Commentary

Octavio has prostate cancer. His prostate growth is large but localized.

“What do your doctors suggest?” I asked him.

“They sent me to two specialists at the medical center,” he said. “One does robotic surgery, the other does radiation. Each one told me why they recommend their technique.”

“How will you decide?”

“I’ll do some reading,” he said.

“What about the doctor who sent you to them?”

“He hasn’t discussed the choice with me, just sent me to get opinions. I have to make up own mind.”

Out of training for some time, I gather from students and family medical interactions that patient autonomy is now a reigning principle. Here is one definition:

Patient autonomy: The right of patients to make decisions about their medical care without their health care provider trying to influence the decision. Patient autonomy does allow for health care providers to educate the patient but does not allow the health care provider to make the decision for the patient.


This sounds sensible, even admirable: no more paternalistic physicians talking down to patients and ordering them around. Yet a closer look shows a contradiction:

1. The second sentence says that patient autonomy “does not allow the health care provider to make the decision for the patient.”

2. But the first one says that patients should decide, “without their health care provider trying to influence the decision.”

Is “trying to influence” the same as making the decision for the patient?

Some would argue that it is: The power discrepancy between the parties makes a doctor’s attempt to influence amount to coercion.

Do you agree, esteemed colleagues, those of you who, like me, treat patients all day? If the choice is between freezing an actinic keratosis, burning it, or using topical chemotherapy, do you just lay all three options out there and ask the patient to pick one? What if your patient works in public and doesn’t have 2 weeks to wait while the reaction to topical 5-fluorouracil that makes his skin look like raw lobster subsides? Can you point that out? Or would that be “trying to influence” and thus not allowed?

FatCamera/Getty Images

You and I can think of many other examples, about medical choices large and small, where we could pose similar questions. This is not abstract philosophy; it is what we do all day.

Look up robot-assisted surgery and radiation for prostate cancer. You will find proponents of both, each making claims concerning survival, recurrence, discomfort, complications. Which is more important – a 15% greater chance of living 2 years longer or a 22% lower risk of incontinence? Will reading such statistics make your choice easier? What if other studies show different numbers?

Octavio chose surgery. I asked him how he decided.

“I talked with an internist I know socially,” he said. “He shared his experience with patients he’s referred for my problem and advised surgery as the better choice. I also saw a story online about a lawyer who chose one method, then 5 years later had to do the other.”

Octavio is sophisticated and well read. He lives near Boston, the self-described hub of medical expertise and academic excellence. Yet he makes up his mind the way everybody does: by asking a trusted adviser, by hearing an arresting anecdote. It’s not science. It’s how people think.

You don’t have to be a behavioral psychologist to know how hard it is for patients, especially frightened ones, to interpret statistical variances or compare disparate categories. Which is better – shorter life with less pain or longer life with more? How much less? How much more? There are ways to address such questions, but having an expert, trusted, and sympathetic adviser is a pretty good way to start. Only an abstract ethicist with no practical exposure to (or sympathy with) actual existing patients and their actual existing providers could possibly think otherwise.

“Let’s freeze those actinics off,” I suggest to a patient. “That won’t scar, you won’t need a dozen shots of lidocaine, and you won’t have to hide for 3 weeks.”

Dr. Rockoff practices dermatology in Brookline, Mass., and is a longtime contributor to Dermatology News. He serves on the clinical faculty at Tufts University, Boston, and has taught senior medical students and other trainees for 30 years. His second book, “Act Like a Doctor, Think Like a Patient,” is available at amazon.com and barnesandnoble.com. Write to him at dermnews@mdedge.com.

Octavio has prostate cancer. His prostate growth is large but localized.

“What do your doctors suggest?” I asked him.

“They sent me to two specialists at the medical center,” he said. “One does robotic surgery, the other does radiation. Each one told me why they recommend their technique.”

“How will you decide?”

“I’ll do some reading,” he said.

“What about the doctor who sent you to them?”

“He hasn’t discussed the choice with me, just sent me to get opinions. I have to make up own mind.”

Out of training for some time, I gather from students and family medical interactions that patient autonomy is now a reigning principle. Here is one definition:

Patient autonomy: The right of patients to make decisions about their medical care without their health care provider trying to influence the decision. Patient autonomy does allow for health care providers to educate the patient but does not allow the health care provider to make the decision for the patient.


This sounds sensible, even admirable: no more paternalistic physicians talking down to patients and ordering them around. Yet a closer look shows a contradiction:

1. The second sentence says that patient autonomy “does not allow the health care provider to make the decision for the patient.”

2. But the first one says that patients should decide, “without their health care provider trying to influence the decision.”

Is “trying to influence” the same as making the decision for the patient?

Some would argue that it is: The power discrepancy between the parties makes a doctor’s attempt to influence amount to coercion.

Do you agree, esteemed colleagues, those of you who, like me, treat patients all day? If the choice is between freezing an actinic keratosis, burning it, or using topical chemotherapy, do you just lay all three options out there and ask the patient to pick one? What if your patient works in public and doesn’t have 2 weeks to wait while the reaction to topical 5-fluorouracil that makes his skin look like raw lobster subsides? Can you point that out? Or would that be “trying to influence” and thus not allowed?

FatCamera/Getty Images

You and I can think of many other examples, about medical choices large and small, where we could pose similar questions. This is not abstract philosophy; it is what we do all day.

Look up robot-assisted surgery and radiation for prostate cancer. You will find proponents of both, each making claims concerning survival, recurrence, discomfort, complications. Which is more important – a 15% greater chance of living 2 years longer or a 22% lower risk of incontinence? Will reading such statistics make your choice easier? What if other studies show different numbers?

Octavio chose surgery. I asked him how he decided.

“I talked with an internist I know socially,” he said. “He shared his experience with patients he’s referred for my problem and advised surgery as the better choice. I also saw a story online about a lawyer who chose one method, then 5 years later had to do the other.”

Octavio is sophisticated and well read. He lives near Boston, the self-described hub of medical expertise and academic excellence. Yet he makes up his mind the way everybody does: by asking a trusted adviser, by hearing an arresting anecdote. It’s not science. It’s how people think.

You don’t have to be a behavioral psychologist to know how hard it is for patients, especially frightened ones, to interpret statistical variances or compare disparate categories. Which is better – shorter life with less pain or longer life with more? How much less? How much more? There are ways to address such questions, but having an expert, trusted, and sympathetic adviser is a pretty good way to start. Only an abstract ethicist with no practical exposure to (or sympathy with) actual existing patients and their actual existing providers could possibly think otherwise.

“Let’s freeze those actinics off,” I suggest to a patient. “That won’t scar, you won’t need a dozen shots of lidocaine, and you won’t have to hide for 3 weeks.”

Dr. Rockoff practices dermatology in Brookline, Mass., and is a longtime contributor to Dermatology News. He serves on the clinical faculty at Tufts University, Boston, and has taught senior medical students and other trainees for 30 years. His second book, “Act Like a Doctor, Think Like a Patient,” is available at amazon.com and barnesandnoble.com. Write to him at dermnews@mdedge.com.

Octavio has prostate cancer. His prostate growth is large but localized.

“What do your doctors suggest?” I asked him.

“They sent me to two specialists at the medical center,” he said. “One does robotic surgery, the other does radiation. Each one told me why they recommend their technique.”

“How will you decide?”

“I’ll do some reading,” he said.

“What about the doctor who sent you to them?”

“He hasn’t discussed the choice with me, just sent me to get opinions. I have to make up own mind.”

Out of training for some time, I gather from students and family medical interactions that patient autonomy is now a reigning principle. Here is one definition:

Patient autonomy: The right of patients to make decisions about their medical care without their health care provider trying to influence the decision. Patient autonomy does allow for health care providers to educate the patient but does not allow the health care provider to make the decision for the patient.


This sounds sensible, even admirable: no more paternalistic physicians talking down to patients and ordering them around. Yet a closer look shows a contradiction:

1. The second sentence says that patient autonomy “does not allow the health care provider to make the decision for the patient.”

2. But the first one says that patients should decide, “without their health care provider trying to influence the decision.”

Is “trying to influence” the same as making the decision for the patient?

Some would argue that it is: The power discrepancy between the parties makes a doctor’s attempt to influence amount to coercion.

Do you agree, esteemed colleagues, those of you who, like me, treat patients all day? If the choice is between freezing an actinic keratosis, burning it, or using topical chemotherapy, do you just lay all three options out there and ask the patient to pick one? What if your patient works in public and doesn’t have 2 weeks to wait while the reaction to topical 5-fluorouracil that makes his skin look like raw lobster subsides? Can you point that out? Or would that be “trying to influence” and thus not allowed?

FatCamera/Getty Images

You and I can think of many other examples, about medical choices large and small, where we could pose similar questions. This is not abstract philosophy; it is what we do all day.

Look up robot-assisted surgery and radiation for prostate cancer. You will find proponents of both, each making claims concerning survival, recurrence, discomfort, complications. Which is more important – a 15% greater chance of living 2 years longer or a 22% lower risk of incontinence? Will reading such statistics make your choice easier? What if other studies show different numbers?

Octavio chose surgery. I asked him how he decided.

“I talked with an internist I know socially,” he said. “He shared his experience with patients he’s referred for my problem and advised surgery as the better choice. I also saw a story online about a lawyer who chose one method, then 5 years later had to do the other.”

Octavio is sophisticated and well read. He lives near Boston, the self-described hub of medical expertise and academic excellence. Yet he makes up his mind the way everybody does: by asking a trusted adviser, by hearing an arresting anecdote. It’s not science. It’s how people think.

You don’t have to be a behavioral psychologist to know how hard it is for patients, especially frightened ones, to interpret statistical variances or compare disparate categories. Which is better – shorter life with less pain or longer life with more? How much less? How much more? There are ways to address such questions, but having an expert, trusted, and sympathetic adviser is a pretty good way to start. Only an abstract ethicist with no practical exposure to (or sympathy with) actual existing patients and their actual existing providers could possibly think otherwise.

“Let’s freeze those actinics off,” I suggest to a patient. “That won’t scar, you won’t need a dozen shots of lidocaine, and you won’t have to hide for 3 weeks.”

Dr. Rockoff practices dermatology in Brookline, Mass., and is a longtime contributor to Dermatology News. He serves on the clinical faculty at Tufts University, Boston, and has taught senior medical students and other trainees for 30 years. His second book, “Act Like a Doctor, Think Like a Patient,” is available at amazon.com and barnesandnoble.com. Write to him at dermnews@mdedge.com.

To the Editor: Even one death by suicide is too many. Suicide is complex and a serious national public health issue that affects people from all walks of life—not just veterans—for a variety of reasons. While there is still a lot we can learn about suicide, we know that suicide is preventable, treatment works, and there is hope.

At the US Department of Veterans Affairs (VA), our suicide prevention efforts are guided by the National Strategy for Preventing Veteran Suicide.¹ Published in 2018, this long-term strategy expands beyond crisis intervention and provides a framework for identifying priorities, organizing efforts, and focusing national attention and community resources to prevent suicide among veterans through a broad public health approach with an emphasis on comprehensive, community-based engagement.

This approach is grounded in 4 key areas: Primary prevention focuses on preventing suicidal behavior before it occurs; whole health considers factors beyond mental health, such as physical health, alcohol or substance misuse, and life events; application of data and research emphasizes evidence-based approaches that can be tailored to the needs of veterans in local communities; and collaboration educates and empowers diverse communities to participate in suicide prevention efforts through coordination.

A recent article by Russell Lemle, PhD, noted that the National Strategy does not emphasize the work of the VA, and he is correct.² Rather than perpetuate the myth that VA can address suicide alone, the strategy was intended to guide veteran suicide prevention efforts across the entire nation, not just within VA’s walls. It is a plan for how we can ALL work together to prevent veteran suicide. The National Strategy does not minimize VA’s role in suicide prevention. It enhances VA’s ability and expectation to engage in collaborative efforts across the nation.

Every year, about 6,000 veterans die by suicide, the majority of whom have not received recent VA care. We are mindful that some veterans may not receive any or all of their health care services from the VA, for various reasons, and want to be respectful and cognizant of those choices. To save lives, VA needs the support of partners across sectors. We need to ensure that multiple systems are working in a coordinated way to reach veterans where they live, work, and thrive.

Our philosophy is that there is no wrong door to care. That is why we focused on universal, non-VA community interventions. Preventing suicide among all of the nation’s 20 million veterans cannot be the sole responsibility of VA—it requires a nationwide effort. As there is no single cause of suicide, no single organization can tackle suicide prevention alone. Put simply, VA must ensure suicide prevention is a part of every aspect of veterans’ lives, not just their VA interactions. At VA, we know that the care and support that veterans need often comes before a mental health crisis occurs, and communities and families may be better equipped to provide these types of supports.

Activities or special interest groups can boost protective factors against suicide and combat risk factors. Communities can foster an environment where veterans can find connection and camaraderie, achieve a sense of purpose, bolster their coping skills, and live healthily. And partners like the National Shooting Sports Foundation help VA to address sensitive issues, such as lethal means safety, while correcting misconceptions about how VA handles gun ownership.

Data also are an integral piece of our public health approach, driving how VA defines the problem, targets its programs, and delivers and implements interventions. VA was one of the first institutions to implement comprehensive suicide analysis and predictive analytics, and VA has continuously improved data surveillance related to veteran suicide.

We began comprehensive suicide monitoring for the entire VA patient population in 2006, and in 2012, VA released its first report of suicide surveillance among all veterans in select partnering states. Though we are able to share data, we acknowledge the limitations Dr. Lemle highlighted in implementing predictive analytics program outside the VA. However, VA continues to improve reporting and surveillance efforts, especially to better understand the 20 veterans and service members who die by suicide each day.

As Lemle noted, little was previously known about the 14 of 20 veterans who die by suicide every day who weren’t recent users of VA health services. Since the September 2018 release of the National Strategy, VA has obtained additional data. In addition to sharing data, VA will focus on helping non-VA entities understand the problem so that they can help reach veterans who may never go to VA for care. Efforts are underway to better understand specific groups that are at elevated risk, such as veterans aged 18 to 34 years, women veterans, never federally activated guardsmen and reservists, recently separated veterans, and former service members with Other Than Honorable discharges.

To end veteran suicide, VA is relentlessly working to make improvements to existing suicide prevention programs, develop VA-specific plans to advance the National Strategy, find innovative ways to get people into care, and educate veterans and family members about VA care. Through Executive Order 13822, for example, VA has partnered with the Departments of Defense and Homeland Security, which allows us to educate service members about VA offerings before they become veterans. We also are making it easier for them to quickly find information online about VA mental health services.

We acknowledge VA is not a perfect organization, and a negative image can turn away veterans. VA is actively working with the media to get more good news stories published. We have many exciting things to talk about, such as a newly implemented Comprehensive Suicide Risk Assessment, and it is important for people to know that VA is providing the gold standard of care. Sometimes, those stories are better messaged and amplified by partners and non-VA entities, and this is a key part of our approach.

Lemle also raised a concern around funding this new public health initiative. While we recognize the challenges in advancing this new public health approach without additional funding, we are hopeful we can energize communities to work with us to find a solution.

The National Strategy is not the end of the conversation. It is a starting point. We are thankful for Lemle’s thoughtful questions and are actively pursuing and investigating solutions regarding veteran suicide studies, peer support, and community care guidelines for partners as we seek to improve our services. We also are putting pen to paper on a plan to strengthen family involvement and integrate suicide prevention within VA’s whole health and social services strategies.

The National Strategy is a call to action to every organization, system, and institution interested in preventing veteran suicide to help do this work where we cannot. For our part, VA will continue to energize communities to increase local involvement to reach all veterans, and we will continue to empower and equip ALL veterans with the resources and care they need to thrive.

To learn about the resources available for veterans and how you can #BeThere as a VA employee, family member, friend, community partner, or clinician, visit www.mentalhealth.va.gov/suicide_prevention/resources.asp. If you or someone you know is having thoughts of suicide, contact the Veterans Crisis Line to receive free, confidential support and crisis intervention available 24 hours a day, 7 days a week, 365 days a year. Call 800-273-8255 and press 1, text to 838255, or chat online at VeteransCrisisLine.net/Chat.

- Keita Franklin, LCSD, PhD

Author affiliations: Executive Director, Suicide Prevention VA Office of Mental Health and Suicide Prevention.

Author disclosures: Keita Franklin participated in the development of the National Strategy for Preventing Veteran Suicide .

Disclaimer: The opinions expressed herein are those of the author and do not necessarily reflect those of Federal Practitioner , Frontline Medical Communications Inc., the US Government, or any of its agencies.

Author Response: Keita Franklin, PhD, offers a valuable response to my December critique of the VA National Strategy to Prevent Veteran Suicide. Dr. Franklin thoughtfully articulates why public health approaches to prevent suicide must be a core component of a multifaceted strategy. She is right about that.

While I see considerable overlap between our statements, there are 2 important points where we diverge: (1) Unless Congress appropriates sufficient funds for extensive public health outreach, there is a danger that funds to implement it would be diverted from VA’s extant effective VA suicide prevention programs. (2) A prospective suicide prevention plan requires 3 prongs of universal, group, and individually focused strategies, because suicide cannot be prevented by any single strategy. The VA National Strategy as well as the March 2019 Executive Order on a National Roadmap to Empower Veterans and End Suicide, focus predominantly on universal strategies, and I believe its overall approach would be improved by also explicitly supporting VA’s targeted programs for at-risk veterans.

- Russell B. Lemle, PhD

Author affiliations: Policy Analyst at the Veterans Healthcare Policy Institute in Oakland, California.

To the Editor: Even one death by suicide is too many. Suicide is complex and a serious national public health issue that affects people from all walks of life—not just veterans—for a variety of reasons. While there is still a lot we can learn about suicide, we know that suicide is preventable, treatment works, and there is hope.

At the US Department of Veterans Affairs (VA), our suicide prevention efforts are guided by the National Strategy for Preventing Veteran Suicide.¹ Published in 2018, this long-term strategy expands beyond crisis intervention and provides a framework for identifying priorities, organizing efforts, and focusing national attention and community resources to prevent suicide among veterans through a broad public health approach with an emphasis on comprehensive, community-based engagement.

This approach is grounded in 4 key areas: Primary prevention focuses on preventing suicidal behavior before it occurs; whole health considers factors beyond mental health, such as physical health, alcohol or substance misuse, and life events; application of data and research emphasizes evidence-based approaches that can be tailored to the needs of veterans in local communities; and collaboration educates and empowers diverse communities to participate in suicide prevention efforts through coordination.

A recent article by Russell Lemle, PhD, noted that the National Strategy does not emphasize the work of the VA, and he is correct.² Rather than perpetuate the myth that VA can address suicide alone, the strategy was intended to guide veteran suicide prevention efforts across the entire nation, not just within VA’s walls. It is a plan for how we can ALL work together to prevent veteran suicide. The National Strategy does not minimize VA’s role in suicide prevention. It enhances VA’s ability and expectation to engage in collaborative efforts across the nation.

Every year, about 6,000 veterans die by suicide, the majority of whom have not received recent VA care. We are mindful that some veterans may not receive any or all of their health care services from the VA, for various reasons, and want to be respectful and cognizant of those choices. To save lives, VA needs the support of partners across sectors. We need to ensure that multiple systems are working in a coordinated way to reach veterans where they live, work, and thrive.

Our philosophy is that there is no wrong door to care. That is why we focused on universal, non-VA community interventions. Preventing suicide among all of the nation’s 20 million veterans cannot be the sole responsibility of VA—it requires a nationwide effort. As there is no single cause of suicide, no single organization can tackle suicide prevention alone. Put simply, VA must ensure suicide prevention is a part of every aspect of veterans’ lives, not just their VA interactions. At VA, we know that the care and support that veterans need often comes before a mental health crisis occurs, and communities and families may be better equipped to provide these types of supports.

Activities or special interest groups can boost protective factors against suicide and combat risk factors. Communities can foster an environment where veterans can find connection and camaraderie, achieve a sense of purpose, bolster their coping skills, and live healthily. And partners like the National Shooting Sports Foundation help VA to address sensitive issues, such as lethal means safety, while correcting misconceptions about how VA handles gun ownership.

Data also are an integral piece of our public health approach, driving how VA defines the problem, targets its programs, and delivers and implements interventions. VA was one of the first institutions to implement comprehensive suicide analysis and predictive analytics, and VA has continuously improved data surveillance related to veteran suicide.

We began comprehensive suicide monitoring for the entire VA patient population in 2006, and in 2012, VA released its first report of suicide surveillance among all veterans in select partnering states. Though we are able to share data, we acknowledge the limitations Dr. Lemle highlighted in implementing predictive analytics program outside the VA. However, VA continues to improve reporting and surveillance efforts, especially to better understand the 20 veterans and service members who die by suicide each day.

As Lemle noted, little was previously known about the 14 of 20 veterans who die by suicide every day who weren’t recent users of VA health services. Since the September 2018 release of the National Strategy, VA has obtained additional data. In addition to sharing data, VA will focus on helping non-VA entities understand the problem so that they can help reach veterans who may never go to VA for care. Efforts are underway to better understand specific groups that are at elevated risk, such as veterans aged 18 to 34 years, women veterans, never federally activated guardsmen and reservists, recently separated veterans, and former service members with Other Than Honorable discharges.

To end veteran suicide, VA is relentlessly working to make improvements to existing suicide prevention programs, develop VA-specific plans to advance the National Strategy, find innovative ways to get people into care, and educate veterans and family members about VA care. Through Executive Order 13822, for example, VA has partnered with the Departments of Defense and Homeland Security, which allows us to educate service members about VA offerings before they become veterans. We also are making it easier for them to quickly find information online about VA mental health services.

We acknowledge VA is not a perfect organization, and a negative image can turn away veterans. VA is actively working with the media to get more good news stories published. We have many exciting things to talk about, such as a newly implemented Comprehensive Suicide Risk Assessment, and it is important for people to know that VA is providing the gold standard of care. Sometimes, those stories are better messaged and amplified by partners and non-VA entities, and this is a key part of our approach.

Lemle also raised a concern around funding this new public health initiative. While we recognize the challenges in advancing this new public health approach without additional funding, we are hopeful we can energize communities to work with us to find a solution.

The National Strategy is not the end of the conversation. It is a starting point. We are thankful for Lemle’s thoughtful questions and are actively pursuing and investigating solutions regarding veteran suicide studies, peer support, and community care guidelines for partners as we seek to improve our services. We also are putting pen to paper on a plan to strengthen family involvement and integrate suicide prevention within VA’s whole health and social services strategies.

The National Strategy is a call to action to every organization, system, and institution interested in preventing veteran suicide to help do this work where we cannot. For our part, VA will continue to energize communities to increase local involvement to reach all veterans, and we will continue to empower and equip ALL veterans with the resources and care they need to thrive.

To learn about the resources available for veterans and how you can #BeThere as a VA employee, family member, friend, community partner, or clinician, visit www.mentalhealth.va.gov/suicide_prevention/resources.asp. If you or someone you know is having thoughts of suicide, contact the Veterans Crisis Line to receive free, confidential support and crisis intervention available 24 hours a day, 7 days a week, 365 days a year. Call 800-273-8255 and press 1, text to 838255, or chat online at VeteransCrisisLine.net/Chat.

- Keita Franklin, LCSD, PhD

Author affiliations: Executive Director, Suicide Prevention VA Office of Mental Health and Suicide Prevention.

Author disclosures: Keita Franklin participated in the development of the National Strategy for Preventing Veteran Suicide .

Disclaimer: The opinions expressed herein are those of the author and do not necessarily reflect those of Federal Practitioner , Frontline Medical Communications Inc., the US Government, or any of its agencies.

Author Response: Keita Franklin, PhD, offers a valuable response to my December critique of the VA National Strategy to Prevent Veteran Suicide. Dr. Franklin thoughtfully articulates why public health approaches to prevent suicide must be a core component of a multifaceted strategy. She is right about that.

While I see considerable overlap between our statements, there are 2 important points where we diverge: (1) Unless Congress appropriates sufficient funds for extensive public health outreach, there is a danger that funds to implement it would be diverted from VA’s extant effective VA suicide prevention programs. (2) A prospective suicide prevention plan requires 3 prongs of universal, group, and individually focused strategies, because suicide cannot be prevented by any single strategy. The VA National Strategy as well as the March 2019 Executive Order on a National Roadmap to Empower Veterans and End Suicide, focus predominantly on universal strategies, and I believe its overall approach would be improved by also explicitly supporting VA’s targeted programs for at-risk veterans.

- Russell B. Lemle, PhD

Author affiliations: Policy Analyst at the Veterans Healthcare Policy Institute in Oakland, California.

To the Editor: Even one death by suicide is too many. Suicide is complex and a serious national public health issue that affects people from all walks of life—not just veterans—for a variety of reasons. While there is still a lot we can learn about suicide, we know that suicide is preventable, treatment works, and there is hope.

At the US Department of Veterans Affairs (VA), our suicide prevention efforts are guided by the National Strategy for Preventing Veteran Suicide.¹ Published in 2018, this long-term strategy expands beyond crisis intervention and provides a framework for identifying priorities, organizing efforts, and focusing national attention and community resources to prevent suicide among veterans through a broad public health approach with an emphasis on comprehensive, community-based engagement.

This approach is grounded in 4 key areas: Primary prevention focuses on preventing suicidal behavior before it occurs; whole health considers factors beyond mental health, such as physical health, alcohol or substance misuse, and life events; application of data and research emphasizes evidence-based approaches that can be tailored to the needs of veterans in local communities; and collaboration educates and empowers diverse communities to participate in suicide prevention efforts through coordination.

A recent article by Russell Lemle, PhD, noted that the National Strategy does not emphasize the work of the VA, and he is correct.² Rather than perpetuate the myth that VA can address suicide alone, the strategy was intended to guide veteran suicide prevention efforts across the entire nation, not just within VA’s walls. It is a plan for how we can ALL work together to prevent veteran suicide. The National Strategy does not minimize VA’s role in suicide prevention. It enhances VA’s ability and expectation to engage in collaborative efforts across the nation.

Every year, about 6,000 veterans die by suicide, the majority of whom have not received recent VA care. We are mindful that some veterans may not receive any or all of their health care services from the VA, for various reasons, and want to be respectful and cognizant of those choices. To save lives, VA needs the support of partners across sectors. We need to ensure that multiple systems are working in a coordinated way to reach veterans where they live, work, and thrive.

Our philosophy is that there is no wrong door to care. That is why we focused on universal, non-VA community interventions. Preventing suicide among all of the nation’s 20 million veterans cannot be the sole responsibility of VA—it requires a nationwide effort. As there is no single cause of suicide, no single organization can tackle suicide prevention alone. Put simply, VA must ensure suicide prevention is a part of every aspect of veterans’ lives, not just their VA interactions. At VA, we know that the care and support that veterans need often comes before a mental health crisis occurs, and communities and families may be better equipped to provide these types of supports.

Activities or special interest groups can boost protective factors against suicide and combat risk factors. Communities can foster an environment where veterans can find connection and camaraderie, achieve a sense of purpose, bolster their coping skills, and live healthily. And partners like the National Shooting Sports Foundation help VA to address sensitive issues, such as lethal means safety, while correcting misconceptions about how VA handles gun ownership.

Data also are an integral piece of our public health approach, driving how VA defines the problem, targets its programs, and delivers and implements interventions. VA was one of the first institutions to implement comprehensive suicide analysis and predictive analytics, and VA has continuously improved data surveillance related to veteran suicide.

We began comprehensive suicide monitoring for the entire VA patient population in 2006, and in 2012, VA released its first report of suicide surveillance among all veterans in select partnering states. Though we are able to share data, we acknowledge the limitations Dr. Lemle highlighted in implementing predictive analytics program outside the VA. However, VA continues to improve reporting and surveillance efforts, especially to better understand the 20 veterans and service members who die by suicide each day.

As Lemle noted, little was previously known about the 14 of 20 veterans who die by suicide every day who weren’t recent users of VA health services. Since the September 2018 release of the National Strategy, VA has obtained additional data. In addition to sharing data, VA will focus on helping non-VA entities understand the problem so that they can help reach veterans who may never go to VA for care. Efforts are underway to better understand specific groups that are at elevated risk, such as veterans aged 18 to 34 years, women veterans, never federally activated guardsmen and reservists, recently separated veterans, and former service members with Other Than Honorable discharges.

To end veteran suicide, VA is relentlessly working to make improvements to existing suicide prevention programs, develop VA-specific plans to advance the National Strategy, find innovative ways to get people into care, and educate veterans and family members about VA care. Through Executive Order 13822, for example, VA has partnered with the Departments of Defense and Homeland Security, which allows us to educate service members about VA offerings before they become veterans. We also are making it easier for them to quickly find information online about VA mental health services.

We acknowledge VA is not a perfect organization, and a negative image can turn away veterans. VA is actively working with the media to get more good news stories published. We have many exciting things to talk about, such as a newly implemented Comprehensive Suicide Risk Assessment, and it is important for people to know that VA is providing the gold standard of care. Sometimes, those stories are better messaged and amplified by partners and non-VA entities, and this is a key part of our approach.

Lemle also raised a concern around funding this new public health initiative. While we recognize the challenges in advancing this new public health approach without additional funding, we are hopeful we can energize communities to work with us to find a solution.

The National Strategy is not the end of the conversation. It is a starting point. We are thankful for Lemle’s thoughtful questions and are actively pursuing and investigating solutions regarding veteran suicide studies, peer support, and community care guidelines for partners as we seek to improve our services. We also are putting pen to paper on a plan to strengthen family involvement and integrate suicide prevention within VA’s whole health and social services strategies.

The National Strategy is a call to action to every organization, system, and institution interested in preventing veteran suicide to help do this work where we cannot. For our part, VA will continue to energize communities to increase local involvement to reach all veterans, and we will continue to empower and equip ALL veterans with the resources and care they need to thrive.

To learn about the resources available for veterans and how you can #BeThere as a VA employee, family member, friend, community partner, or clinician, visit www.mentalhealth.va.gov/suicide_prevention/resources.asp. If you or someone you know is having thoughts of suicide, contact the Veterans Crisis Line to receive free, confidential support and crisis intervention available 24 hours a day, 7 days a week, 365 days a year. Call 800-273-8255 and press 1, text to 838255, or chat online at VeteransCrisisLine.net/Chat.

- Keita Franklin, LCSD, PhD

Author affiliations: Executive Director, Suicide Prevention VA Office of Mental Health and Suicide Prevention.

Author disclosures: Keita Franklin participated in the development of the National Strategy for Preventing Veteran Suicide .

Disclaimer: The opinions expressed herein are those of the author and do not necessarily reflect those of Federal Practitioner , Frontline Medical Communications Inc., the US Government, or any of its agencies.

Author Response: Keita Franklin, PhD, offers a valuable response to my December critique of the VA National Strategy to Prevent Veteran Suicide. Dr. Franklin thoughtfully articulates why public health approaches to prevent suicide must be a core component of a multifaceted strategy. She is right about that.

While I see considerable overlap between our statements, there are 2 important points where we diverge: (1) Unless Congress appropriates sufficient funds for extensive public health outreach, there is a danger that funds to implement it would be diverted from VA’s extant effective VA suicide prevention programs. (2) A prospective suicide prevention plan requires 3 prongs of universal, group, and individually focused strategies, because suicide cannot be prevented by any single strategy. The VA National Strategy as well as the March 2019 Executive Order on a National Roadmap to Empower Veterans and End Suicide, focus predominantly on universal strategies, and I believe its overall approach would be improved by also explicitly supporting VA’s targeted programs for at-risk veterans.

- Russell B. Lemle, PhD

Author affiliations: Policy Analyst at the Veterans Healthcare Policy Institute in Oakland, California.

Clinical trials represent future hope for patients seeking better care, and there is no disease more in need of better care than Alzheimer’s disease. While death rates among most cancers, as well as heart disease, HIV-related illness, and other categories, have declined in the past decade, there has been no progress for Alzheimer’s disease. Better health and wellness overall may be having a beneficial effect that has produced a reduction in age-adjusted dementia rates, but with the aging of the population there are a greater absolute number of dementia cases than ever before, and that number is expected to continue rising. Finding a disease-modifying therapy seems to be the best hope for changing this dim outlook. Clinical trials intend to do just that but are hampered by patient enrollment rates that remain low. Far fewer eligible patients enroll than are needed, causing studies to take longer to complete, driving up their costs and essentially slowing progress. There is a need to increase patient enrollment, and there has been a variety of efforts intended to address this, not the least of which has been an explosion of media coverage of Alzheimer’s disease.

The Global Alzheimer’s Platform (GAP) Foundation, a nonprofit, self-described patient-centric entity dedicated to reducing the time and cost of Alzheimer’s disease clinical trials, recently announced an initiative to increase participation in Alzheimer’s clinical trials by supporting and collaborating with “memory fitness programs” through select Medicare Advantage plans. At worst, this seems a harmless way to increase attention and hopefully interest in clinical trial participation. At best, this may be a cost-effective way to increase enrollment and even improve dementia care. Dementia is notoriously underdiagnosed, especially by overworked, busy primary care providers who simply lack the time to perform the time-consuming testing that is typically required to diagnose and follow such patients.

There are some caveats to consider. First, memory fitness programs are of dubious benefit. They generally fit the description of being harmless, but there is little compelling evidence that they preserve or improve memory.

Second, enrollment in a clinical trial, for a patient, is not always a winning proposition. To date, there has been little success and in the absence of benefit, any downside – even if simply an inconvenience – is a net negative. Recently at the 2018 Clinical Trials on Alzheimer’s Disease meeting, Merck reported that patients with mild cognitive impairment receiving active treatment in the BACE1 inhibitor verubecestat trial actually declined at a more rapid rate than did those on placebo. While the absolute difference was small, and one could argue whether it was clinically significant or simply a random occurrence, it was a reminder that intervention with an experimental agent is not necessarily benign.

Third, Medicare Advantage plans, while popular in some circles, are not considered advantageous to providers so that the proliferation of inadequate reimbursement will potentially fuel the accelerating number of providers who opt out of insurance plans altogether. This is not necessarily an issue for the GAP Foundation specifically but is nonetheless an issue for anything that promotes MA plans).

Finally, it remains important to help patients and families maintain a positive outlook, especially when we have nothing better to offer. Alzheimer’s disease is not a death sentence for every patient affected. While many have difficult and heartbreaking courses, some have slowly progressive courses with relatively little impairment for an extended period of time. There are also the dementia-phobic, cognitively unimpaired individuals (or who simply have normal age-associated cognitive changes) in whom the continued drumbeat of dementia awareness and memory testing raises their paranoia ever higher. We treat deficits (or try to), but we have to live based on our preserved skills. The challenge clinicians must face with patients and families is how to maximize function while compensating for deficits and making sure that patients and families maintain their hope.

Dr. Caselli is professor of neurology at the Mayo Clinic Arizona in Scottsdale and associate director and clinical core director of the Arizona Alzheimer’s Disease Center.

Clinical trials represent future hope for patients seeking better care, and there is no disease more in need of better care than Alzheimer’s disease. While death rates among most cancers, as well as heart disease, HIV-related illness, and other categories, have declined in the past decade, there has been no progress for Alzheimer’s disease. Better health and wellness overall may be having a beneficial effect that has produced a reduction in age-adjusted dementia rates, but with the aging of the population there are a greater absolute number of dementia cases than ever before, and that number is expected to continue rising. Finding a disease-modifying therapy seems to be the best hope for changing this dim outlook. Clinical trials intend to do just that but are hampered by patient enrollment rates that remain low. Far fewer eligible patients enroll than are needed, causing studies to take longer to complete, driving up their costs and essentially slowing progress. There is a need to increase patient enrollment, and there has been a variety of efforts intended to address this, not the least of which has been an explosion of media coverage of Alzheimer’s disease.

The Global Alzheimer’s Platform (GAP) Foundation, a nonprofit, self-described patient-centric entity dedicated to reducing the time and cost of Alzheimer’s disease clinical trials, recently announced an initiative to increase participation in Alzheimer’s clinical trials by supporting and collaborating with “memory fitness programs” through select Medicare Advantage plans. At worst, this seems a harmless way to increase attention and hopefully interest in clinical trial participation. At best, this may be a cost-effective way to increase enrollment and even improve dementia care. Dementia is notoriously underdiagnosed, especially by overworked, busy primary care providers who simply lack the time to perform the time-consuming testing that is typically required to diagnose and follow such patients.

There are some caveats to consider. First, memory fitness programs are of dubious benefit. They generally fit the description of being harmless, but there is little compelling evidence that they preserve or improve memory.

Second, enrollment in a clinical trial, for a patient, is not always a winning proposition. To date, there has been little success and in the absence of benefit, any downside – even if simply an inconvenience – is a net negative. Recently at the 2018 Clinical Trials on Alzheimer’s Disease meeting, Merck reported that patients with mild cognitive impairment receiving active treatment in the BACE1 inhibitor verubecestat trial actually declined at a more rapid rate than did those on placebo. While the absolute difference was small, and one could argue whether it was clinically significant or simply a random occurrence, it was a reminder that intervention with an experimental agent is not necessarily benign.

Third, Medicare Advantage plans, while popular in some circles, are not considered advantageous to providers so that the proliferation of inadequate reimbursement will potentially fuel the accelerating number of providers who opt out of insurance plans altogether. This is not necessarily an issue for the GAP Foundation specifically but is nonetheless an issue for anything that promotes MA plans).

Finally, it remains important to help patients and families maintain a positive outlook, especially when we have nothing better to offer. Alzheimer’s disease is not a death sentence for every patient affected. While many have difficult and heartbreaking courses, some have slowly progressive courses with relatively little impairment for an extended period of time. There are also the dementia-phobic, cognitively unimpaired individuals (or who simply have normal age-associated cognitive changes) in whom the continued drumbeat of dementia awareness and memory testing raises their paranoia ever higher. We treat deficits (or try to), but we have to live based on our preserved skills. The challenge clinicians must face with patients and families is how to maximize function while compensating for deficits and making sure that patients and families maintain their hope.

Dr. Caselli is professor of neurology at the Mayo Clinic Arizona in Scottsdale and associate director and clinical core director of the Arizona Alzheimer’s Disease Center.

Clinical trials represent future hope for patients seeking better care, and there is no disease more in need of better care than Alzheimer’s disease. While death rates among most cancers, as well as heart disease, HIV-related illness, and other categories, have declined in the past decade, there has been no progress for Alzheimer’s disease. Better health and wellness overall may be having a beneficial effect that has produced a reduction in age-adjusted dementia rates, but with the aging of the population there are a greater absolute number of dementia cases than ever before, and that number is expected to continue rising. Finding a disease-modifying therapy seems to be the best hope for changing this dim outlook. Clinical trials intend to do just that but are hampered by patient enrollment rates that remain low. Far fewer eligible patients enroll than are needed, causing studies to take longer to complete, driving up their costs and essentially slowing progress. There is a need to increase patient enrollment, and there has been a variety of efforts intended to address this, not the least of which has been an explosion of media coverage of Alzheimer’s disease.

The Global Alzheimer’s Platform (GAP) Foundation, a nonprofit, self-described patient-centric entity dedicated to reducing the time and cost of Alzheimer’s disease clinical trials, recently announced an initiative to increase participation in Alzheimer’s clinical trials by supporting and collaborating with “memory fitness programs” through select Medicare Advantage plans. At worst, this seems a harmless way to increase attention and hopefully interest in clinical trial participation. At best, this may be a cost-effective way to increase enrollment and even improve dementia care. Dementia is notoriously underdiagnosed, especially by overworked, busy primary care providers who simply lack the time to perform the time-consuming testing that is typically required to diagnose and follow such patients.

There are some caveats to consider. First, memory fitness programs are of dubious benefit. They generally fit the description of being harmless, but there is little compelling evidence that they preserve or improve memory.

Second, enrollment in a clinical trial, for a patient, is not always a winning proposition. To date, there has been little success and in the absence of benefit, any downside – even if simply an inconvenience – is a net negative. Recently at the 2018 Clinical Trials on Alzheimer’s Disease meeting, Merck reported that patients with mild cognitive impairment receiving active treatment in the BACE1 inhibitor verubecestat trial actually declined at a more rapid rate than did those on placebo. While the absolute difference was small, and one could argue whether it was clinically significant or simply a random occurrence, it was a reminder that intervention with an experimental agent is not necessarily benign.

Third, Medicare Advantage plans, while popular in some circles, are not considered advantageous to providers so that the proliferation of inadequate reimbursement will potentially fuel the accelerating number of providers who opt out of insurance plans altogether. This is not necessarily an issue for the GAP Foundation specifically but is nonetheless an issue for anything that promotes MA plans).

Finally, it remains important to help patients and families maintain a positive outlook, especially when we have nothing better to offer. Alzheimer’s disease is not a death sentence for every patient affected. While many have difficult and heartbreaking courses, some have slowly progressive courses with relatively little impairment for an extended period of time. There are also the dementia-phobic, cognitively unimpaired individuals (or who simply have normal age-associated cognitive changes) in whom the continued drumbeat of dementia awareness and memory testing raises their paranoia ever higher. We treat deficits (or try to), but we have to live based on our preserved skills. The challenge clinicians must face with patients and families is how to maximize function while compensating for deficits and making sure that patients and families maintain their hope.

Dr. Caselli is professor of neurology at the Mayo Clinic Arizona in Scottsdale and associate director and clinical core director of the Arizona Alzheimer’s Disease Center.

Q: Why is this a “banner day” for psychiatry?

A: This is truly the first new option for depression in 60 years. The selective serotonin reuptake inhibitors (SSRIs) developed in the mid-’80s were not truly new, not much different from the monoamine oxidase inhibitors (MAOI) and tricyclic antidepressants. In fact, they work much like watered-down MAOIs. Esketamine works by a truly novel mechanism.

Q: What is esketamine’s method of action, and how long will a dose last?

A: Ketamine and esketamine bind to and block glutamate N-methyl-D-aspartate (NMDA) receptors. This leads to the release of several chemical messengers, the result of which increases the production of neurotrophic factors, in particular brain-derived neurotrophic factor (BDNF), that play a key role in healing damaged connections in the brain. A single dose of esketamine would only be expected to relieve depression symptoms for days, up to a week or 2. Multiple doses over the first few weeks can extend the durability of response to several weeks and sometimes months.

It is not true for every patient, but some do have improvement within 2-4 hours that correlates with physiologic changes. Others can be later responders and require up to 6 exposures.

Q: The FDA approval requires those who administer the drug to complete special training and meet licensure requirements. Is this realistic for small practices?

A: Initially, not every psychiatrist will be able to offer esketamine, and I think it might be beyond the reach of small practices, and that’s probably okay. Enough people and enough centers will be able to offer it to meet the initial demand.

Q: Is esketamine “better” than ketamine infusions? With the approved drug available, will ketamine infusion clinics still have a place?

A: There are major pros with this. The FDA approval takes out of the gray area of off-label administration. It will most likely be covered by insurance now – a huge advantage that will put this in the reach of so many patients who haven’t been able to access this treatment.

I think that, because there are advantages and disadvantages for both IV ketamine and nasal esketamine, they will happily coexist for years to come. However, because nasal esketamine will likely be restricted to prescription by psychiatrists, it may have more impact on non-psychiatrist-led practices. In this way, esketamine may push the delivery of these treatments more exclusively into the hands of psychiatrists.

Dr. Steven Levine is the founder of Actify Neurotherapies, which operates nine clinics providing ketamine treatment for depression.

Q: Why is this a “banner day” for psychiatry?

A: This is truly the first new option for depression in 60 years. The selective serotonin reuptake inhibitors (SSRIs) developed in the mid-’80s were not truly new, not much different from the monoamine oxidase inhibitors (MAOI) and tricyclic antidepressants. In fact, they work much like watered-down MAOIs. Esketamine works by a truly novel mechanism.

Q: What is esketamine’s method of action, and how long will a dose last?

A: Ketamine and esketamine bind to and block glutamate N-methyl-D-aspartate (NMDA) receptors. This leads to the release of several chemical messengers, the result of which increases the production of neurotrophic factors, in particular brain-derived neurotrophic factor (BDNF), that play a key role in healing damaged connections in the brain. A single dose of esketamine would only be expected to relieve depression symptoms for days, up to a week or 2. Multiple doses over the first few weeks can extend the durability of response to several weeks and sometimes months.

It is not true for every patient, but some do have improvement within 2-4 hours that correlates with physiologic changes. Others can be later responders and require up to 6 exposures.

Q: The FDA approval requires those who administer the drug to complete special training and meet licensure requirements. Is this realistic for small practices?

A: Initially, not every psychiatrist will be able to offer esketamine, and I think it might be beyond the reach of small practices, and that’s probably okay. Enough people and enough centers will be able to offer it to meet the initial demand.

Q: Is esketamine “better” than ketamine infusions? With the approved drug available, will ketamine infusion clinics still have a place?

A: There are major pros with this. The FDA approval takes out of the gray area of off-label administration. It will most likely be covered by insurance now – a huge advantage that will put this in the reach of so many patients who haven’t been able to access this treatment.

I think that, because there are advantages and disadvantages for both IV ketamine and nasal esketamine, they will happily coexist for years to come. However, because nasal esketamine will likely be restricted to prescription by psychiatrists, it may have more impact on non-psychiatrist-led practices. In this way, esketamine may push the delivery of these treatments more exclusively into the hands of psychiatrists.

Dr. Steven Levine is the founder of Actify Neurotherapies, which operates nine clinics providing ketamine treatment for depression.

Q: Why is this a “banner day” for psychiatry?

A: This is truly the first new option for depression in 60 years. The selective serotonin reuptake inhibitors (SSRIs) developed in the mid-’80s were not truly new, not much different from the monoamine oxidase inhibitors (MAOI) and tricyclic antidepressants. In fact, they work much like watered-down MAOIs. Esketamine works by a truly novel mechanism.

Q: What is esketamine’s method of action, and how long will a dose last?

A: Ketamine and esketamine bind to and block glutamate N-methyl-D-aspartate (NMDA) receptors. This leads to the release of several chemical messengers, the result of which increases the production of neurotrophic factors, in particular brain-derived neurotrophic factor (BDNF), that play a key role in healing damaged connections in the brain. A single dose of esketamine would only be expected to relieve depression symptoms for days, up to a week or 2. Multiple doses over the first few weeks can extend the durability of response to several weeks and sometimes months.

It is not true for every patient, but some do have improvement within 2-4 hours that correlates with physiologic changes. Others can be later responders and require up to 6 exposures.

Q: The FDA approval requires those who administer the drug to complete special training and meet licensure requirements. Is this realistic for small practices?

A: Initially, not every psychiatrist will be able to offer esketamine, and I think it might be beyond the reach of small practices, and that’s probably okay. Enough people and enough centers will be able to offer it to meet the initial demand.

Q: Is esketamine “better” than ketamine infusions? With the approved drug available, will ketamine infusion clinics still have a place?

A: There are major pros with this. The FDA approval takes out of the gray area of off-label administration. It will most likely be covered by insurance now – a huge advantage that will put this in the reach of so many patients who haven’t been able to access this treatment.

I think that, because there are advantages and disadvantages for both IV ketamine and nasal esketamine, they will happily coexist for years to come. However, because nasal esketamine will likely be restricted to prescription by psychiatrists, it may have more impact on non-psychiatrist-led practices. In this way, esketamine may push the delivery of these treatments more exclusively into the hands of psychiatrists.

Dr. Steven Levine is the founder of Actify Neurotherapies, which operates nine clinics providing ketamine treatment for depression.

“The greatest medicine of all is teaching people how not to need it.” – Hippocrates
 

For many years, over-the-counter and prescription medications indicated for sleep problems/disorders have been available to patients. But the side effects associated with some of these medications are many. In light of the numerous nonpharmacologic interventions that are available to patients, they should be offered first when appropriate.

klebercordeiro/Getty Images

One of the top nonpharmacologic interventions is cognitive-behavioral therapy for insomnia, or CBT-I, which the American Academy of Sleep Medicine’s clinical guidelines say should be used as initial treatment if possible.¹ Elements of CBT-I include cognitive therapy, which is aimed at reducing dysfunctional beliefs about sleep. Common distortions expressed by patients include: “I cannot sleep without medications” and “I must get 8 hours of sleep to feel refreshed and function well the next day.” It helps in dealing with anxiety and catastrophic thinking to establish realistic expectations and treatment related to insomnia.

CBT-I can be delivered in the form of monotherapy or in a combined manner. The individual components include psychoeducation, behavioral strategies, cognitive therapy, and relaxation training. CBT-I combines cognitive therapy with behavioral interventions. Behavioral elements include stimulus control therapy and sleep restriction therapy. Relaxation therapy might or might not be included. Sleep hygiene education usually is a part of it.²

Two other kinds of CBT that can be effective options are telephone-based CBT-I and Internet-based CBT-I.^3,4 Meanwhile, among the disadvantages of CBT for insomnia are longer duration of therapy and lack of skilled clinicians.⁵

Many other kinds of behavioral interventions are available to patients with problems related to sleep, including stimulus control therapy, relaxation therapy, exercise therapy, and sleep restriction therapy.
 

Stimulus control therapy

This is a strategy aimed at strengthening the association of bed and bedroom to sleep, establishing a consistent sleep-wake rhythm, and reducing the activities that might interfere with sleep. This behavioral therapy is based on the idea that arousal occurs as a conditioned response to the stimulus of sleep environment, and it is among the most effective behavioral treatments.^6,7 Strategies include the following:

1. Lie down with the intention of sleeping when sleepy.

2. Do not watch television, read, eat or worry while in bed. Use bed only for sleep and sex.

3. Get out of bed if unable to fall asleep within 10-15 minutes and go to another room. Return to bed only when sleepy. Do not watch the clock. Repeat this step as many times as necessary throughout the night.

4. Set an alarm clock to wake up at a fixed time each morning, including weekends, regardless of how much sleep you got during the night.

5. Do not take a nap during the day.

The goal of these strategies is to extinguish negative associations between bed and undesirable outcomes, such as wakefulness and frustration. One study showed that stimulus control participants, unlike control group participants, experienced significant improvement at follow-up for total sleep time, sleep efficiency, and sleep quality.⁸

Relaxation therapy

This encompasses different techniques that produce a relaxation response and reduce somatic arousal. It can be implemented before each sleep period. Progressive muscle relaxation, autogenic training, and biofeedback help reduce somatic arousal. Attention-focused procedures, such as imagery training and meditation, tend to lower presleep cognitive arousal (for example, intrusive thoughts, racing minds).⁹ Slow paced breathing prior to onset of sleep enhances vagal activity, which results in improved sleep parameters.¹⁰ One study showed improved quality of sleep and cognitive functions in the elderly by self-relaxation training.¹¹

Exercise training

Participating in physical exercise can be useful in the treatment of insomnia.¹² One randomized, controlled trial found that exercising regularly for at least 150 minutes per week was optimal.¹³ Another study found that, among overweight and obese men with insomnia, aerobic exercise over a 6-month period reduced difficulty in initiating and improving sleep.¹⁴

Sleep restriction therapy

The goal of this therapy is to increase the homeostatic drive to sleep. This is carried out by limiting the amount of time spent in bed to the same amount of time that the person reports sleeping. Naps are not allowed. Patients improve with increased drive to sleep in successive nights. In patients with bipolar disorder, however, sleep restriction should be used with caution as it can trigger manic episodes.¹⁵

Always ask about sleep

Clinicians should always ask patients about sleep during visits. Sleep duration and sleep quality should be assessed. Insomnia, which is an independent condition, may or may not coexist with other conditions. It is important to determine whether another sleep disorder, or a physical (such as pain, heart, or lung disease), neurological (such as Parkinson’s disease or cerebrovascular disease), or psychiatric disorder (such as depressive illness, anxiety disorder, or substance misuse) is the primary diagnosis. Treatment of insomnia can improve comorbidities.¹⁶

In addition, it is important to teach patients about basic sleep hygiene, which includes abiding by a consistent bedtime, and avoiding coffee, alcohol, and nicotine. Eliminating a bedroom clock, not exercising in the late afternoon/early evening, and consuming light bedtime snacks are other measures that can be taken. Avoiding the prolonged use of light-emitting screens before bedtime is another positive step.¹⁷

In conclusion, cognitive and behavioral methods are just as effective as prescription medications for short-term treatment of chronic insomnia and should be considered as first line before considering medications. The beneficial effects of CBT-I, in contrast to those produced by medication, might last well beyond the termination of active treatment.
 

References

1. J Clin Sleep Med. 2008 Oct 15;4(5):487-504.

2. J Clin Psychol. 2010;66(11):1148-60.

3. Sleep. 2013 Mar 1;36(3):353-62.

4. Sleep Med Rev. 2016 Dec;30:1-10.

5. BMC Family Prac. 2012;13:40.

6. Sleep. 2006 Nov;29(11):1398-414.

7. Behavioral Treatments for Sleep Disorders. 1991. doi: 10.1016/13978-0-12-381522-4.00002-X.

8. Behav Modif 1998 Jan;22(1):3-28.

9. Am Fam Physician. 1999 Jun;59(11):3029-38.

10. Psychophysiology. 2015 Mar;52(3):388-96.

11. J Clin Nursing. 2013 April 10. doi: 10.1111/jocn.12096.

12. J Physiother. 2012;58(3):157-63.

13. J Sleep Res. 2015 Oct;24(5):526-34.

14 Sleep Med. 2016 Sep;25:113-121.

15. Am J Psychiatry. 2013 Jul;170(7):716-20.

16. JAMA Intern Med. 2015 Sep;175(9):1461-72.

17. Proc Natl Acad Sci USA. 2015;112(4):1232-7.
 

Dr. Lamba is a psychiatrist and medical director at Bayridge Hospital in Lynn, Mass. Dr. Rana is assistant professor of pediatrics at Boston University.

“The greatest medicine of all is teaching people how not to need it.” – Hippocrates
 

For many years, over-the-counter and prescription medications indicated for sleep problems/disorders have been available to patients. But the side effects associated with some of these medications are many. In light of the numerous nonpharmacologic interventions that are available to patients, they should be offered first when appropriate.

klebercordeiro/Getty Images

One of the top nonpharmacologic interventions is cognitive-behavioral therapy for insomnia, or CBT-I, which the American Academy of Sleep Medicine’s clinical guidelines say should be used as initial treatment if possible.¹ Elements of CBT-I include cognitive therapy, which is aimed at reducing dysfunctional beliefs about sleep. Common distortions expressed by patients include: “I cannot sleep without medications” and “I must get 8 hours of sleep to feel refreshed and function well the next day.” It helps in dealing with anxiety and catastrophic thinking to establish realistic expectations and treatment related to insomnia.

CBT-I can be delivered in the form of monotherapy or in a combined manner. The individual components include psychoeducation, behavioral strategies, cognitive therapy, and relaxation training. CBT-I combines cognitive therapy with behavioral interventions. Behavioral elements include stimulus control therapy and sleep restriction therapy. Relaxation therapy might or might not be included. Sleep hygiene education usually is a part of it.²

Two other kinds of CBT that can be effective options are telephone-based CBT-I and Internet-based CBT-I.^3,4 Meanwhile, among the disadvantages of CBT for insomnia are longer duration of therapy and lack of skilled clinicians.⁵

Many other kinds of behavioral interventions are available to patients with problems related to sleep, including stimulus control therapy, relaxation therapy, exercise therapy, and sleep restriction therapy.
 

Stimulus control therapy

This is a strategy aimed at strengthening the association of bed and bedroom to sleep, establishing a consistent sleep-wake rhythm, and reducing the activities that might interfere with sleep. This behavioral therapy is based on the idea that arousal occurs as a conditioned response to the stimulus of sleep environment, and it is among the most effective behavioral treatments.^6,7 Strategies include the following:

1. Lie down with the intention of sleeping when sleepy.

2. Do not watch television, read, eat or worry while in bed. Use bed only for sleep and sex.

3. Get out of bed if unable to fall asleep within 10-15 minutes and go to another room. Return to bed only when sleepy. Do not watch the clock. Repeat this step as many times as necessary throughout the night.

4. Set an alarm clock to wake up at a fixed time each morning, including weekends, regardless of how much sleep you got during the night.

5. Do not take a nap during the day.

The goal of these strategies is to extinguish negative associations between bed and undesirable outcomes, such as wakefulness and frustration. One study showed that stimulus control participants, unlike control group participants, experienced significant improvement at follow-up for total sleep time, sleep efficiency, and sleep quality.⁸

Relaxation therapy

This encompasses different techniques that produce a relaxation response and reduce somatic arousal. It can be implemented before each sleep period. Progressive muscle relaxation, autogenic training, and biofeedback help reduce somatic arousal. Attention-focused procedures, such as imagery training and meditation, tend to lower presleep cognitive arousal (for example, intrusive thoughts, racing minds).⁹ Slow paced breathing prior to onset of sleep enhances vagal activity, which results in improved sleep parameters.¹⁰ One study showed improved quality of sleep and cognitive functions in the elderly by self-relaxation training.¹¹

Exercise training

Participating in physical exercise can be useful in the treatment of insomnia.¹² One randomized, controlled trial found that exercising regularly for at least 150 minutes per week was optimal.¹³ Another study found that, among overweight and obese men with insomnia, aerobic exercise over a 6-month period reduced difficulty in initiating and improving sleep.¹⁴

Sleep restriction therapy

The goal of this therapy is to increase the homeostatic drive to sleep. This is carried out by limiting the amount of time spent in bed to the same amount of time that the person reports sleeping. Naps are not allowed. Patients improve with increased drive to sleep in successive nights. In patients with bipolar disorder, however, sleep restriction should be used with caution as it can trigger manic episodes.¹⁵

Always ask about sleep

Clinicians should always ask patients about sleep during visits. Sleep duration and sleep quality should be assessed. Insomnia, which is an independent condition, may or may not coexist with other conditions. It is important to determine whether another sleep disorder, or a physical (such as pain, heart, or lung disease), neurological (such as Parkinson’s disease or cerebrovascular disease), or psychiatric disorder (such as depressive illness, anxiety disorder, or substance misuse) is the primary diagnosis. Treatment of insomnia can improve comorbidities.¹⁶

In addition, it is important to teach patients about basic sleep hygiene, which includes abiding by a consistent bedtime, and avoiding coffee, alcohol, and nicotine. Eliminating a bedroom clock, not exercising in the late afternoon/early evening, and consuming light bedtime snacks are other measures that can be taken. Avoiding the prolonged use of light-emitting screens before bedtime is another positive step.¹⁷

In conclusion, cognitive and behavioral methods are just as effective as prescription medications for short-term treatment of chronic insomnia and should be considered as first line before considering medications. The beneficial effects of CBT-I, in contrast to those produced by medication, might last well beyond the termination of active treatment.
 

References

1. J Clin Sleep Med. 2008 Oct 15;4(5):487-504.

2. J Clin Psychol. 2010;66(11):1148-60.

3. Sleep. 2013 Mar 1;36(3):353-62.

4. Sleep Med Rev. 2016 Dec;30:1-10.

5. BMC Family Prac. 2012;13:40.

6. Sleep. 2006 Nov;29(11):1398-414.

7. Behavioral Treatments for Sleep Disorders. 1991. doi: 10.1016/13978-0-12-381522-4.00002-X.

8. Behav Modif 1998 Jan;22(1):3-28.

9. Am Fam Physician. 1999 Jun;59(11):3029-38.

10. Psychophysiology. 2015 Mar;52(3):388-96.

11. J Clin Nursing. 2013 April 10. doi: 10.1111/jocn.12096.

12. J Physiother. 2012;58(3):157-63.

13. J Sleep Res. 2015 Oct;24(5):526-34.

14 Sleep Med. 2016 Sep;25:113-121.

15. Am J Psychiatry. 2013 Jul;170(7):716-20.

16. JAMA Intern Med. 2015 Sep;175(9):1461-72.

17. Proc Natl Acad Sci USA. 2015;112(4):1232-7.
 

Dr. Lamba is a psychiatrist and medical director at Bayridge Hospital in Lynn, Mass. Dr. Rana is assistant professor of pediatrics at Boston University.

“The greatest medicine of all is teaching people how not to need it.” – Hippocrates
 

For many years, over-the-counter and prescription medications indicated for sleep problems/disorders have been available to patients. But the side effects associated with some of these medications are many. In light of the numerous nonpharmacologic interventions that are available to patients, they should be offered first when appropriate.

klebercordeiro/Getty Images

One of the top nonpharmacologic interventions is cognitive-behavioral therapy for insomnia, or CBT-I, which the American Academy of Sleep Medicine’s clinical guidelines say should be used as initial treatment if possible.¹ Elements of CBT-I include cognitive therapy, which is aimed at reducing dysfunctional beliefs about sleep. Common distortions expressed by patients include: “I cannot sleep without medications” and “I must get 8 hours of sleep to feel refreshed and function well the next day.” It helps in dealing with anxiety and catastrophic thinking to establish realistic expectations and treatment related to insomnia.

CBT-I can be delivered in the form of monotherapy or in a combined manner. The individual components include psychoeducation, behavioral strategies, cognitive therapy, and relaxation training. CBT-I combines cognitive therapy with behavioral interventions. Behavioral elements include stimulus control therapy and sleep restriction therapy. Relaxation therapy might or might not be included. Sleep hygiene education usually is a part of it.²

Two other kinds of CBT that can be effective options are telephone-based CBT-I and Internet-based CBT-I.^3,4 Meanwhile, among the disadvantages of CBT for insomnia are longer duration of therapy and lack of skilled clinicians.⁵

Many other kinds of behavioral interventions are available to patients with problems related to sleep, including stimulus control therapy, relaxation therapy, exercise therapy, and sleep restriction therapy.
 

Stimulus control therapy

This is a strategy aimed at strengthening the association of bed and bedroom to sleep, establishing a consistent sleep-wake rhythm, and reducing the activities that might interfere with sleep. This behavioral therapy is based on the idea that arousal occurs as a conditioned response to the stimulus of sleep environment, and it is among the most effective behavioral treatments.^6,7 Strategies include the following:

1. Lie down with the intention of sleeping when sleepy.

2. Do not watch television, read, eat or worry while in bed. Use bed only for sleep and sex.

3. Get out of bed if unable to fall asleep within 10-15 minutes and go to another room. Return to bed only when sleepy. Do not watch the clock. Repeat this step as many times as necessary throughout the night.

4. Set an alarm clock to wake up at a fixed time each morning, including weekends, regardless of how much sleep you got during the night.

5. Do not take a nap during the day.

The goal of these strategies is to extinguish negative associations between bed and undesirable outcomes, such as wakefulness and frustration. One study showed that stimulus control participants, unlike control group participants, experienced significant improvement at follow-up for total sleep time, sleep efficiency, and sleep quality.⁸

Relaxation therapy

This encompasses different techniques that produce a relaxation response and reduce somatic arousal. It can be implemented before each sleep period. Progressive muscle relaxation, autogenic training, and biofeedback help reduce somatic arousal. Attention-focused procedures, such as imagery training and meditation, tend to lower presleep cognitive arousal (for example, intrusive thoughts, racing minds).⁹ Slow paced breathing prior to onset of sleep enhances vagal activity, which results in improved sleep parameters.¹⁰ One study showed improved quality of sleep and cognitive functions in the elderly by self-relaxation training.¹¹

Exercise training

Participating in physical exercise can be useful in the treatment of insomnia.¹² One randomized, controlled trial found that exercising regularly for at least 150 minutes per week was optimal.¹³ Another study found that, among overweight and obese men with insomnia, aerobic exercise over a 6-month period reduced difficulty in initiating and improving sleep.¹⁴

Sleep restriction therapy

The goal of this therapy is to increase the homeostatic drive to sleep. This is carried out by limiting the amount of time spent in bed to the same amount of time that the person reports sleeping. Naps are not allowed. Patients improve with increased drive to sleep in successive nights. In patients with bipolar disorder, however, sleep restriction should be used with caution as it can trigger manic episodes.¹⁵

Always ask about sleep

Clinicians should always ask patients about sleep during visits. Sleep duration and sleep quality should be assessed. Insomnia, which is an independent condition, may or may not coexist with other conditions. It is important to determine whether another sleep disorder, or a physical (such as pain, heart, or lung disease), neurological (such as Parkinson’s disease or cerebrovascular disease), or psychiatric disorder (such as depressive illness, anxiety disorder, or substance misuse) is the primary diagnosis. Treatment of insomnia can improve comorbidities.¹⁶

In addition, it is important to teach patients about basic sleep hygiene, which includes abiding by a consistent bedtime, and avoiding coffee, alcohol, and nicotine. Eliminating a bedroom clock, not exercising in the late afternoon/early evening, and consuming light bedtime snacks are other measures that can be taken. Avoiding the prolonged use of light-emitting screens before bedtime is another positive step.¹⁷

In conclusion, cognitive and behavioral methods are just as effective as prescription medications for short-term treatment of chronic insomnia and should be considered as first line before considering medications. The beneficial effects of CBT-I, in contrast to those produced by medication, might last well beyond the termination of active treatment.
 

References

1. J Clin Sleep Med. 2008 Oct 15;4(5):487-504.

2. J Clin Psychol. 2010;66(11):1148-60.

3. Sleep. 2013 Mar 1;36(3):353-62.

4. Sleep Med Rev. 2016 Dec;30:1-10.

5. BMC Family Prac. 2012;13:40.

6. Sleep. 2006 Nov;29(11):1398-414.

7. Behavioral Treatments for Sleep Disorders. 1991. doi: 10.1016/13978-0-12-381522-4.00002-X.

8. Behav Modif 1998 Jan;22(1):3-28.

9. Am Fam Physician. 1999 Jun;59(11):3029-38.

10. Psychophysiology. 2015 Mar;52(3):388-96.

11. J Clin Nursing. 2013 April 10. doi: 10.1111/jocn.12096.

12. J Physiother. 2012;58(3):157-63.

13. J Sleep Res. 2015 Oct;24(5):526-34.

14 Sleep Med. 2016 Sep;25:113-121.

15. Am J Psychiatry. 2013 Jul;170(7):716-20.

16. JAMA Intern Med. 2015 Sep;175(9):1461-72.

17. Proc Natl Acad Sci USA. 2015;112(4):1232-7.
 

Dr. Lamba is a psychiatrist and medical director at Bayridge Hospital in Lynn, Mass. Dr. Rana is assistant professor of pediatrics at Boston University.

A 46-year-old woman with diabetes and seizure disorder presents with nausea and fatigue. Her physical exam is unremarkable.

Meds: Glyburide 5 mg daily, metformin 850 mg b.i.d., phenytoin 300 mg daily, topiramate 400 mg daily, pantoprazole 40 mg daily.

Labs: Na 133, K 3.9, Cl 112, HCO₃ 13, Glu 158, Bun 18, Cr 1.0.

What is the most likely cause of this patient’s acidosis?

A. Phenytoin

B. Topiramate

C. Metformin

D. Pantoprazole



The correct answer to this question is topiramate.

Metformin has had warnings about risk of lactic acidosis occurring in patients with kidney disease, but there is no evidence that metformin is associated with lactic acidosis or raised serum lactate levels in patients with diabetes with normal renal function.¹Metformin is actually safer than previously believed in patients with chronic kidney disease (CKD), and its use may decrease CV risk in patients with stage 3 CKD.² This patient has a non–anion gap acidosis (anion gap is 8).

Topiramate acts as a carbonic anhydrase inhibitor, which causes impairment of both the normal reabsorption of filtered HCO₃ by the proximal renal tubule and the excretion of hydrogen ion by the distal tubule.³ Acidosis occurs in most patients who are treated with topiramate. Dr. Ture and colleagues did a cross-sectional study to assess the frequency of metabolic acidosis in patients who were taking topiramate.⁴ Eighty patients who were on topiramate for seizure prevention prior to elective craniotomy were studied. Metabolic acidosis was present in 71% of the patients. Patients treated with topiramate also have a higher risk for kidney stones and uric acid elevation.
 

A 60-year-old patient presents with right great toe pain. On exam he has warmth and erythema of the 1st MTP joint. Aspiration of the joint shows uric acid crystals. He has had BP’s of 150-160 mm Hg systolic on his home BP monitoring over the past 6 months. In clinic today BP is 156/90 mm Hg. Labs: Bun 10, Cr 1.0, K 3.8, Uric acid 7.4.

Which blood pressure medication would you recommend?

A. Hydrochlorothiazide

B. Chlorthalidone

C. Lisinopril

D. Losartan

E. Irbesartan

In a patient with gout, diuretics should be avoided if possible, as they increase uric acid levels. Of the other three options, losartan offers the added benefit of lowering uric acid levels. Losartan has uricosuric effects and lowers uric acid levels, a property that is unique to losartan of the angiotensin receptor blockers (ARBs) that have been studied.^5-6 The uric acid lowering appears to be a probenecid-like effect. Losartan has also been evaluated to see whether using it in combination with a thiazide diuretic can reduce the rise in uric acid that occurs with thiazides. Dr. Matsumura et al. looked at data from the COMFORT trial, focusing on the effect of combining losartan with hydrochlorothiazide on uric acid levels.⁷ They looked at a group of 118 patients on an ARB other than losartan plus a diuretic, who were then randomly assigned to losartan 50 mg/hydrochlorothiazide 12.5 mg or continuation of another ARB plus a diuretic. Blood pressure control was the same between groups, but the patients who received the losartan combination had lower uric acid levels (P = .01).


Pearls: Topiramate acts as a cerbonic anhydrase inhibitor and can cause a non–anion gap acidosis. Losartan has a modest uricosuric effect and can modestly lower uric acid levels. This is a unique property of losartan and is not shared by other ARBs.
 

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and serves as third-year medical student clerkship director at the University of Washington. Contact Dr. Paauw at dpaauw@uw.edu.

References

1. Salpeter SR et al. Risk of fatal and nonfatal lactic acidosis with metformin use in type 2 diabetes mellitus. Cochrane Database Syst Rev. 2010;4:CD002967.

2. Charytan DM et al. Metformin use and cardiovascular events in patients with type 2 diabetes and chronic kidney disease. Diabetes Obes Metab. 2019 Jan 22. doi: 10.1111/dom.13642.

3. Mirza N et al. Effect of topiramate on acid-base balance: extent, mechanism and effects. Br J Clin Pharmacol. 2009 Nov;68(5):655-61.

4. Ture H et al. The frequency and severity of metabolic acidosis related to topiramate. J Int Med Res. 2016;44(6):1376-80.

5. Würzner G et al. Comparative effects of losartan and irbesartan on serum uric acid in hypertensive patients with hyperuricaemia and gout. J Hypertens. 2001 Oct;19(10):1855-60.

6. Puig JG et al. Effect of eprosartan and losartan on uric acid metabolism in patients with essential hypertension. J Hypertens. 1999 Jul;17(7):1033-9.

7. Matsumura K et al. Effect of losartan on serum uric acid in hypertension treated with a diuretic: the COMFORT study. Clin Exp Hypertens. 2015;37(3):192-6.

A 46-year-old woman with diabetes and seizure disorder presents with nausea and fatigue. Her physical exam is unremarkable.

Meds: Glyburide 5 mg daily, metformin 850 mg b.i.d., phenytoin 300 mg daily, topiramate 400 mg daily, pantoprazole 40 mg daily.

Labs: Na 133, K 3.9, Cl 112, HCO₃ 13, Glu 158, Bun 18, Cr 1.0.

What is the most likely cause of this patient’s acidosis?

A. Phenytoin

B. Topiramate

C. Metformin

D. Pantoprazole



The correct answer to this question is topiramate.

Metformin has had warnings about risk of lactic acidosis occurring in patients with kidney disease, but there is no evidence that metformin is associated with lactic acidosis or raised serum lactate levels in patients with diabetes with normal renal function.¹Metformin is actually safer than previously believed in patients with chronic kidney disease (CKD), and its use may decrease CV risk in patients with stage 3 CKD.² This patient has a non–anion gap acidosis (anion gap is 8).

Topiramate acts as a carbonic anhydrase inhibitor, which causes impairment of both the normal reabsorption of filtered HCO₃ by the proximal renal tubule and the excretion of hydrogen ion by the distal tubule.³ Acidosis occurs in most patients who are treated with topiramate. Dr. Ture and colleagues did a cross-sectional study to assess the frequency of metabolic acidosis in patients who were taking topiramate.⁴ Eighty patients who were on topiramate for seizure prevention prior to elective craniotomy were studied. Metabolic acidosis was present in 71% of the patients. Patients treated with topiramate also have a higher risk for kidney stones and uric acid elevation.
 

A 60-year-old patient presents with right great toe pain. On exam he has warmth and erythema of the 1st MTP joint. Aspiration of the joint shows uric acid crystals. He has had BP’s of 150-160 mm Hg systolic on his home BP monitoring over the past 6 months. In clinic today BP is 156/90 mm Hg. Labs: Bun 10, Cr 1.0, K 3.8, Uric acid 7.4.

Which blood pressure medication would you recommend?

A. Hydrochlorothiazide

B. Chlorthalidone

C. Lisinopril

D. Losartan

E. Irbesartan

In a patient with gout, diuretics should be avoided if possible, as they increase uric acid levels. Of the other three options, losartan offers the added benefit of lowering uric acid levels. Losartan has uricosuric effects and lowers uric acid levels, a property that is unique to losartan of the angiotensin receptor blockers (ARBs) that have been studied.^5-6 The uric acid lowering appears to be a probenecid-like effect. Losartan has also been evaluated to see whether using it in combination with a thiazide diuretic can reduce the rise in uric acid that occurs with thiazides. Dr. Matsumura et al. looked at data from the COMFORT trial, focusing on the effect of combining losartan with hydrochlorothiazide on uric acid levels.⁷ They looked at a group of 118 patients on an ARB other than losartan plus a diuretic, who were then randomly assigned to losartan 50 mg/hydrochlorothiazide 12.5 mg or continuation of another ARB plus a diuretic. Blood pressure control was the same between groups, but the patients who received the losartan combination had lower uric acid levels (P = .01).


Pearls: Topiramate acts as a cerbonic anhydrase inhibitor and can cause a non–anion gap acidosis. Losartan has a modest uricosuric effect and can modestly lower uric acid levels. This is a unique property of losartan and is not shared by other ARBs.
 

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and serves as third-year medical student clerkship director at the University of Washington. Contact Dr. Paauw at dpaauw@uw.edu.

References

1. Salpeter SR et al. Risk of fatal and nonfatal lactic acidosis with metformin use in type 2 diabetes mellitus. Cochrane Database Syst Rev. 2010;4:CD002967.

2. Charytan DM et al. Metformin use and cardiovascular events in patients with type 2 diabetes and chronic kidney disease. Diabetes Obes Metab. 2019 Jan 22. doi: 10.1111/dom.13642.

3. Mirza N et al. Effect of topiramate on acid-base balance: extent, mechanism and effects. Br J Clin Pharmacol. 2009 Nov;68(5):655-61.

4. Ture H et al. The frequency and severity of metabolic acidosis related to topiramate. J Int Med Res. 2016;44(6):1376-80.

5. Würzner G et al. Comparative effects of losartan and irbesartan on serum uric acid in hypertensive patients with hyperuricaemia and gout. J Hypertens. 2001 Oct;19(10):1855-60.

6. Puig JG et al. Effect of eprosartan and losartan on uric acid metabolism in patients with essential hypertension. J Hypertens. 1999 Jul;17(7):1033-9.

7. Matsumura K et al. Effect of losartan on serum uric acid in hypertension treated with a diuretic: the COMFORT study. Clin Exp Hypertens. 2015;37(3):192-6.

A 46-year-old woman with diabetes and seizure disorder presents with nausea and fatigue. Her physical exam is unremarkable.

Meds: Glyburide 5 mg daily, metformin 850 mg b.i.d., phenytoin 300 mg daily, topiramate 400 mg daily, pantoprazole 40 mg daily.

Labs: Na 133, K 3.9, Cl 112, HCO₃ 13, Glu 158, Bun 18, Cr 1.0.

What is the most likely cause of this patient’s acidosis?

A. Phenytoin

B. Topiramate

C. Metformin

D. Pantoprazole



The correct answer to this question is topiramate.

Metformin has had warnings about risk of lactic acidosis occurring in patients with kidney disease, but there is no evidence that metformin is associated with lactic acidosis or raised serum lactate levels in patients with diabetes with normal renal function.¹Metformin is actually safer than previously believed in patients with chronic kidney disease (CKD), and its use may decrease CV risk in patients with stage 3 CKD.² This patient has a non–anion gap acidosis (anion gap is 8).

Topiramate acts as a carbonic anhydrase inhibitor, which causes impairment of both the normal reabsorption of filtered HCO₃ by the proximal renal tubule and the excretion of hydrogen ion by the distal tubule.³ Acidosis occurs in most patients who are treated with topiramate. Dr. Ture and colleagues did a cross-sectional study to assess the frequency of metabolic acidosis in patients who were taking topiramate.⁴ Eighty patients who were on topiramate for seizure prevention prior to elective craniotomy were studied. Metabolic acidosis was present in 71% of the patients. Patients treated with topiramate also have a higher risk for kidney stones and uric acid elevation.
 

A 60-year-old patient presents with right great toe pain. On exam he has warmth and erythema of the 1st MTP joint. Aspiration of the joint shows uric acid crystals. He has had BP’s of 150-160 mm Hg systolic on his home BP monitoring over the past 6 months. In clinic today BP is 156/90 mm Hg. Labs: Bun 10, Cr 1.0, K 3.8, Uric acid 7.4.

Which blood pressure medication would you recommend?

A. Hydrochlorothiazide

B. Chlorthalidone

C. Lisinopril

D. Losartan

E. Irbesartan

In a patient with gout, diuretics should be avoided if possible, as they increase uric acid levels. Of the other three options, losartan offers the added benefit of lowering uric acid levels. Losartan has uricosuric effects and lowers uric acid levels, a property that is unique to losartan of the angiotensin receptor blockers (ARBs) that have been studied.^5-6 The uric acid lowering appears to be a probenecid-like effect. Losartan has also been evaluated to see whether using it in combination with a thiazide diuretic can reduce the rise in uric acid that occurs with thiazides. Dr. Matsumura et al. looked at data from the COMFORT trial, focusing on the effect of combining losartan with hydrochlorothiazide on uric acid levels.⁷ They looked at a group of 118 patients on an ARB other than losartan plus a diuretic, who were then randomly assigned to losartan 50 mg/hydrochlorothiazide 12.5 mg or continuation of another ARB plus a diuretic. Blood pressure control was the same between groups, but the patients who received the losartan combination had lower uric acid levels (P = .01).


Pearls: Topiramate acts as a cerbonic anhydrase inhibitor and can cause a non–anion gap acidosis. Losartan has a modest uricosuric effect and can modestly lower uric acid levels. This is a unique property of losartan and is not shared by other ARBs.
 

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and serves as third-year medical student clerkship director at the University of Washington. Contact Dr. Paauw at dpaauw@uw.edu.

References

1. Salpeter SR et al. Risk of fatal and nonfatal lactic acidosis with metformin use in type 2 diabetes mellitus. Cochrane Database Syst Rev. 2010;4:CD002967.

2. Charytan DM et al. Metformin use and cardiovascular events in patients with type 2 diabetes and chronic kidney disease. Diabetes Obes Metab. 2019 Jan 22. doi: 10.1111/dom.13642.

3. Mirza N et al. Effect of topiramate on acid-base balance: extent, mechanism and effects. Br J Clin Pharmacol. 2009 Nov;68(5):655-61.

4. Ture H et al. The frequency and severity of metabolic acidosis related to topiramate. J Int Med Res. 2016;44(6):1376-80.

5. Würzner G et al. Comparative effects of losartan and irbesartan on serum uric acid in hypertensive patients with hyperuricaemia and gout. J Hypertens. 2001 Oct;19(10):1855-60.

6. Puig JG et al. Effect of eprosartan and losartan on uric acid metabolism in patients with essential hypertension. J Hypertens. 1999 Jul;17(7):1033-9.

7. Matsumura K et al. Effect of losartan on serum uric acid in hypertension treated with a diuretic: the COMFORT study. Clin Exp Hypertens. 2015;37(3):192-6.

I was at a meeting in Orlando, sitting in the front row. The speaker was a former Disney executive who was telling us how to improve our offices. He kept walking very close to the edge of the stage – so close I was worried he might step off with the Klieg lights in his eyes. Then he got to the heart of his message, telling us that we need to make each patient encounter a marvelous experience, and how he and his staff had done so for millions of mouseketeers. “You need to make each customer feel special,” he said. He went on with saccharine examples of staff going above and beyond – for example, replacing toddlers’ dropped ice creams before they could cry.

That hit my trigger. From that point on, I was almost hoping he would fall off the stage.

Of course, there is a story behind my reaction.

One sunny day, while I was sitting at the most cluttered desk in the world, one of my staff came into my office to tell me a patient had called. The patient was very unhappy, I was told, and she planned to stink bomb me on social media. Concerned, I pulled the patient’s before-and-after photos. It looked as though she had a great result from her treatment, so I was perplexed. I phoned the patient, but she refused to tell me why she was unhappy. “I’m very unhappy, and I’m going to punish you,” she said. I urged her to come to the office and see me, at her convenience.

When we spoke face-to-face, I examined her nose and took a picture. I explained that her cancer was cured; her result was beautiful, the site was almost imperceptible. I added that I thought the appearance would continue to improve with time.

My patient refused to look at me, and refused to look at the site in the mirror. She shoved the preop defect photo away without giving it a glance. Instead, she told me how inconvenient it was for her to have had a skin cancer at all. Traffic had been terrible coming into the office on the morning of the procedure. There had been a 45-minute backup on the bridge on her way home. Her ex-husband had refused to help with her wound care. She continued in a similar vein for 15 minutes as I waited for her to accuse me of my transgressions. She concluded with a scowl and a whimper, “You just didn’t make me feel special.”

Everyone has difficult patients, and everyone has bad days, but I can’t recall ever being ambushed quite so adroitly in my 30 years of practice. I recognized my patient was being passive-aggressive and was playing a social media–augmented game of “Now I’ve got you, you S.O.B,” right out of Eric Berne’s book “Games People Play.” I’d say that this book should still be required reading for dealing with difficult patients.

There are ways to defuse such patients. One of the best is to slow things down and spread them around. The wider the array of interactions with people (the medical assistant, the nurse, the fellow, the Mohs surgeon, maybe the plastic surgeon), the more times the patient has to vent and the anger is defused across many targets. This also speaks to the value of requiring a preoperative consultation days before the procedure As I thought about this patient, I recalled that, because of the distance she was traveling, I had not done so.

I looked my patient in the eye and told her I was sorry she was unhappy. I told her I would be glad to see her again. I told her I realized how far she was driving and thought the traffic would not be a problem this early in the afternoon. I thanked her and showed her to the door. She stalked out of the office.

Technically and emotionally difficult patients are sometimes referred to you. They are patients who you might prefer not to take on but you do because, as a specialist, you may be at the end of the referral pipeline. Sometimes you can win the day, striking up a friendship or jollying them past their resentment at the world.

And there are times when, as a physician and healer, you must recognize that patient criticism cannot be taken personally. The third law of surviving internship from Samuel Shem’s book “The House of God” is germane here. Remember, “the patient is the one with the disease.” And sometimes the disease is complicated by the patient’s emotional baggage. This is one of the reasons social media ratings can be so unfair. We have to realize that we are all going to be trashed unfairly at some point, and probably sued unfairly as well. As a malpractice attorney told me once, “You doctors shouldn’t take this so personally; it’s just business.”

And my patient? Despite my admonishments to you not to take things personally, I did feel bad for a week or so after our encounter. I did mail her a copy of her pre- and postoperative photographs. I have not seen her again. I did not look to see whether she burned me online.

But, by gosh, I’d really like to lock that Disney executive in a room with her for five minutes.

Dr. Coldiron is in private practice but maintains a clinical assistant professorship at the University of Cincinnati. He cares for patients, teaches medical students and residents, and has several active clinical research projects. Dr. Coldiron is the author of more than 80 scientific letters, papers, and book chapters, and he speaks frequently on a variety of topics. He is a past president of the American Academy of Dermatology. Write to him at dermnews@mdedge.com.

I was at a meeting in Orlando, sitting in the front row. The speaker was a former Disney executive who was telling us how to improve our offices. He kept walking very close to the edge of the stage – so close I was worried he might step off with the Klieg lights in his eyes. Then he got to the heart of his message, telling us that we need to make each patient encounter a marvelous experience, and how he and his staff had done so for millions of mouseketeers. “You need to make each customer feel special,” he said. He went on with saccharine examples of staff going above and beyond – for example, replacing toddlers’ dropped ice creams before they could cry.

That hit my trigger. From that point on, I was almost hoping he would fall off the stage.

Of course, there is a story behind my reaction.

One sunny day, while I was sitting at the most cluttered desk in the world, one of my staff came into my office to tell me a patient had called. The patient was very unhappy, I was told, and she planned to stink bomb me on social media. Concerned, I pulled the patient’s before-and-after photos. It looked as though she had a great result from her treatment, so I was perplexed. I phoned the patient, but she refused to tell me why she was unhappy. “I’m very unhappy, and I’m going to punish you,” she said. I urged her to come to the office and see me, at her convenience.

When we spoke face-to-face, I examined her nose and took a picture. I explained that her cancer was cured; her result was beautiful, the site was almost imperceptible. I added that I thought the appearance would continue to improve with time.

My patient refused to look at me, and refused to look at the site in the mirror. She shoved the preop defect photo away without giving it a glance. Instead, she told me how inconvenient it was for her to have had a skin cancer at all. Traffic had been terrible coming into the office on the morning of the procedure. There had been a 45-minute backup on the bridge on her way home. Her ex-husband had refused to help with her wound care. She continued in a similar vein for 15 minutes as I waited for her to accuse me of my transgressions. She concluded with a scowl and a whimper, “You just didn’t make me feel special.”

Everyone has difficult patients, and everyone has bad days, but I can’t recall ever being ambushed quite so adroitly in my 30 years of practice. I recognized my patient was being passive-aggressive and was playing a social media–augmented game of “Now I’ve got you, you S.O.B,” right out of Eric Berne’s book “Games People Play.” I’d say that this book should still be required reading for dealing with difficult patients.

There are ways to defuse such patients. One of the best is to slow things down and spread them around. The wider the array of interactions with people (the medical assistant, the nurse, the fellow, the Mohs surgeon, maybe the plastic surgeon), the more times the patient has to vent and the anger is defused across many targets. This also speaks to the value of requiring a preoperative consultation days before the procedure As I thought about this patient, I recalled that, because of the distance she was traveling, I had not done so.

I looked my patient in the eye and told her I was sorry she was unhappy. I told her I would be glad to see her again. I told her I realized how far she was driving and thought the traffic would not be a problem this early in the afternoon. I thanked her and showed her to the door. She stalked out of the office.

Technically and emotionally difficult patients are sometimes referred to you. They are patients who you might prefer not to take on but you do because, as a specialist, you may be at the end of the referral pipeline. Sometimes you can win the day, striking up a friendship or jollying them past their resentment at the world.

And there are times when, as a physician and healer, you must recognize that patient criticism cannot be taken personally. The third law of surviving internship from Samuel Shem’s book “The House of God” is germane here. Remember, “the patient is the one with the disease.” And sometimes the disease is complicated by the patient’s emotional baggage. This is one of the reasons social media ratings can be so unfair. We have to realize that we are all going to be trashed unfairly at some point, and probably sued unfairly as well. As a malpractice attorney told me once, “You doctors shouldn’t take this so personally; it’s just business.”

And my patient? Despite my admonishments to you not to take things personally, I did feel bad for a week or so after our encounter. I did mail her a copy of her pre- and postoperative photographs. I have not seen her again. I did not look to see whether she burned me online.

But, by gosh, I’d really like to lock that Disney executive in a room with her for five minutes.

Dr. Coldiron is in private practice but maintains a clinical assistant professorship at the University of Cincinnati. He cares for patients, teaches medical students and residents, and has several active clinical research projects. Dr. Coldiron is the author of more than 80 scientific letters, papers, and book chapters, and he speaks frequently on a variety of topics. He is a past president of the American Academy of Dermatology. Write to him at dermnews@mdedge.com.

I was at a meeting in Orlando, sitting in the front row. The speaker was a former Disney executive who was telling us how to improve our offices. He kept walking very close to the edge of the stage – so close I was worried he might step off with the Klieg lights in his eyes. Then he got to the heart of his message, telling us that we need to make each patient encounter a marvelous experience, and how he and his staff had done so for millions of mouseketeers. “You need to make each customer feel special,” he said. He went on with saccharine examples of staff going above and beyond – for example, replacing toddlers’ dropped ice creams before they could cry.

That hit my trigger. From that point on, I was almost hoping he would fall off the stage.

Of course, there is a story behind my reaction.

One sunny day, while I was sitting at the most cluttered desk in the world, one of my staff came into my office to tell me a patient had called. The patient was very unhappy, I was told, and she planned to stink bomb me on social media. Concerned, I pulled the patient’s before-and-after photos. It looked as though she had a great result from her treatment, so I was perplexed. I phoned the patient, but she refused to tell me why she was unhappy. “I’m very unhappy, and I’m going to punish you,” she said. I urged her to come to the office and see me, at her convenience.

When we spoke face-to-face, I examined her nose and took a picture. I explained that her cancer was cured; her result was beautiful, the site was almost imperceptible. I added that I thought the appearance would continue to improve with time.

My patient refused to look at me, and refused to look at the site in the mirror. She shoved the preop defect photo away without giving it a glance. Instead, she told me how inconvenient it was for her to have had a skin cancer at all. Traffic had been terrible coming into the office on the morning of the procedure. There had been a 45-minute backup on the bridge on her way home. Her ex-husband had refused to help with her wound care. She continued in a similar vein for 15 minutes as I waited for her to accuse me of my transgressions. She concluded with a scowl and a whimper, “You just didn’t make me feel special.”

Everyone has difficult patients, and everyone has bad days, but I can’t recall ever being ambushed quite so adroitly in my 30 years of practice. I recognized my patient was being passive-aggressive and was playing a social media–augmented game of “Now I’ve got you, you S.O.B,” right out of Eric Berne’s book “Games People Play.” I’d say that this book should still be required reading for dealing with difficult patients.

There are ways to defuse such patients. One of the best is to slow things down and spread them around. The wider the array of interactions with people (the medical assistant, the nurse, the fellow, the Mohs surgeon, maybe the plastic surgeon), the more times the patient has to vent and the anger is defused across many targets. This also speaks to the value of requiring a preoperative consultation days before the procedure As I thought about this patient, I recalled that, because of the distance she was traveling, I had not done so.

I looked my patient in the eye and told her I was sorry she was unhappy. I told her I would be glad to see her again. I told her I realized how far she was driving and thought the traffic would not be a problem this early in the afternoon. I thanked her and showed her to the door. She stalked out of the office.

Technically and emotionally difficult patients are sometimes referred to you. They are patients who you might prefer not to take on but you do because, as a specialist, you may be at the end of the referral pipeline. Sometimes you can win the day, striking up a friendship or jollying them past their resentment at the world.

And there are times when, as a physician and healer, you must recognize that patient criticism cannot be taken personally. The third law of surviving internship from Samuel Shem’s book “The House of God” is germane here. Remember, “the patient is the one with the disease.” And sometimes the disease is complicated by the patient’s emotional baggage. This is one of the reasons social media ratings can be so unfair. We have to realize that we are all going to be trashed unfairly at some point, and probably sued unfairly as well. As a malpractice attorney told me once, “You doctors shouldn’t take this so personally; it’s just business.”

And my patient? Despite my admonishments to you not to take things personally, I did feel bad for a week or so after our encounter. I did mail her a copy of her pre- and postoperative photographs. I have not seen her again. I did not look to see whether she burned me online.

But, by gosh, I’d really like to lock that Disney executive in a room with her for five minutes.

Dr. Coldiron is in private practice but maintains a clinical assistant professorship at the University of Cincinnati. He cares for patients, teaches medical students and residents, and has several active clinical research projects. Dr. Coldiron is the author of more than 80 scientific letters, papers, and book chapters, and he speaks frequently on a variety of topics. He is a past president of the American Academy of Dermatology. Write to him at dermnews@mdedge.com.