSV-associated EM recurrence includes oral acyclovir or valacyclovir.²

In this patient, a punch biopsy was performed, confirming the diagnosis. A DIF was negative, and a chest x-ray was negative. Treatment was initiated with oral acyclovir, doxycycline, and a prednisone taper. In addition, topical clobetasol propionate and magic mouthwash (Maalox/lidocaine/nystatin) was prescribed. The patient was placed on daily suppressive valacyclovir to prevent frequent recurrence of EM.

This case and photo were submitted by Ms. Pham, the University of California, Los Angeles, and Dr. Sateesh, San Diego Family Dermatology. Dr. Bilu-Martin edited the column.

Dr. Bilu Martin is a board-certified dermatologist in private practice at Premier Dermatology, MD, in Aventura, Fla. More diagnostic cases are available at mdedge.com/dermatology. To submit a case for possible publication, send an email to dermnews@mdedge.com.

References

1. Hafsi W and Badri T. Erythema Multiforme, in “StatPearls [Internet].” Treasure Island, Fla.: StatPearls Publishing, 2022 Jan.

2. Bolognia J et al. Dermatology. St. Louis: Mosby/Elsevier, 2008.

3. Oakley A. Erythema Multiforme. DermNet NZ. 2015 Oct.

Erythema multiforme (EM) is a hypersensitivity reaction commonly caused by herpes simplex virus (HSV) infection. Less frequently observable infectious agents associated with EM are Mycoplasma pneumoniae, Histoplasma capsulatum, and parapoxvirus (orf). Rarely, EM is triggered by drug eruption or systemic disease. Individuals of all age groups and races can be affected by EM. However, it is predominantly observed in young adult patients (20-40 years of age), and there is a male predominance.

Patients typically present with the abrupt onset of symmetrical red papules that evolve into typical and atypical targetoid lesions. Lesions evolve in 48-72 hours, favoring acrofacial sites that then spread down towards the trunk. Systemic symptoms such as fever and arthralgia may accompany the skin lesions.^1-3

Erythema multiforme is recognized in two forms: EM minor and EM major. Both forms share the same characteristic of target lesions. However, the presence of mucosal involvement distinguishes the two. Mucosal involvement is absent or mild in EM minor, while mucosal involvement in EM major is often severe.^2,3 Painful bullous lesions are commonly present in the mouth, genital, and ocular mucous membranes. Severe symptoms can often result in difficulty eating and drinking.

Diagnosis is largely clinical. Further histologic study may accompany diagnoses to exclude differential diagnosis. In EM, direct immunofluorescence (DIF) is negative. Histopathology reveals apoptosis of individual keratinocytes.^1,2

Therapeutic treatment for painful bullous lesions in the mouth involve antiseptic rinses and anesthetic solutions. Preventive treatment for patients with HSV-associated EM recurrence includes oral acyclovir or valacyclovir.²

In this patient, a punch biopsy was performed, confirming the diagnosis. A DIF was negative, and a chest x-ray was negative. Treatment was initiated with oral acyclovir, doxycycline, and a prednisone taper. In addition, topical clobetasol propionate and magic mouthwash (Maalox/lidocaine/nystatin) was prescribed. The patient was placed on daily suppressive valacyclovir to prevent frequent recurrence of EM.

This case and photo were submitted by Ms. Pham, the University of California, Los Angeles, and Dr. Sateesh, San Diego Family Dermatology. Dr. Bilu-Martin edited the column.

Dr. Bilu Martin is a board-certified dermatologist in private practice at Premier Dermatology, MD, in Aventura, Fla. More diagnostic cases are available at mdedge.com/dermatology. To submit a case for possible publication, send an email to dermnews@mdedge.com.

References

1. Hafsi W and Badri T. Erythema Multiforme, in “StatPearls [Internet].” Treasure Island, Fla.: StatPearls Publishing, 2022 Jan.

2. Bolognia J et al. Dermatology. St. Louis: Mosby/Elsevier, 2008.

3. Oakley A. Erythema Multiforme. DermNet NZ. 2015 Oct.

Erythema multiforme (EM) is a hypersensitivity reaction commonly caused by herpes simplex virus (HSV) infection. Less frequently observable infectious agents associated with EM are Mycoplasma pneumoniae, Histoplasma capsulatum, and parapoxvirus (orf). Rarely, EM is triggered by drug eruption or systemic disease. Individuals of all age groups and races can be affected by EM. However, it is predominantly observed in young adult patients (20-40 years of age), and there is a male predominance.

Patients typically present with the abrupt onset of symmetrical red papules that evolve into typical and atypical targetoid lesions. Lesions evolve in 48-72 hours, favoring acrofacial sites that then spread down towards the trunk. Systemic symptoms such as fever and arthralgia may accompany the skin lesions.^1-3

Erythema multiforme is recognized in two forms: EM minor and EM major. Both forms share the same characteristic of target lesions. However, the presence of mucosal involvement distinguishes the two. Mucosal involvement is absent or mild in EM minor, while mucosal involvement in EM major is often severe.^2,3 Painful bullous lesions are commonly present in the mouth, genital, and ocular mucous membranes. Severe symptoms can often result in difficulty eating and drinking.

Diagnosis is largely clinical. Further histologic study may accompany diagnoses to exclude differential diagnosis. In EM, direct immunofluorescence (DIF) is negative. Histopathology reveals apoptosis of individual keratinocytes.^1,2

Therapeutic treatment for painful bullous lesions in the mouth involve antiseptic rinses and anesthetic solutions. Preventive treatment for patients with HSV-associated EM recurrence includes oral acyclovir or valacyclovir.²

In this patient, a punch biopsy was performed, confirming the diagnosis. A DIF was negative, and a chest x-ray was negative. Treatment was initiated with oral acyclovir, doxycycline, and a prednisone taper. In addition, topical clobetasol propionate and magic mouthwash (Maalox/lidocaine/nystatin) was prescribed. The patient was placed on daily suppressive valacyclovir to prevent frequent recurrence of EM.

This case and photo were submitted by Ms. Pham, the University of California, Los Angeles, and Dr. Sateesh, San Diego Family Dermatology. Dr. Bilu-Martin edited the column.

Dr. Bilu Martin is a board-certified dermatologist in private practice at Premier Dermatology, MD, in Aventura, Fla. More diagnostic cases are available at mdedge.com/dermatology. To submit a case for possible publication, send an email to dermnews@mdedge.com.

References

1. Hafsi W and Badri T. Erythema Multiforme, in “StatPearls [Internet].” Treasure Island, Fla.: StatPearls Publishing, 2022 Jan.

2. Bolognia J et al. Dermatology. St. Louis: Mosby/Elsevier, 2008.

3. Oakley A. Erythema Multiforme. DermNet NZ. 2015 Oct.

Improved treatments for breast cancer (BC) and effective screening programs have resulted in a BC mortality rate reduction of 41% since 1989.¹ Because BC is the leading cause of cancer in women, these mortality improvements have resulted in more than 3 million BC survivors in the United States.^2,3 With longer-term survival, there is increasing interest in late-onset recurrences.^4,5 A recent study has provided an improved understanding of the risk of lateonset recurrence in women with 10 years of disease-free survival, an important finding for women’s health providers because oncologists do not typically follow survivors after 10 years of disease-free survival.⁴

Recent study looks at incidence of late-onset recurrence

Pederson and colleagues evaluated all patients diagnosed with BC in Denmark from 1987 through 2004.⁴ Those patients without evidence of recurrence at 10 years were then followed utilizing population-based linked registries to identify patients who subsequently developed a local, regional, or distant late-onset recurrence. The authors evaluated the frequency of late recurrence and identified associations with demographic and tumor characteristics.

What they found

A total of 36,920 patients were diagnosed with BC in Denmark between 1987-2004, of whom 20,315 (55%) were identified as disease free for at least 10 years. Late-onset recurrence occurred in 2,595 (12.8%) with the strongest associations of recurrence seen in patients who had a tumor size >2 cm and lymph node‒positive (involving 4 or more nodes) disease (24.6%), compared with 12.7% in patients with tumors <2 cm and node-negative disease. Several other factors were associated with a higher risk of late-onset recurrence and are included in the TABLE. Half of the recurrences occurred between 10 and 15 years after the primary diagnosis.

Prior research

These findings are consistent with another recent study showing that BC patients have a 1% to 2%/year risk of recurrence after 10 disease-free years.⁵ Strengths of this study include:

• population-based, including all women with BC
• long-term follow-up for up to 32 years
• universal health care in Denmark, which results in robust and linked databases and very few missing data points.

There were two notable weaknesses to consider:

• Treatment regimens changed considerably during the time frame of the study (1997-2018), particularly the duration of tamoxifen use in patients with HR-positive disease. In this study nearly all patients received 5 years or less of tamoxifen. Since the mid-2010s, 10 years of hormonal adjuvant therapy has become routine in HR-positive BC, which reduces recurrences, including late-onset recurrence.⁶ The effect of 10 years of tamoxifen would very likely have resulted in less late-onset recurrence in the HR-positive population in this study.
• There is a lack of racial diversity in the Danish population, and the study findings may not translate to Black patients who have a higher frequency of triple-negative BC with a different risk of late-onset recurrence.⁷

Practice takeaways

Cancer surveillance. There are 3+ million BC survivors in the United States, and a 55%+ likelihood that they will be disease free for 10 years. This is clearly an important population to the women’s health care provider. This study, and previous research, suggests that among 10-year-disease-free survivors, 1% to 2% will recur annually, with higher rates amongst HR-positive, lymph-node positive women under age 40, and in the first 5 years following the 10-year post–initial diagnosis mark, so ongoing surveillance is imperative. Annual clinical breast examinations along with annual (not biennial) mammography should be performed.⁸ Digital breast tomosynthesis has improved specificity and sensitivity for BC detection and is the preferred modality when it is available.

Management of menopausal symptoms. These findings also have implications for menopausal hormone therapy for patients with symptoms. Because HR-positive patients have an increased risk of late-onset recurrence, nonhormonal therapies should be considered as first-line therapy for patients with menopausal symptoms. If hormone therapy is being considered, providers and patients should use shared decision making to balance the potential benefits (reduction in symptoms, possible cardiovascular benefits, and reduction in bone loss) with the risks (increased risk of recurrence and venous thromboembolism), even if patients are remote from the original diagnosis (ie, 10-year disease-free survival).

Topical estrogen therapies would be preferred for patients with significant urogenital atrophic symptoms who fail nonhormonal therapies due to substantially less systemic absorption and the lack of need to add a progestin.^9,10 If oral therapy is being considered, I carefully counsel these women about the likely increased risk of recurrence and, if possible, include their breast oncologist in the discussion. ●

Improved treatments for breast cancer (BC) and effective screening programs have resulted in a BC mortality rate reduction of 41% since 1989.¹ Because BC is the leading cause of cancer in women, these mortality improvements have resulted in more than 3 million BC survivors in the United States.^2,3 With longer-term survival, there is increasing interest in late-onset recurrences.^4,5 A recent study has provided an improved understanding of the risk of lateonset recurrence in women with 10 years of disease-free survival, an important finding for women’s health providers because oncologists do not typically follow survivors after 10 years of disease-free survival.⁴

Recent study looks at incidence of late-onset recurrence

Pederson and colleagues evaluated all patients diagnosed with BC in Denmark from 1987 through 2004.⁴ Those patients without evidence of recurrence at 10 years were then followed utilizing population-based linked registries to identify patients who subsequently developed a local, regional, or distant late-onset recurrence. The authors evaluated the frequency of late recurrence and identified associations with demographic and tumor characteristics.

What they found

A total of 36,920 patients were diagnosed with BC in Denmark between 1987-2004, of whom 20,315 (55%) were identified as disease free for at least 10 years. Late-onset recurrence occurred in 2,595 (12.8%) with the strongest associations of recurrence seen in patients who had a tumor size >2 cm and lymph node‒positive (involving 4 or more nodes) disease (24.6%), compared with 12.7% in patients with tumors <2 cm and node-negative disease. Several other factors were associated with a higher risk of late-onset recurrence and are included in the TABLE. Half of the recurrences occurred between 10 and 15 years after the primary diagnosis.

Prior research

These findings are consistent with another recent study showing that BC patients have a 1% to 2%/year risk of recurrence after 10 disease-free years.⁵ Strengths of this study include:

• population-based, including all women with BC
• long-term follow-up for up to 32 years
• universal health care in Denmark, which results in robust and linked databases and very few missing data points.

There were two notable weaknesses to consider:

• Treatment regimens changed considerably during the time frame of the study (1997-2018), particularly the duration of tamoxifen use in patients with HR-positive disease. In this study nearly all patients received 5 years or less of tamoxifen. Since the mid-2010s, 10 years of hormonal adjuvant therapy has become routine in HR-positive BC, which reduces recurrences, including late-onset recurrence.⁶ The effect of 10 years of tamoxifen would very likely have resulted in less late-onset recurrence in the HR-positive population in this study.
• There is a lack of racial diversity in the Danish population, and the study findings may not translate to Black patients who have a higher frequency of triple-negative BC with a different risk of late-onset recurrence.⁷

Practice takeaways

Cancer surveillance. There are 3+ million BC survivors in the United States, and a 55%+ likelihood that they will be disease free for 10 years. This is clearly an important population to the women’s health care provider. This study, and previous research, suggests that among 10-year-disease-free survivors, 1% to 2% will recur annually, with higher rates amongst HR-positive, lymph-node positive women under age 40, and in the first 5 years following the 10-year post–initial diagnosis mark, so ongoing surveillance is imperative. Annual clinical breast examinations along with annual (not biennial) mammography should be performed.⁸ Digital breast tomosynthesis has improved specificity and sensitivity for BC detection and is the preferred modality when it is available.

Management of menopausal symptoms. These findings also have implications for menopausal hormone therapy for patients with symptoms. Because HR-positive patients have an increased risk of late-onset recurrence, nonhormonal therapies should be considered as first-line therapy for patients with menopausal symptoms. If hormone therapy is being considered, providers and patients should use shared decision making to balance the potential benefits (reduction in symptoms, possible cardiovascular benefits, and reduction in bone loss) with the risks (increased risk of recurrence and venous thromboembolism), even if patients are remote from the original diagnosis (ie, 10-year disease-free survival).

Topical estrogen therapies would be preferred for patients with significant urogenital atrophic symptoms who fail nonhormonal therapies due to substantially less systemic absorption and the lack of need to add a progestin.^9,10 If oral therapy is being considered, I carefully counsel these women about the likely increased risk of recurrence and, if possible, include their breast oncologist in the discussion. ●

Improved treatments for breast cancer (BC) and effective screening programs have resulted in a BC mortality rate reduction of 41% since 1989.¹ Because BC is the leading cause of cancer in women, these mortality improvements have resulted in more than 3 million BC survivors in the United States.^2,3 With longer-term survival, there is increasing interest in late-onset recurrences.^4,5 A recent study has provided an improved understanding of the risk of lateonset recurrence in women with 10 years of disease-free survival, an important finding for women’s health providers because oncologists do not typically follow survivors after 10 years of disease-free survival.⁴

Recent study looks at incidence of late-onset recurrence

Pederson and colleagues evaluated all patients diagnosed with BC in Denmark from 1987 through 2004.⁴ Those patients without evidence of recurrence at 10 years were then followed utilizing population-based linked registries to identify patients who subsequently developed a local, regional, or distant late-onset recurrence. The authors evaluated the frequency of late recurrence and identified associations with demographic and tumor characteristics.

What they found

A total of 36,920 patients were diagnosed with BC in Denmark between 1987-2004, of whom 20,315 (55%) were identified as disease free for at least 10 years. Late-onset recurrence occurred in 2,595 (12.8%) with the strongest associations of recurrence seen in patients who had a tumor size >2 cm and lymph node‒positive (involving 4 or more nodes) disease (24.6%), compared with 12.7% in patients with tumors <2 cm and node-negative disease. Several other factors were associated with a higher risk of late-onset recurrence and are included in the TABLE. Half of the recurrences occurred between 10 and 15 years after the primary diagnosis.

Prior research

These findings are consistent with another recent study showing that BC patients have a 1% to 2%/year risk of recurrence after 10 disease-free years.⁵ Strengths of this study include:

• population-based, including all women with BC
• long-term follow-up for up to 32 years
• universal health care in Denmark, which results in robust and linked databases and very few missing data points.

There were two notable weaknesses to consider:

• Treatment regimens changed considerably during the time frame of the study (1997-2018), particularly the duration of tamoxifen use in patients with HR-positive disease. In this study nearly all patients received 5 years or less of tamoxifen. Since the mid-2010s, 10 years of hormonal adjuvant therapy has become routine in HR-positive BC, which reduces recurrences, including late-onset recurrence.⁶ The effect of 10 years of tamoxifen would very likely have resulted in less late-onset recurrence in the HR-positive population in this study.
• There is a lack of racial diversity in the Danish population, and the study findings may not translate to Black patients who have a higher frequency of triple-negative BC with a different risk of late-onset recurrence.⁷

Practice takeaways

Cancer surveillance. There are 3+ million BC survivors in the United States, and a 55%+ likelihood that they will be disease free for 10 years. This is clearly an important population to the women’s health care provider. This study, and previous research, suggests that among 10-year-disease-free survivors, 1% to 2% will recur annually, with higher rates amongst HR-positive, lymph-node positive women under age 40, and in the first 5 years following the 10-year post–initial diagnosis mark, so ongoing surveillance is imperative. Annual clinical breast examinations along with annual (not biennial) mammography should be performed.⁸ Digital breast tomosynthesis has improved specificity and sensitivity for BC detection and is the preferred modality when it is available.

Management of menopausal symptoms. These findings also have implications for menopausal hormone therapy for patients with symptoms. Because HR-positive patients have an increased risk of late-onset recurrence, nonhormonal therapies should be considered as first-line therapy for patients with menopausal symptoms. If hormone therapy is being considered, providers and patients should use shared decision making to balance the potential benefits (reduction in symptoms, possible cardiovascular benefits, and reduction in bone loss) with the risks (increased risk of recurrence and venous thromboembolism), even if patients are remote from the original diagnosis (ie, 10-year disease-free survival).

Topical estrogen therapies would be preferred for patients with significant urogenital atrophic symptoms who fail nonhormonal therapies due to substantially less systemic absorption and the lack of need to add a progestin.^9,10 If oral therapy is being considered, I carefully counsel these women about the likely increased risk of recurrence and, if possible, include their breast oncologist in the discussion. ●

“Dr. Lilley, you’ll always be my favorite doctor; you helped me grow.”

These were the parting words from the last patient that I treated during my endocrinology fellowship. I had watched this young man grow from a prepubertal 17-year-old to a young man who had reached his predicted family height as I treated his delayed puberty caused by Kallmann syndrome, a problem that had been missed for years. It was the appropriate bookend for my chosen specialty.

Watching children grow and develop into who they were meant to be is one of my favorite things about endocrinology, as well as forming meaningful relationships with families. Treating detectable deficiencies in logical and measurable ways is also extremely satisfying.

Too little testosterone? That’s a problem I can solve. Too much thyroid hormone? There’s a blocker for that! Endocrinology can be a straightforward field, and when all goes well, everyone leaves happy.

Except when they don’t.
 

Gatekeepers for treatment for children’s growth

“Nice to meet you. We’re here to get growth hormone.”

“We’re here because his pediatrician made us come. We’ve already decided we’re not going to put hormones into his body.”

These are common statements I hear when I first meet new patients whose parents are concerned about their children’s growth. Pediatric endocrinologists, after all, are the usual gatekeepers for this treatment.

Growth hormone (GH) often makes the news for controversial reasons – most commonly for its abuse by elite athletes hoping to exploit its anabolic effects – causing parents to have varied opinions about its possible use in their children.

Some refuse endocrinology referrals at all owing to concerns that we will push daily injections on their children. Others demand referrals for their children of average height, hoping for every perceived advantage.

GH deficiency (GHD) – a condition where the pituitary gland fails to produce enough GH – can occur because of congenital pituitary malformations; anatomic, surgical, or traumatic interruptions to the gland; or enzyme deficiencies leading to faulty production.

GHD is just one reason for poor growth, however.

Growth is one of the most important indicators of health in children. A waning growth rate may be an early symptom of serious problems. In my clinic, I’ve diagnosed severe hypothyroidism in a marathon runner, a brain tumor, celiac disease in a teenager with no gastrointestinal complaints, autoimmune hepatitis, and several other diseases needing treatment in children who show no symptoms other than poor growth.
 

Barriers to normal growth

Sometimes, the die is cast for children to have barriers to normal growth. Several genetic conditions can lead to poor GH production or response, and GH treatment is often necessary to approximate normal height.

These may include:

• Turner syndrome (in females who are missing an X chromosome in whole or part) should be considered in every girl with abnormally short stature; mosaic forms of the condition may be subtle and lack classic features.
• Noonan syndrome is important to detect owing to the possibility of cardiac or renal malformations that may also occur in this condition, caused by a mutation in one of the genes in the RAS-MAPK pathway.
• Russell-Silver syndrome can cause intrauterine GH restriction and has been traced to uniparental disomy of chromosome 7 or duplications, mutations, or methylation defects in chromosome 11.
• Individuals with Prader-Willi syndrome, which is characterized by low muscle tone, hyperphagia, and hypogonadism, have demonstrated dramatic benefits from GH therapy, primarily in maintaining a normal body mass index.

Children who are small for their gestational age may be GH resistant, and those who do not catch up to their growth curve by the age of 2 years may require GH treatment to reach their height potential.

GH therapy isn’t entirely benign. Rare adverse effects of overtreatment can include slipped capital femoral epiphysis (a fracture to the growth plate) and pseudotumor cerebri (idiopathic intracranial hypertension).

Overtreatment can cause acromegaly, which results in coarsened features and large hands and feet.
 

When is GH therapy warranted?

“Growth hormone therapy has been denied by her insurer. They want you to fill out an appeal.”

Insurance approval in the United States can be a herculean effort because GH is expensive: Out-of-pocket costs are prohibitive for most people without insurance assistance, ranging from $7,000 to $30,000 annually.

Pediatric endocrinologists aren’t in the business of cosmetic endocrinology. Treatment of idiopathic short stature has been controversial since this became an indication for GH treatment.

GH isn’t always necessary. Diagnosing the underlying cause for poor growth is the most important step.

Often, we find constitutional delay of growth and puberty, or “late bloomers.” This condition is characterized by a delayed bone age (growth plates more open than expected for age) and delayed pubertal onset. These children will often reach a normal height despite starting as some of the smallest of their peers.

However, GH plays other roles in the body than simply propelling height. Children with congenital GHD will require GH treatment to prevent hypoglycemia, especially in infancy.

GH is needed even in adults with fused growth plates for normal lipid metabolism, bone accrual, and maintaining normal muscle mass.

I have noticed marked improvements in muscle tone in many children with developmental delays who are treated with GH, and research supports cognitive benefits for certain populations.

The most common regimens for GH focus on treatment via subcutaneous injection nightly, when GH is naturally produced; sometimes, injections are given six nights out of seven to provide a break or for splitting time between households.

Newer once-weekly formulations have recently received approval, as reported by this news organization, and are coming into use.

Pediatric endocrinologists measure height and follow growth factors closely with visits every 3-6 months. GH levels are not useful outside of provocative diagnostic (stimulation) testing.

Insulinlike growth factor 1 or insulinlike growth factor binding protein levels are analyzed per Tanner stage of puberty to assess appropriate response and to make dose adjustments.

Annual standardized films of the left hand help predict progress and anticipated adult height. Treatment usually persists through puberty until growth plates are closed; if true GHD is noticed, much smaller doses are continued through adulthood.

Regardless, conversations about GH happen with your friendly local pediatric endocrinologist.

We are thrilled to help shepherd patients through their growing age to meet their potential. For more information about GH treatment for children, the MAGIC Foundation is the perfect place to start.

Dr. Lilley is director of the pediatric diabetes and lipid program, Mississippi Center for Advanced Medicine, Madison. She disclosed no relevant conflicts of interest. A version of this article first appeared on Medscape.com.

“Dr. Lilley, you’ll always be my favorite doctor; you helped me grow.”

These were the parting words from the last patient that I treated during my endocrinology fellowship. I had watched this young man grow from a prepubertal 17-year-old to a young man who had reached his predicted family height as I treated his delayed puberty caused by Kallmann syndrome, a problem that had been missed for years. It was the appropriate bookend for my chosen specialty.

Watching children grow and develop into who they were meant to be is one of my favorite things about endocrinology, as well as forming meaningful relationships with families. Treating detectable deficiencies in logical and measurable ways is also extremely satisfying.

Too little testosterone? That’s a problem I can solve. Too much thyroid hormone? There’s a blocker for that! Endocrinology can be a straightforward field, and when all goes well, everyone leaves happy.

Except when they don’t.
 

Gatekeepers for treatment for children’s growth

“Nice to meet you. We’re here to get growth hormone.”

“We’re here because his pediatrician made us come. We’ve already decided we’re not going to put hormones into his body.”

These are common statements I hear when I first meet new patients whose parents are concerned about their children’s growth. Pediatric endocrinologists, after all, are the usual gatekeepers for this treatment.

Growth hormone (GH) often makes the news for controversial reasons – most commonly for its abuse by elite athletes hoping to exploit its anabolic effects – causing parents to have varied opinions about its possible use in their children.

Some refuse endocrinology referrals at all owing to concerns that we will push daily injections on their children. Others demand referrals for their children of average height, hoping for every perceived advantage.

GH deficiency (GHD) – a condition where the pituitary gland fails to produce enough GH – can occur because of congenital pituitary malformations; anatomic, surgical, or traumatic interruptions to the gland; or enzyme deficiencies leading to faulty production.

GHD is just one reason for poor growth, however.

Growth is one of the most important indicators of health in children. A waning growth rate may be an early symptom of serious problems. In my clinic, I’ve diagnosed severe hypothyroidism in a marathon runner, a brain tumor, celiac disease in a teenager with no gastrointestinal complaints, autoimmune hepatitis, and several other diseases needing treatment in children who show no symptoms other than poor growth.
 

Barriers to normal growth

Sometimes, the die is cast for children to have barriers to normal growth. Several genetic conditions can lead to poor GH production or response, and GH treatment is often necessary to approximate normal height.

These may include:

• Turner syndrome (in females who are missing an X chromosome in whole or part) should be considered in every girl with abnormally short stature; mosaic forms of the condition may be subtle and lack classic features.
• Noonan syndrome is important to detect owing to the possibility of cardiac or renal malformations that may also occur in this condition, caused by a mutation in one of the genes in the RAS-MAPK pathway.
• Russell-Silver syndrome can cause intrauterine GH restriction and has been traced to uniparental disomy of chromosome 7 or duplications, mutations, or methylation defects in chromosome 11.
• Individuals with Prader-Willi syndrome, which is characterized by low muscle tone, hyperphagia, and hypogonadism, have demonstrated dramatic benefits from GH therapy, primarily in maintaining a normal body mass index.

Children who are small for their gestational age may be GH resistant, and those who do not catch up to their growth curve by the age of 2 years may require GH treatment to reach their height potential.

GH therapy isn’t entirely benign. Rare adverse effects of overtreatment can include slipped capital femoral epiphysis (a fracture to the growth plate) and pseudotumor cerebri (idiopathic intracranial hypertension).

Overtreatment can cause acromegaly, which results in coarsened features and large hands and feet.
 

When is GH therapy warranted?

“Growth hormone therapy has been denied by her insurer. They want you to fill out an appeal.”

Insurance approval in the United States can be a herculean effort because GH is expensive: Out-of-pocket costs are prohibitive for most people without insurance assistance, ranging from $7,000 to $30,000 annually.

Pediatric endocrinologists aren’t in the business of cosmetic endocrinology. Treatment of idiopathic short stature has been controversial since this became an indication for GH treatment.

GH isn’t always necessary. Diagnosing the underlying cause for poor growth is the most important step.

Often, we find constitutional delay of growth and puberty, or “late bloomers.” This condition is characterized by a delayed bone age (growth plates more open than expected for age) and delayed pubertal onset. These children will often reach a normal height despite starting as some of the smallest of their peers.

However, GH plays other roles in the body than simply propelling height. Children with congenital GHD will require GH treatment to prevent hypoglycemia, especially in infancy.

GH is needed even in adults with fused growth plates for normal lipid metabolism, bone accrual, and maintaining normal muscle mass.

I have noticed marked improvements in muscle tone in many children with developmental delays who are treated with GH, and research supports cognitive benefits for certain populations.

The most common regimens for GH focus on treatment via subcutaneous injection nightly, when GH is naturally produced; sometimes, injections are given six nights out of seven to provide a break or for splitting time between households.

Newer once-weekly formulations have recently received approval, as reported by this news organization, and are coming into use.

Pediatric endocrinologists measure height and follow growth factors closely with visits every 3-6 months. GH levels are not useful outside of provocative diagnostic (stimulation) testing.

Insulinlike growth factor 1 or insulinlike growth factor binding protein levels are analyzed per Tanner stage of puberty to assess appropriate response and to make dose adjustments.

Annual standardized films of the left hand help predict progress and anticipated adult height. Treatment usually persists through puberty until growth plates are closed; if true GHD is noticed, much smaller doses are continued through adulthood.

Regardless, conversations about GH happen with your friendly local pediatric endocrinologist.

We are thrilled to help shepherd patients through their growing age to meet their potential. For more information about GH treatment for children, the MAGIC Foundation is the perfect place to start.

Dr. Lilley is director of the pediatric diabetes and lipid program, Mississippi Center for Advanced Medicine, Madison. She disclosed no relevant conflicts of interest. A version of this article first appeared on Medscape.com.

“Dr. Lilley, you’ll always be my favorite doctor; you helped me grow.”

These were the parting words from the last patient that I treated during my endocrinology fellowship. I had watched this young man grow from a prepubertal 17-year-old to a young man who had reached his predicted family height as I treated his delayed puberty caused by Kallmann syndrome, a problem that had been missed for years. It was the appropriate bookend for my chosen specialty.

Watching children grow and develop into who they were meant to be is one of my favorite things about endocrinology, as well as forming meaningful relationships with families. Treating detectable deficiencies in logical and measurable ways is also extremely satisfying.

Too little testosterone? That’s a problem I can solve. Too much thyroid hormone? There’s a blocker for that! Endocrinology can be a straightforward field, and when all goes well, everyone leaves happy.

Except when they don’t.
 

Gatekeepers for treatment for children’s growth

“Nice to meet you. We’re here to get growth hormone.”

“We’re here because his pediatrician made us come. We’ve already decided we’re not going to put hormones into his body.”

These are common statements I hear when I first meet new patients whose parents are concerned about their children’s growth. Pediatric endocrinologists, after all, are the usual gatekeepers for this treatment.

Growth hormone (GH) often makes the news for controversial reasons – most commonly for its abuse by elite athletes hoping to exploit its anabolic effects – causing parents to have varied opinions about its possible use in their children.

Some refuse endocrinology referrals at all owing to concerns that we will push daily injections on their children. Others demand referrals for their children of average height, hoping for every perceived advantage.

GH deficiency (GHD) – a condition where the pituitary gland fails to produce enough GH – can occur because of congenital pituitary malformations; anatomic, surgical, or traumatic interruptions to the gland; or enzyme deficiencies leading to faulty production.

GHD is just one reason for poor growth, however.

Growth is one of the most important indicators of health in children. A waning growth rate may be an early symptom of serious problems. In my clinic, I’ve diagnosed severe hypothyroidism in a marathon runner, a brain tumor, celiac disease in a teenager with no gastrointestinal complaints, autoimmune hepatitis, and several other diseases needing treatment in children who show no symptoms other than poor growth.
 

Barriers to normal growth

Sometimes, the die is cast for children to have barriers to normal growth. Several genetic conditions can lead to poor GH production or response, and GH treatment is often necessary to approximate normal height.

These may include:

• Turner syndrome (in females who are missing an X chromosome in whole or part) should be considered in every girl with abnormally short stature; mosaic forms of the condition may be subtle and lack classic features.
• Noonan syndrome is important to detect owing to the possibility of cardiac or renal malformations that may also occur in this condition, caused by a mutation in one of the genes in the RAS-MAPK pathway.
• Russell-Silver syndrome can cause intrauterine GH restriction and has been traced to uniparental disomy of chromosome 7 or duplications, mutations, or methylation defects in chromosome 11.
• Individuals with Prader-Willi syndrome, which is characterized by low muscle tone, hyperphagia, and hypogonadism, have demonstrated dramatic benefits from GH therapy, primarily in maintaining a normal body mass index.

Children who are small for their gestational age may be GH resistant, and those who do not catch up to their growth curve by the age of 2 years may require GH treatment to reach their height potential.

GH therapy isn’t entirely benign. Rare adverse effects of overtreatment can include slipped capital femoral epiphysis (a fracture to the growth plate) and pseudotumor cerebri (idiopathic intracranial hypertension).

Overtreatment can cause acromegaly, which results in coarsened features and large hands and feet.
 

When is GH therapy warranted?

“Growth hormone therapy has been denied by her insurer. They want you to fill out an appeal.”

Insurance approval in the United States can be a herculean effort because GH is expensive: Out-of-pocket costs are prohibitive for most people without insurance assistance, ranging from $7,000 to $30,000 annually.

Pediatric endocrinologists aren’t in the business of cosmetic endocrinology. Treatment of idiopathic short stature has been controversial since this became an indication for GH treatment.

GH isn’t always necessary. Diagnosing the underlying cause for poor growth is the most important step.

Often, we find constitutional delay of growth and puberty, or “late bloomers.” This condition is characterized by a delayed bone age (growth plates more open than expected for age) and delayed pubertal onset. These children will often reach a normal height despite starting as some of the smallest of their peers.

However, GH plays other roles in the body than simply propelling height. Children with congenital GHD will require GH treatment to prevent hypoglycemia, especially in infancy.

GH is needed even in adults with fused growth plates for normal lipid metabolism, bone accrual, and maintaining normal muscle mass.

I have noticed marked improvements in muscle tone in many children with developmental delays who are treated with GH, and research supports cognitive benefits for certain populations.

The most common regimens for GH focus on treatment via subcutaneous injection nightly, when GH is naturally produced; sometimes, injections are given six nights out of seven to provide a break or for splitting time between households.

Newer once-weekly formulations have recently received approval, as reported by this news organization, and are coming into use.

Pediatric endocrinologists measure height and follow growth factors closely with visits every 3-6 months. GH levels are not useful outside of provocative diagnostic (stimulation) testing.

Insulinlike growth factor 1 or insulinlike growth factor binding protein levels are analyzed per Tanner stage of puberty to assess appropriate response and to make dose adjustments.

Annual standardized films of the left hand help predict progress and anticipated adult height. Treatment usually persists through puberty until growth plates are closed; if true GHD is noticed, much smaller doses are continued through adulthood.

Regardless, conversations about GH happen with your friendly local pediatric endocrinologist.

We are thrilled to help shepherd patients through their growing age to meet their potential. For more information about GH treatment for children, the MAGIC Foundation is the perfect place to start.

Dr. Lilley is director of the pediatric diabetes and lipid program, Mississippi Center for Advanced Medicine, Madison. She disclosed no relevant conflicts of interest. A version of this article first appeared on Medscape.com.

In the age of COVID, what exactly does it mean to be optimistic? I get this question quite a bit from virtually everyone I meet in one form or another through my work with the George Washington Resiliency and Well-Being Center in Washington, D.C. Giving a lecture on resilience and staying positive can be a significant challenge. Especially when we wake up to the news that 1 of every 100 older Americans has died secondary to COVID. The mind doesn’t really know how to process this type of loss. It is hard to maintain any form of a positive attitude when you’re still struggling just to accept the magnitude of what humanity has experienced over the past 2 years.

In “Resilience: The Science of Mastering Life’s Greatest Challenges,” (Cambridge, England: Cambridge University Press, 2018), Steven M. Southwick, MD, and Dennis S. Charney, MD, identify 10 critical factors associated with very resilient individuals. The authors based their work on science, personal experience, and interviews of people who have literally been through hell and back. One of the critical factors they identified is optimism.
“Optimism ignites resilience, providing energy to power the other resilience factors. It facilitates an active and creative approach to coping with challenging situations.”

Dr. Southwick and Dr. Charney are a lot smarter than me and far more patient to weave all this data together into a coherent story about optimism. Sounds like a damn good factor to focus a lecture on in my book! Slight problem: In my experience, many health professionals are already expert optimists. They literally eat, sleep, and sincerely breathe this stuff. So if we are going to talk about optimism, then we need to discuss realistic optimism.

How does realistic optimism differ from, say, blind optimism? Dr. Southwick and Dr. Charney’s review of the literature points to three features worthy of highlighting.
 

Realistic vs. blind optimism: Take-home points

• In realistic optimism, we notice the negative but don’t stay engaged with it. Realistic optimists moved on from problems that were not solvable.
• Blind optimism can involve optimistic biases that affect self-deception or convincing oneself of desired beliefs without reality checks.
• Blind optimism can lead to underestimating risk, overestimating abilities, and inadequate preparation.

Growing up in northeast Ohio, I can absolutely embrace the concept of realistic optimism. It’s overcast in Cleveland 8 months out of the year. To hope for 3 sunny days in a row in April is genuinely a fools’ errand. So you learn over time, the sun will shine; you just have to at times wait 3-4 months for it to occur.

 

From a skill perspective, realistic optimism could be conceptualized as a great mix of radical acceptance, emotion regulation, and focused problem solving. This is all fine, but to be realistically optimistic, we must first stop wishing for a better tomorrow. You may say, I don’t wish for or see rainbows and unicorns, et cetera, et cetera. Okay, so you don’t verbalize your wishes, but on a small level, you may engage in wishful thinking. Here are a few wishful thoughts that I would daydream about, which were not realistically optimistic at various points:

• “Once we get enough COVID-19 tests, things will improve.”
• “All we need to do is get vaccines, and then the new normal is right there.”
• “Once everyone gets the booster, then we got this thing beat.”

At this point, you could argue that I was engaged in blind optimism. I consider the above statements blind for a couple of reasons. They weren’t balanced (both positive and negative), didn’t have a clear definition of the outcome, and were more focused on external events I couldn’t control. These statements were the equivalent of wishes, and I don’t have a magic lamp with a genie, so I need to let go of my wishful thinking first. Let me rephrase that: I need to forcefully toss it into the sea of COVID variants and start figuring out how I’m going to tread water for another 6-12 months. So with this in mind, here are my initial thoughts on ways to navigate the next year of the pandemic:

• A multilayered form of protection gives me the best chance to survive the next 6 months of the pandemic.
• It will take time, but I’ll process the loss associated with a workplace that will never be the same.
• Until we have positivity test rates lower than 2% across the globe, COVID will remain a substantial disruption to humanity.
• I can’t bring back missed graduation or the first day of school, but I can share ways that I’ve countered and survived loneliness in my life with my children.

Okay, this is the starting point – hopefully not pessimistic, or blindly optimistic, just realistic. Now I can address other important topics, such as planning to rebuild my disappointing fantasy football team. I was No. 1 in our GW department of psychiatry fantasy football league until my star running back Derrick Henry went down. My residents will become attendings and still give me grief about this for many years to follow, and that is a very good thing.

Everyone be well and safe.

Dr. Norris is associate dean of student affairs; associate professor, department of psychiatry, George Washington University; chief wellness officer, GW Hospital, GW Medical Faculty Associates, and the GW School of Medicine and Health Sciences (GWU Medical Enterprise), Washington. He has disclosed having no relevant financial relationships. A version of this article first appeared on Medscape.com.

In the age of COVID, what exactly does it mean to be optimistic? I get this question quite a bit from virtually everyone I meet in one form or another through my work with the George Washington Resiliency and Well-Being Center in Washington, D.C. Giving a lecture on resilience and staying positive can be a significant challenge. Especially when we wake up to the news that 1 of every 100 older Americans has died secondary to COVID. The mind doesn’t really know how to process this type of loss. It is hard to maintain any form of a positive attitude when you’re still struggling just to accept the magnitude of what humanity has experienced over the past 2 years.

In “Resilience: The Science of Mastering Life’s Greatest Challenges,” (Cambridge, England: Cambridge University Press, 2018), Steven M. Southwick, MD, and Dennis S. Charney, MD, identify 10 critical factors associated with very resilient individuals. The authors based their work on science, personal experience, and interviews of people who have literally been through hell and back. One of the critical factors they identified is optimism.
“Optimism ignites resilience, providing energy to power the other resilience factors. It facilitates an active and creative approach to coping with challenging situations.”

Dr. Southwick and Dr. Charney are a lot smarter than me and far more patient to weave all this data together into a coherent story about optimism. Sounds like a damn good factor to focus a lecture on in my book! Slight problem: In my experience, many health professionals are already expert optimists. They literally eat, sleep, and sincerely breathe this stuff. So if we are going to talk about optimism, then we need to discuss realistic optimism.

How does realistic optimism differ from, say, blind optimism? Dr. Southwick and Dr. Charney’s review of the literature points to three features worthy of highlighting.
 

Realistic vs. blind optimism: Take-home points

• In realistic optimism, we notice the negative but don’t stay engaged with it. Realistic optimists moved on from problems that were not solvable.
• Blind optimism can involve optimistic biases that affect self-deception or convincing oneself of desired beliefs without reality checks.
• Blind optimism can lead to underestimating risk, overestimating abilities, and inadequate preparation.

Growing up in northeast Ohio, I can absolutely embrace the concept of realistic optimism. It’s overcast in Cleveland 8 months out of the year. To hope for 3 sunny days in a row in April is genuinely a fools’ errand. So you learn over time, the sun will shine; you just have to at times wait 3-4 months for it to occur.

 

From a skill perspective, realistic optimism could be conceptualized as a great mix of radical acceptance, emotion regulation, and focused problem solving. This is all fine, but to be realistically optimistic, we must first stop wishing for a better tomorrow. You may say, I don’t wish for or see rainbows and unicorns, et cetera, et cetera. Okay, so you don’t verbalize your wishes, but on a small level, you may engage in wishful thinking. Here are a few wishful thoughts that I would daydream about, which were not realistically optimistic at various points:

• “Once we get enough COVID-19 tests, things will improve.”
• “All we need to do is get vaccines, and then the new normal is right there.”
• “Once everyone gets the booster, then we got this thing beat.”

At this point, you could argue that I was engaged in blind optimism. I consider the above statements blind for a couple of reasons. They weren’t balanced (both positive and negative), didn’t have a clear definition of the outcome, and were more focused on external events I couldn’t control. These statements were the equivalent of wishes, and I don’t have a magic lamp with a genie, so I need to let go of my wishful thinking first. Let me rephrase that: I need to forcefully toss it into the sea of COVID variants and start figuring out how I’m going to tread water for another 6-12 months. So with this in mind, here are my initial thoughts on ways to navigate the next year of the pandemic:

• A multilayered form of protection gives me the best chance to survive the next 6 months of the pandemic.
• It will take time, but I’ll process the loss associated with a workplace that will never be the same.
• Until we have positivity test rates lower than 2% across the globe, COVID will remain a substantial disruption to humanity.
• I can’t bring back missed graduation or the first day of school, but I can share ways that I’ve countered and survived loneliness in my life with my children.

Okay, this is the starting point – hopefully not pessimistic, or blindly optimistic, just realistic. Now I can address other important topics, such as planning to rebuild my disappointing fantasy football team. I was No. 1 in our GW department of psychiatry fantasy football league until my star running back Derrick Henry went down. My residents will become attendings and still give me grief about this for many years to follow, and that is a very good thing.

Everyone be well and safe.

Dr. Norris is associate dean of student affairs; associate professor, department of psychiatry, George Washington University; chief wellness officer, GW Hospital, GW Medical Faculty Associates, and the GW School of Medicine and Health Sciences (GWU Medical Enterprise), Washington. He has disclosed having no relevant financial relationships. A version of this article first appeared on Medscape.com.

In the age of COVID, what exactly does it mean to be optimistic? I get this question quite a bit from virtually everyone I meet in one form or another through my work with the George Washington Resiliency and Well-Being Center in Washington, D.C. Giving a lecture on resilience and staying positive can be a significant challenge. Especially when we wake up to the news that 1 of every 100 older Americans has died secondary to COVID. The mind doesn’t really know how to process this type of loss. It is hard to maintain any form of a positive attitude when you’re still struggling just to accept the magnitude of what humanity has experienced over the past 2 years.

In “Resilience: The Science of Mastering Life’s Greatest Challenges,” (Cambridge, England: Cambridge University Press, 2018), Steven M. Southwick, MD, and Dennis S. Charney, MD, identify 10 critical factors associated with very resilient individuals. The authors based their work on science, personal experience, and interviews of people who have literally been through hell and back. One of the critical factors they identified is optimism.
“Optimism ignites resilience, providing energy to power the other resilience factors. It facilitates an active and creative approach to coping with challenging situations.”

Dr. Southwick and Dr. Charney are a lot smarter than me and far more patient to weave all this data together into a coherent story about optimism. Sounds like a damn good factor to focus a lecture on in my book! Slight problem: In my experience, many health professionals are already expert optimists. They literally eat, sleep, and sincerely breathe this stuff. So if we are going to talk about optimism, then we need to discuss realistic optimism.

How does realistic optimism differ from, say, blind optimism? Dr. Southwick and Dr. Charney’s review of the literature points to three features worthy of highlighting.
 

Realistic vs. blind optimism: Take-home points

• In realistic optimism, we notice the negative but don’t stay engaged with it. Realistic optimists moved on from problems that were not solvable.
• Blind optimism can involve optimistic biases that affect self-deception or convincing oneself of desired beliefs without reality checks.
• Blind optimism can lead to underestimating risk, overestimating abilities, and inadequate preparation.

Growing up in northeast Ohio, I can absolutely embrace the concept of realistic optimism. It’s overcast in Cleveland 8 months out of the year. To hope for 3 sunny days in a row in April is genuinely a fools’ errand. So you learn over time, the sun will shine; you just have to at times wait 3-4 months for it to occur.

 

From a skill perspective, realistic optimism could be conceptualized as a great mix of radical acceptance, emotion regulation, and focused problem solving. This is all fine, but to be realistically optimistic, we must first stop wishing for a better tomorrow. You may say, I don’t wish for or see rainbows and unicorns, et cetera, et cetera. Okay, so you don’t verbalize your wishes, but on a small level, you may engage in wishful thinking. Here are a few wishful thoughts that I would daydream about, which were not realistically optimistic at various points:

• “Once we get enough COVID-19 tests, things will improve.”
• “All we need to do is get vaccines, and then the new normal is right there.”
• “Once everyone gets the booster, then we got this thing beat.”

At this point, you could argue that I was engaged in blind optimism. I consider the above statements blind for a couple of reasons. They weren’t balanced (both positive and negative), didn’t have a clear definition of the outcome, and were more focused on external events I couldn’t control. These statements were the equivalent of wishes, and I don’t have a magic lamp with a genie, so I need to let go of my wishful thinking first. Let me rephrase that: I need to forcefully toss it into the sea of COVID variants and start figuring out how I’m going to tread water for another 6-12 months. So with this in mind, here are my initial thoughts on ways to navigate the next year of the pandemic:

• A multilayered form of protection gives me the best chance to survive the next 6 months of the pandemic.
• It will take time, but I’ll process the loss associated with a workplace that will never be the same.
• Until we have positivity test rates lower than 2% across the globe, COVID will remain a substantial disruption to humanity.
• I can’t bring back missed graduation or the first day of school, but I can share ways that I’ve countered and survived loneliness in my life with my children.

Okay, this is the starting point – hopefully not pessimistic, or blindly optimistic, just realistic. Now I can address other important topics, such as planning to rebuild my disappointing fantasy football team. I was No. 1 in our GW department of psychiatry fantasy football league until my star running back Derrick Henry went down. My residents will become attendings and still give me grief about this for many years to follow, and that is a very good thing.

Everyone be well and safe.

Dr. Norris is associate dean of student affairs; associate professor, department of psychiatry, George Washington University; chief wellness officer, GW Hospital, GW Medical Faculty Associates, and the GW School of Medicine and Health Sciences (GWU Medical Enterprise), Washington. He has disclosed having no relevant financial relationships. A version of this article first appeared on Medscape.com.

Twenty years ago, the dilemma in treating acute otitis media (AOM) was which among 10-plus antibiotics to prescribe. A recent column discussed the evolving pathogen distribution in AOM and its effects on antibiotic choices.¹ But here we consider treatment duration. Until the past decade, AOM treatment (except azithromycin) involved 10-day courses. But lately, 10-day antibiotic regimens for uncomplicated infections are disappearing. Shorter-course recommendations are the new norm because of the evolving clinical data showing that an appropriately chosen antibiotic (in partnership with host defenses and source control) resolves infection faster than was previously thought. Shorter courses make sense because of fewer adverse effects, less distortion of normal flora, and less likely induction of pathogen resistance. Table 4.12 in the newest 2021-2024 SOID Redbook lists three antibiotic durations for AOM, and actually there are more than that.

Why so many duration options? Clinical data show that not all AOM is alike and short courses work for subsets of AOM because, besides antibiotics, key elements in AOM resolution are host anatomy and immunity. Bacterial AOM results from a combination of refluxed pathogens in the middle ear being trapped when the eustachian tube malfunctions (infection occurs when middle ear plumbing gets stopped up). If the eustachian tube spontaneously drains and the host immune response slows/stops pathogen growth, no antibiotics are needed. Indeed, a sizable proportion of mild/moderate AOM episodes spontaneously resolve, particularly in children over 2 years old. So a high likelihood of spontaneous remission allows an initial 0-days duration option (watchful waiting) or delayed antibiotics (rescue prescriptions) for older children.

That said, when one chooses to initially prescribe antibiotics for AOM, different durations are recommended. Table 1 has my suggestions.

Data that gave me better microbiological understanding of why oral AOM trials less than 10 days were successful involved purulent AOM drainage from children who had pressure-equalizing (PE) tubes.² The authors randomized children to either standard-dose amoxicillin-clavulanate or placebo. Of note, 95% of pathogens were susceptible to the antibiotic; 5% were pneumococcus intermediately resistant to penicillin. The authors sampled ear drainage daily for 7 days. Figure 1 shows that cultures remained positive in only around 5% of children by day 3-5 of antibiotics, but viable bacteria persisted through 7 days in over half of placebo recipients. Remember, both groups benefited from a form of source control (drainage of the middle ear via PE tubes). So, if antibiotics can do the job in 3-5 days, why continue antibiotics beyond 5 days?

Anatomy and severity. In children over 5 years old (reasonably mature eustachian tube anatomy) with nonrecurrent (no AOM in past month), nonsevere (no otalgia or high fever) AOM, 5 days is enough. But 2- to 5-year-olds (less mature anatomy) need 7 days and those <2 years old (least mature plumbing) need 10 days. Likewise, severe AOM usually warrants 10 days. Some experts recommend 10 days for bilateral AOM as well.

These age/severity differences make sense because failures are more frequent with:

1. Younger age.³ While not proven, my hypothesis is that “natural” source control (spontaneous internal draining the middle ear into the nasopharynx [NP]) is less frequent in younger children because they have less mature eustachian tube systems. Further, reflux of persisting NP organisms could restart a new AOM episode even if the original pathogen was eliminated by a short 5-day course.

2. Severe AOM. A rationale for longer courses in severe AOM (ear pain, high fever) is that high middle-ear pressures (indicated by degree of tympanic membrane bulging and ear pain) could impede antibiotic penetration, or that high initial bacterial loads (perhaps indicated by systemic fever) require more antibiotic. And finally, return to baseline eustachian tube function may take longer if severe AOM caused enhanced inflammation.

3. Recurrent AOM. (AOM within 1 prior month) – With recurrent AOM, the second “hit” to the eustachian tube may lead to more dysfunction, so a longer antibiotic course may be required to allow more complete source control and more time for more complete functional recovery after a repeated inflammatory injury.

4. Bilateral AOM. Two independent but infected sites mean twice the chance for failure. So, a longer course could allow more time for both sites to undergo “natural” source control.⁴

More bacteria – more antibiotic? So, is more antibiotic really needed for a higher bacterial load? In vitro this is known as the “inoculum effect,” particularly for beta-lactam drugs, for example, amoxicillin and cephalosporins. Laboratory susceptibility testing is performed with a specifically defined quantity of bacteria (10⁵ bacteria/mL) and the minimum inhibitory concentration (MIC) is the lowest antibiotic concentration that stops bacterial growth. We know that drugs will likely fail if the MIC exceeds the achievable antibiotic concentration at the infection site. But is it as simple as just exceeding the MIC at the infection site? No, pharmacodynamics tell us that overall antibiotic exposure is also important. For example, to be successful, beta-lactam concentrations need to be above the MIC for 40%-50% of the day.

Higher MIC with higher bacterial load. Particularly for beta-lactams, testing with a quantity of bacteria >10⁵/mL produces a higher MIC in vitro. This suggests that clinical failure could occur, even when our in vivo dosing leads to 40%-50% above the “standard” MIC that was obtained from testing the lab standard of 10⁵/mL bacteria, when the infected site’s (middle ear) bacterial load is >10⁵/mL (such higher bacterial loads occur in up to 30% of AOM).⁵ One way to negate inoculum effect is source control (drain the abscess or debridement), which reduces the bacterial load as well as allowing better antibiotic penetration– both favoring infection resolution. But with suboptimal source control, for example, the middle ear is not drained externally or internally, longer courses (more antibiotic exposure) could aid resolution. Whether the exposure can be administered as higher doses in fewer days or standard doses for more days is debatable but consider that a single parenteral dose of ceftriaxone successfully resolves AOM not attributable to penicillin-nonsusceptible pneumococcus.⁶Bottom line: Even though the number of potential antibiotics has contracted in the past 20 years, the need to individualize AOM treatment remains important and duration choices are more complex. Indeed, AOM comes in different flavors with patient age, clinical presentation, and episode frequency dictating the choice of duration.
 

Dr. Christopher J. Harrison is professor of pediatrics and pediatric infectious diseases at Children’s Mercy Hospitals and Clinics in Kansas City, Mo. Email him at pdnews@mdedge.com.

References

1. Pichichero ME. MDedge. 2022 Jan 11.

2. Ruohola A et al. Pediatrics. 2003;111(5):1061-7.

3. Hoberman A et al. N Engl J Med. 2016;375(25):2446-56.

4. Pichichero ME et al. Otolaryngol Head Neck Surg. 2001;124(4):381-7.

5. Harrison CJ et al. Pediatr Infect Dis. 1985;4(6):641-6.

6. Leibovitz E et al. Pediatr Infect Dis. 2000;19(11):1040-5.

Twenty years ago, the dilemma in treating acute otitis media (AOM) was which among 10-plus antibiotics to prescribe. A recent column discussed the evolving pathogen distribution in AOM and its effects on antibiotic choices.¹ But here we consider treatment duration. Until the past decade, AOM treatment (except azithromycin) involved 10-day courses. But lately, 10-day antibiotic regimens for uncomplicated infections are disappearing. Shorter-course recommendations are the new norm because of the evolving clinical data showing that an appropriately chosen antibiotic (in partnership with host defenses and source control) resolves infection faster than was previously thought. Shorter courses make sense because of fewer adverse effects, less distortion of normal flora, and less likely induction of pathogen resistance. Table 4.12 in the newest 2021-2024 SOID Redbook lists three antibiotic durations for AOM, and actually there are more than that.

Why so many duration options? Clinical data show that not all AOM is alike and short courses work for subsets of AOM because, besides antibiotics, key elements in AOM resolution are host anatomy and immunity. Bacterial AOM results from a combination of refluxed pathogens in the middle ear being trapped when the eustachian tube malfunctions (infection occurs when middle ear plumbing gets stopped up). If the eustachian tube spontaneously drains and the host immune response slows/stops pathogen growth, no antibiotics are needed. Indeed, a sizable proportion of mild/moderate AOM episodes spontaneously resolve, particularly in children over 2 years old. So a high likelihood of spontaneous remission allows an initial 0-days duration option (watchful waiting) or delayed antibiotics (rescue prescriptions) for older children.

That said, when one chooses to initially prescribe antibiotics for AOM, different durations are recommended. Table 1 has my suggestions.

Data that gave me better microbiological understanding of why oral AOM trials less than 10 days were successful involved purulent AOM drainage from children who had pressure-equalizing (PE) tubes.² The authors randomized children to either standard-dose amoxicillin-clavulanate or placebo. Of note, 95% of pathogens were susceptible to the antibiotic; 5% were pneumococcus intermediately resistant to penicillin. The authors sampled ear drainage daily for 7 days. Figure 1 shows that cultures remained positive in only around 5% of children by day 3-5 of antibiotics, but viable bacteria persisted through 7 days in over half of placebo recipients. Remember, both groups benefited from a form of source control (drainage of the middle ear via PE tubes). So, if antibiotics can do the job in 3-5 days, why continue antibiotics beyond 5 days?

Anatomy and severity. In children over 5 years old (reasonably mature eustachian tube anatomy) with nonrecurrent (no AOM in past month), nonsevere (no otalgia or high fever) AOM, 5 days is enough. But 2- to 5-year-olds (less mature anatomy) need 7 days and those <2 years old (least mature plumbing) need 10 days. Likewise, severe AOM usually warrants 10 days. Some experts recommend 10 days for bilateral AOM as well.

These age/severity differences make sense because failures are more frequent with:

1. Younger age.³ While not proven, my hypothesis is that “natural” source control (spontaneous internal draining the middle ear into the nasopharynx [NP]) is less frequent in younger children because they have less mature eustachian tube systems. Further, reflux of persisting NP organisms could restart a new AOM episode even if the original pathogen was eliminated by a short 5-day course.

2. Severe AOM. A rationale for longer courses in severe AOM (ear pain, high fever) is that high middle-ear pressures (indicated by degree of tympanic membrane bulging and ear pain) could impede antibiotic penetration, or that high initial bacterial loads (perhaps indicated by systemic fever) require more antibiotic. And finally, return to baseline eustachian tube function may take longer if severe AOM caused enhanced inflammation.

3. Recurrent AOM. (AOM within 1 prior month) – With recurrent AOM, the second “hit” to the eustachian tube may lead to more dysfunction, so a longer antibiotic course may be required to allow more complete source control and more time for more complete functional recovery after a repeated inflammatory injury.

4. Bilateral AOM. Two independent but infected sites mean twice the chance for failure. So, a longer course could allow more time for both sites to undergo “natural” source control.⁴

More bacteria – more antibiotic? So, is more antibiotic really needed for a higher bacterial load? In vitro this is known as the “inoculum effect,” particularly for beta-lactam drugs, for example, amoxicillin and cephalosporins. Laboratory susceptibility testing is performed with a specifically defined quantity of bacteria (10⁵ bacteria/mL) and the minimum inhibitory concentration (MIC) is the lowest antibiotic concentration that stops bacterial growth. We know that drugs will likely fail if the MIC exceeds the achievable antibiotic concentration at the infection site. But is it as simple as just exceeding the MIC at the infection site? No, pharmacodynamics tell us that overall antibiotic exposure is also important. For example, to be successful, beta-lactam concentrations need to be above the MIC for 40%-50% of the day.

Higher MIC with higher bacterial load. Particularly for beta-lactams, testing with a quantity of bacteria >10⁵/mL produces a higher MIC in vitro. This suggests that clinical failure could occur, even when our in vivo dosing leads to 40%-50% above the “standard” MIC that was obtained from testing the lab standard of 10⁵/mL bacteria, when the infected site’s (middle ear) bacterial load is >10⁵/mL (such higher bacterial loads occur in up to 30% of AOM).⁵ One way to negate inoculum effect is source control (drain the abscess or debridement), which reduces the bacterial load as well as allowing better antibiotic penetration– both favoring infection resolution. But with suboptimal source control, for example, the middle ear is not drained externally or internally, longer courses (more antibiotic exposure) could aid resolution. Whether the exposure can be administered as higher doses in fewer days or standard doses for more days is debatable but consider that a single parenteral dose of ceftriaxone successfully resolves AOM not attributable to penicillin-nonsusceptible pneumococcus.⁶Bottom line: Even though the number of potential antibiotics has contracted in the past 20 years, the need to individualize AOM treatment remains important and duration choices are more complex. Indeed, AOM comes in different flavors with patient age, clinical presentation, and episode frequency dictating the choice of duration.
 

Dr. Christopher J. Harrison is professor of pediatrics and pediatric infectious diseases at Children’s Mercy Hospitals and Clinics in Kansas City, Mo. Email him at pdnews@mdedge.com.

References

1. Pichichero ME. MDedge. 2022 Jan 11.

2. Ruohola A et al. Pediatrics. 2003;111(5):1061-7.

3. Hoberman A et al. N Engl J Med. 2016;375(25):2446-56.

4. Pichichero ME et al. Otolaryngol Head Neck Surg. 2001;124(4):381-7.

5. Harrison CJ et al. Pediatr Infect Dis. 1985;4(6):641-6.

6. Leibovitz E et al. Pediatr Infect Dis. 2000;19(11):1040-5.

Twenty years ago, the dilemma in treating acute otitis media (AOM) was which among 10-plus antibiotics to prescribe. A recent column discussed the evolving pathogen distribution in AOM and its effects on antibiotic choices.¹ But here we consider treatment duration. Until the past decade, AOM treatment (except azithromycin) involved 10-day courses. But lately, 10-day antibiotic regimens for uncomplicated infections are disappearing. Shorter-course recommendations are the new norm because of the evolving clinical data showing that an appropriately chosen antibiotic (in partnership with host defenses and source control) resolves infection faster than was previously thought. Shorter courses make sense because of fewer adverse effects, less distortion of normal flora, and less likely induction of pathogen resistance. Table 4.12 in the newest 2021-2024 SOID Redbook lists three antibiotic durations for AOM, and actually there are more than that.

Why so many duration options? Clinical data show that not all AOM is alike and short courses work for subsets of AOM because, besides antibiotics, key elements in AOM resolution are host anatomy and immunity. Bacterial AOM results from a combination of refluxed pathogens in the middle ear being trapped when the eustachian tube malfunctions (infection occurs when middle ear plumbing gets stopped up). If the eustachian tube spontaneously drains and the host immune response slows/stops pathogen growth, no antibiotics are needed. Indeed, a sizable proportion of mild/moderate AOM episodes spontaneously resolve, particularly in children over 2 years old. So a high likelihood of spontaneous remission allows an initial 0-days duration option (watchful waiting) or delayed antibiotics (rescue prescriptions) for older children.

That said, when one chooses to initially prescribe antibiotics for AOM, different durations are recommended. Table 1 has my suggestions.

Data that gave me better microbiological understanding of why oral AOM trials less than 10 days were successful involved purulent AOM drainage from children who had pressure-equalizing (PE) tubes.² The authors randomized children to either standard-dose amoxicillin-clavulanate or placebo. Of note, 95% of pathogens were susceptible to the antibiotic; 5% were pneumococcus intermediately resistant to penicillin. The authors sampled ear drainage daily for 7 days. Figure 1 shows that cultures remained positive in only around 5% of children by day 3-5 of antibiotics, but viable bacteria persisted through 7 days in over half of placebo recipients. Remember, both groups benefited from a form of source control (drainage of the middle ear via PE tubes). So, if antibiotics can do the job in 3-5 days, why continue antibiotics beyond 5 days?

Anatomy and severity. In children over 5 years old (reasonably mature eustachian tube anatomy) with nonrecurrent (no AOM in past month), nonsevere (no otalgia or high fever) AOM, 5 days is enough. But 2- to 5-year-olds (less mature anatomy) need 7 days and those <2 years old (least mature plumbing) need 10 days. Likewise, severe AOM usually warrants 10 days. Some experts recommend 10 days for bilateral AOM as well.

These age/severity differences make sense because failures are more frequent with:

1. Younger age.³ While not proven, my hypothesis is that “natural” source control (spontaneous internal draining the middle ear into the nasopharynx [NP]) is less frequent in younger children because they have less mature eustachian tube systems. Further, reflux of persisting NP organisms could restart a new AOM episode even if the original pathogen was eliminated by a short 5-day course.

2. Severe AOM. A rationale for longer courses in severe AOM (ear pain, high fever) is that high middle-ear pressures (indicated by degree of tympanic membrane bulging and ear pain) could impede antibiotic penetration, or that high initial bacterial loads (perhaps indicated by systemic fever) require more antibiotic. And finally, return to baseline eustachian tube function may take longer if severe AOM caused enhanced inflammation.

3. Recurrent AOM. (AOM within 1 prior month) – With recurrent AOM, the second “hit” to the eustachian tube may lead to more dysfunction, so a longer antibiotic course may be required to allow more complete source control and more time for more complete functional recovery after a repeated inflammatory injury.

4. Bilateral AOM. Two independent but infected sites mean twice the chance for failure. So, a longer course could allow more time for both sites to undergo “natural” source control.⁴

More bacteria – more antibiotic? So, is more antibiotic really needed for a higher bacterial load? In vitro this is known as the “inoculum effect,” particularly for beta-lactam drugs, for example, amoxicillin and cephalosporins. Laboratory susceptibility testing is performed with a specifically defined quantity of bacteria (10⁵ bacteria/mL) and the minimum inhibitory concentration (MIC) is the lowest antibiotic concentration that stops bacterial growth. We know that drugs will likely fail if the MIC exceeds the achievable antibiotic concentration at the infection site. But is it as simple as just exceeding the MIC at the infection site? No, pharmacodynamics tell us that overall antibiotic exposure is also important. For example, to be successful, beta-lactam concentrations need to be above the MIC for 40%-50% of the day.

Higher MIC with higher bacterial load. Particularly for beta-lactams, testing with a quantity of bacteria >10⁵/mL produces a higher MIC in vitro. This suggests that clinical failure could occur, even when our in vivo dosing leads to 40%-50% above the “standard” MIC that was obtained from testing the lab standard of 10⁵/mL bacteria, when the infected site’s (middle ear) bacterial load is >10⁵/mL (such higher bacterial loads occur in up to 30% of AOM).⁵ One way to negate inoculum effect is source control (drain the abscess or debridement), which reduces the bacterial load as well as allowing better antibiotic penetration– both favoring infection resolution. But with suboptimal source control, for example, the middle ear is not drained externally or internally, longer courses (more antibiotic exposure) could aid resolution. Whether the exposure can be administered as higher doses in fewer days or standard doses for more days is debatable but consider that a single parenteral dose of ceftriaxone successfully resolves AOM not attributable to penicillin-nonsusceptible pneumococcus.⁶Bottom line: Even though the number of potential antibiotics has contracted in the past 20 years, the need to individualize AOM treatment remains important and duration choices are more complex. Indeed, AOM comes in different flavors with patient age, clinical presentation, and episode frequency dictating the choice of duration.
 

Dr. Christopher J. Harrison is professor of pediatrics and pediatric infectious diseases at Children’s Mercy Hospitals and Clinics in Kansas City, Mo. Email him at pdnews@mdedge.com.

References

1. Pichichero ME. MDedge. 2022 Jan 11.

2. Ruohola A et al. Pediatrics. 2003;111(5):1061-7.

3. Hoberman A et al. N Engl J Med. 2016;375(25):2446-56.

4. Pichichero ME et al. Otolaryngol Head Neck Surg. 2001;124(4):381-7.

5. Harrison CJ et al. Pediatr Infect Dis. 1985;4(6):641-6.

6. Leibovitz E et al. Pediatr Infect Dis. 2000;19(11):1040-5.

I agree with most advice given by the affable TV character Ted Lasso. “Every choice is a chance,” he said. Pandemic-era physicians must now consider whether a politically motivated choice to decline COVID-19 vaccination should negatively affect the chance to receive an organ donation.

And in confronting these choices, we have a chance to educate the public on the complexities of the organ allocation process.

A well-informed patient’s personal choice should be honored, even if clinicians disagree, if it does not affect the well-being of others. For example, I once had a patient in acute leukemic crisis who declined blood products because she was a Jehovah’s Witness. She died. Her choice affected her longevity only.

Compare that decision with awarding an organ to an individual who has declined readily available protection of that organ. Weigh that choice against the fact that said protection is against an infectious disease that has killed over 5.5 million worldwide.
 

Some institutions stand strong, others hedge their bets

Admirably, Loyola University Health System understands that difference. They published a firm stand on transplant candidacy and COVID-19 vaccination status in the Journal of Heart and Lung Transplant. Daniel Dilling, MD, medical director of the lung transplantation program , and Mark Kuczewski, PhD, a professor of medical ethics at Loyola University Chicago, Maywood, Ill., wrote that: “We believe that requiring vaccination against COVID-19 should not be controversial when we focus strictly on established frameworks and practices surrounding eligibility for wait-listing to receive a solid organ transplant.”

The Cleveland Clinic apparently agrees. In October 2021, they denied a liver transplant to Michelle Vitullo of Ohio, whose daughter had been deemed “a perfect match.” Her daughter, also unvaccinated, stated: “Being denied for a nonmedical reason for someone’s beliefs that are different to yours, I mean that’s not how that should be.”

But vaccination status is a medical reason, given well-established data regarding increased mortality  among the immunosuppressed. Ms. Vitullo then said: “We are trying to get to UPMC [University of Pittsburgh Medical Center] as they don’t require a vaccination.”

The public information page on transplant candidacy from UPMC reads (my italics): It is recommended that all transplant candidates, transplant recipients, and their household members receive COVID-19 vaccination when the vaccine is available to them. It is preferred that transplant candidates are vaccinated more than 2 weeks before transplantation.

I reached out to UPMC for clarification and was told by email that “we do not have a policy regarding COVID-19 vaccination requirement for current transplant candidates.” Houston Methodist shares the same agnostic stance.

Compare these opinions with Brigham and Women’s Hospital, where the requirements are resolute: “Like most other transplant programs across the country, the COVID-19 vaccine is one of several vaccines and lifestyle behaviors that are required for patients awaiting solid organ transplant.”

They add that “transplant candidates must also receive the seasonal influenza and hepatitis B vaccines, follow other healthy behaviors, and demonstrate they can commit to taking the required medications following transplant.”

In January 2022, Brigham and Women’s Hospital declared 31-year-old D.J. Ferguson ineligible for a heart transplant because he declined to be vaccinated against COVID-19. According to the New York Post and ABC News, his physicians resorted to left ventricular assist device support. His mother, Tracy Ferguson, is quoted as saying: “He’s not an antivaxxer. He has all of his vaccines.” I’ll just leave that right there.

Unfortunately, Michelle Vitullo’s obituary was published in December 2021. Regardless of whether she received her liver transplant, the outcome is tragic, and whatever you think of this family’s battle playing out in the glare of the national spotlight, their loss is no less devastating.

The directed-donation aspect of this case poses an interesting question. A news anchor asked the mother and daughter: “If you both accept the risks, why doesn’t the hospital just let you try?” The answers are obvious to us clinicians. Performing a transplantation in an unvaccinated patient could lead to their early death if they became infected because of their immunocompromised state, would open the door for transplantation of any patient who is unvaccinated for anything, including influenza and hepatitis B, which could result in the preventable waste of organs, and puts other vulnerable hospitalized patients at risk during the initial transplant stay and follow-up.

That’s not to mention the potential legal suit. Never has a consent form dissuaded any party from lodging an accusation of wrongful death or medical malpractice. In the face of strong data on higher mortality in unvaccinated, immunocompromised patients, a good lawyer could charge that the institution and transplant surgeons should have known better, regardless of the donor and recipient’s willingness to accept the risks.

The Vitullo and Ferguson cases are among many similar dilemmas surrounding transplant candidacy across the United States.

University of Virginia Health in Charlottesville denied 42-year-old Shamgar Connors a kidney transplant because he is unvaccinated, despite a previous COVID-19 infection. In October 2021, Leilani Lutali of Colorado was denied a kidney by UCHealth because she declined vaccination. 

AppleTV

As Ted Lasso says: “There’s a bunch of crazy stuff on Twitter.”

Predictably, social media is full of public outcry. “Some cold-hearted people on here” tweeted one. “What if it was one of your loved ones who needed a transplant?” Another tweeted the Hippocratic oath with the comment that “They all swore under this noble ‘oat’, but I guess it’s been forgotten.” (This was followed with a photo of a box of Quaker Oats in a failed attempt at humor.) These discussions among the Twitterati highlight the depths of misunderstanding on organ transplantation.

To be fair, unless you have been personally involved in the decision-making process for transplant candidacy, there is little opportunity to be educated. I explain to my anxious patients and their families that a donor organ is like a fumbled football. There may be well over 100 patients at all levels of transplant status in many geographic locations diving for that same organ.

The transplant team is tasked with finding the best match, determining who is the sickest, assessing time for transport of that organ, and, above all, who will be the best steward of that organ.

Take heart transplantation, for instance. Approximately 3,500 patients in the United States are awaiting one each year. Instead of facing an almost certain death within 5 years, a transplant recipient has a chance at a median survival of 12-13 years. The cost of a heart transplant is approximately $1.38 million, according to Milliman, a consulting firm. This is “an incredibly resource intensive procedure,” including expenditures for transportation, antirejection medication, office visits, physician fees, ICU stays, rejection surveillance, and acute rejection therapies.
 

 

Transplant denial is nothing new

People get turned down for organ transplants all the time. My patient with end-stage dilated cardiomyopathy was denied a heart transplant when it was discovered that he had scores of outstanding parking tickets. This was seen as a surrogate for an inability to afford his antirejection medication.

Another patient swore that her positive cotinine levels were caused by endless hours at the bingo hall where second-hand smoke swirled. She was also denied. Many potential candidates who are in acute decline hold precariously to newfound sobriety. They are denied. A patient’s boyfriend told the transplant team that he couldn’t be relied upon to drive her to her appointments. She was denied.

Many people who engage in antisocial behaviors have no idea that these actions may result in the denial of an organ transplant should their future selves need one. These are hard lines, but everyone should agree that the odds of survival are heavily in favor of the consistently adherent.

We should take this opportunity to educate the public on how complicated obtaining an organ transplant can be. More than 6,000 people die each year waiting for an organ because of the supply-and-demand disparities in the transplantation arena. I’m willing to bet that many of the loudest protesters in favor of unvaccinated transplant recipients have not signed the organ donor box on the back of their driver’s license. This conversation is an opportunity to change that and remind people that organ donation may be their only opportunity to save a fellow human’s life.

Again, to quote Ted Lasso: “If you care about someone and you got a little love in your heart, there ain’t nothing you can’t get through together.” That philosophy should apply to the tasks of selecting the best organ donors as well as the best organ recipients.

And every organ should go to the one who will honor their donor and their donor’s family by taking the best care of that ultimate gift of life, including being vaccinated against COVID-19.

Dr. Walton-Shirley is a native Kentuckian who retired from full-time invasive cardiology. She enjoys locums work in Montana and is a champion of physician rights and patient safety. She disclosed no relevant conflicts of interest. A version of this article first appeared on Medscape.com.

I agree with most advice given by the affable TV character Ted Lasso. “Every choice is a chance,” he said. Pandemic-era physicians must now consider whether a politically motivated choice to decline COVID-19 vaccination should negatively affect the chance to receive an organ donation.

And in confronting these choices, we have a chance to educate the public on the complexities of the organ allocation process.

A well-informed patient’s personal choice should be honored, even if clinicians disagree, if it does not affect the well-being of others. For example, I once had a patient in acute leukemic crisis who declined blood products because she was a Jehovah’s Witness. She died. Her choice affected her longevity only.

Compare that decision with awarding an organ to an individual who has declined readily available protection of that organ. Weigh that choice against the fact that said protection is against an infectious disease that has killed over 5.5 million worldwide.
 

Some institutions stand strong, others hedge their bets

Admirably, Loyola University Health System understands that difference. They published a firm stand on transplant candidacy and COVID-19 vaccination status in the Journal of Heart and Lung Transplant. Daniel Dilling, MD, medical director of the lung transplantation program , and Mark Kuczewski, PhD, a professor of medical ethics at Loyola University Chicago, Maywood, Ill., wrote that: “We believe that requiring vaccination against COVID-19 should not be controversial when we focus strictly on established frameworks and practices surrounding eligibility for wait-listing to receive a solid organ transplant.”

The Cleveland Clinic apparently agrees. In October 2021, they denied a liver transplant to Michelle Vitullo of Ohio, whose daughter had been deemed “a perfect match.” Her daughter, also unvaccinated, stated: “Being denied for a nonmedical reason for someone’s beliefs that are different to yours, I mean that’s not how that should be.”

But vaccination status is a medical reason, given well-established data regarding increased mortality  among the immunosuppressed. Ms. Vitullo then said: “We are trying to get to UPMC [University of Pittsburgh Medical Center] as they don’t require a vaccination.”

The public information page on transplant candidacy from UPMC reads (my italics): It is recommended that all transplant candidates, transplant recipients, and their household members receive COVID-19 vaccination when the vaccine is available to them. It is preferred that transplant candidates are vaccinated more than 2 weeks before transplantation.

I reached out to UPMC for clarification and was told by email that “we do not have a policy regarding COVID-19 vaccination requirement for current transplant candidates.” Houston Methodist shares the same agnostic stance.

Compare these opinions with Brigham and Women’s Hospital, where the requirements are resolute: “Like most other transplant programs across the country, the COVID-19 vaccine is one of several vaccines and lifestyle behaviors that are required for patients awaiting solid organ transplant.”

They add that “transplant candidates must also receive the seasonal influenza and hepatitis B vaccines, follow other healthy behaviors, and demonstrate they can commit to taking the required medications following transplant.”

In January 2022, Brigham and Women’s Hospital declared 31-year-old D.J. Ferguson ineligible for a heart transplant because he declined to be vaccinated against COVID-19. According to the New York Post and ABC News, his physicians resorted to left ventricular assist device support. His mother, Tracy Ferguson, is quoted as saying: “He’s not an antivaxxer. He has all of his vaccines.” I’ll just leave that right there.

Unfortunately, Michelle Vitullo’s obituary was published in December 2021. Regardless of whether she received her liver transplant, the outcome is tragic, and whatever you think of this family’s battle playing out in the glare of the national spotlight, their loss is no less devastating.

The directed-donation aspect of this case poses an interesting question. A news anchor asked the mother and daughter: “If you both accept the risks, why doesn’t the hospital just let you try?” The answers are obvious to us clinicians. Performing a transplantation in an unvaccinated patient could lead to their early death if they became infected because of their immunocompromised state, would open the door for transplantation of any patient who is unvaccinated for anything, including influenza and hepatitis B, which could result in the preventable waste of organs, and puts other vulnerable hospitalized patients at risk during the initial transplant stay and follow-up.

That’s not to mention the potential legal suit. Never has a consent form dissuaded any party from lodging an accusation of wrongful death or medical malpractice. In the face of strong data on higher mortality in unvaccinated, immunocompromised patients, a good lawyer could charge that the institution and transplant surgeons should have known better, regardless of the donor and recipient’s willingness to accept the risks.

The Vitullo and Ferguson cases are among many similar dilemmas surrounding transplant candidacy across the United States.

University of Virginia Health in Charlottesville denied 42-year-old Shamgar Connors a kidney transplant because he is unvaccinated, despite a previous COVID-19 infection. In October 2021, Leilani Lutali of Colorado was denied a kidney by UCHealth because she declined vaccination. 

AppleTV

As Ted Lasso says: “There’s a bunch of crazy stuff on Twitter.”

Predictably, social media is full of public outcry. “Some cold-hearted people on here” tweeted one. “What if it was one of your loved ones who needed a transplant?” Another tweeted the Hippocratic oath with the comment that “They all swore under this noble ‘oat’, but I guess it’s been forgotten.” (This was followed with a photo of a box of Quaker Oats in a failed attempt at humor.) These discussions among the Twitterati highlight the depths of misunderstanding on organ transplantation.

To be fair, unless you have been personally involved in the decision-making process for transplant candidacy, there is little opportunity to be educated. I explain to my anxious patients and their families that a donor organ is like a fumbled football. There may be well over 100 patients at all levels of transplant status in many geographic locations diving for that same organ.

The transplant team is tasked with finding the best match, determining who is the sickest, assessing time for transport of that organ, and, above all, who will be the best steward of that organ.

Take heart transplantation, for instance. Approximately 3,500 patients in the United States are awaiting one each year. Instead of facing an almost certain death within 5 years, a transplant recipient has a chance at a median survival of 12-13 years. The cost of a heart transplant is approximately $1.38 million, according to Milliman, a consulting firm. This is “an incredibly resource intensive procedure,” including expenditures for transportation, antirejection medication, office visits, physician fees, ICU stays, rejection surveillance, and acute rejection therapies.
 

 

Transplant denial is nothing new

People get turned down for organ transplants all the time. My patient with end-stage dilated cardiomyopathy was denied a heart transplant when it was discovered that he had scores of outstanding parking tickets. This was seen as a surrogate for an inability to afford his antirejection medication.

Another patient swore that her positive cotinine levels were caused by endless hours at the bingo hall where second-hand smoke swirled. She was also denied. Many potential candidates who are in acute decline hold precariously to newfound sobriety. They are denied. A patient’s boyfriend told the transplant team that he couldn’t be relied upon to drive her to her appointments. She was denied.

Many people who engage in antisocial behaviors have no idea that these actions may result in the denial of an organ transplant should their future selves need one. These are hard lines, but everyone should agree that the odds of survival are heavily in favor of the consistently adherent.

We should take this opportunity to educate the public on how complicated obtaining an organ transplant can be. More than 6,000 people die each year waiting for an organ because of the supply-and-demand disparities in the transplantation arena. I’m willing to bet that many of the loudest protesters in favor of unvaccinated transplant recipients have not signed the organ donor box on the back of their driver’s license. This conversation is an opportunity to change that and remind people that organ donation may be their only opportunity to save a fellow human’s life.

Again, to quote Ted Lasso: “If you care about someone and you got a little love in your heart, there ain’t nothing you can’t get through together.” That philosophy should apply to the tasks of selecting the best organ donors as well as the best organ recipients.

And every organ should go to the one who will honor their donor and their donor’s family by taking the best care of that ultimate gift of life, including being vaccinated against COVID-19.

Dr. Walton-Shirley is a native Kentuckian who retired from full-time invasive cardiology. She enjoys locums work in Montana and is a champion of physician rights and patient safety. She disclosed no relevant conflicts of interest. A version of this article first appeared on Medscape.com.

I agree with most advice given by the affable TV character Ted Lasso. “Every choice is a chance,” he said. Pandemic-era physicians must now consider whether a politically motivated choice to decline COVID-19 vaccination should negatively affect the chance to receive an organ donation.

And in confronting these choices, we have a chance to educate the public on the complexities of the organ allocation process.

A well-informed patient’s personal choice should be honored, even if clinicians disagree, if it does not affect the well-being of others. For example, I once had a patient in acute leukemic crisis who declined blood products because she was a Jehovah’s Witness. She died. Her choice affected her longevity only.

Compare that decision with awarding an organ to an individual who has declined readily available protection of that organ. Weigh that choice against the fact that said protection is against an infectious disease that has killed over 5.5 million worldwide.
 

Some institutions stand strong, others hedge their bets

Admirably, Loyola University Health System understands that difference. They published a firm stand on transplant candidacy and COVID-19 vaccination status in the Journal of Heart and Lung Transplant. Daniel Dilling, MD, medical director of the lung transplantation program , and Mark Kuczewski, PhD, a professor of medical ethics at Loyola University Chicago, Maywood, Ill., wrote that: “We believe that requiring vaccination against COVID-19 should not be controversial when we focus strictly on established frameworks and practices surrounding eligibility for wait-listing to receive a solid organ transplant.”

The Cleveland Clinic apparently agrees. In October 2021, they denied a liver transplant to Michelle Vitullo of Ohio, whose daughter had been deemed “a perfect match.” Her daughter, also unvaccinated, stated: “Being denied for a nonmedical reason for someone’s beliefs that are different to yours, I mean that’s not how that should be.”

But vaccination status is a medical reason, given well-established data regarding increased mortality  among the immunosuppressed. Ms. Vitullo then said: “We are trying to get to UPMC [University of Pittsburgh Medical Center] as they don’t require a vaccination.”

The public information page on transplant candidacy from UPMC reads (my italics): It is recommended that all transplant candidates, transplant recipients, and their household members receive COVID-19 vaccination when the vaccine is available to them. It is preferred that transplant candidates are vaccinated more than 2 weeks before transplantation.

I reached out to UPMC for clarification and was told by email that “we do not have a policy regarding COVID-19 vaccination requirement for current transplant candidates.” Houston Methodist shares the same agnostic stance.

Compare these opinions with Brigham and Women’s Hospital, where the requirements are resolute: “Like most other transplant programs across the country, the COVID-19 vaccine is one of several vaccines and lifestyle behaviors that are required for patients awaiting solid organ transplant.”

They add that “transplant candidates must also receive the seasonal influenza and hepatitis B vaccines, follow other healthy behaviors, and demonstrate they can commit to taking the required medications following transplant.”

In January 2022, Brigham and Women’s Hospital declared 31-year-old D.J. Ferguson ineligible for a heart transplant because he declined to be vaccinated against COVID-19. According to the New York Post and ABC News, his physicians resorted to left ventricular assist device support. His mother, Tracy Ferguson, is quoted as saying: “He’s not an antivaxxer. He has all of his vaccines.” I’ll just leave that right there.

Unfortunately, Michelle Vitullo’s obituary was published in December 2021. Regardless of whether she received her liver transplant, the outcome is tragic, and whatever you think of this family’s battle playing out in the glare of the national spotlight, their loss is no less devastating.

The directed-donation aspect of this case poses an interesting question. A news anchor asked the mother and daughter: “If you both accept the risks, why doesn’t the hospital just let you try?” The answers are obvious to us clinicians. Performing a transplantation in an unvaccinated patient could lead to their early death if they became infected because of their immunocompromised state, would open the door for transplantation of any patient who is unvaccinated for anything, including influenza and hepatitis B, which could result in the preventable waste of organs, and puts other vulnerable hospitalized patients at risk during the initial transplant stay and follow-up.

That’s not to mention the potential legal suit. Never has a consent form dissuaded any party from lodging an accusation of wrongful death or medical malpractice. In the face of strong data on higher mortality in unvaccinated, immunocompromised patients, a good lawyer could charge that the institution and transplant surgeons should have known better, regardless of the donor and recipient’s willingness to accept the risks.

The Vitullo and Ferguson cases are among many similar dilemmas surrounding transplant candidacy across the United States.

University of Virginia Health in Charlottesville denied 42-year-old Shamgar Connors a kidney transplant because he is unvaccinated, despite a previous COVID-19 infection. In October 2021, Leilani Lutali of Colorado was denied a kidney by UCHealth because she declined vaccination. 

AppleTV

As Ted Lasso says: “There’s a bunch of crazy stuff on Twitter.”

Predictably, social media is full of public outcry. “Some cold-hearted people on here” tweeted one. “What if it was one of your loved ones who needed a transplant?” Another tweeted the Hippocratic oath with the comment that “They all swore under this noble ‘oat’, but I guess it’s been forgotten.” (This was followed with a photo of a box of Quaker Oats in a failed attempt at humor.) These discussions among the Twitterati highlight the depths of misunderstanding on organ transplantation.

To be fair, unless you have been personally involved in the decision-making process for transplant candidacy, there is little opportunity to be educated. I explain to my anxious patients and their families that a donor organ is like a fumbled football. There may be well over 100 patients at all levels of transplant status in many geographic locations diving for that same organ.

The transplant team is tasked with finding the best match, determining who is the sickest, assessing time for transport of that organ, and, above all, who will be the best steward of that organ.

Take heart transplantation, for instance. Approximately 3,500 patients in the United States are awaiting one each year. Instead of facing an almost certain death within 5 years, a transplant recipient has a chance at a median survival of 12-13 years. The cost of a heart transplant is approximately $1.38 million, according to Milliman, a consulting firm. This is “an incredibly resource intensive procedure,” including expenditures for transportation, antirejection medication, office visits, physician fees, ICU stays, rejection surveillance, and acute rejection therapies.
 

 

Transplant denial is nothing new

People get turned down for organ transplants all the time. My patient with end-stage dilated cardiomyopathy was denied a heart transplant when it was discovered that he had scores of outstanding parking tickets. This was seen as a surrogate for an inability to afford his antirejection medication.

Another patient swore that her positive cotinine levels were caused by endless hours at the bingo hall where second-hand smoke swirled. She was also denied. Many potential candidates who are in acute decline hold precariously to newfound sobriety. They are denied. A patient’s boyfriend told the transplant team that he couldn’t be relied upon to drive her to her appointments. She was denied.

Many people who engage in antisocial behaviors have no idea that these actions may result in the denial of an organ transplant should their future selves need one. These are hard lines, but everyone should agree that the odds of survival are heavily in favor of the consistently adherent.

We should take this opportunity to educate the public on how complicated obtaining an organ transplant can be. More than 6,000 people die each year waiting for an organ because of the supply-and-demand disparities in the transplantation arena. I’m willing to bet that many of the loudest protesters in favor of unvaccinated transplant recipients have not signed the organ donor box on the back of their driver’s license. This conversation is an opportunity to change that and remind people that organ donation may be their only opportunity to save a fellow human’s life.

Again, to quote Ted Lasso: “If you care about someone and you got a little love in your heart, there ain’t nothing you can’t get through together.” That philosophy should apply to the tasks of selecting the best organ donors as well as the best organ recipients.

And every organ should go to the one who will honor their donor and their donor’s family by taking the best care of that ultimate gift of life, including being vaccinated against COVID-19.

Dr. Walton-Shirley is a native Kentuckian who retired from full-time invasive cardiology. She enjoys locums work in Montana and is a champion of physician rights and patient safety. She disclosed no relevant conflicts of interest. A version of this article first appeared on Medscape.com.